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Functional gastrointestinal disorders (FGID), also known as disorders of gut–brain interaction, include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and motility disturbances. Classification
Terms such as functional colonic disease (or functional bowel disorder) refer in medicine to a group of bowel disorders which are characterised by chronic abdominal complaints without a structural or biochemical cause that could explain symptoms. Other functional disorders relate to other aspects of the process of digestion.The consensus review process of meetings and publications organised by the Rome Foundation, known as the Rome process, has helped to define the functional gastrointestinal disorders. Successively, the Rome I, Rome II, Rome III and Rome IV proposed consensual classification system and terminology, as recommended by the Rome Coordinating Committee. These now include classifications appropriate for adults, children and neonates/toddlers.The current Rome IV classification, published in 2016, is as follows:A. Esophageal disorders
A1. Functional chest pain
A2. Functional heartburn
A3. Reflux hypersensitivity
A4. Globus
A5. Functional dysphagiaB. Gastroduodenal disorders
B1. Functional dyspepsia
B1a. Postprandial distress syndrome (PDS)
B1b. Epigastric pain syndrome (EPS)
B2. Belching disorders
B2a. Excessive supragastric belching
B2b. Excessive gastric belching
B3. Nausea and vomiting disorders
B3a. Chronic nausea vomiting syndrome (CNVS)
B3b. Cyclic vomiting syndrome (CVS)
B3c. Cannabinoid hyperemesis syndrome (CHS)
B4. Rumination syndromeC. Bowel disorders
C1. Irritable bowel syndrome (IBS)
IBS with predominant constipation (IBS-C)
IBS with predominant diarrhea (IBS-D)
IBS with mixed bowel habits (IBS-M)
IBS unclassified (IBS-U)
C2. Functional constipation
C3. Functional diarrhea
C4. Functional abdominal bloating/distension
C5. Unspecified functional bowel disorder
C6. Opioid-induced constipationD. Centrally mediated disorders of gastrointestinal pain
D1. Centrally mediated abdominal pain syndrome (CAPS)
D2. Narcotic bowel syndrome (NBS)/ Opioid-induced GI hyperalgesiaE. | If necessary, measuring cAMP (cyclic AMP) in the urine after an intravenous dose of PTH can help in the distinction between hypoparathyroidism and other causes.Differential diagnoses are:
Pseudohypoparathyroidism (normal PTH levels but tissue insensitivity to the hormone, associated with intellectual disability and skeletal deformities) and pseudopseudohypoparathyroidism. Vitamin D deficiency or hereditary insensitivity to this vitamin (X-linked dominant). Malabsorption
Kidney disease
Medication: steroids, diuretics, some antiepileptics.Other tests include ECG for abnormal heart rhythms, and measurement of blood magnesium levels. Treatment
Severe hypocalcaemia, a potentially life-threatening condition, is treated as soon as possible with intravenous calcium (e.g. as calcium gluconate). Generally, a central venous catheter is recommended, as the calcium can irritate peripheral veins and cause phlebitis. In the event of a life-threatening attack of low calcium levels or tetany (prolonged muscle contractions), calcium is administered by intravenous (IV) infusion. Precautions are taken to prevent seizures or larynx spasms. The heart is monitored for abnormal rhythms until the person is stable. When the life-threatening attack has been controlled, treatment continues with medicine taken by mouth as often as four times a day.Long-term treatment of hypoparathyroidism is with vitamin D analogs and calcium supplementation, but may be ineffective in some due to potential renal damage. The N-terminal fragment of parathyroid hormone (PTH 1-34) has full biological activity. The use of pump delivery of synthetic PTH 1-34 provides the closest approach to physiologic PTH replacement therapy. Injections of recombinant human parathyroid hormone are available as treatment in those with low blood calcium levels. See also
Hyperparathyroidism
References
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One survey of 5,713 American residents identified habitual snoring in 24% of men and 13.8% of women, rising to 60% of men and 40% of women aged 60 to 65 years; this suggests an increased susceptibility to snoring with age.An observational study in the UK Biobank estimated that ~37% of 408,317 participants were habitual snorers, and confirmed positive associations with larger body-mass index, lower socio-economic status and more frequent smoking and alcohol consumption. Further reading
Nestor, James (2020). Breath: The New Science of a Lost Art. Riverhead Books. ISBN 978-0735213616. == References == | The forces responsible for the movement of the lateral body wall folds are poorly understood, and a better understanding of these forces would help to explain why gastroschisis occurs mostly to the right of the umbilicus, while other ventral body wall defects occur in the midline.At least six hypotheses have been proposed for the pathophysiology:
Failure of mesoderm to form in the body wall
Rupture of the amnion around the umbilical ring with subsequent herniation of bowel
Abnormal involution of the right umbilical vein leading to weakening of the body wall and gut herniation
Disruption of the right vitelline (yolk sac) artery with subsequent body wall damage and gut herniation
Abnormal folding of the body wall results in a ventral body wall defect through which the gut herniates
Failure to incorporate the yolk sac and related vitelline structures into the umbilical stalkThe first hypothesis does not explain why the mesoderm defect would occur in such a specific small area. The second hypothesis does not explain the low percentage of associated abnormality compared with omphalocele. The third hypothesis was criticized due to no vascular supplement of anterior abdominal wall by umbilical vein. The fourth hypothesis was commonly accepted, but it was later shown that the right vitelline artery (right omphalomesenteric artery) did not supply the anterior abdominal wall in this area. More evidence is needed to support the fifth hypothesis. | 0-1
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CT scans can be used to check lymph nodes in the chest, though this is uncommon.Despite the use of these methods to diagnose whether or not a person has leukemia, many people have not been diagnosed because many of the symptoms are vague, non-specific, and can refer to other diseases. For this reason, the American Cancer Society estimates that at least one-fifth of the people with leukemia have not yet been diagnosed. Treatment
Most forms of leukemia are treated with pharmaceutical medication, typically combined into a multi-drug chemotherapy regimen. Some are also treated with radiation therapy. In some cases, a bone marrow transplant is effective. Acute lymphoblastic
Management of ALL is directed towards control of bone marrow and systemic (whole-body) disease. Additionally, treatment must prevent leukemic cells from spreading to other sites, particularly the central nervous system (CNS) e.g. monthly lumbar punctures. In general, ALL treatment is divided into several phases:
Induction chemotherapy to bring about bone marrow remission. For adults, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L-asparaginase or cyclophosphamide. For children with low-risk ALL, standard therapy usually consists of three drugs (prednisone, L-asparaginase, and vincristine) for the first month of treatment. Consolidation therapy or intensification therapy to eliminate any remaining leukemia cells. There are many different approaches to consolidation, but it is typically a high-dose, multi-drug treatment that is undertaken for a few months. People with low- to average-risk ALL receive therapy with antimetabolite drugs such as methotrexate and 6-mercaptopurine (6-MP). | Radiation
Large doses of Sr-90 emission from nuclear reactor accidents, nicknamed bone seeker increases the risk of bone cancer and leukemia in animals and is presumed to do so in people. Genetic conditions
Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia.Chronic myelogenous leukemia is associated with a genetic abnormality called the Philadelphia translocation; 95% of people with CML carry the Philadelphia mutation, although this is not exclusive to CML and can be observed in people with other types of leukemia. Non-ionizing radiation
Whether or not non-ionizing radiation causes leukemia has been studied for several decades. The International Agency for Research on Cancer expert working group undertook a detailed review of all data on static and extremely low frequency electromagnetic energy, which occurs naturally and in association with the generation, transmission, and use of electrical power. | 11
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Other names, such as Antelepsin, Clonoten, Ravotril, Rivotril, Iktorivil, Clonex (Israel), Paxam, Petril, Naze, Zilepam and Kriadex, are used throughout the world. References
Further reading
Poisons Information Monograph - Clonazepam
External links
"Clonazepam". Drug Information Portal. U.S. National Library of Medicine. | Because of this inconsistency, extended assessment may be required to determine if a simple response (e.g. a finger movement or a blink) occurred because of a specific environmental event (e.g. a command to move the finger or to blink) or was merely a coincidental behavior. Distinguishing between VS and MCS is often difficult because the diagnosis is dependent on observation of behavior that show self or environmental awareness and because those behavioral responses are markedly reduced. One of the more common diagnostic errors involving disorders of consciousness is mistaking MCS for VS which may lead to serious repercussions related to clinical management.Giacino et al. have suggested demonstration of the following behaviors in order to make the diagnosis of MCS. Following simple commands. Gestural or verbal yes/no responses (regardless of accuracy). Intelligible verbalization. Purposeful behavior such as those that are contingent due to appropriate environmental stimuli and are not reflexive. Some examples of purposeful behavior include:
appropriate smiling or crying in response to the linguistic or visual content of emotional but not to neutral topics or stimuli. vocalizations or gestures that occur in direct response to the linguistic content of questions. reaching for objects that demonstrates a clear relationship between object location and direction of reach. touching or holding objects in a manner that accommodates the size and shape of the object. pursuit eye movement or sustained fixation that occurs in direct response to moving or salient stimuli. Treatment
There is currently no definitive evidence that support altering the course of the recovery of minimally conscious state. | 0-1
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MRI provides information regarding features of the articular cartilage and bone under the cartilage, including edema, fractures, fluid interfaces, articular surface integrity, and fragment displacement. A low T1 and high T2 signal at the fragment interface is seen in active lesions. This indicates an unstable lesion or recent microfractures. While MRI and arthroscopy have a close correlation, X-ray films tend to be less inductive of similar MRI results.Computed tomography (CT) scans and Technetium-99m bone scans are also sometimes used to monitor the progress of treatment. Unlike plain radiographs (X-rays), CT scans and MRI scans can show the exact location and extent of the lesion. Technetium bone scans can detect regional blood flow and the amount of osseous uptake. Both of these seem to be closely correlated to the potential for healing in the fragment. Classification
OCD is classified by the progression of the disease in stages. There are two main staging classifications used; one is determined by MRI diagnostic imaging while the other is determined arthroscopically. However, both stagings represent the pathological conditions associated with OCDs natural progression.While the arthroscopic classification of bone and cartilage lesions is considered standard, the Anderson MRI staging is the main form of staging used in this article. Stages I and II are stable lesions. Stages III and IV describe unstable lesions in which a lesion of the cartilage has allowed synovial fluid between the fragment and bone. | It is not recommended in severe disease or in those with abnormal factor VIII. Usefulness in type 2A, 2M, or 2N von Willebrand disease is variable. Generally not recommended in 2B and type 3 von Willebrand disease.Desmopressin is only recommended in mild hemophilia A. It may be used both for bleeding due to trauma or to try to prevent bleeding due to surgery. It is not effective in the treatment of hemophilia B (factor IX deficiency) or severe hemophilia A. May also be used in uremia induced bleeding. Diabetes insipidus
Desmopressin is used in the treatment of central diabetes insipidus (DI) as a replacement for endogenous antidiuretic hormone (ADH) that is in insufficient quantity due to decreased or non-existent secretion or production of ADH by the posterior pituitary or hypothalamus, respectively. It is also used in the diagnostic workup for diabetes insipidus, in order to distinguish central from DI due to the kidneys. Desmopressin is not effective at treating nephrogenic DI, thus a positive response is generally indicative of central DI. Side effects
headaches
facial flushing
nausea
hyponatremia
seizuresUS drug regulators added warning to the nasal sprays after two people died and fifty-nine other people had seizures. This occurred due to hyponatremia, a deficit of the bodys sodium levels, and the nasal spray is no longer approved for use in children in the United States. However, US drug regulators have said that desmopressin tablets can still be considered safe for treatment of nocturnal enuresis in children as long as the person is otherwise healthy. | 0-1
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After this point in time, however, there is a theoretical concern of increased risks of infection if closed immediately. Thus some healthcare providers may delay closure while others may be willing to immediately close up to 24 hours after the injury. Using clean non-sterile gloves is equivalent to using sterile gloves during wound closure.If closure of a wound is decided upon a number of techniques can be used. These include bandages, a cyanoacrylate glue, staples, and sutures. Absorbable sutures have the benefit over non absorbable sutures of not requiring removal. They are often preferred in children. Buffering the pH of lidocaine makes the injection less painful. Adhesive glue and sutures have comparable cosmetic outcomes for minor lacerations <5 cm in adults and children. The use of adhesive glue involves considerably less time for the doctor and less pain for the person. The wound opens at a slightly higher rate but there is less redness. The risk for infections (1.1%) is the same for both. Adhesive glue should not be used in areas of high tension or repetitive movements, such as joints or the posterior trunk. Split-thickness skin grafting (STSG) is also a surgical technique that features rapid wound closure, multiple possible donor sites with minimal morbidity. Dressings
In the case of clean surgical wounds, there is no evidence that the use of topical antibiotics reduces infection rates in comparison with non-antibiotic ointment or no ointment at all. Antibiotic ointments can irritate the skin, slow healing, and greatly increase the risk of developing contact dermatitis and antibiotic resistance. | A type of amputation where the extremity is pulled off rather than cut off. When used in reference to skin avulsions, the term degloving is also sometimes used as a synonym. Puncture wounds – caused by an object puncturing the skin, such as a splinter, nail or needle. Penetration wounds – caused by an object such as a knife entering and coming out from the skin. Gunshot wounds – caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a "through-and-through." Critical wounds- Including large burns that have been split. These wounds can cause serious hydroelectrolytic and metabolic alterations including fluid loss, electrolyte imbalances, and increased catabolism
Closed
Closed wounds have fewer categories, but are just as dangerous as open wounds:
Hematomas (or blood tumor) – caused by damage to a blood vessel that in turn causes blood to collect under the skin. Hematomas that originate from internal blood vessel pathology are petechiae, purpura, and ecchymosis. The different classifications are based on size. Hematomas that originate from an external source of trauma are contusions, also commonly called bruises. Crush injury – caused by a great or extreme amount of force applied over a long period of time. Presentation
Complications
Bacterial infection of wound can impede the healing process and lead to life-threatening complications. | 11
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delirium or hallucinations. difficult urination. difficulty swallowing. dry eyes, mouth, nose, or throat.As with any other general anesthetic agent, propofol should be administered only where appropriately trained staff and facilities for monitoring are available, as well as proper airway management, a supply of supplemental oxygen, artificial ventilation, and cardiovascular resuscitation.Because of its lipid base, some hospital facilities require the IV tubing (of continuous propofol infusions) to be changed after 12 hours. This is a preventive measure against microbial growth and infection. Propofol infusion syndrome
A rare, but serious, side effect is propofol infusion syndrome. This potentially lethal metabolic derangement has been reported in critically ill patients after a prolonged infusion of high-dose propofol, sometimes in combination with catecholamines and/or corticosteroids. Interactions
The respiratory effects of propofol are increased if given with other respiratory depressants, including benzodiazepines. Pharmacology
Pharmacodynamics
Propofol has been proposed as having several mechanisms of action, both through potentiation of GABAA receptor activity and therefore acting as a GABAA receptor positive allosteric modulator, thereby slowing the channel-closing time. At high doses, propofol may be able to activate GABAA receptors in the absence of GABA, behaving as a GABAA receptor agonist as well. Propofol analogs have been shown to also act as sodium channel blockers. Some research has also suggested that the endocannabinoid system may contribute significantly to propofols anesthetic action and to its unique properties. An EEG study on patients undergoing general anesthesia with propofol found that it causes a prominent reduction in the brains information integration capacity. | Patients die due to bacterial or viral infections. Aggressive treatment with antibiotics is required and bone marrow transplant is common. Patients undergoing bone marrow transplant, specifically from a matched sibling, have a higher 5 year survival rate than those receiving a transplant from other donors. Research
Gene Therapy
Gene therapy is a relatively new concept in the field of SCID. This therapy is currently undergoing clinical trial and has cured a small number of children suffering from X-linked SCID and recessive allele SCID. Gene therapy aims to correct the underlying genetic abnormality in SCID. In the case of RD, the genetic abnormality would be AK2 malfunction. Stem cells are taken from an affected childs blood or bone marrow. Then in laboratory conditions the stem cells are manipulated and corrected with gene technology. They are then injected back into the patient. Similarly, in bone transplant, stem cells are able to find their way back through tracking mechanisms. References
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Tafluprost (trade names Taflotan by Santen Pharmaceutical, Zioptan by Merck in the US and Saflutan by Mundipharma in Australia) is a prostaglandin analogue. It is used topically (as eye drops) to control the progression of open-angle glaucoma and in the management of ocular hypertension, alone or in combination with other medication. It reduces intraocular pressure by increasing the outflow of aqueous fluid from the eyes. Adverse effects
The most common side effect is conjunctival hyperemia, which occurs in 4 to 20% of patients. Less common side effects include stinging of the eyes, headache, and respiratory infections. Rare side effects are dyspnoea (breathing difficulties), worsening of asthma, and macular oedema. Interactions
Nonsteroidal anti-inflammatory drugs (NSAIDs) can either reduce or increase the effect of tafluprost. Timolol eye drops, a common kind of glaucoma medication, does not negatively interact with this drug.No interactions with systemic (for example, oral) drugs are expected because tafluprost does not reach relevant concentrations in the bloodstream. Pharmacology
Mechanism of action
Tafluprost is a prodrug of the active substance, tafluprost acid, a structural and functional analogue of prostaglandin F2α (PGF2α). Tafluprost acid is a selective agonist at the prostaglandin F receptor, increasing outflow of aqueous fluid from the eyes and thus lowering intraocular pressure.Other PGF2α analogues with the same mechanism include latanoprost and travoprost. Pharmacokinetics
Tafluprost, as a lipophilic ester, easily penetrates the cornea and is then activated to the carboxylic acid, tafluprost acid. | Onset of action is 2 to 4 hours after application, the maximal effect is reached after 12 hours, and ocular pressure remains lowered for at least 24 hours.Tafluprost acid is inactivated by beta oxidation to 1,2-dinortafluprost acid, 1,2,3,4-tetranortafluprost acid, and its lactone, which are subsequently glucuronidated or hydroxylated. The cytochrome P450 liver enzymes play no role in the metabolism.An analogous pathway (at least up to the tetranor-metabolites) has been found for latanoprost and travoprost. == References == | 11
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Nasal mucosa, particularly in the region of middle meatus becomes swollen due to collection of extracellular fluid. This extracellular fluid collection causes polyp formation and protrusion into the nasal cavity or sinuses. Polyps which are sessile in the beginning become pedunculated due to gravity.In people with nasal polyps due to aspirin or NSAID sensitivity, the underlying mechanism is due to disorders in the metabolism of arachidonic acid. Exposure to cycloxygenase inhibitors such as aspirin and NSAIDs leads to shunting of products through the lipoxygenase pathway leading to an increased production of products that cause inflammation. In the airway, these inflammatory products lead to symptoms of asthma such as wheezing as well as nasal polyp formation. Diagnosis
Nasal polyps can be seen on physical examination inside of the nose and are often detected during the evaluation of symptoms. On examination, a polyp will appear as a visible mass in the nostril. Some polyps may be seen with anterior rhinoscopy (looking in the nose with a nasal speculum and a light), but frequently, they are farther back in the nose and must be seen by nasal endoscopy. Nasal endoscopy involves passing a small, rigid camera with a light source into the nose. An image is projected onto a screen in the office so the doctor can examine the nasal passages and sinuses in greater detail. | Brodalumab, sold under the brand name Siliq in the US and Kyntheum in the EU, is a human monoclonal antibody designed for the treatment of inflammatory diseases.In February 2017, it received US FDA approval to treat moderate to severe plaque psoriasis in people who have not improved with other treatments. Mechanism of action
Brodalumab binds to the interleukin-17 receptor and so prevents interleukin 17 (IL-17) from activating the receptor. This mechanism is similar to that of another anti-psoriasis antibody, ixekizumab, which however binds to IL-17 itself. History
Brodalumab was developed by Amgen, Inc. as AMG 827. In 2013, it was in two phase III clinical trials for the treatment of moderate to severe psoriasis.In November 2014, Amgen and AstraZeneca reported encouraging results for the compound. The companies stated that the compound met the primary endpoint showing superior skin clearance in a Phase III trial when compared to ustekinumab and a placebo.However, in May 2015, Amgen announced that it was ending its participation in co-development of the compound because of reports of patients having "events of suicidal ideation and behavior". AstraZeneca will be solely responsible for any future development and marketing of brodalumab in all territories except for certain Asian territories such as Japan, where Kyowa Hakko Kirin has rights to brodalumab and continued as KHK4827. In September 2015, AstraZeneca announced a partnership with Valeant Pharmaceuticals in which Valeant took over exclusive rights to develop and commercialize brodalumab. | 0-1
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Vaccination
Spanish physician Jaume Ferran i Clua developed a cholera inoculation in 1885, the first to immunize humans against a bacterial disease. However, his vaccine and inoculation was rather controversial and was rejected by his peers and several investigation commissions. Russian-Jewish bacteriologist Waldemar Haffkine successfully developed the first human cholera vaccine in July 1892. He conducted a massive inoculation program in British India.Persons who survive an episode of cholera have long-lasting immunity for at least 3 years (the period tested.) A number of safe and effective oral vaccines for cholera are available. The World Health Organization (WHO) has three prequalified oral cholera vaccines (OCVs): Dukoral, Sanchol, and Euvichol. Dukoral, an orally administered, inactivated whole cell vaccine, has an overall efficacy of about 52% during the first year after being given and 62% in the second year, with minimal side effects. It is available in over 60 countries. However, it is not currently recommended by the Centers for Disease Control and Prevention (CDC) for most people traveling from the United States to endemic countries. The vaccine that the US Food and Drug Administration (FDA) recommends, Vaxchora, is an oral attenuated live vaccine, that is effective for adults aged 18-64 as a single dose.One injectable vaccine was found to be effective for two to three years. The protective efficacy was 28% lower in children less than five years old. However, as of 2010, it has limited availability. Work is under way to investigate the role of mass vaccination. | With intensification of the rains, new cases increased on a daily basis reaching a peak on the first week of January 2018 with over 700 cases reported.In collaboration with partners, the Zambia Ministry of Health (MoH) launched a multifaceted public health response that included increased chlorination of the Lusaka municipal water supply, provision of emergency water supplies, water quality monitoring and testing, enhanced surveillance, epidemiologic investigations, a cholera vaccination campaign, aggressive case management and health care worker training, and laboratory testing of clinical samples.The Zambian Ministry of Health implemented a reactive one-dose Oral Cholera Vaccine (OCV) campaign in April 2016 in three Lusaka compounds, followed by a pre-emptive second-round in December. India
The city of Kolkata, India in the state of West Bengal in the Ganges delta has been described as the "homeland of cholera", with regular outbreaks and pronounced seasonality. In India, where the disease is endemic, cholera outbreaks occur every year between dry seasons and rainy seasons. India is also characterized by high population density, unsafe drinking water, open drains, and poor sanitation which provide an optimal niche for survival, sustenance and transmission of Vibrio cholerae. Democratic Republic of Congo
In Goma in the Democratic Republic of Congo, cholera has left an enduring mark on human and medical history. | 11
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In contrast, the homeless experience, according to Moore, constitutes more as a "lack of belonging" and a loss of identity that leads to individuals or communities feeling "out of place" once they can no longer call a place of their own home.This new perspective on homelessness sheds light on the plight of refugees, a population of stateless people who are not normally included in the mainstream definition of homelessness. It has also created problems for researchers because the nature of "counting" homeless people across the globe relies heavily on who is considered a homeless person. Homeless individuals, and by extension refugees, can be seen as lacking lack the "crucible of our modern society" and lacking a way of actively belonging to and engaging with their respective communities or cultures. As Casavant demonstrates, a spectrum of definitions for homelessness, called the "continuum of homelessness", should refer to refugees as homeless individuals because they not only lose their home, but they are also afflicted with a myriad of problems that parallel those affecting the domestic homeless, such as "[a lack of] stable, safe and healthy housing, an extremely low income, adverse discrimination in access to services, with problems of mental health, alcohol, and drug abuse or social disorganization". Refugees, like the domestic homeless, lose their source of identity and way of connecting with their culture for an indefinite period of time. | Osteonecrosis of the jaws refers to the death of bone marrow in the maxilla or the mandible due to inadequate blood supply. It is not necessarily a painful condition, typically there will be no pain at all unless bone necrotic bone becomes exposed to the mouth or through the facial skin, and even then this continues to be painless in some cases. When pain does occur, it is variable in severity, and may be neuralgiform or neuropathic in nature. The term NICO is used to describe pain caused by ischemic osteonecrosis of the jaws, where degenerative extracellular cystic spaces (cavitations inside the bone) are said to develop as a result of ischemia and infarctions in the bone marrow, possibly in relation to other factors such as a hereditary predisposition for thrombus formation within blood vessels, chronic low-grade dental infections and the use of vasoconstrictors in local anesthetics during dental procedures. This proposed phenomenon has been postulated to be the cause of pain in some patients with AFP or trigeminal neuralgia, but this is controversial. NICO is said to be significantly more common in females, and the lesions may or may not be visible on radiographs. When they are visible, the appearance is very variable. About 60% of the lesions appear as a "hot spot" on an technetium 99 bone scan. | 0-1
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Autoimmune estrogen dermatitis
Autoimmune progesterone dermatitis
Autosensitization dermatitis
Breast eczema (nipple eczema)
Chronic vesiculobullous hand eczema
Circumostomy eczema
Dyshidrosis (acute vesiculobullous hand eczema, cheiropompholyx, dyshidrotic eczema, pompholyx, podopompholyx)
Ear eczema
Eyelid dermatitis
Hand eczema
Hyperkeratotic hand dermatitis
Id reaction (disseminated eczema, generalized eczema)
Irritant diaper dermatitis (diaper dermatitis, napkin dermatitis)
Juvenile plantar dermatosis (atopic winter feet, dermatitis plantaris sicca, forefoot dermatitis, moon-boot foot syndrome, sweaty sock dermatitis)
Molluscum dermatitis
Nummular dermatitis (discoid eczema, microbial eczema, nummular eczema, nummular neurodermatitis)
Nutritional deficiency eczema
Sulzberger–Garbe syndrome (oid-oid disease)
Xerotic eczema (asteatotic eczema, desiccation dermatitis, eczema craquelé, pruritus hiemalis, winter eczema, winter itch)
Pustular
Pustular dermatitis is an inflammation of the skin that presents with pustular lesions. Eosinophilic pustular folliculitis (Ofujis disease, sterile eosinophilic pustulosis)
Reactive arthritis
Subcorneal pustular dermatosis (Sneddon–Wilkinson disease)
Seborrheic
Seborrheic dermatitis is a chronic, superficial, inflammatory disease characterized by scaling on an erythematous base. Infantile seborrheic dermatitis
Leiners disease
Pityriasis simplex capillitii (dandruff)
Seborrheic dermatitis (seborrheic eczema)
Disturbances of pigmentation
Disturbances of human pigmentation, either loss or reduction, may be related to loss of melanocytes or the inability of melanocytes to produce melanin or transport melanosomes correctly. | Albinism–black lock–cell migration disorder of the neurocytes of the gut–deafness syndrome (ABCD syndrome)
Albinism–deafness syndrome (Woolf syndrome, Ziprkowski–Margolis syndrome)
Alezzandrini syndrome
Argyria
Arsenic poisoning
Berlin syndrome
Canthaxanthin
Chédiak–Higashi syndrome
Chrysiasis
Cross–McKusick–Breen syndrome (Cross syndrome, oculocerebral-hypopigmentation syndrome)
Dermatopathia pigmentosa reticularis (dermatopathia pigmentosa reticularis hyperkeratotica et mutilans, dermatopathia pigmentosa reticularis hypohidotica et atrophica, dermatopathic pigmentosa reticularis)
Dyschromatosis symmetrica hereditaria (reticulate acropigmentation of Dohi, symmetrical dyschromatosis of the extremities)
Dyschromatosis universalis hereditaria
Elejalde syndrome (Griscelli syndrome type 1)
Eruptive hypomelanosis
Familial progressive hyperpigmentation
Galli–Galli disease
Griscelli syndrome type 2 (partial albinism with immunodeficiency)
Griscelli syndrome type 3
Hemochromatosis (bronze diabetes)
Hemosiderin hyperpigmentation
Hermansky–Pudlak syndrome
Idiopathic guttate hypomelanosis (leukopathia symmetrica progressiva)
Iron metallic discoloration
Klein–Waardenburg syndrome
Lead poisoning
Leukoderma
Melanoma-associated leukoderma
Melasma (chloasma faciei, mask of pregnancy)
Mukamel syndrome
Necklace of Venus
Nevus anemicus
Nevus depigmentosus (nevus achromicus)
Ocular albinism
Oculocutaneous albinism
Pallister–Killian syndrome
Periorbital hyperpigmentation
Photoleukomelanodermatitis of Kobori
Phylloid hypomelanosis
Piebaldism
Pigmentatio reticularis faciei et colli
Pityriasis alba
Poikiloderma of Civatte
Poikiloderma vasculare atrophicans
Postinflammatory hyperpigmentation (postinflammatory hypermelanosis)
Postinflammatory hypopigmentation
Progressive macular hypomelanosis
Quadrichrome vitiligo
Reticular pigmented anomaly of the flexures (dark dot disease, Dowling–Degos disease)
Reticulate acropigmentation of Kitamura
Revesz syndrome
Riehl melanosis
Scratch dermatitis (flagellate pigmentation from bleomycin)
Segmental vitiligo
Shah–Waardenburg syndrome
Shiitake mushroom dermatitis (flagellate mushroom dermatitis, mushroom workers disease, shiitake-induced toxicoderma)
Tar melanosis (melanodermatitis toxica lichenoides)
Tietz syndrome
Titanium metallic discoloration
Transient neonatal pustular melanosis (transient neonatal pustulosis, lentigines neonatorum)
Trichrome vitiligo
Vagabonds leukomelanoderma
Vasospastic macule
Vitiligo
Vitiligo ponctué
Vogt–Koyanagi–Harada syndrome
Waardenburg syndrome
Wende–Bauckus syndrome (Pegum syndrome)
Woronoffs ring
X-linked reticulate pigmentary disorder (familial cutaneous amyloidosis, Partington amyloidosis, Partington cutaneous amyloidosis, Partington syndrome type II, reticulate pigmentary disorder, X-linked reticulate pigmentary disorder with systemic manifestations)
Yemenite deaf-blind hypopigmentation syndrome
Drug eruptions
Drug eruptions are adverse drug reactions that present with cutaneous manifestations. | 11
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Furthermore, with what little information is currently known about post-schizophrenic depression, the onset may be caused by not giving patients with schizophrenia antipsychotic medications. After being taken off of antipsychotic medication, schizophrenic patients antidepressant medication had to be increased, while those under antipsychotic medication reported having fewer depressive symptoms, further giving reason to believe that a lack of antipsychotic medication in earlier stages of schizophrenia may lead to post-schizophrenic depression. However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression. Suicide
Those with post-schizophrenic depression are also commonly at risk for suicidal tendencies. There is a trend correlated between suicide and post-schizophrenic depression according to Mulholland and Coopers research in "The Symptoms of Depression in Schizophrenia and its Management." Furthermore, depression and schizophrenia have both been studied individually to try to determine if there is a correlation, and research has indicated that there is a very strong tendency for people with depression or schizophrenia to attempt suicide. | Statistically, out of all patients with schizophrenia, "10%...commit suicide. Depressed patients with schizophrenia are at a particularly high risk for suicide the first few months after diagnosis and after hospital discharge." Risk factors increasing the chance of suicide are, from highest to lowest, previous depressive orders, previous suicide attempts, drug abuse, and several other factors. Surprisingly, the suicide risk actually decreased with the presence of hallucinations. The ICD-10 Classification of Mental and Behavioural Disorders officially recognizes suicide as being a prominent aspect of post-schizophrenic depression. Because of this drastic increase in suicide, it can be difficult to study post-schizophrenic depression as many of those affected take their own lives. Treatment
For a number of years, scholars debated amongst themselves whether or not antipsychotic drugs had a tendency to increase depression or simply help the patient manage their mental illness. However, conclusive evidence points to antipsychotic drugs actually helping patients with their depression while simultaneously assisting in the suppression of schizophrenic episodes. Specifically risperidone, olanzapine, quetiapine, fluphenazine, haloperidol, and L-sulpiride have done the best in drug trials pertaining to people with schizophrenia. Along with antipsychotic drugs, post-schizophrenic patients may receive antidepressants to actively treat the depression. Drugs are certainly not the only answer, though. At the base of both depression and schizophrenia, social withdrawal is a shared symptom between the two. People with schizophrenia require a strong support system to be healthy, just as is the case with the rest the human population. | 11
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Pseudomembranous colitis and Clostridium difficile have been reported with use of cefalexin.Signs and symptoms of an allergic reaction include rash, itching, swelling, trouble breathing, or red, blistered, swollen, or peeling skin. Overall, cefalexin allergy occurs in less than 0.1% of patients, but it is seen in 1% to 10% of patients with a penicillin allergy. Interactions
Like other β-lactam antibiotics, renal excretion of cefalexin is delayed by probenecid. Alcohol consumption reduces the rate at which it is absorbed. Cefalexin also interacts with metformin, an antidiabetic drug, and this can lead to higher concentrations of metformin in the body. Histamine H2 receptor antagonists like cimetidine and ranitidine may reduce the efficacy of cefalexin by delaying its absorption and altering its antimicrobial pharmacodynamics. Pharmacology
Mechanism of action
Cefalexin is a beta-lactam antibiotic of the cephalosporin family. It is bactericidal and acts by inhibiting synthesis of the peptidoglycan layer of the bacterial cell wall. As cefalexin closely resembles d-alanyl-d-alanine, an amino acid ending on the peptidoglycan layer of the cell wall, it is able to irreversibly bind to the active site of PBP, which is essential for the synthesis of the cell wall. It is most active against gram-positive cocci, and has moderate activity against some gram-negative bacilli. However, some bacterial cells have the enzyme β-lactamase, which hydrolyzes the beta-lactam ring, rendering the drug inactive. This contributes to antibacterial resistance towards cefalexin. Pharmacokinetics
Cefalexin is rapidly and almost completely absorbed from the gastrointestinal tract with oral administration. | It is on the World Health Organizations List of Essential Medicines. In 2019, it was the 83rd most commonly prescribed medication in the United States, with more than 9 million prescriptions. In Canada, it was the fifth most common antibiotic used in 2013. In Australia, it is one of the top 15 most prescribed medications. Medical uses
Cefalexin can treat a number of bacterial infections including otitis media, streptococcal pharyngitis, bone and joint infections, pneumonia, cellulitis, and urinary tract infections. It may be used to prevent bacterial endocarditis. It can also be used for the prevention of recurrent urinary-tract infections.Cefalexin does not treat methicillin-resistant Staphylococcus aureus infections.Cefalexin is a useful alternative to penicillins in patients with penicillin intolerance. For example, penicillin is the treatment of choice for respiratory tract infections caused by Streptococcus, but cefalexin may be used as an alternative in penicillin-intolerant patients. Caution must be exercised when administering cephalosporin antibiotics to penicillin-sensitive patients, because cross-sensitivity with beta-lactam antibiotics has been documented in up to 10% of patients with a documented penicillin allergy. Pregnancy and breastfeeding
It is category A in Australia meaning that no evidence of harm has been found after being taken by many pregnant women. Use during breast feeding is generally safe. Adverse effects
The most common adverse effects of cefalexin, like other oral cephalosporins, are gastrointestinal (stomach area) disturbances and hypersensitivity reactions. Gastrointestinal disturbances include nausea, vomiting, and diarrhea, the latter being the most common. Hypersensitivity reactions include skin rashes, urticaria, fever, and anaphylaxis. | 11
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Examples of such environmental modifications include using the bed for sleep and sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not occur in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during nighttime hours, and eliminating daytime naps.A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy may be effective for insomnia.Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). | Common misconceptions and expectations that can be modified include
Unrealistic sleep expectations
Misconceptions about insomnia causes
Amplifying the consequences of insomnia
Performance anxiety after trying for so long to have a good nights sleep by controlling the sleep processNumerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia, but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem, CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.Common forms of CBT-I treatments include stimulus control therapy, sleep restriction, sleep hygiene, improved sleeping environments, relaxation training, paradoxical intention, and biofeedback. CBT is the well-accepted form of therapy for insomnia since it has no known adverse effects, whereas taking medications to alleviate insomnia symptoms have been shown to have adverse side effects. Nevertheless, the downside of CBT is that it may take a lot of time and motivation.Metacognition is a recent trend in approach to behaviour therapy of insomnia. | 11
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The flushing also results from secretion of kallikrein, the enzyme that catalyzes the conversion of kininogen to lysyl-bradykinin. The latter is further converted to bradykinin, one of the most powerful vasodilators known. Other components of the carcinoid syndrome are diarrhea (probably caused by the increased serotonin, which greatly increases peristalsis, leaving less time for fluid absorption), a pellagra-like syndrome (probably caused by diversion of large amounts of tryptophan from synthesis of the vitamin B3 niacin, which is needed for NAD production, to the synthesis of serotonin and other 5-hydroxyindoles), fibrotic lesions of the endocardium, particularly on the right side of the heart resulting in insufficiency of the tricuspid valve and, less frequently, the pulmonary valve and, uncommonly, bronchoconstriction.The pathogenesis of the cardiac lesions and the bronchoconstriction is unknown, but the former probably involves activation of serotonin 5-HT2B receptors by serotonin. When the primary tumor is in the gastrointestinal tract, as it is in the great majority of cases, the serotonin and kallikrein are inactivated in the liver; manifestations of carcinoid syndrome do not occur until there are metastases to the liver or when the cancer is accompanied by liver failure (cirrhosis). Carcinoid tumors arising in the bronchi may be associated with manifestations of carcinoid syndrome without liver metastases because their biologically active products reach the systemic circulation before passing through the liver and being metabolized.In most patients, there is an increased urinary excretion of 5-HIAA (5-hydroxyindoleacetic acid), a degradation product of serotonin.The biology of these tumors differs from many other tumor types. | A tracer agent of Indium 111 is injected into a vein where then the tumors absorb the radionuclide Indium 111 and become visible on the scanner. Only the tumors absorb the somatostatin agent Indium 111 making the scan highly effective. Treatment
For symptomatic relief of carcinoid syndrome:
Octreotide (a somatostatin analogue which decreases the secretion of serotonin by the tumor and, secondarily, decreases the breakdown product of serotonin (5-HIAA))
Telotristat ethyl (Xermelo) along with a somatostatin analogue in patients not responding to somatostatin analogue monotherapy. It is a tryptophan hydroxylase inhibitor and reduces the production of serotonin. Peptide receptor radionuclide therapy (PRRT) with lutetium-177, yttrium-90 or indium-111 labeled to octreotate is highly effective
Methysergide maleate (antiserotonin agent but not used because of the serious side effect of retroperitoneal fibrosis)
Cyproheptadine (an antihistamine drug with antiserotonergic effects)Alternative treatment for qualifying patients:
Surgical resection of tumor and chemotherapy (5-FU and doxorubicin)
Endovascular, chemoembolization, targeted chemotherapy directly delivered to the liver through special catheters mixed with embolic beads (particles that block blood vessels), used for patients with liver metastases. Uncertainties
Disease progression is difficult to ascertain because the disease can metastasize anywhere in the body and can be too small to identify with any current technology. Markers of the condition such as chromogranin-A are imperfect indicators of disease progression. Prognosis
Prognosis varies from individual to individual. It ranges from a 95% 5-year survival for localized disease to an 80% 5-year survival for those with liver metastases. The average survival time from the start of octreotide treatment has increased to about 12 years. | 11
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According to AASLD guidelines, "omega-3 fatty acids should not be used as a specific treatment of NAFLD or NASH, but they may be considered to treat hypertriglyceridemia for patients with NAFLD". Surgery
Bariatric surgery is an effective method for obese and diabetic individuals with NAFLD to induce weight loss and reduce or resolve NASH inflammation, including fibrosis, and improve longevity. For the AASLD, bariatric surgery can be considered only for NASH on a case-by-case basis by an experienced bariatric surgery program. Indeed, some individuals might develop new or worsened features of NAFLD.About 92% of people with NAFLD saw an improvement in steatosis and 70% a complete resolution after bariatric surgery.A preoperative diet such as a low-calorie diet or a very-low-calorie diet is usually recommended to reduce liver volume by 16–20%. Preoperative weight loss is the only factor associated with postoperative weight loss. Preoperative weight loss can reduce operative time and hospital stay, although there is insufficient evidence whether preoperative weight loss reduces long-term morbidity or complications. Weight loss and decreases in liver size may be independent of the amount of calorie restriction.The APWG on NAFLD recommends bariatric surgery as a treatment option for those with class II obesity (BMI >32.5 kg/m2 for Asians, 35 kg/m2 for Caucasians). They consider its effects on improving liver-related complications as unproven yet, but it effectively increases longevity by improving cardiovascular factors.Surgery carries more risks for individuals with NASH cirrhosis, with a review estimating overall morbidity to be 21%. | Organic material may then be further decomposed by detritivores, organisms which recycle detritus, returning it to the environment for reuse in the food chain, where these chemicals may eventually end up being consumed and assimilated into the cells of an organism. Examples of detritivores include earthworms, woodlice and dung beetles. Microorganisms also play a vital role, raising the temperature of the decomposing matter as they break it down into yet simpler molecules. Not all materials need to be fully decomposed. Coal, a fossil fuel formed over vast tracts of time in swamp ecosystems, is one example. Natural selection
Contemporary evolutionary theory sees death as an important part of the process of natural selection. It is considered that organisms less adapted to their environment are more likely to die having produced fewer offspring, thereby reducing their contribution to the gene pool. Their genes are thus eventually bred out of a population, leading at worst to extinction and, more positively, making the process possible, referred to as speciation. Frequency of reproduction plays an equally important role in determining species survival: an organism that dies young but leaves numerous offspring displays, according to Darwinian criteria, much greater fitness than a long-lived organism leaving only one. Extinction
Extinction is the cessation of existence of a species or group of taxa, reducing biodiversity. The moment of extinction is generally considered to be the death of the last individual of that species (although the capacity to breed and recover may have been lost before this point). | 0-1
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The findings are based on low quality evidence suggesting it may be safe to stop anti-hypertensive medications. However, older adults should not stop any of their medications without talking to a healthcare professional. See also
Chemical dependency
Craving, a psychological withdrawal symptom
Drug detoxification
Drug tolerance
Hangover
Neonatal withdrawal
Rebound effect
Post-acute withdrawal syndrome (PAWS)
== References == | Atrial tachycardia is a type of heart rhythm problem in which the hearts electrical impulse comes from an ectopic pacemaker (that is, an abnormally located cardiac pacemaker) in the upper chambers (atria) of the heart, rather than from the sinoatrial node, the normal origin of the hearts electrical activity. As with any other form of tachycardia (rapid heart beat), the underlying mechanism can be either the rapid discharge of an abnormal focus, the presence of a ring of cardiac tissue that gives rise to a circle movement (reentry), or a triggered rapid rhythm due to other pathological circumstances (as would be the case with some drug toxicities, such as digoxin toxicity). Classification
Forms of atrial tachycardia (ATach) include multifocal atrial tachycardia (MAT), focal atrial tachycardia and atrial flutter. Paroxysmal atrial tachycardia (PAT) is an episode of arrhythmia that begins and ends abruptly. Etiology
Atrial tachycardia tends to occur in individuals with structural heart disease, with or without heart failure, and ischemic coronary artery disease. However, focal atrial tachycardia often occurs in healthy individuals without structural heart disease. Other possible etiologies are listed below:
Hypoxia
Pulmonary disease
Ischemic heart disease
Stimulants: cocaine, caffeine, chocolate, ephedra
Alcohol
Metabolic disturbances
Digoxin toxicity
Heightened sympathetic toneA study noted 10 to 15% of patients presenting for supraventricular tachycardia ablation had atrial tachycardia. | 0-1
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Antiandrogen therapy, hormonal therapy with antiandrogenic medications such as spironolactone, flutamide, cyproterone acetate, ethinylestradiol, finasteride, dutasteride, and metformin, have been found to be effective in clinical studies. However, the quality of available evidence is low and does not presently allow for robust evidence-based recommendations. Intravenous infusion or subcutaneous injection of anti-inflammatory (TNF inhibitors; anti-TNF-alpha) drugs such as infliximab, and etanercept This use of these drugs is not currently Food and Drug Administration (FDA) approved and is somewhat controversial, so may not be covered by insurance. TNF inhibitor: Studies have supported that various TNF inhibitors have a positive effect on HS lesions. Specifically adalimumab at weekly intervals is useful. Adalimumab is the only medication approved by the FDA for the treatment of HS as of 2021. Topical isotretinoin is usually ineffective in people with HS, and is more commonly known as a medication for the treatment of acne vulgaris. Individuals affected by HS who responded to isotretinoin treatment tended to have milder cases of the condition. Surgery
When the process becomes chronic, wide surgical excision is the procedure of choice. Wounds in the affected area do not heal by secondary intention, and immediate or delayed application of a split-thickness skin graft is an option. Another option is covering the defect with a perforator flap. With this technique, the (mostly totally excised) defect is covered with tissue from an area nearby. For example, the axilla with a fully excised defect of 15 × 7 cm can be covered with a thoracodorsal artery perforator flap. | Laser hair removal
The 1064-nm wavelength laser for hair removal may aid in the treatment of HS. A randomized control study has shown improvement in HS lesions with the use of an Nd:YAG laser. Prognosis
In stage III disease, as classified by the Hurleys staging system, fistulae left undiscovered, undiagnosed, or untreated, can rarely lead to the development of squamous cell carcinoma in the anus or other affected areas. Other stage III chronic sequelae may also include anemia, multilocalized infections, amyloidosis, and arthropathy. Stage III complications have been known to lead to sepsis, but clinical data are still uncertain. Potential complications
Contractures and reduced mobility of the lower limbs and axillae due to fibrosis and scarring occur. Severe lymphedema may develop in the lower limbs. Local and systemic infections (meningitis, bronchitis, pneumonia, etc. ), are seen, which may even progress to sepsis. Interstitial keratitis
Anal, rectal, or urethral fistulae
Normochromic or hypochromic anemia
People with HS may be at increased risk for autoimmune disorders including ankylosing spondylitis, rheumatoid arthritis, and psoriatic arthritis. Squamous cell carcinoma has been found on rare occasions in chronic hidradenitis suppurativa of the anogenital region. The mean time to the onset of this type of lesion is 10 years or more and the tumors are usually highly aggressive. Tumors of the lung and oral cavity, and liver cancer
Hypoproteinemia and amyloidosis, which can lead to kidney failure and death
Seronegative and usually asymmetric arthropathy: pauciarticular arthritis, polyarthritis/polyarthralgia syndrome
History
From 1833 to 1839, in a series of three publications, Velpeau identified and described a disease now known as hidradenitis suppurativa. | 11
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A primordial cyst is a developmental odontogenic cyst. It is found in an area where a tooth should have formed but is missing. Primordial cysts most commonly arise in the area of mandibular third molars. Under microscopes, the cyst looks like an odontogenic keratocyst (also called a Keratocyst odontogenic tumor) whereby the lesions displays a parakeratinized epithelium with palisading basal epithelial cells. The term "Primordial cyst" is considered an outdated term and should be avoided. Most "primordial cysts" are actually Keratocyst odontogenic tumors (KOTs). References
Kahn, Michael A. Basic Oral and Maxillofacial Pathology. Volume 1. 2001. | Chondrocalcinosis or cartilage calcification is calcification (accumulation of calcium salts) in hyaline cartilage and/or fibrocartilage. It can be seen on radiography. Causes
Buildup of calcium phosphate in the ankle joints has been found in about 50% of the general population, and may be associated with osteoarthritis.Another common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD). CPPD is estimated to affect 4% to 7% of the adult populations of Europe and the United States. Previous studies have overestimated the prevalence by simply estimating the prevalence of chondrocalcinosis regardless of cause.A magnesium deficiency may cause chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis. Other causes of chondrocalcinosis include:
Hypercalcaemia, especially when caused by hyperparathyroidism
Arthritis
Pseudogout
Wilson disease
Hemochromatosis
Ochronosis
Hypophosphatasia
Hypothyroidism
Hyperoxalemia
Acromegaly
Gitelman syndrome
Diagnosis
Chondrocalcinosis can be visualized on projectional radiography, CT scan, MRI, US, and nuclear medicine. CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule), however radiography is more successful. At ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage. As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis and gout. == References == | 0-1
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The FDA approved the drug (via the then-new FDA accelerated approval system) for use against HIV, AIDS, and AIDS Related Complex (ARC, a now-obsolete medical term for pre-AIDS illness) on March 20, 1987. The time between the first demonstration that AZT was active against HIV in the laboratory and its approval was 25 months, the shortest period of drug development in recent history.AZT was subsequently approved unanimously for infants and children in 1990. AZT was initially administered in significantly higher dosages than today, typically 400 mg every four hours, day and night, compared to modern dosage of 300 mg twice daily. The paucity of alternatives for treating HIV/AIDS at that time unambiguously affirmed the health risk/benefit ratio, with inevitable slow, disfiguring, and painful death from HIV outweighing the drugs side-effect of transient anemia and malaise. Society and culture
In 1991, the advocacy group Public Citizen filed a lawsuit claiming that the patents were invalid. Subsequently, Barr Laboratories and Novopharm Ltd. also challenged the patent, in part based on the assertion that NCI scientists Samuel Broder, Hiroaki Mitsuya, and Robert Yarchoan should have been named as inventors, and those two companies applied to the FDA to sell AZT as a generic drug. In response, Burroughs Wellcome Co. filed a lawsuit against the two companies. The United States Court of Appeals for the Federal Circuit ruled in 1992 in favor of Burroughs Wellcome, ruling that even though they had never tested it against HIV, they had conceived of it working before they sent it to the NCI scientists. | In order to expedite the process of discovering a drug, the NCI researchers actively sought collaborations with pharmaceutical companies having access to libraries of compounds with potential antiviral activity. This assay could simultaneously test both the anti-HIV effect of the compounds and their toxicity against infected T cells. In June 1984, Burroughs-Wellcome virologist Marty St. Clair set up a program to discover drugs with the potential to inhibit HIV replication. Burroughs-Wellcome had expertise in nucleoside analogs and viral diseases, led by researchers including George Hitchings, Gertrude Elion, David Barry, Paul (Chip) McGuirt Jr., Philip Furman, Martha St. Clair, Janet Rideout, Sandra Lehrman and others. Their research efforts were focused in part on the viral enzyme reverse transcriptase. Reverse transcriptase is an enzyme that retroviruses, including HIV, utilize to replicate themselves. Secondary testing was performed in mouse cells infected with the retroviruses Friend virus or Harvey sarcoma virus, as the Wellcome group did not have a viable in-house HIV antiviral assay in place at that time, and these other retroviruses were believed to represent reasonable surrogates. AZT proved to be a remarkably potent inhibitor of both Friend virus and Harvey sarcoma virus, and a search of the companys records showed that it had demonstrated low toxicity when tested for its antibacterial activity in rats many years earlier. | 11
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In Ancient Greece, the physician Hippocrates (460-370 BCE) described symptoms of scurvy, specifically a "swelling and obstruction of the spleen." In 406 CE, the Chinese monk Faxian wrote that ginger was carried on Chinese ships to prevent scurvy.The knowledge that consuming foods containing vitamin C is a cure for scurvy has been repeatedly forgotten and rediscovered into the early 20th century. Early modern era
In the 13th century, the Crusaders frequently developed scurvy. In the 1497 expedition of Vasco da Gama, the curative effects of citrus fruit were already known and confirmed by Pedro Álvares Cabral and his crew in 1507.The Portuguese planted fruit trees and vegetables in Saint Helena, a stopping point for homebound voyages from Asia, and left their sick, who had scurvy and other ailments, to be taken home by the next ship if they recovered.In 1500, one of the pilots of Cabrals fleet bound for India noted that in Malindi, its king offered the expedition fresh supplies such as lambs, chickens, and ducks, along with lemons and oranges, due to which "some of our ill were cured of scurvy".Unfortunately, these travel accounts did not stop further maritime tragedies caused by scurvy, first because of the lack of communication between travelers and those responsible for their health, and because fruits and vegetables could not be kept for long on ships.In 1536, the French explorer Jacques Cartier, exploring the St. Lawrence River, used the local natives knowledge to save his men who were dying of scurvy. | However, the condition may be present in association with other syndromes: Turner syndrome, Noonan syndrome, Loeys–Dietz syndrome, Marfan syndrome, Ehlers–Danlos syndrome, Morquio syndrome, trisomy 18, trisomy 21, homocystinuria, osteogenesis imperfecta, multiple lentigines syndrome (LEOPARD syndrome), Sly syndrome (mucopolysaccharidosis type VII), and scoliosis. In about 25% of cases of pectus carinatum, the patient has a family member with the condition. Diagnosis
The pectus carinatum can be easily diagnosed by certain tests like a CT scan (2D and 3D). It may then be found out that the rib cage is in normal structure. If there is more than average growth of sternum than pectus carinatum protrudes. Also it is of two types, as pectus carinatum is symmetrical or unsymmetrical. On the basis of that further treatment is given to the patient. Treatment
External bracing technique
The use of orthotic bracing, pioneered by Sydney Haje as of 1977, is finding increasing acceptance as an alternative to surgery in select cases of pectus carinatum. In children, teenagers, and young adults who have pectus carinatum and are motivated to avoid surgery, the use of a customized chest-wall brace that applies direct pressure on the protruding area of the chest produces excellent outcomes. Willingness to wear the brace as required is essential for the success of this treatment approach. The brace works in much the same way as orthodontics (braces that correct the alignment of teeth). The brace consists of front and back compression plates that are anchored to aluminum bars. | 0-1
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Adult worms have a lifespan of 1–2 years which means that individuals may be infected all their lives as worms die and new worms are acquired.Eggs can survive potentially for 15 years and a single worm may produce 200,000 eggs a day. They maintain their position by swimming against the intestinal flow. Mechanism
Ascaris takes most of its nutrients from the partially digested host food in the intestine. There is some evidence that it can secrete enzyme inhibitors, presumably to protect itself from digestion by the hosts enzymes. Children are often more severely affected. Diagnosis
Most diagnoses are made by identifying the appearance of the worm or eggs in feces. Due to the large quantity of eggs laid, diagnosis can generally be made using only one or two fecal smears. The diagnosis is usually incidental when the host passes a worm in the stool or vomit. The eggs can be seen in a smear of fresh feces examined on a glass slide under a microscope and there are various techniques to concentrate them first or increase their visibility, such as the ether sedimentation method or the Kato technique. The eggs have a characteristic shape: they are oval with a thick, mamillated shell (covered with rounded mounds or lumps), measuring 35–50 micrometer in diameter and 40–70 in length. During pulmonary disease, larvae may be found in fluids aspirated from the lungs. White blood cell counts may demonstrate peripheral eosinophilia; this is common in many parasitic infections and is not specific to ascariasis. | Other effective agents include tribendimidine and nitazoxanide.About 0.8 to 1.2 billion people globally have ascariasis, with the most heavily affected populations being in sub-Saharan Africa, Latin America, and Asia. This makes ascariasis the most common form of soil-transmitted helminthiasis. As of 2010 it caused about 2,700 deaths a year, down from 3,400 in 1990. Another type of Ascaris infects pigs. Ascariasis is classified as a neglected tropical disease. Signs and symptoms
In populations where worm infections are widespread, it is common to find that most people are infected by a small number of worms, while a small number of people are heavily infected. This is characteristic of many types of worm infections. Those people who are infected with only a small number of worms usually have no symptoms. Migrating larvae
As larval stages travel through the body, they may cause visceral damage, peritonitis and inflammation, enlargement of the liver or spleen, and an inflammation of the lungs. Pulmonary manifestations take place during larval migration and may present as Loefflers syndrome, a transient respiratory illness associated with blood eosinophilia and pulmonary infiltrates with radiographic shadowing. Intestinal blockage
The worms can occasionally cause intestinal blockage when large numbers get tangled into a bolus or they may migrate from the small intestine, which may require surgery. More than 796 A. lumbricoides worms weighing up to 550 g (19 oz) were recovered at autopsy from a two-year-old South African girl. The worms had caused torsion and gangrene of the ileum, which was interpreted as the cause of death.The worms lack teeth. | 11
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Ischemia or ischaemia is a restriction in blood supply to any tissues, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also means local hypoxia in a given part of a body sometimes resulting from constriction (such as vasoconstriction, thrombosis or embolism). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial (poor perfusion) or total blockage. The inadequate delivery of oxygenated blood to the organs must be resolved either by treating the cause of the inadequate delivery or reducing the oxygen demand of the system that needs it. For example, patients with myocardial ischemia have a decreased blood flow to the heart and are prescribed with medications that reduce chronotrophy and ionotrophy to meet the new level of blood delivery supplied by the stenosed so that it is adequate. Signs and symptoms
The signs and symptoms of ischemia vary, as it can occur anywhere in the body and depends on the degree to which blood flow is interrupted. For example, clinical manifestations of acute limb ischemia (which can be summarized as the "six Ps") include pain, pallor, pulseless, paresthesia, paralysis, and poikilothermia.Without immediate intervention, ischemia may progress quickly to tissue necrosis and gangrene within a few hours. | Limb
Inadequate blood supply to a limb may results in acute limb ischemia or chronic limb threatening ischemia. Cutaneous
Reduced blood flow to the skin layers may result in mottling or uneven, patchy discoloration of the skin. Kidney Ischemia
Kidney Ischemia is a loss of blood flow to the kidney cells. Several physical symptoms include shrinkage of one or both kidneys, renovascular hypertension, acute renal failure, progressive azotemia, and acute pulmonary edema. It is a disease with high mortality rate and high morbidity. Failure to treat could cause chronic kidney disease and a need for renal surgery. Causes
Ischemia is a vascular disease involving an interruption in the arterial blood supply to a tissue, organ, or extremity that, if untreated, can lead to tissue death. It can be caused by embolism, thrombosis of an atherosclerotic artery, or trauma. Venous problems like venous outflow obstruction and low-flow states can cause acute arterial ischemia. An aneurysm is one of the most frequent causes of acute arterial ischemia. Other causes are heart conditions including myocardial infarction, mitral valve disease, chronic atrial fibrillation, cardiomyopathies, and prosthesis, in all of which thrombi are prone to develop. Occlusion
The thrombi may dislodge and may travel anywhere in the circulatory system, where they may lead to pulmonary embolus, an acute arterial occlusion causing the oxygen and blood supply distal to the embolus to decrease suddenly. The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD). | 11
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These are factors which all must be excluded for a diagnosis of functional FI, and are abnormal innervation caused by lesion(s) within the brain (e.g., dementia), spinal cord (at or below T12), or sacral nerve roots, or mixed lesions (e.g., multiple sclerosis), or as part of a generalized peripheral or autonomic neuropathy (e.g., due to diabetes), anal sphincter abnormalities associated with a multisystem disease (e.g., scleroderma), and structural or neurogenic abnormalities that are the major cause. Definition
There is no globally accepted definition, but fecal incontinence is generally defined as the recurrent inability to voluntarily control the passage of bowel contents through the anal canal and expel it at a socially acceptable location and time, occurring in individuals over the age of four. "Social continence" has been given various precise definitions for the purposes of research; however, generally it refers to symptoms being controlled to an extent that is acceptable to the individual in question, with no significant effect on their life. There is no consensus about the best way to classify FI, and several methods are used. Symptoms can be directly or indirectly related to the loss of bowel control. The direct (primary) symptom is a lack of control over bowel contents which tends to worsen without treatment. Indirect (secondary) symptoms, which are the result of leakage, include pruritus ani (an intense itching sensation from the anus), perianal dermatitis (irritation and inflammation of the skin around the anus), and urinary tract infections. Due to embarrassment, people may only mention secondary symptoms rather than acknowledge incontinence. | Smiths Recognizable Patterns of Human Malformation (6th ed.). Philadelphia: WB Saunders. ISBN 978-0-7216-2359-7. Orrico A.; Galli L.; Cavaliere ML. ; et al. (2004). "Phenotypic and molecular characterisation of the Aarskog–Scott syndrome: a survey of the clinical variability in light of FGD1 mutation analysis in 46 patients". Eur. J. Hum. Genet. 12 (1): 16–23. doi:10.1038/sj.ejhg.5201081. PMID 14560308. External links
Aarskog–Scott syndrome, detailed up-to-date information in OMIM (Online Mendelian Inheritance in Man)
Aarskogs syndrome at Who Named It? | 0-1
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Epiploic appendagitis (EA) is an uncommon, benign, self-limiting inflammatory process of the epiploic appendices. Other, older terms for the process include appendicitis epiploica and appendagitis, but these terms are used less now in order to avoid confusion with acute appendicitis. Epiploic appendices are small, fat-filled sacs or finger-like projections along the surface of the upper and lower colon and rectum. They may become acutely inflamed as a result of torsion (twisting) or venous thrombosis. The inflammation causes pain, often described as sharp or stabbing, located on the left, right, or central regions of the abdomen. There is sometimes nausea and vomiting. The symptoms may mimic those of acute appendicitis, diverticulitis, or cholecystitis. The pain is characteristically intense during/after defecation or micturition (espec. in the sigmoid type) due to the effect of traction on the pedicle of the lesion caused by straining and emptying of the bowel and bladder. Initial lab studies are usually normal. EA is usually diagnosed incidentally on CT scan which is performed to exclude more serious conditions. Although it is self-limiting, epiploic appendagitis can cause severe pain and discomfort. It is usually thought to be best treated with an anti-inflammatory and a moderate to severe pain medication (depending on the case) as needed. Surgery is not recommended in nearly all cases. Sand and colleagues, however, recommend laparoscopic surgery to excise the inflamed appendage in most cases in order to prevent recurrence. Signs and symptoms
The condition commonly occurs in patients in their 40s and 50s predominantly in men. | Segmented genomes: Bunyaviridae, Orthomyxoviridae, Arenaviridae, and Reoviridae (acronym BOAR). All are RNA viruses. Viruses transmitted almost exclusively by arthropods: Bunyavirus, Flavivirus, and Togavirus. Some Reoviruses are transmitted from arthropod vectors. All are RNA viruses. One family of enveloped viruses causes gastroenteritis (Coronaviridae). All other viruses associated with gastroenteritis are non-enveloped. Baltimore Group
This group of analysts defined multiple categories of virus. Groups:
I - dsDNA
II - ssDNA
III - dsRNA
IV - positive-sense ssRNA
V - negative-sense ssRNA
VI - ssRNA-RT
VII - dsDNA-RT
Clinical characteristics
The clinical characteristics of viruses may differ substantially among species within the same family:
See also
List of latent human viral infections
Pathogenic bacteria
References
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The observation about the self and storage of those observations by the I-self creates three types of knowledge, which collectively account for the Me-self, according to James. These are the material self, social self, and spiritual self. The social self comes closest to self-esteem, comprising all characteristics recognized by others. The material self consists of representations of the body and possessions and the spiritual self of descriptive representations and evaluative dispositions regarding the self. This view of self-esteem as the collection of an individuals attitudes toward itself remains today.In the mid-1960s, social psychologist Morris Rosenberg defined self-esteem as a feeling of self-worth and developed the Rosenberg self-esteem scale (RSES), which became the most-widely used scale to measure self-esteem in the social sciences.In the early 20th century, the behaviorist movement minimized introspective study of mental processes, emotions, and feelings, replacing introspection with objective study through experiments on behaviors observed in relation with the environment. Behaviorism viewed the human being as an animal subject to reinforcements, and suggested placing psychology as an experimental science, similar to chemistry or biology. As a consequence, clinical trials on self-esteem were overlooked, since behaviorists considered the idea less liable to rigorous measurement. In the mid-20th century, the rise of phenomenology and humanistic psychology led to renewed interest in self-esteem. Self-esteem then took a central role in personal self-actualization and in the treatment of psychic disorders. Psychologists started to consider the relationship between psychotherapy and the personal satisfaction of people with high self-esteem as useful to the field. | Defensive high self-esteem individuals internalize subconscious self-doubts and insecurities, causing them to react very negatively to any criticism they may receive. There is a need for constant positive feedback from others for these individuals to maintain their feelings of self-worth. The necessity of repeated praise can be associated with boastful, arrogant behavior or sometimes even aggressive and hostile feelings toward anyone who questions the individuals self-worth, an example of threatened egotism.The Journal of Educational Psychology conducted a study in which they used a sample of 383 Malaysian undergraduates participating in work integrated learning (WIL) programs across five public universities to test the relationship between self-esteem and other psychological attributes such as self-efficacy and self-confidence. The results demonstrated that self-esteem has a positive and significant relationship with self-confidence and self-efficacy since students with higher self-esteem had better performances at university than those with lower self-esteem. It was concluded that higher education institutions and employers should emphasize the importance of undergraduates self-esteem development. Implicit and explicit
Implicit self-esteem refers to a persons disposition to evaluate themselves positively or negatively in a spontaneous, automatic, or unconscious manner. It contrasts with explicit self-esteem, which entails more conscious and reflective self-evaluation. Both explicit self-esteem and implicit self-esteem are theoretically subtypes of self-esteem proper. | 11
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Pharmacology
Mechanism of action
Amikacin irreversibly binds to 16S rRNA and the RNA-binding S12 protein of the 30S subunit of prokaryotic ribosome and inhibits protein synthesis by changing the ribosomes shape so that it cannot read the mRNA codons correctly. It also interferes with the region that interacts with the wobble base of the tRNA anticodon. It works in a concentration-dependent manner, and has better action in an alkaline environment.At normal doses, amikacin-sensitive bacteria respond within 24–48 hours. Resistance
Amikacin evades attacks by all antibiotic-inactivating enzymes that are responsible for antibiotic resistance in bacteria, except for aminoacetyltransferase and nucleotidyltransferase. This is accomplished by the L-hydroxyaminobuteroyl amide (L-HABA) moiety attached to N-1 (compare to kanamycin, which simply has a hydrogen), which blocks the access and decreases the affinity of aminoglycoside-inactivating enzymes. Amikacin ends up with only one site where these enzymes can attack, while gentamicin and tobramycin have six.Bacteria that are resistant to streptomycin and capreomycin are still susceptible to amikacin; bacteria that are resistant to kanamycin have varying susceptibility to amikacin. Resistance to amikacin also confers resistance to kanamycin and capreomycin.Resistance to amikacin and kanamycin in Mycobacterium, the causative agent of tuberculosis, is due to a mutation in the rrs gene, which codes for the 16S rRNA. Mutations such as these reduce the binding affinity of amikacin to the bacterias ribosome. | Recurrent disease in transplanted kidneys is common, although there have been reports of successful transplantations.Associated autoimmune diseases (e.g., systemic lupus erythematosus, thyroiditis) contribute significantly to increased morbidity in these patients compared with the general population. Although uncommon, insulin resistance increases cardiovascular risk. Susceptibility to bacterial infections probably results from a C3 deficiency (due to complement activation and consumption of C3). Low C3 levels may impair complement-mediated phagocytosis and bacterial killing. Epidemiology
Around 250 cases have been reported since the recognition of this syndrome. It is a rare syndrome with no known prevalence, although it is more common than the generalized form of acquired lipodystrophy (Lawrence syndrome). Race: No clear relationship exists between incidence and race in this syndrome; however, most reported patients have been of European descent. Age: The median age of onset of lipodystrophy has been reported to be around seven years; however, onset occurring as late as the fourth or fifth decade of life also has been reported. The median age at presentation has been about 25 years, and women have been found to present later than men (age 28 for women, age 18 for men). Sex: Analysis of the pooled data revealed female patients were affected about four times more often than males. See also
Lipodystrophy
Laminopathy
List of cutaneous conditions
References
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The U.S. Preventive Services Task Force found "insufficient evidence" to recommend that doctors counsel patients on exercise but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease, morbidity, and mortality", only the effectiveness of counseling itself. The American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.Psychological symptoms are common in people with CHD, and while many psychological treatments may be offered following cardiac events, there is no evidence that they change mortality, the risk of revascularization procedures, or the rate of non-fatal myocardial infarction.Antibiotics for secondary prevention of coronary heart disease
Antibiotics may help patients with coronary disease to reduce the risk of heart attacks and strokes. However, the latest evidence suggests that antibiotics for secondary prevention of coronary heart disease are harmful with increased mortality and occurrence of stroke. So, the use of antibiotics is not currently supported for preventing secondary coronary heart disease. Neuropsychological Assessment
A thorough systematic review found that indeed there is a link between a CHD condition and brain dysfunction in females/women. Consequently, since research is showing that cardiovascular diseases, like CHD, can play a role as a precursor for dementia, like Alzheimers disease, individuals with CHD should have a neuropsychological assessment. Treatment
There are a number of treatment options for coronary artery disease:
Lifestyle changes
Medical treatment – commonly prescribed drugs (e.g., cholesterol lowering medications, beta-blockers, nitroglycerin, calcium channel blockers, etc. | The number of categories of adverse childhood experiences (psychological, physical, or sexual abuse; violence against mother; or living with household members who used substances, mentally ill, suicidal, or incarcerated) showed a graded correlation with the presence of adult diseases including coronary artery (ischemic heart) disease. Hemostatic factors: High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD. Low hemoglobin. In the Asian population, the b fibrinogen gene G-455A polymorphism was associated with the risk of CAD. Pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the hearts muscle cells. The hearts muscle cells may die from lack of oxygen and this is called a myocardial infarction (commonly referred to as a heart attack). It leads to damage, death, and eventual scarring of the heart muscle without regrowth of heart muscle cells. Chronic high-grade narrowing of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into a dangerous heart rhythm known as ventricular fibrillation, which often leads to death.Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis, the arterys lining becomes hardened, stiffened, and accumulates deposits of calcium, fatty lipids, and abnormal inflammatory cells – to form a plaque. | 11
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However, as discussed below, many scholars now hold that culture bound disorders may often be an artifact of colonial encounters, and contemporary discussions of piblokto in medical anthropology and cross-cultural psychiatry consider it to be an example of the suspect nature of culture bound syndromes. Origin
Piblokto is most often found in but not confined to the Inughuit culture in the polar regions of northern Greenland. Similar symptoms have been reported in European sailors stranded in Arctic regions in the 1800s. Among the Inughuit, the attacks are not considered out of the ordinary. No native theory of the disorder is currently reported. This condition is most often seen in Inughuit women. Piblokto is most common during long Arctic nights. Symptoms
Piblokto is an abrupt dissociative episode with four phases: social withdrawal, excitement, convulsions and stupor, and recovery. In his book Handbook of Cultural Psychiatry, Wen-Shing Tseng provides the following example adapted from Foulks:
Mrs. A is a 30-year-old woman who has had periodic episodes of "strange experiences" in the past 3 years (since her mothers death). Three years ago, in the winter, during her first episode, she was acutely assaultive and tried to harm herself. The attack lasted about 15 min and she remembered nothing about it afterward. Two years ago, she had her second attack, which lasted about half an hour, during which time she ran from her home into the snow, tearing off her clothing. | Causes
Although there is no known cause for piblokto, Western scientists have attributed the disorder to the lack of sun, the extreme cold, and the desolate state of most villages in the region. A cause for this disorder present in this culture may be the isolation of their cultural group.This culture-bound syndrome is possibly linked to vitamin A toxicity (hypervitaminosis A). The native Inughuit diet or Eskimo nutrition provides rich sources of vitamin A through the ingestion of livers, kidneys, and fat of arctic fish and mammals and is possibly the cause or a causative factor. This causative factor is through the toxicity that has been reported for males, females, adults, children, and dogs. The ingestion of organ meats, particularly the livers of some Arctic mammals, such as the polar bear and bearded seal, in whom the vitamin is stored at levels toxic to humans, can be fatal to most people. Inughuit tradition states that it is caused by evil spirits possessing the living. Shamanism and animism are dominant themes in Inughuit traditional beliefs with the angakkuq (healer) acting as a mediator with the supernatural forces. Angakkuit use trance states to communicate with spirits and carry out faith healing. There is a view among the Inughuit that individuals entering trance states should be treated with respect, given the possibility of a new "revelation" emerging as a result. Treatment in piblokto cases usually involves allowing the episode to run its course without interference. | 11
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Actavis appealed and in May a panel of the Second Circuit Court of Appeals upheld the injunction, and in June Actavis asked that its case be heard by the full Second Circuit panel. In August 2015, Actavis request was denied. Society and culture
Recreational use
One preclinical study on monkeys showed that memantine was capable of inducing a PCP-like intoxication. Because of its very long biological half-life, memantine was previously thought not to be recreational, although a few cases of sporadic recreational use have been described.A study examining self-reported use of memantine on the social network Reddit showed that the drug was used recreationally and as a nootropic, but also that it was misused in various illnesses as self-medication without strong scientific basis. | Common adverse drug reactions (≥1% of people) include confusion, dizziness, drowsiness, headache, insomnia, agitation, and/or hallucinations. Less common adverse effects include vomiting, anxiety, hypertonia, cystitis, and increased libido.Like many other NMDA antagonists, memantine behaves as a dissociative anesthetic at supratherapeutic doses. Despite isolated reports, recreational use of memantine is rare due to the drugs long duration and limited availability. Also memantine seems to lack effects such as euphoria or hallucinations.Memantine appears to be generally well tolerated by children with autism spectrum disorder. Pharmacology
Glutamate
A dysfunction of glutamatergic neurotransmission, manifested as neuronal excitotoxicity, is hypothesized to be involved in the etiology of Alzheimers disease. Targeting the glutamatergic system, specifically NMDA receptors, offers a novel approach to treatment in view of the limited efficacy of existing drugs targeting the cholinergic system.Memantine is a low-affinity voltage-dependent uncompetitive antagonist at glutamatergic NMDA receptors. By binding to the NMDA receptor with a higher affinity than Mg2+ ions, memantine is able to inhibit the prolonged influx of Ca2+ ions, particularly from extrasynaptic receptors, which forms the basis of neuronal excitotoxicity. The low affinity, uncompetitive nature, and rapid off-rate kinetics of memantine at the level of the NMDA receptor-channel, however, preserves the function of the receptor at synapses, as it can still be activated by physiological release of glutamate following depolarization of the postsynaptic neuron. The interaction of memantine with NMDA receptors plays a major role in the symptomatic improvement that the drug produces in Alzheimers disease. | 11
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Maculopathy has been reported in rare cases, and may be linked effects from the mutation on the ATXN1 locus on genes in neighboring loci. Task specific dystonias have been reported in individual cases, often in the form of writers cramps or cervical dystonia.SCAs can also be detected before serious atrophy with electrophysiologic techniques, using electrodes on the scalp to detect changes in electric potential within the brain in response to sensations or movements. Individuals with SCA1 often exhibit abnormal brainstem auditory evoked potential, including prolonged latency and absent or poorly defined waveforms, with one study reporting 73.3% of test subjects exhibiting abnormalities. The same study also found abnormalities in visual evoked potential and median somatosensory evoked potential in some SCA1 persons. These results were similar to those exhibited in other SCAs and differences between the SCAs were not statistically significant, so electrophysiologic techniques cannot replace genetic testing for specific diagnoses of SCAs.All SCAs cause atrophy in various neural tissues that are detectable using magnetic resonance imaging, computed tomography, or other imaging techniques. In SCA1 some degradation in the grey matter of the cerebellum and brain stem can sometimes be detected in presymptomatic individuals with the expansion in ATXN1. Typically, grey matter loss can be observed in cerebellar vermis in all lobules of the cerebellum and in the paramedian portions of both hemispheres. White matter loss can also be observed in the middle cerebellar peduncles. | Axanthism is a condition common in reptiles and amphibians, in which xanthophore metabolism is affected rather than synthesis of melanin, resulting in reduction or absence of red and yellow pteridine pigments. Leucism differs from albinism in that the melanin is, at least, partially absent but the eyes retain their usual colour. Some leucistic animals are white or pale because of chromatophore (pigment cell) defects, and do not lack melanin. Melanism is the direct opposite of albinism. An unusually high level of melanin pigmentation (and sometimes absence of other types of pigment in species that have more than one) results in an appearance darker than non-melanistic specimens from the same gene pool. In plants
In plants, albinism is characterised by partial or complete loss of chlorophyll pigments and incomplete differentiation of chloroplast membranes. Albinism in plants interferes with photosynthesis, which can reduce survivability. Some plant variations may have white flowers or other parts. However, these plants are not totally devoid of chlorophyll. Terms associated with this phenomenon are "hypochromia" and "albiflora".Plants that are pale simply from being in the dark are termed etiolated. Albino redwoods are rare examples of an albino tree with white needles; despite its lack of chlorophyll it may grow to substantial size as a parasite, usually on the base of the (normal) redwood tree from which it first grew. Only about sixty examples of albino redwoods are known. Additionally, an even smaller number of "chimeric" redwood trees have both normal and white needles. | 0-1
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Diagnosis
Classification
The definitions of the pressure ulcer stages are revised periodically by the National Pressure Injury Advisory Panel (NPUAP) in the United States and the European Pressure Ulcer Advisory Panel (EPUAP) in Europe. Different classification systems are used around the world, depending upon the health system, the health discipline and the purpose for the classifying (e.g. health care versus, prevalence studies versus funding. Briefly, they are as follows:
Stage I: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area differs in characteristics such as thickness and temperature as compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk). Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation. Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. | Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders and individuals with impaired mobility such as wheelchair users (especially where spinal injury is involved). Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is important.The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23%, and the prevalence was 26% in Canadian healthcare settings from 1990 to 2003. In 2013, there were 29,000 documented deaths from pressure ulcers globally, up from 14,000 deaths in 1990. Presentation
Complications
Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthrosis, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolins ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis. | 11
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This means that the child can move, smile, suckle and breathe without the aid of devices. Causes
Folic acid has been shown to be important in neural tube formation since at least 1991, and as a subtype of neural tube defect, folic acid may play a role in anencephaly. Studies have shown that the addition of folic acid to the diet of women of child-bearing age may significantly reduce, although not eliminate, the incidence of neural tube defects. Therefore, it is recommended that all women of child-bearing age consume 0.4 mg of folic acid daily, especially those attempting to conceive or who may possibly conceive, as this can reduce the risk to 0.03%. It is not advisable to wait until pregnancy has begun, since, by the time a woman knows she is pregnant, the critical time for the formation of a neural tube defect has usually already passed. A physician may prescribe even higher dosages of folic acid (5 mg/day) for women having had a previous pregnancy with a neural tube defect.Neural tube defects can follow patterns of heredity, with direct evidence of autosomal recessive inheritance. As reported by Bruno Reversade and colleagues, the homozygous inactivation of the NUAK2 kinase leads to anencephaly in humans. Animal models indicate a possible association with deficiencies of the transcription factor TEAD2. | Anencephaly is the absence of a major portion of the brain, skull, and scalp that occurs during embryonic development. It is a cephalic disorder that results from a neural tube defect that occurs when the rostral (head) end of the neural tube fails to close, usually between the 23rd and 26th day following conception. Strictly speaking, the Greek term translates as "without a brain" (or totally lacking the inside part of the head), but it is accepted that children born with this disorder usually only lack a telencephalon, the largest part of the brain consisting mainly of the cerebral hemispheres, including the neocortex, which is responsible for cognition. The remaining structure is usually covered only by a thin layer of membrane—skin, bone, meninges, etc., are all lacking. With very few exceptions, infants with this disorder do not survive longer than a few hours or days after birth. Signs and symptoms
The National Institute of Neurological Disorders and Stroke (NINDS) describes the presentation of this condition as follows: "A baby born with anencephaly is usually blind, deaf, unaware of its surroundings and unable to feel pain. Although some individuals with anencephaly may be born with a main brain stem, the lack of a functioning cerebrum permanently rules out the possibility of ever gaining awareness of their surroundings. Reflex actions such as breathing and responses to sound or touch may occur. "Due to the presence of the brainstem, children with anencephaly have almost all the primitive reflexes of a newborn, responding to auditory, vestibular and painful stimuli. | 11
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A study on identification of viruses in bats that could spread to other mammals used the workflow: sequencing of genomic samples → “cleaning” of raw reads → elimination of host reads and eukaryotic contaminants → de novo assembly of the remaining reads → annotation of viral contigs → molecular detection of specific viruses → phylogenetic analysis → interpretation of data.Detecting CST and estimating its rate based on prevalence data is challenging. Due to these difficulties, computational methods are used to analyse CST events and the pathogens associated with them. The explosive development of molecular techniques has opened new possibilities for using phylogenetic analysis of pathogen genetics to infer epidemiological parameters. This provides some insight into the origins of these events and how they could be addressed. Methods of CST prevention are currently using both biological and computational data. An example of this is using both cellular assays and phylogenetic comparisons to support a role for TRIM5α, the product of the TRIM5 gene, in suppressing interspecies transmission and emergence of retroviruses in nature. Analysis
Phylogeny
The comparison of genomic data is very important for the study of cross-species transmission. Phylogenetic analysis is used to compare genetic variation in both pathogens associated with CST and the host species that they infect. Taken together, it is possible to infer what allowed a pathogen to crossover to a new host (i.e. mutation in a pathogen, change in host susceptibility) and how this can be prevented in the future. | The pain has been described as either a hot electric stabbing pain, an ever-increasing pressure sensation around the bones (especially before electrical storms) or as a constant ache that radiates through several long bones at once. Pain may also occur in the hips, wrists, knees and other joints as they essentially just lock-up (often becoming very stiff, immobile and sore), mostly when walking up or down staircases, writing for extended periods of time, or during the colder months of the year. Those with the disease tend to have a very characteristic walk medically diagnosed as a waddling gait. This is observed by the broad-based gait with a duck-like waddle to the swing phase, the pelvis drops to the side of the leg being raised, notable forward curvature of the lumbar spine and a marked body swing.The pain is especially severe during a flare-up, these can be unpredictable, exhausting and last anywhere from a few hours to several weeks. This is a common occurrence for several CED patients, often causing myopathy and extensive sleep deprivation from the chronic, severe and disabling pain. Patients may even require the use of a wheelchair (or additional carers help with getting dressed, showering, mobility/shopping, preparing meals or lifting heavy items) especially when bedridden or housebound for days or weeks at a time. | 0-1
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Use of glue, paint and gasoline became more common after the 1950s. Model airplane glue-sniffing as problematic behavior among youth was first reported in 1959 and increased in the 1960s. Use of aerosol sprays became more common in the 1980s, as older propellants such as CFCs were phased out and replaced by more environmentally friendly compounds such as propane and butane. Most inhalant solvents and gases are not regulated under drug laws such as the United States Controlled Substances Act. However, many US states and Canadian cities have placed restrictions on the sale of some solvent-containing products to minors, particularly for products widely associated with sniffing, such as model cement. The practice of inhaling such substances is sometimes colloquially referred to as huffing, sniffing (or glue sniffing), dusting, or chroming. Australia
Australia has long faced a petrol (gasoline) sniffing problem in isolated and impoverished aboriginal communities. Although some sources argue that sniffing was introduced by United States servicemen stationed in the nations Top End during World War II or through experimentation by 1940s-era Cobourg Peninsula sawmill workers, other sources claim that inhalant abuse (such as glue inhalation) emerged in Australia in the late 1960s. Chronic, heavy petrol sniffing appears to occur among remote, impoverished indigenous communities, where the ready accessibility of petrol has helped to make it a common addictive substance. In Australia, petrol sniffing now occurs widely throughout remote Aboriginal communities in the Northern Territory, Western Australia, northern parts of South Australia, and Queensland. | It also has more consistently observed non-genomic antimineralocorticoid effects relative to spironolactone (see membrane mineralocorticoid receptor). Eplerenone differs from spironolactone in its extensive metabolism, with a short half-life and inactive metabolites.Eplerenone seems to be about 50 to 75% as potent as spironolactone as an antimineralocorticoid. Hence, 25 mg/day spironolactone may be equivalent to approximately 50 mg/day eplerenone. Regulatory and Patent History
Eplerenone was patented in 1983 and approved for medical use in the United States in 2002. Eplerenone is currently approved for sale in Canada, the US, EU, Netherlands and Japan. Eplerenone costs an estimated $2.93 per day when treating congestive heart failure and $5.86 per day when treating hypertension. See also
Finerenone
Mexrenone
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Additionally, heavy drinking over time has been found to have a negative effect on reproductive functioning in women. This results in reproductive dysfunction such as anovulation, decreased ovarian mass, problems or irregularity of the menstrual cycle, and early menopause. Alcoholic ketoacidosis can occur in individuals who chronically misuse alcohol and have a recent history of binge drinking. The amount of alcohol that can be biologically processed and its effects differ between sexes. Equal dosages of alcohol consumed by men and women generally result in women having higher blood alcohol concentrations (BACs), since women generally have a lower weight and higher percentage of body fat and therefore a lower volume of distribution for alcohol than men. Psychiatric
Long-term misuse of alcohol can cause a wide range of mental health problems. Severe cognitive problems are common; approximately 10% of all dementia cases are related to alcohol consumption, making it the second leading cause of dementia. Excessive alcohol use causes damage to brain function, and psychological health can be increasingly affected over time. Social skills are significantly impaired in people with alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The social skills that are impaired by alcohol use disorder include impairments in perceiving facial emotions, prosody, perception problems, and theory of mind deficits; the ability to understand humor is also impaired in people who misuse alcohol. Psychiatric disorders are common in people with alcohol use disorders, with as many as 25% also having severe psychiatric disturbances. | Hurler syndrome, also known as mucopolysaccharidosis Type IH (MPS-IH), Hurlers disease, and formerly gargoylism, is a genetic disorder that results in the buildup of large sugar molecules called glycosaminoglycans (GAGs) in lysosomes. The inability to break down these molecules results in a wide variety of symptoms caused by damage to several different organ systems, including but not limited to the nervous system, skeletal system, eyes, and heart. The underlying mechanism is a deficiency of alpha-L iduronidase, an enzyme responsible for breaking down GAGs. : 544 Without this enzyme, a buildup of dermatan sulfate and heparan sulfate occurs in the body. Symptoms appear during childhood, and early death usually occurs. Other, less severe forms of MPS Type I include Hurler-Scheie Syndrome (MPS-IHS) and Scheie Syndrome (MPS-IS). Hurler syndrome is classified as a lysosomal storage disease. It is clinically related to Hunter syndrome (MPS II); however, Hunter syndrome is X-linked, while Hurler syndrome is autosomal recessive. Signs and symptoms
Children with Hurler syndrome may appear normal at birth and develop symptoms over the first years of life. Symptoms vary between patients.One of the first abnormalities that may be detected is coarsening of the facial features; these symptoms can begin at 3–6 months of age. The head can be large with prominent frontal bones. The skull can be elongated. The nose can have a flattened nasal bridge with continuous nasal discharge. The eye sockets may be widely spaced, and the eyes may protrude from the skull. The lips can be large, and affected children may hold their jaws open constantly. | 0-1
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Pathophysiology
In terms of the mechanism of congenital hyperinsulinism one sees that channel trafficking requires KATP channels need the shielding of ER retention signal.E282K prevents the KATP channel surface expression, the C-terminus (SUR1 subunit) is needed in KATP channel mechanism.R1215Q mutations (ABCC8 gene) affect ADP gating which in turn inhibits KATP channel. Diagnostic
In terms of the investigation of congenital hyperinsulinism, valuable diagnostic information is obtained from a blood sample drawn during hypoglycemia, detectable amounts of insulin during hypoglycemia are abnormal and indicate that hyperinsulinism is likely to be the cause. Inappropriately low levels of free fatty acids and ketones provide additional evidence of insulin excess. An additional piece of evidence indicating hyperinsulinism is a usually high requirement for intravenous glucose to maintain adequate glucose levels, the minimum glucose required to maintain a plasma glucose above 70 mg/dl. A GIR above 8 mg/kg/minute in infancy suggests hyperinsulinism. A third form of evidence suggesting hyperinsulinism is a rise of the glucose level after injection of glucagon at the time of the low glucose.Diagnostic efforts then shift to determining the type- elevated ammonia levels or abnormal organic acids can indicate specific, rare types. Intrauterine growth retardation and other perinatal problems raise the possibility of transience, while large birthweight suggests one of the more persistent conditions. Genetic screening is now available within a useful time frame for some of the specific conditions. It is worthwhile to identify the minority of severe cases with focal forms of hyperinsulinism because these can be completely cured by partial pancreatectomy. | A variety of pre-operative diagnostic procedures have been investigated but none has been established as infallibly reliable. Positron emission tomography is becoming the most useful imaging technique. Differential diagnosis
The differential diagnosis of congenital hyperinsulinism is consistent with PMM2-CDG, as well as several syndromes. Among other diagnoses, the following are listed:
MPI-CDG
Beckwith-Wiedemann syndrome
Sotos syndrome
Usher 1 syndromes
Types
Congenital hyperinsulinism has two types, diffuse and focal, as indicated below:
Treatment
In terms of treatment, acute hypoglycemia is reversed by raising the blood glucose, but in most forms of congenital hyperinsulinism hypoglycemia recurs and the therapeutic effort is directed toward preventing falls and maintaining a certain glucose level. Some of the following measures are often tried:
Corn starch can be used in feeding; unexpected interruptions of continuous feeding regimens can result in sudden hypoglycemia, gastrostomy tube insertion (requires a minor surgical procedure) is used for such feeding. Prolonged glucocorticoid use incurs the many unpleasant side effects of Cushings syndrome, while diazoxide can cause fluid retention requiring concomitant use of a diuretic, and prolonged use causes hypertrichosis. Diazoxide works by opening the KATP channels of the beta cells. Octreotide must be given by injection several times a day or a subcutaneous pump must be inserted every few days, octreotide can cause abdominal discomfort and responsiveness to octreotide often wanes over time. Glucagon requires continuous intravenous infusion, and has a very short half-life.Nifedipine is effective only in a minority, and dose is often limited by hypotension. | 11
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The CSF of patients with treated TB meningitis is commonly abnormal even at 12 months; the rate of resolution of the abnormality bears no correlation with clinical progress or outcome, and is not an indication for extending or repeating treatment; repeated sampling of CSF by lumbar puncture to monitor treatment progress should therefore not be done.Although TB meningitis and TB cerebritis are classified together, the experience of many clinicians is that their progression and response to treatment is not the same. TB meningitis usually responds well to treatment, but TB cerebritis may require prolonged treatment (up to two years) and the steroid course needed is often also prolonged (up to six months). Unlike TB meningitis, TB cerebritis often required repeated CT or MRI imaging of the brain to monitor progress.Central nervous system TB may be secondary to blood-borne spread: therefore some experts advocate the routine sampling of CSF in patients with miliary TB.The anti-TB drugs that are most useful for the treatment of Central nervous system TB are:
INH (CSF penetration 100%)
RMP (10–20%)
EMB (25–50% inflamed meninges only)
PZA (100%)
STM (20% inflamed meninges only)
LZD (20%)
Cycloserine (80–100%)
Ethionamide (100%)
PAS (10–50%) (inflamed meninges only)The use of steroids is routine in TB meningitis (see section below). There is evidence from one poorly designed trial that aspirin may be beneficial, but further work is required before this can be recommended routinely. Steroids
The usefulness of corticosteroids (e.g., prednisolone or dexamethasone) in the treatment of TB is proven for TB meningitis and TB pericarditis. | Another meta-analysis came to a similar conclusion, namely that rifamycin-containing regimens taken for 3 months or longer had a better profile in preventing TB reactivation. Research
There is some evidence from animal and clinical studies that suggests that moxifloxacin-containing regimens as short as four months may be as effective as six months of conventional therapy.Bayer is currently running a phase II clinical trial in collaboration with the TB Alliance to evaluate shorter treatment regimens for TB; encouragingly, Bayer have also promised that if the trials are successful, Bayer will make moxifloxacin affordable and accessible in countries that need it. Another approach for anti-TB drug development, which does not rely on antibiotics, consists of targeting NAD+ synthase, an essential enzyme in tuberculosis bacteria but not in humans. Low level laser therapy for treating tuberculosis is not supported by reliable evidence. History
Streptomycin and para-aminosalicylic acid were developed by the mid-1940s. In 1960, Edinburgh City Hospital physician Sir John Crofton, addressed the Royal College of Physicians in London with a lecture titled "Tuberculosis Undefeated", and proposed that "the disease could be conquered, once and for all". With his colleagues at Edinburgh, he recognised that germs that developed only a mild resistance to one drug was significant. His team showed that when treating new cases of TB, strict compliance to a combination of three therapies, or the triple therapy, (streptomycin, para-aminosalicylic acid and isoniazid) could provide a complete cure. It became known as the Edinburgh method and became standard treatment for at least 15 years. | 11
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Therefore, a lack of testosterone would alter this metabolic process, leading to a decrease in muscle mass.Signs and symptoms of testicular atrophy that are due to a secondary medical condition include:
inflammation
fever
sensitivity or pain of the testicle(s)
nauseaSecondary medical conditions that may cause the signs and symptoms listed above include testicular cancer, chronic alcohol use, sexually transmitted infections, COVID-19, orchitis, varicoceles, or torsion of the testes. Causes
Age
Shrinkage of the testicles is common with advanced age, as overall reproductive function declines. Alcohol use
High alcohol usage lowers testosterone levels by direct damage to the Leydig cells (which produce testosterone) and by affecting hormones involved in signaling to the Leydig cells to produce testosterone. As a result, testicular atrophy is a common feature among individuals with high alcohol use. Testicular malformations and low testosterone levels is also commonly found in people with alcoholic cirrhosis as the negative effect of alcohol use is worsened by the liver damage itself. Excessive alcohol intake can cause inflammation and the degradation of cells in the liver, which can then cause testicular abnormalities (including testicular atrophy). Anabolic steroid use and hormone therapy
Anabolic steroid use and testosterone replacement therapy (TRT) have been found to cause testicular atrophy through similar mechanisms. Anabolic steroids and TRT are both used (either by prescription or illicitly) to mimic the effects of testosterone produced by the body, such as building muscle and maintaining sex drive. | Individuals can get genetic testing done to see if they are a carrier of the trait, and if so may choose to complete genetic counseling to better understand the disorder and help manage family planning. Parents can choose to do prenatal genetic testing for the disorder to determine if their child will have the disease. The only risk factor is if both parents of a child carry the recessive allele linked to the disorder. Mechanism
Individuals with the disorder have a mutation to their fibrinogen gene that prevents the formation of the protein. In normal conditions, fibrinogen is converted to fibrin when it is cleaved by the enzyme thrombin in the blood. The newly formed fibrin forms a fiber-rich network that helps trap red blood cells to start the coagulation process and form a clot. Since there is no fibrinogen present during afibrinogenemia, fibrin can not be formed to aid in this process. Diagnosis
Diagnostic tests
When a problem of fibrinogen is suspected, the following tests can be ordered:
PT
PTT
Fibrinogen level in blood (total and clottable)
Reptilase time
Thrombin timeBlood fibrinogen levels of less than 0.1 g/L and prolonged bleeding test times are indicators of an individual having afibrinogenemia.A suspicion of congenital afibrinogenemia may appear on a platelet aggregation function test. Treatment
The most common treatment is fibrinogen replacement therapy, including cryoprecipitate, blood plasma, and fibrinogen concentration transfusions to help with bleeding episodes or prior to surgery. Although some thrombotic complications have been reported following replacement theory, transfusions of fibrinogen concentrate are widely considered to be the most beneficial. | 0-1
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The presence of eosinophils in the mucous lining of the nose and paranasal sinuses has been demonstrated for many people, and this has been termed eosinophilic mucin rhinosinusitis (EMRS). Cases of EMRS may be related to an allergic response, but allergy is not often documented, resulting in further subcategorization into allergic and nonallergic EMRS.A more recent, and still debated, development in chronic sinusitis is the role that fungi play in this disease. Whether fungi are a definite factor in the development of chronic sinusitis remains unclear, and if they are, what is the difference between those who develop the disease and those who remain free of symptoms. Trials of antifungal treatments have had mixed results.Recent theories of sinusitis indicate that it often occurs as part of a spectrum of diseases that affect the respiratory tract (i.e., the "one airway" theory) and is often linked to asthma.Both smoking and secondhand smoke are associated with chronic rhinosinusitis.Other diseases such as cystic fibrosis and granulomatosis with polyangiitis can also cause chronic sinusitis. Pathophysiology
Biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and interdependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis. | The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.A short-course (3–7 days) of antibiotics seems to be just as effective as the typical longer-course (10–14 days) of antibiotics for those with clinically diagnosed acute bacterial sinusitis without any other severe disease or complicating factors. The IDSA guideline suggest five to seven days of antibiotics is long enough to treat a bacterial infection without encouraging resistance. The guidelines still recommend children receive antibiotic treatment for ten days to two weeks. Corticosteroids
For unconfirmed acute sinusitis, nasal sprays using corticosteroids have not been found to be better than a placebo either alone or in combination with antibiotics. For cases confirmed by radiology or nasal endoscopy, treatment with intranasal corticosteroids alone or in combination with antibiotics is supported. The benefit, however, is small.For confirmed chronic rhinosinusitis, there is limited evidence that intranasal steroids improve symptoms and insufficient evidence that one type of steroid is more effective.There is only limited evidence to support short treatment with corticosteroids by mouth for chronic rhinosinusitis with nasal polyps. There is limited evidence to support corticosteroids by mouth in combination with antibiotics for acute sinusitis; it has only short-term effect improving the symptoms. Surgery
For sinusitis of dental origin, treatment focuses on removing the infection and preventing reinfection, by removal of the microorganisms, their byproducts, and pulpal debris from the infected root canal. | 11
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Cisapride may enhance the absorption, and therefore the sedative activity, of diazepam. Small doses of theophylline may inhibit the action of diazepam. Diazepam may block the action of levodopa (used in the treatment of Parkinsons disease). Diazepam may alter digoxin serum concentrations. Other drugs that may have interactions with diazepam include antipsychotics (e.g. chlorpromazine), MAO inhibitors, and ranitidine. Because it acts on the GABA receptor, the herb valerian may produce an adverse effect. Foods that acidify the urine can lead to faster absorption and elimination of diazepam, reducing drug levels and activity. Foods that alkalinize the urine can lead to slower absorption and elimination of diazepam, increasing drug levels and activity. Reports conflict as to whether food in general has any effects on the absorption and activity of orally administered diazepam. Pharmacology
Diazepam is a long-acting "classical" benzodiazepine. Other classical benzodiazepines include chlordiazepoxide, clonazepam, lorazepam, oxazepam, nitrazepam, temazepam, flurazepam, bromazepam, and clorazepate. Diazepam has anticonvulsant properties. Benzodiazepines act via micromolar benzodiazepine binding sites as calcium channel blockers and significantly inhibit depolarization-sensitive calcium uptake in rat nerve cell preparations.Diazepam inhibits acetylcholine release in mouse hippocampal synaptosomes. This has been found by measuring sodium-dependent high-affinity choline uptake in mouse brain cells in vitro, after pretreatment of the mice with diazepam in vivo. This may play a role in explaining diazepams anticonvulsant properties.Diazepam binds with high affinity to glial cells in animal cell cultures. Diazepam at high doses has been found to decrease histamine turnover in mouse brain via diazepams action at the benzodiazepine-GABA receptor complex. | Polysyndactyly is a hereditary anatomical malformation combining polydactyly and syndactyly. There is also a type called crossed polysyndactyly. Signs and symptoms
The way polysyndactyly presents itself varies; when the webbing is mild, it gives the appearance of the extra digit being partially connected to the (otherwise normal) digit next to it, when the webbing is extreme, the extra digit and the digit next to it will have the appearance of one rather enlarged digit (macrodactyly) and will have two or more finger/toe nails growing in the same digit (polyonychia). How the nails look will also vary, from separate supernumerary finger/toe nails to one very wide finger/toe nail. References
External links
Polysyndactyly and Marfans syndrome The case of an Egyptian Jewish family with 17 affected members. The mother also had Marfans syndrome, which she passed on to a daughter who did not have polysyndactyly. | 0-1
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Life cycle
The adult Spirometra live in the small intestine of the definitive host—a dog, cat, raccoon, or other mammal—for up to 9 years, where they produce many eggs. When the host defecates, the unembryonated eggs leave the body in the feces and hatch when they reach fresh water. The eggs are eaten by copepods (crustaceans of the genus Cyclops), which are the first intermediate hosts. In the copepods, the eggs develop into procercoid larvae that live in the body cavity. The second intermediate hosts include fish, reptiles, or amphibians that consume the copepods. The larvae penetrate the intestinal tract of the second intermediate host, where they become plerocercoid larvae and proliferate to the subcutaneous tissues and muscles. The second intermediate host is eventually eaten by a definitive host predator, such as a dog, and the cycle begins again. Humans are accidental hosts in the cycle, becoming infected with the plerocercoid larvae by contact with or ingestion of the first or second intermediate hosts. The larvae migrate to the subcutaneous tissues in humans; however, no development takes place and the human is not capable of transmitting the disease. In S. proliferum, many larvae, rather than just a few, proliferate throughout the subcutaneous tissues of humans. Diagnosis
Sparganosis is typically diagnosed following surgical removal of the worms, although the infection may also be diagnosed by identification of eosinophilia or identification of the parasite in a tissue specimen. If such biopsy and excision procedures are not feasible, the antisparganum ELISA test may be used. | If untreated, ocular sparganosis can lead to blindness.In one case of brain infestation by Spirometra erinaceieuropaei, a man sought treatment for headaches, seizures, memory flashbacks and strange smells. Magnetic resonance imaging (MRI) scans showed a cluster of rings, initially in the right medial temporal lobe, but moving over time to the other side of the brain. The cause was not determined for four years; ultimately a biopsy was performed and a 1 cm-long tapeworm was found and removed. The patient continued to have symptoms. Transmission
The parasite is transmitted to humans in three different ways. First, humans may acquire the infection by drinking water that is contaminated with copepods housing Spirometra larvae. Second, humans may acquire the infection by consuming the raw flesh of one of the second intermediate hosts, such as frogs or snakes. For example, humans consume raw snakes or tadpoles for medicinal purposes in some Asian cultures; if the snakes or tadpoles are infected, the larvae may be transmitted to humans. Third, humans may acquire the infection by placing raw poultices of the second intermediate hosts on open wounds, lesions, or the eyes for medicinal or ritualistic reasons. If the poultice is infected with plerocercoid larvae, the human may become infected. According to Zunt et al., human infection most often occurs following ingestion of infected raw snake, frog, or pig, although contact with infected flesh of an intermediate host can also cause infection. The high prevalence in Korea may be explained by the ingestion of dog meat. | 11
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Boys are twice as likely as girls to be admitted to hospital. Rotavirus infections occur primarily during cool, dry seasons. The number attributable to food contamination is unknown.Outbreaks of rotavirus A diarrhoea are common among hospitalised infants, young children attending day care centres, and elderly people in nursing homes. An outbreak caused by contaminated municipal water occurred in Colorado in 1981. During 2005, the largest recorded epidemic of diarrhoea occurred in Nicaragua. This unusually large and severe outbreak was associated with mutations in the rotavirus A genome, possibly helping the virus escape the prevalent immunity in the population. A similar large outbreak occurred in Brazil in 1977.Rotavirus B, also called adult diarrhoea rotavirus or ADRV, has caused major epidemics of severe diarrhoea affecting thousands of people of all ages in China. These epidemics occurred as a result of sewage contamination of drinking water. Rotavirus B infections also occurred in India in 1998; the causative strain was named CAL. Unlike ADRV, the CAL strain is endemic. To date, epidemics caused by rotavirus B have been confined to mainland China, and surveys indicate a lack of immunity to this species in the United States. History
In 1943, Jacob Light and Horace Hodes proved that a filterable agent in the faeces of children with infectious diarrhoea also caused scours (livestock diarrhoea) in cattle. Three decades later, preserved samples of the agent were shown to be rotavirus. In the intervening years, a virus in mice was shown to be related to the virus causing scours. | Ellis–Van Creveld syndrome (also called mesoectodermal dysplasia but see Nomenclature section below) is a rare genetic disorder of the skeletal dysplasia type. Signs and symptoms
It involves numerous anomalies including:
Post-axial polydactyly
Congenital heart defects (most commonly an atrial septal defect producing a common atrium, occurring in 60% of affected individuals)
Teeth present at birth (natal teeth)
Fingernail dysplasia
Short-limbed dwarfism, mesomelic pattern
Short ribs
Cleft palate
Malformation of the wrist bones (fusion of the hamate and capitate bones). Genetics
Ellis–Van Creveld syndrome often is the result of founder effects in isolated human populations, such as the Amish and some small island inhabitants. Although relatively rare, this disorder does occur with higher incidence within founder-effect populations due to lack of genetic variability. Observation of the inheritance pattern has illustrated that the disease is autosomal recessive, meaning that both parents have to carry the gene in order for an individual to be affected by the disorder.Ellis–Van Creveld syndrome is caused by a mutation in the EVC gene, as well as by a mutation in a nonhomologous gene, EVC2, located close to the EVC gene in a head-to-head configuration. The gene was identified by positional cloning. The EVC gene maps to the chromosome 4 short arm (4p16). The function of a healthy EVC gene is not well understood at this time. Relation to other rare disorders: genetic ciliopathy
Until recently, the medical literature did not indicate a connection among many genetic disorders, both genetic syndromes and genetic diseases, that are now being found to be related. | 0-1
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Another way the Norris lab is attempting to find this gene is by looking at genes involved in the formation of the aorta and mitral valves, as these valves are often prolapsed or malformed as a symptom of EDS. Because hEDS is such a complex, multi-organ disease, focusing on one hallmark trait has proven successful. One gene found this way is DZIP1, which regulates cardiac valve development in mammals through a Cby1-beta-catenin mechanism. Mutations at this gene affect the beta-catenin cascade involved in development, causing malformation of the extra-cellular matrix, resulting in loss of collagen. A lack of collagen here is both consistent with hEDS and explains the "floppy" mitral and aortic valve heart defects. A second genetic study specific to mitral valve prolapse focused on the PDGF signaling pathway, which is involved in growth factor ligands and receptor isoforms. Mutations in this pathway affect the ability to localize cilia in various cell types, including cardiac cells. With the resulting ciliopathies, structures such as the cardiac outflow tract, heart tube assembly, and cardiac fusion are limited and/or damaged. Classical EDS
Classical EDS (formerly categorized as type 1) is characterized by extremely elastic skin that is fragile and bruises easily and hypermobility of the joints. Molluscoid pseudotumors (calcified hematomas that occur over pressure points) and spheroids (cysts that contain fat occurring over forearms and shins) are also often seen. A side complication of the hyperelasticity presented in many EDS cases makes wounds closing on their own more difficult. Sometimes, motor development is delayed and hypotonia occurs. | Further out into the fibrous shell there is a zone that contains T cells and plasma cells in association with blood vessels. The histology of pulmonary nodules are similar to that of subcutaneous nodules, with central necrosis surrounded by palisading macrophages and inflammatory infiltrate. Risk Factors
Rheumatoid nodules develop if a person currently has rheumatoid arthritis. However, not all people with rheumatoid arthritis develop rheumatoid nodules. Some risk factors for rheumatoid nodules for people with rheumatoid arthritis may include:
Smoking (strong association)
Elevated levels of serum rheumatoid factors
HLA-DRB1 gene (weak association)
Trauma to small vessels
Having severe rheumatoid arthritis
Taking Methotrexate over other arthritis drugs
Diagnosis
Differential diagnosis of rheumatoid nodules can be classified from localization, depth pathology, age of onset, persistence, rheumatoid factor, concomitant joint disease, and bone erosions. Diagnosis is typically determined clinically by a rheumatologist. Rheumatoid arthritis associated rheumatoid nodules are typically subcutaneous and occur at extensor sites. The onset typically starts in adulthood and presents with rheumatoid factors and bone erosions, and concomitant joint diseases. The pathology is characterized by central necrosis, palisading mononuclear cells, and perivascular lymphocytic infiltrations.Rheumatoid nodulosis is characterized by multiple subcutaneous nodules presenting with rheumatoid factors but an absence of joint complaints. The nodules are typically small and concentrated on the extensor sites of the hands and feet, sometimes accompanied by bone erosions. The onset typically starts in adulthood with a pathology similar to rheumatoid arthritis associated rheumatoid nodules.Benign rheumatoid nodules are often not associated with rheumatoid factors or concomitant joint diseases. They are typically found on the feet, scalp, and pretibial regions. | 0-1
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Bleeding is more frequent and severe in women of child-bearing age; these women may suffer miscarriages, menometrorrhagia, and excessive bleeding during child birth and/or the postpartum period. Excessive bleeding following major or minor surgery, including dental extractions, occurs in both females and males with the disorder. Thrombotic complications of the disorder are often (~50%) recurrent and can involve central and peripheral arteries, deep and superficial veins. Thrombotic events may be serious and involve occlusion of a cerebral artery leading to stroke, splanchnic venous thrombosis, and pulmonary thrombosis presumptively secondary to deep vein thrombosis. Fibrinogen
Circulating fibrinogen is a glycoprotein made of two trimers each of which is composed of three polypeptide chains, Aα (also termed α) encoded by the FGA gene, Bβ (also termed β) encoded by the FGB gene, and γ encoded by the FGG gene. All three genes are located on the long or "q" arm of human chromosome 4 (at positions 4q31.3, 4q31.3, and 4q32.1, respectively) and are the sites where mutations occur that code for a dysfunctional fibrinogen and/or reduced fibrinogen levels which are the cause of congenital hypodysfibrinogenemia. Pathophysiology
Congenital hypodysfibrinogenemia is inherited as an autosomal dominant disorder caused by at least 32 different types of single mutations. Ten of these mutations are in the fibrinogen alpha chain gene (also termed the FGA gene), 5 in the fibrinogen beta chain gene (also termed the FGB gene), and 17 in the fibrinogen gamma chain gene (also termed the FGG gen). | Sandifer syndrome (or Sandifers syndrome) is an eponymous paediatric medical disorder, characterised by gastrointestinal symptoms and associated neurological features. There is a significant correlation between the syndrome and gastro-oesophageal reflux disease (GORD); however, it is estimated to occur in less than 1% of children with reflux. Symptoms and signs
Onset is usually confined to infancy and early childhood, with peak prevalence at 18–36 months. In rare cases, particularly where the child is severely mentally impaired, onset may extend to adolescence.The classical symptoms of the syndrome are spasmodic torticollis and dystonia. Nodding and rotation of the head, neck extension, gurgling, writhing movements of the limbs, and severe hypotonia have also been noted.Spasms may last for 1–3 minutes and may occur up to 10 times a day. Ingestion of food is often associated with occurrence of symptoms; this may result in reluctance to feed. Associated symptoms, such as epigastric discomfort, vomiting (which may involve blood) and abnormal eye movements have been reported. Clinical signs may also include anaemia. Diagnosis
Diagnosis is made on the basis of the association of gastro-oesophageal reflux with the characteristic movement disorder. Neurological examination is usually normal. Misdiagnosis as benign infantile spasms or epileptic seizures is common, particularly where clear signs or symptoms of gastro-oesophageal reflux are not apparent. Early diagnosis is critical, as treatment is simple and leads to prompt resolution of the movement disorder. Treatment
Successful treatment of the associated underlying disorder, such as GORD or hiatus hernia, may provide relief. Prognosis
Sandifer syndrome is not typically life-threatening and the prognosis is typically good. | 0-1
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Heparin-induced thrombocytopenia (HIT) is the development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin, an anticoagulant. HIT predisposes to thrombosis (the abnormal formation of blood clots inside a blood vessel) because platelets release microparticles that activate thrombin, thereby leading to thrombosis. When thrombosis is identified the condition is called heparin-induced thrombocytopenia and thrombosis (HITT). HIT is caused by the formation of abnormal antibodies that activate platelets. If someone receiving heparin develops new or worsening thrombosis, or if the platelet count falls, HIT can be confirmed with specific blood tests.The treatment of HIT requires stopping heparin treatment, and both protection from thrombosis and choice of an agent that will not reduce the platelet count any further. Several alternatives are available for this purpose; mainly used are danaparoid, fondaparinux, argatroban, and bivalirudin.While heparin was discovered in the 1930s, HIT was not reported until the 1960s. Signs and symptoms
Heparin may be used for both prevention and the treatment of thrombosis. It exists in two main forms: an "unfractionated" form that can be injected under the skin (subcutaneously) or through an intravenous infusion, and a "low molecular weight" form that is generally given subcutaneously. Commonly used low molecular weight heparins are enoxaparin, dalteparin, nadroparin and tinzaparin.In HIT, the platelet count in the blood falls below the normal range, a condition called thrombocytopenia. However, it is generally not low enough to lead to an increased risk of bleeding. Most people with HIT, therefore, do not experience any symptoms. | Body odor or body odour (BO) is present in all animals and its intensity can be influenced by many factors (behavioral patterns, survival strategies). Body odor has a strong genetic basis, but can also be strongly influenced by various diseases and physiological conditions. Though body odor has played an important role (and continues to do so in many life forms) in early humankind, it is generally considered to be an unpleasant odor amongst many human cultures. Causes
In humans, the formation of body odors is caused by factors such as diet, sex, health, and medication, but the major contribution comes from bacterial activity on skin gland secretions. Humans have three types of sweat glands: eccrine sweat glands, apocrine sweat glands and sebaceous glands. Eccrine sweat glands are present from birth, while the latter two become activated during puberty. Among the different types of human skin glands, body odor is primarily the result of the apocrine sweat glands, which secrete the majority of chemical compounds that the skin flora metabolize into odorant substances. This happens mostly in the axillary (armpit) region, although the gland can also be found in the areola, anogenital region, and around the navel. In humans, the armpit regions seem more important than the genital region for body odor, which may be related to human bipedalism. | 0-1
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Vitreous touch syndrome is a late complication of intra capsular cataract extraction wherein the vitreous bulges through the pupillary aperture, and touches and attaches to the corneal endothelium. References
Further reading
Dr. Kushal Banerjee (2006). "A review and clinical evaluation of per-operative and post-operative complications in case of manual small incision cataract surgery and extracapsular cataract extraction with posterior chamber intra-ocular lens implantation" (PDF). Archived from the original (PDF) on 5 June 2014. Retrieved 1 June 2014. Dissertation submitted Rajib Gandhi University of Health Sciences
== External links == | Cilostazol, sold under the brand name Pletal among others, is a medication used to help the symptoms of intermittent claudication in peripheral vascular disease. If no improvement is seen after 3 months, stopping the medication is reasonable. It may also be used to prevent stroke. It is taken by mouth.Common side effects include headache, diarrhea, dizziness, and cough. Serious side effects may include decreased survival in those with heart failure, low platelets, and low white blood cells. Cilostazol is a phosphodiesterase 3 inhibitor which works by inhibiting platelet aggregation and dilating arteries.Cilostazol was approved for medical use in the United States in 1999. It is available as a generic medication. In 2017, it was the 301st most commonly prescribed medication in the United States, with more than one million prescriptions. Medical uses
Cilostazol is approved for the treatment of intermittent claudication in the United States and United Kingdom.Cilostazol is also used for secondary stroke prevention, though to date no regulatory body has approved it specifically for that indication. Heart failure
Cilostazol is dangerous for people with severe heart failure. Cilostazol has been studied in people without heart failure, without evidence of harm, but much more data would be needed to determine no risk exists. Although cilostazol would not be approvable for a trivial condition the Cardio-Renal Advisory Committee and FDA concluded that fully informed patients and physicians should be able to choose to use it to treat intermittent claudication. Patient and physician labeling will describe the basis for concern and the incomplete information available. | 0-1
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A tear of a meniscus is a rupturing of one or more of the fibrocartilage strips in the knee called menisci. When doctors and patients refer to "torn cartilage" in the knee, they actually may be referring to an injury to a meniscus at the top of one of the tibiae. Menisci can be torn during innocuous activities such as walking or squatting. They can also be torn by traumatic force encountered in sports or other forms of physical exertion. The traumatic action is most often a twisting movement at the knee while the leg is bent. In older adults, the meniscus can be damaged following prolonged wear and tear. Especially acute injuries (typically in younger, more active patients) can lead to displaced tears which can cause mechanical symptoms such as clicking, catching, or locking during motion of the joint. The joint will be in pain when in use, but when there is no load, the pain goes away. A tear of the medial meniscus can occur as part of the unhappy triad, together with a tear of the anterior cruciate ligament and medial collateral ligament. Signs and symptoms
The common signs and symptoms of a torn meniscus are knee pain, particularly along the joint line, and swelling. These are worse when the knee bears more weight (for example, when running). Another typical complaint is joint locking, when the affected person is unable to straighten the leg fully. This can be accompanied by a clicking feeling. | Diagnosis
Syringomas can often be diagnosed clinically based on presentation, distribution patterns over the body, lack of associated symptoms, and family history. A definitive diagnosis requires a skin biopsy to allow the tissue to be examined under a microscope. Histologically, syringomas have a characteristic comma-shaped ("tadpole") tail of dilated, cystic eccrine ducts. Treatment
The goal of treatment is to improve the appearance of lesions, since they are otherwise not serious and typically do not cause symptoms. Many treatment methods have been attempted, but complete removal is uncommon. No single treatment method has been shown to work consistently. Both medical and surgical treatments have been studied, each with variable success. Common destructive treatment methods include carbon dioxide lasers, dermabrasion, surgical excision, electrocoagulation, and chemical peels. Many of these methods are very time-consuming and require multiple treatment sessions. Carbon dioxide lasers are the most commonly practiced method; they can cause thermal damage, though, leading to scarring in the area. Medical therapies include topical atropine, topical retinoids, and oral tranilast. The most common adverse effects include redness, skin discoloration, and pain. Other side effects include blistering and scarring. See also
Acrospiroma
List of cutaneous conditions
List of cutaneous neoplasms associated with systemic syndromes
References
External links
eMedicine entry on syringomas
DermNet NZ | 0-1
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Auricular hypertrichosis (hypertrichosis lanuginosa acquisita, hypertrichosis pinnae auris) is a genetic condition expressed as long and strong hairs growing from the helix of the pinna. Presentation
Ear hair generally refers to the terminal hair arising from follicles inside the external auditory meatus in humans. In its broader sense, ear hair may also include the fine vellus hair covering much of the ear, particularly at the prominent parts of the anterior ear, or even the abnormal hair growth as seen in hypertrichosis and hirsutism. Medical research on the function of ear hair is currently very scarce. Hair growth within the ear canal is often observed to increase in older men, together with increased growth of nose hair. Excessive hair growth within or on the ear is known medically as auricular hypertrichosis. Some men, particularly in the male population of India, have coarse hair growth along the lower portion of the helix, a condition referred to as "having hairy pinnae" (hypertrichosis lanuginosa acquisita). Genetics
The genetic basis of auricular hypertrichosis has not been settled. Some researchers have proposed a Y-linked pattern of inheritance and others have suggested an autosomal gene is responsible. A third hypothesis predicts the phenotype results from the interaction of two loci, one on the homologous part of the X and Y and one on the nonhomologous sequence of the Y. These hypotheses are not mutually exclusive, and there may be a variety of genetic mechanisms underlying this phenotype. Lee et al. | Nadolol, sold under the brand name Corgard among others, is a medication used to treat high blood pressure, heart pain, atrial fibrillation, and some inherited arrhythmic syndromes. It has also been used to prevent migraine headaches and complications of cirrhosis. It is taken orally.Common side effects include dizziness, feeling tired, a slow heart rate, and Raynaud syndrome. Serious side effects may include heart failure and bronchospasm. Its use in pregnancy and breastfeeding is of unclear safety. It is a non-selective beta blocker and works by blocking β1-adrenergic receptors in the heart and β2-adrenergic receptors in blood vessels.Nadolol was patented in 1970 and came into medical use in 1978. It is available as a generic medication. In 2016, it was the 283rd most commonly prescribed medication in the United States, with more than a million prescriptions. Medical uses
Nadolol is used to treat hypertension and for long-term treatment of angina pectoris and is approved by the FDA for these purposes.It is regularly used off-label for control of heart rate in people with atrial fibrillation, prevention of migraine headaches; prevention of bleeding veins in people with portal hypertension caused by cirrhosis; and to treat people with high levels of thyroid hormone.Nadolol is the preferred beta-blockers in the management of patients with LQTS for prevention of ventricular arrhythmia. It is more efficacious than selective beta blockers or propranolol in the prevention of breakthrough cardiac events. | 0-1
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Thus any cause that influences the rate or volume of air entering the lungs (ventilation) or any cause that influences the transfer of air from the lungs to the blood may cause hypoxemia. As well as these respiratory causes, cardiovascular causes such as shunts may also result in hypoxemia. Hypoxemia is caused by five categories of etiologies: hypoventilation, ventilation/perfusion mismatch, right-to-left shunt, diffusion impairment, and low PO2. Low PO2 and hypoventilation are associated with a normal alveolar–arterial gradient (A-a gradient) whereas the other categories are associated with an increased A-a gradient. : 229
Ventilation
If the alveolar ventilation is low, there will not be enough oxygen delivered to the alveoli for the bodys use. This can cause hypoxemia even if the lungs are normal, as the cause is in the brainstems control of ventilation or in the bodys inability to breathe effectively. Respiratory drive
Respiration is controlled by centers in the medulla, which influence the rate of breathing and the depth of each breath. This is influenced by the blood level of carbon dioxide, as determined by central and peripheral chemoreceptors located in the central nervous system and carotid and aortic bodies, respectively. Hypoxia occurs when the breathing center doesnt function correctly or when the signal is not appropriate:
Strokes, epilepsy and cervical neck fractures can all damage the medullary respiratory centres that generates rhythmic impulses and transmit them along the phrenic nerve to the diaphragm, the muscle that is responsible for breathing. | These results suggest that 5-HT7 receptor antagonism mediates the antidepressant effects of amisulpride.Amisulpride also appears to bind with high affinity to the serotonin 5-HT2B receptor (Ki = 13 nM), where it acts as an antagonist. The clinical implications of this, if any, are unclear. In any case, there is no evidence that this action mediates any of the therapeutic effects of amisulpride.Amisulpride shows stereoselectivity in its actions. Aramisulpride ((R)-amisulpride) has higher affinity for the 5-HT7 receptor (Ki = 47 nM vs. 1,900 nM) while esamisulpride ((S)-amisulpride) has higher affinity for the D2 receptor (4.0 nM vs. 140 nM). An 85:15 ratio of aramisulpride to esamisulpride (SEP-4199) which provides more balanced 5-HT7 and D2 receptor antagonism than racemic amisulpride (50:50 ratio of enantiomers) is under development for the treatment of bipolar depression. Society and culture
Brand names
Brand names include: Amazeo, Amipride (AU), Amival, Solian (AU, IE, RU, UK, ZA), Soltus, Sulpitac (IN), Sulprix (AU), Midora (RO) and Socian (BR). Availability
Amisulpride was not approved by the Food and Drug Administration for use in the United States until February 2020, but it is used in Europe, Israel, Mexico, India, New Zealand and Australia to treat psychosis and schizophrenia.An IV formulation of Amisulpride was approved for the treatment of postoperative nausea and vomiting ("PONV") in the United States in February 2020. History
The U.S. Food and Drug Administration (FDA) approved amisulpride based on evidence from four clinical trials of 2323 subjects undergoing surgery or experiencing nausea and vomiting after the surgery. | 0-1
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Prevention
Michael Beach, a recreational waterborne illness specialist for the Centers for Disease Control and Prevention, stated in remarks to the Associated Press that wearing of nose clips to prevent insufflation of contaminated water would be effective protection against contracting PAM, noting that "Youd have to have water going way up in your nose to begin with".Advice stated in the press release from Taiwans Centers for Disease Control recommended people prevent fresh water from entering the nostrils and avoid putting their heads down into fresh water or stirring mud in the water with feet. When starting to suffer from fever, headache, nausea, or vomiting subsequent to any kind of exposure to fresh water, even in the belief that no fresh water has traveled through the nostrils, people with such conditions should be carried to hospital quickly and make sure doctors are well-informed about the history of exposure to fresh water. Treatment
On the basis of the laboratory evidence and case reports, heroic doses of amphotericin B have been the traditional mainstay of PAM treatment since the first reported survivor in the United States in 1982.Treatment has often also used combination therapy with multiple other antimicrobials in addition to amphotericin, such as fluconazole, miconazole, rifampicin and azithromycin. They have shown limited success only when administered early in the course of an infection. | Dacryoadenitis is inflammation of the lacrimal glands. Symptoms
Swelling of the outer portion of the upper lid, with possible redness and tenderness
Pain in the area of swelling
Excess tearing or discharge
Swelling of lymph nodes in front of the ear
Complications
Swelling may be severe enough to put pressure on the eye and distort vision. Some patients first thought to have dacryoadenitis may turn out to have a malignancy of the lacrimal gland. Causes
Acute dacryoadenitis is most commonly due to viral or bacterial infection. Common causes include mumps, Epstein-Barr virus, staphylococcus, and gonococcus. Chronic dacryoadenitis is usually due to noninfectious inflammatory disorders. Examples include sarcoidosis, thyroid eye disease, and orbital pseudotumor. Diagnosis
Dacryoadenitis can be diagnosed by examination of the eyes and lids. Special tests such as a CT scan may be required to search for the cause. Sometimes biopsy will be needed to be sure that a tumor of the lacrimal gland is not present. Prevention
Mumps can be prevented by immunization. Gonococcus, bacteria can be avoided by the use of condoms. Most other causes cannot be prevented. Treatment
If the cause of dacryoadenitis is a viral condition such as mumps, simple rest and warm compresses may be all that is needed. For other causes, the treatment is specific to the causative disease. Prognosis
Most patients will fully recover from dacryoadenitis. For conditions with more serious causes, such as sarcoidosis, the prognosis is that of the underlying condition. References
External links
Source (NIH/Medline)
eMedicine
Diseases Database (DDB): 3430 | 0-1
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Bioethics
A person in a coma is said to be in an unconscious state. Perspectives on personhood, identity and consciousness come into play when discussing the metaphysical and bioethical views on comas. It has been argued that unawareness should be just as ethically relevant and important as a state of awareness and that there should be metaphysical support of unawareness as a state.In the ethical discussions about disorders of consciousness (DOCs), two abilities are usually considered as central: experiencing well-being and having interest. Well-being can broadly be understood as the positive effect related to what makes life good (according to specific standards) for the individual in question. The only condition for well-being broadly considered is the ability to experience its ‘positiveness’. That said, because experiencing positiveness is a basic emotional process with phylogenetic roots, it is likely to occur at a completely unaware level and therefore, introduces the idea of an unconscious well-being. As such, the ability of having interests, is crucial for describing two abilities which those with comas are deficient in. Having an interest in a certain domain can be understood as having a stake in something that can affect what makes our life good in that domain. An interest is what directly and immediately improves life from a certain point of view or within a particular domain, or greatly increases the likelihood of life improvement enabling the subject to realize some good. That said, sensitivity to reward signals is a fundamental element in the learning process, both consciously and unconsciously. | Body-focused repetitive behavior (BFRB) is an umbrella name for impulse control behaviors involving compulsively damaging ones physical appearance or causing physical injury.Body-focused repetitive behavior disorders (BFRBDs) in ICD-11 is in development.BFRB disorders are currently estimated to be under the obsessive-compulsive spectrum. They are also associated with ADHD and anxiety. Causes
The cause of BFRBs is unknown.Emotional variables may have a differential impact on the expression of BFRBs.Research has suggested that the urge to repetitive self-injury is similar to a body-focused repetitive behavior but others have argued that for some the condition is more akin to a substance abuse disorder.Researchers are investigating a possible genetic component. Onset
BFRBs most often begin in late childhood or in the early teens. Diagnosis
Types
The main BFRB disorders are:
Skin
Dermatillomania (excoriation disorder), skin picking
Dermatophagia, skin nibbling
Mouth
Morsicatio buccarum, cheek biting
Morsicatio labiorum, inner lip biting
Morsicatio linguarum, tongue biting
Hands
Onychophagia, nail biting
Onychotillomania, nail picking
Nose
Rhinotillexomania, compulsive nose picking
Hair
Trichophagia, hair nibbling
Trichotemnomania, hair cutting
Trichotillomania, hair pulling
Eyes
Mucus fishing syndrome - compulsion to remove or "fish" strands of mucus from the eye
Treatment
Psychotherapy
Treatment can include behavior modification therapy, medication, and family therapy. The evidence base criteria for BFRBs is strict and methodical. Individual behavioral therapy has been shown as a "probably effective" evidence-based therapy to help with thumb sucking, and possibly nail biting. Cognitive behavioral therapy was cited as experimental evidence based therapy to treat trichotillomania and nail biting; a systematic review found best evidence for habit reversal training and decoupling. Another form of treatment that focuses on mindfulness, stimuli and rewards has proven effective in some people. | 0-1
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Some of the clinical findings described in their first papers do not match current criteria for Creutzfeldt–Jakob disease, and it has been speculated that at least two of the people in initial studies had a different ailment. An early description of familial CJD stems from the German psychiatrist and neurologist Friedrich Meggendorfer (1880–1953). A study published in 1997 counted more than 100 cases worldwide of transmissible CJD and new cases continued to appear at the time.The first report of suspected iatrogenic CJD was published in 1974. Animal experiments showed that corneas of infected animals could transmit CJD, and the causative agent spreads along visual pathways. A second case of CJD associated with a corneal transplant was reported without details. In 1977, CJD transmission caused by silver electrodes previously used in the brain of a person with CJD was first reported. Transmission occurred despite the decontamination of the electrodes with ethanol and formaldehyde. Retrospective studies identified four other cases likely of similar cause. The rate of transmission from a single contaminated instrument is unknown, although it is not 100%. In some cases, the exposure occurred weeks after the instruments were used on a person with CJD. In the 1980s it was discovered that Lyodura, a dura mater transplant product, was shown to transmit CJD from the donor to the recipient. | Medical uses
Anticholinergic drugs are used to treat a variety of conditions:
Dizziness (including vertigo and motion sickness-related symptoms)
Extrapyramidal symptoms, a potential side-effect of antipsychotic medications
Gastrointestinal disorders (e.g., peptic ulcers, diarrhea, pylorospasm, diverticulitis, ulcerative colitis, nausea, and vomiting)
Genitourinary disorders (e.g., cystitis, urethritis, and prostatitis)
Insomnia, although usually only on a short-term basis
Respiratory disorders (e.g., asthma, chronic bronchitis, and chronic obstructive pulmonary disease [COPD])
Sinus bradycardia due to a hypersensitive vagus nerve
Organophosphate based nerve agent poisoning, such as VX, sarin, tabun, and soman (atropine is favoured in conjunction with an oxime, usually pralidoxime)Anticholinergics generally have antisialagogue effects (decreasing saliva production), and most produce some level of sedation, both being advantageous in surgical procedures.Until the beginning of the 20th century anticholinergic drugs were widely used to treat psychiatric disorders. Physiological effects
Delirium (often with hallucinations and delusions indistinguishable from reality)
Ocular symptoms (from eye drops): mydriasis, pupil dilation, and acute angle-closure glaucoma in those with shallow anterior chamber
Anhidrosis, dry mouth, dry skin
Fever
Constipation
Tachycardia
Urinary retention
Cutaneous vasodilationClinically the most significant feature is delirium, particularly in the elderly, who are most likely to be affected by the toxidrome. Side effects
Long-term use may increase the risk of both cognitive and physical decline. It is unclear whether they affect the risk of death generally. However, in older adults they do appear to increase the risk of death.Possible effects of anticholinergics include:
Possible effects in the central nervous system resemble those associated with delirium, and may include:
Older patients are at a higher risk of experiencing CNS side effects. | 0-1
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Gephyrophobia is the anxiety disorder or specific phobia characterized by the fear of bridges and tunnels. As a result, sufferers of gephyrophobia may avoid routes that will take them over bridges, or if they are a passenger, will act very apprehensively when passing over a bridge. The term gephyrophobia comes from the Greek γέφυρα (gephura), meaning "bridge", and φόβος (phobos), meaning "fear".Some possible manifestations of gephyrophobia may be fear of driving off the bridge, fear of a gust of wind blowing one off the bridge, or fear that the bridge will collapse when crossing it (e.g., fear that the bridge lacks structural integrity). The fear overlaps with acrophobia (the fear of heights) as gephyrophobia tends to be exacerbated in taller bridges as compared to those closer to the water or ground beneath. Dr. Michael Liebowitz, founder of the Anxiety Disorders Clinic at the New York State Psychiatric Institute, says, "Its not an isolated phobia, but usually part of a larger constellation ... Its people who get panic attacks. You get light-headed, dizzy; your heart races. You become afraid that youll feel trapped." It is a situational phobia.As of 2008, the New York State Thruway Authority would lead gephyrophobiacs over the Tappan Zee Bridge. A driver could call the authority in advance and arrange for someone to drive their car over the bridge for them. | The authority performed the service about six times a year.The Maryland Transportation Authority previously offered a similar service for crossing the Chesapeake Bay Bridge, but that role is now filled by private companies.The Mackinac Bridge Authority, which oversees the Mackinac Bridge connecting Michigans Upper and Lower peninsulas, will drive needy gephyrophobiacs cars across the bridge for a nominal fee. Some one thousand drivers take advantage of this program annually. Leslie Ann Pluhar had her Yugo blown off the bridge in 1989. Later investigation concluded she had stopped her car over the open steel grating on the bridges span and that a gust of wind blowing through the grating pushed her vehicle off the bridge, but this assertion is not supported by recorded wind speed measurements taken on and around the bridge at the time of the accident. In media
Gephyrophobia is the main plot in "The Bridge" episode of The Middle. The character Brick is plagued by the phobia. In 1965s A Charlie Brown Christmas, Lucy references gephyrophobia (albeit with a slight mispronunciation) when attempting to diagnose Charlie Browns problems at her psychiatric help stand. See also
Galloping Gertie
List of bridge disasters
List of structural failures and collapses
List of phobias
== References == | 11
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For example, a primary viral infection that weakens the immune system could lead to a secondary bacterial infection. Similarly, a primary burn that creates an open wound could provide an entry point for bacteria, and lead to a secondary bacterial infection. Terminal disease
A terminal disease is one that is expected to have the inevitable result of death. Previously, AIDS was a terminal disease; it is now incurable, but can be managed indefinitely using medications. Illness
The terms illness and sickness are both generally used as synonyms for disease; however, the term illness is occasionally used to refer specifically to the patients personal experience of his or her disease. In this model, it is possible for a person to have a disease without being ill (to have an objectively definable, but asymptomatic, medical condition, such as a subclinical infection, or to have a clinically apparent physical impairment but not feel sick or distressed by it), and to be ill without being diseased (such as when a person perceives a normal experience as a medical condition, or medicalizes a non-disease situation in his or her life – for example, a person who feels unwell as a result of embarrassment, and who interprets those feelings as sickness rather than normal emotions). Symptoms of illness are often not directly the result of infection, but a collection of evolved responses – sickness behavior by the body – that helps clear infection and promote recovery. Such aspects of illness can include lethargy, depression, loss of appetite, sleepiness, hyperalgesia, and inability to concentrate. | The risks, benefits, and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Vaccine
No vaccines are currently available to protect against S. pyogenes infection, although research is underway to develop one. Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine. Infection
People with positive cultures for Streptococcus pyogenes should be treated with penicillin as long as allergy is not present. The use of antibiotics will not alter cardiac involvement in the development of rheumatic fever. Some suggest the use of benzathine benzylpenicillin.Monthly injections of long-acting penicillin must be given for a period of five years in patients having one attack of rheumatic fever. If there is evidence of carditis, the length of therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence. Inflammation
While corticosteroids are often used, evidence to support this is poor. Salicylates are useful for pain.Steroids are reserved for cases where there is evidence of an involvement of the heart. The use of steroids may prevent further scarring of tissue and may prevent the development of sequelae such as mitral stenosis. | 0-1
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Step therapy or stepladder therapy is a specific type of prioritization by lines of therapy. It is controversial in American health care because unlike conventional decision-making about what constitutes first-line, second-line, and third-line therapy, which in the U.S. reflects safety and efficacy first and cost only according to the patients wishes, step therapy attempts to mix cost containment by someone other than the patient (third-party payers) into the algorithm. Therapy freedom and the negotiation between individual and group rights are involved. | By intent
By therapy composition
Treatments can be classified according to the method of treatment:
By matter
by drugs: pharmacotherapy, chemotherapy (also, medical therapy often means specifically pharmacotherapy)
by medical devices: implantation
cardiac resynchronization therapy
by specific molecules: molecular therapy (although most drugs are specific molecules, molecular medicine refers in particular to medicine relying on molecular biology)
by specific biomolecular targets: targeted therapy
molecular chaperone therapy
by chelation: chelation therapy
by specific chemical elements:
by metals:
by heavy metals:
by gold: chrysotherapy (aurotherapy)
by platinum-containing drugs: platin therapy
by biometals
by lithium: lithium therapy
by potassium: potassium supplementation
by magnesium: magnesium supplementation
by chromium: chromium supplementation; phonemic neurological hypochromium therapy
by copper: copper supplementation
by nonmetals:
by diatomic oxygen: oxygen therapy, hyperbaric oxygen therapy (hyperbaric medicine)
transdermal continuous oxygen therapy
by triatomic oxygen (ozone): ozone therapy
by fluoride: fluoride therapy
by other gases: medical gas therapy
by water:
hydrotherapy
aquatic therapy
rehydration therapy
oral rehydration therapy
water cure (therapy)
by biological materials (biogenic substances, biomolecules, biotic materials, natural products), including their synthetic equivalents: biotherapy
by whole organisms
by viruses: virotherapy
by bacteriophages: phage therapy
by animal interaction: see animal interaction section
by constituents or products of organisms
by plant parts or extracts (but many drugs are derived from plants, even when the term phytotherapy is not used)
scientific type: phytotherapy
traditional (prescientific) type: herbalism
by animal parts: quackery involving shark fins, tiger parts, and so on, often driving threat or endangerment of species
by genes: gene therapy
gene therapy for epilepsy
gene therapy for osteoarthritis
gene therapy for color blindness
gene therapy of the human retina
gene therapy in Parkinsons disease
by epigenetics: epigenetic therapy
by proteins: protein therapy (but many drugs are proteins despite not being called protein therapy)
by enzymes: enzyme replacement therapy
by hormones: hormone therapy
hormonal therapy (oncology)
hormone replacement therapy
estrogen replacement therapy
androgen replacement therapy
hormone replacement therapy (menopause)
transgender hormone therapy
feminizing hormone therapy
masculinizing hormone therapy
antihormone therapy
androgen deprivation therapy
by whole cells: cell therapy (cytotherapy)
by stem cells: stem cell therapy
by immune cells: see immune system products below
by immune system products: immunotherapy, host modulatory therapy
by immune cells:
T-cell vaccination
cell transfer therapy
autologous immune enhancement therapy
TK cell therapy
by humoral immune factors: antibody therapy
by whole serum: serotherapy, including antiserum therapy
by immunoglobulins: immunoglobulin therapy
by monoclonal antibodies: monoclonal antibody therapy
by urine: urine therapy (some scientific forms; many prescientific or pseudoscientific forms)
by food and dietary choices:
medical nutrition therapy
grape therapy (quackery)
by salts (but many drugs are the salts of organic acids, even when drug therapy is not called by names reflecting that)
by salts in the air
by natural dry salt air: "taking the cure" in desert locales (especially common in prescientific medicine; for example, one 19th-century way to treat tuberculosis)
by artificial dry salt air:
low-humidity forms of speleotherapy
negative air ionization therapy
by moist salt air:
by natural moist salt air: seaside cure (especially common in prescientific medicine)
by artificial moist salt air: water vapor forms of speleotherapy
by salts in the water
by mineral water: spa cure ("taking the waters") (especially common in prescientific medicine)
by seawater: seaside cure (especially common in prescientific medicine)
by aroma: aromatherapy
by other materials with mechanism of action unknown
by occlusion with duct tape: duct tape occlusion therapy
By energy
by electric energy as electric current: electrotherapy, electroconvulsive therapy
Transcranial magnetic stimulation
Vagus nerve stimulation
by magnetic energy:
magnet therapy
pulsed electromagnetic field therapy
magnetic resonance therapy
by electromagnetic radiation (EMR):
by light: light therapy (phototherapy)
ultraviolet light therapy
PUVA therapy
photodynamic therapy
photothermal therapy
cytoluminescent therapy
blood irradiation therapy
by darkness: dark therapy
by lasers: laser therapy
low level laser therapy
by gamma rays: radiosurgery
Gamma Knife radiosurgery
stereotactic radiation therapy
cobalt therapy
by radiation generally: radiation therapy (radiotherapy)
intraoperative radiation therapy
by EMR particles:
particle therapy
proton therapy
electron therapy
intraoperative electron radiation therapy
Auger therapy
neutron therapy
fast neutron therapy
neutron capture therapy of cancer
by radioisotopes emitting EMR:
by nuclear medicine
by brachytherapy
quackery type: electromagnetic therapy (alternative medicine)
by mechanical: manual therapy as massotherapy and therapy by exercise as in physical therapy
inversion therapy
by sound:
by ultrasound:
ultrasonic lithotripsy
extracorporeal shockwave therapy
sonodynamic therapy
by music: music therapy
by temperature
by heat: heat therapy (thermotherapy)
by moderately elevated ambient temperatures: hyperthermia therapy
by dry warm surroundings: Waon therapy
by dry or humid warm surroundings: sauna, including infrared sauna, for sweat therapy
by cold:
by extreme cold to specific tissue volumes: cryotherapy
by ice and compression: cold compression therapy
by ambient cold: hypothermia therapy for neonatal encephalopathy
by hot and cold alternation: contrast bath therapy
By procedure and human interaction
Surgery
by counseling, such as psychotherapy (see also: list of psychotherapies)
systemic therapy
by group psychotherapy
by cognitive behavioral therapy
by cognitive therapy
by behaviour therapy
by dialectical behavior therapy
by cognitive emotional behavioral therapy
by cognitive rehabilitation therapy
by family therapy
by education
by psychoeducation
by information therapy
by speech therapy, physical therapy, occupational therapy, vision therapy, massage therapy, chiropractic or acupuncture
by lifestyle modifications, such as avoiding unhealthy food or maintaining a predictable sleep schedule
by coaching
By animal interaction
by pets, assistance animals, or working animals: animal-assisted therapy
by horses: equine therapy, hippotherapy
by dogs: pet therapy with therapy dogs, including grief therapy dogs
by cats: pet therapy with therapy cats
by fish: ichthyotherapy (wading with fish), aquarium therapy (watching fish)
by maggots: maggot therapy
by worms:
by internal worms: helminthic therapy
by leeches: leech therapy
by immersion: animal bath
By meditation
by mindfulness: mindfulness-based cognitive therapy
By reading
by bibliotherapy
By creativity
by expression: expressive therapy
by writing: writing therapy
journal therapy
by play: play therapy
by art: art therapy
sensory art therapy
comic book therapy
by gardening: horticultural therapy
by dance: dance therapy
by drama: drama therapy
by recreation: recreational therapy
by music: music therapy
By sleeping and waking
by deep sleep: deep sleep therapy
by sleep deprivation: wake therapy
See also
Biophilia hypothesis
Classification of Pharmaco-Therapeutic Referrals
Cure
Interventionism (medicine)
Inverse benefit law
List of therapies
Greyhound therapy
Mature minor doctrine
Medicine
Medication
Nutraceutical
Prevention
Psychotherapy
Treatment as prevention
Therapeutic inertia
Therapeutic nihilism, the idea that treatment is useless
References
External links
Media related to Therapies at Wikimedia Commons
The dictionary definition of therapy at Wiktionary
"Chapter Nine of the Book of Medicine Dedicated to Mansur, with the Commentary of Sillanus de Nigris" is a Latin book by Rhazes, from 1483, that is known for its ninth chapter, which is about therapeutics | 11
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Other reviews, however, concluded that there is some evidence that higher caffeine intake by pregnant women may be associated with a higher risk of giving birth to a low birth weight baby, and may be associated with a higher risk of pregnancy loss. A systematic review, analyzing the results of observational studies, suggests that women who consume large amounts of caffeine (greater than 300 mg/day) prior to becoming pregnant may have a higher risk of experiencing pregnancy loss. Adverse effects
Physical
Caffeine in coffee and other caffeinated drinks can affect gastrointestinal motility and gastric acid secretion. In postmenopausal women, high caffeine consumption can accelerate bone loss.Acute ingestion of caffeine in large doses (at least 250–300 mg, equivalent to the amount found in 2–3 cups of coffee or 5–8 cups of tea) results in a short-term stimulation of urine output in individuals who have been deprived of caffeine for a period of days or weeks. This increase is due to both a diuresis (increase in water excretion) and a natriuresis (increase in saline excretion); it is mediated via proximal tubular adenosine receptor blockade. The acute increase in urinary output may increase the risk of dehydration. However, chronic users of caffeine develop a tolerance to this effect and experience no increase in urinary output. Psychological
Minor undesired symptoms from caffeine ingestion not sufficiently severe to warrant a psychiatric diagnosis are common and include mild anxiety, jitteriness, insomnia, increased sleep latency, and reduced coordination. Caffeine can have negative effects on anxiety disorders. | Lower urinary tract symptoms (LUTS) refer to a group of clinical symptoms involving the bladder, urinary sphincter, urethra and, in men, the prostate. The term is more commonly applied to men—over 40% of older men are afected—but lower urinary tract symptoms also affect women. The condition is also termed prostatism in men, but LUTS is preferred. Symptoms and signs
Symptoms can be categorised into:
Filling (storage) or irritative symptoms
Increased frequency of urination
Increased urgency of urination
Urge incontinence
Excessive passage of urine at night
Voiding or obstructive symptoms
Poor stream (unimproved by straining)
Hesitancy (worsened if bladder is very full)
Terminal dribbling
Incomplete voiding
Urinary retention
Overflow incontinence (occurs in chronic retention)
Episodes of near retentionAs the symptoms are common and non-specific, LUTS is not necessarily a reason to suspect prostate cancer. Large studies of patients have also failed to show any correlation between lower urinary tract symptoms and a specific diagnosis. Also, recently a report of lower urinary tract symptoms even with malignant features in the prostate failed to be associated with prostate cancer after further laboratory investigation of the biopsy. Causes
Benign prostatic hyperplasia (BPH)
Bladder stone
Cancer of the bladder and prostate
Detrusor muscle weakness and/or instability
Diabetes
Use of ketamine
Neurological conditions; for example multiple sclerosis, spinal cord injury, cauda equina syndrome
Prostatitis, including IgG4-related prostatitis
Urethral stricture
Urinary tract infections (UTIs)
Diagnosis
The International Prostate Symptom Score (IPSS) can be used to gauge the symptoms, along with physician examination. Other primary and secondary tests are often carried out, such as a PSA (Prostate-specific antigen) test, urinalysis, ultrasound, urinary flow studies, imaging, temporary prostatic stent placement, prostate biopsy and/or cystoscopy. | 0-1
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Also studies shown to us, failure of the immune system caused by blood transfusion can be categorized as one of the main factors leading to more than 10 different cancer types that are fully associated with blood transfusion and the innate and adaptive immune system. Allogeneic blood transfusion, through five major mechanisms including the lymphocyte-T set, myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), natural killer cells (NKCs), and dendritic cells (DCs) can help the recipients defense mechanisms. On the other hand, the role for each of the listed items includes activation of the antitumor CD8+ cytotoxic T lymphocytes (CD8+/CTL), temporal inactivation of Tregs, inactivation of the STAT3 signaling pathway, the use of bacteria to enhance the antitumor immune response and cellular Immunotherapy. Transfusion-associated volume overload is a common complication simply because blood products have a certain amount of volume. This is especially the case in recipients with underlying cardiac or kidney disease. Red cell transfusions can lead to volume overload when they must be repeated because of insufficient efficacy (see above). Plasma transfusion is especially prone to causing volume overload because large volumes are usually required to give any therapeutic benefit. It has been proved that blood transfusion produce worse outcomes after cytoreductive surgery and HIPEC. Hypothermia can occur with transfusions with large quantities of blood products which normally are stored at cold temperatures. Core body temperature can go down as low as 32 °C and can produce physiologic disturbances. Prevention should be done with warming the blood to ambient temperature prior to transfusions. | Hypospadias is a common variation in fetal development of the penis in which the urethra does not open from its usual location in the head of the penis. It is the second-most common birth abnormality of the male reproductive system, affecting about one of every 250 males at birth. Roughly 90% of cases are the less serious distal hypospadias, in which the urethral opening (the meatus) is on or near the head of the penis (glans). The remainder have proximal hypospadias, in which the meatus is all the way back on the shaft of the penis, near or within the scrotum. Shiny tissue that should have made the urethra extends from the meatus to the tip of the glans; this tissue is called the urethral plate. In most cases, the foreskin is less developed and does not wrap completely around the penis, leaving the underside of the glans uncovered. Also, a downward bending of the penis, commonly referred to as chordee, may occur. Chordee is found in 10% of distal hypospadias and 50% of proximal hypospadias cases at the time of surgery. Also, the scrotum may be higher than usual on either side of the penis (called penoscrotal transposition). The cause of hypospadias is unknown. | 0-1
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Classically, the increased pain when tilting the head forwards separates sinusitis from pulpitis.For cases of maxillary sinusitis, limited field CBCT imaging, as compared to periapical radiographs, improves the ability to detect the teeth as the sources for sinusitis. A coronal CT picture may also be useful. Chronic
For sinusitis lasting more than 12 weeks, a CT scan is recommended. On a CT scan, acute sinus secretions have a radiodensity of 10 to 25 Hounsfield units (HU), but in a more chronic state they become more viscous, with a radiodensity of 30 to 60 HU.Nasal endoscopy and clinical symptoms are also used to make a positive diagnosis. A tissue sample for histology and cultures can also be collected and tested. Nasal endoscopy involves inserting a flexible fiber-optic tube with a light and camera at its tip into the nose to examine the nasal passages and sinuses. Sinus infections, if they result in tooth pain, usually present with pain involving more than one of the upper teeth, whereas a toothache usually involves a single tooth. Dental examination and appropriate radiography aid in ruling out pain arises from a tooth. Treatment
Recommended treatments for most cases of sinusitis include rest and drinking enough water to thin the mucus. Antibiotics are not recommended for most cases.Breathing low-temperature steam such as from a hot shower or gargling can relieve symptoms. There is tentative evidence for nasal irrigation in acute sinusitis, for example during upper respiratory infections. | Decongestant nasal sprays containing oxymetazoline may provide relief, but these medications should not be used for more than the recommended period. Longer use may cause rebound sinusitis. It is unclear if nasal irrigation, antihistamines, or decongestants work in children with acute sinusitis. There is no clear evidence that plant extracts such as Cyclamen europaeum are effective as an intranasal wash to treat acute sinusitis. Evidence is inconclusive on whether anti-fungal treatments improve symptoms or quality of life. Antibiotics
Most sinusitis cases are caused by viruses and resolve without antibiotics. However, if symptoms do not resolve within 10 days, amoxicillin/clavulanate is a reasonable antibiotic association for first treatment. A 2018 Cochrane review, however, found no evidence that people with symptoms lasting seven days or more before consulting their physician are more likely to have bacterial sinusitis as one study found that about 80% of patients have symptoms lasting more than 7 days and another about 70%. Antibiotics are specifically not recommended in those with mild / moderate disease during the first week of infection due to risk of adverse effects, antibiotic resistance, and cost.Fluoroquinolones, and a newer macrolide antibiotic such as clarithromycin or a tetracycline like doxycycline, are used in those who have severe allergies to penicillins. Because of increasing resistance to amoxicillin the 2012 guideline of the Infectious Diseases Society of America recommends amoxicillin-clavulanate as the initial treatment of choice for bacterial sinusitis. The guidelines also recommend against other commonly used antibiotics, including azithromycin, clarithromycin, and trimethoprim/sulfamethoxazole, because of growing antibiotic resistance. | 11
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Though all forms of MCD involve excessive production of cytokines and a cytokine storm, iMCD has important differences in symptoms, disease course, and treatment from POEMS-associated MCD and HHV-8-associated MCD. First line treatment for iMCD is anti-IL-6 therapy with siltuximab (or tocilizumab, if siltuximab is not available). Siltuximab is the only FDA-approved treatment for iMCD and patients who respond to siltuximab tend to have long-term responses. In critically ill patients, chemotherapy and corticosteroids are recommended if the patient is demonstrating disease progression while on siltuximab. Approximately half of iMCD patients do not improve with anti-IL-6 therapy. In patients where siltuximab is not effective, other treatments such as rituximab and sirolimus can be used.iMCD can be further sub-classified into three clinical subgroups:
iMCD with TAFRO Syndrome (iMCD-TAFRO): characterized by acute episodes of Thrombocytopenia, Anasarca, Fever, Renal dysfunction or mylefibrosis, and Organomegaly.iMCD with idiopathic plasmacytic lymphadenopathy (iMCD-IPL): characterized by thrombocytosis, hypergammaglobulinemia, and a more chronic disease course.iMCD, not otherwise specified (iMCD-NOS): is diagnosed in iMCD patients who do not have iMCD-TAFRO or iMCD-IPL. Pathology
Castleman disease is defined by a range of characteristic features seen on microscopic analysis (histology) of tissue from enlarged lymph nodes. Variations in the lymph node tissues of patients with CD have led to 4 histological classifications:
Plasmacytic: increased number of follicles with large hyperplastic germinal centers and sheetlike plasmacytosis (increased number plasma cells). Germinal centers may also show regressed features
Hyaline vascular: regressed germinal centers, follicular dendritic cell prominence or dysplasia, hypervascularity in interfollicular regions, sclerotic vessels, prominent mantle zones with an "onion-skin" appearance. | Hypervascular: similar to hyaline vascular features, but seen in iMCD rather than UCD. Includes regressed germinal centers, follicular dendritic cell prominence, hypervascularity in interfollicular regions, and prominent mantle zones with an "onion-skin" appearance. Mixed: presence of a combination of hyaline vascular/hypervascular and plasmacytic features in the same lymph node.UCD most commonly demonstrates hyaline vascular features, but plasmacytic features or a mix of features may also be seen. iMCD more commonly demonstrates plasmacytic features, but hypervascular features or a mix of features are also seen. All cases of HHV-8-associated MCD are thought to demonstrate plasmablastic features—similar to plasmacytic features, but with plasmablasts present. The clinical utility of subtyping Castleman disease by histologic features is uncertain, as histologic subtypes do not consistently predict disease severity or treatment response. Guidelines recommend against using histologic subtype to guide treatment decisions. Staining with latency-associated nuclear antigen (LANA-1), a marker for HHV-8 infection, should be measured in all forms of Castleman disease but is positive only in HHV-8-associated MCD.Diseases other than Castleman disease can present with similar histologic findings in lymph node tissue, including:
Infectious causes: Epstein-Barr virus, human immunodeficiency virus, tuberculosis
Autoimmune diseases: Systemic lupus erythematosus, rheumatoid arthritis
Lymphoproliferative disorders: lymphoma, autoimmune lymphoproliferative syndrome
History
Unicentric Castleman disease was first described in a case series by Benjamin Castleman in 1956. By 1984, a number of case reports had been published describing a multicentric variant of the disease and with some reports describing an association with Kaposis sarcoma. In 1995, the association between HHV-8 and Castleman disease was described in patients with HIV. | 11
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While the exact role of zinc in dysgeusia is unknown, it has been cited that zinc is partly responsible for the repair and production of taste buds. Zinc somehow directly or indirectly interacts with carbonic anhydrase VI, influencing the concentration of gustin, which is linked to the production of taste buds. It has also been reported that patients treated with zinc experience an elevation in calcium concentration in the saliva. In order to work properly, taste buds rely on calcium receptors. Zinc “is an important cofactor for alkaline phosphatase, the most abundant enzyme in taste bud membranes; it is also a component of a parotid salivary protein important to the development and maintenance of normal taste buds.”
Drugs
There are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H1-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste, including Paxlovid, a drug used to treat COVID-19. Some describe so-called "Paxlovid mouth" as like a "mouthful of dirty pennies and rotten soymilk," according to the Wall Street Journal.The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. | Type IV cells are normally rooted at the posterior end of the taste bud. Every cell in the taste bud forms microvilli at the ends. Diagnosis
In general, gustatory disorders are challenging to diagnose and evaluate. Because gustatory functions are tied to the sense of smell, the somatosensory system, and the perception of pain (such as in tasting spicy foods), it is difficult to examine sensations mediated through an individual system. In addition, gustatory dysfunction is rare when compared to olfactory disorders.Diagnosis of dysgeusia begins with the patient being questioned about salivation, swallowing, chewing, oral pain, previous ear infections (possibly indicated by hearing or balance problems), oral hygiene, and stomach problems. The initial history assessment also considers the possibility of accompanying diseases such as diabetes mellitus, hypothyroidism, or cancer. A clinical examination is conducted and includes an inspection of the tongue and the oral cavity. Furthermore, the ear canal is inspected, as lesions of the chorda tympani have a predilection for this site. Gustatory testing
In order to further classify the extent of dysgeusia and clinically measure the sense of taste, gustatory testing may be performed. Gustatory testing is performed either as a whole-mouth procedure or as a regional test. In both techniques, natural or electrical stimuli can be used. In regional testing, 20 to 50 µL of liquid stimulus is presented to the anterior and posterior tongue using a pipette, soaked filter-paper disks, or cotton swabs. | 11
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IHs are usually absent at birth or a small area of pallor, telangiectasias, or duskiness may be seen. A fully formed mass at birth usually indicates a diagnosis other than IH. Superficial hemangiomas in the upper dermis have a bright-red strawberry color, whereas those in the deep dermis and subcutis, deep hemangiomas, may appear blue and be firm or rubbery on palpation. Mixed hemangiomas can have both features. A minimally proliferative IH is an uncommon type that presents with fine macular telangiectasias with an occasional bright-red, papular, proliferative component. Minimally proliferative IHs are more common in the lower body.A precise history of the growth characteristics of the IH can be very helpful in making the diagnosis. In the first 4 to 8 weeks of life, IHs grow rapidly with primarily volumetric rather than radial growth. This is usually followed by a period of slower growth that can last 6–9 months, with 80% of the growth completed by 3 months. Finally, IHs involute over a period of years. The exceptions to these growth characteristics include minimally proliferative His, which do not substantially proliferate and large, deep IHs in which noticeable growth starts later and lasts longer. If the diagnosis is not clear based on physical examination and growth history (most often in deep hemangiomas with little cutaneous involvement), then either imaging or histopathology can help confirm the diagnosis. On Doppler ultrasound, an IH in the proliferative phase appears as a high-flow, soft-tissue mass usually without direct arteriovenous shunting. | It is generally applied two to three times daily. Surgery
Surgical excision of hemangiomas is rarely indicated, and limited to lesions which fail medical therapy (or when it is contraindicated), which are anatomically distributed in a location which is amenable to resection, and in which resection would likely be necessary and the scar will be similar regardless of timing of the surgery. Surgery may also be useful for removal of residual fibrofatty tissue (following hemangioma involution) and reconstruction of damaged structures. Laser
Laser therapy, most often the pulsed dye laser (PDL), plays a limited role in hemangioma management. PDL is most often used for treatment of ulcerated hemangiomas, often in conjunction with topical therapies and wound care, and may speed healing and diminish pain. Laser therapy may also be useful for early superficial IHs (although rapidly proliferating lesions may be more prone to ulceration following PDL treatment), and for the treatment of cutaneous telangiectasias which persist following involution. Prognosis
In the involution phase, an IH finally begins to diminish in size. While IHs were previously thought to improve by about 10% each year, newer evidence suggests that maximal improvement and involution is typically reached by 3.5 years of age. Most IHs resolve by age 10, but in some patients, the hemangioma does not completely resolve. Residual redness may be noted and can be improved with laser therapy, most commonly PDL. Ablative fractional resurfacing may be considered for textural skin changes. | 11
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This effect was shown in animals when a nitric oxide precursor, L-arginine, reversed morphine-induced changes in gut motility. Hormone imbalance
Clinical studies consistently conclude that morphine, like other opioids, often causes hypogonadism and hormone imbalances in chronic users of both sexes. This side effect is dose-dependent and occurs in both therapeutic and recreational users. Morphine can interfere with menstruation in women by suppressing levels of luteinizing hormone. Many studies suggest the majority (perhaps as many as 90%) of chronic opioid users have opioid-induced hypogonadism. This effect may cause the increased likelihood of osteoporosis and bone fracture observed in chronic morphine users. Studies suggest the effect is temporary. As of 2013, the effect of low-dose or acute use of morphine on the endocrine system is unclear. Effects on human performance
Most reviews conclude that opioids produce minimal impairment of human performance on tests of sensory, motor, or attentional abilities. However, recent studies have been able to show some impairments caused by morphine, which is not surprising, given that morphine is a central nervous system depressant. Morphine has resulted in impaired functioning on critical flicker frequency (a measure of overall CNS arousal) and impaired performance on the Maddox wing test (a measure of the deviation of the visual axes of the eyes). Few studies have investigated the effects of morphine on motor abilities; a high dose of morphine can impair finger tapping and the ability to maintain a low constant level of isometric force (i.e. | Heroin is converted to morphine before binding to the opioid receptors in the brain and spinal cord, where morphine causes the subjective effects, which is what the addicted individuals are seeking. Tolerance
Several hypotheses are given about how tolerance develops, including opioid receptor phosphorylation (which would change the receptor conformation), functional decoupling of receptors from G-proteins (leading to receptor desensitization), μ-opioid receptor internalization or receptor down-regulation (reducing the number of available receptors for morphine to act on), and upregulation of the cAMP pathway (a counterregulatory mechanism to opioid effects) (For a review of these processes, see Koch and Hollt.) CCK might mediate some counter-regulatory pathways responsible for opioid tolerance. CCK-antagonist drugs, specifically proglumide, have been shown to slow the development of tolerance to morphine. Dependence and withdrawal
Cessation of dosing with morphine creates the prototypical opioid withdrawal syndrome, which, unlike that of barbiturates, benzodiazepines, alcohol, or sedative-hypnotics, is not fatal by itself in otherwise healthy people. Acute morphine withdrawal, along with that of any other opioid, proceeds through a number of stages. Other opioids differ in the intensity and length of each, and weak opioids and mixed agonist-antagonists may have acute withdrawal syndromes that do not reach the highest level. | 11
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White blood cells may also bind to the endothelium of small capillaries, obstructing them and leading to more ischemia.Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are involved in brain failure following reversal of cardiac arrest; control of these processes is the subject of ongoing research. Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ulcer. Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. As this process is repeated, it eventually damages tissue enough to cause a wound.The main reason for the acute phase of ischemia-reperfusion injury is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced. Mitochondrial complex I is thought to be the most vulnerable enzyme to tissue ischemia/reperfusion but the mechanism of damage is different in different tissues. For example brain ischemia/reperfusion injury is mediated via complex I redox-dependent inactivation. It was found that lack of oxygen leads to conditions in which mitochondrial complex I loses its natural cofactor, flavin mononucleotide (FMN) and become inactive. When oxygen is present the enzyme catalyzes a physiological reaction of NADH oxidation by ubiquinone, supplying electrons downstream of the respiratory chain (complexes III and IV). | More specifically, calcium overload and excessive production of reactive oxygen species in the first few minutes after reperfusion set off a cascade of biochemical changes that result in the opening of the so-called mitochondrial permeability transition pore (MPT pore) in the mitochondrial membrane of cardiac cells.The opening of the MPT pore leads to the inrush of water into the mitochondria, resulting in mitochondrial dysfunction and collapse. Upon collapse, the calcium is then released to overwhelm the next mitochondria in a cascading series of events that cause mitochondrial energy production supporting the cell to be reduced or stopped completely. The cessation of energy production results in cellular death. Protecting mitochondria is a viable cardioprotective strategy.In 2008, an editorial in the New England Journal of Medicine called for more studies to determine if cyclosporin can become a treatment to ameliorate reperfusion injury by protecting mitochondria. To that end, in 2011 the researchers involved in the original 2008 NEJM study initiated a phase III clinical study of reperfusion injury in 1000 myocardial infarction patients in centers throughout Europe. Results of that study were announced in 2015 and indicated that "intravenous cyclosporine did not result in better clinical outcomes than those with placebo and did not prevent adverse left ventricular remodeling at 1 year." This same process of mitochondrial destruction through the opening of the MPT pore is implicated in making traumatic brain injuries much worse. TRO40303
TRO40303 is a new cardioprotective compound that was shown to inhibit the MPT pore and reduce infarct size after ischemia-reperfusion. | 11
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Serological tests (detection of antibodies in the serum of the patients) are available and widely used. Cross reactivity with Brucella can confuse interpretation of the results, so diagnosis should not rely only on serology. Molecular methods such as PCR are available in reference laboratories. Prevention
There are no safe, available, approved vaccines against tularemia. However, vaccination research and development continues, with live attenuated vaccines being the most thoroughly researched and most likely candidate for approval. Sub-unit vaccine candidates, such as killed-whole cell vaccines, are also under investigation, however research has not reached a state of public use.Optimal preventative practices include limiting direct exposure when handling potentially infected animals by wearing gloves and face masks (importantly when skinning deceased animals). Treatment
If infection occurs or is suspected, treatment is generally with the antibiotics streptomycin or Gentamicin. Doxycycline was previously used. Gentamicin may be easier to obtain than streptomycin. There is also tentative evidence to support the use of quinolone antibiotics. Prognosis
Since the invention of antibiotics, the rate of death associated with tularemia has decreased from 60% to less than 4%. Epidemiology
Tularemia is most common in the Northern Hemisphere, including North America and parts of Europe and Asia. It occurs between 30º and 71º north latitude.In the United States, although records show that tularemia was never particularly common, incidence rates continued to drop over the course of the 20th century. | A gastrojejunocolic fistula is a disorder of the human gastrointestinal tract. It may form between the transverse colon and the upper jejunum after a Billroth II surgical procedure. (The Billroth procedure attaches the jejunum to the remainder of the stomach.) Fecal matter thereby passes improperly from the colon to the stomach, and causes halitosis.Patients may present with diarrhea, weight loss and halitosis as a result of fecal matter passing through the fistula from the colon into the stomach. == References == | 0-1
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Symptoms of the resultant hyperthyroidism are mainly insomnia, hand tremor, hyperactivity, hair loss, excessive sweating, oligomenorrhea, itching, heat intolerance, weight loss despite increased appetite, diarrhea, frequent defecation, palpitations, periodic partial muscle weakness or paralysis in those especially of Asian descent, and skin warmth and moistness. Further signs that may be seen on physical examination are most commonly a diffusely enlarged (usually symmetric), nontender thyroid, lid lag, excessive lacrimation due to Graves ophthalmopathy, arrhythmias of the heart, such as sinus tachycardia, atrial fibrillation, and premature ventricular contractions, and hypertension. Cause
The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. While a theoretical mechanism occurs by which exposure to severe stressors and high levels of subsequent distress such as PTSD (Post traumatic stress disorder) could increase the risk of immune disease and cause an aggravation of the autoimmune response that leads to Graves disease, more robust clinical data are needed for a firm conclusion. Genetics
A genetic predisposition for Graves disease is seen, with some people more prone to develop TSH receptor activating antibodies due to a genetic cause. Human leukocyte antigen DR (especially DR3) appears to play a role. To date, no clear genetic defect has been found to point to a single-gene cause.Genes believed to be involved include those for thyroglobulin, thyrotropin receptor, protein tyrosine phosphatase nonreceptor type 22 (PTPN22), and cytotoxic T-lymphocyte–associated antigen 4, among others. | A glycogen storage disease (GSD, also glycogenosis and dextrinosis) is a metabolic disorder caused by an enzyme deficiency affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.GSD has two classes of cause: genetic and acquired. Genetic GSD is caused by any inborn error of metabolism (genetically defective enzymes) involved in these processes. In livestock, acquired GSD is caused by intoxication with the alkaloid castanospermine. Types
Remarks:
Some GSDs have different forms, e.g. infantile, juvenile, adult (late-onset). Some GSDs have different subtypes, e.g. GSD1a / GSD1b, GSD9A1 / GSD9A2 / GSD9B / GSD9C / GSD9D. GSD type 0: Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often classified with the GSDs as type 0 because it is another defect of glycogen storage and can cause similar problems. GSD type VIII (GSD 8): In the past it was considered a distinct condition, however it is now classified with GSD type VI or GSD IXa1; it has been described as X-linked recessive inherited. GSD type XI (GSD 11): Fanconi-Bickel syndrome, hepatorenal glycogenosis with renal Fanconi syndrome, no longer considered a glycogen storage disease. GSD type XIV (GSD 14): Now classed as Congenital disorder of glycosylation type 1 (CDG1T), affects the phosphoglucomutase enzyme (gene PGM1). Lafora disease is considered a complex neurodegenerative disease and also a glycogen metabolism disorder. Diagnosis
Treatment
Treatment is dependent on the type of glycogen storage disease. | 0-1
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No result
the outcome of a limited overs match in which each team does not face the minimum number of overs required for a result to be recorded, usually due to a rain delay. This is generally equivalent to a draw, but differs in the recording of some statistics. Non-striker
the batsman standing at the bowling end. Nothing shot
An overly-tentative shot by the batsman: neither a committed attempt to hit the ball, nor a deliberate leave. This often results in an edge, beating the bat, or playing on. Not out
1. a batsman who is in and has not yet been dismissed, particularly when play has ceased. 2. the call of the umpire when turning down an appeal for a wicket. Nurdle
To score runs, usually in singles, by using low-risk shots to gently nudge the ball into vacant areas of the field. O
Obstructing the field
An extremely rare method of dismissal. The batsman is given out if they wilfully interfere with the fielding, such as blocking a run out or preventing a fielder from taking a catch. Since 2017 obstructing the field includes the offence of handled the ball, which was previously considered a separate method of dismissal. Occupying the crease
The act of a batsman staying in for a long time, without trying to score many runs. This tires the bowler and may frustrate the fielding side in a timed match, but requires skilled defensive batting technique. It is particularly prized among opening batsmen or when batting for a draw. | Epidemiology
Currently, no research has shown a higher prevalence of most leukodystrophy types in any one place around the world. There is, however, a higher prevalence of the Canavan disease in the Jewish population. 1 in 40 individuals of Ashkenazi Jewish descent are carriers of Canavan disease. This estimates to roughly 2.5%. Additionally, due to an autosomal recessive inheritance patterns, there is no significant difference found between affected males and affected females for most types of leukodystrophy including, but not limited to, metachromatic leukodystrophy, Krabbe disease, Canavan disease, and Alexander disease. The one exception to this is any type of leukodystrophy carried on a sex chromosome, such as X-linked adrenoleukodystrophy, which is carried on the X-chromosome. Because of the inheritance pattern of X-linked diseases, males are more often affected by this type of leukodystrophy, although female carriers are often symptomatic, though not as severely so as males. Research
The National Institute of Neurological Disorders and Stroke (NINDS, under the U.S. National Institutes of Health) supports research on genetic disorders, including the leukodystrophies. NINDS also supports researchers who are working with the Global Leukodystrophy Initiative Clinical Trials Network (GLIA-CTN) which promotes advances in the diagnosis and treatment of leukodystrophies.The European Leukodystrophy Association also supports research into leukodystrophy. As of 2020, more than 387 research projects have been funded. Each year, ELA invites the international scientific community to submit research projects in the field of genetic leukodystrophies, the cerebral white matter in premature infants, and of myelin repair. | 0-1
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Treatment
Ulnar polydactyly
Ulnar polydactyly usually does not interfere with hand function, but for social reasons it can be treated operatively. Type A ulnar polydactyly
The treatment of Type A ulnar polydactyly is complex as its goal is to remove the accessory digit while maintaining a stable, functional small finger. When the duplicated proximal phalanx articulates with a common, broad metacarpal head, the ulnar collateral ligament must be considered. In those cases with a common articulation or with a sixth metacarpal the muscle executing the abduction of the little finger (abductor digiti minimi) must be preserved. In patients with a common metacarpal articulation an elliptical incision at the base of the post-axial digit is made. This incision may be extended proximally in order to adequately expose the abductor digiti minimi. The ulnar collateral ligament and the insertions of the abductor digiti minimi are then elevated with a periosteal sleeve. The duplicated extensor and flexor tendons to the ulnar digit are transected and after that the digit is amputated at its articulation with the metacarpal. If the articular surface is wide the metacarpal may be shaved. At last the collateral ligament and abductor digiti minimi are reinserted at the base of the preserved proximal phalanx and a wire is then placed across the reconstructed joint. In patients with a duplicated metacarpal, the accessory digit is amputated in a standard ray fashion with transfer of the abductor digiti minimi to the retained small finger. Type B ulnar polydactyly
In this situation there is an absence of osseous and ligamentous structures. | The neurovascular bundle which supplies the distal component is reserved and transferred proximally. Central polydactyly
Early osteotomy and ligament reconstructions should be done to prevent deformities, such as angular growth deformities.The surgical treatment of central polydactyly is highly variable. After the surgery the hand must be functional and stable, but also aesthetically pleasing. This requires intraoperative creativity and flexibility. The surgeon must also consider whether retention of a fully functional supranumerary digit is preferable to surgical intervention. In contrast, a functional, four-fingered hand achieved via ray amputation may be preferable to a five-fingered hand with a deformed or stiff reconstructed finger.Cases of polysyndactyly are approached through a standard opposing zig-zag incision. The incision is favored toward the accessory digit, preserving extra skin for subsequent closure. Depending on the level and extent of duplication, the flexor and extensor tendons may require centralization or rebalancing. Also, the collateral ligaments must be preserved or reconstructed. Wide articular surfaces should be narrowed and phalangeal wedge osteotomies may be required to provide an axial alignment. Attention must also be given to reconstruct the intermetacarpal ligament. Furthermore, one should take in mind the provision for adequate web-space soft tissue. Prognosis
Ulnar polydactyly
Type A ulnar polydactyly
There are no substantive outcome studies regarding the function of these hands following surgical intervention. This is mainly caused by the fact that there is a generally normal function of these patients’ hands following ablation with collateral ligament reconstruction. | 11
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Afrin may refer to:
Places
Afrin Canton, one of the cantons of the de facto autonomous Democratic Federation of Northern Syria
Afrin District, a district of Aleppo Governorate in northern Syria. The administrative centre is the city of Afrin
Afrin Subdistrict, a subdistrict of the Afrin District
Afrin Region, the westernmost of the three regions of the de facto autonomous Democratic Federation of Northern Syria
Afrin River, a river in Turkey and Syria
Afrin Dam, dam on the Afrin River in northwest Syria
Afrin, Syria, a city in northwestern Syria, administratively part of Aleppo Governorate
Institutions
Afrin SC, a football club based in Afrin, Syria
University of Afrin, an unrecognized university established in the city of Afrin by the Afrin Canton Board of Education
Products
Afrin (nasal spray), a nasal decongestant
People
Given name
Afrin Ali (born 1986), Indian politician
Surname
Jill Afrin (born 1962), psychiatrist
Nahid Afrin (born 2001), Indian playback singer
Narin Afrin, resistance leader | Manganese deficiency may refer to:
Manganese deficiency (medicine)
Manganese deficiency (plant) | 0-1
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Blood pressure medication, levodopa and medications for Parkinsons disease have also been known to cause nightmares.The nightmares may be idiopathic or could be associated with psychiatric disorders like post-traumatic stress disorder, schizophrenia, and borderline personality disorder. Nightmares can also be triggered by stress and anxiety and substance abuse, such as drugs that affect the neurotransmitters norepinephrine and dopamine and serotonin. Nevertheless, causality between drugs such as beta-blockers or alpha-agonists and nightmares is still unclear and further research needs to be done to investigate the biochemical mechanisms of nightmares.Eighty percent of patients who have PTSD report nightmares. Patients with PTSD have symptoms that are classified into three clusters: intrusive/re-experiencing, numbing, and hyperarousal. Nightmares are usually considered to be part of the intrusive/re-experiencing symptom.Some differences are existing between idiopathic and PTSD related nightmares. A PTSD person having nightmares would wake up during the night more frequently and for a longer time than with idiopathic nightmares. Consequently, people with PTSD would have a poorer sleep quality. Furthermore, nightmares related to PTSD would be more stressful than idiopathic ones. However, further studies have to be conducted in this area to obtain more reliable results. Assessment
Polysomnography records physiological parameters, such as electroencephalography (EEG), electromyography (EMG) and electrooculography (EOG) in a sleep laboratory. However, the frequency of posttraumatic nightmares tends to decrease in an artificial lab setting, which would impact the content of nightmares. | The two main types of myotonia congenita are Thomsen disease, which begins in infancy, and Becker disease (sometimes called generalized myotonia), which usually begins between the ages four and 12. References
External links
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Diagnosis is determined by a specific test for DNA repair, which measures the recovery of RNA after exposure to UV radiation. Despite being associated with genes involved in nucleotide excision repair (NER), unlike xeroderma pigmentosum, CS is not associated with an increased risk of cancer. Laboratory Studies
In Cockayne syndrome patients, UV-irradiated cells show decreased DNA and RNA synthesis. https://emedicine.medscape.com/article/1115866-workup#c5
Laboratory studies are mainly useful to eliminate other disorders. For example, skeletal radiography, endocrinologic tests, and chromosomal breakage studies can help in excluding disorders included in the differential diagnosis. Imaging Studies
Brain CT scanning in Cockayne syndrome patients may reveal calcifications and cortical atrophy. Other Tests
Prenatal evaluation is possible. Amniotic fluid cell culturing is used to demonstrate that fetal cells are deficient in RNA synthesis after UV irradiation. Neurology
Imaging studies reveal a widespread absence of the myelin sheaths of the neurons in the white matter of the brain and general atrophy of the cortex. Calcifications have also been found in the putamen, an area of the forebrain that regulates movements and aids in some forms of learning, along with the cortex. Additionally, atrophy of the central area of the cerebellum found in patients with Cockayne syndrome could also result in the lack of muscle control, particularly involuntary, and poor posture typically seen. Treatment
There is no permanent cure for this syndrome, although patients can be symptomatically treated. Treatment usually involves physical therapy and minor surgeries to the affected organs, such as cataract removal. | Also wearing high-factor sunscreen and protective clothing is recommended because Cockayne Syndrome patients are very sensitive to UV radiation. Optimal nutrition can also help. Genetic counseling for the parents is recommended, as the disorder has a 25% chance of being passed to any future children, and prenatal testing is also a possibility. Another important aspect is the prevention of recurrence of CS in other siblings. Identification of gene defects involved makes it possible to offer genetic counseling and antenatal
diagnostic testing to the parents who already have one affected child. Prognosis
The prognosis for those with Cockayne syndrome is poor, as death typically occurs by the age of 12. The prognosis for Cockayne syndrome varies by disease type. There are three types of Cockayne syndrome according to the severity and onset of the symptoms. However, the differences between the types are not always clear-cut, and some researchers believe the signs and symptoms reflect a spectrum instead of distinct types:
Cockayne syndrome Type A (CSA) is marked by normal development until a child is 1 or 2 years old, at which point growth slows and developmental delays are noticed. Symptoms are not apparent until they are 1 year. Life expectancy for type A is approximately 10 to 20 years. These symptoms are seen in CS type 1 children. Cockayne syndrome type B (CSB), also known as "cerebro-oculo-facio-skeletal (COFS) syndrome" (or "Pena-Shokeir syndrome type B"), is the most severe subtype. Symptoms are present at birth and normal brain development stops after birth. | 11
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Islam is the only major religion that puts a cap on polygamy, limiting the number of a mans wives to four—provided the husband can do justice to all of them. Although some religions, such as Catholicism for instance, puts a cap on polygamy all together, or even serial monogamy, allowing one spouse until death does them apart, not even accepting divorce. According to the teachings of Islam a Muslim man should have a valid reason and have to get permission from his existing wife (without any force) if he requires to marry again. Islam vehemently abhors any intimate relationship outside the bond of marriage. There is no external sign to show his status as a husband, unless he adopted the tradition of wearing a wedding ring. Hinduism
A Hindu husband traditionally takes his wife to his home. He is expected to provide for her and to prove his abilities to do so. The marriage in Hinduism is a relationship for Seven births (सात जन्मों का सम्बन्ध). Before 1951 there was no divorce allowed in Hindu marriage. In modern times once again after 1951, equal rights for women through society and law jurisdiction is given. In Hinduism, based on the different regions, marriage process is observed differently with the same Saat Pheras around agni kund (light pyre) to be taken to become a husband and wife. The Encyclopædia Britannica mentions that "In Hindu law, the male members of a joint family, together with their wives, widows, and children, are entitled to support out of the joint property." | A husband is a male in a marital relationship, who may also be referred to as a spouse. The rights and obligations of a husband regarding his spouse and others, and his status in the community and in law, vary between societies and cultures, and have varied over time. In monogamous cultures, there are only two parties to a marriage, which is enforced by laws against bigamy and polygamy. Traditionally, the husband was regarded as the head of the household and was expected to be the sole provider or breadwinner, a role that continues in some cultures (sometimes described as paternalistic). Today, a husband is not necessarily considered the breadwinner of the family, especially if his spouse has a more financially rewarding occupation or career. In such cases, it is not uncommon for a husband to be considered a stay-at-home father if the married couple have children. The term continues to be applied to such a man who has separated from his spouse and ceases to be applied to him only when his marriage has come to an end following a legally recognized divorce or the death of his spouse. On the death of his spouse, a husband is referred to as a widower; after a divorce a man may be referred to as the "ex-husband" of his former spouse. Origin and etymology
The term husband refers to Middle English huseband, from Old English hūsbōnda, from Old Norse hūsbōndi (hūs, house + bōndi, būandi, present participle of būa, to dwell, so, etymologically, a householder). | 11
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Dementia, aging, and intellectual disabilities: a handbook. Philadelphia, PA: Brunner/Mazel. p. 12. ISBN 0-87630-916-3. OCLC 39223703. Australian Institute of Health and Welfare paper The Definition and Prevalence of Intellectual Disability in Australia
Harris, James C. (2010). Intellectual Disability: A Guide for Families and Professionals. Oxford University Press. 2001 New Zealand Snapshot of Intellectual Disability
Kovago, Emese. (2003). People with Intellectual Disabilities: from Invisible to Visible Citizens of the EU Accession Countries Archived Copy
Endicott, Orville (1991). Persons with intellectual disability who are incarcerated for criminal offences: A literature review (PDF). Communications and Corporate Development, Research Branch. : Correctional Service of Canada. Archived from the original (PDF) on 1 July 2013. Retrieved 30 June 2022. "John F. Kennedy and people with intellectual disabilities". Presidential Library and Museum. Archived from the original on 21 January 2022. Jones, Jessica (December 2007). "Persons with intellectual disabilities in the criminal justice system: Review of issues". International Journal of Offender Therapy and Comparative Criminology. Sage. 51 (6): 723–733. doi:10.1177/0306624X07299343. eISSN 1552-6933. ISSN 0306-624X. PMID 17636203. S2CID 27995011. Petersilia, Joan (2000). "Invisible Victims Violence against persons with developmental disabilities". Human Rights. American Bar Association. 27 (1): 9–12. Archived from the original on 1 September 2000. Retrieved 12 July 2022. Søndenaa, Erik; Linaker, Olav Martin; Nøttestad, Jim Aage (September 2009). "Effects of the changes in legislation governing offenders with intellectual disabilities in Norway: A descriptive study". Journal of Policy and Practice in Intellectual Disabilities. International Association for the Scientific Study of Intellectual Disabilities. 6 (3): 229–235. doi:10.1111/j.1741-1130.2009.00206.x. ISSN 1741-1130. Wehmeyer, Michael L. (2013). | Other groups may include veterinarians, researchers, or people planning to travel to regions where rabies is common. Three doses of the vaccine are given over a one-month period on days zero, seven, and either twenty-one or twenty-eight. After exposure
For individuals who have been potentially exposed to the virus, four doses over two weeks are recommended, as well as an injection of rabies immunoglobulin with the first dose. This is known as post-exposure vaccination. For people who have previously been vaccinated, only a single dose of the rabies vaccine is required. However, vaccination after exposure is neither a treatment nor a cure for rabies; it can only prevent the development of rabies in a person if given before the virus reaches the brain. Because the rabies virus has a relatively long incubation period, post-exposure vaccinations are typically highly effective. Additional doses
Immunity following a course of doses is typically long lasting, and additional doses are usually not needed unless the person has a high risk of contracting the virus. Those at risk may have tests done to measure the amount of rabies antibodies in the blood, and then get rabies boosters as needed. Following administration of a booster dose, one study found 97% of immunocompetent individuals demonstrated protective levels of neutralizing antibodies after ten years. Safety
Rabies vaccines are safe in all age groups. About 35 to 45 percent of people develop a brief period of redness and pain at the injection site, and 5 to 15 percent of people may experience fever, headaches, or nausea. | 0-1
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A Meckels diverticulum, a true congenital diverticulum, is a slight bulge in the small intestine present at birth and a vestigial remnant of the omphalomesenteric duct (also called the vitelline duct or yolk stalk). It is the most common malformation of the gastrointestinal tract and is present in approximately 2% of the population, with males more frequently experiencing symptoms. Meckels diverticulum was first explained by Fabricius Hildanus in the sixteenth century and later named after Johann Friedrich Meckel, who described the embryological origin of this type of diverticulum in 1809. Signs and symptoms
The majority of people with a Meckels diverticulum are asymptomatic. An asymptomatic Meckels diverticulum is called a silent Meckels diverticulum. If symptoms do occur, they typically appear before the age of two years. The most common presenting symptom is painless rectal bleeding such as melaena-like black offensive stools, followed by intestinal obstruction, volvulus and intussusception. Occasionally, Meckels diverticulitis may present with all the features of acute appendicitis. Also, severe pain in the epigastric region is experienced by the person along with bloating in the epigastric and umbilical regions. At times, the symptoms are so painful that they may cause sleepless nights with acute pain felt in the foregut region, specifically in the epigastric and umbilical regions. In some cases, bleeding occurs without warning and may stop spontaneously. The symptoms can be extremely painful, often mistaken as just stomach pain resulting from not eating or constipation. | Biological models
Biological models explaining the origins of kleptomania have been based mostly on pharmacotherapy treatment studies that used selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, and opioid receptor antagonists.Some studies using SSRIs have observed that opioid antagonists appear to reduce the urge to steal and mute the "rush" typically experienced immediately after stealing by some subjects with kleptomania. This would suggest that poor regulation of serotonin, dopamine, and/or natural opioids within the brain are to blame for kleptomania, linking it with impulse control and affective disorders.An alternative explanation too based on opioid antagonist studies states that kleptomania is similar to the "self-medication" model, in which stealing stimulates the persons natural opioid system. "The opioid release soothes the patients, treats their sadness, or reduces their anxiety. Thus, stealing is a mechanism to relieve oneself from a chronic state of hyperarousal, perhaps produced by prior stressful or traumatic events, and thereby modulate affective states. ": 354
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Disagreement surrounds the method by which kleptomania is considered and diagnosed. On one hand, some researchers believe that kleptomania is merely theft and dispute the suggestion that there are psychological mechanisms involved, while others observe kleptomania as part of a substance-related addiction. Yet others categorize kleptomania as a variation of an impulse control disorder, such as obsessive-compulsive disorder or eating disorders. | 0-1
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Their treatment usually includes chemotherapy. Radiotherapy can also be given to places where the cancer has spread, e.g. the brain.Women who undergo chemotherapy are advised not to conceive for one year after completion of treatment. These women also are likely to have an earlier menopause. It has been estimated by the Royal College of Obstetricians and Gynaecologists that the age at menopause for women who receive single agent chemotherapy is advanced by one year, and by three years for women who receive multi agent chemotherapy. Follow up
Follow up is necessary in all women with gestational trophoblastic disease, because of the possibility of persistent disease, or because of the risk of developing malignant uterine invasion or malignant metastatic disease even after treatment in some women with certain risk factors.The use of a reliable contraception method is very important during the entire follow up period, as patients are strongly advised against pregnancy at that time. If a reliable contraception method is not used during the follow-up, it could be initially unclear to clinicians as to whether a rising hCG level is caused by the patient becoming pregnant again, or by the continued presence of GTD. In women who have a malignant form of GTD, hCG concentrations stay the same (plateau) or they rise. | When the LCS tumor is readily accessible, the best treatment method is usually surgical removal. There is, however, an observed increased risk of tumor relapse following surgical resection. Both chemotherapy and radiation therapy are useful as treatments, either as monotherapy or in conjunction with other treatments. Chemotherapy is currently the most common treatment method, either alone or in combination. The most common chemotherapeutic regimen consisted of cyclophosphamide, doxorubicin, vincristine, and prednisolone (otherwise known as CHOP therapy). Other common chemotherapeutic regimens include MAID (mesna, doxorubicin, ifosfamide, and dacarbazine), ESHAP (etoposide, carboplatin, cytarabine, and methylprednisolone), EPIG (etoposide, cisplatin, ifosfamide, mesna, and gemcitabine), and AIM (doxorubicin, ifosfamide, and mesna). Other regimens have been used with mixed levels of success. In an effort to prevent recurrence, sometimes combination therapy is used. Following surgical resection, additional radiation therapy or chemotherapy may be performed to prevent relapse. Patients receiving combined chemotherapy and radiation therapy has only shown limited benefit.There are a variety of other therapies under research with varying levels of reported success. These include high-dose chemotherapy, bone marrow transplants, and somatostatin analogues.When there is only one site of LCS involvement, monotherapy may be sufficient treatment. But when the disease has multiple sites or has metastasized, combination therapy will be necessary to achieve any level of adequate treatment. Prognosis
Overall prognosis of patients with LCS depends heavily on the bodily organ involved and the extent of involvement of the tumor. Organs associated with a poor prognosis include the liver, lungs, and bone marrow. | 0-1
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BAL cytology analyses (differential cell counts) should be considered in the evaluation of patients with IPF at the discretion of the treating physician based on availability and experience at their institution. BAL may reveal alternative specific diagnoses: malignancy, infections, eosinophilic pneumonia, histiocytosis X, or alveolar proteinosis. In the evaluation of patients with suspected IPF, the most important application of BAL is in the exclusion of other diagnoses. Prominent lymphocytosis (>30%) generally allows excluding a diagnosis of IPF. Pulmonary function tests
Spirometry classically reveals a reduction in the vital capacity (VC) with either a proportionate reduction in airflows, or increased airflows for the observed vital capacity. The latter finding reflects the increased lung stiffness (reduced lung compliance) associated with pulmonary fibrosis, which leads to increased lung elastic recoil.Measurement of static lung volumes using body plethysmography or other techniques typically reveals reduced lung volumes (restriction). This reflects the difficulty encountered in inflating the fibrotic lungs. The diffusing capacity for carbon monoxide (DLCO) is invariably reduced in IPF and may be the only abnormality in mild or early disease. Its impairment underlies the propensity of patients with IPF to exhibit oxygen desaturation with exercise which can also be evaluated using the 6-minute walk test (6MWT).Terms such as mild, moderate, and severe are sometimes used for staging disease and are commonly based on resting pulmonary function test measurements. However, there is no clear consensus regarding the staging of IPF patients and what are the best criteria and values to use. | Updated international guidelines were published in 2022, which some simplification in diagnosis and the removal of antacids as a possible adjunct therapy. Signs and symptoms
In many people, symptoms are present for a considerable time before diagnosis. The most common clinical features of IPF include the following:
Age over 50 years
Dry, non-productive cough on exertion
Progressive exertional dyspnea (shortness of breath with exercise)
Dry, inspiratory bibasilar "velcro-like" crackles on auscultation (a crackling sound in the lungs during inhalation similar to Velcro being torn apart slowly, heard with a stethoscope). Clubbing of the digits, a disfigurement of the finger tips or toes (see image)
Abnormal pulmonary function test results, with evidence of restriction and impaired gas exchange.Some of these features are due to chronic hypoxemia (oxygen deficiency in the blood), are not specific for IPF, and can occur in other pulmonary disorders. IPF should be considered in all patients with unexplained chronic exertional dyspnea who present with cough, inspiratory bibasilar crackles, or finger clubbing.Assessment of "velcro" crackles on lung auscultation is a practical way to improve the earlier diagnosis of IPF. Fine crackles are easily recognized by clinicians and are characteristic of IPF.If bilateral fine crackles are present throughout the inspiratory time and are persisting after several deep breaths, and if remaining present on several occasions several weeks apart in a subject aged ≥60 years, this should raise the suspicion of IPF and lead to consideration of an HRCT scan of the chest which is more sensitive than a chest X-ray. | 11
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Thus, the physiological range of GCs is monitored by the negative feedback loop GCs exert on any portion of the HPA axis. Methylprednisolone structurally and functionally mimics endogenous corticoids and will act upon the HPA axis in a similar fashion. Pharmacokinetics
Methylprednisolone is approved for oral and parenteral administration. Methylprednisolone (Medrol) for oral administration is available in a tablet formulation in 2 mg, 4 mg, 8 mg, 16 mg or 32 mg strengths. Both methylprednisolone acetate (Depo-Medrol) and methylprednisolone succinate (Solu-Medrol) are approved for intramuscular injection. Depo-Medrol is additionally approved for intralesional, intra-articular, and soft tissue injections. Depo-Medrol is available as sterile aqueous solution in 20 mg/mL, 40 mg/mL, or 80 mg/mL strengths. Solu-Medrol is the only derivative of methylprednisolone that is approved for intravenous infusion, as the sterile powder is soluble in water and can be mixed with a diluent. Strengths vary from 40 mg to 2g.Synthetic glucocorticoids are similar to endogenous steroids in metabolism, but differ in affinity for glucocorticoid and mineralocorticoid receptors, affinity for protein-binding, rate of elimination, and metabolic products.Oral methylprednisolone is readily absorbed from the gastrointestinal tract with a bioavailability of 89.9%. In contrast to endogenous GCs, methylprednisolone does not bind to the glycoprotein transcortin (corticosteroid binding globulin, CBG) but does have moderate protein binding to albumin. Thus, pharmacokinetics of methylprednisolone is linear and show no dose dependency. Patients exhibiting low albumin concentrations are at risk for adverse effects during glucocorticoid therapy. | Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol) is a synthetic glucocorticoid, primarily prescribed for its anti-inflammatory and immunosuppressive effects. It is either used at low doses for chronic illnesses or used concomitantly at high doses during acute flares. Methylprednisolone and its derivatives can be administered orally or parenterally.Regardless of route of administration, methylprednisolone integrates systemically as exhibited by its effectiveness to quickly reduce inflammation during acute flares. It is associated with many adverse reactions that require tapering off the drug as soon as the disease is under control. Serious side effects include iatrogenic Cushings Syndrome, hypertension, osteoporosis, diabetes, infection, and skin atrophy.Chemically, methylprednisolone is a synthetic pregnane steroid hormone derived from hydrocortisone and prednisolone. It belongs to a class of synthetic glucocorticoids and more generally, corticosteroids. It acts as a mineralocorticoid and glucocorticoid receptor agonist. In comparison to other exogenous glucocorticoids, methylprednisolone has a higher affinity to glucocorticoid receptors than to mineralocorticoid receptors. Glucocorticoids name was derived after the discovery of their involvement in regulating carbohydrate metabolism. The cellular functions of glucocorticoids, such as methylprednisolone, are now understood to regulate homeostasis, metabolism, development, cognition, and inflammation. They play a critical role in adapting and responding to environmental, physical and emotional stress.Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and FDA approved in the United States in October 1957. In 2019, it was the 161st most commonly prescribed medication in the United States, with more than 3 million prescriptions. | 11
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They may be unusually sensitive or insensitive to sound, light, and other stimuli; these sensory responses are found in other developmental disorders and are not specific to AS or to ASD. There is little support for increased fight-or-flight response or failure of habituation in autism; there is more evidence of decreased responsiveness to sensory stimuli, although several studies show no differences.Hans Aspergers initial accounts and other diagnostic schemes include descriptions of physical clumsiness. Children with AS may be delayed in acquiring skills requiring dexterity, such as riding a bicycle or opening a jar, and may seem to move awkwardly or feel "uncomfortable in their own skin". They may be poorly coordinated or have an odd or bouncy gait or posture, poor handwriting, or problems with motor coordination. They may show problems with proprioception (sensation of body position) on measures of developmental coordination disorder (motor planning disorder), balance, tandem gait, and finger-thumb apposition. There is no evidence that these motor skills problems differentiate AS from other high-functioning ASDs.Children with AS are more likely to have sleep problems, including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. AS is also associated with high levels of alexithymia, which is difficulty in identifying and describing ones emotions. Although AS, lower sleep quality, and alexithymia are associated with each other, their causal relationship is unclear. Causes
Hans Asperger described common traits among his patients family members, especially fathers, and research supports this observation and suggests a genetic contribution to Asperger syndrome. | Causes
Diabetes mellitus is classified into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes, hyperglycemia first detected during pregnancy, "unclassified diabetes", and "other specific types". "Hybrid forms of diabetes" include slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes. "Hyperglycemia first detected during pregnancy" includes gestational diabetes mellitus and diabetes mellitus in pregnancy (type 1 or type 2 diabetes first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes. Diabetes is a more variable disease than once thought and people may have combinations of forms. Type 1
Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile diabetes" due to the frequent onset in children, the majority of individuals living with type 1 diabetes are now adults. | 0-1
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Epiploic appendagitis (EA) is an uncommon, benign, self-limiting inflammatory process of the epiploic appendices. Other, older terms for the process include appendicitis epiploica and appendagitis, but these terms are used less now in order to avoid confusion with acute appendicitis. Epiploic appendices are small, fat-filled sacs or finger-like projections along the surface of the upper and lower colon and rectum. They may become acutely inflamed as a result of torsion (twisting) or venous thrombosis. The inflammation causes pain, often described as sharp or stabbing, located on the left, right, or central regions of the abdomen. There is sometimes nausea and vomiting. The symptoms may mimic those of acute appendicitis, diverticulitis, or cholecystitis. The pain is characteristically intense during/after defecation or micturition (espec. in the sigmoid type) due to the effect of traction on the pedicle of the lesion caused by straining and emptying of the bowel and bladder. Initial lab studies are usually normal. EA is usually diagnosed incidentally on CT scan which is performed to exclude more serious conditions. Although it is self-limiting, epiploic appendagitis can cause severe pain and discomfort. It is usually thought to be best treated with an anti-inflammatory and a moderate to severe pain medication (depending on the case) as needed. Surgery is not recommended in nearly all cases. Sand and colleagues, however, recommend laparoscopic surgery to excise the inflamed appendage in most cases in order to prevent recurrence. Signs and symptoms
The condition commonly occurs in patients in their 40s and 50s predominantly in men. | Pathognomonic CT scan data represent EA as 2–4 cm, oval shaped, fat density lesions, surrounded by inflammation. Contrasting with diverticulitis findings, the colonic wall is mostly unchanged. Management
Epiploic appendagitis is self-limiting and can be managed conservatively with NSAIDs. Epidemiology
Acute epiploic appendigitis is usually associated with obesity, hernia and unaccustomed exercise. The inflammation of the epiploic appendages normally resolves on its own for most patients. It is possible however uncommon for acute epiploic appendigitis to result in adhesion, bowel obstruction, intussusception, intraperitoneal loose body, peritonitis, and/or abscess formation. Treatment consists of reassurance of the patient and analgesics. Under non invasive treatment, symptoms resolve in two weeks. Hospitalization is not necessary. References
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Post-traumatic epilepsy (PTE) is a form of acquired epilepsy that results from brain damage caused by physical trauma to the brain (traumatic brain injury, abbreviated TBI). A person with PTE experiences repeated post-traumatic seizures (PTS, seizures that result from TBI) more than a week after the initial injury. PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of acquired epilepsy (in which seizures are caused by an identifiable organic brain condition).It is not known who will develop epilepsy after TBI and who will not. However, the likelihood that a person will develop PTE is influenced by the severity and type of injury; for example penetrating injuries and those that involve bleeding within the brain confer a higher risk. The onset of PTE can occur within a short time of the physical trauma that causes it, or months or years after. People with head trauma may remain at a higher risk for post-traumatic seizures than the general population even decades after the injury. PTE may be caused by several biochemical processes that occur in the brain after trauma, including overexcitation of brain cells and damage to brain tissues by free radicals.Diagnostic measures include electroencephalography (EEG) and brain imaging techniques such as magnetic resonance imaging, but these are not totally reliable. Antiepileptic drugs do not prevent the development of PTE after head injury, but may be used to treat the condition if it does occur. When medication does not work to control the seizures, surgery may be needed. | Although infection is not the reason or cause of chronic bronchitis, it is seen to aid in sustaining the bronchitis. Diagnosis
A physical examination will often reveal decreased intensity of breath sounds, wheezing, rhonchi, and prolonged expiration. During examination for physicians rely on history and the presence of persistent or acute onset of cough, followed by a URTI with no traces of pneumonia. Acute bronchitis is typically a clinical diagnosis that relies on patients history and exam, and should be suspected in patients with an acute onset of cough, which often follows a URTI without traces of pneumonia.Although there is no universally-accepted clinical definition for acute bronchitis, there is a proposed set of practical criteria (Macfarlane, 2001) that include:
An acute illness of less than three weeks. Cough as the predominant symptom. At least one other lower respiratory tract symptom, such as sputum production, wheezing, chest pain. No alternative explanation for the symptoms.A variety of tests may be performed in people presenting with cough and shortness of breath:
A chest X-ray is useful to exclude pneumonia which is more common in those with a fever, fast heart rate, fast respiratory rate, or who are old. A sputum sample showing neutrophil granulocytes (inflammatory white blood cells) and culture showing that has pathogenic microorganisms such as Streptococcus species. A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein).Decreased breath sounds, crackles, wheezing, and rhonchi that clears with coughs may be heard in the chest. | 0-1
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These animals all consume diets that require little storage of food, no predigestion with gastric juices, or both.The gastric lining is usually divided into two regions, an anterior portion lined by fundic glands and a posterior portion lined with pyloric glands. Cardiac glands are unique to mammals, and even then are absent in a number of species. The distributions of these glands vary between species, and do not always correspond with the same regions as in humans. Furthermore, in many non-human mammals, a portion of the stomach anterior to the cardiac glands is lined with epithelium essentially identical to that of the oesophagus. Ruminants, in particular, have a complex stomach, the first three chambers of which are all lined with oesophageal mucosa.In birds and crocodilians, the stomach is divided into two regions. Anteriorly is a narrow tubular region, the proventriculus, lined by fundic glands, and connecting the true stomach to the crop. Beyond lies the powerful muscular gizzard, lined by pyloric glands, and, in some species, containing stones that the animal swallows to help grind up food.In insects there is also a crop. The insect stomach is called the midgut. Information about the stomach in echinoderms or molluscs can be found under the respective articles. Additional images
See also
Gastroesophageal reflux disease
Human gastrointestinal microbiota
Proton-pump inhibitor
References
External links
Stomach at the Human Protein Atlas
"Stomach" article from the Encyclopedia of Nursing & Allied Health, from enotes.com
Digestion of proteins in the stomach or tiyan
Site with details of how ruminants process food
Control of Gastric Emptying Archived 2019-11-12 at the Wayback Machine | This procedure has been shown to be beneficial in 50% of cases. Epidemiology
This syndrome is predominantly found in young women, but also occurs in children, teenagers and octogenarians. == References == | 0-1
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During pregnancy, the placenta converts the androgenic hormones dehydroepiandrosterone (DHEA) and DHEA sulfate to the estrogenic hormones estrone and estradiol, respectively; after these estrogens are produced by the placenta, they are transferred into the babys circulation, thereby leading to temporary gynecomastia in the baby. In some infants, neonatal milk (also known as "witchs milk") can leak from the nipples. The temporary gynecomastia seen in newborn babies usually resolves after two or three weeks. Adolescents
Hormonal imbalance (elevated ratio of estrogen to androgen) during early puberty, either due to decreased androgen production from the adrenals and/or increased conversion of androgens to estrogens, leads to transient gynecomastia in adolescent males. It can occur in up to 65% of adolescents as early as age 10 and peaks at ages 13 and 14. It is self-limited in 75-90% of adolescents and usually resolves spontaneously within 1 to 3 years as pubertal progression increases testosterone levels and cause regression of breast tissue. By age 17, only 10% of adolescent males have persistent gynecomastia. Older adults
Declining testosterone levels and an increase in the level of subcutaneous fatty tissue seen as part of the normal aging process can lead to gynecomastia in older males. Increased fatty tissue, a major site of aromatase activity, leads to increased conversion of androgenic hormones such as testosterone to estrogens. Additionally, levels of sex hormone binding globulin (SHBG) increase with age and bind with less affinity to estrogen than androgens. | Bowel infarction or gangrenous bowel represents an irreversible injury to the intestine resulting from insufficient blood flow. It is considered a medical emergency because it can quickly result in life-threatening infection and death. Any cause of bowel ischemia, the earlier reversible form of injury, may ultimately lead to infarction if uncorrected. The causes of bowel ischemia or infarction include primary vascular causes (for example, mesenteric ischemia) and other causes of bowel obstruction. Causes
Primary vascular causes of bowel infarction, also known as mesenteric ischemia, are due to blockages in the arteries or veins that supply the bowel. Types of mesenteric ischemia are generally separated into acute and chronic processes, because this helps determine treatment and prognosis.Bowel obstruction is most often caused by intestinal adhesions, which frequently form after abdominal surgeries, or by chronic infections such as diverticulitis, hepatitis, and inflammatory bowel disease. The condition may be difficult to diagnose, as the symptoms may resemble those of other bowel disorders. Bowel volvulus describes a specific form of bowel obstruction, where the intestine and/or mesentery are twisted, resulting in ischemia. Management
An infarcted or dead intestinal segment is a serious medical problem because intestines contain non-sterile contents within the lumen. Although the fecal content and high bacterial loads of the intestine are normally safely contained, progressive ischemia causes tissue breakdown and inevitably leads to bacteria spreading to the bloodstream. | 0-1
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Controlled decisions are effortful and largely conscious processes in which an individual weighs alternatives and makes a more deliberate decision. Automatic Process: Automatic processes have four main features. They occur unintentionally or without a conscious decision, the cost of the decision is very low in mental resources, they cannot be easily stopped, and they occur without conscious thought on the part of the individual making them. Controlled Process: Controlled processes also have four main features that are very close to the opposite in spectrum from their automatic counterparts. Controlled processes occur intentionally, they require the expenditure of cognitive resources, the individual making the decision can stop the process voluntarily, and the mental process is a conscious one.Dual process theories at one time considered any single action/thought as either being automatic or controlled. However, currently they are seen as operating more along a continuum as most impulsive actions will have both controlled and automatic attributes. Automatic processes are classified according to whether they are meant to inhibit or to facilitate a thought process. For example, in one study researchers offered individuals a choice between a 1 in 10 chance of winning a prize and a 10 in 100 chance. Many participants chose one of the choices over the other without identifying that the chances inherent in each were the same as they saw either only 10 chances total as more beneficial, or of having 10 chances to win as more beneficial. | Individual differences in discounting curves are affected by personality characteristics such as self-reports of impulsivity and locus of control; personal characteristics such as age, gender, IQ, race, and culture; socioeconomic characteristics such as income and education; and many other variables. to drug addiction. Lesions of the nucleus accumbens core subregion or basolateral amygdala produce shifts towards choosing the smaller-sooner reward, suggesting the involvement of these brain regions in the preference for delayed reinforcers. There is also evidence that the orbitofrontal cortex is involved in delay discounting, although there is currently debate on whether lesions in this region result in more or less impulsivity.Economic theory suggests that optimal discounting involves the exponential discounting of value over time. This model assumes that people and institutions should discount the value of rewards and punishments at a constant rate according to how delayed they are in time. While economically rational, recent evidence suggests that people and animals do not discount exponentially. Many studies suggest that humans and animals discount future values according to a hyperbolic discounting curve where the discount factor decreases with the length of the delay (for example, waiting from today to tomorrow involves more loss of value than waiting from twenty days to twenty-one days). Further evidence for non-constant delay discounting is suggested by the differential involvement of various brain regions in evaluating immediate versus delayed consequences. | 11
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The fact that the CIA organized a fake vaccination program in 2011 to help find Osama Bin Laden is an additional cause of distrust. In 2015, the WHO announced a deal with the Taliban to encourage them to distribute the vaccine in areas they control. However, the Pakistani Taliban was not supportive. On 11 September 2016, two unidentified gunmen associated with the Pakistani Taliban, Jamaat-ul-Ahrar, shot Zakaullah Khan, a doctor who was administering polio vaccines in Pakistan. The leader of the Jamaat-ul-Ahrar claimed responsibility for the shooting and stated that the group would continue this type of attack. Such resistance to and scepticism of vaccinations has consequently slowed down the polio eradication process within the two remaining endemic countries. Travel requirements
Travellers who wish to enter or leave certain countries must be vaccinated against polio, usually at most 12 months and at least 4 weeks before crossing the border, and be able to present a vaccination record/certificate at the border checks. : 25–27 Most requirements apply only to travel to or from so-called polio-endemic, polio-affected, polio-exporting, polio-transmission, or high-risk countries. As of August 2020, Afghanistan and Pakistan are the only polio-endemic countries in the world (where wild polio has not yet been eradicated). Several countries have additional precautionary polio vaccination travel requirements, for example to and from key at-risk countries, which as of December 2020 include China, Indonesia, Mozambique, Myanmar, and Papua New Guinea. | This resulted in the APHA arranging a Symposium on Poliomyelitis to be delivered at the Annual Meeting of their Southern Branch the following month. It was during the discussion at this meeting that Dr. James Leake of the U.S. Public Health Service stood to immediately present clinical evidence that the Kolmer vaccine had caused several deaths and then allegedly accused Kolmer of being a murderer. As Rivers recalled in his oral history, "All hell broke loose, and it seemed as if everybody was trying to talk at the same time....Jimmy Leake used the strongest language that I have ever heard used at a scientific meeting." In response to the attacks from all sides, Brodie was reported to have stood up and stated, "It looks as though, according to Dr. Rivers, my vaccine is no good, and, according to Dr. Leake, Dr Kolmers is dangerous." Kolmer simply responded by stating, "Gentlemen, this is one time I wish the floor would open up and swallow me." Ultimately, Kolmers live vaccine was undoubtedly shown to be dangerous and had already been withdrawn in September 1935 prior to the Milwaukee meeting. While the consensus of the symposium was largely sceptical of the efficacy of Brodies vaccine, its safety was not in question and the recommendation was for a much larger well-controlled trial. | 11
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Rhizomelic chondrodysplasia punctata is a rare developmental brain disorder characterized by systemic shortening of the proximal bones (i.e. rhizomelia), seizures, recurrent respiratory tract infections and congenital cataracts. The affected individuals have low levels of plasmalogens. Signs and symptoms
Rhizomelic chondrodysplasia punctata has the following symptoms:
Bilateral shortening of the femur
Post-natal growth problems (deficiency)
Cataracts
Intellectual disability
Possible seizures
Possible infections of respiratory tract
Genetics
This condition is a consequence of mutations in the PEX7 gene, the GNPAT gene (which is located on chromosome 1) or the AGPS gene. The condition is acquired in an autosomal recessive manner. Pathophysiology
The mechanism of rhizomelic chondrodysplasia punctata in the case of type 1 of this condition one finds that peroxisome objective is PEX7, in peroxisome assembly. There are 3 pathways that count on PEX7 and are:
AGPS (catalyzes plasmalogen biosynthesis)
PhYH (catalyzes catabolism of phytanic acid)
ACAA1 (catalyzes beta-oxidation of VLCFA - straight)
Diagnosis
The diagnosis of rhizomelic chondrodysplasia punctata can be based on genetic testing as well as radiography results, plus a physical examination of the individual. Types
Type 1 (RCDP1) is associated with PEX7 mutations; these are peroxisome biogenesis disorders where proper assembly of peroxisomes is impaired. Type 2 (RCDP2) is associated with DHAPAT mutations
Type 3 (RCDP3) is associated with AGPS mutations
Treatment
Management of rhizomelic chondrodysplasia punctata can include physical therapy; additionally orthopedic procedures improved function sometimes in affected people. However, the prognosis is poor in this condition. See also
Plasmalogen
Peroxisomal disorder
References
Further reading
== External links == | The etiology or duration of renal failure seems not to be relevant, but NSF risk greatly depends on the residual kidney function. The majority of NSF cases have been identified in patients with stage 5 CKD, but NSF has also developed in patients with stage 4 and 3 CKD, and those with acute kidney injury, even if kidney function subsequently returned to normal following GBCA administration. Thus NSF should be considered as a differential diagnosis in any patient who has been exposed to a GBCA, regardless of the kidney function level.Three GBCAs have been principally implicated in NSF: gadodiamide, gadopentetate dimeglumine, and gadoversetamide, though cases have been reported with majority of GBCAs on the market. High doses in individual GBCA administrations and high cumulative doses of GBCA over the lifetime of patients with renal dysfunction are associated with increased risk of NSF. Mechanism
De-chelation of Gd(III) is responsible for the toxicity associated with gadolinium complexes such as GBCAs, and the toxicity appears to be a consequence of Zn2+, Cu2+, and Ca2+ transmetallation in vivo. This hypothesis is supported by acute toxicity experiments, which demonstrate that despite a 50-fold range of LDse values for four Gd(III) complexes, all become lethally toxic when they release precisely the same quantity of Gd(III). It is also supported by subchronic rodent toxicity experiments, which demonstrate a set of gross and microscopic findings similar to those known to be caused by Zn2+ deficiency. | 0-1
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Chronic mountain sickness (CMS) is a disease in which the proportion of blood volume that is occupied by red blood cells increases (polycythaemia) and there is an abnormally low level of oxygen in the blood (hypoxemia). CMS typically develops after extended time living at high altitude (over 2,500 metres (8,200 ft)). It is most common amongst native populations of high altitude nations. The most frequent symptoms of CMS are headache, dizziness, tinnitus, breathlessness, palpitations, sleep disturbance, fatigue, loss of appetite, confusion, cyanosis, and dilation of veins.CMS was first described in 1925 by Carlos Monge Medrano, a Peruvian doctor who specialised in diseases of high altitude. While acute mountain sickness is experienced shortly after ascent to high altitude, chronic mountain sickness may develop only after many years of living at high altitude. In medicine, high altitude is defined as over 2,500 metres (8,200 ft), but most cases of CMS occur at over 3,000 metres (9,800 ft). It has recently been correlated with increased expression of the genes ANP32D and SENP1. Diagnosis
CMS is characterised by polycythaemia (with subsequent increased haematocrit) and hypoxaemia; raised blood pressure in the lungs (pulmonary hypertension) can develop over time and in some cases progress to heart failure (cor pulmonale). CMS is believed to arise because of an excessive production of red blood cells (erythrocytes) due to the low oxygen levels at altitude, which increases the oxygen carrying capacity of the blood[1]. The increased levels of erythrocytes causes increased blood viscosity and uneven blood flow through the lungs (V/Q mismatch). | CMS prevalence rates reported from the study are summarised below:
Ethiopia [3600–4100 m]: 0%
Tibetan Plateau (Tibetans): 0.91–1.2%
Indian Himalayas [3000–4200 m]: 4–7%
Kyrgyzstan [3000–4200 m]: 4.6%
Tibetan Plateau (Han Chinese): 5.6%
La Paz, Bolivia [3600 m]: 6% to 8%
Bolivia: 8–10%
Cerro de Pasco, Peru [4300 m]: 14.8–18.2%
References
External links
^ Online calculator illustrating blood oxygen carrying capacity at altitude | 11
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In Blum & Ritters study in West Germany (1990), they found that 27% of their population had only minor issues, 72% had a palpable mass at the site, and 23% reported pain and other signs of inflammation such as hyperthermia, pulsation, and cystic, pustular, or papular lesions. Size of masses were an average of 2 cm in diameter ranging up to 4 cm, some being associated with purulent drainage, continuous discharge, and crusting. Dystrophic calcinosis cutis has also been reported. Other serious sequelae include sialolithiasis of the submandibular gland and adenolymphoma of the parotid gland.The histopathology of fiddlers neck frequently shows hyperkeratosis and acanthosis, along with plugging of follicles. Histiocytic infiltration with granulomas to foreign body and follicular cysts are also common. Foreign body granulomas are thought to derive from abrasion of the wooden surface of the chin rest and its absorption into the superficial dermis. The location and complex mechanism of causation for fiddlers neck give rise to a wider spectrum of skin changes when compared to contact dermatitis from more common irritants. Fiddlers neck can be differentiated from rosacea and sarcoid reaction with granulomas. Causes
The proximal causes of fiddlers neck are friction and pressure, but both repetitive shearing stress and occlusion with consequent trapping of sweat give rise to progressive damage. This damage along with poor hygiene predisposes the area to local infection, and such infection can progress to scarring and other long-term effects. | Diagnosis
The following tests have been promoted as supposedly diagnosing placental insufficiency, but all have been unsuccessful at predicting stillbirth due to placental insufficiency:
Placental grading
Amniotic fluid index
Fetal biophysical profile test scoring
Doppler velocimetry
Routine ultrasound scanning
Detection and management of maternal diabetes mellitus
Antenatal fetal heart rate monitoring using cardiotocography
Vibroacoustic stimulation, fetal movement counting
Home vs. hospital-based bed rest and monitoring in high-risk pregnancy
In-hospital fetal surveillance unit
Use of the partograph during labor
Cardiotocography during labor with or without pulse oximetry
See also
Small for gestational age
References
== External links == | 0-1
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Surgically
This procedure is done through open heart surgery (sternotomy or thoracotomy) using an ECC where the heart is stopped to allow a system of special cannulas to be placed. The hole is closed by a direct suture (sewing) if the hole is small enough or if the hole is larger, suturing (sewing) a small patch of pericardium (heart tissue or skin) or fabric to close the hole.To increase quality life following ASD procedures/surgeries, patients should have a physical exam and ECG every 3, 6, and 12 months with their cardiologist. For many patients with secundum ASD closure repair, they can return to their normal activities unless their procedure was heart catheterization which in this case they should rest for a few days. All patients should remain on blood thinner medication for at least 6 months and up to a year unless the patient had a stroke in which they would always be on blood thinners. Patients with coronary artery disease or pulmonary hypertension will take additional medicines described by their physician. For patients who had heart surgery to repair the defect or received a transcatheter closure device, they will need to take some form of antibiotics to prevent infections such as endocarditis for at least 6 months following the procedure.Success with ASD closure is very high, 96% for percutaneous procedures and 100% of ASD surgeries as found by one research group. | Signs and symptoms
A list of the common side effects broken down by frequency.Very frequent
Abnormal gastrointestinal tract
Absent pectoral muscles
Brachydactyly (Short fingers)
Dextrocardia
Diaphragmatic hernia/defect
Humerus absent/abnormal
Liver/biliary tract anomalies
Maternal diabetes
Oligodactyly/missing fingers
Radius absent/abnormal
Rhizomelic micromelia (relatively shorter proximal segment of the limbs compared to the middle and the distal segments)
Sparsity or abnormality of axillary hair on affected side
Syndactyly of fingers (webbing)
Ulna absent/abnormal
Upper limb asymmetry
Abnormal rib
Simian crease on affected sideFrequent
Hypoplastic/absent nipples
Scapula anomalyOccasional
Agenesis/hypoplasia of kidneys
Encephalocele/exencephaly
Abnormal morphology of hypothalamic-hypophyseal axis
Abnormal function of hypothalamic-hypophyseal axis
Microcephaly
Preaxial polydactyly
Ureteric anomalies (reflux/duplex system)
Vertebral segmentation anomalyIt is usually considered a unilateral condition. Some have claimed that the term can be applied in bilateral presentation, but others recommend using alternate terminology in those cases. Causes
The cause of Poland syndrome is unknown. However, an interruption of the embryonic blood supply to the arteries that lie under the collarbone (subclavian arteries) at about the 46th day of embryonic development is the prevailing theory.The subclavian arteries normally supply blood to embryonic tissues that give rise to the chest wall and hand. Variations in the site and extent of the disruption may explain the range of signs and symptoms that occur in Poland syndrome. Abnormality of an embryonic structure called the apical ectodermal ridge, which helps direct early limb development, may also be involved in this disorder. Diagnosis
Poland syndrome is usually diagnosed at birth, based upon the physical characteristics. Imaging techniques such as a CT scan may reveal the extent to which the muscles are affected. The syndrome varies in severity and as such is often not reported until puberty, when lopsided growth becomes apparent. | 0-1
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Tay–Sachs disease belongs to the latter. Other
Other lipid storage disorders that generally are not classified as sphingolipidoses include fucosidosis, Schindler disease, and Wolman disease. Genetics
Lipid storage diseases can be inherited two ways:
Autosomal recessive inheritance occurs when both parents carry and pass on a copy of the faulty gene, but neither parent show signs and symptoms of the condition and is not affected by the disorder. Each child born to these parents have a 25 percent chance of inheriting both copies of the defective gene, a 50 percent chance of being a carrier, and a 25 percent chance of not inheriting either copy of the defective gene. Children of either gender may be affected by an autosomal recessive this pattern of inheritance.X-linked recessive (or sex linked) inheritance occurs when the mother carries the affected gene on the X chromosome that has determined the childs gender and passes it to her son. Sons of carriers have a 50 percent chance of inheriting the disorder. Daughters have a 50 percent chance of inheriting the X-linked chromosome, but usually are not severely affected by the disorder. Affected men do not pass the disorder to their sons, but their daughters will be carriers for the disorder. Diagnosis
Diagnosis of the lipid storage disorders can be achieved through the use of several tests. These tests include clinical examination, biopsy, genetic testing, molecular analysis of cells or tissues, and enzyme assays. Certain forms of this disease also can be diagnosed through urine testing, which detects the stored material. | The enzymes OxyA, OxyB, OxyC, and OxyD are cytochrome P450 enzymes. OxyB catalyzes oxidative cross-linking between residues 4 and 6, OxyA between residues 2 and 4, and OxyC between residues 5 and 7. This cross-linking occurs while the heptapeptide is covalently bound to the PCP domain of the 7th NRPS module. These P450s are recruited by the X domain present in the 7th NRPS module, which is unique to glycopeptide antibiotic biosynthesis. The cross-linked heptapeptide is then released by the action of the TE domain, and methyltransferase Vmt then N-methylates the terminal leucine residue. GtfE then joins D-glucose to the phenolic oxygen of residue 4, followed by the addition of vancosamine catalyzed by GtfD. Some of the glycosyltransferases capable of glycosylating vancomycin and related nonribosomal peptides display notable permissivity and have been employed for generating libraries of differentially glycosylated analogs through a process known as glycorandomization. Total synthesis
Both the vancomycin aglycone and the complete vancomycin molecule have been targets successfully reached by total synthesis. The target was first achieved by David Evans in October 1998, KC Nicolaou in December 1998, Dale Boger in 1999, and has recently been more selectively synthesized again by Dale Boger in 2020. Pharmacology and chemistry
Vancomycin is a branched tricyclic glycosylated nonribosomal peptide produced by the Actinomycetota species Amycolatopsis orientalis (formerly designated Nocardia orientalis). Vancomycin exhibits atropisomerism — it has multiple chemically distinct rotamers owing to the rotational restriction of some of the bonds. The form present in the drug is the thermodynamically more stable conformer. | 0-1
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DNA test
The muscle-specific isoform of the dystrophin gene is composed of 79 exons, and DNA testing (blood test) and analysis can usually identify the specific type of mutation of the exon or exons that are affected. DNA testing confirms the diagnosis in most cases. Muscle biopsy
If DNA testing fails to find the mutation, a muscle biopsy test may be performed. A small sample of muscle tissue is extracted using a biopsy needle. The key tests performed on the biopsy sample for DMD are immunohistochemistry, immunocytochemistry, and immunoblotting for dystrophin, and should be interpreted by an experienced neuromuscular pathologist. These tests provide information on the presence or absence of the protein. Absence of the protein is a positive test for DMD. Where dystrophin is present, the tests indicate the amount and molecular size of dystrophin, helping to distinguish DMD from milder dystrophinopathy phenotypes. Over the past several years, DNA tests have been developed that detect more of the many mutations that cause the condition, and muscle biopsy is not required as often to confirm the presence of DMD. Prenatal tests
A prenatal test can be considered when the mother is a known or suspected carrier.Prenatal tests can tell whether the unborn child has one of the most common mutations. | This functional, yet truncated, form of dystrophin gave rise to the notion that shorter dystrophin can still be therapeutically beneficial. Concurrently, Kole et al. had modified splicing by targeting pre-mRNA with antisense oligonucleotides (AONs). Kole demonstrated success using splice-targeted AONs to correct missplicing in cells removed from beta-thalassemia patients Wiltons group tested exon skipping for muscular dystrophy. Gene therapy
Researchers are working on a gene editing method to correct a mutation that leads to Duchenne muscular dystrophy (DMD). Researchers used a technique called CRISPR/Cas9-mediated genome editing, which can precisely remove a mutation in the dystrophin gene in DNA, allowing the bodys DNA repair mechanisms to replace it with a normal copy of the gene. The benefit of this over other gene therapy techniques is that it can permanently correct the "defect" in a gene rather than just transiently adding a "functional" one.Genome editing through the CRISPR/Cas9 system is not currently feasible in humans. However, it may be possible, through advancements in technology, to use this technique to develop therapies for DMD in the future. In 2007, researchers did the worlds first clinical (viral-mediated) gene therapy trial for Duchenne MD.Biostrophin is a delivery vector for gene therapy in the treatment of Duchenne muscular dystrophy and Becker muscular dystrophy. References
Further reading
Birnkrant DJ, Bushby K, Bann CM, Apkon SD, Blackwell A, Brumbaugh D, et al. (March 2018). "Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management". Lancet Neurol. 17 (3): 251–267. doi:10.1016/S1474-4422(18)30024-3. PMC 5869704. PMID 29395989. | 11
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It is not useful for spasticity due to neurologic conditions such as cerebral palsy.A 2004 review found benefit for fibromyalgia symptoms, with a reported number needed to treat of 4.8 (meaning that 1 person out of every 4.8 benefits from treatment) for pain reduction, but no change in fatigue or tender points. A 2009 Cochrane review found insufficient evidence to justify its use in myofascial pain syndrome. It may also be used along with other treatments for tetanus. Side effects
Cyclobenzaprine results in increased rates of drowsiness (38%), dry mouth (24%), and dizziness (10%). Drowsiness and dry mouth appear to intensify with increasing dose. The sedative effects of cyclobenzaprine are likely due to its antagonistic effect on histamine, serotonin, and muscarinic receptors.Agitation is a common side effect observed, especially in the elderly. Some experts believe that cyclobenzaprine should be avoided in elderly patients because it can cause confusion, delirium, and cognitive impairment. In general, the National Committee for Quality Assurance recommends avoiding the use of cyclobenzaprine in the elderly because of the potential for more severe side effects.Dysphagia, a life-threatening side-effect, may rarely occur. Treatment protocols and support should follow the same as for any structurally related tricyclic, such as tricyclic antidepressants. Overdose
The most common effects of overdose are drowsiness and tachycardia. Rare but potentially critical complications are cardiac arrest, abnormal heart rhythms, severe low blood pressure, seizures, and neuroleptic malignant syndrome. Life-threatening overdose is rare, however, as the median lethal dose is about 338 milligrams/kilogram in mice and 425 mg/kg in rats. | Host genetic factors
For genotype 1 hepatitis C treated with pegylated interferon alfa-2a or pegylated interferon alfa-2b combined with ribavirin, it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in response to the treatment. This finding, originally reported in Nature, showed genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more likely to achieve sustained virological response after the treatment than others. Another report in Nature demonstrated the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus. Other infections
Has also been used for Middle East respiratory syndrome and hepatitis E.
Manufacture
It is pegylated with a branched 40 kg/mol PEG chain. The drug has been manufactured under the brand name Pegasys by Roche Pharmaceuticals. Due to changes in clinical practice - antiviral hepatitis drugs such as sofosbuvir have become much more important - Roche announced in 2020 that it would withdraw Pegasys from the market worldwide, but subsequently sold the worldwide rights to pharma&, an Austrian / Swiss pharmaceutical company that ensures supply in the medium and long term almost worldwide (excluding China and Japan). Research
A Cochrane Review sought to determine whether interferon alfa-2a could be used as a treatment for individuals with neovascular age-related macular degeneration. They found no evidence of improved visual acuity with potential harm. References
External links
"Peginterferon alfa-2a". Drug Information Portal. U.S. National Library of Medicine. Pegasys at the US National Library of Medicine Medical Subject Headings (MeSH) | 0-1
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Whole grains are another source of the vitamin, but milling to make white rice or white flour removes much of the pantothenic acid, as it is found in the outer layers of whole grains. In animal feeds, the most important sources are alfalfa, cereal, fish meal, peanut meal, molasses, rice bran, wheat bran, and yeasts. Supplements
Dietary supplements of pantothenic acid commonly use pantothenol (or panthenol), a shelf-stable analog, which is converted to pantothenic acid once consumed. Calcium pantothenate – a salt – may be used in manufacturing because it is more resistant than pantothenic acid to factors that deteriorate stability, such as acid, alkali or heat. The amount of pantothenic acid in dietary supplement products may contain up to 1,000 mg (200 times the Adequate Intake level for adults), without evidence that such large amounts provide any benefit. According to WebMD, pantothenic acid supplements have a long list of claimed uses, but there is insufficient scientific evidence to support any of them.As a dietary supplement, pantothenic acid is not the same as pantethine, which is composed of two pantothenic acid molecules linked by a disulfide bridge. Sold as a high-dose supplement (600 mg), pantethine may be effective for lowering blood levels of LDL cholesterol – a risk factor for cardiovascular diseases – but its long-term effects are unknown, requiring that its use be supervised by a physician. Dietary supplementation with pantothenic acid does not have the same effect on LDL. | Pantothenic acid, also called vitamin B5 is a water-soluble B vitamin and therefore an essential nutrient. All animals require pantothenic acid in order to synthesize coenzyme A (CoA) – essential for fatty acid metabolism – as well as to, in general, synthesize and metabolize proteins, carbohydrates, and fats.Pantothenic acid is the combination of pantoic acid and β-alanine. Its name derives from the Greek pantos, meaning "from everywhere", as minimally, at least small quantities of pantothenic acid are found in nearly every food. Human deficiency is very rare. As a dietary supplement or animal feed ingredient, the form commonly used is calcium pantothenate because of chemical stability, and hence long product shelf life, compared to sodium pantothenate or free pantothenic acid. Definition
Pantothenic acid is a water-soluble vitamin, one of the B vitamins. It is synthesized from the amino acid β-alanine and pantoic acid (see biosynthesis and structure of coenzyme A figures). Unlike vitamin E or vitamin K, which occurs in several chemically related forms known as vitamers, pantothenic acid is only one chemical compound. It is a starting compound in the synthesis of coenzyme A (CoA), a cofactor for many enzyme processes. Use in biosynthesis of coenzyme A
Pantothenic acid is a precursor to CoA via a five-step process. The biosynthesis requires pantothenic acid, cysteine, four equivalents of ATP (see figure). Pantothenic acid is phosphorylated to 4′-phosphopantothenate by the enzyme pantothenate kinase. This is the committed step in CoA biosynthesis and requires ATP. | 11
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In the most malignant form of plasma cell dyscrasias, primary plasma cell leukemia, the plasma cell population contains >1900 distinct DNA alterations in >600 genes.In general, the plasma cell dyscrasias are defined by 1) the presence of these genetically unstable clonal plasma cells, lymphoplasmacytoid cells, or B cells infiltrating the bone marrow or forming distinct masses in bone, and/or other tissues as defined by biopsy of involved tissues and 2) the presence of these cells myeloma proteins (i.e. intact monoclonal antibody, free light chain, free heavy chain, shortened version of these proteins, or any combination of these proteins) in blood and/or urine as defined by various types of gel electrophoresis. Obviously, the latter criterion does not apply to the rare cases of true non-secretory myeloma. Myeloma protein toxicity
Myeloma proteins form as a result of gene mutations rather than physiological gene remodeling responses to an instigating foreign antigen: typically these proteins are non-functional. However, they sometimes cause serious tissue damage with the kidney being a particularly vulnerable target. The toxic effects of monoclonal proteins may occur at early stages in the plasma cell dyscrasia spectrum and require treatment independently of the mass or tissue-destructive effects of the myeloma protein-producing cells. | In general, patients with plasma cell myeloma with concomitant chronic Lymphocytic Leukemia/monoclonal B-cell Lymphocytosis have been treated with the same regimens used for multiple myeloma patients unless significant complications related to the lymphocytic component of their disease (e.g. autoimmune hemolytic anemia) require treatments used in chronic lymphocytic leukemia. Some patients who lack appreciable symptoms have been followed with no specific treatment of their disease. Waldenström macroglobulinemia
According to the International Workshop on Waldenströms Macroglobulinemia, the disease is diagnosed in patients that have a serum IgM monoclonal protein and a bone marrow that contains ≥10% of its nucleated cells as lymphoplasmacytic cells. There is no requirement for symptomatic disease, a particular level of IgM protein, or presence of extramedullary (i.e. non-bone) lymphoplasmacytic cell infiltrates. The overall survival for this malignancy at 5 and 10 years among >5,000 patients is 62% and 39%, respectively, with newer treatment regimens anticipated to improve these survival rates in the future. Multiple myeloma
Multiple myeloma is diagnosed in patients that (except for non-secretory multiple myeloma patients) have a clonal IgG, IgA, IgD, or IgE myeloma protein in their serum and/or a clonal κ or λ light chain in their serum or urine plus either one of two sets of criteria. | 11
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In addition, there is a genetic component: a woman whose mother or sister had the condition is at higher risk than otherwise. Patients who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy. The occurrence of pre-eclampsia was 5% in white, 9% in Hispanic, and 11% in African American patients and this may reflect disproportionate risk of developing pre-eclampsia among ethnic groups. Additionally, black patients were also shown to have a disproportionately higher risk of dying from eclampsia. Mechanism
The mechanisms of eclampsia and preeclampsia are not definitively understood, but following provides some insight. The presence of a placenta is required, and eclampsia resolves if it is removed. Reduced blood flow to the placenta (placental hypoperfusion) may be a key feature of the process. It is typically accompanied by increased sensitivity of the maternal vasculature to agents which cause constriction of the small arteries, leading to reduced blood flow to multiple organs. Vascular dysfunction-associated maternal conditions such as Lupus, hypertension, and renal disease, or obstetric conditions that increase placental volume without an increase in placental blood flow (such as multifetal gestation) may increase risk for pre-eclampsia. Also, activation of the coagulation cascade can lead to microthrombi formation, which may further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from the blood to the interstitial space which reduces blood flow and causes edema. These events can lead to hypertension, renal dysfunction, pulmonary dysfunction, hepatic dysfunction, and cerebral edema with cerebral dysfunction and convulsions. | A median mandibular cyst is a type of cyst that occurs in the midline of the mandible, thought to be created by proliferation and cystic degeneration of resting epithelial tissue that is left trapped within the substance of the bone during embryologic fusion of the two halves of the mandible, along the plane of fusion later termed the symphysis menti. A true median mandibular cyst would therefore be classified as a non-odontogenic, fissural cyst. The existence of this lesion as a unique clinical entity is controversial, and some reported cases may have represented misdiagnosed odontogenic cysts, which are by far the most common type of intrabony cyst occurring in the jaws. It has also been suggested that the mandible develops as a bilobed proliferation of mesenchyme connected with a central isthmus. Therefore, it is unlikely that epithelial tissue would become trapped as there is no ectoderm separating the lobes in the first instance. == References == | 0-1
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Immobility can lead to pressure sores, particularly in bony areas, requiring precautions such as extra cushioning and turning in bed every two hours (in the acute setting) to relieve pressure. In the long term, people in wheelchairs must shift periodically to relieve pressure. Another complication is pain, including nociceptive pain (indication of potential or actual tissue damage) and neuropathic pain, when nerves affected by damage convey erroneous pain signals in the absence of noxious stimuli. Spasticity, the uncontrollable tensing of muscles below the level of injury, occurs in 65–78% of chronic SCI. It results from lack of input from the brain that quells muscle responses to stretch reflexes. It can be treated with drugs and physical therapy. Spasticity increases the risk of contractures (shortening of muscles, tendons, or ligaments that result from lack of use of a limb); this problem can be prevented by moving the limb through its full range of motion multiple times a day. Another problem lack of mobility can cause is loss of bone density and changes in bone structure. Loss of bone density (bone demineralization), thought to be due to lack of input from weakened or paralysed muscles, can increase the risk of fractures. Conversely, a poorly understood phenomenon is the overgrowth of bone tissue in soft tissue areas, called heterotopic ossification. It occurs below the level of injury, possibly as a result of inflammation, and happens to a clinically significant extent in 27% of people. | The constant interval between the sinus beat and PVC suggests a reentrant etiology rather than spontaneous automaticity of the ventricle.Premature atrial contractions by contrast do not have a compensatory pause, since they reset the sinus node, but atrial or supraventricular bigeminy can occur. If the PACs are very premature, the wavefront can encounter a refractory AV node and not be conducted. This can be mistaken for sinus bradycardia if the PAC is buried in the T wave since the PAC will reset the SA node and lead to a long P–P interval. Diagnosis
Rule of bigeminy
When the atrial rhythm is irregular (as in atrial fibrillation or sinus arrythmia) the presence of bigeminy depends on the length of the P–P interval and happens more frequently with a longer interval. As with post PVC pauses, a longer P–P interval leads to a higher chance of re-entrant circuits and thus PVCs. The term "rule of bigeminy" is used to refer to the dependence of bigeminy on the ventricular cycle length in irregular rhythms. Classification
There can be similar patterns depending on the frequency of abnormal beats. If every other beat is abnormal, it is described as bigeminal. If every third beat is aberrant, it is trigeminal; every fourth would be quadrigeminal. Typically, if every fifth or more beat is abnormal, the aberrant beat would be termed occasional.Bigeminy is contrasted with couplets, which are paired abnormal beats. | 0-1
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The condition was described at least as early as the 300s BC by Hippocrates. Prior to the availability of antibiotics, the risk of death was significant. Signs and symptoms
Symptoms may include pain in a specific bone with overlying redness, fever, and weakness and inability to walk especially in children with acute bacterial osteomyelitis. Onset may be sudden or gradual. Enlarged lymph nodes may be present. In fungal osteomyelitis, there is usually a history of walking bare-footed, especially in rural and farming areas. Contrary to the mode of infection in bacterial osteomyelitis, which is primarily blood-borne, fungal osteomyelitis starts as a skin infection, then invades deeper tissues until it reaches bone. Cause
In children, the metaphyses, the ends of long bones, are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.Acute osteomyelitis almost invariably occurs in children who are otherwise healthy, because of rich blood supply to the growing bones. When adults are affected, it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).Osteomyelitis is a secondary complication in 1–3% of patients with pulmonary tuberculosis. In this case, the bacteria, in general, spread to the bone through the circulatory system, first infecting the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone. | The latter smells faintly of ethanol; a 1% aqueous solution has a pH of 2–3; and the specific rotation is
[
α
]
D
25
{\displaystyle [\alpha ]_{D}^{25}}
−110° cm³/dm·g in 0.01 N methanolic hydrochloric acid. History
After penicillin revolutionized the treatment of bacterial infections in WWII, many chemical companies moved into the field of discovering antibiotics by bioprospecting. American Cyanamid was one of these, and in the late 1940s chemists there discovered chlortetracycline, the first member of the tetracycline class of antibiotics. Shortly thereafter, scientists at Pfizer discovered terramycin and it was brought to market. Both compounds, like penicillin, were natural products and it was commonly believed that nature had perfected them, and further chemical changes could only degrade their effectiveness. | 0-1
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Azelaic acid (AzA) is an organic compound with the formula HOOC(CH2)7COOH. This saturated dicarboxylic acid exists as a white powder. It is found in wheat, rye, and barley. It is a precursor to diverse industrial products including polymers and plasticizers, as well as being a component of a number of hair and skin conditioners. AzA inhibits tyrosinase. Production
Azelaic acid is industrially produced by the ozonolysis of oleic acid. The side product is nonanoic acid. It is produced naturally by Malassezia furfur (also known as Pityrosporum ovale), a yeast that lives on normal skin. The bacterial degradation of nonanoic acid gives azelaic acid. Biological function
In plants, azelaic acid serves as a "distress flare" involved in defense responses after infection. It serves as a signal that induces the accumulation of salicylic acid, an important component of a plants defensive response. Applications
Polymers and related materials
Esters of this dicarboxylic acid find applications in lubrication and plasticizers. In lubricant industries it is used as a thickening agent in lithium complex grease. With hexamethylenediamine, azelaic acid forms Nylon-6,9, which finds specialized uses as a plastic. Medical
Azelaic acid is used to treat mild to moderate acne, both comedonal acne and inflammatory acne. It belongs to a class of medication called dicarboxylic acids. It works by killing acne bacteria that infect skin pores. It also decreases the production of keratin, which is a natural substance that promotes the growth of acne bacteria. Azelaic acid is also used as a topical gel treatment for rosacea, due to its ability to reduce inflammation. | According to one report in 1988, azelaic acid in combination with zinc sulfate in vitro was found to be a potent (90% inhibition) 5α-reductase inhibitor, similar to the hair loss drugs finasteride and dutasteride. In vitro research during mid-1980s evaluating azelaic acids depigmenting (whitening) capability concluded it is effective (cytotoxic to melanocytes) at only high concentrations.A 1996 review claimed 20% AzA is as potent as 4% hydroquinone after a period of application of three months without the latters adverse effects and even more effective if applied along with tretinoin for the same period of time. Brand names
Brand names for azelaic acid include Dermaz 99, Crema Pella Perfetta (micronized azelaic acid, kojic dipalmitate, and liquorice extract), Azepur99, Azetec99, Azaclear (azelaic acid and niacinamide), AzClear Action, Azelex, White Action cream, Finacea, Finevin, Melazepam, Skinoren, Ezanic, Azelac, Azaderm, (Acnegen, Eziderm, Acnicam, Azelexin in Pakistan)
References
External links
DermNet treatments/azelaic-acid"Azelaic Acid Topical". MedlinePlus. | 11
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Twilight sedation is, however, inherently safer than general anesthesia; it also allows the patients to follow simple commands and even to watch the procedure on a closed-circuit monitor. Tens of millions of adults annually need to have colonoscopies, and yet many dont because of concerns about the procedure.Colonoscopy can be carried out without any sedation and without problems with pain, which is practised in several institutions in many countries with the patients agreement. This allows the patient to shift the body position to help the doctor carry out the procedure and significantly reduces recovery time and side-effects. There is some discomfort when the colon is distended with air, but this is not usually particularly painful, and it passes relatively quickly. Unsedated patients can be released from the hospital on their own without any feelings of nausea, able to continue with normal activities, and without the need for an escort as recommended after sedation. Ultrasound
Duodenography and colonography are performed like a standard abdominal examination using B-mode and color flow Doppler ultrasonography using a low frequency transducer — for example a 2.5 MHz — and a high frequency transducer, for example a 7.5 MHz probe. Detailed examination of duodenal walls and folds, colonic walls and haustra was performed using a 7.5 MHz probe. Deeply located abdominal structures were examined using 2.5 MHz probe. All ultrasound examinations are performed after overnight fasting (for at least 16 hours) using standard scanning procedure. Subjects are examined with and without water contrast. | Anthrax immune globulin, tradename Anthrasil, is a human immune globulin that is used in combination with antibiotics to treat anthrax. It was developed by Cangene and purchased in 2011 by the Biomedical Advanced Research and Development Authority (BARDA) under Project Bioshield. On 24 March 2015 it was granted approval by the United States Food and Drug Administration for use in treating inhalation anthrax in conjunction with antibiotics. Preparation
Anthrax immune globulin is prepared from the plasma of donors who have been vaccinated against anthrax. Safety and efficacy testing
Due to the ethical and feasibility concerns with testing the efficacy of anthrax immune globulin in humans, it was tested in rabbits and monkeys under the FDAs animal efficacy rule. Following efficacy testing, anthrax immune globulin was tested for safety in human volunteers, where the most common side effects were headache, back pain, nausea and infusion site pain and swelling. == References == | 0-1
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Other common adverse effects include abdominal pain, asthenia, headache, vomiting and, particularly in children, rash.Raised liver enzymes and hyperlipidemia (both hypertriglyceridemia and hypercholesterolemia) are also commonly observed during lopinavir/ritonavir treatment.Lopinavir/ritonavir is anticipated to have varying degrees of interaction with other medications that are also CYP3A and/or P-gp substrates.People with a structural heart disease, preexisting conduction system abnormalities, ischaemic heart disease, or cardiomyopathies should use lopinavir/ritonavir with caution.On 8 March 2011 the U.S. Food and Drug Administration notified healthcare professionals of serious health problems that have been reported in premature babies receiving lopinavir/ritonavir oral solution, probably because of its propylene glycol content. They recommend the use should be avoided in premature babies. History
Abbott Laboratories (now, via spinoff, Abbvie) was one of the earliest users of the Advanced Photon Source (APS), a national synchrotron-radiation light source at Argonne National Laboratory. One of the early research projects undertaken at the APS focused on proteins from the human immunodeficiency virus (HIV). Using the APS beam line for X-ray crystallography, researchers determined viral protein structures that allowed them to determine their approach to the development of HIV protease inhibitors, a key enzyme target that processes HIV polyproteins after infection, the function of which allows the lifecycle of the virus to proceed. | Constipation in children refers to the medical condition of constipation in children. It is a functional gastrointestinal disorder. Presentation
Children have different bowel movement patterns than adults. In addition, there is a wide spectrum of normalcy when considering childrens bowel habits. On average, infants have 3-4 bowel movements/day, and toddlers have 2-3 bowel movements per day. At around age 4, children develop an adult-like pattern of bowel movements (1-2 stools/day). Children benefit from scheduled toilet breaks, once early in the morning and 30 minutes after meals. The Rome III Criteria for constipation in children helps to define constipation for various age groups. Causes
While it is difficult to assess an exact age at which constipation most commonly arises, children frequently experience constipation in conjunction with life-changes. Examples include: toilet training, starting or transferring to a new school, and changes in diet. Especially in infants, changes in formula or transitioning from breast milk to formula can cause constipation. Fortunately, the majority of constipation cases are not tied to a medical disease, and treatment can be focused on simply relieving the symptoms. Congenital causes
A number of diseases present at birth can result in constipation. They are as a group uncommon with Hirschsprungs disease (HD) being the most common. HD is more common in males than females, affecting 1 out of 5000 babies. In people with HD, specific types of cells called neural crest cells fail to migrate to parts of the colon. | 0-1
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