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Apart from the mainstream approaches detailed above, there are numerous treatments of unproven effectiveness, ranging from herbal remedies to otherwise alternative treatments, including Aloe vera, Myrtus communis, Rosa damascena, potassium alum, zinc sulfate, nicotine, polio virus vaccine and prostaglandin E2. Prognosis
By definition, there is no serious underlying medical condition, and most importantly, the ulcers do not represent oral cancer nor are they infectious. However, aphthae are capable of causing significant discomfort. There is a spectrum of severity, with symptoms ranging from a minor nuisance to disabling. Due to pain during eating, weight loss may develop as a result of not eating in severe cases of aphthous stomatitis. Usually, the condition lasts for several years before spontaneously disappearing in later life. Epidemiology
Aphthous stomatitis affects between 5% and 66% of people, with about 20% of individuals in most populations having the condition to some degree. This makes it the most common disease of the oral mucosa. Aphthous stomatitis occurs worldwide, but is more common in developed countries.Within nations, it is more common in higher socioeconomic groups. Males and females are affected in an equal ratio, and the peak age of onset between 10 and 19 years. About 80% of people with aphthous stomatitis first developed the condition before the age of 30. There have been reports of ethnic variation. For example, in the United States, aphthous stomatitis may be three times more common in white-skinned people than black-skinned people. | Some suggest that screening for celiac disease should form part of the routine work up for individuals complaining of recurrent oral ulceration. Many of the systemic diseases cause other symptoms apart from oral ulceration, which is in contrast to aphthous stomatitis where there is isolated oral ulceration. Patch testing may be indicated if allergies are suspected (e.g. a strong relationship between certain foods and episodes of ulceration). Several drugs can cause oral ulceration (e.g. nicorandil), and a trial substitution to an alternative drug may highlight a causal relationship.Tissue biopsy is not usually required, unless to rule out other suspected conditions such as oral squamous cell carcinoma. The histopathologic appearance is not pathognomonic (the microscopic appearance is not specific to the condition). Early lesions have a central zone of ulceration covered by a fibrinous membrane. In the connective tissue deep to the ulcer there is increased vascularity and a mixed inflammatory infiltrate composed of lymphocytes, histiocytes and polymorphonuclear leukocytes. The epithelium on the margins of the ulcer shows spongiosis and there are many mononuclear cells in the basal third. There are also lymphocytes and histiocytes in the connective tissue surrounding deeper blood vessels near to the ulcer, described histologically as "perivascular cuffing". Classification
Aphthous stomatitis has been classified as a type of non-infectious stomatitis (inflammation of the mouth). | 11
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The actual variability between gestational age as estimated from the beginning of the last menstrual period (without the use of any additional method mentioned in previous section) is substantially larger because of uncertainty which menstrual cycle gave rise to the pregnancy. For example, the menstruation may be scarce enough to give the false appearance that an earlier menstruation gave rise to the pregnancy, potentially giving an estimated gestational age that is approximately one month too large. Also, vaginal bleeding occurs during 15-25% of first trimester pregnancies, and may be mistaken as menstruation, potentially giving an estimated gestational age that is too low. Uses
Gestational age is used for example for:
The events of prenatal development, which usually occur at specific gestational ages. Hence, the gestational timing of a fetal toxin exposure, fetal drug exposure or vertically transmitted infection can be used to predict the potential consequences to the fetus. Estimated date of delivery
Scheduling prenatal care
Estimation of fetal viability
Calculating the results of various prenatal tests, (for example, in the triple test). Birth classification into for example preterm, term or postterm. Classification of infant deaths and stillbirths
Postnatally (after birth) to estimate various risk factors
Estimation of due date
The mean pregnancy length has been estimated to be 283.4 days of gestational age as timed from the first day of the last menstrual period and 280.6 days when retrospectively estimated by obstetric ultrasound measurement of the fetal biparietal diameter (BPD) in the second trimester. | In a similar manner EDTA is used in the cement industry for the determination of free lime and free magnesia in cement and clinkers.The solubilisation of Fe3+ ions at or below near neutral pH can be accomplished using EDTA. This property is useful in agriculture including hydroponics. However, given the pH dependence of ligand formation, EDTA is not helpful for improving iron solubility in above neutral soils. Otherwise, at near-neutral pH and above, iron(III) forms insoluble salts, which are less bioavailable to susceptible plant species. Scrubbing
Aqueous [Fe(EDTA)]− is used for removing ("scrubbing") hydrogen sulfide from gas streams. This conversion is achieved by oxidising the hydrogen sulfide to elemental sulfur, which is non-volatile:
2 [Fe(EDTA)]− + H2S → 2 [Fe(EDTA)]2− + S + 2 H+In this application, the iron(III) centre is reduced to its iron(II) derivative, which can then be reoxidised by air. In similar manner, nitrogen oxides are removed from gas streams using [Fe(EDTA)]2−. The oxidising properties of [Fe(EDTA)]− are also exploited in photography, where it is used to solubilise silver particles. Ion-exchange chromatography
EDTA was used in separation of the lanthanide metals by ion-exchange chromatography. Perfected by F. H. Spedding et al. in 1954, the method relies on the steady increase in stability constant of the lanthanide EDTA complexes with atomic number. Using sulfonated polystyrene beads and Cu2+ as a retaining ion, EDTA causes the lanthanides to migrate down the column of resin while separating into bands of pure lanthanides. | 0-1
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They are generally more common on toes than on fingers, develop at 15–29 years, and are more common in women than in men. Fibrous cephalic plaques are present in about 25% of people with TSC. These are raised, discoloured areas usually found on the forehead, but sometimes on the face or elsewhere on the scalp. Shagreen patches are present in about half of people with TSC, appearing in childhood. They are areas of thick leathery skin that are dimpled like an orange peel, and pigmented, they are usually found on the lower back or nape of the neck, or scattered across the trunk or thighs. The frequency of these lesions rises with age. Dental enamel pits are found in almost all adults with TSC. Intraoral fibromas are small surface-tumours found in the gums, inside the cheeks or tongue. Gum (gingival) fibromas are found in about 20-50% of people with TSC, more commonly in adults. Eyes
Retinal lesions, called astrocytic hamartomas (or "phakomas"), which appear as a greyish or yellowish-white lesion in the back of the globe on the ophthalmic examination. Astrocytic hamartomas can calcify, and they are in the differential diagnosis of a calcified globe mass on a CT scan.Nonretinal lesions associated with TSC include:
Coloboma
Angiofibromas of the eyelids
Papilledema (related to hydrocephalus)
Pancreas
Pancreatic neuroendocrine tumours have been described in rare cases of TSC. Variability
Individuals with TSC may experience none or all of the clinical signs discussed above. The following table shows the prevalence of some of the clinical signs in individuals diagnosed with TSC. | Neurological
Three types of brain tumours are associated with TSC:
Giant cell astrocytoma: (grows and blocks the cerebrospinal fluid flow, leading to dilatation of ventricles causing headache and vomiting)
Cortical tubers: after which the disease is named
Subependymal nodules: form in the walls of ventriclesClassic intracranial manifestations of TSC include subependymal nodules and cortical/subcortical tubers.The tubers are typically triangular in configuration, with the apex pointed towards the ventricles, and are thought to represent foci of abnormal neuronal migration. The T2 signal abnormalities may subside in adulthood, but will still be visible on histopathological analysis. On magnetic resonance imaging (MRI), TSC patients can exhibit other signs consistent with abnormal neuron migration such as radial white matter tracts hyperintense on T2WI and heterotopic grey matter.Subependymal nodules are composed of abnormal, swollen glial cells and bizarre multinucleated cells which are indeterminate for glial or neuronal origin. Interposed neural tissue is not present. These nodules have a tendency to calcify as the patient ages. A nodule that markedly enhances and enlarges over time should be considered suspicious for transformation into a subependymal giant cell astrocytoma, which typically develops in the region of the foramen of Monro, in which case it is at risk of developing an obstructive hydrocephalus.A variable degree of ventricular enlargement is seen, either obstructive (e.g. by a subependymal nodule in the region of the foramen of Monro) or idiopathic in nature. Neuropsychiatric
About 90% of people with TSC develop a range of neurodevelopmental, behavioural, psychiatric, and psychosocial difficulties. The "TSC‐associated neuropsychiatric disorders" are abbreviated TAND. | 11
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At the height of their career, they had the highest paid act in vaudeville. They also appeared in the movies Freaks and Chained for Life. Lucio and Simplicio Godina of Samar, Philippines (1908–1936)
Masha and Dasha Krivoshlyapova of Moscow, Russia (1950–2003), the rarest form of conjoined twins, one of few cases of dicephalus tetrabrachius tripus (two heads, four arms, three legs)
Ronnie and Donnie Galyon of Ohio (1951–2020), omphalopagus; longest-lived conjoined twins in the world at 68 years and 250 days. Tjitske and Folkje de Vries of Mûnein, Netherlands (b. 1953)
Wariboko and Tamunotonye Davies, born July 25, 1953, in Kano, Nigeria. Separated in London by a team led by Ian Aird. Tamunotonye died postoperatively. Wariboko became a nurse. Lori and George Schappell, born September 18, 1961, in Reading, Pennsylvania, American entertainers, craniopagus. As of 2022, they are the worlds oldest living conjoined twins. Ganga and Jamuna Mondal of India, born 1969 or 1970, known professionally as The Spider Girls and The Spider Sisters. Ischiopagus. Anna and Barbara Rozycki (born 1970), the first conjoined twins successfully separated. Ma Nan Soe and Ma Nan San (born 1971 in Myanmar), separated in July 1971 at Yangon Pediatric Hospital. They were joined from chest to belly button. Ma Nan San died after one month and seven days after operation. Elisa and Lisa Hansen, Ogden, Utah (1977–2020). Born by Caesarean section on October 18, 1977, were conjoined at the top of their head (craniopagus). They were separated 1979 after 16-hour surgery, were first to both survive surgery. | See also
Craniopagus parasiticus is another form of partial twinning which results in two heads kept alive by a single torso. In these cases a second, vestigial torso is present, and the heads are joined directly to one another. Diprosopus is a condition in which there are duplicated facial features on one head. Polycephaly is a general term about organisms with more than one head. == References == | 0-1
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These include Haemophilus, Moraxella and Neisseria pathogens, and infections caused by Acinectobacter baumannii.The antibacterial spectrum of ceftazidime/avibactam includes nearly all Enterobacteriaceae, including ceftazidime-resistant strains. The activity of ceftazidime/avibactam against the important hospital pathogen Pseudomonas aeruginosa is variable, due to the potential presence of other resistance mechanisms in addition to β-lactamase production. Synergy was observed for avibactam with ceftazidime in the Burkholderia cepacia complex. Adverse events
When used to treat life-threatening infections, ceftazidime/avibactam is more likely than carbapenem antibiotics to cause serious adverse events, including worsening kidney function and gastrointestinal adverse effects. Mechanism of action
Bacterial resistance to cephalosporins is often due to bacterial production of β-lactamase enzymes that deactivate these antibiotics. Avibactam inhibits some (but not all) bacterial β-lactamases. Also, some bacteria are resistant to cephalosporins by other mechanisms, and therefore avibactam doesnt work. Avibactam is not active against New Delhi metallo-β-lactamase 1 (NDM-1). Avibactam inhibits Klebsiella pneumoniae carbapenemases (KPCs), and AmpC-type β-lactamases, which are resistant to the other clinically-available β-lactamases, tazobactam and clavulanic acid. Regulatory
It was granted approval for marketing in the United States by the Food and Drug Administration (FDA) in February 2015. It was granted approval for marketing in Europe by the European Medicines Agency in 2016. During its clinical development, ceftazidime/avibactam was designated as a Qualified Infectious Disease Product under the Generating Antibiotic Incentives Now provision of the Food and Drug Administration Safety and Innovation Act. Development of ceftazidime/avibactam was fast-tracked by the FDA due to the shortage of drugs for treatment of infections due to antibiotic-resistant bacteria. References
External links
"Avibactam mixture with ceftazidime". | Drug Information Portal. U.S. National Library of Medicine. | 11
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They develop from cells that line both the hollow cavities of the brain and the canal containing the spinal cord, but they usually arise from the floor of the fourth ventricle, situated in the lower back portion of the brain, where they may produce headache, nausea and vomiting by obstructing the flow of cerebrospinal fluid. This obstruction may also cause hydrocephalus. They may also arise in the spinal cord, conus medullaris and supratentorial locations. Other symptoms can include (but are not limited to): loss of appetite, difficulty sleeping, temporary inability to distinguish colors, uncontrollable twitching, seeing vertical or horizontal lines when in bright light, and temporary memory loss. It should be remembered that these symptoms also are prevalent in many other illnesses not associated with ependymoma.About 10% of ependymomas are benign myxopapillary ependymoma (MPE). MPE is a localized and slow-growing low-grade tumor, which originates almost exclusively from the lumbosacral nervous tissue of young patients. On the other hand, it is the most common tumor of the lumbosacral canal comprising about 90% of all tumoral lesions in this region.Although some ependymomas are of a more anaplastic and malignant type, most of them are not anaplastic. Well-differentiated ependymomas are usually treated with surgery. For other ependymomas, total surgical removal is the preferred treatment in addition to radiation therapy. The malignant (anaplastic) varieties of this tumor, malignant ependymoma and the ependymoblastoma, are treated similarly to medulloblastoma but the prognosis is much less favorable. Malignant ependymomas may be treated with a combination of radiation therapy and chemotherapy. | Ependymoblastomas, which occur in infants and children younger than 5 years of age, may spread through the cerebrospinal fluid and usually require radiation therapy. The subependymoma, a variant of the ependymoma, is apt to arise in the fourth ventricle but may occur in the septum pellucidum and the cervical spinal cord. It usually affects people over 40 years of age and more often affects men than women.Extraspinal ependymoma (EEP), also known as extradural ependymoma, may be an unusual form of teratoma or may be confused with a sacrococcygeal teratoma. Treatment
Guidelines for initial management for ependymoma are maximum surgical resection followed by radiation. Chemotherapy is of limited use and reserved for special cases including young children and those with tumor present after resection. Prophylactic craniospinal irradiation is of variable use and is a source of controversy given that most recurrence occurs at the site of resection and therefore is of debatable efficacy. Confirmation of cerebrospinal infiltration warrants more expansive radiation fields.Prognosis of recurrence is poor and often indicates palliative care to manage symptoms. References
External links
Brain and Spinal Tumors: Hope Through Research (National Institute of Neurological Disorders and Stroke) | 11
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Iatrogenesis is the causation of a disease, a harmful complication, or other ill effect by any medical activity, including diagnosis, intervention, error, or negligence. First used in this sense in 1924, the term was introduced to sociology in 1976 by Ivan Illich, alleging that industrialized societies impair quality of life by overmedicalizing life. Iatrogenesis may thus include mental suffering via medical beliefs or a practitioners statements. Some iatrogenic events are obvious, like amputation of the wrong limb, whereas others, like drug interactions, can evade recognition. In a 2013 estimate, about 20 million negative effects from treatment had occurred globally. In 2013, an estimated 142,000 persons died from adverse effects of medical treatment, up from an estimated 94,000 in 1990. Iatrogenic avenues
Risk associated with medical interventions
Adverse effects of prescription drugs
Overuse of drugs (causing, for example, antibiotic resistance in bacteria)
Prescription drug interaction
Medical errors
Incorrect prescription, perhaps due to illegible handwriting or computer typos
Faulty procedures, techniques, information, methods, or equipment
Negligence
Hospital-acquired infections
Causes and consequences
Medical error and negligence
Iatrogenic conditions need not result from medical errors, such as mistakes made in surgery, or the prescription or dispensing of the wrong therapy, such as a drug. In fact, intrinsic and sometimes adverse effects of a medical treatment are iatrogenic. For example, radiation therapy and chemotherapy—necessarily aggressive for therapeutic effect – frequently produce such iatrogenic effects as hair loss, hemolytic anemia, diabetes insipidus, vomiting, nausea, brain damage, lymphedema, infertility, etc. | Iridodonesis () is the vibration or agitated motion of the iris with eye movement. This may be caused by lens subluxation, the incomplete or partial dislocation of the lens; or by aphakia, the absence of a lens. The term originated from irido- (Latin: iris) + doneo (Greek: δονεο, to shake to and fro). See also
Phacodonesis
References
External links
An example of iridodonesis on YouTube | 0-1
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This is part of a normal process in which bacteria from the environment start to grow on a babys skin. It is unknown whether the immune response that causes erythema toxicum neonatorum is helpful to the baby. Recent research indicates an association with Demodex mites infestation (demodicosis). Diagnosis
Health professionals can diagnose erythema toxicum neonatorum with a skin exam. Most cases of erythema toxicum neonatorum can be diagnosed without further testing. If more testing is needed to make a diagnosis, the contents of a lesion can be examined under a microscope. A health professional may make a small cut into a pus-filled lesion and collect a swab of pus for testing. Lesions caused by erythema toxicum neonatorum contain eosinophils and other immune cells. These cells can be seen under a microscope when a special stain is applied to the sample.Since the appearance of erythema toxicum neonatorum varies, it may be confused with other newborn rashes. Some newborn infections cause bumps or boils, which may look like erythema toxicum neonatorum. Bacterial infections, including Staphylococcus and Streptococcus infections, almost always cause additional symptoms. These symptoms may be severe, and they are usually not limited to rash. Bacterial rashes can be diagnosed by testing pus from a lesion along with a blood sample. Bacteria can be seen under a microscope with a special stain or may be found on a culture. Fungal infection with Candida may also cause a similar rash in newborns, but it usually causes additional symptoms like thrush. | Erythema toxicum neonatorum is a common, non-threatening rash in newborns. It appears in 4-70% of newborns within the first week of life, and it typically improves within 1–2 weeks. It only occurs during the newborn period, but may appear slightly later in premature babies. The rash has a variable appearance. It typically includes blotchy red spots, often with overlying firm, yellow-white bumps or pus-filled boils. There may be only a few or many lesions. The lesions can appear almost anywhere on the body, and individual lesions may appear and disappear within hours. There are no other symptoms associated with erythema toxicum neonatorum, and the rash does not have any long-term effects on the skin. Erythema toxicum neonatorum is not harmful and does not require any treatment. Epidemiology
The exact prevalence of erythema toxicum neonatorum is unknown, and studies estimate prevalence as low as 3.7 percent to as high as 72 percent. It is one of the most commonly diagnosed rashes in healthy babies. It is more common among infants born at higher gestational age and is rare among premature infants. Erythema toxicum neonatorum is more likely to develop in infants delivered vaginally. Higher birth weight is an additional risk factor. There may be a slightly increased risk in males, but this association is unclear. There are no known associations with race or ethnicity. Presentation
Erythema toxicum neonatorum usually appears during the first week of life, most often on day two. | 11
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Trimipramine is unique in that it is an exception and produces antidepressant effects without compromising or otherwise affecting REM sleep. Even long-term treatment with trimipramine for up to 2 years has not been found to suppress REM sleep. In addition, trimipramine has been found to decrease nocturnal cortisol levels to normal and to normalize cortisol response in depressed patients; hence, it normalizes the hypothalamic–pituitary–adrenal axis, whereas imipramine and other antidepressants tend to increase nocturnal cortisol secretion.In clinical studies, trimipramine has been found in doses of 50 to 200 mg/day to significantly increase sleep efficiency and total sleep time and to decrease waking time for up to 3 weeks in patients with insomnia. It also improved subjectively perceived sleep quality and well-being during daytime. Monitoring of patients upon discontinuation of trimipramine found that it did not cause rebound insomnia or worsening of sleep quality in subjective evaluations of sleep, although objective measurements found total sleep time below baseline in a subset of patients during trimipramine withdrawal. Antidopaminergic activity
Trimipramine is a weak but significant antagonist of the dopamine D1 and D2 receptors, and also binds to the D4 receptor (Ki = 275 nM). Its affinities for various monoamine receptors including the D2 and 5-HT2A receptors closely resemble those of the atypical antipsychotic clozapine. In accordance, high doses of trimipramine have been found to have antipsychotic effects in schizophrenic patients, notably without causing extrapyramidal symptoms, and trimipramine has recently been found to be effective in reducing psychotic symptoms in patients with delusional depression. | Two-thirds of the parent compound breaks down into the active metabolite N-desmethyl-zolmitriptan (183C91), while the remaining one-third separates into the other two inactive metabolites: zolmitriptan N-oxide and an indole acetic acid derivative. It has an elimination half-life of about three hours before it undergoes renal elimination; its clearance is greater than the glomerular filtration rate suggesting that there is some renal tubular secretion of the compound. Economics
Brand names
Zolmitriptan is marketed by AstraZeneca with the brand names Zomig, Zomigon (Argentina, Canada & Greece), AscoTop (Germany) and Zomigoro (France). Economics
In 2008, Zomig generated nearly $154 million in sales.AstraZenecas U.S. patent on Zomig tablets expired on November 14, 2012, and its pediatric exclusivity extension expired on May 14, 2013. The patent in certain European countries has already expired too, and generic drug maker Actavis released a generic version in those countries, starting in March 2012. Legal status
In Russia versions of zolmitriptan, which are not registered in the National registry of medications, may be regarded as narcotic drugs (derivatives of dimethyltriptamine). References
Further reading
MacGregor EA (1998). "Zolmitriptan clinical studies". Drugs Today. 34 (12): 1027–1033. doi:10.1358/dot.1998.34.12.487488. PMID 14743270. External links
"Zolmitriptan". Drug Information Portal. U.S. National Library of Medicine. "Zolmitriptan Nasal Spray". MedlinePlus. | 0-1
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Metabolism
The IDH1 gene encodes for the enzyme isocitrate dehydrogenase 1 and is uncommonly mutated in glioblastoma (primary GBM: 5%, secondary GBM >80%). By producing very high concentrations of the oncometabolite D-2-hydroxyglutarate and dysregulating the function of the wild-type IDH1 enzyme, it induces profound changes to the metabolism of IDH1-mutated glioblastoma, compared with IDH1 wild-type glioblastoma or healthy astrocytes. Among others, it increases the glioblastoma cells dependence on glutamine or glutamate as an energy source. IDH1-mutated glioblastomas are thought to have a very high demand for glutamate and use this amino acid and neurotransmitter as a chemotactic signal. Since healthy astrocytes excrete glutamate, IDH1-mutated glioblastoma cells do not favor dense tumor structures, but instead migrate, invade, and disperse into healthy parts of the brain where glutamate concentrations are higher. This may explain the invasive behavior of these IDH1-mutated glioblastoma. Ion channels
Furthermore, GBM exhibits numerous alterations in genes that encode for ion channels, including upregulation of gBK potassium channels and ClC-3 chloride channels. By upregulating these ion channels, glioblastoma tumor cells are hypothesized to facilitate increased ion movement over the cell membrane, thereby increasing H2O movement through osmosis, which aids glioblastoma cells in changing cellular volume very rapidly. This is helpful in their extremely aggressive invasive behavior because quick adaptations in cellular volume can facilitate movement through the sinuous extracellular matrix of the brain. MicroRNA
As of 2012, RNA interference, usually microRNA, was under investigation in tissue culture, pathology specimens, and preclinical animal models of glioblastoma. | A pivotal clinical trial carried out in the early 1970s showed that among 303 GBM patients randomized to radiation or nonradiation therapy, those who received radiation had a median survival more than double those who did not. Subsequent clinical research has attempted to build on the backbone of surgery followed by radiation. On average, radiotherapy after surgery can reduce the tumor size to 107 cells. Whole-brain radiotherapy does not improve when compared to the more precise and targeted three-dimensional conformal radiotherapy. A total radiation dose of 60–65 Gy has been found to be optimal for treatment.GBM tumors are well known to contain zones of tissue exhibiting hypoxia, which are highly resistant to radiotherapy. Various approaches to chemotherapy radiosensitizers have been pursued, with limited success as of 2016. As of 2010, newer research approaches included preclinical and clinical investigations into the use of an oxygen diffusion-enhancing compound such as trans sodium crocetinate as radiosensitizers, and as of 2015 a clinical trial was underway. Boron neutron capture therapy has been tested as an alternative treatment for glioblastoma, but is not in common use. Chemotherapy
Most studies show no benefit from the addition of chemotherapy. However, a large clinical trial of 575 participants randomized to standard radiation versus radiation plus temozolomide chemotherapy showed that the group receiving temozolomide survived a median of 14.6 months as opposed to 12.1 months for the group receiving radiation alone. This treatment regimen is now standard for most cases of glioblastoma where the person is not enrolled in a clinical trial. | 11
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For example, the Asp816Phe and Asp816Val mutations (the aspartate normally at position 816 in the c-kit protein has been replaced with phenylalanine or valine respectively) have been associated with early manifestation of the disease (mean age of onset: 1.3 and 5.9 months respectively). The c-kit gene is encoded on the q12 locus of chromosome 4. Irritants
Several factors can worsen the symptoms of urticaria pigmentosa:
Emotional stress
Physical stimuli such as heat, friction, and excessive exercise
Bacterial toxins
Venom
Eye drops containing dextran
NSAIDs
Alcohol
MorphineThe classification of NSAIDs can be disputed. Aspirin, for example, causes the mast cells to degranulate, releasing histamines and causing symptoms to flare. However, daily intake of 81 mg aspirin may keep the mast cells degranulated. Thus, while symptoms may be worsened at first, they can get better as the mast cells are unable to recharge with histamine. Diagnosis
The disease is most often diagnosed as an infant, when parents take their baby in for what appears to be bug bites. The bug bites are actually the clumps of mast cells. Doctors can confirm the presence of mast cells by rubbing the babys skin. If hives appear, it most likely signifies the presence of urticaria pigmentosa. Treatments
There are no permanent cures for urticaria pigmentosa. However, treatments are possible. Most treatments for mastocytosis can be used to treat urticaria pigmentosa. | Urticaria pigmentosa (also known as generalized eruption of cutaneous mastocytosis (childhood type): 616
) is the most common form of cutaneous mastocytosis. It is a rare disease caused by excessive numbers of mast cells in the skin that produce hives or lesions on the skin when irritated. Signs and symptoms
Urticaria pigmentosa is characterized by excessive amounts of mast cells in the skin. Red or brown spots are often seen on the skin, typically around the chest, forehead, and back. These mast cells, when irritated (e.g. by rubbing the skin, heat exposure), produce too much histamine, triggering an allergic reaction that leads to hives localized to the area of irritation, sometimes referred to as Dariers sign. Severe itching usually follows, and scratching the area only serves to further symptoms. Symptoms can be mild (flushing and hives that require no treatment), moderate (diarrhea, tachycardia, nausea/vomiting, headache, and fainting), or life-threatening (vascular collapse requiring emergency treatment and hospitalization). Cause
The majority of urticaria pigmentosa cases are caused by a point mutation at amino acid 816 of the proto-oncogene c-kit. c-kit is a transmembrane protein which, when bound to Mast Cell Growth Factor (MCGF), signals the cell to divide. Mutations in position 816 of c-kit can result in a constant division signal being sent to the mast cells, resulting in abnormal proliferation. Different mutations have been linked to different onset times of the disease. | 11
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Chemical methods can also be used, including sanitizing surgical equipment after each use. Tetracycline drugs are the most common treatment for anaplasmosis, and can provide the animal with immunity for a period of time. The disease is more common in the South and West parts of the United States, but is no longer considered a major problem since the use of tetracycline drugs. Transmission
Mechanical and biological vector transmission work in different ways but both lead to infection of the red blood cells. Mechanical transmission happens in two ways, one when red blood cells are inoculated with the blood parasite through surgical equipment including needles, dehorners, ear taggers, castrating knives, and tattoo instruments. Another mechanical transmission mode is through the mouthparts of biting flies who carry an Anaplasma species of blood parasite.Biological vector transmission is through ticks that carry a blood parasite able to cause anaplasmosis. The most common Anaplasmosis-causing tick is Ixodes scapularis, also known as the black-legged tick or the deer tick. Ticks who contain species of many different Anaplasma species can transmit this disease through a bite. The blood parasite survives and can multiply in the tick, and can sit dormant for months without being transmitted to an animal. When bitten by a tick carrying a blood parasite, the blood parasite can then enter the new host and cause infection.Once infected with a species of Anaplasma, the parasite multiplies in the blood stream and attaches to red blood cells. | Anaplasma marginale is found worldwide and is transmitted by Rhipicephalus ticks. Anaplasma phagocytophilum is also found worldwide, mainly transmitted by Ixodes ticks. Other species that cause anaplasmosis in specific species include:
Cattle:
Anaplasma centrale - found mainly in South America, Africa and the Middle East
Sheep and goats:
Anaplasma ovis - found worldwide. There is a prevalence of 82.9% in sheep, and 74.9% in goats. This species is the most prevalent for causing anaplasmosis in sheep and goats, although Anaplasma phagocytophilium can also cause the disease. Anaplasma phagocytophilium has a prevalence of 11.9% in sheep, and 15.2% in goats. Morphology
There are many strains of Anaplasma marginale, all with differing morphology, antigenic properties, protein sequence, and ability to be transmitted by ticks. Major surface proteins (MSP) have been found to play a major role in the infection by Anaplasma marginale. Out of the six MSP found on this species, three of the major surface proteins do not seem to differ between all strains, those including MSP1a, MSP4, and MSP5. The msp1a gene, which codes for MSP1a, is used as a marker for the identification of Anaplasma marginale because it has shown to be conserved in the multiplication of rickettsia in cattle and ticks and has been shown to be involved in adhesion to bovine erythrocytes and tick cells.Anaplasma phagocytophilum is a gram-negative bacterium that does not have lipopolysaccharides or peptidoglycan. The outer membrane does not have a capsule, and is coarse with irregular periplasmic spaces. | 11
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In that study of 550 RA patients, logistic regression analysis of data collected on the 237 (43%) with ILD revealed that age, smoking, RF positivity, and elevated lactate dehydrogenase closely correlated with ILD.Recent studies have identified risk factors for disease progression and mortality. A retrospective study of 167 patients with RA-ILD determined that the usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) was a risk factor for progression, as were severe disease upon diagnosis and rate of change in pulmonary function test results in the first 6 months after diagnosis. A study of 59 RA-ILD patients found no median survival difference between those with the UIP pattern and those without it. But the UIP group had more deaths, hospital admissions, need for supplemental oxygen, and decline in lung function. == References == | If topical corticosteroids and moisturisers fail, short-term treatment with topical calcineurin inhibitors such as tacrolimus or pimecrolimus may be tried, although their use is controversial, as some studies indicate that they increase the risk of developing skin cancer or lymphoma. A 2007 meta-analysis showed that topical pimecrolimus is not as effective as corticosteroids and tacrolimus. A 2015 meta-analysis, though, indicated that topical tacrolimus and pimecrolimus are more effective than low-dose topical corticosteroids, and found no evidence for increased risk of malignancy or skin atrophy. In 2016, crisaborole, an inhibitor of PDE-4, was approved as a topical treatment for mild-to-moderate eczema.Other medications used for AD include systemic immunosuppressants such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil, and azathioprine. Antidepressants and naltrexone may be used to control pruritus (itchiness). Leukotriene inhibitors such as monteleukast are of unclear benefit as of 2018.In 2017, the monoclonal antibody(mAb) dupilumab under the trade name Dupixent was approved to treat moderate-to-severe eczema. In 2021, an additional monoclonal antibody, tralokinumab, was approved in the EU & UK with the trade name Adtralza then later in the US as Adbry for similarly severe cases. | 0-1
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Pathophysiology
In terms of the mechanism of congenital hyperinsulinism one sees that channel trafficking requires KATP channels need the shielding of ER retention signal.E282K prevents the KATP channel surface expression, the C-terminus (SUR1 subunit) is needed in KATP channel mechanism.R1215Q mutations (ABCC8 gene) affect ADP gating which in turn inhibits KATP channel. Diagnostic
In terms of the investigation of congenital hyperinsulinism, valuable diagnostic information is obtained from a blood sample drawn during hypoglycemia, detectable amounts of insulin during hypoglycemia are abnormal and indicate that hyperinsulinism is likely to be the cause. Inappropriately low levels of free fatty acids and ketones provide additional evidence of insulin excess. An additional piece of evidence indicating hyperinsulinism is a usually high requirement for intravenous glucose to maintain adequate glucose levels, the minimum glucose required to maintain a plasma glucose above 70 mg/dl. A GIR above 8 mg/kg/minute in infancy suggests hyperinsulinism. A third form of evidence suggesting hyperinsulinism is a rise of the glucose level after injection of glucagon at the time of the low glucose.Diagnostic efforts then shift to determining the type- elevated ammonia levels or abnormal organic acids can indicate specific, rare types. Intrauterine growth retardation and other perinatal problems raise the possibility of transience, while large birthweight suggests one of the more persistent conditions. Genetic screening is now available within a useful time frame for some of the specific conditions. It is worthwhile to identify the minority of severe cases with focal forms of hyperinsulinism because these can be completely cured by partial pancreatectomy. | Fetus in fetu differs from fetiform teratoma in having an apparent spine and bilateral symmetry.Most authorities agree that fetiform teratomas are highly developed mature teratomas; the natural history of fetus in fetu is controversial. There also may be a cultural difference, with fetiform teratoma being reported more often in ovarian teratomas (by gynecologists) and fetus in fetu being reported more often in retroperitoneal teratomas (by general surgeons). Fetus in fetu has often been interpreted as a fetus growing within its twin. As such, this interpretation assumes a special complication of twinning, one of several grouped under the term parasitic twin. In this regard, in many cases the fetus in fetu is reported to occupy a fluid-filled cyst within a mature teratoma. Cysts within mature teratoma may have partially developed organ systems; reports include cases of partial cranial bones, long bones and a rudimentary beating heart.Regardless of whether fetus in fetu and fetiform teratoma are one entity or two, they are distinct from and not to be confused with ectopic pregnancy. Struma ovarii
A struma ovarii (also known as goitre of the ovary or ovarian goiter) is a rare form of mature teratoma that contains mostly thyroid tissue. Epignathus
Epignathus is a rare teratoma originating in the oropharyngeal area that occurs in utero. It presents with a mass protruding from the mouth at birth. Untreated, breathing is impossible. An EXIT procedure is the recommended initial treatment. Signs and symptoms
Teratomas may be found in babies, children, and adults. | 0-1
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Genetic mutations thought to be involved in the development and/or progression of the latter disease include the L265P mutation in the MYD88 gene found in >90% of Waldenström macroglobulinaemia patients as well as various mutations in the CXCR gene found in 27% to 40% of Waldenström macroglobulinaemia patients.The clonal plasma cells involved in plasma cell dyscrasias exhibit a high degree of genetic instability. For example, the clonal plasma cell population formed by initial genetic alterations that lead to multiple myeloma contains cells that develop further genetic changes that enhance their survival, proliferation, tissue-injuring, and metastatic capacities. This allows the new cell clones to crowd out older cell clones and thereby establish a more malignant disease. Repetition of such genetic changes underlie the evolution of a clinically silent plasma cell dyscrasia to an overt malignancy. The progressive genetic changes in clonal plasma cells include accumulating numerous single nucleotide polymorphisms, increases and decreases in gene and chromosome copy numbers, and chromosomal translocations. Genes affected include those regulating genome stability itself (e.g. KIF2B) as well as cellular activation, proliferation, and apoptosis (e.g. CIDEC, TP52, ATM, KRAS, NRAS, Wnt, and NF-κB). | Infections
Bacterial, viral, and protozoal infections may occur in the area surround the rectum. These may be the result of a sexually transmitted disease. Other
Hemorrhoids or rectal foreign body. References
== External links == | 0-1
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Long term steroid use can cause contribute to the development of cataracts.Macrophage activation syndrome (MAS) is a severe, potentially life-threatening complication that can occur in patients with the systemic subtype of JIA. MAS involves uncontrolled activation of the immune system, sometimes referred to as a cytokine storm, which can present with a sepsis-like picture of fever, rash, enlarged liver and spleen, enlarged lymph nodes and cardiorespiratory compromise. It is recognised by a series of characteristic changes in laboratory parameters, including a high ferritin and a paradoxically low erythrocyte sedimentation rate. Causes
The cause of JIA remains unknown. However, the disorder is autoimmune — meaning that the bodys own immune system starts to attack and destroy cells and tissues (particularly in the joints) for no apparent reason. The immune system is thought to be provoked by changes in the environment, in combination with mutations in many associated genes and/or other causes of differential expression of genes. Experimental studies have shown that certain mutated viruses may be able to trigger JIA. The disease appears to be more common in girls, and is most common in Caucasians.The cause of JIA, as the word "idiopathic" suggests, is unknown and an area of active research. Current understanding of JIA suggests that it arises in a genetically susceptible individual due to environmental factors. Diagnosis
The diagnosis of JIA can be difficult, in part because joint pain in children is so common and may be from many causes other than JIA. | Complications
JIA is a chronic disorder, which if neglected, can lead to serious complications. However, with regular follow-up and modern treatments, complications have reduced and outcomes improved. If inflammation is not treated, it can damage the joint, the cartilage and the bone. With the advent of modern therapies, these complications of JIA have become much less common.Children with JIA may have a reduced overall rate of growth, especially if the disease involves many joints or other body systems. This may be due to a combination of the disease itself, as well as its treatments, particularly corticosteroid use. Paradoxically, limbs where a large joint (such as the knee) is inflamed may have increased growth in the short term, leading to limb-length discrepancy (i.e. one arm or leg is slightly longer than the other). This is due to increased blood supply to the bony growth plates surrounding the inflamed joints. Bone density and bone strength may be reduced through a combination of inflammation, corticosteroid use and reduced physical activity levels. Other musculoskeletal complications may include joint contractures, muscle weakness or muscle wasting.Uveitis, if left untreated, can result in scarring, glaucoma, cataracts, and even blindness. Regular monitoring allows for early detection and treatment. Steroid eye drops are usually the first line treatment for anterior uveitis. However, other treatments – many of which also treat arthritis (e.g. methotrexate, biologics) – may be required to keep the inflammation under control, and to minimise steroid use over the longer term. | 11
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Immunohistochemical staining for antibodies against T. whipplei has been used to detect the organism in a variety of tissues, and a polymerase chain reaction-based assay is also available, which can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipples disease, but that a negative PCR is most likely indicative of a healthy individual. Treatment
Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has a relapse rate around 40%. Expert opinion as of 2007 is that Whipples disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms. Epidemiology
The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries, the rate of women receiving a diagnosis of Whipples disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population. T. whipplei appears to be an environmental organism that is commonly present in the gastrointestinal tract, but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. | The possible immunological defect may be specific for T. whipplei, since the disease is not associated with a substantially increased risk of other infections. The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s. History
Whipple described the disease in 1907 in a paper in the now-defunct Bulletin of Johns Hopkins Hospital. The patient was a 36-year-old medical missionary. Whipple referred to the disease as "intestinal lipodystrophy". It was long presumed to be an infectious disease, but the causative organism was only fully identified in 1992. In 2003, doctors from Johns Hopkins Hospital, together with the French microbiologist Didier Raoult applied novel diagnostic methods to stored tissue samples from Whipples original patient, and demonstrated T. whipplei in these tissues. See also
Tropheryma whipplei
Notes
References
External links
"Whipples Disease". National Digestive Disease Information Clearinghouse NDDIC. | 11
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Distal spinal muscular atrophy type 1 (DSMA1), also known as spinal muscular atrophy with respiratory distress type 1 (SMARD1), is a rare neuromuscular disorder involving death of motor neurons in the spinal cord which leads to a generalised progressive atrophy of body muscles. The condition is caused by a genetic mutation in the IGHMBP2 gene and is inherited in an autosomal recessive manner. There is no known cure to DSMA1, and research of the disorder is still in early stages due to low incidence and high mortality rates. Signs and symptoms
Usually, the first respiratory symptoms are shortness of breath (dyspnea) and paradoxical respirations which then escalate within the first few months of life to diaphragmatic paralysis. The symptoms of diaphragmatic paralysis come on very rapidly and without warning, and the patient is often rushed to a hospital where they are placed on a ventilator for respiratory support. Due to the severe nature of diaphragmatic paralysis, the patient eventually needs continuous ventilation support to survive. Continuous ventilation, however, may in itself cause damage to the anatomy of the lungs.In addition to diaphragmatic paralysis, other issues may arise: as the name suggests, the distal limbs are most affected with symptoms of weakness, restricting mobility due to (near-)paralysis of the distal limbs as well as the head and neck. Also, dysfunction of the peripheral nerves and the autonomic nervous system may occur. Due to these dysfunctions, the patients have been shown to suffer from excessive sweating and irregular heartbeat. | So, the patient uses excessive accommodation to stimulate accommodative convergence to overcome reduced PFV. Risk factors
A large amount of near work is the main precipitating factor of accommodative excess. Pseudomyopia
Pseudomyopia also known as artificial myopia refers to an intermittent and temporary shift in refractive error of the eye towards myopia. It may occur due to excessive accommodation or spasm of accommodation. Diagnosis
Differential diagnosis
Parinaud’s syndrome, which can mimic some aspects of spasm of the near reflex, such as excessive accommodation and convergence; however, pupillary near-light dissociation, not miosis, is a feature of Parinaud’s syndrome. Treatment
Optical: Cycloplegic refraction, and correction of Refractive errors if any
Vision therapy
General: Relax from near work
See also
Spasm of accommodation
Convergence excess
== References == | 0-1
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As a naval surgeon on HMS Salisbury, Lind had compared several suggested scurvy cures: hard cider, vitriol, vinegar, seawater, oranges, lemons, and a mixture of balsam of Peru, garlic, myrrh, mustard seed and radish root. In A Treatise on the Scurvy (1753)
Lind explained the details of his clinical trial and concluded "the results of all my experiments was, that oranges and lemons were the most effectual remedies for this distemper at sea." However, the experiment and its results occupied only a few paragraphs in a work that was long and complex and had little impact. Lind himself never actively promoted lemon juice as a single cure. He shared medical opinion at the time that scurvy had multiple causes – notably hard work, bad water, and the consumption of salt meat in a damp atmosphere which inhibited healthful perspiration and normal excretion – and therefore required multiple solutions. Lind was also sidetracked by the possibilities of producing a concentrated rob of lemon juice by boiling it. This process destroyed the vitamin C and was therefore unsuccessful.During the 18th century, scurvy killed more British sailors than wartime enemy action. It was mainly by scurvy that George Anson, in his celebrated voyage of 1740–1744, lost nearly two-thirds of his crew (1,300 out of 2,000) within the first 10 months of the voyage. | While pasteurization killed bacteria, it also destroyed vitamin C. This was eventually resolved by supplementing with onion juice or cooked potatoes. Native Americans helped save some newcomers from scurvy by directing them to eat wild onions. 20th century
By the early 20th century, when Robert Falcon Scott made his first expedition to the Antarctic (1901–1904), the prevailing theory was that scurvy was caused by "ptomaine poisoning", particularly in tinned meat. However, Scott discovered that a diet of fresh meat from Antarctic seals cured scurvy before any fatalities occurred.In 1907, an animal model which would eventually help to isolate and identify the "antiscorbutic factor" was discovered. Axel Holst and Theodor Frølich, two Norwegian physicians studying shipboard beriberi contracted by ships crews in the Norwegian Fishing Fleet, wanted a small test mammal to substitute for the pigeons then used in beriberi research. They fed guinea pigs their test diet of grains and flour, which had earlier produced beriberi in their pigeons, and were surprised when classic scurvy resulted instead. This was a serendipitous choice of animal. Until that time, scurvy had not been observed in any organism apart from humans and had been considered an exclusively human disease. Certain birds, mammals, and fish are susceptible to scurvy, but pigeons are unaffected, since they can synthesize ascorbic acid internally. Holst and Frølich found they could cure scurvy in guinea pigs with the addition of various fresh foods and extracts. | 11
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In recent years, homicide rates have been highest in developing countries in Sub-Saharan Africa and Latin America and the Caribbean and lowest in East Asia, the western Pacific, and some countries in northern Africa. Studies show a strong, inverse relationship between homicide rates and both economic development and economic equality. Poorer countries, especially those with large gaps between the rich and the poor, tend to have higher rates of homicide than wealthier countries. Homicide rates differ markedly by age and sex. Gender differences are least marked for children. For the 15 to 29 age group, male rates were nearly six times those for female rates; for the remaining age groups, male rates were from two to four times those for females.Studies in a number of countries show that, for every homicide among young people age 10 to 24, 20 to 40 other young people receive hospital treatment for a violent injury.Forms of violence such as child maltreatment and intimate partner violence are highly prevalent. Approximately 20% of women and 5–10% of men report being sexually abused as children, while 25–50% of all children report being physically abused. A WHO multi-country study found that between 15 and 71% of women reported experiencing physical and/or sexual violence by an intimate partner at some point in their lives. Collective violence
Wars grab headlines, but the individual risk of dying violently in an armed conflict is today relatively low—much lower than the risk of violent death in many countries that are not suffering from an armed conflict. | Glycation (sometimes called non-enzymatic glycosylation) is the covalent attachment of a sugar to a protein or lipid. Typical sugars that participate in glycation are glucose, fructose, and their derivatives. Glycation is the non-enzymatic process responsible for many (e.g. micro and macrovascular) complications in diabetes mellitus and is implicated in some diseases and in aging. Glycation end products are believed to play a causative role in the vascular complications of diabetes mellitus.In contrast with glycation, glycosylation is the enzyme-mediated ATP-dependent attachment of sugars to protein or lipid. Glycosylation occurs at defined sites on the target molecule. It is a common form of post-translational modification of proteins and is required for the functioning of the mature protein. Biochemistry
Glycations occur mainly in the bloodstream to a small proportion of the absorbed simple sugars: glucose, fructose, and galactose. It appears that fructose has approximately ten times the glycation activity of glucose, the primary body fuel. Glycation can occur through Amadori reactions, Schiff base reactions, and Maillard reactions; which lead to advanced glycation end products (AGEs). Biomedical implications
Red blood cells have a consistent lifespan of 120 days and are accessible for measurement of glycated hemoglobin. Measurement of HbA1c—the predominant form of glycated hemoglobin—enables medium-term blood sugar control to be monitored in diabetes. | 0-1
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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. | It should be used with caution in people with arrhythmias or long QT.No dose adjustment is necessary for renal impairment or advanced age, but children seem to clear voriconazole faster than adults and drug levels may need monitoring. Side effects
The labels carry several warnings of the risk of injection site reactions, hypersensitivity reactions; kidney, liver, and pancreas damage; trouble with vision; and adverse effects in skin including damage due to phototoxicity, squamous cell skin cancer, and Stevens–Johnson syndrome; in long-term use there is a warning of the risk of bone fluorosis and periostitis.Additionally, very common adverse effects, occurring in more than 10% of people, include peripheral edema, headaches, trouble breathing, diarrhea, vomiting, abdominal pain, nausea, rashes, and fever.Common adverse effects, occurring in between 1 and 10% of people, include sinus infections, low numbers of white and red blood cells (agranulocytosis, pancytopenia, thrombocytopenia, leukopenia, and anemia), low blood sugar, reduced amount of potassium and sodium, depression, hallucinations, anxiety, insomnia, agitation, confusion, convulsions, fainting, tremor, weakness, tingling, sleepiness, dizziness, bleeding retina, irregular heart beats, slow or fast heart beats, low blood pressure, inflamed veins, acute respiratory distress syndrome, pulmonary edema, inflamed lips, swollen face, stomach upset, constipation, gingivitis, jaundice, hair loss, flaky skin, itchiness, red skin, back pain, chest pain, and chills. Interactions
Being metabolized by hepatic cytochrome P450, voriconazole interacts with many drugs. | 11
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This proposal split the members of the patients society, many of whom were extremely wary of entrusting their fate to a third party, as they had done in 1959 with unfortunate results. At a meeting on the 5 April 1969, the opposing views within the society could not be reconciled and the organisation split into the pro-arbitration group and the litigation group (who decided to sue the company). That summer, Chisso sent gifts to the families who opted for arbitration rather than litigation. An arbitration committee was duly set up by the Ministry of Health and Welfare on 25 April, but it took almost a year to draw up a draft compensation plan. A newspaper leak in March 1970 revealed that the committee would ask Chisso to pay only ¥2 million ($5,600) for dead patients and ¥140,000 to ¥200,000 ($390 to $560) per year to surviving patients. The arbitration group were dismayed by the sums on offer. They petitioned the committee, together with patients and supporters of the litigation group, for a fairer deal. The arbitration committee announced their compensation plan on 25 May in a disorderly session at the Ministry of Health and Welfare in Tokyo. Thirteen protesters were arrested. Instead of accepting the agreement as they had promised, the arbitration group asked for increases. The committee was forced to revise its plan and the patients waited inside the ministry building for two days while they did so. The final agreement was signed on 27 May. | Infections
Bacterial, viral or fungal infections can cause glossitis. Chronic Candida infections of the tongue can cause an atrophic glossitis known as median rhomboid glossitis.Syphilis is now relatively rare, but the tertiary stage can cause diffuse glossitis and atrophy of lingual papillae, termed "syphilitic glossitis", "luetic glossitis" or "atrophic glossitis of tertiary syphilis". It is caused by Treponema pallidum and is a sexually transmitted infection. Other causes
Many conditions can cause glossitis via malnutrition or malabsorption, which creates the nutritional deficiencies described above, although other mechanisms may be involved in some of those conditions listed. Alcoholism
Sprue (celiac disease, or tropical sprue), secondary to nutritional deficiencies
Crohn’s disease
Whipple disease
Glucagonoma syndrome
Cowden disease
Acquired immunodeficiency syndrome (AIDS)
Carcinoid syndrome
Kwashiorkor amyloidosis
Veganism and other specialized diets, without B12 supplementation. Poor hydration and low saliva in the mouth, which allows bacteria to grow more readily
Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma
Tongue piercing Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament
Exposure to irritants such as tobacco, alcohol, hot foods, or spices
Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors)
Administration of ganglion blockers (e.g., Tubocurarine, Mecamylamine). Oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris
Heredity
Albuterol (bronchodilator medicine)A painful tongue may be an indication of an underlying serious medical condition and nearly always merits assessment by a physician or dental surgeon. Diagnosis
Classification
Glossitis could be classified as a group of tongue diseases or gastrointestinal diseases. | 0-1
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Retinoblastoma can be curable after the initial sign and up to six months, if the tumor is intraocular. If you do not visit an ophthalmologist with signs of leucocoria within a reasonable amount of time, the delay in the diagnosis could lead to a more severe prognosis. Due to a delay in the diagnosis, it could result in proptosis which is then considered extraocular, the most severe.The most common and obvious sign of retinoblastoma is an abnormal appearance of the retina as viewed through the pupil, the medical term for which is leukocoria, also known as amaurotic cats eye reflex. Other signs and symptoms include deterioration of vision, a red and irritated eye with glaucoma, and faltering growth or delayed development. Some children with retinoblastoma can develop a squint, commonly referred to as "cross-eyed" or "wall-eyed" (strabismus). Retinoblastoma presents with advanced disease in developing countries and eye enlargement is a common finding.Depending on the position of the tumors, they may be visible during a simple eye exam using an ophthalmoscope to look through the pupil. A positive diagnosis is usually made only with an examination under anesthetic (EUA). A white eye reflection is not always a positive indication of retinoblastoma and can be caused by light being reflected badly or by other conditions such as Coats disease.The presence of the photographic fault red eye in only one eye and not in the other may be a sign of retinoblastoma. A clearer sign is "white eye" or "cats eye" (leukocoria). | According to Reese and Ellsworth, there were different groups that had various features in order to classify the globe salvage as very favorable to the category of very unfavorable. In order to salvage the affected eye, the disc diameter had to be around 4DD and behind the equator to have higher favorability. If the tumor was around ten in disc diameter and involved roughly 50% of the retina, it was considered unfavorable to salvage the globe which could result in enucleation. According to Murphree, the different groups were classified from very low risk to very high risk which was determined by features of the given tumor. Very low risk means that the tumor has to be less than 3mm and there must be no seeding of the vitreous or sub-retinal area. When a patient is very high risk, the tumor presents itself with multiple features and is going to have to be treated with conservative treatment modalities or enucleation. International Classification for Intraocular Retinoblastoma
Treatment
The priority of retinoblastoma treatment is to preserve the life of the child, then to preserve vision, and then to minimize complications or side effects of treatment. The exact course of treatment depends on the individual case and is decided by the ophthalmologist in discussion with the paediatric oncologist. Correct treatment also depends on the mutation type, whether it is a germline RB1 mutation, a sporadic RB1 mutation or MYCN amplification with functional RB1. Children with involvement of both eyes at diagnosis usually require multimodality therapy (chemotherapy, local therapies). | 11
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Supportive therapy is given if necessary, including respiratory assistance and maintenance of body temperature. Once a person has had a normal ECG for more than 24 hours they are generally medically clear. Decontamination
Initial treatment of an acute overdose includes gastric decontamination. This is achieved by giving activated charcoal, which adsorbs the drug in the gastrointestinal tract either by mouth or via a nasogastric tube. Activated charcoal is most useful if given within 1 to 2 hours of ingestion. Other decontamination methods such as stomach pumps, ipecac induced emesis, or whole bowel irrigation are generally not recommended in TCA poisoning. Stomach pumps may be considered within an hour of ingestion but evidence to support the practice is poor. Medication
Administration of intravenous sodium bicarbonate as an antidote has been shown to be an effective treatment for resolving the metabolic acidosis and cardiovascular complications of TCA poisoning. If sodium bicarbonate therapy fails to improve cardiac symptoms, conventional antidysrhythmic drugs or magnesium can be used to reverse any cardiac abnormalities. However, no benefit has been shown from Class 1 antiarrhythmic drugs; it appears they worsen the sodium channel blockade, slow conduction velocity, and depress contractility and should be avoided in TCA poisoning. | Superficial lymphatic malformation is a congenital malformation of the superficial lymphatics, presenting as groups of deep-seated, vesicle-like papules resembling frog spawn, at birth or shortly thereafter. Lymphangioma circumscriptum is the most common congenital lymphatic malformation. It is a benign condition and treatment is not required if the person who has it does not have symptoms from it. Signs and symptoms
Lymphangioma circumscriptum is characterized by a rash on the skin featuring clear vesicles. The rash may be painful and is sometimes itchy. The vesicles often leak lymph and may bleed. The rash may appear similar to warts if the vesicles frequently break open. Diagnosis
A biopsy of the affected skin and histological examination under the microscope is necessary to diagnose lymphangioma circumscriptum. Differential diagnosis
Several other conditions may mimic lymphangioma circumscriptum. These conditions include infections such as an outbreak of herpes simplex, herpes simplex vegetans, molluscum contagiosum, verruca vulgaris, and condyloma acuminatum. Similarly, benign and cancerous non-infectious conditions may also present in a similar manner and include conditions such as angiokeratoma, dermatitis herpetiformis, hemangioma, epidermal nevus, lymphangiectasia, melanoma, angiosarcoma, and metastatic carcinomas. Treatment
The condition is benign and does not require treatment if the affected person does not have symptoms. Lymphangioma circumscriptum is often treated when it causes troubling symptoms to the affected person (itching, pain) or due to concerns about its cosmetic appearance. Surgical removal (excision) of the affected layers of skin is the most common and effective treatment. | 0-1
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Drug Information Portal. U.S. National Library of Medicine. | Monoclonal gammopathy, also known as paraproteinemia, is the presence of excessive amounts of myeloma protein or monoclonal gamma globulin in the blood. It is usually due to an underlying immunoproliferative disorder or hematologic neoplasms, especially multiple myeloma. It is sometimes considered equivalent to plasma cell dyscrasia. The most common form of the disease is monoclonal gammopathy of undetermined significance. Causes
Causes of paraproteinemia include the following:
Leukemias and lymphomas of various types, but usually B-cell non-Hodgkin lymphomas with a plasma cell component. Myeloma
Plasmacytoma
Lymphoplasmacytic lymphoma
Idiopathic (no discernible cause): some of these will be revealed as leukemias or lymphomas over the years. AL amyloidosis
Diagnosis
These are characterized by the presence of any abnormal protein that is involved in the immune system, which are most often immunoglobulins and are associated with the clonal proliferation of lymphocytes.When a paraproteinemia is present in the blood, there will be a narrow band, or spike, in the serum protein electrophoresis because there will be an excess of production of one protein.There are two large classes of blood proteins: albumin and globulin. They are generally equal in proportion, but albumin is much smaller than globulin, and slightly negatively charged, which leads to an accumulation at the end of the electrophoretic gel. The globulins separate out into three regions on the electrophoretic gel, which are the α band, the β band, and the γ band. The α band can be separated into two components: α1 and α2. The α1 region consists mostly of α1-antitrypsin and α1-acid glycoprotein. The α2 region is mostly haptoglobin, α2-macroglobulin, α2-antiplasmin, and ceruloplasmin. | 0-1
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Epidemiology
The incidence of central nervous system toxicity among divers has decreased since the Second World War, as protocols have developed to limit exposure and partial pressure of oxygen inspired. In 1947, Donald recommended limiting the depth allowed for breathing pure oxygen to 7.6 m (25 ft), which equates to an oxygen partial pressure of 1.8 bar (180 kPa). Over time this limit has been reduced, until today a limit of 1.4 bar (140 kPa) during a recreational dive and 1.6 bar (160 kPa) during shallow decompression stops is generally recommended. Oxygen toxicity has now become a rare occurrence other than when caused by equipment malfunction and human error. Historically, the U.S. Navy has refined its Navy Diving Manual Tables to reduce oxygen toxicity incidents. Between 1995 and 1999, reports showed 405 surface-supported dives using the helium–oxygen tables; of these, oxygen toxicity symptoms were observed on 6 dives (1.5%). As a result, the U.S. Navy in 2000 modified the schedules and conducted field tests of 150 dives, none of which produced symptoms of oxygen toxicity. Revised tables were published in 2001.The variability in tolerance and other variable factors such as workload have resulted in the U.S. Navy abandoning screening for oxygen tolerance. Of the 6,250 oxygen-tolerance tests performed between 1976 and 1997, only 6 episodes of oxygen toxicity were observed (0.1%).Central nervous system oxygen toxicity among patients undergoing hyperbaric oxygen therapy is rare, and is influenced by a number of a factors: individual sensitivity and treatment protocol; and probably therapy indication and equipment used. | Therefore, current guidelines for patients on mechanical ventilation in intensive care recommends keeping oxygen concentration less than 60%. Likewise, divers who undergo treatment of decompression sickness are at increased risk of oxygen toxicity as treatment entails exposure to long periods of oxygen breathing under hyperbaric conditions, in addition to any oxygen exposure during the dive. Ocular toxicity
Prolonged exposure to high inspired fractions of oxygen causes damage to the retina. Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions. Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants. In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications.Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures. It also occurs frequently in those undergoing repeated hyperbaric oxygen therapy. | 11
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In addition, due to the high risk of serious hepatotoxicity, flutamide should not be used in the absence of a serious indication.The mechanism of action of flutamide-induced hepatotoxicity is thought to be due to mitochondrial toxicity. Specifically, flutamide and particularly its major metabolite hydroxyflutamide inhibit enzymes in the mitochondrial electron transport chain in hepatocytes, including respiratory complexes I (NADH ubiquinone oxidoreductase), II (succinate dehydrogenase), and V (ATP synthase), and thereby reduce cellular respiration via ATP depletion and hence decrease cell survival. Inhibition of taurocholate (a bile acid) efflux has also been implicated in flutamide-induced hepatotoxicity. In contrast to flutamide and hydroxyflutamide, which severely compromise hepatocyte cellular respiration in vitro, bicalutamide does not significantly do so at the same concentrations and is regarded as non-mitotoxic. It is thought that the nitroaromatic group of flutamide and hydroxyflutamide enhance their mitochondrial toxicity; bicalutamide, in contrast, possesses a cyano group in place of the nitro moiety, greatly reducing the potential for such toxicity.The hepatotoxicity of flutamide appears to depend on hydrolysis of flutamide catalyzed by an arylacetamide deacetalyse enzyme. This is analogous to the hepatotoxicity that occurs with the withdrawn paracetamol (acetominophen)-related medication phenacetin. In accordance, the combination of paracetamol (acetaminophen) and flutamide appears to result in additive to synergistic hepatotoxicity, indicating a potential drug interaction. Others
Flutamide has also been associated with interstitial pneumonitis (which can progress to pulmonary fibrosis). The incidence of interstitial pneumonitis with flutamide was found to be 0.04% (4 per 10,000) in a large clinical cohort of 41,700 prostate cancer patients. | Metamorphopsia is a type of distorted vision in which a grid of straight lines appears wavy and parts of the grid may appear blank. People can first notice they suffer with the condition when looking at mini-blinds in their home. For example, straight lines might be wavy or bendy. Things may appear closer or further than they are. Initially characterized in the 1800s, metamorphopsia was described as one of the primary and most notable indications of myopic and senile maculopathies. Metamorphopsia can present itself as unbalanced vision, resulting from small unintentional movements of the eye as it tries to stabilize the field of vision. Metamorphopsia can also lead to the misrepresentation of an object’s size or shape.It is mainly associated with macular degeneration, particularly age-related macular degeneration with choroidal neovascularization. Other conditions that can present with complaints of metamorphopsia include: pathological myopia, presumed ocular histoplasmosis syndrome, choroidal rupture and multifocal choroiditis. Pathology
The mechanisms that result in the development of metamorphopsia involve structural changes in the retina of the eye (retinal mechanism) as well as processing changes in the cerebral cortex of the brain (cortical mechanism). The retinal mechanism involves the displacement of retinal layers which results in the mislocation of light on the retina. The cortical mechanism, which was discovered after the retinal mechanism, is affected by perceptual “filling-in” and visual crowding effects. The cortical mechanism was found to work in combination with the retinal mechanism to contribute to metamorphopsia in long-standing maculopathy or after the treatment of macular disorders. | 0-1
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"Vaccination schedules generally require a primary course of two doses, 3–6 weeks apart, followed by boosters at 6–12 month intervals. It is generally recognized that in many cases such schedules may not maintain protective levels of antibody and more frequent administration is advised in high-risk situations. "It is a common requirement at shows in the United Kingdom that horses be vaccinated against equine flu and a vaccination card must be produced; the International Federation for Equestrian Sports (FEI) requires vaccination every six months. Poultry
Poultry vaccines for bird flu are made inexpensively and are not filtered and purified like human vaccines to remove bits of bacteria or other viruses. They usually contain whole virus, not just hemagglutinin as in most human flu vaccines. Another difference between human and poultry vaccines is that poultry vaccines are adjuvated with mineral oil, which induces a strong immune reaction but can cause inflammation and abscesses. "Chicken vaccinators who have accidentally jabbed themselves have developed painful swollen fingers or even lost thumbs, doctors said. Effectiveness may also be limited. Chicken vaccines are often only vaguely similar to circulating flu strains – some contain an H5N2 strain isolated in Mexico years ago. With a chicken, if you use a vaccine thats only 85 percent related, youll get protection, Dr. Cardona said. In humans, you can get a single point mutation, and a vaccine thats 99.99 percent related wont protect you. And they are weaker [than human vaccines]. | Other methods of manufacture
Methods of vaccine generation that bypass the need for eggs include the construction of influenza virus-like particles (VLP). VLP resemble viruses, but there is no need for inactivation, as they do not include viral coding elements, but merely present antigens in a similar manner to a virion. Some methods of producing VLP include cultures of Spodoptera frugiperda Sf9 insect cells and plant-based vaccine production (e.g., production in Nicotiana benthamiana). There is evidence that some VLPs elicit antibodies that recognize a broader panel of antigenically distinct viral isolates compared to other vaccines in the hemagglutination-inhibition assay (HIA).A gene-based DNA vaccine, used to prime the immune system after boosting with an inactivated H5N1 vaccine, underwent clinical trials in 2011.On November 20, 2012, Novartis received FDA approval for the first cell-culture vaccine. In 2013, the recombinant influenza vaccine, Flublok, was approved for use in the United States.On September 17, 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for Supemtek, a quadrivalent influenza vaccine (recombinant, prepared in cell culture). The applicant for this medicinal product is Sanofi Pasteur. Supemtek was approved for medical use in the European Union in November 2020.Australia authorised its first and cell-based vaccine in March 2021, based on an "eternal cell line" of a dog kidney. Because of the way it is produced, it produces better-matched vaccine (to the flu strains). | 11
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Twelfth man
Traditionally, the first substitute player who fields when a member of the fielding side is injured. In Test matches, twelve players are named to a team prior to the match, with the final reduction to eleven occurring immediately prior to play commencing on the first day. This gives the captain some flexibility in team selection, dependent on the conditions (e.g. a spin bowler may be named to the team, but omitted if the captain feels that the pitch is not suitable for spin bowling). Twenty20 (or T20)
a form of limited overs cricket in which each team has one innings with a maximum length of twenty overs. Two
batsmans call for a probable two runs, requiring their partner to commit to a fast turn. See No, Push, Yes, Wait. U
Umpire
An official who enforces the laws and adjudicates play. One umpire stands behind the wicket at the non-strikers end, while a second (usually) stands at square leg, with the positions alternating for each over. The two on-field umpires use a system of arm signals to indicate decisions to the players and the scorer. Televised matches usually also have a third umpire to adjudicate on replays and the umpire decision review system. Umpire Decision Review System (UDRS)
(or Decision Review System, DRS)Official system to challenge certain decisions made by an umpire. The third umpire then reviews the decision using various technological aids, such as slow motion television replays, ball tracking, a snickometer etc. | It is done when the opposition plays a heavy off-side field and then bowl outside off. This shot was originally invented by Kevin Pietersen. It is also played by James Taylor and by New Zealand tailender Trent Boult
Flash
to wield the bat aggressively, often hitting good line and length deliveries indiscriminately. Flat pitch
a pitch which is advantageous to the batsmen and offers little or no help to the bowlers, due to predictable bounce. Also known as a "flat deck"
Flat hit
an aerial shot hit with significant power by the batsman which travels fast enough to make the ballistic trajectory of the ball appear flat
Flat throw
a ball thrown by the fielder which is almost parallel to the ground. Considered to be a hallmark of good fielding if the throw is also accurate because flat throws travel at a fast pace. Flat-track bully
a batsman high in the batting order who is very good only when the pitch is not giving the bowlers much help. Track is Australian slang for the pitch. When the track is said to be flat it is at its easiest for the batsman, but these are the only conditions under which some players can dominate. When conditions are tough, or when it really counts – they dont. Flick
a gentle movement of the wrist to move the bat, often associated with shots on the leg side. Flight
a delivery which is thrown up at a more arched trajectory by a spinner. Considered to be good bowling. Also loop. | 11
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The second stream of expansion of cannabis use encompasses "the use of hemp for commercial manufacturers utilizing large-scale cultivation primarily as a fiber for mercantile purposes"; but it is also linked to the search for psychedelic experiences (which can be traced back to the formation of the Parisian Club des Hashischins). Legal status
Since the beginning of the 20th century, most countries have enacted laws against the cultivation, possession or transfer of cannabis. These laws have had an adverse effect on cannabis cultivation for non-recreational purposes, but there are many regions where handling of cannabis is legal or licensed. Many jurisdictions have lessened the penalties for possession of small quantities of cannabis so that it is punished by confiscation and sometimes a fine, rather than imprisonment, focusing more on those who traffic the drug on the black market. In some areas where cannabis use had been historically tolerated, new restrictions were instituted, such as the closing of cannabis coffee shops near the borders of the Netherlands, and closing of coffee shops near secondary schools in the Netherlands. In Copenhagen, Denmark in 2014, mayor Frank Jensen discussed possibilities for the city to legalize cannabis production and commerce.Some jurisdictions use free voluntary treatment programs and/or mandatory treatment programs for frequent known users. Simple possession can carry long prison terms in some countries, particularly in East Asia, where the sale of cannabis may lead to a sentence of life in prison or even execution. | Neuroimaging
Although global abnormalities in white matter and grey matter are not consistently associated with heavy cannabis use, reduced hippocampal volume is consistently found. Amygdala abnormalities are sometimes reported, although findings are inconsistent.Cannabis use is associated with increased recruitment of task-related areas, such as the dorsolateral prefrontal cortex, which is thought to reflect compensatory activity due to reduced processing efficiency. Cannabis use is also associated with downregulation of CB1 receptors. The magnitude of down regulation is associated with cumulative cannabis exposure, and is reversed after one month of abstinence. There is limited evidence that chronic cannabis use can reduce levels of glutamate metabolites in the human brain. Cannabis dependence
About 9% of those who experiment with marijuana eventually become dependent according to DSM-IV (1994) criteria. A 2013 review estimates daily use is associated with a 10–20% rate of dependence. The highest risk of cannabis dependence is found in those with a history of poor academic achievement, deviant behavior in childhood and adolescence, rebelliousness, poor parental relationships, or a parental history of drug and alcohol problems. Of daily users, about 50% experience withdrawal upon cessation of use (i.e. are dependent), characterized by sleep problems, irritability, dysphoria, and craving. Cannabis withdrawal is less severe than withdrawal from alcohol.According to DSM-V criteria, 9% of those who are exposed to cannabis develop cannabis use disorder, compared to 20% for cocaine, 23% for alcohol and 68% for nicotine. | 11
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While it may occur with any weather conditions, it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma, however, oral doses may improve endurance and strength. Occupational
Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational disease. Many cases, however, are not reported or recognized as such. It is estimated that 5–25% of asthma cases in adults are work-related. A few hundred different agents have been implicated, with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers. Aspirin-induced asthma
Aspirin-exacerbated respiratory disease (AERD), also known as aspirin-induced asthma, affects up to 9% of asthmatics. AERD consists of asthma, nasal polyps, sinus disease, and respiratory reactions to aspirin and other NSAID medications (such as ibuprofen and naproxen). People often also develop loss of smell and most experience respiratory reactions to alcohol. Alcohol-induced asthma
Alcohol may worsen asthmatic symptoms in up to a third of people. This may be even more common in some ethnic groups such as the Japanese and those with aspirin-induced asthma. Other studies have found improvement in asthmatic symptoms from alcohol. Non-atopic asthma
Non-atopic asthma, also known as intrinsic or non-allergic, makes up between 10 and 33% of cases. There is negative skin test to common inhalant allergens. | Does the amino acid sequence of the transferred proteins resemble the sequence of known allergenic proteins? Are the transferred proteins resistant to digestion - a trait shared by many allergenic proteins? Genes approved for animal use can be restricted from human consumption due to potential for allergic reactions. In 1998 Starlink brand corn restricted to animals was detected in the human food supply, leading to first a voluntary and then a FDA mandated recall. There are requirements in some countries and recommendations in others that all foods containing GMO ingredients be so labeled, and that there be a post-launch monitoring system to report adverse effects (much there exists in some countries for drug and dietary supplement reporting). Restaurants
In the US, the FDA Food Code states that the person in charge in restaurants should have knowledge about major food allergens, cross-contacts, and symptoms of food allergy
reactions. Restaurant staff, including wait staff and kitchen staff, may not be adequately informed about allergenic ingredients, or the risk of cross-contact when kitchen utensils used to prepare food may have been in previous contact with an allergenic food. The problem may be compounded when customers have a hard time describing their food allergies or when wait staff have a hard time understanding those with food allergies when taking an order. Diagnosing issues
There exists both over-reporting and under-reporting of the prevalence of food allergies. | 0-1
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Persistent generalized lymphadenopathy (PGL) is enlarged, painless, non-tender lymph nodes occurring in a couple of different areas for more than three to six months for which no other reason can be found. This condition frequently occurs in people in the latency period of HIV/AIDS.The lymphatic system is part of the immune surveillance system. Blood contains fluid and blood cells. The fluid, which may contain suspended foreign material such as bacteria and viruses, seeps through blood vessel walls into the tissues, where it bathes the body cells and exchanges substances with them. Some of this lymph fluid is then taken up by lymphatic vessels and passed back to the heart, where it is again mixed with the blood. On its way, the fluid passes through the lymph nodes, small nodular organs located throughout the body but concentrated in certain areas such as the armpits or groin. These lymph nodes are also known as glands or lymphoid tissue. If they detect something foreign passing through them, they enlarge. This is called lymphadenopathy or swollen glands. Usually this is localized (for example, an infected spot on the scalp will cause lymph nodes in the neck on that same side to swell). However, when two or more lymph node groups are involved, it is called generalized lymphadenopathy. Usually this is in response to significant systemic disease and will subside once the person has recovered. | Signs and symptoms
The main symptom of dysmenorrhea is pain concentrated in the lower abdomen or pelvis. It is also commonly felt in the right or left side of the abdomen. It may radiate to the thighs and lower back.Symptoms often co-occurring with menstrual pain include nausea and vomiting, diarrhea, headache, dizziness, disorientation, fainting and fatigue. Symptoms of dysmenorrhea often begin immediately after ovulation and can last until the end of menstruation. This is because dysmenorrhea is often associated with changes in hormonal levels in the body that occur with ovulation. In particular, prostaglandins induce abdominal contractions that can cause pain and gastrointestinal symptoms. The use of certain types of birth control pills can prevent the symptoms of dysmenorrhea because they stop ovulation from occurring. Dysmenorrhea is associated with increased pain sensitivity and heavy menstrual bleeding.For many women, primary dysmenorrhea gradually subsides in late second generation. Pregnancy has also been demonstrated to lessen the severity of dysmenorrhea, when menstruation resumes. However, dysmenorrhea can continue until menopause. 5–15% of women with dysmenorrhea experience symptoms severe enough to interfere with daily activities. Causes
Dysmenorrhea can be classified as either primary or secondary based on the absence or presence of an underlying cause. Primary dysmenorrhea occurs without an associated underlying condition, while secondary dysmenorrhea has a specific underlying cause, typically a condition that affects the uterus or other reproductive organs.Painful menstrual cramps that result from an excess of prostaglandin release are referred to as primary dysmenorrhea. | 0-1
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It is thought that normal neuron migration during the second trimester of intrauterine development, when primitive neuron precursors (germinal matrix) migrate from just beneath the ventricular ependyma to the peripheral hemispheres where they form the cortical grey matter. Genetic
There was once thought to be a genetic association with the EMX2 gene, although this theory has recently lost support. However it has been confirmed that mutations in the COL4A1 gene occur in some patients with schizencephaly. In utero infections
Schizencephaly may also be caused by environmental toxin exposure during pregnancy, infection during pregnancy (such as Cytomegalovirus), or a vascular insult. Often there are additional associated heterotopias (isolated islands of neurons) which indicate a failure of migration of the neurons to their final position in the brain caused by possible stroke. Diagnosis
Radiological methods like computed tomography (CT) and/or magnetic resonance imaging (MRI) - unilateral or bilateral clefting of the brain. Genetic testing for confirmation of mutations in the genes associated with susceptibility to the condition. Treatment
Treatment for individuals with schizencephaly generally consists of physical therapy (KG-ZNS with Vojta Methode), occupational therapy (with specific emphasis on neuro-developmental therapy techniques), treatment for seizures, and, in cases that are complicated by hydrocephalus, a shunt. Prognosis
The prognosis for individuals with schizencephaly varies depending on the size of the clefts and the degree of neurological deficit. Frequency
In some cases, the defect is linked to mutations of the EMX2, SIX3, and Collagen, type IV, alpha 1 genes. | Headache is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.Headaches can occur as a result of many conditions. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society, which classifies it into more than 150 types of primary and secondary headaches. Causes of headaches may include dehydration; fatigue; sleep deprivation; stress; the effects of medications (overuse) and recreational drugs, including withdrawal; viral infections; loud noises; head injury; rapid ingestion of a very cold food or beverage; and dental or sinus issues (such as sinusitis).Treatment of a headache depends on the underlying cause, but commonly involves pain medication (especially in case of migraine or cluster headache). A headache is one of the most commonly experienced of all physical discomforts.About half of adults have a headache in a given year. Tension headaches are the most common, affecting about 1.6 billion people (21.8% of the population) followed by migraine headaches which affect about 848 million (11.7%). Causes
There are more than 200 types of headaches. Some are harmless and some are life-threatening. The description of the headache and findings on neurological examination, determine whether additional tests are needed and what treatment is best.Headaches are broadly classified as "primary" or "secondary". Primary headaches are benign, recurrent headaches not caused by underlying disease or structural problems. For example, migraine is a type of primary headache. | 0-1
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Trimethoprim/sulfamethoxazole, sold under the brand name Bactrim among others, is a fixed-dose combination antibiotic medication used to treat a variety of bacterial infections. It consists of one part trimethoprim to five parts sulfamethoxazole. It is used to treat urinary tract infections, methicillin-resistant Staphylococcus aureus (MRSA) skin infections, travelers diarrhea, respiratory tract infections, and cholera, among others. It is used both to treat and prevent pneumocystis pneumonia and toxoplasmosis in people with HIV/AIDS and other causes of immunosuppression. It can be given by mouth or intravenously.Trimethoprim/sulfamethoxazole is on the World Health Organizations List of Essential Medicines and is also available as a generic medication. In 2019, it was the 100th most commonly prescribed medication in the United States, with more than 6 million prescriptions. Medical uses
Pneumocystis jirovecii pneumonia
Trimethoprim/sulfamethoxazole (TMP/SMX) is the medicine most commonly used to prevent Pneumocystis jirovecii pneumonia (PCP) People who get Pneumocystis pneumonia have a medical condition that weakens their immune system, like HIV/AIDS, or take medicines (such as corticosteroids) that reduce the bodys ability to fight bacterial and viral infections. People with HIV/AIDS are less likely to get Pneumocystis pneumonia as a result of antiretroviral therapy (ART). However, Pneumocystis pneumonia is still a substantial public health problem. Most of what is scientifically known about Pneumocystis pneumonia and its treatment comes from studying people with HIV/AIDS. Susceptibility
Organisms against which trimethoprim/sulfamethoxazole can be effective include:
The only notable nonsusceptible organisms are Pseudomonas aeruginosa, the mycoplasmae and Francisella tularensis (the causative organism of tularaemia). | Pregnancy and breast feeding
Its use during pregnancy is contraindicated, although it has been placed in Australian pregnancy category C. Its use during the first trimester (during organogenesis) and 12 weeks prior to pregnancy has been associated with an increased risk of congenital malformations, especially malformations associated with maternal folic acid deficiency (which is most likely related to the mechanism of action of co-trimoxazole) such as neural tube defects such as spina bifida, cardiovascular malformations (e.g. Ebsteins anomaly), urinary tract defects, oral clefts, and club foot in epidemiological studies. Its use later on during pregnancy also increases the risk of preterm labour (odds ratio: 1.51) and low birth weight (odds ratio: 1.67). Animal studies have yielded similarly discouraging results.It appears to be safe for use during breastfeeding as long as the baby is healthy. Babies
Its use in those less than 2 months of age is not recommended due to the risk of adverse side effects. Adverse effects
Common side effects include nausea, vomiting, rash, and diarrhea. Severe allergic reactions and Clostridium difficile infection may occasionally occur. Its use in pregnancy is not recommended. It appears to be safe for use during breastfeeding as long as the baby is healthy. Trimethoprim/sulfamethoxazole generally results in bacterial death. It works by blocking the making and use of folate by the microorganisms. Contraindications
Contraindications include the following:
Interactions
Its use is advised against in people being concomitantly treated with:
Overdose
Likely signs of toxicity include:
The recommended treatment for overdose includes:
Administration of activated charcoal
Stomach pumping
General supportive measures
Haemodialysis, which is moderately effective in clearing co-trimoxazole from the plasma. | 11
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This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye, causing pain and redness (symptomatic, or so-called "acute" angle closure). In this situation, the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include a headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. However, the majority of cases are asymptomatic. Prior to the very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse and prevent contact between the iris and trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser iridoplasty, medication (pilocarpine) or incisional surgery may be required. Primary open-angle glaucoma is when optic nerve damage results in a progressive loss of the visual field. | 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". | 0-1
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Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:
Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism,
Basic electrolytes and serum calcium to rule out a metabolic disturbance,
Full blood count including ESR to rule out a systemic infection or chronic disease, and
Serology to exclude syphilis or HIV infection.Other investigations include:
EEG to exclude epilepsy, and an
MRI or CT scan of the head to exclude brain lesions.Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using toxicology screening. Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individuals family, partner, or friends should be asked whether the patient is currently taking any dietary supplements.Common mistakes made when diagnosing people who are psychotic include:
Not properly excluding delirium,
Not appreciating medical abnormalities (e.g., vital signs),
Not obtaining a medical history and family history,
Indiscriminate screening without an organizing framework,
Missing a toxic psychosis by not screening for substances and medications,
Not asking their family or others about dietary supplements,
Premature diagnostic closure, and
Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a persons family history, incorporating information from the person with psychosis, and information from family, friends, or significant others. Types of psychosis in psychiatric disorders may be established by formal rating scales. | Linear gingival erythema (LGE) is a periodontal disorder diagnosed based on distinct clinical characteristics. It was originally thought that LGE was directly associated with HIV, and it was thus called HIV-associated gingivitis (HIV-G). Later research confirmed that LGE also occurs in HIV negative immunocompromised patients, and it was thus renamed. Presentation
LGE is limited to the soft tissue of the periodontium, appearing as a red line 2–3 mm in width adjacent to the free gingival margin. Unlike conventional periodontal disease, though, LGE is not significantly associated with increased levels of dental plaque.The prevalence of LGE remains unclear and there is no known treatment. == References == | 0-1
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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. | Heparin, also known as unfractionated heparin (UFH), is a medication and naturally occurring glycosaminoglycan. Since heparins depend on the activity of antithrombin, they are considered anticoagulants. Specifically it is also used in the treatment of heart attacks and unstable angina. It is given by injection into a vein or under the skin. Other uses for its anticoagulant properties include inside blood specimen test tubes and kidney dialysis machines.Common side effects include bleeding, pain at the injection site, and low blood platelets. Serious side effects include heparin-induced thrombocytopenia. Greater care is needed in those with poor kidney function.Heparin is contraindicated for suspected cases of vaccine-induced pro-thrombotic immune thrombocytopenia (VIPIT) secondary to SARS-CoV-2 vaccination, as heparin may further increase the risk of bleeding in an anti-PF4/heparin complex autoimmune manner, in favor of alternative anticoagulant medications (such as argatroban or danaparoid).Heparin appears to be relatively safe for use during pregnancy and breastfeeding. Heparin is produced by basophils and mast cells in all mammals.The discovery of heparin was announced in 1916. It is on the World Health Organizations List of Essential Medicines. A fractionated version of heparin, known as low molecular weight heparin, is also available. History
Heparin was discovered by Jay McLean and William Henry Howell in 1916, although it did not enter clinical trials until 1935. It was originally isolated from dog liver cells, hence its name (hepar or "ήπαρ" is Greek for "liver"; hepar + -in). | 0-1
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Richters syndrome (RS), also known as Richters transformation, is a transformation of B cell chronic lymphocytic leukemia (CLL) or hairy cell leukemia into a fast-growing diffuse large B cell lymphoma, a variety of non-Hodgkin lymphoma which is refractory to treatment and carries a bad prognosis. There is also a less common variant in which the CLL changes into a Hodgkins lymphoma. Rarely, transformations to a form of myeloid leukemia have been observed. These extraordinarily rare transformations carry a very poor prognosis. Richters transformation affects about 5% of CLL patients at some point during their lives. Signs and symptoms
Symptoms of Richter’s transformation in a CLL patient include fever (without infection), elevated serum levels of lactate dehydrogenase, and rapidly enlarging lymph nodes. While about 8% of all CLL patients will have elevated levels of serum lactate dehydrogenase (LDH), more than 50% of CLL patients with Richters transformation will have elevated LDH levels.Richters can appear suddenly, even in patients who were in remission. Cause
A case of RS may have arisen by one of two different routes: a transformation of the CLL cells into lymphoma, or the appearance of an unrelated lymphoma.It is thought that genetic defects may introduce the additional abnormalities necessary to transform CLL cells into Richters syndrome cells. Treatment
Treatment with conventional immunochemotherapy is usually indicated; in younger patients, allogeneic bone marrow transplantation may be curative. Prognosis
The prognosis is generally poor. | PMID 16710033. S2CID 25490586. | 11
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The only long-term treatment option for the condition is liver transplantation. While awaiting transplantation, people with HRS often receive other treatments that improve the abnormalities in blood vessel tone, including supportive care with medications, or the insertion of a transjugular intrahepatic portosystemic shunt (TIPS), which is a small shunt placed to reduce blood pressure in the portal vein. Some patients may require hemodialysis to support kidney function, or a newer technique called liver dialysis which uses a dialysis circuit with albumin-bound membranes to bind and remove toxins normally cleared by the liver, providing a means of extracorporeal liver support until transplantation can be performed. Classification
Hepatorenal syndrome is a particular and common type of kidney failure that affects individuals with liver cirrhosis or, less commonly, with fulminant liver failure. The syndrome involves constriction of the blood vessels of the kidneys and dilation of blood vessels in the splanchnic circulation, which supplies the intestines. The classification of hepatorenal syndrome identifies two categories of kidney failure, termed type 1 and type 2 HRS, which both occur in individuals with either cirrhosis or fulminant liver failure. In both categories, the deterioration in kidney function is quantified either by an elevation in creatinine level in the blood, or by decreased clearance of creatinine in the urine. | Nitric oxide, prostaglandins, and other vasoactive substances have been hypothesized as powerful mediators of splanchnic vasodilation in cirrhosis. The consequence of this phenomenon is a decrease in the "effective" volume of blood sensed by the juxtaglomerular apparatus, leading to the secretion of renin and the activation of the renin–angiotensin system, which results in the vasoconstriction of vessels systemically and in the kidney specifically. However, the effect of this is insufficient to counteract the mediators of vasodilation in the splanchnic circulation, leading to persistent "underfilling" of the kidney circulation and worsening kidney vasoconstriction, leading to kidney failure.Studies to quantify this theory have shown that there is an overall decreased systemic vascular resistance in hepatorenal syndrome, but that the measured femoral and kidney fractions of cardiac output are respectively increased and reduced, suggesting that splanchnic vasodilation is implicated in the kidney failure. Many vasoactive chemicals have been hypothesized as being involved in mediating the systemic hemodynamic changes, including atrial natriuretic factor, prostacyclin, thromboxane A2, and endotoxin. In addition to this, it has been observed that the administration of medications to counteract splanchnic vasodilation (such as ornipressin, terlipressin, and octreotide) leads to improvement in glomerular filtration rate (which is a quantitative measure of kidney function) in patients with hepatorenal syndrome, providing further evidence that splanchnic vasodilation is a key feature of its pathogenesis. | 11
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Pulmonary (or pulmonic) insufficiency (or incompetence, or regurgitation) is a condition in which the pulmonary valve is incompetent and allows backflow from the pulmonary artery to the right ventricle of the heart during diastole. While a small amount of backflow may occur ordinarily, it is usually only shown on an echocardiogram and is harmless. More pronounced regurgitation that is noticed through a routine physical examination is a medical sign of disease and warrants further investigation. If it is secondary to pulmonary hypertension it is referred to as a Graham Steell murmur. Signs and symptoms
Because pulmonic regurgitation is the result of other factors in the body, any noticeable symptoms are ultimately caused by an underlying medical condition rather than the regurgitation itself. However, more severe regurgitation may contribute to right ventricular enlargement by dilation, and in later stages, right heart failure. A diastolic decrescendo murmur can sometimes be identified,( heard best) over the left lower sternal border. Causes
Among the causes of pulmonary insufficiency are:
Pathophysiology
The pathophysiology is due to diastolic pressure variations between the pulmonary artery and right ventricle, differences are often very small, but increase regurgitation. An elevation in pulmonary insufficiency due to elevated intrathoracic pressure is relevant in ventilated patients (having acute restrictive right ventricular physiology). The reasons for changes in stiffness of the right ventricles walls are not well understood, but such stiffness is thought to increase with hypertrophy of the ventricle. | Diagnosis
In the diagnosis of pulmonary insufficiency both echocardiograms and ECG is used to ascertain if the individual has this condition, as well as, the use of a chest x-ray to expose enlargement of the right atrium or ventricle. Treatment
In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced. See also
Pulmonary valve stenosis
References
Further reading
Lake, Carol L.; Booker, Peter D. (2005-01-01). Pediatric Cardiac Anesthesia. Lippincott Williams & Wilkins. ISBN 9780781751759. Bruce, Charles J.; Connolly, Heidi M. (2009-05-26). "Right-Sided Valve Disease Deserves a Little More Respect". Circulation. 119 (20): 2726–2734. doi:10.1161/CIRCULATIONAHA.108.776021. ISSN 0009-7322. PMID 19470901. M.D, Steven Lehrer (2011-12-27). Understanding Pediatric Heart Sounds. Steven Lehrer. ISBN 9781468138030. External links
"Problem: Pulmonary Valve Regurgitation". www.heart.org. Retrieved 2015-08-29. | 11
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The donation was announced to be split between the Alzheimers Society and Music for Dementia. Notes
References
External links
Dementia at Curlie | A malignant acrospiroma is a sweat gland carcinoma of the hand, which may recur locally in 50% of patients after excision, with distant metastases occurring in 60% of patients. See also
Acrospiroma
Syringoma
Hidrocystoma
List of cutaneous conditions
References
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Gait apraxia is the loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions. Ideational/conceptual apraxia is having an inability to conceptualize a task and impaired ability to complete multistep actions. This form of apraxia consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. Also, a loss occurs in the ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, these patients may try to write with it as if it were a pen, or try to comb their hair with a toothbrush. Ideomotor apraxia is having deficits in the ability to plan or complete motor actions that rely on semantic memory. These patients are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." When the ability to perform an action automatically when cued remains intact, though, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings. Limb-kinetic apraxia is having the inability to perform precise, voluntary movements of extremities. | The term acne cosmetica refers to acne caused by or aggravated by cosmetics. : 240 The mechanism is thought to be chemically induced plugging of the pilosebaceous orifice. This became a significant problem for dermatologists in the 1970s and 1980s, but with the improved formulations produced by cosmetic chemists in the decades since, a diagnosis of acne cosmetica has become relatively rare in dermatological practice. The terms "non-comedogenic" and "non-acne(i)genic" appeared on moisturizers and other cosmetic compounds as manufacturers introduced re-formulations—sometimes associated with claims that the products were "oil-free" or "water-based". Although early work produced lists of comedogenic chemicals in various strengths and vehicles, it became apparent that one could not predict the actual comedogenicity of a product from its contents; rather, the finished product itself needed use-testing.The production of a low-grade folliculitis by some components of cosmetic products has led to misdiagnosis on occasion. People may not attribute skin reactions to their cosmetics at first, but may notice worsening symptoms after using certain face makeup, sunblock or lip products. Reactions are more likely to occur if applied cosmetics are left on and not stripped after wearing them. See also
List of cutaneous conditions
References
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Lamellar ichthyosis, also known as ichthyosis lamellaris and nonbullous congenital ichthyosis, is a rare inherited skin disorder, affecting around 1 in 600,000 people. Presentation
Affected babies are born in a collodion membrane, a shiny, waxy-appearing outer layer to the skin. This is shed 10–14 days after birth, revealing the main symptom of the disease, extensive scaling of the skin caused by hyperkeratosis. With increasing age, the scaling tends to be concentrated around joints in areas such as the groin, the armpits, the inside of the elbow and the neck. The scales often tile the skin and may resemble fish scales. Collodion baby
In medicine, the term collodion baby applies to newborns who appear to have an extra layer of skin (known as a collodion membrane) that has a collodion-like quality. It is a descriptive term, not a specific diagnosis or disorder (as such, it is a syndrome). Appearance and treatment at birth
The appearance is often described as a shiny film looking like a layer of Vaseline. The eyelids and mouth may have the appearance of being forced open due to the tightness of the skin. There can be associated eversion of the eyelids (ectropion). Collodion babies can have severe medical consequences, mainly because the baby can lose heat and fluid through the abnormal skin. This can lead to hypothermia and dehydration. Strategies to prevent these problems are the use of emollients or nursing the baby in a humidified incubator. | There is also an increased risk of skin infection and mechanical compression, leading to problems like limb ischemia. There is also a risk of intoxication by cutaneous absorption of topical products, for example salicylate intoxication (similar to aspirin overdose) due to keratolytics.The condition is not thought to be painful or in itself distressing to the child. Nursing usually takes place in a neonatal intensive care unit, and good intensive care seems to have improved the prognosis markedly. The collodion membrane should peel off or "shed" 2 to 4 weeks after birth, revealing the underlying skin disorder. The condition can resemble but is different from harlequin type ichthyosis. Long term course
The appearance can be caused by several skin diseases, and it is most often not associated with other birth defects. In most cases, the baby develops an ichthyosis or ichthyosis-like condition or other rare skin disorder. Most cases (approximately 75%) of collodion baby will go on to develop a type of autosomal recessive congenital ichthyosis (either lamellar ichthyosis or congenital ichthyosiform erythrodema).In around 10% of cases the baby sheds this layer of skin and has normal skin for the rest of its life. This is known as self-healing collodion baby. The remaining 15% of cases are caused by a variety of diseases involving keratinization disorders. Known causes of collodion baby include ichthyosis vulgaris and trichothiodystrophy. Less well documented causes include Sjögren-Larsson syndrome, Netherton syndrome, Gaucher disease type 2, congenital hypothyroidism, Conradi syndrome, Dorfman-Chanarin syndrome, ketoadipiaciduria, koraxitrachitic syndrome, ichthyosis variegata and palmoplantar keratoderma with anogenital leukokeratosis. | 11
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The eponym was bestowed by Charcot after and on behalf of Gilles de la Tourette, who later became Charcots senior resident.Following the 19th-century descriptions, a psychogenic view prevailed and little progress was made in explaining or treating tics until well into the 20th century. The possibility that movement disorders, including Tourette syndrome, might have an organic origin was raised when an encephalitis lethargica epidemic from 1918 to 1926 was linked to an increase in tic disorders.During the 1960s and 1970s, as the beneficial effects of haloperidol on tics became known, the psychoanalytic approach to Tourette syndrome was questioned. The turning point came in 1965, when Arthur K. Shapiro—described as "the father of modern tic disorder research"—used haloperidol to treat a person with Tourettes, and published a paper criticizing the psychoanalytic approach. In 1975, The New York Times headlined an article with "Bizarre outbursts of Tourettes disease victims linked to chemical disorder in brain", and Shapiro said: "The bizarre symptoms of this illness are rivaled only by the bizarre treatments used to treat it. "During the 1990s, a more neutral view of Tourettes emerged, in which a genetic predisposition is seen to interact with non-genetic and environmental factors. | In this context, correction of the nasal deformities is one of the more difficult procedures. Bone and cartilage grafts may be necessary to create a nasal frame and local rotation with for example forehead flaps, or advancement flaps can be used to cover the nose. Complications from surgery
As with almost every kind of surgery, the main complications in both treatments of hypertelorism include excessive bleeding, risk of infection and CSF leaks and dural fistulas. Infections and leaks can be prevented by giving perioperative antibiotics and identifying and closing of any dural tears. The risk of significant bleeding can be prevented by meticulous technique and blood loss is compensated by transfusions. Blood loss can also be reduced by giving hypotensive anesthesia. Major eye injuries, including blindness, are rarely seen. Visual disturbances can occur due to the eye muscle imbalance after orbital mobilization. Ptosis and diplopia can also occur postoperatively, but this usually self-corrects. A quite difficult problem to correct postoperatively is canthal drift, which can be managed best by carefully preserving the canthal tendon attachments as much as possible. Despite the extensiveness in these procedures, mortality is rarely seen in operative correction of hypertelorism. See also
Hypotelorism
Telecanthus
References
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The other three explanatory modes might be rendered material composition, structure and dynamics, and, again, criterion of completion. The word that Aristotle used was αἰτία. For the present purpose, that Greek word would be better translated as "explanation" than as "cause" as those words are most often used in current English. Another translation of Aristotle is that he meant "the four Becauses" as four kinds of answer to "why" questions.Aristotle assumed efficient causality as referring to a basic fact of experience, not explicable by, or reducible to, anything more fundamental or basic. In some works of Aristotle, the four causes are listed as (1) the essential cause, (2) the logical ground, (3) the moving cause, and (4) the final cause. In this listing, a statement of essential cause is a demonstration that an indicated object conforms to a definition of the word that refers to it. A statement of logical ground is an argument as to why an object statement is true. These are further examples of the idea that a "cause" in general in the context of Aristotles usage is an "explanation".The word "efficient" used here can also be translated from Aristotle as "moving" or "initiating".Efficient causation was connected with Aristotelian physics, which recognized the four elements (earth, air, fire, water), and added the fifth element (aether). | Microcystic adnexal carcinoma (MAC) is a rare sweat gland cancer, which often appears as a yellow spot or bump in the skin. It usually occurs in the neck or head, although cases have been documented in other areas of the body. Most diagnosis occur past the age of 50. Although considered an invasive cancer, metastasis rarely occurs. If the tumor spreads, it can grow and invade fat, muscles, and other types of tissue. Main treatments are wide local excision or Mohs micrographic surgery, which ensures that most, if not all, cancer cells are removed surgically. Presentation
MACs usually present as a smooth, flesh or yellow colored, slow-growing nodule or bump somewhere on the face or neck with typical development being 3–5 years. The most common location is the mouth (occurring in 74% of cases), however cases have been documented on the scalp, tongue, trunk, upper extremities, and genitals. Patients are more likely to be white, female, and middle aged or elderly, although cases have been documented in children. Although usually presenting with no visual or physical symptoms, some patients do experience numbness, paresthesia, burning, or tingling. This may be due to the invasive nature of MACs, which can burrow deep into underlying tissues and nerves in the face. MAC is very difficult to recognize and differentiate from other conditions. Specialists may suggest a series of tests including a biopsy, an MRI, or a CT scan. The average tumor size is less than 2 cm, however cases have been documented where tumor size exceeds 7.9 cm. | 0-1
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Light transmission aggregometry
In light transmission aggregometry (LTA), platelet-rich plasma is placed between a light source and a photocell. Unaggregated plasma allows relatively little light to pass through. After adding an agonist, the platelets aggregate, resulting in greater light transmission, which is detected by the photocell. PFA-100
The PFA-100 (Platelet Function Assay - 100) is a system for analysing platelet function in which citrated whole blood is aspirated through a disposable cartridge containing an aperture within a membrane coated with either collagen and epinephrine or collagen and ADP. These agonists induce platelet adhesion, activation and aggregation, leading to rapid occlusion of the aperture and cessation of blood flow termed the closure time (CT). An elevated CT with EPI and collagen can indicate intrinsic defects such as von Willebrand disease, uremia, or circulating platelet inhibitors. The follow-up test involving collagen and ADP is used to indicate if the abnormal CT with collagen and EPI was caused by the effects of acetyl sulfosalicylic acid (aspirin) or medications containing inhibitors. Disorders
Adapted from:: vii The three broad categories of platelet disorders are "not enough", "dysfunctional", and "too many". | Primary dysmenorrhea usually begins within a year or two of menarche, typically with the onset of ovulatory cycles. Perimenstrual pain is often included as a component of premenstrual syndrome (PMS). Secondary dysmenorrhea is the diagnosis given when menstruation pain is a secondary cause to another disorder. Conditions causing secondary dysmenorrhea include endometriosis, uterine fibroids, uterine adenomyosis, and polycystic ovary syndrome. Rarely, congenital malformations, intrauterine devices, certain cancers, and pelvic infections cause secondary dysmenorrhea. If the pain occurs between menstrual periods, lasts longer than the first few days of the period, or is not adequately relieved by the use of non-steroidal anti-inflammatory drugs (NSAIDs) or hormonal contraceptives, this could be a sign for secondary causes of dysmenorrhea.When laparoscopy is used for diagnosis, the most common cause of dysmenorrhea is endometriosis, in approximately 70% of adolescents.Other causes of secondary dysmenorrhea include leiomyoma, adenomyosis, ovarian cysts, pelvic congestion, and cavitated and accessory uterine mass. Risk factors
Genetic factors, stress and depression are risk factors for dysmenorrhea. Risk factors for primary dysmenorrhea include: early age at menarche, long or heavy menstrual periods, smoking, and a family history of dysmenorrhea.Dysmenorrhea is a highly polygenic and heritable condition. There is strong evidence of familial predisposition and genetic factors increasing susceptibility to dysmenorrhea. There have been multiple polymorphisms and genetic variants in both metabolic genes and genes responsible for immunity which have been associated with the disorder.Three distinct possible phenotypes have been identified for dysmenorrhea which include "multiple severe symptoms", "mild localized pain", and "severe localized pain". | 0-1
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A third group of muscles below the bladder (pelvic floor muscles) can contract to keep urine back.A babys bladder fills to a set point, then automatically contracts and empties. As the child gets older, the nervous system develops. The childs brain begins to get messages from the filling bladder and begins to send messages to the bladder to keep it from automatically emptying until the child decides it is the time and place to void.Failures in this control mechanism result in incontinence. Reasons for this failure range from the simple to the complex. Diagnosis
The pattern of voiding and urine leakage is important as it suggests the type of incontinence. Other points include straining and discomfort, use of drugs, recent surgery, and illness.The physical examination looks for signs of medical conditions causing incontinence, such as tumors that block the urinary tract, stool impaction, and poor reflexes or sensations, which may be evidence of a nerve-related cause.Other tests include:
Stress test – the patient relaxes, then coughs vigorously as the doctor watches for loss of urine. Urinalysis – urine is tested for evidence of infection, urinary stones, or other contributing causes. Blood tests – blood is taken, sent to a laboratory, and examined for substances related to causes of incontinence. Ultrasound – sound waves are used to visualize the kidneys and urinary bladder, assess the capacity of the bladder before voiding, and the remaining amount of urine after voiding. This helps know if theres a problem in emptying. | They are widely available in pharmacies and supermarkets. The advantages of using these are that they barely need any fitting or introduction by a healthcare specialist. The disadvantages with absorbent products are that they can be bulky, leak, have odors and can cause skin breakdown due to the constant dampness. Intermittent catheters are single-use catheters that are inserted into the bladder to empty it, and once the bladder is empty they are removed and discarded. Intermittent catheters are primarily used for urinary retention (inability to empty the bladder), but for some people they can be used to reduce or avoid incontinence. These are prescription-only medical devices. Indwelling catheters (also known as foleys) are often used in hospital settings, or if the user is not able to handle any of the above solutions himself/herself (e.g. severe neurologic injury or neurodegenerative disease). These are also prescription-only medical devices. The indwelling catheter is typically connected to a urine bag that can be worn on the leg or hung on the side of the bed. Indwelling catheters need to be monitored and changed on a regular basis by a healthcare professional. The advantage of indwelling catheters is that because the urine is funneled away from the body, the skin remains dry. However, the disadvantage is that it is very common to incur urinary tract infections when using indwelling catheters. Bladder spasms and other problems can also occur with long-term use of indwelling catheters. | 11
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The biologic mechanisms of mutual recognition of the two cabinets, and the way they are glued together, are quite complex and obscure despite intensive scientific research.Orofacial clefts may be associated with a syndrome (syndromic) or may not be associated with a syndrome (nonsyndromic). Syndromic clefts are part of syndromes that are caused by a variety of factors such as environment and genetics or an unknown cause. Nonsyndromic clefts, which are not as common as syndromic clefts, also have a genetic cause. Genetics
Genetic factors contributing to cleft lip and cleft palate formation have been identified for some syndromic cases. Many clefts run in families, even though in some cases there does not seem to be an identifiable syndrome present. A number of genes are involved including cleft lip and palate transmembrane protein 1 and GAD1, One study found an association between mutations in the HYAL2 gene and cleft lip and cleft palate formation. Syndromes
The Van der Woude syndrome is caused by a specific variation in the gene IRF6 that increases the occurrence of these deformities threefold. Mutations in interferon regulatory factor 6 (IRF6) that cause cleft lip palate are also implicated in neural tube defects such as spina bifida. Another syndrome, Siderius X-linked intellectual disability, is caused by mutations in the PHF8 gene (OMIM: 300263); in addition to cleft lip or palate, symptoms include facial dysmorphism and mild intellectual disability.In some cases, cleft palate is caused by syndromes that also cause other problems:
Stickler syndrome can cause cleft lip and palate, joint pain, and myopia. | Craniodiaphyseal dysplasia (CDD), also known as lionitis, is an extremely rare autosomal recessive bone disorder that causes calcium to build up in the skull, disfiguring the facial features and reducing life expectancy. These calcium deposits decrease the size of cranial foramina, and can decrease the circumference of the cervical spinal canal. In the few cases recorded, most died in childhood. Cause
The underlying genetics are uncertain. Diagnosis
Among the medical signs are dacryocystitis, seizures, intellectual disability, and paralysis, each of which is a complication resulting from the diminutive foramina. A common sign reported as a result of the disease has been widely spaced eyes. Society
Peter Bogdanovichs 1985 drama film Mask drew public attention to the case of Roy L. "Rocky" Dennis, an American boy who died of the disorder in 1978.In the American medical drama Greys Anatomy episode "Yesterday", Jesse Plemons plays a teenage boy with lionitis. The main character of the two-issue comic book miniseries Friday the 13th: How I Spent My Summer Vacation by Wildstorm Productions is a 13-year-old boy with the disorder. In the anthology television series American Horror Story season 1, Beauregard, the brother of Tate and Adelaide, had lionitis. See also
Leontiasis ossea
References
External links
Craniodiaphyseal dysplasia at orpha.net | 0-1
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Also, the rate of lymphocytic infiltration increased in areas where the iodine intake was once low, but increased due to iodine supplementation. "The prevalence of positive serum tests in such areas rises to over 40 percent within 0.5 to 5 years." Age
It has been shown that "the prevalence of positive tests for thyroid antibodies increases with age, with a frequency as high as 33 percent in women 70 years old or older." The mean age of prevalence in women is higher than in men by one year, (58 and 59 years old respectively).Autoimmune thyroiditis can affect children. It is very rare in children under the age of five, but can occur; it accounts for around 40 percent of cases in adolescents with goiters.People with hypothyroidism over the age of 40 have an increased chance of developing autoimmune thyroiditis. Mechanism
Thyroid autoantibodies appear mostly with the presence of lymphocytes in the targeted organ. Lymphocytes produce antibodies targeting three different thyroid proteins: Thyroid peroxidase Antibodies (TPOAb), Thyroglobulin Antibodies (TgAb), and Thyroid stimulating hormone receptor Antibodies (TRAb). The antibody attacks ultimately lead to hypothyroidism, which is caused by replacement of follicular cells with parenchymatous tissue.Some patients who are healthy may be positive for more than one of these antibodies. Doctors who attend to such patients will most likely do routine follow-ups on the patients health since, even though it is highly unlikely that they will present any thyroid problems, there is still a chance that they will develop some type of dysfunction with time. | Prevention includes drinking clean water, better sanitation, and better handwashing. Treatment of the disease is with antibiotics such as azithromycin. Resistance to a number of other previously effective antibiotics is common.Paratyphoid affects about six million people a year. It is most common in parts of Asia and rare in the developed world. Most cases are due to Paratyphi A rather than Paratyphi B or C. In 2015, paratyphoid fever resulted in about 29,200 deaths, down from 63,000 deaths in 1990. The risk of death is between 10 and 15% without treatment, while with treatment, it may be less than 1%. Signs and symptoms
Paratyphoid fever resembles typhoid fever. Infection is characterized by a sustained fever, headache, abdominal pain, malaise, anorexia, a nonproductive cough (in early stage of illness), a relative bradycardia (slow heart rate), and hepatosplenomegaly (an enlargement of the liver and spleen). About 30% of Caucasians develop rosy spots on the central body. In adults, constipation is more common than diarrhea.Only 20 to 40% of people initially have abdominal pain. Nonspecific symptoms such as chills, sweating, headache, loss of appetite, cough, weakness, sore throat, dizziness, and muscle pains are frequently present before the onset of fever. Some very rare symptoms are psychosis (mental disorder), confusion, and seizures. Cause
Paratyphoid fever is caused by any of three serovars of Salmonella enterica subsp. enterica: S. Paratyphi A, S. Paratyphi B (invalid alias S. schottmuelleri), S. Paratyphi C (invalid alias S. hirschfeldii). | 0-1
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Delayed crawling or walking are the usual concerns that arise in infants with paralysis of the limb. In these cases, abnormalities of the legs are the main focus of the attention. Diagnosis
Monoplegia is diagnosed by a physician after a physical examination and sometimes after further neurologic examination as well. As monoplegia is fairly rare, after physical examination of a patient complaining of monoplegia, sometimes weakness of an additional limb is also identified and the patient is diagnosed with hemiplegia or paraplegia instead. After neurologic examination of the limb, a diagnosis of a monoplegic limb can be given if the patient receives a Medical Research Council power grade of 0, which is a measurement of the patients limb strength. Needle Electromyography is often used to study all limbs, essentially showing the extent in each limb involvement. Furthermore, magnetic resonance imaging (MRI) is the diagnostic modality of choice for investigating all forms of hemiplegia. It is especially informative to show migrational defects in hemiplegic cerebral palsy associated with seizures.An approach called single-pulse transcranial magnetic stimulation (spTMS) has also been used to help diagnose motor deficits such as monoplegia. This is done by evaluating the functional level of the corticospinal tract through stimulation of the corticospinal lesions in order to obtain neurophysiologic evidence on the integrity of the corticospinal tracts. Single-pulse transcranial magnetic stimulation provides neuropsychological feedback such as motor-evoked potentials (MEPs) and central motor conduction time (CMCT). | While chronic progressive brachial monoplegia is uncommon, syringomyelia and tumors of the cervical cord or brachial plexus may be the cause. The onset of brachial plexus paralysis is usually explosive where pain is the initial feature. Pain localizes to the shoulder but may be more diffuse, or could be limited to the lower arm. Pain is severe and often described as sharp, stabbing, throbbing, or aching. The duration of pain, which is constant, varies from a span of several hours to 3 weeks. As the pain subsides, weakness usually appears. In addition, chronicle progressive weakness of one leg suggests a tumor of the spinal cord of the lumbar plexus. Fever is often the first symptom of lumbar plexus paralysis, followed by pain in one or both legs. The pain has an abrupt onset and may occur in a femoral or sciatic distribution. Weakness may develop concurrently with pain or be delayed for as long as 3 weeks. Furthermore, a monomeric form of spinal muscular atrophy, affecting only one leg or arm, should be considered when progressive weakness is not accompanied by sensory loss. Causes
Some potential causes of monoplegia are listed below. | 11
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Brass, an alloy of copper and zinc in various proportions, was used as early as the third millennium BC in the Aegean area and the region which currently includes Iraq, the United Arab Emirates, Kalmykia, Turkmenistan and Georgia. In the second millennium BC it was used in the regions currently including West India, Uzbekistan, Iran, Syria, Iraq, and Israel. Zinc metal was not produced on a large scale until the 12th century in India, though it was known to the ancient Romans and Greeks. The mines of Rajasthan have given definite evidence of zinc production going back to the 6th century BC. To date, the oldest evidence of pure zinc comes from Zawar, in Rajasthan, as early as the 9th century AD when a distillation process was employed to make pure zinc. Alchemists burned zinc in air to form what they called "philosophers wool" or "white snow". The element was probably named by the alchemist Paracelsus after the German word Zinke (prong, tooth). German chemist Andreas Sigismund Marggraf is credited with discovering pure metallic zinc in 1746. Work by Luigi Galvani and Alessandro Volta uncovered the electrochemical properties of zinc by 1800. Corrosion-resistant zinc plating of iron (hot-dip galvanizing) is the major application for zinc. Other applications are in electrical batteries, small non-structural castings, and alloys such as brass. | Classically, hemoperitoneum was an indication for emergency surgery to locate the source of bleeding and also to recover spilled blood from the peritoneal cavity and to use it for auto-transfusion if it has not been contaminated by ruptured bowel contents. The method of control depends on the source of blood loss. Vascular bleeding, i.e. from a blood vessel, would be treated by clamping and ligation of the offending vessel, or repair of the vessel in the case of major arteries such as the aorta or mesenteric arteries. Bleeding from the spleen most often requires splenectomy, or removal of the spleen, usually but not always in the form of a total splenectomy. Bleeding from the liver might be controlled by application of hemostatic sponges, thrombin, or more recently, argon beam cauterization.With modern diagnostic aids such as computed tomography (CT) scans, certain injuries such as low-grade lacerations of the spleen may be diagnosed early and observed, with surgical options deferred unless clinical deterioration obligates them. In rare occasions, rupture of an Abdominal Aortic Aneurysm may be repaired via an endovascular technique, though this is generally not performed in the setting of acute rupture. References
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Spondyloperipheral dysplasia is an autosomal dominant disorder of bone growth. The condition is characterized by flattened bones of the spine (platyspondyly) and unusually short fingers and toes (brachydactyly). Some affected individuals also have other skeletal abnormalities, short stature, nearsightedness (myopia), hearing loss, and mental retardation. Spondyloperipheral dysplasia is a subtype of collagenopathy, types II and XI. Genetics
Spondyloperipheral dysplasia is one of a spectrum of skeletal disorders caused by mutations in the COL2A1 gene, located on chromosome 12q13.11-q13.2. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the vitreous humour (the eyeball). Type II collagen is essential for the normal development of bones and other connective tissues (the tissues that form the bodys supportive framework).Mutations in the COL2A1 gene interfere with the assembly of type II collagen molecules. The protein made by the altered COL2A1 gene cannot be used to make type II collagen, resulting in a reduced amount of this type of collagen in the body. Instead of forming collagen molecules, the abnormal protein builds up in cartilage cells (chondrocytes). These changes disrupt the normal development of bones, leading to the signs and symptoms of spondyloperipheral dysplasia.The disorder is believed to be inherited in an autosomal dominant manner. This indicates that the defective gene responsible for the disorder is located on an autosome (chromosome 12 is an autosome), and only one copy of the defective gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. | Diagnosis
Management
References
This article incorporates public domain text from
Spondyloperipheral dysplasia at NLM Genetics Home Reference
External links
Spondyloperipheral dysplasia short ulna at NIHs Office of Rare Diseases | 11
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A positive test for the MECP2 mutation is not enough to make a diagnosis.Ruling in
Decreased or loss of use of fine motor skills
Decreased or loss of verbal speech
Abnormalities during gait
Repetitive hand movements such as wringing/squeezing or clapping/tappingRuling out
Traumatic or anoxic/hypoxic brain injury, neurometabolic disease, or severe infection that may better explain symptoms
Abnormal psychomotor development during the first six months of lifeSupportive criteria
Breathing disturbances when awake
Bruxism while awake
Impaired sleep pattern
Abnormal muscle tone
Peripheral vasomotor disturbances
Scoliosis/kyphosis
Growth retardation
Small cold hands and feet
Inappropriate laughing/screaming spells
Diminished response to pain
Intense eye communication (eye pointing)
Differential diagnosis
Signs of Rett syndrome that are similar to autism:
Signs of Rett syndrome that are also present in cerebral palsy (regression of the type seen in Rett syndrome would be unusual in cerebral palsy; this confusion could rarely be made):
Treatment
Currently there is no cure for Rett syndrome. Treatment is directed towards improving function and addressing symptoms. A multi-disciplinary team approach is typically used to treat the person throughout life. This team may include primary care physician, physical therapist, occupational therapist, speech-language pathologist, nutritionist, and support services in academic and occupational settings. Some children may require special equipment and aids such as braces to arrest scoliosis, splints to modify hand movements, and nutritional programs to help them maintain adequate weight.Because of the increased risk of sudden cardiac death, when long QT syndrome is found on an annual screening EKG it is treated with an anti-arrhythmic such as a beta-blocker. | Because the correlation between in vitro data and clinical response has not been demonstrated, there is insufficient evidence to recommend either posaconazole or voriconazole for treatment of sporotrichosis at this time.SurgeryIn cases of bone infection and cavitary nodules in the lungs, surgery may be necessary.Heat therapyHeat creates higher tissue temperatures, which may inhibit fungus growth while the immune system counteracts the infection. The "pocket warmer" used for this purpose has the advantage of being able to maintain a constant temperature of 44 degrees-45 degrees C on the skin surface for several hours, while permitting unrestricted freedom of movement. The duration of treatment depends on the type of lesion, location, depth, and size. Generally, local application for 1-2 h per day, or in sleep time, for 5-6 weeks seems to be sufficient. Other animals
Sporotrichosis can be diagnosed in domestic and wild mammals. In veterinary medicine it is most frequently seen in cats and horses. Cats have a particularly severe form of cutaneous sporotrichosis. Infected cats may exhibit abscesses, cellulitis, or draining wounds that fail to respond to antibiotic treatment.Sporotrichosis can spread from nonhuman animals to humans (zoonosis). Infected cats in particular exude large quantities of Sporothrix organisms from their skin leasions and can spread the infection to people who handle them. Although cats are the most common animal source, the infection has also been known to spread to humans from dogs, rats, squirrels, and armadillos. See also
Mucormycosis
List of cutaneous conditions
References
External links
Sporotrichosis by Health in Plain English (with pictures)
Sporotrichosis by Centers for Disease Control and Prevention (CDC) | 0-1
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The court reported that "the unified hypothesis [could] no longer be regarded as a credible or alternative cause of the triad of injuries": subdural haemorrhage, retinal bleeding and encephalopathy due to hypoxemia (low blood oxygen) found in suspected SBS.On 31 January 2008, the Wisconsin Court of Appeals granted Audrey A. Edmunds a new trial based on "competing credible medical opinions in determining whether there is a reasonable doubt as to Edmundss guilt." Specifically, the appeals court found that "Edmunds presented evidence that was not discovered until after her conviction, in the form of expert medical testimony, that a significant and legitimate debate in the medical community has developed in the past ten years over whether infants can be fatally injured through shaking alone, whether an infant may suffer head trauma and yet experience a significant lucid interval prior to death, and whether other causes may mimic the symptoms traditionally viewed as indicating shaken baby or shaken impact syndrome. "In 2012, A. Norman Guthkelch, the neurosurgeon often credited with "discovering" the diagnosis of SBS, published an article "after 40 years of consideration," which is harshly critical of shaken baby prosecutions based solely on the triad of injuries. | Shaken baby syndrome (SBS), also known as abusive head trauma (AHT), is the leading cause of fatal head injuries in children younger than two years. Diagnosing the syndrome has proved both challenging and contentious for medical professionals, in that objective witnesses to the initial trauma are generally unavailable. This is said to be particularly problematic when the trauma is deemed non accidental. Some medical professionals propose that SBS is the result of respiratory abnormalities leading to hypoxia and swelling of the brain The courtroom has become a forum for conflicting theories with which generally accepted medical literature has not been reconciled. Often there are no outwardly visible signs of trauma, despite the presence of severe internal brain and eye . Complications include seizures, visual impairment, cerebral palsy, cognitive impairment, and death.The cause may be blunt trauma, vigorous shaking, or a combination of both. Often this occurs as a result of a caregiver becoming frustrated due to the child crying. Diagnosis can be difficult as symptoms may be nonspecific. A CT scan of the head is typically recommended if a concern is present. If there are concerning findings on the CT scan, a full work-up for child abuse should occur, including an eye exam and skeletal survey. Retinal hemorrhage is highly associated with AHT, occurring in 78% of cases of AHT versus 5% of cases of non-abusive head trauma.Educating new parents appears to be beneficial in decreasing rates of the condition. SBS is estimated to occur in three to four per 10,000 babies a year. | 11
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After incubation the enrichment broth is subcultured to blood agar plates and GBS like colonies are identified by the CAMP test or using latex agglutination with GBS antisera. After incubation the enrichment broth can also be subcultured to granada medium agar where GBS grows as pink-red colonies or to chromogenic agars, where GBS grows as colored colonies. GBS-like colonies that develop in chromogenic media should be confirmed as GBS using additional reliable tests to avoid mis-identification.Nucleic acid amplification tests (NAAT) such as polymerase chain reaction (PCR) and DNA hybridization probes have been developed for identifying GBS directly from recto-vaginal samples, but they still cannot replace antenatal culture for the most accurate detection of GBS carriers. Intrapartum NAAT without enrichment has a high false negative rate and the use of intrapartum NAAT without enrichment to rule out the need for IAP. Vaccination
Though IAP for EOD prevention is associated with a large decline in the incidence of the disease, there is, however, no effective strategy for preventing late-onset neonatal GBS disease.Vaccination is considered an ideal solution to prevent not only EOD and LOD but also GBS infections in adults at risk. Nevertheless, though research and clinical trials for the development of an effective vaccine to prevent GBS infections are underway, no vaccine was available in 2020. The capsular polysaccharide of GBS is not only an important GBS virulence factor but it is also an excellent candidate for the development of an effective vaccine. Protein-based vaccines are also in development. | In Africa, a number of wildlife hosts have been identified as carriers, including the banded mongoose, Egyptian fox, Rusa deer, and shrews. There are various mechanisms whereby animals can infect each other. Dogs may lick the urine of an infected animal off the grass or soil, or drink from an infected puddle. House-bound domestic dogs have contracted leptospirosis, apparently from licking the urine of infected mice in the house. Leptospirosis can also be transmitted via the semen of infected animals. The duration of bacteria being consistently present in animal urine may persist for years.Humans are the accidental host of Leptospira. Humans become infected through contact with water or moist soil that contains urine from infected animals. The bacteria enter through cuts, abrasions, ingestion of contaminated food, or contact with mucous membrane of the body (e.g. mouth, nose, and eyes). Occupations at risk of contracting leptospirosis include farmers, fishermen, garbage collectors and sewage workers. The disease is also related to adventure tourism and recreational activities. It is common among water-sports enthusiasts in specific areas, including triathlons, water rafting, canoeing and swimming, as prolonged immersion in water promotes the entry of the bacteria. However, Leptospira are unlikely to penetrate intact skin. The disease is not known to spread between humans, and bacterial dissemination in recovery period is extremely rare in humans. Once humans are infected, bacterial shedding from the kidneys usually persists for up to 60 days.Rarely, leptospirosis can be transmitted through an organ transplant. Infection through the placenta during pregnancy is also possible. | 0-1
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In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently developed deep vein thrombosis) the insertion of a vena cava filter. In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis, and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines. Treatment
The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment. Anticoagulation
Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reduce thromboembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin. | Hemochromatosis type 4 is a hereditary iron overload disorder that affects ferroportin, an iron transport protein needed to export iron from cells into circulation. Although the disease is rare, it is found throughout the world and affects people from various ethnic groups. While the majority of individuals with type 4 hemochromatosis have a relatively mild form of the disease, some affected individuals have a more severe form. As the disease progresses, iron may accumulate in the tissues of affected individuals over time, potentially resulting in organ damage. Signs and symptoms
Symptoms vary greatly between individuals with type 4 hemochromatosis. This difference in symptoms is likely due to the different types of SLC40A1 mutations patients may have. In general, signs and symptoms of type 4 hemochromatosis are caused by excess iron in cells, which leads to tissue damage. The damage is largely due to iron-catalyzed oxidative reactions. Iron can exchange electrons with a variety of substrates, which can lead to generation of reactive oxygen species. This can lead to oxidative stress, lipid peroxidation, and DNA damage, which may result in cell death. Two main forms of hemochromatosis type 4 exist (A and B), and the symptoms of these forms are distinct from one another.Type 4A hemochromatosis typically has milder symptoms than other types of hemochromatosis. Individuals with type 4A hemochromatosis tend to have hyperferritinemia (elevated ferritin in the blood plasma) and low saturated transferrin levels. These individuals are likely to have liver and spleen iron overload, primarily in Kupffer cells and other macrophages. | 0-1
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Pathophysiology
Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years.Obesity and diabetes mellitus are linked to cardiovascular disease, as are a history of chronic kidney disease and hypercholesterolaemia. In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics. Screening
Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive. Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms. Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the value of some biomarkers is questionable. Ankle-brachial index (ABI), high-sensitivity C-reactive protein (hsCRP), and coronary artery calcium, are also of unclear benefit in those without symptoms as of 2018.The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. | The Commission on Social Determinants of Health recommended that more equal distributions of power, wealth, education, housing, environmental factors, nutrition, and health care were needed to address inequalities in cardiovascular disease and non-communicable diseases. Air pollution
Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, airborne particles under 2.5 micrometers in diameter (PM2.5) are the major focus, in which gradients are used to determine CVD risk. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5. Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction. Cardiovascular risk assessment
Existing cardiovascular disease or a previous cardiovascular event, such as a heart attack or stroke, is the strongest predictor of a future cardiovascular event. Age, sex, smoking, blood pressure, blood lipids and diabetes are important predictors of future cardiovascular disease in people who are not known to have cardiovascular disease. These measures, and sometimes others, may be combined into composite risk scores to estimate an individuals future risk of cardiovascular disease. Numerous risk scores exist although their respective merits are debated. | 11
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The unspoken assumption is that by the age of five, unusual behaviors will either resolve or develop into diagnosable autism. However, some parents view the PDD label as no more than a euphemism for autism spectrum disorders, problematic because this label makes it more difficult to receive aid for early childhood intervention. Classification
The pervasive developmental disorders were:
Pervasive developmental disorder not otherwise specified (PDD-NOS), which includes atypical autism, and is the most common (47% of autism diagnoses);
Typical autism, the best-known;
Asperger syndrome (9% of autism diagnoses);
Rett syndrome; and
Childhood disintegrative disorder (CDD).The first three of these disorders are commonly called the autism spectrum disorders; the last two disorders are much rarer, and are sometimes placed in the autism spectrum and sometimes not.In May 2013, the Diagnostic and Statistical Manual–5th Edition (DSM-V) was released, updating the classification for pervasive developmental disorders. The grouping of disorders, including PDD-NOS, Autism, Asperger Syndrome, Rett Syndrome, and CDD, has been removed and replaced with the general term of Autism Spectrum Disorders. The American Psychiatric Association has concluded that using the general diagnosis of ASD supports more accurate diagnoses. The combination of these disorders was also fueled by the standpoint that Autism is characterized by common symptoms and should therefore bear a single diagnostic term. In order to distinguish between the different disorders, the DSM-V employs severity levels. The severity levels take into account required support, restricted interests and repetitive behaviors, and deficits in social communication. PDD and PDD-NOS
There is a division among doctors on the use of the term PDD. | Other known environmental conditions that have led to anophthalmia are maternal vitamin A deficiency, exposure to X-rays during gestation, solvent abuse, and exposure to thalidomide. Chromosome 14
An interstitial deletion of chromosome 14 has been known to occasionally be the source of anophthalmia. The deletion of this region of chromosome has also been associated with patients having a small tongue, and high arched palate, developmental and growth retardation, undescended testes with a micropenis, and hypothyroidism. The region that has been deleted is region q22.1-q22.3. This confirms that region 22 on chromosome 14 influences the development of the eye. Classifications
There are three classifications for this condition:
Primary anophthalmia is a complete absence of eye tissue due to a failure of the part of the brain that forms the eye. Secondary anophthalmia the eye starts to develop and for some reason stops, leaving the infant with only residual eye tissue or extremely small eyes which can only be seen under close examination. Degenerative anophthalmia the eye started to form and, for some reason, degenerated. One reason for this occurring could be a lack of blood supply to the eye. Prenatal diagnosis
Ultrasounds
Ultrasounds can be used to diagnose anophthalmia during gestation. Due to the resolution of the ultrasound, it is difficult to diagnose it until the second trimester. The earliest time to detect anophthalmia this way is approximately 20 weeks. Amniocentesis
It is possible to diagnose prenatally with amniocentesis, but it may not show a correct negative result. Amniocentesis can only diagnose anophthalmia when there is a chromosomal abnormality. | 0-1
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Voluntary apnea can be achieved by closing the vocal cords, simultaneously keeping the mouth closed and blocking the nasal vestibule, or constantly activating expiratory muscles, not allowing any inspiration. Complications
Under normal conditions, humans cannot store much oxygen in the body. Prolonged apnea leads to severe lack of oxygen in the blood circulation, leading to dysfunction of organ systems. Permanent brain damage can occur after as little as three minutes and death will inevitably ensue after a few more minutes unless ventilation is restored. However, under special circumstances such as hypothermia, hyperbaric oxygenation, apneic oxygenation (see below), or extracorporeal membrane oxygenation, much longer periods of apnea may be tolerated without severe detrimental consequences. Untrained humans usually cannot sustain voluntary apnea for more than one or two minutes, since the urge to breathe becomes unbearable. The reason for the time limit of voluntary apnea is that the rate of breathing and the volume of each breath are tightly regulated to maintain constant values of CO2 tension and pH of the blood more than oxygen levels. In apnea, CO2 is not removed through the lungs and accumulates in the blood. The consequent rise in CO2 tension and drop in pH result in stimulation of the respiratory centre in the brain which eventually cannot be overcome voluntarily. The accumulation of carbon dioxide in the lungs will eventually irritate and trigger impulses from the respiratory center part of the brain and the phrenic nerve. Rising levels of carbon dioxide signal the body to breathe and resume unconscious respiration forcibly. | These entities must be clinically excluded. Clinical condition characterized by ovarian mass, ascites, and right-sided pleural effusion. Ovarian malignancy and the other causes of pelvic mass, ascites, and pleural effusion to be considered, History of early satiety, weight loss with increased abdominal girth, bloating, intermittent abdominal pain, dyspnea, nonproductive cough may help in differentiating potential local factor causing such symptoms. Treatment
Treatment of Meigs syndrome consists of thoracentesis and paracentesis to drain off the excess fluid (exudate), and unilateral salpingo-oophorectomy or wedge resection to correct the underlying cause. Eponym
Meigs syndrome is named for Joe Vincent Meigs. References
== External links == | 0-1
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Baclofen, sold under the brand name Lioresal among others, is a medication used to treat muscle spasticity such as from a spinal cord injury or multiple sclerosis. It may also be used for hiccups and muscle spasms near the end of life. It is taken by mouth or by delivery into the spinal canal.Common side effects include sleepiness, weakness, and dizziness. Serious side effects may occur if baclofen is rapidly stopped including seizures and rhabdomyolysis. Use in pregnancy is of unclear safety while use during breastfeeding is probably safe. It is believed to work by decreasing levels of certain neurotransmitters.Baclofen was approved for medical use in the United States in 1977. It is available as a generic medication. In 2019, it was the 125th most commonly prescribed medication in the United States, with more than 5 million prescriptions. Medical uses
Baclofen is primarily used for the treatment of spastic movement disorders, especially in instances of spinal cord injury, cerebral palsy, and multiple sclerosis. Its use in people with stroke or Parkinsons disease is not recommended. Baclofen has also been used for the treatment of alcohol use disorder but evidence as of a systematic review conducted in 2018 shows that the evidence of its use as a first line intervention remains uncertain. Adverse Drug Reactions
Adverse effects include drowsiness, dizziness, weakness, fatigue, headache, trouble sleeping, nausea and vomiting, urinary retention, or constipation. Withdrawal syndrome
Discontinuation of baclofen can be associated with a withdrawal syndrome which resembles benzodiazepine withdrawal and alcohol withdrawal. | Acute bronchitis, also known as a chest cold, is short-term bronchitis – inflammation of the bronchi (large and medium-sized airways) of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.In more than 90% of cases, the cause is a viral infection. These viruses may be spread through the air when people cough or by direct contact. Risk factors include exposure to tobacco smoke, dust, and other air pollution. A small number of cases are due to high levels of air pollution or bacteria such as Mycoplasma pneumoniae or Bordetella pertussis. Diagnosis is typically based on a persons signs and symptom. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is typically not needed. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing and flu vaccination may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. Antibiotics should generally not be used. | 0-1
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Precipitating factors include sleep deprivation, use of hypnotics or tranquilisers before bedtime, and sudden awakening from sleep (e.g., telephone ringing, alarm clock).In the ICSD-2 alcohol intake had been considered as a precipitating factor of confusional arousals. In the ICSD-3 the relation between alcohol use and disorder or arousal have been excluded. Moreover, the alcohol blackout has been added as a differential diagnosis. These changes have important implications for forensic cases. == References == | Molindone, sold under the brand name Moban, is an antipsychotic which is used in the United States in the treatment of schizophrenia. It works by blocking the effects of dopamine in the brain, leading to diminished symptoms of psychosis. It is rapidly absorbed when taken orally. It is sometimes described as a typical antipsychotic, and sometimes described as an atypical antipsychotic.Molindone was discontinued by its original supplier, Endo Pharmaceuticals, on January 13, 2010. Availability and Marketing in the USA
After having been produced and subsequently discontinued by Core Pharma in 2015-2017, Molindone is available again from Epic Pharma effective December, 2018. Adverse effects
The side effect profile of molindone is similar to that of other typical antipsychotics. Unlike most antipsychotics, however, molindone use is associated with weight loss. Chemistry
Synthesis
Condensation of oximinoketone 2 (from nitrosation of 3-pentanone), with cyclohexane-1,3-dione (1) in the presence of zinc and acetic acid leads directly to the partly reduced indole derivative 6. The transformation may be rationalized by assuming as the first step, reduction of 2 to the corresponding α-aminoketone. Conjugate addition of the amine to 1 followed by elimination of hydroxide (as water) would give ene-aminoketone 3. This enamine may be assumed to be in tautomeric equilibrium with imine 4. Aldol condensation of the side chain carbonyl group with the doubly activated ring methylene group would then result in cyclization to pyrrole 5; simple tautomeric transformation would then give the observed product. Mannich reaction of 6 with formaldehyde and morpholine gives the tranquilizer molindone (7). See also
L-741,626
Losindole
Piquindone
== References == | 0-1
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In narcolepsy, the reflex inhibition of the motor system seen in cataplexy has features normally seen only in normal REM sleep. Diagnosis
The third edition of the International Classification of Sleep Disorders (ICSD-3) differentiates between narcolepsy with cataplexy (type 1) and narcolepsy without cataplexy (type 2), while the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) uses the diagnosis of narcolepsy to refer to type 1 narcolepsy only. The DSM-5 refers to narcolepsy without cataplexy as hypersomnolence disorder. The most recent edition of the International Classification of Diseases, ICD-11, currently identifies three types of narcolepsy: type 1 narcolepsy, type 2 narcolepsy, and unspecified narcolepsy.ICSD-3 diagnostic criteria posits that the individual must experience "daily periods of irrepressible need to sleep or daytime lapses into sleep" for both subtypes of narcolepsy. This symptom must last for at least three months. For a diagnosis of type 1 narcolepsy, the person must present with either cataplexy, a mean sleep latency of less than 8 minutes, and two or more sleep-onset REM periods (SOREMPs), or they must present with a hypocretin-1 concentration of less than 110 pg/mL. A diagnosis of type 2 narcolepsy requires a mean sleep latency of less than 8 minutes, two or more SOREMPs, and a hypocretin-1 concentration of more than 110 pg/mL. | This can feel like living their entire lives in a constant state of sleep deprivation.Excessive sleepiness can vary in severity, and it appears most commonly during monotonous situations that dont require much interaction. Daytime naps may occur with little warning and may be physically irresistible. These naps can occur several times a day. They are typically refreshing, but only for a few hours or less. Vivid dreams may be experienced on a regular basis, even during very brief naps. Drowsiness may persist for prolonged periods or remain constant. In addition, night-time sleep may be fragmented, with frequent awakenings. A second prominent symptom of narcolepsy is abnormal REM sleep. Narcoleptics are unique in that they enter into the REM phase of sleep in the beginnings of sleep, even when sleeping during the day.The classic symptoms of the disorder, often referred to as the "tetrad of narcolepsy," are cataplexy, sleep paralysis, hypnagogic hallucinations, and excessive daytime sleepiness. Other symptoms may include automatic behaviors and night-time wakefulness. These symptoms may not occur in all people with narcolepsy. Cataplexy is an episodic loss of muscle function, ranging from slight weakness such as limpness at the neck or knees, sagging facial muscles, weakness at the knees often referred to as "knee buckling", or inability to speak clearly, to a complete body collapse. Episodes may be triggered by sudden emotional reactions such as laughter, anger, surprise, or fear. The person remains conscious throughout the episode. In some cases, cataplexy may resemble epileptic seizures. | 11
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About half of those living to age 85 will have at least one attack, and fewer than 5% will have more than one attack. Although symptoms can be severe, risk of death is very low: 0.28 to 0.69 deaths per million.The disease has been recognized since ancient times. Signs and symptoms
The earliest symptoms of shingles, which include headache, fever, and malaise, are nonspecific, and may result in an incorrect diagnosis. These symptoms are commonly followed by sensations of burning pain, itching, hyperesthesia (oversensitivity), or paresthesia ("pins and needles": tingling, pricking, or numbness). Pain can be mild to severe in the affected dermatome, with sensations that are often described as stinging, tingling, aching, numbing or throbbing, and can be interspersed with quick stabs of agonizing pain.Shingles in children is often painless, but people are more likely to get shingles as they age, and the disease tends to be more severe.In most cases, after one to two days – but sometimes as long as three weeks – the initial phase is followed by the appearance of the characteristic skin rash. The pain and rash most commonly occur on the torso but can appear on the face, eyes, or other parts of the body. At first, the rash appears similar to the first appearance of hives; however, unlike hives, shingles causes skin changes limited to a dermatome, normally resulting in a stripe or belt-like pattern that is limited to one side of the body and does not cross the midline. | However, herpes simplex virus (HSV) can occasionally produce a rash in such a pattern (zosteriform herpes simplex).When the rash is absent (early or late in the disease, or in the case of zoster sine herpete), shingles can be difficult to diagnose. Apart from the rash, most symptoms can occur also in other conditions. Laboratory tests are available to diagnose shingles. The most popular test detects VZV-specific IgM antibody in blood; this appears only during chickenpox or shingles and not while the virus is dormant. In larger laboratories, lymph collected from a blister is tested by polymerase chain reaction (PCR) for VZV DNA, or examined with an electron microscope for virus particles. Molecular biology tests based on in vitro nucleic acid amplification (PCR tests) are currently considered the most reliable. Nested PCR test has high sensitivity, but is susceptible to contamination leading to false positive results. The latest real-time PCR tests are rapid, easy to perform, and as sensitive as nested PCR, and have a lower risk of contamination. They also have more sensitivity than viral cultures. Differential diagnosis
Shingles can be confused with herpes simplex, dermatitis herpetiformis and impetigo, and skin reactions caused by contact dermatitis, candidiasis, certain drugs and insect bites. Prevention
Shingles can be prevented by the chickenpox vaccine if the vaccine is administered before the individual gets chickenpox. If primary infection has already occurred, there are shingles vaccines that reduce the risk of developing shingles or developing severe shingles if the disease occurs. | 11
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In people with chronic kidney failure, treatment consists of dietary restriction of phosphorus; supplements containing an active form of vitamin D, such as calcitriol, doxercalciferol, paricalcitol; and phosphate binders, which are either calcium-based and non-calcium based.Extended Release Calcifediol was recently approved by the FDA as a treatment for secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic kidney disease (CKD) and low vitamin D blood levels (25-hydroxyvitamin D less than 30 ng/mL). It can help treat SHPT by increasing Vitamin D levels and lowering parathyroid hormone or PTH. It is not indicated for people with stage 5 CKD or on dialysis.In the treatment of secondary hyperparathyroidism due to chronic kidney disease on dialysis calcimimetics do not appear to affect the risk of early death. It does decrease the need for a parathyroidectomy but caused more issues with low blood calcium levels and vomiting.Most people with hyperparathyroidism secondary to chronic kidney disease will improve after renal transplantation, but many will continue to have a degree of residual hyperparathyroidism (tertiary hyperparathyroidism) post-transplant with associated risk of bone loss, etc. Prognosis
If left untreated, the disease will progress to tertiary hyperparathyroidism, where correction of the underlying cause will not stop excess PTH secretion, i.e. parathyroid gland hypertrophy becomes irreversible. In contrast with secondary hyperparathyroidism, tertiary hyperparathyroidism is associated with hypercalcemia rather than hypocalcemia. See also
Primary hyperparathyroidism
Tertiary hyperparathyroidism
References
== External links == | Megalocornea (MGCN, MGCN1) is an extremely rare nonprogressive condition in which the cornea has an enlarged diameter, reaching and exceeding 13 mm. It is thought to have two subforms, one with autosomal inheritance and the other X-linked (Xq21.3-q22). The X-linked form is more common and males generally constitute 90% of cases.It may be associated with Alport syndrome, craniosynostosis, dwarfism, Down syndrome, Parry–Romberg syndrome, Marfan syndrome, mucolipidosis, Frank–ter Haar syndrome, crouzon syndrome, megalocornea-mental retardation syndrome etc. Clinical features
Eyes are usually highly myopic. There may be with the rule astigmatism. Lens may be luxated due to zonular streaching.In rare cases, it might be associated with intellectual disabilities. References
External links
Megalocornea - eMedicine ophthalmology; May 15, 2009; Thomas A Oetting, MD, Mark A Hendrix, MD
An Infant With Enlarged Corneas - medscape | 0-1
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They may also be problematic in those who have difficulties in processing past experiencesAnimal-assisted therapy has been found to be helpful. Drawbacks may be that pets are not always welcomed in a communal space in the care setting. An animal may pose a risk to residents, or may be perceived to be dangerous. Certain animals may also be regarded as "unclean" or "dangerous" by some cultural groups.Occupational therapy also addresses psychological and psychosocial needs of patients with dementia through improving daily occupational performance and caregivers competence. When compensatory intervention strategies are added to their daily routine, the level of performance is enhanced and reduces the burden commonly placed on their caregivers. Occupational therapists can also work with other disciplines to create a client centered intervention. To manage cognitive disability, and coping with behavioral and psychological symptoms of dementia, combined occupational and behavioral therapies can support patients with dementia even further. Cognitive training
There is no strong evidence to suggest that cognitive training is beneficial for people with Parkinsons disease, dementia, or mild cognitive impairment. Personally tailored activities
Offering personally tailored activity sessions to people with dementia in long-term care homes may help manage challenging behavior. Medications
No medications have been shown to prevent or cure dementia. Medications may be used to treat the behavioral and cognitive symptoms, but have no effect on the underlying disease process.Acetylcholinesterase inhibitors, such as donepezil, may be useful for Alzheimers disease, Parkinsons disease dementia, DLB, or vascular dementia. The quality of the evidence is poor and the benefit is small. | The last two he described as the "senium", a period of mental and physical decay, and that the final phase was when "the scene of mortal existence closes after a great length of time that very fortunately, few of the human species arrive at, where the mind is reduced to the imbecility of the first epoch of infancy". In 550 BC, the Athenian statesman and poet Solon argued that the terms of a mans will might be invalidated if he exhibited loss of judgement due to advanced age. Chinese medical texts made allusions to the condition as well, and the characters for "dementia" translate literally to "foolish old person".Athenian philosophers Aristotle and Plato discussed the mental decline that can come with old age and predicted that this affects everyone who becomes old and nothing can be done to stop this decline from taking place. Plato specifically talked about how the elderly should not be in positions that require responsibility because, "There is not much acumen of the mind that once carried them in their youth, those characteristics one would call judgement, imagination, power of reasoning, and memory. They see them gradually blunted by deterioration and can hardly fulfill their function. "For comparison, the Roman statesman Cicero held a view much more in line with modern-day medical wisdom that loss of mental function was not inevitable in the elderly and "affected only those old men who were weak-willed". He spoke of how those who remained mentally active and eager to learn new things could stave off dementia. | 11
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The eyes appeared to be lumps of coagulated blood, turned out, about the bigness of a plum, ghastly to behold. It had no external ears, but holes where the ears should be. The hands and feet appeared to be swollen, were cramped up and felt quite hard. The back part of the head was much open. It made a strange kind of noise, very low, which I cannot describe. It lived about forty-eight hours and was alive when I saw it." The harlequin-type designation comes from the diamond shape of the scales at birth (resembling the costume of Arlecchino). Gallery
Notable cases
Nusrit "Nelly" Shaheen (born in 1984) is possibly the oldest known survivor; she resides in Coventry, England, and was one of nine children in a Pakistani Muslim household. Four of her eight siblings also had the condition but died as young children. Ryan Gonzalez (born in 1986) is the oldest person in the United States living with the disease. He was featured in an episode of Medical Incredible. Stephanie Turner (1993 – 2017) was the second oldest person in the United States living with the disease, and the first ever to give birth. Turners two children do not have the disease. She died on March 3, 2017, at age 23. Mason van Dyk (born 2013), despite being given a life expectancy of one to five days, was five years old as of July 2018. | Signs and symptoms
Newborns with harlequin-type ichthyosis present with thick, fissured armor-plate hyperkeratosis. Sufferers feature severe cranial and facial deformities. The ears may be very poorly developed or absent entirely, as may the nose. The eyelids may be everted (ectropion), which leaves the eyes and the area around them very susceptible to infection. Babies with this condition often bleed during birth. The lips are pulled back by the dry skin (eclabium).Joints are sometimes lacking in movement, and may be below the normal size. Hypoplasia is sometimes found in the fingers. Polydactyly has also been found on occasion. In addition, the fish mouth appearance, mouth breathing, and xerostomia place affected individuals at extremely high risk for developing rampant dental decay.Patients with this condition are extremely sensitive to changes in temperature due to their hard, cracked skin, which prevents normal heat loss. The skin also restricts respiration, which impedes the chest wall from expanding and drawing in enough air. This can lead to hypoventilation and respiratory failure. Patients are often dehydrated, as their plated skin is not well suited to retaining water. Cause
Harlequin-type ichthyosis is caused by a loss-of-function mutation in the ABCA12 gene. This gene is important in the regulation of protein synthesis for the development of the skin layer. Mutations in the gene cause impaired transport of lipids in the skin layer and may also lead to shrunken versions of the proteins responsible for skin development. | 11
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There are many measures that can improve the quality of life of people with dementia and their caregivers. Cognitive and behavioral interventions may be appropriate for treating associated symptoms of depression. Signs and symptoms
The signs and symptoms of dementia are termed as the neuropsychiatric symptoms, also known as the behavioral and psychological symptoms of dementia. Behavioral symptoms can include agitation, restlessness, inappropriate behavior, sexual disinhibition, and aggression, which can be verbal or physical. These symptoms may result from impairments in cognitive inhibition. Psychological symptoms can include depression, psychotic hallucinations and delusions, apathy, and anxiety. The most commonly affected areas include memory, visuospatial function affecting perception and orientation, language, attention and problem solving. The rate at which symptoms progress occurs on a continuum over several stages, and they vary across the dementia subtypes. Most types of dementia are slowly progressive with some deterioration of the brain well established before signs of the disorder become apparent. Often there are other conditions present such as high blood pressure, or diabetes, and there can sometimes be as many as four of these comorbidities.People with dementia are also more likely to have problems with incontinence: they are three times more likely to have urinary and four times more likely to have fecal incontinence compared to people of similar ages.Dementia symptoms can vary widely from person to person. It affects memory, attention span, communication, reasoning, judgement, problem solving and visual perception, etc. | This is mainly a problem with producing speech. They have trouble finding the right words, but mostly they have a difficulty coordinating the muscles they need to speak. Eventually, someone with NFA-PPA only uses one-syllable words or may become totally mute. A frontotemporal dementia associated with amyotrophic lateral sclerosis (ALS) known as (FTD-ALS) includes the symptoms of FTD (behavior, language and movement problems) co-occurring with amyotrophic lateral sclerosis (loss of motor neurons). Two FTD-related disorders are progressive supranuclear palsy (also classed as a Parkinson-plus syndrome), and corticobasal degeneration. These disorders are tau-associated. Huntingtons disease
Huntingtons disease is a neurodegenerative disease caused by mutations in a single gene HTT, that encodes for huntingtin protein. Symptoms include cognitive impairment and this usually declines further into dementia.The first main symptoms of Huntingtons disease often include:
difficulty concentrating
memory lapses
depression - this can include low mood, lack of interest in things, or just abnormal feelings of hopelessness
stumbling and clumsiness that is out of the ordinary
mood swings, such as irritability or aggressive behavior to insignificant things
HIV
HIV-associated dementia results as a late stage from HIV infection, and mostly affects younger people. The essential features of HIV-associated dementia are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. | 11
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It has less commonly been associated with spasm of accommodation on attempted upward gaze, pseudoabducens palsy (also known as thalamic esotropia) or slower movements of the abducting eye than the adducting eye during horizontal saccades, see-saw nystagmus and associated ocular motility deficits including skew deviation, oculomotor nerve palsy, trochlear nerve palsy and internuclear ophthalmoplegia. Causes
Parinauds syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye. Classically, it has been associated with three major groups:
Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome. Women in their 20s-30s with multiple sclerosis
Older patients following stroke of the upper brainstemHowever, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome. Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilsons disease, kernicterus, and barbiturate overdose. Diagnosis
Diagnosis can be made via combination of physical exam, particularly deficits of the relevant cranial nerves. Confirmation can be made via imaging, such as CT scan or MRI. Treatment
Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. | A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well. Prognosis
The eye findings of Parinauds syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported. References
Further reading
Aguilar-Rebolledo F, Zárate-Moysén A, Quintana-Roldán G (1998). "Parinauds syndrome in children". Rev. Invest. Clin. (in Spanish). 50 (3): 217–20. PMID 9763886. Waga S, Okada M, Yamamoto Y (1979). "Reversibility of Parinaud syndrome in thalamic hemorrhage". Neurology. 29 (3): 407–9. doi:10.1212/wnl.29.3.407. PMID 571990. S2CID 42247406. == External links == | 11
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Cancer can be difficult to diagnose and can be considered a "great imitator. "People may become anxious or depressed post-diagnosis. The risk of suicide in people with cancer is approximately double. Local symptoms
Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can block the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, affecting bowel habits. Masses in breasts or testicles may produce observable lumps. Ulceration can cause bleeding that can lead to symptoms such as coughing up blood (lung cancer), anemia or rectal bleeding (colon cancer), blood in the urine (bladder cancer), or abnormal vaginal bleeding (endometrial or cervical cancer). Although localized pain may occur in advanced cancer, the initial tumor is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen. Systemic symptoms
Systemic symptoms may occur due to the bodys response to the cancer. This may include fatigue, unintentional weight loss, or skin changes. Some cancers can cause a systemic inflammatory state that leads to ongoing muscle loss and weakness, known as cachexia.Some cancers, such as Hodgkins disease, leukemias, and liver or kidney cancers, can cause a persistent fever.Some systemic symptoms of cancer are caused by hormones or other molecules produced by the tumor, known as paraneoplastic syndromes. | Mutations in the cathepsin K gene are associated with pycnodysostosis, a hereditary osteopetrotic disease, characterised by a lack of functional cathepsin K expression. Knockout studies of cathepsin K in mice lead to an osteopetrotic phenotype, which, is partially compensated by increased expression of proteases other that cathepsin K and enhanced osteoclastogenesis. Cathepsin K has an optimal enzymatic activity in acidic conditions. It is synthesized as a proenzyme with a molecular weight of 37kDa, and upon activation by autocatalytic cleavage, is transformed into the mature, active form with a molecular weight of ~27kDa. Upon polarization of the osteoclast over the site of resorption, cathepsin K is secreted from the ruffled border into the resorptive pit. Cathepsin K transmigrates across the ruffled border by intercellular vesicles and is then released by the functional secretory domain. Within these intercellular vesicles, cathepsin K, along with reactive oxygen species generated by TRAP, further degrades the bone extracellular matrix. Several other cathepsins are expressed in osteoclasts including cathepsins B, C, D, E, G, and L. The function of these cysteine and aspartic proteases is generally unknown within bone, and they are expressed at much lower levels than cathepsin K.
Studies on cathepsin L knockout mice have been mixed, with a report of reduced trabecular bone in homozygous and heterozygous cathepsin L knockout mice compared to wild-type and another report finding no skeletal abnormalities. Matrix metalloproteinases
The matrix metalloproteinases (MMPs) comprise a family of more than 20 zinc-dependent endopeptidases. | 0-1
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This has become particularly common since the HIV epidemic began. The arts
The first sculptural representations of the human body 20,000–35,000 years ago depict obese females. Some attribute the Venus figurines to the tendency to emphasize fertility while others feel they represent "fatness" in the people of the time. Corpulence is, however, absent in both Greek and Roman art, probably in keeping with their ideals regarding moderation. This continued through much of Christian European history, with only those of low socioeconomic status being depicted as obese.During the Renaissance some of the upper class began flaunting their large size, as can be seen in portraits of Henry VIII of England and Alessandro dal Borro. Rubens (1577–1640) regularly depicted heavyset women in his pictures, from which derives the term Rubenesque. These women, however, still maintained the "hourglass" shape with its relationship to fertility. During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard. In his 1819 print, The Belle Alliance, or the Female Reformers of Blackburn!! !, artist George Cruikshank criticised the work of female reformers in Blackburn and used fatness as a means to portray them as unfeminine. Society and culture
Economic impact
In addition to its health impacts, obesity leads to many problems including disadvantages in employment and increased business costs. These effects are felt by all levels of society from individuals, to corporations, to governments. | As of 2008, the WHO estimates that at least 500 million adults (greater than 10%) are obese, with higher rates among women than men. The global prevalence of obesity more than doubled between 1980 and 2014. In 2014, more than 600 million adults were obese, equal to about 13 percent of the worlds adult population. The percentage of adults affected in the United States as of 2015–2016 is about 39.6% overall (37.9% of males and 41.1% of females).The rate of obesity also increases with age at least up to 50 or 60 years old and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity. The OECD has projected an increase in obesity rates until at least 2030, especially in the United States, Mexico and England with rates reaching 47%, 39% and 35%, respectively.Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world. These increases have been felt most dramatically in urban settings. The only remaining region of the world where obesity is not common is sub-Saharan Africa. History
Etymology
Obesity is from the Latin obesitas, which means "stout, fat, or plump". Ēsus is the past participle of edere (to eat), with ob (over) added to it. The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave. Historical attitudes
Ancient Greek medicine recognizes obesity as a medical disorder, and records that the Ancient Egyptians saw it in the same way. | 11
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AK with cutaneous horn: A cutaneous horn is a keratinic projection with its height at least one-half of its diameter, often conical in shape. They can be seen in the setting of actinic keratosis as a progression of an HAK, but are also present in other skin conditions. 38–40% of cutaneous horns represent AKs. Pigmented AK: Pigmented AKs are rare variants that often present as macules or plaques that are tan to brown in color. They can be difficult to distinguish from a solar lentigo or lentigo maligna. Actinic cheilitis: When an AK forms on the lip, it is called actinic cheilitis. This usually presents as a rough, scaly patch on the lip, often accompanied by the sensation of dry mouth and symptomatic splitting of the lips. Bowenoid AK: Usually presents as a solitary, erythematous, scaly patch or plaque with well-defined borders. Bowenoid AKs are differentiated from Bowens disease by degree of epithelial involvement as seen on histology.The presence of ulceration, nodularity, or bleeding should raise concern for malignancy. Specifically, clinical findings suggesting an increased risk of progression to squamous cell carcinoma can be recognized as "IDRBEU": I (induration/inflammation), D (diameter > 1 cm), R (rapid enlargement), B (bleeding), E (erythema), and U (ulceration). AKs are usually diagnosed clinically, but because they are difficult to clinically differentiate from squamous cell carcinoma, any concerning features warrant biopsy for diagnostic confirmation. Causes
The most important cause of AK formation is solar radiation, through a variety of mechanisms. | This altitude is known as Armstrongs Line. In practice bodily fluids do not boil off at this altitude. This is because the skin and outer organs have enough strength to withstand this pressure, thus pressure inside the body would be significantly higher—however, nitrogen bubbles are starting to form, creating a hazard. Prevention
To prevent ebullism, a pure oxygen (O2) atmosphere was used in early space flights to eliminate nitrogen in the blood. There are major fire hazards associated with using pure O2 as a breathing gas, which was central to the death of three astronauts in a fire during a ground test with Apollo 1. Nonetheless, NASA continued to use a nominally pure oxygen atmosphere throughout the Apollo Program but switched to air for the follow-on Space Transport System "Space Shuttle". Russian cosmonauts used pure oxygen before changing to a higher-pressure nitrox mixture, leading to incompatibility problems in 1975 on the Apollo-Soyuz Test Project. Space suits are often pressurized to several psi lower than stations capsules or shuttles and since they still use pure O2, an acclimation period is common in the airlock to remove nitrogen and other gases from the bloodstream. Etymology
The term "space ebullism" was introduced by Captain Julian E. Ward in his paper "The True Nature of the Boiling of Body Fluids in Space", published in Aviation Medicine in October 1956. It was suggested "because the word ebullism does not connote the addition of heat to produce vapor." It comes from Latin ebullire, meaning "to bubble out, or to boil up." | 0-1
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While the individuals in the BPD reported many of the symptoms of PTSD and CPTSD, the BPD class was clearly distinct in its endorsement of symptoms unique to BPD. The RR ratios presented in Table 5 revealed that the following symptoms were highly indicative of placement in the BPD rather than the CPTSD class: (1) frantic efforts to avoid real or imagined abandonment, (2) unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation, (3) markedly and persistently unstable self-image or sense of self, and (4) impulsiveness. Given the gravity of suicidal and self-injurious behaviors, it is important to note that there were also marked differences in the presence of suicidal and self-injurious behaviors with approximately 50% of individuals in the BPD class reporting this symptom but much fewer and an equivalent number doing so in the CPTSD and PTSD classes (14.3 and 16.7%, respectively). The only BPD symptom that individuals in the BPD class did not differ from the CPTSD class was chronic feelings of emptiness, suggesting that in this sample, this symptom is not specific to either BPD or CPTSD and does not discriminate between them. Overall, the findings indicate that there are several ways in which complex PTSD and BPD differ, consistent with the proposed diagnostic formulation of CPTSD. BPD is characterized by fears of abandonment, unstable sense of self, unstable relationships with others, and impulsive and self-harming behaviors. In contrast, in CPTSD as in PTSD, there was little endorsement of items related to instability in self-representation or relationships. | Endometrial: Endometrial causes of abnormal bleeding include infection of the endometrium, endometritis, which may occur after a miscarriage (spontaneous abortion) or a delivery, or may be related to a sexually-transmitted infection of the uterus, fallopian tubes or pelvis generally termed pelvic inflammatory disease (PID). Other endometrial causes of abnormal bleeding may relate to the ways that the endometrium heals itself or develops blood vessels. Iatrogenic (caused by medical treatment or procedures): The most common Iatrogenic cause of abnormal bleeding relates to treatment with hormonal medications such as birth control pills, patches, rings, injections, implants, and intrauterine devices (IUDs). Hormone therapy for treatment of menopausal symptoms can also cause abnormal bleeding. Unscheduled bleeding that occurs during such hormonal treatment is termed "breakthrough bleeding" (BTB) Breakthrough bleeding may result from inconsistent use of hormonal treatment, although in the initial months after initiation of a method, it may occur even with perfect use, and may ultimately affect adherence to the medication regimen. The risk of breakthrough bleeding with oral contraceptives is greater if pills are missed. Not classified: The Not Classified category of the PALM-COEIN system includes conditions that may be rare, or whose contribution to abnormal bleeding has not been well established or understood. Pregnancy
Vaginal bleeding occurs during 15–25% of first trimester pregnancies. Of these, half go on to miscarry and half bring the fetus to term. There are a number of causes including complications to the placenta, such as placental abruption and placenta previa. | 0-1
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Sometimes called smile surgery by the media, muscle transfers grafted from the thigh to the corners of the mouth can be performed to provide the ability to smile. Although "smile surgery" may provide the ability to smile, the procedure is complex and can take twelve hours for each side of the face. Also, the surgery cannot be considered a "cure" for Möbius syndrome, because it does not improve the ability to form other facial expressions. Epidemiology
It is estimated that there are, on average, 2 to 20 cases of Möbius syndrome per million births. Although its rarity often leads to late diagnosis, infants with this disorder can be identified at birth by a "mask-like" lack of expression that is detectable during crying or laughing and by an inability to suck while nursing because of paresis (palsy) of the sixth and seventh cranial nerves. Also, because a person with Möbius syndrome cannot follow objects by moving their eyes from side to side, they turn their head instead. Society and culture
Literature and media with mentions of Möbius syndrome include:
The protagonist of the novel Painted by Eliza Wyatt and Christian Leffler has Möbius syndrome. In the second season of Scream Queens, Daira Janessen (Riley McKenna Weinstein), also known as Chanel 8, has Möbius syndrome. In the first season of American medical drama The Good Doctor, a teenage patient is depicted with Möbius syndrome. In the BBC TV series Face, Loraine Deveney, a Möbius syndrome patient, was portrayed as a successful example of "smile surgery" performed by R. M. Zuker, M.D. | Suberosis is a type of hypersensitivity pneumonitis usually caused by the fungus Penicillium glabrum (formerly called Penicillium frequentans) from exposure to moldy cork dust. Chrysonilia sitophilia, Aspergillus fumigatus, uncontaminated cork dust, and Mucor macedo may also have significant roles in the pathogenesis of the disease. Cause
Cork is often harvested from the cork oak (Quercus suber) and stored in slabs in a hot and humid environment until covered in mold. Cork workers may be exposed to organic dusts in this process, leading to this disease. Diagnosis
Chest radiography, high-resolution chest CT, pulmonary function testing, bronchofibroscopy with BAL and transbronchial biopsy, delayed cutaneous hypersensitivity tests, fungal and suberin antigen testing, immediate hypersensitivity specific skin tests, and specific bronchial challenge tests can all be used for diagnosis. Chest radiography can show fine miliary mottling. Obtaining a history of antigen exposure and asking about symptoms (e.g. dyspnea, cough) can also be useful. Treatment
Avoidance of antigen exposure is beneficial. History
Vinte-e-Um Mendes first reported respiratory disease in Portuguese cork workers in 1947 at the Portuguese Medical Reunion. Cancella dAbreu first described the disease in 1955. See also
Hypersensitivity pneumonitis
References
Further reading
Cancella de Abreu, LC (1955) On a special kind of pneumoconiosis: the suberosis [in Portuguese]. Med Contemp 73,235-243
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Mitapivat, sold under the brand name Pyrukynd, is a medication used to treat hemolytic anemia. It is taken as the sulfate hydrate salt by mouth. Mitapivat is a pyruvate kinase activator.Mitapivat was approved for medical use in the United States in February 2022. Medical uses
Mitapivat is indicated for the treatment of hemolytic anemia in adults with pyruvate kinase deficiency. Pharmacology
Mechanism of action
Mitapivat binds to and activates pyruvate kinase, thereby enhancing glycolytic pathway activity, improving adenosine triphosphate (ATP) levels and reducing 2,3-diphosphoglycerate (2,3-DPG) levels. Mutations in pyruvate kinase cause deficiency in pyruvate kinase which prevents adequate red blood cell (RBC) glycolysis, leading to a buildup of the upstream glycolytic intermediate 2,3-DPG and deficiency in the pyruvate kinase product ATP. Society and culture
Legal status
On 15 September 2022, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Pyrukynd, intended for the treatment of an inherited condition called pyruvate kinase deficiency. The applicant for this medicinal product is Agios Netherlands B.V.
Names
Mitapivat is the international nonproprietary name (INN). References
Further reading
Kung C, Hixon J, Kosinski PA, Cianchetta G, Histen G, Chen Y, et al. (September 2017). "AG-348 enhances pyruvate kinase activity in red blood cells from patients with pyruvate kinase deficiency". Blood. 130 (11): 1347–1356. doi:10.1182/blood-2016-11-753525. PMC 5609468. PMID 28760888. Rab MA, Van Oirschot BA, Kosinski PA, Hixon J, Johnson K, Chubukov V, et al. (January 2021). | "AG-348 (Mitapivat), an allosteric activator of red blood cell pyruvate kinase, increases enzymatic activity, protein stability, and ATP levels over a broad range of PKLR genotypes". Haematologica. 106 (1): 238–249. doi:10.3324/haematol.2019.238865. PMC 7776327. PMID 31974203. External links
"Mitapivat sulfate". Drug Information Portal. U.S. National Library of Medicine. Clinical trial number NCT03548220 for "A Study to Evaluate Efficacy and Safety of AG-348 in Not Regularly Transfused Adult Participants With Pyruvate Kinase Deficiency (PKD)" at ClinicalTrials.gov
Clinical trial number NCT03559699 for "A Study Evaluating the Efficacy and Safety of AG-348 in Regularly Transfused Adult Participants With Pyruvate Kinase Deficiency (PKD)" at ClinicalTrials.gov | 11
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Although these results reflect a laboratory setting, the general lack of success for T. penetrans’s reproductive (opportunistic) R-strategy is surprising given the number of fleas that a single person can attract. The low survival rate suggests that a concentrated public health effort directed at any point in the flea’s life cycle is likely to deal a crippling blow to the overall population of the flea in the area. Diagnosis
There are no diagnostic tests for tungiasis. This is most likely because the parasite is ectoparasitic with visible symptoms. Identification of the parasite through removal, and a patient’s traveling history, should suffice for diagnosis, though the latter is clearly more useful than the former. Localization of the lesion may be a useful diagnostic method for the clinician. A biopsy may be done, though again, it is not required for diagnosis. Prevention
Due to the high number of hosts, eradication of tungiasis is not feasible, at least not easily so. Public health and prevention strategies should then be done with elimination as the target. Better household hygiene, including having a cemented rather than a sand floor, and washing it often, would lower the rates of tungiasis significantly.Though vaccines would be useful, due to the ectoparasitic nature of chigoe flea, they are neither a feasible nor an effective tool against tungiasis. Nevertheless, due to the high incidence of secondary infection, those at risk of tungiasis should get vaccinated against tetanus. A better approach is to use repellents that specifically target the chigoe flea. | Controlled, in-home spraying of DDT is effective as it gives the home immunity against arthropods while not contaminating the local water supplies and doing as much ecological damage as was once the case when DDT was first introduced.While other species gradually gained resistance to DDT and other insecticides that were used, T. penetrans did not; as a result, the incidence of tungiasis in Mexico is very low when compared to the rest of Latin America, especially Brazil, where rates in poor areas have been known to be as high or higher than 50%. There was a 40-year period with no tungiasis cases in Mexico. It was not until August 1989 that three Mexican patients presented with the disease. Though there were other cases of tungiasis reported thereafter, all were acquired in Africa. Treatment
As the disease is self-limiting, at least when exposure to the parasite is limited, management is mostly confined to treatment. Due to the secondary infection that can cause serious medical issues, the recommended course of action upon diagnosis is a surgical extraction of the fleas followed by the application of a topical antibiotic. Care should be taken to avoid tearing the flea during the extraction procedures as severe inflammation will result. The same will occur if part of the flea is left behind. Sterile equipment should always be used, as contaminated instruments could act as mechanical vectors for pathogens to enter the body.There is no drug that has proven to be effective against embedded fleas. | 11
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Specific activities that have been postulated as potential risk factors include intensive computer mouse use, trackball use, and typing, as well as some pastimes, including bowling, golf, fly-fishing, piano-playing, sewing, and knitting.Women are diagnosed more often than men. The syndrome commonly occurs during and, even more so, after pregnancy. Contributory factors may include hormonal changes, fluid retention and—again, more debatably and potentially harmfully—increased housework and lifting. Pathophysiology
De Quervain syndrome involves noninflammatory thickening of the tendons and the synovial sheaths that the tendons run through. The two tendons concerned are those of the extensor pollicis brevis and abductor pollicis longus muscles. These two muscles run side by side and function to bring the thumb away from the hand; the extensor pollicis brevis brings the thumb outwards radially, and the abductor pollicis longus brings the thumb forward away from the palm. De Quervain tendinopathy affects the tendons of these muscles as they pass from the forearm into the hand via a fibro-osseous tunnel (the first dorsal compartment). Evaluation of histopathological specimens shows a thickening and myxoid degeneration consistent with a chronic degenerative process, as opposed to inflammation. The pathology is identical in de Quervain seen in new mothers. Diagnosis
De Quervain syndrome is diagnosed clinically, based on history and physical examination, though diagnostic imaging such as X-ray may be used to rule out fracture, arthritis, or other causes, based on the persons history and presentation. The modified Eichoff maneuver, commonly called the Finkelsteins test, is a physical exam maneuver used to diagnose de Quervain syndrome. | This renders eight possible categories, six of which Mellor was able to find multiple criminal offenders to exemplify:
This typology is compatible with the necrophilia typology, producing hybrid categories which help to understand the totality of the offenders paraphilic desires. See also
Sexual masochism disorder
Biastophilia
Lust murder
Marquis de Sade, after whom sadism is named
Sadistic personality disorder
References
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Diabulimia, which is characterized by the deliberate manipulation of insulin levels by diabetics in an effort to control their weight. Drunkorexia, which is commonly characterized by purposely restricting food intake in order to reserve food calories for alcoholic calories, exercising excessively in order to burn calories from drinking, and over-drinking alcohol in order to purge previously consumed food. Food maintenance, which is characterized by a set of aberrant eating behaviors of children in foster care. Night eating syndrome, which is characterized by nocturnal hyperphagia (consumption of 25% or more of the total daily calories after the evening meal) with nocturnal ingestions, insomnia, loss of morning appetite and depression. Nocturnal sleep-related eating disorder, which is a parasomnia characterized by eating, habitually out-of-control, while in a state of NREM sleep, with no memory of this the next morning. Gourmand syndrome, a rare condition occurring after damage to the frontal lobe. Individuals develop an obsessive focus on fine foods. Orthorexia nervosa, a term used by Steven Bratman to describie an obsession with a "pure" diet, in which a person develops an obsession with avoiding unhealthy foods to the point where it interferes with the persons life. Klüver-Bucy syndrome, caused by bilateral lesions of the medial temporal lobe, includes compulsive eating, hypersexuality, hyperorality, visual agnosia, and docility. Prader-Willi syndrome, a genetic disorder associated with insatiable appetite and morbid obesity. Pregorexia, which is characterized by extreme dieting and over-exercising in order to control pregnancy weight gain. | Dysregulation of the HPA axis has been associated with eating disorders, such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones or neuropeptides and amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.Serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior. Norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior. Dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food. Neuropeptide Y also known as NPY is a hormone that encourages eating and decreases metabolic rate. Blood levels of NPY are elevated in patients with anorexia nervosa, and studies have shown that injection of this hormone into the brain of rats with restricted food intake increases their time spent running on a wheel. Normally the hormone stimulates eating in healthy patients, but under conditions of starvation it increases their activity rate, probably to increase the chance of finding food. The increased levels of NPY in the blood of patients with eating disorders can in some ways explain the instances of extreme over-exercising found in most anorexia nervosa patients. Leptin and ghrelin: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of satiety. Ghrelin is an appetite inducing hormone produced in the stomach and the upper portion of the small intestine. | 11
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As is revealed in many of the Cochrane systematic reviews listed below, studies of these medications for the treatment of neuropathic pain are often methodologically flawed and the evidence is potentially subject to major bias. In general, the evidence does not support the usage of antiepileptic and antidepressant medications for the treatment of neuropathic pain. Better designed clinical trials and further review from non-biased third parties are necessary to gauge just how useful for patients these medications truly are. Reviews of these systematic reviews are also necessary to assess for their failings. It is also often the case that the aforementioned medications are prescribed for neuropathic pain conditions for which they had not been explicitly tested on or for which controlled research is severely lacking; or even for which evidence suggests that these medications are not effective. The NHS for example explicitly state that amitriptyline and gabapentin can be used for treating the pain of sciatica. This is despite both the lack of high quality evidence that demonstrates efficacy of these medications for that symptom, and also the prominence of generally moderate to high quality evidence that reveals that antiepileptics in specific, including gabapentin, demonstrate no efficacy in treating it. Antidepressants
In general, according to Cochranes systematic reviews, antidepressants have shown to either be ineffective for the treatment of neuropathic pain or the evidence available is inconclusive. | This usually picks out either the motor neurons (known as motor neuron disease) or the sensory neurons (known as sensory neuronopathy or dorsal root ganglionopathy).The effect of this is to cause symptoms in more than one part of the body, often symmetrically on left and right sides. As for any neuropathy, the chief symptoms include motor symptoms such as weakness or clumsiness of movement; and sensory symptoms such as unusual or unpleasant sensations such as tingling or burning; reduced ability to feel sensations such as texture or temperature, and impaired balance when standing or walking. In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms also may occur, such as dizziness on standing up, erectile dysfunction, and difficulty controlling urination.Polyneuropathies usually are caused by processes that affect the body as a whole. Diabetes and impaired glucose tolerance are the most common causes. Hyperglycemia-induced formation of advanced glycation end products (AGEs) is related to diabetic neuropathy. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as Lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs). Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. | 11
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Classification by severity
The ICSD-R described three different severities of sleep bruxism, defining mild as occurring less than nightly, with no damage to teeth or psychosocial impairment; moderate as occurring nightly, with mild impairment of psychosocial functioning; and severe as occurring nightly, and with damage to the teeth, tempormandibular disorders and other physical injuries, and severe psychosocial impairment. Classification by duration
The ICSD-R also described three different types of sleep bruxism according to the duration the condition is present, namely acute, which lasts for less than one week; subacute, which lasts for more than a week and less than one month; and chronic which lasts for over a month. Management
Treatment for bruxism revolves around repairing the damage to teeth that has already occurred, and also often, via one or more of several available methods, attempting to prevent further damage and manage symptoms, but there is no widely accepted, best treatment. Since bruxism is not life-threatening, and there is little evidence of the efficacy of any treatment, it has been recommended that only conservative treatment which is reversible and that carries low risk of morbidity should be used. The main treatments that have been described in awake and sleep bruxism are described below. Psychosocial interventions
Given the strong association between awake bruxism and psychosocial factors (the relationship between sleep bruxism and psychosocial factors being unclear), the role of psychosocial interventions could be argued to be central to the management. | The pain may be felt over the angle of the jaw (masseter) or in the temple (temporalis), and may be described as a headache or an aching jaw. Most (but not all) bruxism includes clenching force provided by masseter and temporalis muscle groups; but some bruxers clench and grind front teeth only, which involves minimal action of the masseter and temporalis muscles. The temporomandibular joints themselves may also become painful, which is usually felt just in front of the ear, or inside the ear itself. Clicking of the jaw joint may also develop. The forces exerted on the teeth are more than the periodontal ligament is biologically designed to handle, and so inflammation may result. A tooth may become sore to bite on, and further, tooth wear may reduce the insulating width of enamel and dentin that protects the pulp of the tooth and result in hypersensitivity, e.g. to cold stimuli. The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. Indeed, the symptoms of TMD overlap with those of bruxism. Others suggest that there is no strong association between TMD and bruxism. A systematic review investigating the possible relationship concluded that when self-reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when stricter diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. | 11
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These signs disappear with treatment of the hyperthyroidism.Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball), which occurs specifically and uniquely in hyperthyroidism caused by Graves disease (note that not all exophthalmos is caused by Graves disease, but when present with hyperthyroidism is diagnostic of Graves disease). This forward protrusion of the eyes is due to immune-mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare. Thyroid storm
Thyroid storm is a severe form of thyrotoxicosis characterized by rapid and often irregular heart beat, high temperature, vomiting, diarrhea, and mental agitation. Symptoms may not be typical in the young, old, or pregnant. It usually occurs due to untreated hyperthyroidism and can be provoked by infections. It is a medical emergency and requires hospital care to control the symptoms rapidly. Even with treatment, death occurs in 20% to 50% of cases. Hypothyroidism
Hyperthyroidism due to certain types of thyroiditis can eventually lead to hypothyroidism (a lack of thyroid hormone), as the thyroid gland is damaged. Also, radioiodine treatment of Graves disease often eventually leads to hypothyroidism. Such hypothyroidism may be diagnosed with thyroid hormone testing and treated by oral thyroid hormone supplementation. Causes
There are several causes of hyperthyroidism. Most often, the entire gland is overproducing thyroid hormone. Less commonly, a single nodule is responsible for the excess hormone secretion, called a "hot" nodule. Thyroiditis (inflammation of the thyroid) can also cause hyperthyroidism. | Sebelipase alfa, sold under the brand name Kanuma, is a recombinant form of the enzyme lysosomal acid lipase (LAL) that is used as a medication for the treatment of lysosomal acid lipase deficiency (LAL-D). It is administered via intraveneous infusion. It was approved for medical use in the European Union and in the United States in 2015. Medical uses
Sebelipase alfa is indicated for long-term enzyme replacement therapy (ERT) in people of all ages with lysosomal acid lipase (LAL) deficiency. History
Sebelipase was developed by Synageva that became part of Alexion Pharmaceuticals in 2015. For its production, chickens are genetically modified to produce the recombinant form of LAL (rhLAL) in their egg white. After extraction and purification it becomes available as the medication. On 8 December 2015 the FDA announced that its approval came from two centers: The Center for Drug Evaluation and Research (CDER) approved the human therapeutic application of the medication, while the Center for Veterinary Medicine (CVM) approved the application for a recombinant DNA construct in genetically engineered chicken to produce rhLAL in their egg whites. At the time it gained FDA approval Kanuma was the first only drug manufactured in chicken eggs and intended for use in humans.Sebelipase alfa is an orphan drug; its effectiveness was published after a phase 3 trial in 2015. The disease of LAL affects < 0.2 in 10,000 people in the EU. References
External links
"Sebelipase alfa". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Controversy
ADHD controversies include concerns about its existence as a disorder, its causes, the methods by which ADHD is diagnosed and treated including the use of stimulant medications in children, possible overdiagnosis, misdiagnosis as ADHD leading to undertreatment of the real underlying disease, alleged hegemonic practices of the American Psychiatric Association and negative stereotypes of children diagnosed with ADHD. These controversies have surrounded the subject since at least the 1970s. References
Further reading
External links
"Publications About ADHD". National Institute for Mental Health. Rockville, Maryland. Archived from the original on 2017-01-18. Retrieved 2015-04-13. | Vibratory angioedema is a form of physical urticaria that may be an inherited autosomal dominant trait, or may be acquired after prolonged exposure to occupational vibration. : 155
See also
Urticaria
Skin lesion
List of cutaneous conditions
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Pseudohermaphroditism is a condition in which an individual has a matching chromosomal and gonadal tissue (ovary or testis) sex, but mismatching external genitalia. Female pseudohermaphroditism refers to an individual with ovaries and external genitalia resembling those of a male. Male pseudohermaphroditism refers to an individual with testes and external genitalia resembling those of a female. In some cases, external sex organs associated with pseudohermaphroditism appear intermediate between a typical clitoris and penis. Thus, pseudohermaphroditism is sometimes not identified until puberty or adulthood. The term contrasts with true hermaphroditism, a condition describing an individual with both female and male reproductive organs. Associated conditions include 5-α-reductase deficiency and androgen insensitivity syndrome. Mechanism
Sex is determined by chromosomes during fertilization. In the early stages of human development, a human embryo has the precursors of female (paramesonephric or Müllerian ducts) and male (mesonephric ducts or Wolffian) gonads. If a Y chromosome is lacking, or defective as seen in Swyer syndrome, the embryo will reabsorb the mesonephric ducts and proceed with paramesonephric ducts, which give rise to ovaries. The Y chromosome contains a sex-determining region called the SRY gene. Thus, the developmental plan of the embryo is altered only if this gene is present and functional.Mutations affecting the androgen receptor (AR) gene may cause either complete or partial androgen insensitivity syndrome. Androgens are a group of hormones which regulate the development and maintenance of male characteristics. | Between 8 and 12 weeks, human male fetuses become externally distinct as androgens enlarge the phallus and produce a penis with a urethra and scrotum.Persistent Müllerian duct syndrome is a form of pseudohermaphroditism, developed through Müllerian-inhibiting factor defects. In such instances, duct derivatives are present in males, including the uterus, fallopian tubes, and upper vagina. Management
Surgery is sometimes performed to alter the appearance of the genitals. Sex-specific cancers present on the gonads may require surgical removal. History
John Money is perhaps the best-known early researcher in this area. His doctoral thesis was titled Hermaphroditism: An Inquiry into the Nature of a Human Paradox, and awarded by Harvard University in 1952. Terminology
The term "Pseudohermaphroditimus" (pseudohermaphroditism) was coined in German by Edwin Klebs in 1876. Klebs had included the term as a synonym for the earlier coined, "spurious hermaphroditism" (which he referred to as Schein-Zwitter in German). | 11
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Thus, this sign is reasonably predictive when present, but not helpful when absent, as only one-third to one-half of children who are anemic (depending on severity) will show pallor.In severe cases, shortness of breath can occur. Pica may also develop; of which consumption of ice, known as pagophagia, has been suggested to be the most specific for iron deficiency anemia.Other possible symptoms and signs of iron-deficiency anemia include:
Child development
Iron-deficiency anemia is associated with poor neurological development, including decreased learning ability and altered motor functions. This is because iron deficiency impacts the development of the cells of the brain called neurons. When the body is low on iron, the red blood cells get priority on iron and it is shifted away from the neurons of the brain. Exact causation has not been established, but there is a possible long-term impact from these neurological issues. Cause
A diagnosis of iron-deficiency anemia requires further investigation into its cause. It can be caused by increased iron demand, increased iron loss, or decreased iron intake. Increased iron demand often occurs during periods of growth, such as in children and pregnant women. For example, during stages of rapid growth, babies and adolescents may outpace their dietary intake of iron which can result in deficiency in the absence of disease or a grossly abnormal diet. Iron loss is typically from blood loss. One example of blood loss is by chronic gastrointestinal blood loss, which could be linked to a possible cancer. | Upon awakening, the sleeper is usually alert and oriented within their surroundings, but may have an increased heart rate and symptoms of anxiety, like sweating. They may have trouble falling back to sleep for fear they will experience another nightmare. A person experiencing nightmare disorder may have trouble going through everyday tasks; anxiety and lack of sleep caused by the fearful dreams may hinder the individual from completing everyday tasks efficiently and correctly. Upon experiencing this, these nightmare sufferers may consult with a psychiatrist. The sleeper may have recurring episodes of awakening while recalling the intensely disturbing dream manifestations which usually result from fear or anxiety, but can also be triggered by anger, sadness, disgust, and other dysphoric emotions. Additionally, the sleeper may experience at least one of the following two features: delayed return of going back to sleep after episodes, and having episodes in the latter half of the sleep period. Consequences
Nightmare disorder is common: it affects about 4% of the adult population. Even if children have more nightmares than adults, only 1% of children meet the criteria of the disorder. Nightmare disorder can impair the quality of life for people who are affected by the condition. It can make the patient avoid sleep, which leads to sleep deprivation, which in turn may lead to even more intense nightmares. Some other consequences of the nightmare disorder are fatigue and insomnia.Nightmare disorders have negative consequences on several aspects of the patients life, such as sleep, cognitive and emotional functioning and well-being. | 0-1
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Cysts by location
Female reproductive system
Nabothian cyst (on the surface of the cervix)
Ovarian cyst (ovary)
Paratubal cyst (in front of fallopian tube behind the ovary)
Vaginal cystsGartners duct cyst (lateral to vaginal wall)
Bartholins cyst (at vaginal introitus)
Skenes duct cyst (Beside the urinary meatus)
Ectopic ureterocoele (around the urinary meatus)
Urethral diverticulum (In front of vaginal wall)
Male reproductive system
Rete tubular ectasia (within the rete testis)
Epididymal cyst (in the epididymis)
Hydrocele testis (testicle): clear fluid within the cavum vaginale
Spermatocele (testicle): fluid within the head of epididymis
Cutaneous and subcutaneous
Acne cyst – Pseudocysts associated with cystic acne - an inflammatory nodule with or without an associated epidermoid inclusion cyst
Arachnoid cyst (between the surface of the brain and the cranial base or on the arachnoid membrane)
Epidermoid cyst
Myxoid cyst (cutaneous condition often characterized by nail plate depression and grooves)
Pilar cyst (cyst of the scalp)
Pilonidal cyst (skin infection near tailbone)
Sebaceous cyst – sac below skin
Trichilemmal cyst – same as a pilar cyst, a familial cyst of the scalp
Head and neck
Odontogenic cyst
Ceruminous cyst (ear)
Chalazion cyst (eyelid)
Mucous cyst of the oral mucosa
Nasolabial cyst
Thyroglossal cyst
Vocal fold cyst
Chest
Fibrous cyst (breast cyst)
Pulmonary cyst (air pocket in the lung)
Pericardial cyst (abnormal dilatation of pericardium)
Abdomen
Liver cysts
Simple cysts
Hydatid cysts
Biliary cystadenoma
Biliary cystadenocarcinoma
Polycystic liver disease
Adrenal cyst (glands located above the kidneys) - It is a rare disease, affecting 0.06 to 0.18% of autopsy studies. It constitutes 5.4 to 6.0% of adrenal gland diseases. There are five major types of adrenal cysts: simple or endothelial cysts, true or epithelial cysts, pseudocysts, parasitic cysts, and cysts not classified elsewhere. 7% of the cysts can be malignant. | A cyst is a closed sac, having a distinct envelope and division compared with the nearby tissue. Hence, it is a cluster of cells that have grouped together to form a sac (like the manner in which water molecules group together to form a bubble); however, the distinguishing aspect of a cyst is that the cells forming the "shell" of such a sac are distinctly abnormal (in both appearance and behaviour) when compared with all surrounding cells for that given location. A cyst may contain air, fluids, or semi-solid material. A collection of pus is called an abscess, not a cyst. Once formed, a cyst may resolve on its own. When a cyst fails to resolve, it may need to be removed surgically, but that would depend upon its type and location. Cancer-related cysts are formed as a defense mechanism for the body following the development of mutations that lead to an uncontrolled cellular division. Once that mutation has occurred, the affected cells divide incessantly and become cancerous, forming a tumor. The body encapsulates those cells to try to prevent them from continuing their division and contain the tumor, which becomes known as a cyst. That said, the cancerous cells still may mutate further and gain the ability to form their own blood vessels, from which they receive nourishment before being contained. Once that happens, the capsule becomes useless, and the tumor may advance from benign to cancerous. Some cysts are neoplastic, and thus are called cystic tumors. | 11
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There was low- to moderate-strength evidence of no benefit for most of the other medications used in RCTs, which included antidepressants (bupropion, mirtazapine, sertraline), antipsychotics (aripiprazole), anticonvulsants (topiramate, baclofen, gabapentin), naltrexone, varenicline, citicoline, ondansetron, prometa, riluzole, atomoxetine, dextroamphetamine, and modafinil. Behavioral treatments
A 2018 systematic review and network meta-analysis of 50 trials involving 12 different psychosocial interventions for amphetamine, methamphetamine, or cocaine addiction found that combination therapy with both contingency management and community reinforcement approach had the highest efficacy (i.e., abstinence rate) and acceptability (i.e., lowest dropout rate). Other treatment modalities examined in the analysis included monotherapy with contingency management or community reinforcement approach, cognitive behavioral therapy, 12-step programs, non-contingent reward-based therapies, psychodynamic therapy, and other combination therapies involving these.Additionally, research on the neurobiological effects of physical exercise suggests that daily aerobic exercise, especially endurance exercise (e.g., marathon running), prevents the development of drug addiction and is an effective adjunct therapy (i.e., a supplemental treatment) for amphetamine addiction. Exercise leads to better treatment outcomes when used as an adjunct treatment, particularly for psychostimulant addictions. In particular, aerobic exercise decreases psychostimulant self-administration, reduces the reinstatement (i.e., relapse) of drug-seeking, and induces increased dopamine receptor D2 (DRD2) density in the striatum. This is the opposite of pathological stimulant use, which induces decreased striatal DRD2 density. One review noted that exercise may also prevent the development of a drug addiction by altering ΔFosB or c-Fos immunoreactivity in the striatum or other parts of the reward system. | Once nucleus accumbens ΔFosB is sufficiently overexpressed, it begins to increase the severity of addictive behavior (i.e., compulsive drug-seeking) with further increases in its expression. While there are currently no effective drugs for treating amphetamine addiction, regularly engaging in sustained aerobic exercise appears to reduce the risk of developing such an addiction. Sustained aerobic exercise on a regular basis also appears to be an effective treatment for amphetamine addiction; exercise therapy improves clinical treatment outcomes and may be used as an adjunct therapy with behavioral therapies for addiction. Biomolecular mechanisms
Chronic use of amphetamine at excessive doses causes alterations in gene expression in the mesocorticolimbic projection, which arise through transcriptional and epigenetic mechanisms. The most important transcription factors that produce these alterations are Delta FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB), cAMP response element binding protein (CREB), and nuclear factor-kappa B (NF-κB). ΔFosB is the most significant biomolecular mechanism in addiction because ΔFosB overexpression (i.e., an abnormally high level of gene expression which produces a pronounced gene-related phenotype) in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and regulates multiple behavioral effects (e.g., reward sensitization and escalating drug self-administration) involved in addiction. Once ΔFosB is sufficiently overexpressed, it induces an addictive state that becomes increasingly more severe with further increases in ΔFosB expression. | 11
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Thus, quantum physics casts reasonable doubt on the traditional determinism of classical, Newtonian physics in so far as reality does not seem to be absolutely determined. This was the subject of the famous Bohr–Einstein debates between Einstein and Niels Bohr and there is still no consensus.Adequate determinism (see Varieties, above) is the reason that Stephen Hawking calls libertarian free will "just an illusion". See also
References
Notes
Bibliography
Daniel Dennett (2003) Freedom Evolves. Viking Penguin. John Earman (2007) "Aspects of Determinism in Modern Physics" in Butterfield, J., and Earman, J., eds., Philosophy of Physics, Part B. North Holland: 1369–1434. George Ellis (2005) "Physics and the Real World", Physics Today. Epstein, J.M. (1999). "Agent Based Models and Generative Social Science". Complexity. IV (5): 41–60. Bibcode:1999Cmplx...4e..41E. CiteSeerX 10.1.1.118.546. doi:10.1002/(sici)1099-0526(199905/06)4:5<41::aid-cplx9>3.0.co;2-f.
Epstein, J.M. and Axtell R. (1996) Growing Artificial Societies – Social Science from the Bottom. MIT Press. Harris, James A. (2005) Of Liberty and Necessity: The Free Will Debate in Eighteenth-Century British Philosophy. Clarendon Press. Kenrick, D. T.; Li, N. P.; Butner, J. (2003). "Dynamical evolutionary psychology: Individual decision rules and emergent social norms" (PDF). Psychological Review. 110 (1): 3–28. CiteSeerX 10.1.1.526.5218. doi:10.1037/0033-295x.110.1.3. PMID 12529056. S2CID 43306158. Albert Messiah, Quantum Mechanics, English translation by G. M. Temmer of Mécanique Quantique, 1966, John Wiley and Sons, vol. I, chapter IV, section III. Ernest Nagel (3 March 1960). "Determinism in history". Philosophy and Phenomenological Research. 20 (3): 291–317. doi:10.2307/2105051. JSTOR 2105051. (Online version found here)
John T Roberts (2006). "Determinism". In Sahotra Sarkar; Jessica Pfeifer (eds.). The Philosophy of Science: A-M. Taylor & Francis. pp. 197 ff. | Industry workers often have NIHL because the discomfort threshold is not a relevant indicator of the harmfulness of a sound. Gradually developing
Gradually developing NIHL refers to permanent cochlear damage from repeated exposure to loud sounds over a period of time. Unlike acoustic trauma, this form of NIHL does not occur from a single exposure to a high-intensity sound pressure level. Gradually developing NIHL can be caused by multiple exposures to excessive noise in the workplace or any source of repetitive, frequent exposures to sounds of excessive volume, such as home and vehicle stereos, concerts, nightclubs, and personal media players. Earplugs have been recommended for those people who regularly attend live music concerts. A range of earplugs are now available ranging from inexpensive disposable sets to custom fit, attenuated earplugs which provide true fidelity at reduced audio levels. Personal listening devices
Although research is limited, it suggests that increased exposure to loud noise through personal listening devices is a risk factor for noise induced hearing loss. More than half of people are exposed to sound through music exposure on personal devices greater than recommended levels. Research suggests stronger correlations between extended duration or elevated usage of personal listening devices and hearing loss. Workplace
About 22 million workers are exposed to hazardous noise, with additional millions exposed to solvents and metals that could put them at increased risk for hearing loss. Occupational hearing loss is one of the most common occupational diseases. 49% of male miners have hearing loss by the age of 50. | 0-1
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Patients have markedly reduced whole-body cholesterol biosynthesis associated with suppressed hepatic, ileal, and mononuclear leukocyte hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate-controlling enzyme in the cholesterol biosynthetic pathway. Whether or not the down-regulation is due to accumulated sitosterol is still debatable, but most recent data indicate that secondary effects of unknown regulators other than sitosterol can lead to reduced HMG-CoA reductase activity in the disease. This is coupled with significantly increased low-density lipoprotein (LDL) receptor expression. Diagnosis
Diagnosis is made by measuring serum plant sterol concentrations. Treatment
The disorder is treated by strictly reducing the intake of foods rich in plant sterols (e.g., vegetable oils, olives and avocados). However, dietary therapy is often never fully sufficient to control this disease since plant sterols are constituents of all plant-based foods. Statins have been used, and while these lower cholesterol levels and may ameliorate atherosclerotic disease, plant sterol levels are insufficiently lowered by their use alone. If dietary treatment alone is insufficient, bile acid-binding resins (e.g., cholestyramine, colestipol) could be considered. In October 2002, a new cholesterol absorption inhibitor, ezetimibe, received US Food and Drug Administration (FDA) approval for use in sitosterolemia. This drug is now the standard of care, as it blocks sterol entry and can be used in combination with bile-acid resins. Finally, ileal bypass has been performed in select cases to decrease the levels of plant sterols in the body, though this therapy was undertaken prior to the advent of ezetimibe. | Pruritus vulvae is itchiness of the vulva, which is the counterpart of pruritus scroti, and may have many different causes. : 56 Patch testing may be used to diagnose the cause. Causes
This condition is a symptom of an underlying condition more often than it is a primary condition. Vulva irritation can be caused by any moisture left on the skin. This moisture may be perspiration, urine, vaginal discharge or small amounts of stool. It may be caused by vaginal infections, vulvitis, HPV (human papilloma virus) infection, anal incontinence, Bowens disease, or dietary irritants (caffeine, potatoes, chilli, capsicum, tomatoes, and peanuts). Treatment with antibiotics can lead to a yeast infection and irritation of the vulva. Some diseases increase the possibility of yeast infections, such as diabetes mellitus. Chronic inflammation of the vulva predisposes to the development of premalignant or malignant changes. == References == | 0-1
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IVIG works as well as plasmapheresis when started within two weeks of the onset of symptoms, and has fewer complications. IVIG is usually used first because of its ease of administration and safety; the risks include occasionally causing liver inflammation, or in rare cases, kidney failure. Glucocorticoids alone have not been found to be effective in speeding recovery and could potentially delay recovery. Respiratory failure
Respiratory failure may require intubation of the trachea and breathing support through mechanical ventilation, generally on an intensive care unit. The need for ventilatory support can be anticipated by measurement of two spirometry-based breathing tests: the forced vital capacity (FVC) and the negative inspiratory force (NIF). An FVC of less than 15 mL per kilogram body weight or an NIF of less than 60 cmH2O are considered markers of severe respiratory failure. Pain
While pain is common in people with Guillain–Barré syndrome, studies comparing different types of pain medication are insufficient to make a recommendation as to which should be used. Rehabilitation
Following the acute phase, around 40% of people require intensive rehabilitation with the help of a multidisciplinary team to focus on improving activities of daily living (ADLs). Studies into the subject have been limited, but it is likely that intensive rehabilitation improves long-term symptoms. Teams may include physical therapists, occupational therapists, speech language pathologists, social workers, psychologists, other allied health professionals and nurses. | Officially, diagnosing post-schizophrenia depression in a patient requires for the patient to be experiencing a depressive episode of either short or long term following the overcoming of schizophrenia. The patient must still demonstrate some schizophrenic symptoms but those symptoms must no longer be the focus of the illness. Typically, the depressive symptoms are not severe enough to be classified as a severe depressive episode. Formally, diagnosis entails the patient having had schizophrenia within the past year, a number of schizophrenic symptoms, and depression being present for two weeks or more. Mild schizophrenic signs may be withdrawing socially, agitation or hostility, and irregular sleep such as in the case of insomnia and hypersomnia. Causes
There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those with post-schizophrenic depression often experience social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those with mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those with schizophrenia, as depressants such as alcohol and cannabis can be relaxing. | 0-1
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This technique, where one or two cells are extracted from a typically 4- to 8-cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos affected with HD genes are not implanted, so any offspring will not inherit the disease. Some forms of preimplantation genetic diagnosis—non-disclosure or exclusion testing—allow at-risk people to have HD-free offspring without revealing their own parental genotype, giving no information about whether they themselves are destined to develop HD. In exclusion testing, the embryos DNA is compared with that of the parents and grandparents to avoid inheritance of the chromosomal region containing the HD gene from the affected grandparent. In nondisclosure testing, only disease-free embryos are replaced in the uterus while the parental genotype and hence parental risk for HD are never disclosed. Prenatal testing
Obtaining a prenatal diagnosis for an embryo or fetus in the womb is also possible, using fetal genetic material acquired through chorionic villus sampling. An amniocentesis can be performed if the pregnancy is further along, within 14–18 weeks. This procedure looks at the amniotic fluid surrounding the baby for indicators of the HD mutation. This, too, can be paired with exclusion testing to avoid disclosure of parental genotype. Prenatal testing can be done when parents have been diagnosed with HD, when they have had genetic testing showing the expansion of the HTTgene, or when they have a 50% chance of inheriting the disease. | Accordingly, the disease is thought not to be caused by inadequate production of Htt, but by a toxic gain-of-function of mHtt in the body. Cellular changes
The toxic action of mHtt may manifest and produce the HD pathology through multiple cellular changes. In its mutant (polyglutamine expanded) form, the protein is more prone to cleavage that creates shorter fragments containing the polyglutamine expansion. These protein fragments have a propensity to undergo misfolding and aggregation, yielding fibrillar aggregates in which non-native polyglutamine β-strands from multiple proteins are bonded together by hydrogen bonds. These aggregates share the same fundamental cross-beta amyloid architecture seen in other protein deposition diseases. Over time, the aggregates accumulate to form inclusion bodies within cells, ultimately interfering with neuronal function. Inclusion bodies have been found in both the cell nucleus and cytoplasm. Inclusion bodies in cells of the brain are one of the earliest pathological changes, and some experiments have found that they can be toxic for the cell, but other experiments have shown that they may form as part of the bodys defense mechanism and help protect cells.Several pathways by which mHtt may cause cell death have been identified. These include effects on chaperone proteins, which help fold proteins and remove misfolded ones; interactions with caspases, which play a role in the process of removing cells; the toxic effects of glutamine on nerve cells; impairment of energy production within cells; and effects on the expression of genes.Mutant huntingtin protein has been found to play a key role in mitochondrial dysfunction. | 11
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At these doses of doxepin, dry mouth, an anticholinergic effect, was common (71%), and other side effects such as headache (25%), increased appetite (21%), and dizziness (21%) were also frequently observed, although these adverse effects were notably not significantly more frequent than with placebo in the study in question. In any case, taken together, higher doses of doxepin than very low doses are associated with an increased rate of side effects as well as apparent loss of hypnotic effectiveness with chronic treatment.Doxepin at a dose of 25 mg/day for 3 weeks has been found to decrease cortisol levels by 16% in adults with chronic insomnia and to increase melatonin production by 26% in healthy volunteers. In individuals with neuroendocrine dysregulation in the form of nocturnal melatonin deficiency presumably due to chronic insomnia, very-low-dose doxepin was found to restore melatonin levels to near-normal values after 3 weeks of treatment. These findings suggest that normalization of the hypothalamic–pituitary–adrenal axis and the circadian sleep–wake cycle may be involved in the beneficial effects of doxepin on sleep and insomnia. CYP2D6 inhibition
Doxepin has been identified as an inhibitor of CYP2D6 in vivo in a study of human patients being treated with 75 to 250 mg/day for depression. While it significantly altered metabolic ratios for sparteine and its metabolites, doxepin did not convert any of the patients to a different metabolizer phenotype (e.g., extensive to intermediate or poor). Nonetheless, inhibition of CYP2D6 by doxepin could be of clinical importance. | Acute intermittent porphyria (AIP) is a rare metabolic disorder affecting the production of heme resulting from a deficiency of the porphobilinogen deaminase. It is the most common of the acute porphyrias. Signs and symptoms
The clinical presentation of AIP is highly variable and non-specific. The patients are typically asymptomatic, with most gene carriers having no family history because the condition had remained latent for several generations. The syndrome marked by acute attacks affects only 10% of gene carriers. The mean age at diagnosis is 33 years old. Like other porphyrias, AIP is more likely to present in women. A distinguishing feature of AIP that separates it from other porphyrias is the absence of photosensitive cutaneous symptoms that occur in addition to acute attacks. Acute attacks
AIP is one of the four porphyrias that presents as an acute attack. 90% of affected individuals never experience an acute attack and are asymptomatic, while an estimated 5% of affected individuals experience repeat attacks. Attacks are most common in young adult women and are rare before puberty or after menopause. Severe acute attacks may require hospitalization. Patients usually experience symptoms in attacks that last from several hours to a few days. Between attacks, patients are asymptomatic.The most frequent presenting symptoms are abdominal pain and tachycardia. The abdominal pain is typically severe, colicky, poorly localized, and often associated with pain in back and legs. Patients may also present with vomiting and constipation, but diarrhea is unusual. | 0-1
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The FDA gave the drug a 1C rating, meaning that it found little difference between felodipine and the drugs already approved for the same use.In 1994 Astra AB and Merck changed their partnership to a joint venture called Astra Merck, and in 1998 Astra (by that time, AstraZeneca) bought out Mercks rights in the joint venture.The first generics became available in Sweden in 2003 and in the US in 2004.: 155 In April 2016, AstraZeneca announced that they were selling the right to market felodipine in China to China Medical System Holdings for $310 million; AZ would continue to manufacture the drug. Society and culture
As of 2016, felodipine was marketed under many brand names worldwide: Auronal, Cardioplen, Catrazil, Dewei, Dilahex, Enfelo, Erding, Fedil, Fedisyn, Feldil, Felicipin, Felo, Felocard, Felocor, Feloday, Felodil, Felodin, Felodip, Felodipin, Felodipina, Felodipine, Felodipino, Felodistad, Felogard, Felohexal, Felop, Felopine, Felostad, Feloten, Felotens, Felpin, Flodicar, Flodil, Keliping, Keydipin, Lodistad, Modip, Munobal, Nirmadil, Parmid, Penedil, Perfudal, Phelop, Phenodical, Plendil, Plentopine, Polo, Presid, Preslow, Prevex, Renedil, Sistar, Splendil, Stapin, Topidil, Vascalpha, Versant, and XiaoDing.The combination of felodipine and candesartan was marketed as Atacand.The combination of felodipine and ramipril was marketed as Delmuno, Tazko, Triacor, Triapin, Triasyn, Tri-Plen, Unimax, and Unitens.The combination of felodipine and enalapril was marketed as Lexxel.The combination of felodipine and metoprolol was marketed as Logimat, Logimax, and Mobloc. == References == | Laurence–Moon syndrome (LMS) is a rare autosomal recessive genetic disorder associated with retinitis pigmentosa, spastic paraplegia, and mental disabilities. Signs and symptoms
Intellectual disability, hexadactyly, central diabetes insipidus, blindness (usually by 30 years due to central retinal degeneration). Genetics
LMS is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on 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. Diagnosis
The syndrome was originally thought to have five cardinal features (and recently a sixth was added), on the basis of which a diagnostic criterion was developed:
4 primary features or 3 primary features and 2 secondary features must be present. The primary features are:
1. Polydactyly
2. Rod-cone dystrophy
3. Learning disabilities
4. Obesity
5. Hypogonadism in males
6. Renal abnormalities
While the secondary features are stated to be as:
1. Speech disorder and/or developmental delay
2. Ophthalmic abnormalities other than rod-cone dystrophy (strabismus, cataract, astigmatism etc.) 3. Brachydactyly or Syndactyly
4. Polyuria and/or polydipsia (nephrogenic diabetes insipidus)
5. Ataxia, poor coordination, imbalance
6. Mild spasticity (especially lower limbs)
7. Diabetes mellitus
8. Dental crowding, hypodontia, small roots, high arched palate
9. Congenital heart disease
10. Hepatic fibrosis
Treatment
There is no cure to LNMS. However, symptomatic treatment is often provided. The patients with LNMS often experience ataxia, spasticity and contractures, restricting their movements and daily activities. | 0-1
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A parathyroid adenoma is a benign tumor of the parathyroid gland. It generally causes hyperparathyroidism; there are very few reports of parathyroid adenomas that were not associated with hyperparathyroidism.A human being usually has four parathyroid glands located on the posterior surface of the thyroid in the neck. In order to maintain calcium metabolism, the parathyroid glands secrete parathyroid hormone (PTH) which stimulates the bones to release calcium and the kidneys to reabsorb it from the urine into the blood, thereby increasing its serum level. The action of calcitonin opposes PTH. When a parathyroid adenoma causes hyperparathyroidism, more parathyroid hormone is secreted, causing the calcium concentration of the blood to rise, resulting in hypercalcemia. Signs and symptoms
The first signs of a parathyroid adenoma and the resulting primary hyperparathyroidism can include bone fractures and urinary calculi such as kidney stones.Often, a parathyroid adenoma is diagnosed by an incidental finding on blood tests that reveal high calcium levels. Patients may not be experiencing any noticeable symptoms but could be producing excessive amounts of calcium and eventually experience problems later in life if untreated. However, if symptomatic, patients can experience: pain or discomfort in the joints, muscles, and abdomen; depression and mood changes due to the hormonal imbalance. ; constipation; exhaustion; and kidney damage. Genetics
Parathyroid adenoma can be associated with overexpression of the cyclin D1 gene. It is also associated with multiple endocrine neoplasia (MEN). Diagnosis
Hyperparathyroidism is confirmed by blood tests such as calcium and PTH levels. | Dens invaginatus (DI), also known as tooth within a tooth, is a rare dental malformation where there is an infolding of enamel into dentine. The prevalence of condition is 0.3 - 10%, affecting more males than females. The condition is presented in two forms, coronal and radicular, with the coronal form being more common. DI is a malformation of teeth most likely resulting from an infolding of the dental papilla during tooth development or invagination of all layers of the enamel organ in dental papillae. Affected teeth show a deep infolding of enamel and dentine starting from the foramen coecum or even the tip of the cusps and which may extend deep into the root. Teeth most affected are maxillary lateral incisors (80%), followed by maxillary canines (20%). Bilateral occurrence is not uncommon (25%). Signs and symptoms
Tooth affected by this condition has a higher risk of developing caries and periradicular pathology. The thin layer of the infolding enamel could be chipped off easily, providing entrance for microorganisms into the tooth canal. This can cause abscess formation, displacement of dental structures (i.e. teeth). Preventive measures should be taken. Cause
Cause of DI is unclear. However, there are several theories:
Infection
Trauma
Growth pressure of the dental arches during odontogenesis
Rapid proliferation of the internal enamel epithelium invades the underlying dental papilla
Diagnosis
During clinical examination, abnormally shaped tooth can be observed. Teeth with this condition can have a conical shape or deep pit on the lingual side or have an exaggerated talon cusp. | 0-1
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Donnatal is a combination medication that provides natural belladonna alkaloids in a specific fixed ratio combined with phenobarbital to provide peripheral anticholinergic/antispasmodic action and mild sedation. Donnatal is manufactured for Concordia Pharmaceuticals by IriSys, LLC. It is available as tablets and 5 mL elixir. Active ingredients are listed as: phenobarbital (16.2 mg), hyoscyamine sulfate (0.1037 mg), atropine sulfate (0.0194 mg), and scopolamine hydrobromide (0.0065 mg). The latter two ingredients are found in plants of the family Solanaceae, such as belladonna. Indication
Based on a review of this drug by the National Academy of Sciences–National Research Council and/or other information, FDA has classified the indications as follows: "possibly" effective: For use as adjunctive therapy in the treatment of irritable bowel syndrome (irritable colon, spastic colon, mucous colitis) and acute enterocolitis. May also be useful as adjunctive therapy in the treatment of duodenal ulcer. History
Clinical Research with Combinations of Belladonna Alkaloids and Phenobarbital
Clinical studies have been performed on different combinations of belladonna alkaloids and phenobarbital over the last 70 years. For example, Steigmann et al. evaluated a combination of 0.25 mg belladonna alkaloids and 50 mg phenobarbital on gastrointestinal symptoms in 93 patients. The population included 33 IBS patients. Eighteen out of 33 patients reported complete relief of symptoms and 13 reported fair response with partial relief within 24 hours. Only 2 IBS patients reported no response. | After 1 day, patients exhibited significant improvement in day and night pain as well as clinician global evaluation when taking Donnatal® tablets and belladonna alkaloids, but the phenobarbital group also was statistically better for day and night pain, and the placebo group for day pain. Females taking Donnatal® tablets were 4 times more likely to experience weeks free of daytime pain compared to phenobarbital alone and twice as likely to experience weeks free of nighttime pain compared to belladonna alkaloids. Only the phenobarbital group demonstrated a significant change in pain type compared to belladonna alkaloids at the end of the study with an approximate 48% response rate. Patients on Donnatal® tablets, belladonna alkaloids, and placebo all had non-significant (p > 0.149) shifts to dull pain, 39.5%, 52.3%, and 40.4%, respectively compared to belladonna alkaloids eline. Males also showed a greater response for pain free-weeks on phenobarbital in comparison to Donnatal® tablets. All groups demonstrated an improvement in bowel movement frequency. FDA status
Donnatal® is considered part of the DESI drug category and currently is listed as one of 14 drugs still under evaluation by the FDA. In response to FDA questions about Donnatal® efficacy, A. H. Robins Co. filed abbreviated new drug applications for Donnatal® tablets (ANDA 86-676), capsules (ANDA 86-677), and Elixir (ANDA 86-661). These ANDAs, with the exception of the capsule formulation, are still in force today and the FDA has not changed the review status of Donnatal® as being conditionally approved for its indication. | 11
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One example of such equipment is the 360 gamma, a radiation protection belt that applies selective shielding to protect the bone marrow stored in the pelvic area as well as other radio sensitive organs in the abdominal region without hindering functional mobility. More information on bone marrow shielding can be found in the "Health Physics Radiation Safety Journal". article Waterman, Gideon; Kase, Kenneth; Orion, Itzhak; Broisman, Andrey; Milstein, Oren (September 2017). "Selective Shielding of Bone Marrow: An Approach to Protecting Humans from External Gamma Radiation". Health Physics. 113 (3): 195–208. doi:10.1097/HP.0000000000000688. PMID 28749810. S2CID 3300412., or in the Organisation for Economic Co-operation and Development (OECD) and the Nuclear Energy Agency (NEA)s 2015 report: "Occupational Radiation Protection in Severe Accident Management" (PDF). Reduction of incorporation
Where radioactive contamination is present, an elastomeric respirator, dust mask, or good hygiene practices may offer protection, depending on the nature of the contaminant. Potassium iodide (KI) tablets can reduce the risk of cancer in some situations due to slower uptake of ambient radioiodine. Although this does not protect any organ other than the thyroid gland, their effectiveness is still highly dependent on the time of ingestion, which would protect the gland for the duration of a twenty-four-hour period. They do not prevent ARS as they provide no shielding from other environmental radionuclides. Fractionation of dose
If an intentional dose is broken up into a number of smaller doses, with time allowed for recovery between irradiations, the same total dose causes less cell death. | Ichthyosis acquisita is a disorder clinically and histologically similar to ichthyosis vulgaris. : 565
Presentation
Associated conditions
The development of ichthyosis in adulthood can be a manifestation of systemic disease, and it has been described in association with malignancies, drugs, endocrine and metabolic disease, HIV, infection, and autoimmune conditions. : 494 It usually is associated with people who have Hodgkins disease but it is also occurs in people with mycosis fungoides, other malignant sarcomas, Kaposis sarcoma and visceral carcinomas. It can occur in people with leprosy, AIDS, tuberculosis, and typhoid fever. See also
Ichthyosis
Confluent and reticulated papillomatosis of Gougerot and Carteaud
List of cutaneous conditions
References
== External links == | 0-1
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Heat syncope is fainting or dizziness as a result of overheating (syncope is the medical term for fainting). It is a type of heat illness. The basic symptom of heat syncope is fainting, with or without mental confusion. Heat syncope is caused by peripheral vessel dilation, resulting in diminished blood flow to the brain and dehydration. Signs and symptoms
Faintness, dizziness, headache, increased pulse, restlessness, nausea, vomiting, pale/clammy skin, and brief loss of consciousness. Causes
Heat syncope occurs in a warm environment when blood pressure is lowered as the body dilates (widens) arterioles (small blood vessels) in the skin to radiate heat. This condition occurs within five days of heat acclimatization, before the blood volume expands. The result is less blood to the brain, causing light-headedness and fainting when a person stands up quickly or stands for a long period of time. Those who perform strenuous work outside in warm climates are at particular risk. Diagnosis
The diagnosis of heat syncope is done during a physical examination. During the physical exam the practitioner will test the blood pressure of the patient, and the pulse. If the patient is experiencing heat syncope the blood pressure will be low, and the pulse will be elevated. Observation of excess sweating will also be a key sign. Finally, the practitioner will ask questions figuring out the history of the patients symptoms. If the patient developed symptoms while engaging in physical activity and high temperatures it will then be a true case of heat syncope. | Alzheimers disease, for example, is much more likely to develop in a person who has experienced a head injury. Brain damage, which is the destruction or degeneration of brain cells, is a common occurrence in those who experience a head injury. Neurotoxicity is another cause of brain damage that typically refers to selective, chemically induced neuron/brain damage. Classification
Head injuries include both injuries to the brain and those to other parts of the head, such as the scalp and skull. Head injuries can be closed or open. A closed (non-missile) head injury is where the dura mater remains intact. The skull can be fractured, but not necessarily. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater. Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area. A head injury may cause skull fracture, which may or may not be associated with injury to the brain. Some patients may have linear or depressed skull fractures. If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of intracranial hemorrhage include subdural, subarachnoid, extradural, and intraparenchymal hematoma. Craniotomy surgeries are used in these cases to lessen the pressure by draining off the blood. | 0-1
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Signs and symptoms
Two of the symptoms of flail chest are chest pain and shortness of breath.The characteristic paradoxical motion of the flail segment occurs due to pressure changes associated with respiration that the rib cage normally resists:
During normal inspiration, the diaphragm contracts and intercostal muscles pull the rib cage out. Pressure in the thorax decreases below atmospheric pressure, and air rushes in through the trachea. The flail segment will be pulled in with the decrease in pressure while the rest of the rib cage expands. During normal expiration, the diaphragm and intercostal muscles relax increasing internal pressure, allowing the abdominal organs to push air upwards and out of the thorax. However, a flail segment will also be pushed out while the rest of the rib cage contracts.Paradoxical motion is a late sign of flail segment; therefore, an absence of paradoxical motion does not mean the patient does not have a flail segment. The constant motion of the ribs in the flail segment at the site of the fracture is extremely painful, and, untreated, the sharp broken edges of the ribs are likely to eventually puncture the pleural sac and lung, possibly causing a pneumothorax. The concern about "mediastinal flutter" (the shift of the mediastinum with paradoxical diaphragm movement) does not appear to be merited. Pulmonary contusions are commonly associated with flail chest and that can lead to respiratory failure. This is due to the paradoxical motions of the chest wall from the fragments interrupting normal breathing and chest movement. | The knees should come in toward the chest while the person inhales, and exhale when the knees are lowered. This exercise can be done in 3 sets of 6–8 repetitions with a pause in between sets. The person should always make sure to maintain controlled breaths.Eventually, the person will be progressed to walking and posture correction while walking. Before the person is discharged from the hospital, the person should be able to perform mobility exercises to the core and should have attained good posture. Prognosis
The death rate of people with flail chest depends on the severity of their condition, ranging from 10 to 25%. A systematic review comparing the safety and effectiveness of surgical fixation versus non-surgical methods for the treatment of flail chest, reported that there was no statistically significant difference in the reported deaths between patients treated surgically and those treated non-surgically i.e. with conservative management methods. The results of the systematic review suggested that surgical intervention reduces the need for tracheostomy, reduces the time spent in the intensive care unit following a traumatic flail chest injury and could reduce the risk of acquiring pneumonia after such an event. Epidemiology
Approximately 1 out of 13 people admitted to the hospital with fractured ribs are found to have flail chest. References
External links
Rib Fractures & Flail Chest at Trauma.org – info, images, and video of paradoxical flail-segment motion | 11
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When given intravenously, clonidine can temporarily increase blood pressure by stimulating α1 receptors in smooth muscles in blood vessels. This hypertensive effect is not usual when clonidine is given by mouth or by the transdermal route. : 201–203 Plasma concentration of clonidine exceeding 2.0 ng/mL does not provide further blood pressure reduction. Attention deficit hyperactivity disorder
In the setting of attention deficit hyperactivity disorder (ADHD), clonidines molecular mechanism of action occurs due to its agonism at the alpha-2A adrenergic receptor, the subtype of the adrenergic receptor that is most principally found in the brain. Within the brain, the alpha-2A adrenergic receptors are found within the prefrontal cortex (PFC), among other areas. The alpha-2A adrenergic receptors are found on the presynaptic cleft of a given neuron, and, when activated by an agonist, the effect on downstream neurons is inhibitory. The inhibition is accomplished by preventing the secretion of the neurotransmitter norepinephrine. Thus, clonidines agonism on alpha-2A adrenergic receptors in the PFC inhibits the action of downstream neurons by preventing the secretion of norepinephrine.This mechanism is similar to the brains physiological inhibition of PFC neurons by the locus ceruleus (LC), which secretes norepinephrine into the PFC. Although norepinephrine can also bind to target adrenergic receptors on the downstream neuron (otherwise inducing a stimulatory effect), norepinephrine also binds to alpha-2A adrenergic receptors (akin to clonidines mechanism of action), inhibiting the release of norepinephrine by that neuron and inducing an inhibitory effect. | Clonidine, sold under the brand name Catapres among others, is an α2-adrenergic agonist medication used to treat high blood pressure, ADHD, drug withdrawal (alcohol, opioids, or nicotine), menopausal flushing, diarrhea, spasticity, and certain pain conditions. It is used by mouth, by injection, or as a skin patch. Onset of action is typically within an hour with the effects on blood pressure lasting for up to eight hours.Common side effect include dry mouth, dizziness, headaches, hypotension, and sleepiness. Severe side effects may include hallucinations, heart arrhythmias, and confusion. If rapidly stopped, withdrawal effects may occur. Use during pregnancy or breastfeeding is not recommended. Clonidine lowers blood pressure by stimulating α2 receptors in the brain, which results in relaxation of many arteries.Clonidine was patented in 1961 and came into medical use in 1966. It is available as a generic medication. In 2019, it was the 64th most commonly prescribed medication in the United States, with more than 11 million prescriptions. Medical uses
Clonidine is used to treat high blood pressure, attention deficit hyperactivity disorder (ADHD), drug withdrawal (alcohol, opioids, or smoking), menopausal flushing, diarrhea, and certain pain conditions. It also sees some use off-label for episodic insomnia, restless-legs syndrome, and anxiety, among other uses. Resistant hypertension
Clonidine may be effective for lowering blood pressure in people with resistant hypertension.Clonidine works by slowing the pulse rate and exerts a reduction of serum concentrations of renin, aldosterone, and catecholamines. | 11
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PBA is most commonly observed in people with neurologic injuries such as traumatic brain injury (TBI) and stroke, and neurologic diseases such as dementias including Alzheimers disease, attention deficit/hyperactivity disorder (ADHD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and Parkinsons disease (PD). It has been reported as a symptom of hyperthyroidism, Graves disease, or hypothyroidism in combination with depression.PBA has also been observed in association with a variety of other brain disorders, including brain tumors, Wilsons disease, syphilitic pseudobulbar palsy, and various encephalitides. Rarer conditions associated with PBA include gelastic epilepsy, dacrystic epilepsy, central pontine myelinolysis, olivopontinocerebellar atrophy, lipid storage diseases, chemical exposure (e.g., nitrous oxide and insecticides), fou rire prodromique, and Angelman syndrome. It is hypothesized that these primary neurologic injuries and diseases affect chemical signaling in the brain, which in turn disrupts the neurologic pathways that control emotional expression. Stroke
PBA is one of the most frequently reported post-stroke behavioral disorders, with a range of reported prevalence rates from 28% to 52%. The higher prevalence rates tend to be reported in stroke patients who are older or who have a history of prior stroke. The relationship between post-stroke depression and PBA is complicated, because the depressive syndrome also occurs with high frequency in stroke survivors. Post-stroke patients with PBA are more depressed than post-stroke patients without PBA, and the presence of a depressive syndrome may exacerbate the weeping side of PBA symptoms. Multiple sclerosis
Recent studies suggest that approximately 10% of patients with multiple sclerosis (MS) will experience at least one episode of emotional lability. | Inclisiran, sold under the brand name Leqvio, is a medication for the treatment of people with atherosclerotic cardiovascular disease (ASCVD), ASCVD risk-equivalents, and heterozygous familial hypercholesterolemia (HeFH). It is a small interfering RNA (siRNA) that acts as an inhibitor of a proprotein convertase, specifically, inhibiting translation of the protein PCSK9.Inclisiran was approved for use in the European Union in December 2020. In August 2021, it received NICE approval for use by the National Health Service in the UK. In December 2021, it was approved for medical use in the United States. Medical uses
In the European Union, inclisiran is indicated in adults with primary hypercholesterolemia (heterozygous familial and non-familial) or mixed dyslipidaemia, as an adjunct to diet in combination with a statin or statin with other lipid-lowering therapies in people unable to reach LDL-C goals with the maximum tolerated dose of a statin, or alone or in combination with other lipid-lowering therapies in people who are statin-intolerant, or for whom a statin is contraindicated.In the United States, it is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (ASCVD), who require additional lowering of low- density lipoprotein cholesterol (LDL-C). Discovery and mechanism of action
Inclisiran is a small interfering RNA that acts as an inhibitor of a proprotein convertase, specifically, inhibiting translation of the protein termed proprotein convertase subtilisin/kexin type 9 (PCSK9). | 0-1
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Initial treatment of an overdose involves resuscitation measures such as maintaining an adequate airway and adequate circulation followed by gastric decontamination by administering activated charcoal, which adsorbs the salicylate in the gastrointestinal tract. Stomach pumping is no longer routinely used in the treatment of poisonings, but is sometimes considered if the patient has ingested a potentially lethal amount less than one hour before presentation. Inducing vomiting with syrup of ipecac is not recommended. Repeated doses of activated charcoal have been proposed to be beneficial in cases of salicylate poisoning, especially in ingestion of enteric coated and extended release salicylic acid formulations which are able to remain in the gastrointestinal (GI) tract for longer periods of time. Repeated doses of activated charcoal are also useful to re-adsorb salicylates in the GI tract that may have desorbed from the previous administration of activated charcoal. The initial dose of activated charcoal is most useful if given within 2 hours of initial ingestion. Contraindications to the use of activated charcoal include altered mental status (due to the risk of aspiration), GI bleeding (often due to salicylates) or poor gastric motility. Whole bowel irrigation using the laxative polyethylene glycol can be useful to induce the gastrointestinal elimination of salicylates, particularly if there is partial or diminished response to activated charcoal.Alkalinization of the urine and plasma, by giving a bolus of sodium bicarbonate then adding sodium bicarbonate to maintenance fluids, is an effective method to increase the clearance of salicylates from the body. | Other truths being actively revealed include data suggesting that the pathogen itself (i.e., chlamydia) might play an equally important role, or perhaps even more important, than the host with disease susceptibility; asymptomatic chlamydial infections might be a common cause of reactive arthritis and the two variants of reactive arthritis might respond differently to treatment in spite of the congruent clinical presentation. However, much about this syndrome remains shrouded in mystery. Recent data has been suggesting that Chlamydia-induced reactive arthritis might be a common condition that clinicians are simply failing to recognise. Therefore, an emphasis is placed on disease awareness since viable treatment options are emerging. Treatment
Balanitis circinata is one out of multiple manifestations of the reactive arthritis.Right now, topical corticosteroid therapy is the most commonly used treatment, and topical calcineurin inhibitors have also been used successfully. Newer tests on patients showed that a less harmful off-label topical treatment with the immunomodulator pimecrolimus or the immunosuppressant tacrolimus can prevent all visible symptoms of this disease. Since reactive arthritis cannot be healed as such, affected people are forced to a continuous topical treatment – otherwise they will again note first symptoms after three to four days without it.However, strong debates and controversies continue regarding the exact indications of immunomodulators like pimecrolimus and their duration of use in the absence of active controlled trials. A study released in 2015 (tested were 7,457 children with a total of 26,792 person-years) did not find any evidence that pimecrolimus could cause cancer. == References == | 0-1
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It attenuates "second pain" with primary effects on slow-conducting, unmyelintated C-fibers and is less effective on neuropathic pain and "first pain" signals through small, myelinated A-fibers.Fentanyl can produce the following clinical effects strongly, through μ-receptor agonism. Supraspinal analgesia (μ1)
Respiratory depression (μ2)
Physical dependence
Muscle rigidityIt produces sedation and spinal analgesia through Κ-receptor agonism. Therapeutic effects
Pain relief: Primarily, fentanyl provides the relief of pain by acting on the brain and spinal μ-receptors. Sedation: Fentanyl produces sleep and drowsiness, as the dosage is increased, and can produce the δ-waves often seen in natural sleep on electroencephalogram. Suppression of the cough reflex: Fentanyl can decrease the struggle against an endotracheal tube and excessive coughing by decreasing the cough reflex, becoming useful when intubating people who are awake and have compromised airways. After receiving a bolus dose of fentanyl, people can also experience paradoxical coughing, which is a phenomenon that is not well understood. Detection in biological fluids
Fentanyl may be measured in blood or urine to monitor for abuse, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Commercially available immunoassays are often used as initial screening tests, but chromatographic techniques are generally used for confirmation and quantitation. The Marquis Color test may also be used to detect the presence of fentanyl. Using formaldehyde and sulfuric acid, the solution will turn purple when introduced to opium drugs. | Dyschromatosis universalis hereditaria is a rare genodermatosis characterized by reticulate hyper- and hypo- pigmentated macules in a generalized distribution. : 856 Both autosomal dominant and recessive inheritance have been reported with the disorder.It has been associated with mutations in genes SASH1 and ABCB6. References
External links
Dyschromatosis universalis hereditaria: Two cases, Dermatology Online Journal. | 0-1
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