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It can be tried for depression as a second-line therapy, after the failure of other treatments. For treatment-resistant adolescent depression or for cancer-related depression amitriptyline is no better than placebo. It is sometimes used for the treatment of depression in Parkinsons disease, but supporting evidence for that is lacking. Pain
Amitriptyline alleviates painful diabetic neuropathy. It is recommended by a variety of guidelines as a first or second line treatment. It is as effective for this indication as gabapentin or pregabalin but less well tolerated.Low doses of amitriptyline moderately improve sleep disturbances and reduce pain and fatigue associated with fibromyalgia. It is recommended for fibromyalgia accompanied by depression by Association of the Scientific Medical Societies in Germany and as a second-line option for fibromyalgia, with exercise being the first line option, by European League Against Rheumatism. Combinations of amitriptyline and fluoxetine or melatonin may reduce fibromyalgia pain better than either medication alone.There is some (low-quality) evidence that amitriptyline may reduce pain in cancer patients. It is recommended only as a second line therapy for non-chemotherapy-induced neuropathic or mixed neuropathic pain, if opioids did not provide the desired effect.Moderate evidence exists in favor of amitriptyline use for atypical facial pain. Amitriptyline is ineffective for HIV-associated neuropathy. Headache
Amitriptyline is probably effective for the prevention of periodic migraine in adults. Amitriptyline is similar in efficacy to venlafaxine and topiramate but carries a higher burden of adverse effects than topiramate. For many patients, even very small doses of amitriptyline are helpful, which may allow for minimization of side effects. | Benzodiazepines are recommended to control seizures. Dialysis is of no use due to the high degree of protein binding with amitriptyline. Interactions
Since amitriptyline and its active metabolite nortriptyline are primarily metabolized by cytochromes CYP2D6 and CYP2C19 (see Amitriptyline#Pharmacology), the inhibitors of these enzymes are expected to exhibit pharmacokinetic interactions with amitriptyline. According to the prescribing information, the interaction with CYP2D6 inhibitors may increase the plasma level of amitriptyline. However, the results in the other literature are inconsistent: the co-administration of amitriptyline with a potent CYP2D6 inhibitor paroxetine does increase the plasma levels of amitriptyline two-fold and of the main active metabolite nortriptyline 1.5-fold, but combination with less potent CYP2D6 inhibitors thioridazine or levomepromazine does not affect the levels of amitriptyline and increases nortriptyline by about 1.5-fold; a moderate CYP2D6 inhibitor fluoxetine does not seem to have a significant effect on the levels of amitriptyline or nortriptyline. A case of clinically significant interaction with potent CYP2D6 inhibitor terbinafine has been reported.A potent inhibitor of CYP2C19 and other cytochromes fluvoxamine increases the level of amitriptyline two-fold while slightly decreasing the level of nortriptyline. Similar changes occur with a moderate inhibitor of CYP2C19 and other cytochromes cimetidine: amitriptyline level increases by about 70%, while nortriptyline decreases by 50%. CYP3A4 inhibitor ketoconazole elevates amitriptyline level by about a quarter. On the other hand, cytochrome P450 inducers such as carbamazepine and St. Johns Wort decrease the levels of both amitriptyline and nortriptylineOral contraceptives may increase the blood level of amitriptyline by as high as 90%. | 11
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Current studies funded by the GWIRP and the VA are also investigating yoga as a treatment for GWI. An amino acid supplement containing L-carnosine was found to reduce irritable bowel syndrome-associated diarrhea in a randomized, controlled GWIRP-funded trial in GW Veterans (Baraniuk, 2013). Veterans receiving L-carnosine showed a significant improvement in performance in a cognitive task, but no improvement in fatigue, pain, hyperalgesia, or activity levels. Results from a 26 week GWIRP-funded trial comparing standard care to nasal irrigation with either saline or a xylitol solution revealed that both irrigation protocols reduced GWI respiratory (chronic rhinosinusitis) and fatigue symptoms (Hayer, 2015). Administration of the glucocorticoid receptor antagonist mifepristone to GW Veterans in a GWIRP-funded randomized trial resulted in an improvement in verbal learning, but no improvement in self-reported physical health or other self-reported measures of mental health (Golier, 2016).Ongoing Intervention Studies
The GWIRP is currently funding many early-phase clinical trials aimed at GWI. Interventions include direct electrical nerve stimulation, repurposing FDA-approved pharmaceuticals, and dietary protocols and/or nutraceuticals. Both ongoing and closed GWIRP-supported clinical treatment trials and pilot studies can be found at [1]. A Clinical Consortium Award was offered [in FY2017] to support a group of institutions, coordinated through an Operations Center that will conceive, design, develop, and conduct collaborative Phase I and II clinical evaluations of promising therapeutic agents for the management or treatment of GWI. These mechanisms were designed to build on the achievements of the previously established consortia and to further promote collaboration and resource sharing. | The report called for a substantial commitment to improving identification and treatment of multisymptom illness in Gulf War veterans focussing on continued monitoring of Gulf War veterans, improved medical care, examination of genetic differences between symptomatic and asymptomatic groups and studies of environment-gene interactions.A variety of signs and symptoms have been associated with GWI:
* This table applies only to coalition forces involved in combat.Birth defects have been suggested as a consequence of Gulf War deployment. However, a 2006 review of several studies of international coalition veterans children found no strong or consistent evidence of an increase in birth defects, finding a modest increase in birth defects that was within the range of the general population, in addition to being unable to exclude recall bias as an explanation for the results. A 2008 report stated that "it is difficult to draw firm conclusions related to birth defects and pregnancy outcomes in Gulf War veterans", observing that while there have been "significant, but modest, excess rates of birth defects in children of Gulf War veterans", the "overall rates are still within the normal range found in the general population". The same report called for more research on the issue. | 11
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No special blood tests or diagnostic procedures are usually required to make the diagnosis.The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema, seborrheic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis). Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy shows clubbed epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions. The stratum granulosum layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin are also abnormal as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nuclei. Inflammatory infiltrates can typically be seen on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells, while a predominance of CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and the joints. Classification
Morphological
Psoriasis is classified as a papulosquamous disorder and is most commonly subdivided into different categories based on histological characteristics. Variants include plaque, pustular, guttate, and flexural psoriasis. | Tepotinib, sold under the brand name Tepmetko, is a medication used for the treatment of adults with non-small cell lung cancer (NSCLC).Tepotinib first received marketing approval in Japan, in March 2020, as a "line-agnostic" drug, meaning it is approved both for treatment-naive patients and for those in whom previous attempts at treatment have failed. U.S. approval followed in February 2021. It is the second therapy approved by the U.S. Food and Drug Administration (FDA) to treat non-small cell lung cancer with these particular mutations, after capmatinib. Medical uses
Tepotinib is indicated for the treatment of adults with metastatic non-small cell lung cancer (NSCLC) whose tumors have a mutation that leads to mesenchymal-epithelial transition (MET) exon 14 skipping. Adverse effects
The most common side effects seen in clinical trials were edema, fatigue, nausea, diarrhea, muscle aches, and shortness of breath. Like capmatinib, tepotinib can also cause interstitial lung disease and liver damage, and is toxic to a developing fetus. The most common treatment-related adverse effect in a 2021 study were peripheral edema (54.1%), nausea (20.0%), diarrhea (19.6%), blood creatinine increased (17.6%), and hypoalbuminemia (14.5%), which were mostly mild or moderate. Society and culture
Legal status
On 16 December 2021, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Tepmetko, intended for the treatment of patients with advanced non-small cell lung cancer (NSCLC) harboring alterations leading to mesenchymal-epithelial transition factor gene exon 14 (METex14) skipping. | 0-1
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The first mutational event can be inherited (germline or constitutional), which will then be present in all cells in the body. The second “hit” results in the loss of the remaining normal allele (gene) and occurs within a particular retinal cell. In the sporadic, nonheritable form of retinoblastoma, both mutational events occur within a single retinal cell after fertilization (somatic events); sporadic retinoblastoma tends to be unilateral. Several methods have been developed to detect the RB1 gene mutations. Attempts to correlate gene mutations to the stage at presentation have not shown convincing evidence of a correlation. MYCN
Not all retinoblastoma cases are with RB1 inactivation. There are cases reported with only one RB1 mutation or even two functional RB1 alleles, which indicates other oncogenic lesions of retinoblastoma. Somatic amplification of the MYCN oncogene is responsible for some cases of nonhereditary, early-onset, aggressive, unilateral retinoblastoma. MYCN can act as a transcription factor and promotes proliferation by regulating the expression of cell cycle genes. Although MYCN amplification accounted for only 1.4% of retinoblastoma cases, researchers identified it in 18% of infants diagnosed at less than 6 months of age. Median age at diagnosis for MYCN retinoblastoma was 4.5 months, compared with 24 months for those who had nonfamilial unilateral disease with two RB1 gene mutations. | Using cloned α1G, α1H, and α1I T-type calcium channels, Gomoras team found that ethosuximide blocked the channels with an IC50 of 12 ± 2 mmol/L and that of N-desmethylmethsuximide (the active metabolite of mesuximide) is 1.95 ± 0.19 mmol/L for α1G, 1.82 ± 0.16 mmol/L for α1I, and 3.0 ± 0.3 mmol/L for α1H. It was suggested that the blockade of open channels is facilitated by ethosuximides physically plugging the channels when current flows inward. Stereochemistry
Ethosuximide is a chiral drug with a stereocenter. Therapeutically, the racemate, the 1: 1 mixture of ( S ) and ( R ) - isomers used. Society and culture
Cost
As of 2019 there were concerns in the United States that the price of ethosuximide was inflated by manufacturers. Availability
Availability of ethosuximide is limited in many countries. It was marketed under the trade names Emeside and Zarontin. However, both capsule preparations were discontinued from production, leaving only generic preparations available. Emeside capsules were discontinued by their manufacturer, Laboratories for Applied Biology, in 2005. Similarly, Zarontin capsules were discontinued by Pfizer in 2007. Syrup preparations of both brands remained available. See also
Phensuximide
Methsuximide
References
External links
"Ethosuximide". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Between 4% and 20% of stones are mixed.Gallstones can vary in size and shape from as small as a grain of sand to as large as a golf ball. The gallbladder may contain a single large stone or many smaller ones. Pseudoliths, sometimes referred to as sludge, are thick secretions that may be present within the gallbladder, either alone or in conjunction with fully formed gallstones. Diagnosis
Diagnosis is typically confirmed by abdominal ultrasound. Other imaging techniques used are ERCP and MRCP. Gallstone complications may be detected on blood tests.On abdominal ultrasound, sinking gallstones usually have posterior acoustic shadowing. In floating gallstones, reverberation echoes (or comet-tail artifact) is seen instead in a clinical condition called adenomyomatosis. Another sign is wall-echo-shadow (WES) triad (or double-arc shadow) which is also characteristic of gallstones.A positive Murphys sign is a common finding on physical examination during a gallbladder attack. Prevention
Maintaining a healthy weight by getting sufficient exercise and eating a healthy diet that is high in fiber may help prevent gallstone formation.Ursodeoxycholic acid (UDCA) appears to prevent formation of gallstones during weight loss. A high fat diet during weight loss also appears to prevent gallstones. Treatment
Lithotripsy
Extracorporeal shock wave lithotripsy is a non-invasive method to manage gallstones that uses high-energy sound waves to disintegrate them first applied in January 1985. Side effects of extracorporeal shock wave lithotripsy include biliary pancreatitis and liver haematoma. Surgical
Cholecystectomy (gallbladder removal) has a 99% chance of eliminating the recurrence of cholelithiasis. | The lack of a gallbladder has no negative consequences in most people, however 10 to 15% of people develop postcholecystectomy syndrome, which may cause nausea, indigestion, diarrhea, and episodes of abdominal pain.There are two surgical options for cholecystectomy:
Open cholecystectomy is performed via an abdominal incision (laparotomy) below the lower right ribs. Recovery typically requires 3–5 days of hospitalization, with a return to normal diet a week after release and to normal activity several weeks after release. Laparoscopic cholecystectomy, introduced in the 1980s, is performed via three to four small puncture holes for a camera and instruments. Post-operative care typically includes a same-day release or a one-night hospital stay, followed by a few days of home rest and pain medication. Perforation of the gall bladder is not uncommon—it has been reported in the range of 10% to 40%. Unretrieved gallstone spillage has been reported as 6% to 30%, but gallstones that are not retrieved rarely cause complications (0.08%–0.3%).Obstruction of the common bile duct with gallstones can sometimes be relieved by endoscopic retrograde sphincterotomy (ERS) following endoscopic retrograde cholangiopancreatography (ERCP). Medical
The medications ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) have been used in treatment to dissolve gallstones. A 2013 meta-analysis concluded that UDCA or higher dietary fat content appeared to prevent formation of gallstones during weight loss. Medical therapy with oral bile acids has been used to treat small cholesterol stones, and for larger cholesterol gallstones when surgery is either not possible or unwanted. | 11
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Nausea is a diffuse sensation of unease and discomfort, sometimes perceived as an urge to vomit. While not painful, it can be a debilitating symptom if prolonged and has been described as placing discomfort on the chest, abdomen, or back of the throat.Over 30 definitions of nausea were proposed in a 2011 book on the topic.Nausea is a non-specific symptom, which means that it has many possible causes. Some common causes of nausea are gastroenteritis and other gastrointestinal disorders, food poisoning, motion sickness, dizziness, migraine, fainting, low blood sugar, anxiety, and lack of sleep. Nausea is a side effect of many medications including chemotherapy, or morning sickness in early pregnancy. Nausea may also be caused by disgust and depression.Medications taken to prevent and treat nausea and vomiting are called antiemetics. The most commonly prescribed antiemetics in the US are promethazine, metoclopramide, and the newer ondansetron. The word nausea is from Latin nausea, from Greek ναυσία – nausia, "ναυτία" – nautia, motion sickness, "feeling sick or queasy". Causes
Gastrointestinal infections (37%) and food poisoning are the two most common causes of acute nausea and vomiting. Side effects from medications (3%) and pregnancy are also relatively frequent. There are many causes of chronic nausea. Nausea and vomiting remain undiagnosed in 10% of the cases. Aside from morning sickness, there are no sex differences in complaints of nausea. After childhood, doctor consultations decrease steadily with age. Only a fraction of one percent of doctor visits by those over 65 are due to nausea. | According to Apollodorus, the Cyclopes also provided Poseidon with his trident and Hades with his cap of invisibility, and the gods used these weapons to defeat the Titans. Although the primordial Cyclopes of the Theogony were presumably immortal (as were their brothers the Titans), the sixth-century BC Hesiodic Catalogue of Women, has them being killed by Apollo. Later sources tell us why: Apollos son Asclepius had been killed by Zeus thunderbolt, and Apollo killed the Cyclopes, the makers of the thunderbolt, in revenge. According to a scholiast on Euripides Alcestis, the fifth-century BC mythographer Pherecydes supplied the same motive, but said that Apollo, rather than killing the Cyclopes, killed their sons (one of whom he named Aortes) instead. No other source mentions any offspring of the Cyclopes. A Pindar fragment suggests that Zeus himself killed the Cyclopes to prevent them from making thunderbolts for anyone else.The Cyclopes prowess as craftsmen is stressed by Hesiod who says "strength and force and contrivances were in their works." Being such skilled craftsmen of great size and strength, later poets, beginning with the third-century BC poet Callimachus, imagine these Cyclopes, the primordial makers of Zeus thunderbolt, becoming the assistants of the smith-god Hephaestus, at his forge in Sicily, underneath Mount Etna, or perhaps the nearby Aeolian Islands. In his Hymn to Artemis, Callimachus has the Cyclopes on the Aeolian island of Lipari, working "at the anvils of Hephaestus", make the bows and arrows used by Apollo and Artemis. | 0-1
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Hemifacial microsomia (HFM) is a congenital disorder that affects the development of the lower half of the face, most commonly the ears, the mouth and the mandible. It usually occurs on one side of the face, but both sides are sometimes affected. If severe, it may result in difficulties in breathing due to obstruction of the trachea—sometimes even requiring a tracheotomy. With an incidence in the range of 1:3500 to 1:4500, it is the second most common birth defect of the face, after cleft lip and cleft palate. [1] HFM shares many similarities with Treacher Collins syndrome. Presentation
The clinical presentation of HFM is quite variable. The severity may depend on the extent of the area with an insufficient blood supply in utero, and the gestational age of the fetus at which this occurs. In some people, the only physical manifestation may be a small and underdeveloped external ear. In more severe cases, multiple parts of the face may be affected. Some people with HFM may have sensorineural hearing loss and decreased visual acuity or even blindness.It can be thought of as a particularly severe form of HFM, in which extracranial anomalies are present to some extent. Some of the internal organs (especially the heart, kidneys, and lungs) may be underdeveloped, or in some cases even absent altogether. The affected organs are typically on the same side as the affected facial features, but bilateral involvement occurs in approximately 10% of cases. | Christianson syndrome is an X linked syndrome associated with intellectual disability, microcephaly, seizures, ataxia and absent speech. Presentation
Onset of symptoms is normally within the first year of life with truncal ataxia and seizures. The head is small (microcephaly). Common facial abnormalities include:
Long narrow face
Prominent nose
Prominent jaw
Large ears
Open mouth
Thick eyebrowsOther common features include:
Uncontrolled drooling
Abnormal eye movementsThe associated intellectual disability is usually in the profound range. Those affected often have a happy demeanor with frequent smiling and spontaneous laughter. Genetics
This condition is caused by mutations in the SLC9A6 gene. This gene is located on the long arm of the X chromosome (Xq26.3). The gene encodes a sodium/hydrogen exchanger located in the endosomes. Mutations in this gene cause a rise in the pH of the endosomes.How this causes the clinical features is not known presently. The inheritance of this condition is X-linked dominant. Diagnosis
The diagnosis may be suspected on clinical grounds.It is made by sequencing the SLC9A6 gene. Differential diagnosis
Angelman syndrome
Spinocerebellar ataxia type 29
Management
There is presently no curative treatment. Management is supportive. Epidemiology
The prevalence is not known but this is considered to be a rare disease. History
This condition was first described in 1999. The causative mutation was discovered in 2008. == References == | 0-1
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In terms of weather, both unusually dry weather and unusually moist weather have been cited. The seemingly contradictory data can most likely be reconciled by proposing that B. dermatitidis prospers in its natural habitats in times of moisture and moderate warmth, but that inoculum formed during these periods remains alive for some time and can be released into the air by subsequent dust formation under dry conditions. Indeed, dust per se or construction potentially linked to dust has been associated with several outbreaks The data, then, tend to link blastomycosis to all weather, climate and atmospheric conditions except freezing weather, periods of snow cover, and extended periods of hot, dry summer weather in which soil is not agitated. Gender bias
Sex is another factor inconstantly linked to contraction of blastomycosis: though many studies show more men than women affected, some show no sex-related bias. As mentioned above, most cases are in middle aged adults, but all age groups are affected, and cases in children are not uncommon. Ethnic populations
Ethnic group or race is frequently investigated in epidemiological studies of blastomycosis, but is potentially confounded by differences in residence and in quality and accessibility of medical care, factors that have not been stringently controlled for to date. In the United States, some studies show a disproportionately high incidence and/or mortality rate for blastomycosis among Black people.In Canada, some studies, but not others, indicate that First Nations people have a disproportionately high incidence of blastomycosis. Incidence in First Nations children may be unusually high. | In these areas, there are about 1 to 2 cases per 100,000 per year. Less frequently, blastomycosis also occurs in Africa, the Middle East, India, and western North America. Blastomycosis also affects a broad range of non-human mammals, and dogs in particular are an order of magnitude more likely to contract the disease than humans. The ecological niche of Blastomyces in the wild is poorly understood, and it is unknown if there are any significant host animals.Blastomycosis has existed for millions of years but was first described by Thomas Caspar Gilchrist in 1894. Because of this, it is sometimes called "Gilchrists disease". Signs and symptoms
The symptoms of blastomycosis cover a wide range, overlapping with more common conditions; for this reason, blastomycosis has often been called "the great pretender". Many cases are asymptomatic or subclinical. Lung symptoms are common, because the lungs are infected in 79% of blastomycosis cases. However, in 25-40% of cases the disease also disseminates to other organs, including the skin.The extent and severity of symptoms depends in part on a persons immune status; less than 50% of healthy people with blastomycosis have symptoms, while immunocompromised patients are especially likely to have the disease spread beyond the lungs to other organs like the skin and bones.Blastomycosis manifests as a primary lung infection in about 79% of cases. The onset is relatively slow and symptoms are suggestive of bacterial pneumonia, often leading to initial treatment with antibacterials. | 11
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There is tentative evidence that children with recurrent acute otitis media (AOM) who receive tubes have a modest improvement in the number of further AOM episodes (around one fewer episode at six months and less of an improvement at 12 months following the tubes being inserted). Evidence does not support an effect on long-term hearing or language development. A common complication of having a tympanostomy tube is otorrhea, which is a discharge from the ear. The risk of persistent tympanic membrane perforation after children have grommets inserted may be low. It is still uncertain whether or not grommets are more effective than a course of antibiotics.Oral antibiotics should not be used to treat uncomplicated acute tympanostomy tube otorrhea. They are not sufficient for the bacteria that cause this condition and have side effects including increased risk of opportunistic infection. In contrast, topical antibiotic eardrops are useful. Otitis media with effusion
The decision to treat is usually made after a combination of physical exam and laboratory diagnosis, with additional testing including audiometry, tympanogram, temporal bone CT and MRI. Decongestants, glucocorticoids, and topical antibiotics are generally not effective as treatment for non-infectious, or serous, causes of mastoid effusion. Moreover, it is recommended against using antihistamines and decongestants in children with OME. In less severe cases or those without significant hearing impairment, the effusion can resolve spontaneously or with more conservative measures such as autoinflation. | Furthermore, it has been demonstrated that individuals with otitis media have more depression/anxiety-related disorders compared to individuals with normal hearing. Once the infections resolve and hearing thresholds return to normal, childhood otitis media may still cause minor and irreversible damage to the middle ear and cochlea. More research on the importance of screening all children under 4 years old for otitis media with effusion needs to be performed. Epidemiology
Acute otitis media is very common in childhood. It is the most common condition for which medical care is provided in children under five years of age in the US. Acute otitis media affects 11% of people each year (709 million cases) with half occurring in those below five years. Chronic suppurative otitis media affects about 5% or 31 million of these cases with 22.6% of cases occurring annually under the age of five years. Otitis media resulted in 2,400 deaths in 2013—down from 4,900 deaths in 1990. Etymology
The term otitis media is composed of otitis, Ancient Greek for "inflammation of the ear", and media, Latin for "middle". References
External links
Neff MJ (June 2004). "AAP, AAFP, AAO-HNS release guideline on diagnosis and management of otitis media with effusion". American Family Physician. 69 (12): 2929–31. PMID 15222658. | 11
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Treatment of P. vivax requires both treatment of blood stages (with chloroquine or artemisinin-based combination therapy) and clearance of liver forms with an 8-aminoquinoline agent such as primaquine or tafenoquine.To treat malaria during pregnancy, the WHO recommends the use of quinine plus clindamycin early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters). There is limited safety data on the antimalarial drugs in pregnancy. Severe and complicated malaria
Cases of severe and complicated malaria are almost always caused by infection with P. falciparum. The other species usually cause only febrile disease. Severe and complicated malaria cases are medical emergencies since mortality rates are high (10% to 50%).Recommended treatment for severe malaria is the intravenous use of antimalarial drugs. For severe malaria, parenteral artesunate was superior to quinine in both children and adults. In another systematic review, artemisinin derivatives (artemether and arteether) were as efficacious as quinine in the treatment of cerebral malaria in children. Treatment of severe malaria involves supportive measures that are best done in a critical care unit. This includes the management of high fevers and the seizures that may result from it. It also includes monitoring for poor breathing effort, low blood sugar, and low blood potassium. Artemisinin derivatives have the same or better efficacy than quinolones in preventing deaths in severe or complicated malaria. Quinine loading dose helps to shorten the duration of fever and increases parasite clearance from the body. | Recrudescence is when symptoms return after a symptom-free period and the origin is parasites that survived in the blood as a result of inadequate or ineffective treatment. Relapse is when symptoms reappear after the parasites have been eliminated from the blood and the recurrence source is activated parasites which had persisted as dormant hypnozoites in liver cells. Relapse commonly occurs after 8–24 weeks and is often seen in P. vivax and P. ovale infections. However, relapse-like P. vivax recurrences are probably being over-attributed to hypnozoite activation. Some of them might have an extra-vascular or sequestered merozoite origin, making those recurrences recrudescences, not relapses. Newly recognised, non-hypnozoite, possible contributing sources to recurrent peripheral P. vivax parasitemia are erythrocytic forms in the bone marrow and spleen. P. vivax malaria cases in temperate areas often involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite. Reinfection means that the parasites responsible for the past infection were eliminated from the body but a new parasite(s) was introduced. Reinfection cannot readily be distinguished from relapse and recrudescence, although recurrence of infection within two weeks of treatment for the initial malarial manifestations is typically attributed to treatment failure. But doing this is not necessarily correct. People may develop some immunity when exposed to frequent infections. Pathophysiology
Malaria infection develops via two phases: one that involves the liver (exoerythrocytic phase), and one that involves red blood cells, or erythrocytes (erythrocytic phase). | 11
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In his landmark work On the Sacred Disease, he proposed that epilepsy was not divine in origin and instead was a medically treatable problem originating in the brain. He accused those of attributing a sacred cause to the disease of spreading ignorance through a belief in superstitious magic. Hippocrates proposed that heredity was important as a cause, described worse outcomes if the disease presents at an early age, and made note of the physical characteristics as well as the social shame associated with it. Instead of referring to it as the sacred disease, he used the term great disease, giving rise to the modern term grand mal, used for tonic–clonic seizures. Despite his work detailing the physical origins of the disease, his view was not accepted at the time. Evil spirits continued to be blamed until at least the 17th century.In Ancient Rome people did not eat or drink with the same pottery as that used by someone who was affected. People of the time would spit on their chest believing that this would keep the problem from affecting them. According to Apuleius and other ancient physicians, in order to detect epilepsy, it was common to light a piece of gagates, whose smoke would trigger the seizure. Occasionally a spinning potters wheel was used, perhaps a reference to photosensitive epilepsy.In most cultures, persons with epilepsy have been stigmatized, shunned, or even imprisoned. | A phoenix abscess is an acute exacerbation of a chronic periapical lesion. It is a dental abscess that can occur immediately following root canal treatment. Another cause is due to untreated necrotic pulp (chronic apical periodontitis). It is also the result of inadequate debridement during the endodontic procedure. Risk of occurrence of a phoenix abscess is minimised by correct identification and instrumentation of the entire root canal, ensuring no missed anatomy. Treatment involves repeating the endodontic treatment with improved debridement, or tooth extraction. Antibiotics might be indicated to control a spreading or systemic infection. Causes
Phoenix abscesses are believed to be due to a changing internal environment of the root canal system during the instrumentation stage of root canal treatment, causing a sudden worsening of the symptoms of chronic periradicular periodontitis. This instrumentation is thought to stimulate the residual microbes in the root canal space to cause an inflammatory reaction. These microbes are predominantly facultative anaerobic gram-positive bacteria, such as Streptococcus, Enterococcus and Actinomyces species. Another cause of a phoenix abscess is a decrease in a patients resistance to these bacteria and their products. Signs & Symptoms
Clinical Features
PainA common clinical feature is exacerbated and exaggerated pain. There may or may not be associated with pus & suppuration. The signs & symptoms are similar to that of an acute periradicular abscess, but with a periradicular radiolucency present as well. Loss of VitalityThe problematic tooth will have a non-vital pulp with no previous symptoms. Vitality of teeth can be assessed through various means. | 0-1
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Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries, and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss; it is not the result of increased CSF pressure. Mechanism
Hydrocephalus is usually due to blockage of CSF outflow in the ventricles or in the subarachnoid space over the brain. In a person without hydrocephalus, CSF continuously circulates through the brain, its ventricles and the spinal cord and is continuously drained away into the circulatory system. Alternatively, the condition may result from an overproduction of the CSF, from a congenital malformation blocking normal drainage of the fluid, or from complications of head injuries or infections.Compression of the brain by the accumulating fluid eventually may cause neurological symptoms such as convulsions, intellectual disability, and epileptic seizures. These signs occur sooner in adults, whose skulls are no longer able to expand to accommodate the increasing fluid volume within. Fetuses, infants, and young children with hydrocephalus typically have an abnormally large head, excluding the face, because the pressure of the fluid causes the individual skull bones—which have yet to fuse—to bulge outward at their juncture points. | Hydrocephalus was described more clearly by the ancient Greek physician Hippocrates in the fourth century BC, while a more accurate description was later given by the Roman physician Galen in the second century AD.The first clinical description of an operative procedure for hydrocephalus appears in the Al-Tasrif (1,000 AD) by the Arab surgeon Abulcasis, who clearly described the evacuation of superficial intracranial fluid in hydrocephalic children. He described it in his chapter on neurosurgical disease, describing infantile hydrocephalus as being caused by mechanical compression. He wrote:
The skull of a newborn baby is often full of liquid, either because the matron has compressed it excessively or for other, unknown reasons. The volume of the skull then increases daily, so that the bones of the skull fail to close. In this case, we must open the middle of the skull in three places, make the liquid flow out, then close the wound and tighten the skull with a bandage. In 1881, a few years after the landmark study of Retzius and Key, Carl Wernicke pioneered sterile ventricular puncture and external drainage of CSF for the treatment of hydrocephalus. It remained an intractable condition until the 20th century, when cerebral shunt and other neurosurgical treatment modalities were developed.It is a lesser-known medical condition; relatively little research is conducted to improve treatment, and still no cure has been found. In developing countries, the condition often goes untreated at birth. Before birth, the condition is difficult to diagnose, and access to medical treatment is limited. | 11
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To date there are no ultrasound courses which teach the identification of nuchal cord to physicians or technicians. A recent review by Wilson of the American Academy of Ultrasonography Technicians recommends the documentation of umbilical cord issues. Classification
A "Type A" nuchal cord is wrapped around the neck but is free sliding
A "Type B" pattern is described as a hitch which cannot be undone and ends up as a true knot. Treatment
Management of a presenting nuchal cord should be tailored to prevent umbilical cord compression whenever possible. Techniques to preserve an intact nuchal cord depend on how tightly the cord is wrapped around the infant’s neck. If the cord is loose, it can easily be slipped over the infant’s head. The infant can be delivered normally and placed on maternal abdomen as desired. If the cord is too tight to go over the infant’s head, the provider may be able to slip it over the infant’s shoulders and deliver the body through the cord. The cord can then be unwrapped from around the baby after birth. Finally, if the cord is too tight to slip back over the shoulders, one may use the somersault maneuver to allow the body to be delivered. The birth attendant may also choose to clamp and cut the umbilical cord to allow for vaginal delivery if other methods of nuchal cord management are not feasible. | Localized hypertrichosis may refer to:
Localized acquired hypertrichosis
Localized congenital hypertrichosisSee also:
Hypertrichosis | 0-1
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Canada
In Canada, prasterone is a Controlled Drug listed under Section 23 of Schedule IV of the Controlled Drugs and Substances Act and as such is available by prescription only. United Kingdom
Prasterone is listed as an anabolic steroid and is thus a class C controlled drug. United States
Prasterone is legal to sell in the United States as a dietary supplement. It is currently grandfathered in as an "Old Dietary Ingredient" being on sale prior to 1994. Prasterone is specifically exempted from the Anabolic Steroid Control Act of 1990 and 2004. Sports and athletics
Prasterone is banned from use in athletic competition. It is a prohibited substance under the World Anti-Doping Code of the World Anti-Doping Agency, which manages drug testing for Olympics and other sports. Yulia Efimova, who holds the world record pace for both the 50-meter and 200-meter breaststroke, and won the bronze medal in the 200-meter breaststroke in the 2012 London Olympic Games, tested positive for prasterone in an out-of-competition doping test. Rashard Lewis, then with the Orlando Magic, tested positive for prasterone and was suspended 10 games before the start of the 2009–10 season. In 2016 MMA fighter Fabio Maldonado revealed he was taking prasterone during his time with the UFC. In January 2011, NBA player O. J. Mayo was given a 10-game suspension after testing positive for prasterone. Mayo termed his use of prasterone as "an honest mistake," saying the prasterone was in an over-the-counter supplement and that he was unaware the supplement was banned by the NBA. | Prasterone was under development for the treatment of systemic lupus erythematosus in the United States and Europe in the 1990s and 2000s and reached phase III clinical trials and preregistration for this indication, respectively, but ultimately development was not continued past 2010. Memory
Prasterone supplementation has not been found to be useful for memory function in normal middle aged or older adults. It has been studied as a treatment for Alzheimers disease, but there is no evidence that it is effective or ineffective. More research is needed to determine its benefits. Mood
A few small, short term clinical studies have found that prasterone improves mood but its long-term efficacy and safety, and how it compares to antidepressants, was unknown as of 2015. References
Further reading
Keppel Hesselink JM (December 1997). "[Prasterone (dihydroepiandrosterone): a modern source of eternal youth?]". Ned Tijdschr Geneeskd (in Dutch). 141 (51): 2484–7. PMID 9555138. Zelissen PM, Thijssen JH (October 2001). "[Role of prasterone (dehydroepiandrosterone) in substitution therapy for adrenocortical insufficiency]". Ned Tijdschr Geneeskd (in Dutch). 145 (42): 2018–22. PMID 11695098. Pope, JE; Cupp, MJ; Tracy, TS (2003). Dehydroepiandrosterone (DHEA) (Prasterone). Dietary Supplements. Totowa, NJ: Humana Press. pp. 123–147. doi:10.1007/978-1-59259-303-3_8 (inactive 31 July 2022). ISBN 9781592593033. {{cite book}}: CS1 maint: DOI inactive as of July 2022 (link)
Kocis P (November 2006). "Prasterone". Am J Health Syst Pharm. 63 (22): 2201–10. doi:10.2146/ajhp060100. PMID 17090740. Mendivil Dacal JM, Borges VM (April 2009). "[Dehydroepiandrosterone (DHEA), review of its efficiency in the managing of the libido decrease and other symptoms of aging]". Actas Urol Esp (in Spanish). 33 (4): 390–401. doi:10.4321/s0210-48062009000400009. | 11
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One way in which a vertical jaw abnormality can occur is if the condylar growth process is damaged, and thus the intramembranous growth continues along the posterior condylar margin, becoming predominant, thus resulting in a high angle type.Assessing a patient for vertical and horizontal excess
The Maxillary Mandibular Plane Angle (MMPA) is important in assessing a patient for vertical jaw abnormality. The important landmarks are the Frankfurt plane and the Mandibular plane. The Frankfurt plane is a line charted from the upper border of external auditory meatus to the lower border of the orbit. It is similar to the ala-tragus line however should not be confused with it. Whereas the Mandibular angle is a line measured along the natural lower border of the patients mandible. The intersection of the Frankfurt and Mandibular plane is what determines the pattern of vertical growth. If the intersection occurs behind the occiput i.e. decreased angle, then the patient is considered to have horizontal growth. On the other hand, if the intersection occurs in front of the occiput, then the patient is considered to have vertical growth. The normal range is considered to be between 25 and 30 degrees in a typical Caucasian person. Those with excess vertical jaw growth are most often seen having an anterior open bite, as the mandible is growing away from the maxilla. Whereas those with excessive horizontal growth are seen as having an overbite. | Supraclavicular lymph nodes are lymph nodes found above the clavicle, that can be felt in the supraclavicular fossa. The supraclavicular lymph nodes on the left side are called Virchows nodes. It leads to an appreciable mass that can be recognized clinically, called Troisier sign. Structure
A Virchows node is a left-sided supraclavicular lymph node. Clinical significance
Malignancies of the internal organs can reach an advanced stage before giving symptoms. Stomach cancer, for example, can remain asymptomatic while metastasizing. One of the first visible spots where these tumors metastasize is one of the left supraclavicular lymph node. Virchows nodes take their supply from lymph vessels in the abdominal cavity, and are therefore sentinel lymph nodes of cancer in the abdomen, particularly gastric cancer, ovarian cancer, testicular cancer and kidney cancer, that has spread through the lymph vessels, and Hodgkins lymphoma. Such spread typically results in Troisiers sign, which is the finding of an enlarged, hard Virchows node.The left supraclavicular nodes are the classical Virchows node because they receive lymphatic drainage of most of the body (from the thoracic duct) and enters the venous circulation via the left subclavian vein. The metastasis may block the thoracic duct leading to regurgitation into the surrounding Virchows nodes. Another concept is that one of the supraclavicular nodes corresponds to the end node along the thoracic duct and hence the enlargement.Differential diagnosis of an enlarged Virchows node includes lymphoma, various intra-abdominal malignancies, breast cancer, and infection (e.g. of the arm). | 0-1
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This is because in both the hip and shoulder joints the metaphysis is intra-articular which in turn facilitates the spread of hematogenous osteomyelitis into the joint cavity. Conversely, joint sepsis may spread to the metaphysis and induce osteomyelitis. Acute exacerbation of juvenile idiopathic arthritis and transient synovitis of the hip both of which are non-septic conditions may mimic septic arthritis. More serious and life-threatening disorders as bone malignancies e.g. Ewing sarcoma and osteosarcoma may mimic septic arthritis associated with concurrent acute hematogenous osteomyelitis. In this regard, Magnetic resonance imaging may play an important role in the differential diagnosis. Joint aspiration
In children, joint synovial fluid aspiration techniques aim at isolating the infectious organism by culture and sensitivity analysis. Cytological analysis of the joint aspirate can point to septic arthritis. However, a negative culture and sensitivity test does not rule out the presence of septic arthritis. Various clinical scenarios and technique-related factors may impact the validity of results of the culture and sensitivity. Additionally, results of cytological analysis, though important, should not be interpreted in isolation of the clinical settings. In the joint fluid, the typical white blood cell count in septic arthritis is over 50,000-100,000 cells per 10−6/l (50,000-100,000 cell/mm3); where more than 90% are neutrophils is suggestive of septic arthritis. For those with prosthetic joints, white cell count more than 1,100 per mm3 with neutrophil count greater than 64% is suggestive of septic arthritis. However, septic synovial fluid can have white blood cell counts as low as a few thousand in the early stages. | One or multiple joints can be affected at the same time.Laboratory studies such as blood cultures, white blood cell count with differential, ESR, and CRP should also be included. However, white cell count, ESR, and CRP are nonspecific and could be elevated due to infection elsewhere in the body. Serologic studies should be done if lyme disease is suspected. Blood cultures can be positive in 25 to 50% of those with septic arthritis due to spread of infection from the blood. CRP more than 20 mg/L and ESR greater than 20 mm/hour together with typical signs and symptoms of septic arthritis should prompt arthrocentesis from the affected joint for synovial fluid examination.The synovial fluid should be collected before the administration of antibiotics and should be sent for gram stain, culture, leukocyte count with differential, and crystal studies. This can include NAAT testing for N. gonorrhoeae if suspected in a sexually active person.In children, the Kocher criteria is used for diagnosis of septic arthritis. Differential diagnosis
The differential diagnosis of septic arthritis is broad and challenging. First, it has to be differentiated from acute hematogenous osteomyelitis. This is because the treatment lines of both conditions are not identical. Noteworthy, septic arthritis and acute hematogenous osteomyelitis can co-occur. Especially in the hip and shoulder joints their co-occurrence is likely and represents a diagnostic challenge. Therefore, physicians should have a high suspicion index in that regard. | 11
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One reviewer has commented on the difficulty of clarifying the core characteristics of and differences between atypical attachment styles and ways of categorizing more severe disorders of attachment.As of 2010, the American Psychiatric Association has proposed to redefine RAD into two distinct disorders in the DSM-V. Corresponding with the inhibited type, one disorder will be reclassified as Reactive Attachment Disorder of Infancy and Early Childhood.In regards to pathogenic care, or the type of care in which these behaviors are present, a new criterion for Disinhibited Social Engagement Disorder now includes chronically harsh punishment or other types of severely inept caregiving. Relating to pathogenic care for both proposed disorders, a new criterion is rearing in atypical environments such as institutions with high child/caregiver ratios that cut down on opportunities to form attachments with a caregiver. Differential diagnosis
The diagnostic complexities of RAD mean that careful diagnostic evaluation by a trained mental health expert with particular expertise in differential diagnosis is considered essential. Several other disorders, such as conduct disorders, oppositional defiant disorder, anxiety disorders, post traumatic stress disorder and social phobia share many symptoms and are often comorbid with or confused with RAD, leading to over and under diagnosis. RAD can also be confused with neuropsychiatric disorders such as autism, pervasive developmental disorder, childhood schizophrenia and some genetic syndromes. Infants with this disorder can be distinguished from those with organic illness by their rapid physical improvement after hospitalization. Autistic children are likely to be of normal size and weight and often exhibit a degree of intellectual disability. | Surgery is the last option for most cases as the result may not be satisfactory. Etymology
The name is derived from the ancient Greek words kamptos (bent) and daktylos (finger). See also
Clinodactyly
References
External links
Media related to camptodactyly at Wikimedia Commons
The dictionary definition of camptodactyly at Wiktionary | 0-1
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Gene conversion occurs when the intact SBDS gene and its pseudogene copy aberrantly recombine at meiosis, leading to an incorporation of pseudogene-like sequences into the otherwise functional copy of the SBDS gene, thereby inactivating it.Two gene conversion mutations predominate in SDS patients. One is a splice site mutation affecting the 5 splice site of intron two, while the second is an exon two nonsense mutation. The marked absence of patients homozygous for the otherwise common nonsense mutation suggested that the SBDS gene is essential. Consistent with this, knockout of the mouse gene leads to early embryonic lethality. This, in turn, suggests that the common splice site mutation seen in patients may be hypomorphic, i.e. that it results in only a partial loss of function, whereas the complete loss of SBDS function is likely to be lethal. Mechanisms
The SBDS gene is expressed in all tissues and encodes a protein of 250 amino acid residues. A great deal of indirect evidence suggested that the SBDS protein may be involved in an aspect of cellular RNA metabolism or ribosome assembly or function. The wide occurrence of the gene in all archaea and eukaryotes supported a role for this protein in a very fundamental and evolutionarily conserved aspect of cellular biology. The homologous genes in archaea also tend to be present in conserved cluster enriched for RNA processing and ribosomal genes. A specific function for SBDS in RNA metabolism or ribosome assembly or function is further supported by its localization to the nucleolus, the nuclear subdomain where these processes occur. | APP tends to occur in women more frequently than in men, and is usually less severe than other forms of generalized pustular psoriasis such as impetigo herpetiformis. This form of psoriasis is characterized by ring-shaped plaques with pustules around the edges and yellow crusting. APP most often affects the torso, neck, arms, and legs. Diagnosis
Classification
Pustular psoriasis is classified into two major forms: localized and generalized pustular psoriasis. Within these two categories there are several variants:
Management
injection of methotrexate
References
== External links == | 0-1
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H, or h, is the eighth letter in the Latin alphabet, used in the modern English alphabet, the alphabets of other western European languages and others worldwide. Its name in English is aitch (pronounced , plural aitches), or regionally haitch . History
The original Semitic letter Heth most likely represented the voiceless pharyngeal fricative (ħ). The form of the letter probably stood for a fence or posts. The Greek Eta Η in archaic Greek alphabets, before coming to represent a long vowel, /ɛː/, still represented a similar sound, the voiceless glottal fricative /h/. In this context, the letter eta is also known as Heta to underline this fact. Thus, in the Old Italic alphabets, the letter Heta of the Euboean alphabet was adopted with its original sound value /h/. While Etruscan and Latin had /h/ as a phoneme, almost all Romance languages lost the sound—Romanian later re-borrowed the /h/ phoneme from its neighbouring Slavic languages, and Spanish developed a secondary /h/ from /f/, before losing it again; various Spanish dialects have developed [h] as an allophone of /s/ or /x/ in most Spanish-speaking countries, and various dialects of Portuguese use it as an allophone of /ʀ/. H is also used in many spelling systems in digraphs and trigraphs, such as ch, which represents /tʃ/ in Spanish, Galician, and Old Portuguese; /ʃ/ in French and modern Portuguese; /k/ in Italian and French. Name in English
For most English speakers, the name for the letter is pronounced as and spelled "aitch" or occasionally "eitch". | These conditions are relatively uncommon.Conditions where the secondary polycythemia is not caused by physiologic adaptation, and occurs irrespective of body needs include:
Neoplasms – Renal cell carcinoma or liver tumors, von Hippel-Lindau disease, and endocrine abnormalities including pheochromocytoma and adrenal adenoma with Cushings syndrome. People whose testosterone levels are high because of the use of anabolic steroids, including athletes who abuse steroids, or people on testosterone replacement for hypogonadism or transgender hormone replacement therapy, may develop secondary polycythemia. Blood doping - Secondary polycythemia can be induced by endurance athletes that take erythropoietin-stimulating agents, receive blood transfusions, and take other measures to increase their red blood cell mass in an effort to increase oxygen transport capacity. Altered oxygen sensing
Inherited mutations in three genes which all result in increased stability of hypoxia-inducible factors, leading to increased erythropoietin production, have been shown to cause erythrocytosis:
Chuvash erythrocytosis is an autosomal recessive form of erythrocytosis which is endemic in patients from the Chuvash Republic in Russia. Chuvash erythrocytosis is associated with homozygosity for a C598T mutation in the von Hippel-Lindau gene (VHL), which is needed for the destruction of hypoxia-inducible factors in the presence of oxygen. Clusters of patients with Chuvash erythrocytosis have been found in other populations, such as on the Italian island of Ischia, located in the Bay of Naples. PHD2 erythrocytosis: Heterozygosity for loss-of-function mutations of the PHD2 gene are associated with autosomal dominant erythrocytosis and increased hypoxia-inducible factors activity. HIF2α erythrocytosis: Gain-of-function mutations in HIF2α are associated with autosomal dominant erythrocytosis and pulmonary hypertension. | 0-1
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Distraction
Research suggests that the drivers attention is affected by distracting sounds such as conversations and operating a mobile phone while driving. Many jurisdictions now restrict or outlaw the use of some types of phone within the car. Recent research conducted by British scientists suggests that music can also have an effect; classical music is considered to be calming, yet too much could relax the driver to a condition of distraction. On the other hand, hard rock may encourage the driver to step on the acceleration pedal, thus creating a potentially dangerous situation on the road.Cell phone use is an increasingly significant problem on the roads and as the U.S. National Safety Council compiled more than 30 studies postulating that hands-free is not a safer option, because the brain remains distracted by the conversation and cannot focus solely on the task of driving. Intent
Some traffic collisions are caused intentionally by a driver. For example, a collision may be caused by a driver who intends to commit vehicular suicide. Collisions may also be intentionally caused by people who hope to make an insurance claim against the other driver, or may be staged for such purposes as insurance fraud. Motor vehicles may also be involved in collisions as part of a deliberate effort to hurt other people, such as in a vehicle-ramming attack. Combinations of factors
Several conditions can combine to create a much worse situation, for example:
Combining low doses of alcohol and cannabis has a more severe effect on driving performance than either cannabis or alcohol in isolation. | The summary says:
The evidence shows the risk of having a crash is increased both for vehicles traveling slower than the average speed, and for those traveling above the average speed. The risk of being injured increases exponentially with speeds much faster than the median speed. The severity / lethality of a crash depends on the vehicle speed change at impact. There is limited evidence suggesting lower speed limits result in lower speeds on a system-wide basis. Most crashes related to speed involve speed too fast for the conditions. More research is needed to determine the effectiveness of traffic calming.In the U.S. in 2018, 9,378 people were killed in motor vehicle crashes involving at least one speeding driver, which accounted for 26% of all traffic-related deaths for the year.In Michigan in 2019, excessive speed was a factor in 18.8% of the fatalities that resulted from fatal motor vehicle crashes and in 15.6% of the suspected serious injuries resulting from crashes.The Road and Traffic Authority (RTA) of the Australian state of New South Wales (NSW) asserts speeding (traveling too fast for the prevailing conditions or above the posted speed limit) is a factor in about 40 percent of road deaths. The RTA also say speeding increases the risk of a crash and its severity. | 11
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In humans a similar mutation (G595E) has been associated with Schmid metaphyseal chondrodysplasia (SMCD), a relatively mild skeletal disorder that is also associated with dwarfism.The now-extinct Ancon sheep was created by humans through the selective breeding of common domestic sheep with achondroplasia. The average-sized torso combined with the relatively smaller legs produced by achondroplasia was valued for making affected sheep less likely to escape without affecting the amount of wool or meat each sheep produced. See also
Achondroplasia in children
List of radiographic findings associated with cutaneous conditions
References
External links
Achondroplasia at Curlie
Pauli RM (1998). "Achondroplasia". In Pagon RA, Bird TD, Dolan CR, et al. (eds.). GeneReviews. Seattle WA: University of Washington, Seattle. PMID 20301331. NBK1152. | Hypotonia is a condition that can be helped with early intervention. Signs and symptoms
Central hypotonia accounts for 60 to 80% of all hypotonia in infants. Hypotonic patients may display a variety of objective manifestations that indicate decreased muscle tone. Motor skills delay is often observed, along with hypermobile or hyperflexible joints, drooling and speech difficulties, poor reflexes, decreased strength, decreased activity tolerance, rounded shoulder posture, with leaning onto supports, and poor attention. The extent and occurrence of specific objective manifestations depends upon the age of the patient, the severity of the hypotonia, the specific muscles affected, and sometimes the underlying cause. For instance, some people with hypotonia may experience constipation, while others have no bowel problems. Floppy baby syndrome
The term "floppy infant syndrome" is used to describe abnormal limpness when an infant is born, affecting limbs, trunk, and head. Such condition may appear immediately after birth or during early life as inability to maintain proper posture during movement and rest. In severe cases, hypotonic infants often have difficulty feeding, as their mouth muscles cannot maintain a proper suck-swallow pattern, or a good breastfeeding latch. Developmental delay
Children with normal muscle tone are expected to achieve certain physical abilities within an average timeframe after birth. Most low-tone infants have delayed developmental milestones, but the length of delay can vary widely. Motor skills are particularly susceptible to the low-tone disability. They can be divided into two areas, gross motor skills, and fine motor skills, both of which are affected. | 0-1
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Often psychotherapy teaches coping skills while allowing the teens or children to explore feelings and events in a safe environment.Severe depression, low global functioning, higher scores on suicidality scales, co-existing anxiety, distorted thought processes and feelings of hopelessness are characteristics of adolescent depression that are associated with a poor response to psychotherapy. If there is concomitant family conflict then interpersonal therapy is more effective than cognitive therapy. Talk therapy is one of the best forms of therapy, as the depressed person finds a solace in the one whom he/she is talking to. Through this means, the counselor is able to know and understood fully the mind of the depressed individual. Many people are depressed and simply needs the right person to talk to. This is where the talk therapy comes in as a very helpful solution to those who are in need of it. Cognitive therapy
Cognitive therapy aims to change harmful ways of thinking and reframe negative thoughts in a more positive way. Aims of cognitive therapy include various steps of patient learning. During cognitive behavioral therapy, children and adolescents with depression work with therapists to learn about their diagnosis, how to identify and reshape negative thought patterns, and how to increase engagement in enjoyable activities. CBT-trained therapists work with individuals, families, and groups. The approach can be used to help anyone irrespective of ability, culture, race, gender, or sexual preference. It can be applied with or without concurrent psychopharmacological medication, depending on the severity or nature of each patients problem. | Hyperpituitarism is a condition due to the primary hypersecretion of pituitary hormones; it typically results from a pituitary adenoma. In children with hyperpituitarism, disruption of growth regulation is rare, either because of hormone hypersecretion or because of manifestations caused by local compression of the adenoma. Symptoms and signs
Symptoms caused by hormone excess and associated mass effects include:
Cause
The cause of hyperpituitarism in most cases is due to pituitary adenomas. They usually come from the anterior lobe, are functional and secrete the hormone, GH and prolactin. Mechanism
Evidence indicates that the mechanism of hyperpituitarism can originate from genetic disruption causing pituitary tumorigenesis, most pituitary adenomas are monoclonal, which in turn indicates their origin from an event in a single cell. There are three hormones that are oversecreted resulting in the pituitary adenoma: prolactin, adrenocorticotropic hormone (ACTH), and growth hormone (GH).Excess prolactin may result in a prolactinoma Excess GH results in gigantism, the severity of gigantism depends on whether the epiphyseal plate is open. The four most common types of hyperpituitarism are caused by 4 types of pituitary adenoma, as follows: prolactinoma, corticotropinoma (Cushings disease), somatotropinoma (gigantism), and thyrotropinoma . Diagnosis
For the diagnosis of hyperpituitarism it depends on the cell type(s) affected, clinical manifestations of hormone excess may include, gigantism or acromegaly, which can be identified by clinical and radiographic results. | 0-1
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However, similarly to the case of prostate cancer, arguments have been made for the use of bioidentical estrogens like estradiol instead of DES for breast cancer.Oral DES at 0.25 to 0.5 mg/day is effective in the treatment of hot flashes in men undergoing androgen deprivation therapy for prostate cancer.Although DES was used to support pregnancy, it was later found not to be effective for this use. Side effects
At more than 1 mg/day, DES is associated with high rates of side effects including nausea, vomiting, abdominal discomfort, headache, and bloating (incidence of 15–50%). Breast changes and feminization
The pigmentation of the breast areolae are often very dark and almost black with DES therapy. The pigmentation that occurs with synthetic estrogens such as DES is much greater than with natural estrogens such as estradiol. The mechanism of the difference is unknown. Progestogens like hydroxyprogesterone caproate have been reported to reduce the nipple hyperpigmentation induced by high-dose estrogen therapy.In men treated with it for prostate cancer, DES has been found to produce high rates of gynecomastia (breast development) of 41 to 77%. Blood clots and cardiovascular issues
In studies of DES as a form of high-dose estrogen therapy for men with prostate cancer, it has been associated with considerable cardiovascular morbidity and mortality. The risk is dose-dependent. A dosage of 5 mg/day DES has been associated with a 36% increase in non-cancer-related (mostly cardiovascular) deaths. In addition, there is an up to 15% incidence of venous thromboembolism. | A 3 mg/day dosage of DES has been associated with an incidence of thromboembolism of 9.6 to 17%, with an incidence of cardiovascular complications of 33.3%. A lower dosage of 1 mg/day DES has been associated with a rate of death due to cardiovascular events of 14.8% (relative to 8.3% for orchiectomy alone). Other long-term effects
DES has been linked to a variety of long-term adverse effects, such as increased risk of
vaginal clear-cell adenocarcinoma
vaginal adenosis
T-shaped uterus
uterine fibroids
cervical weakness
breast cancer
infertility
hypogonadism
intersexual gestational defects
depression,
and others,in women who were treated with it during pregnancy, and/or in their offspring.A comprehensive animal study in 1993 found a plethora of adverse effects from DES such as (but not limited to)
genotoxicity (due to quinone metabolite)
teratogenicity
penile and testicular hypoplasia
cryptorchidism (in rats and rhesus monkeys),
liver and renal cancer (in hamsters), ovarian papillary carcinoma (in canines), and
malignant uterine mesothelioma (in squirrel monkeys). Evidence was also found linking ADHD to F2 generations, demonstrating that there is at least some neurological and transgenerational effects in addition to the carcinogenic.Rodent studies reveal female reproductive tract cancers and abnormalities reaching to the F2 generation, and there is evidence of adverse effects such as irregular menstrual cycles intersexual in grandchildren of DES mothers. Additionally, evidence also points to transgenerational effects in F2 sons, such as hypospadias. At this time however, the extent of DES transgenerational effects in humans is not fully understood. Overdose
DES has been assessed in the past in clinical studies at extremely high doses of as much as 1,500 to 5,000 mg/day. | 11
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For another member of the gene family, mutations in the Notch1 gene are associated with bicuspid aortic valve, a valve with two leaflets instead of three. Notch1 is also associated with calcification of the aortic valve, the third most common cause of heart disease in adults.Mutations of a cell regulatory mechanism, the Ras/MAPK pathway are responsible for a variety of syndromes, including Noonan syndrome, LEOPARD syndrome, Costello syndrome and cardiofaciocutaneous syndrome in which there is cardiac involvement. While the conditions listed are known genetic causes, there are likely many other genes which are more subtle. It is known that the risk for congenital heart defects is higher when there is a close relative with one. Environmental
Known environmental factors include certain infections during pregnancy such as rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus). Alcohol exposure in the father also appears to increase the risk of congenital heart defects.Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both pre-pregnancy folate deficiency and diabetes have been implicated in some studies. Mechanism
There is a complex sequence of events that result in a well formed heart at birth and disruption of any portion may result in a defect. | Heart valve dysplasia is a congenital heart defect which affects the aortic, pulmonary, mitral, and tricuspid heart valves. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium. In dogs, tricuspid valve dysplasia can be similar to Ebsteins anomaly in humans.Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, Great Pyrenees, and sometimes the Papillon. It is inherited in the Labrador Retriever.The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. The prognosis is poor with significant heart enlargement. == References == | 0-1
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In particular, individuals who are homozygous for the G allele at the single nucleotide polymorphism (SNP) rs776746 (also known as CYP3A5 *3/*3) have a non-functional CYP3A5 protein. The frequency of the G allele varies worldwide, from 4% in some African populations to 80–90% in Caucasian populations. Across a large number of studies, individuals homozygous for the G allele have been shown to have higher concentrations of tacrolimus and require lower doses of the drug, as compared to individuals who are not homozygous for the G allele. Achieving target concentrations of tacrolimus is important – if levels are too low, then there is a risk of transplant rejection, if levels are too high, there is a risk of drug toxicities. There is evidence to suggest that dosing patients based on rs776746 genotype can result in faster and more frequent achievement of target tacrolimus levels. However, there is a lack of consistent evidence as to whether dosing based on rs776746 genotype results in improved clinical outcomes (such as a decreased risk for transplant rejection or drug toxicities), likely because patients taking tacrolimus are subject to therapeutic drug monitoring.Studies have shown that genetic polymorphisms of genes other than CYP3A5, such as NR1I2 (encoding PXR), also significantly influence the pharmacokinetics of tacrolimus. History
Tacrolimus was discovered in 1987; it was among the first macrolide immunosuppressants discovered, preceded by the discovery of rapamycin (sirolimus) on Rapa Nui (Easter Island) in 1975. It is produced by a soil bacterium, Streptomyces tsukubensis. | The name tacrolimus is derived from "Tsukuba macrolide immunosuppressant".Tacrolimus was first approved by the US Food and Drug Administration (FDA) in 1994, for use in liver transplantation; the indications were extended to include kidney transplants. Generic versions of tacrolimus were approved in the US in 2017.Tacrolimus was approved for medical use in the European Union in 2002, for the treatment of moderate to severe atopic dermatitis. In 2007, the indications were expanded to include the prophylaxis of transplant rejection in adult kidney or liver allograft recipients and the treatment of allograft rejection resistant to treatment with other immunosuppressive medicinal products in adults. In 2009, the indications were expanded to include the prophylaxis of transplant rejection in adult and paediatric, kidney, liver or heart allograft recipients and the treatment of allograft rejection resistant to treatment with other immunosuppressive medicinal products in adults and children. Available forms
A branded version of the drug is owned by Astellas Pharma, and is sold under the brand name Prograf, given twice daily. A number of other manufacturers hold marketing authorisation for alternative brands of the twice-daily formulation.Once-daily formulations with marketing authorisation include Advagraf (Astellas Pharma) and Envarsus (marketed as Envarsus XR in US by Veloxis Pharmaceuticals and marketed in Europe by Chiesi). These formulations are intended to reduce pharmacokinetic variation in blood levels and facilitate compliance with dosing.The topical formulation is marketed by LEO Pharma under the name Protopic. Biosynthesis
The biosynthesis of tacrolimus is hybrid synthesis of both type 1 polyketide synthases (PKS 1) and nonribosomal peptide syntheses (NRPS). | 11
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Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one third of people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those have permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial Doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm.The pathogenesis of cerebral vasospasm following subarachnoid hemorrhage is attributed to the higher levels of endothelin 1, a potent vasoconstrictor, and the lower levels of endothelial NOS (eNOS), a potent vasodilator. Both of which are produced from a series of events that begin from the inflammatory reaction caused by the products released from erythrocytes degradation. Following subarachnoid hemorrhage, different clotting factors and blood products are released into the surrounding perivascular spaces known as (Virchow-Robin spaces). The released clotting factors like; fibrinopeptides, thromboxane A2 and others lead to microthrombosis around near vessels that leads to extrinsic vasoconstriction of these vessels. | While it becomes more common with age, about 50% of people present under 55 years old. It is a form of stroke and comprises about 5 percent of all strokes. Surgery for aneurysms was introduced in the 1930s. Since the 1990s many aneurysms are treated by a less invasive procedure called endovascular coiling, which is carried out through a large blood vessel. Signs and symptoms
The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the head", or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head). About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage. Vomiting may be present, and 1 in 14 have seizures. Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.Neck stiffness usually presents six hours after initial onset of SAH. Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull). Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the hyaloid membrane, which envelops the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. | 11
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Defects in nuclear-encoded mitochondrial genes are associated with hundreds of clinical disease phenotypes including anemia, dementia, hypertension, lymphoma, retinopathy, seizures, and neurodevelopmental disorders.A study by Yale University researchers (published in the February 12, 2004, issue of the New England Journal of Medicine) explored the role of mitochondria in insulin resistance among the offspring of patients with type 2 diabetes. Other studies have shown that the mechanism may involve the interruption of the mitochondrial signaling process in body cells (intramyocellular lipids). A study conducted at the Pennington Biomedical Research Center in Baton Rouge, Louisiana showed that this, in turn, partially disables the genes that produce mitochondria. Mechanisms
The effective overall energy unit for the available body energy is referred to as the daily glycogen generation capacity, and is used to compare the mitochondrial output of affected or chronically glycogen-depleted individuals to healthy individuals. This value is slow to change in a given individual, as it takes between 18 and 24 months to complete a full cycle.The glycogen generation capacity is entirely dependent on, and determined by, the operating levels of the mitochondria in all of the cells of the human body; however, the relation between the energy generated by the mitochondria and the glycogen capacity is very loose and is mediated by many biochemical pathways. The energy output of full healthy mitochondrial function can be predicted exactly by a complicated theoretical argument, but this argument is not straightforward, as most energy is consumed by the brain and is not easily measurable. | Amyloid-related imaging abnormalities (ARIA) are abnormal differences seen in magnetic resonance imaging of the brain in patients with Alzheimers disease. ARIA is associated with amyloid-modifying therapies, particularly human monoclonal antibodies such as aducanumab. There are two types of ARIA: ARIA-E and ARIA-H. The phenomenon was first seen in trials of bapineuzumab. ARIA-E
ARIA-E refers to cerebral edema, involving the breakdown of the tight endothelial junctions of the blood-brain barrier and subsequent accumulation of fluid. In a double-blind trial of the humanised monoclonal antibody solanezumab (n = 2042), sixteen patients (11 taking the drug, 5 taking a placebo), or 0.78% developed ARIA-E. A further 7 patients developed ARIA-E during an open-label extension of the trial.The effect of ARIA-E depends on the severity and location of the edema. Symptoms may include headache, changes in mental state, confusion, vomiting, nausea, tremor and gait disturbances. ARIA-H
ARIA-H refers to cerebral microhaemorrhages (mH), small haemorrhages on the brain, often accompanied by hemosiderosis. mH are usually seen as small, round and low intensity lesions and are small haemosiderin deposits. Some studies define mH as being less than or equal to 10mm, while others define the cut-off as ≤ 5mm. The prevalence of mH in healthy elderly people is approximately 6%, but this value increases to between 50% and 80% in elderly people with cerebrovascular disease. ARIA MRI Classification Criteria
References
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Juvenile xanthogranuloma is a form of histiocytosis, classified as "non-Langerhans cell histiocytosis", or more specifically, "type 2".It is a rare skin disorder that primarily affects children under one year of age but can also be found in older children and adults. It was first described in 1905 by Adamson. In 5% to 17% of people, the disorder is present at birth, but the median age of onset is two years. JXG is a benign idiopathic cutaneous granulomatous tumor and the most common form of non-Langerhans cell histiocytosis (non-LHC). The lesions appear as orange-red macules or papules and are usually located on the face, neck, and upper trunk. They may also appear at the groin, scrotum, penis, clitoris, toenail, palms, soles, lips, lungs, bone, heart, and gastrointestinal tract more rarely. JXG usually manifests with multiple lesions on the head and neck in cases with children under six months of age. The condition usually resolves spontaneously over one to five years. A biopsy of the lesion is critical to confirm the diagnosis. Ocular JXG manifests in up to 10% of people with JXG and may affect their vision. The presence of JXG in the eye can cause spontaneous hyphema, secondary glaucoma or even blindness. It is most often seen in the iris but may be found on the eyelid, corneoscleral limbus, conjunctiva, orbit, retina, choroid, disc, or optic nerve. Of patients with ocular JXG, 92% are younger than the age of two. Although cutaneous JXG usually disappear spontaneously, ocular lesions rarely improve spontaneously and require treatment. | Treatments that have been used include surgical excision, intralesional steroid injection, cryotherapy, and low dose radiotherapy. In the case of a resistant or reoccurring lesion, chemotherapy has been used as a treatment. Ocular JXG is usually unilateral and presents with a tumor, a red eye with signs of uveitis, unilateral glaucoma, spontaneous hyphema or heterochromia iridis. Diagnosing and treating the patient as early as possible contributes to the most positive visual outcome. Histiocytic disorders like JXG are identified by the cells that make them up. Immunohistochemical analysis is used to discern the immunoreactivity to certain antibodies in these analyses. JXG is a non-LHC disorder which is a varied group of disorders defined by the accumulation of histiocytes that do not meet criteria to be diagnosed as Langerhans cells. JXG is not metastatic and may be present with lipid deposits. JXG is often accompanied with other disorders such as neurofibromatosis type one and juvenile chronic myelogenous leukemia. Juvenile variety xanthogranuloma can be distinguished from xanthoma by the spread of the lesion and the lack of lipid abnormalities. Other similar diagnoses include molluscum contagiosum, hemangioma and neurofibroma. See also
Non-X histiocytoses
List of cutaneous conditions
References
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In the same year, the Council of Europe became the first institution to state that intersex people have the right not to undergo sex affirmation interventions. Anti-discrimination and equal treatment
People born with intersex bodies are seen as different. Intersex infants, children, adolescents and adults "are often stigmatized and subjected to multiple human rights violations", including discrimination in education, healthcare, employment, sport, and public services. Several countries have so far explicitly protected intersex people from discrimination, with landmarks including South Africa, Australia, and, most comprehensively, Malta. Remedies and claims for compensation
Claims for compensation and remedies for human rights abuses include the 2011 case of Christiane Völling in Germany. A second case was adjudicated in Chile in 2012, involving a child and his parents. A further successful case in Germany, taken by Michaela Raab, was reported in 2015. In the United States, the Minor Child (M.C. v Aaronson) lawsuit was "a medical malpractice case related to the informed consent for a surgery performed on the Crawfords adopted child (known as M.C.) at [Medical University of South Carolina] in April 2006". The case was one of the first lawsuit of its kind to challenge "legal, ethical, and medical issues regarding genital-normalizing surgery" in minors, and was eventually settled out of court by the Medical University of South Carolina for $440,000 in 2017. Information and support
Access to information, medical records, peer and other counselling and support. | Dicheirus is a genus of beetles in the family Carabidae, containing the following species:
Dicheirus dilatatus Dejean, 1829
Dicheirus obtusus LeConte, 1852
Dicheirus piceus Menetries, 1845
Dicheirus pilosus G. Horn, 1880
Dicheirus strenuus G. Horn, 1868
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MDR-TB has a mortality rate of about 15% with treatment, which further depends on a number of factors, including:
How many drugs the organism is resistant to (the fewer the better)
How many drugs the patient is given (patients treated with five or more drugs do better)
The expertise and experience of the physician responsible
How co-operative the patient is with treatment (treatment is arduous and long, and requires persistence and determination on the part of the patient)
Whether the patient is HIV-positive or not (HIV co-infection is associated with increased mortality).The majority of patients with multidrug-resistant tuberculosis do not receive treatment, as they are found in underdeveloped countries or in poverty. Denial of treatment remains a difficult human rights issue, as the high cost of second-line medications often precludes those who cannot afford therapy.A study of cost-effective strategies for tuberculosis control supported three major policies. First, the treatment of smear-positive cases in DOTS programs must be the foundation of any tuberculosis control approach, and should be a basic practice for all control programs. Second, there is a powerful economic case for treating smear-negative and extra-pulmonary cases in DOTS programs along with treating smear-negative and extra-pulmonary cases in DOTS programs as a new WHO "STOP TB" approach and the second global plan for tuberculosis control. Last, but not least, the study shows that significant scaling-up of all interventions is needed in the next 10 years if the millennium development goal and related goals for tuberculosis control are to be achieved. | The structure of Aureomycin was elucidated in 1952 and published in 1954 by the Pfizer-Woodward group. After the discovery of the structure, researchers at Pfizer began chemically modifying aureomycin by treating it with hydrogen in the presence of a palladized carbon catalyst. This chemical reaction replaced a chlorine moiety with a hydrogen, creating a compound named tetracycline via hydrogenolysis. Tetracycline displayed higher potency, better solubility, and more favorable pharmacology than the other antibiotics in its class, leading to its FDA approval in 1954. The new compound was one of the first commercially successful semi-synthetic antibiotics that was used, and laid the foundation for the development of Sancycline, Minocycline, and later the Glycylcyclines. Evidence in antiquity
Our modern understanding of tetracyclines dates their discovery to 1948, but there is evidence that early inhabitants of Northeastern Africa consumed tetracycline antibiotics. Nubian mummies from between 350 and 550 C.E. were found to exhibit patterns of fluorescence identical with that of modern tetracycline labelled bone.Tetracycline has a high affinity for calcium and is incorporated into bones during the active mineralization of hydroxyapatite. When incorporated into bones, tetracycline can be identified using ultraviolet light.It is conjectured that the beer brewed at the time was the source of the tetracycline found in these bones. Society and culture
Price
According to data from EvaluatePharma and published in the Boston Globe, in the USA the price of tetracycline rose from $0.06 per 250-mg pill in 2013 to $4.06 a pill in 2015. | 0-1
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Cochlear hydrops (or cochlear Menieres or cochlear endolymphatic hydrops) is a condition of the inner ear involving a pathological increase of fluid affecting the cochlea. This results in swelling that can lead to hearing loss or changes in hearing perception. It is a form of endolymphatic hydrops and related to Menieres disease. Cochlear hydrops refers to a case of inner-ear hydrops that only involves auditory symptoms and does not cause vestibular issues. Cause and behavior
Cochlear hydrops refers to an increase in endolymphatic fluid in the inner ear. This build-up is either due to an overproduction or insufficient drainage of endolymph in the constant regulation of fluid in the inner ear. Usually, only one ear is affected. The root cause of the process is unclear and may vary from patient to patient, but can have auto-immune, viral, and/or allergic triggers, among others.The build-up of endolymph creates pressure in the scala media. This causes its diameter to increase, and the vestibular membrane to curve outwards in the direction of the vestibule. The changes to the membrane can result in changes to either the hearing perception or hearing threshold of a patient.Episodes are usually cyclical and symptoms fluctuate through time. Patients may be symptom-free between episodes, which themselves may progressively worsen, improve, or remain constant in severity or duration. | Depression or anxiety that the condition will worsen or progress to Menieres disease.As with Menieres disease, atypical, early, or mild cases may only present some symptoms. Diagnosis
Diagnosis is based on symptoms and a hearing test that documents a loss in the low and mid frequencies, usually only in one ear. For patients with mild or atypical hydrops, the hearing thresholds may be normal, but they may experience a subjective, unilateral distortion of sounds in lower frequencies, such as diplacusis or that voices are sounding "robotic". Patients may also mention a feeling of pressure or fullness in the ear.To objectively test for the presence of hydrops, an electrocochleography (or ECOG) procedure can be done to detect elevated inner ear pressure. It is also possible to reveal the presence of hydrops with an MRI.If vertigo is experienced, the diagnosis progresses to Menieres disease. This occurs if the fluid increase leads to a leak or rupture of the membranes in the inner ear, causing a mixture of perilymph and endolymph. Treatment
Treatment for cochlear hydrops is the same as for Menieres disease. Currently, no cure exists for either.If a patient has undergone sudden sensorineural hearing loss, a course of steroids is often prescribed in an attempt to recover the hearing. Steroids may be injected directly through the eardrum.Like Menieres Disease, a low salt diet is recommended as a preventative measure. A diuretic may be prescribed to help lower salt content.Betahistine is the most widely prescribed medication for the treatment of Menieres disease. | 11
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Menopause has been described as a subjective experience, with social and cultural factors playing a prominent role in the way menopause is experienced and perceived. The word menopause was invented by French doctors at the beginning of the nineteenth century. Some of them noted that peasant women had no complaints about the end of menses, while urban middle-class women had many troubling symptoms. Doctors at this time considered the symptoms to be the result of urban lifestyles of sedentary behaviour, alcohol consumption, too much time indoors, and over-eating, with a lack of fresh fruit and vegetables. Within the United States, social location affects the way women perceive menopause and its related biological effects. Research indicates that whether a woman views menopause as a medical issue or an expected life change is correlated with her socio-economic status. The paradigm within which a woman considers menopause influences the way she views it: Women who understand menopause as a medical condition rate it significantly more negatively than those who view it as a life transition or a symbol of aging.Ethnicity and geography play roles in the experience of menopause. American women of different ethnicities report significantly different types of menopausal effects. One major study found Caucasian women most likely to report what are sometimes described as psychosomatic symptoms, while African-American women were more likely to report vasomotor symptoms.It seems that Japanese women experience menopause effects, or konenki, in a different way from American women. | For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and increasing the urine osmolality.A low level of evidence, predominantly from observational studies, suggests that thiazide diuretics have a modest beneficial effect on bone mineral density and are associated with a decreased fracture risk when compared with people not taking thiazides. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation.The combination of fixed-dose preparation such as losartan/hydrochlorothiazide has added advantages of a more potent antihypertensive effect with additional antihypertensive efficacy at the dose of 100 mg/25 mg when compared to monotherapy. Adverse effects
Hypokalemia, or low blood levels of potassium are an occasional side effect. It can be usually prevented by potassium supplements or by combining hydrochlorothiazide with a potassium-sparing diuretic
Other disturbances in the levels of serum electrolytes, including hypomagnesemia (low magnesium), hyponatremia (low sodium), and hypercalcemia (high calcium)
Hyperuricemia (high levels of uric acid in the blood). All thiazide diuretics including hydrochlorothiazide can inhibit excretion of uric acid by the kidneys, thereby increasing serum concentrations of uric acid.This may increase the incidence of gout in doses of ≥ 25 mg per day and in more susceptible patients such as male gender of <60 years old. | 0-1
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Rubinstein–Taybi syndrome (RTS) is a rare genetic condition characterized by short stature, moderate to severe learning difficulties, distinctive facial features, and broad thumbs and first toes. Other features of the disorder vary among affected individuals. These characteristics are caused by a mutation or deletion in the CREBBP and/or EP300 gene located on chromosome 16. People with this condition have an increased risk of developing noncancerous and cancerous tumors, leukemia, and lymphoma. This condition is sometimes inherited as an autosomal dominant pattern and is uncommon. Many times it occurs as a de novo (not inherited) occurrence. It occurs in an estimated 1 in 125,000-300,000 births. Presentation
Rubinstein–Taybi syndrome presents itself from birth, and is usually hallmarked by delayed physical and cognitive growth.Typical features of the disorder include:
Broad thumbs and broad first toes and clinodactyly of the 5th finger
Mental disability
Small height, low bone growth, small head
Cryptorchidism in males
Unusual facies involving the eyes, nose, and palate
Anesthesia may be dangerous in these patients: "According to the medical literature, in some cases, individuals with Rubinstein–Taybi syndrome may have complications (e.g., respiratory distress and/or irregular heart beats [cardiac arrythmias]) associated with a certain muscle relaxant (succinylcholine) and certain anesthesia. Any situations requiring the administration of anesthesia or succinylcholine (e.g., surgical procedures) should be closely monitored by skilled professionals (Anesthesiologists)." Primary literature suggests the children may have a higher rate of cardiac physical and conduction abnormalities which may cause unexpected results with cardioactive medications. | Medical uses
Attention deficit hyperactivity disorder
Viloxazine is indicated to treat attention deficit hyperactivity disorder (ADHD) in children age 6 to 12 years, adolescents age 13 to 17 years, and adults.In a phase 3 regulatory randomized controlled trial of viloxazine for ADHD in adults, scores on the Attention-Deficit/Hyperactivity Disorder Investigator Symptom Rating Scale (AISRS) with viloxazine therapy decreased from 38.5 points at baseline to 23.0 points following treatment (–40%) and with placebo decreased from 37.6 points at baseline to 25.9 points (–31%). This gave a placebo-subtracted score difference (drug minus placebo), or improvement in scores attributable to the effects of viloxazine, of –3.7 points (–9%). Depression
Viloxazine was previously marketed as an antidepressant for the treatment of major depressive disorder. It was considered to be effective in mild to moderate as well as severe depression with or without co-morbid symptoms. The typical dose range for depression was 100 to 400 mg per day in divided doses administered generally two to three times per day. Available forms
Viloxazine is available for ADHD in the form of 100, 150, and 200 mg extended-release capsules. These capsules can be opened and sprinkled into food for easier administration. | 0-1
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In particular, HER2 is overexpressed in 13–22% of patients with gastric cancer. Of note, HER2 overexpression in gastric neoplasia is heterogeneous and comprises a minority of tumor cells (less than 10% of gastric cancers overexpress HER2 in more than 5% of tumor cells). Hence, this heterogeneous expression should be taken into account for HER2 testing, particularly in small samples such as biopsies, requiring the evaluation of more than one bioptic sample. Radiation
Radiation therapy (also called radiotherapy) may be used to treat stomach cancer, often as an adjuvant to chemotherapy and/or surgery. Lymphoma
MALT lymphomas can often be fully treated by treating an underlying H. pylori infection. This results in remission in about 80% of cases. Prognosis
The prognosis of stomach cancer is generally poor, because the tumor has often metastasized by the time of discovery, and most people with the condition are elderly (median age is between 70 and 75 years) at presentation. The average life expectancy after being diagnosed is around 24 months, and the five-year survival rate for stomach cancer is less than 10%.Almost 300 genes are related to outcomes in stomach cancer, with both unfavorable genes where high expression is related to poor survival and favorable genes where high expression is associated with longer survival times. Examples of poor prognosis genes include ITGAV, DUSP1 and P2RX7. Epidemiology
Worldwide, stomach cancer is the fifth most-common cancer with 952,000 cases diagnosed in 2012. It is more common both in men and in developing countries. | Tentative evidence indicates that treating H. pylori decreases the future risk. If stomach cancer is treated early, it can be cured. Treatments may include some combination of surgery, chemotherapy, radiation therapy, and targeted therapy. For certain subtypes of gastric cancer, cancer immunotherapy is an option as well. If treated late, palliative care may be advised. Some types of lymphoma can be cured by eliminating H. pylori. Outcomes are often poor, with a less than 10% five-year survival rate in the Western world for advanced cases. This is largely because most people with the condition present with advanced disease. In the United States, five-year survival is 31.5%, while in South Korea it is over 65% and Japan over 70%, partly due to screening efforts.Globally, stomach cancer is the fifth-leading type of cancer and the third-leading cause of death from cancer, making up 7% of cases and 9% of deaths. In 2018, it newly occurred in 1.03 million people and caused 783,000 deaths. Before the 1930s, in much of the world, including most Western developed countries, it was the most common cause of death from cancer. Rates of death have been decreasing in many areas of the world since then. This is believed to be due to the eating of less salted and pickled foods as a result of the development of refrigeration as a method of storing food. Stomach cancer occurs most commonly in East Asia and Eastern Europe. It occurs twice as often in males as in females. | 11
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Latency antibiotics: The time from PROM to labor is termed the latency period, and there is an inverse relationship between gestational age and the length of latency, meaning that the earlier the rupture, the longer it will take for labor to begin naturally. As expected, antibiotics given to mothers that experience PPROM serve to protect against infections during this lengthened latency period. Additionally, antibiotics increase the time that babies stay in the womb. Antibiotics dont seem to prevent death or make a difference in the long-term (years after the baby is born). But, because of the short-term benefits, routine use of antibiotics in PPROM is still recommended. The American Congress of Obstetricians and Gynecologists (ACOG) recommends a seven-day course of intravenous ampicillin and erythromycin followed by oral amoxicillin and erythromycin if watchful waiting is attempted before 34 weeks. Amoxicillin/clavulanic acid increases the risk of fetal bowel death (necrotizing enterocolitis) and should be avoided in pregnancy. Prophylactic antibiotics: If a woman is colonized with GBS, than the typical use of antibiotics during labor is recommended to prevent transmission of this bacteria to the fetus, regardless of earlier treatments. Controversial or not recommended
Preventative tocolysis (medications to prevent contractions): the use of tocolytic medications to prevent labor contractions is controversial. On the one hand, this can delay delivery and allow the fetus more time to develop and benefit from antenatal corticosteroid medication, on the other hand it increases the risk of infection or chorioamnionitis. | The use of tocolysis has not shown to benefit mom or baby and currently there is not enough data to recommend or discourage its use in the case of preterm PROM. Therapeutic tocolysis (medications to stop contractions): Once labor has started, using tocolysis to stop labor has not been shown to help, and is not recommended. Amnioinfusion: This treatment attempts to replace the lost amniotic fluid from the uterus by infusing normal saline fluid into the uterine cavity. This can be done through the vagina and cervix (transcervical amnioinfusion) or by passing a needle through the abdominal wall (transabdominal amnioinfusion). Current data suggests that this treatment prevents infection, lung problems, and fetal death. However, there have not been enough trials to recommend its routine use in all cases of PPROM. Home care: Typically women with PPROM are managed in the hospital, but, occasionally they opt to go home if watchful waiting is attempted. Since labor usually starts soon after PPROM, and infection, umbilical cord compression, and other fetal emergencies can happen very suddenly, it is recommended that women stay in the hospital in cases of PPROM after 24 weeks. Currently, there is not enough evidence to determine meaningful differences in safety, cost, and womens views between management at home vs. the hospital. Sealing membranes after rupture: Infection is the major risk associated with PROM and PPROM. | 11
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For the best care, patients should see a physician who regularly treats leptomeningeal cancer and is most up-to-date on medicines that penetrate the blood-brain barrier, how to treat the symptoms, and clinical trials that might include patients with leptomeningeal cancer. Risks of treatments
Both Chemotherapy and Radiotherapy are harmful to the body and most definitely the brain. Caution must be utilized in treating patients with NM. Another factor that makes treatment difficult is that there is no suitable method to evaluate the disease progression. Prognosis
The prognosis is generally poor with survival typically measured in months. The median survival time of patients without treatment is four to six weeks. The best prognoses are seen from NM due to breast cancer with the median overall survival of no more than six months after diagnosis of NM. Death is generally due to progressive neurological dysfunction. Treatment is meant to stabilize neurological function and prolong survival. Neurological dysfunction usually cannot be fixed but progressive dysfunction can be halted and survival may be increased to four to six months. It occurs in approximately 3-5% of cancer patients. The disease is usually terminal and if left untreated, the median survival is 4–6 weeks whereas if treated, the median survival can increase to 2–3 months. Treatment will be more effective if it is done on the primary tumor before it metastasizes to the brain or spinal cord. Patients with leukaemia achieve better results compared to patients with solid tumours who have undergone treatment. | Venous spread may occur when intra-abdominal or thoracic pressure increases and venous flow is retrograde which then allows tumor cells in the systemic venous system to enter the vertebral venous system. Centripetal migration from systemic tumors along perineural, invasion of nerve space, or perivascular spaces. Malignant cells can migrate along spinal or cranial nerve epineurium-perineurium, invade the subpial space, and travel along blood vessels into the endoneurial space, or invade the nerve parenchyma.Infiltration happens most often at the base of the brain, dorsal surface, and especially at the cauda equina, which is largely due to the effect of gravity. Once in the CSF, malignant cells can extend along the membrane surfaces or spread freely in the CSF and attach to other locations. These cells have the ability to penetrate the pial membrane and invade the spinal cord and cranial nerves. Infiltration to spinal cord
Infiltration from the subarachnoid space into the spinal cord occurs primarily along the perivascular tissues that surround blood vessels at the brain entrance. Infiltration from the anterior median fissure, a 3mm deep furrow on the anterior side of the spinal cord, to the anterior horn of the spinal cord, the ventral grey matter of the spinal cord, is found along the central artery. | 11
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Side effects
Dry mouth, urinary retention, headaches, vomiting, diarrhea, constipation, blurry vision are possible side effects of the medication. Since glycopyrronium reduces the bodys sweating ability, it can even cause hyperthermia and heat stroke in hot environments. The medication also induces drowsiness, an effect exacerbated by the consumption of alcohol. Pharmacology
Mechanism of action
Glycopyrronium competitively blocks muscarinic receptors, thus inhibiting cholinergic transmission. Pharmacokinetics
Glycopyrronium bromide affects the gastrointestinal tracts, liver and kidney but has a very limited effect on the brain and the central nervous system. In horse studies, after a single intravenous infusion, the observed tendencies of glycopyrronium followed a tri-exponential equation, by rapid disappearance from the blood followed by a prolonged terminal phase. Excretion was mainly in urine and in the form of an unchanged drug. Glycopyrronium has a relatively slow diffusion rate, and in a standard comparison to atropine, is more resistant to penetration through the blood-brain barrier and placenta. Research
It has been studied in asthma. References
External links
"Glycopyrronium bromide". Drug Information Portal. U.S. National Library of Medicine. "Glycopyrronium". Drug Information Portal. U.S. National Library of Medicine. | Follow-up
Within 3–7 days after commencing treatment, patients should be re-examined to determine whether the treatment was successful. Within 3 days, symptoms of ulcers should improve. Healing time of the ulcer depends mainly on size and can take more than two weeks for larger ulcers. In uncircumcised men, healing is slower if the ulcer is under the foreskin. Sometimes, needle aspiration or incision and drainage are necessary. Epidemiology
Although the prevalence of chancroid has decreased in the United States and worldwide, sporadic outbreaks can still occur in regions of the Caribbean and Africa. Like other sexually transmitted diseases, having chancroid increases the risk of transmitting and acquiring HIV. History
Chancroid has been known to humans since time of ancient Greeks. Some of important events on historical timeline of chancre are:
References
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Neurological effects
reducing electrical excitation
modulating release of acetylcholine
antagonising N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system and thus providing neuroprotection from excitoxicity. Diabetes mellitus
Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11.0 and 47.7%. Magnesium deficiency is strongly associated with high glucose and insulin resistance, which indicate that it is common in poorly controlled diabetes. Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications. Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile. However, their effect on cardiovascular risk in diabetes are to be determined. Homeostasis
Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll (chloroplasts), cocoa derivatives, nuts, wheat, seafood, and meat. It is absorbed primarily in the duodenum of the small intestine. The rectum and sigmoid colon can absorb magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.The body contains 21–28 grams of magnesium (0.864–1.152 mol). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium.The majority of serum magnesium is bound to chelators, including proteins and citrate. Roughly 33% is bound to proteins, and 5–10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7–2.3 mg/dL (0.69–0.94 mmol/L). | Replacement by mouth is appropriate for people with mild symptoms, while intravenous replacement is recommended for people with severe effects.Numerous oral magnesium preparations are available. In two trials of magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was less bioavailable than magnesium citrate, chloride, lactate or aspartate. Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate forms.Intravenous magnesium sulfate (MgSO4) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma. Food
Food sources of magnesium include leafy green vegetables, beans, nuts, and seeds. Epidemiology
The condition is relatively common among people in hospital. History
Magnesium deficiency in humans was first described in the medical literature in 1934. Plants
Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants dry matter and is necessary for normal plant growth. Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency, as does aluminium toxicity.Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll. Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal chlorosis, or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. | 11
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Physicians can biopsy the skin with a 3-mm circular punch tool and immediately fix the specimen in 2% paraformaldehyde lysine-periodate or Zambonis fixative. Specimens are sent to a specialized laboratory for processing and analysis where the small nerve fibers are quantified by a neuropathologist to obtain a diagnostic result.This skin punch biopsy measurement technique is called intraepidermal nerve fiber density (IENFD). The following table describes the IENFD values in males and females of a 3 mm biopsy 10 cm above the lateral malleolus (above ankle outer side of leg). Any value measured below the 0.05 Quantile IENFD values per age span, is considered a reliable positive diagnosis for small fiber peripheral neuropathy. Treatment
Treatment is based on the underlying cause, if any. Where the likely underlying condition is known, treatment of this condition is indicated to reduce progression of the disease and symptoms. For cases without those conditions, there is only symptomatic treatment. See also
Neuropathy
Polyneuropathy
Wartenbergs migratory sensory neuropathy
Burning feet syndrome
Electrochemical skin conductance
References
External links
Peripheral Neuropathy Fact Sheet – NINDS
[1] | Gustatory hyperhidrosis is excessive sweating classified under focal hyperhidrosis, that is, it is restricted to certain regions of the body. Affected people regularly experience this on the forehead (scalp), upper lip, perioral region, or sternum a few moments after eating spicy foods, tomato sauce, chocolate, coffee, tea, or hot soups.A common cause is trauma or damage to the nerve that passes through the parotid gland, which can be due to surgery of the parotid gland (parotidectomy). This type of sweating is known as Freys syndrome. Gustatory hyperhidrosis has been observed in diabetics with autonomic neuropathy, and a variant of this disorder has been reported following surgical sympathectomy.Around 10% of affected people require treatment. One of the more effective treatments is oral or topically applied glycopyrrolate. == References == | 0-1
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Hyperchloremia is an electrolyte disturbance in which there is an elevated level of chloride ions in the blood. The normal serum range for chloride is 96 to 106 mEq/L, therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. As of now there are no specific symptoms of hyperchloremia; however, it can be influenced by multiple abnormalities that cause a loss of electrolyte-free fluid, loss of hypotonic fluid, or increased administration of sodium chloride. These abnormalities are caused by diarrhea, vomiting, increased sodium chloride intake, renal dysfunction, diuretic use, and diabetes. Hyperchloremia should not be mistaken for hyperchloremic metabolic acidosis as hyperchloremic metabolic acidosis is characterized by two major changes: a decrease in blood pH and bicarbonate levels, as well as an increase in blood chloride levels. Instead those with hyperchloremic metabolic acidosis are usually predisposed to hyperchloremia. Hyperchloremia prevalence in hospital settings has been researched in the medical field since one of the major sources of treatment at hospitals is administering saline solution. Previously, animal models with elevated chloride have displayed more inflammation markers, changes in blood pressure, increased renal vasoconstriction, and less renal blood flow as well at glomerulus filtration, all of which are prompting researchers to investigate if these changes or others may exist in patients. Some studies have reported a possible relationship between increased chloride levels and death or acute kidney injury in severely ill patients that may frequent the hospital or have prolonged visits. | Initial randomized trials in septic shock comparing Plasma-Lyte and 0.9% saline (SPLIT and SALT trials) did not show any risk reduction in AKI. However, the later trials with larger sample size in critically and non critically ill adults (SMART and SALT-ED trials) showed reduction in major adverse kidney events. Extrapolating from the findings of septic shock, a recent trial comparing plasmalyte with 0.9% saline in DKA also did not show any significant difference in AKI. Hence, the causal link between hyperchloremia and AKI is yet to be conclusively established.As studies continue, it is important to include a large patient sample size, a diverse patient population, and a diverse range of hospitals involved in these studies. References
== External links == | 11
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Umbilical granuloma is the most common umbilical abnormality in newborn children or neonates, causing inflammation and drainage. It may appear in the first few weeks of newborn infants during the healing process of the umbilical cord due to an umbilical mass. It is the overgrowth of the umbilical tissue. It develops in about 1 out of 500 newborns. With appropriate treatment, it is expected to heal in 1~2 weeks. Causes
Following umbilical cord clamping during delivery, the umbilicus base will spontaneously separate within 7-15 days. With routine cord care and proper hygienic conditions, the remaining umbilical base will heal and new skin tissue will form. In some instances, a mass of tissue, or granuloma, will form at the base.Umbilical granulomas occur after umbilical cord removal when the remaining ring of the umbilicus undergoes incomplete wound healing and there is excessive healing tissue, also known as granulation tissue.Delayed cord separation, mild infections and hygienic conditions are all factors which may contribute to the incidence of umbilical granuloma. Although the exact cause of umbilical granulomas is unknown, it is hypothesized that inflammation of the remaining umbilical stump drives skin cell division, resulting in a tissue mass, rather than proper healing at the site. Histophysiology
An umbilical granuloma is a physiological response which surpasses the normal processes of skin restoration following umbilical cord clamping. Once the skin lesion is formed, there is an excess of fibroblast production. | Diagnosis
Umbilical granuloma can be diagnosed from physical examination. If there is a discharge around the navel and the granulation tissue is large enough to be visible with the open eye, umbilical granuloma is the first to be suspected. Open eye inspection and/or dermoscopy is commonly used to recognize the granular tissue at the site. If the granuloma is not visible with the open eye, gentle pressure on the surrounding site or a surgical tweezer can be used to expose the small granuloma hidden within the umbilical pit. An otoscope may also be used by physicians in order to expose a small, sessile granuloma. Other additional tests are usually not required, but if continued, ultrasonography (US) can be used for initial diagnosis of umbilical lesions. Treatment
Topical
Although there is no singular method of treatment for umbilical granulomas, some treatment options available include common salt, silver nitrate, corticosteroids, and cleaning with alcohol. Home care following treatments include gentle cleaning the navel area with soap and sterile water, followed by open exposure of the belly button to air. Silver nitrate
Silver nitrate is the most common treatment and practiced worldwide. Neonatology textbooks suggest silver nitrate as a first-line treatment option. The application of silver nitrate to granulomas was first noted in early 1800s as a cauterizing agent.Silver nitrate can be used as an antiseptic, an astringent, and as a caustic agent, depending on the indication. Its application requires medical personnel for treatment and may have unfavorable adverse effects if applied improperly. | 11
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In Slovak, it is known as "z očí", meaning "(coming) from eyes". In Slovene, it is known as "Zlobno oko", meaning "evil eye". In Somali, it is called "il", or "ilaaco" or "sixir" (the first two words literally meaning "eye" and the other word meaning black magic)
In Sinhala it is known as "ඇස්වහ" (æsvaha). In Spanish, mal de ojo literally means "evil from the Eye" as the name does not refer to the actual eye but to the evil that supposedly comes from it. Casting the evil eye is then echar mal de ojo, i.e. "to cast evil from the Eye". In Berber languages(Tamazight/Tamaziɣt/ⵜⴰⵎⴰⵣⵉⵖⵜ/ⵜⵎⵣⵗⵜ) it is called Tafust (ⵜⴰⴼⵓⵙⵜ) which means little hand
In Tagalog, it is known as ohiya or usog, which is a culture-bound syndrome where a visit by a stranger afflicts a child with sudden illness and convulsions. In Tamil, "கண் படுதல்" (kan padudhal) literally means "casting an eye" (with an intention to cause harm). "கண்ணூறு" (kannooru) "harm from the eye"
In Trinidadian Creole it is called maljo, derived from the French mal yeux meaning "bad eye"
In Turkish kem göz means evil eye and the cure is having a "nazar boncuğu", the nazar amulet. In Urdu, nazar (نظر) Chashm-é bad (چشمِ بد) or Nazar-é bad (نظرِبد); nazar lagna means to be afflicted by the evil eye. | Blue ornaments may be used to protect a household, and blue bottles from Milk of Magnesia have been hung on trees or placed in the yard surrounding a property.Blue soap and Albion Blue (an indigo dye referred to Trinbagonians simply as ‘blue’) are traditionally used for domestic washing, but are also considered to prevent maljo if used in bath water or to anoint the soles of the feet. Jumbie beads are the poisonous seeds of the Rosary Pea tree which are used to make jewelry that also wards off maljo and evil spirits. One superstition is that a pinch can reverse maljo following interpersonal interactions, especially if one is stared at or given a compliment. Some also believe that rubbing ones own saliva in their hair will counteract maljo in general, but particularly from envy of the hair texture and length. A bath in the sea is also thought to relieve an afflicted person. Maljo believers are particularly concerned with safeguarding babies and children, who are considered to be most vulnerable to its effects. It may be ‘caused by someone born with a "blight" in the eye when such a person looks admiringly at a child. It can also occur with a pat on the head, or with just a glance. Whether it is intended or not, compliments (...) can cause maljo. It can be caused by a stranger, a member of the childs immediate family, or by another relative.’ It may even be passed on by a parent who is obsessed with their own child. | 11
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Cutis verticis gyrata is a medical condition usually associated with thickening of the scalp. The condition is identified by excessive thickening of the soft tissues of the scalp and characterized by ridges and furrows, which give the scalp a cerebriform appearance. Clinically, the ridges are hard and cannot be flattened on applying pressure. Patients show visible folds, ridges or creases on the surface of the top of the scalp. The number of folds can vary from two to roughly ten and are typically soft and spongy. The condition typically affects the central and rear regions of the scalp, but sometimes can involve the entire scalp. Hair loss can occur over time where the scalp thickens, though hair within any furrows remains normal. Thus far, due to the (apparent) rarity of the condition, limited research exists and causes are as yet undetermined. What is known, is that the condition is not exclusively congenital. The condition was first reported by Jean-Louis-Marc Alibert in 1837, who called it cutis sulcata. A clinical description of the condition was provided by Robert in 1843 and it was named by Paul Gerson Unna in 1907. It has also been called Robert-Unna syndrome, bulldog scalp, corrugated skin, cutis verticis plicata, and pachydermia verticis gyrata. Cause
At this time, causes are unknown, but it is believed to not be congenital. Diagnosis
There is no clinical diagnosis for CVG as cases are rarely seen and are often comorbid with other conditions. Classifications
CVG is classified according to the presence, or lack of underlying cause. | Studies suggest that CVG often occurs in individuals in a secondary form to other ailments. However, the condition can also be present on its own. CVG can be classified into two forms: ‘primary’ (essential and non-essential) and ‘secondary’.The classifications are:
Primary essential
Primary non-essential
SecondaryPrimary essential CVG is where the cause of the condition in unknown. It has no other associated abnormalities. This occurs mainly in men, with a male:female ratio of 5:1 or 6:1, and develops during or soon after puberty. Because of the slow progression of the condition, which usually occurs without symptom, it often passes unnoticed in the early stage.Primary non-essential CVG can be associated with neuropsychiatric disorders including cerebral palsy, epilepsy, seizures, and ophthalmologic abnormalities, most commonly cataracts.Secondary CVG occurs as a consequence of a number of diseases or drugs that produce changes in scalp structure. These include: acromegaly (excessive growth hormone levels due to pituitary gland tumours), and theoretically, the use of growth hormone itself or the use of drugs that mimic the effect of growth hormone (such as GHRP-6 and CJC-1295). It may also arise in association with melanocytic naevi (moles), birthmarks (including connective tissue naevi, fibromas and naevus lipomatosus), and inflammatory processes (e.g. eczema, psoriasis, Darier disease, folliculitis, impetigo, atopic dermatitis, acne). Treatment
Options for medical treatment for this condition have been limited to plastic surgery with excision of the folds by means of scalp reduction/surgical resection. Scalp subcision has also been suggested as a treatment. Additional suggestions also include injections of a dermal filler (e.g. | 11
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Micropsia is a condition affecting human visual perception in which objects are perceived to be smaller than they actually are. Micropsia can be caused by optical factors (such as wearing glasses), by distortion of images in the eye (such as optically, via swelling of the cornea or from changes in the shape of the retina such as from retinal edema, macular degeneration, or central serous retinopathy), by changes in the brain (such as from traumatic brain injury, epilepsy, migraines, prescription drugs, and illicit drugs), and from psychological factors. Dissociative phenomena are linked with micropsia, which may be the result of brain-lateralization disturbance.Micropsia is also commonly reported when the eyes are fixating at (convergence), or focusing at (accommodation), a distance closer than that of the object in accord with Emmerts law. Specific types of micropsia include hemimicropsia, a form of micropsia that is localized to one half of the visual field and can be caused by brain lesions in one of the cerebral hemispheres. Related visual distortion conditions include macropsia, a less common condition with the reverse effect, and Alice in Wonderland syndrome, a condition that has symptoms that can include both micropsia and macropsia. Signs and symptoms
Micropsia causes affected individuals to perceive objects as being smaller or more distant than they actually are.The majority of individuals with micropsia are aware that their perceptions do not mimic reality. Many can imagine the actual sizes of objects and distances between objects. | Johnson–McMillin syndrome, also known as Johnson neuroectodermal syndrome, is a neuroectodermal syndrome characterized by conductive hearing loss and alopecia, microtia, conductive hearing loss, anosmia/hyposmia, and hypogonadotropic hypogonadism. See also
List of cutaneous conditions
References
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Human babies require large and steady supplies of glucose to feed the growing brain. In infants in the first year of life, the brain consumes 60% of all calories, so both babies and their mothers require a dependable food supply. Some evidence suggests that hunters contribute less than half the total food budget of most hunter-gatherer societies, and often much less than half, so that foraging grandmothers can contribute substantially to the survival of grandchildren at times when mothers and fathers are unable to gather enough food for all of their children. In general, selection operates most powerfully during times of famine or other privation. So although grandmothers might not be necessary during good times, many grandchildren cannot survive without them during times of famine. Post-reproductive female orcas tend to lead their pods, especially during years of food scarcity. Furthermore, the increased mortality risk of an orca due to losing a grandmother is stronger in years of food scarcityAnalysis of historical data found that the length of a females post-reproductive lifespan was reflected in the reproductive success of her offspring and the survival of her grandchildren. Another study found comparative effects but only in the maternal grandmother—paternal grandmothers had a detrimental effect on infant mortality (probably due to paternity uncertainty). Differing assistance strategies for maternal and paternal grandmothers have also been demonstrated. | Yoga may help with postmenopausal symptoms similar to other exercise. There is insufficient evidence to suggest that relaxation techniques reduce menopausal symptoms. Alternative medicine
There is no evidence of consistent benefit of alternative therapies for menopausal symptoms despite their popularity.The effect of soy isoflavones on menopausal symptoms is promising for reduction of hot flashes and vaginal dryness. Evidence does not support a benefit from phytoestrogens such as coumestrol, femarelle, or the non-phytoestrogen black cohosh. As of 2011 there is no support for herbal or dietary supplements in the prevention or treatment of the mental changes that occur around menopause.Hypnosis may reduce the severity of hot flashes. In addition, relaxation training with at-home relaxation audiotapes such as deep breathing, paced respiration, and guided imagery may have positive effects on relaxing muscles and reducing stress.There is no evidence to support the efficacy of acupuncture as a management for menopausal symptoms. A 2016 Cochrane review found not enough evidence to show a difference between Chinese herbal medicine and placebo for the vasomotor symptoms. Other efforts
Lack of lubrication is a common problem during and after perimenopause. Vaginal moisturizers can help women with overall dryness, and lubricants can help with lubrication difficulties that may be present during intercourse. It is worth pointing out that moisturizers and lubricants are different products for different issues: some women complain that their genitalia are uncomfortably dry all the time, and they may do better with moisturizers. Those who need only lubricants do well using them only during intercourse. | 11
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Strains were characterized by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Serologic tests and enzyme linked immunosorbent assays (ELISA), which measured Variola virus-specific immunoglobulin and antigen were also developed to assist in the diagnosis of infection.Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox could be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly. A variety of laboratory methods were available for detecting chickenpox in the evaluation of suspected smallpox cases. Prevention
The earliest procedure used to prevent smallpox was inoculation with variola minor (known as variolation after the introduction of smallpox vaccine to avoid possible confusion), which likely occurred in India, Africa, and China well before the practice arrived in Europe. The idea that inoculation originated in India has been challenged, as few of the ancient Sanskrit medical texts described the process of inoculation. Accounts of inoculation against smallpox in China can be found as early as the late 10th century, and the procedure was widely practiced by the 16th century, during the Ming dynasty. If successful, inoculation produced lasting immunity to smallpox. Because the person was infected with Variola virus, a severe infection could result, and the person could transmit smallpox to others. | Based on one study, it has the highest affinity for the norepinephrine transporter (NET) of any other TCA, and is said to be the most noradrenergic and the most selective for the NET of the TCAs. The observed effectiveness of desipramine in the treatment of ADHD was the basis for the development of the selective NRI atomoxetine and its use in ADHD.Desipramine has the weakest antihistamine and anticholinergic effects of the TCAs. It tends to be slightly activating/stimulating rather than sedating, unlike most others TCAs. Whereas other TCAs are useful for treating insomnia, desipramine can cause insomnia as a side effect due to its activating properties. The drug is also not associated with weight gain, in contrast to many other TCAs. Secondary amine TCAs like desipramine and nortriptyline have a lower risk of orthostatic hypotension than other TCAs, although desipramine can still cause moderate orthostatic hypotension. Pharmacokinetics
Desipramine is the major metabolite of imipramine and lofepramine. Chemistry
Desipramine is a tricyclic compound, specifically a dibenzazepine, and possesses three rings fused together with a side chain attached in its chemical structure. Other dibenzazepine TCAs include imipramine (N-methyldesipramine), clomipramine, trimipramine, and lofepramine (N-(4-chlorobenzoylmethyl)desipramine). Desipramine is a secondary amine TCA, with its N-methylated parent imipramine being a tertiary amine. Other secondary amine TCAs include nortriptyline and protriptyline. The chemical name of desipramine is 3-(10,11-dihydro-5H-dibenzo[b,f]azepin-5-yl)-N-methylpropan-1-amine and its free base form has a chemical formula of C18H22N2 with a molecular weight of 266.381 g/mol. | 0-1
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In hereditary cases, evidence of dental germ developing after surrounding tissues have closed the space required for development may be a large contributing factor, as well as such genetic disorders as Down syndrome, ectodermal dysplasia, cleidocranial dysplasia, and cleft lip and cleft palate. MSX1
MSX1 (muscle segment homeobox 1) is involved in condensation of ectomesenchyme in the tooth germ. Among the members of homeobox genes, MSX1 and MSX2 are crucial in mediating direct epithelial-mesenchymal interactions during tooth development by expressing in regions of condensing ectomesenchyme in the tooth germ. MSX1 mutations have been identified as a contributing factor in missing second premolars, third molars, and a small percentage of first molars. MSX1 is less likely to cause anterior agenesis.Heterozygous mutations in PAX9 (paired box gene 9) could arrest tooth morphogenesis as it plays a role of transcription the gene expressed in tooth mesenchyme at the bud stage during tooth development. A study showed that single nucleotide polymorphisms in PAX9 were highly associated with missing upper lateral incisors. AXIN2
The AXIN2 (AXIS inhibition protein 2) gene is a negative regulator of the Wnt signalling pathway, which is important in regulating cell fate, proliferation, differentiation and apoptosis. Its polymorphic variant may be associated with hypodontia such as missing lower incisors or in a more severe form of agenesis like oligontia (lack of six or more permanent teeth). EDA
EDA provides instructions for making a protein called ectodysplasin A. It encodes transmembrane protein that is part of TNF (tumour necrosis factor) family of ligands. | Management of retained primary teeth
When there is a case of hypodontia of the permanent premolar teeth, the primary molar teeth would often remain in the mouth beyond the time they are meant to be lost. Therefore, with a presence of healthy primary teeth in the absence of a permanent successor, retaining the primary teeth can be a feasible management of hypodontia. The primary molars present also functions as a space maintainer, prevent alveolar bone resorption and delays future prosthodontic space replacement by acting as a semi permanent solution going into adulthood Previous studies also shown a good prognosis of retained primary molars going into adulthood. However, leaving the primary teeth in place may run the risk of tooth infraocclusion where the occlusal surface is below that of adjacent teeth.Despite this, the retention of primary teeth, particularly molars, are more susceptible to occlusal wear, over-eruption of opposing teeth and the loss of inter-occlusal space. Orthodontic space closure
Orthodontic space closure is a way of using orthodontics in order to close spaces in the mouth where the teeth are missing. The ideal age for definitive orthodontic treatment is early adolescence but it is important to consider the patients age, severity of hypodontia, patient expectations and their commitment to treatment. It can be an option for hypodontia management in the case of missing maxillary lateral incisors through the reshaping, and mesial re-positioning of the adjacent canine. | 11
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The organization recommends healthy sleep habits for ideal cardiac health along with other well known factors like blood pressure, cholesterol, diet, glucose, weight, smoking, and physical activity. The Centers for Disease Control and Prevention has noted that adults who sleep less than 7 hours per day are more likely to have chronic health conditions including heart attack, coronary heart disease, and stroke compared to those with adequate amount of sleep.In a study that followed over 160,000 healthy, non-obese adults, the subjects who self-reported sleep duration less than 6 hours a day were at an increased risk for developing multiple cardiometabolic risk factors. They presented with increased central obesity, elevated fasting glucose, hypertension, low high-density lipoprotein, hypertriglyceridemia, and metabolic syndrome. The presence or lack of insomnia symptoms did not modify the effects of sleep duration in this study.The United Kingdom Biobank studied nearly 500,000 adults who had no cardiovascular disease, and the subjects who slept less than 6 hours a day were associated with a 20 percent increase in the risk of developing myocardial infarction (MI) over 7 years of follow-up period. Interestingly, long sleep duration of more than 9 hours a night was also a risk factor. Immunosuppression
Among the myriad of health consequences that sleep deprivation can cause, disruption of the immune system is one of them. While it is not clearly understood, researchers believe that sleep is essential to providing sufficient energy for the immune system to work and allow inflammation to take place during sleep. | Haverhill fever (or epidemic arthritic erythema) is a systemic illness caused by the bacterium Streptobacillus moniliformis, an organism common in rats and mice. If untreated, the illness can have a mortality rate of up to 13%. Among the two types of rat-bite fever, Haverhill fever caused by Streptobacillus moniliformis is most common in North America. The other type of infection caused by Spirillum minus is more common in Asia and is also known as Sodoku.The initial non-specific presentation of the disease and hurdles in culturing the causative microorganism are at times responsible for a delay or failure in the diagnosis of the disease. Although non-specific in nature, initial symptoms like relapsing fever, rash and migratory polyarthralgia are the most common symptoms of epidemic arthritic erythema.Bites and scratches from rodents carrying the bacteria are generally responsible for the affliction. However, the disease can be spread even without physical lacerations by rodents. In fact, the disease was first recognized from a milk-associated outbreak which occurred in Haverhill, Massachusetts in January, 1926. The organism S. moniliformis was isolated from the patients and epidemiologically, consumption of milk from one particular dairy was implicated in association with the infection. Hence, ingestion of food and drink contaminated with the bacteria can also result in the development of the disease. Symptoms and signs
The illness resembles a severe influenza, with a moderate fever (38-40 °C, or 101-104 °F), sore throat, chills, myalgia, headache, vomiting, and a diffuse red rash (maculopapular, petechial, or purpuric), located mostly on the hands and feet. | 0-1
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Premenstrual syndrome (PMS) refers to emotional and physical symptoms that regularly occur in the one to two weeks before the start of each menstrual period. Symptoms resolve around the time menstrual bleeding begins. Different women experience different symptoms. The common emotional symptoms include irritability and mood changes. The common physical symptoms include acne, tender breasts, bloating, and feeling tired. These are nonspecific symptoms and may be seen in women without PMS. Often PMS-related symptoms are present for about six days. An individuals pattern of symptoms may change over time. Symptoms do not occur during pregnancy or following menopause.Diagnosis requires a consistent pattern of emotional and physical symptoms occurring after ovulation and before menstruation to a degree that interferes with normal life. Emotional symptoms must not be present during the initial part of the menstrual cycle. A daily list of symptoms over a few months may help in diagnosis. Other disorders that cause similar symptoms need to be excluded before a diagnosis is made.The cause of PMS is unknown, but the underlying mechanism is believed to involve changes in hormone levels. Reducing salt, alcohol, caffeine, and stress along with increasing exercise is typically all that is recommended in those with mild symptoms. Calcium and vitamin D supplementation may be useful in some. Anti-inflammatory drugs such as ibuprofen or naproxen may help with physical symptoms. | In those with more significant symptoms birth control pills or the diuretic spironolactone may be useful.Up to 80% of women report having some symptoms after ovulation and before the beginning of menstruation, but these symptoms generally do not cause substantial disruption. These symptoms qualify as PMS in approximately 20 to 30% of pre-menopausal women. Premenstrual dysphoric disorder (PMDD) is a more severe form of PMS that has greater psychological symptoms. PMDD affects 3 to 8% of pre-menopausal individuals. Antidepressant medication of the selective serotonin reuptake inhibitors class may be used for PMDD in addition to the usual measures for PMS. Signs and symptoms
More than 200 different symptoms have been associated with PMS. Common emotional and non-specific symptoms include stress, anxiety, difficulty with sleep, headache, feeling tired, mood swings, increased emotional sensitivity, and changes in interest in sex. Problems with concentration and memory may occur. There may also be depression or anxiety.Physical symptoms associated with the menstrual cycle – but not necessarily with PMS, which is symptoms that appear before menstruation, rather than during menstruation – include bloating, lower back pain, cramps in the pelvic area, constipation/diarrhea, swelling or tenderness in the breasts, cyclic acne (acne that appears and disappears at predictable times during the menstrual cycle), joint or muscle pain, and food cravings. The exact symptoms and their intensity vary significantly from person to person, and even somewhat from cycle to cycle and over time. | 11
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These include:
Assault with further specific intent
Acts done to the person with intent to murder
Wounding or grievous bodily harm
Use or possession of a weapon to resist arrest
Assault causing certain injuries
Actual bodily harm – the term is not defined in the Crimes Act, but case law indicates actual bodily harm may include injuries such as bruises and scratches, as well as psychological injuries if the injury inflicted is more than merely transient (the injury does not necessarily need to be permanent)
Wounding – where there is breaking of the skin;
Grievous bodily harm – which includes the destruction of a foetus, permanent or serious disfiguring, and transmission of a grievous bodily disease
Assault causing death
Death
Death when intoxicated (in regards to the offender)
Canada
Assault is an offence under s. 265 of the Canadian Criminal Code. There is a wide range of the types of assault that can occur. Generally, an assault occurs when a person directly or indirectly applies force intentionally to another person without their consent. It can also occur when a person attempts to apply such force, or threatens to do so, without the consent of the other person. An injury need not occur for an assault to be committed, but the force used in the assault must be offensive in nature with an intention to apply force. It can be an assault to "tap", "pinch", "push", or direct another such minor action toward another, but an accidental application of force is not an assault. | Attacks on internationally protected persons
Section 1(1)(a) of the Internationally Protected Persons Act 1978 (c.17) makes provision for assault occasioning actual bodily harm or causing injury on "protected persons" (including Heads of State). Attacks on UN Staff workers
Section 1(2)(a) of the United Nations Personnel Act 1997 (c.13) makes provision for assault causing injury, and section 1(2)(b) makes provision for assault occasioning actual bodily harm, on UN staff. Assault by person committing an offence under the Night Poaching Act 1828
This offence is created by section 2 of the Night Poaching Act 1828.Abolished offences:
Assault on customs and excise officers, etc. Section 16(1)(a) of the Customs and Excise Management Act 1979 (c.2) provided that it was an offence to, amongst other things, assault any person duly engaged in the performance of any duty or the exercise of any power imposed or conferred on him by or under any enactment relating to an assigned matter, or any person acting in his aid. For the meaning of "assault" in this provision, see Logdon v. DPP [1976] Crim LR 121, DC. This offence was abolished and replaced by the Commissioners for Revenue and Customs Act 2005. Assaulting a person designated under section 43 of the Serious Organised Crime and Police Act 2005
This offence was created by section 51(1) of the Serious Organised Crime and Police Act 2005. It related to officers of the Serious Organized Crime Agency and was repealed when that agency was abolished. England and Wales
English law provides for two offences of assault: common assault and battery. | 11
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CAA occurring in the Flemish type has been observed to be linked to large dense-core plaques observed in this pedigree.The reason for increased deposition of Aβ in sporadic CAA is still unclear with both increased production of the peptide and abnormal clearance having been proposed as potential causes. Under normal physiology Aβ is cleared from the brain by four pathways: (1) endocytosis by astrocytes and microglial cells, (2) enzymatic degradation by neprilysin or insulysin (3) cleared by way of the blood brain barrier or (4) drained along periarterial spaces. Abnormalities in each of these identified clearance pathways have been linked to CAA.In familial forms of CAA, the cause of Aβ build up is likely due to increased production rather than poor clearance. Mutations in the amyloid precursor protein (APP), Presenilin (PS) 1 and PS2 genes can result in increased rates of cleavage of the APP into Aβ. An immune mechanism has also been proposed. apolipoprotein E (APOE) ε2 and ε4 are associated with increased risk of getting cerebral amyloid antipathy. The use of antiplatelet and anticoagulant therapy increases the risk of getting intracerebral haemorrhage in CAA. Types
Several familial variants exist. The condition is usually associated with amyloid beta. However, there are types involving other amyloid peptides:
the "Icelandic type" is associated with Cystatin C amyloid (ACys). the "British type" and "Danish type" are associated with British amyloid (ABri) and Danish amyloid (ADan) respectively. Both peptides are linked to mutations in ITM2B. Familial amyloidosis-Finnish type is associated with gelsolin amyloid (AGel). | Pathophysiology
The vascular amyloid pathology characteristic of CAA can be classified as either Type 1 or Type 2, the latter type being the more common. Type 1 CAA pathology entails detectable amyloid deposits within cortical capillaries as well as within the leptomeningeal and cortical arteries and arterioles. In type 2 CAA pathology, amyloid deposits are present in leptomeningeal and cortical arteries and arterioles, but not in capillaries. Deposits in veins or venules are possible in either type but are far less prevalent. Diagnosis
CAA can only be definitively diagnosed by a post-mortem autopsy. Biopsies can play a role in diagnosing probable cases. When no tissue is available for biopsy, the Boston Criteria are used to determine probable CAA cases from MRI or CT scan data. The Boston Criteria require evidence of multiple lobar or cortical hemorrhages to label a patient as probably having CAA. Susceptibility weighted imaging has been proposed as a tool for identifying CAA-related microhemorrhages. Imaging
Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding usually occurs on the surfaces of the brain in contrast with intracranial haemorrhage due to high blood pressure which occurs in deep locations of the brain such as basal ganglia and pons. In lobar intracerebral bleed, computed tomography (CT) scan would show hyperdense haemorrhage area and hypodense odema around the haemorrhagic site.MRI sequence of gradient echo and susceptibility weighted imaging (SWI) are useful in detecting microbleeds and deposition of iron on the brain cortex (cortical superficial siderosis). | 11
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: p104 Aside from a subjective change in perception and mood, the most common short-term physical and neurological effects include increased heart rate, increased appetite, impairment of short-term and working memory, and psychomotor coordination.Additional desired effects from consuming cannabis include relaxation, a general alteration of conscious perception, increased awareness of sensation, increased libido and distortions in the perception of time and space. At higher doses, effects can include altered body image, auditory and/or visual illusions, pseudohallucinations and ataxia from selective impairment of polysynaptic reflexes. In some cases, cannabis can lead to dissociative states such as depersonalization and derealization. Spiritual
Cannabis has held sacred status in several religions and has served as an entheogen – a chemical substance used in religious, shamanic, or spiritual contexts – in the Indian subcontinent since the Vedic period. The earliest known reports regarding the sacred status of cannabis in the Indian subcontinent come from the Atharva Veda, estimated to have been composed sometime around 1400 BCE. The Hindu god Shiva is described as a cannabis user, known as the "Lord of bhang. : p19 In modern culture, the spiritual use of cannabis has been spread by the disciples of the Rastafari movement who use cannabis as a sacrament and as an aid to meditation. Modes of cannabis consumption
Cannabis is consumed in many different ways, all of which involve heating to decarboxylate THCA in the plant into THC. | However, the benzodiazepines, temazepam and triazolam at 30 mg and 0.5 mg, respectively, are highly effective if aggression, agitation, or violent behaviour is apparent. In the instance of persistent psychosis after repeated use of stimulants, there are cases in which electroconvulsive therapy has been beneficial. This is followed by abstinence from psychostimulants supported with counselling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state. See also
References
== External links == | 0-1
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Beheading is often threatened if the government fails to heed the wishes of the hostage takers. Sometimes, the beheadings are videotaped and made available on the Internet. One of the most publicized of such executions was that of Nick Berg.Judicial execution is practiced in Iraq, but is generally carried out by hanging. Saudi Arabia
Saudi Arabia has a criminal justice system based on Shariah law reflecting a particular state-sanctioned interpretation of Islam. Crimes such as rape, murder, apostasy, and sorcery are punishable by beheading. It is usually carried out publicly by beheading with a sword. A public beheading will typically take place around 9am. The convicted person is walked into the square and kneels in front of the executioner. The executioner uses a sword to remove the condemned persons head from his or her body at the neck with a single strike. After the convicted person is pronounced dead, a police official announces the crimes committed by the beheaded alleged criminal and the process is complete. The official might announce the same before the actual execution. This is the most common method of execution in Saudi Arabia.According to Amnesty International, at least 79 people were executed in Saudi Arabia in 2013. Foreigners are not exempt, accounting for "almost half" of executions in 2013. Syria
The Syrian government employs hanging as its method of capital punishment. However, the terrorist organisation known as the Islamic State, which controlled territory in much of eastern Syria, had regularly carried out beheadings of people. | Eight points recommended to explain the diagnosis to the person and their caregivers are:
Reasons for concluding they do not have epilepsy
What they do have (describe FND)
Emphasize they are not suspected of "putting on" the attacks, and the symptoms are not "all in their head"
There may be no triggering "stresses"
Maintaining factors
May improve after correct diagnosis
Caution that anticonvulsant drug withdrawal should be done in conjunction with their physician
Describe treatment to help regain control of symptomsPsychotherapy is the most frequently used treatment, which might include cognitive behavioral therapy or therapy to retrain the physical symptoms and allow the individual to regain control of the attacks (ReACT). There is also some evidence supporting selective serotonin reuptake inhibitor antidepressants.Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) treatments for PNES typically target fear avoidance and work to reattribute patients symptoms to psychosocial issues. Retraining and Control Therapy (ReACT)
ReACT, while new and understudied, has shown extremely promising outcomes for reduction of PNES episodes in pediatric patients. This therapy focuses on the idea that PNES are caused by a learned physical reaction or habit the body develops, similar to a reflex. ReACT aims to retrain the learned reaction (PNES episodes) by targeting symptom catastrophizing and restoring sense of control over symptoms. Prognosis
Though there is limited evidence, outcomes appear to be relatively poor with a review of outcome studies finding that two thirds of people with PNES continue to experience episodes and more than half are dependent on the Social Security program at three-year follow-up. | 0-1
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These mutants also demonstrated diminished dopamine binding affinity, reduced cell surface transporter, loss of post-translational dopamine transporter glycosylation, and failure of amphetamine-mediated dopamine efflux.The age at which signs and symptoms appear seems to be related to the severity of DAT dysfunction. Early-onset DTDS movement problems in infancy most often have transporter activity that is less than 5 percent of normal. Those whose movement problems appear in childhood or later tend to have somewhat higher levels of transporter activity, although they are still lower than normal. Researchers speculate that higher levels of transporter activity may delay the onset of the disease in these individuals. DTDS is inherited in an autosomal recessive pattern, which means, for affected individuals, both copies of the gene in each cell have SLC6A3 mutations. As such, each sibling of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and 25% chance of being unaffected and not a carrier. Once a SLC6A3 pathogenic variant is identified within an affected family member, carrier testing for at-risk relatives and prenatal testing or preimplantation genetic diagnosis for pregnancies can be options considered for genetic counseling. Diagnosis
Diagnosis of SLC6A3-negative DTDS is established in a proband via molecular genetic testing, looking for biallelic (i.e. homozygous or compound heterozygous) pathogenic SLC6A3 variants. DTDS-positive patients are further identified by matching their genetic testing results with known characteristic clinical, laboratory, and imaging findings.To date, another potential diagnostic tool is neurotransmitter analysis of patient cerebrospinal fluid. | Bronchospasms and hypoglycemia occur because at high doses, the drug can be an antagonist for β2 adrenergic receptors located in the lungs and liver. Bronchospasm occurs due to the blockage of β2 receptors in the lungs. Hypoglycemia occurs due to decreased stimulation of glycogenolysis and gluconeogenesis in the liver via β2 receptors. Cautions
Non-selective beta-blockers should be avoided in people with asthma or bronchospasm as they may cause exacerbations and worsening of symptoms. A β1 selective beta-blocker like bisoprolol may be cautiously tried in those with controlled, mild-to-moderate asthma with cardiac comorbidities. A 2014 meta-analysis found that cardioselective beta-blockers may cause detrimental changes in lung function and partially blunts β2-agonist response. However, a 2017 control study found no significant association with asthma exacerbations by dose and exposure duration while a 2020 clinical trial found bisoprolol being non-inferior to placebo in bronchodilator response to salbutamol. Pharmacology
Mechanism of action
Bisoprolol is cardioprotective because it selectively and competitively blocks catecholamine (adrenaline) stimulation of β1 adrenergic receptors (adrenoreceptors), which are mainly found in the heart muscle cells and heart conduction tissue (cardiospecific), but also found in juxtaglomerular cells in the kidney. Normally, adrenaline and noradrenaline stimulation of the β1 adrenoreceptor activates a signalling cascade (Gs protein and cAMP) which ultimately leads to increased myocardial contractility and increased heart rate of the heart muscle and heart pacemaker, respectively. Bisoprolol competitively blocks the activation of this cascade, so decreases the adrenergic tone/stimulation of the heart muscle and pacemaker cells. Decreased adrenergic tone shows less contractility of heart muscle and lowered heart rate of pacemakers. | 0-1
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Removal of calculus after formation
The College of Registered Dental Hygienists of Alberta defines a dental hygienist as "a health care professional whose work focuses on the oral health of an individual or community." These dental professionals aim to improve oral health by educating patients on the prevention and management of oral disease. Dental hygienists can be found performing oral health services in various settings, including private dental offices, schools, and other community settings, such as long-term care facilities. As mentioned above in the clinical significance section, plaque and calculus deposits are a major etiological factor in the development and progression of oral disease. An important part of the scope of practice of a dental hygienist is the removal of plaque and calculus deposits. This is achieved through the use of specifically designed instruments for debridement of tooth surfaces. Treatment with these types of instruments is necessary as calculus deposits cannot be removed by brushing or flossing alone. To effectively manage disease or maintain oral health, thorough removal of calculus deposits should be completed at frequent intervals. The recommended frequency of dental hygiene treatment can be made by a registered professional, and is dependent on individual patient needs. Factors that are taken into consideration include an individuals overall health status, tobacco use, amount of calculus present, and adherence to a professionally recommended home care routine.Hand instruments are specially designed tools used by dental professionals to remove plaque and calculus deposits that have formed on the teeth. These tools include scalers, curettes, jaquettes, hoes, files and chisels. | In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival ("above the gum"), and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival ("below the gum"). Calculus formation is associated with a number of clinical manifestations, including bad breath, receding gums and chronically inflamed gingiva. Brushing and flossing can remove plaque from which calculus forms; however, once formed, calculus is too hard (firmly attached) to be removed with a toothbrush. Calculus buildup can be removed with ultrasonic tools or dental hand instruments (such as a periodontal scaler). Etymology
The word comes from Latin calculus "small stone", from calx "limestone, lime", probably related to Greek χάλιξ chalix "small stone, pebble, rubble", which many trace to a Proto-Indo-European root for "split, break up". Calculus was a term used for various kinds of stones. | 11
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Acute Interstitial Pneumonitis can result from many different irritants in the lungs and usually is resolved in under a month. Chemical Pneumonitis is caused by toxic substances reaching the lower airways of the bronchial tree. This causes a chemical burn and severe inflammation. (oxford)
Radiation Pneumonitis, also known as Radiation Induced Lung Injury, describes the initial damage done to the lung tissue by ionization radiation. Radiation, used to treat cancer, can cause pneumonitis when applied to the chest or full body. Radiation pneumonitis occurs in approximately 30% of advanced lung cancer patients treated with radiation therapy. Aspiration pneumonitis is caused by a chemical inhalation of harmful gastric contents which include causes such as:
Aspiration due to a drug overdose
A lung injury after the inhalation of habitual gastric contents. The development of colonized oropharyngeal material after inhalation. Bacteria entering the lungs
Treatment
Typical treatment for pneumonitis includes conservative use of corticosteroids such as a short course of oral prednisone or methylprednisolone. Inhaled corticosteroids such as fluticasone or budesonide may also be effective for reducing inflammation and preventing re-inflammation on a chronic level by suppressing inflammatory processes that may be triggered by environmental exposures such as allergens. Severe cases of pneumonitis may require corticosteroids and oxygen therapy, as well as elimination of exposure to known irritants.Corticosteroid dose and treatment duration vary from case to case. | The Centers for Disease Control and Prevention (CDC) recommends all teenagers receive MenACWY vaccine and booster, with optional MenB. MenACWY and MenB are also recommended for people of other ages with various medical conditions and social risk factors.A meningococcal polysaccharide vaccine (MPSV4) has been available since the 1970s and is the only meningococcal vaccine licensed for people older than 55. MPSV4 may be used in people 2–55 years old if the MCV4 vaccines are not available or contraindicated. Two meningococcal conjugate vaccines (MCV4) are licensed for use in the U.S. The first conjugate vaccine was licensed in 2005, the second in 2010. Conjugate vaccines are the preferred vaccine for people 2 through 55 years of age. It is indicated in those with impaired immunity, such as nephrotic syndrome or splenectomy. In June 2012, the U.S. Food and Drug Administration (FDA) approved a combination vaccine against two types of meningococcal diseases and Hib disease for infants and children 6 weeks to 18 months old. The vaccine, Menhibrix, was designed to prevent disease caused by Neisseria meningitidis serogroups C and Y, and Haemophilus influenzae type b (Hib). It was the first meningococcal vaccine that could be given to infants as young as six weeks old.In October 2014 the FDA approved the first vaccine effective against serogroup B, named Trumenba, for use in 10- to 25-year-old individuals. Africa
In 2010, the Meningitis Vaccine Project introduced a vaccine called MenAfriVac in the African meningitis belt. | 0-1
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Hyperthyroidism must also be distinguished from gestational transient thyrotoxicosis; as it can increase the risk of complications for mother and child. Such risks include pregnancy-related hypertension, pregnancy loss, low-birth weight, still birth and behavioral disorders later in the childs life. Nonetheless, high maternal FT4 levels during pregnancy have been associated with impaired brain developmental outcomes of the offspring and this was independent of for example hCG levels. Other animals
Cats
Hyperthyroidism is one of the most common endocrine conditions affecting older domesticated housecats. In the United States, up to 10% of cats over ten years old have hyperthyroidism. The disease has become significantly more common since the first reports of feline hyperthyroidism in the 1970s. The most common cause of hyperthyroidism in cats is the presence of benign tumors called adenomas. 98% of cases are caused by the presence of an adenoma, but the reason these cats develop such tumors continues to be studied. The most common presenting symptoms are: rapid weight loss, tachycardia (rapid heart rate), vomiting, diarrhea, increased consumption of fluids (polydipsia), increased appetite (polyphagia), and increased urine production (polyuria). Other symptoms include hyperactivity, possible aggression, an unkempt appearance, and large, thick claws. Heart murmurs and a gallop rhythm can develop due to secondary hypertrophic cardiomyopathy. About 70% of affected cats also have enlarged thyroid glands (goiter). 10% of cats exhibit "apathetic hyperthyroidism", which is characterized by anorexia and lethargy.The same three treatments used with humans are also options in treating feline hyperthyroidism (surgery, radioiodine treatment, and anti-thyroid drugs). | Diet
People with autoimmune hyperthyroidism (such as in Graves disease) should not eat foods high in iodine, such as edible seaweed and kelps.From a public health perspective, the general introduction of iodized salt in the United States in 1924 resulted in lower disease, goiters, as well as improving the lives of children whose mothers would not have eaten enough iodine during pregnancy which would have lowered the IQs of their children. Surgery
Surgery (thyroidectomy to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult, and even simply generalized staphylococcal infection as with any major surgery. Some people with Graves may opt for surgical intervention. This includes those that cannot tolerate medicines for one reason or another, people that are allergic to iodine, or people that refuse radioiodine.If people have toxic nodules treatments typically include either removal or injection of the nodule with alcohol. Radioiodine
In iodine-131 (radioiodine) radioisotope therapy, which was first pioneered by Dr. Saul Hertz, radioactive iodine-131 is given orally (either by pill or liquid) on a one-time basis, to severely restrict, or altogether destroy the function of a hyperactive thyroid gland. This isotope of radioactive iodine used for ablative treatment is more potent than diagnostic radioiodine (usually iodine-123 or a very low amount of iodine-131), which has a biological half-life from 8–13 hours. | 11
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Cisplatin and pemetrexed together give patients a median survival of 12.1 months.Cisplatin in combination with raltitrexed has shown an improvement in survival similar to that reported for pemetrexed in combination with cisplatin, but raltitrexed is no longer commercially available for this indication. For patients unable to tolerate pemetrexed, cisplatin in combination with gemcitabine or vinorelbine is an alternative, or vinorelbine on its own, although a survival benefit has not been shown for these drugs. For patients in whom cisplatin cannot be used, carboplatin can be substituted but non-randomised data have shown lower response rates and high rates of haematological toxicity for carboplatin-based combinations, albeit with similar survival figures to patients receiving cisplatin. Cisplatin in combination with premetrexed disodium, folic acid, and vitamin B12 may also improve survival for people who are responding to chemotherapy.In January 2009, the United States FDA approved using conventional therapies such as surgery in combination with radiation and or chemotherapy on stage I or II Mesothelioma after research conducted by a nationwide study by Duke University concluded an almost 50 point increase in remission rates.In pericardial mesothelioma, chemotherapy – typically adriamycin or cisplatin – is primarily used to shrink the tumor and is not curative. Immunotherapy
Treatment regimens involving immunotherapy have yielded variable results. For example, intrapleural inoculation of Bacillus Calmette-Guérin (BCG) in an attempt to boost the immune response, was found to be of no benefit to the patient (while it may benefit patients with bladder cancer). | This trial was the first to report a survival advantage from chemotherapy in malignant pleural mesothelioma, showing a statistically significant improvement in median survival from 10 months in the patients treated with cisplatin alone to 13.3 months in the group of patients treated with cisplatin in the combination with pemetrexed and who also received supplementation with folate and vitamin B12. Vitamin supplementation was given to most patients in the trial and pemetrexed related side effects were significantly less in patients receiving pemetrexed when they also received daily oral folate 500mcg and intramuscular vitamin B12 1000mcg every 9 weeks compared with patients receiving pemetrexed without vitamin supplementation. The objective response rate increased from 20% in the cisplatin group to 46% in the combination pemetrexed group. Some side effects such as nausea and vomiting, stomatitis, and diarrhoea were more common in the combination pemetrexed group but only affected a minority of patients and overall the combination of pemetrexed and cisplatin was well tolerated when patients received vitamin supplementation; both quality of life and lung function tests improved in the combination pemetrexed group. In February 2004, the United States Food and Drug Administration (FDA) approved pemetrexed for treatment of malignant pleural mesothelioma. However, there are still unanswered questions about the optimal use of chemotherapy, including when to start treatment, and the optimal number of cycles to give. | 11
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Osteochondromas are the most common benign tumors of the bones. The tumors take the form of cartilage-capped bony projections or outgrowth on the surface of bones exostoses. It is characterized as a type of overgrowth that can occur in any bone where cartilage forms bone. Tumors most commonly affect long bones about the knee and in the forearm. Additionally, flat bones such as the pelvis and scapula (shoulder blade) may be affected. Hereditary multiple exostoses usually present during childhood. Yet, the vast majority of affected individuals become clinically manifest by the time they reach adolescence. Osteochondromas occur in 3% of the general population and represent 35% of all benign tumors and 8% of all bone tumors. The majority of these tumors are solitary non-hereditary lesions and approximately 15% of osteochondromas occur as hereditary multiple exostoses preferably known as hereditary multiple osteochondromas (HMOs). Osteochondromas do not result from injury and the exact cause remains unknown. Recent research has indicated that multiple osteochondromas is an autosomal dominant inherited disease. Germ line mutations in EXT1 and EXT2 genes located on chromosomes 8 and 11 have been associated with the cause of the disease. The treatment choice for osteochondroma is surgical removal of solitary lesion or partial excision of the outgrowth, when symptoms cause motion limitations or nerve and blood vessel impingements. In hereditary multiple exostoses the indications of surgery are based upon multiple factors that are taken collectively, namely: patients age, tumor location and number, accompanying symptomatology, esthetic concerns, family history and underlying gene mutation. | They show a clear picture of dense structures of bones, and will also indicate bone growth pertaining to osteochondroma. Computed tomography (CT) scan can identify the bony lesion in great details and show the presence of calcification. These tests also provide great details, especially in soft tissues with the aide of cross-sectional images. Magnetic resonance imaging (MRI) is the most accurate method for detecting bone masses in symptomatic cases to depict precise morphology of a tumor. It is used to verify if the palpable mass is continuous with the cortex of the affected bone and to differentiate an osteochondroma from other lesions on the surface of the bone. MRI can also be used to look for cartilage on the surface of tumor and can depict any vascular complications caused by the tumor. An MRI can identify tumors of the spinal column and is often used to diagnose low grade osteosarcoma. Ultrasound is done if aneurysms or pseudoaneurysms and venous or arterial thrombosis is suspected. Ultrasound is an accurate method for examining the cartilaginous cap of the osteochondroma. It is also a way of pinpointing bursitis. However, it cannot be used to predict if the growth of tumor is inward in regards to the cap. Angiography is used to detect vascular lesions caused by osteochondroma due to ossified cartilaginous cap. It is also used to characterize malignant transformation lesions through neovascularity. Clinical testing such as sequence analysis can be done of the entire coding regions of both EXT1 and EXT2 to detect mutations. | 11
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CYP3A inhibitors, by nature of inhibiting the enzyme that metabolizes amlodipine, CYP3A4, are one such class of drugs. Others include the calcium-channel blocker diltiazem, the antibiotic clarithromycin, and possibly some antifungals. Amlodipine causes several drugs to increase in levels, including cyclosporine, simvastatin, and tacrolimus (the increase in the last one being more likely in people with CYP3A5*3 genetic polymorphisms). When more than 20 mg of simvastatin, a lipid-lowering agent, are given with amlodipine, the risk of myopathy increases. Giving amlodipine with Viagra increases the risk of hypotension. Pharmacology
Amlodipine is a long-acting calcium channel antagonist that selectively inhibits calcium ion influx across cell membranes. It targets L-type calcium channels in muscle cells and N-type calcium channels in the central nervous system which are involved in nociceptive signalling and pain perception. Amlodipine has an inhibitory effect on calcium influx in smooth muscle cells to inhibit contraction. Amlodipine ends up significantly reducing total vascular resistance without decreasing cardiac output expressed by pressure-rate product and cardiac contractability in comparison with verapamil, a non-dihydropyridine. In turn, following treatment lasting a month, with amlodipine, cardiac output is significantly enhanced. Unlike verapamil which has efficacy in moderation of emotional arousal and reduces cardiac load without lowering cardiac output demands, amlodipine increases the cardiac output response concomitantly with increased functional cardiac load. Mechanism of action
Amlodipine is an angioselective calcium channel blocker and inhibits the movement of calcium ions into vascular smooth muscle cells and cardiac muscle cells which inhibits the contraction of cardiac muscle and vascular smooth muscle cells. | In cats, it is the first line of treatment due to its efficacy and few side effects. Systemic hypertension in cats is usually secondary to another abnormality, such as chronic kidney disease, and so amlodipine is most often administered to cats with kidney disease. While amlodipine is used in dogs with systemic hypertension, it is not as efficacious. Amlodipine is also used to treat congestive heart failure due to mitral valve regurgitation in dogs. By decreasing resistance to forward flow in the systemic circulation it results in a decrease in regurgitant flow into the left atrium. Similarly, it can be used on dogs and cats with left-to-right shunting lesions such as ventricular septal defect to reduce the shunt. Side effects are rare in cats. In dogs, the primary side effect is gingival hyperplasia. References
External links
"Amlodipine". Drug Information Portal. U.S. National Library of Medicine. onog | 11
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Avindra Nath, clinical director of the National Institute of Neurological Disorders and Stroke and president of the International Society for NeuroVirology, compared the situation to the prolonged investigations that led to confirmation of HIV as the cause of AIDS. In response to the suggestion that the enterovirus might be taking over the role of polio, Nath said that EV-D68 was far less virulent and spread much more slowly than polio, and that unlike in polio, only a few cases of paralysis were seen per thousand children infected. He also suggested that adults with respiratory diseases should also be evaluated for neurological deficits, and that infectious disease should be considered as a cause when patients presented with neurological symptoms.A subsequent report described 29 cases of EV-D68-associated AFM in Europe in 2016, noting, "these probably represent only the tip of the iceberg. "CDC sees 2018 as a record year, annual documented cases of AFM reached a record 238 nationwide. The relatively lower circulation in 2020 may reflect the use of COVID-19 pandemic infection mitigation measures. Because of the EV-D68 surge in 2022 Health Alert Network (HAN) released a notice for Healthcare providers and hospitals. The CDC warned clinicians that EV-D68 detections have continued to be high. "Sentinel surveillance sites are reporting a higher proportion of EV-D68 positivity in children who are [rhinovirus and/or enterovirus] positive compared to previous years," the agency wrote. Clinicians should be aware of "the potential for an increase in AFM cases in the upcoming weeks." | It you lift the arm up, it literally drops. Sensation is usually intact. There might be slightly decreased sensation in the other arm, but these are younger kids, so theyre not always so cooperative in giving you a good sensory exam. Childrens Mercy Hospital, which had three or four cases in 2014, reported that the MRI images and symptoms closely mimicked polio. They reported: "The sudden onset of flaccid paralysis in single or multiple limbs with absolutely no sensory findings, the MRIs all showing uniformly a signal increase in the ventral horns of the spinal cord — this is exactly the same region of the spinal cord affected in polio ... Almost all of the patients have an increase in their white blood cells in the cerebrospinal fluid. Some of the patients have brainstem findings and cranial-nerve findings. "Of 64 patients meeting the CDC criteria before October 29, 2014, 80% had had a preceding respiratory illness and 75% reported fever in the days leading up to limb weakness, the onset of which was generally abrupt. By November 20, the number of confirmed cases stood at 88 from 29 states.The CDC requested that physicians provide information about cases meeting these criteria: patients diagnosed after August 1, 2014, who are no older than 21 years of age, showing acute onset of focal limb weakness, with a spinal-cord lesion largely restricted to grey matter visualized by MRI.In November 2018, the CDC reported that they were investigating 286 cases, with at least 116 confirmed cases in 31 states. | 11
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Therefore, an interprofessional team approach with occupational therapy (OT), physical therapy (PT), orthotist, podiatrist, and or orthopedic surgeon is recommended. PT typically focuses on muscle-strength training, muscle stretching, and aerobic exercise, while OT can provide education on energy conservation strategies and activities of daily living. Physical therapy should be involved in designing an exercise program that fits a persons personal strengths and flexibility. Bracing can also be used to correct problems caused by CMT. An orthotist may address gait abnormalities by prescribing the use of orthotics.Appropriate footwear is also very important for people with CMT, but they often have difficulty finding well-fitting shoes because of their high arched feet and hammertoes. Due to the lack of good sensory reception in the feet, CMT patients may also need to see a podiatrist for assistance in trimming nails or removing calluses that develop on the pads of the feet. Lastly, patients can also decide to have surgery performed by a podiatrist or an orthopedic surgeon. Surgery may help to stabilize the patients feet or correct progressive problems. These procedures include straightening and pinning the toes, lowering the arch, and sometimes, fusing the ankle joint to provide stability. CMT patients must take extra care to avoid falling as fractures take longer to heal in someone with an underlying disease process. Additionally, the resulting inactivity may cause the CMT to worsen. | Charcot–Marie–Tooth disease (CMT) is a hereditary motor and sensory neuropathy of the peripheral nervous system characterized by progressive loss of muscle tissue and touch sensation across various parts of the body. This disease is the most commonly inherited neurological disorder, affecting about one in 2,500 people. It is named after those who classically described it: the Frenchman Jean-Martin Charcot (1825–1893), his pupil Pierre Marie (1853–1940), and the Briton Howard Henry Tooth (1856–1925).There is no known cure. Care focuses on maintaining function. CMT was previously classified as a subtype of muscular dystrophy. Signs and symptoms
Symptoms of CMT usually begin in early childhood or early adulthood but can begin later. Some people do not experience symptoms until their early 30s or 40s. Usually, the initial symptom is foot drop early in the course of the disease. This can also cause hammertoe, where the toes are always curled. Wasting of muscle tissue of the lower parts of the legs may give rise to a "stork leg" or "inverted champagne bottle" appearance. Weakness in the hands and forearms occurs in many people as the disease progresses.Loss of touch sensation in the feet, ankles, and legs as well as in the hands, wrists, and arms occurs with various types of the disease. Early- and late-onset forms occur with on and off painful spasmodic muscular contractions that can be disabling when the disease activates. High-arched feet (pes cavus) or flat-arched feet (pes planus) are classically associated with the disorder. | 11
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A person may have only one kind of the malformation or can have a mixture of both macro- and microcysts. Cystic hygroma can be associated with a nuchal lymphangioma or a fetal hydrops. Additionally, it can be associated with Down syndrome, Turner syndrome, or Noonan syndrome. If it is diagnosed in the third trimester, then chances of association with Down syndrome are increased, but if diagnosed in the second trimester, then it is associated with Turner syndrome. A lethal version of this condition exists, known as Cowchock–Wapner–Kurtz syndrome, that, in addition to cystic hygroma, includes cleft palate and lymphedema, a condition of localized edema and tissue swelling caused by a compromised lymphatic system. Signs and symptoms
Cystic hygromas are increasingly diagnosed by prenatal ultrasonography. A common sign is a neck growth. It may be found at birth, or discovered later in an infant after an upper respiratory tract infection. Cystic hygromas can grow very large and may affect breathing and swallowing. Some symptoms may include a mass or lump in the mouth, neck, cheek, or tongue. It feels like a large, fluid-filled sac. In addition, cystic hygromas can be found in other body parts, such as the arms, chest, legs, groin, and buttocks. Cystic hygromas are also often seen in Turners syndrome, although a patient who does not have the syndrome can present with this condition. Diagnosis
Lymphatic malformations may be detected in the human fetus by ultrasound if they are of sufficient size. | It was redescribed by Johann Weyer during an epidemic in lower Germany between 1564 and 1565; he referred to it as scarlatina anginosa. The first unequivocal description of scarlet fever appeared in a book by Joannes Coyttarus of Poitiers, De febre purpura epidemiale et contagiosa libri duo, which was published in 1578 in Paris. Daniel Sennert of Wittenberg described the classical scarlatinal desquamation in 1572 and was also the first to describe the early arthritis, scarlatinal dropsy, and ascites associated with the disease.In 1675 the term that has been commonly used to refer to scarlet fever, "scarlatina", was written by Thomas Sydenham, an English physician. In 1827, Richard Bright was the first to recognize the involvement of the renal system in scarlet fever.The association between streptococci and disease was first described in 1874 by Theodor Billroth, discussing people with skin infections. Billroth also coined the genus name Streptococcus. In 1884 Friedrich Julius Rosenbach edited the name to its current one, Streptococcus pyogenes, after further looking at the bacteria in the skin lesions. The organism was first cultured in 1883 by the German surgeon Friedrich Fehleisen from erysipelas lesions.Also in 1884, the German physician Friedrich Loeffler was the first to show the presence of streptococci in the throats of people with scarlet fever. Because not all people with pharyngeal streptococci developed scarlet fever, these findings remained controversial for some time. | 0-1
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About three-quarters of patients acquire PLE after UV-A exposure only, one-tenth after UV-B exposure only, and the rest after a combination of UV-A and UV-B exposure.People vary in the amount of sun exposure needed to trigger the rash. Oxidative stress
Oxidative stress and the modification of the redox status of the skin has been implicated in the expression of PLE. Photosensitizer
It has been suggested that an undefined endogenous or exogenous photo-allergen may trigger a delayed immune reaction resulting in PLE. Genetics
Half of patients have a family history of PLE, demonstrating a clear genetic influence. Oestrogen effect
The preponderance in women with a decline in severity following menopause has been thought to be associated with oestrogen effects, A natural fall in oestrogens may account for the tendency to remit after the menopause. Diagnosis
The diagnosis of PLE is typically made by assessing the history and clinical observations. Any investigations are usually to exclude other conditions, particularly lupus and porphyria.Blood tests are usually normal. However, positive antinuclear antibody and extractable nuclear antigen (anti-Ro/La) in low titre may be found, even in the absence of other criteria to suggest a diagnosis of lupus erythematosus. If clinical findings suggest a possibility of porphyria, urinary and red cell porphyrin screening may be performed and are negative in PLE.Photoprovocation tests are usually not required but may be undertaken by specialised centres in winter. | 7 Up
As with cocaine in Coca-Cola, lithium was widely marketed as one of a number of patent medicine products popular in the late-19th and early-20th centuries, and was the medicinal ingredient of a refreshment beverage. Charles Leiper Grigg, who launched his St. Louis-based company The Howdy Corporation, invented a formula for a lemon-lime soft drink in 1920. The product, originally named "Bib-Label Lithiated Lemon-Lime Soda", was launched two weeks before the Wall Street Crash of 1929. It contained the mood stabilizer lithium citrate, and was one of a number of patent medicine products popular in the late-19th and early-20th centuries. Its name was soon changed to 7 Up. All American beverage makers were forced to remove lithium in 1948. Despite the 1948 ban, in 1950 the Painesville Telegraph still carried an advertisement for a lithiated lemon beverage. Salts and product names
Many different lithium salts can be used as medication, including lithium carbonate, lithium acetate, lithium sulfate, lithium citrate, lithium orotate and lithium gluconate. Lithium carbonate (Li2CO3), sold under several trade names, is the most commonly prescribed, while lithium citrate (Li3C6H5O7) is also used in conventional pharmacological treatments. Lithium orotate (C5H3LiN2O4), has been presented as an alternative. Lithium bromide and lithium chloride have been used in the past as table salt; however, they fell out of use in the 1940s, when it was discovered they were toxic in those large doses. | 0-1
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There are more pressing challenges to address, such as access to treatment, veracity and availability of information, and quality of health care. Public health messaging is perhaps the most important challenge. The multiple levels of interconnectivity and negotiated social meanings inherent to the disease require cooperation between medical professionals and patients to achieve correct public health communication. Therefore, Scalvini argues in the BMJ that it is necessary a "new ethic of shared responsibility" to educate people about dangers and give people from underprivileged groups the tools they need to make better decisions. Treatment
In the European Union and the United States, tecovirimat is approved for the treatment of several poxviruses, including monkeypox. BMJ Best Practice recommends tecovirimat or the smallpox treatment brincidofovir as the first line antiviral treatment if required, alongside supportive care (including antipyretic, fluid balance and oxygenation). Empirical antibiotic therapy or aciclovir may be used if secondary bacterial or varicella zoster infection is suspected, respectively. Outcome
After healing, the scabs may leave pale marks before becoming darker scars. The risk of death in those infected ranges from 0% to 11%, depending on the type of monkeypox and location in the world. Fatality rates have been reported as around 3.6% in West Africa and 10.6% in Central Africa. Most reported deaths have occurred in young children and people with HIV infection. Epidemiology
In 1970, monkeypox was first associated with an illness as a disease in humans in the Democratic Republic of the Congo (formerly Zaire), in the town of Basankusu, Équateur Province. | Cases were also reported in travellers to Israel and Singapore. The UK saw further cases in 2019 and 2021.In June 2022, the World Health Organization announced that it would find a new name for the disease, in line with its policy to avoid misleading associations with specific regions or animals.On 31 July 2022, the first death from monkeypox was recorded in India: a 22-year-old man who had returned from the UAE died. See also
2003 Midwest monkeypox outbreak
2022 monkeypox outbreak
2022 monkeypox outbreak in Canada
2022 monkeypox outbreak in the United States
2022 monkeypox outbreak in the United Kingdom
References
External links
CDC – Monkeypox Fact Sheet
WHO – Monkeypox Fact Sheet
Virology.net Picturebook: Monkeypox
"Could Monkeypox Take Over Where Smallpox Left Off? Smallpox may be gone, but its viral cousins – monkeypox and cowpox – are staging a comeback". Scientific American, March 4, 2013. More than 80 cases confirmed in 12 countries, May 23, 2022. Monkeypox DNA sequencing hints virus circulating since 2017, June 7, 2022. MonkeypoxTracker – Monkeypox statistics visualization site
PoxApp - the monkeypox app – Assess skin lesions and symptoms with artificial intelligence developed by Stanford University | 11
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Aneurysm of the left ventricle myocardium develops in about 10% of MI and is itself a risk factor for heart failure, ventricular arrhythmia, and the development of clots.Risk factors for complications and death include age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers. Epidemiology
Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease; with it being the leading cause of death in high- or middle-income countries and second only to lower respiratory infections in lower-income countries. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as women.Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the US in 2008. For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.In contrast, IHD is becoming a more common cause of death in the developing world. For example, in India, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985–2015. | Papular eruption of blacks is a cutaneous condition characterized clinically by small, pruritic papules and histologically by a mononuclear cell-eosinophil perivascular infiltrate. See also
Pachydermatous eosinophilic dermatitis
List of cutaneous conditions
== References == | 0-1
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Dosages are titrated to target blood levels at specific times after medication administration. Skin
As an ointment, tacrolimus is used in the treatment of eczema, in particular atopic dermatitis. It suppresses inflammation in a similar way to steroids, and is equally as effective as a mid-potency steroid. An important advantage of tacrolimus is that, unlike steroids, it does not cause skin thinning (atrophy), or other steroid related side effects.It is applied on the active lesions until they heal off, but may also be used continuously in low doses (twice a week), and applied to the thinner skin over the face and eyelids. Clinical trials of up to one year have been conducted. Recently it has also been used to treat segmental vitiligo in children, especially in areas on the face. Eyes
Tacrolimus solution, as drops, is sometimes prescribed by veterinarians for keratoconjunctivitis, and other dry eye maladies, in the eyes of domestic cats, dogs, and horses. It has been studied for use in human eyes. | Dysregulation of the HPA axis has been associated with eating disorders, such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones or neuropeptides and amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.Serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior. Norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior. Dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food. Neuropeptide Y also known as NPY is a hormone that encourages eating and decreases metabolic rate. Blood levels of NPY are elevated in patients with anorexia nervosa, and studies have shown that injection of this hormone into the brain of rats with restricted food intake increases their time spent running on a wheel. Normally the hormone stimulates eating in healthy patients, but under conditions of starvation it increases their activity rate, probably to increase the chance of finding food. The increased levels of NPY in the blood of patients with eating disorders can in some ways explain the instances of extreme over-exercising found in most anorexia nervosa patients. Leptin and ghrelin: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of satiety. Ghrelin is an appetite inducing hormone produced in the stomach and the upper portion of the small intestine. | 0-1
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After infection, the viruses are transported along sensory nerves to the nerve cell bodies, where they reside lifelong. Causes of recurrence may include: decreased immune function, stress, and sunlight exposure. Oral and genital herpes is usually diagnosed based on the presenting symptoms. The diagnosis may be confirmed by viral culture or detecting herpes DNA in fluid from blisters. Testing the blood for antibodies against the virus can confirm a previous infection but will be negative in new infections.The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex. Condom use decreases the risk. Daily antiviral medication taken by someone who has the infection can also reduce spread. There is no available vaccine and once infected, there is no cure. Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms. Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. HSV-1 is usually acquired during childhood. Since there is no cure for either HSV-1 or HSV-2, rates of both inherently increase as people age. Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world. Most people with HSV-2 do not realize that they are infected. | Drug induced pigmentation may take on many different appearances, one of the most common being a change in the color, or pigmentation, of the skin. Presentation
Cause
Drug-induced pigmentation of the skin may occur as a consequence of drug administration, and the mechanism may be postinflammatory hyperpigmentation in some cases, but frequently is related to actual deposition of the offending drug in the skin. : 125–6 The incidence of this change varies, and depends on the type of medication involved. Some of the most common drugs involved are NSAIDs, antimalarials, psychotropic drugs, Amiodarone, cytotoxic drugs, tetracyclines, and heavy metals such as silver and gold (which must be ingested, not just worn). Pathophysiology
There are 4 possible mechanisms to how this change may occur:
Accumulation of melanin, the skin pigment
Accumulation of drug or one of its products under any layer of the skin (usually the dermis or epidermis)
Accumulation of iron throughout the dermis from drug-induced post-inflammatory changes
The synthesis of special pigments, under direct influence of the drug
See also
Skin lesion
References
== External links == | 0-1
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Originally termed EMG syndrome (for exomphalos, macroglossia, and gigantism), this syndrome over time became known as Beckwith–Wiedemann syndrome or Wiedemann Beckwith syndrome. Originally, Dr. Hans-Rudolf Wiedemann (born 16 February 1915, Bremen, Germany, died 4 August 2006, Kiel) coined the term exomphalos-macroglossia-gigantism (EMG) syndrome to describe the combination of congenital abdominal wall defects as hernia (exomphalos), large tongues (macroglossia), and large bodies and/or long limbs (gigantism). Over time, this constellation was renamed Beckwith–Wiedemann syndrome following the autoptical observations of Prof. John Bruce Beckwith (born 18 September 1933, Spokane, Washington), who also observed a severe increase in the size of the adrenal glands in some of these patients. See also
Perlman syndrome
References
Further reading
GeneReview/UW/NIH entry on Beckwith-Wiedemann syndrome
== External links == | Vaccination is an effective method to prevent pathogenic
diseases in aquaculture and different kinds vaccines to prevent GBS infections have been developed recently.GBS has also been found in many other animals, such as camels, dogs, cats, crocodiles, seals, elephants and dolphins. References
External links
CDC—Group B Strep (GBS)
Group B Strep Association US
Group B Strep Support UK
Type strain of Streptococcus agalactiae at BacDive - the Bacterial Diversity Metadatabase | 0-1
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CES mainly affects middle-aged individuals, particularly those in their forties and fifties, and presents more often in men. It is not a typical diagnosis, developing in only 4 to 7 out of every 10,000 to 100,000 patients, and is more likely to occur proximally. Disc herniation is reportedly the most common cause of CES, and it is thought that 1 to 2% of all surgical disc herniation cases result in CES. CES is often concurrent with congenital or degenerative diseases and represents a high cost of care to those admitted to the hospital for surgery. Hospital stays generally last 4 to 5 days, and cost an average of $100,000 to $150,000. Delays in care for cauda equina results in the English NHS paying about £23 million a year in compensation. In animals
Degenerative lumbosacral stenosis (DLSS), also known as cauda equina syndrome, is a pathologic degeneration in the lumbosacral disk in dogs. DLSS affects the articulation, nerve progression, and tissue and joint connections of the disk. This degeneration causes compressions in soft tissues and nerve root locations in the caudal area of the medulla, causing neuropathic pain in the lumbar vertebrae. References
External links
06-093c. at Merck Manual of Diagnosis and Therapy Home Edition | A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die. Small placental infarcts, especially at the edge of the placental disc, are considered to be normal at term. Large placental infarcts are associated with vascular abnormalities, e.g. hypertrophic decidual vasculopathy, as seen in hypertension. Very large infarcts lead to placental insufficiency and may result in fetal death. Relation to maternal floor infarct
Maternal floor infarcts are not considered to be true placental infarcts, as they result from deposition of fibrin around the chorionic villi, i.e. perivillous fibrin deposition. See also
Placental disease
References
External links
Gross pathology of a placental infarct (utah.edu) | 0-1
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Side effects
Common side effects include: bladder pain; bloating or swelling of the face, arms, hands, lower legs, or feet; bloody or cloudy urine; body aches or pain; chest pain; chills; confusion; cough; diarrhea; difficult, burning, or painful urination; difficulty with breathing; difficulty with speaking up to inability to speak; double vision; sleeplessness; and inability to move the arms, legs, or facial muscles. Society and culture
Legal status
Sipuleucel-T was approved by the U.S. Food and Drug Administration (FDA) on April 29, 2010, to treat asymptomatic or minimally symptomatic metastatic HRPC.Shortly afterward, sipuleucel-T was added to the compendium of cancer treatments published by the National Comprehensive Cancer Network (NCCN) as a "category 1" (highest recommendation) treatment for HRPC. The NCCN Compendium is used by Medicare and major health care insurance providers to decide whether a treatment should be reimbursed. Research
Clinical trials
Completed
Sipuleucel-T showed overall survival (OS) benefit to patients in three double-blind randomized phase III clinical trials, D9901, D9902a, and IMPACT.The IMPACT trial served as the basis for FDA licensing. This trial enrolled 512 patients with asymptomatic or minimally symptomatic metastatic HRPC randomized in a 2:1 ratio. The median survival time for sipuleucel-T patients was 25.8 months comparing to 21.7 months for placebo-treated patients, an increase of 4.1 months. 31.7% of treated patients survived for 36 months vs. 23.0% in the control arm. Overall survival was statistically significant (P=0.032). The longer survival without tumor shrinkage or change in progression is surprising. This may suggest the effect of an unmeasured variable. | Sipuleucel-T, sold under the brand name Provenge, developed by Dendreon Pharmaceuticals, LLC, is a cell-based cancer immunotherapy for prostate cancer (CaP). It is an autologous cellular immunotherapy. Medical uses
Sipuleucel-T is indicated for the treatment of metastatic, asymptomatic or minimally symptomatic, metastatic castrate-resistant hormone-refractory prostate cancer (HRPC). Other names for this stage are metastatic castrate-resistant (mCRPC) and androgen independent (AI) or (AIPC). This stage leads to mCRPC with lymph node involvement and distal (distant) tumors; this is the lethal stage of CaP. The prostate cancer staging designation is T4,N1,M1c. Treatment method
A course of treatment consists of three basic steps:
The patients white blood cells, primarily dendritic cells, a type of antigen-presenting cells (APCs), are extracted in a leukapheresis procedure. The blood product is sent to a production facility and incubated with a fusion protein (PA2024) consisting of two parts:
The antigen prostatic acid phosphatase (PAP), which is present in 95% of prostate cancer cells and
An immune signaling factor granulocyte-macrophage colony stimulating factor (GM-CSF) that helps the APCs to mature. The activated blood product (APC8015) is returned from the production facility to the infusion center and reinfused into the patient.Premedication with acetaminophen and antihistamine is recommended to minimize side effects. | 11
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This disorder became politically controversial when associated with domestic violence which was considered to be mostly caused by males. However a number of studies suggest that the disorder is common. In spite of its exclusion from DSM-IV in 1994, it continues to enjoy widespread currency amongst clinicians as a construct that explains a great many facets of human behaviour.Sexual masochism that "causes clinically significant distress or impairment in social, occupational, or other important areas of functioning" is still in DSM-IV. Millons subtypes
Theodore Millon has proposed four subtypes of masochist. Any individual masochist may fit into none, one or more of the following subtypes:
See also
Sadistic personality disorder
Self-handicapping
Self-preservation
Setting up to fail
Autosadism
Algolagnia
Learned helplessness
Notes
References
External links
http://www.psychnet-uk.com/x_new_site/personality_psychology/personality_disorders_self_defeating.html
https://www.scribd.com/doc/55533833/The-Riddle-of-Masochism | A bee sting is the wound and pain caused by the stinger of a female bee puncturing skin. Bee stings differ from insect bites, with the venom of stinging insects having considerable chemical variation. The reaction of a person to a bee sting may vary according to the bee species. While bee stinger venom is slightly acidic and causes only mild pain in most people, allergic reactions may occur in people with allergies to venom components. Honey bee stings
A honey bee that is away from the hive foraging for nectar or pollen will rarely sting, except when stepped on or roughly handled. Honey bees will actively seek out and sting when they perceive the hive to be threatened, often being alerted to this by the release of attack pheromones (below). Although it is widely believed that a worker honey bee can sting only once, this is a partial misconception: although the stinger is in fact barbed so that it lodges in the victims skin, tearing loose from the bees abdomen and leading to its death in minutes, this only happens if the skin of the victim is sufficiently thick, such as a mammals. Honey bees are the only hymenoptera with a strongly barbed sting, though yellow jackets and some other wasps have small barbs. The venom of the honeybee contains histamine, mast cell degranulating peptide, melittin, phospholipase A2, hyaluronidase and acid phosphatase. The three proteins in honeybee venom which are important allergens are phospholipase A2, hyaluronidase and acid phosphatase. | 0-1
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The star witness for the case against Bendectin, William McBride, was later found to have falsified research on teratogenic effects of the drug, and was struck off the medical register in Australia.An extensive review of the evidence submitted in legal proceedings regarding Bendectin has been summarized and found no evidence that the drug in clinical use was linked to birth defects.The FDA, in 1999, published a statement in the Federal Register that summarized their opinion regarding the safety of pyridoxine/doxylamine during pregnancy: “The FDA has determined that the drug product Bendectin, a tablet composed of pyridoxine hydrochloride 10 mg, and doxylamine succinate 10 mg, for the prevention of nausea of pregnancy was not withdrawn from the market for reasons of safety or effectiveness”. On Monday April 8, 2013, the FDA approved the return of the doxylamine-pyridoxine combination under the new trademark name of Diclegis. The medication is manufactured by Duchesnay Inc, a company later shown to not disclose conflict of interests with authors, leading to Canadian Family Physician to correct several articles because of their behavior and the lack of research that shows that there was medically significant results.In July 2015, the drug company came under considerable scrutiny for promoting its drug through the American celebrity Kim Kardashian through the social media platforms Facebook and Instagram.In October 2015, Toronto, Canada physicians Drs. | Crigler–Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. The disorder results in a form of nonhemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants. The disorder is inherited in an autosomal recessive manner. The annual incidence is estimated at 1 in 1,000,000.This syndrome is divided into types I and II, with the latter sometimes called Arias syndrome. These two types, along with Gilberts syndrome, Dubin–Johnson syndrome, and Rotor syndrome, make up the five known hereditary defects in bilirubin metabolism. Unlike Gilberts syndrome, only a few causes of Crigler–Najjar syndrome are known. Signs and symptoms
Jaundice
Diarrhea
Vomiting
Fever
Confusion
Slurred speech
Difficulty swallowing
Change in gait, staggering frequent falling
Seizures
Cause
It is caused by abnormalities in the gene coding for uridine diphosphoglucuronate glucuronosyltransferase (UGT1A1). UGT1A1 normally catalyzes the conjugation of bilirubin and glucuronic acid within hepatocytes. Conjugated bilirubin is more water-soluble and is excreted in bile. Diagnosis
Type I
This is a very rare disease (estimated at 0.6–1.0 per million live births), and consanguinity increases the risk of this condition (other rare diseases may be present). Inheritance is autosomal recessive. Intense jaundice appears in the first days of life and persists thereafter. Type 1 is characterised by a serum bilirubin usually above 345 μmol/L [20 mg/dL] (range 310–755 μmol/L [18–44 mg/dL]) (whereas the reference range for total bilirubin is 2–14 μmol/L [0.1–0.8 mg/dL]). No UDP glucuronosyltransferase 1-A1 expression can be detected in the liver tissue. | 0-1
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There is not a definite cause for the development of the disease, but one that was hypothesized is that it originates from a blood vessel tissue and smooth muscle fiber residue in an embryo. Imaging and histopathological examination is used for diagnosis of the disease. Furthermore, treatment of the disease is to surgically remove the tumor.Vulvar Leiomyomas are one the most prominent types of genital leiomyomas. Lesions to the vulva may be up to 15 cm in length and they are reported to be acutely painful. Enlargement of these leiomyomas may occur during pregnancy. Scrotal
Scrotal leiomyoma is considered to be an extremely rare type of genital leiomyoma. Because leiomyomas in the scrotum are usually painless and slowly grows over time, there is a delay in physician referral, with an average of 6–7 years. Physician referral usually occurs when people notice their testicles growing and getting heavier. A review of 11,000 cases of benign and malignant tumors of the scrotum found 11 cases of scrotal leiomyoma. Scrotal leiomyomas can affect males of any age and race, but are more common in Caucasians from the ages of 40-60. The tumor in the scrotum has an average diameter of 6.4 cm. Signs and symptoms
People with leiomyoma can be presented as asymptomatic, or having no symptoms. However, some people may experience severe symptoms that can interfere with daily activities. Common symptoms are recurrent pain and pressure in the affected region. People with uterine leiomyoma can experience pain during urination, bowel movements, and sexual intercourse. | This produces a rounded appearance on X-ray that doctors may mistake for a tumor. Rounded atelectasis is usually a complication of asbestos-induced disease of the pleura, but it may also result from other types of chronic scarring and thickening of the pleura. Treatment
Treatment is directed at correcting the underlying cause. In atelectasis manifestations that result from the mucus plugging of the airways as seen in patients with cystic fibrosis and pneumonia, mucolytic agents such as acetylcysteine (NAC) is used. This nebulized treatment works by reducing mucous viscosity and elasticity by breaking disulfide bonds in mucoproteins within the mucus complex, thus facilitating mucus clearance. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. One method is continuous positive airway pressure, which delivers pressurized air or oxygen through a nose or face mask to help ensure that the alveoli do not collapse, even at the end of a breath. This is helpful, as partially inflated alveoli can be expanded more easily than collapsed alveoli. Sometimes additional respiratory support is needed with a mechanical ventilator. The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. | 0-1
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Muscle spasticity
Botulinum toxin is used to treat a number of disorders characterized by overactive muscle movement, including cerebral palsy, post-stroke spasticity, post-spinal cord injury spasticity, spasms of the head and neck, eyelid, vagina, limbs, jaw, and vocal cords. Similarly, botulinum toxin is used to relax the clenching of muscles, including those of the esophagus, jaw, lower urinary tract and bladder, or clenching of the anus which can exacerbate anal fissure. Botulinum toxin appears to be effective for refractory overactive bladder. Other muscle disorders
Strabismus, otherwise known as improper eye alignment, is caused by imbalances in the actions of muscles that rotate the eyes. This condition can sometimes be relieved by weakening a muscle that pulls too strongly, or pulls against one that has been weakened by disease or trauma. Muscles weakened by toxin injection recover from paralysis after several months, so injection might seem to need to be repeated, but muscles adapt to the lengths at which they are chronically held, so that if a paralyzed muscle is stretched by its antagonist, it grows longer, while the antagonist shortens, yielding a permanent effect. | Society and culture
Economics
As of 2018, botulinum toxin injections are the most common cosmetic operation, with 7.4 million procedures in the United States, according to the American Society of Plastic Surgeons. Qualifications for Botox injectors vary by county, state, and country. Botox cosmetic providers include dermatologists, plastic surgeons, aesthetic spa physicians, dentists, nurse practitioners, nurses, and physician assistants.The global market for botulinum toxin products, driven by their cosmetic applications, was forecast to reach $2.9 billion by 2018. The facial aesthetics market, of which they are a component, was forecast to reach $4.7 billion ($2 billion in the U.S.) in the same timeframe. Global Market
In 2019, 6,271,488 Botulinum Toxin procedures were administered worldwide. The Global Botulinum Toxin market size was US$4.83 billion in 2019 and is projected to reach US$7.71 billion by 2027.US Market
In 2020, 4,401,536 Botulinum Toxin Type A procedures were administered. In 2019 the botulinum Toxin market made US$3.19 billion.Botox cost
Botox cost is generally determined by the number of units administered (avg. | 11
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This commonly occurs as a result of chest trauma (both blunt and penetrating), but can also be caused by myocardial infarction, myocardial rupture, cancer (most often Hodgkin lymphoma), uremia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissection, or while the person is taking anticoagulant therapy. The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances. Surgery
One of the most common settings for cardiac tamponade is in the first 7 days after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade. Pathophysiology
The pericardium, the double-walled sac surrounding the heart, consists of a fibrous pericardium layer on the outside and a double-layered serous pericardium on the inside. Between the two layers of the serous pericardium is the pericardial space, which is filled with lubricating serous fluid that prevents friction as the heart contracts. The outer layer of the heart is made of fibrous tissue which does not easily stretch, so once excess fluid begins to enter the pericardial space, pressure starts to increase. Consequently, the heart becomes compressed due to its inability to fully relax.If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. | Sowda is a cutaneous condition, a localized type of onchocerciasis. : 440
This is mostly seen in patients with the disease from Yemen, Saudi Arabia, East and West Africa
See also
Skin lesion
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Epidemiology
The prevalence of this disease is estimated to be < 1/million.The usual age at presentation is between 20 and 40 but it has been reported in the newborn. History
This condition was first described in 1978. Animals
This condition has been reported in cats. and dogs. References
== External links == | Dasiglucagon, sold under the brand name Zegalogue, is a medication used to treat severe hypoglycemia in people with diabetes.The most common side effects include nausea, vomiting, headache, diarrhea, and injection site pain.Dasiglucagon was approved for medical use in the United States in March 2021. It was designated an orphan drug in August 2017. Medical uses
Dasiglucagon is indicated for the treatment of severe hypoglycemia in people aged six years of age and older with diabetes. Contraindications
Dasiglucagon is contraindicated in people with pheochromocytoma or insulinoma. References
External links
"Dasiglucagon". Drug Information Portal. U.S. National Library of Medicine. Clinical trial number NCT03378635 for "A Trial to Confirm the Efficacy and Safety of Dasiglucagon in the Treatment of Hypoglycemia in Type 1 Diabetes Subjects" at ClinicalTrials.gov
Clinical trial number NCT03688711 for "Trial to Confirm the Clinical Efficacy and Safety of Dasiglucagon in the Treatment of Hypoglycemia in Subjects With T1DM" at ClinicalTrials.gov
Clinical trial number NCT03667053 for "Trial to Confirm the Efficacy and Safety of Dasiglucagon in the Treatment of Hypoglycemia in T1DM Children" at ClinicalTrials.gov | 0-1
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A large body of evidence demonstrates an association between this condition and both poor emotional well-being and reduced health-related quality of life. A link between stress and this condition has also been shown. A recent study has demonstrated an association between stressful life events (e.g. bereavement, divorce, etc.) and chronic idiopathic urticaria and also an association between post-traumatic stress and chronic idiopathic hives. Diagnosis
Diagnosis is typically based on the appearance. The cause of chronic hives can rarely be determined. Patch testing may be useful to determine the allergy. In some cases regular extensive allergy testing over a long period of time is requested in hopes of getting new insight. No evidence shows regular allergy testing results in identification of a problem or relief for people with chronic hives. Regular allergy testing for people with chronic hives is not recommended. Acute versus chronic
Acute urticaria is defined as the presence of evanescent wheals which completely resolve within six weeks. Acute urticaria becomes evident a few minutes after the person has been exposed to an allergen. The outbreak may last several weeks, but usually the hives are gone in six weeks. Typically, the hives are a reaction to food, but in about half the cases, the trigger is unknown. Common foods may be the cause, as well as bee or wasp stings, or skin contact with certain fragrances. Acute viral infection is another common cause of acute urticaria (viral exanthem). Less common causes of hives include friction, pressure, temperature extremes, exercise, and sunlight. | Hyperoxaluria is an excessive urinary excretion of oxalate. Individuals with hyperoxaluria often have calcium oxalate kidney stones. It is sometimes called Birds disease, after Golding Bird, who first described the condition. Causes
Hyperoxaluria can be primary (as a result of a genetic defect) or secondary to another disease process. Type I primary hyperoxaluria (PH1) is associated mutations in the gene encoding AGXT, a key enzyme involved in oxalate metabolism. PH1 is an example of a protein mistargeting disease, wherein AGXT shows a trafficking defect. Instead of being trafficked to peroxisomes, it is targeted to mitochondria, where it is metabolically deficient despite being catalytically active. Type II is associated with GRHPR.Secondary hyperoxaluria can occur as a complication of jejunoileal bypass, or in a patient who has lost much of the ileum with an intact colon. In these cases, hyperoxaluria is caused by excessive gastrointestinal oxalate absorption.Excessive intake of oxalate-containing food, such as rhubarb, may also be a cause in rare cases. Diagnosis
Types
Primary hyperoxaluria
Enteric hyperoxaluria
Idiopathic hyperoxaluria
Oxalate poisoning
Treatment
The main therapeutic approach to primary hyperoxaluria is still restricted to symptomatic treatment, i.e. kidney transplantation once the disease has already reached mature or terminal stages. However, through genomics and proteomics approaches, efforts are currently being made to elucidate the kinetics of AGXT folding which has a direct bearing on its targeting to appropriate subcellular localization. Secondary hyperoxaluria is much more common than primary hyperoxaluria, and should be treated by limiting dietary oxalate and providing calcium supplementation. A child with primary hyperoxaluria was treated with a liver and kidney transplant. | 0-1
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Medical uses
Treatment of PCP caused by Pneumocystis jirovecii
Prevention of PCP in adults with HIV who have one or both of the following:
History of PCP
CD4+ count ≤ 200mm³
Treatment of leishmaniasis
Treatment of African trypanosomiasis caused by Trypanosoma brucei gambiense
Balamuthia infections
Pentamidine is classified as an orphan drug by the U.S. Food and Drug Administration
Other uses
Use as an antitumor drug has also been proposed. Pentamidine is also identified as a potential small molecule antagonist that disrupts this interaction between S100P and RAGE receptor. Special Populations
Pregnancy
It has not been shown to cause birth defects in animal studies when given intravenously. There are no controlled studies to show if pentamidine can harm the fetus in pregnant women. It is only recommended if the drug of choice trimethoprim-sulfamethoxazole is contraindicated. Breastfeeding
There is no information regarding the excretion of pentamidine in breast milk, but since the adverse effects on breastfed infants are unknown currently, it is recommended by the manufacturer for the infant to not be breastfed or for the mother to stop the drug. Risks versus benefits for the mother should be considered when making this decision. Children
Pentamidine can be used in the prevention of PCP in children with HIV who cannot tolerate Trimethoprim/Sulfamethoxazole and can use a nebulizer. Intranvenous solutions of pentamidine should only be used in children with HIV older than 2 years old when other treatments are unavailable
Elderly
There is no data for the use of pentamidine in this specific population. | See also
Restasis (ciclosporin eye drops for keratoconjunctivitis sicca)
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The oldest drugs on the market are not prescribed often, but may be a good option for some women. These include tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). TCAs may cause side effects like dry mouth, constipation, or dizziness. MAOIs can cause sedation, insomnia, dizziness, and weight gain. To avoid the risk of a rapid rise in blood pressure, people taking MAOIs must also avoid eating a substance called tyramine, found in yogurt, aged cheese, pickles, beer, and red wine. Some drug side effects subside with time, while others may lessen when a drug dose is lowered. Research
Differences in the brains structure and function appear to be present in adolescents with depression though this may depend on age. Younger adolescents, mostly under the age of 18, with depression have shown greater white matter volume within frontal regions of the brain, greater cortical thickness in the anterior cingulate cortex and medial orbitofrontal cortex, as well as greater functional connectivity between cortico-limbic brain regions. Whereas older adolescents, mostly above the age of 18, appear to show lower cortical surface area in regions including the lingual, occipital gyri, as well as medial orbitofrontal and motor cortices. Results such as these have led to the hypothesis that the biological causes of depression may in part be neurodevelopmental, with its biological underpinnings forming early on in brain development. | Depression is a mental disorder characterized by prolonged unhappiness or irritability, accompanied by a constellation of somatic and cognitive signs and symptoms such as fatigue, apathy, sleep problems, loss of appetite, loss of engagement; low self-regard or worthlessness; difficulty concentrating or indecisiveness; or recurrent thoughts of death or suicide. Depression in childhood and adolescence is similar to adult major depressive disorder, although young sufferers may exhibit increased irritability or behavioral dyscontrol instead of the more common sad, empty, or hopeless feelings seen with adults. Children who are under stress, experiencing loss, or have other underlying disorders are at a higher risk for depression. Childhood depression is often comorbid with mental disorders outside of other mood disorders; most commonly anxiety disorder and conduct disorder. Depression also tends to run in families. In a 2016 Cochrane review cognitive behavior therapy (CBT), third wave CBT and interpersonal therapy demonstrated small positive benefits in the prevention of depression. Psychologists have developed different treatments to assist children and adolescents suffering from depression, though the legitimacy of the diagnosis of childhood depression as a psychiatric disorder, as well as the efficacy of various methods of assessment and treatment, remains controversial. Base rates and prevalence
About 8% of children and adolescents suffer from depression. In 2016, 51 percent of students (teens) who visited a counseling center reported having anxiety, followed by depression (41 percent), relationship concerns (34 percent) and suicidal ideation (20.5 percent). Many students reported experiencing multiple conditions at once. | 11
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Blood pressure control is often achieved using diuretics or a combination of diuretics and angiotensin converter enzyme inhibitors, although the optimal treatment regimen depends on the individual.Studies that evaluated the application of Blood pressure‐lowering drugs in people who had a TIA or stroke, concluded that this type of medication helps to reduce the possibility of a recurrent stroke, of a major vascular event and dementia. The effects achieved in stroke recurrence were mainly obtained through the ingestion of angiotensin-converting enzyme (ACE) inhibitor or a diuretic. Cholesterol control
There is inconsistent evidence regarding the effect of LDL-cholesterol levels on stroke risk after TIA. Elevated cholesterol may increase ischemic stroke risk while decreasing the risk of hemorrhagic stroke. While its role in stroke prevention is currently unclear, statin therapy has been shown to reduce all-cause mortality and may be recommended after TIA. Diabetes control
Diabetes mellitus increases the risk of ischemic stroke by 1.5-3.7 times, and may account for at least 8% of first ischemic strokes. While intensive glucose control can prevent certain complications of diabetes such as kidney damage and retinal damage, there has previously been little evidence that it decreases the risk of stroke or death. However, data from 2017 suggests that metformin, pioglitazone and semaglutide may reduce stroke risk. Surgery
If the TIA affects an area that is supplied by the carotid arteries, a carotid ultrasound scan may demonstrate stenosis, or narrowing, of the carotid artery. | Anonychia is the absence of fingernails or toenails, an anomaly which may be the result of a congenital ectodermal defect, ichthyosis, severe infection, severe allergic contact dermatitis, self-inflicted trauma, Raynaud phenomenon, lichen planus, epidermolysis bullosa, or severe exfoliative diseases. : 784
Congenital form
This is rare and is usually due to mutations in the R-spondin 4 (RSPO4) gene which is located on the short arm of chromosome 20 (20p13). Clinically it is manifest by the absence (anonychia) or hypoplasia (hyponychia) of finger- or toenails. See also
List of cutaneous conditions
References
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There is also not enough evidence on effectiveness of giving intermittent twice or thrice weekly short course regimen compared to daily dosing regimen in treating children with tuberculosis. Medication resistance
Primary resistance occurs when a person becomes infected with a resistant strain of TB. A person with fully susceptible MTB may develop secondary (acquired) resistance during therapy because of inadequate treatment, not taking the prescribed regimen appropriately (lack of compliance), or using low-quality medication. Drug-resistant TB is a serious public health issue in many developing countries, as its treatment is longer and requires more expensive drugs. MDR-TB is defined as resistance to the two most effective first-line TB drugs: rifampicin and isoniazid. Extensively drug-resistant TB is also resistant to three or more of the six classes of second-line drugs. Totally drug-resistant TB is resistant to all currently used drugs. It was first observed in 2003 in Italy, but not widely reported until 2012, and has also been found in Iran and India. There is some efficacy for linezolid to treat those with XDR-TB but side effects and discontinuation of medications were common. Bedaquiline is tentatively supported for use in multiple drug-resistant TB.XDR-TB is a term sometimes used to define extensively resistant TB, and constitutes one in ten cases of MDR-TB. Cases of XDR TB have been identified in more than 90% of countries.For those with known rifampicin or MDR-TB, molecular tests such as the Genotype® MTBDRsl Assay (performed on culture isolates or smear positive specimens) may be useful to detect second-line anti-tubercular drug resistance. | Effective TB treatment is difficult, due to the unusual structure and chemical composition of the mycobacterial cell wall, which hinders the entry of drugs and makes many antibiotics ineffective.Active TB is best treated with combinations of several antibiotics to reduce the risk of the bacteria developing antibiotic resistance. The routine use of rifabutin instead of rifampicin in HIV-positive people with tuberculosis is of unclear benefit as of 2007. Latent TB
Latent TB is treated with either isoniazid or rifampin alone, or a combination of isoniazid with either rifampicin or rifapentine.The treatment takes three to nine months depending on the medications used. People with latent infections are treated to prevent them from progressing to active TB disease later in life.Education or counselling may improve the latent tuberculosis treatment completion rates. New onset
The recommended treatment of new-onset pulmonary tuberculosis, as of 2010, is six months of a combination of antibiotics containing rifampicin, isoniazid, pyrazinamide, and ethambutol for the first two months, and only rifampicin and isoniazid for the last four months. Where resistance to isoniazid is high, ethambutol may be added for the last four months as an alternative. Treatment with anti-TB drugs for at least 6 months results in higher success rates when compared with treatment less than 6 months, even though the difference is small. Shorter treatment regimen may be recommended for those with compliance issues. There is also no evidence to support shorter anti-tuberculosis treatment regimens when compared to a 6-month treatment regimen. | 11
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"In August 2010, Wired reported that a man in Hawaii, Craig Smallwood, sued the gaming company NCSoft for negligence and for not specifying that their game, Lineage II, was so addictive. He alleged he would not have begun playing if he was aware he would become addicted. Smallwood says he has played Lineage for 20,000 hours between 2004 and 2009.In 2013, a man from China observed his sons addiction to video games, and decided to take action. He hired online assassins to kill his sons virtual avatar every time he logged in. He hoped that being relentlessly killed would help his son lose interest in this destructive habit. Inclusion in the ICD-11
In the draft versions leading to the final ICD-11 document, gaming disorder was included alongside gambling disorder under "Disorders Due to Addictive Behaviors". The addition defines as "a pattern of persistent or recurrent gaming behaviour (digital gaming or video-gaming)", defined by three criteria: the lack of control over playing video games, priority given to video games over other interests, and the inability to stop playing video games even after being affected by negative consequences. For gaming disorder to be diagnosed, the behavior pattern must be of sufficient severity to result in significant impairment in personal, family, social, educational, occupational or other important areas of functioning and would normally have been evident for at least 12 months. | Video game addiction (VGA), also known as gaming disorder or internet gaming disorder, is generally defined as the problematic, compulsive use of video games that results in significant impairment to an individuals ability to function in various life domains over a prolonged period of time. This and associated concepts have been the subject of considerable research, debate, and discussion among experts in several disciplines and has generated controversy within the medical, scientific, and gaming communities. Such disorders can be diagnosed when an individual engages in gaming activities at the cost of fulfilling daily responsibilities or pursuing other interests without regard for the negative consequences. As defined by the ICD-11, the main criterion for this disorder is a lack of self control over gaming.The World Health Organization included gaming disorder in the 11th revision of its International Classification of Diseases (ICD). The American Psychiatric Association (APA), while stating there is insufficient evidence for the inclusion of Internet gaming disorder in the Diagnostic and Statistical Manual of Mental Disorders in 2013, considered it worthy of further study.Controversy around the diagnosis includes whether the disorder is a separate clinical entity or a manifestation of underlying psychiatric disorders. Research has approached the question from a variety of viewpoints, with no universally standardized or agreed definitions, leading to difficulties in developing evidence-based recommendations. | 11
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Significant levels of inflammatory infiltrate have been found in transitional hair follicles. Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss.The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains a mystery, but possible explanations are higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress. The mechanism by which the androgen receptor triggers dermal papilla permanent senescence is not known, but may involve IL6, TGFB-1 and oxidative stress. Senescence of the dermal papilla is measured by lack of mobility, different size and shape, lower replication and altered output of molecules and different expression of markers. The dermal papilla is the primary location of androgen action and its migration towards the hair bulge and subsequent signaling and size increase are required to maintain the hair follicle so senescence via the androgen receptor explains much of the physiology. Inheritance
Male pattern baldness is an X-linked recessive condition, because of its "particularly strong signals on the X chromosome". Metabolic syndrome
Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome, with low HDL being the component of metabolic syndrome with highest association. | The envelope is reinforced structurally by matrix proteins on the interior that enclose the RNPs, and the envelope contains HA and NA (or HEF) proteins extending outward from the exterior surface of the envelope. HA and HEF proteins have a distinct "head" and "stalk" structure. M2 proteins form proton ion channels through the viral envelope that are required for viral entry and exit. IBVs contain a surface protein named NB that is anchored in the envelope, but its function is unknown. Life cycle
The viral life cycle begins by binding to a target cell. Binding is mediated by the viral HA proteins on the surface of the evelope, which bind to cells that contain sialic acid receptors on the surface of the cell membrane. For N1 subtypes with the "G147R" mutation and N2 subtypes, the NA protein can initiate entry. Prior to binding, NA proteins promote access to target cells by degrading mucous, which helps to remove extracellular decoy receptors that would impede access to target cells. After binding, the virus is internalized into the cell by an endosome that contains the virion inside it. The endosome is acidified by cellular vATPase to have lower pH, which triggers a conformational change in HA that allows fusion of the viral envelope with the endosomal membrane. At the same time, hydrogen ions diffuse into the virion through M2 ion channels, disrupting internal protein-protein interactions to release RNPs into the host cells cytosol. | 0-1
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This led to the disease being known as "Asturian leprosy", and it is recognized as the first modern pathological description of a syndrome. It was an endemic disease in northern Italy, where it was named, from Lombard, as "pell agra" (agra = holly-like or serum-like; pell = skin) by Francesco Frapolli of Milan. With pellagra affecting over 100,000 people in Italy by the 1880s, debates raged as to how to classify the disease (as a form of scurvy, elephantiasis or as something new), and over its causation. In the 19th century, Roussel started a campaign in France to restrict consumption of maize and eradicated the disease in France, but it remained endemic in many rural areas of Europe. Because pellagra outbreaks occurred in regions where maize was a dominant food crop, the most convincing hypothesis during the late 19thcentury, as espoused by Cesare Lombroso, was that the maize either carried a toxic substance or was a carrier of disease. Louis Sambon, an Anglo-Italian doctor working at the London School of Tropical Medicine, was convinced that pellagra was carried by an insect, along the lines of malaria. Later, the lack of pellagra outbreaks in Mesoamerica, where maize is a major food crop, led researchers to investigate processing techniques in that region. Pellagra was studied mostly in Europe until the late 19th century when it became epidemic especially in the southern United States. In the early 1900s, pellagra reached epidemic proportions in the American South. | It also incorporates itself into viral DNA, hence inhibiting viral DNA synthesis during reproduction.It possesses in vitro activity against the following viruses:
Human herpesviruses
Adenoviruses
Human poxviruses (including the smallpox virus)
Human papillomavirus
History
Cidofovir was discovered at the Institute of Organic Chemistry and Biochemistry, Prague, by Antonín Holý, and developed by Gilead Sciences and is marketed with the brand name Vistide by Gilead in the US, and by Pfizer elsewhere. Synthesis
Cidofovir can be synthesized from a pyrimidone derivative and a protected derivative of glycidol. See also
Brincidofovir, a novel prodrug of cidofovir that can be taken orally
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Pain and physical violence are not essential in Krafft-Ebings conception, and he defined "masochism" (German Masochismus) entirely in terms of control. Sigmund Freud, a psychoanalyst and a contemporary of Krafft-Ebing, noted that both were often found in the same individuals, and combined the two into a single dichotomous entity known as "sadomasochism" (German Sadomasochismus, often abbreviated as S&M or S/M). This observation is commonly verified in both literature and practice; many practitioners, both sadists and masochists, define themselves as switches and "switchable" — capable of taking and deriving pleasure in either role. However, French philosopher Gilles Deleuze argued that the concurrence of sadism and masochism proposed in Freuds model is the result of "careless reasoning," and should not be taken for granted.Freud introduced the terms "primary" and "secondary" masochism. Though this idea has come under a number of interpretations, in a primary masochism the masochist undergoes a complete, rather than partial, rejection by the model or courted object (or sadist), possibly involving the model taking a rival as a preferred mate. This complete rejection is related to the death drive (Todestrieb) in Freuds psychoanalysis. In a secondary masochism, by contrast, the masochist experiences a less serious, more feigned rejection and punishment by the model. | Secondary masochism, in other words, is the relatively casual version, more akin to a charade, and most commentators are quick to point out its contrivedness.Rejection is not desired by a primary masochist in quite the same sense as the feigned rejection occurring within a mutually consensual relationship—or even where the masochist happens to be the one having actual initiative power. In Things Hidden Since the Foundation of the World, René Girard attempts to resuscitate and reinterpret Freuds distinction of primary and secondary masochism, in connection with his own philosophy.Both Krafft-Ebing and Freud assumed that sadism in men resulted from the distortion of the aggressive component of the male sexual instinct. Masochism in men, however, was seen as a more significant aberration, contrary to the nature of male sexuality. Freud doubted that masochism in men was ever a primary tendency, and speculated that it may exist only as a transformation of sadism. Sadomasochism in women received comparatively little discussion, as it was believed that it occurred primarily in men. Both also assumed that masochism was so inherent to female sexuality that it would be difficult to distinguish as a separate inclination. Havelock Ellis, in Studies in the Psychology of Sex, argued that there is no clear distinction between the aspects of sadism and masochism, and that they may be regarded as complementary emotional states. He also made the important point that sadomasochism is concerned only with pain in regard to sexual pleasure, and not in regard to cruelty, as Freud had suggested. | 11
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Especially common are selenides (R2Se, analogues of thioethers), diselenides (R2Se2, analogues of disulfides), and selenols (RSeH, analogues of thiols). Representatives of selenides, diselenides, and selenols include respectively selenomethionine, diphenyldiselenide, and benzeneselenol. The sulfoxide in sulfur chemistry is represented in selenium chemistry by the selenoxides (formula RSe(O)R), which are intermediates in organic synthesis, as illustrated by the selenoxide elimination reaction. Consistent with trends indicated by the double bond rule, selenoketones, R(C=Se)R, and selenaldehydes, R(C=Se)H, are rarely observed. History
Selenium (Greek σελήνη selene meaning "Moon") was discovered in 1817 by Jöns Jacob Berzelius and Johan Gottlieb Gahn. Both chemists owned a chemistry plant near Gripsholm, Sweden, producing sulfuric acid by the lead chamber process. The pyrite from the Falun Mine created a red precipitate in the lead chambers which was presumed to be an arsenic compound, so the pyrites use to make acid was discontinued. Berzelius and Gahn wanted to use the pyrite and they also observed that the red precipitate gave off a smell like horseradish when burned. This smell was not typical of arsenic, but a similar odor was known from tellurium compounds. Hence, Berzeliuss first letter to Alexander Marcet stated that this was a tellurium compound. However, the lack of tellurium compounds in the Falun Mine minerals eventually led Berzelius to reanalyze the red precipitate, and in 1818 he wrote a second letter to Marcet describing a newly found element similar to sulfur and tellurium. | BritLofex is only available by prescription. Lofexidine was first approved by the US FDA on May 16, 2018, under the brand name Lucemyra, produced by US WorldMeds. It was noted as the first, non-opioid drug approved in the US for the treatment of opioid withdrawal. See also
Methadone
Naltrexone
Clonidine
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Non-Hodgkin lymphoma (NHL), also known as non-Hodgkins lymphoma, is a group of blood cancers that includes all types of lymphomas except Hodgkin lymphomas. Symptoms include enlarged lymph nodes, fever, night sweats, weight loss, and tiredness. Other symptoms may include bone pain, chest pain, or itchiness. Some forms are slow-growing while others are fast-growing.Lymphomas are types of cancer that develop from lymphocytes, a type of white blood cell. Risk factors include poor immune function, autoimmune diseases, Helicobacter pylori infection, hepatitis C, obesity, and Epstein–Barr virus infection. The World Health Organization classifies lymphomas into five major groups, including one for Hodgkin lymphoma. Within the four groups for NHL are over 60 specific types of lymphoma. Diagnosis is by examination of a bone marrow or lymph node biopsy. Medical imaging is done to help with cancer staging.Treatment depends on whether the lymphoma is slow- or fast-growing and if it is in one area or many areas. Treatments may include chemotherapy, radiation, immunotherapy, targeted therapy, stem-cell transplantation, surgery, or watchful waiting. If the blood becomes overly thick due to high numbers of antibodies, plasmapheresis may be used. Radiation and some chemotherapy, however, increase the risk of other cancers, heart disease, or nerve problems over the subsequent decades.In 2015, about 4.3 million people had non-Hodgkin lymphoma, and 231,400 (5.4%) died. In the United States, 2.1% of people are affected at some point in their life. The most common age of diagnosis is between 65 and 75 years old. The five-year survival rate in the United States is 71%. | Signs and symptoms
The signs and symptoms of non-Hodgkin lymphoma vary depending upon its location within the body. Symptoms include enlarged lymph nodes, fever, night sweats, weight loss, and tiredness. Other symptoms may include bone pain, chest pain, or itchiness. Some forms are slow growing, while others are fast growing. Enlarged lymph nodes may cause lumps to be felt under the skin when they are close to the surface of the body. Lymphomas in the skin may also result in lumps, which are commonly itchy, red, or purple. Lymphomas in the brain can cause weakness, seizures, problems with thinking, and personality changes.While an association between non-Hodgkin lymphoma and endometriosis has been described, these associations are tentative. Causes
The many different forms of lymphoma probably have different causes. These possible causes and associations with at least some forms of NHL include:
Infectious agents:
Epstein–Barr virus: associated with Burkitts lymphoma, follicular dendritic cell sarcoma, extranodal NK-T-cell lymphoma and diffuse large B-cell lymphoma. Human T-cell leukemia virus: associated with adult T-cell lymphoma. Helicobacter pylori: associated with gastric lymphoma. HHV-8: associated with primary effusion lymphoma, multicentric Castleman disease. Hepatitis C virus: associated with splenic marginal zone lymphoma, lymphoplasmacytic lymphoma and diffuse large B-cell lymphoma. HIV infection. Some chemicals, like polychlorinated biphenyls (PCBs), diphenylhydantoin, dioxin, and phenoxy herbicides. Medical treatments, like radiation therapy and chemotherapy. Genetic diseases, like Klinefelter syndrome, Chédiak–Higashi syndrome, ataxia–telangiectasia syndrome. Autoimmune diseases, like Sjögren syndrome, celiac disease, rheumatoid arthritis, and systemic lupus erythematosus. Bone trauma and microfractures associated with diffuse large B-cell lymphoma originating in bone marrow. | 11
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In addition, unaffected gyri are also present in especially bilateral watershed regions indicating delayed effects of perinatal hypoxic damage. However, there are three main criteria for diagnosing ulegyria using MRI in addition to the features mentioned above:
1.The presence of a poorly demarcated lesion
2. Atrophy and thinning of the cortex resulting in the characteristic “mushroom” like shape of ulegyria. 3. Presence of white matter signal abnormalities as a result of FLAIR signaling (fluid attenuated inversion recovery).Another sign of ulegyria that is visible on an MRI scan is the presence of a widened subarachnoid space, signifying cortex atrophy. FLAIR signaling can help visualize the depths of the parietal-occipital sulci, which also allows ulegyria-affected gyri to be identified. Though there is still confusion in differentiating ulegyria and polymicrogyria in patients, MRI allows for the proper identification in the majority of the cases. In addition, most of the current research regarding ulegyria is focused on improving this identification. Furthermore, MRI can diagnose whether ulegyria presence is unilateral or bilateral. Electroencephalography, EEG, can also be used to screen for ulegyria, though MRI is still preferred. This is mainly done for epilepsy patients as abnormalities in EEG recordings indicate the presence of ulegyria in the area of the brain being tested. For example, when EEG tests in epileptic patients show deviations in the frontal and central-parietal regions, ulegyria can be considered to be present in that area. Treatment
Presently, there is no well-defined treatment for ulegyria mainly because of the irreversible ischaemic damage done to neurons of an affected area. | Polymicrogyria is characterized by excessive folding of the surface gyri and a thickening of the cerebral cortex, rather than the sulcal scarring that is typical of ulegyria. In addition to morphological differences, the period in which polmicrogyria and ulegyria emerge is also different. Polymicrogyria typically forms while the embryos central nervous system is maturing. Ulegyria is acquired later in development during the perinatal period after neuronal migration has already occurred. It is also suspected that polymicrogyra is genetically linked, whereas ulegyria is caused by environmental factors—namely lack of oxygen.Polymicrogyria can lead to similar conditions that are linked to ulegyria such as mental retardation, cerebral palsy, and epilepsy. It has been observed that patients with polymicrogyria are not receptive to epilepsy surgery. However, responses of patients with ulegyria to similar surgeries are still not fully known, which makes distinction of these two disorders significant. In vivo neuroimaging techniques, namely MRI, have been instrumental in making this distinction. An MRI image of ulegyria is identified by mushroom shaped gyri, deformities in white matter, and localization mainly in the posterior cerebral region. Polymicrogyria is typically recognized by a scalloped appearance at the bordering region between grey and white matter. Although these distinctions have been made with many patients, there is still some difficulty in defining distinct boundaries between these two similar conditions. Detection
Primarily, the main method of detecting ulegyria is through the use of MRI screening for epilepsy. Normally an MRI of an ulegyria affected region will reveal groups of deteriorated neurons with gliosis present. | 11
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However, the evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option.Evidence supports the use of cannabinoids for some forms of neuropathic pain. A 2018 Cochrane review of cannabis-based medicines for the treatment of chronic neuropathic pain included 16 studies. All of these studies included THC as a pharmacological component of the test group. The authors rated the quality of evidence as very low to moderate. The primary outcome was quoted as, "Cannabis-based medicines may increase the number of people achieving 50% or greater pain relief compared with placebo" but "the evidence for improvement in Patient Global Impression of Change (PGIC) with cannabis to be of very low quality". The authors also conclude, "The potential benefits of cannabis-based medicine... might be outweighed by their potential harms. "A 2014 Cochrane review of topical lidocaine for the treatment of various peripheral neuropathies found its usage supported by a few low quality studies. The authors state that there are no high quality randomised control trials demonstrating its efficacy or safety profile.A 2015 (updated in 2022) Cochrane review of topical clonidine for the treatment of diabetic neuropathy included two studies of 8 and 12 weeks in length; both of which compared topical clonidine to placebo and both of which were funded by the same drug manufacturer. The review found that topical clonidine may provide some benefit versus placebo. | Transplanting skin derived from genetically modified stem cells onto the wound surfaces has been studied with a report of improvements in one person.A 2017 clinical trial with male RDEB (recessive dystrophic EB) patients conducted successful grafting of type VII gene corrected keratinocytes (COL7A1 gene correction using retrovirus transduction), without any serious adverse effects. Type VII collage formation was observed at the dermis-epidermis junction in significant amounts.A 2020 study demonstrated the safe allogenic grafting of acellular dermal matrix/scaffolds in EB patients without any observed infection or necrosis and instead noted fewer required dressing changes, promoted wound healing, pain reduction, and an overall improvement in the quality of life of the patients. Monitoring
The Epidermolysis Bullosa Disease Activity and Scarring index (EBDASI) is a scoring system that objectively quantifies the severity of EB. The EBDASI is a tool for clinicians and patients to monitor the severity of the disease. It has also been designed to evaluate the response to new therapies for the treatment of EB. The EBDASI was developed and validated by Professor Dedee Murrell and her team of students and fellows at the St George Hospital, University of New South Wales, in Sydney, Australia. It was presented at the International Investigative Dermatology congress in Edinburgh in 2013 and a paper-based version was published in the Journal of the American Academy of Dermatology in 2014. Prognosis
A 2014 study classified cases into three types—EBS, JEB and DEB—and reviewed their times of death. The first two types tended to die in infancy and the last in early adulthood. | 0-1
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Surgery to cut the adhesions (capsular release) may be indicated in prolonged and severe cases; the procedure is usually performed by arthroscopy. Surgical evaluation of other problems with the shoulder, e.g., subacromial bursitis or rotator cuff tear, may be needed. Resistant adhesive capsulitis may respond to open release surgery. This technique allows the surgeon to find and correct the underlying cause of restricted glenohumeral movement such as contracture of coracohumeral ligament and rotator interval. Physical therapy may achieve improved results after surgical procedure and postoperative rehabilitation.Physical therapy is an effective procedure that provides essential exercises to improve range of motion. Patients who receive the proper training from an authorized physiotherapist can perform these exercises independently at home. The physiotherapy treatment for frozen shoulder will include manual therapy to mobilize the affected joints and release their muscles. "Pendulum stretch", "finger walk", "towel stretch", "armpit stretch" and "crossbody reach" are some essential mobility exercises specifically designed to improve the shoulder mobility of patients with frozen shoulders. There are also limited case reports of therapy utilizing vibration platforms obtaining fast results, not as a post-operative aid, but instead of surgery.Acupuncture has been found to decrease pain levels and improve shoulder function and range of motion, particularly in shoulder flexion. Acupuncture combined with shoulder exercises was found to be more effective than shoulder exercise alone. However, further studies with longer follow-up times are needed to assess mid- and long term benefits. Prognosis
Most cases of adhesive capsulitis are self limiting, but may take 1 to 3 years to fully resolve. | Mafenide (INN; usually as mafenide acetate, trade name Sulfamylon) is a sulfonamide-type medication used as an antibiotic. It was approved by the FDA in 1948. Uses
Mafenide is used to treat severe burns. It is used topically as an adjunctive therapy for second- and third-degree burns. It is bacteriostatic against many gram-positive and gram-negative organisms, including Pseudomonas aeruginosa. Some sources state that mafenide is more appropriate for non-facial burns, while chloramphenicol/prednisolone or bacitracin are more appropriate for facial burns. Mechanism of action
Mafenide works by reducing the bacterial population present in the avascular tissues of burns and permits spontaneous healing of deep partial-thickness burns. Adverse reactions
Adverse reactions can include superinfection, pain or burning upon application, rash, pruritus, tachypnea, or hyperventilation. Mafenide is metabolized to a carbonic anhydrase inhibitor, which could potentially result in metabolic acidosis. Drug interactions
There are no significant interactions. Contraindications
Mafenide is contraindicated in those with sulfonamide hypersensitivity or renal impairment. Dosage
For use as adjunctive therapy for second- and third-degree burns to prevent infection, adults and children should apply topically to a thickness of approximately 1.6 mm to cleaned and debrided wound once or twice per day with a sterile gloved hand. The burned area should be covered with cream at all times. References
External links
Mafenide information on RxList | 0-1
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Other medications and treatments are available, but have only anecdotal evidence.Medications that may worsen RBD and should be stopped if possible are tramadol, mirtazapine, antidepressants, and beta blockers.In addition to medication, it is wise to secure the sleepers environment by removing potentially dangerous objects from the bedroom and either place a cushion around the bed or move the mattress to the floor for added protection against injuries. In extreme cases, an affected individual has slept in a sleeping bag zipped up to their neck, wearing mittens so they cannot unzip it until they awake.Patients are advised to maintain a normal sleep schedule, avoid sleep deprivation, and keep track of any sleepiness they may have. Treatment includes regulating neurologic symptoms and treating any other sleep disorders that might interfere with sleep. Sleep deprivation, alcohol, certain medications, and other sleep disorders can all increase RBD and should be avoided if possible. Prognosis
Patients with RBD are at risk for sleep-related injury.Almost 92% of patients with idiopathic RBD will go on to develop a neurodegenerative disorder. The disorders most strongly associated with RBD are the synucleinopathies, particularly Parkinsons disease, dementia with Lewy bodies, and to a lesser extent, multiple system atrophy. Most people with RBD will convert to a synucleinopathy—usually Parkinsons disease or dementia with Lewy bodies—within 4 to 9 years from diagnosis of RBD, and 11 to 16 years from onset of symptoms. Epidemiology
RBD prevalence as of 2017 is estimated to be 0.5–2% overall, and 5–13% of those aged 60 to 99. | Umbilical-urachal sinus is a congenital disorder of the urinary bladder caused by failure of obliteration of proximal or distal part of the allantois, and the presentation of this anomaly is more common in children and rarer in adults.It is thought have been first described by Cabriolus in 1550. Complications
Infection, with possible abscess formation. Concurrent occurrence of a tumour. See also
Urachus
== References == | 0-1
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GRMF affects primarily the liver (rather than the kidneys) for some physiological processes.High-potassium media (which stimulates aldosterone secretion in vitro) also stimulate cortisol secretion from the fasciculata zone of canine adrenals — unlike corticosterone, upon which potassium has no effect.Potassium loading also increases ACTH and cortisol in humans. This is probably the reason why potassium deficiency causes cortisol to decline (as mentioned) and causes a decrease in conversion of 11-deoxycortisol to cortisol. This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA.Ascorbic acid presence, particularly in high doses has also been shown to mediate response to psychological stress and speed the decrease of the levels of circulating cortisol in the body post-stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol levels after treatment with ascorbic acid. Factors increasing cortisol levels
Viral infections increase cortisol levels through activation of the HPA axis by cytokines. Intense (high VO2 max) or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose; however, cortisol declines to normal levels after eating (i.e., restoring a neutral energy balance)
Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods. Low-carbohydrate diets cause a short-term increase in resting cortisol (~3 weeks), and increase the cortisol response to aerobic exercise in the short- and long-term. Biochemistry
Biosynthesis
Cortisol is synthesized from cholesterol. Synthesis takes place in the zona fasciculata of the adrenal cortex. (The name cortisol is derived from cortex.) | The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown. Bone and collagen
Cortisol reduces bone formation, favoring long-term development of osteoporosis (progressive bone disease). The mechanism behind this is two-fold: cortisol stimulates the production of RANKL by osteoblasts which stimulates, through binding to RANK receptors, the activity of osteoclasts – cells responsible for calcium resorption from bone – and also inhibits the production of osteoprotegerin (OPG) which acts as a decoy receptor and captures some RANKL before it can activate the osteoclasts through RANK. In other words, when RANKL binds to OPG, no response occurs as opposed to the binding to RANK which leads to the activation of osteoclasts. It transports potassium out of cells in exchange for an equal number of sodium ions (see above). This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine. Cortisol down-regulates the synthesis of collagen. Amino acid
Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis. Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves. Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE. Electrolyte balance
Cortisol decreases glomerular filtration rate, and renal plasma flow from the kidneys thus increasing phosphate excretion, as well as increasing sodium and water retention and potassium excretion by acting on mineralocorticoid receptors. | 11
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In classifying perinatal deaths, stillbirths and infant deaths
For most of the 20th Century, official definitions of a live birth and infant death in the Soviet Union and Russia differed from common international standards, such as those established by the World Health Organization in the latter part of the century. Babies who were fewer than 28 weeks of gestational age, or weighed fewer than 1000 grams, or fewer than 35 cm in length – even if they showed some sign of life (breathing, heartbeat, voluntary muscle movement) – were classified as "live fetuses" rather than "live births." Only if such newborns survived seven days (168 hours) were they then classified as live births. If, however, they died within that interval, they were classified as stillbirths. If they survived that interval but died within the first 365 days they were classified as infant deaths. More recently, thresholds for "fetal death" continue to vary widely internationally, sometimes incorporating weight as well as gestational age. The gestational age for statistical recording of fetal deaths ranges from 16 weeks in Norway, to 20 weeks in the US and Australia, 24 weeks in the UK, and 26 weeks in Italy and Spain.The WHO defines the perinatal period as "The perinatal period commences at 22 completed weeks (154 days) of gestation and ends seven completed days after birth." Perinatal mortality is the death of fetuses or neonates during the perinatal period. | Therefore, fracture of the bone may not only lead to lesion of the radial nerve, but also haematoma of the internal structures of the arm. The artery then continues on to anastamose with the recurrent radial branch of the brachial artery, providing a diffuse blood supply for the elbow joint. Veins
The veins of the arm carry blood from the extremities of the limb, as well as drain the arm itself. The two main veins are the basilic and the cephalic veins. There is a connecting vein between the two, the median cubital vein, which passes through the cubital fossa and is clinically important for venepuncture (withdrawing blood). The basilic vein travels on the medial side of the arm and terminates at the level of the seventh rib. The cephalic vein travels on the lateral side of the arm and terminates as the axillary vein. It passes through the deltopectoral triangle, a space between the deltoid and the pectoralis major muscles. Society and culture
In Hindu, Buddhist and Egyptian iconography the symbol of the arm is used to illustrate the power of the sovereign. In Hindu tradition gods are depicted with several arms which carry specific symbols of their powers. It is believed that several arms depict omnipotence of gods. In popular culture Thakur did not have arms in the movie Sholay. In West Africa, the Bambara use forearm to symbolize the spirit, which is a link between God and man. Symbolic gestures of raising both hands signal surrender, appeals for mercy, and justice. | 0-1
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The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause. Prevention
There is no known preventive measure for type 1 diabetes. Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment. | However, these subgroups do not affect how the disease is diagnosed or treated. Treatment
Prostaglandins
If the diagnosis is made prenatally, prostaglandin E1 (PGE1) is started after birth to avoid closure of the ductus arteriosus. Prostaglandin therapy is performed via a continuous infusion, due to how quickly prostaglandins are metabolized in the body. However, the diagnosis may go undetected, delaying treatment until closure of the ductus arteriosus produces symptoms. Surgery
Curative treatment consists of open heart surgery soon after birth, preferably immediately after diagnosis. Often, a synthetic patch is used to recreate the lost section of aorta. Recent research has revealed that an initial single-stage repair using direct anastomoses and repair of any existing cardiac defects is the preferred surgical technique, as opposed to a two-stage surgical repair.Awaiting surgery, prostaglandin can be administered to keep the ductus arteriosus open, thereby allowing blood flow to the lower body. After successful treatment, the patient is monitored for the rest of their life by a specialist to ensure that problems do not occur. Prognosis
Failure to treat the condition yields a mortality rate of 90% at a median age of 4 days. Death occurs due to increased blood flow from the left side of the heart (oxygenated blood) to the right side (deoxygenated blood), inducing heart failure; pulmonary edema; and eventual closing of the ductus arteriosus. For an infant with an interrupted aortic arch, a patent (open) ductus arteriosus allows for blood to bypass the "interruption," without which blood will be unable to reach the lower half of the body. | 0-1
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Psychological
According to a 2011 study, those with vaginismus are twice as likely to have a history of childhood sexual interference and held less positive attitudes about their sexuality, whereas no correlation was noted for lack of sexual knowledge or (nonsexual) physical abuse. Physical
Often, when faced with a person experiencing painful intercourse, a gynecologist will recommend reverse Kegel exercises and provide some additional lubricants. Although vaginismus has not been shown to affect a persons ability to produce lubrication, providing additional lubricant can be helpful in achieving successful penetration. This is due to the fact that women may not produce natural lubrication if anxious or in pain. Achieving sufficient arousal during foreplay is crucial for the release of lubrication which can contribute to the ease of sexual penetration and pain-free intercourse. Though strengthening exercises such as Kegel exercises were previously considered to be a helpful intervention for pelvic pain, new research suggests that these exercises, which function to strengthen the pelvic floor, may not be helpful or may make conditions that are caused by over-active muscles such as vaginismus worse. Exercises that stretch or relax the pelvic floor may be a better treatment option for vaginismus.To help develop a treatment plan that best fits the needs of their patient, a gynecologist or general practitioner may refer a person experiencing painful intercourse to a Pelvic floor physical therapist or occupational therapist. These therapists specialize in the treatment of disorders of the pelvic floor muscles such as vaginismus, dyspareunia, vulvodynia, constipation, and fecal or urinary incontinence. | Spasm of the entry muscle accounts for the common complaint that people often report when trying to have intercourse: "Its like hitting a brick wall". Secondary vaginismus
Secondary vaginismus occurs when a person who has previously been able to achieve penetration develops vaginismus. This may be due to physical causes such as a yeast infection or trauma during childbirth, while in some cases it may be due to psychological causes, or to a combination of causes. The treatment for secondary vaginismus is the same as for primary vaginismus, although, in these cases, previous experience with successful penetration can assist in a more rapid resolution of the condition. Peri-menopausal and menopausal vaginismus, often due to a drying of the vulvar and vaginal tissues as a result of reduced estrogen, may occur as a result of "micro-tears" first causing sexual pain then leading to vaginismus. Mechanism
Specific muscle involvement is unclear, but the condition may involve the pubococcygeus muscle, levator ani, bulbocavernosus, circumvaginal, or perivaginal muscles. Diagnosis
The diagnosis of vaginismus, as well as other diagnoses of female sexual dysfunction, can be made when "symptoms are sufficient to result in personal distress." The DSM-IV-TR defines vaginismus as "recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with sexual intercourse, causing marked distress or interpersonal difficulty". Treatment
A Cochrane review found little high quality evidence regarding the treatment of vaginismus in 2012. Specifically it is unclear if systematic desensitisation is better than other measures including nothing. | 11
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Glycogen serves as a carbohydrate storage molecule, primarily found in muscle, liver and brain. Its breakdown frees up glucose for energy. PLP also catalyzes transamination reactions that are essential for providing amino acids as a substrate for gluconeogenesis, the biosynthesis of glucose. Lipid metabolism
PLP is an essential component of enzymes that facilitate the biosynthesis of sphingolipids. Particularly, the synthesis of ceramide requires PLP. In this reaction, serine is decarboxylated and combined with palmitoyl-CoA to form sphinganine, which is combined with a fatty acyl-CoA to form dihydroceramide. This compound is then further desaturated to form ceramide. In addition, the breakdown of sphingolipids is also dependent on vitamin B6 because sphingosine-1-phosphate lyase, the enzyme responsible for breaking down sphingosine-1-phosphate, is also PLP-dependent. Hemoglobin synthesis and function
PLP aids in the synthesis of hemoglobin, by serving as a coenzyme for the enzyme aminolevulinic acid synthase. It also binds to two sites on hemoglobin to enhance the oxygen binding of hemoglobin. Gene expression
PLP has been implicated in increasing or decreasing the expression of certain genes. Increased intracellular levels of the vitamin lead to a decrease in the transcription of glucocorticoids. Vitamin B6 deficiency leads to the increased gene expression of albumin mRNA. Also, PLP influences expression of glycoprotein IIb by interacting with various transcription factors; the result is inhibition of platelet aggregation. In plants
Plant synthesis of vitamin B6 contributes to protection from sunlight. Ultraviolet-B radiation (UV-B) from sunlight stimulates plant growth, but in high amounts can increase production of tissue-damaging reactive oxygen species (ROS), i.e., oxidants. | Surgical excision may be required if its presence is resulting in atrophy of the adrenal glands and the surrounding tissues.In order to acquire better treatment strategies, it is important to further examine, study and discern the distinct molecular mechanisms involved in the formation of endogenous Adrenal Adenomas, hyperplasias, and ACTH-independent Cushings Syndrome to improve the available diagnostic and prognostic markers that can assist clinicians in the management and advance-treatment of such conditions. Prognosis
The long-term outlook for individuals diagnosed with non-functional adrenocortical adenoma is usually excellent. The long-term outlook for individuals diagnosed with functional adrenocortical adenoma is good with early diagnosis and treatment. Epidemiology
Prevalence: Female > Male
More common in adults
Relatively earlier onset in females (ages ≤ 20) than males (ages ≤ 30)
Most common cause of ACTH-independent Cushings syndrome
See also
Hyperplasia
Adrenal tumor
Cushings syndrome
Conns syndrome
Hypercortisolism
Hyperaldosteronism
Hyperandrogenism
Adrenal gland
Adrenal paraganglioma
Adrenal Pheochromocytoma
Adrenal ganglioneuroma
References
== External links == | 0-1
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This mutation produced a frameshift mutation, which led to a stop codon at position 131. SOD1 activity was decreased by about 30%. The patient’s histological examination showed severe reduction in lower motor neurons. Upon further study, this case proved to be important because it demonstrated that SOD1 mutations might not effect steady neuropathological changes, and that environmental and genetic factors might affect the phenotype of the SOD1 mutations. Treatment
PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders. History
The disease was first recognized by the French neurologist Guillaume Duchenne in 1860 and termed, “labioglossolaryngeal paralysis”. In 1859, Wachsmuth changed the name to progressive bulbar palsy. In 1869, Charcot studied the involvement of the corticospinal tracts and with Joffroy, who noted the loss of the bulbar motor nuclei, discovered the similarities to amyotrophic lateral sclerosis (ALS). It was observed that a distinction from ALS was fatigue that predominated in muscles innervated by lower cranial nerve nuclei, rather than the upper motor neurons. See also
Amyotrophic lateral sclerosis
Motor neuron disease
References
Bibliography
Lapiedra RC, Moreno Lopez LA, and Esparza Gomez GC. Progressive bulbar palsy: a case report diagnosed by lingual symptoms. J Oral Pathol Med. 31: 277-279. (2002)
Hughes TAT and Wiles CM. Neurogenic dysphagia: the role of the neurologist. J Neurol Neurosurg Psychiatry. 64:569-572. | Co-administration with ketoconazole, a strong CYP3A4 inhibitor, results in a 22% increase in the AUC, and potentially an increase in the rate of adverse effects experiencedSince bedaquiline can also prolong the QT interval, use of other QT prolonging drugs should be avoided. Other medications for tuberculosis that can prolong the QT interval include fluoroquinolones and clofazimine. Mechanism of action
Bedaquiline blocks the proton pump for ATP synthase of mycobacteria. It is the first member of a new class of drugs called the diarylquinolines. Bedaquiline is bactericidal. ATP production is required for cellular energy production and its loss leads inhibition of mycobacterial growth within hours of the addition of bedaquiline. The onset of bedaquiline-induced mycobacterial cell death does not occur until several days after treatment, but nonetheless kills consistently thereafter. Resistance
The specific part of ATP synthase affected by bedaquiline is subunit c which is encoded by the gene atpE. Mutations in atpE can lead to resistance. Mutations in drug efflux pumps have also been linked to resistance. Ongoing research
In vitro experiments have indicated that Bedaquiline may also target the mitochondrial ATP synthase of malignant mammalian cells and reduce the rate of metastasis. History
Bedaquiline was described for the first time in 2004 at the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) meeting, after the drug had been in development for over seven years. | 0-1
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Cases of pediatric XDR-TB have been reported in most countries including the United States.In 2006 an outbreak of XDR-TB South Africa was first reported as a cluster of 53 patients in a rural hospital in KwaZulu-Natal, with all but one dying. What was particularly worrying was that the mean survival from sputum specimen collection to death was only 16 days and that the majority of patients had never previously received treatment for tuberculosis. This is the epidemic for which the acronym XDR-TB was first used, although TB strains that fulfil the current definition have been identified retrospectively, this was the largest group of linked cases ever found. Since the initial report in September 2006, cases have now been reported in most provinces in South Africa. As of 16 March 2007, there were 314 cases reported, with 215 deaths. It is clear that the spread of this strain of TB is closely associated with a high prevalence of HIV and poor infection control; in other countries where XDR-TB strains have arisen, drug-resistance has arisen from mismanagement of cases or poor patient compliance with drug treatment instead of being transmitted from person to person. This strain of TB does not respond to any of the drugs currently available in South Africa for first- or second-line treatment. It is now clear that the problem has been around for much longer than health department officials have suggested, and is far more extensive. By 23 November 2006, 303 cases of XDR-TB had been reported, of which 263 were in KwaZulu-Natal. | The probability of resistance is higher in those patients who relapse and every effort must be made to obtain a specimen that can be cultured for sensitivities. That said, most patients who relapse do so with a fully sensitive strain and it is possible that these patients have not relapsed, but have instead been re-infected; these patients can be re-treated with the same regimen as before (no drugs need to be added to the regimen and the duration need not be any longer). The WHO recommends a regimen of 2SHREZ/6HRE when microbiology is not available (the majority of countries where TB is highly endemic). This regimen was designed to provide optimal treatment for fully sensitive TB (the most common finding in patients who have relapsed) as well as to cover the possibility of INH-resistant TB (the most common form of resistance found). Because of the lifelong risk of relapse, all patients should be warned of the symptoms of TB relapse upon finishing treatment and given strict instructions to return to their doctor if symptoms recur. Public health and health policy
As of 2010, India has more reported cases of TB than any other country. This is in part due to severe mismanagement of diagnosis and treatment of TB within the private health care sector of India that serves about 50% of the population. There are therefore calls for the private sector to engage in the public Revised National Tuberculosis Control Program that has proved effective in reducing TB amongst the patients receiving health care through the government. | 11
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The over-exposure to excessive loud noise is partially attributed to recreational exposure, such as the use of personal audio devices with music at high volumes for long durations, or social settings such as bars, entertainment and sporting events.The International Organization for Standardization (ISO) developed the ISO 1999 standards for the estimation of hearing thresholds and noise-induced hearing impairment. They used data from two noise and hearing study databases, one presented by Burns and Robinson (Hearing and Noise in Industry, Her Majestys Stationery Office, London, 1970) and by Passchier-Vermeer (1968). As race and ethnicity are some of the factors that can affect the expected distribution of pure-tone hearing thresholds several other national or regional datasets exist, from Sweden, Norway, South Korea, the United States and Spain. In the United States hearing is one of the health outcomes measure by the National Health and Nutrition Examination Survey (NHANES), a survey research program conducted by the National Center for Health Statistics. It examines health and nutritional status of adults and children in the United States. While there is no perfect way to pinpoint hearing loss from excessive noise, researchers look for audiometric notches in a hearing test—dips in the ability to hear certain frequencies—as signs of possible NIHL. As of 2011 data, approximately 24% adults age 20–69 in the United States has an audiometric notch. This data identified differences in NIHL based on age, gender, race/ethnicity, and whether or not a person is exposed to noise at work. | While healing, an over-expression of glutamate receptors can result in temporary tinnitus, or ringing in the ears. Repeated ruptures at the same synapse may eventually fail to heal, leading to permanent hearing loss.Prolonged exposure to high intensity noise has also been linked to the disruption of ribbon synapses located in the synaptic cleft between inner hair cells and spiral ganglion nerve fibers, leading to a disorder referred to as cochlear synaptopathy or hidden hearing loss. This disorder is cumulative and over time, leads to degeneration of the spiral ganglion cells of the inner ear and overall dysfunction in the neural transmission between auditory nerve fibers and the central auditory pathway. The most common symptom of cochlear synaptopathy is difficulty understanding speech, especially in the presence of competing noise. However, this type of hearing impairment is often undetectable by conventional pure tone audiometry, thus the name "hidden" hearing loss. Acoustic over-exposure can also result in decreased myelination at specific points on the auditory nerve. Myelin, an insulating sheath surrounding nerve axons, expedites electrical impulses along nerves throughout the nervous system. Thinning of the myelin sheath on the auditory nerve significantly slows the transmission of electrical signals from hair cell to auditory cortex, reducing comprehension of auditory stimuli by delaying auditory perception, particularly in noisy environments. Individual susceptibility towards noise
There appear to be large differences in individual susceptibility to NIHL. | 11
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