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Myelophthisic anemia (or myelophthisis) is a severe type of anemia found in some people with diseases that affect the bone marrow. Myelophthisis refers to the displacement of hemopoietic bone-marrow tissue by fibrosis, tumors, or granulomas. The word comes from the roots myelo-, which refers to bone marrow, and phthysis, shrinkage or atrophy. Causes
Myelophthisis can occur in the setting of chronic myeloproliferative disease (e.g. myelofibrosis), leukemia, lymphoma, and metastatic carcinoma or myeloma. It is common in people who have chronic idiopathic myelofibrosis. It has been linked to small-cell lung cancer, breast cancer or prostate cancer that metastasizes to the bone marrow.Currently, the most common cause is displacement of bone marrow by metastatic cancer (extramedullary hematopoiesis tends to be modest). Other causes include myeloproliferative disorders (especially late-stage or spent polycythemia vera), granulomatous diseases, and (lipid) storage diseases. Myelofibrosis can occur in all of these. Factors that may contribute to decreased RBC production include a decreased quantity of functioning hematopoietic tissue, disordered metabolism related to the underlying disorder, and, in some cases, erythrophagocytosis. Pathophysiology
Some cases of myelophthisis are thought to be related to the release of cytokines that simulate fibroblastic proliferation and fibrosis in the marrow. Diagnosis
The first test for diagnosis myelophthisis involves looking at a small sample of blood under a microscope. Myelophthisis is suggested by the presence of red blood cells that contain nuclei or are teardrop-shaped (dacryocytes), or immature granulocyte precursor cells which indicates leukoerythroblastosis is occurring because the displaced hematopoietic cells begin to undergo extramedullary hematopoiesis. | Before the 17th century, the joint pain which was thought to be caused by viscous humours seeping into the joints was always referred to as gout, a word adopted in Middle English from Old French gote "a drop; the gout, rheumatism", not to be confused with the present day specific term referring to excess of uric acid.The English term rheumatism in the current sense has been in use since the late 17th century, as it was believed that chronic joint pain was caused by excessive flow of rheum which means bodily fluids into a joint. See also
Corbetts electrostatic machine
References
Further reading
Callan, Margaret (2011). The Rheumatology Handbook. 15th World Congress of Pain Clinicians, (WSPC 2012) (Illustrated ed.). World Scientific. ISBN 978-1-84816-320-1. External links
American College of Rheumatology
National Institute of Arthritis and Musculoskeletal and Skin Diseases - US National Institute of Arthritis and Musculoskeletal and Skin Diseases | 0-1
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Photokeratitis or ultraviolet keratitis is a painful eye condition caused by exposure of insufficiently protected eyes to the ultraviolet (UV) rays from either natural (e.g. intense sunlight) or artificial (e.g. the electric arc during welding) sources. Photokeratitis is akin to a sunburn of the cornea and conjunctiva. The injury may be prevented by wearing eye protection that blocks most of the ultraviolet radiation, such as welding goggles with the proper filters, a welders helmet, sunglasses rated for sufficient UV protection, or appropriate snow goggles. The condition is usually managed by removal from the source of ultraviolet radiation, covering the corneas, and administration of pain relief. Photokeratitis is known by a number of different terms including: snow blindness, arc eye, welders flash, bake eyes, corneal flash burns, flash burns, niphablepsia, or keratoconjunctivitis photoelectrica. Signs and symptoms
Common symptoms include pain, intense tears, eyelid twitching, discomfort from bright light, and constricted pupils. Cause
Any intense exposure to UV light can lead to photokeratitis. In 2010, the Department of Optometry at the Dublin Institute of Technology published that the threshold for photokeratitis is 0.12 J/m2. (Prior to this, in 1975, the Division of Biological Effects at the US Bureau of Radiological Health had published that the human threshold for photokeratitis is 50 J/m2.) Common causes include welding with failure to use adequate eye protection such as an appropriate welding helmet or welding goggles. This is termed arc eye, while photokeratitis caused by exposure to sunlight reflected from ice and snow, particularly at elevation, is commonly called snow blindness. | It can also occur due to using tanning beds without proper eyewear. Natural sources include bright sunlight reflected from snow or ice or, less commonly, from sea or sand. Fresh snow reflects about 80% of the UV radiation compared to a dry, sandy beach (15%) or sea foam (25%). This is especially a problem in polar regions and at high altitudes, as with about every 300 m (1,000 ft) of elevation (above sea level), the intensity of UV rays increases by four percent. Diagnosis
Fluorescein dye staining will reveal damage to the cornea under ultraviolet light. Prevention
Photokeratitis can be prevented by using sunglasses or eye protection that transmits 5–10% of visible light and absorbs almost all UV rays. Additionally, these glasses should have large lenses and side shields to avoid incidental light exposure. Sunglasses should always be worn, even when the sky is overcast, as UV rays can pass through clouds.The Inuit, Yupik, and other Arctic peoples carved snow goggles from materials such as driftwood or caribou antlers to help prevent snow blindness. Curved to fit the users face with a large groove cut in the back to allow for the nose, the goggles allowed in a small amount of light through a long thin slit cut along their length. The goggles were held to the head by a cord made of caribou sinew.In the event of missing sunglass lenses, emergency lenses can be made by cutting slits in dark fabric or tape folded back onto itself. | 11
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Epidermolysis bullosa simplex (EBS) is a disorder resulting from mutations in the genes encoding keratin 5 or keratin 14.: 598 Blister formation of EBS occurs at the dermoepidermal junction. Sometimes EBS is called epidermolytic. Cause
Absence of keratin-5,14 since birth. Diagnosis
Classification
Epidermolysis bullosa simplex may be divided into multiple types:
Management
No cure for EB
Treat symptoms
Protect skin, stop blister formation, promote healing
Prevent complications
Necessary treatment: use oral and topical steroid for healing and prevent complication
Maintain cool environment, avoid overheating and decreases friction
See also
Epidermolysis bullosa
List of cutaneous conditions caused by mutations in keratins
References
Further reading
GeneReviews/NCBI/UW/NIH entry on Epidermolysis Bullosa Simplex
== External links == | Treatments
As with many diseases in developing nations, (including trypanosomiasis and malaria) effective and affordable chemotherapy is sorely lacking and parasites or insect vectors are becoming increasingly resistant to existing anti-parasite drugs. Possibly due to the lack of financial return, new drugs are slow to emerge and much of the basic research into potential drug targets takes place in universities, funded by charitable organizations. Product Development Partnership, Drugs for Neglected Diseases initiative works on the development of new treatments (combination treatments and new chemical entities) for visceral leishmaniasis.The traditional treatment is with pentavalent antimonials such as sodium stibogluconate and meglumine antimoniate. Resistance is now common in India, and rates of resistance have been shown to be as high as 60% in parts of Bihar, India.The treatment of choice for visceral leishmaniasis acquired in India is now amphotericin B in its various liposomal preparations. In East Africa, the WHO recommended treatment is SSG&PM (sodium stibogluconate and paromomycin) developed by Drugs for Neglected Diseases initiative (DNDi) in 2010.Miltefosine is the first oral treatment for this disease. The cure rate of miltefosine in Phase III clinical trials is 95%; Studies in Ethiopia show that is also effective in Africa. In HIV immunosuppressed people which are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment. Miltefosine has received approval by the Indian regulatory authorities in 2002, in Germany in 2004 and in U.S.A. in 2014. It is now registered in many countries.The drug is generally better tolerated than other drugs. | 0-1
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Trichothiodystrophy (TTD) is an autosomal recessive inherited disorder characterised by brittle hair and intellectual impairment. The word breaks down into tricho – "hair", thio – "sulphur", and dystrophy – "wasting away" or literally "bad nourishment". TTD is associated with a range of symptoms connected with organs of the ectoderm and neuroectoderm. TTD may be subclassified into four syndromes: Approximately half of all patients with trichothiodystrophy have photosensitivity, which divides the classification into syndromes with or without photosensitivity; BIDS and PBIDS, and IBIDS and PIBIDS. Modern covering usage is TTD-P (photosensitive), and TTD. Presentation
Features of TTD can include photosensitivity, icthyosis, brittle hair and nails, intellectual impairment, decreased fertility and short stature. A more subtle feature associated with this syndrome is a "tiger tail" banding pattern in hair shafts, seen in microscopy under polarized light. The acronyms PIBIDS, IBIDS, BIDS and PBIDS give the initials of the words involved. BIDS syndrome, also called Amish brittle hair brain syndrome and hair-brain syndrome, is an autosomal recessive inherited disease. It is nonphotosensitive. BIDS is characterized by brittle hair, intellectual impairment, decreased fertility, and short stature. : 501 There is a photosensitive syndrome, PBIDS.BIDS is associated with the gene MPLKIP (TTDN1). IBIDS syndrome, following the acronym from ichthyosis, brittle hair and nails, intellectual impairment and short stature, is the Tay syndrome or sulfur-deficient brittle hair syndrome, first described by Tay in 1971. (Chong Hai Tay was the Singaporean doctor who was the first doctor in South East Asia to have a disease named after him.) | Mesenteric pseudocyst (Pseudomesenteric cyst) is a mass in the abdomen that is devoid of any epithelial lining. They are caused either due to trauma or infection. The term mesenteric pseudocyst was first used by Ros et al in 1987. Mesenteric pseudocysts are very rare, making up only about less than one in 250,000 hospital admissions. == References == | 0-1
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Although barium is superior in demonstrating small perforations, the spillage of barium sulfate into the mediastinal and pleural cavities can cause an inflammatory response and subsequent fibrosis and is therefore not used as the primary diagnostic study. If, however, the water-soluble study is negative, a barium study should be performed for better definition.Endoscopy has no role in the diagnosis of spontaneous esophageal perforation. Both the endoscope and insufflation of air can extend the perforation and introduce air into the mediastinum.Patients may also have a pleural effusion high in amylase (from saliva), low pH, and may contain particles of food. Differential diagnosis
Common misdiagnoses include myocardial infarction, pancreatitis, lung abscess, pericarditis, and spontaneous pneumothorax. If esophageal perforation is suspected, even in the absence of physical findings, chest xray, water soluble contrast radiographic studies of the esophagus and a CT scan should be promptly obtained. In most cases, non-operative management is administered based on radiological evidence contained in mediastinal collection. Treatment
With the exception of a few case reports describing survival without surgery, the mortality of untreated Boerhaave syndrome is 100%. Its treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation, and if there is significant fluid loss it should be replaced with IV fluid therapy since oral rehydration is not possible. Even with early surgical intervention (within 24 hours) the risk of death is 25%. References
Further reading
Radiology Esophageal rupture
Arens, Ann; Ben-Youssef, Leila; Hayashi, Sandra; Smollin, Craig (2016). "Esophageal Rupture After Ghost Pepper Ingestion". The Journal of Emergency Medicine. 51 (6): e141–e143. | Tolerance, dependence and withdrawal
Oxazepam, as with other benzodiazepine drugs, can cause tolerance, physical dependence, addiction, and benzodiazepine withdrawal syndrome. Withdrawal from oxazepam or other benzodiazepines often leads to withdrawal symptoms which are similar to those seen during alcohol and barbiturate withdrawal. The higher the dose and the longer the drug is taken, the greater the risk of experiencing unpleasant withdrawal symptoms. Withdrawal symptoms can occur, though, at standard dosages and also after short-term use. Benzodiazepine treatment should be discontinued as soon as possible by a slow and gradual dose reduction regimen. Contraindications
Oxazepam is contraindicated in myasthenia gravis, chronic obstructive pulmonary disease, and limited pulmonary reserve, as well as severe hepatic disease. Special precautions
Benzodiazepines require special precautions if used in the elderly, during pregnancy, in children, alcohol- or drug-dependent individuals, and individuals with comorbid psychiatric disorders. Benzodiazepines including oxazepam are lipophilic drugs and rapidly penetrate membranes, so rapidly crosses over into the placenta with significant uptake of the drug. Use of benzodiazepines in late pregnancy, especially high doses, may result in floppy infant syndrome. Pregnancy
Oxazepam when taken during the third trimester, causes a definite risk to the neonate including a severe benzodiazepine withdrawal syndrome including hypotonia, and reluctance to suck, to apnoeic spells, cyanosis, and impaired metabolic responses to cold stress. Floppy infant syndrome and sedation in the newborn may also occur. Symptoms of floppy infant syndrome and the neonatal benzodiazepine withdrawal syndrome have been reported to persist from hours to months after birth. | 0-1
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Headache and dizziness occur immediately after the injury, but also can be long lasting.The condition is associated with a wide range of non-specific symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. Many of the symptoms associated with PCS are common or may be exacerbated by other disorders, so there is considerable risk of misdiagnosis. Headaches that occur after a concussion may feel like migraine headaches or tension-type headaches. Most headaches are tension-type headaches, which may be associated with a neck injury that occurred at the same time of the head injury. Physical
A common condition associated with PCS is headache. While most people have headaches of the same type they experienced before the injury, people diagnosed with PCS often report more frequent or longer-lasting headaches. Between 30% and 90% of people treated for PCS report having more frequent headaches and between 8% and 32% still report them a year after the injury.Dizziness is another common symptom reported in about half of people diagnosed with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness, which can contribute to subsequent injuries and higher rates of mortality due to falls.About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% report blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. | PCS may cause insomnia, fatigue, or other problems with sleep. Psychological and behavioral
Psychological conditions, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality. Other emotional and behavioral symptoms include restlessness, aggression, and mood swings. Some common symptoms, such as apathy, insomnia, irritability, or lack of motivation, may result from other co-occurring conditions, such as depression. Higher mental functions
Common symptoms associated with a diagnosis of PCS are related to cognition, attention, and memory, especially short-term memory, which can also worsen other problems such as forgetting appointments or difficulties at work. In one study, one in four people diagnosed with PCS continued to report memory problems a year after the injury, but most experts agree that cognitive symptoms clear within six months to a year after injury in the vast majority of individuals. Causes
The question of the cause or causes of PCS has been heavily debated for many years and remain controversial. It is not known to exactly what degree the symptoms are due to physiological changes or to other factors, such as pre-existing psychiatric disorders or factors related to secondary gain or disability compensation. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.PCS may also be exacerbated by psychosocial factors, chronic pain, or an interaction of some or all of these. | 11
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Niacin, also known as nicotinic acid, is an organic compound and a form of vitamin B3, an essential human nutrient. It can be manufactured by plants and animals from the amino acid tryptophan. Niacin is obtained in the diet from a variety of whole and processed foods, with highest contents in fortified packaged foods, meat, poultry, red fish such as tuna and salmon, lesser amounts in nuts, legumes and seeds. Niacin as a dietary supplement is used to treat pellagra, a disease caused by niacin deficiency. Signs and symptoms of pellagra include skin and mouth lesions, anemia, headaches, and tiredness. Many countries mandate its addition to wheat flour or other food grains, thereby reducing the risk of pellagra.The amide derivative nicotinamide (niacinamide) is a component of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP+). Although niacin and nicotinamide are identical in their vitamin activity, nicotinamide does not have the same pharmacological, lipid-modifying effects or side effects as niacin, i.e., when niacin takes on the -amide group, it does not reduce cholesterol nor cause flushing. Nicotinamide is recommended as a treatment for niacin deficiency because it can be administered in remedial amounts without causing the flushing, considered an adverse effect.Niacin is also a prescription medication. Amounts far in excess of the recommended dietary intake for vitamin functions will lower blood triglycerides and low density lipoprotein cholesterol (LDL-C), and raise blood high density lipoprotein cholesterol (HDL-C, often referred to as "good" cholesterol). There are two forms: immediate-release and sustained-release niacin. | It also tends to occur in less developed areas where people eat maize (corn) as a staple food, as maize is the only grain low in digestible niacin. A cooking technique called nixtamalization i.e., pretreating with alkali ingredients, increases the bioavailability of niacin during maize meal/flour production. For this reason, people who consume corn as tortillas or hominy are at less risk of niacin deficiency. For treating deficiency, the World Health Organization (WHO) recommends administering niacinamide(i.e. nicotinamide) instead of niacin, to avoid the flushing side effect commonly caused by the latter. Guidelines suggest using 300 mg/day for three to four weeks. Dementia and dermatitis show improvement within a week. Because deficiencies of other B-vitamins may be present, the WHO recommends a multi-vitamin in addition to the niacinamide.Hartnup disease is a hereditary nutritional disorder resulting in niacin deficiency. It is named after an English family with a genetic disorder that resulted in a failure to absorb the essential amino acid tryptophan, tryptophan being a precursor for niacin synthesis. The symptoms are similar to pellagra, including red, scaly rash and sensitivity to sunlight. Oral niacin or niacinamide is given as a treatment for this condition in doses ranging from 50 to 100 mg twice a day, with a good prognosis if identified and treated early. Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin. Measuring vitamin status
Plasma concentrations of niacin and niacin metabolites are not useful markers of niacin status. | 11
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It is thus recommended that children with ADHD be regularly assessed for sleep problems. Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to hyperactivity and inattentiveness. Obstructive sleep apnea can also cause ADHD-type symptoms. Management
The management of ADHD typically involves counseling or medications, either alone or in combination. While treatment may improve long-term outcomes, it does not get rid of negative outcomes entirely. Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants. In those who have trouble focusing on long-term rewards, a large amount of positive reinforcement improves task performance. ADHD stimulants also improve persistence and task performance in children with ADHD. "Recent evidence from observational and registry studies indicates that pharmacological treatment of ADHD is associated with increased achievement and decreased absenteeism at school, a reduced risk of trauma-related emergency hospital visits, reduced risks of suicide and attempted suicide, and decreased rates of substance abuse and criminality". Behavioral therapies
There is good evidence for the use of behavioral therapies in ADHD. They are the recommended first-line treatment in those who have mild symptoms or who are preschool-aged. Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy, interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioral peer intervention, organization training, and parent management training. | A high index of suspicion is therefore required especially in women at risk of thyroid disease e.g. women with a personal or family history of thyroid disease, goitre, or co-existing primary autoimmune disorder like type 1 diabetes. Risks of hypothyroidism on fetal and maternal well-being
Hypothyroidism is diagnosed by noting a high TSH associated with a subnormal T4 concentration. Subclinical hypothyroidism (SCH) is present when the TSH is high but the T4 level is in the normal range but usually low normal. SCH is the commonest form of hypothyroidism in pregnancy and is usually due to progressive thyroid destruction due to autoimmune thyroid disease.Several studies, mostly retrospective, have shown an association between overt hypothyroidism and adverse fetal and obstetric outcomes (e.g. Glinoer 1991). Maternal complications such as miscarriages, anaemia in pregnancy, pre-eclampsia, abruptio placenta and postpartum haemorrhage can occur in pregnant women with overt hypothyroidism. Also, the offspring of these mothers can have complications such as premature birth, low birth weight and increased neonatal respiratory distress. Similar complications have been reported in mothers with subclinical hypothyroidism. A three-fold risk of placental abruption and a two-fold risk of pre-term delivery were reported in mothers with subclinical hypothyroidism. Another study showed a higher prevalence of subclinical hypothyroidism in women with pre-term delivery (before 32 weeks) compared to matched controls delivering at term. An association with adverse obstetrics outcome has also been demonstrated in pregnant women with thyroid autoimmunity independent of thyroid function. | 0-1
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There are also three polar capsules, each of which contains a coiled polar filament between 170 and 180 μm long. Polar filaments in both this stage and in the myxospore stage (see picture above) rapidly shoot into the body of the host, creating an opening through which the sporoplasm can enter. Sporoplasm stage
Upon contact with fish hosts and firing of the polar capsules, the sporoplasm contained within the central style of the triactinomyxon migrates into the epithelium or gut lining. Firstly, this sporoplasm undergoes mitosis to produce more amoeboid cells, which migrate into deeper tissue layers, to reach the cerebral cartilage. Myxosporean stage
Myxospores, which develop from sporogonic cell stages inside fish hosts, are lenticular. They have a diameter of about 10 micrometers and are made of six cells. Two of these cells form polar capsules, two merge to form a binucleate sporoplasm, and two form protective valves. Myxospores are infective to oligochaetes, and are found among the remains of digested fish cartilage. They are often difficult to distinguish from related species because of morphological similarities across genera. Though M. cerebralis is the only myxosporean ever found in salmonid cartilage, other visually similar species may be present in the skin, nervous system, or muscle. Life cycle
Myxobolus cerebralis has a two-host life cycle involving a salmonid fish and a tubificid oligochaete. So far, the only worm known to be susceptible to M. cerebralis infection is Tubifex tubifex, though what scientists currently call T. tubifex may in fact be more than one species. | History
Unlike rejection and infection, CAV in the transplanted heart was not initially a predicted outcome. Early survivors of heart transplants soon developed this form of vasculopathy of their coronary arteries, initially identified at post-mortems. There were early suggestions that preventing cytomegalovirus (CMV) infection could decrease the prevalence of CAV. The impact of CAV has changed over time, with early recipients being younger, having more rejection and cardiovascular risk factors and less use of statins. Later recipients used statins routinely and were introduced to the immunosuppressive agent mycophenolate mofetil (MMF) and CMV prophylaxis. In addition, the later recipients were monitored for antibody-mediated cardiac allograft rejection (AMR).Before 2010 there was no uniform international standards for the nomenclature of CAV. A consensus statement on a standard language for CAV was first published in 2010 by the ISHLT. This was devised in a similar way to the earlier acute rejection grading system by endomyocardial biopsy. Research directions
Antibody-mediated cardiac allograft rejection (AMR) is a significant factor leading to the rapid progression of CAV. Future research directions in this area may include prospective databases that correlate clinical factors with surveillance of the incidence and severity of AMR, the frequency of CMV infection, and the use of immunosuppressants. The role of inducing immune tolerance has yet to be established. == References == | 0-1
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UK only
Capsules – Episenta prolonged release by Beacon
Sachets – Episenta prolonged release by Beacon
Intravenous solution for injection – Episenta solution for injection by Beacon
Germany, Switzerland, Norway, Finland, Sweden
Tablets – Orfiril by Desitin Pharmaceuticals
Intravenous injection – Orfiril IV by Desitin Pharmaceuticals
South Africa
Syrup – Convulex by Byk Madaus
Tablets – Epilim by Sanofi-synthelabo
Malaysia
Tablets – Epilim by Sanofi-Aventis
Romania
Companies are SANOFI-AVENTIS FRANCE, GEROT PHARMAZEUTIKA GMBH and DESITIN ARZNEIMITTEL GMBH
Types are Syrup, Extended release mini tablets, Gastric resistant coated tablets, Gastric resistant soft capsules, Extended release capsules, Extended release tablets and Extended release coated tablets
Canada
Intravenous injection – Epival or Epiject by Abbott Laboratories. Syrup – Depakene by Abbott Laboratories its generic formulations include Apo-Valproic and ratio-Valproic. Japan
Tablets – Depakene by Kyowa Hakko Kirin
Extended release tablets – Depakene-R by Kyowa Hakko Kogyo and Selenica-R by Kowa
Syrup – Depakene by Kyowa Hakko Kogyo
Europe
In much of Europe, Dépakine and Depakine Chrono (tablets) are equivalent to Epilim and Epilim Chrono above. Taiwan
Tablets (white round tablet) – Depakine (Chinese: 帝拔癲; pinyin: di-ba-dian) by Sanofi Winthrop Industrie (France)
Iran
Tablets – Epival 200 (enteric coated tablet) and Epival 500 (extended release tablet) by Iran Najo
Slow release tablets – Depakine Chrono by Sanofi Winthrop Industrie (France)
Israel
Depalept and Depalept Chrono (extended release tablets) are equivalent to Epilim and Epilim Chrono above. Manufactured and distributed by Sanofi-Aventis. | Other probable examples have been discovered in other continents around the world, including North and South America, and Africa.The earliest written record of what was probably a meningioma is from the 1600s, when Felix Plater (1536–1614) of the University of Basel performed an autopsy on Sir Caspar Bonecurtius. Surgery for removal of meningiomata was first attempted in the sixteenth century, but the first known successful surgery for removal of a meningioma of the convexity (parasagittal) was performed in 1770 by Anoine Luis. The first documented successful removal of a skull base meningioma was performed in 1835 by Zanobi Pecchioli, Professor of Surgery at the University of Siena. Other notable meningioma researchers have been William Macewen (1848–1924), and William W. Keen (1837–1932).Improvements in meningioma research and treatment over the last century have occurred in terms of the surgical techniques for removal of the tumor, and related improvements in anesthesia, antiseptic methods, techniques to control blood loss, better ability to determine which tumors are and are not operable, and to effectively differentiate between the different meningioma subtypes. Notable cases
Leonard Wood (1860–1927), underwent successful surgery by Dr. Harvey Cushing for a meningioma circa 1910, a major advance in neurosurgery at the time. Crystal Lee Sutton (1940–2009), American union organizer and inspiration for the film Norma Rae, died of a malignant meningioma. Elizabeth Taylor (1932–2011), American actress, underwent surgery in February 1997 to remove a benign meningioma. Kathi Goertzen (1958–2012), television news anchor in Seattle who underwent a very public battle with recurring tumors. | 0-1
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Pharmacokinetics
As with all potent bisphosphonates, the fraction of the drug that reaches the circulatory system intact (systemic bioavailability) after oral dosing is low, averaging only 0.6–0.7% in women and in men under fasting conditions. Intake together with meals and beverages other than water further reduces the bioavailability. The absorbed drug rapidly partitions, with approximately 50% binding to the exposed bone surface; the remainder is excreted unchanged by the kidneys. Unlike with most drugs, the strong negative charge on the two phosphonate moieties limits oral bioavailability, and, in turn, the exposure to tissues other than bone is very low. After absorption in the bone, alendronate has an estimated terminal elimination half-life of 10 years. References
External links
"Alendronic acid". Drug Information Portal. U.S. National Library of Medicine. "Alendronate sodium". Drug Information Portal. U.S. National Library of Medicine. | See also
The Myelin Project
The Stennis Foundation
References
External links
OMIM entries on Alexander disease
Infantile-onset Alexander disease in a child with long-term follow-up by serial magnetic resonance imaging: a case report
Alexander Disease: New Insights From Genetics | 0-1
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If symptoms continue after behavioral strategies have been implemented, some medications can be recommended to target specific symptoms or co-existing problems such as restricted and repetitive behaviors (RRBs), anxiety, depression, hyperactivity/inattention and sleep disturbance. Melatonin for example can be used for sleep problems.While there are a number of parent-mediated behavioral therapies to target social communication deficits in children with autism, there is uncertainty regarding the efficacy of interventions to treat RRBs. Education
Educational interventions often used include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy and social skills therapy. Among these approaches, interventions either treat autistic features comprehensively, or focalize treatment on a specific area of deficit. The quality of research for early intensive behavioral intervention (EIBI)—a treatment procedure incorporating over thirty hours per week of the structured type of ABA that is carried out with very young children—is currently low, and more vigorous research designs with larger sample sizes are needed. Two theoretical frameworks outlined for early childhood intervention include structured and naturalistic ABA interventions, and developmental social pragmatic models (DSP). One interventional strategy utilizes a parent training model, which teaches parents how to implement various ABA and DSP techniques, allowing for parents to disseminate interventions themselves. Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation. Despite the recent development of parent training models, these interventions have demonstrated effectiveness in numerous studies, being evaluated as a probable efficacious mode of treatment. | Noma neonatorum is a cutaneous condition, a manifestation of infection, usually Pseudomonas aeruginosa sepsis, and has been reported almost exclusively in developing countries. Despite the similarity of facial lesions, noma neonatorum is not related to noma. See also
Green nail syndrome
List of cutaneous conditions
== References == | 0-1
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Except for members of the order Taeniidae, the first intermediate host is an arthropod, and except for in the case of Archigetes spp. (which can attain sexual maturity in freshwater oligochaeta), the second host is usually a fish, but can be another invertebrate or vertebrate. After the scolex has differentiated and matured in the larval stage, growth will stop until a vertebrate eats the intermediate host, and then the strobila develops. Adult tapeworms often have a high final host specificity, with some species only found in one host vertebrate. Common infective species
Medical importance
Taeniasis
Taeniasis is an infection within the intestines by adult tapeworms belonging to the genus Taenia. It is due to eating contaminated undercooked beef or pork. There are generally no or only mild symptoms. Symptoms may occasionally include weight loss or abdominal pain. Segments of tapeworm may be seen in the stool. Cysticercosis
Cysticercosis is a tissue infection caused by the young form of the pork tapeworm. Infection occurs through swallowing or antiperistaltic contractions during regurgitation carrying eggs or gravid proglottids to the stomach. At this point, larvae hatch when exposed to enzymes and penetrate the intestinal wall, travelling through the body through blood vessels to tissues like the brain, the eye, muscles, and the nervous system (called neurocysticercosis).At these sites, the parasites lodge and form cysts, a condition called cysticercosis, producing inflammatory reactions and clinical issues when they die, sometimes causing serious or fatal damage. | Brain infection can cause granulomas, hematomas, and abscesses. Subdivisions
The evolutionary history of the Eucestoda has been studied using ribosomal RNA, mitochondrial and other DNA, and morphological analysis and continues to be revised. "Tetraphyllidea" is seen to be paraphyletic; "Pseudophyllidea" has been broken up into two orders, Bothriocephalidea and Diphyllobothriidea. Hosts, whose phylogeny often mirrors that of the parasites (Fahrenholzs rule), are indicated in italics and parentheses, the life-cycle sequence (where known) shown by arrows as (intermediate host1 [→ intermediate host2 ] → definitive host). Alternatives, generally for different species within an order, are shown in square brackets. References
Bale, James F. "Cysticercosis." Current Treatment Options in Neurology. 2000. pp. 355–360. Dunn, J., and Philip E. S. Palmer. "Sparganosis." Seminars in Roentgenology. 1998. pp. 86–88. Esteban, J. G., Munoz-Antoli, C., and R. Toledo. "Human Infection by a "Fish Tapeworm," Diphyllobothrium latum, in a Non-Endemic Country." Infection. 2014. pp. 191–194. Kim, Bong Jin, et al. "Heavy Hymenoleptis nana Infection Possibly Through Organic Food: Report of a Case." The Korean Journal of Parasitology. 2014. pp. 85–87. Mehlhorn, Heinz. "Eucestoda Classification." Encyclopedia of Parasitology. 2008. pp. 495–497. Rohde, Klaus. "Eucestoda." AccessScience. McGraw-Hill Ryerson. Usharani, A., et al. "Case Reports of Hydatid Disease." Journal of Epidemiology and Global Health. 2013. p. 63–66. | 11
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Thus, EHS has been worked into conspiracy theories, but there is no scientific evidence that EHS has non-natural origins. Diagnosis
Classification
Exploding head syndrome is classified under other parasomnias by the 2014 International Classification of Sleep Disorders (ICSD, 3rd.Ed.) and is an unusual type of auditory hallucination in that it occurs in people who are not fully awake.According to ICD-10 and DSM-5 EHS is classified as either other specified sleep-wake disorder (codes:780.59 or G47.8) or unspecified sleep-wake disorder (codes: 780.59 or G47.9). Treatment
As of 2018, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals. Epidemiology
There have not been sufficient studies to make conclusive statements about how common or who is most often affected. One study found that 14% of a sample of undergrads reported at least one episode over the course of their lives, with higher rates in those who also have sleep paralysis. History
Case reports of EHS have been published since at least 1876, which Silas Weir Mitchell described as "sensory discharges" in a patient. However, it has been suggested that the earliest written account of EHS was described in the biography of the French philosopher René Descartes in 1691. | The drug should not be used in children under two years of age, people with kidney disease, or people who are allergic to aspirin.Side effects are primarily gastrointestinal but may also include headache; GI effects include nausea, diarrhea and abdominal pain. There have been scattered reports of various problems when the oral form is used, including: problems caused by myelosuppression (leukopenia, neutropenia, agranulocytosis, aplastic anaemia, and thrombocytopenia), as well as hair loss, peripheral neuropathy, pancreatitis, liver problems, myocarditis and pericarditis, allergic and fibrotic lung reactions, lupus erythematosus-like reactions and rash (including urticaria), drug fever, interstitial nephritis and nephrotic syndrome, usually reversible on withdrawal. Very rarely, use of mesalazine has been associated with an exacerbation of the symptoms of colitis, Stevens Johnson syndrome and erythema multiforme. Chemistry
Mesalazine is the active moiety of sulfasalazine, which is metabolized to sulfapyridine and mesalazine. It is also the active component of the prodrug balsalazide along with the inert carrier molecule 4-aminobenzoyl-beta-alanine. It is in the category of disease-modifying antirheumatic drugs (DMARDs) family of medications. It is unclear exactly how it works. Mechanism of action
Exact mechanism of mesalazine is unknown, but is speculated that mesalazine decreases synthesis of prostaglandin and leukotriene, modulating the inflammatory response derived from the cyclooxygenase and lipooxygenase pathways. It appears to act locally on colonic mucosa. Society and culture
Brand names
Mesalazine is sold under various names including Apriso, Asacol, Asacol HD, Canasa, Delzicol, Fivasa, Lialda, Pentasa, Rowasa, and Sfrowasa. References
External links
"Mesalamine". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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No or less frequent placebos
If the pill formulation is monophasic, meaning each hormonal pill contains a fixed dose of hormones, it is possible to skip withdrawal bleeding and still remain protected against conception by skipping the placebo pills altogether and starting directly with the next packet. Attempting this with bi- or tri-phasic pill formulations carries an increased risk of breakthrough bleeding and may be undesirable. It will not, however, increase the risk of getting pregnant. Starting in 2003, women have also been able to use a three-month version of the pill. Similar to the effect of using a constant-dosage formulation and skipping the placebo weeks for three months, Seasonale gives the benefit of less frequent periods, at the potential drawback of breakthrough bleeding. Seasonique is another version in which the placebo week every three months is replaced with a week of low-dose estrogen. A version of the combined pill has also been packaged to eliminate placebo pills and withdrawal bleeds. Marketed as Anya or Lybrel, studies have shown that after seven months, 71% of users no longer had any breakthrough bleeding, the most common side effect of going longer periods of time without breaks from active pills. While more research needs to be done to assess the long term safety of using COCPs continuously, studies have shown there may be no difference in short term adverse effects when comparing continuous use versus cyclic use of birth control pills. | In July 1961, Searle finally began marketing Enovid 5 mg (5 mg noretynodrel and 75 µg mestranol) to physicians as a contraceptive.Although the FDA approved the first oral contraceptive in 1960, contraceptives were not available to married women in all states until Griswold v. Connecticut in 1965 and were not available to unmarried women in all states until Eisenstadt v. Baird in 1972.The first published case report of a blood clot and pulmonary embolism in a woman using Enavid (Enovid 10 mg in the U.S.) at a dose of 20 mg/day did not appear until November 1961, four years after its approval, by which time it had been used by over one million women. It would take almost a decade of epidemiological studies to conclusively establish an increased risk of venous thrombosis in oral contraceptive users and an increased risk of stroke and myocardial infarction in oral contraceptive users who smoke or have high blood pressure or other cardiovascular or cerebrovascular risk factors. These risks of oral contraceptives were dramatized in the 1969 book The Doctors Case Against the Pill by feminist journalist Barbara Seaman who helped arrange the 1970 Nelson Pill Hearings called by Senator Gaylord Nelson. The hearings were conducted by senators who were all men and the witnesses in the first round of hearings were all men, leading Alice Wolfson and other feminists to protest the hearings and generate media attention. | 11
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The weak but significant androgenic activity of MGA may serve to limit its clinical effectiveness in the treatment of prostate cancer. Glucocorticoid activity
MGA is an agonist of the glucocorticoid receptor (GR), the biological target of glucocorticoids like cortisol. It has been found to possess 30% of the affinity of the corticosteroid dexamethasone for this receptor. MGA shows the lowest ratio of PR affinity to GR affinity of a broad selection of marketed progestins, suggesting that it may have among the highest relative glucocorticoid effect of the progestins used in medicine. MGA produces observable glucocorticoid effects, with one study finding that, in the dose range tested, it possessed about 50% of the eosinopenic and hyperglycemic activity (markers of glucocorticoid activity) of an equal amount of medroxyprogesterone acetate and about 25% that of hydrocortisone. Accordingly, manifestations of its glucocorticoid activity, including symptoms of Cushings syndrome, steroid diabetes, and adrenal insufficiency, have been reported with the use of MGA in the literature, albeit sporadically. Appetite stimulation
MGA is frequently used as an appetite stimulant to promote weight gain. The direct mechanism of appetite enhancement is unclear, but it is known that MGA induces a variety of downstream changes to cause the effect, including stimulation of the release of neuropeptide Y in the hypothalamus, neurosteroid-like modulation of calcium channels in the ventromedial hypothalamus, and inhibition of the secretion of proinflammatory cytokines including interleukin 1α, interleukin 1β, interleukin 6, and tumor necrosis factor α, all of which have been implicated in facilitation of appetite. | Hyperpituitarism is a condition due to the primary hypersecretion of pituitary hormones; it typically results from a pituitary adenoma. In children with hyperpituitarism, disruption of growth regulation is rare, either because of hormone hypersecretion or because of manifestations caused by local compression of the adenoma. Symptoms and signs
Symptoms caused by hormone excess and associated mass effects include:
Cause
The cause of hyperpituitarism in most cases is due to pituitary adenomas. They usually come from the anterior lobe, are functional and secrete the hormone, GH and prolactin. Mechanism
Evidence indicates that the mechanism of hyperpituitarism can originate from genetic disruption causing pituitary tumorigenesis, most pituitary adenomas are monoclonal, which in turn indicates their origin from an event in a single cell. There are three hormones that are oversecreted resulting in the pituitary adenoma: prolactin, adrenocorticotropic hormone (ACTH), and growth hormone (GH).Excess prolactin may result in a prolactinoma Excess GH results in gigantism, the severity of gigantism depends on whether the epiphyseal plate is open. The four most common types of hyperpituitarism are caused by 4 types of pituitary adenoma, as follows: prolactinoma, corticotropinoma (Cushings disease), somatotropinoma (gigantism), and thyrotropinoma . Diagnosis
For the diagnosis of hyperpituitarism it depends on the cell type(s) affected, clinical manifestations of hormone excess may include, gigantism or acromegaly, which can be identified by clinical and radiographic results. | 0-1
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Entamoeba histolytica is a protozoan parasite that causes intestinal inflammation. A few cases have been misdiagnosed as UC with poor outcomes occurring due to the use of corticosteroids.The most common disease that mimics the symptoms of ulcerative colitis is Crohns disease, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases since their courses and treatments may differ. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis. Crohns disease can be distinguished from ulcerative colitis in several ways. Characteristics that indicate Crohns include evidence of disease around the anus (perianal disease). This includes anal fissures and abscesses as well as fistulas, which are abnormal connections between various bodily structures.Infectious colitis is another condition that may present in similar manner to ulcerative colitis. Endoscopic findings are also oftentimes similar. One can discern whether a patient has infectious colitis by employing tissue cultures and stool studies. Biopsy of the colon is another beneficial test but is more invasive. Other forms of colitis that may present similarly include radiation and diversion colitis. Radiation colitis occurs after irradiation and often affects the rectum or sigmoid colon, similar to ulcerative colitis. Upon histology radiation colitis may indicate eosinophilic infiltrates, abnormal epithelial cells, or fibrosis. Diversion colitis, on the other hand, occurs after portions of bowel loops have been removed. Histology in this condition often shows increased growth of lymphoid tissue. | The most common type of skin manifestation, erythema nodosum, presents in up to 3% of UC patients and almost 8% in patients afflicted with Crohns disease. It develops as raised, tender red nodules usually appearing on the outer areas of the arms or legs, especially in the anterior tibial area (shins). The nodules have diameters that measure approximately 1–5 cm. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue (panniculitis), and biopsy will display focal panniculitis (although is often unnecessary in diagnosis). In contrast to joint-related manifestations, erythema nodosum often occurs alongside intestinal disease. Thus, treatment of UC can often lead to resolution of skin nodules.A lesser common skin complication associated with UC, pyoderma gangrenosum, is typically more severe. One study discovered this skin manifestation in only 0.75% pf patients. Pyoderma gangrenosum is characterized by painful lesions or nodules that become ulcers which progressively grow. It often starts as many small raised red spots (papules) or pus-filled lesions (pustules) that are usually detected on lower extremities. The inner layer of the skin, or dermis, slowly undergoes necrosis (process of dying) causing the ulcerations that are typical of pyoderma gangrenosum. The ulcers are often filled with sterile pus-like material, so biopsy often displays an abscess that is sterile. Whereas erythema nodosum tends to correlate with the activity of the ulcerative colitis and often improves with treatment of the colonic inflammation, pyoderma gangrenosum may occur independently of UC disease activity. In some cases, pyoderma gangrenosum may require injection with corticosteroids. | 11
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In line with this, the yeast homologue, SdoI, has been shown to be critical for maturation of pre-60S ribosomes, by effecting release and recycling of the nucleolar shuttling factor Tif6. This is required for 60S maturation and translational activation of ribosomes. It has also been shown that the Dictyostelium discoideum homologue catalyzes the removal of eukaryotic initiation factor 6 (eIF6), which is required for the translational activation of ribosomes. Cells from SDS patients were shown to have a defect in assembly of ribosome subunits.At present, it is not obvious how disruption of the basic cellular process of translation leads to the tissue- and organ-specific manifestations seen in SDS. However, unusual and combinations of tissues and organs are also affected in Diamond–Blackfan anemia, X-linked dyskeratosis congenita, and cartilage–hair hypoplasia—three diseases that may also be linked to defective ribosome function. Pleiotropic disease features may be the result of cell-specific effects of reduced levels of SBDS activity provided by hypomorphic mutations. Diagnosis
Initially, the clinical presentation of SDS may appear similar to cystic fibrosis. However, CF can be excluded with a normal chloride in sweat test but faecal elastase as a marker of pancreatic function will be reduced. The variation, intermittent nature, and potential for long-term improvement of some clinical features make this syndrome difficult to diagnose. SDS may present with either malabsorption, or hematological problems. Rarely, SDS may present with skeletal defects, including severe rib cage abnormalities that lead to difficulty in breathing. Diagnosis is generally based on evidence of exocrine pancreatic dysfunction and neutropenia. | Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. It should be avoided or used with caution in patients with severe chronic kidney disease, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease. Prognosis
One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Becks triad). | 0-1
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Atopy patch testing has been used in some cases for the potential identification of delayed, non-IgE (cell-mediated) reactions. Diagnostic criteria
The diagnosis of eosinophilic esophagitis requires all of the following:
Symptoms related to esophageal dysfunction. Eosinophil-predominant inflammation on esophageal biopsy, characteristically consisting of a peak value of ≥15 eosinophils per high power field (HPF). Exclusion of other causes that may be responsible for symptoms and esophageal eosinophilia. Treatment
The goal of EoE treatment is to control the symptoms by decreasing the number of eosinophils in the esophagus and, subsequently, reducing the esophageal inflammation. Management consists of dietary, pharmacological, and endoscopic treatment. Dietary management
Dietary treatment can be effective, as there does appear to be a role of allergy in the development of EOE. Allergy testing is not particularly effective in predicting which foods are driving the disease process. If no specific allergenic food or agent is present, a trial of the six food elimination diet (SFED) can be pursued. Various approaches have been tried, where either six food groups (cows milk, wheat, egg, soy, nuts and fish/seafood), four groups (animal milk, gluten-containing cereals, egg, legumes) or two groups (animal milk and gluten-containing cereals) are excluded for a period of time, usually six weeks. A "top down" (starting with six foods, then reintroducing) approach may be very restrictive. Four- or even two-group exclusion diets may be less difficult to follow and reduce the need for many endoscopies if the response to the limited restriction is good.Alternative options to SFED includes the elemental diet, which is an amino acid based diet. | Pleural thickening is an increase in the bulkiness of one or both of the pulmonary pleurae. Causes
Pleural plaques
Pleural plaques are patchy collections of hyalinized collagen in the parietal pleura. They have a holly leaf appearance on X-ray. They are indicators of asbestos exposure, and the most common asbestos-induced lesion. They usually appear after 20 years or more of exposure and never degenerate into mesothelioma. They appear as fibrous plaques on the parietal pleura, usually on both sides, and at the posterior and inferior part of the chest wall as well as the diaphragm. See also
Pleural disease
== References == | 0-1
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Mural calcification in central pulmonary arteries is most frequently seen in patients with Eisenmengers syndrome. Right heart catheterization
Although pulmonary arterial pressure (PAP) can be estimated on the basis of echocardiography, pressure measurements with a Swan-Ganz catheter inserted through the right side of the heart provide the most definite assessment. [42] Pulmonary hypertension is defined as a mean PAP of at least 20 mm Hg (3300 Pa) at rest, and PAH is defined as precapillary pulmonary hypertension (i.e. mean PAP ≥ 20 mm Hg with pulmonary arterial occlusion pressure [PAOP] ≤ 15 mm Hg and pulmonary vascular resistance [PVR] > 3 Wood Units). PAOP and PVR cannot be measured directly with echocardiography. Therefore, diagnosis of PAH requires right-sided cardiac catheterization. A Swan-Ganz catheter can also measure the cardiac output; this can be used to calculate the cardiac index, which is far more important in measuring disease severity than the pulmonary arterial pressure.Mean PAP (mPAP) should not be confused with systolic PAP (sPAP), which is often reported on echocardiogram reports. A systolic pressure of 40 mm Hg typically implies a mean pressure of more than 25 mm Hg. Roughly, mPAP = 0.61•sPAP + 2. Due to the invasive nature of this procedure, the use of computational fluid dynamics based hemodynamic indices have been postulated. | Some acquired conditions may share some features with EME and should be differentiated from it. These include hypoxic-ischaemic encephalopathy, central nervous system infections, acute metabolic disturbances or acute vascular events. Mechanism
Pathology results in EME consist of multifocal changes in white matter, imperfect lamination of the deep cortical layers, astrocytic proliferation, and demyelination. Diagnosis
Electroencephalogram (EEG) is usually characterized by a burst suppression pattern. Subsequently it may transition to hypsarrhythmia, a chaotic pattern on EEG, or other severely abnormal EEG patterns. Neuroimaging is useful in assessing a possible underlying structural causality that might cause EME. MRI findings depend on the underlying etiology and may be normal or not at diagnosis. Prevention
Early identification of metabolism error defects is very essential in prevention as the traditional antiepileptic drug are usually not very effective, proper treatment aiming to the conditions can prevent neurological worsening. Genetic counselling is critical given the high prevalence of genetic mutations and early genetic testing also helps to avoid unnecessary procedures and unsuccessful treatment. The families who are at risk, prophylactic treatment is suggested as it may stop the seizure and help in recovering the neurodevelopmental consequences. Management
Antiepileptic drugs are used to treat EME, but it is difficult to control seizures with anti-epileptic drugs alone. Phenobarbital, valproate, pyridoxine, zonisamide, and benzodiazepines have all been used but with inadequate usefulness in seizure control. Some patients show favorable response to sodium channel agents, often at high dose. There are various means to add on the treatment when seizures are resistant. A ketogenic diet can be useful in controlling seizures. | 0-1
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Organic brain syndrome, also known as organic brain disease, organic brain disorder, organic mental syndrome, or organic mental disorder, refers to any syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders (mental disorders). Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but during the era when this distinction was drawn, not enough was known about brain science (including neuroscience, cognitive science, neuropsychology, and mind-brain correlation) for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine. While mental or behavioural abnormalities related to the dysfunction can be permanent, treating the disease early may prevent permanent damage in addition to fully restoring mental functions. An organic cause to brain dysfunction is suspected when there is no indication of a clearly defined psychiatric or "inorganic" cause, such as a mood disorder. Types
Organic brain syndrome can be divided into 2 major subgroups: acute (delirium or acute confusional state) and chronic (dementia). A third entity, encephalopathy (amnestic), denotes a gray zone between delirium and dementia. | Oil folliculitis is inflammation of hair follicles due to exposure to various oils, and typically occurs on forearms or thighs. It is common in refinery workers, road workers, mechanics, and sheep shearers. Even makeup may cause it. Malignancy may also be represented by recalcitrant cases. Treatment
Most simple cases resolve on their own, but first-line treatments are typically topical medications. Topical antiseptic treatment is adequate for most cases. Topical antibiotics, such as mupirocin or neomycin/polymyxin B/bacitracin ointment may be prescribed. Oral antibiotics may also be used. Some patients may benefit from systemic narrow-spectrum penicillinase-resistant penicillins (such as dicloxacillin in the US or flucloxacillin in UK). Fungal folliculitis may require an oral antifungal such as fluconazole. Topical antifungals such as econazole nitrate may also be effective.Folliculitis may recur even after symptoms have gone away. See also
Ingrown hair
Keratosis
References
External links
Folliculitis Treatments
Malassezia (Pityrosporum) Folliculitis Treatment & Management | 0-1
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Nabiximols, a combined THC and cannabidiol (CBD) product that is formulated as an oral (buccal) spray, has been shown to improve withdrawal symptoms without improving abstinence rates. Oral CBD has not shown efficacy in reducing the signs or symptoms of cannabis use, and likely has no benefit in cannabis use withdrawal symptoms. The CB-1 receptor antagonist rimonabant has shown efficacy in reducing the effects of cannabis in users, but with a risk for serious psychiatric side effects.Naltrexone, a mu opioid receptor antagonist, has shown mixed results for cannabis use disorder—both increasing the subjective effects of cannabis when given acutely, but potentially decreasing the overall use of cannabis with chronic administration. N-acetylcysteine (NAC) has shown some limited benefit in decreasing cannabis use in adolescents, though not with adults. Lithium, a mood stabilizer, has shown mixed results for treating symptoms of cannabis withdrawal, but is likely ineffective. Quetiapine, a second-generation antipsychotic, has been shown to treat cannabis withdrawal related insomnia and decreased appetite at the expense of exacerbating cravings. Oxytocin, a neuropeptide that the body produces, has shown some benefit in reducing the use of cannabis when administered intranasally in combination with motivational enhancement therapy sessions, though the treatment effect did not persist between sessions.Finally, CB1 antagonists such as rimonabant have been tested for utility in CUD. These drugs are effective at blocking the subjective effects of cannabis intoxication as well as the somatic components. This is accomplished by preventing THC binding to the CB1 receptor, effectively eliminating the ability to get high. | Zolpidem, a GABA-A receptor agonist and "Z-hypnotic" medication, has shown some efficacy in treating insomnia due to cannabis withdrawal, though there is a potential for misuse. Entacapone was well tolerated and decreased cannabis cravings in a trial on a small number of patients. Topiramate, an antiepileptic drug, has shown mixed results in adolescents, reducing the volume of cannabis consumption without significantly increasing abstinence, with somewhat poor tolerability. Gabapentin, an indirect GABA modulator, has shown some preliminary benefit for reducing cravings and cannabis use.The agonist substitution approach is one that draws upon the analogy of the success of nicotine replacement therapy for nicotine addiction. Dronabinol, which is synthetic THC, has shown benefit in reducing cravings and other symptoms of withdrawal, though without preventing relapse or promoting abstinence. Combination therapy with dronabinol and the alpha 2 adrenergic receptor agonist lofexidine have shown mixed results, with possible benefits towards reducing withdrawal symptoms. However, overall, the combination of dronabinol and lofexidine is likely not effective for the treatment of cannabis use disorder. Nabilone, a synthetic THC analogue, has shown benefits in reducing symptoms of withdrawal such as difficulty sleeping, and decreased overall cannabis use. Despite its psychoactive effects, the slower onset of action and longer duration of action of nabilone make it less likely to be abused than cannabis itself, which makes nabilone a promising harm reduction strategy for the treatment of cannabis use disorder. The combination of nabilone and zolpidem has been shown to decrease sleep-related and mood-related symptoms of cannabis withdrawal, in addition to decreasing cannabis use. | 11
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Role in metabolism
Reduced sulfate availability due to impaired activity of ARSB has been linked to increased aerobic glycolysis, as shown by an increase in NADH and NADPH, reduced oxygen consumption, increased extracellular acidification and serum lactate, and a decline in mitochondrial membrane potential in ARSB-silenced cells and ARSB-null mouse tissues. Extra-lysosomal localization
Although primarily a lysosomal enzyme, ARSB was also found to localize at the cell membrane of hepatocytes, sinusoidal endothelial cells, and Kupffer cells in the liver, as well as in the apical membranes of normal and malignant colonic and prostatic epithelial cells, by immunohistochemistry and immunofluorescence studies. Membrane immunostaining in the colon and prostate was lower in malignant than in normal tissue and also was lower in higher grade malignancies. ARSB activity assay in the membrane and cytosol fractions of cultured bronchial epithelial cells showed that the activity was several-fold greater in the membrane fraction. See also
Aryl
Sulfatase
References
Further reading
Brunelli MJ, Atallah ÁN, da Silva EM (September 2021). "Enzyme replacement therapy with galsulfase for mucopolysaccharidosis type VI". Cochrane Database Syst Rev. 2021 (9): CD009806. doi:10.1002/14651858.CD009806.pub3. PMC 8447860. PMID 34533215. "Galsulfase (Naglazyme)". Common Drug Review. Ottawa (ON): Canadian Agency for Drugs and Technologies in Health (CADTH). November 2016. PMID 28121110. Ferreira CR, Gahl WA (May 2017). "Lysosomal storage diseases". Transl Sci Rare Dis. 2 (1–2): 1–71. doi:10.3233/TRD-160005. PMC 5685203. PMID 29152458. External links
Medical Dictionary, Arylsulfatase B function. Protein Data Base (PDB), Arylsulfatase structure. Genetics Home Reference, Arylsulfatase B function. Overview of all the structural information available in the PDB for UniProt: P15848 (Arylsulfatase B) at the PDBe-KB. "Galsulfase". | CFTR potentiator VRT-532 increased ARSB expression and activity in cystic fibrosis cells to the level in the normal bronchial epithelial cells. Role in malignancy
ARSB has been studied in a variety of cancers. Cultured normal mammary epithelial and myoepithelial cells had significantly higher ARSB activity than cultured malignant mammary cells. Immunohistochemistry in the colon showed decreased membrane ARSB staining in colon cancer compared to normal colon, as well as in higher grade malignancies. ARSB activity was lower in malignant than normal prostate tissue, and immunostaining of prostate tissue microarrays showed not only decreasing ARSB staining in prostate cancer tissue of a higher Gleason score, but also lower staining in patients with recurrent compared to non-recurrent cancer. ARSB staining was a greater predictor of recurrence than Prostate-specific antigen (PSA) test, indicating possible future role of ARSB as a prognostic biomarker of prostate cancer. Further evidence of ARSB as a tumor suppressor was determined by molecular studies in cell cultures where ARSB was silenced by siRNA. The studies showed that decrease of ARSB leads to increase in free galectin-3, which attaches more strongly to less sulfated chondroitin 4-sulfate. Galectin-3 then acts on transcription factors AP-1 to increase expression of chondroitin sulfate proteoglycan versican and SP-1 to increase expression of WNT9A. Another mechanism by which reduced ARSB is associated with carcinogenesis is through increased binding of SHP2 to more sulfated chondroitin 4-sulfate, which leads to increased phosphorylation of p38 and MITF with subsequently increased expression of GPNMB. | 11
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Most cases of intentional pesticide poisoning appear to be impulsive acts undertaken during stressful events, and the availability of pesticides strongly influences the incidence of self poisoning. Pesticides are the agents most frequently used by farmers and students in India to commit suicide. Occupational
Pesticide poisoning is an important occupational health issue because pesticides are used in a large number of industries, which puts many different categories of workers at risk. Extensive use puts agricultural workers in particular at increased risk for pesticide illnesses. Exposure can occur through inhalation of pesticide fumes, and often occurs in settings including greenhouse spraying operations and other closed environments like tractor cabs or while operating rotary fan mist sprayers in facilities or locations with poor ventilation systems. Workers in other industries are at risk for exposure as well. For example, commercial availability of pesticides in stores puts retail workers at risk for exposure and illness when they handle pesticide products. The ubiquity of pesticides puts emergency responders such as fire-fighters and police officers at risk, because they are often the first responders to emergency events and may be unaware of the presence of a poisoning hazard. The process of aircraft disinsection, in which pesticides are used on inbound international flights for insect and disease control, can also make flight attendants sick.Different job functions can lead to different levels of exposure. Most occupational exposures are caused by absorption through exposed skin such as the face, hands, forearms, neck, and chest. | A pesticide poisoning occurs when pesticides, chemicals intended to control a pest, affect non-target organisms such as humans, wildlife, plant, or bees. There are three types of pesticide poisoning. The first of the three is a single and short-term very high level of exposure which can be experienced by individuals who commit suicide, as well as pesticide formulators. Type two poisoning is long-term high-level exposure, which can occur in pesticide formulators and manufacturers. The third type of poisoning is a long-term low-level exposure, which individuals are exposed to from sources such as pesticide residues in food as well as contact with pesticide residues in the air, water, soil, sediment, food materials, plants and animals.In developing countries, such as Sri Lanka, pesticide poisonings from short-term very high level of exposure (acute poisoning) is the most worrisome type of poisoning. However, in developed countries, such as Canada, it is the complete opposite: acute pesticide poisoning is controlled, thus making the main issue long-term low-level exposure of pesticides. Cause
The most common exposure scenarios for pesticide-poisoning cases are accidental or suicidal poisonings, occupational exposure, by-stander exposure to off-target drift, and the general public who are exposed through environmental contamination. Accidental or suicidal
Self-poisoning with agricultural pesticides represents a major hidden public health problem accounting for approximately one-third of all suicides worldwide. It is one of the most common forms of self-injury in the Global South. The World Health Organization estimates that 300,000 people die from self-harm each year in the Asia-Pacific region alone. | 11
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Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has. In a 2019 Cochrane review on beginning reading interventions for children and adolescents with intellectual disability small to moderate improvements in phonological awareness, word reading, decoding, expressive and receptive language skills and reading fluency were noted when these elements were part of the teaching intervention.Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. | Diuresis is usually complete within 6–8 hours of oral administration, but there is significant variation between individuals. Adverse effects
Furosemide also can lead to gout caused by hyperuricemia. Hyperglycemia is also a common side effect. The tendency, as for all loop diuretics, to cause low serum potassium concentration (hypokalemia) has given rise to combination products, either with potassium or with the potassium-sparing diuretic amiloride (Co-amilofruse). Other electrolyte abnormalities that can result from furosemide use include hyponatremia, hypochloremia, hypomagnesemia, and hypocalcemia.In the treatment of heart failure, many studies have shown that the long-term use of furosemide can cause varying degrees of thiamine deficiency, so thiamine supplementation is also suggested.Furosemide is a known ototoxic agent generally causing transient hearing loss but can be permanent. Reported cases of furosemide induced hearing loss appeared to be associated with rapid intravenous administration, high dosages, concomitant renal disease and coadministration with other ototoxic medication. However, a recently reported longitudinal study showed that participants treated with loop diuretics over 10 years were 40% more likely to develop hearing loss and 33% more likely of progressive hearing loss compared to participants who did not use loop diuretics. This suggests the long-term consequences of loop diuretics on hearing could be a more significant than previously thought and further research is required in this area. Other precautions include: nephrotoxicity, sulfonamide (sulfa) allergy, and increases free thyroid hormone effects with large doses. Interactions
Furosemide has potential interactions with these medications:
Aspirin and other salicylates
Other diuretics (e.g. ethacrynic acid, hydrochlorothiazide)
Synergistic effects with other antihypertensives (e.g. | 0-1
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The genetic relationship of ADHD to Tourette syndrome, however, has not been fully established. A genetic link between autism and Tourettes has not been established as of 2017. Mechanism
The exact mechanism affecting the inherited vulnerability to Tourettes is not well established. Tics are believed to result from dysfunction in cortical and subcortical brain regions: the thalamus, basal ganglia and frontal cortex. Neuroanatomic models suggest failures in circuits connecting the brains cortex and subcortex; imaging techniques implicate the frontal cortex and basal ganglia. In the 2010s, neuroimaging and postmortem brain studies, as well as animal and genetic studies, made progress towards better understanding the neurobiological mechanisms leading to Tourettes. These studies support the basal ganglia model, in which neurons in the striatum are activated and inhibit outputs from the basal ganglia.Cortico-striato-thalamo-cortical (CSTC) circuits, or neural pathways, provide inputs to the basal ganglia from the cortex. These circuits connect the basal ganglia with other areas of the brain to transfer information that regulates planning and control of movements, behavior, decision-making, and learning. Behavior is regulated by cross-connections that "allow the integration of information" from these circuits. Involuntary movements may result from impairments in these CSTC circuits, including the sensorimotor, limbic, language and decision making pathways. Abnormalities in these circuits may be responsible for tics and premonitory urges.The caudate nuclei may be smaller in subjects with tics compared to those without tics, supporting the hypothesis of pathology in CSTC circuits in Tourettes. | Children may be less aware of it than are adults, but their awareness tends to increase with maturity; by the age of ten, most children recognize the premonitory urge.Premonitory urges which precede the tic make suppression of the impending tic possible. Because of the urges that precede them, tics are described as semi-voluntary or "unvoluntary", rather than specifically involuntary; they may be experienced as a voluntary, suppressible response to the unwanted premonitory urge. The ability to suppress tics varies among individuals, and may be more developed in adults than children. People with tics are sometimes able to suppress them for limited periods of time, but doing so often results in tension or mental exhaustion. People with Tourettes may seek a secluded spot to release the suppressed urge, or there may be a marked increase in tics after a period of suppression at school or work. Children may suppress tics while in the doctors office, so they may need to be observed when not aware of being watched.Complex tics related to speech include coprolalia, echolalia and palilalia. Coprolalia is the spontaneous utterance of socially objectionable or taboo words or phrases. Although it is the most publicized symptom of Tourettes, only about 10% of people with Tourettes exhibit it, and it is not required for a diagnosis. Echolalia (repeating the words of others) and palilalia (repeating ones own words) occur in a minority of cases. | 11
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Ichthyosis prematurity syndrome (IPS) is a dermatological disease with known genetic causes. This syndrome is a rare subcategory of autosomal recessive congenital ichthyosis (ARCI). It is associated with complications in the mid-trimester of a pregnancy leading to premature births. Although most prevalent in individuals of Scandinavian origin, there have also been scattered cases in people of Japanese, Italian and Indian ethnicity. This disorder is also referred to as ichthyosis congenital type IV. Signs and symptoms
The symptoms associated with the disorder are often confused for other dermatological disorders. The symptoms below are ones specifically associated with IPS. Premature birth
Pregnancies that have a foetus affected with this syndrome are complicated because of polyhydramnion. Complications arise because of opaque amnionic fluid resulting from the shedding of skin. As a result, ultrasounds are difficult to conduct. Triggered by the harsh environment in the uterus, delivery results around 30– 34 weeks of gestation (pregnancy) and the baby is born in prematurely. Thick caseous layer of skin
A white layer of thick scaly substance covers the surface of the skin of the infant. This is characterized by aggregating membranes in the upper layer of skin on epidermal cells. Desquamating skin
Red endemic skin as well as spongy and desquamating (peeling) skin are consistent with this syndrome. Respiratory problems
After premature delivery, the baby often has neonatal asphyxia from breathing amnionic debris mainly composed of shedding skin cells. Neonatal refers to the very young infant and amniotic fluid refers to the liquid environment the baby is bathed in inside the uterus. | Flashing may refer to:
Technology
Firmware#Flashing, overwriting an EEPROM module in a device
BIOS flashing, overwriting a BIOS image
Flashing (cinematography), a technique that desaturates the color so that one sees more in shadowed areas
Flashing (weatherproofing), construction material used to prevent the passage of water around objects
Flash evaporation, causing evaporation by lowering a fluids pressure below its vapour pressure
Flashing light, such as a light bulb or computers cursor
Flash (manufacturing), excess material attached to a moulded product which must usually be removed
Other
Flashing (horse)
Flashing, a 1981 album by Himiko Kikuchi
Exhibitionism, sexual body exposure
Indecent exposure, inappropriate public nudity
Headlight flashing, to alert other drivers
Facing (retail), moving shelved products to the front
See also
Flash (disambiguation) | 0-1
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Melphalan, sold under the brand name Alkeran among others, is a chemotherapy medication used to treat multiple myeloma, ovarian cancer, melanoma, and AL amyloidosis. It is taken by mouth or by injection into a vein.Common side effects include nausea and bone marrow suppression. Other severe side effects may include anaphylaxis and the development of other cancers. Use during pregnancy may result in harm to the fetus. Melphalan belongs to the class of nitrogen mustard alkylating agents. It works by interfering with the creation of DNA and RNA.Melphalan was approved for medical use in the United States in 1964. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. Medical uses
It is used to treat multiple myeloma, ovarian cancer, AL amyloidosis, and occasionally malignant melanoma. The agent was first investigated as a possible drug for use in melanoma, it was not found to be effective.In 2016, it was approved in the U.S. for:
use as a high-dose conditioning treatment prior to hematopoietic progenitor (stem) cell transplantation in multiple myeloma (MM) patients
the palliative treatment of MM patients for whom oral therapy is not appropriateMelphalan is used to treat ocular retinoblastoma, a pediatric solid tumor. This is accomplished via transarterial catheter based slow pulsed infusion into the ophthalmic artery. | The applicant for this medicinal product is ADIENNE S.r.l. S.U. Melphalan was approved for medical use in the European Union in November 2020. References
External links
"Melphalan". Drug Information Portal. U.S. National Library of Medicine. | 11
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Radiation as a treatment for malignant head and neck tumors can reduce the number of blood vessels in the treatment area and lead to scarring. In some cases, this can paralyze the vagus nerve, of which the RLNs are branches. Tumors of the vagus nerve, called vagal neurilemmomas, can also paralyze the vocal folds. Trauma
VF paresis can result from trauma to one of more laryngeal nerves during intubation, surgery (e.g. thyroidectomy, spine surgery, carotid endartectomy, vagal nerve stimulator implantation), injection of botulinum neurotoxin, or penetrating neck trauma. Thyroid disease
Causes of VF paresis also include diseases of the thyroid gland, such as hypothyroidism, goiter, and thyroiditis. Systemic neurologic diseases
Several neurological diseases can cause VF paresis including:
Myasthenia Gravis (MG), a rare neuromuscular autoimmune disease. MGs dominant characteristic is muscles weakness including facial, jaw, pharyngeal and laryngeal muscles. Charcot-Marie-Tooth (CMT), a neurological heredity disease that affects both motor and sensory functions. CMT affects the nerve cells and interrupts the transmission of nerve impulses as it concerns the axons and the myelination of the nerve cells. Multiple Sclerosis (MS), which is an autoimmune disease that damages the myelin sheet surrounding the axons of the cranial nerves and the spinal nerves. There are several types of MS depending on the course of the disease. Spinocerebellar Degeneration, a term that refers to a rare yet diverse chronic disease that affects the brain and the spinal cord. | Vocal cord paresis, also known as recurrent laryngeal nerve paralysis or vocal fold paralysis, is an injury to one or both recurrent laryngeal nerves (RLNs), which control all intrinsic muscles of the larynx except for the cricothyroid muscle. The RLN is important for speaking, breathing and swallowing.The primary larynx-related functions of the mainly efferent nerve fiber RLN, include the transmission of nerve signals to the muscles responsible for regulation of the vocal folds position and tension to enable vocalization, as well as the transmission of sensory nerve signals from the mucous membrane of the larynx to the brain. A unilateral injury of the nerve typically results in hoarseness caused by a reduced mobility of one of the vocal folds. It may also cause minor shortages of breath as well as aspiration problems especially concerning liquids. A bilateral injury causes the vocal folds to impair the air flow resulting in breathing problems, stridor and snoring sounds, and fast physical exhaustion. This strongly depends on the median or paramedian position of the paralyzed vocal folds. Hoarseness rarely occurs in bilaterally paralyzed vocal folds. Signs and symptoms
Typically, patients with vocal fold paresis or paralysis are able to identify the onset of their symptoms. The most commonly reported symptom patients with either vocal fold paresis or paralysis make is having a rough voice quality. It is important to note that the symptoms of vocal fold paresis are not specific to the condition and tend to be common symptoms of other voice disorders as well. | 11
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Several treatments including Promiseb, lactamide MEA gel, hydrocortisone 1% lotion, licochalcone 0.025%, flumethasone pivalate 0.02% ointment, and eosin 2% aqueous solution have been studied, however there is uncertainty regarding the efficacy and safety of these treatments.For adults: see the article on seborrheic dermatitis (the adult version of cradle cap). Scalp, behind ears, eyebrows
If the cradle cap is not severe, it could simply be combed out gently after bathing. The softened scales can then be brushed away with a soft brush, comb or cloth, but if not done very gently, this could worsen the condition and bring about temporary hair loss. Applying petroleum jelly (e.g., Vaseline) liberally overnight is another popular treatment. The softened scales either fall off during the night, or can be brushed off in the morning.There is broad disagreement regarding the role of shampoos. Some sources warn against frequent shampooing, others recommend it. Mild baby shampoo is often recommended, but the exact denotation of the label "mild" in this context is not quite clear. Baby shampoos often contain detergent surfactants, perfumes, quaternium-15 and other eczemagenic irritants. No studies have been performed on non-prescription shampoos.In stubborn cases some doctors may recommend keratolytic (dandruff) shampoos (e.g. with sulfur, selenium, zinc pyrithione, or salicylic acid) while others warn against the use of medicated shampoos in newborns due to systemic absorption. Dandruff shampoos often contain sodium dodecyl sulfate, a noted skin irritant.Steroid and tar preparations have also been used but may have drawbacks. The immunomodulators tacrolimus/Protopic and pimecrolimus/Elidel have not been approved for children under two years. | In descending perineum syndrome the anal canal is situated several cm below this imaginary line, or it descends 3–4 cm during straining. Defecography may also demonstrate abnormal perineal descent. Treatment
Surgical treatments may be used to treat the condition, and include retro-rectal levatorplasty, post-anal repair, retro-anal levator plate myorrhaphy. Epidemiology
The condition mainly occurs in women, and it is thought by some to be one of the main defects encountered problem in perineology. == References == | 0-1
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Further scratching may remove scabs, inhibiting the healing process. Scratching infected areas may also spread the fungus to the fingers and under the fingernails. If not washed away soon enough, it can infect the fingers and fingernails, growing in the skin and in the nails (not just underneath). After scratching, it can be spread to wherever the person touches, including other parts of the body and to ones environment. Scratching also causes infected skin scales to fall off into ones environment, leading to further possible spread. When athletes foot fungus or infested skin particles spread to ones environment (such as to clothes, shoes, bathroom, etc.) whether through scratching, falling, or rubbing off, not only can they infect other people, they can also reinfect (or further infect) the host they came from. For example, infected feet infest ones socks and shoes which further expose the feet to the fungus and its spores when worn again.The ease with which the fungus spreads to other areas of the body (on ones fingers) poses another complication. When the fungus is spread to other parts of the body, it can easily be spread back to the feet after the feet have been treated. And because the condition is called something else in each place it takes hold (e.g., tinea corporis (ringworm) or tinea cruris (jock itch)), persons infected may not be aware it is the same disease. | Symptoms in SSPs tend to be more severe than in PSPs, as the unaffected lungs are generally unable to replace the loss of function in the affected lungs. Hypoxemia (decreased blood-oxygen levels) is usually present and may be observed as cyanosis (blue discoloration of the lips and skin). Hypercapnia (accumulation of carbon dioxide in the blood) is sometimes encountered; this may cause confusion and – if very severe – may result in comas. The sudden onset of breathlessness in someone with chronic obstructive pulmonary disease (COPD), cystic fibrosis, or other serious lung diseases should therefore prompt investigations to identify the possibility of a pneumothorax.Traumatic pneumothorax most commonly occurs when the chest wall is pierced, such as when a stab wound or gunshot wound allows air to enter the pleural space, or because some other mechanical injury to the lung compromises the integrity of the involved structures. Traumatic pneumothoraces have been found to occur in up to half of all cases of chest trauma, with only rib fractures being more common in this group. The pneumothorax can be occult (not readily apparent) in half of these cases, but may enlarge – particularly if mechanical ventilation is required. They are also encountered in people already receiving mechanical ventilation for some other reason.Upon physical examination, breath sounds (heard with a stethoscope) may be diminished on the affected side, partly because air in the pleural space dampens the transmission of sound. Measures of the conduction of vocal vibrations to the surface of the chest may be altered. | 0-1
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With a few exceptions (snakes, placental mammals), most organisms avoid these effects by having absorbent oil droplets around their cone cells. The alternative, developed by organisms that had lost these oil droplets in the course of evolution, is to make the lens impervious to UV light—this precludes the possibility of any UV light being detected, as it does not even reach the retina. Rods and cones
The retina contains two major types of light-sensitive photoreceptor cells used for vision: the rods and the cones. Rods cannot distinguish colours, but are responsible for low-light (scotopic) monochrome (black-and-white) vision; they work well in dim light as they contain a pigment, rhodopsin (visual purple), which is sensitive at low light intensity, but saturates at higher (photopic) intensities. Rods are distributed throughout the retina but there are none at the fovea and none at the blind spot. Rod density is greater in the peripheral retina than in the central retina. Cones are responsible for colour vision. They require brighter light to function than rods require. In humans, there are three types of cones, maximally sensitive to long-wavelength, medium-wavelength, and short-wavelength light (often referred to as red, green, and blue, respectively, though the sensitivity peaks are not actually at these colours). The colour seen is the combined effect of stimuli to, and responses from, these three types of cone cells. Cones are mostly concentrated in and near the fovea. Only a few are present at the sides of the retina. | Spinal stenosis is an abnormal narrowing of the spinal canal or neural foramen that results in pressure on the spinal cord or nerve roots. Symptoms may include pain, numbness, or weakness in the arms or legs. Symptoms are typically gradual in onset and improve with leaning forward. Severe symptoms may include loss of bladder control, loss of bowel control, or sexual dysfunction.Causes may include osteoarthritis, rheumatoid arthritis, spinal tumors, trauma, Pagets disease of the bone, scoliosis, spondylolisthesis, and the genetic condition achondroplasia. It can be classified by the part of the spine affected into cervical, thoracic, and lumbar stenosis. Lumbar stenosis is the most common, followed by cervical stenosis. Diagnosis is generally based on symptoms and medical imaging.Treatment may involve medications, bracing, or surgery. Medications may include NSAIDs, acetaminophen, or steroid injections. Stretching and strengthening exercises may also be useful. Limiting certain activities may be recommended. Surgery is typically only done if other treatments are not effective, with the usual procedure being a decompressive laminectomy.Spinal stenosis occurs in as many as 8% of people. It occurs most commonly in people over the age of 50. Males and females are affected equally often. The first modern description of the condition is from 1803 by Antoine Portal, and there is evidence of the condition dating back to Ancient Egypt. Types
The most common forms are lumbar spinal stenosis, at the level of the lower back, and cervical spinal stenosis, which are at the level of the neck. | 0-1
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Drug reactions
Drug-induced lupus erythematosus is a (generally) reversible condition that usually occurs in people being treated for a long-term illness. Drug-induced lupus mimics SLE. However, symptoms of drug-induced lupus generally disappear once the medication that triggered the episode is stopped. More than 38 medications can cause this condition, the most common of which are procainamide, isoniazid, hydralazine, quinidine, and phenytoin. Non-systemic forms of lupus
Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of rash on the face, neck, scalp or arms. Approximately 5% of people with DLE progress to SLE. Pathophysiology
SLE is triggered by environmental factors that are unknown. In SLE, the bodys immune system produces antibodies against self-protein, particularly against proteins in the cell nucleus. These antibody attacks are the immediate cause of SLE.SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement. Reticulate and stellate acral pigmentation should be considered a possible manifestation of SLE and high titers of anti-cardiolipin antibodies, or a consequence of therapy.People with SLE have intense polyclonal B-cell activation, with a population shift towards immature B cells. Memory B cells with increased CD27+/IgD—are less susceptible to immunosuppression. CD27-/IgD- memory B cells are associated with increased disease activity and renal lupus. T cells, which regulate B-cell responses and infiltrate target tissues, have defects in signaling, adhesion, co-stimulation, gene transcription, and alternative splicing. | Discovered by a team of researchers at the Mayo Clinic, they discovered that the white blood cells contained the nucleus of another cell that was pushing against the whites cell proper nucleus.Noting that the invading nucleus was coated with antibody that allowed it to be ingested by a phagocytic or scavenger cell, they named the antibody that causes one cell to ingest another the LE factor and the two nuclei cell result in the LE cell. The LE cell, it was determined, was a part of an anti-nuclear antibody (ANA) reaction; the body produces antibodies against its own tissue. This discovery led to one of the first definitive tests for lupus since LE cells are found in approximately 60% of all people diagnosed with lupus. The LE cell test is rarely performed as a definitive lupus test today as LE cells do not always occur in people with SLE and can occur in individuals with other autoimmune diseases. Their presence can help establish a diagnosis but no longer indicates a definitive SLE diagnosis. The discovery of the LE cell led to further research and this resulted in more definitive tests for lupus. Building on the knowledge that those with SLE had auto-antibodies that would attach themselves to the nuclei of normal cells, causing the immune system to send white blood cells to fight off these "invaders", a test was developed to look for the anti-nuclear antibody (ANA) rather than the LE cell specifically. | 11
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Cystica profunda is characterized by formation of mucin cysts in the muscle layers of the gut lining, and it can occur anywhere along the gastrointestinal tract. When it occurs in the rectum, some believe to be an interchangeable diagnosis with SRUS since the histologic features of the conditions overlap. Indeed, CCP is managed identically to SRUS.Electromyography may show pudendal nerve motor latency. Complications
Complications are uncommon, but include massive rectal bleeding, ulceration into the prostate gland or formation of a stricture. Very rarely, cancer can arise on the section of prolapsed rectal lining. Diagnosis and investigations
SRUS is commonly misdiagnosed, and the diagnosis is not made for 5–7 years. Clinicians may not be familiar with the condition, and treat for Inflammatory bowel disease, or simple constipation.The thickened lining or ulceration can also be mistaken for types of cancer.The differential diagnosis of SRUS (and CCP) includes:
polyps
endometriosis
inflammatory granulomas
infectious disorders
drug-induced colitis
mucus-producing adenocarcinomaDefecography, sigmoidoscopy, transrectal ultrasound, mucosal biopsy, anorectal manometry and electromyography have all been used to diagnose and study SRUS. Some recommend biopsy as essential for diagnosis since ulcerations may not always be present, and others state defecography as the investigation of choice to diagnose SRUS. Treatment
Although SRUS is not a medically serious disease, it can be the cause of significantly reduced quality of life for patients. It is difficult to treat, and treatment is aimed at minimizing symptoms. Stopping straining during bowel movements, by use of correct posture, dietary fiber intake (possibly included bulk forming laxatives such as psyllium), stool softeners (e.g. | Negative interim PET scan results may result in an increase in progression-free survival compared if the adjusted result was measured. Negative interim PET scan results probably result in a large increase in the overall survival compared to those with a positive interim PET scan result.Current research evaluated whether Nivolumab can be used for the treatment of a Hodgkins lymphoma. The evidence is very uncertain about the effect of Nivolumab for patients with a Hodgkins lymphoma on the overall survival, the quality of life, the survival without a progression, the response rate (=complete disappear) and grade 3 or 4 serious adverse events. Palliative care
Palliative care, a specialized medical care focused on the symptoms, pain, and stress of a serious illness, is recommended by multiple national cancer treatment guidelines as an accompaniment to curative treatments for people with lymphoma. It is used to address both the direct symptoms of lymphoma and many unwanted side effects that arise from treatments. Palliative care can be especially helpful for children who develop lymphoma, helping both children and their families deal with the physical and emotional symptoms of the disease. For these reasons, palliative care is especially important for people requiring bone marrow transplants. Supportive treatment
Adding physical exercises to the standard treatment for adult patients with haematological malignancies like lymphomas may result in little to no difference in the mortality, the quality of life and the physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue. | 0-1
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The active metabolite of progesterone has been found to enhance the binding of benzodiazepines to the benzodiazepine binding sites on the GABAA receptor. The cross-tolerance between GABAA receptor positive modulators, including benzodiazepines, occurs because of the similar mechanism of action and the subunit changes that occur from chronic use from one or more of these compounds in expressed receptor isoforms. Abrupt withdrawal from any of these compounds, e.g., barbiturates, benzodiazepines, alcohol, corticosteroids, neuroactive steroids, and nonbenzodiazepines, precipitate similar withdrawal effects characterized by central nervous system hyper-excitability, resulting in symptoms such as increased seizure susceptibility and anxiety. While many of the neuroactive steroids do not produce full tolerance to their therapeutic effects, cross-tolerance to benzodiazepines still occurs as had been demonstrated between the neuroactive steroid ganaxolone and diazepam. Alterations of levels of neuroactive steroids in the body during the menstrual cycle, menopause, pregnancy, and stressful circumstances can lead to a reduction in the effectiveness of benzodiazepines and a reduced therapeutic effect. During withdrawal of neuroactive steroids, benzodiazepines become less effective. Physiology of withdrawal
Withdrawal symptoms are a normal response in individuals having chronically used benzodiazepines, and an adverse effect and result of drug tolerance. Symptoms typically emerge when dosage of the drug is reduced. GABA is the second-most-common neurotransmitter in the central nervous system (the most common being glutamate) and by far the most abundant inhibitory neurotransmitter; roughly one-quarter to one-third of synapses use GABA. | Benzodiazepines have also been linked to an increased risk of road traffic accidents and falls in the elderly. The long-term effects of benzodiazepines are still not fully understood. Long-term benzodiazepine use is associated with attentional and visuospatial functional impairments. Withdrawal from benzodiazepines can lead to improved alertness and decreased forgetfulness in the elderly. Withdrawal led to statistically significant improvements in memory function and performance-related skills in those having withdrawn successfully from benzodiazepines, whereas those having remained on benzodiazepines experienced worsening symptoms. People having withdrawn from benzodiazepines also felt their sleep was more refreshing, making statements such as "I feel sharper when I wake up" or "I feel better, more awake", or "It used to take me an hour to fully wake up." This suggests that benzodiazepines may actually make insomnia worse in the elderly. Cause
Tolerance occurs to the muscle-relaxant, anticonvulsant, and sleep-inducing effects of benzodiazepines, and upon cessation a benzodiazepine withdrawal syndrome occurs. This can lead to benzodiazepines being taken for longer than originally intended, as people continue to take the drugs over a long period of time to suppress withdrawal symptoms. Some people use benzodiazepines at very high doses and devote a lot of time to doing so, satisfying the diagnostic criteria in DSM V for substance use disorder. Another group of people include those on low to moderate therapeutic doses of benzodiazepines who do not use their benzodiazepines differently than recommended by their prescriber but develop a physical tolerance and benzodiazepine dependence. | 11
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Nine of them will be in developing countries: Mumbai, India – 27.4 million; Lagos, Nigeria – 24.4; Shanghai, China – 23.4; Jakarta, Indonesia – 21.2; São Paulo, Brazil – 20.8; Karachi, Pakistan – 20.6; Beijing, China – 19.4; Dhaka, Bangladesh – 19; Mexico City, Mexico – 18.8. The only city in a developed country that will be in the top ten is Tokyo, Japan – 28.7 million. "In 2008, Dr. Anna Tibaijuka, executive director of UN-HABITAT, referring to the recent report "State of the Worlds Cities Report 2008/2009", said that the world economic crisis we are in should be viewed as a "housing finance crisis" in which the poorest of poor were left to fend for themselves. Refuges and alternative accommodation
There are various places where a homeless person might seek refuge:
24-hour Internet cafes are now used by over 5,000 Japanese "Net cafe refugees". An estimated 75% of Japans 3,200 all-night internet cafes cater to regular overnight guests, who in some cases have become their main source of income. 24-hour McDonalds restaurants are used by "McRefugees" in Japan, China and Hong Kong. There are about 250 McRefugees in Hong Kong. Couch surfing: temporary sleeping arrangements in dwellings of friends or family members ("couch surfing"). This can also include housing in exchange for labor or sex. Couch surfers may be harder to recognize than street homeless people and are often omitted from housing counts. | In 2009 it was estimated that one out of 50 children or 1.5 million children in the United States would experience some form of homelessness each year.In 2010 in New York City, where there were over 36,000 homeless people in 2009, there was a mobile video exhibit in the streets showing a homeless person on a screen and asking onlookers and passersby to text with their cellphones a message for him, and they also could donate money by cellphones to the organization Pathways to Housing. In September 2010, it was reported that the Housing First Initiative had significantly reduced the chronic homeless single person population in Boston, Massachusetts, although homeless families were still increasing in number. Some shelters were reducing the number of beds due to lowered numbers of homeless, and some emergency shelter facilities were closing, especially the emergency Boston Night Center. In 2011, the Department of Veterans Affairs Supportive Services for Veterans Families Initiative, SSVF, began funding private non-profit organizations and consumer cooperatives to provide supportive services to very low-income veteran families living in or transitioning to permanent housing.In 2019, in an interview with CBS News, scholar Sara Goldrick-Rab said that her study on college student homelessness found that "[n]early one in ten college students said they were homeless in the last year, meaning they had at least one night where they did not know where they were going to sleep." Puerto Rico
According to the count by the Puerto Rico Department of Family, in January 2017 there were 3,501 homeless persons in the territory. | 11
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The contraceptive effects of desogestrel in women are mediated not only by prevention of ovulation via its antigonadotropic effects but also by its marked progestogenic and antiestrogenic effects on cervical mucus and the endometrium.Aside from its progestogenic activity, desogestrel also has some off-target hormonal activity at other steroid hormone receptors (see below). However, these activities are relatively weak, and desogestrel is said to be one of the most selective and pure progestogens used in oral contraceptives. Antigonadotropic effects
Desogestrel has antigonadotropic effects via its progestogenic activity, similarly to other progestogens. It has been found to reduce testosterone levels by 15% in women at a dosage of 125 μg/day. In addition, desogestrel has been extensively investigated as an antigonadotropin at dosages of 150 to 300 μg/day in combination with testosterone in male contraceptive regimens. One study found that 150 μg/day and 300 μg/day desogestrel alone in healthy young men suppressed luteinizing hormone (LH) levels by about 35% and 42%, respectively; follicle-stimulating hormone (FSH) levels by about 47% and 55%, respectively; and testosterone levels by about 59% and 68%, respectively. LH levels were suppressed maximally by desogestrel within 3 days, whereas 14 days were necessary for maximal suppression of FSH and testosterone levels. A previous study by the same authors found that increasing the dosage of desogestrel from 300 μg/day to 450 μg/day resulted in no further suppression of gonadotropin concentrations. | The addition of a low dose of 50 or 100 mg/week intramuscular testosterone enanthate after 3 weeks increased testosterone levels and further suppressed LH and FSH levels, to the limits of assay detection (i.e., to undetectable or near-undetectable levels), in both the 150 μg/day and 300 μg/day desogestrel groups. Upon cessation of treatment, levels of LH, FSH, and testosterone all recovered to baseline values within 4 weeks. Androgenic activity
Etonogestrel has about 20% of the affinity of metribolone and 50% of the affinity of levonorgestrel for the androgen receptor (AR) while desogestrel has no affinity for this receptor. The 5α-reduced metabolite of etonogestrel, 5α-dihydroetonogestrel (3-keto-5α-dihydrodesogestrel), also has some affinity for the AR (about 17% of that of metribolone). Desogestrel (via etonogestrel) has very low androgenic potency, about 1.9 to 7.4% of that of methyltestosterone in animal assays, and hence is considered to be a very weak androgen. Although etonogestrel has about the same affinity for the AR as norethisterone, due to the relatively increased progestogenic potency and decreased androgenic activity of etonogestrel, the drug has markedly higher selectivity for the PR over the AR than older 19-nortestosterone progestins like norethisterone and levonorgestrel. Conversely, its selectivity for the PR over the AR is similar to other newer 19-nortestosterone progestins like gestodene and norgestimate. It has been estimated that 150 μg/day desogestrel has less than one-sixth of the androgenic effect of 1 mg/day norethisterone (these being common dosages of the drugs used in combined oral contraceptives). | 11
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in Quebec civil law), if the mother is married to another man, the latter will be defined as the father
Presumed father – Where a presumption of paternity has determined that a man is a childs father regardless of if he actually is or is not the biological father
Social father – where a man takes de facto responsibility for a child, such as caring for one who has been abandoned or orphaned (the child is known as a "child of the family" in English law)
Stepfather – a married non-biological father where the child is from a previous relationship
Fatherhood defined by contact level
Absent father – father who cannot or will not spend time with his child(ren)
Second father – a non-parent whose contact and support is robust enough that near parental bond occurs (often used for older male siblings who significantly aid in raising a child, sometimes for older men who took care of younger friends who have no families)
Stay-at-home dad – the male equivalent of a housewife with child, where his spouse is breadwinner
Weekend/holiday father – where child(ren) only stay(s) with father on weekends, holidays, etc. Non-human fatherhood
For some animals, it is the fathers who take care of the young. Darwins frog (Rhinoderma darwini) fathers carry eggs in the vocal pouch. Most male waterfowl are very protective in raising their offspring, sharing scout duties with the female. Examples are the geese, swans, gulls, loons, and a few species of ducks. | These contain additional material from chromosome 21 and occur in about 2.5% of cases. An isochromosome results when the two long arms of a chromosome separate together rather than the long and short arm separating together during egg or sperm development. Trisomy 21
Trisomy 21 (also known by the karyotype 47,XX,+21 for females and 47,XY,+21 for males) is caused by a failure of the 21st chromosome to separate during egg or sperm development (nondisjunction). As a result, a sperm or egg cell is produced with an extra copy of chromosome 21; this cell thus has 24 chromosomes. When combined with a normal cell from the other parent, the baby has 47 chromosomes, with three copies of chromosome 21. About 88% of cases of trisomy 21 result from nonseparation of the chromosomes in the mother, 8% from nonseparation in the father, and 3% after the egg and sperm have merged. Mosaicism
Mosaicism is diagnosed when there is a mixture of two types of cells: some cells have three copies of chromosome 21 but some cells have the typical two copies of chromosome 21. Mosaicism is the least common form of Down syndrome and accounts for only about 1% of all cases of Down syndrome. Children with mosaic Down syndrome may have the same features as other children with Down syndrome. However, they may have fewer characteristics of the condition due to the presence of some (or many) cells with a typical number of chromosomes. | 0-1
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Adenosine deaminase deficiency (ADA deficiency) is a metabolic disorder that causes immunodeficiency. It is caused by mutations in the ADA gene. It accounts for about 10–15% of all cases of autosomal recessive forms of severe combined immunodeficiency (SCID) among non-inbred populations.ADA deficiency can present in infancy, childhood, adolescence, or adulthood. Age of onset and severity is related to some 29 known genotypes associated with the disorder. It occurs in fewer than one in 100,000 live births worldwide. Signs and symptoms
The main symptoms of ADA deficiency are pneumonia, chronic diarrhea, and widespread skin rashes. Affected children also grow much more slowly than healthy children and some have developmental delay. Most individuals with ADA deficiency are diagnosed with SCID in the first 6 months of life.An association with polyarteritis nodosa has been reported. Genetics
The enzyme adenosine deaminase is encoded by the ADA gene on chromosome 20. ADA deficiency is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome (chromosome 20 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.Age of onset and severity is related to some 29 known genotypes associated with the disorder. Pathophysiology
ADA deficiency is due to a lack of the enzyme adenosine deaminase. | Psychiatists may instead use a definition from the DSM-IV, defining nocturnal enuresis as repeated urination into bed or clothes, occurring twice per week or more for at least three consecutive months in a child of at least 5 years of age and not due to either a drug side effect or a medical condition. Management
There are a number of management options for bedwetting. The following options apply when the bedwetting is not caused by a specifically identifiable medical condition such as a bladder abnormality or diabetes. Treatment is recommended when there is a specific medical condition such as bladder abnormalities, infection, or diabetes. It is also considered when bedwetting may harm the childs self-esteem or relationships with family/friends. Only a small percentage of bedwetting is caused by a specific medical condition, so most treatment is prompted by concern for the childs emotional welfare. Behavioral treatment of bedwetting overall tends to show increased self-esteem for children.Parents become concerned much earlier than doctors. A study in 1980 asked parents and physicians the age that children should stay dry at night. The average parent response was 2.75 years old, while the average physician response was 5.13 years old.Punishment is not effective and can interfere with treatment. Treatment approaches
Simple behavioral methods are recommended as initial treatment. Other treatment methods include the following:
Motivational therapy in nocturnal enuresis mainly involves parent and child education. Guilt should be allayed by providing facts. Fluids should be restricted 2 hours prior to bed. | 0-1
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They may find it difficult to go on a vacation, and even if they book a vacation, they may keep postponing it until it never happens. They may feel uncomfortable when they do go on a vacation and will take something along with them so they can work. They choose hobbies that are organized and structured, and they approach them as a serious task requiring work to perfect. The devotion to productivity in OCPD, however, is distinct from work addiction. OCPD is controlled and egosyntonic, whereas work addiction is uncontrolled and egodystonic, and the affected person may display signs of withdrawal. Rigidity
Individuals with OCPD are overconscientious, scrupulous and rigid, and inflexible on matters of morality, ethics and other areas of life. They may force themselves and others to follow rigid moral principles and strict standards of performance. They are self-critical and harsh about their mistakes. These symptoms should not be accounted for or caused by a persons culture or religion. Their view of the world is polarised and dichotomous; there is no grey area between what is right and what is wrong. Whenever this dichotomous view of the world cannot be applied to a situation, this causes internal conflict as the persons perfectionist tendencies are challenged.People with this disorder are so obsessed with doing everything the "right and correct" way that they have a hard time understanding and appreciating the ideas, beliefs, and values of other people, and are reluctant to change their views, especially on matters of morality and politics. | ISBN 978-1-61537-280-5
External links
MedlinePlus Encyclopedia: Obsessive–compulsive personality disorder | 11
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However the onset to peak effect is 2 hours and the clinical effects remain up to 2 hours after patch has been removed. The absorption is increased when the transdermal patch is applied onto inflamed skin or skin that has been exposed to heat. The absorption lasts for approximately 9 hours after application (onto normal, unexposed to heat and uninflamed skin). 90% of the medication is excreted in the urine as metabolites and unchanged drug. Cost
Brand-name and generic formulations are available. Legal status
Internationally, methylphenidate is a Schedule II drug under the Convention on Psychotropic Substances. In the United States, methylphenidate is classified as a Schedule II controlled substance, the designation used for substances that have a recognized medical value but present a high potential for misuse. In the United Kingdom, methylphenidate is a controlled Class B substance. Possession without prescription carries a sentence up to 5 years or an unlimited fine, or both; supplying methylphenidate is 14 years or an unlimited fine, or both. In Canada, methylphenidate is listed in Schedule III of the Controlled Drugs and Substances Act and is illegal to possess without a prescription, with unlawful possession punishable by up to three years imprisonment, or (via summary conviction) by up to one year imprisonment and/or fines of up to two thousand dollars. Unlawful possession for the purpose of trafficking is punishable by up to ten years imprisonment, or (via summary conviction) by up to eighteen months imprisonment. In New Zealand, methylphenidate is a class B2 controlled substance. | There is evidence to suggest that children diagnosed with ADHD who do not receive treatment will have an increased risk of substance use disorders as adults.The precise magnitude of improvement in ADHD symptoms and quality of life that are produced by methylphenidate treatment remains uncertain as of November 2015. Methylphenidate is not included in the World Health Organization Essential Medicines List, as findings by the World Health Organization indicate that evidence of benefit versus harm to be unclear in the treatment of ADHD. A 2021 systematic review concluded that there is no clear evidence for using IR Methylphenidate (immediate-release) for adults.Since ADHD diagnosis has increased around the world, methylphenidate may be misused as a "study drug" by some populations, which may be harmful. This also applies to people who may be experiencing a different issue and are misdiagnosed with ADHD. People in this category can then experience negative side-effects of the drug which worsen their condition. Narcolepsy
Narcolepsy, a chronic sleep disorder characterized by overwhelming daytime drowsiness and uncontrollable sleep, is treated primarily with stimulants. Methylphenidate is considered effective in increasing wakefulness, vigilance, and performance. Methylphenidate improves measures of somnolence on standardized tests, such as the Multiple Sleep Latency Test (MSLT), but performance does not improve to levels comparable to healthy people. Other medical uses
Methylphenidate may also be prescribed for off-label use in treatment-resistant cases of bipolar disorder and major depressive disorder. It can also improve depression in several groups including stroke, cancer, and HIV-positive patients. | 11
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However, clinical trials have developed certain compounds that could potentially change the future of Alzheimers disease treatments. Currently, diagnoses of Alzheimers is subpar, and better methods need to be utilized for various aspects of clinical diagnoses. Alzheimers has a 20% misdiagnosis rate.AD pathology is primarily characterized by the presence of amyloid plaques and neurofibrillary tangles. Plaques are made up of small peptides, typically 39–43 amino acids in length, called amyloid beta (also written as A-beta or Aβ). Amyloid beta is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neurons membrane. APP appears to play roles in normal neuron growth, survival and post-injury repair. APP is cleaved into smaller fragments by enzymes such as gamma secretase and beta secretase. One of these fragments gives rise to fibrils of amyloid beta which can self-assemble into the dense extracellular amyloid plaques. Parkinsons disease
Parkinsons disease (PD) is the second most common neurodegenerative disorder. It typically manifests as bradykinesia, rigidity, resting tremor and posture instability. The crude prevalence rate of PD has been reported to range from 15 per 100,000 to 12,500 per 100,000, and the incidence of PD from 15 per 100,000 to 328 per 100,000, with the disease being less common in Asian countries. PD is primarily characterized by death of dopaminergic neurons in the substantia nigra, a region of the midbrain. The cause of this selective cell death is unknown. Notably, alpha-synuclein-ubiquitin complexes and aggregates are observed to accumulate in Lewy bodies within affected neurons. | Diseases caused by the aggregation of proteins are known as proteopathies, and they are primarily caused by aggregates in the following structures:
cytosol, e.g. Parkinsons and Huntingtons
nucleus, e.g. Spinocerebellar ataxia type 1 (SCA1)
endoplasmic reticulum (ER), (as seen with neuroserpin mutations that cause familial encephalopathy with neuroserpin inclusion bodies)
extracellularly excreted proteins, amyloid-beta in Alzheimers diseaseThere are two main avenues eukaryotic cells use to remove troublesome proteins or organelles:
ubiquitin–proteasome: protein ubiquitin along with enzymes is key for the degradation of many proteins that cause proteopathies including polyQ expansions and alpha-synucleins. Research indicates proteasome enzymes may not be able to correctly cleave these irregular proteins, which could possibly result in a more toxic species. This is the primary route cells use to degrade proteins.Decreased proteasome activity is consistent with models in which intracellular protein aggregates form. It is still unknown whether or not these aggregates are a cause or a result of neurodegeneration. autophagy–lysosome pathways: a form of programmed cell death (PCD), this becomes the favorable route when a protein is aggregate-prone meaning it is a poor proteasome substrate. This can be split into two forms of autophagy: macroautophagy and chaperone-mediated autophagy (CMA).macroautophagy is involved with nutrient recycling of macromolecules under conditions of starvation, certain apoptotic pathways, and if absent, leads to the formation of ubiquinated inclusions. Experiments in mice with neuronally confined macroautophagy-gene knockouts develop intraneuronal aggregates leading to neurodegeneration. chaperone-mediated autophagy defects may also lead to neurodegeneration. | 11
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One of them is decapitation, both a fearsome way to intimidate victims as well as an act that may include ritualistic elements. According to an UN report from Congolese refugees, they believed the Bana Mura and Kamuina Nsapu militias have "magical powers" as a result of drinking the blood of decapitated victims, making them invincible. According to some reports, they indeed feed the blood from their victims heads to younger members as an initiation rite, then they often burn the remains or sometimes consume these, committing cannibalism.Besides the massive decapitations (like the beheading of 40 members of the State Police), a globally notorious case happened in March 2017 to Swedish politician Zaida Catalán and American UN expert Michael Sharp, who were kidnapped and executed during a mission near the village of Ngombe in Kasaï Province. | Robert Devereux, 2nd Earl of Essex, and Mary, Queen of Scots required three strikes at their respective executions. The same could be said for the execution of Johann Friedrich Struensee, favorite of the Danish queen Caroline Matilda of Great Britain. Margaret Pole, 8th Countess of Salisbury, is said to have required up to 10 strokes before decapitation was achieved. This particular story may, however, be apocryphal (since highly divergent accounts exist). Historian and philosopher David Hume, for example, relates the following about her death:She refused to lay her head on the block, or submit to a sentence where she had received no trial. She told the executioner, that if he would have her head, he must win it the best way he could: and thus, shaking her venerable grey locks, she ran about the scaffold; and the executioner followed her with his axe, aiming many fruitless blows at her neck before he was able to give the fatal stroke. To ensure that the blow would be fatal, executioners swords usually were blade-heavy two-handed swords. Likewise, if an axe was used, it almost invariably was wielded with both hands. In England a bearded axe was used for beheading, with the blades edge extending downwards from the tip of the shaft.Finlands official beheading axe resides today at the Museum of Crime in Vantaa. It is a broad-bladed two-handed axe. It was last used when murderer Tahvo Putkonen was executed in 1825, the last execution in peacetime in Finland. | 11
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Side effects
More than 10% of people taking ledipasvir/sofosbuvir have headaches or fatigue; rashes, nausea, diarrhea, and insomnia occur in between 1% and 10% of people taking it.More severe reactions are connected with allergic reactions to the medications and cardiovascular problems. Harvoni side effects are considered relatively mild compared to older interferon-based treatment. Ledipasvir/sofosbuvir could cause hepatitis B re-activation in people co-infected with hepatitis B and C viruses. The European Medicines Agency recommended screening all people for hepatitis B before starting ledipasvir/sofosbuvir for hepatitis C in order to minimize the risk of hepatitis B reactivation. Drug interactions
Ledipasvir/sofosbuvir is a substrate for the drug transporters P-Glycoprotein (P-gp) and breast cancer resistance protein (BCRP). Intestinal absorption of these drug transporter substrates may be decreased by inducers such as rifampin and St. Johns wort .Patients are also advised to stay away from H2 receptor antagonists (H2RA) and proton-pump inhibitors (PPI) because they decrease the concentration of ledipasvir (its solubility is pH-dependent and is higher under acidic conditions). Therefore, it is advised to take a PPI at least two hours after ledipasvir/sofosbuvir with a dose less than or equal to 20 mg daily and H2RAs with a dose of less than or equal to 40 mg twice daily.Ledipasvir/sofosbuvir should additionally be avoided when taking amiodarone or other drugs that lower heart rate; there is a serious risk of the heart slowing or stopping when ledipasvir/sofosbuvir is used with such drugs. | Mechanisms of action
The most commonly associated mechanism associated with ledipasvir/sofosbuvir is the hyperphosphorylation of NS5A, a viral polymerase important in proper viral assembly and interferes with proper liver metabolism. Ledipasvir/sofosbuvir inhibits the proper viral assembly by re-positioning NS5As sub-cellular localization.NS5B, a viral polymerase that can initiate RNA synthesis de novo, is also allosterically inhibited by ledipasvir/sofosbuvir.NS5A and NS5B inhibitors in combination have a synergistic effect. Pharmacokinetics
Sofosbuvir is absorbed fast in the plasma with a peak concentration (Cmax) at 0.8 to 1 hour after the administered dosage and undergoes extra hepatic metabolism with 61 to 65% bound to human plasma proteins. It is then predominantly converted to the inactive phosphate free circulating metabolite GS-331007 (eliminated 76% through renal passive filtration) which has a median peak plasma concentration at 3.5 to 4 hours after the medication is ingested. Sofosbuvir does not appear to be affected by different levels of macronutrients when compared with fasting states.Ledipasvir has a maximum concentration at 4 to 4.5 hours after ingestion and is not affected by macronutrients. It is more than 98% protein bound and is predominantly eliminated fecally, with minimal metabolism in the liver. Elimination
The median terminal half life after a dosage of ledipasvir/sofosbuvir for 90 mg of [14C]-Ledipasvir is 47 hours; for 400 mg of [14C]-Sofosbuvir it is 0.5 hours (after the initial distribution of medication in body tissue) and 27 hours (the eventual excretion of the medication). | 11
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Researchers have observed in some studies that brain tumor patients (or their mothers) have generally consumed more cured foods (also known as Curing) than control groups. Recently, Drs. Lee, Wrensch and others found that adults with glioma were more likely to consume diets high in cured foods and low in vitamin C-rich fruits and vegetables, and to consume diets high in nitrites and low in vitamin C. The effect was more pronounced in men than women. However, the pattern of increased risk with increased consumption of cured foods, and decreased risk with greater consumption of fruits, vegetables, and antioxidant vitamins is compatible with other cancer studies that show increased consumption of vegetables and possibly of fruits is associated with decreased cancer risk. Radiation
A link between gliomas and electromagnetic radiation from cell phones has not been conclusively proven. It was considered possible, though several large studies have found no conclusive evidence, as summarized by the NIHs National Cancer Institute review of the topic and its numerous citations, and the FCC. However, further research is still being pursued to obtain more robust evidence and verify that there is no relationship (the NIHs National Institute of Environmental Health Sciences most recent press release discussed an ongoing study showing mildly positive results, although it appears there may have been issues with the control group dying prematurely). Infection with cytomegalovirus
Some studies have reported that glioblastomas are infected with cytomegalovirus, with suggestions that this may speed the development of tumors. | pointed out that IDH1 and IDH2 mutant cells produce an excess metabolic intermediate, 2-hydroxyglutarate, which binds to catalytic sites in key enzymes that are important in altering histone and DNA promoter methylation. Thus, mutations in IDH1 and IDH2 generate a "DNA CpG island methylator phenotype or CIMP" that causes promoter hypermethylation and concomitant silencing of tumor suppressor genes such as DNA repair genes MGMT and ERCC1. On the other hand, Cohen et al. and Molenaar et al. pointed out that mutations in IDH1 or IDH2 can cause increased oxidative stress. Increased oxidative damage to DNA could be mutagenic. This is supported by an increased number of DNA double-strand breaks in IDH1-mutated glioma cells. Thus, IDH1 or IDH2 mutations act as driver mutations in glioma carcinogenesis, though it is not clear by which role they are primarily acting. A study, involving 51 patients with brain gliomas who had two or more biopsies over time, showed that mutation in the IDH1 gene occurred prior to the occurrence of a p53 mutation or a 1p/19q loss of heterozygosity, indicating that an IDH1 mutation is an early driver mutation. Pathophysiology
High-grade gliomas are highly vascular tumors and have a tendency to infiltrate diffusely. They have extensive areas of necrosis and hypoxia. Often, tumor growth causes a breakdown of the blood–brain barrier in the vicinity of the tumor. | 11
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The secondary stage occurs months to two years later (but usually 1–2 months later), and may thus begin when the mother yaw has not yet healed. It happens when the bacterium spreads in the blood and lymph. It begins as multiple, pinhead-like papules; these initial lesions grow and change in appearance and may last weeks before healing, with or without scarring.Secondary yaws typically shows widespread skin lesions that vary in appearance, including "crab yaws" (areas of skin of abnormal colour) on the palms of the hands and soles of the feet (named for the crab-like gait they cause people with painful soles to assume). These may show desquamation. These secondary lesions frequently ulcerate and are then highly infectious, but heal after 6 months or more.Secondary yaws affects the skin and bones. The most common bone-related problem is periostitis, an inflammation around the bone, often occurs in the bones of the fingers and the long bones of the lower arms and legs, causing swollen fingers and limbs. This causes pain at night and thickening of the affected bones (periostitis). About 75% of infected children surveyed in Papua New Guinea reported joint pain. Swollen lymph nodes, fever, and malaise are also common.After primary and secondary yaws (and possibly, in some cases, without these phases), a latent infection develops. Within five years (rarely, within ten years) it can relapse and become active again, causing further secondary lesions, which may infect others. These relapse lesions are most commonly found around the armpits, mouth, and anus. | Yaws is a tropical infection of the skin, bones, and joints caused by the spirochete bacterium Treponema pallidum pertenue. The disease begins with a round, hard swelling of the skin, 2 to 5 cm (0.79 to 1.97 in) in diameter. The center may break open and form an ulcer. This initial skin lesion typically heals after 3–6 months. After weeks to years, joints and bones may become painful, fatigue may develop, and new skin lesions may appear. The skin of the palms of the hands and the soles of the feet may become thick and break open. The bones (especially those of the nose) may become misshapen. After 5 years or more, large areas of skin may die, leaving scars.Yaws is spread by direct contact with the fluid from a lesion of an infected person. The contact is usually of a nonsexual nature. The disease is most common among children, who spread it by playing together. Other related treponemal diseases are bejel (T. pallidum endemicum), pinta (T. carateum), and syphilis (T. p. pallidum). Yaws is often diagnosed by the appearance of the lesions. Blood antibody tests may be useful, but cannot separate previous from current infections. Polymerase chain reaction is the most accurate method of diagnosis.No vaccine has yet been found. Prevention is, in part, done by curing those who have the disease, thereby decreasing the risk of transmission. Where the disease is common, treating the entire community is effective. Improving cleanliness and sanitation also decreases spread. | 11
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Biomechanical loading
As well as medication, rehabilitation programmes and surgical interventions, the application of biomechanical loading on tremor movement has been shown to be a technique that is able to suppress the effects of tremor on the human body. It has been established in the literature that most of the different types of tremor respond to biomechanical loading. In particular, it has been clinically tested that the increase of damping or inertia in the upper limb leads to a reduction of the tremorous motion. Biomechanical loading relies on an external device that either passively or actively acts mechanically in parallel to the upper limb to counteract tremor movement. This phenomenon gives rise to the possibility of an orthotic management of tremor.Starting from this principle, the development of upper-limb non-invasive ambulatory robotic exoskeletons is presented as a promising solution for patients who cannot benefit from medication to suppress the tremor. In this area robotic exoskeletons have emerged, in the form of orthoses, to provide motor assistance and functional compensation to disabled people. An orthosis is a wearable device that acts in parallel to the affected limb. In the case of tremor management, the orthosis must apply a damping or inertial load to a selected set of limb articulations.Recently, some studies demonstrated that exoskeletons could achieve a consistent 40% of tremor power reduction for all users, being able to attain a reduction ratio in the order of 80% tremor power in specific joints of users with severe tremor. | Byssinosis is an occupational lung disease caused by inhalation of cotton or jute dust in inadequately ventilated working environments and can develop over time with repeated exposure. Byssinosis commonly occurs in textile workers who are employed in yarn and fabric manufacture industries. It is now thought that the cotton dust directly causes the disease and some believe that the causative agents are endotoxins that come from the cell walls of gram-negative bacteria that grow on the cotton. Although bacterial endotoxin is a likely cause, the absence of similar symptoms in workers in other industries exposed to endotoxins makes this uncertain. Current smokers are also at risk for developing byssinosis or having complications relating to byssinosis.Of the 81 byssinosis-related fatalities reported in the United States between 1990 and 1999, 48% included an occupation in the yarn, thread, and fabric industry on their death certificate. This disease often occurred in the times of the Industrial Revolution. Most commonly young girls working in mills or other textile factories would be affected by this disease. In the United States, from 1996 to 2005, North Carolina accounted for about 37% of all deaths caused by byssinosis, with 31, followed by South Carolina (8) and Georgia (7).There is a lack of information regarding the prevalence and impact of byssinosis in low and middle income countries (LMIC) despite the fact that of the 25 million tons of cotton produced worldwide, about two thirds of this production comes from LMICs like India, Pakistan, and China. | 0-1
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Phylloid hypomelanosis is a cutaneous condition, a syndrome occurring in patients with mosaic trisomy 13 or translocation trisomy 13. See also
Riehl melanosis
List of cutaneous conditions
== References == | This also ensures that important things such as letters are not completely hidden behind any scotomas (small defects in parts of the functioning visual field), and reduces the chances of getting lost in the text. However, the simplification of the view should not be done in such a way that it requires too rapid a movement to navigate around a large document, since too much motion can cause other problems (see above). In viewing an array of objects, people with CVI can more easily see them if they only have to look at one or two at a time. People with CVI also see familiar objects more easily than new ones. Placing objects against a plain background also makes them easier for the person with CVI to see. For the same reason (simplified view), the person may also dislike crowded rooms and other situations where their functioning is dependent on making sense of a lot of visual clutter. Visual processing can take a lot of effort. Often the person has to make a conscious choice about how to divide mental effort between making sense of visual data and performing other tasks. For some people, maintaining eye contact is difficult, which can create problems in Western culture (for example, bonding can be difficult for some parents who have an infant with CVI, and lack of contact in an older child can cause others to regard him or her with suspicion). | 0-1
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The parrilla was commonly used at Villa Grimaldi, a prison complex maintained by Dirección de Inteligencia Nacional, a part of the Pinochet regime. In the 1970s, during the Dirty War, the parrilla was used in Argentina. Francisco Tenório Júnior (known as Tenorinho), a Brazilian piano player, was subjected to the parrilla during the military dictatorship in Brazil.Advocates for the mentally ill and some psychiatrists such as Thomas Szasz have asserted that electroconvulsive therapy (ECT) is torture when used without a bona fide medical benefit against recalcitrant or non-responsive patients.The Judge Rotenberg Center in Canton, Massachusetts has been condemned for torture by the United Nations special rapporteur on torture for its use of electric shocks as punishment as part of its behavior modification program.Japanese serial killer Futoshi Matsunaga used electric shocks to control his victims. Capital punishment
Electric shock delivered by an electric chair is sometimes used as an official means of capital punishment in the United States, although its use has become rare from the 1990s onward due to the adoption of lethal injection. Although some original proponents of the electric chair considered it to be a more humane execution method than hanging, shooting, poison gassing, etc., it has now generally been replaced by lethal injections in states that practice capital punishment. Modern reporting has claimed that it sometimes takes several shocks to be lethal, and that the condemned person may actually catch fire before death. Other than in parts of the United States, only the Philippines reportedly has used this method, from 1926 to 1976. | Ruskin reported in his diaries having visual disturbances consistent with the disease, and it has also been suggested that it might have been a factor in causing him to describe James Whistlers Nocturne in Black and Gold – The Falling Rocket as "ask[ing] two hundred guineas for throwing a pot of paint in the publics face". This resulted in the famous libel trial that resulted in a jurys awarding Whistler one farthing damages.Recent research into the illness of philosopher Friedrich Nietzsche has suggested that his mental illness and death may have been caused by CADASIL rather than tertiary syphilis. Likewise, the early death of the composer Felix Mendelssohn, at age 37, from a stroke has been potentially linked to CADASIL. His sister, Fanny Mendelssohn, was similarly affected. And James Dewar, best known as vocalist for Robin Trower, died age 59 from complications of CADASIL.In the movie The Sea Inside, one of the characters is stated to have CADASIL. See also
Proteopathy
CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy)
References
Further reading
Lesnik Oberstein SA, Boon EM, Terwindt GM (June 28, 2012). CADASIL. University of Washington, Seattle. PMID 20301673. NBK1500. In Adam MP, Everman DB, Mirzaa GM, Pagon RA, Wallace SE, Bean LJH, Gripp KW, Amemiya A (1993). Pagon RA, Bird TD, Dolan CR, et al. (eds.). GeneReviews [Internet]. Seattle WA: University of Washington, Seattle. PMID 20301295. External links
A patient story at The New York Times | 0-1
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If the above five steps fails to help people who suspected of having a genodermatosis to obtain the diagnosis result, they should keep all their information such as the diagnosis record and the clinical manifestations at different stages, and continue to record the changes of the body, waiting with a positive attitude, the future medicine may give the answer. Therapy
The therapy of genodermatosis not only needs to take care of patients skin, reduce their pain and prevent complications, but also needs to carry out mental support for patients and their families. Prevention and care
Different types of genodermatosis require different kinds of prevention and care. Ichthyosis
There is no radical therapeutic method for ichthyosis, but some care can ease the symptoms. To prevent skin thickening and hydrate skin, patients can apply a cream containing alpha hydroxy acids and patients can also be treated with antibiotics for subsequent infections. Epidermolysis bullosa
For epidermolysis bullosa, daily care is important. When treating a wound, keep it clean and reduce friction, the bandages and dressing used must be non-sticky and gentle, and the patient should wear loose clothing to avoid damaging the wound. Epidermolytic hyperkeratosis
The treatment of Epidermolytic hyperkeratosis is mainly control and alleviate symptoms, and good nursing can reduce the incidence of complications like electrolyte disturbances and sepsis. To improve the look and feeling of the skin, patients can apply a cream containing alpha hydroxy acids, glycerol and urea, and if necessary, patients can use antibiotics to control secondary infections. | A trichilemmal cyst is a common cyst that forms from a hair follicle, most often on the scalp, and is smooth, mobile, and filled with keratin, a protein component found in hair, nails, skin, and horns. Trichilemmal cysts are clinically and histologically distinct from trichilemmal horns, hard tissue that is much rarer and not limited to the scalp. Rarely, these cysts may grow more extensively and form rapidly multiplying trichilemmal tumors, also called proliferating trichilemmal cysts, which are benign, but may grow aggressively at the cyst site. Very rarely, trichilemmal cysts can become cancerous. Classification
Trichilemmal cysts may be classified as sebaceous cysts, although technically speaking are not sebaceous. "True" sebaceous cysts, which originate from sebaceous glands and which contain sebum, are relatively rare and are known as steatocystoma simplex or, if multiple, as steatocystoma multiplex. Medical professionals have suggested that the term "sebaceous cyst" be avoided since it can be misleading. : 31 In practice, however, the term is still often used for epidermoid and pilar cysts. Pathogenesis
Trichilemmal cysts are derived from the outer root sheath of the hair follicle. Their origin is currently unknown, but they may be produced by budding from the external root sheath as a genetically determined structural aberration. They arise preferentially in areas of high hair follicle concentrations, so 90% of cases occur on the scalp. They are solitary in 30% and multiple in 70% of cases.Histologically, they are lined by stratified squamous epithelium that lacks a granular cell layer and are filled with compact "wet" keratin. | 0-1
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Hand, foot, and mouth disease (HFMD) is a common infection caused by a group of enteroviruses. It typically begins with a fever and feeling generally unwell. This is followed a day or two later by flat discolored spots or bumps that may blister, on the hands, feet and mouth and occasionally buttocks and groin. Signs and symptoms normally appear 3–6 days after exposure to the virus. The rash generally resolves on its own in about a week. Fingernail and toenail loss may occur a few weeks later, but they will regrow with time.The viruses that cause HFMD are spread through close personal contact, through the air from coughing and the feces of an infected person. Contaminated objects can also spread the disease. Coxsackievirus A16 is the most common cause, and enterovirus 71 is the second-most common cause. Other strains of coxsackievirus and enterovirus can also be responsible. Some people may carry and pass on the virus despite having no symptoms of disease. Other animals are not involved. Diagnosis can often be made based on symptoms. Occasionally, a throat or stool sample may be tested for the virus.Handwashing may prevent spread, and those infected should not go to work, daycare or school. No antiviral medication or vaccine is available, but development efforts are underway. Most cases require no specific treatment. Simple pain medication such as ibuprofen or numbing mouth gel may be used. Occasionally, intravenous fluids are given to children who are unable to drink enough. | History
HFMD cases were first described clinically in Canada and New Zealand in 1957. The disease was termed "Hand Foot and Mouth Disease", by Thomas Henry Flewett, after a similar outbreak in 1960. Research
Novel antiviral agents to prevent and treat infection with the viruses responsible for HFMD are currently under development. Preliminary studies have shown inhibitors of the EV-71 viral capsid to have potent antiviral activity. References
External links
Media related to Hand, foot and mouth disease at Wikimedia Commons
Highly contagious Hand, foot and mouth disease killing Chinas children at Wikinews | 11
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A nasogastric tube from the stomach may appear on the film in the chest cavity; this sign is pathognomonic for diaphragmatic rupture, but it is rare. The X-ray is better able to detect the injury when taken from the back with the person upright, but this is not usually possible because the person is usually not stable enough; thus it is usually taken from the front with the person lying supine. Positive pressure ventilation helps keep the abdominal organs from herniating into the chest cavity, but this also can prevent the injury from being discovered on an X-ray.A CT scan has an increased accuracy of diagnosis over X-ray, but no specific findings on a CT scan exist to establish a diagnosis. The free edge of a ruptured diaphragm may curl and become perpendicular to the chest wall, a sign known as a dangling diaphragm. A herniated organ may constrict at the location of a rupture, a sign known as the collar sign. If the liver herniates through a rupture on the right side, it may produce two signs known as the hump and band signs. The hump sign is a form of the collar sign on the right. The band sign is a bright line that intersects the liver. it is believed to result due to the ruptured diaphragm compressing. Although CT scanning increases chances that diaphragmatic rupture will be diagnosed before surgery, the rate of diagnosis before surgery is still only 31–43.5%. | This is done be debriding nonviable tissue and closing the rupture. Most of the time, the injury is repaired during laparotomy. Early surgery is important, as diaphragmatic atrophy and adhesions occur over time. Sutures are used in the repair. Other injuries, such as hemothorax, may present a more immediate threat and may need to be treated first if they accompany diaphragmatic rupture. Video-assisted thoracoscopy may be used. Prognosis
In most cases, isolated diaphragmatic rupture is associated with good outcome if it is surgically repaired. The death rate (mortality) for diaphragmatic rupture after blunt and penetrating trauma is estimated to be 15–40% and 10–30% respectively, but other injuries play a large role in determining outcome. Herniation of abdominal organs is present in 3–4% of people with abdominal trauma who present to a trauma center. Epidemiology
Diaphragmatic injuries are present in 1–7% of people with significant blunt trauma and an average of 3% of abdominal injuries. A high body mass index may be associated with a higher risk of diaphragmatic rupture in people involved in vehicle accidents. Over 90% occur due to trauma from vehicle accidents. Due to the great force needed to rupture the diaphragm, it is rare for the diaphragm alone to be injured, especially in blunt trauma; other injuries are associated in as many as 80–100% of cases. In fact, if the diaphragm is injured, it is an indication that more severe injuries to organs may have occurred. Thus, the mortality after a diagnosis of diaphragmatic rupture is 17%, with most deaths due to lung complications. | 11
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A lack of family history may indicate that the condition was acquired.It is suggested that the dental/medical professional establish if the condition is a syndrome of another inherited condition such as:
Osteogenesis imperfecta - indicates Type I Dentinogenesis Imperfecta (see Shields Classification in Classification section)
Ehlers Danlos syndrome
Goldblatt syndrome
Schimke immune-osseus dysplasia
Brachio-skeleto-genital syndrome
Osteodysplastic and primordial short stature with severe microdontia
Opalescent teeth
Rootless molars[This is not a comprehensive list]
It can be useful to enquire about symptoms of osteogenesis imperfecta, as Type I Dentinogenesis Imperfecta (Shields Classification) is associated with osteogenesis imperfecta. Notable information includes:
History of bone fracture caused by minimal trauma
Short stature
Blue sclera
Hearing lossCommon dental features of osteogenesis imperfecta include:
Hypodontia
Oligodontia
Taurodontism
Unerupted permanent 2nd molars, with no obstruction in the path of eruption
Retrognathic maxilla
Differential diagnosis
Hypocalcified forms of amelogenesis imperfecta
Congenital erythropoietic porphyria
Conditions that can cause early loss of teeth e.g. Kostmanns disease, cyclic neutropenia, Chediak-Hegashi syndrome, histiocytosis X, Papillon-Lefevre syndrome
Permanent tooth discolouration caused by medications such as tetracyclines, or medical conditions such as rickets
Treatment
Preventive and restorative care are important as well as esthetics as a consideration. This ensures preservation of the patients vertical face height between their upper and lower teeth when they bite together. The basis of treatment is standard throughout the different types of DI where prevention, preservation of occlusal face height, maintenance of function, and aesthetic needs are priority. Preventive efforts can limit pathology occurring within the pulp, which may render future endodontic procedures less challenging, with better outcomes. | Type of DI with similar dental abnormalities usually an autosomal dominant trait with variable expressivity but can be recessive if the associated osteogenesis imperfecta is of recessive type.Recent genetic studies have identified that mutations in the genes coding for the collagen type 1 proteins, COL1A1 and COL1A2, are associated with this type of DI.Not all individuals with OI have dentinogenesis imperfecta, and the prevalence of DI varies depending on the sub-type of OI:
Higher prevalence of DI among individuals with OI type III and IV at 43-82% and 37-100%, respectively
Lower prevalence of DI among individuals with OI type I at 8-40%
No data available for other OI sub-types
Type II
DI not associated with OI. Occurs in people without other inherited disorders (i.e. Osteogenesis imperfecta). It is an autosomal dominant trait. A few families with type II have progressive hearing loss in addition to dental abnormalities. Also called hereditary opalescent dentin. Type III
Brandywine isolate. This type is rare with occurrences only in the secluded populations in Maryland, USA. Similar to DI type II, this type is also not associated with OI. Its predominant characteristic is bell-shaped crowns, especially in the permanent dentition. Unlike Types I and II, it involves teeth with shell-like appearance and multiple pulp exposures.Mutations in the gene coding for the dentine sialophosphoprotein (DSPP) are associated with DI type II and III. DSPP is a polypeptide which gives rise to 3 proteins; dentine sialoprotein (DSP), dentine glycoprotein (DGP), and dentine phosphoprotein (DPP). | 11
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A dermoid cyst is a teratoma of a cystic nature that contains an array of developmentally mature, solid tissues. It frequently consists of skin, hair follicles, and sweat glands, while other commonly found components include clumps of long hair, pockets of sebum, blood, fat, bone, nail, teeth, eyes, cartilage, and thyroid tissue. As dermoid cysts grow slowly and contain mature tissue, this type of cystic teratoma is nearly always benign. In those rare cases wherein the dermoid cyst is malignant, a squamous cell carcinoma usually develops in adults, while infants and children usually present with an endodermal sinus tumor. : 781
Location
Due to its classification, a dermoid cyst can occur wherever a teratoma can occur. Vaginal and ovarian dermoid cysts
Ovaries normally grow cyst-like structures called follicles each month. Once an egg is released from its follicle during ovulation, follicles typically deflate. Sometimes fluid accumulates inside the follicle, forming a simple (containing only fluid) cyst. The majority of these functional cysts resolve spontaneously.While all ovarian cysts can range in size from very small to quite large, dermoid cysts are not classified as functional cysts. Dermoid cysts originate from pluripotent germ cells (which are present at birth) that differentiate abnormally, developing characteristics of mature dermal cells. Complications exist, such as torsion (twisting), rupture, and infection, although their incidence is rare. Dermoid ovarian cysts which are larger present complications which might require removal by either laparoscopy or laparotomy (traditional surgery). Rarely, a dermoid cyst can develop in the vagina. | Spinal dermoid cysts
Spinal dermoid cysts are benign ectopic growths thought to be a consequence of embryology errors during neural tube closure. Their reported incidence is extremely rare, accounting for less than 1% of intramedullary spinal cord tumours. It has been proposed that a possible 180 cases of spinal dermoid tumours have been identified over the past century in the literature.Dermoid cysts more often involve the lumbosacral region than the thoracic vertebrae and are extramedullary presenting in the first decade of life. Various hypotheses have been advanced to explain the pathogenesis of spinal dermoids, the origin of which may be acquired or congenital. Acquired or iatrogenic dermoids may arise from the implantation of epidermal tissue into the subdural space i.e. spinal cutaneous inclusion, during needle puncture (e.g. lumbar puncture) or during surgical procedures on closure of a dysraphic malformation. Congenital dermoids, however, are thought to arise from cells whose position is correct but which fail to differentiate into the correct cell-type. The long-time held belief was that the inclusion of cutaneous ectodermal cells occurred early in embryonic life, and the displaced pluripotent cells developed into a dermoid lesion.Spinal abnormalities, e.g. intramedullary dermoid cysts may arise more frequently in the lumbosacral region (quite often at the level of the conus medullaris) and may be seen with other congenital anomalies of the spine including posterior spina bifida occulta as identified by the neuroradiological analysis. Diagnosis
Differential diagnosis
A small dermoid cyst on the coccyx can be difficult to distinguish from a pilonidal cyst. | 11
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In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and—in the case of additional (co-morbid) disorders such as eating disorders—a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.The treatment of chronic depersonalization is considered in depersonalization disorder. A 2001 Russian study showed that naloxone, a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization." The anti convulsion drug Lamotrigine has shown some success in treating symptoms of depersonalization, often in combination with a selective serotonin reuptake inhibitor and is the first drug of choice at the depersonalisation research unit at Kings College London. Research
The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research into depersonalization disorder. Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder. In a 2020 article in the journal Nature, Vesuna, et al. describe experimental findings which show that layer 5 of the retrosplenial cortex is likely responsible for dissociative states of consciousness in mammals. | Depersonalization can consist of a detachment within the self, regarding ones mind or body, or being a detached observer of oneself. Subjects feel they have changed and that the world has become vague, dreamlike, less real, lacking in significance or being outside reality while looking in. It can be described as feeling like one is on “autopilot” and that the persons sense of individuality or selfhood has been hindered or suppressed.Chronic depersonalization refers to depersonalization/derealization disorder, which is classified by the DSM-5 as a dissociative disorder, based on the findings that depersonalization and derealization are prevalent in other dissociative disorders including dissociative identity disorder.Though degrees of depersonalization and derealization can happen to anyone who is subject to temporary anxiety or stress, chronic depersonalization is more related to individuals who have experienced a severe trauma or prolonged stress/anxiety. Depersonalization-derealization is the single most important symptom in the spectrum of dissociative disorders, including dissociative identity disorder and "dissociative disorder not otherwise specified" (DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such as anxiety disorders, clinical depression, bipolar disorder, schizophrenia, schizoid personality disorder, hypothyroidism or endocrine disorders, schizotypal personality disorder, borderline personality disorder, obsessive–compulsive disorder, migraines, and sleep deprivation; it can also be a symptom of some types of neurological seizure. In social psychology, and in particular self-categorization theory, the term depersonalization has a different meaning and refers to "the stereotypical perception of the self as an example of some defining social category". | 11
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Epidemiology
Because T. pallidum pertenue is temperature- and humidity-dependent, yaws is found in humid tropical forest regions in South America, Africa, Asia and Oceania.About three quarters of people affected are children under 15 years of age, with the greatest incidence in children 6–10 years old. Therefore, children are the main reservoir of infection.It is more common in remote areas, where access to treatment is poorer. It is associated with poverty and poor sanitation facilities and personal hygiene.Worldwide, almost 85% of yaws cases are in Ghana, Papua New Guinea, and the Solomon Islands. Rates in sub-Saharan Africa are low, but tend to be concentrated in specific populations. As of 2015, it is estimated that about 89 million people live in yaws-endemic areas, but data are poor, and this is likely an over-estimate.In the early 1900s, yaws was very common; in sub-saharan Africa, it was more frequently treated than malaria, sometimes making up more than half of treatments.Mass treatment campaigns in the 1950s reduced the worldwide prevalence from 50 to 150 million to fewer than 2.5 million; however, during the 1970s there were outbreaks in South-East Asia, and there have been continued sporadic cases in South America. As of 2011, it was unclear how many people worldwide were currently infected.From 2008 to 2012, 13 countries reported over 300,000 new cases to the WHO. There was no system for certifying local elimination of yaws, and it is not known whether the lack of reports from some countries is because they stopped having yaws cases or because they stopped reporting them. | Hypopnea is overly shallow breathing or an abnormally low respiratory rate. Hypopnea is defined by some to be less severe than apnea (the complete cessation of breathing), while other researchers have discovered hypopnea to have a "similar if not indistinguishable impact" on the negative outcomes of sleep breathing disorders. In sleep clinics, obstructive sleep apnea syndrome or obstructive sleep apnea–hypopnea syndrome is normally diagnosed based on the frequent presence of apneas and/or hypopneas rather than differentiating between the two phenomena. Hypopnea is typically defined by a decreased amount of air movement into the lungs and can cause oxygen levels in the blood to drop. It commonly is due to partial obstruction of the upper airway. Hypopnea during sleep is classed as a sleep disorder. With moderate to severe hypopnea, sleep is disturbed such that patients may get a full nights sleep but still not feel rested because they did not get the right kind of sleep. The disruption in breathing causes a drop in blood oxygen level, which may in turn disrupt the stages of sleep. Daytime hypopnea events, however, are mostly limited to those with severely compromised respiratory muscles, as occurs in certain neuromuscular diseases or compromised central respiratory drive, as occurs in conditions such as acquired or congenital central hypoventilation syndrome (ACHS or CCHS). Daytime hypopnea can also cause a drop in blood oxygen level. Symptoms
The most common hypopnea symptom is excessive sleepiness, which results from constant sleep interruption. | 0-1
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Early research suggested that the number of IC/BPS cases ranged from 1 in 100,000 to 5.1 in 1,000 of the general population. In recent years, the scientific community has achieved a much deeper understanding of the epidemiology of interstitial cystitis. Recent studies have revealed that between 2.7 and 6.53 million women in the USA have symptoms of IC and up to 12% of women may have early symptoms of IC/BPS. Further study has estimated that the condition is far more prevalent in men than previously thought ranging from 1.8 to 4.2 million men having symptoms of interstitial cystitis.The condition is officially recognized as a disability in the United States. History
Philadelphia surgeon Joseph Parrish published the earliest record of interstitial cystitis in 1836 describing three cases of severe lower urinary tract symptoms without the presence of a bladder stone. The term "interstitial cystitis" was coined by Dr. Alexander Skene in 1887 to describe the disease. In 2002, the United States amended the Social Security Act to include interstitial cystitis as a disability. The first guideline for diagnosis and treatment of interstitial cystitis is released by a Japanese research team in 2009. The American Urological Association released the first American clinical practice guideline for diagnosing and treating IC/BPS in 2011. Names
Originally called interstitial cystitis, this disorder was renamed to interstitial cystitis/bladder pain syndrome (IC/BPS) in the 2002–2010 timeframe. | ), urinary chemicals can "leak" into surrounding tissues, causing pain, inflammation, and urinary symptoms. Oral medications like pentosan polysulfate and medications placed directly into the bladder via a catheter sometimes work to repair and rebuild this damaged/wounded lining, allowing for a reduction in symptoms. Most literature supports the belief that ICs symptoms are associated with a defect in the bladder epithelium lining, allowing irritating substances in the urine to penetrate into the bladder—a breakdown of the bladder lining (also known as the adherence theory). Deficiency in this glycosaminoglycan layer on the surface of the bladder results in increased permeability of the underlying submucosal tissues.GP51 has been identified as a possible urinary biomarker for IC with significant variations in GP51 levels in those with IC when compared to individuals without interstitial cystitis.Numerous studies have noted the link between IC, anxiety, stress, hyper-responsiveness, and panic. Another proposed cause for interstitial cystitis is that the bodys immune system attacks the bladder. Biopsies on the bladder walls of people with IC usually contain mast cells. Mast cells containing histamine packets gather when an allergic reaction is occurring. The body identifies the bladder wall as a foreign agent, and the histamine packets burst open and attack. The body attacks itself, which is the basis of autoimmune disorders. Additionally, IC may be triggered by an unknown toxin or stimulus which causes nerves in the bladder wall to fire uncontrollably. When they fire, they release substances called neuropeptides that induce a cascade of reactions that cause pain in the bladder wall. | 11
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Diagnosis
In terms of the diagnosis for this condition one sees the following (though this is not a complete list):
CBC
PT/PTT
Blood gases
Urine test
Prevention
The risk of heat stroke can be reduced by observing precautions to avoid overheating and dehydration. Light, loose-fitting clothes will allow perspiration to evaporate and cool the body. Wide-brimmed hats in light colors help prevent the sun from warming the head and neck. Vents on a hat will help cool the head, as will sweatbands wetted with cool water. Strenuous exercise should be avoided during hot weather, especially in the sun peak hours as well as avoiding confined spaces (such as automobiles) without air-conditioning or adequate ventilation.In hot weather, people need to drink plenty of cool liquids and mineral salts to replace fluids lost from sweating. Thirst is not a reliable sign that a person needs fluids. A better indicator is the color of urine. A dark yellow color may indicate dehydration.Example of a checklist designed to help protect workers from heat stress:
Know signs/symptoms of heat-related illnesses. Block out direct sun and other heat sources. Drink fluids often, and before you are thirsty. Wear lightweight, light-colored, loose-fitting clothes. Avoid beverages containing alcohol or caffeine. Treatment
Treatment of heat stroke involves rapid mechanical cooling along with standard resuscitation measures.The body temperature must be lowered quickly via conduction, convection, or evaporation. The person should be moved to a cool area, such as indoors or to a shaded area. Clothing should be removed to promote heat loss through passive cooling. | Conductive cooling methods such as ice-water immersion should also be used, if possible. Evaporative and convective cooling by a combination of cool water spray or cold compresses with constant air flow over the body, such as with a fan or air-conditioning unit, is also an effective alternative. The person should not be wrapped in wet towels or clothing as this can act as insulation and increase the body temperature.Aggressive ice-water immersion remains the gold standard for life-threatening heat stroke. This method may require the effort of several people and the person should be monitored carefully during the treatment process. Immersion should be avoided for an unconscious person, but if there is no alternative, the persons head must be held above water. Immersion in very cold water was once thought to be counterproductive by reducing blood flow to the skin and thereby preventing heat from escaping the body core. However, research has shown that this mechanism does not play a dominant role in the decrease in core body temperature brought on by cold water. Dantrolene, a muscle relaxant used to treat other forms of hyperthermia, is not an effective treatment for heat stroke.Hydration is important in cooling the person. In mild cases of concomitant dehydration, this can be achieved by drinking water, or commercial isotonic sports drinks may be used as a substitute. In either exercise- or heat-induced dehydration, electrolyte imbalance can result, and can be worsened by excess consumption of water. Hyponatremia can be corrected by intake of hypertonic fluids. | 11
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In more severe cases, treatment consists of:
Diuretics to increase urination, which are most effective for excess blood volume. Vasopressin receptor antagonists
Notable cases
1097: During the First Crusade, according to at least one chronicle, many crusaders died after drinking too much from a river while marching to Antioch. 1991, Andy Warhol: Five years after his death, Warhols family publicly accused the hospital where he had his gallbladder removed of causing his death by water intoxication administered post-operatively. A claimed autopsy weight of 68 kg (150 lb), with his weight being 58 kg (128 lb) when admitted, was cited as evidence that too much fluid had been given. October 24, 1995: Anna Wood, a 15-year-old Australian schoolgirl, died from the effects of water intoxication. November 16, 1995: Leah Betts, a British schoolgirl, died as the result of drinking too much water, though in the media her death was mistakenly attributed to taking an ecstasy tablet at her 18th birthday party. 2003: British actor Anthony Andrews survived a case of water intoxication. He was performing as Henry Higgins in a revival of the musical My Fair Lady at the time, and consumed up to eight litres of water a day. He was unconscious and in intensive care for three days. February 2, 2005: Matthew Carrington, a student at Chico State University in Chico, California, died as a direct result of a fraternity hazing ritual involving forced water intoxication. | CRS has been controlled by universal vaccination (MMR or MMRV vaccine). Cytomegalovirus (CMV) infection is the most common cause of progressive sensorineural hearing loss in children. It is a common viral infection contracted by contact with infected bodily fluids such as saliva or urine and easily transmitted in nurseries and thus from toddlers to expectant mothers. CMV infection during pregnancy can affect the developing foetus and lead to learning difficulties as well as hearing loss. Toxoplasmosis, a parasitic disease affecting 23% of the population in the U.S., can cause sensorineural deafness to the fetus in utero. Hypoplastic auditory nerves or abnormalities of the cochlea. Abnormal development of the inner ear can occur in some genetic syndromes such as LAMM syndrome (labyrinthine aplasia, microtia and microdontia), Pendred syndrome, branchio-oto-renal syndrome, CHARGE syndrome
GATA2 deficiency, a grouping of several disorders caused by common defect, viz., familial or sporadic inactivating mutations in one of the two parental GATA2 genes. These autosomal dominant mutations cause a reduction, i.e. a haploinsufficiency, in the cellular levels of the genes product, GATA2. The GATA2 protein is a transcription factor critical for the embryonic development, maintenance, and functionality of blood-forming, lympathic-forming, and other tissue-forming stem cells. In consequence of these mutations, cellular levels of GATA2 are deficient and individuals develop over time hematological, immunological, lymphatic, and/or other disorders. GATA2 deficiency-induced abnormalities in the lymphatic system are proposed to be responsible for a failure in generating the perilymphatic space around the inner ears semicircular canals, which in turn underlies the development of sensorineural hearing loss. | 0-1
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Treatment
Although research is ongoing, currently there is no genetic-level cure for the myriad of mutations that cause the various presentations of hereditary spherocytosis. Common current management focuses on interventions prevent the body from inappropriately destroying the functional spherocytes produced by erythrocyte progenitor cells within the bone marrow. Typical treatment options include:
Splenectomy (operative): This is the operative removal of the entire spleen by a surgeon, thus stopping the extravascular hemolysis, but also removing the immune functions the spleen naturally provide to the body. Partial splenectomy (operative): This is when only a section of the spleen is removed, instead of the entire organ. The goal is to lower the extravascular hemolysis to a level compatible with homeostasis of the patient, while preserving the immune function of the spleens presence. Research on outcomes is currently ongoing, and is routine at childrens hospitals within the United States of America. Splenic ablation (interventional radiology): This option is non-operative, and is when an interventional radiologist (instead of a surgeon) uses radiologic techniques to coil or cauterize vasculature within the splenic circulation. There are various points in the circulatory pathway where the treatment can be applied to produces varying amounts of retained viability of the spleen, thus giving the option to attempt to preserve splenic immune function.All operative and interventional treaments require the immunization of HS patients against the influenza virus, SARS-CoV-2, and encapsulated bacteria such as Streptococcus pneumoniae and meningococcus. Antibiotics are no longer recommended for maintenance use, even in post-splenectomy HS patients. | Since the spleen is important for protecting against encapsulated organisms, sepsis caused by encapsulated organisms is a possible complication of splenectomy.Additional elective treatments offered:
Surgical removal of the gallbladder.Experimental treatment:
Bone marrow transplant (heme-oncology intervention): The replacement of the bone marrow with bone marrow from an individual without spherocytosis. The transplanted progenitor cells do not have the genetic mutations found in individuals with hereditary spherocytosis, and therefore do not produce spherocytes. This results in an individual with biconcave-disc-shaped erythrocytes. This treatment is not standard of care, and is not offered as it has only been documented incidentally during treatment for other diseases, such as myelodysplastic sydnrome.Symptomatic treatments:
Folic acid supplementation. Complications
Common Complications
Hemolytic crisis, with more pronounced jaundice due to accelerated hemolysis (may be precipitated by infection). Aplastic crisis with dramatic fall in hemoglobin level and (reticulocyte count)-decompensation, usually due to maturation arrest and often associated with megaloblastic changes; may be precipitated by infection, such as influenza, notably with parvovirus B19. Folate deficiency caused by increased bone marrow requirement. Pigmented gallstones occur in approximately half of untreated patients. Increased hemolysis of red blood cells leads to increased bilirubin levels, because bilirubin is a breakdown product of heme. The high levels of bilirubin must be excreted into the bile by the liver, which may cause the formation of a pigmented gallstone, which is composed of calcium bilirubinate. Since these stones contain high levels of calcium carbonates and phosphate, they are radiopaque and are visible on x-ray. Hyperglycemia with concomitant low hemoglobin A1C levels. | 11
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People with this type are hypertonic and have a neuromuscular condition stemming from damage to the corticospinal tract or the motor cortex that affects the nervous systems ability to receive gamma amino butyric acid in the area(s) affected by the disability.Spastic CP is further classified by topography dependent on the region of the body affected; these include:
Spastic hemiplegia (one side being affected). Generally, injury to muscle-nerves controlled by the brains left side will cause a right body deficit, and vice versa. Typically, people that have spastic hemiplegia are the most ambulatory, although they generally have dynamic equinus on the affected side and are primarily prescribed ankle-foot orthoses to prevent said equinus. [11]
Spastic diplegia (the lower extremities are affected with little to no upper-body spasticity). The most common form of the spastic forms. Most people with spastic diplegia are fully ambulatory and have a scissors gait. Flexed knees and hips to varying degrees are common. Hip problems, dislocations, and in three-quarters of spastic diplegics, also strabismus (crossed eyes), can be present as well. In addition, these individuals are often nearsighted. The intelligence of a person with spastic diplegia is unaffected by the condition. Spastic tetraplegia (all four limbs affected equally). People with spastic quadriplegia are the least likely to be able to walk, or if they can, to want to walk, because their muscles are too tight and it is too much effort to do so. | Concentrations reached in the blood plasma are so low that they are generally not detectable. To judge from animal models, the drug acts for at least 24 hours. Its elimination half-life is 16 to 17 hours (in rabbits). Chemistry
The drug is used in form of a salt, netarsudil dimesilate, which is a white to light yellow crystalline powder. It is a weak acid and moderately hygroscopic, freely soluble in water and soluble in methanol. See also
Netarsudil/latanoprost, a combination drug
References
External links
"Netarsudil". Drug Information Portal. U.S. National Library of Medicine. "Netarsudil mesylate". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Some cancer patients treat the loss of their hair from chemotherapy as a metonymy or metaphor for all the losses caused by the disease.Some diseases are used as metaphors for social ills: "Cancer" is a common description for anything that is endemic and destructive in society, such as poverty, injustice, or racism. AIDS was seen as a divine judgment for moral decadence, and only by purging itself from the "pollution" of the "invader" could society become healthy again. More recently, when AIDS seemed less threatening, this type of emotive language was applied to avian flu and type 2 diabetes mellitus. Authors in the 19th century commonly used tuberculosis as a symbol and a metaphor for transcendence. People with the disease were portrayed in literature as having risen above daily life to become ephemeral objects of spiritual or artistic achievement. In the 20th century, after its cause was better understood, the same disease became the emblem of poverty, squalor, and other social problems. See also
References
External links
Health Topics, MedlinePlus descriptions of most diseases, with access to current research articles. OMIM Comprehensive information on genes that cause disease at Online Mendelian Inheritance in Man
CTD The Comparative Toxicogenomics Database is a scientific resource connecting chemicals, genes, and human diseases. | Enalapril/hydrochlorothiazide, sold under the brand name Vaseretic among others, is a fixed-dose combination medication used for the treatment of hypertension (high blood pressure). It contains enalapril, an angiotensin converting enzyme inhibitor, and hydrochlorothiazide a diuretic. It is taken by mouth.The most frequent side effects include dizziness, headache, fatigue, and cough. History
Enalapril/hydrochlorothiazide was approved for medical use in the United States in October 1986. References
Further reading
Frishman WH, Goldberger J, Sherman D (December 1987). "Enalapril, hydrochlorothiazide, and combination therapy in patients with moderate hypertension". J Clin Hypertens. 3 (4): 520–7. PMID 2839628. External links
"Enalapril". Drug Information Portal. U.S. National Library of Medicine. "Hydrochlorothiazide". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Mast cells reside in connective tissues and mucous membranes, and regulate the inflammatory response. They are most often associated with allergy and anaphylaxis. Basophils and eosinophils are related to neutrophils. They secrete chemical mediators that are involved in defending against parasites and play a role in allergic reactions, such as asthma.Innate lymphoid cells (ILCs) are a group of innate immune cells that are derived from common lymphoid progenitor and belong to the lymphoid lineage. These cells are defined by absence of antigen specific B or T cell receptor (TCR) because of the lack of recombination activating gene. ILCs do not express myeloid or dendritic cell markers.Natural killer cells (NK) are lymphocytes and a component of the innate immune system which does not directly attack invading microbes. Rather, NK cells destroy compromised host cells, such as tumor cells or virus-infected cells, recognizing such cells by a condition known as "missing self." This term describes cells with low levels of a cell-surface marker called MHC I (major histocompatibility complex)—a situation that can arise in viral infections of host cells. Normal body cells are not recognized and attacked by NK cells because they express intact self MHC antigens. Those MHC antigens are recognized by killer cell immunoglobulin receptors which essentially put the brakes on NK cells. Inflammation
Inflammation is one of the first responses of the immune system to infection. The symptoms of inflammation are redness, swelling, heat, and pain, which are caused by increased blood flow into tissue. | Inflammation would cause serious cognitive and physical impairments if it were to occur during wake times, and inflammation may occur during sleep times due to the presence of melatonin. Inflammation causes a great deal of oxidative stress and the presence of melatonin during sleep times could actively counteract free radical production during this time. Physical exercise
Physical exercise has a positive effect on the immune system and depending on the frequency and intensity, the pathogenic effects of diseases caused by bacteria and viruses are moderated. Immediately after intense exercise there is a transient immunodepression, where the number of circulating lymphocytes decreases and antibody production declines. This may give rise to a window of opportunity for infection and reactivation of latent virus infections, but the evidence is inconclusive. Changes at the cellular level
During exercise there is an increase in circulating white blood cells of all types. This is caused by the frictional force of blood flowing on the endothelial cell surface and catecholamines affecting β-adrenergic receptors (βARs). The number of neutrophils in the blood increases and remains raised for up to six hours and immature forms are present. Although the increase in neutrophils ("neutrophilia") is similar to that seen during bacterial infections, after exercise the cell population returns to normal by around 24 hours.The number of circulating lymphocytes (mainly natural killer cells) decreases during intense exercise but returns to normal after 4 to 6 hours. | 11
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Blood flow is selectively redirected to the myocardium, adrenal glands, and in particular to the brain in a brain-sparing effect.In late stage, the redistribution becomes ineffective, there is decrease in cardiac output, ineffective preload handling and elevation of central venous pressure. This deterioration in circulation may ultimately lead to tricuspid insufficiency and death of the fetus. Peripheral circulatory disturbances also accompany these central circulatory changes. Fetal behavioral changes
Chronic hypoxemia leads to delay in all aspects of CNS maturation. With worsening fetal hypoxemia, there is decline in fetal activity. With further hypoxemia, fetal breathing ceases. Gross body movements and tone decrease further. Fetal heart rate decreases due to spontaneous deceleration due to direct depression of cardiac contractility. This leads to intrauterine fetal death. Risk of later metabolic disease
According to the theory of thrifty phenotype, placental insufficiency triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes. | 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 == | 11
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Onychoatrophy is a faulty underdevelopment of the nail that may be congenital or acquired, in which the nail is thinned and smaller. : 784
== References == | One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male,
Signs and symptoms
There is usually an itch, with generalised dry flaky thick skin of the palm of a hand. Frequently, one hand is affected, but it can be in both. If the back of the hand is affected, it may appear as reddish circles like in ringworm. Sometimes there are no symptoms. The feet may be affected as in two feet-one hand syndrome. Cause and mechanism
The most common cause is Trichophyton rubrum. Other causes include Trichophyton verrucosum (from cattle), Microsporum canis (from a cat or dog), Trichophyton erinacei (from a hedgehog), Trichophyton mentagrophytes, Epidermophyton floccosum, Trichophyton interdigitale, and more rarely Microsporum gypseum, Trichophyton eriotrephon, and Arhroderma benhamiae.Tinea manuum can result from touching another area of the body with a fungal infection such as athletes foot or tinea cruris, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors
Diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet are risk factors for tinea manuum. Pet owners and farmworkers are also at higher risk. Diagnosis
Diagnosis is by visualization, direct microscopy and culture. Differential diagnosis
Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment
Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole by mouth might be options. Other options include clotrimazole, fluconazole and ketoconazole. | 0-1
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Medical uses
Metformin is used to lower the blood sugar in those with type 2 diabetes. It is also used as a second-line agent for infertility in those with polycystic ovary syndrome. Type 2 diabetes
The American Diabetes Association and the American College of Physicians both recommend metformin as a first-line agent to treat type 2 diabetes. It is as effective as repaglinide and more effective than all other oral diabetes mellitus type 2 drugs. Efficacy
Treatment guidelines for major professional associations, including the European Association for the Study of Diabetes, the European Society for Cardiology, and the American Diabetes Association, describe evidence for the cardiovascular benefits of metformin as equivocal. A 2020 Cochrane systematic review did not find enough evidence of reduction of cardiovascular mortality, non-fatal myocardial infarction or non-fatal stroke when comparing metformin monotherapy to other glucose-lowering drugs, behaviour change interventions, placebo or no intervention.The use of metformin reduces body weight in people with type 2 diabetes mellitus in contrast to sulfonylureas, which are associated with weight gain. Some evidence shows that metformin is associated with weight loss in obesity in the absence of diabetes. Metformin has a lower risk of hypoglycemia than the sulfonylureas, although hypoglycemia has uncommonly occurred during intense exercise, calorie deficit, or when used with other agents to lower blood glucose. Metformin modestly reduces low density lipoprotein and triglyceride levels. Polycystic ovarian syndrome
In those with polycystic ovarian syndrome (PCOS), tentative evidence shows that metformin use increases the rate of live births. | In a normal person, this redistribution of blood has little effect on respiratory function as the left ventricle has the adequate capacity to suddenly increase its stroke volume (as a result of the Frank-Starling mechanism). In a person with heart failure, the left ventricle has an inadequate capacity to respond to increased arrival of blood from the pulmonary circulation. This leads to the pooling up of blood in the pulmonary circulation and doesnt change its volume enough. The increased intra-parenchymal pulmonary intravascular pressure can also result in hydrostatic pressure related fluid transudation into the alveoli, thus causing cardiogenic pulmonary edema and further worsening shortness of breath. Thus, shortness of breath is commonly experienced after a reasonably short time lying near to flat for a person with left ventricular failure. This is different from the dyspnea experienced by someone with lung parenchymal pathology (both restrictive and obstructive) when lying down, which is sudden and instead related to an acute change in diaphragmatic/accessory respiratory muscle mechanical advantage lost when moving the body into a more horizontal position. Diagnosis
Diagnosis is based mostly on the clinical features and symptoms, as well as finding causes like heart failure. Treatment
Based on the cause, Orthopnea can be treated with respiratory support devices such as CPAP or biPAP while the disease causing it is addressed. Etymology
The word orthopnea uses combining forms of ortho- + -pnea, from Greek ortho, straight, regular, + pnoia, breath. See pronunciation information at dyspnea. See also
Paroxysmal nocturnal dyspnoea
Platypnea
Trepopnea
Bendopnea
Shortness of breath
References
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[1] Specific resources are available for administrators, faculty and staff, and students. The use of the documents is voluntary and are not to be used as standards or as part of accreditation procedures. Despite these recommendations, musicians continue to face unique challenges in protecting their hearing when compared to individuals in industrial settings. Typically environmental controls are the first line of defense in a hearing conservation program, and depending on the type of musicians some recommendations have been proposed. These recommendations can include adjusting risers or level of the speakers and adjusting the layout of a band or orchestra. These changes in the environment can be beneficial to musicians, but the ability to accomplish them is not always possible. In the cases where these changes cannot be made, hearing protection is recommended. Hearing protection in musicians offers its own sets of benefits and complications. When used properly, hearing protection can limit the exposure of noise in individuals. Musicians have the ability to pick from several different types of hearing protection from conventional ear plugs to custom or high fidelity hearing protection. Despite this, use of hearing protection among musicians is low for several different reasons. Musicians often feel that hearing protective devices can distort how music sounds or makes it too quiet for them to hear important cues which makes them less likely to wear hearing protection even when aware of the risks. | Superficial pustular folliculitis is a superficial folliculitis with thin-walled pustules at the follicular openings. : 252
See also
Streptococcal intertrigo
List of cutaneous conditions
References
External links
Special types of folliculitis which should be differentiated from acne, US National Library of Medicine, Published 2017 Sep 27 | 0-1
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Labyrinthitis is inflammation of the labyrinth – a maze of fluid-filled channels in the inner ear. Vestibular neuritis is inflammation of the vestibular nerve – the nerve in the inner ear that sends messages related to motion and position to the brain. Both conditions involve inflammation of the inner ear. Labyrinths that house the vestibular system sense changes in the heads position or the heads motion. Inflammation of these inner ear parts results in a sensation of the world spinning and also possible hearing loss or ringing in the ears. It can occur as a single attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea, vomiting, and eye nystagmus. The cause is often not clear. It may be due to a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy, or as a reaction to medication. 30% of affected people had a common cold prior to developing the disease. Either bacterial or viral labyrinthitis can cause a permanent hearing loss in rare cases. This appears to result from an imbalance of neuronal input between the left and right inner ears. Signs and symptoms
The main symptoms are severe vertigo and nystagmus. The most common symptom for vestibular neuritis is the onset of vertigo that has formed from an ongoing infection or trauma. The dizziness sensation that is associated with vertigo is thought to be from the inner ear labyrinth. | Additionally, irrigating the bladder with distilled water three times daily with 3 way Foleys catheter and urinary antiseptics like pyridium may be used to help relieve urinary symptoms. Antibiotics such as trimethoprim-sulfamethoxazole or ciprofloxacin may be used. History
Leonor Michaelis and Carl Gutmann first described malakoplakia in 1902 after analyzing a patients tumor at the request of David Paul von Hansemann. See also
List of inclusion bodies that aid in diagnosis of cutaneous conditions
References
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The Department of Justices Drug Enforcement Administration (DEA) enforces controlled substances laws and regulations. The Department of Health and Human Services Food and Drug Administration (FDA) serve to protect and promote public health by controlling the manufacturing, marketing, and distribution of products, like medications. The United States approach to substance abuse has shifted over the last decade, and is continuing to change. The federal government was minimally involved in the 19th century. The federal government transitioned from using taxation of drugs in the early 20th century to criminalizing drug abuse with legislations and agencies like the Federal Bureau of Narcotics (FBN) mid-20th century in response to the nations growing substance abuse issue. These strict punishments for drug offenses shined light on the fact that drug abuse was a multi-faceted problem. The Presidents Advisory Commission on Narcotics and Drug Abuse of 1963 addressed the need for a medical solution to drug abuse. However, drug abuse continued to be enforced by the federal government through agencies such as the DEA and further legislations such as The Controlled Substances Act (CSA), the Comprehensive Crime Control Act of 1984, and Anti-Drug Abuse Acts. In the past decade, there have been growing efforts through state and local legislations to shift from criminalizing drug abuse to treating it as a health condition requiring medical intervention. 28 states currently allow for the establishment of needle exchanges. Florida, Iowa, Missouri and Arizona all introduced bills to allow for the establishment of needle exchanges in 2019. | The supporters of programs with total abstinence from drugs as a goal believe that enabling further drug use means prolonged drug use and risks an increase in addiction and complications from addiction. Residential
Residential drug treatment can be broadly divided into two camps: 12-step programs and therapeutic communities. 12-step programs are a nonclinical support-group and spiritual-based approach to treating addiction. Therapy typically involves the use of cognitive-behavioral therapy, an approach that looks at the relationship between thoughts, feelings and behaviors, addressing the root cause of maladaptive behavior. Cognitive-behavioral therapy treats addiction as a behavior rather than a disease, and so is subsequently curable, or rather, unlearnable. Cognitive-behavioral therapy programs recognize that, for some individuals, controlled use is a more realistic possibility.One of many recovery methods are 12-step recovery programs, with prominent examples including Alcoholics Anonymous, Narcotics Anonymous, Drug Addicts Anonymous and Pills Anonymous. They are commonly known and used for a variety of addictions for the individual addicted and the family of the individual. Substance-abuse rehabilitation (rehab) centers offer a residential treatment program for some of the more seriously addicted, in order to isolate the patient from drugs and interactions with other users and dealers. Outpatient clinics usually offer a combination of individual counseling and group counseling. Frequently, a physician or psychiatrist will prescribe medications in order to help patients cope with the side effects of their addiction. Medications can help immensely with anxiety and insomnia, can treat underlying mental disorders (cf. | 11
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Relationship to Menieres Disease
The data on how often progression to Menieres disease occurs is mixed, but the majority of recent studies suggest a low likelihood. A 1984 study from Japan looked at patients with Menieres disease and classified them into subcategories based on their first symptoms. The study found that the majority of patients with Menieres disease (104 out of 163, or 63.80%) presented vertigo with their first symptoms, and only 59 out of 163 (36.19%) of patients presented with cochlear symptoms first, such as "tinnitus or deafness." However, the study found that 59 out of 74 (79.72%) patients who started out with a cochlear hydrops diagnosis progressed to Menieres disease, and concluded that "cochlear Menieres disease frequently develops into Menieres disease. "Conversely, A 2006 study from doctors at the House Ear Institute found that “conversion from cochlear hydrops to Menieres disease occurred in 33%” of diagnosed patients in a study including 46 subjects. A 2009 study from Japan found that only about 10% of their diagnosed patients with sudden low-frequency hearing loss (SLFHL) went on to develop full Menieres disease, and about 18% with recurring SLFHL developed Menieres disease. From this study, about 70% of patients who did not develop Menieres Disease maintained their hearing in the end. | 6-MP is metabolized analogously to natural purines, giving thioguanosine triphosphate (TGTP) and thiodeoxyguanosine triphosphate (TdGTP) via thioinosine monophosphate (TIMP) and several further intermediates. On a second path, the sulfur atom of 6-MP and TIMP is methylated. The end products of azathioprine metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine. Mechanism of action
Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression. Azathioprine is converted within tissues to 6-MP, some of which is converted, in turn, to 6-thioguanine by the addition of an amino group. Both 6-MP and 6-thioguanine are conjugated with ribose, and then phosphorylated to form the nucleotides thioinosinic acid and thioguanylic acid, respectively. These nucleotides masquerade, respectively, as inosinic acid and guanylic acid; the former is the starting point for purine nucleotide biosynthesis, while the latter is one of the building blocks of DNA and RNA. The nucleotides are incorporated into newly synthesized (but nonfunctional) DNA, halting replication. The nucleotides act to inhibit glutamine-phosphoribosyl pyrophosphate amidotransferase (GPAT), one of the enzymes involved in purine biosynthesis, one of the earlier steps in the synthesis of DNA and RNA. They achieve GPAT inhibition through a form of negative feedback called product inhibition. | 0-1
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The point mutation A8344G is mostly associated with MERRF, in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama stated that 80% of the patients with MERRF disease exhibited this point mutation. The remaining mutations only account for 10% of cases, and the remaining 10% of the patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.If a patient does not exhibit mitochondrial DNA mutations, there are other ways that they can be diagnosed with MERRF. They can go through computed tomography (CT) or magnetic resonance imaging (MRI).The classification for the severity of MERRF syndrome is difficult to distinguish since most individuals will exhibit multi-symptoms. This is often necessary for children with complex neurologic or multi-system involvement, as described below. History and physical examination of the patient
A detailed family history should be obtained from at least three generations, particularly if there have been any neonatal and childhood deaths. A family history may also indicate if any family members exhibit features of the multi-system disease, specifically if there has been maternal inheritance. This would show transmission of the disease only to females, or if there is a family member who experienced a multi-system involvement such as: brain condition that a family member has been record to have such as seizures, dystonia, ataxia, or stroke-like episodes. There may also be optic atrophy, skeletal muscle with a history of myalgia, weakness, or ptosis. Family history may also include neuropathy and dysautonomia, or heart conditions such as cardiomyopathy. | This study suggests that a buccal swab approach can be used to informatively examine mitochondrial dysfunction in children with seizures and may be applicable to screening mitochondrial disease with other clinical presentations.Proceedings of the National Academy of Science of the United States of America published an article investigating the human mitochondrial tRNA (hmt-tRNA) mutations which are associated with mitochondrial myopathies. Since the current understanding of the precise molecular mechanisms of these mutations is limited, there is no efficient method to treat their associated mitochondrial diseases. All pathogenic mutants displayed pleiotropic phenotypes, with the exception of the G34A anticodon mutation, which solely affected aminoacylation. See also
Epilepsy
Mitochondrial disease
Myoclonus
Ragged red fibers
References
External links
MERRF+Syndrome at the US National Library of Medicine Medical Subject Headings (MeSH)
merrf at NIH/UW GeneTests | 11
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Acute intermittent porphyria
Adrenoleukodystrophy (Schilders disease)
Alkaptonuria
Aminolevulinic acid dehydratase deficiency porphyria (Doss porphyria, plumboporphyria)
B-mannosidase deficiency
Carotenosis
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy syndrome (CADASIL syndrome)
Cerebrotendinous xanthomatosis
Citrullinemia
Congenital erythropoietic porphyria (Gunthers disease)
Diabetic bulla (bullosis diabeticorum, bullous eruption of diabetes mellitus)
Diabetic cheiroarthropathy
Diabetic dermopathy (shin spots)
Dystrophic calcinosis cutis
Eruptive xanthoma
Erythropoietic protoporphyria
Fabry disease (Anderson–Fabry disease, angiokeratoma corporis diffusum)
Familial alpha-lipoprotein deficiency (Tangier disease)
Familial amyloid polyneuropathy
Familial apoprotein CII deficiency
Familial combined hyperlipidemia (multiple-type hyperlipoproteinemia)
Familial defective apolipoprotein B-100
Familial dysbetalipoproteinemia (broad beta disease, remnant removal disease)
Familial hypertriglyceridemia
Farber disease (fibrocytic dysmucopolysaccharidosis, lipogranulomatosis)
Fucosidosis
Gauchers disease
Gout (podagra, urate crystal arthropathy, urate deposition disease)
Hartnup disease (pellagra-like dermatosis)
Hemodialysis-associated amyloidosis
Hepatoerythropoietic porphyria
Hereditary coproporphyria
Hereditary gelsolin amyloidosis
Heredofamilial amyloidosis
Hunter syndrome
Hurler syndrome (gargoylism, mucopolysaccharidosis type I)
Hurler–Scheie syndrome (mucopolysaccharidosis type I H-S)
Hyaluronidase deficiency (mucopolysaccharidosis type IX)
Iatrogenic calcinosis cutis
Idiopathic scrotal calcinosis (idiopathic calcified nodules of the scrotum)
Lafora disease
Lesch–Nyhan syndrome (juvenile gout)
Lichen amyloidosis
Limited joint mobility
Lipoid proteinosis (hyalinosis cutis et mucosae, Urbach–Wiethe disease)
Lipoprotein lipase deficiency (chylomicronemia, chylomicronemia syndrome)
Macular amyloidosis
Maroteaux–Lamy syndrome (mucopolysaccharidosis type VI)
Medication-induced hyperlipoproteinemia
Metastatic calcinosis cutis
Milia-like calcinosis
Morquios disease (mucopolysaccharidosis type IV)
Necrobiosis lipoidica (necrobiosis lipoidica diabeticorum)
Niemann–Pick disease
Nodular amyloidosis
Nodular xanthoma
Normolipoproteinemic xanthomatosis
Obstructive liver disease (xanthomatous biliary cirrhosis)
Ochronosis
Osteoma cutis
Palmar xanthoma
Phenylketonuria
Phytosterolemia (sitosterolemia)
Porphyria cutanea tarda
Primary cutaneous amyloidosis
Primary systemic amyloidosis
Prolidase deficiency
Pseudoporphyria (pseudoporphyria cutanea tarda)
Sanfilippo syndrome
Scheie syndrome (mucopolysaccharidosis type I S)
Secondary cutaneous amyloidosis
Secondary systemic amyloidosis
Sialidosis
Sly syndrome (mucopolysaccharidosis type VII)
Subepidermal calcified nodule (solitary congenital nodular calcification, Winers nodular calcinosis)
Transient erythroporphyria of infancy (purpuric phototherapy-induced eruption)
Traumatic calcinosis cutis
Tuberoeruptive xanthoma (tuberous xanthoma)
Tumoral calcinosis
Variegate porphyria (mixed hepatic porphyria, mixed porphyria, South African genetic porphyria, South African porphyria)
Verruciform xanthoma
Waxy skin
Wilsons disease (hepatolenticular degeneration)
Xanthelasma palpebrarum (xanthelasma)
Xanthoma diabeticorum
Xanthoma planum (plane xanthoma)
Xanthoma striatum palmare
Xanthoma tendinosum (tendinous xanthoma)
Xanthoma tuberosum
Resulting from physical factors
Skin conditions resulting from physical factors occur from a number of causes, including, but not limited to, hot and cold temperatures, friction, and moisture. | Uveitis () is the inflammation of the uvea, the pigmented layer that lies between the inner retina and the outer fibrous layer composed of the sclera and cornea. The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is described anatomically, by the part of the eye affected, as anterior, intermediate or posterior, from front to back. In the panuveitic form, all parts are involved. The most common form is the anterior one. Symptoms include pain, floaters and blurred vision, and clinical examination may show redness and an irregular pupil, while ophthalmic examination shows dilated ciliary blood vessels and the presence of cells in the anterior chamber. Uveitis may arise spontaneously and associated with some genetic factors, or be associated with a wide range of conditions including autoimmune disease and infections. While the eye is a relatively protected environment, its immune mechanisms may be overcome resulting in inflammation and tissue destruction associated with T-cell activation. The incidence is approximately 1:4500, most commonly between the ages of 20–60. Uveitis is an ophthalmic emergency and requires a thorough examination by an ophthalmologist or optometrist, including dilation of the pupil to allow better visualisation. Urgent treatment is required to control the inflammation. Further procedures may be required to identify any underlying disease. Treatment usually involves the use of steroids, most commonly as eye drops. Any underlying disease, for instance herpes zoster (shingles) will also require treatment. | 0-1
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Fludarabine is a purine analogue and antineoplastic agent. It is generally used as its 5-O-phosphorylated form known as fludarabine phosphate,
sold under the brand name Fludara among others. It is a chemotherapy medication used in the treatment of leukemia and lymphoma. These include chronic lymphocytic leukemia, non-Hodgkins lymphoma, acute myeloid leukemia, and acute lymphocytic leukemia. It is given by injection into a vein or by mouth.Common side effects include nausea, diarrhea, fever, rash, shortness of breath, numbness, vision changes, and feeling tired. Severe side effects include brain dysfunction, low blood cell counts, and lung inflammation. Use in pregnancy will likely result in harm to the fetus. Fludarabine is in the purine analog family of medications and works by interfering with the duplication of DNA.Fludarabine was approved for medical use in the United States in 1991. It is on the World Health Organizations List of Essential Medicines. Medical uses
Fludarabine is highly effective in the treatment of chronic lymphocytic leukemia, producing higher response rates than alkylating agents such as chlorambucil alone. Fludarabine is used in various combinations with cyclophosphamide, mitoxantrone, dexamethasone and rituximab in the treatment of indolent non-Hodgkins lymphomas. As part of the FLAG or FLAMSA regimen, fludarabine is used together with cytarabine and granulocyte colony-stimulating factor in the treatment of acute myeloid leukaemia. Because of its immunosuppressive effects, fludarabine is also used in some conditioning regimens prior to allogeneic stem cell transplant. Side effects
Fludarabine is associated with profound lymphopenia, and as a consequence, increases the risk of opportunistic infections. | People who have been treated with fludarabine will usually be asked to take co-trimoxazole or to use monthly nebulised pentamidine to prevent Pneumocystis jiroveci pneumonia. The profound lymphopenia caused by fludarabine renders patients susceptible to transfusion-associated graft versus host disease, an oftentimes fatal complication of blood transfusion. For this reason, all patients who have ever received fludarabine should only be given irradiated blood components. Fludarabine causes anemia, thrombocytopenia and neutropenia, requiring regular blood count monitoring. Some patients require blood and platelet transfusion, or G-CSF injections to boost neutrophil counts. Fludarabine is associated with the development of severe autoimmune hemolytic anemia in a proportion of patients.Difficulties are often encountered when harvesting peripheral blood stem cells from patients previously treated with fludarabine. Pharmacology
Fludarabine is a purine analog, and can be given both orally and intravenously. Fludarabine inhibits DNA synthesis by interfering with ribonucleotide reductase and DNA polymerase. It is active against both dividing and resting cells. Being phosphorylated, fludarabine is ionized at physiologic pH and is effectually trapped in blood. This provides some level of specificity for blood cells, both cancerous and healthy. History
Fludarabine was produced by John Montgomery and Kathleen Hewson of the Southern Research Institute in 1968. Names
Fludarabine is generally administered as its 5-O-phosphorylated form known as fludarabine phosphate, which is rapidly dephosphorylated to fludarabine in the plasma. References
External links
"Fludarabine". Drug Information Portal. U.S. National Library of Medicine. | 11
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Patients with bipolar affective disorder should not receive antidepressants whilst in a manic phase, as antidepressants can worsen mania. Absolute
Hypersensitivity to maprotiline or to other TCAs and TeCAs
Hypertrophy of the prostate gland with urine hesitancy
Closed angle glaucoma
Special caution needed
Concomitant treatment with a MAO inhibitor
Serious impairment of liver and kidney function
Epilepsy and other conditions that lower the seizure threshold (active brain tumors, alcohol withdrawal, other medications)
Serious cardiovascular conditions (arrhythmias, heart insufficience, state after myocardial infarction etc.) Treatment of patients under age 18
Suicidal patients
Same as other antidepressants, maprotiline increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders. Anyone considering the use of maprotiline or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need. Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older. Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide. Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. Maprotiline is not approved for use in pediatric patients. | Cryofibrinogenemic purpura is a skin condition that manifests as painful purpura with slow healing ulcerations and edema of both feet during winter months. : 823
See also
Cryofibrinogenemia
Skin lesion
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Vocal cord hemorrhage occurs when a blood vessel in the vocal cords ruptures, which results in leakage of blood into the superficial lamina propria and dysphonia (hoarseness). The rupture usually results from overly forceful or incorrect vocalization, and may be a one-time occurrence or occur repeatedly. According to News Medical.net, "professional singers are at an increased risk of vocal hemorrhage, particularly in cases where gruelling performance schedules are followed". The treatment is vocal rest as failure to rest the voice can result in permanent scarring. == References == | Crouzonodermoskeletal syndrome is a disorder characterized by the premature joining of certain bones of the skull (craniosynostosis) during development and a skin condition called acanthosis nigricans.Some of the signs and symptoms of Crouzonodermoskeletal syndrome are similar to those seen with Crouzon syndrome. They include prematurely fused skull bones, which affect the shape of the head and face; wide-set, bulging eyes due to shallow eye sockets; eyes that do not point in the same direction (strabismus); a small, beaked nose; and an underdeveloped upper jaw. People with these conditions are generally of normal intelligence.Several features distinguish Crouzonodermoskeletal syndrome from Crouzon syndrome. People with Crouzonodermoskeletal syndrome have acanthosis nigricans, a skin condition characterized by thick, dark, velvety skin in body folds and creases, including the neck and underarms. In addition, subtle changes may be seen in the bones of the spine (vertebrae). Noncancerous growths called cementomas may develop in the jaw during young adulthood.Crouzonodermoskeletal syndrome is rare; the condition is seen in about 1 per million people. Genetics
Mutations in the FGFR3 gene cause Crouzonodermoskeletal syndrome. The protein made by the FGFR3 gene is a receptor that plays a role in the development and maintenance of bone and brain tissue. | 0-1
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Raloxifene, already proven effective against Mers and Sars in preclinical tests, has been indicated as effective against SARS-CoV-2 by the “in-silico” research conducted by the consortium which has shown efficacy in countering the replication of the virus in cells. The IP for its use against SARS-CoV-2 has already been protected on May 6 2020 in the name Dompé farmaceutici, Fraunhofer Institute and KU Leuven, to facilitate the largest possible access. Raloxifene would be used in mildly symptomatic COVID-19 patients to halt the spread of infection. This result emerged from the first virtual (in silico) screening conducted on the Consortium’s supercomputers of more than 400.000 molecules (safe-in-man drugs and natural products) made available by Dompé farmaceutici and the partner Fraunhofer (IME) to the Consortium. The molecules were prioritized if in clinical stage or already on the market. 7.000 molecules with certain promising characteristics were tested. References
Further reading
Barrett-Connor E (2001). "Raloxifene: risks and benefits". Ann N Y Acad Sci. 949 (1): 295–303. Bibcode:2001NYASA.949..295B. doi:10.1111/j.1749-6632.2001.tb04036.x. PMID 11795366. S2CID 41412601. Heringa M (2003). "Review on raloxifene: profile of a selective estrogen receptor modulator". Int J Clin Pharmacol Ther. 41 (8): 331–45. doi:10.5414/cpp41331. PMID 12940590. Sporn MB, Dowsett SA, Mershon J, Bryant HU (2004). "Role of raloxifene in breast cancer prevention in postmenopausal women: clinical evidence and potential mechanisms of action". Clin Ther. 26 (6): 830–40. doi:10.1016/s0149-2918(04)90127-0. PMID 15262454. Vogel VG (2009). "The NSABP Study of Tamoxifen and Raloxifene (STAR) trial". Expert Rev Anticancer Ther. 9 (1): 51–60. doi:10.1586/14737140.9.1.51. PMC 2785111. PMID 19105706. | Wickerham DL, Costantino JP, Vogel VG, Cronin WM, Cecchini RS, Ford LG, Wolmark N (2009). "The use of tamoxifen and raloxifene for the prevention of breast cancer". Recent Results Cancer Res. Recent Results in Cancer Research. 181: 113–9. doi:10.1007/978-3-540-69297-3_12. ISBN 978-3-540-69296-6. PMC 5110043. PMID 19213563. Vogel VG (2011). "Update on raloxifene: role in reducing the risk of invasive breast cancer in postmenopausal women". Breast Cancer: Targets and Therapy. 3: 127–37. doi:10.2147/BCTT.S11288. PMC 3846694. PMID 24367182. Yang ZD, Yu J, Zhang Q (2013). "Effects of raloxifene on cognition, mental health, sleep and sexual function in menopausal women: a systematic review of randomized controlled trials". Maturitas. 75 (4): 341–8. doi:10.1016/j.maturitas.2013.05.010. PMID 23764354. External links
"Raloxifene". Drug Information Portal. U.S. National Library of Medicine. "Raloxifene hydrochloride". Drug Information Portal. U.S. National Library of Medicine. | 11
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One small study, which used a dose of 2 mg slow-release melatonin at bedtime, found that 50% of participants had “shortened nocturnal sleep duration, decreased sleep drunkenness and relieved daytime sleepiness.” Other studies have shown that melatonin synchronizes the circadian rhythms, and improves the “onset, duration and quality of sleep.”
Levothyroxine
There have been some studies suggesting levothyroxine as a possible treatment for IH, especially for patients with subclinical hypothyroidism. This treatment does carry potential risks (especially for patients without hypothyroidism or subclinical hypothroidism), which include cardiac arrhythmia. Hypocretin agonists
Hypocretin-1 has been shown to be strongly wake-promoting in animal models, but it does not cross the blood-brain barrier. Suvorexant, a hypocretin receptor antagonist, has been developed to limit the natural effects of hypocretin in patients with insomnia. It is therefore possible that a hypocretin agonist may be similarly developed for the treatment of hypersomnia. Acetylcholinesterase inhibitor
Antidepressants seems to have some therapeutic effects as they enhance synaptic levels of noradrenaline and serotonin and for same reason enhancing the levels of acetylcholine may have some therapeutic effect. Donepezil showed improvement in one patient by decreasing ESS score from 20 up to 14. Memantine has also shown some positive effect on a patient with narcolepsy. Levodopa
Levodopa is an amino acid and is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). | However, "even in the presence of other specific causes of hypersomnia, one should carefully assess the contribution of these etiological factors to the complaint of EDS and when specific treatments of these conditions fail to suppress EDS, the additional diagnosis of IH should be considered. "The severity of EDS can be quantified by subjective scales, such as the Epworth Sleepiness Scale and the Stanford Sleepiness Scale, and also by objective tests, like actigraphy, psychomotor vigilance task, maintenance of wakefulness test (MWT), multiple sleep latency test (MSLT) although as per latest research studies, the effectiveness of MSLT has been called into question. Several groups of researchers have found normal MSLT results in patients who otherwise seem to have IH. Therefore, when IH is suspected, researchers suggest appending a 24-hour continuous polysomnography to the standard overnight/MSLT study in order to record total sleep time.The recent studies have also found that reports of sleepiness in IH relate more to mental fatigue rather than physiological sleepiness per se and the subjective scales like ESS, IH symptom diary (IHSD) and PGIC better captures the severity of symptoms consistently.It is also important to note that whereas narcolepsy is strongly associated with the HLA-DQB1*0602 genotype, "HLA typing is of no help in the positive diagnosis of idiopathic hypersomnia." This is "despite some reports that suggest an increase [sic] frequency of HLA Cw2 and DRS in idiopathic hypersomnia subjects. "In patients with IH, polysomnography typically shows short sleep latency, increased mean slow wave sleep, and a high mean sleep efficiency. | 11
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Angiostrongylus cantonensis is a parasitic nematode (roundworm) that causes angiostrongyliasis, the most common cause of eosinophilic meningitis in Southeast Asia and the Pacific Basin. The nematode commonly resides in the pulmonary arteries of rats, giving it the common name rat lungworm. Snails are the primary intermediate hosts, where larvae develop until they are infectious. Humans are incidental hosts of this roundworm, and may become infected through ingestion of larvae in raw or undercooked snails or other vectors, or from contaminated water and vegetables. The larvae are then transported via the blood to the central nervous system, where they are the most common cause of eosinophilic meningitis, a serious condition that can lead to death or permanent brain and nerve damage. Angiostrongyliasis is an infection of increasing public health importance, as globalization contributes to the geographic spread of the disease. History
First described by the renowned Chinese parasitologist Hsin-Tao Chen (1904–1977) in 1935, after examining Cantonese rat specimens, the nematode Angiostrongylus cantonensis was identified in the cerebrospinal fluid of a patient with eosinophilic meningitis by Nomura and Lim in Taiwan in 1944. They noted that raw food eaten by the patient may have been contaminated by rats. In 1955, Mackerass and Sanders identified the lifecycle of the worm in rats, defining snails and slugs as the intermediate hosts, and noting the path of transmission through the blood, brain, and lungs in rats. Infectious agent
A. cantonensis is a helminth of the phylum Nematoda, order Strongylida, and superfamily Metastrongyloidea. | Freshwater snails: Pila spp., Pomacea canaliculata, Cipangopaludina chinensis, Bellamya aeruginosa and Bellamya quadrata
Slugs: Limax maximus, Limax flavus Deroceras laeve, Deroceras reticulatum, Laevicaulis alte, Sarasinula plebeia, Vaginulus yuxjsjs, Lehmannia valentiana, Phiolomycus bilineatus, Macrochlamys loana, Meghimatium bilineatum and probably other species of slugs.Definitive hosts of A. cantonensis include wild rodents, especially the brown rat (Rattus norvegicus) and the black rat (Rattus rattus).Paratenic hosts of A. cantonensis include the predatory land flatworm Platydemus manokwari and the amphibians, Bufo asiaticus, Rana catesbeiana, Rhacophorus leucomystax and Rana limnocharis.In 2004, a captive yellow-tailed black cockatoo (Calyptorhynchus funereus) and two free-living tawny frogmouths (Podargus strigoides) suffering neurological symptoms were shown to have the parasite. They were the first avian hosts discovered for the organism. In 2018, in Mallorca two North African hedgehogs with signs of acute neurological disease were found to have A. cantonensis in their brains, one of them with a gravid female. It was the first report of hedgehogs as hosts of Angiostrongylus.The Hawaiʻi Dept. of Health states that fresh water opihi can carry the parasite, as well as other aquatic organisms such as prawns, frogs, and water monitor lizards. House pets may interact with A. cantonensis-carrying animals yet not well studied. Cats are known to carry and spread feline lungworm in rat and snail interactions. Pathogenesis of human angiostrongylosis
The presence of parasitic worms burrowed in the neural tissue of the human central nervous system (CNS) causes complications. | 11
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Voriconazole, sold under the brand name Vfend among others, is an antifungal medication used to treat a number of fungal infections. This includes aspergillosis, candidiasis, coccidioidomycosis, histoplasmosis, penicilliosis, and infections by Scedosporium or Fusarium. It can be taken by mouth or used by injection into a vein.Common side effects include vision problems, nausea, abdominal pain, rash, headache, and seeing or hearing things that are not present. Use during pregnancy may result in harm to the baby. It is in the triazole family of medications. It works by affecting fungal metabolism and fungal cell membranes.Voriconazole was patented in 1990 and approved for medical use in the United States in 2002. It is on the World Health Organizations List of Essential Medicines. Medical uses
Voriconazole is used to treat invasive aspergillosis and candidiasis and fungal infections caused by Scedosporium and Fusarium species, which may occur in immunocompromised patients, including people undergoing allogeneic bone marrow transplant (BMT), who have hematologic cancers or who undergo organ transplants.It is also used to prevent fungal infection in people as they undergo BMT.It is also the recommended treatment for the CNS fungal infections transmitted by epidural injection of contaminated steroids.It can be taken by mouth or given in a doctors office or clinic by intravenous infusion. Contraindications
It is toxic to the fetus; pregnant women should not take it and women taking it should not become pregnant.People who have hereditary intolerance for galactose, Lapp lactase deficiency, or glucose-galactose malabsorption should not take this drug. | CD20 is widely expressed on B cells, from early pre-B cells to later in differentiation, but it is absent on terminally differentiated plasma cells. Although the function of CD20 is unknown, it may play a role in Ca2+ influx across plasma membranes, maintaining intracellular Ca2+ concentration and allowing activation of B cells. Rituximab is relatively ineffective in elimination of cells with low CD20 cell-surface levels. It tends to stick to one side of B cells, where CD20 is, forming a cap and drawing proteins over to that side. The presence of the cap changes the effectiveness of natural killer (NK) cells in destroying these B cells. When an NK cell latched onto the cap, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this asymmetric protein cluster, it was killed only 40% of the time.The following effects have been found:
The Fc portion of rituximab mediates antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Rituximab has a general regulatory effect on the cell cycle. Preferential elimination of malignant B cells with high CD20 levels and high BCR signaling propensity, especially in chronic lymphocytic leukemia (CLL). It increases MHC II and adhesion molecules LFA-1 and LFA-3 (lymphocyte function-associated antigen). It elicits shedding of CD23. It downregulates the B cell receptor. It induces apoptosis of CD20+ cells. | 0-1
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Dicephalic parapagus () is a rare form of partial twinning with two heads side by side on one torso. Infants conjoined this way are sometimes called "two-headed babies" in popular media. The condition is also called parapagus dicephalus.If carried to term, most dicephalic twins are stillborn, or die soon after birth. A small number are known to have survived to adulthood.The extent to which limbs and organs are duplicated varies from case to case. One head may be only partially developed (anencephalic), or both may be complete. In some cases, two complete hearts are present as well, which improves their chances of survival. The total number of arms may be two, three or four.Their prospects are best if no attempt is made to separate them, except in cases in which one twin is clearly dying. Terminology
Dicephalus means two-headed. Parapagus means joined side by side.Dicephalic twins are called:
dibrachius if they have two arms altogether (one for each twin),
tribrachius, if they have three arms altogether,
tetrabrachius, if they have four arms altogether,
dipus, if they have two legs altogether (one for each twin). Incidence
Conjoined twins appear in one in 50,000 to one in 100,000 births. Dicephalic twins represent about 11 percent of all conjoined twins. Medical and social response
As late as the 1960s, some medical publications argued that newborn dicephalic twins should not be actively treated or resuscitated. An attempt at surgical separation was reported in a paper published in 1982, but did not result in long-term survival of either twin. | A phytobezoar is a type of bezoar, or trapped mass in the gastrointestinal system, that consists of components of indigestible plant material, such as fibres, skins and seeds. While phytobezoars may be discovered incidentally on barium x-ray or endoscopic testing of the stomach, individuals with phytobezoars may develop symptoms: nausea, vomiting, gastric outlet obstruction, perforation, abdominal pain, and bleeding have been reported. Conditions that lead to decreased motility in the stomach (gastroparesis) and surgeries on the stomach (such as vagotomy or gastric bypass) are associated with the development of phytobezoars. A specific type of phytobezoar, termed a diospyrobezoar, is associated with ingestion of unripe persimmons, which contain a soluble tannin called shibuol that polymerizes into a coagulative cellulose-protein compound in the acid environment of the stomach, to form the bezoar. In addition to their presence in human stomachs, phytobezoars have been documented in the stomachs of slaughtered plant-eating animals. Cause
Gastric phytobezoars are a form of intestinal blockage and are seen in those with poor gastric motility. The preferred treatment of bezoars includes different therapies and/or fragmentation to avoid surgery. Phytobezoars are most common and consist of undigested lignin, cellulose, tannins, celery, pumpkin skin, grape skins, prunes, raisins, vegetables and fruits. Phytobezoars can form after eating persimmons and pineapples. These are more difficult to treat and are referred to as diospyrobezoars. Phytobezoars are more likely to form due to the ingestion of raw plant foods, even in persons without predisposing factors, as cooking softens them for easier digestion. Treatment
Several treatments for phytobezoars have been described. | 0-1
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Individual psychological and social work factors, as well as worker-employer relations are also likely to be associated with time and rates of recovery.A Finnish study of return to work in patients with spinal stenosis treated by surgery found that: (1) none of the patients who had retired before the operation returned to work afterward. (2) The variables that predicted postoperative ability to work for women were: being fit to work at the time of operation, age < 50 years at the time of operation, and duration of lumbar spinal stenosis symptoms < 2 years. (3) For men, these variables were: being fit to work at the time of operation, age < 50 years at the time of operation, no prior surgery, and the extent of the surgical procedure equal to or less than one laminectomy. Womens and mens working capacity do not differ after lumbar spinal stenosis operation. If the aim is to maximize working capacity, then, when a lumbar spinal stenosis operation is indicated, it should be performed without delay. In lumbar spinal stenosis patients who are > 50 years old and on sick leave, it is unrealistic to expect that they will return to work. Therefore, after such an extensive surgical procedure, re-education of patients for lighter jobs could improve the chances of these patients returning to work.In a related Finnish study, a total of 439 patients operated on for lumbar spinal stenosis during the period 1974–1987 was re-examined and evaluated for working and functional capacity approximately 4 years after the decompressive surgery. | Neoplasia also includes direct seeding of the cerebrospinal fluid (CSF) from primary central nervous system (CNS) tumors such as glioblastoma multiforme, medulloblastoma, ependymoma, and choroid plexus carcinoma. Strictly speaking, the most common cause of arachnoiditis in failed back syndrome is not infectious or from cancer. It is due to non-specific scarring secondary to the surgery or the underlying pathology. Nerve injury
Laceration of a nerve root, or damage from cautery or traction can lead to chronic pain, however this can be difficult to determine. Chronic compression of the nerve root by a persistent agent such as disc, bone (osteophyte) or scarring can also permanently damage the nerve root. Epidural scarring caused by the initial pathology or occurring after the surgery can also contribute to nerve damage. In one study of failed back patients, the presence of pathology was noted to be at the same site as the level of surgery performed in 57% of cases. The remaining cases developed pathology at a different level, or on the opposite side, but at the same level as the surgery was performed. In theory, all failed back patients have some sort of nerve injury or damage which leads to a persistence of symptoms after a reasonable healing time. Diagnosis
Avoiding post-laminectomy/laminotomy syndrome
Smaller procedures that do not remove bone (such as Endoscopic Transforaminal Lumbar Discectomy and Reconfiguration) do not cause post laminectomy/laminotomy syndrome. Management
Failed back syndrome (FBS) is a well-recognized complication of surgery of the lumbar spine. | 11
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(1996) administered fluoxetine to 21 children for nine weeks and found that 76% of the children had reduced or no symptoms by the end of the experiment. This indicates that fluoxetine is an SSRI that is indeed helpful in treating selective mutism. History
In 1877, German physician Adolph Kussmaul described children who were able to speak normally but often refused to as having a disorder he named aphasia voluntaria. Although this is now an obsolete term, it was part of an early effort to describe the concept now called selective mutism. In 1980, a study by Torey Hayden identified what she called four "subtypes" of elective mutism (as it was called then), although this set of subtypes is not in current diagnostic use. These subtypes are no longer recognized, though "speech phobia" is sometimes used to describe a selectively mute person who appears not to have any symptoms of social anxiety. The Diagnostic and Statistical Manual of Mental Disorders (DSM), first published in 1952, first included selective mutism in its third edition, published in 1980. Selective mutism was described as "a continuous refusal to speak in almost all social situations" despite normal ability to speak. While "excessive shyness" and other anxiety-related traits were listed as associated features, predisposing factors included "maternal overprotection", "mental retardation", and trauma. Elective mutism in the third edition revised (DSM III-R) is described similarly to the third edition except for specifying that the disorder is not related to social phobia. | Melanonychia is a black or brown pigmentation of the normal nail plate, and may be present as a normal finding on many digits in Afro-Caribbeans, as a result of trauma, systemic disease, or medications, or as a postinflammatory event from such localized events as lichen planus or fixed drug eruption. : 790 : 665 There are two types, longitudinal and transverse melanonychia. : 671 Longitudinal melanonychia may be a sign of subungual melanoma (acral lentiginous melanoma), although there are other diagnoses such as chronic paronychia, onychomycosis, subungual hematoma, pyogenic granuloma, glomus tumour, subungual verruca, mucous cyst, subungual fibroma, keratoacanthoma, carcinoma of the nail bed, and subungual exostosis. See also
Nail anatomy
List of cutaneous conditions
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Herpetiform ulceration is often extremely painful, and the lesions recur more frequently than minor or major aphthous ulcers. Recurrence may be so frequent that ulceration is virtually continuous. It generally occurs in a slightly older age group than the other subtypes, and females are affected slightly more frequently than males. RAS type ulceration
Recurrent oral ulceration associated with systemic conditions is termed "RAS-type ulceration", "RAS-like ulceration", or "aphthous-like ulcers". Aphthous stomatitis occurs in individuals with no associated systemic disease. Persons with certain systemic diseases may be prone to oral ulceration, but this is secondary to the underlying medical condition (see the systemic disease section). This kind of ulceration is considered by some to be separate from true aphthous stomatitis. However, this definition is not strictly applied. For example, many sources refer to oral ulceration caused by anemia and/or nutritional deficiencies as aphthous stomatitis, and some also consider Behçets disease to be a variant. Treatment
The vast majority of people with aphthous stomatitis have minor symptoms and do not require any specific therapy. The pain is often tolerable with simple dietary modification during an episode of ulceration such as avoiding spicy and acidic foods and beverages. Many different topical and systemic medications have been proposed (see table), sometimes showing little or no evidence of usefulness when formally investigated. Some of the results of interventions for RAS may in truth represent a placebo effect. No therapy is curative, with treatment aiming to relieve pain, promote healing and reduce the frequency of episodes of ulceration. | )Unknown frequency
Anemia
Headache
Increased respiratory rate
Orthostatic hypotension
Prolonged QT interval
Visual disturbancesRare (<1% incidence)
Contraindications
Pre-existing coma, acute stroke
Severe intoxication with alcohol or other central depressant drugs
Known allergy against haloperidol or other butyrophenones or other drug ingredients
Known heart disease, when combined will tend towards cardiac arrest
Special cautions
A multiple-year study suggested this drug and other neuroleptic antipsychotic drugs commonly given to people with Alzheimers with mild behavioral problems often make their condition worse and its withdrawal was even beneficial for some cognitive and functional measures. Elderly patients with dementia-related psychosis: analysis of 17 trials showed the risk of death in this group of patients was 1.6 to 1.7 times that of placebo-treated patients. Most of the causes of death were either cardiovascular or infectious in nature. It is not clear to what extent this observation is attributed to antipsychotic drugs rather than the characteristics of the patients. The drug bears a boxed warning about this risk. Impaired liver function, as haloperidol is metabolized and eliminated mainly by the liver
In patients with hyperthyroidism, the action of haloperidol is intensified and side effects are more likely. IV injections: risk of hypotension or orthostatic collapse
Patients at special risk for the development of QT prolongation (hypokalemia, concomitant use of other drugs causing QT prolongation)
Patients with a history of leukopenia: a complete blood count should be monitored frequently during the first few months of therapy and discontinuation of the drug should be considered at the first sign of a clinically significant decline in white blood cells. | 0-1
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Worry refers to the thoughts, images, emotions, and actions of a negative nature in a repetitive, uncontrollable manner that results from a proactive cognitive risk analysis made to avoid or solve anticipated potential threats and their potential consequences. Introduction
Psychologically, worry is part of
Perseverative Cognition (a collective term for continuous thinking about negative events in the past or in the future). As an emotion "worry" is experienced from anxiety or concern about a real or imagined issue, often personal issues such as health or finances, or external broader issues such as environmental pollution, social structure or technological change. It is a natural response to anticipated future problems. Excessive worry is a primary diagnostic feature of generalized anxiety disorder, but also is pervasive in other psychological disorders, like schizophrenia. Most people experience short-lived periods of worry in their lives without incident; indeed, a mild amount of worrying have positive effects, if it prompts people to take precautions (e.g., fastening their seat belt or buying insurance) or avoid risky behaviors (e.g., angering dangerous animals, or binge drinking), but with excessive worrisome people they overestimate future dangers in their assessments and in its extremities tend to magnify the situation as a dead end which results stress. Overestimation happens because analytic resources are a combination of external locus of control, personal experience and belief fallacies. | At a pre-conscious level, these processes influence the competition among mental representations in which some correspond to the assertive power of worry with impaired cognitive process and others to the preventive power of worry with attentional control or exhaustive vigilance. The biases determine threatening degree and nature of worry content the worrier attempts to resolve the perceived threat and the redirection of anticipations, responses and coping in such situations.There are some who respond to mental representations in an uncertain or ambiguous state in regard to the stressful or upsetting event. In this state the worrier is held in a perpetual state of worry. This is because availability of an overwhelming number(maybe 2 or 3, depending upon the worry-prone individual) of possibilities of outcomes which can be generated, it puts the worrier in a threatening crisis and they focus their attentional control voluntarily on the potential negative outcomes, whereas others engage in a constructive problem solving manner and in a benign approach rather than to engage with heightened anticipation on the possible negative outcome. Philosophical perspectives
Greek thinkers such as stoic philosopher Epictetus and Seneca advised against worry. Albert Ellis, the creator of Rational Emotive Behavior Therapy, was inspired by the Stoics’ therapeutic ideas. Religious perspectives
The biblical word used in Hebrew for worry (Hebrew: דָּאַג, daag) regards worry as a combined form of fear and sorrow which affects nephesh, the totality of our being. The bible takes a fortitude-strengthening approach regarding worrying e.g. | 11
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These outcomes concluded that there was a reduction in urgency to urinate, a decrease in micturitions and a decrease in average volume voided per micturition. There is also an improvement observed of the symptoms when Vibegron is administered over a longer period (52 weeks) concluding that it is effective and safe for longer use. In severe patients, increasing the dose was accompanied by similar beneficial effects when there was first a lack of these. Quality of life of the patients is improved, including a reduction of nocturia. Adverse effects
The most common side effects of Vibegron are a dry mouth, constipation, headache, nasopharyngitis, diarrhea, nausea, bronchitis, urinary tract infection and upper respiratory tract infection. An indication is made that upon urinary retention development, the patient should stop using the drug. Risk assessment for the drug in pregnant women has yet to be evaluated. Interactions
Vibegron is in contrast to other OAB drugs very selective and leads to a lesser degree in unwanted side effects. Vibegron is found to be a substrate for CYP3A4 in vivo, but does not actually induce or inhibit any of the cytochrome P450 enzymes and is thus less likely to take part in drug–drug interactions (DDI). Here vibegron differs from the previous overactive bladder drug mirabegron, which was known to be associated in various drug–drug interactions by inhibiting CYP2D6 or inducing CYP3A4, CYP2D6 and CYP2C9 in the liver.Using Vibegron only (monotherapy) has positive effects on OAB and UUI, but a combination with other drugs can have additional effects. | It was globally approved on September 21, 2018, in Japan for OAB.Vibegron has been proven effective in 5 key clinical trials.A phase IIb global trial completed in 2013 of 1395 patients, of which 89.7% were women and 63.3% had not been treated previously, demonstrated a significant decrease in daily micturitions and urgent urinary incontinence episodes upon administration of vibegron.An international phase III trial of 506 participants completed in 2019 found statistically significant efficacy of vibegron after 2 weeks of daily administration. The adverse effect rates in patients treated with vibegron were comparable to those in patients who received a placebo.GEMTESA, a drug using vibegron as an active ingredient was approved by the FDA on December 23, 2020, after an additional phase III international trial of 1085 patients. Society and culture
Legal status
Vibegron was approved for medical use in the United States in December 2020. Names
Vibegron is the international nonproprietary name (INN). Mechanism of action
Vibegron is a selective agonist for the beta-3 adrenergic receptor (β3-AR). The receptors are located in the kidneys, urinary tract and bladder tissue. Upon binding, the β3 receptor undergoes a conformational change. This induces the activation of adenylate cyclases via G proteins and thereby promotes the formation of cyclic adenosine monophosphate (cAMP). The consequence of this cascade is an increased intracellular cAMP concentration which triggers activation of cAMP-dependent protein kinase A and causes a reduction of Ca2+ concentration in the cytoplasm. The kinase then phosphorylates myosin chains and thereby inhibits muscle contraction.The final effect of vibegron is muscle relaxation in the bladder. | 11
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In the lower doses used for water fluoridation, the only clear adverse effect is dental fluorosis, which can alter the appearance of childrens teeth during tooth development; this is mostly mild and is unlikely to represent any real effect on aesthetic appearance or on public health. A chronic fluoride ingestion of 1 ppm of fluoride in drinking water can cause mottling of the teeth (fluorosis) and an exposure of 1.7 ppm will produce mottling in 30%–50% of patients. Chemical structure
Sodium fluoride is an inorganic ionic compound, dissolving in water to give separated Na+ and F− ions. Like sodium chloride, it crystallizes in a cubic motif where both Na+ and F− occupy octahedral coordination sites; its lattice spacing, approximately 462 pm, is somewhat smaller than that of sodium chloride. Occurrence
The mineral form of NaF, villiaumite, is moderately rare. It is known from plutonic nepheline syenite rocks. Production
NaF is prepared by neutralizing hydrofluoric acid or hexafluorosilicic acid (H2SiF6), both byproducts of the reaction of fluorapatite (Ca5(PO4)3F) from phosphate rock during the production of superphosphate fertilizer. Neutralizing agents include sodium hydroxide and sodium carbonate. Alcohols are sometimes used to precipitate the NaF:
HF + NaOH → NaF + H2OFrom solutions containing HF, sodium fluoride precipitates as the bifluoride salt sodium bifluoride (NaHF2). Heating the latter releases HF and gives NaF. HF + NaF ⇌ NaHF2In a 1986 report, the annual worldwide consumption of NaF was estimated to be several million tonnes. See also
Cryolite
Fluoride therapy
References
External links
"Sodium fluoride". | Fluorine-18 has a half-life of 110 min, which requires it to be used promptly once produced; this logistical limitation hampered its adoption in the face of the more convenient technetium-99m-labelled radiopharmaceuticals. However fluorine-18 is generally considered to be a superior radiopharmaceutical for skeletal imaging. In particular it has a high and rapid bone uptake accompanied by very rapid blood clearance, which results in a high bone-to-background ratio in a short time. Additionally the annihilation photons produced by decay of 18F have a high energy of 511 keV compared to the 140 keV photons of 99mTc. Chemistry
Sodium fluoride has a variety of specialty chemical applications in synthesis and extractive metallurgy. It reacts with electrophilic chlorides including acyl chlorides, sulfur chlorides, and phosphorus chloride. Like other fluorides, sodium fluoride finds use in desilylation in organic synthesis. Sodium fluoride can be used to produce fluorocarbons via the Finkelstein reaction; this process has the advantage of being simple to perform on a small scale but is rarely used on an industrial scale due to the existence of more effective techniques (e.g. Electrofluorination, Fowler process). Other uses
Sodium fluoride is used as a cleaning agent (e.g., as a "laundry sour").Sodium fluoride can be used in a nuclear molten salt reactor. Over a century ago, sodium fluoride was used as a stomach poison for plant-feeding insects. Inorganic fluorides such as fluorosilicates and sodium fluoride complex magnesium ions as magnesium fluorophosphate. They inhibit enzymes such as enolase that require Mg2+ as a prosthetic group. Thus, fluoride poisoning prevents phosphate transfer in oxidative metabolism. | 11
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Urine alkalinisation has not been found to be useful.If a person is drowsy but awake and can swallow and breathe without difficulty, the treatment can be as simple as monitoring the person closely. If the person is not breathing, it may involve mechanical ventilation until the drug has worn off. Psychiatric consult is generally recommended. Notable cases
People who are known to have died by suicide from barbiturate overdose include, Gillian Bennett, Charles Boyer, Ruan Lingyu, Victor Folke Nelson, Dalida, Jeannine "The Singing Nun" Deckers, Felix Hausdorff, Abbie Hoffman, Phyllis Hyman, Marilyn Monroe, C. P. Ramanujam, George Sanders, Jean Seberg, Lupe Vélez and the members of Heavens Gate cult. Others who have died as a result of barbiturate overdose include Pier Angeli, Brian Epstein, Judy Garland, Jimi Hendrix, Inger Stevens, Dinah Washington, Ellen Wilkinson, and Alan Wilson; in some cases these have been speculated to be suicides as well. Those who died of a combination of barbiturates and other drugs include Rainer Werner Fassbinder, Dorothy Kilgallen, Malcolm Lowry, Edie Sedgwick and Kenneth Williams. Dorothy Dandridge died of either an overdose or an unrelated embolism. Ingeborg Bachmann may have died of the consequences of barbiturate withdrawal (she was hospitalized with burns, the doctors treating her not being aware of her barbiturate addiction). Maurice Chevalier attempted suicide in March 1971 by swallowing a large amount of barbiturates and slitting his wrists. While he lived, he suffered severe organ damage as a result and died from multiple organ failure nine months later. | Transient erythroblastopenia of childhood (TEC) is a slowly developing anemia of early childhood characterized by gradual onset of pallor. Signs and symptoms
Individuals with TEC have a median age of presentation of 18–26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years. Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels. Cause
The cause of TEC is unknown, but it thought to be triggered by a viral infection. While rare cases have been attributed to infection with Parvovirus B19, the majority of cases are not related to Parvovirus infection. This is in contrast to transient aplastic crisis, seen in patients with hemoglobinopathies such as sickle cell disease, which is usually caused by Parvovirus infection. Diagnosis
Children typically present with a moderate normocytic anemia (usual range: Hemoglobin 5-8 g/dL) and reticulocytopenia. Mean corpuscular volume (MCV) is usually normal for age. Hemoglobin F levels are also typically normal. Prognosis
Most patients recover completely within 1–2 months. However many reported cases have lasted 18–24 months and longer. References
External links
ped/2279 at eMedicine | 0-1
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There was very little difference between mothers who had high caffeine consumption during pregnancy as opposed to mothers who did not have high consumption of caffeine during their pregnancy.Caffeine in younger children has been found to shorten their sleep duration and increase daytime sleepiness. One study, which looked at children ages six to ten years of age, found that those who consistently consumed caffeine lost about 15 minutes of sleep each night. In most cases where younger children are drinking high amounts of caffeine, parents usually buy their children soft drinks, iced tea, or energy drinks without realizing the amount of caffeine these drinks contain or the implications they have on their children.30% of adolescent adults in a survey were found to consume caffeine daily. Individuals with higher caffeine consumption, tended to feel an increase in wakefulness after sleep onset, shorter sleep durations, and longer daytime sleep. Those who consumed high amounts of caffeine daily, were found to be 1.9 times more likely to have difficulty sleeping and 1.8 times more likely to feel sleepy in the morning compared to those who consume almost no caffeine. Individuals with higher caffeine consumption felt an increase in wakefulness after sleep onset, shorter sleep durations, and longer daytime sleep. The higher consumption time for adolescent adults tends to be on the weekends, while the lowest consumption is midweek. This is assumed to be from greater social opportunities among adolescence. Mechanism of caffeine
Caffeine is an adenosine receptor antagonist. | The neurologic deficits related to central venous thromboses does not necessarily affect one side of the body or one arterial or brain territory as is more common "arterial" strokes. Bilateral 6th cranial nerve palsies may occur, causing abnormalities related to eye movement, but this is rare.40% of people have seizures, although it is more common in women who develop sinus thrombosis peripartum (in the period before and after giving birth). These are mostly seizures affecting only one part of the body and unilateral (occurring on one side), but occasionally the seizures are generalised and rarely they lead to status epilepticus (persistent or recurrent seizure activity for a long period of time).In the elderly, many of the aforementioned symptoms may not occur. Common symptoms in the elderly with this condition are otherwise unexplained changes in mental status and a depressed level of consciousness.The pressure around the brain may rise, causing papilledema (swelling of the optic disc) which may be experienced as visual obscurations. In severely raised intracranial pressure, the level of consciousness is decreased, the blood pressure rises, the heart rate falls and there is abnormal posturing.Focal neurologic deficits may occur hours to days after the headache in 50% of cases, this may present as hemiparesis (unilateral weakness) if due to infarction of the frontal or parietal lobe which are drained by the vein of Trolard. Focal deficits may also present as aphasia or confusion if the vein of Labbe (responsible for draining the temporal lobe) is affected. | 0-1
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Normocytic anemia is a type of anemia and is a common issue that occurs for men and women typically over 85 years old. Its prevalence increases with age, reaching 44 percent in men older than 85 years. The most common type of normocytic anemia is anemia of chronic disease. Classification
A normocytic anemia is when the red blood cells (RBCs) are of normal size. Normocytic anemia is defined when the mean corpuscular volume (MCV) is between 80 and 100 femtolitres (fL), which is within the normal and expected range. However, the hematocrit and hemoglobin are decreased. In contrast, microcytic anemias are defined as an anemia with a mean corpuscular volume (MCV) less than 80 fL and macrocytic anemias have a mean corpuscular volume over 100 fL. Diagnosis
To aid with determining the underlying cause of the normocytic anemia, a lab test is done on reticulocyte count. A reticulocyte count that is high, normal or low will aid with the classification process. A high reticulocyte count signifies that bone marrow processes are normal. A low reticulocyte count would signify there is a problem at the level of the bone marrow, which produce the stem cells. Acute blood loss would result in a high reticulocyte count, as bone marrow processes are normal and the bone marrow responds accordingly to the bodys need for blood. | Treatment for anemia due to chronic diseases, such as kidney disease, focus on healing the primary condition first. Dietary foods or supplements should be added if anemia is due to a lack of a particular vitamin. Erythropoietin may be considered if anemia is severe. Erythropoietin will stimulate the bone marrow to make more blood cells. References
External links
Entry on aafp.org | 11
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Individuals with pre-existing conditions such as diabetes are also at a higher risk. Age also affects the severity of the disease, with more than one-third of deaths being in the 65-84 age group. History
The first case of what was later named coccidioidomycosis was described in 1892 in Buenos Aires by Alejandro Posadas, a medical intern at the Hospital de Clínicas "José de San Martín". Posadas established an infectious character of the disease after being able to transfer it in laboratory conditions to lab animals. In the U.S., Dr. E. Rixford, a physician from a San Francisco hospital, and T. C. Gilchrist, a pathologist at Johns Hopkins Medical School, became early pioneers of clinical studies of the infection. They decided that the causative organism was a Coccidia-type protozoan and named it Coccidioides immitis (resembling Coccidia, not mild).Dr. William Ophüls, a professor at Stanford University Hospital (San Francisco), discovered that the causative agent of the disease that was at first called Coccidioides infection and later coccidioidomycosis was a fungal pathogen, and coccidioidomycosis was also distinguished from Histoplasmosis and Blastomycosis. Further, Coccidioides immitis was identified as the culprit of respiratory disorders previously called San Joaquin Valley fever, desert fever, and Valley fever, and a serum precipitin test was developed by Charles E. Smith that was able to detect an acute form of the infection. | By including the cost for trichiasis treatment, the estimated overall cost for the disease increases to about $US 8 billion. References
External links
CDC Disease Info trachomaCelia W. Dugger (31 March 2006), "Preventable Disease Blinds Poor in Third World", The New York Times
Photographs of trachoma patients
Trachoma Atlas
International Trachoma Initiative | 0-1
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Diagnosis
A rare autoimmune disease characterized by recurrent urticaria (nettle rash), first described in the 1970s. There is no defined paradigm for the syndrome aetiology and severity in progression. Diagnosis is confirmed with the identification of at least two conditions from: venulitis on skin biopsy, arthritis, ocular inflammation, abdominal pain or positive C1q antibodies to immune complexes. It is this last category, anti-C1q antibodies, that all HUV patients test positive for. In vitro experiments and mouse models of the disease have not thoroughly determined the link between these antibodies and the disease, even though the link is so pronounced. Treatment
Unfortunately there are no known specific therapies for HUV. The regime of prescription steroids and other immunosuppressive drugs aims to dampen the bodys production of anti-C1q antibodies. However, this again renders the individual immunocompromised. Popular culture
Urticarial vasculitis is featured prominently in the 2010 documentary film Fat, Sick and Nearly Dead. The main character and narrator has the disease. See also
Cutaneous small-vessel vasculitis
List of cutaneous conditions
References
== External links == | Bakers itch is a cutaneous reaction caused by bites of Acarus siro, the flour mite. See also
List of mites associated with cutaneous reactions
List of cutaneous conditions
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It must be emphasised that this is by no means an exhaustive list of stressful life events, because the events which trigger brief reactive psychosis tend, due to the individualistic nature of human psychology, to be extremely personalized. BRP may be the first breakdown for someone with a chronic psychiatric disorder but only time will tell whether the disorder will be brief or lifelong, whether BRP or a chronic condition that is controlled well enough by medication that symptoms do not return.The condition usually resolves spontaneously within a time span of weeks to months, with the severity of the symptoms reducing continuously over the period in question. A primary goal of treatment is to prevent patients who are either suicidal or homicidal from harming themselves or others during the episode. Cause/pathophysiology
The exact cause of brief psychotic disorder is not known. One theory suggests a genetic link, because the disorder is more common in people who have family members with mood disorders, such as depression or bipolar disorder. Another theory suggests that the disorder is caused by poor coping skills, as a defense against or escape from a particularly frightening or stressful situation. These factors may create a vulnerability to develop brief psychotic disorder. In most cases, the disorder is triggered by a major stress or traumatic event. In females, a low estrogen state (which may occur premenstrual, postpartum, or perimenopausal) can trigger sudden, short-lived psychosis. The psychosis is often linked to an underlying bipolar or schizophrenic condition. | Long-term use of topical steroids can lead to secondary infection with fungus or bacteria (see tinea incognito), skin atrophy, telangiectasia (prominent blood vessels), skin bruising and fragility.The use of the finger tip unit may be helpful in guiding how much topical steroid is required to cover different areas of the body. Adverse effects
Hypothalamic–pituitary–adrenal axis (HPA) suppression
Cushings syndrome
Diabetes mellitus
Osteoporosis
Topical steroid addiction
Allergic contact dermatitis (see steroid allergy)
Steroid atrophy
Perioral dermatitis: This is a rash that occurs around the mouth and the eye region that has been associated with topical steroids. Ocular effects: Topical steroid drops are frequently used after eye surgery but can also raise intraocular pressure (IOP) and increase the risk of glaucoma, cataract, retinopathy as well as systemic adverse effects. Tachyphylaxis: The acute development of tolerance to the action of a drug after repeated doses. Significant tachyphylaxis can occur by day 4 of therapy. Recovery usually occurs after 3 to 4 days rest. This has led to therapies such as 3 days on, 4 days off; or one week on therapy, and one week off therapy. Delivery-related adverse effects
Other local adverse effects: These include facial hypertrichosis, folliculitis, miliaria, genital ulcers, and granuloma gluteale infantum. Long-term use has resulted in Norwegian scabies, Kaposis sarcoma, and other unusual dermatosis. Safety in pregnancy
A 2015 meta-analysis of observational studies of pregnancies found no association between mothers use of topical steroids and type of delivery, APGAR score, birth defects, or prematurity. Classification systems
Seven-class System
The U.S. utilizes 7 classes, which are classified by their ability to constrict capillaries and cause skin blanching. | 0-1
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The centre–surround structures are mathematically equivalent to the edge detection algorithms used by computer programmers to extract or enhance the edges in a digital photograph. Thus, the retina performs operations on the image-representing impulses to enhance the edges of objects within its visual field. For example, in a picture of a dog, a cat and a car, it is the edges of these objects that contain the most information. In order for higher functions in the brain (or in a computer for that matter) to extract and classify objects such as a dog and a cat, the retina is the first step to separating out the various objects within the scene. As an example, the following matrix is at the heart of a computer algorithm that implements edge detection. This matrix is the computer equivalent to the centre–surround structure. In this example, each box (element) within this matrix would be connected to one photoreceptor. The photoreceptor in the centre is the current receptor being processed. The centre photoreceptor is multiplied by the +1 weight factor. The surrounding photoreceptors are the "nearest neighbors" to the centre and are multiplied by the −1/8 value. The sum of all nine of these elements is finally calculated. This summation is repeated for every photoreceptor in the image by shifting left to the end of a row and then down to the next line. The total sum of this matrix is zero, if all the inputs from the nine photoreceptors are of the same value. | It passes through the other layers, creating the optic disc in primates.Additional structures, not directly associated with vision, are found as outgrowths of the retina in some vertebrate groups. In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it supplies oxygen and nutrients to the eye, and may also aid in vision. Reptiles have a similar, but much simpler, structure.In adult humans, the entire retina is approximately 72% of a sphere about 22 mm in diameter. The entire retina contains about 7 million cones and 75 to 150 million rods. The optic disc, a part of the retina sometimes called "the blind spot" because it lacks photoreceptors, is located at the optic papilla, where the optic-nerve fibres leave the eye. It appears as an oval white area of 3 mm². Temporal (in the direction of the temples) to this disc is the macula, at whose centre is the fovea, a pit that is responsible for our sharp central vision but is actually less sensitive to light because of its lack of rods. Human and non-human primates possess one fovea, as opposed to certain bird species, such as hawks, who are bifoviate, and dogs and cats, who possess no fovea but a central band known as the visual streak. Around the fovea extends the central retina for about 6 mm and then the peripheral retina. The farthest edge of the retina is defined by the ora serrata. | 11
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The Charcot–Marie–Tooth Association classifies the chemotherapy drug vincristine as a "definite high risk" and states, "vincristine has been proven hazardous and should be avoided by all CMT patients, including those with no symptoms." Several corrective surgical procedures can be done to improve the physical condition of the affected individuals. Orthotics
If the muscles of the lower extremities are weak, it makes sense to prescribe custom-fabricated orthotics. Depending on which muscle groups are affected, the correct orthoses with appropriate functional elements should be prescribed. A weakness of the Musculus tibialis anterior, which lifts the feet, is usually accompanied by an atrophy of the Musculus gastrocnemius which, together with the Musculus soleus, forms the Musculus triceps surae (distal calf muscles), occurs causing the known "stork leg deformity". In most cases, ankle-foot orthoses that have functional elements for the foot lifting and adjustable control of the lowering of the forefoot make sense. Weak calf muscles lead to insufficient activation of the forefoot lever. This leads to an additional increasing uncertainty when standing and walking. If the calf muscles are weak, an orthosis should therefore be equipped with functional elements to activate the forefoot lever. An orthotic joint with an adjustable dynamic dorsiflexion stop with strong spring in combination with a lower leg shell in front of the shin is recommended for this. Such orthoses help to control foot drop, instability of the foot and ankle and offer the patient a better sense of balance when standing and walking without restricting mobility and the dynamics of the ankle joint. | Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménières disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the persons symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition. Surgery
Surgical treatments, such as a semi-circular canal occlusion, exist for severe and persistent cases that fail vestibular rehabilitation (including particle repositioning and habituation therapy). As they carry the same risks as any neurosurgical procedure, they are reserved as last resorts. References
Further reading
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Breast development, also known as mammogenesis, is a complex biological process in primates that takes place throughout a females life. It occurs across several phases, including prenatal development, puberty, and pregnancy. At menopause, breast development ceases and the breasts atrophy. Breast development results in prominent and developed structures on the chest known as breasts in primates, which serve primarily as mammary glands. The process is mediated by an assortment of hormones (and growth factors), the most important of which include estrogen, progesterone, prolactin, and growth hormone. Biochemistry
Hormones
The master regulators of breast development are the steroid hormones, estrogen and progesterone, growth hormone (GH), mostly via its secretory product, insulin-like growth factor 1 (IGF-1), and prolactin. These regulators induce the expression of growth factors, such as amphiregulin, epidermal growth factor (EGF), IGF-1, and fibroblast growth factor (FGF), which in turn have specific roles in breast growth and maturation.At puberty, gonadotropin-releasing hormone (GnRH) is secreted in a pulsatile manner from the hypothalamus. GnRH induces the secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), from the pituitary gland. The secreted gonadotropins travel through the bloodstream to the ovaries and trigger the secretion of estrogen and progesterone in fluctuating amounts during each menstrual cycle. Growth hormone (GH), which is secreted from the pituitary gland, and insulin-like growth factor 1 (IGF-1), which is produced in the body in response to GH, are growth-mediating hormones. | As both the IGF-1R and the EGFR are independently essential for mammary gland development, and as combined application of IGF-1 and EGF, through their respective receptors, has been found to synergistically stimulate the growth of human breast epithelial cells, these growth factor systems appear to work together in mediating breast development.Elevated levels of HGF and, to a lesser extent, IGF-1 (by 5.4-fold and 1.8-fold, respectively), in breast stromal tissue, have been found in macromastia, a very rare condition of extremely and excessively large breast size. Exposure of macromastic breast stromal tissue to non-macromastic breast epithelial tissue was found to cause increased alveolar morphogenesis and epithelial proliferation in the latter. A neutralizing antibody for HGF, but not for IGF-1 or EGF, was found to attenuate the proliferation of breast epithelial tissue caused by exposure to macromastic breast stromal cells, potentially directly implicating HGF in the breast growth and enlargement seen in macromastia. Also, a genome-wide association study has highly implicated HGF and its receptor, c-Met, in breast cancer aggressiveness. Lactation
Upon parturition (childbirth), estrogen and progesterone rapidly drop to very low levels, with progesterone levels being undetectable. Conversely, prolactin levels remain elevated. As estrogen and progesterone block prolactin-induced lactogenesis by suppressing prolactin receptor (PRLR) expression in breast tissue, their sudden absence results in the commencement of milk production and lactation by prolactin. Expression of the PRLR in breast tissue may increase by as much as 20-fold when estrogen and progesterone levels drop upon childbirth. | 11
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In this situation, the individual would have three copies of part of one chromosome (two normal copies and the portion that exists on the derivative chromosome) and only one copy of part of the other chromosome involved in the derivative chromosome. Robertsonian translocations, for example, account for a very small minority of Down syndrome cases (<5%). The formation of one isochromosome results in partial trisomy of the genes present in the isochromosome and partial monosomy of the genes in the lost arm. Aneugens
Agents capable of causing aneuploidy are called aneugens. Many mutagenic carcinogens are aneugens. X-rays, for example, may cause aneuploidy by fragmenting the chromosome; it may also target the spindle apparatus. Other chemicals such as colchicine can also produce aneuploidy by affecting microtubule polymerization. Exposure of males to lifestyle, environmental and/or occupational hazards may increase the risk of spermatozoa aneuploidy. Tobacco smoke contains chemicals that cause DNA damage. Smoking also can induce aneuploidy. For instance, smoking increases chromosome 13 disomy in spermatozoa by 3-fold, and YY disomy by 2-fold.Occupational exposure to benzene is associated with a 2.8-fold increase of XX disomy and a 2.6-fold increase of YY disomy in spermatozoa.Pesticides are released to the environment in large quantities so that most individuals have some degree of exposure. The insecticides fenvalerate and carbaryl have been reported to increase spermatozoa aneuploidy. Occupational exposure of pesticide factory workers to fenvalerate is associated with increased spermatozoa DNA damage. Exposure to fenvalerate raised sex chromosome disomy 1.9-fold and disomy of chromosome 18 by 2.6-fold. | For example, in melanoma patients, high somatic copy number alterations are associated with less effective response to immune checkpoint blockade anti–CTLA4 (cytotoxic T lymphocyte–associated protein 4) therapy.A research work published in 2008 focuses on the mechanisms involved in aneuploidy formation, specifically on the epigenetic origin of aneuploid cells. Epigenetic inheritance is defined as cellular information other than the DNA sequence itself, that is still heritable during cell division. DNA methylation and histone modifications comprise two of the main epigenetic modifications important for many physiological and pathological conditions, including cancer. Aberrant DNA methylation is the most common molecular lesion in cancer-cells, even more frequent than gene mutations. Tumor suppressor gene silencing by CpG island promoter hypermethylation is supposed to be the most frequent epigenetic modification in cancer cells. Epigenetic characteristics of cells may be modified by several factors including environmental exposure, deficiencies of certain nutrients, radiation, etc. Some of the alterations have been correlated with the formation of aneuploid cells in vivo. In this study it is suggested on a growing basis of evidence, that not only genetics but also epigenetics, contribute to aneuploid cell formation. Partial aneuploidy
The terms "partial monosomy" and "partial trisomy" are used to describe an imbalance of genetic material caused by loss or gain of part of a chromosome. In particular, these terms would be used in the situation of an unbalanced translocation, where an individual carries a derivative chromosome formed through the breakage and fusion of two different chromosomes. | 11
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Linguistically responsive psychologist understand that second language acquisition is a process and they understand how to support ELLs growth in language and academically.</ref> When ELLs are referred for a psychoeducational assessment, it is difficult to isolate and disentangle what are the effects of the language acquisition process, from poor quality educational services, from what may be academic difficulties that result from processing disorders, attention problems, and learning disabilities. Additionally not having trained staff and faculty becomes more of an issue when staff is unaware of numerous types of psychological factors that immigrant children in the U.S dealing could be potentially dealing with. These factors that include acculturation, fear and/or worry of deportation, separation from social supports such as parents, language barriers, disruptions in learning experiences, stigmatization, economic challenge, and risk factors associated with poverty. In the United States, there are no set policies mandating that all districts employ bilingual school psychologist, nor are schools equipped with specific tools and resources to assist immigrant children and families. Many school districts do not have the proper personnel that is able to communicate with this population. Spanish-speaking ELL
A well trained bilingual school psychologist will be able to administer and interpret assessment all psychological testing tool. Also, an emphasis is placed on informal assessment measures such as language samples, observations, interviews, and rating scales as well as curriculum-based measurement to complement information gathered from formal assessments. | ISBN 9780205320103 OCLC 888129572
"Learning Difficulties Australia" (PDF). Vol. 40, no. 2. June 2008. Archived from the original (PDF) on 2021-01-21. Retrieved 2019-07-20. {{cite magazine}}: Cite magazine requires |magazine= (help)
"Learning Disabilities Mortality Review (LeDeR) Programme" (Annual report). National Health Service. UK. December 2017. Retrieved 3 July 2022. "Learning Disabilities: Prevalence". Social Work, Alcohol & Drugs. University of Bedfordshire. Archived from the original on 2014-10-26. Retrieved 2014-10-18. "Special Educational Needs and Disability: A. Cognition and Learning Needs". teachernet. Archived from the original on 2010-05-01. Retrieved 2010-12-08. Vickerman, Philip (2009-07-08). "Severe Learning Difficulties". Teacher Training Resource Bank. UK. Archived from the original on 2014-10-26. Retrieved 2014-10-19. Extensive further references. External links
Learning Disabilities at Curlie | 11
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Research surveys have revealed a paucity of professional, emotional support for women struggling in the weeks following delivery despite there being a heightened risk for PPD for new mothers during this transitional period. Community-based support
A lack of social support has been identified as a barrier to seeking help for postpartum depression. Peer-support programs have been identified as an effective intervention for women experiencing symptoms of postpartum depression. In-person, online, and telephone support groups are available to both women and men throughout the United States. Peer-support models are appealing to many women because they are offered in a group and outside of the mental-health setting. The website Postpartum Progress provides a comprehensive list of support groups separated by state and includes the contact information for each group. The National Alliance on Mental Illness lists a virtual support group titled "The Shades of Blue project," which is available to all women via the submission of a name and email address. Additionally, NAMI recommends the website "National Association of Professional and Peer Lactation Supports of Color" for mothers in need of a lactation supporter. Lactation assistance is available either online or in-person, if there is support nearby. Personal narratives & memoirs
Postpartum Progress is a blog focused on being a community of mothers talking openly about postpartum depression and other mental health conditions associated. Story-telling and online communities reduce the stigma around PPD and promote peer-based care. Postpartum Progress is specifically relevant to people of color and queer folks due to an emphasis on cultural competency. | Regarding gender of the child, many studies have suggested dissatisfaction in infants gender (birth of a baby girl) is a risk factor for PPD. This is because in some Asian cultures, married couples are expected by the family to have at least one son to maintain the continuity of the bloodline which might lead a woman to experience PPD if she cannot give birth to a baby boy. Europe
There is a general assumption that Western cultures are homogenous and that there are no significant differences in psychiatric disorders across Europe and the USA. However, in reality factors associated with maternal depression, including work and environmental demands, access to universal maternity leave, health care, and financial security, are regulated and influenced by local policies that differ across countries. For example, European social policies differ from country-to-country contrary to the US, all countries provide some form of paid universal maternity leave and free health care. Studies also found differences in symptomatic manifestations of PPD between European and American women. Women from Europe reported higher scores of anhedonia, self-blaming, and anxiety, while women from the USA disclosed more severe insomnia, depressive feelings, and thoughts of self-harming. Additionally, there are differences in prescribing patterns and attitudes towards certain medications between the US and Europe which are indicative of how different countries approach treatment, and their different stigmas. Africa
Africa, like all other parts of the world struggles with a burden of postpartum depression. | 11
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Disks or balls, consisting of concentric blue and white circles (usually, from inside to outside, dark blue, light blue, white, and dark blue) representing an evil eye are common apotropaic talismans in West Asia and the Balkans, found on the prows of boats and elsewhere; in some forms of the folklore, the staring eyes are supposed to bend the malicious gaze back to the sorcerer. Known as nazar (Turkish: nazar boncuğu or nazarlık), this talisman is most frequently seen in Turkey, found in or on houses and vehicles or worn as beads. The word hamsa, also spelled khamsa and hamesh, means "five" referring to the fingers of the hand. In Jewish culture, the hamsa is called the Hand of Miriam; in the Levantine Christian culture is called the Hand of Mary, in some Muslim and Balkan cultures, the Hand of Fatima. Though condemned as superstition by doctrinaire Muslims, it is almost exclusively among the Near East and Mediterranean that the belief in envious looks containing destructive power or the talismanic power of a nazar to defend against them. To adherents of other faiths in the region, the nazar is an attractive decoration. A variety of motifs to ward off the evil eye are commonly woven into tribal kilim rugs. Such motifs include a cross (Turkish: Haç) to divide the evil eye into four, a hook (Turkish: Çengel) to destroy the evil eye, or a human eye (Turkish: Göz) to avert the evil gaze. | Clinical significance
Anything arising from the intervertebral disc may be termed discogenic in particular when referring to associated pain as discogenic pain. Herniation
A spinal disc herniation, commonly referred to as a slipped disc, can happen when unbalanced mechanical pressures substantially deform the anulus fibrosus, allowing part of the nucleus to obtrude. These events can occur during peak physical performance, during traumas, or as a result of chronic deterioration (typically accompanied with poor posture), and has been associated with a Propionbacterium acnes infection. Both the deformed anulus and the gel-like material of the nucleus pulposus can be forced laterally or posteriorly, distorting local muscle function and putting pressure on the nearby nerve. This can give symptoms typical of nerve root entrapment, which can vary between paresthesia, numbness, chronic and/or acute pain, either locally or along the dermatome served by the entrapped nerve, loss of muscle tone and decreased homeostatic performance. The disc is not physically slipped; it bulges, usually in just one direction. Another kind of herniation, of the nucleus pulposus, can happen as a result of the formation of Schmorls nodes on the intervertebral disc. This is referred to as vertical disc herniation. Degeneration
Before age 40, approximately 25% of people show evidence of disc degeneration at one or more levels. Beyond age 40, more than 60% of people show evidence of disc degeneration at one or more levels on magnetic resonance imaging (MRI). These degenerative changes are a normal part of the ageing process and do not correlate to pain. | 0-1
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These include medications such as methadone, amiodarone, citalopram, and fluconazole. Other medications may increase the risk for a low level of potassium in the blood, thereby indirectly increasing the risk for QT prolongation. For example, dexamethasone, hydrochlorothiazide, and theophylline can lower the level of potassium in the blood. CNS depression
Lofexidine can depress the central nervous system (CNS), which, in combination with other CNS depressants, may reduce a persons ability to perform tasks that require skills and attention. For example, clobazam, gabapentin, and levetiracetam all can depress the CNS. Hypotension
The risk of hypotension (low blood pressure) is increased when lofexidine is combined with other drugs that lower blood pressure. These may include losartan, metoprolol, and pramipexole. Pharmacology
Lofexidine is an agonist at the α-2A, 2B, and 2C adrenergic receptor subtypes, with the highest activity at the alpha-2A receptor. Ki represents the dissociation constant for lofexidines binding to a specific subtype of alpha-2 receptor. The smaller the Ki value, the stronger the drug binds to the receptor to exert its activity. Lofexidine inhibits the release of norepinephrine in the central and peripheral nervous system, thereby reducing some of the symptoms of opioid withdrawal, but it has no documented effect on drug craving and endogenous opioid levels. Pharmacokinetics
Lofexidines oral bioavailability is about 90%, with extensive oral absorption. Peak plasma concentrations occur at 3 hours after a single administration, with a half-life of 11 hours. Lofexidine is extensively metabolized by the liver, and primarily cleared by the kidney. It is 80-90% plasma protein bound. | Anemia is common in fetuses exposed to warfarin as blood constantly seeps into the interstitial fluid or amniotic cavity. High doses of warfarin and heavy bleeding lead to abortion and stillbirth. Osteocalcin is another protein dependent on vitamin K for correct folding and function. Osteocalcin is normally secreted by osteoblast cells and plays a role in aiding correct bone mineralization and bone maturation. In the presence of warfarin and subsequent absence of vitamin K and active osteocalcin, bone mineralization and growth are stunted. Prevention
Fetal warfarin syndrome is prevented by withholding prescription to pregnant women or those trying to conceive. As warfarin can remain in the mothers body for up to five days, warfarin should not be administered in the days leading up to conception. Doctors must take care to ensure women of reproductive age are aware of the risks to the baby should they get pregnant, before prescribing warfarin. For some women, such as those with prosthetic heart valves, anticoagulation medication cannot be suspended during pregnancy as the risk of thrombus and emboli is too high. In such cases an alternate anticoagulant, which cannot pass through the placental barrier to the fetus, is proscribed in place of warfarin. Heparin is one such anticoagulant medication, although its efficacy in patients with prosthetic heart valves is not well established. New anticoagulant medications, which are efficacious and non-teratogenic such as ximelagatran continue to be developed. | 0-1
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