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Other signs include high blood pressure in the lung (pulmonary hypertension), heart failure, difficulties getting enough oxygen to the body (hypoxia), and respiratory failure requiring support with breathing masks, such as bilevel positive airway pressure machines or ventilators. Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa are the three most common organisms causing lung infections in CF patients. : 1254 In addition, opportunistic infection due to Burkholderia cepacia complex can occur, especially through transmission from patient to patient.In addition to typical bacterial infections, people with CF more commonly develop other types of lung diseases. Among these is allergic bronchopulmonary aspergillosis, in which the bodys response to the common fungus Aspergillus fumigatus causes worsening of breathing problems. Another is infection with Mycobacterium avium complex, a group of bacteria related to tuberculosis, which can cause lung damage and do not respond to common antibiotics.Mucus in the paranasal sinuses is equally thick and may also cause blockage of the sinus passages, leading to infection. This may cause facial pain, fever, nasal drainage, and headaches. Individuals with CF may develop overgrowth of the nasal tissue (nasal polyps) due to inflammation from chronic sinus infections. Recurrent sinonasal polyps can occur in 10% to 25% of CF patients. : 1254 These polyps can block the nasal passages and increase breathing difficulties.Cardiorespiratory complications are the most common causes of death (about 80%) in patients at most CF centers in the United States. | : 1254
Gastrointestinal
In addition, protrusion of internal rectal membranes (rectal prolapse) is more common, occurring in as many as 10% of children with CF, and it is caused by increased fecal volume, malnutrition, and increased intra–abdominal pressure due to coughing.The thick mucus seen in the lungs has a counterpart in thickened secretions from the pancreas, an organ responsible for providing digestive juices that help break down food. These secretions block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas, often with painful inflammation (pancreatitis). The pancreatic ducts are totally plugged in more advanced cases, usually seen in older children or adolescents. This causes atrophy of the exocrine glands and progressive fibrosis.Individuals with CF also have difficulties absorbing the fat-soluble vitamins A, D, E, and K.In addition to the pancreas problems, people with CF experience more heartburn, intestinal blockage by intussusception, and constipation. Older individuals with CF may develop distal intestinal obstruction syndrome, which occurs when feces becomes thick with mucus (inspissated) and can cause bloating, pain, and incomplete or complete bowel obstruction.Exocrine pancreatic insufficiency occurs in the majority (85% to 90%) of patients with CF. : 1253 It is mainly associated with "severe" CFTR mutations, where both alleles are completely nonfunctional (e.g. ΔF508/ΔF508). : 1253 It occurs in 10% to 15% of patients with one "severe" and one "mild" CFTR mutation where little CFTR activity still occurs, or where two "mild" CFTR mutations exist. | 11
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Therapy
Physical and occupational therapy is important when dealing with a brachial plexus injuries. One of the main goals of rehabilitation is to prevent muscle atrophy until the nerves regain function. Electrical stimulation is an effective treatment to help patients reach this fundamental goal. Exercises that involve shoulder extension, flexion, elevation, depression, abduction and adduction facilitate healing by engaging the nerves in the damaged sites as well as improve muscle function. Stretching is done on a daily basis to improve or maintain range of motion. Stretching is important in order to rehabilitate since it increases the blood flow to the injury as well as facilitates nerves in functioning properly.A study has also shown that a sensory-motor deficit in the upper limbs after a brachial plexus injury can affect the corporal balance in the vertical positioning. Examined patients had a lower score in the Berg balance scale, a greater difficulty in maintaining in the unipodal stance during one minute and leaned the body weight distribution to the side affected by the lesion. Patients also exhibited a greater variability in the postural oscillation, evaluated by the directional stability index. The results alert the clinical community about the necessity to prevent and treat secondary effects of this condition. Epidemiology
Brachial plexus injury is found in both children and adults, but there is a difference between children and adults with BPI. Adults
The prevalence of brachial plexus injuries in North American adults in the 1900s was about 1.2%. | Rifampicin/isoniazid/pyrazinamide, also known as rifampin/isoniazid/pyrazinamide, and sold under the trade name Rifater, is a medication used to treat tuberculosis. It is a fixed dose combination of rifampicin, isoniazid, and pyrazinamide. It is used either by itself or along with other antituberculosis medication. It is taken by mouth.Side effects are those of the underlying medications. These may include poor coordination, loss of appetite, nausea, joint pain, feeling tired, and numbness. Severe side effects include liver problems. Use in those under the age of 15 may not be appropriate. It is unclear if use in pregnancy is safe for the baby.Rifampicin/isoniazid/pyrazinamide was approved for medical use in the United States in 1994. It is on the World Health Organizations List of Essential Medicines. Medical uses
The hope of a fixed-dose combination pill is to increase the likelihood that people will take all of three medications. Also, if people forget to take one or two of their drugs, they might not then develop resistance to the remaining drugs. Society and culture
It is manufactured by Aventis. See also
Tuberculosis treatment
Rifampicin + isoniazid + ethambutol
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Microscopic examination by a pathologist is then necessary to identify molecular, cellular, or tissue architectural characteristics of epithelial cells. Types
Oral: Most oral cancers are squamous-cell carcinoma
Lung: Carcinoma comprises >98% of all lung cancers. Breast: Nearly all breast cancers are ductal carcinoma. Prostate: The most common form of carcinoma of the prostate is adenocarcinoma. Colon and rectum: Nearly all malignancies of the colon and rectum are either adenocarcinoma or squamous cell carcinoma. Pancreas: Pancreatic carcinoma is almost always of the adenocarcinoma type and is highly lethal. Ovaries: One of the most deadly forms due to late detection.Some carcinomas are named for their or the putative cell of origin, (e.g.hepatocellular carcinoma, renal cell carcinoma). Staging
Staging of carcinoma refers to the process of combining physical/clinical examination, pathological review of cells and tissues, surgical techniques, laboratory tests, and imaging studies in a logical fashion to obtain information about the size of the neoplasm and the extent of its invasion and metastasis. Carcinomas are usually staged with Roman numerals. In most classifications, Stage I and Stage II carcinomas are confirmed when the tumor has been found to be small and/or to have spread to local structures only. Stage III carcinomas typically have been found to have spread to regional lymph nodes, tissues, and/or organ structures, while Stage IV tumors have already metastasized through the blood to distant sites, tissues, or organs. | An orthotopic liver transplant is another option, used only when antibiotics have no effect, in combination with recurring cholangitis. With a liver transplant, cholangiocarcinoma is usually avoided in the long run.Family studies are necessary to determine if Caroli disease is due to inheritable causes. Regular follow-ups, including ultrasounds and liver biopsies, are performed. Prognosis
Mortality is indirect and caused by complications. After cholangitis occurs, patients typically die within 5–10 years. Epidemiology
Caroli disease is typically found in Asia, and diagnosed in persons under the age of 22. Cases have also been found in infants and adults. As medical imaging technology improves, diagnostic age decreases. History
Jacques Caroli, a gastroenterologist, first described a rare congenital condition in 1958 in Paris, France. He described it as "nonobstructive saccular or fusiform multifocal segmental dilatation of the intrahepatic bile ducts"; basically, he observed cavernous ectasia in the biliary tree causing a chronic, often life-threatening hepatobiliary disease. Caroli, born in France in 1902, learned and practiced medicine in Angers. After World War II, he was chief of service for 30 years at Saint-Antoine in Paris. Before dying in 1979, he was honored with the rank of commander in the Legion of Honour in 1976. References
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Respiratory infections, including bronchitis, pharyngitis
Sinusitis
Sepsis
Whooping cough, to prevent and treat secondary infectionsAmpicillin used to also be used to treat gonorrhea, but there are now too many strains resistant to penicillins. Bacteria
Ampicillin is used to treat infections by many gram-positive and gram-negative bacteria. It was the first "broad spectrum" penicillin with activity against gram-positive bacteria, including Streptococcus pneumoniae, Streptococcus pyogenes, some isolates of Staphylococcus aureus (but not penicillin-resistant or methicillin-resistant strains), Trueperella, and some Enterococcus. It is one of the few antibiotics that works against multidrug resistant Enterococcus faecalis and E. faecium. Activity against gram-negative bacteria includes Neisseria meningitidis, some Haemophilus influenzae, and some of the Enterobacteriaceae (though most Enterobacteriaceae and Pseudomonas are resistant). Its spectrum of activity is enhanced by co-administration of sulbactam, a drug that inhibits beta lactamase, an enzyme produced by bacteria to inactivate ampicillin and related antibiotics. It is sometimes used in combination with other antibiotics that have different mechanisms of action, like vancomycin, linezolid, daptomycin, and tigecycline. Available forms
Ampicillin can be administered by mouth, an intramuscular injection (shot) or by intravenous infusion. The oral form, available as capsules or oral suspensions, is not given as an initial treatment for severe infections, but rather as a follow-up to an IM or IV injection. For IV and IM injections, ampicillin is kept as a powder that must be reconstituted.IV injections must be given slowly, as rapid IV injections can lead to convulsive seizures. | In the kidneys, it is filtered out mostly by tubular secretion; some also undergoes glomerular filtration, and the rest is excreted in the feces and bile. Hetacillin and pivampicillin are ampicillin esters that have been developed to increase bioavailability. History
Ampicillin has been used extensively to treat bacterial infections since 1961. Until the introduction of ampicillin by the British company Beecham, penicillin therapies had only been effective against gram-positive organisms such as staphylococci and streptococci. Ampicillin (originally branded as "Penbritin") also demonstrated activity against gram-negative organisms such as H. influenzae, coliforms, and Proteus spp. Cost
Ampicillin is relatively inexpensive. In the United States, it is available as a generic medication. Veterinary use
In veterinary medicine, ampicillin is used in cats, dogs, and farm animals to treat:
Anal gland infections
Cutaneous infections, such as abscesses, cellulitis, and pustular dermatitis
E. coli and Salmonella infections in cattle, sheep, and goats (oral form). Ampicillin use for this purpose had declined as bacterial resistance has increased. Mastitis in sows
Mixed aerobic–anaerobic infections, such as from cat bites
Multidrug-resistant Enterococcus faecalis and E. faecium
Prophylactic use in poultry against Salmonella and sepsis from E. coli or Staphylococcus aureus
Respiratory tract infections, including tonsilitis, bovine respiratory disease, shipping fever, bronchopneumonia, and calf and bovine pneumonia
Urinary tract infections in dogsHorses are generally not treated with ampicillin, as they have low bioavailability of beta-lactams.The half-life in animals is around that same of that in humans (just over an hour). Oral absorption is less than 50% in cats and dogs, and less than 4% in horses. | 11
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Nine years later however, the USPSTF issued a grade B recommendation for the use of low-dose aspirin (75 to 100 mg/day) "for the primary prevention of CVD [cardiovascular disease] and CRC in adults 50 to 59 years of age who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years".A meta-analysis through 2019 said that there was an association between taking aspirin and lower risk of cancer of the colorectum, esophagus, and stomach.In 2021, the U.S. Preventive services Task Force raised questions about the use of aspirin in cancer prevention. It notes the results of the 2018 ASPREE (Aspirin in Reducing Events in the Elderly) Trial, in which the risk of cancer-related death was higher in the aspirin-treated group than in the placebo group. Psychiatry
Bipolar disorder
Aspirin, along with several other agents with anti-inflammatory properties, has been repurposed as an add-on treatment for depressive episodes in subjects with bipolar disorder in light of the possible role of inflammation in the pathogenesis of severe mental disorders. However, meta-analytic evidence is based on very few studies and does not suggest any efficacy of aspirin in the treatment of bipolar depression. Thus, notwithstanding the biological rationale, the clinical perspectives of aspirin and anti-inflammatory agents in the treatment of bipolar depression remain uncertain. | For those weighing less than 70 kilograms (154 lb), low dose is effective for preventing cardiovascular disease; for patients above this weight, higher doses are required.In general, for adults, doses are taken four times a day for fever or arthritis, with doses near the maximal daily dose used historically for the treatment of rheumatic fever. For the prevention of myocardial infarction (MI) in someone with documented or suspected coronary artery disease, much lower doses are taken once daily.March 2009 recommendations from the USPSTF on the use of aspirin for the primary prevention of coronary heart disease encourage men aged 45–79 and women aged 55–79 to use aspirin when the potential benefit of a reduction in MI for men or stroke for women outweighs the potential harm of an increase in gastrointestinal hemorrhage. The WHI study of postmenopausal women found that aspirin resulted in a 25% lower risk of death from cardiovascular disease and a 14% lower risk of death from any cause, though there was no significant difference between 81 mg and 325 mg aspirin doses. | 11
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People with a narrowed airway may develop dyspnea, coughing, wheezing, respiratory tract infection, and difficulty with clearing secretions. If the bronchiole is completely obstructed, atelectasis occurs: the alveoli of the lung collapse. Lung tissue distal to a completely obstructed bronchiole often does not become infected. Because it is filled with mucus, this tissue remains functional. When the secretions are removed, the affected portion of the lung is commonly able to function almost normally. However, infection is common in lungs distal to a partially obstructed bronchiole. Infected lung tissue distal to a stricture can be damaged, and wheezing and coughing may develop due to the narrowing. In addition to pneumonia, the stenosis may cause bronchiectasis, in which bronchi are dilated, to develop. Even after an airway with a stricture is restored to normal, the resulting loss of lung function may be permanent.Complications may also occur with treatment; for example, a granuloma can form at the suture site. Also, the sutured wound can tear again, as occurs when there is excessive pressure in the airways from ventilation. However, for people who do receive surgery soon after the injury to repair the lesion, outcome is usually good; the long-term outcome is good for over 90% of people who have TBI surgically repaired early in treatment. Even when surgery is performed years after the injury, the outlook is good, with low rates of death and disability and good chances of preserving lung function. Epidemiology
Rupture of the trachea or bronchus is the most common type of blunt injury to the airway. | At higher doses during the last weeks of life, midazolam is considered a first line agent in palliative continuous deep sedation therapy when it is necessary to alleviate intolerable suffering not responsive to other treatments, but the need for this is rare. Administration
Routes of administration of midazolam can be oral, intranasal, buccal, intravenous, and intramuscular. Contraindications
Benzodiazepines require special precaution if used in the elderly, during pregnancy, in children, in alcohol- or other drug-dependent individuals or those with comorbid psychiatric disorders. Additional caution is required in critically ill patients, as accumulation of midazolam and its active metabolites may occur. Kidney or liver impairments may slow down the elimination of midazolam leading to prolonged and enhanced effects. Contraindications include hypersensitivity, acute narrow-angle glaucoma, shock, hypotension, or head injury. Most are relative contraindications. Side effects
Side effects of midazolam in the elderly are listed above. People experiencing amnesia as a side effect of midazolam are generally unaware their memory is impaired, unless they had previously known it as a side effect.Long-term use of benzodiazepines has been associated with long-lasting deficits in memory, and show only partial recovery six months after stopping benzodiazepines. It is unclear whether full recovery occurs after longer periods of abstinence. Benzodiazepines can cause or worsen depression. Paradoxical excitement occasionally occurs with benzodiazepines, including a worsening of seizures. Children and elderly individuals or those with a history of excessive alcohol use and individuals with a history of aggressive behavior or anger are at increased risk of paradoxical effects. Paradoxical reactions are particularly associated with intravenous administration. | 0-1
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The sadist attempts to destroy the ego in an effort to unify the id and super-ego, in effect gratifying the most base desires the sadist can express while ignoring or completely suppressing the will of the ego, or of the conscience. Thus, Deleuze attempts to argue that masochism and sadism arise from such different impulses that the combination of the two terms is meaningless and misleading. A masochists perception of their own self-subjugating sadistic desires and capacities are treated by Deleuze as reactions to prior experience of sadistic objectification. (For example, in terms of psychology, compulsively defensive appeasement of pathological guilt feelings as opposed to the volition of a strong free will.) The epilogue of Venus In Furs shows the character of Severin has become embittered by his experiment in the alleged control of masochism, and advocates instead the domination of women.Before Deleuze, however, Sartre had presented his own theory of sadism and masochism, at which Deleuzes deconstructive argument, which took away the symmetry of the two roles, was probably directed. Because the pleasure or power in looking at the victim figures prominently in sadism and masochism, Sartre was able to link these phenomena to his famous philosophy of the "Look of the Other". Sartre argued that masochism is an attempt by the "For-itself" (consciousness) to reduce itself to nothing, becoming an object that is drowned out by the "abyss of the Others subjectivity". | GMS syndrome is a syndrome characterised by goniodysgenesis, intellectual disability, and short stature. References
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Outcomes
Array-based karyotyping of 260 medulloblastomas resulted in the following clinical subgroups based on cytogenetic profiles:
Poor prognosis: gain of 6q or amplification of MYC or MYCN
Intermediate: gain of 17q or an i(17q) without gain of 6q or amplification of MYC or MYCN
Excellent prognosis: 6q and 17q balanced or 6q deletionTranscriptional profiling shows the existence of four main subgroups (Wnt, Shh, Group 3, and Group 4). Very good prognosis: WNT group, CTNNB1 mutation
Infants good prognosis, others intermediate: SHH group, PTCH1/SMO/SUFU mutation, GLI2 amplification, or MYCN amplification
Poor prognosis: Group 3, MYC amplification, photoreceptor/GABAergic gene expression
Intermediate prognosis: Group 4, gene expression of neuronal/glutamatergic, CDK6 amplification, MYCN amplification
Survival
The historical cumulative relative survival rate for all age groups and histology follow-up was 60%, 52%, and 47% at 5 years, 10 years, and 20 years, respectively. Patients diagnosed with a medulloblastoma or PNET are 50 times more likely to die than a matched member of the general population. The most recent population-based (SEER) 5-year relative survival rates are 69% overall: 72% in children (1–9 years) and 67% in adults (20+ years). The 20-year survival rate is 51% in children. Children and adults have different survival profiles, with adults faring worse than children only after the fourth year after diagnosis (after controlling for increased background mortality). Before the fourth year, survival probabilities are nearly identical. Long-term sequelae of standard treatment include hypothalamic-pituitary and thyroid dysfunction and intellectual impairment. | The child typically becomes listless, with repeated episodes of vomiting, and a morning headache, which may lead to a misdiagnosis of gastrointestinal disease or migraine. Soon after, the child will develop a stumbling gait, truncal ataxia, frequent falls, diplopia, papilledema, and sixth cranial nerve palsy. Positional vertigo and nystagmus are also frequent, and facial sensory loss or motor weakness may be present. Decerebrate attacks appear late in the disease. Extraneural metastasis to the rest of the body is rare, and when it occurs, it is in the setting of relapse, more commonly in the era prior to routine chemotherapy. Pathogenesis
Medulloblastomas are usually found in the vicinity of the fourth ventricle, between the brainstem and the cerebellum. Tumors with similar appearance and characteristics originate in other parts of the brain, but they are not identical to medulloblastoma.Although medulloblastomas are thought to originate from immature or embryonal cells at their earliest stage of development, the cell of origin depends on the subgroup of medulloblastoma. WNT tumors originate from the lower rhombic lip of the brainstem, while SHH tumors originate from the external granular layer.Currently, medulloblastomas are thought to arise from cerebellar stem cells that have been prevented from dividing and differentiating into their normal cell types. This accounts for the histologic variants seen on biopsy. Both perivascular pseudorosette and Homer Wright pseudorosette formations are highly characteristic of medulloblastomas and are seen in up to half of cases. | 11
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Oral vaccines can be safely distributed in baits, a practice that has successfully reduced rabies in rural areas of Canada, France, and the United States. In Montreal, Quebec, Canada, baits are successfully used on raccoons in the Mount-Royal Park area. Vaccination campaigns may be expensive, but cost-benefit analysis suggests baits may be a cost-effective method of control. In Ontario, a dramatic drop in rabies was recorded when an aerial bait-vaccination campaign was launched.The number of recorded human deaths from rabies in the United States has dropped from 100 or more annually in the early 20th century to one or two per year due to widespread vaccination of domestic dogs and cats and the development of human vaccines and immunoglobulin treatments. Most deaths now result from bat bites, which may go unnoticed by the victim and hence untreated. Treatment
After exposure
Treatment after exposure can prevent the disease if given within 10 days. The rabies vaccine is 100% effective if given early, and still has a chance of success if delivery is delayed. Every year, more than 15 million people get vaccinated after potential exposure. While this works well, the cost is significant. In the US it is recommended people receive one dose of human rabies immunoglobulin (HRIG) and four doses of rabies vaccine over a 14-day period. HRIG is expensive and makes up most of the cost of post-exposure treatment, ranging as high as several thousand dollars. | Tramline shadowing, finger-in-glove opacities and toothpaste shadows are also prevalent findings.When utilising high-resolution CT scans, there can be a better assessment of the distribution and pattern of bronchiectasis within the lungs, and hence this is the tool of choice in the radiological diagnosis of ABPA. Central (confined to medial two-thirds of the medial half of the lung) bronchiectasis that peripherally tapers bronchi is considered a requirement for ABPA pathophysiology, though in up to 43% of cases there is a considerable extension to the periphery of the lung.Mucoid impaction of the upper and lower airways is a common finding. Plugs are hypodense but appear on CT with high attenuation (over 70 Hounsfield units) in up to 20% of patients. Where present it is a strong diagnostic factor of ABPA and distinguishes symptoms from other causes of bronchiectasis.CT scans may more rarely reveal mosaic-appearance attenuation, centrilobular lung nodules, tree-in-bud opacities and pleuropulmonary fibrosis (a finding consistent with CPA, a disease with ABPA as a known precursor). Rarely other manifestations can be seen on CT scans, including military nodular opacities, perihilar opacities (that mimic hilar lymphadenopathy), pleural effusions and pulmonary masses. Cavitation and aspergilloma are rarer findings, not exceeding 20% of patients, and likely represent a shift from ABPA to CPA if accompanied by pleural thickening or fibrocavitary disease. Culture
Culturing fungi from sputum is a supportive test in the diagnosis of ABPA, but is not 100% specific for ABPA as A. fumigatus is ubiquitous and commonly isolated from lung expectorant in other diseases. | 0-1
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Tropical ataxic neuropathy (TAN, also known as Strachan-Scott Syndrome and prisoners of war neuropathy) is a disease or category of diseases that commonly causes disability and increases mortality. The causes of TAN are not understood; there is no generally accepted treatment, and the reported outcomes are inconsistent. The disease affects poor tropical populations; there are no good statistics on how many people are affected worldwide, but in some populations, more than a quarter of people are affected. Malnutrition may play a role. Classification and signs and symptoms
TAN is one of many tropical myeloneuropathies. It was first described in Jamaica in 1897, by postmortems of 510 cases; in 1959, it was dubbed "tropical ataxic neuropathy". The diagnostic criteria were defined in 1968. TAN is defined by "bilateral optic atrophy, bilateral sensory neural deafness, predominant posterior column involvement, and pyramidal tract myelopathy, with ataxic polyneuropathy". The classification of TAN is still not settled, and researchers disagree about it.There are thought to be two neurological syndromes lumped together as TAN. One affects adolescents, appears with retrobulbar optic neuropathy and evidence of malnutrition, and improves with better nutrition. Half of these adolescents are seen to have spinal ataxia.The other affects middle-aged and elderly people. They suffer sensory polyneuropathy, including weakness and paresthesic sensations. Paresthesias include sensations of numbness, heat, cold, tightness, crawling motion, tingling, pins and needles, and a feeling of walking on cotton or pebbles. Weaknesses show as gait ataxia (lack of co-ordination). | Historical data suggests that, in the 1960s, TAN in Africa was most common in people in their 30s and 40s.While the areas affected roughly correspond to the areas in which cassava is grown, some people in non-cassava-growing populations get TAN, and some cassava-growing populations do not get TAN. It is possible that there are several diseases being categorized as TAN.It has been estimated that 5% of surviving World War II prisoners of war held in the Far East acquired TAN; while they were held for 3.5 years or less, the TAN symptoms persisted chronically after they returned to temperate climates. Other animals
The behaviour and neurology of malnourished and cassava-fed rats has been compared to that of humans with TAN. See also
Konzo, a diet-based tropical neuropathy
Lathyrism, a diet-based neuropathy
Tropical spastic paraparesis, and infectious tropical myeloneuropathy
Neglected tropical diseases
Beri-beri
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Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain. Atenolol, however, does not seem to improve mortality in those with high blood pressure. Other uses include the prevention of migraines and treatment of certain irregular heart beats. It is taken by mouth or by injection into a vein. It can also be used with other blood pressure medications.Common side effects include feeling tired, heart failure, dizziness, depression, and shortness of breath. Other serious side effects include bronchospasm. Use is not recommended during pregnancy and alternative drugs are preferred when breastfeeding. It works by blocking β1-adrenergic receptors in the heart, thus decreasing the heart rate and workload.Atenolol was patented in 1969 and approved for medical use in 1975. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. In 2020, it was the 53rd most commonly prescribed medication in the United States, with more than 12 million prescriptions. Medical uses
Atenolol is used for a number of conditions including hyperthyroidism, hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, and the symptoms of alcohol withdrawal.The role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than other agents such as ACE inhibitors, calcium channel blockers, thiazide diuretics and angiotensin receptor blockers, particularly in the elderly. | In the population overall, the greatest likelihood of experiencing the first episode of any of these three TEAEs was greatest in the first week of treatment and decreased thereafter.According to Medscape, the most common (>10%) were: Nausea , Diarrhea (7-12%), Headache (2-11%). Less common side effects (1-10%) included: Abdominal pain (4-8%), Abdominal distension (3-6%), Flatulence (4-6%), Vomiting (3%), Loose stools (3%), Edema (1-3%), Abdominal discomfort (1-3%), Dizziness (3%), Chest discomfort/pain (2%), Dyspnea (2%), Dyspepsia (2%), Fatigue (2%), Dry mouth (1%). Contraindications
Known or suspected mechanical GI obstruction. Known hypersensitivity to lubiprostone or any ingredient in the formulation.There is no current data on use in people with liver or kidney complications. The effects on pregnancy have not been studied in humans but testing in guinea pigs resulted in fetal loss. Amitiza is not approved for use in children. Lubiprostone is contraindicated in patients exhibiting chronic diarrhea, bowel obstruction, or diarrhea-predominant irritable bowel syndrome. Mechanism of action
Lubiprostone is a bicyclic fatty acid derived from prostaglandin E1 that acts by specifically activating ClC-2 chloride channels on the apical aspect of gastrointestinal epithelial cells, producing a chloride-rich fluid secretion. These secretions soften the stool, increase motility, and promote spontaneous bowel movements (SBM). Symptoms of constipation such as pain and bloating are usually improved within one week, and SBM may occur within one day. Pharmacokinetics
Unlike many laxative products, lubiprostone does not show signs of drug tolerance, chemical dependency, or altered serum electrolyte concentration. | 0-1
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Researchers theorize that anhedonia may result from the breakdown in the brains reward system, involving the neurotransmitter dopamine. Anhedonia can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness".The conditions of akinetic mutism and negative symptoms are closely related. In akinetic mutism, a stroke or other lesion to the anterior cingulate cortex causes reduction in movement (akinetic) and speech (mutism). Occurrence
Major depressive disorder
Anhedonia occurs in roughly 70% of people with a major depressive disorder. Anhedonia is a core symptom of major depressive disorder; therefore, individuals experiencing this symptom can be diagnosed with depression, even in the absence of low/depressed mood. The Diagnostic and Statistical Manual of Mental Disorders (DSM) describes a "lack of interest or pleasure", but these can be difficult to discern given that people tend to become less interested in things which do not give them pleasure. The DSM criterion of weight loss is probably related, and many individuals with this symptom describe a lack of enjoyment of food. They can portray any of the non-psychotic symptoms and signs of depression. Schizophrenia
Anhedonia is one of the negative symptoms of schizophrenia. Although five domains are usually used to classify negative symptoms, factor analysis of questionnaires yield two factors, with one including deficits in pleasure and motivation. People with schizophrenia retrospectively report experiencing fewer positive emotions than healthy individuals. | In the Northern Bolivian Altiplano, some authors suggested that several aquatic plants such as bero-bero (watercress), algas (algae), kjosco and tortora could act as a source of infection for humans. Because F. hepatica cercariae also encyst on water surface, humans can be infected by drinking of fresh untreated water containing cercariae. In addition, an experimental study suggested that humans consuming raw liver dishes from fresh livers infected with juvenile flukes could become infected. Intermediate hosts
Intermediate hosts of F. hepatica are freshwater snails from family Lymnaeidae. Snails from family Planorbidae act as an intermediate host of F. hepatica very occasionally. Mechanism
The development of infection in definitive host is divided into two phases: the parenchymal (migratory) phase and the biliary phase. The parenchymal phase begins when excysted juvenile flukes penetrate the intestinal wall. After the penetration of the intestine, flukes migrate within the abdominal cavity and penetrate the liver or other organs. F. hepatica has a strong predilection for the tissues of the liver. Occasionally, ectopic locations of flukes such as the lungs, diaphragm, intestinal wall, kidneys, and subcutaneous tissue can occur. During the migration of flukes, tissues are mechanically destroyed and inflammation appears around migratory tracks of flukes. The second phase (the biliary phase) begins when parasites enter the biliary ducts of the liver. In biliary ducts, flukes mature, feed on blood, and produce eggs. Hypertrophy of biliar ducts associated with obstruction of the lumen occurs as a result of tissue damage. Resistance to infection
Mechanisms of resistance have been studied by several authors in different animal species. | 0-1
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Chemistry
EMP, also known as estradiol 3-normustine 17β-phosphate or as estradiol 3-(bis(2-chloroethyl)carbamate) 17β-(dihydrogen phosphate), is a synthetic estrane steroid and a derivative of estradiol. It is an estrogen ester; specifically, EMP is a diester of estradiol with a C3 normustine (nitrogen mustard–carbamate moiety) ester and a C17β phosphate ester. EMP is provided as the sodium or meglumine salt. EMP is similar as a compound to other estradiol esters such as estradiol sulfate and estradiol valerate, but differs in the presence of its nitrogen mustard ester moiety. Antineoplastic agents related to EMP, although none of them were marketed, include alestramustine, atrimustine, cytestrol acetate, estradiol mustard, ICI-85966, and phenestrol.Due to its hydrophilic phosphate ester moiety, EMP is a readily water-soluble compound. This is in contrast to most other estradiol esters, which are fatty acid esters and lipophilic compounds that are not particularly soluble in water. Unlike EMP, estramustine is highly lipophilic, practically insoluble in water, and non-ionizable. The phosphate ester of EMP was incorporated into the molecule in order to increase its water solubility and allow for intravenous administration.The molecular weight of EMP sodium is 564.3 g/mol, of EMP meglumine is 715.6 g/mol, of EMP is 520.4 g/mol, of estramustine is 440.4 g/mol, and of estradiol is 272.4 g/mol. As a result of these differences in molecular weights, EMP contains about 52%, EMP sodium about 48%, and EMP meglumine about 38% of the amount of estradiol within their structures as does an equal-mass quantity of estradiol. History
EMP was first synthesized in the mid-1960s and was patented in 1967. | Hormonal – related to the increasing amounts of estrogen and progesterone and their effect on the LES
Mechanical – the enlarging uterus increasing intra-abdominal pressure, inducing reflux of gastric acid
Behavioral – as with other instances of heartburn, behavioral modifications can exacerbate or alleviate symptoms
Unknown origin
Functional heartburn is heartburn of unknown cause. It is commonly associated with psychiatric conditions like depression, anxiety, and panic attacks. It is also seen with other functional gastrointestinal disorders like irritable bowel syndrome and is the primary cause of lack of improvement post treatment with proton pump inhibitors (PPIs). Despite this, PPIs are still the primary treatment with response rates in about 50% of people. The diagnosis is one of elimination, based upon the Rome III criteria. It was found to be present in 22.3% of Canadians in one survey. Diagnostic approach
Heartburn can be caused by several conditions and a preliminary diagnosis of GERD is based on additional signs and symptoms. The chest pain caused by GERD has a distinct burning sensation, occurs after eating or at night, and worsens when a person lies down or bends over. It also is common in pregnant women, and may be triggered by consuming food in large quantities, or specific foods containing certain spices, high fat content, or high acid content. In young persons (typically <40 years) who present with heartburn symptoms consistent with GERD (onset after eating, when laying down, when pregnant), a physician may begin a course of PPIs to assess clinical improvement before additional testing is undergone. | 0-1
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The various treatment modalities for retinoblastoma includes:
Enucleation of the eye – Most patients with unilateral disease present with advanced intraocular disease, so usually undergo enucleation, which results in a cure rate of 95%. In bilateral Rb, enucleation is usually reserved for eyes that have failed all known effective therapies or without useful vision. External beam radiotherapy (EBR) – The most common indication for EBR is for the eye in a young child with bilateral retinoblastoma who has active or recurrent disease after completion of chemotherapy and local therapies. However, patients with hereditary disease who received EBR therapy are reported to have a 35% risk of second cancers. Brachytherapy involves the placement of a radioactive implant (plaque), usually on the sclera adjacent to the base of a tumor. It used as the primary treatment, or more frequently, in patients with small tumors or in those who had failed initial therapy including previous EBR therapy. Thermotherapy involves the application of heat directly to the tumor, usually in the form of infrared radiation. It is also used for small tumors. Laser photocoagulation is recommended only for small posterior tumors. An argon or diode laser or a xenon arc is used to coagulate all the blood supply to the tumor. Cryotherapy induces damage to the vascular endothelium with secondary thrombosis and infarction of the tumor tissue by rapidly freezing it. It may be used as primary therapy for small peripheral tumors or for small recurrent tumors previously treated with other methods. | With proper medical attention, infections can usually be successfully treated without long-term visual loss. In non-humans
Feline eosinophilic keratitis — affecting cats and horses; possibly initiated by feline herpesvirus 1 or other viral infection. See also
Chronic superficial keratitis, or pannus, for the disease in dogs
Thygesons superficial punctate keratopathy
Keratoendotheliitis fugax hereditaria
References
External links
Facts About the Cornea and Corneal Disease The National Eye Institute (NEI)
Filimentary keratitis | 0-1
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This is not an issue in the reform community for two reasons. First, only one parent must be Jewish for the child to be considered Jewish; thus, if the father is Jewish, the mothers religion is irrelevant. Second, if the mother who carries the pregnancy and gives birth is Jewish, reform Jews will generally consider that child to be Jewish from birth because it was born of a Jewish mother. See also
Donor conceived person
Sperm donation
Surrogacy
Third-party reproduction
References
External links
Egg Donation at Curlie | Brainerd diarrhea is a sudden-onset watery, explosive diarrhea that lasts for months and does not respond to antibiotics; the cause of Brainerd diarrhea is unknown. Brainerd diarrhea was first described in Brainerd, Minnesota in 1983. It has been associated with the consumption of raw milk and untreated water. Of the ten outbreaks reported since 1983, nine have been in the U.S. The characteristics of each outbreak have been similar to that caused by an infectious agent. Although a comparatively large outbreak (117 patients) occurred in 1996 in Fannin County, Texas., the largest outbreak (122 patients) was the original one in Brainerd, MN. There have been no secondary cases reported in any of the outbreaks, suggesting that the
causative agent cannot be passed from person to person, but boiling water appears to inactivate the Brainerd agent. Although there is no treatment available, the disease does appear to resolve itself, although this process takes months if not years. References
External link
CDC information on Brainerd Diarrhea | 0-1
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When the thorax is fixed, they can pull up the pelvis and finally, they can bend the vertebral column sideways and assist in the trunks rotation. Posture
The transverse abdominis muscle is the deepest muscle, therefore, it cannot be touched from the outside. It can greatly affect the bodys posture. The internal obliques are also deep and also affect body posture. Both of them are involved in rotation and lateral flexion of the spine and are used to bend and support the spine from the front. The external obliques are more superficial and they are also involved in rotation and lateral flexion of the spine. Also they stabilize the spine when upright. The rectus abdominis muscle is not the most superficial abdominal muscle. The tendonous sheath extending from the external obliques cover the rectus abdominis. The rectus abdominis is the muscle that very fit people develop into the 6-pack ab look. Although it should really be a 10 pack as there are 5 vertical sections on each side. The 2 bottom sections are just above the pubic bone and usually not visible, hence, the 6 pack abs. The rectus abdominals function is to bend ones back forward (flexion). The main work of the abdominal muscles is to bend the spine forward when contracting concentrically. Society and culture
Social and cultural perceptions of the outward appearance of the abdomen has varying significance around the world. | The abdomen in vertebrates contains a number of organs belonging to, for instance, the digestive system, urinary system, and muscular system. Contents
The abdominal cavity contains most organs of the digestive system, including the stomach, the small intestine, and the colon with its attached appendix. Other digestive organs are known as the accessory digestive organs and include the liver, its attached gallbladder, and the pancreas, and these communicate with the rest of the system via various ducts. The spleen, and organs of the urinary system including the kidneys, and adrenal glands also lie within the abdomen, along with many blood vessels including the aorta and inferior vena cava. The urinary bladder, uterus, fallopian tubes, and ovaries may be seen as either abdominal organs or as pelvic organs. Finally, the abdomen contains an extensive membrane called the peritoneum. A fold of peritoneum may completely cover certain organs, whereas it may cover only one side of organs that usually lie closer to the abdominal wall. This is called the retroperitoneum, and the kidneys and ureters are known as retroperitoneal organs. Abdominal organs can be highly specialized in some animals. For example, the stomach of ruminants, (a suborder of mammals that includes cattle and sheep), is divided into four chambers – rumen, reticulum, omasum and abomasum. Muscles
There are three layers of muscles in the abdominal wall. They are, from the outside to the inside: external oblique, internal oblique, and transverse abdominal. | 11
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Signs and symptoms
Most people who have taken too much of a calcium channel blocker, especially diltiazem, get slow heart rate and low blood pressure (vasodilatory shock). This can progress to the heart stopping altogether. CCBs of the dihydropyridine group, as well as flunarizine, predominantly cause reflex tachycardia as a reaction to the low blood pressure.Other potential symptoms include: nausea and vomiting, a decreased level of consciousness, and breathing difficulties. Symptoms usually begin within 6 hours of taking the medication by mouth. With extended release formulations symptoms may not occur for up to a day. Seizures are rare in adults but in children occur more often. Hypocalcaemia may also occur. Cause
Calcium channel blockers, also known as calcium channel antagonists, are widely used for a number of health conditions. Thus they are commonly present in many peoples homes. In young children one pill may cause serious health problems and potentially death. The calcium channel blocker that caused the greatest number of deaths in 2010 in the United States was verapamil. This agent is believed to cause more heart problems than many of the others. Diagnosis
A blood or urine test to diagnose overdose is not generally available. CCB overdose may cause high blood sugar levels, and this is often a sign of how severe the problem will become. Electrocardiogram
CCB toxicity can cause a number of electrocardiogram abnormalities with a low sinus rhythm being the most common. Others include: QT prolongation, bundle branch block, first-degree atrioventricular block, and even sinus tachycardia. | Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe that occurs due to disease or frontal lobe injury. The frontal lobe of the brain plays a key role in executive functions such as motivation, planning, social behaviour, and speech production. Frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, neurodegenerative diseases, Neurodevelopmental disorders, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical signs and symptoms, use of simple screening tests, and specialist neurological testing. Signs and symptoms
The signs and symptoms of frontal lobe disorder can be indicated by dysexecutive syndrome which consists of a number of symptoms which tend to occur together. Broadly speaking, these symptoms fall into three main categories; cognitive (movement and speech), emotional or behavioral. Although many of these symptoms regularly co-occur, it is common to encounter patients who have several, but not all of these symptoms. This is one reason why some researchers are beginning to argue that dysexecutive syndrome is not the best term to describe these various symptoms. The fact that many of the dysexecutive syndrome symptoms can occur alone has led some researchers to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research on frontal cortex areas suggests that executive functions may be more discrete than was previously thought. Signs/symptoms can be divided as follows:
Causes
The causes of frontal lobe disorders can be closed head injury. | 0-1
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A typical wafer weighs about half a gram. Wheat flour contains around 10 to 13% gluten, so a single communion wafer may have more than 50 mg of gluten, an amount that harms many people with coeliac, especially if consumed every day (see Diet above). Many Christian churches offer their communicants gluten-free alternatives, usually in the form of a rice-based cracker or gluten-free bread. These include the United Methodist, Christian Reformed, Episcopal, the Anglican Church (Church of England, UK) and Lutheran. Catholics may receive from the Chalice alone, or ask for gluten-reduced hosts; gluten-free ones however are not considered to still be wheat bread and hence invalid matter. Roman Catholic position
Roman Catholic doctrine states that for a valid Eucharist, the bread to be used at Mass must be made from wheat. Low-gluten hosts meet all of the Catholic Churchs requirements, but they are not entirely gluten free. Requests to use rice wafers have been denied.The issue is more complex for priests. As a celebrant, a priest is, for the fullness of the sacrifice of the Mass, absolutely required to receive under both species. On 24 July 2003, the Congregation for the Doctrine of the Faith stated, "Given the centrality of the celebration of the Eucharist in the life of a priest, one must proceed with great caution before admitting to Holy Orders those candidates unable to ingest gluten or alcohol without serious harm. "By January 2004, extremely low-gluten Church-approved hosts had become available in the United States, Italy and Australia. | However, more sensitive methods of detecting urinary and serum light chain myeloma proteins using enzyme-linked immunosorbent assays indicate that >60% of cases initially diagnosed as non-secretory multiple myeloma had abnormal levels of either a clonal κ or λ light chain in their urine or serum and therefore were better diagnosed as having light chain multiple myeloma. Based on the latter definition, non-secretory multiple myeloma represents ~1% of all multiple myeloma cases with formerly diagnosed non-secretory myelomas considered to be cases primarily of light chain multiple myeloma but on occasion "false non-secretors", i.e. cases in which there is evidence of myeloma protein secretion such as renal myeloma protein deposits.A Mayo Clinic study of 124 patients initially diagnosed as having non-secretory multiple myeloma were later found to be composed of 65% free light chain secretors and 35% true non-secretors. As a group, these patients response to therapy, time to disease recurrence, and overall survival were similar to typical myeloma patients. However, in a subset of patients diagnosed after 2001 and therefore treated with more effective therapy that included autologous stem-cell transplantation, prognosis was significantly better in non-secretory multiple myeloma patients (median survival 8.3 years) compared to typical myeloma patients (median survival 5.4 years). In addition, non-secretory patients exhibited a better prognosis than light chain-secretory patients. | 0-1
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Moreover, diagnosis of PLMD cannot be used when narcolepsy, restless legs syndrome (RLS), REM sleep behaviour disorder (RBD) or untreated obstructive sleep apnea (OSA) is already diagnosed, since abnormal movements during sleep are frequent in these disorders. Signs and symptoms
People with PLMD often have excessive daytime sleepiness (EDS), falling asleep during the day, trouble falling asleep at night, and difficulty staying asleep throughout the night. Patients also display involuntary limb movements that occur at periodic intervals anywhere from 20 to 40 seconds apart. They often only last the first half of the night during non-REM sleep stages. Movements do not occur during REM because of muscle atonia. PLMS can be unilateral or bilateral and not really symmetrical or simultaneous. PLMS is often a symptom of RLS but evidence for differences between those two sleep disorders was found in literature. Sleep structure differed, when RLS patients had significantly more REM sleep and less stage 1 sleep compared to PLMD patients. Besides, PLMI was significantly higher in patients with PLMD. Causes
It is mostly unknown what causes PLMD, but in many cases the patient also has other medical problems such as Parkinsons disease or narcolepsy. Medical agents must be taken into consideration: several psychopharmacological drugs (serotonergic and tricyclic antidepressants, venlafaxine and mirtazapine) heighten the risk of PLMD. | The mean effective half-life of elexacaftor, tezacaftor, and ivacaftor is 27.4 hours, 25.1 hours, and 15 hours, respectively. History
A phase III trial showed people treated with elexacaftor/tezacaftor/ivacaftor improved in FEV1 at four weeks with sustained improvement at 24 weeks. Rate of pulmonary exacerbation was 63% lower and sweat chloride concentration was 41.8 mmol/L lower. Its effectiveness is dependent on the type of CF mutations the patient has. Society and culture
Legal status
United States
The combination was approved for use in the United States in 2019 for people twelve years and older with cystic fibrosis who have at least one F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which is estimated to represent 90% of the cystic fibrosis population. In December 2020, after an additional clinical trial was completed, and FDA approval was expanded for 177 other cystic fibrosis mutations. FDA approval for children aged 6–11 was added in January 2021, after a third clinical trial was completed.The U.S. Food and Drug Administration (FDA) granted the application priority review, in addition to fast track, breakthrough therapy, and orphan drug designations. The drugs manufacturer Vertex Pharmaceuticals will receive a rare pediatric disease priority review voucher for having developed this therapy. Australia
In March 2021, health regulators in Australia approved trikafta for patients aged 12 years and older with at least one copy of the F508del mutation. At the end of April 2022, it was placed on PBS, thus reducing the cost from tens of thousands of dollars a month, to tens of dollars a month. | 0-1
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Specific symptoms attributable to early hypercapnia are dyspnea (breathlessness), headache, confusion and lethargy. Clinical signs include flushed skin, full pulse (bounding pulse), rapid breathing, premature heart beats, muscle twitches, and hand flaps (asterixis). The risk of dangerous irregularities of the heart beat is increased. | Diagnosis
Clinical features of myxedema coma:
Cardiovascular
Bradycardia
Bundle branch blocks
Complete heart block and arrhythmias
Cardiomegaly
Elevated diastolic blood pressure—early
Hypotension—late
Low cardiac output
Non-specific ECG findings
Pericardial effusion
Polymorphic ventricular tachycardia (torsades de pointes)
Prolonged QT interval
Respiratory
Hypoxia
Hypercapnia
Hyperventilation
Myxedema of the larynx
Pleural effusion
Gastrointestinal
Abdominal distention
Abdominal pain
Anasarca
Anorexia and nausea
Decreased motility
Fecal impaction and constipation
Gastrointestinal atony or ileus
Myxedema or toxic megacolon—late
Neurogenic oropharyngeal dysphagia
ileus
Neurological
Altered mentation
Coma
Confusion and obtundation
Delayed tendon reflexes
Depression
Poor cognitive function
Psychosis
Seizures
Renal and urinary function
Bladder dystonia and distension
Fluid retention
Appearance and dermatological
Alopecia
Coarse, sparse hair
Dry, cool, doughy skin
Myxedematous face
Generalized swelling
Goiter
Macroglossia
Non-pitting edema
Ptosis
Periorbital edema
Surgical scar from prior thyroidectomy
HypothermiaLaboratory features in myxedema coma:
Anemia
Elevated creatine kinase (CPK)
Elevated creatinine
Elevated transaminases
Hypercapnia
Hypercholesterolemia (elevated LDL)
Hyperlipidemia
Hypoglycemia
Hyponatremia
Hypoxia
Leukopenia
Respiratory acidosis
Epidemiology
Hypothyroidism is four times more common in women than men. The incidence of myxedema coma has been reported to be 0.22 per 1000000 per year but the data is limited and especially lacking in countries outside the western world and countries along the equator. Myxedema coma is most common in people 60 years old and older and is most common in the winter months when hypothermia is more common. See also
Thyroid storm
Euthyroid sick syndrome
References
== External links == | 0-1
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This codec API is also available in C++ as libFLAC++. The reference implementation of FLAC compiles on many platforms, including most Unix (such as Solaris, BSD) and Unix-like (including Linux), Microsoft Windows, BeOS, and OS/2 operating systems. There are build-systems for autoconf/automake, MSVC, Watcom C, and Xcode. There is currently no multicore support in libFLAC, but utilities such as GNU parallel and various graphical frontends can be used to spin up multiple instances of the encoder. FLAC playback support in portable audio devices and dedicated audio systems is limited compared to formats such as MP3 or uncompressed PCM. FLAC support is included by default in Windows 10, Android, BlackBerry 10 and Jolla devices. In 2014, several aftermarket mobile electronics companies introduced multimedia solutions that include support for FLAC. These include the NEX series from Pioneer Electronics and the VX404 and NX404 from Clarion. The European Broadcasting Union (EBU) has adopted the FLAC format for the distribution of high quality audio over its Euroradio network. The Windows operating system has supported native FLAC integration since the introduction of Windows 10. The Android operating system has supported native FLAC playback since version 3.1. macOS High Sierra and iOS 11 add native FLAC playback support.Among others the Pono music player and streaming service used the FLAC format. Bandcamp insists on a lossless format for uploading, and has FLAC as a download option. The Wikimedia Foundation sponsored a free and open-source online ECMAScript FLAC tool for browsers supporting the required HTML5 features. | Carotidynia is a syndrome characterized by unilateral (one-sided) tenderness of the carotid artery, near the bifurcation. It was first described in 1927 by Temple Fay. The most common cause of carotidynia may be migraine, and then it is usually self-correcting. Common migraine treatments may help alleviate the carotidynia symptoms. Recent histological evidence has implicated an inflammatory component of carotidynia, but studies are limited. Carotid arteritis is a much less common cause of carotidynia, but has much more serious consequences. It is a form of giant cell arteritis, which is a condition that usually affects arteries in the head. Due to this serious condition possibly causing carotidynia, and the possibility that neck pain is related to some other non-carotidynia and serious condition, the case should be investigated by a medical doctor. Because carotidynia can be caused by numerous causes, Biousse and Bousser in 1994 recommended the term not be used in the medical literature. However, recent MRI and ultrasound studies have supported the existence of a differential diagnosis of carotidynia consistent with Fays characterization. References
External links
Family Practice notebook.com | 0-1
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Of admittees 16% either went on their own, or were referred by family or friends.In the European Union (data as available in 2018, information for individual countries was collected between 2012 and 2017), 26.3% of adults aged 15–64 used cannabis at least once in their lives, and 7.2% used cannabis in the last year. The highest prevalence of cannabis use among 15 to 64 years old in the EU was reported in France, with 41.4% having used cannabis at least once in their life, and 2.17% used cannabis daily or almost daily. Among young adults (15–34 years old), 14.1% used cannabis in the last year.Among adolescents (15–16 years old) in a European school based study (ESPAD), 16% of students have used cannabis at least once in their life, and 7% (boys: 8%, girls: 5%) of students had used cannabis in the last 30 days.Globally, 22.1 million people (0.3% of the worlds population) were estimated to have cannabis dependence. Research
Medications such as SSRI antidepressants, mixed action antidepressants, bupropion, buspirone and atomoxetine may not be helpful to treat cannabis use disorder, but the evidence is very weak and further research is required. THC preparations, gabapentin, oxytocin, and N-acetylcysteine also require more research to determine if they are effective as the evidence base is weak.Heavy cannabis use has been associated with impaired cognitive functioning, however, its specific details are difficult to elucidate due to the potential use of additional substances of users, and lack of longitudinal studies. | Psychological
Psychological intervention includes cognitive behavioral therapy (CBT), motivational enhancement therapy (MET), contingency management (CM), supportive-expressive psychotherapy (SEP), family and systems interventions, and twelve-step programs.Evaluations of Marijuana Anonymous programs, modelled on the 12-step lines of Alcoholics Anonymous and Narcotics Anonymous, have shown small beneficial effects for general drug use reduction. In 2006, the Wisconsin Initiative to Promote Healthy Lifestyles implemented a program that helps primary care physicians identify and address marijuana use problems in patients. Medication
As of 2020, there is no single medication that has been proven effective for treating cannabis use disorder; research is focused on three treatment approaches: agonist substitution, antagonist, and modulation of other neurotransmitter systems. More broadly, the goal of medication therapy for cannabis use disorder centers around targeting the stages of the addiction: acute intoxication/binge, withdrawal/negative affect, and preoccupation/anticipation.For the treatment of the withdrawal/negative affect symptom domain of cannabis use disorder, medications may work by alleviating restlessness, irritable or depressed mood, anxiety, and insomnia. Bupropion, which is a norepinephrine–dopamine reuptake inhibitor, has been studied for the treatment of withdrawal with largely poor results. Atomoxetine has also shown poor results, and is as a norepinephrine reuptake inhibitor, though it does increase the release of dopamine through downstream effects in the prefrontal cortex (an area of the brain responsible for planning complex tasks and behavior). Venlafaxine, a serotonin–norepinephrine reuptake inhibitor, has also been studied for cannabis use disorder, with the thought that the serotonergic component may be useful for the depressed mood or anxious dimensions of the withdrawal symptom domain. | 11
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Dentigerous cyst, also known as follicular cyst is an epithelial-lined developmental cyst formed by accumulation of fluid between the reduced enamel epithelium and crown of an unerupted tooth. It is formed when there is an alteration in the reduced enamel epithelium and encloses the crown of an unerupted tooth at the cemento-enamel junction. Fluid is accumulated between reduced enamel epithelium and the crown of an unerupted tooth. Dentigerous cyst is the second most common form of benign developmental odontogenic cysts. Dentigerous cyst is the second most prevalent type of odontogenic cysts after radicular cyst. 70 percent of the cases occurs in the mandible. Dentigerous cyst is usually painless. Patient usually comes with a concern of delayed tooth eruption or facial swelling. Dentigerous cyst can go unnoticed and may be discovered coincidentally on a regular radiographic examination. Pathogenesis
Odontogenesis happens by means of a complex interaction between oral epithelium and surrounding mesenchymal tissue. Abnormal tissue interaction during this process can result in ectopic tooth development. Ectopic tooth eruption may result due to pathological process, such as a tumor or cyst or developmental disturbance. The pathogenesis of dentigerous cyst is still controversial. The accumulation of fluid either between the reduced enamel epithelium and enamel or in between the layers of enamel organ seems to be the key to the formation of dentigerous cysts. A potentially erupting tooth on an impacted follicle can obstruct the venous outflow, inducing rapid transudation of serum across the capillary walls. Main suggested that this may exert pressure, causing the accumulation of fluid. | Some dentigerous cysts may result in considerable displacement of the involved tooth. Infrequently, a third molar may be displaced to the lower border of the mandible or into the ascending ramus. On the other hand, maxillary anterior teeth may be displaced into the floor of the nasal cavity, while other maxillary teeth may be displaced through the maxillary sinus to the floor of the orbit. Furthermore, larger cysts can lead to resorption of adjacent unerupted teeth. Some dentigerous cysts may also grow to considerable size and produce bony expansion that is usually painless, unless secondarily infected. However, any particularly large dentigerous radiolucency should clinically be suspected of a more aggressive odontogenic lesion such as an odontogenic keratocyst or ameloblastoma. For this reason, biopsy is mandated for all significant pericoronal radiolucencies to confirm the diagnosis. The role of CT (computerized tomography) imaging in the evaluation of cystic lesions has been well-documented. CT imaging aids to rule out solid and fibro-osseous lesions, displays bony detail, and provides precise information about the size, origin, content, and relationships of the lesions.On CT imaging, a mandibular dentigerous cyst appears as a well-circumscribed unilocular area of osteolysis that incorporates the crown of a tooth. Displacement of adjacent teeth may be seen and they may be partly eroded. Dentigerous cysts in the maxilla often extend into the antrum, displacing and remodeling the bony sinus wall. Large cysts which may project into the nasal cavity or infratemporal fossa and may elevate the floor of the orbit can be noted on CT imaging. | 11
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Just like endothelial cells, nerve cells cannot regulate their glucose uptake and suffer the same type of damages listed above. Therefore, the diabetic heart shows clear denervation as the pathology progresses. This denervation correlates with echocardiographic evidence of diastolic dysfunction and results in a decline of survival in patients with diabetes from 85% to 44%. Other causes of denervation are ischemia from microvascular disease and thus appear following the development of microangiopathy. Inflammation
Diabetes is associated with increased inflammation, which is mediated by generation of abnormal fatty acids, AGEs and other mechanisms. The resulting cytokine profile promotes hypertrophy and apoptosis of cardiomyocytes, abnormal calcium signaling, impaired myocardial contractility and myocardial fibrosis. Additionally, it may lead to microvascular dysfunction, either directly or via endothelial damage, thereby promoting myocardial ischemia. Diagnosis
Diagnostic approaches for diabetic cardiomyopathy include echocardiography, cardiac MRI investigations, Multi‐slice computed tomography (MsCT), and nuclear imaging. Potential risks of the investigation (e.g. exposure to radiation) and diagnostic utility should be weighed for an optimised personalised procedure. Treatment
At present, there is no effective specific treatment available for diabetic cardiomyopathy. Treatment centers around intense glycemic control through diet, oral hypoglycemics and frequently insulin and management of heart failure symptoms. There is a clear correlation between increased glycemia and risk of developing diabetic cardiomyopathy, therefore, keeping glucose concentrations as controlled as possible is paramount. Thiazolidinediones are not recommended in patients with NYHA Class III or IV heart failure secondary to fluid retention.As with most other heart diseases, ACE inhibitors can also be administered. | The protozoan is in the smaller of its two forms, called an amastigote, which is round, non-motile, and only 3–7 micrometers in diameter. Inside the stomach of the sandfly, the amastigotes quickly transform into elongated and motile forms called the promastigotes. Promastigote is spindle-shaped, triple the size of the amastigote, and has a single flagellum that allows mobility. The promastigotes live extracellularly in the alimentary canal, reproducing asexually, then migrate to the proximal end of the gut where they become poised for a regurgitational transmission. As the fly bites, the promastigotes are released from the proboscis and introduced locally at the bite site.Once inside the human host, promastigotes invade macrophages. Inside the cells they transform back into the smaller amastigote form. The amastigotes replicate in the most hostile part of the macrophage cell, inside the phagolysosome, whose normal defensive response they are able to prevent. After repeated multiplication, they break down their host cell by sheer pressure of mass, but there is some recent speculation that they are able to leave the cell by triggering the exocytosis response of the macrophage. The daughter cells protozoans then migrate to fresh cells or through the bloodstream to find new hosts. In this way the infection is progressive, spreading to the hosts mononuclear phagocyte system, particularly the spleen and liver. The free amastigotes in peripheral tissues are then ingested by sandfly to enter another cycle. Regulatory T and B cells
The cell-mediated immunity (CMI) that kills Leishmania also produces inflammation. If the inflammation is excessive, it can cause tissue damage. | 0-1
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The pain may also be misdiagnosed as a behavior disorder or Munchausen by proxy.The pain associated with EDS ranges from mild to debilitating. Causes
Every type of EDS except the hypermobile type (which affects the vast majority of people with EDS) can be positively tied to specific genetic variation. Variations in these genes can cause EDS:
Collagen primary structure and collagen processing: ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2
Collagen folding and collagen cross-linking: PLOD1, FKBP14
Structure and function of myomatrix: TNXB, COL12A1
Glycosaminoglycan biosynthesis: B4GALT7, B3GALT6, CHST14, DSE
Complement pathway: C1R, C1S
Intracellular processes: SLC39A13, ZNF469, PRDM5Variations in these genes usually alter the structure, production, or processing of collagen or proteins that interact with collagen. Collagen provides structure and strength to connective tissue. A defect in collagen can weaken connective tissue in the skin, bones, blood vessels, and organs, resulting in the features of the disorder. Inheritance patterns depend on the specific syndrome. Most forms of EDS are inherited in an autosomal dominant pattern, which means only one of the two copies of the gene in question must be altered to cause a disorder. A few are inherited in an autosomal recessive pattern, which means both copies of the gene must be altered for a person to be affected. It can also be an individual (de novo or "sporadic") variation. Sporadic variations occur without any inheritance. Diagnosis
A diagnosis can be made by an evaluation of medical history and clinical observation. The Beighton criteria are widely used to assess the degree of joint hypermobility. DNA and biochemical studies can help identify affected people. | Along with these general signs and side effects, patients can have trouble healing.Women who are pregnant should be warned about things such as pre-labor rupture of membranes, drop in blood pressure with anesthesia, precipitate birth (very fast, active labor), malposition of bleeding, and more. New mothers with hEDS should pay extra attention to taking care of their babies. Mothers may have trouble taking care of babies because of the risk of dropping a baby due to weak connective tissue in arms and legs, falling, postpartum depression (more than the general population), and healing from the birthing process. Genetics of Hypermobile EDS
While 12 of the 13 subtypes of EDS have genetic variations that can be tested for by genetic testing, there is no known genetic cause of hEDS. Despite the unknown gene, hEDS appears to follow an autosomal dominant pattern of inheritance. This means that in order to be affected, a person needs a mutation in only one copy of the responsible gene in each cell. This mutation can be inherited from a parent or a de novo (new) mutation. A person with hEDS has a 50% chance of passing their mutated gene on to their children.Recently, several labs and research initiatives have been attempting to uncover a potential hEDS gene. In 2018, the Ehlers–Danlos Society began the Hypermobile Ehlers–Danlos Genetic Evaluation (HEDGE) study. The ongoing study has screened over 1,000 people who have been diagnosed with hEDS by the 2017 criteria to evaluate their genome for a common mutation. | 11
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Two years later, measles was responsible for the deaths of half the population of Honduras, and it has ravaged Mexico, Central America, and the Inca civilization.Between roughly 1855 and 2005, measles is estimated to have killed about 200 million people worldwide.The 1846 measles outbreak in the Faroe Islands was unusual for being well-studied. Measles had not been seen on the islands for 60 years, so almost no residents had any acquired immunity. Three-quarters of the residents got sick, and more than 100 (1–2%) died from it before the epidemic burned itself out. Peter Ludvig Panum observed the outbreak and determined that measles was spread through direct contact of contagious people with people who had never had measles.Measles killed 20 percent of Hawaiis population in the 1850s. In 1875, measles killed over 40,000 Fijians, approximately one-third of the population. In the 19th century, the disease killed more than half of the Great Andamanese population. Seven to eight million children are thought to have died from measles each year before the vaccine was introduced.In 1914, a statistician for the Prudential Insurance Company estimated from a survey of 22 countries that 1% of all deaths in the temperate zone were caused by measles. He observed also that 1–6% of cases of measles ended fatally, the difference depending on age (0–3 being the worst), social conditions (e.g. overcrowded tenements) and pre-existing health conditions.In 1954, the virus causing the disease was isolated from a 13-year-old boy from the United States, David Edmonston, and adapted and propagated on chick embryo tissue culture. | Even in countries where vaccination has been introduced, rates may remain high. Measles is a leading cause of vaccine-preventable childhood mortality. Worldwide, the fatality rate has been significantly reduced by a vaccination campaign led by partners in the Measles Initiative: the American Red Cross, the United States CDC, the United Nations Foundation, UNICEF and the WHO. Globally, measles fell 60% from an estimated 873,000 deaths in 1999 to 345,000 in 2005. Estimates for 2008 indicate deaths fell further to 164,000 globally, with 77% of the remaining measles deaths in 2008 occurring within the Southeast Asian region. There were 142,300 measles related deaths globally in 2018, of which most cases were reported from African and eastern Mediterranean regions. These estimates were slightly higher than that of 2017, when 124,000 deaths were reported due to measles infection globally.In 2000, the WHO established the Global Measles and Rubella Laboratory Network (GMRLN) to provide laboratory surveillance for measles, rubella, and congenital rubella syndrome. Data from 2016 to 2018 show that the most frequently detected measles virus genotypes are decreasing, suggesting that increasing global population immunity has decreased the number of chains of transmission.Cases reported in the first three months of 2019, were 300% higher than in the first three months of 2018, with outbreaks in every region of the world, even in countries with high overall vaccination coverage where it spread among clusters of unvaccinated people. | 11
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Ambiguous phenotypic states include a phallic structure that is intermediate between a clitoris and a penis, and a single perineal orifice that connects to both the urethra and the vagina (i.e. urogenital sinus). At birth, it may not be possible to immediately differentiate the external genitalia of individuals with PAIS as being either male or female, although the majority of individuals with PAIS are raised male. Given the wide diversity of phenotypes associated with PAIS, the diagnosis is often further specified by assessing genital masculinization. Grades 2 through 5 of the Quigley scale quantify four degrees of increasingly feminized genitalia that correspond to PAIS.Grade 2, the mildest form of PAIS, presents with a predominantly male phenotype that presents with minor signs of undermasculinized genitalia, such as isolated hypospadias, which can be severe. Hypospadias may manifest with a partially formed channel from the urethral opening to the glans. Until recently, it was thought that isolated micropenis was not a manifestation of PAIS. However, in 2010, two cases of PAIS manifesting with isolated micropenis were documented. Grade 3, the most common phenotypic form of PAIS, features a predominantly male phenotype that is more severely undermasculinized, and typically presents with micropenis and pseudovaginal perineoscrotal hypospadias with bifid scrotum.Grade 4 presents with a gender ambiguous phenotype, including a phallic structure that is intermediate between a clitoris and a penis. The urethra typically opens into a common channel with the vagina (i.e. | Sigmoid colon volvulus, also known as sigmoid volvulus, is volvulus affecting the sigmoid colon. It is a common cause of bowel obstruction and constipation. It is common in Asia, India (7% of intestinal obstruction) and especially South India because of the high fibre diet. It is a very common cause of large bowel obstruction in Peru and Bolivia due to high altitude. Signs and symptoms
Pain in abdomen – initially left-sided, eventually all over
Absolute constipation
Enormous distension of abdomen
Late vomiting and eventually dehydration
Features of peritonitis
Hiccup and retching may occur
Tyre-like feel of the abdomen is diagnostic
Cause
The condition is more common in males and with old age. It is also common in people with chronic constipation and laxative abuse. It is common in:
Ogilvie syndrome
Individuals with learning difficulties
Chagas disease
Hypothyroidism
Anticholinergic drugs
Multiple sclerosis
Scleroderma
Parkinsons diseaseIn sigmoid, volvulus rotation is always anticlockwise. It requires one and a half rotation to cause vascular obstruction and gangrene which eventually leads to perforation either at the root or at the summit of the sigmoid loop. Diagnosis
Plain X-ray (diagnostic in 70–80%): coffee bean sign is seen
Contrast enema: bird beak sign
CT scan: shows characteristic whirl pattern
Blood: haematocrit, renal functions, serum electrolytes
Treatment
RT aspiration
IV fluids
Catheterisation
Antibiotics
By flatus tube or sigmoidoscope, derotation is done
If derotation does not occur, then laparotomy through midline incision should be done. It is derotated manually. If viable, it can be fixed to lateral wall of abdomen or pelvis
If sigmoid colon is gangrenous, then Hartmanns operation or Paul Mikulicz operation is done
References
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Flunisolide (marketed as AeroBid among others) is a corticosteroid often prescribed as treatment for allergic rhinitis. Intranasal corticosteroids are the most effective medication for controlling symptoms. The principal mechanism of action of flunisolide is to activate glucocorticoid receptors, meaning it has an anti-inflammatory action. The effects of topical corticosteroids is not immediate and requires regular use and at least a few days to start experiencing noticeable symptom relief. As-needed use has been shown to be not as effective as regular recommended use. Flunisolide should not be used in the presence of nasal infection. It should not be continued if there is no relief of symptoms after regular use over two to three weeks. It was patented in 1958 and approved for medical use in 1978. It is on the World Health Organizations List of Essential Medicines. Side effects
Temporary nose and throat dryness, irritation, bleeding or unpleasant taste or smell may occur. Nasal septum perforation is rarely reported. Rare, but localized infections of the nose and pharynx with Candida albicans have been reported and long-term use may raise the chance of cataracts or glaucoma.Flunisolide nasal spray is absorbed into the circulatory system (blood). Corticosteroid nasal sprays may affect the hypothalamic-pituitary-adrenal axis function in humans. After the desired clinical effect is obtained, the maintenance dose should be reduced to the smallest amount necessary to control symptoms, which can be as low as 1 spray in each nostril a day. Utilizing the minimum effective dose will reduce possibility of side effects. | The typical age of adolescent onset is 12.9, give or take 0.4 years (±), with males affected sooner than females (11.0 ± 0.8 for males versus 13.8 ± 0.5 for females).There is little evidence concerning the impact of hereditary influence in rumination syndrome. However, case reports involving entire families with rumination exist. History
The term rumination is derived from the Latin word ruminare, which means to chew the cud. First described in ancient times, and mentioned in the writings of Aristotle, rumination syndrome was clinically documented in 1618 by Italian anatomist Fabricus ab Aquapendente, who wrote of the symptoms in a patient of his.Among the earliest cases of rumination was that of a physician in the nineteenth century, Charles-Édouard Brown-Séquard, who acquired the condition as the result of experiments upon himself. As a way of evaluating and testing the acid response of the stomach to various foods, the doctor would swallow sponges tied to a string, then intentionally regurgitate them to analyze the contents. As a result of these experiments, the doctor eventually regurgitated his meals habitually by reflex.Numerous case reports exist from before the twentieth century, but were influenced greatly by the methods and thinking used in that time. By the early twentieth century, it was becoming increasingly evident that rumination presented itself in a variety of ways in response to a variety of conditions. | 0-1
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The tumor may be localized at the end of the long bone (commonly in the metaphysis). Most often it affects the proximal end of tibia or humerus, or distal end of femur. Osteosarcoma tends to affect regions around the knee in 60% of cases, 15% around the hip, 10% at the shoulder, and 8% in the jaw. The tumor is solid, hard, irregular ("fir-tree," "moth-eaten", or "sun-burst" appearance on X-ray examination) due to the tumor spicules of calcified bone radiating at right angles. These right angles form what is known as a Codman triangle, which is characteristic but not diagnostic of osteosarcoma. Surrounding tissues are infiltrated. Microscopically: The characteristic feature of osteosarcoma is presence of osteoid (bone formation) within the tumor. Tumor cells are very pleomorphic (anaplastic), some are giant, numerous atypical mitoses. These cells produce osteoid describing irregular trabeculae (amorphous, eosinophilic/pink) with or without central calcification (hematoxylinophilic/blue, granular)—tumor bone. Tumor cells are included in the osteoid matrix. Depending on the features of the tumor cells present (whether they resemble bone cells, cartilage cells, or fibroblast cells), the tumor can be subclassified. Osteosarcomas may exhibit multinucleated osteoclast-like giant cells. Diagnosis
X-rays is the initial imaging of choice to diagnose osteosarcoma. Some characteristics of osteosarcoma on X-rays are sunburst appearance and Codman triangle (elevation of bony cortex by the tumour that caused new bone formation). CT scan is helpful in defining the bony anatomy, the integrity of the bony cortex, detecting pathologic fracture, and assessing ossification (laying of new bone materials) and calcification of the cartilage. | Surgical techniques designed to save the leg (limb-sparing procedures) do not improve the prognosis.Some current studies indicate osteoclast inhibitors such as alendronate and pamidronate may have beneficial effects on the quality of life by reducing osteolysis, thus reducing the degree of pain, as well as the risk of pathological fractures. Cats
Osteosarcoma is also the most common bone tumor in cats, although not as frequently encountered, and most typically affect the rear legs. The cancer is generally less aggressive in cats than in dogs, so amputation alone can lead to a significant survival time in many affected cats, though post-amputation chemotherapy is recommended when a high grade is confirmed on histopathology. References
Further reading
Jaffe, N. (2010). Pediatric and Adolescent Osteosarcoma. New York: Springer. ISBN 978-1-4419-0283-2. Osteosarcoma research: past, present and future. External links
National Cancer Institute—patient information on osteosarcoma
Osteosarcoma – An Introduction Archived 2020-10-27 at the Wayback Machine
What is osteosarcoma? | 11
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It is often claimed that sativa strains provide a more stimulating psychoactive high while indica strains are more sedating with a body high. However, this is disputed by researchers.A 2015 review found that the use of high CBD-to-THC strains of cannabis showed significantly fewer positive symptoms, such as delusions and hallucinations, better cognitive function and both lower risk for developing psychosis, as well as a later age of onset of the illness, compared to cannabis with low CBD-to-THC ratios. Psychoactive ingredients
According to the United Nations Office on Drugs and Crime (UNODC), "the amount of THC present in a cannabis sample is generally used as a measure of cannabis potency." The three main forms of cannabis products are the flower/fruit, resin (hashish), and oil (hash oil). The UNODC states that cannabis often contains 5% THC content, resin "can contain up to 20% THC content", and that "Cannabis oil may contain more than 60% THC content. "A 2012 review found that the THC content in marijuana had increased worldwide from 1970 to 2009. It is unclear, however, whether the increase in THC content has caused people to consume more THC or if users adjust based on the potency of the cannabis. It is likely that the higher THC content allows people to ingest less tar. At the same time, CBD levels in seized samples have lowered, in part because of the desire to produce higher THC levels and because more illegal growers cultivate indoors using artificial lights. | Valsalva retinopathy is a form of retinopathy due to retinal bleeding secondary to rupture of retinal vessels caused by intrathoracic or intra-abdominal pressure due to physical activities. It can occur in any person irrespective of age, gender, race or health status. Pathophysiology
Valsalva retinopathy is a form of sub-retinal, sub-hyaloid or sub-internal limiting membrane hemorrhage occur due to rupture of retinal vessels caused by a strenuous physical activity. Physical exertion like weight lifting and aerobic exercise, coughing, sneezing, straining at stool, vomiting, sexual intercourse, pregnancy, asthma, blowing up balloons, blowing musical instruments, cardiopulmonary resuscitation or compression injuries may cause sudden increase in intrathoracic or intra-abdominal pressure may lead to rupture of superficial retinal blood vessels. A sudden increase in venous pressure due to intrathoracic or intra-abdominal pressure cause the small perifoveal capillaries of retina to rupture, leading to premacular hemorrhage of varying intensity. Signs and symptoms
The main symptom of valsalva retinopathy is painless sudden loss of vision. Sudden-onset floaters and central or paracentral visual field defects and nausea resulting from increased intraocular pressure are other symptoms. Diagnosis
Patients may have a history of sudden vision loss after a strenuous physical activity. Physical examination and eye examination is needed for diagnosis of valsalava retinopathy. OCT scanning can be used to identify the location of the bleeding. Complications
One of the main complications of valsalva retinopathy is vitreous hemorrhage. Epidemiology
As of 2022, there is currently no specific age, gender or racial preference noted for this retinopathy in the medical literature. | 0-1
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Adult polyglucosan body disease (APBD) is a rare genetic glycogen storage disorder caused by an inborn error of metabolism. Symptoms can emerge any time after the age of 30; early symptoms include trouble controlling urination, trouble walking, and lack of sensation in the legs. People eventually develop dementia. A person inherits loss-of-function mutations in the GBE1 gene from each parent, and the lack of glycogen branching enzyme (the protein encoded by GBE1) leads to buildup of unbranched glycogen in cells, which harms neurons more than other kinds of cells. Most people first go to the doctor due to trouble with urination. The condition is diagnosed by gathering symptoms, a neurological examination, laboratory tests including genetic testing, and medical imaging. As of 2015 there was no cure or treatment, but the symptoms could be managed. People diagnosed with APBD can live a long time after diagnosis, but will probably die earlier than people without the condition. Signs and symptoms
Adult polyglucosan body disease is a condition that affects the nervous system. People with this condition have problems walking due to reduced sensation in their legs (peripheral neuropathy) and progressive muscle weakness and stiffness (spasticity). Damage to the nerves that control bladder function (neurogenic bladder) causes progressive difficulty in controlling the flow of urine. About half of people with adult polyglucosan body disease experience dementia. Most people with the condition first complain of bladder issues.People with adult polyglucosan body disease typically first experience signs and symptoms related to the condition between ages 30 and 60. | Examination of tissue biopsied from the sural nerve under a microscope can reveal the presence of polyglucosan bodies. There will also be white matter changes visible in a magnetic resonance imaging scans. Classification
Adult polyglucosan body disease is an orphan disease and a glycogen storage disorder that is caused by an inborn error of metabolism, that affects the central and peripheral nervous systems.The condition in newborns caused by the same mutations is called glycogen storage disease type IV. Prevention
APBD can only be prevented if parents undergo genetic screening to understand their risk of producing a child with the condition; if in vitro fertilization is used, then preimplantation genetic diagnosis can be done to identify fertilized eggs that do not carry two copies of mutated GBE1. Management
As of 2015 there was no cure for APDB, instead symptoms are managed. There are various approaches to managing neurogenic bladder dysfunction, physical therapy and mobility aids to help with walking, and dementia can be managed with occupational therapy, counseling and drugs. Presently a number of promising research initiatives are underway in universities and hospitals in the United States, Canada, and Israel. These studies are in need of funding but due to the small number of known cases both research funding and participation is small. It is estimated that there are upwards of 12,000 cases in the United States, most of which are undiagnosed. | 11
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While its true that children diagnosed with PDD-NOS, as a whole, show fewer intellectual deficits and are higher-functioning than autistic children, many others who fit the criteria for PDD-NOS have some autistic features but also have intellectual deficits that are so severe that its difficult or impossible to tell whether some of the deficits come from the autism or from the severe to profound degree of intellectual disability itself. Furthermore, some others who fit the criteria for PDD-NOS come to professional attention at a later age, compared to those diagnosed with autism. Subgroups
Studies suggest that persons with PDD-NOS belong to one of three very different subgroups:
A high-functioning group (around 25 percent) whose symptoms more or less overlap with that of Asperger syndrome, while also not meeting the criteria for autistic disorder, but who completely differ from those with Asperger syndrome in terms of having a lag in language development and/or mild cognitive impairment. (The criteria for Asperger syndrome excludes a speech delay or a cognitive delay in early life.) Another group (around 25 percent) whose symptoms more closely resemble those of autism, but do not fully meet all its diagnostic signs and symptoms. This is because either the symptoms were recognized at a later age or because they were too young or have cognitive deficits that are too severe to properly identify all the symptoms of autism that they may have. | The biggest group (around 50 percent) consists of those who meet all the diagnostic criteria for autistic disorder but whose stereotypical and repetitive behaviors are noticeably mild. Treatment
There is no known cure for PDD-NOS, but there are interventions that can have a positive influence. Some of the more common therapies and services include:
Visual and environmental supports, visual schedules
Social stories and comic strip conversations
Speech therapy
Physical and occupational therapy
References
== External links == | 11
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Causes
Hormonal disorders or fluctuations can lead to the formation of a lot of visceral fat and a protruding abdomen. Medications such as protease inhibitors that are used to treat HIV and AIDS also form visceral fat. Android fat can be controlled with proper diet and exercise. A poor diet with lack of exercise is likely to increase android fat level. Health consequences
Differences in body fat distribution are found to be associated with high blood pressure, high triglyceride, lower high-density lipoprotein (HDL) cholesterol levels and high fasting and post-oral glucose insulin levels The android, or male pattern, fat distribution has been associated with a higher incidence of coronary artery disease, in addition to an increase in resistance to insulin in both obese children and adolescents. Studies have also related central abdominal obesity (indicated via increased waist–hip ratio) with increases in peripheral fasting insulin levels.Android fat is also associated with a change in pressor response in circulation. Specifically, in response to stress in a subject with central obesity the cardiac output dependent pressor response is shifted toward a generalised rise in peripheral resistance with an associated decrease in cardiac output.There are differences in android and gynoid fat distribution among individuals, which relates to various health issues among individuals. Android body fat distribution is related to high cardiovascular disease and mortality rate. People with android obesity have higher hematocrit and red blood cell count and higher blood viscosity than people with gynoid obesity. | Blood pressure is also higher in those with android obesity which leads to cardiovascular disease.Women who are infertile and have polycystic ovary syndrome show high amounts of android fat tissue. In contrast, patients with anorexia nervosa have increased gynoid fat percentage Women normally have small amounts of androgen, however when the amount is too high they develop male psychological characteristics and male physical characteristics of muscle mass, structure and function and an android adipose tissue distribution. Women who have high amounts of androgen and thus an increase tendency for android fat distribution are in the lowest quintiles of levels of sex-hormone-binding globulin and more are at high risks of ill health associated with android fat High levels of android fat have been associated with obesity and diseases caused by insulin insensitivity, such as diabetes. Insulin responsiveness is dependent on adipose cell size. The larger the adipose cell size the less sensitive the insulin. Diabetes is more likely to occur in obese women with android fat distribution and hypertrophic fat cells. It is not just general obesity that is a consequence of android fat distribution but also other health consequences. There are connections between high android fat distributions and the severity of diseases such as acute pancreatitis - where the higher the levels of android fat are, the more severe the pancreatitis can be. An increase in android fat distribution is positively correlated with foot pain and disability associated with foot pain. | 11
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The poorer classes worked outdoors and got darker skin from exposure to the sun, while the upper class stayed indoors and had light skin. Hence light skin became associated with wealth and high position. Women would put lead-based cosmetics on their skin to whiten their skin tone artificially. However, when not strictly monitored, these cosmetics caused lead poisoning. Other methods also aimed at achieving a light-skinned appearance, including the use of arsenic to whiten skin, and powders. Women would wear full-length clothes when outdoors, and would use gloves and parasols to provide shade from the sun. Colonization and enslavement as carried out by European countries became involved with colorism and racism, associated with the belief that people with dark skin were uncivilized, inferior, and should be subordinate to lighter-skinned invaders. This belief exists to an extent in modern times as well. Institutionalized slavery in North America led people to perceive lighter-skinned African-Americans as more intelligent, cooperative, and beautiful. Such lighter-skinned individuals had a greater likelihood of working as house slaves and of receiving preferential treatment from plantation owners and from overseers. For example, they had a chance to get an education. The preference for fair skin remained prominent until the end of the Gilded Age, but racial stereotypes about worth and beauty persisted in the last half of the 20th century and continue in the present day. | One concern is that bevacizumab will interfere with these normal processes, and worsen conditions like coronary artery disease or peripheral artery disease.The main side effects are hypertension and heightened risk of bleeding. Bowel perforation has been reported. Fatigue and infection are also common. In advanced lung cancer, less than half of patients qualify for treatment. Nasal septum perforation and renal thrombotic microangiopathy have been reported. In December 2010, the FDA warned of the risk of developing perforations in the body, including in the nose, stomach, and intestines. In 2013, Hoffmann-La Roche announced that the drug was associated with 52 cases of necrotizing fasciitis from 1997 to 2012, of which 17 patients died. About 2/3 of cases involved patients with colorectal cancer, or patients with gastrointestinal perforations or fistulas. These effects are largely avoided in ophthalmological use since the drug is introduced directly into the eye thus minimizing any effects on the rest of the body.Neurological adverse events include reversible posterior encephalopathy syndrome. Ischemic and hemorrhagic strokes are also possible.Protein in the urine occurs in approximately 20% of people. This does not require permanent discontinuation of the drug. Nonetheless, the presence of nephrotic syndrome necessitates permanent discontinuation of bevacizumab. Mechanism of action
Bevacizumab is a recombinant humanized monoclonal antibody that blocks angiogenesis by inhibiting vascular endothelial growth factor A (VEGF-A). VEGF-A is a growth factor protein that stimulates angiogenesis in a variety of diseases, especially in cancer. Bevacizumab is the first available angiogenesis inhibitor in the United States. | 0-1
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Neither lidocaine nor amiodarone, in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation, improves survival to hospital discharge but both equally improve survival to hospital admission.Thrombolytics when used generally may cause harm but may be of benefit in those with a confirmed pulmonary embolism as the cause of arrest. Evidence for use of naloxone in those with cardiac arrest due to opioids is unclear but it may still be used. In those with cardiac arrest due to local anesthetic, lipid emulsion may be used. Targeted temperature management
Current international guidelines suggest cooling adults after cardiac arrest using targeted temperature management (TTM), which was previously known as therapeutic hypothermia. People are typically cooled for a 24-hour period, with a target temperature of 32–36 °C (90–97 °F). There are a number of methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body, or infusing cold saline. This is followed by gradual rewarming over the next 12 to 24 hrs.Effectiveness of TTM after out-of-hospital cardiac arrest is an area of ongoing study. Pre-hospital TTM after out-of-hospital cardiac arrest has been shown to increase the risk of adverse outcomes. The rates of re-arrest may be higher in people who were treated with pre-hospital TTM, however, more research is needed on the effectiveness and risks of TTM. TTM in post-arrest care has not been found to improve mortality or neurological outcomes. Moreover, TTM may have adverse neurological effects in people who survive post cardiac arrest. | There is currently uncertainty about the effectiveness of anaesthesia or analgesia for manual extraction, in terms of pain and the risk of postpartum haemorrhage. Very rarely a curettage is necessary to ensure that no remnants of the placenta remain (in rare conditions with very adherent placenta such as a placenta accreta). However, in birth centers and attended home birth environments, it is common for licensed care providers to wait for the placentas birth up to 2 hours in some instances. Other animals
Retention of fetal membranes (afterbirth) is observed more frequently in cattle than in other animals. In a normal condition, a cow’s placenta is expelled within a 12-hour period after calving. == References == | 0-1
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Some include gastrointestinal hemorrhage as a fourth criterion; this occurs in 33% of cases, sometimes, but not necessarily always, due to intussusception. The purpura typically appear on the legs and buttocks, but may also be seen on the arms, face and trunk. The abdominal pain is colicky in character, and may be accompanied by nausea, vomiting, constipation or diarrhea. There may be blood or mucus in the stools. The joints involved tend to be the ankles, knees, and elbows, but arthritis in the hands and feet is possible; the arthritis is nonerosive and hence causes no permanent deformity. Forty percent have evidence of kidney involvement, mainly in the form of hematuria (blood in the urine), but only a quarter will have this in sufficient quantities to be noticeable without laboratory tests. Problems in other organs, such as the central nervous system (brain and spinal cord) and lungs may occur, but is much less common than in the skin, bowel and kidneys.Of the 40% of patients who develop kidney involvement, almost all have evidence (visible or on urinalysis) of blood in the urine. More than half also have proteinuria (protein in the urine), which in one eighth is severe enough to cause nephrotic syndrome (generalised swelling due to low protein content of the blood). While abnormalities on urinalysis may continue for a long time, only 1% of all HSP patients develop chronic kidney disease. Hypertension (high blood pressure) may occur. | Distal intestinal obstruction syndrome (DIOS) involves obstruction of the distal part of the small intestines by thickened intestinal content and occurs in about 20% of mainly adult individuals with cystic fibrosis. DIOS was previously known as meconium ileus equivalent, a name which highlights its similarity to the intestinal obstruction seen in newborn infants with cystic fibrosis. DIOS tends to occur in older individuals with pancreatic insufficiency. Individuals with DIOS may be predisposed to bowel obstruction, though it is a separate entity than true constipation. Signs and symptoms
Signs and symptoms of DIOS include a sudden onset of crampy abdominal pain, vomiting, and a palpable mass (often in the right lower quadrant) in the abdomen. The characteristic abdominal pain is typically located in the center or right lower quadrant of the abdomen. X-rays of the abdomen may reveal stool in the colon and air-fluid levels in the small intestines. Diagnosis
A complete history and physical examination can be suggestive, especially if a palpable mass in the right lower quadrant of the abdomen is present (though this can be present in the absence of DIOS). Ultrasound and computed tomography (CT) imaging of the abdomen can confirm the diagnosis by demonstrating dilated loops of intestine with material in the intestinal lumen with bubbles. Air-fluid levels may be seen in those affected by DIOS. Classification
DIOS is sometimes classified by the degree of obstruction as incomplete or complete DIOS. Differential diagnosis
Additional diagnoses which may present with similar symptoms to DIOS include severe constipation, appendicitis, and intussusception. | 0-1
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A full mouth examination and recording is required to document and track periodontal disease including:
Pocket Depth (PD)
Clinical Attachment Loss (CAL)
Bleeding On Probing (BOP)
Plaque index/score
Furcation involvement
Suppuration
Mobility
RadiographsMeasuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding indices using a periodontal probe. Pockets greater than 3mm in depth are considered to be unhealthy. True pocket formation of 4 mm or more are specifically related to chronic periodontitis. Bleeding on probing is considered to be a sign of active disease. Discharge of pus, involvement of the root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth. Evidence of alveolar bone loss is also required to differentiate between true bone loss and not attributions of gingival oedema. Usually, a horizontal pattern of bone loss would be found however, vertical (infrabony) bone loss may also be present on specific sites. A Basic Periodontal Examination (BPE) or Periodontal Screening and Recording (PSR) should give a score of 3 or 4. A correct diagnosis is vital to allow the formation of a specific treatment plan for the patient and to arrest the disease progression. Chronic periodontitis can be further classified into:
Extent (can be either localised affecting < 30% of sites; or generalised if > 30% of sites are affected)
Severity (slight = 1–2 mm CAL; moderate = 3–4 mm CAL; severe ≥5 mm CAL)
2017 classification
Chronic periodontitis is not included within the newer 2017 World Workshop classification. | The anterior dentition occasionally have recession and maxillary anterior and palatal surfaces are more adversely affected. Pathophysiology
Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast-derived enzymes. Plaque hypothesis
At least two mechanisms of the microbiology of periodontitis have been described: the specific plaque hypothesis and the non-specific plaque hypothesis. Consensus is that neither view is entirely correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque. This is called the ecological plaque hypothesis. The disease is associated with a variable microbial pattern.Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in chronic periodontitis.Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, and Eikenella corrodens also may play a role in chronic periodontitis. Signs and symptoms
In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following:
Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g. | 11
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China officially apologized for early slowness in dealing with the SARS epidemic.The viral outbreak was subsequently genetically traced to a colony of cave-dwelling horseshoe bats in Xiyang Yi Ethnic Township, Yunnan.The outbreak first came to the attention of the international medical community on 27 November 2002, when Canadas Global Public Health Intelligence Network (GPHIN), an electronic warning system that is part of the World Health Organizations Global Outbreak Alert and Response Network (GOARN), picked up reports of a "flu outbreak" in China through Internet media monitoring and analysis and sent them to the WHO. While GPHINs capability had recently been upgraded to enable Arabic, Chinese, English, French, Russian, and Spanish translation, the system was limited to English or French in presenting this information. Thus, while the first reports of an unusual outbreak were in Chinese, an English report was not generated until 21 January 2003. The first super-spreader was admitted to the Sun Yat-sen Memorial Hospital in Guangzhou on 31 January, which soon spread the disease to nearby hospitals.In early April 2003, after a prominent physician, Jiang Yanyong, pushed to report the danger to China, there appeared to be a change in official policy when SARS began to receive a much greater prominence in the official media. Some have directly attributed this to the death of an American teacher, James Earl Salisbury, in Hong Kong. It was around this same time that Jiang Yanyong made accusations regarding the undercounting of cases in Beijing military hospitals. | The WHO officially removed Toronto from its list of infected areas by the end of June 2003.The official response by the Ontario provincial government and Canadian federal government has been widely criticized in the years following the outbreak. Brian Schwartz, vice-chair of Ontarios SARS Scientific Advisory Committee, described public health officials preparedness and emergency response at the time of the outbreak as "very, very basic and minimal at best". Critics of the response often cite poorly outlined and enforced protocol for protecting healthcare workers and identifying infected patients as a major contributing factor to the continued spread of the virus. The atmosphere of fear and uncertainty surrounding the outbreak resulted in staffing issues in area hospitals when healthcare workers elected to resign rather than risk exposure to SARS. Identification of virus
In late February 2003, Italian doctor Carlo Urbani was called into The French Hospital of Hanoi to look at Johnny Chen, an American businessman who had fallen ill with what doctors thought was a bad case of influenza. Urbani realized that Chens ailment was probably a new and highly contagious disease. He immediately notified the WHO. He also persuaded the Vietnamese Health Ministry to begin isolating patients and screening travelers, thus slowing the early pace of the epidemic. He subsequently contracted the disease himself, and died in March 2003.The CDC and Canadas National Microbiology Laboratory identified the SARS genome in April 2003. Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS coronavirus fulfilled Kochs postulates thereby suggesting it as the causative agent. | 11
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See also
Cholestasis
Cholestatic pruritus
List of cutaneous conditions
Pruritic urticarial papules and plaques of pregnancy (PUPPP) an itchy condition of pregnancy that is associated with a rash. References
External links
E A Fagan "Intrahepatic cholestasis of pregnancy" | A potential complication of phimosis is paraphimosis, where the tight foreskin becomes trapped behind the glans. Signs and symptoms
At birth, the inner layer of the foreskin is sealed to the glans penis. The foreskin is usually non-retractable in early childhood, and some males may reach the age of 18 before their foreskin can be fully retracted.Medical associations advise not to retract the foreskin of an infant, in order to prevent scarring. Some argue that non-retractability may "be considered normal for males up to and including adolescence." Hill states that full retractability of the foreskin may not be achieved until late childhood or early adulthood. A Danish survey found that the mean age of first foreskin retraction is 10.4 years.Rickwood, as well as other authors, has suggested that true phimosis is over-diagnosed due to failure to distinguish between normal developmental non-retractability and a pathological condition. Some authors use the terms "physiologic" and "pathologic" to distinguish between these types of phimosis; others use the term "non-retractile foreskin" to distinguish this developmental condition from pathologic phimosis.In some cases a cause may not be clear, or it may be difficult to distinguish physiological phimosis from pathological phimosis if an infant appears to have discomfort while urinating or demonstrates obvious ballooning of the foreskin. However, ballooning does not indicate urinary obstruction.In women, a comparable condition is known as "clitoral phimosis", whereby the clitoral hood cannot be retracted, limiting exposure of the glans clitoridis. Severity
Score 1: full retraction of foreskin, tight behind the glans. | 0-1
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Mechanisms
Though the pathophysiology of schizoaffective disorder remains unclear, studies suggest that dopamine, norepinephrine, and serotonin may be factors in the development of the disorder.White matter and Grey Matter reductions in the right lentiform nucleus, left superior temporal gyrus, and right precuneus, and other areas in the brain are also characteristic of schizoaffective disorder. Deformities in white matter have also been found to worsen with time in individuals with schizoaffective disorder. Due to its role in emotional regulation, researchers believe that the hippocampus is also involved in the progression of schizoaffective disorder. Specifically, psychotic disorders (such as schizoaffective disorder) have been associated with lower hippocampal volumes. Moreover, deformities in the medial and thalamic regions of the brain have been implicated as contributing factors to the disorder as well. Diagnosis
Psychosis as a symptom of a psychiatric disorder is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis cannot be considered to be a symptom of a psychiatric disorder until other relevant and known medical causes of psychosis are excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.An initial assessment includes a comprehensive history and physical examination. Although no biological laboratory tests exist which confirm schizoaffective disorder, biological tests should be performed to exclude psychosis associated with or caused by substance use, medications, toxins or poisons, surgical complications, or other medical illnesses. | But DSM-IV schizoaffective disorder carries an unnecessarily worse prognosis than a "mood disorder with psychotic features" diagnosis, because long-term data revealed that a significant proportion of DSM-IV schizoaffective disorder patients had 15-year outcomes indistinguishable from patients with mood disorders with or without psychotic features, even though the clinical picture at the time of first diagnosis looked different from both schizophrenia and mood disorders.These problems with the DSM-IV schizoaffective disorder definition result in most people the diagnosis is used on being misdiagnosed; furthermore, outcome studies done 10 years after the diagnosis was released showed that the group of patients defined by the DSM-IV and ICD-10 schizoaffective diagnosis had significantly better outcomes than predicted, so the diagnosis carries a misleading and unnecessarily poor prognosis. The DSM-IV criteria for schizoaffective disorder will continue to be used on U.S. board examinations in psychiatry through the end of 2014; established practitioners may continue to use the problematic DSM-IV definition much further into the future also. DSM-5 research directions
The new schizoaffective disorder criteria continue to have questionable diagnostic validity. Questionable diagnostic validity does not doubt that people with symptoms of psychosis and mood disorder need treatment—psychosis and mood disorder must be treated. Instead, questionable diagnostic validity means there are unresolved problems with the way the DSM-5 categorizes and defines schizoaffective disorder. A core concept in modern psychiatry since DSM-III was released in 1980, is the categorical separation of mood disorders from schizophrenia, known as the Kraepelinian dichotomy. | 11
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Multiple sulfatase deficiency (MSD), also known as Austin disease, or mucosulfatidosis, is a very rare autosomal recessive: 561 lysosomal storage disease caused by a deficiency in multiple sulfatase enzymes, or in formylglycine-generating enzyme, which activates sulfatases. : 502 It is similar to mucopolysaccharidosis. Signs and symptoms
Symptoms of this disorder commonly appear between one and two years of age. Symptoms include mildly coarsened facial features, deafness, ichthyosis and an enlarged liver and spleen (hepatosplenomegaly). Abnormalities of the skeleton, such as a curving of the spine and breast bone may occur. The skin of individuals afflicted with this disorder, is typically dry. Children affected by this disorder develop more slowly than normal and may display delayed speech and walking skills.The disease is fatal, with symptoms that include neurological damage and severe mental retardation. These sulfatase enzymes are responsible for breaking down and recycling complex sulfate-containing sugars from lipids and mucopolysaccharides within the lysosome. The accumulation of lipids and mucopolysaccharides inside the lysosome results in symptoms associated with this disorder. As of 2018, 75–100 cases of MSD had been reported worldwide. Causes
Multiple sulfatase deficiency is caused by any mutation of the SUMF1 gene which renders its protein product, the formylglycine-generating enzyme (FGE), defective. These mutations result in inactive forms of FGE. This enzyme is required for posttranslational modification of a cysteine residue in the sulfatase enzyme active site into formylglycine, which is required for its proper function. Genetics
MSD has an autosomal recessive inheritance pattern. | : 561
The inheritance probabilities per birth are as follows:
If both parents are carriers:
25% (1 in 4) children will have the disorder
50% (2 in 4) children will be carriers (but unaffected)
25% (1 in 4) children will be free of MSD - unaffected child that is not a carrier
If one parent is affected and one is free of MSD:
0% (0) children will have the disorder - only one parent is affected, other parent always gives normal gene
100% (4 in 4) children will be carriers (but unaffected)
If one parent is a carrier and the other is free of MSD:
50% (2 in 4) children will be carriers (but unaffected)
50% (2 in 4) children will be free of MSD - unaffected child that is not a carrier
Diagnosis
MSD may be diagnosed when deficiency of more than one sulfatase enzyme is identified in leukocytes or fibroblasts, or by molecular genetic testing which shows pathogenic variation in both alleles of the SUMF1 gene. Treatment
As there is no cure for MSD, treatment is restricted to management of symptoms. There is much research on MSD that is currently underway. MSD Action Foundation have initiated more than 15 research projects on MSD in the last 6 years. Many of these have a translational focus. It is hoped that clinical trials for MSD will happen in the not too distant future- Alan Finglas. [Ref 17. Finglas 2020]
See also
Linear porokeratosis
List of cutaneous conditions
References
[17] View from inside: When multiple sulfatase deficiency changes everything about how you live and becomes your life
Alan Finglas,
https://doi.org/10.1002/jimd.12305
== External links ==SavingDylan.com | 11
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As a result of low oxygen levels, infants with PPHN are at an increased risk of developing complications, such as asphyxia, chronic lung disease, neurodevelopment issues, and death.Nosocomial infections are another type of complication that may contribute to mortality in someone with PPHN. If the newborn acquires an infection while hospitalized, this could result in deterioration of the condition even after days of improvement. Pathophysiology
Typically, a fetus experiences pulmonary hypertension in utero since it is relying on the placenta for oxygen rather than its lungs. When the fetus is born, it is no longer attached to the placenta and must use the lungs to receive oxygen. To facilitate this change from fetus to newborn, the baby must change from a state of high PVR to low PVR, allowing for increased blood flow to circulate throughout the body. This inability of the newborn to adapt to these changes is caused by various processes, such as:
Normal vascular anatomy with functional vasoconstriction: This has a good prognosis, as it is reversible. Causes include hypoxia, meconium aspiration, and respiratory distress syndrome. Left untreated, this can lead to hypoxic respiratory failure (HRF). Decreased diameter of pulmonary vessels with hypertrophy of vessel walls: This has a poor prognosis, as it is a fixed abnormality. Causes include post-term pregnancy, placental insufficiency, and NSAID use by the mother. Decreased size of pulmonary vascular bed: This has a poor prognosis, as it is a fixed abnormality. It is caused by space occupying lesions such as pleural effusions and diaphragmatic hernias. | In June 2015, the U.S. Supreme Court ruled that they had failed to prove that midazolam was cruel and unusual when compared to known, available alternatives.The state of Nevada is also known to use midazolam in execution procedures. In July 2018, one of the manufacturers accused state officials of obtaining the medication under pretences. This incident was the first time a drug company successfully, though temporarily, halted an execution. A previous attempt in 2017, to halt an execution in the state of Arizona by another drug manufacturer was not successful. References
External links
"Midazolam". Drug Information Portal. U.S. National Library of Medicine. "Midazolam hydrochloride". Drug Information Portal. U.S. National Library of Medicine. Inchem - Midazolam | 0-1
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There is some evidence that phenytoin may be more effective than a beta-blocker.While medicinal interventions to mitigate breathing challenges in children with Rett Syndrome (RTT) are still being developed, children with RTT may be prescribed rebreathing techniques (e.g., rebreathing masks), oxygen delivery, or non-invasive ventilation as preventative or rescue breathing treatments. High oxidative stress levels in individuals with RTT have exacerbated effects on their cardiorespiratory health and functionality, dramatically increasing the risk for sudden cardiac death—an anomaly that has an associated 300x increased occurrence risk in children with Rett Syndrome. Due to this, it is vital to closely monitor atypical breathing behaviors in children with RTT, making sure to effectively use lifesaving respiratory improvement devices and strategies as prescribed. Prescribed treatment methods may vary depending on the breathing characteristic phenotype expressed by the child. Physicians have identified three major RTT breathing phenotypes; forceful breathers, feeble breathers, and apneustic breathers. For forceful breathers, for example, rebreathing masks may be used while the child is awake. Prognosis
Males with pathogenic MECP2 mutations usually die within the first 2 years from severe encephalopathy, unless they have one or more extra X chromosomes, or have somatic mosaicism. Male fetuses with the disorder rarely survive to term. | Molecular Functions of MECP2 in Rett Syndrome Pathology
As reviewed by Sharifi and Yasui, MECP2 protein, encoded by the MECP2 gene binds to DNA with a high affinity for CpG methylated DNA sites and affects transcription. MECP2 can bind to 5mc (5-methylcytosine) and 5hmc (5-hydroxymethylcytosine) with similar affinity, and these dinucleotides account for the majority of MECP2 binding sites in the mammalian genome. MECP2 is involved in higher order chromatin organization and appears necessary for compacting chromosomes. MECP2 binding to DNA influences mRNA splicing events. MECP2 also appears to function in DNA repair processes. MECP2-/+ deficient female mice have elevated rates of cell death when exposed to DNA damaging agents and are prone to early senescence. Interactive pathway map
An interactive pathway map of Rett syndrome has been published. Diagnosis
Prior to the discovery of a genetic cause, Rett syndrome had been designated as a pervasive developmental disorder by the Diagnostic and Statistical Manual of Mental Disorders (DSM), together with the autism spectrum disorders. Some argued against this conclusive assignment because RTT resembles non-autistic disorders such as fragile X syndrome, tuberous sclerosis, or Down syndrome that also exhibit autistic features. After research proved the molecular mechanism, in 2013 the DSM-5 removed the syndrome altogether from classification as a mental disorder.Rett syndrome diagnosis involves close observation of the childs growth and development to observe any abnormalities in regards to developmental milestones. A diagnosis is considered when decreased head growth is observed. | 11
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The incidence of side effects with doxepin and its safety at these doses was similar to that of placebo in clinical trials; the most frequent side effects were headache and somnolence/sedation, both with an incidence of less than 5%. Other side effects sometimes associated with antihistamines, including daytime sedation, increased appetite, and weight gain, all were not observed. Clinical evidence of H1 receptor antagonists and TCAs for the treatment insomnia shows mixed effectiveness and is limited in its quality due to weaknesses like small sample sizes and poor generalizability. However, doxepin is a unique and notable exception; it has been well-studied in the treatment of insomnia and shows consistent benefits with excellent tolerability and safety. Aside from diphenhydramine and doxylamine, which have historical approval as hypnotics, doxepin is the only H1 receptor antagonist that is specifically approved for the treatment of insomnia in the United States.The effect sizes of very low-dose doxepin in the treatment of insomnia range from small to medium. These include subjective and objective measures of sleep maintenance, sleep duration, and sleep efficiency. Conversely, very low-dose doxepin shows relatively weak effects on sleep initiation and does not significantly separate from placebo on this measure. This is in contrast to benzodiazepines and nonbenzodiazepine (Z-drug) hypnotics, which are additionally effective in improving sleep onset latency. However, it is also in contrast to higher doses of doxepin (50 to 300 mg/day), which have been found to significantly reduce latency to sleep onset. | These cases have revealed that the cause of the disease likely exhibits genetic heterogeneity, meaning the disease involves mutations in other locations within the genome (although no other loci have been identified in the development of BD as of now). Diagnosis
Diagnosis of BD begins with clinical evaluation of individuals for characteristic symptoms of cramping and stiffness of exercised muscles. A few techniques are involved in confirming a diagnosis of BD.Blood testing may be used to measure serum creatine kinase, which ranges from normal to slightly elevated in those with BD. Skeletal muscle biopsies are used to examine muscle fibers. Biopsies in individuals with BD often show variation in muscle fiber size, atrophied fast-twitch muscle fibers, and increased nuclei number. Electromyography (EMG) can be used in diagnosis to rule out myotonia, or muscle stiffness that is detected by EMG. Individuals with BD have stiff muscles but normal EMG results (pseudo-myotonia), where no myotonic discharges are detected. Genetic testing may also be used in the diagnosis of BD to look for mutations in ATP2A1. Since only some forms of the disease are associated with ATP2A1, results of genetic testing do not always confirm a diagnosis of BD, but are useful to rule out other similar disorders. Treatment
There is no cure for BD, although treatment options are available for reducing the negative symptoms of BD. The drugs dantrolene and verapamil are used in BD treatment due to their effects on Ca2+. | 0-1
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Ectopic ACTH syndrome describes conditions leading to excess production of adrenocorticotropic hormone (ACTH) subsequently leading to mineralocorticoid production. This can arise in ectopic forms of Cushings syndrome associated with small-cell lung cancers and other ACTH-producing tumors. The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects. Metabolic and dietary forms
Metabolic causes include conditions of glucocorticoid resistance and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy. Dietary causes include overconsumption of licorice-containing products. Glycyrrhetinic acid in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the mineralocorticoid receptor by cortisol leading to aldosterone-like effects. Diagnosis
In patients with hypertension, diagnostic clues pointing to pseudohyperaldosteronism can be found on routine labwork. These include low serum potassium (hypokalemia), elevated serum sodium (hypernatremia), and elevated serum bicarbonate (metabolic alkalosis). Urine studies may show elevated urine potassium (kaliuresis). To further differentiate between hyperaldosteronism and pseudohyperaldosteronism, studies including plasma renin activity (PRA) and plasma aldosterone concentration (PAC) can be obtained. Pseudohyperaldosteronism will exhibit low levels of both PRA and PAC while hyperaldosteronism will demonstrate elevated PAC. Confirmatory tests to diagnose the specific forms of pseudohyperaldosteronism vary depending on the cause. The genetic conditions such as Liddles syndrome and CAH can be confirmed with genetic tests for the affected genes. CAH can also be confirmed by analyzing enzyme levels following ACTH stimulation testing. AME can be diagnosed with a 24 hour urine collection exhibiting an increased ratio of urinary cortisol to urinary cortisone. | Although media reports have suggested that eye exposure to the agent can lead to temporary or permanent blindness, the risk of permanent blindness is not supported by existing research.Phytophotodermatitis can affect people of any age. In children, it has sometimes been mistaken for child abuse. Phototoxic species
Plants associated with phytophotodermatitis mainly come from four plant families: the carrot family (Apiaceae), the citrus family (Rutaceae), the mulberry family (Moraceae), and the legume family (Fabaceae). Apiaceae
The carrot family Apiaceae (or Umbelliferae) is the main family of plants associated with phytophotodermatitis. Of all the plant species that have been reported to induce phytophotodermatitis, approximately half belong to the family Apiaceae.False bishops weed (Ammi majus), the worlds major source of the linear furanocoumarin xanthotoxin, has been used since antiquity to treat vitiligo but accidental or inappropriate use of this plant can lead to phytophotodermatitis. Despite this danger, A. majus continues to be cultivated for its furanocoumarins, which are still used for the treatment of skin disease. Numerous species in the family Apiaceae are cultivated as food products, some of which exhibit phototoxic effects. In particular, celery, parsnip, and parsley have been reported to cause phytophotodermatitis among agricultural workers, grocery workers, and other occupational food handlers.A number of phototoxic plant species in the carrot family have become invasive species, including wild parsnip (Pastinaca sativa) and the tall hogweeds of the genus Heracleum, namely, Persian hogweed (Heracleum persicum), Sosnowskys hogweed (Heracleum sosnowskyi), and giant hogweed (Heracleum mantegazzianum). | 0-1
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When fully mature, C. silacea and C. dimidiata assume the day-biting tendencies of all tabanids.The bite of the mango fly can be very painful, possibly because of the laceration style employed; rather than puncturing the skin as a mosquito does, the mango fly (and deer fly) makes a laceration in the skin and subsequently laps up the blood. Female flies require a fair amount of blood for their aforementioned reproductive purposes and thus may take multiple blood meals from the same host if disturbed during the first one.Although Chrysops silacea and C. dimidiata are attracted to canopied rainforests, they do not do their biting there. Instead, they leave the forest and take most blood meals in open areas. The flies are attracted to smoke from wood fires and they use visual cues and sensation of carbon dioxide plumes to find their preferred host, humans.A study of Chrysops spp. biting habits showed that C. silacea and C. dimidiata take human blood meals approximately 90% of the time, with hippopotamus, wild ruminant, rodent and lizard blood meals making up the other 10%. Morphology
Adult Loa worms are sexually dimorphic, with males considerably smaller than females at 30–34 mm long and 0.35–0.42 mm wide compared to 40–70 mm long and 0.5 mm wide. Adults live in the subcutaneous tissues of humans, where they mate and produce wormlike eggs called microfilariae. | Studies have sought to delineate the sequence of events following Ivermectin treatment that lead to neurologic SAE and sometimes death, while also trying to understand the mechanisms of adverse reactions to develop more appropriate treatments.In a study looking at mass Ivermectin treatment in Cameroon, one of the greatest endemic regions for both onchocerciasis and loiasis, a sequence of events in the clinical manifestation of adverse effects was outlined.It was noted that the patients used in this study had a L. loa microfilarial load of greater than 3,000 per ml of blood.Within 12–24 hours post-Ivermectin treatment (D1), individuals complained of fatigue, anorexia, and headache, joint and lumbar pain—a bent forward walk was characteristic during this initial stage accompanied by fever. Stomach pain and diarrhea were also reported in several individuals.By day 2 (D2), many patients experienced confusion, agitation, dysarthria, mutism and incontinence. Some cases of coma were reported as early as D2. The severity of adverse effects increased with higher microfilarial loads. Hemorrhaging of the eye, particularly the retinal and conjunctiva regions, is another common sign associated with SAE of Ivermectin treatment in patients with L. loa infections and is observed between D2 and D5 post-treatment. This can be visible for up to 5 weeks following treatment and has increased severity with higher microfilarial loads.Haematuria and proteinuria have also been observed following Ivermectin treatment, but this is common when using Ivermectin to treat onchocerciasis. The effect is exacerbated when there are high L. loa microfilarial loads however, and microfilariae can be observed in the urine occasionally. | 11
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Initially, glaucoma drops may reasonably be started in either one or in both eyes.The possible neuroprotective effects of various topical and systemic medications are also being investigated. Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow. Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body. Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow. Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrines mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor). Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma. Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. Adherence
Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-quarter failed to refill their prescriptions a second time. | Often, the optic nerve shows an abnormal amount of cupping.If treated early, it is possible to slow or stop the progression of disease with medication, laser treatment, or surgery. The goal of these treatments is to decrease eye pressure. A number of different classes of glaucoma medication are available. Laser treatments may be effective in both open-angle and closed-angle glaucoma. A number of types of glaucoma surgeries may be used in people who do not respond sufficiently to other measures. Treatment of closed-angle glaucoma is a medical emergency.About 70 million people have glaucoma globally, with about two million patients in the United States. It is the leading cause of blindness in African Americans. It occurs more commonly among older people, and closed-angle glaucoma is more common in women. Glaucoma has been called the "silent thief of sight", because the loss of vision usually occurs slowly over a long period of time. Worldwide, glaucoma is the second-leading cause of blindness after cataracts. Cataracts caused 51% of blindness in 2010, while glaucoma caused 8%. The word "glaucoma" is from the Ancient Greek glaukos, which means "shimmering." In English, the word was used as early as 1587 but did not become commonly used until after 1850, when the development of the ophthalmoscope allowed doctors to see the optic nerve damage. Signs and symptoms
As open-angle glaucoma is usually painless with no symptoms early in the disease process, screening through regular eye exams is important. | 11
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However, a large-scale investigation based on data of nearly 700 patients showed "that aspirin or other antiplatelet aggregating agents or anticoagulants adversely influence the visual outcome in patients with CRVO and hemi-CRVO, without any evidence of protective or beneficial effect". Several expert groups, including the Royal College of Ophthalmologists, recommended against the use of antithrombotic drugs (incl. aspirin) for patients with RVO. Central effects
Large doses of salicylate, a metabolite of aspirin, cause temporary tinnitus (ringing in the ears) based on experiments in rats, via the action on arachidonic acid and NMDA receptors cascade. Reyes syndrome
Reyes syndrome, a rare but severe illness characterized by acute encephalopathy and fatty liver, can occur when children or adolescents are given aspirin for a fever or other illness or infection. From 1981 to 1997, 1207 cases of Reyes syndrome in people younger than 18 were reported to the US Centers for Disease Control and Prevention (CDC). Of these, 93% reported being ill in the three weeks preceding the onset of Reyes syndrome, most commonly with a respiratory infection, chickenpox, or diarrhea. Salicylates were detectable in 81.9% of children for whom test results were reported. | The National Institute for Occupational Safety and Health (NIOSH) has set a recommended exposure limit in the United States of 5 mg/m3 (time-weighted average). In 1989, the Occupational Safety and Health Administration (OSHA) set a legal permissible exposure limit for aspirin of 5 mg/m3, but this was vacated by the AFL-CIO v. OSHA decision in 1993. Synthesis
The synthesis of aspirin is classified as an esterification reaction. Salicylic acid is treated with acetic anhydride, an acid derivative, causing a chemical reaction that turns salicylic acids hydroxyl group into an ester group (R-OH → R-OCOCH3). This process yields aspirin and acetic acid, which is considered a byproduct of this reaction. Small amounts of sulfuric acid (and occasionally phosphoric acid) are almost always used as a catalyst. This method is commonly demonstrated in undergraduate teaching labs. Reaction mechanism
Formulations containing high concentrations of aspirin often smell like vinegar because aspirin can decompose through hydrolysis in moist conditions, yielding salicylic and acetic acids. Physical properties
Aspirin, an acetyl derivative of salicylic acid, is a white, crystalline, weakly acidic substance, with a melting point of 136 °C (277 °F), and a boiling point of 140 °C (284 °F). Its acid dissociation constant (pKa) is 3.5 at 25 °C (77 °F). Polymorphism
Polymorphism, or the ability of a substance to form more than one crystal structure, is important in the development of pharmaceutical ingredients. Many drugs receive regulatory approval for only a single crystal form or polymorph. For a long time, only one crystal structure for aspirin was known. | 11
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Tretinoin, also known as all-trans retinoic acid (ATRA), is a medication used for the treatment of acne and acute promyelocytic leukemia. For acne, it is applied to the skin as a cream, gel or ointment. For leukemia, it is taken by mouth for up to three months. Topical tretinoin is also the most extensively investigated retinoid therapy for photoaging.Common side effects when used as a cream are limited to the skin and include skin redness, peeling, and sun sensitivity. When used by mouth, side effects include shortness of breath, headache, numbness, depression, skin dryness, itchiness, hair loss, vomiting, muscle pains, and vision changes. Other severe side effects include high white blood cell counts and blood clots. Use during pregnancy is contraindicated due to the risk of birth defects. It is in the retinoid family of medications.Tretinoin was patented in 1957, and approved for medical use in 1962. It is on the World Health Organizations List of Essential Medicines. Tretinoin is available as a generic medication. In 2019, it was the 244th most commonly prescribed medication in the United States, with more than 1 million prescriptions. Medical uses
Skin use
Tretinoin is most commonly used to treat acne, both inflammatory and noninflammatory. Multiple studies support the efficacy of topical retinoids in the treatment of acne vulgaris. It is sometimes used in conjunction with other topical acne medications to enhance their penetration. In addition to treating active acne, retinoids accelerate the resolution of acne-induced postinflammatory hyperpigmentation. | Mechanism of action
For its use in cancer, its mechanism of action is unknown, but on a cellular level, laboratory tests show that tretinoin forces APL cells to differentiate and stops them from proliferating; in people there is evidence that it forces the primary cancerous promyelocytes to differentiate into their final form, allowing normal cells to take over the bone marrow. Recent study shows that ATRA inhibits and degrades active PIN1.For its use in acne, tretinoin (along with other retinoids) are vitamin A derivatives that act by binding to two nuclear receptor families within keratinocytes: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). These events contribute to the normalization of follicular keratinization and decreased cohesiveness of keratinocytes, resulting in reduced follicular occlusion and microcomedone formation. The retinoid-receptor complex competes for coactivator proteins of AP-1, a key transcription factor involved in inflammation. Retinoids also down-regulate expression of toll-like receptor (TLR)-2, which has been implicated in the inflammatory response in acne. Moreover, tretinoin and retinoids may enhance the penetration of other topical acne medications.The combination of the 10% benzoyl peroxide and light results in more than 50% degradation of tretinoin in about 2 hours and 95% in 24 hours. This lack of stability in the presence of light and oxidizing agents has led to the development of novel formulations of the drug. When microencapsulated tretinoin is exposed to benzoyl peroxide and light only 1% degradation takes place in about 4 hours and only 13% after 24 hours. Biosynthesis
Tretinoin is synthesized from beta-carotene. | 11
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Diagnosis
Clinical signs of cerebral edema, such as focal neurological deficits, papilledema and decreased level of consciousness, if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes.MRI of the head has been used in research to better understand DDS. Treatment
Avoidance is the primary treatment. Better alternatives are Nocturnal or Daily Dialysis, which are far more gentle processes for the new dialysis patient. Dialysis disequilibrium syndrome is a reason why hemodialysis initiation should be done gradually, i.e. it is a reason why the first few dialysis sessions are shorter and less aggressive than the typical dialysis treatment for end-stage renal disease patients. See also
Kidney failure
References
External links
Dialysis disequilibrium syndrome at the United States National Library of Medicine
Dialysis Disequilibrium Syndrome (DDS) – Rare but serious complication of dialysis | Intense itching or burning sensations are sometimes felt before the blisters appear in a particular area.The signs and symptoms of DH typically appear around 30 to 40 years of age, although all ages may be affected. Although the first signs and symptoms of dermatitis herpetiformis are intense itching and burning, the first visible signs are the small papules or vesicles that usually look like red bumps or blisters. The rash rarely occurs on other mucous membranes, excepting the mouth or lips. The symptoms range in severity from mild to serious, but they are likely to disappear if gluten ingestion is avoided and appropriate treatment is administered. Dermatitis herpetiformis symptoms are chronic, and they tend to come and go, mostly in short periods of time in response to the amount of gluten ingested. Sometimes, these symptoms may be accompanied by symptoms of coeliac disease, which typically include abdominal pain, bloating or loose stool, weight loss, and fatigue. However, individuals with DH often have no gastrointestinal symptoms even if they have associated intestinal damage.The rash caused by dermatitis herpetiformis forms and disappears in three stages. In the first stage, the patient may notice a slight discoloration of the skin at the site where the lesions appear. In the next stage, the skin lesions transform into obvious vesicles and papules that are likely to occur in groups. Healing of the lesions is the last stage of the development of the symptoms, usually characterized by a change in the skin color. | 0-1
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In both cases, supplementation with biotin can often restore normal metabolic function and proper catabolism of leucine and isoleucine.The symptoms of biotinidase deficiency (and dietary deficiency of biotin) can be quite severe. A 2004 case study from Metametrix detailed the effects of biotin deficiency, including aggression, cognitive delay, and reduced immune function. Genetics
Mutations in the BTD gene cause biotinidase deficiency. Biotinidase is the enzyme that is made by the BTD gene. Many mutations that cause the enzyme to be nonfunctional or to be produced at extremely low levels have been identified. Biotin is a vitamin that is chemically bound to proteins. (Most vitamins are only loosely associated with proteins.) Without biotinidase activity, the vitamin biotin cannot be separated from foods and therefore cannot be used by the body. Another function of the biotinidase enzyme is to recycle biotin from enzymes that are important in metabolism (processing of substances in cells). When biotin is lacking, specific enzymes called carboxylases cannot process certain proteins, fats, or carbohydrates. Specifically, two essential branched-chain amino acids (leucine and isoleucine) are metabolized differently.Individuals lacking functional biotinidase enzymes can still have normal carboxylase activity if they ingest adequate amounts of biotin. The standard treatment regimen calls for 5–10 mg of biotin per day.Biotinidase deficiency is inherited in an autosomal recessive pattern, which means the defective gene is located on an autosome, and two copies of the defective gene - one from each parent - must be inherited for a person to be affected by the disorder. | Flurbiprofen is a member of the phenylalkanoic acid derivative family of nonsteroidal anti-inflammatory drugs (NSAIDs). It is primarily indicated as a pre-operative anti-miotic (in an ophthalmic solution) as well as orally for arthritis or dental pain. Side effects are analogous to those of ibuprofen.It was derived from propionic acid by the research arm of Boots UK during the 1960s, a period which also included the discovery of ibuprofen, indometacin, diclofenac, naproxen, ketoprofen, and sulindac. : 34 It was patented in 1964 by Boots UK and approved for medical use in 1987. It was approved in the US in 1988; the first generic was approved in 1994.: 158
Adverse effects
In October 2020, the U.S. Food and Drug Administration (FDA) required the drug label to be updated for all nonsteroidal anti-inflammatory medications to describe the risk of kidney problems in unborn babies that result in low amniotic fluid. They recommend avoiding NSAIDs in pregnant women at 20 weeks or later in pregnancy. | 0-1
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Definitive diagnosis is typically made in a laboratory by employing some combination of blood tests, particularly immunologic, serologic and/or virologic techniques such as ELISA, complement fixation, polymerase chain reaction, neutralization test, and hemagglutination-inhibition test. Classification
In the past, arboviruses were organized into one of four groups: A, B, C, and D. Group A denoted members of the genus Alphavirus, Group B were members of the genus Flavivirus, and Group C remains as the Group C serogroup of the genus Orthobunyavirus. Group D was renamed in the mid-1950s to the Guama group and is currently the Guama serogroup in the genus Orthobunyavirus. Currently, viruses are jointly classified according to Baltimore classification and a virus-specific system based on standard biological classification. With the exception of the African swine fever virus, which belongs to the Asfarviridae family of viruses, all major clinically important arboviruses belong to one of the following four groups:
Prevention
Vector control measures, especially mosquito control, are essential to reducing the transmission of disease by arboviruses. Habitat control involves draining swamps and removal of other pools of stagnant water (such as old tires, large outdoor potted plants, empty cans, etc.) that often serve as breeding grounds for mosquitoes. Insecticides can be applied in rural and urban areas, inside houses and other buildings, or in outdoor environments. They are often quite effective for controlling arthropod populations, though use of some of these chemicals is controversial, and some organophosphates and organochlorides (such as DDT) have been banned in many countries. | Chromosome 14 is also known to cause particular symptoms such as skeletal abnormalities, intellectual disability, and joint contractures, among others.UPD has rarely been studied prospectively, with most reports focusing on either known conditions or incidental findings. It has been proposed that the incidence may not be as low as believed, rather it may be under-reported. All chromosomes
Genome wide UPD, also called uniparental diploidy, is when all chromosomes are inherited from one parent. Only in mosaic form can this phenomenon be compatible with life. As of 2017, there have only been 18 reported cases of genome wide UPD. History
The first clinical case of UPD was reported in 1988 and involved a girl with cystic fibrosis and short stature who carried two copies of maternal chromosome 7. Since 1991, out of the 47 possible disomies, 29 have been identified among individuals ascertained for medical reasons. This includes chromosomes 2, 5–11, 13–16, 21 and 22. See also
Aneuploidy
References
External links
"Uniparental disomy". Department of Medical Genetics, University of British Columbia. Archived from the original on 2002-06-17. {{cite web}}: CS1 maint: unfit URL (link)
T. Liehr: Cases with uniparental disomy
UPD Animations: UPD AnimationsThis article incorporates public domain text from The U.S. National Library of Medicine | 0-1
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Coxiella burnetii – named for Cox and Burnet – is no longer regarded as closely related to the Rickettsiae, but as similar to Legionella and Francisella, and is a Gammaproteobacterium. Society and culture
An early mention of Q fever was important in one of the early Dr. Kildare films (1939, Calling Dr. Kildare). Kildares mentor Dr. Gillespie (Lionel Barrymore) tires of his protégé working fruitlessly on "exotic diagnoses" ("I think its Q fever!") and sends him to work in a neighborhood clinic, instead.Q fever was also highlighted in an episode of the U.S. television medical drama House ("The Dig", season seven, episode 18). Biological warfare
C. burnetii has been used to develop biological weapons.The United States investigated it as a potential biological warfare agent in the 1950s, with eventual standardization as agent OU. At Fort Detrick and Dugway Proving Ground, human trials were conducted on Whitecoat volunteers to determine the median infective dose (18 MICLD50/person i.h.) and course of infection. The Deseret Test Center dispensed biological Agent OU with ships and aircraft, during Project 112 and Project SHAD. As a standardized biological, it was manufactured in large quantities at Pine Bluff Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970. C. burnetii is currently ranked as a "category B" bioterrorism agent by the CDC. It can be contagious, and is very stable in aerosols in a wide range of temperatures. Q fever microorganisms may survive on surfaces up to 60 days. | Treatment with ablative carbon dioxide lasers is a less invasive method that can be used to improve the appearance of lymphangioma circumscriptum. These laser treatments require local anesthesia and may cause significant wounds. See also
Lymphangioma
Skin lesion
List of cutaneous conditions
References
== External links == | 0-1
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However, this meta-analysis included two large studies of smokers, so it is not clear that the results apply to the general population. The review only studied the influence of synthetic antioxidants and the results should not be translated to potential effects of fruits and vegetables. β-Carotene and photosensitivity
Oral β-carotene is prescribed to people suffering from erythropoietic protoporphyria. It provides them some relief from photosensitivity. Carotenemia
Carotenemia or hypercarotenemia is excess carotene, but unlike excess vitamin A, carotene is non-toxic. Although hypercarotenemia is not particularly dangerous, it can lead to an oranging of the skin (carotenodermia), but not the conjunctiva of eyes (thus easily distinguishing it visually from jaundice). It is most commonly associated with consumption of an abundance of carrots, but it also can be a medical sign of more dangerous conditions. Production
Carotenes are produced in a general manner for other terpenoids and terpenes, i.e. by coupling, cyclization, and oxygenation reactions of isoprene derivatives. Lycopene is the key precursor to carotenoids. It is formed by coupling of geranylgeranyl pyrophosphate and[geranyllinalyl pyrophosphate.Most of the worlds synthetic supply of carotene comes from a manufacturing complex located in Freeport, Texas and owned by DSM. The other major supplier BASF also uses a chemical process to produce β-carotene. Together these suppliers account for about 85% of the β-carotene on the market. In Spain Vitatene produces natural β-carotene from fungus Blakeslea trispora, as does DSM but at much lower amount when compared to its synthetic β-carotene operation. | For example, one association is with mutations in the XBP1 gene, which is involved in the unfolded protein response pathway of the endoplasmic reticulum. The gene variants of NOD2/CARD15 seem to be related with small-bowel involvement. Other well documented genes which increase the risk of developing Crohns disease are ATG16L1, IL23R, IRGM, and SLC11A1. There is considerable overlap between susceptibility loci for IBD and mycobacterial infections. Genome-wide association studies have shown that Crohns disease is genetically linked to coeliac disease.Crohns has been linked to the gene LRRK2 with one variant potentially increasing the risk of developing the disease by 70%, while another lowers it by 25%. The gene is responsible for making a protein, which collects and eliminates waste product in cells, and is also associated with Parkinsons disease. Immune system
There was a prevailing view that Crohns disease is a primary T cell autoimmune disorder; however, a newer theory hypothesizes that Crohns results from an impaired innate immunity. The later hypothesis describes impaired cytokine secretion by macrophages, which contributes to impaired innate immunity and leads to a sustained microbial-induced inflammatory response in the colon, where the bacterial load is high. Another theory is that the inflammation of Crohns was caused by an overactive Th1 and Th17 cytokine response.In 2007, the ATG16L1 gene was implicated in Crohns disease, which may induce autophagy and hinder the bodys ability to attack invasive bacteria. | 0-1
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Along with clinical studies using various drugs with anticholinergic activity, these models have contributed to a "cholinergic deficiency hypothesis" of delirium.Profound systemic inflammation occurring during sepsis is also known to cause delirium (often termed sepsis-associated encephalopathy). Animal models used to study the interactions between prior degenerative disease and overlying systemic inflammation have shown that even mild systemic inflammation causes acute and transient deficits in working memory among diseased animals. Prior dementia or age-associated cognitive impairment is the primary predisposing factor for clinical delirium and "prior pathology" as defined by these new animal models may consist of synaptic loss, abnormal network connectivity, and "primed microglia" brain macrophages stimulated by prior neurodegenerative disease and aging to amplify subsequent inflammatory responses in the central nervous system (CNS). Cerebrospinal fluid
Studies of cerebrospinal fluid (CSF) in delirium are difficult to perform. Apart from the general difficulty of recruiting participants who are often unable to give consent, the inherently invasive nature of CSF sampling makes such research particularly challenging. However, a few studies have exploited the opportunity to sample CSF from persons undergoing spinal anesthesia for elective or emergency surgery.A 2018 systematic review showed that, broadly, delirium may be associated with neurotransmitter imbalance (namely serotonin and dopamine signaling), reversible fall in somatostatin, and increased cortisol. The leading "neuroinflammatory hypothesis" (where neurodegenerative disease and aging leads the brain to respond to peripheral inflammation with an exaggerated CNS inflammatory response) has been described, but current evidence is still conflicting and fails to concretely support this hypothesis. | Predisposing factors
The most important predisposing factors are:
65 or more years of age
Male sex
Cognitive impairment/dementia
Physical comorbidity (biventricular failure, cancer, cerebrovascular disease)
Psychiatric comorbidity (e.g., depression)
Sensory impairment (vision, hearing)
Functional dependence (e.g., requiring assistance for self-care or mobility)
Dehydration/malnutrition
Drugs and drug-dependence
Alcohol dependence
Precipitating factors
Any acute factors that affect neurotransmitter, neuroendocrine, or neuroinflammatory pathways can precipitate an episode of delirium in a vulnerable brain. Clinical environments can also precipitate delirium. Some of the most common precipitating factors are listed below:
Prolonged sleep deprivation
Environmental, physical/psychological stress
Inadequately controlled pain
Admission to an intensive care unit
Immobilization, use of physical restraints
Urinary retention, use of bladder catheter,
Emotional stress
Severe constipation/fecal impaction
MedicationsSedatives (benzodiazepines, opioids), anticholinergics, dopaminergics, corticosteroids, polypharmacy
General anesthetic
Substance intoxication or withdrawal
Primary neurologic diseases
Severe drop in blood pressure, relative to the patients normal blood pressure (orthostatic hypotension) resulting in inadequate blood flow to the brain (cerebral hypoperfusion)
Stroke/Transient ischemic attack(TIA)
Intracranial bleeding
Meningitis, encephalitis
Concurrent illness
Infections – especially respiratory (e.g. pneumonia, COVID-19) and urinary tract infections
Iatrogenic complications
Hypoxia, hypercapnea, anemia
Poor nutritional status, dehydration, electrolyte imbalances, hypoglycemia
Shock, heart attacks, heart failure
Metabolic derangements (e.g. SIADH, Addisons disease, hyperthyroidism, )
Chronic/terminal illness (e.g. cancer)
Post-traumatic event (e.g. fall, fracture)
Mercury poisoning (e.g. Erethism)
Surgery
Cardiac, orthopedic, prolonged cardiopulmonary bypass, thoracic surgeries
Pathophysiology
The pathophysiology of delirium is still not well understood, despite extensive research. Animal models
The lack of animal models that are relevant to delirium has left many key questions in delirium pathophysiology unanswered. Earliest rodent models of delirium used atropine (a muscarinic acetylcholine receptor blocker) to induce cognitive and electroencephalography (EEG) changes similar to delirium, and other anticholinergic drugs, such as biperiden and hyoscine, have produced similar effects. | 11
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Eyes
Adenovirus eye infection may present as a pinky-red eye. Six to nine-days following exposure to adenovirus, one or both eyes, typically in children, may be affected in association with fever, pharyngitis and lymphadenopathy (pharyngoconjunctival fever (PCF)). The onset is usually sudden, and there is often rhinitis. Adenovirus infection can also cause adenoviral keratoconjunctivitis. Typically one eye is affected after an incubation period of up to a week. The eye becomes itchy, painful, burning and reddish and lymphadenopathy may be felt by the ear nearest the affected eye. The symptoms may last around 10-days to three-weeks. It may be is associated with blurred vision, photophobia and swelling of the conjunctiva. A sore throat and nasal congestion may or may not be present. This tends to occur in epidemics, affecting predominantly adults. In very young children, it may be associated with high fever, sore throat, otitis media, diarrhoea, and vomiting. Gastrointestinal tract
Adenovirus infection can cause a gastroenteritis when it may present with diarrhoea, vomiting and abdominal pain, with or without respiratory or general symptoms. Children under the age of one-year appear particularly vulnerable. However, it usually resolves within three-days. It appears similar to diarrhoea diseases caused by other infections. Other organs
Uncommonly the bladder may be affected, presenting with a sudden onset of burning on passing urine and increased frequency of passing urine, followed by seeing blood in the urine a day or two later. Meningism may occur in adenovirus associated meningoencephalitis, which may occur in people with weakened immune systems such as with AIDS or lymphoma. | For some adenovirus serotypes, the clinical spectrum of disease associated with infection varies depending on the site of infection; for example, infection with adenovirus 7 acquired by inhalation is associated with severe lower respiratory tract disease, whereas oral transmission of the virus typically causes no or mild disease. Outbreaks of adenovirus-associated respiratory disease have been more common in the late winter, spring, and early summer; however, adenovirus infections can occur throughout the year.Several adenoviruses, including Ad5, Ad9, Ad31, Ad36, Ad37, and SMAM1, have at least some evidence of causation of obesity in animals, adipogenesis in cells, and/or association with human obesity. Diagnosis
Diagnosis is by signs and symptoms, and a laboratory test is not usually required. In some circumstances such as severe disease, when a diagnosis needs to be confirmed, a PCR test on blood or respiratory secretions may detect adenovirus DNA. Adenovirus can be isolated by growing in cell cultures in a laboratory. Other conditions that appear similar include whooping cough, influenza, parainfluenza, and respiratory syncytial virus. Since adenovirus can be excreted for prolonged periods, the presence of virus does not necessarily mean it is associated with disease. Prevention
Infection by adenovirus may be prevented by washing hands, avoiding touching own eyes, mouth and nose before washing hands and avoiding being near sick people. Strict attention to good infection-control practices is effective for stopping transmission in hospitals of adenovirus-associated disease, such as epidemic keratoconjunctivitis. Maintaining adequate levels of chlorination is necessary for preventing swimming pool-associated outbreaks of adenovirus conjunctivitis. | 11
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There are also situations where the terms are misused to refer to relationships where the younger person is an adult of legal age, but is either considered too young in comparison to their older partner, or the older partner occupies a position of authority over them. Researchers state that the above uses of the term pedophilia are imprecise or suggest that they are best avoided. The Mayo Clinic states that pedophilia "is not a criminal or legal term". Pedophile advocacy groups
From the late 1950s to early 1990s, several pedophile membership organizations advocated age of consent reform to lower or abolish age of consent laws, as well as for the acceptance of pedophilia as a sexual orientation rather than a psychological disorder, and for the legalization of child pornography. The efforts of pedophile advocacy groups did not gain mainstream acceptance, and today those few groups that have not dissolved have only minimal membership and have ceased their activities other than through a few websites. In contrast to these organizations, members of the support group Virtuous Pedophiles believe that child sexual abuse is wrong and seek to raise awareness that some pedophiles do not offend; this is generally not considered pedophile advocacy, as the Virtuous Pedophiles organization does not approve of the legalization of child pornography and does not support age of consent reform. Anti-pedophile activism
Anti-pedophile activism encompasses opposition against pedophiles, against pedophile advocacy groups, and against other phenomena that are seen as related to pedophilia, such as child pornography and child sexual abuse. | Radial neuropathy is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of the arm. It is known as transient paresthesia when sensation is temporarily abnormal. Signs and symptoms
Symptoms of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, numbness on the back of the hand and wrist, and inability to voluntarily straighten the fingers. Loss of wrist extension is due to loss of the ability to move of the posterior compartment of forearm muscles. In the event of lacerations to the wrist area the symptom would therefore be sensory. Additionally, depending on the type of trauma, other nerves may be affected such as the median nerve and axillary nerves. Causes
There are many ways to acquire radial nerve neuropathy, including:
Upper arm - a fracture of the bone
Elbow - entrapment of the nerve
Wrist - elbow deformity and soft-tissue masses
Axilla - here the most common cause is compression. However, a dislocation of the humerus is a possible factor as well. It could also be due to brachial plexus compression. Mechanism
The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal degeneration. These would be caused via laceration or compression of the nerve in question. Diagnosis
Radial neuropathy may be diagnosed using MRI, ultrasound, nerve conduction study or electromyography (EMG). | 0-1
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Wine is important in cuisine not just for its value as an accompanying beverage, but as a flavor agent, primarily in stocks and braising, since its acidity lends balance to rich savory or sweet dishes. Wine sauce is an example of a culinary sauce that uses wine as a primary ingredient. Natural wines may exhibit a broad range of alcohol content, from below 9% to above 16% ABV, with most wines being in the 12.5–14.5% range. Fortified wines (usually with brandy) may contain 20% alcohol or more. Alcohol measurement
Alcohol concentration
The concentration of alcohol in a beverage is usually stated as the percentage of alcohol by volume (ABV, the number of milliliters (ml) of pure ethanol in 100 ml of beverage) or as proof. In the United States, proof is twice the percentage of alcohol by volume at 60 degrees Fahrenheit (e.g. 80 proof = 40% ABV). Degrees proof were formerly used in the United Kingdom, where 100 degrees proof was equivalent to 57.1% ABV. Historically, this was the most dilute spirit that would sustain the combustion of gunpowder. Ordinary distillation cannot produce alcohol of more than 95.6% by weight, which is about 97.2% ABV (194.4 proof) because at that point alcohol is an azeotrope with water. A spirit which contains a very high level of alcohol and does not contain any added flavoring is commonly called a neutral spirit. | Intal may refer to:
Intal, a brand name for the pharmaceutical drug cromoglicic acid
Intal language, an international auxiliary language
JC Intal, a Filipino professional basketball player | 0-1
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Another group of mutations that lead to elliptocytosis are those that cause glycophorin C deficiencies. There are three phenotypes caused by abnormal glycophorin C, these are named Gerbich, Yus and Leach (see glycophorin C for more information). Only the rarest of the three, the Leach phenotype, causes elliptocytosis. Glycophorin C has the function of holding band 4.1 to the cell membrane. It is thought that elliptocytosis in glycophorin C deficiency is actually the consequence of a band 4.1 deficit, as glycophorin C deficient individuals also have reduced intracellular band 4.1 (probably due to the reduced number of binding sites for band 4.1 in the absence of glycoprotein C).Inheritance of multiple mutations tends to infer more serious disease. For instance, the most common genotype responsible for HPP occurs when the affected individual inherits an α-spectrin mutation from one parent (i.e. one parent has hereditary elliptocytosis) and the other parent passes on an as-yet-undefined defect that causes the affected individuals cells to preferentially produce the defective α-spectrin rather than normal α-spectrin. Diagnosis
The diagnosis of hereditary elliptocytosis is usually made by coupling a family history of the condition with an appropriate clinical presentation and confirmation on a blood smear. In general it requires that at least 25% of erythrocytes in the specimen are abnormally elliptical in shape, though the observed percentage of elliptocytes can be 100%. | In the United Kingdom, marketing of paracetamol began in 1956 by Sterling-Winthrop Co. as Panadol, available only by prescription, and promoted as preferable to aspirin since it was safe for children and people with ulcers. In 1963, paracetamol was added to the British Pharmacopoeia, and has gained popularity since then as an analgesic agent with few side-effects and little interaction with other pharmaceutical agents.Concerns about paracetamols safety delayed its widespread acceptance until the 1970s, but in the 1980s paracetamol sales exceeded those of aspirin in many countries, including the United Kingdom. This was accompanied by the commercial demise of phenacetin, blamed as the cause of analgesic nephropathy and hematological toxicity. Available in the US without a prescription since 1955 (1960, according to another source) paracetamol has become a common household drug. In 1988, Sterling Winthrop was acquired by Eastman Kodak which sold the over the counter drug rights to SmithKline Beecham in 1994.In June 2009, an FDA advisory committee recommended that new restrictions be placed on paracetamol use in the United States to help protect people from the potential toxic effects. The maximum single adult dosage would be decreased from 1000 mg to 650 mg, while combinations of paracetamol and other products would be prohibited. | 0-1
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Since that time, it has achieved blockbuster drug status with global sales of US$1.87B in 2004 (with $1.49B coming from the United States). AMRI received royalty payments from Aventis that enabled the growth of AMRI.In January 2011, the FDA approved over-the-counter sales of fexofenadine in the United States, and Sanofi Aventis version became available in March 2011. | Fexofenadine was also shown to inhibit histamine-induced wheal and flare to a significantly greater degree than loratadine or desloratadine, but was slightly less effective than levocetirizine.Fexofenadine at doses above 120 mg a day does not appear to provide additional efficacy in the treatment of allergic rhinitis. Side effects
The most common side effects include headache, back and muscle pain, miosis or pinpoint pupils, nausea, drowsiness, and menstrual cramps. Anxiety and insomnia have also been rarely reported. The most common side effects demonstrated during clinical trials were cough, upper respiratory tract infection, fever, and otitis media for children ages 6 to 11 and fatigue for children ages 6 months to 5 years. Overdose
The safety profile of fexofenadine is quite favorable, as no cardiovascular or sedative effects have been shown to occur even when taking 10 times the recommended dose. Research on humans ranges from a single 800-mg dose, to a twice-daily, 690-mg dose for a month, with no clinically significant adverse effects, when compared to a placebo. No deaths occurred in testing on mice, at 5000 mg/kg body weight, which is 110 times the maximum recommended dose for an adult human. If overdose were to occur, supportive measures are recommended. Theoretically, an overdose could present as dizziness, dry mouth, and/or drowsiness, consistent with an exaggeration of the usual side effects. Hemodialysis does not appear to be an effective means of removing fexofenadine from the blood. Pharmacology
Pharmacodynamics
Fexofenadine is a selective peripheral H1 receptor antagonist. | 11
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More than half of twins are born weighing less than 5.5 pounds (2.5 kg), while the average birth weight of a healthy baby should be around 6–8 pounds (3–4 kg). This is largely due to the fact that twins are typically born premature. Premature birth and low birth weights, especially when under 3.5 pounds (1.6 kg), can increase the risk of several health-related issues, such as vision and hearing loss, mental disabilities, and cerebral palsy. There is an increased possibility of potential complications as the birth weight of the baby decreases. Twin-to-twin transfusion syndrome
Monozygotic twins who share a placenta can develop twin-to-twin transfusion syndrome. This condition means that blood from one twin is being diverted into the other twin. One twin, the donor twin, is small and anemic, the other, the recipient twin, is large and polycythemic. The lives of both twins are endangered by this condition. Stillbirths
Stillbirths occurs when a fetus dies after 20 weeks of gestation. There are two types of stillbirth, including intrauterine death and intrapartum death. Intrauterine death occurs when a baby dies during late pregnancy. Intrapartum death, which is more common, occurs when a baby dies while the mother is giving birth. The cause of stillbirth is often unknown, but the rate of babies who are stillborn is higher in twins and multiple births. Caesareans or inductions are advised after 38 weeks of pregnancy for twins, because the risk of stillbirth increases after this time. | Pulmonary vein stenosis is a rare cardiovascular disorder. It is recognized as being the stenosis of one or more of the four pulmonary veins that return blood from the lungs to the left atrium of the heart. In congenital cases, it is associated with poor prognosis and high mortality rate. In some people, pulmonary vein stenosis occurs after pulmonary vein ablation for the treatment of atrial fibrillation. Some recent research has indicated that it may be genetically linked in congenital cases. == References == | 0-1
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Chronic venous insufficiency (CVI) is a medical condition in which blood pools in the veins, straining the walls of the vein. The most common cause of CVI is superficial venous reflux which is a treatable condition. As functional venous valves are required to provide for efficient blood return from the lower extremities, this condition typically affects the legs. If the impaired vein function causes significant symptoms, such as swelling and ulcer formation, it is referred to as chronic venous disease. It is sometimes called chronic peripheral venous insufficiency and should not be confused with post-thrombotic syndrome in which the deep veins have been damaged by previous deep vein thrombosis. Most cases of CVI can be improved with treatments to the superficial venous system or stenting the deep system. Varicose veins for example can now be treated by local anesthetic endovenous surgery. Rates of CVI are higher in women than in men. Other risk factors include genetics, smoking, obesity, pregnancy, and prolonged standing. Signs and symptoms
Signs and symptoms of CVI in the leg include the following:
Varicose veins
Itching (pruritus)
Hyperpigmentation
Phlebetic lymphedema
Chronic swelling of the legs and ankles
Venous ulcerationCVI in the leg may cause the following:
Venous stasis
Ulcers
Stasis dermatitis, also known as varicose eczema
Contact dermatitis, a disrupted epidermal barrier due to venous insufficiency, making patients more susceptible than the general population to contact sensitization and subsequent dermatitis. Atrophie blanche, an end point of a variety of conditions that appears as atrophic plaques of ivory white skin with telangiectasias. | Starting in the 1950s, ethinylestradiol became widely used in birth control pills. Estradiol-containing birth control pills were initially studied in the 1970s, with the first report published in 1977. Development of birth control pills containing estradiol was motivated by the thrombotic risks of ethinylestradiol that were uncovered in the 1960s and 1970s. More than 15 attempts were made at development of an estradiol-containing birth control pill starting in the 1970s, but were unsuccessful due to unacceptable menstrual bleeding patterns. Estradiol valerate/cyproterone acetate (Femilar) was introduced for use as a birth control pill in Finland in 1993, but was never marketed elsewhere. Subsequently, estradiol valerate/dienogest (Natazia, Qlaira) was marketed as a birth control pill in 2008 and estradiol/nomegestrol acetate (Naemis, Zoely) was introduced in 2012. Society and culture
Generic names
Estradiol is the generic name of estradiol in American English and its INN, USAN, USP, BAN, DCF, and JAN. Estradiolo is the name of estradiol in Italian and the DCIT and estradiolum is its name in Latin, whereas its name remains unchanged as estradiol in Spanish, Portuguese, French, and German. Oestradiol was the former BAN of estradiol and its name in British English, but the spelling was eventually changed to estradiol. When estradiol is provided in its hemihydrate form, its INN is estradiol hemihydrate. Brand names
Estradiol is marketed under a large number of brand names throughout the world. | 0-1
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Endometrial cancer is a cancer that arises from the endometrium (the lining of the uterus or womb). It is the result of the abnormal growth of cells that have the ability to invade or spread to other parts of the body. The first sign is most often vaginal bleeding not associated with a menstrual period. Other symptoms include pain with urination, pain during sexual intercourse, or pelvic pain. Endometrial cancer occurs most commonly after menopause.Approximately 40% of cases are related to obesity. Endometrial cancer is also associated with excessive estrogen exposure, high blood pressure and diabetes. Whereas taking estrogen alone increases the risk of endometrial cancer, taking both estrogen and a progestogen in combination, as in most birth control pills, decreases the risk. Between two and five percent of cases are related to genes inherited from the parents. Endometrial cancer is sometimes loosely referred to as "uterine cancer", although it is distinct from other forms of uterine cancer such as cervical cancer, uterine sarcoma, and trophoblastic disease. The most frequent type of endometrial cancer is endometrioid carcinoma, which accounts for more than 80% of cases. Endometrial cancer is commonly diagnosed by endometrial biopsy or by taking samples during a procedure known as dilation and curettage. A pap smear is not typically sufficient to show endometrial cancer. | Char syndrome is an autosomal dominant congenital disease caused by mutations in TFAP2B gene which affects the development of the bones of the face as well as the heart and limbs. During embryo development, TFAP2B regulates the production of the protein AP-2β, a transcription factor that is active in the neural crest and helps regulate genes that control cell division and apoptosis. There are at least 10 mutations of this gene that have been identified in people presenting Char syndrome, which alters specific regions of the gene preventing production of the transcription factor and disrupting normal development of embryo structures. People with this condition present a very distinct facial appearance with flattened cheek bones, flat and broad tip nose, shortened distance between the nose and upper lip, triangular-shaped mouth with tick lips and strabismus. It is also characterized by a patent ductus arteriosus, which is the failure to close the ductus that connects the aorta and pulmonary artery during pre-birth life and may cause many symptoms including breathing issues and heart failure. Abnormalities of hand and finger development have also been reported in people with this condition, including short or absent fifth finger. Other abnormal findings include supernumerary nipples. These conditions often affect multiple members of a family and there are no reports of non-genetic factors that might be related with incidence of this syndrome. It was first described by Florence Char in 1978. == References == | 0-1
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Pneumatosis is the abnormal presence of air or other gas within tissues.In the lungs, emphysema involves enlargement of the distal airspaces, and is a major feature of chronic obstructive pulmonary disease (COPD). Other pneumatoses in the lungs are focal (localized) blebs and bullae, pulmonary cysts and cavities. Pneumoperitoneum (or peritoneal emphysema) is air or gas in the abdominal cavity, and is most commonly caused by gastrointestinal perforation, often the result of surgery. Pneumarthrosis, the presence of air in a joint, is rarely a serious sign. Lung cysts
A lung cyst, or pulmonary cyst, encloses a small volume of air, and has a wall thickness of up to 4 mm. A minimum wall thickness of 1 mm has been suggested, but thin-walled pockets may be included in the definition as well. Pulmonary cysts are not associated with either smoking or emphysema.A lung cavity has a wall thickness of more than 4 mm. Other thoracic
Pneumothorax, air or gas in the pleural space
Pneumomediastinum, air or gas in the mediastinum
Also called mediastinal emphysema or pneumatosis/emphysema of the mediastinum
Abdominal
Pneumoperitoneum (or peritoneal emphysema), air or gas in the abdominal cavity. The most common cause is a perforated abdominal viscus, generally a perforated peptic ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or abdominal trauma. Pneumatosis intestinalis, air or gas cysts in the bowel wall
Gastric pneumatosis (or gastric emphysema) is air or gas cysts in the stomach wall
Joints
Pneumarthrosis is the presence of air in a joint. | Its presentation on radiography is a radiolucent cleft often called a vacuum phenomenon, or vacuum sign. Pneumarthrosis is associated with osteoarthritis and spondylosis.Pneumarthrosis is a common normal finding in shoulders as well as in sternoclavicular joints. It is believed to be a cause of the sounds of joint cracking. It is also a common normal post-operative finding at least after spinal surgery. Pneumarthrosis is extremely rare in conjunction with fluid or pus in a joint, and its presence can therefore practically exclude infection. Other
Subcutaneous emphysema is found in the deepest layer of the skin. Emphysematous cystitis is a condition of gas in the bladder wall. On occasion this may give rise to secondary subcutaneous emphysema which has a poor prognosis.Pneumoparotitis is the presence of air in the parotid gland caused by raised air pressure in the mouth often as a result of playing wind instruments. In rare cases air may escape from the gland and give rise to subcutaneous emphysema in the face, neck, or mediastinum. Terminology
The term pneumatosis has word roots of pneumat- + -osis, meaning "air problem/injury". References
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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. | Prevention
Physical activity in extremely hot weather should be avoided. If a person starts to experience over heating, and symptoms of heat syncope, they should move or be moved to a shaded or cool area. It is also recommended to avoid alcoholic beverages in hot weather, because they cause dehydration which may worsen symptoms. Finally, drinking plenty of water with electrolytes is imperative when engaging in physical activity in hot weather. Treatment
The basic treatment for heat syncope is like that for other types of fainting: the patient is positioned in a seating or supine position with legs raised. Water containing salt, or another drink containing electrolytes, is administered slowly, and the patient is moved to a cooler area, such as the shade. The affected person should rest and recover, because heat syncope can lead to heat stroke or heat exhaustion. References
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To help with diagnosis, a synovial fluid Gram stain and culture may be performed. Other conditions that can look similar include CPPD (pseudogout), rheumatoid arthritis, psoriatic arthritis, palindromic rheumatism, and reactive arthritis. Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma or other neoplasms. Prevention
Risk of gout attacks can be lowered by complete abstinence from drinking alcoholic beverages, reducing the intake of fructose (e.g. high fructose corn syrup) and purine-rich foods of animal origin, such as organ meats and seafood. Eating dairy products, vitamin C-rich foods, coffee, and cherries may help prevent gout attacks, as does losing weight. Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks. Medications
As of 2020, allopurinol is generally the recommended preventative treatment if medications are used. A number of other medications may occasionally be considered to prevent further episodes of gout, including probenecid, febuxostat, benzbromarone, and colchicine. Long term medications are not recommended until a person has had two attacks of gout, unless destructive joint changes, tophi, or urate nephropathy exist. It is not until this point that medications are cost-effective. They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack. | Plain X-rays are usually normal and are not useful for confirming a diagnosis of early gout. They may show signs of chronic gout such as bone erosion. Synovial fluid
A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or a tophus. All synovial fluid samples obtained from undiagnosed inflamed joints by arthrocentesis should be examined for these crystals. Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform and requires a trained observer. The fluid must be examined relatively soon after aspiration, as temperature and pH affect solubility. Blood tests
Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with raised uric acid levels never develop gout. Thus, the diagnostic utility of measuring uric acid levels is limited. Hyperuricemia is defined as a plasma urate level greater than 420 μmol/L (7.0 mg/dl) in males and 360 μmol/L (6.0 mg/dl) in females. Other blood tests commonly performed are white blood cell count, electrolytes, kidney function and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection. A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented. Differential diagnosis
The most important differential diagnosis in gout is septic arthritis. This should be considered in those with signs of infection or those who do not improve with treatment. | 11
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It was later further studied by Henry Lynch who recognized an autosomal dominant transmission pattern with those affected having relatively early onset of cancer (mean age 44 years), greater occurrence of proximal lesions, mostly mucinous or poorly differentiated adenocarcinoma, greater number of synchronous and metachronous cancer cells, and good outcome after surgical intervention. The Amsterdam Criteria was initially used to define Lynch syndrome before the underlying genetic mechanism had been worked out. The Criteria required that the patient has three family members all first-degree relatives with colorectal cancer that involves at least two generations with at least one affected person being younger than 50 years of age when the diagnosis was made. The Amsterdam Criteria is too restrictive and was later expanded to include cancers of endometrial, ovarian, gastric, pancreatic, small intestinal, ureteral, and renal pelvic origin. The increased risk of cancer seen in patients with by the syndrome is associated with dysfunction of DNA repair mechanism. Molecular biologists have linked the syndrome to specific genes such as hMSH2, hMSH1, hMSH6, and hPMS2. Peutz–Jeghers syndrome
Peutz–Jeghers syndrome is an autosomal dominant syndrome that presents with hamartomatous polyps, which are disorganized growth of tissues of the intestinal tract, and hyperpigmentation of the interlining of the mouth, lips and fingers. The syndrome was first noted in 1896 by Hutchinson, and later separately described by Peutz, and then again in 1940 by Jeghers. | A colorectal polyp is a polyp (fleshy growth) occurring on the lining of the colon or rectum. Untreated colorectal polyps can develop into colorectal cancer.Colorectal polyps are often classified by their behaviour (i.e. benign vs. malignant) or cause (e.g. as a consequence of inflammatory bowel disease). They may be benign (e.g. hyperplastic polyp), pre-malignant (e.g. tubular adenoma) or malignant (e.g. colorectal adenocarcinoma). Signs and symptoms
Colorectal polyps are not usually associated with symptoms. When they occur, symptoms include bloody stools; changes in frequency or consistency of stools (such as a week or more of constipation or diarrhoea); and fatigue arising from blood loss. Anemia arising from iron deficiency can also present due to chronic blood loss, even in the absence of bloody stools. Another symptom may be an increased mucus production especially those involving villous adenomas. Copious production of mucous causes loss of potassium that can occasionally result in symptomatic hypokalemia. Occasionally, if a polyp is big enough to cause a bowel obstruction, there may be nausea, vomiting and severe constipation. Structure
Polyps are either pedunculated (attached to the intestinal wall by a stalk) or sessile (grow directly from the wall). : 1342 In addition to the gross appearance categorization, they are further divided by their histologic appearance as tubular adenoma which are tubular glands, villous adenoma which are long finger like projections on the surface, and tubulovillous adenoma which has features of both. | 11
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This is usually inserted in the posterior fossa, but a shunt in the lateral ventricles may be used instead or in conjunction. Endoscopic third ventriculostomy (ETV) is a less invasive option for patients older than 1 year. Posterior fossa shunts are most effective (80% of the time) but carry the highest risk of complications, while ETV is least effective but has the least risk of complications. The mortality rate is roughly 15%, mostly due to complications from hydrocephalus or its treatment, which can include subdural haematomas or infection. The prognosis after successful hydrocephalus treatment is usually good but depends on any associated condition and its symptoms. Those without hydrocephalus are treated based on any associated symptoms or condition.The prevalence of DWM is estimated at between 1 in 25,000 to 1 in 50,000. DWM is the cause of around 4.3% of cases of congenital hydrocephalus and 2.5% of all cases of hydrocephalus. At least 21% of those with DWM have a sibling with the malformation, and at least 16% have a parent with the malformation. The malformation was first described by English surgeon John Bland-Sutton in 1887, though it was named by German psychiatrist Clemens Ernst Benda in 1954 after American neurosurgeons Walter Dandy and Arthur Earl Walker, who described it in 1914 and 1942, respectively. Signs and symptoms
Hydrocephalus
The most frequent and prominent symptoms of DWM are those associated with hydrocephalus in the postnatal period. Hydrocephalus occurs in an estimated 80% of patients with classic DWM. | The melanocytic tumours in these cases are thought to relate to the same genetic errors in the development of the embryonic neural tube that lead to the DWM, since the subsequent embryonic neural crest gives rise to melanocytes, among other cells. 10% of patients had endocrine or metabolic disorders, and 2.7% had excessive hair growth (hypertrichosis). 9% of patients (almost all with classic DWM) had musculoskeletal abnormalities, which included scoliosis or kyphoscoliosis and arthrogryposis. 5.9% of patients had underdeveloped reproductive organs, such as hypoplastic genitalia or undescended testicles (cryptorchidism). 5.3% of patients had underdeveloped or polycystic kidneys.Occipital encephalocele may occur in DWM. This has generally been found at rates between 6 and 8%. It has been suggested to occur to compensate for the increased pressure in the posterior fossa during foetal life.Syringomyelia occasionally occurs with DWM, though it is not certain how often. One review reported an occurrence of 4.3% in a sample. This may be due to herniation of the bottom of the cyst through the foramen magnum (a similar mechanism to Chiari malformation). Alternatively, it may be a result of hydrocephalus, in which it forms as a "fifth ventricle" due to an enlarged central canal.Rarely, spina bifida has been found with DWM. When it is present, it is usually spina bifida occulta. Cause
DWM is caused by any disruption to embryonic development that affects the formation of the cerebellar vermis. This is usually a genetic mutation that results in impaired cell migration and division. A large number of genetic conditions can result in the anomaly. | 11
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Some degree of non-cyclical breast tenderness can normally be present due to hormonal changes in puberty (both in girls and boys), in menopause and during pregnancy. After pregnancy, breast pain can be caused by breastfeeding. Other causes of non-cyclical breast pain include alcoholism with liver damage (likely due to abnormal steroid metabolism), mastitis and medications such as digitalis, methyldopa (an antihypertensive), spironolactone, certain diuretics, oxymetholone (an anabolic steroid), and chlorpromazine (a typical antipsychotic). Also, shingles can cause a painful blistering rash on the skin of the breasts. Breast cancer
Some women who have pain in one or both breasts may fear breast cancer. However, breast pain is not a common symptom of cancer. The great majority of breast cancer cases do not present with symptoms of pain, though breast pain in older women is more likely to be associated with cancer. Diagnosis
Diagnosis involves breast examination, with medical imaging if only a specific part of the breast hurts. Medical imaging by ultrasound is recommended for all ages, well in those over 30 it is recommended together with mammography.Ruling out the other possible causes of the pain is one way to differentiate the source of the pain. Breast pain can be due to:
Medications can be associated with breast pain and include:
Diagnostic testing can be useful. Typical tests used are mammogram, excisional biopsy for solid lumps, fine-needle aspiration and biopsy, pregnancy test, ultrasonography, and magnetic resonance imaging (MRI). Treatment
In more than 75% of people the pain resolves without any specific treatment. Otherwise treatments may include paracetamol or NSAIDs. | A well fitting bra may also help. In those with severe pain tamoxifen or danazol may be used.Bromocriptine may be used as well.Spironolactone, low dose oral contraceptives, and low-dose estrogen have helped to relieve pain. Topical anti-inflammatory medications can be used for localized pain. Vitamin E is not effective in relieving pain nor is evening primrose oil. Vitamin B6 and vitamin A have not been consistently found to be beneficial. Flaxseed has shown some activity in the treatment of cyclic mastalgia.Pain may be relieved by the use of nonsteroidal anti-inflammatory drugs or, for more severe localized pain, by local anaesthetic. Pain may be relieved by reassurance that it does not signal a serious underlying problem, and an active life style can also effect an improvement.Information regarding how the pain is real but not necessarily caused by disease can help to understand the problem. Counseling can also be to describe changes that vary during the monthly cycle. Women on hormone replacement therapy may benefit from a dose adjustment. Another non-pharmacological measure to help relieve symptoms of pain may be to use good bra support. Breasts change during adolescence and menopause and refitting may be beneficial. Applying heat and/or ice can bring relief. Dietary changes may also help with the pain. Methylxanthines can be eliminated from the diet to see if a sensitivity is present. Some clinicians recommending a reduction in salt, though no evidence supports this practice. See also
Galactagogue
Mammoplasia
Pain management
References
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In the 19th and 20th centuries, some medical experts devised new nomenclature in an attempt to classify the characteristics that they had observed, the first attempt to create a taxonomic classification system of intersex conditions. Intersex people were categorized as either having "true hermaphroditism", "female pseudohermaphroditism", or "male pseudohermaphroditism". These terms are no longer used, and terms including the word "hermaphrodite" are considered to be misleading, stigmatizing, and scientifically specious in reference to humans. In biology, the term "hermaphrodite" is used to describe an organism that can produce both male and female gametes. Some people with intersex traits use the term "intersex", and some prefer other language. In clinical settings, the term "disorders of sex development" (DSD) has been used since 2006, a shift in language considered controversial since its introduction. Intersex people face stigmatization and discrimination from birth, or following the discovery of intersex traits at stages of development such as puberty. Intersex people may face infanticide, abandonment, and stigmatization from their families. Globally, some intersex infants and children, such as those with ambiguous outer genitalia, are surgically or hormonally altered to create more socially acceptable sex characteristics. However, this is considered controversial, with no firm evidence of favorable outcomes. Such treatments may involve sterilization. Adults, including elite female athletes, have also been subjects of such treatment. Increasingly, these issues are considered human rights abuses, with statements from international and national human rights and ethics institutions (see intersex human rights). | Hangmans fracture is the colloquial name given to a fracture of both pedicles, or partes interarticulares, of the axis vertebra (C2). Causes
The injury mainly occurs from falls, usually in elderly adults, and motor accidents mainly due to impacts of high force causing extension of the neck and great axial load onto the C2 vertebra. In a study based in Norway, 60% of reported cervical fractures came from falls and 21% from motor-related accidents. According to the Agency for Healthcare Research and Quality (AHRQ), the group under the highest risk of C2 fractures are elderly people within the age group of 65-84 (39.02%) at risks of falls (61%) or motor accidents (21%) in metropolitan areas (94%). There were 203 discharges from the age group 1-17; 1,843 from 18- to 44-year-olds; 2,147 from 45- to 64-year-olds, 4,890 from 65- to 84-year-olds, and 3440 from 85+-year-olds. Females accounted for 54.45% of occurrences while males accounted for the other 45.38%. Mechanisms
The mechanism of the injury is forcible hyperextension of the head, usually with distraction of the neck. Traditionally this would occur during judicial hanging, when the noose was placed below the condemned subjects chin. When the subject was dropped, the head would be forced into hyperextension by the full weight of the body, a sufficient force to cause the fracture. | 0-1
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Diagnosis
The diagnosis of pruritic folliculitis of pregnancy is established based on clinical features such as redness of the skin consisting of small red bumps that surrounds a hair follicle and histopathologic features such as immune cells within the pus along with microscopic testing that shows there is no bacteria, microorganism, or other conditions that could cause itchy skin. Diagnosis for pruritic folliculitis of pregnancy requires patients to go through a biopsy, which consists of taking samples from the tissue to evaluate whether their lesions match the physical factors of pruritic folliculitis. Other pregnancy associated skin diseases must be ruled out along side obstetric cholestasis, which is a disorder that affects the liver during pregnancy.There is a great deal of overlap between the following conditions in pregnancy: eczema, prurigo, and pruritic folliculitis. Because of this, they are grouped in a class called atopic eruption of pregnancy. Compared to other pregnancy associated skin conditions, conditions in the class of atopic eruption of pregnancy occurs much earlier. Management/Treatment
There is currently no official treatment guidelines for pruritic folliculitis of pregnancy as its etiology and clinical presentations still require further investigation; however, the goal of treatment is to relieve symptoms without causing harm to the mother or fetus. Non-pharmacological intervention is recommended first before using pharmacological agents to treat symptoms. Since pruritic folliculitis of pregnancy appears in later stages of pregnancy and self-resolves post-partum, non-pharmacological interventions are recommended first to relieve itching symptoms. | A plantar wart, or verruca, is a wart occurring on the bottom of the foot or toes. Its color is typically similar to that of the skin. Small black dots often occur on the surface. One or more may occur in an area. They may result in pain with pressure such that walking is difficult.They are caused by the human papillomavirus (HPV). A break in the skin is required for infection to occur. Risk factors include use of communal showers, having had prior warts, and poor immune function. Diagnosis is typically based on symptoms.Treatment is only needed if it is causing symptoms. This may include salicylic acid, cryotherapy, chemo-based fluorouracil or bleomycin, and surgical removal. The skin atop the lesion should generally be removed before treatment. In about a third to two-thirds of cases, they go away without specific treatment, but this may take a few years. Plantar warts are common. Children and young adults are most often affected. Signs and symptoms
Their colors are typically similar to that of the nearby skin. Small, black dots may occur on their surfaces. One or more may occur in an area. They may result in pain with pressure such that walking may be difficult. Cause
Plantar warts are benign epithelial tumors generally caused by infection by human papillomavirus types 1, 2, 4, 60, or 63, but have also been caused by types 57, 65, 66, and 156. These types are classified as clinical (visible symptoms). | 0-1
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Other
Three other treatment modalities also aim at improving LEMS symptoms, namely pyridostigmine, 3,4-diaminopyridine (amifampridine), and guanidine. They work to improve neuromuscular transmission. Tentative evidence supports 3,4-diaminopyridine] at least for a few weeks. The 3,4-diaminopyridine base or the water-soluble 3,4-diaminopyridine phosphate may be used. Both 3,4-diaminopyridine formulations delay the repolarization of nerve terminals after a discharge, thereby allowing more calcium to accumulate in the nerve terminal.Pyridostigmine decreases the degradation of acetylcholine after release into the synaptic cleft, and thereby improves muscle contraction. An older agent, guanidine, causes many side effects and is not recommended. 4-Aminopyridine (dalfampridine), an agent related to 3,4-aminopyridine, causes more side effects than 3,4-DAP and is also not recommended. History
Anderson and colleagues from St Thomas Hospital, London, were the first to mention a case with possible clinical findings of LEMS in 1953, but Edward H. Lambert, Lee Eaton, and E.D. Rooke at the Mayo Clinic were the first physicians to substantially describe the clinical and electrophysiological findings of the disease in 1956. In 1972, the clustering of LEMS with other autoimmune diseases led to the hypothesis that it was caused by autoimmunity. Studies in the 1980s confirmed the autoimmune nature, and research in the 1990s demonstrated the link with antibodies against P/Q-type voltage-gated calcium channels. References
== External links == | Binge eating habits are often associated with changes in food preferences (cravings for more sweets, carbohydrates), eating inedible objects and snatching food from others. Recent findings from structural MRI research have indicated that eating changes in FTD are associated with atrophy (wasting) in the right ventral insula, striatum, and orbitofrontal cortex.People with FTD show marked deficiencies in executive functioning and working memory. Most become unable to perform skills that require complex planning or sequencing. In addition to the characteristic cognitive dysfunction, a number of primitive reflexes known as frontal release signs are often able to be elicited. Usually the first of these frontal release signs to appear is the palmomental reflex which appears relatively early in the disease course whereas the palmar grasp reflex and rooting reflex appear late in the disease course.In rare cases, FTD can occur in people with amyotrophic lateral sclerosis (ALS) a motor neuron disease. The prognosis for people with ALS is worse when combined with FTD, shortening survival by about a year. Genetics
A higher proportion of frontotemporal dementias seem to have a familial component than other neurodegenerative diseases such as Alzheimers disease. More and more mutations and genetic variants are being identified all the time, needing constant updating of genetic influences. Tau-positive frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is caused by mutations in the MAPT gene on chromosome 17 that encodes the tau protein. It has been determined that there is a direct relationship between the type of tau mutation and the neuropathology of gene mutations. | 0-1
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Ingestion of cat feces containing oocysts: This can occur through hand-to-mouth contact following gardening, cleaning a cats litter box, contact with childrens sandpits; the parasite can survive in the environment for months. Ingestion of untreated, unfiltered water through direct consumption or utilization of water for food preparation. Ingestion of unpasteurized milk and milk products, particularly goats milk. Ingestion of raw seafood.Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected intermediate host that could include mammals (like rodents) or birds. Oocyst shedding usually starts from the third day after ingestion of infected intermediate hosts, and may continue for weeks. The oocysts are not infective when excreted. After about a day, the oocyst undergoes a process called sporulation and becomes potentially pathogenic. In addition to cats, birds and mammals including human beings are also intermediate hosts of the parasite and are involved in the transmission process. However the pathogenicity varies with the age and species involved in infection and the mode of transmission of T. gondii.Toxoplasmosis may also be transmitted through solid organ transplants. Toxoplasma-seronegative recipients who receive organs from recently infected Toxoplasma-seropositive donors are at risk. Organ recipients who have latent toxoplasmosis are at risk of the disease reactivating in their system due to the immunosuppression occurring during solid organ transplant. | Recipients of hematogenous stem cell transplants may experience higher risk of infection due to longer periods of immunosuppression.Heart and lung transplants provide the highest risk for toxoplasmosis infection due to the striated muscle making up the heart, which can contain cysts, and risks for other organs and tissues vary widely. Risk of transmission can be reduced by screening donors and recipients prior to the transplant procedure and providing treatment. Pregnancy precautions
Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the placenta. Congenital toxoplasmosis is associated with fetal death and miscarriage, and in infants, it is associated with hydrocephalus, cerebral calcifications and chorioretinitis, leading to encephalopathy and possibly blindness. A positive antibody titer indicates previous exposure and immunity, and largely ensures the unborn fetus safety. A simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to T. gondii while pregnant, the fetus is at particular risk.Not much evidence exists around the effect of education before pregnancy to prevent congenital toxoplasmosis. However educating parents before the baby is born has been suggested to be effective because it may improve food, personal and pet hygiene. | 11
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However, a 2002 study has supported the protocol of precautionary administration of PEP where a child or mentally compromised individual has been alone with a bat, especially in sleep areas, where a bite or exposure may occur with the victim being unaware. After onset
At least two treatment schemes have been proposed for treating rabies after the onset of symptoms, the Milwaukee Protocol and the Recife Protocol. The Milwaukee Protocol was first used in 2004 on Jeanna Giese, who became the first person known to have survived rabies without preventive treatments before symptom onset. The protocol puts a person into a chemically induced coma and uses antiviral medications to prevent fatal dysautonomia. The overall protocol is complex; the sixth version of the protocol last updated in 2018 consists of 17 pages with 22 steps of treatment, detailed monitoring, and a timeline of expected complications. The Recife Protocol follows the same principle but differs in details like termination of sedation and supplementary medication. Prognosis
Vaccination after exposure, PEP, is highly successful in preventing rabies. In unvaccinated humans, rabies is virtually always fatal after neurological symptoms have developed. Epidemiology
In 2010, an estimated 26,000 people died from rabies, down from 54,000 in 1990. The majority of the deaths occurred in Asia and Africa. As of 2015, India, followed by China (approximately 6,000) and the Democratic Republic of the Congo (5,600), had the most cases. | Angel-shaped phalango-epiphyseal dysplasia, also known as peripheral dysostosis, is a rare type of osteochondrodysplasia which is characterized by angel-shaped middle phalanges of the fingers and generalized metaphyseal dysplasia/delayed osseous age. Additional findings include joint hypermobility, hypodontia, and hip osteoarthritis. According to OMIM, 10 cases from multiple families have been described in medical literature. It is thought to be inherited in an autosomal dominant manner. According to ORPHA, 20 cases have been reported. Presentation
The middle phalanges (often those of the 2nd, 3rd and 5th digits of the hands) angel shape is caused by an abnormal development of the epiphysis, metaphysis, and diaphysis of said phalanges; the wings are formed by an abnormal dyaphysis, the angels skirt is from a cone-shaped epiphysis, and the head is formed by an abnormal distal pseudoepophysis. Genetics
This disorder is thought to be caused by autosomal dominant mutations in the GDF5 gene, in chromosome 20. History
This condition was first discovered in 1967, by Bachman et al. when he described a "hereditary peripheral dysostosis" on one woman and 2 of her children. Eponym
This disorders name comes from the fact that Bachman et al. (the researchers who originally described the disorder) and Giedion et al. missed a characteristic feature that the people diagnosed with the disorder shared: a middle phalange that had a striking resemblance to the shape of decorative angels of small size that are often put in Christmas trees. == References == | 0-1
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Therefore, cancer cells which divide much more rapidly than most other cells in the body will be more severely affected by decitabine just because they replicate more. In cancer cells, and more specifically in haematological malignancies, it seems that DNA hypermethylation is really critical for their development. Methylation of CpG islands upstream of tumor suppressor genes in order to silence them seems to be critical for these type of cancers. Thus at optimal doses, decitabine blocks this type of methylation and has an anti-neoplastic effect. Research
Atherosclerosis
A number of investigators have shown a relationship between atherosclerosis and disturbed blood flow. This upregulates DNA methyltransferase expression, which leads to genome-wide DNA methylation alterations and global gene expression changes. These studies have revealed several mechanosensitive genes, such as HoxA5, Klf3, and Klf4, whose promoters were hypermethylated by disturbed blood flow, but rescued by DNA methyltransferases inhibitors such as 5-aza-2-deoxycytidine. It has been found that use of this DNA methyltranferase inhibitor prevents atherosclerosis lesion formation and reduces the production of inflammatory cytokines by macrophages. References
Further reading
Moon C, Kim SH (June 2009). "Use of epigenetic modification to induce FOXP3 expression in naïve T cells". Transplant. Proc. 41 (5): 1848–1854. doi:10.1016/j.transproceed.2009.02.101. PMID 19545742. External links
"Decitabine". Drug Information Portal. U.S. National Library of Medicine. | HIV elimination
Graft-versus-host disease has been implicated in eliminating several cases of HIV, including The Berlin Patient and 6 others in Spain. See also
Graft-versus-tumor effect
Immunosuppression
Transplant rejection
References
Further reading
Ferrara JLM, Deeg HJ, Burakoff SJ. Graft-Vs.-Host Disease: Immunology, Pathophysiology, and Treatment. Marcel Dekker, 1990 ISBN 0-8247-9728-0
Polsdorfer, JR Gale Encyclopedia of Medicine: Graft-vs.-host disease
== External links == | 0-1
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In a 2000 Canadian survey of 130 patients, the majority reported better satisfaction, quality of life, compliance with treatment, thinking, mood, and alertness.Compared to other antipsychotics, clozapine has an increased risk of blood dyscrasias, in particular agranulocytosis, in the first 18 weeks of treatment. After one year, this risk reduces to that associated with most antipsychotics. Clozapines use is therefore reserved for people who have not responded to two other antipsychotics and is only done with stringent blood monitoring. Overall, despite the concerns relating to blood and other side effects, clozapine use is associated with a reduced mortality, especially from suicide which is a major cause of premature death in people with schizophrenia. The risk of clozapine related agranulocytosis and neutropenia warranted the mandatory use of stringent risk monitoring and management systems, which have reduced the risk of death from these adverse events to around 1 in 7,700. The association between clozapine use and specific bloods dyscrasias was first noted in the 1970s when eight deaths from agranulocytosis were noted in Finland. At the time it was not clear if this exceeded the established rate of this side effect which is also found in other antipsychotics and although the drug was not completely withdrawn, its use became limited. Clozapine became widely available in the early 1990s and remains the only treatment likely to be effective in treating resistant schizophrenia. Common adverse effects include drowsiness, constipation, hypersalivation (increased saliva production), tachycardia, low blood pressure, blurred vision, weight gain, and dizziness. | A large meta-analysis of clozapine exposure to over 250,000 people revealed that these occurred in approximately 7 in 1000 patients treated and resulted in death in 3 and 4 in 10,000 patients exposed respectively and although myocarditis occurred almost exclusively within the first 8 weeks of treatment, cardiomyopathy can occur much later on. First manifestations of illness are fever which may be accompanied by symptoms associated with upper respiratory tract, gastrointestinal or urinary tract infection. Typically C-reactive protein (CRP) increases with the onset of fever and rises in the cardiac enzyme, troponin, occur up to 5 days later. Monitoring guidelines advise checking CRP and troponin at baseline and weekly for the first 4 weeks after clozapine initiation and observing the patient for signs and symptoms of illness. Signs of heart failure are less common and may develop with the rise in troponin. A recent case-control study found that the risk of clozapine-induced myocarditis is increased with increasing rate of clozapine dose titration, increasing age and concomitant sodium valproate. A large electronic health register study has revealed that nearly 90% of cases of suspected clozapine related myocarditis are false positives. Rechallenge after clozapine induced myocarditis has been performed and a protocol for this specialist approach has been published. A systematic review of rechallenge after myocarditis has show success in over 60% of reported cases. Gastrointestinal hypomotility
Another underrecognized and potentially life-threatening effect spectrum is gastrointestinal hypomotility, which may manifest as severe constipation, fecal impaction, paralytic ileus, bowel obstruction, acute megacolon, ischemia or necrosis. | 11
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But, certainly, violence is more than killing people, unless one includes all those words and actions that kill people slowly. The effect of limitation to a "killing fields" perspective is the widespread neglect of many other forms of violence. We must insist that violence also refers to that which is psychologically destructive, that which demeans, damages, or depersonalizes others. In view of these considerations, violence may be defined as follows: any action, verbal or nonverbal, oral or written, physical or psychical, active or passive, public or private, individual or institutional/societal, human or divine, in whatever degree of intensity, that abuses, violates, injures, or kills. Some of the most pervasive and most dangerous forms of violence are those that are often hidden from view (against women and children, especially); just beneath the surface in many of our homes, churches, and communities is abuse enough to freeze the
blood. Moreover, many forms of systemic violence often slip past our attention because they are so much a part of the infrastructure of life (e.g., racism, sexism, ageism). See also
Aestheticization of violence
Aggression
Communal violence
Corporal punishment
Domestic violence
Fight-or-flight response
Hunting
Legislative violence
Martial arts
Parasitism
Predation
Religious violence
Resentment
Sectarian violence
War
Notes
References
Sources
Barzilai, Gad (2003). Communities and Law: Politics and Cultures of Legal Identities. Ann Arbor: University of Michigan Press. ISBN 0472113151. Benjamin, Walter, Critique of Violence
Flannery, D.J., Vazsonyi, A.T. & Waldman, I.D. (Eds.) (2007). The Cambridge handbook of violent behavior and aggression. Cambridge University Press. ISBN 052160785X. James, Paul; Sharma, RR (2006). Globalization and Violence, Vol. 4: Transnational Conflict. London: Sage Publications. Malešević, Siniša The Sociology of War and Violence. | Mary Thompson, a vertebrate paleontologist at Idaho Museum of Natural History, has found evidence in many species of early horses and concludes, "The results of this study strongly suggest that man’s intervention (whether by increased usage or improper breeding practices) may not be the sole cause of the syndrome", although she cautions that her results are preliminary. Work
Working on steep hills, galloping, and jumping all contribute to navicular syndrome, as they place greater stress on the DDF tendons, and may cause overextension of the pastern and coffin joints. Regular exercise on hard or irregular ground increases concussion on the hoof, thus increasing the risk of navicular syndrome. It is possible that standing can also increase the chance of navicular disease (such as a horse that spends most of the day in a stall with little turnout, as with some racehorses and show horses). Blood flow to the hoof decreases when the horse is not in motion. The horse is also constantly applying pressure to the navicular bones (which is intermittent as the horse moves). Body weight
Horses with a high weight-to-foot-size ratio may have an increased chance of exhibiting symptoms of navicular syndrome, since the relative load on the foot increases. This might explain why the syndrome is seen more frequently in Thoroughbreds, American Quarter Horses, and Warmbloods as opposed to ponies and Arabians. Signs
Heel pain is very common in horses with navicular syndrome. Lameness may begin as mild and intermittent, and progress to severe. | 0-1
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In cases where ICH already has occurred, aspirin use results in higher mortality, with a dose of about 250 mg per day resulting in a relative risk of death within three months after the ICH around 2.5 (95% confidence interval 1.3 to 4.6).Aspirin and other NSAIDs can cause abnormally high blood levels of potassium by inducing a hyporeninemic hypoaldosteronic state via inhibition of prostaglandin synthesis; however, these agents do not typically cause hyperkalemia by themselves in the setting of normal renal function and euvolemic state.Use of low-dose aspirin before a surgical procedure has been associated with an increased risk of bleeding events in some patients, however, ceasing aspirin prior to surgery has also been associated with an increase in major adverse cardiac events. An analysis of multiple studies found a three-fold increase in adverse events such as myocardial infarction in patients who ceased aspirin prior to surgery. The analysis found that the risk is dependent on the type of surgery being performed and the patient indication for aspirin use.On 9 July 2015, the US Food and Drug Administration (FDA) toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAID). Aspirin is an NSAID but is not affected by the new warnings. Overdose
Aspirin overdose can be acute or chronic. In acute poisoning, a single large dose is taken; in chronic poisoning, higher than normal doses are taken over a period of time. Acute overdose has a mortality rate of 2%. | Kinneret is the Hebrew name of the Sea of Galilee, the largest freshwater lake in Israel. Other meanings of Kinneret and Kineret include:
Places
Camp Kinneret, a summer camp of Canadian Young Judaea
Kinneret (archaeological site), biblical city which gave the Sea of Galilee its Hebrew name; now Tell el-Oreimeh or Tel Kinrot on the northwestern coast of the lake
Kinneret College, college south of the Sea of Galilee
Kinneret Farm, experimental training farm (1908-1949), now museum
Kinneret Subdistrict, Israel
Kvutzat Kinneret, kibbutz southwest of the Sea of Galilee
Moshavat Kinneret, village (moshava) southwest of the Sea of Galilee
People
Kineret (singer), an Orthodox Jewish recording artist
Kinneret Shiryon (born 1955), Reform rabbi, the first female rabbi in Israel
Other
Kineret (medication), brand name of anakinra; no direct relation to the lake
Kinneret, Israeli song based on Rachel Bluwsteins poem "Perhaps" ("VeUlai")
Kinneret bream or Kinneret bleak, Acanthobrama terraesanctae, fish endemic to the Sea of Galilee and a second lake in Syria
Kinneret Zmora-Bitan Dvir, publishing company, Israel
Operation Kinneret, another name of the Israeli military Operation Olive Leaves
See also
All pages with titles containing Kinneret
All pages with titles containing Kineret | 0-1
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recommending that the patient be fit with custom orthotics if they are overprone). Fortunately, subluxed cuboids are generally quite treatable and most patients return to a normal level of activity once the pain is brought under control. See also
Arthritis
Physiatry
Rheumatology
Tarsal tunnel syndrome
== References == | It was soon discovered that some lots of Salk polio vaccine made by Cutter and Wyeth had not been properly inactivated, allowing live poliovirus into more than 100,000 doses of vaccine. In May 1955, the National Institutes of Health and Public Health Services established a Technical Committee on Poliomyelitis Vaccine to test and review all polio vaccine lots and advise the Public Health Service as to which lots should be released for public use. These incidents reduced public confidence in polio vaccine, leading to a drop in vaccination rates. 1961
At the same time that Salk was testing his vaccine, both Albert Sabin and Hilary Koprowski continued working on developing a vaccine using live virus. During a meeting in Stockholm to discuss polio vaccines in November 1955, Sabin presented results obtained on a group of 80 volunteers, while Koprowski read a paper detailing the findings of a trial enrolling 150 people. Sabin and Koprowski both eventually succeeded in developing vaccines. Because of the commitment to the Salk vaccine in America, Sabin and Koprowski both did their testing outside the United States, Sabin in Mexico and the Soviet Union, Koprowski in the Congo and Poland. In 1957, Sabin developed a trivalent vaccine containing attenuated strains of all three types of poliovirus. In 1959, ten million children in the Soviet Union received the Sabin oral vaccine. For this work, Sabin was given the medal of the Order of Friendship of Peoples, described as the Soviet Unions highest civilian honor. | 0-1
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The treatment for this may be to increase signage, post an advisory speed limit, apply a high-friction road surface, add crash barriers or any one of a number of other visible interventions. The immediate result may be to reduce collisions at the bend, but the subconscious relaxation on leaving the "dangerous" bend may cause drivers to act with fractionally less care on the rest of the road, resulting in an increase in collisions elsewhere on the road, and no overall improvement over the area. In the same way, increasing familiarity with the treated area will often result in a reduction over time to the previous level of care and may result in faster speeds around the bend due to perceived increased safety (risk compensation). Epidemiology
In 2004 50 million more were injured in motor vehicle collisions. In 2013, between 1.25 million and 1.4 million people were killed in traffic collisions, up from 1.1 million deaths in 1990. That number represents about 2.5% of all deaths. Approximately 50 million additional people were injured in traffic collisions, a number unchanged from 2004.India recorded 105,000 traffic deaths in a year, followed by China with over 96,000 deaths. This makes motor vehicle collisions the leading cause of injury and death among children worldwide 10–19 years old (260,000 children die a year, 10 million are injured) and the sixth leading preventable cause of death in the United States. In 2019, there were 36,096 people killed and 2.74 million people injured in motor vehicle traffic crashes on roadways in the United States. | The blood-brain barrier breakdown results in vasogenic edema, which promotes the development of RPON. Neuropeptides-induced
Alternatively, it is proposed that migraine-related release of neuropeptides from trigeminal nerve fibers terminating on the circle of Willis might be the cause. Some of the neuropeptides released are potentially toxic, and may induce blood-brain barrier breakdown that accounts for ophthalmoplegia. Neuropathic mechanism
Additional models have been proposed to explain the cause of RPON. The thickened and enhanced symptomatic nerve, as shown in recent MRI findings, might be indicative of the existence of structural nerve damage in RPON. Therefore, neuropathy is suggested as the primary cause of RPON, either induced by recurrent viral infections or immune-mediated inflammation. However, cerebrospinal fluid (CSF) analyses are normal in the vast majority of RPON cases, which is inconsistent with the findings of autoimmune or inflammatory-mediated pathomechanism. Nevertheless, several neuropathic mechanisms have been proposed. Benign viral infection
The enhancement and thickening of the oculomotor nerve can occur in a variety of infectious inflammatory conditions. However, spontaneous resolution is unlikely to occur in viral infection, except for benign viral infection that usually causes mild or no symptoms in humans. Therefore, benign viral infection could be an explanation for the development of RPON. Immune-mediated inflammation
Recent MRI findings have led to the current understanding of RPON as an inflammation-induced neuropathy. Recurrent demyelinating neuropathy is proposed as a pathophysiological pathway because similar MRI findings have been observed in both RPON and chronic inflammatory demyelinating neuropathy. | 0-1
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Treatment
Treatment is a relatively simple surgery in which excess skin of the outer lids is removed or tendons and muscles are shortened with one or two stitches. General anesthesia is sometimes used before local anesthetics are injected into the muscles around the eye. Prognosis is excellent if surgery is performed before the cornea is damaged. Entropion in other species
Entropion has been documented in most dog breeds, although there are some breeds (particularly purebreds) that are more commonly affected than others. These include the Akita, Pug, Chow Chow, Shar Pei, St. Bernard, Cocker Spaniel, Boxer, English Springer Spaniel, Welsh Springer Spaniel, Labrador Retriever, Cavalier King Charles Spaniel, Neapolitan Mastiff, Bull Mastiff, Great Dane, Irish Setter, Shiba Inu, Rottweiler, Poodle and particularly Bloodhound. The condition is usually present by six months of age. If left untreated, the condition can cause such trauma to the eye that it will require removal. Entropion has also been seen in cat breeds. Typically it is secondary to trauma or infection leading to chronic eyelid changes. It is also seen secondary to enophthalmos. Primary entropion might also be encountered : the brachycephalic breeds (mostly the Persian) and the Maine Coon are predisposed.Upper-lid entropion involves the eyelashes rubbing on the eye, but the lower lid usually has no eyelashes, so little or no hair rubs on the eye. Surgical correction is used in more severe cases. A number of techniques for surgical correction exist. | The Hotz-Celsus technique involves the removal of strip of skin and orbicularis oculi muscle parallel to the affected portion of the lid and then the skin is sutured. Alternative techniques such as the Wyman technique focus on tightening the lower eyelid. This technique is not as effective in cases of enophthalmos.Shar Peis, who often are affected as young as two or three weeks old, respond well to temporary eyelid tacking. The entropion is often corrected after three to four weeks, and the sutures are removed. See also
Ectropion
References
External links
HumansMedline Plus - Entropion | 11
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The Predecisional Draft document generated by the workgroup in 1998 recommended additional research in the basic epidemiology of MCS, the performance of case-comparison and challenge studies, and the development of a case definition for MCS. However, the workgroup also concluded that it was unlikely that MCS would receive extensive financial resources from federal agencies because of budgetary constraints and the allocation of funds to other, extensively overlapping syndromes with unknown cause, such as chronic fatigue syndrome, fibromyalgia, and Gulf War syndrome. The Environmental Health Policy Committee is currently inactive, and the workgroup document has not been finalized.The different understandings of MCS over the years have also resulted in different proposals for names. For example, in 1996 the International Programme on Chemical Safety proposed calling it idiopathic environmental illness, because of their belief that chemical exposure may not the sole cause, while another researcher, whose definition includes people with allergies and acute poisoning, calls it chemical sensitivity. See also
Electromagnetic hypersensitivity
Sick building syndrome
Sensory processing disorder
Sensory processing sensitivity
List of questionable diseases
Environmental health
Environmental medicine
Indoor air quality
Sense of smell#Disorders
References
External links
Multiple Chemical Sensitivity Syndrome at the Merck Manual Professional Edition | The FDA said its approval of Zarxio is based on review of evidence that included structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamics data, clinical immunogenicity data and other clinical safety and effectiveness data that demonstrates Zarxio is biosimilar to Neupogen.In 2018, filgrastim-aafi (trade name Nivestym) was approved for use in the United States.In September 2008, Ratiograstim, Tevagrastim, Biograstim, and Filgrastim ratiopharm were approved for use in the European Union. Filgrastim ratiopharm was withdrawn in July 2011 and Biograstim was withdrawn in December 2016. In February 2009, Filgrastim Hexal and Zarzio were approved for use in the European Union.In June 2010, Nivestim was approved for use in the European Union.In October 2013, Grastofil was approved for use in the European Union.In September 2014, Accofil was approved for use in the European Union.In 2016, Fraven was approved for use by Republic of Turkey ministry of health.Nivestym was approved for medical use in Canada in April 2020.In October 2021, Nypozi was approved for medical use in Canada. Economics
Shortly after it was introduced, analyses of whether filgrastim is a cost-effective way of preventing febrile neutropenia depended upon the clinical situation and the financial model used to pay for treatment. The longer-acting pegfilgrastim may in some cases be more cost-effective. The introduction of biosimilars into the market resulted in a price reduction for the original, patent-protected product and increased use. References
Further reading
Santoso B, van Boxtel CJ, Edwards RI, eds. (2001). Drug benefits and risks: international textbook of clinical pharmacology. New York: Wiley. ISBN 0-471-89927-5. External links
"Filgrastim". | 0-1
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Anesthetic strategies to prevent vomiting include using regional anesthesia whenever possible and avoiding medications that cause vomiting. Medications to treat and prevent PONV are limited by both cost and the adverse effects. People with risk factors likely warrant preventive medication, whereas a "wait and see" strategy is appropriate for those without risk factors. Preoperative fasting
Fasting guidelines often restrict the intake of any oral fluid 2-6 hours preoperatively, but in a large retrospective analysis in Torbay Hospital, unrestricted clear oral fluids until transfer to theatre could significantly reduce the incidence of postoperative nausea and vomiting without an increased risk in the adverse outcomes for which such conservative guidance exists. Medications
A multimodal approach to treating a patient with PONV can be efficacious. Numerous patient factors and medication adverse effects must be taken into consideration when selecting a treatment regimen. Serotonin (5-HT3) receptor antagonists can be administered as a single dose at the end of surgery. Adverse effects include prolongation of the QT interval on electrocardiogram (EKG). Medications include ondansetron, granisetron, and dolasetron. Anticholinergics can be used as a long-acting patch placed behind the patients ear. Adverse effects include dry mouth and blurry vision. Care must be taken when handling the patch, as transfer of medication to the eye can induce pupillary dilation. Avoid use in elderly patients. Medications include scopolamine. Glucocorticoids have direct antiemetic effects and can reduce need for postoperative opioids. Adverse effects include a transient increase in serum glucose level, and poor wound healing (controversial). Medications include dexamethasone. | Genitopatellar syndrome is a rare disorder consisting of congenital flexion contractures of the lower extremities, abnormal or missing patellae, and urogenital anomalies. Additional symptoms include microcephaly, severe psychomotor disability. In 2012, it was shown that mutations in the gene KAT6B cause the syndrome. Genitopatellar syndrome (GTPTS) can be caused by heterozygous mutation in the KAT6B gene on chromosome 10q22. The Say-Barber-Biesecker variant of Ohdo syndrome, which has many overlapping features with GTPTS, can also be caused by heterozygous mutation in the KAT6B gene. Signs and symptoms
Genitopatellar syndrome is characterized by genital abnormalities, missing or underdeveloped kneecaps (patellae), intellectual disability and abnormalities affecting other parts of the body. It is also associated with delayed development and intellectual disability, which are often severe. Affected individuals may have an unusually small head (microcephaly) and structural brain abnormalities, including agenesis of the corpus callosum.Major features include:
Patellar hypoplasia/agenesis
Flexion contractures at the hips and knees
Agenesis of the corpus callosum with microcephaly
Hydronephrosis and/or multiple kidney cysts
Atrial septal defect
Intestinal malrotation
Talipes equinovarus (including club feet)
Feeding difficultiesOther features may include:
Dental anomalies (delayed eruption of teeth)
Hearing loss
Thyroid anomalies
Anal anomalies
Hypotonia
Global developmental delay/intellectual disability
Cause
Genitopatellar syndrome is inherited in an autosomal dominant fashion. The mutation responsible for the syndrome occurs in the KAT6B gene. This gene is located on the long arm of chromosome 10 (10q22.2).The KAT6B gene gene product is an enzyme called histone acetyltransferase which functions in regulating and making of histone which are proteins that attach to DNA and give the chromosomes their shape. | 0-1
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The menopausal transition or perimenopause leading up to menopause usually lasts 3–4 years (sometimes as long as 5–14 years).In rare cases, a womans ovaries stop working at a very early age, ranging anywhere from the age of puberty to age 40. This is known as premature ovarian failure and affects 1 to 2% of women by age 40.Undiagnosed and untreated coeliac disease is a risk factor for early menopause. Coeliac disease can present with several non-gastrointestinal symptoms, in the absence of gastrointestinal symptoms, and most cases escape timely recognition and go undiagnosed, leading to a risk of long-term complications. A strict gluten-free diet reduces the risk. Women with early diagnosis and treatment of coeliac disease present a normal duration of fertile life span.Women who have undergone hysterectomy with ovary conservation go through menopause on average 1.5 years earlier than the expected age. Other factors that can promote an earlier onset of menopause (usually 1 to 3 years early) are smoking cigarettes. Premature ovarian insufficiency
Premature ovarian insufficiency (POI) is when the ovaries stop functioning before the age of 40 years. It is diagnosed or confirmed by high blood levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) on at least three occasions at least four weeks apart.Premature ovarian insufficiency may be auto immune and therefore co occur with other autoimmune disorders such as thyroid disease, [adrenal insufficiency], and diabetes mellitus. Other causes include chemotherapy, being a carrier of the fragile X syndrome gene, and radiotherapy. | Iobenguane, or MIBG, is an aralkylguanidine analog of the adrenergic neurotransmitter norepinephrine (noradrenaline), typically used as a radiopharmaceutical. It acts as a blocking agent for adrenergic neurons. When radiolabeled, it can be used in nuclear medicinal diagnostic and therapy techniques as well as in neuroendocrine chemotherapy treatments. It localizes to adrenergic tissue and thus can be used to identify the location of tumors such as pheochromocytomas and neuroblastomas. With iodine-131 it can also be used to treat tumor cells that take up and metabolize norepinephrine. Usage and mechanism
MIBG is absorbed by and accumulated in granules of adrenal medullary chromaffin cells, as well as in pre-synaptic adrenergic neuron granules. The process in which this occurs is closely related to the mechanism employed by norepinephrine and its transporter in vivo. The norepinephrine transporter (NET) functions to provide norepinephrine uptake at the synaptic terminals and adrenal chromaffin cells. MIBG, by bonding to NET, finds its roles in imaging and therapy. Metabolites and excretion
Less than 10% of the administered MIBG gets metabolized into m-iodohippuric acid (MIHA), and the mechanism for how this metabolite is produced is unknown. Diagnostic imaging
MIBG concentrates in endocrine tumors, most commonly neuroblastoma, paraganglioma, and pheochromocytoma. It also accumulates in norepinephrine transporters in adrenergic nerves in the heart, lungs, adrenal medulla, salivary glands, liver, and spleen, as well as in tumors that originate in the neural crest. When labelled with iodine-123 it serves as a whole-body, non-invasive scintigraphic screening for germ-line, somatic, benign, and malignant neoplasms originating in the adrenal glands. | 0-1
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The virus also causes lytic infection in the oropharynx, but is kept in check by a normal, functioning immune system. Uncontrolled lytic infection is manifested as oral hairy leukoplakia in immunocompromised hosts. OHL usually arises where the immunocompromise is secondary to HIV/AIDS. Rarely are other causes of immunocompromise associated with OHL, but it has been reported in people who have received transplants and are taking immunosuppressive medication. OHL may also accompany chronic graft versus host disease. Even more rare are reports of OHL in persons with competent immune systems. Diagnosis
The white lesion cannot be wiped away, unlike some other common oral white lesions, e.g. pseudomembranous candidiasis, and this may aid in the diagnosis. Diagnosis of OHL is mainly clinical, but can be supported by proof of EBV in the lesion (achieved by in situ hybridization, polymerase chain reaction, immunohistochemistry, Southern blotting, or electron microscopy) and HIV serotesting. When clinical appearance alone is used to diagnose OHL, there is a false positive rate of 17% compared to more objective methods. The appearance of OHL in a person who is known to be infected with HIV does not usually require further diagnostic tests as the association is well known. OHL in persons with no known cause of immunocompromise usually triggers investigations to look for an underlying cause. | Hairy leukoplakia is a white patch on the side of the tongue with a corrugated or hairy appearance. It is caused by Epstein-Barr virus (EBV) and occurs usually in persons who are immunocompromised, especially those with human immunodeficiency virus infection/acquired immunodeficiency syndrome (HIV/AIDS). The white lesion, which cannot be scraped off, is benign and does not require any treatment, although its appearance may have diagnostic and prognostic implications for the underlying condition. Depending upon what definition of leukoplakia is used, hairy leukoplakia is sometimes considered a subtype of leukoplakia, or a distinct diagnosis. Signs and symptoms
There are no symptoms associated with the lesion itself, although many and varied symptoms and signs may be associated with the underlying cause of immunosuppression. The lesion is a white patch, which almost exclusively occurs on the lateral surfaces of the tongue, although rarely it may occur on the buccal mucosa, soft palate, pharynx or esophagus. The lesion may grow to involve the dorsal surface of the tongue. The texture is vertically corrugated ("hairy") or thickly furrowed and shaggy in appearance. Causes
The white appearance is created by hyperkeratosis (overproduction of keratin) and epithelial hyperplasia. The causative agent implicated is Epstein-Barr virus, the same virus that causes infectious mononucleosis (glandular fever). After the primary EBV infection has been overcome, the virus will persist for the rest of the hosts life and "hides" from the immune system by latent infection of B lymphocytes. | 11
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Ocular myasthenia gravis (MG) is a disease of the neuromuscular junction resulting in hallmark variability in muscle weakness and fatigability. MG is an autoimmune disease where anomalous antibodies are produced against the naturally occurring acetylcholine receptors in voluntary muscles. MG may be limited to the muscles of the eye (ocular MG), leading to abrupt onset of weakness/fatigability of the eyelids or eye movement. MG may also involve other muscle groups (generalized MG). Signs and symptoms
Although these blocking antibodies may be confined to one of the larger muscles responsible for moving the face or appendages or for breathing, about 90% of MG patients eventually have eye involvement. The most common symptoms are double vision (diplopia) and eyelid drooping (ptosis), whereas the pupil is always spared. Diplopia occurs when MG affects a single extraocular muscle in one eye, limiting eye movement and leading to double vision when the eye is turned toward the affected muscle. Ptosis occurs when the levator palpebrae superioris (the muscle responsible for eyelid elevation) is affected on one or both sides, leading to eyelid drooping. Although these symptoms may not be readily apparent in well-rested patients, weakness can usually be induced with exercise of the commonly affected muscles (e.g. by having the patient look upward for about 60 seconds). In 75% of MG cases, the initial manifestation is in the eye. Within 2 years, 80% of patients with ocular onset of MG will progress to involve other muscle groups, thereby developing generalized MG. | Steroid therapy is controversial, but in another study the results suggested that prednisone does decrease progression to generalized MG. There is no single recommended dosing regimen in light of the side effects commonly associated with chronic corticosteroid therapy, and the difficulty in weaning patients from steroids without exacerbation of symptoms. Response to prednisone therapy is variable. Additionally, MG patients should be examined for thymomas, and if found, should undergo surgery to address this condition. A prophylactic thymectomy is controversial, but has been shown to be helpful in young MG patients with acute disease within 3 years of disease onset, in patients with enlarged thymus glands and for whom surgery is low-risk, and patients with generalized MG who are unresponsive to medical treatment. The symptoms of ocular MG can also be addressed by non-medicinal means. Ptosis can be corrected with placement of crutches on eyeglasses and with ptosis tape to elevate eyelid droop. Diplopia can be addressed by occlusion with eye patching, frosted lens, occluding contact lens, or by simply placing opaque tape over a portion of eyeglasses. Also, plastic prisms (Fresnel prisms) can be attached to eyeglasses of a diplopic patient, allowing for alignment of vision from both eyes in the affected direction, but are often problematic if the degree of muscle weakness, and therefore ocular misalignment, fluctuates frequently. | 11
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Toxicity
The typical amounts of potassium chloride found in the diet appear to be generally safe. In larger quantities, however, potassium chloride is toxic. The LD50 of orally ingested potassium chloride is approximately 2.5 g/kg, or 190 grams (6.7 oz) for a body mass of 75 kilograms (165 lb). In comparison, the LD50 of sodium chloride (table salt) is 3.75 g/kg. Intravenously, the LD50 of potassium chloride is far smaller, at about 57.2 mg/kg to 66.7 mg/kg; this is found by dividing the lethal concentration of positive potassium ions (about 30 to 35 mg/kg) by the proportion by mass of potassium ions in potassium chloride (about 0.52445 mg K+/mg KCl). Chemical properties
Solubility
KCl is soluble in a variety of polar solvents. Solutions of KCl are common standards, for example for calibration of the electrical conductivity of (ionic) solutions, since KCl solutions are stable, allowing for reproducible measurements. In aqueous solution, it is essentially fully ionized into solvated K+ and Cl− ions. | Tricho–rhino–phalangeal syndrome type 2 (also known as Langer–Giedion syndrome) is a genetic disorder consisting of fine and sparse scalp hair, thin nails, pear-shaped broad nose, and cone-shaped epiphyses of the middle phalanges of some fingers and toes. : 578 It has been associated with TRPS1. See also
Skin lesion
List of cutaneous conditions
References
== External links == | 0-1
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It is a controlled substance in the United States and is considered to have a low misuse potential. Pharmacology
Pharmacodynamics
Lemborexant is a dual antagonist of the orexin OX1 and OX2 receptors. It associates and dissociates from the orexin receptors more rapidly than certain other orexin receptor antagonists, such as suvorexant, and this may cause it to have a shorter duration of action. Pharmacokinetics
The bioavailability of lemborexant is good and is at least 87%. The time to peak levels of lemborexant is 1 to 3 hours. A high-fat and high-calorie meal has been found to delay the time to peak levels by 2 hours. Its plasma protein binding in vitro is 94%. Lemborexant is metabolized primarily by CYP3A4 and to a lesser extent by CYP3A5. The "effective" half-life of lemborexant is 17 to 19 hours while its terminal elimination half-life is 55 hours. The medication is excreted in feces (57%) and to a lesser extent urine (29%). Although lemborexant has a longer terminal elimination half-life than suvorexant, it appears to be more rapidly cleared than suvorexant in the earlier phases of elimination. In addition, lemborexant dissociates from the orexin receptors more rapidly than does suvorexant. These differences may allow for comparatively reduced next-day effects such as daytime somnolence with lemborexant. History
In June 2016, Eisai initiated Phase III clinical trials in the United States, France, Germany, Italy, Japan, Poland, Spain and the UK.In December 2019, lemborexant was approved for use in the United States based on results from the SUNRISE 1 and SUNRISE 2 Phase III clinical trials. | Sneddons syndrome is a form of arteriopathy characterized by several symptoms, including:
Severe, transient neurological symptoms or stroke
Livedo reticularis, or livedo racemosa
Signs and symptoms
Sneddons syndrome generally manifests with stroke or severe, transient neurological symptoms, and a skin rash (livedo reticularis). Livedo reticularis appears as a bluish-purple, netlike mottling of the skin. Sneddons syndrome may instead present with livedo racemosa, which involves larger, less organized patches of bluish-purple mottling of the skin. Both are generally found first in the extremities, both worsen in cold and either may occur without Sneddons Syndrome or any other systemic disease.Sneddons Syndrome can be characterized by: transient amnesia, transient aphasia, palsy, headaches, hypertension, transient ischemic attacks (TIA), stroke, coronary disease and dementia. The skin manifestations may precede the neurologic symptoms by years. Pathogenesis
Sneddons syndrome is a progressive, noninflammatory arteriopathy leading to the characteristic skin condition and to cerebrovascular problems, including stroke, transient ischemic attack (TIA), severe but transient neurological symptoms thought to be caused by cerebral vasospasm, coronary disease and early-onset dementia. Progressive compromise of arterial linings in Sneddons produces clotting, for which high-dose warfarin is most commonly prescribed, and can also cause the development of systemic arterial plaque when cholesterol levels are normal. Diagnosis
There are no diagnostic tests on which all Sneddons patients will have abnormal results, although brain MRI and skin biopsy are often abnormal. The diagnosis is based on a detailed history and physical examination. About 40-60% of patients with the syndrome test positive for antiphospholipid antibodies. | 0-1
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Mammograms or breast biopsies are normally performed on women who do not respond to treatment or on non-breastfeeding women. This type of tests is sometimes ordered to exclude the possibility of a rare type of breast cancer which causes symptoms similar to those of mastitis. Differential diagnosis
Breast cancer may coincide with or mimic symptoms of mastitis. Only full resolution of symptoms and careful examination are sufficient to exclude the diagnosis of breast cancer. Lifetime risk for breast cancer is significantly reduced for women who were pregnant and breastfeeding. Mastitis episodes do not appear to influence lifetime risk of breast cancer. Mastitis does however cause great difficulties in diagnosis of breast cancer and delayed diagnosis and treatment can result in worse outcome. Breast cancer may coincide with mastitis or develop shortly afterwards. All suspicious symptoms that do not completely disappear within 5 weeks must be investigated. Breast cancer incidence during pregnancy and lactation is assumed to be the same as in controls. Course and prognosis are also very similar to age matched controls. However diagnosis during lactation is particularly problematic, often leading to delayed diagnosis and treatment. Some data suggest that noninflammatory breast cancer incidence is increased within a year following episodes of nonpuerperal mastitis and special care is required for follow-up cancer prevention screening. So far only data from short term observation is available and total risk increase can not be judged. | One third of these patients die, one third survives with a major neurological condition, and only one third survives in good condition; therefore shaken baby syndrome puts children at risk of long-term disability. The most frequent neurological impairments are learning disabilities, seizure disorders, speech disabilities, hydrocephalus, cerebral palsy, and visual disorders. Epidemiology
Small children are at particularly high risk for the abuse that causes SBS given the large difference in size between the small child and an adult. SBS usually occurs in children under the age of two but may occur in those up to age five. In the US, deaths due to SBS constitute about 10% of deaths due to child abuse. History
In 1971, Norman Guthkelch proposed that whiplash injury caused subdural bleeding in infants by tearing the veins in the subdural space. The term "whiplash shaken infant syndrome" was introduced by Dr. John Caffey, a pediatric radiologist, in 1973, describing a set of symptoms found with little or no external evidence of head trauma, including retinal bleeds and intracranial bleeds with subdural or subarachnoid bleeding or both. Development of computed tomography and magnetic resonance imaging techniques in the 1970s and 1980s advanced the ability to diagnose the syndrome. Legal issues
The Presidents Council of Advisers on Science and Technology (PCAST) noted in its September 2016 report that there are concerns regarding the scientific validity of forensic evidence of abusive head trauma that "require urgent attention". | 0-1
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In such cases, Tdap is recommended to be substituted for one dose of Td, again preferably between 27 and 36 weeks of gestation, and then the series completed with Td. Specific types
The first vaccine is given in infancy. The baby is injected with the DTaP vaccine, which is three inactive toxins in one injection. DTaP protects against diphtheria, pertussis, and tetanus. This vaccine is safer than the previously used DTP. Another option is DT, which is a combination of diphtheria and tetanus vaccines. This is given as an alternative to infants who have conflicts with the DTaP vaccine. Quadrivalent, pentavalent, and hexavalent formulations contain DTaP with one or more of the additional vaccines: inactivated polio virus vaccine (IPV), Haemophilus influenzae type b conjugate, Hepatitis B, with the availability varying in different countries.For the every ten-year booster Td or Tdap may be used, though Tdap is more expensive. Schedule
Because DTaP and DT are administered to children less than a year old, the recommended location for injection is the anterolateral thigh muscle. However, these vaccines can be injected into the deltoid muscle if necessary.The World Health Organization (WHO) recommends six doses in childhood starting at six weeks of age. Four doses of DTaP are to be given in early childhood. The first dose should be around two months of age, the second at four months, the third at six, and the fourth from fifteen to eighteen months of age. | Pyodermatitis vegetans can refer to:
Pyostomatitis vegetans
Blastomycosis-like pyoderma | 0-1
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Cirrhosis is defined by its features on microscopy: (1) the presence of regenerating nodules of hepatocytes and (2) the presence of fibrosis, or the deposition of connective tissue between these nodules. The pattern of fibrosis seen can depend on the underlying insult that led to cirrhosis. Fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: including the sinusoids, the space of Disse, and other vascular structures, which leads to altered resistance to blood flow in the liver, and portal hypertension. As cirrhosis can be caused by many different entities which injure the liver in different ways, cause-specific abnormalities may be seen. For example, in chronic hepatitis B, there is infiltration of the liver parenchyma with lymphocytes. In congestive hepatopathy there are erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins. In primary biliary cholangitis, there is fibrosis around the bile duct, the presence of granulomas and pooling of bile. Lastly in alcoholic cirrhosis, there is infiltration of the liver with neutrophils.Macroscopically, the liver is initially enlarged, but with the progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and if associated with steatosis the color is yellow. Depending on the size of the nodules, there are three macroscopic types: micronodular, macronodular, and mixed cirrhosis. In the micronodular form (Laennecs cirrhosis or portal cirrhosis), regenerating nodules are under 3 mm. | Quantification of Sepiapterin in CSF
This study examined the clinical history of the CSF and urine of two Greek siblings who were both diagnosed with SR deficiency. Both siblings displayed delayed psychomotor development and a movement disorder. The diagnosis was confirmed by measuring the SR enzyme activity and mutation analysis. The mutation analysis of the gene was performed using genomic DNA isolated from blood samples. The results concluded that both patients have low concentrations of HVA and HIAA and high concentrations of sepiapterin in the CSF, but neopterin and biopterin were abnormal in only one sibling. The results of this research indicates that when diagnosing the SR deficiency, the quantification of sepiapterin in the CSF is more important and indicative of SR deficiency than using neopterin and biopterin alone. The results also show that the urine concentrations of neurotransmitter metabolites are abnormal in patients with this disorder. This finding may provide an initial and easier indication of the deficiency before CSF analysis is performed. Figures
See also
Succinic semialdehyde dehydrogenase deficiency
Neurotransmitter
Parkinsons disease
Cerebral palsy
Enzyme
Biochemistry
References
External links
SR deficiency Genetics Home Reference
SR deficiency National Institute of Health | 0-1
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Differential diagnosis
Medical conditions
The differential diagnosis for LUTS is broad and includes various medical conditions, neurologic disorders, and other diseases of the bladder, urethra, and prostate such as bladder cancer, urinary tract infection, urethral stricture, urethral calculi (stones), chronic prostatitis, and prostate cancer. Neurogenic bladder can cause urinary retention and cause symptoms similar to those of BPH. This may occur as a result of uncoordinated contraction of the bladder muscle or impairment in the timing of bladder muscle contraction and urethral sphincter relaxation. Notable causes of neurogenic bladder include disorders of the central nervous system such as Parkinsons disease, multiple sclerosis, and spinal cord injuries as well as disorders of the peripheral nervous system such as diabetes mellitus, vitamin B12 deficiency, and alcohol-induced nerve damage. Individuals affected by heart failure often experience nighttime awakenings to urinate due to redistribution of fluid accumulated in swollen legs. Medications
Certain medications can increase urination difficulties by increasing bladder outlet resistance due to increased smooth muscle tone at the prostate or bladder neck and contribute to LUTS. Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In contrast, calcium channel blockers and anticholinergic medications can worsen urinary retention by promoting bladder muscle relaxation. Diuretic medications such as loop diuretics (e.g., furosemide) or thiazides (e.g., chlorthalidone) can cause or worsen urinary frequency and nighttime awakenings to urinate. Management
When treating and managing benign prostatic hyperplasia, the aim is to prevent complications related to the disease and improve or relieve symptoms. Approaches used include lifestyle modifications, medications, and surgery. | Signs and symptoms
In surgery
Symptoms include:
Hypotension
Shortness of breath
In divers
Symptoms of arterial gas embolism include:
Loss of consciousness
Cessation of breathing
Vertigo
Convulsions
Tremors
Loss of coordination
Loss of control of bodily functions
Numbness
Paralysis
Extreme fatigue
Weakness in the extremities
Areas of abnormal sensation
Visual abnormalities
Hearing abnormalities
Personality changes
Cognitive impairment
Nausea or vomiting
Bloody sputum
Symptoms of other consequences of lung overexpansion such as pneumothorax, subcutaneous or mediastinal emphysema may also be present. Causes
Interventional procedures
Interventional radiology procedures, cardiac, and neurosurgical procedures can predispose to air embolism. Besides, increasing use of pump injectors for contrast delivery, and percutaneous intervention to the lungs also increases the risk of air embolism. Decompression illness
Gas embolism is a diving disorder experienced by underwater divers who breathe gases at ambient pressure, and can happen in two distinct ways:
Pulmonary barotrauma: Air bubbles can enter the bloodstream as a result of gross trauma to the lining of the lung following a rapid ascent while holding the breath; the air held within the lung expands to the point where the tissues tear (pulmonary barotrauma). This is easy to do as the lungs give little warning through pain until they do burst. The diver will usually arrive at the surface in pain and distress and may froth or spit blood. A pulmonary barotrauma is usually obvious and may present quite differently from decompression sickness. Decompression sickness: Inert gas bubbles form in the bloodstream if the gas dissolved in the blood under pressure during the dive is not allowed sufficient time to be eliminated in solution on ascent. | 0-1
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See also
Auditory imagery
Earworm
Hearing Voices Network
Hypnagogic hallucinations
Intrusive thought
Microwave auditory effect
Speech synthesis
Tinnitus
References
Further reading
Johnson FH (1978). The anatomy of hallucinations. Chicago: Nelson-Hall Co. ISBN 978-0-88229-155-0. Bentall RP, Slade PD (1988). Sensory deception: a scientific analysis of hallucination. London: Croom Helm. ISBN 978-0-7099-3961-0. Larøi F, Aleman A (2008). Hallucinations: The Science of Idiosyncratic Perception. American Psychological Association (APA). ISBN 978-1-4338-0311-6. Archived from the original on 2008-12-21. Retrieved 2009-10-27. External links
"Anthropology and Hallucinations", chapter from The Making of Religion
"The voice inside: A practical guide to coping with hearing voices"
A salience dysregulation syndrome, from Jim van Os. The British Journal of Psychiatry, 2009. | Chemical colitis is a type of colitis, an inflammation of the large intestine or colon, caused by the introduction of harsh chemicals to the colon by an enema or other procedure. Chemical colitis can resemble ulcerative colitis, infectious colitis and pseudomembranous colitis endoscopically.Prior to 1950, hydrogen peroxide enemas were commonly used for certain conditions. This practice will often result in chemical colitis.Soap enemas may also cause chemical colitis. Harsh chemicals, such as compounds used to clean colonoscopes, are sometimes accidentally introduced into the colon during colonoscopy or other procedures. This can also lead to chemical colitis.Chemical colitis may trigger a flare of ulcerative colitis or Crohns colitis. Symptoms of colitis are assessed using the Simple Clinical Colitis Activity Index. == References == | 0-1
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The DPP protein is thought to contribute to hydroxyapatite crystal formation and growth, a fundamental crystal which is widely distributed in mineralised dentine and enamel. The function of the DGP and DSP proteins is not well understood.Genetic studies have shown that type II and III may be the same sub-type of dentinogenesis imperfecta, differing only by the severity. de La Dure-Molla, Foruner and Berdal (2015)
de La Dure-Molla, Foruner and Berdal (2015) have proposed a new classification to supersede the Shield Classification (1973). This new classification is designed to overcome the shortcomings of its predecessor, mainly the clinical difficulty in using the Shield classification due to the overlapping signs & symptoms between the sub-types.In this classification, the authors propose that the DSPP (dentine sialophosphoprotein) diseases, that is dentinogenesis imperfecta and dentine dysplasia, are jointly named "Dentinogenesis imperfecta", and sub-types are determined according to the severity of the condition. There are a few exceptions:
Shields Dentine Dysplasia type I - this condition is unique in that it only affects root development, and is separately termed "radicular dentin dysplasia" in the new classification. Shields Dentinogenesis Imperfecta type I - this sub-type is not acknowledged in this new classification as the authors deem it a different disease since it is a syndrome of osteogenesis imperfecta
Mild type
Primary (baby) teeth are moderately affected. Permanent (adult) teeth are not discoloured, or the discolouration is mild (grey colour). Little or no attrition (tooth wear) is evident. The crown of the teeth may be bulbous and markedly constricted at the cemento-enamel junction (CEJ). | Dentinogenesis imperfecta (DI) is a genetic disorder of tooth development. It is inherited in an autosomal dominant pattern, as a result of mutations on chromosome 4q21, in the dentine sialophosphoprotein gene (DSPP). It is one of the most frequently occurring autosomal dominant features in humans. Dentinogenesis imperfecta affects an estimated 1 in 6,000-8,000 people.This condition can cause teeth to be discolored (most often a blue-gray or yellow-brown color) and translucent, giving teeth an opalescent sheen. Teeth are also weaker than normal, making them prone to rapid wear, breakage, and loss. These problems can affect baby (primary/deciduous) teeth alone, or both baby teeth and adult (permanent) teeth, with the baby teeth usually more severely affected.Although genetic factors are the main contributor for the disease, any environmental or systemic upset that impedes calcification or metabolisation of calcium can also result in anomalous dentine. Classification
Shield classification (1973)
This is the most widely used classification for dentinogenesis imperfecta, and sub-divides the condition into 3 types:
Type I
DI associated with Osteogenesis Imperfecta (OI). | 11
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In some types of ED, abnormal development of parts of the eye can result in dryness of the eye, cataracts, and vision defects. Professional eye care can help minimize the effects of ED on vision. Similarly, abnormalities in the development of the ear may cause hearing problems. Respiratory infections can be more common because the normal protective secretions of the mouth and nose are not present. Precautions must be taken to limit infections. Genetics
ED can be classified by inheritance (autosomal dominant, autosomal recessive and X-linked) or by which structures are involved (hair, teeth, nails and/or sweat glands). There are several different types with distinct genetic causes:
Hay–Wells syndrome (Rapp–Hodgkin syndrome) and EEC syndrome are all associated with TP63. Hypohidrotic ectodermal dysplasia can be associated with EDA, EDAR and EDARADD. Margarita Island ectodermal dysplasia is associated with PVRL1. Ectodermal dysplasia with skin fragility is associated with PKP1. Cloustons hidrotic ectodermal dysplasia is associated with GJB6. Naegeli syndrome/Dermatopathia pigmentosa reticulariss is associated with KRT14. Pachyonychia congenita is caused by multiple keratins. Focal dermal hypoplasia is associated with PORCN. Ellis–van Creveld syndrome is associated with EVC. Palmoplantar ectodermal dysplasia refers to several different conditions selectively affecting the hands and feet. | Diagnosis
In terms of the clinical evaluation, clinical features are the classification method
Treatment
Management for this condition is symptom specific
Society and culture
Notable cases
Michael Berryman, American actor with hypohidrotic ectodermal dysplasia
Levi Hawken, New Zealand skateboarder and artist who became well known in 2011 in New Zealand for the "Nek minnit" viral video on YouTube
See also
List of cutaneous conditions
List of cutaneous conditions caused by mutations in keratins
References
== External links == | 11
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In addition, conjunctival resection can be performed to temporarily remove local inflammatory mediators, followed by the use of immunosuppressants. Prognosis
Currently, there are limited studies regarding the prognosis of PUK. However, one study has pointed out possible complications surrounding PUK include moderate to severe vision loss, corneal perforation and increased risk of recurrence. Epidemiology
PUK is a rare condition with an estimated incidence of 3 per million annually. Studies have reported that most patients with PUK are older than 60 years of age (32%). Among them, men have a higher occurrence rate in men (60%). Most patients live in rural areas (66%) and are in the lower socioeconomic groups. The age of those with PUK ranges from 5 to 89 years, with a mean age of 45.5 years.The mortality rate after PUK diagnosis in an investigation of 34 patients with and without immunosuppressive medication is 53% and 5%, respectively. Another single-centre study involving 46 patients with RA reported a mortality rate of 15%. Reports have also shown a possibility of PUK occurrence after any ocular surgery. In a retrospective study of 771 eyes, 1.4% of participants reported developing late-onset PUK at an average of 3–6 months after surgery. == References == | The provisional representation of species addressed by the resource has been indicated in the TaxBox on this page by a superscript yb beside the species name. Development of YersiniaBase was funded by the University of Malaya and the Ministry of Education, Malaysia. Pathogenesis
Y. pestis is the causative agent of plague. The disease caused by Y. enterocolitica is called yersiniosis. Yersinia may be associated with Crohns disease, an inflammatory autoimmune condition of the gut. Iranian sufferers of Crohns disease were more likely to have had earlier exposure to refrigerators at home, consistent with its unusual ability to thrive at low temperatures. Yersinia is implicated as one of the causes of reactive arthritis worldwide.Also, the genus is associated with pseudoappendicitis, which is an incorrect diagnosis of appendicitis due to a similar presentation. History
Y. pestis, the first known species, was identified in 1894 by A.E.J. Yersin, a Swiss bacteriologist, and Kitasato Shibasaburō, a Japanese bacteriologist. It was formerly described as Pasteurella pestis (known trivially as the plague-bacillus) by Lehmann and Neumann in 1896. In 1944, van Loghem reclassified the species P. pestis and P. rondentium into a new genus, Yersinia. Following the introduction of the bacteriological code, it was accepted as valid in 1980. References
External links
Yersinia Enterocolitis Mimicking Crohns Disease in a Toddler
Sweden: Pork warnings over new stomach illness
Yersinia genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
YersiniaBase | 0-1
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Doctors do not agree on what causes cradle cap, but the two most common hypotheses are fungal infection and overactive sebaceous glands. Cradle cap is an inflammatory condition.Possibly it has to do with overactive sebaceous glands in the skin of newborn babies, due to the mothers hormones still in the babys circulation. The glands release a greasy substance that makes old skin cells attach to the scalp instead of falling off as they dry. There is a relationship with skin yeasts (Pityrosporum ovale, newly renamed Malassezia furfur). Warning signs
If the condition thickens, turns red and irritated, starts spreading, appears on other body parts, or if the baby develops thrush (fungal mouth infection), fungal ear infection (an ear infection that does not respond to antibiotics) or a persistent diaper rash, medical intervention is recommended. Severe cases of cradle cap, especially with cracked or bleeding skin, can provide a place for bacteria to grow. If the cradle cap is caused by a fungal infection which has worsened significantly over days or weeks to allow bacterial growth (impetigo, most commonly), a combination treatment of antibiotics and antifungals may be necessary. Since it is difficult for a layperson to distinguish the difference between sebaceous gland cradle cap, fungal cradle cap, or either of these combined with a bacterial infection, medical advice should be sought if the condition appears to worsen. Cradle cap is occasionally linked to immune disorders. If the baby is not thriving and has other problems (e.g. diarrhea), a doctor should be consulted. | Several treatments including Promiseb, lactamide MEA gel, hydrocortisone 1% lotion, licochalcone 0.025%, flumethasone pivalate 0.02% ointment, and eosin 2% aqueous solution have been studied, however there is uncertainty regarding the efficacy and safety of these treatments.For adults: see the article on seborrheic dermatitis (the adult version of cradle cap). Scalp, behind ears, eyebrows
If the cradle cap is not severe, it could simply be combed out gently after bathing. The softened scales can then be brushed away with a soft brush, comb or cloth, but if not done very gently, this could worsen the condition and bring about temporary hair loss. Applying petroleum jelly (e.g., Vaseline) liberally overnight is another popular treatment. The softened scales either fall off during the night, or can be brushed off in the morning.There is broad disagreement regarding the role of shampoos. Some sources warn against frequent shampooing, others recommend it. Mild baby shampoo is often recommended, but the exact denotation of the label "mild" in this context is not quite clear. Baby shampoos often contain detergent surfactants, perfumes, quaternium-15 and other eczemagenic irritants. No studies have been performed on non-prescription shampoos.In stubborn cases some doctors may recommend keratolytic (dandruff) shampoos (e.g. with sulfur, selenium, zinc pyrithione, or salicylic acid) while others warn against the use of medicated shampoos in newborns due to systemic absorption. Dandruff shampoos often contain sodium dodecyl sulfate, a noted skin irritant.Steroid and tar preparations have also been used but may have drawbacks. The immunomodulators tacrolimus/Protopic and pimecrolimus/Elidel have not been approved for children under two years. | 11
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This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia). Diagnosis
Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight. | For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global number of diabetes cases might increase by 48% between 2017 and 2045. History
Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The Ebers papyrus includes a recommendation for a drink to take in such cases. The first described cases are believed to have been type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. | 11
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Canada
Health Canada has investigated the risks and benefits of pseudoephedrine and ephedrine/Ephedra. Near the end of the study, Health Canada issued a warning on their website stating that those who are under the age of 12, or who have heart disease and may have strokes, should avoid taking pseudoephedrine and ephedrine. Also, they warned that everyone should avoid taking ephedrine or pseudoephrine with other stimulants like caffeine. They also banned all products that contain both ephedrine (or pseudoephedrine) and caffeine.Products whose only medicinal ingredient is pseudoephedrine must be kept behind the pharmacy counter. Products containing pseudoephedrine along with other medicinal ingredients may be displayed on store shelves but may be sold only in a pharmacy when a pharmacist is present. Colombia
The Colombian government prohibited the trade of pseudoephedrine in 2010. Japan
Medications that contain more than 10% pseudoephedrine are prohibited under the Stimulants Control Law in Japan. Mexico
On 23 November 2007, the use and trade of pseudoephedrine in Mexico was made illegal as it was argued that it was extremely popular as a precursor in the synthesis of methamphetamine. Netherlands
Pseudoephedrine was withdrawn from sale in 1989 due to concerns about adverse cardiac side effects. New Zealand
In New Zealand, pseudoephedrine is currently classified as a Class B Part II controlled drug in the Misuse of Drugs Act 1975, making it illegal to supply or possess except on prescription.Pseudoephedrine, ephedrine, and any product containing these substances, e.g. | Increase of ectopic pacemaker activity can occur when pseudoephedrine is used concomitantly with digitalis. Antacids increase the rate of pseudoephedrine absorption, while kaolin decreases it. Mechanism of action
Pseudoephedrine is a sympathomimetic amine. Its principal mechanism of action relies on its direct action on the adrenergic receptor system. The vasoconstriction that pseudoephedrine produces is believed to be principally an α-adrenergic receptor response.Pseudoephedrine acts on α- and β2-adrenergic receptors, to cause vasoconstriction and relaxation of smooth muscle in the bronchi, respectively. α-Adrenergic receptors are located on the muscles lining the walls of blood vessels. When these receptors are activated, the muscles contract, causing the blood vessels to constrict (vasoconstriction). The constricted blood vessels now allow less fluid to leave the blood vessels and enter the nose, throat and sinus linings, which results in decreased inflammation of nasal membranes, as well as decreased mucus production. Thus, by constriction of blood vessels, mainly those located in the nasal passages, pseudoephedrine causes a decrease in the symptoms of nasal congestion. Activation of β2-adrenergic receptors produces relaxation of smooth muscle of the bronchi, causing bronchial dilation and in turn decreasing congestion (although not fluid) and difficulty breathing. Other uses
There have been reports of off-label uses of pseudoephedrine for its stimulant properties. Long-distance truck drivers and athletes, for example, have reportedly used pseudoephedrine as a stimulant to increase their state of alertness/awareness.A study has also found that pseudoephedrine can reduce milk production in breastfeeding women. | 11
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A 2012 systematic review found although it was difficult to draw firm conclusions, there was some evidence that prenatal exposure to cannabis was associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence". A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as it may interact with the endocannabinoid system. Effects in pediatrics
Children can become exposed to cannabis, typically through accidental exposure which can lead to very high doses, especially in the case of edibles. Unlike in adults, these levels of exposure can lead to major complications in children. These complications include encephalopathy, hypotension, respiratory depression severe enough to require ventilation, somnolence, coma, and there have been case reports of death. Pediatric exposure to edibles is of increasing concern because these products are typically sweets (gummies, cookies, etc. ), and their prevalence is increasing as cannabis is legalized or decriminalized in many territories. See also
Cannabis smoking
Psychoactive drug
References
Further reading
National Academies of Sciences, Engineering, and Medicine (2017). The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. National Academies of Sciences, Engineering, and Medicine. Washington, DC: The National Academies Press. doi:10.17226/24625. ISBN 978-0-309-45304-2. PMID 28182367. {{cite book}}: CS1 maint: multiple names: authors list (link) | Prax may refer to:
Prax (malware), or Regin, a malware and hacking toolkit
Prax Group, operators of Lindsey Oil Refinery, North Killingholme, North Lincolnshire, England
Praso, Italy (German: Prax), a former comune in Trentino, Italy
Mike Prax (born 1956), American politician from Alaska
Valentine Prax (1897–1981), French expressionist and cubist painter | 0-1
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