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As of 2006, three instances of males with Down syndrome fathering children and 26 cases of females having children have been reported. Without assisted reproductive technologies, around half of the children of someone with Down syndrome will also have the syndrome. Cause
The cause of the extra full or partial chromosome is still unknown. Most of the time, Down syndrome is caused by a random mistake in cell division during early development of the fetus, but not inherited, and no scientific research shows that environmental factors or the parents activities contribute to Down syndrome. The only factor that has been linked to the increased chance of having a baby with Down syndrome is maternal age. Down syndrome is caused by having three copies of the genes on chromosome 21, rather than the usual two. The parents of the affected individual are typically genetically normal. Those who have one child with Down syndrome have about a 1% possibility of having a second child with the syndrome, if both parents are found to have normal karyotypes.The extra chromosome content can arise through several different ways. The most common cause (about 92–95% of cases) is a complete extra copy of chromosome 21, resulting in trisomy 21. In 1.0 to 2.5% of cases, some of the cells in the body are normal and others have trisomy 21, known as mosaic Down syndrome. The other common mechanisms that can give rise to Down syndrome include: a Robertsonian translocation, isochromosome, or ring chromosome. | The thickness of the meniscus, its diminished vascular blood supply, and in some instances, weak capsular attachment, makes it more prone to tears compared to a normal meniscus. The anomaly in itself is asymptomatic; however, a tear of the meniscus can result in pain, swelling, and snapping in the affected knee. The orthopedic classification of discoid menisci includes: complete, incomplete or Wrisberg-ligament types as depicted here. Coverage of the lateral tibial plateau determines the designation of complete or incomplete. The Wrisberg-ligament type has an abnormal posterior attachment by attaching to part of the posterior cruciate ligament. Symptoms
Symptom is usually pain in the knee. And when the knee is bent or stretched it makes the sound of bouncing bones. Diagnosis
The transverse diameter of a normal meniscus is approximately 10 to 11 mm; therefore a normal meniscus body will be visible on only 2 slices of a MR with 4-5-mm sagittal slices. A discoid meniscus should be considered if more than two contiguous body segments are present. However, this method may lead to a false negative when evaluating people with the Wrisberg variant of discoid meniscus since it maintains a narrow crescent shape. Coronal and radial images of the meniscus are useful to demonstrate the extension of the aberrant meniscus into the joint as seen here. On coronal images, it is diagnosed when the horizontal measurement between the free margin and the periphery of the body is more than 1.4 cm. | 0-1
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Diagnostic
Diagnosis of mouth ulcers usually consists of a medical history followed by an oral examination as well as examination of any other involved area. The following details may be pertinent: The duration that the lesion has been present, the location, the number of ulcers, the size, the color and whether it is hard to touch, bleeds or has a rolled edge. As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon, or maxillofacial surgeon). If there have been previous ulcers that have healed, then this again makes cancer unlikely. An ulcer that keeps forming on the same site and then healing may be caused by a nearby sharp surface, and ulcers that heal and then recur at different sites are likely to be RAS. Malignant ulcers are likely to be single in number, and conversely, multiple ulcers are very unlikely to be oral cancer. The size of the ulcers may be helpful in distinguishing the types of RAS, as can the location (minor RAS mainly occurs on non-keratinizing mucosa, major RAS occurs anywhere in the mouth or oropharynx). Induration, contact bleeding and rolled margins are features of a malignant ulcer. There may be nearby causative factor, e.g. a broken tooth with a sharp edge that is traumatizing the tissues. Otherwise, the person may be asked about problems elsewhere, e.g. | Findings found that the use of “fecal/sewage” as a description, and the use of multiple descriptors of the smell, and incorrect locations of smell origin effectively differentiated ORS from TMAU. In the literature on body odour identification, emphasis is frequently placed on multiple consultations to reduce the risk of misdiagnosis, and also asking the individual to have a reliable confidant accompany them to the consultation who can confirm the reality of the reported symptom. ORS patients are unable to provide such confidants as they have no objective odor.A fecal smell (fecal body odour) is often a self reported symptom associated with TMAU, however there is no recorded evidence of fecal body odour present in any study related to TMAU. Cashman JR found that 53% of TMAU and 59% of non-TMAU subjects suffered from regular halitosis, dental plaque on the back of the tongue, which produced on average "200-600 ppb of sulfurous/fecal smelling volatile sulfur compounds (i.e., VSC: hydrogen sulfide; methylmercaptan; dimethylsulfide) with each exhalation, creating a “malodorous cloud” in their vicinity. It is likely that halitosis, ORS or in severe cases, a bowel obstruction leading to fecal vomiting may be the cause. There is the possibility that someone may suffer from both Trimethylaminuria and ORS-like paranoia, due to the potential lack of ability to smell the odour oneself and the worry that it generates. It is recommended to organise reliable confidants, colleagues, friends or relatives ("smell buddies") to work with the sufferer to discretely inform them if they are presenting an odour. | 0-1
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as a result of the improving job market, but until they have actually found a position, they are counted as unemployed. Similarly, during a recession, the increase in the unemployment rate is moderated by people leaving the labour force or being otherwise discounted from the labour force, such as with the self-employed. For the fourth quarter of 2004, according to OECD (Employment Outlook 2005 ISBN 92-64-01045-9), normalized unemployment for men aged 25 to 54 was 4.6% in the US and 7.4% in France. At the same time and for the same population, the employment rate (number of workers divided by population) was 86.3% in the US and 86.7% in France. That example shows that the unemployment rate was 60% higher in France than in the US, but more people in that demographic were working in France than in the US, which is counterintuitive if it is expected that the unemployment rate reflects the health of the labour market.Those deficiencies make many labour market economists prefer to look at a range of economic statistics such as labour market participation rate, the percentage of people between 15 and 64 who are currently employed or searching for employment, the total number of full-time jobs in an economy, the number of people seeking work as a raw number and not a percentage, and the total number of person-hours worked in a month compared to the total number of person-hours people would like to work. | Rising unemployment has traditionally been regarded by the public and the media in any country as a key guarantor of electoral defeat for any government that oversees it. That was very much the consensus in the United Kingdom until 1983, when Thatchers Conservative government won a landslide in the general election, despite overseeing a rise in unemployment from 1.5 million to 3.2 million since the 1979 election. Benefits
The primary benefit of unemployment is that people are available for hire, without being headhunted away from their existing employers. That permits both new and old businesses to take on staff. Unemployment is argued to be "beneficial" to the people who are not unemployed in the sense that it averts inflation, which itself has damaging effects, by providing (in Marxian terms) a reserve army of labour, which keeps wages in check. However, the direct connection between full local employment and local inflation has been disputed by some because of the recent increase in international trade that supplies low-priced goods even while local employment rates rise to full employment. Full employment cannot be achieved because workers would shirk if they were not threatened with the possibility of unemployment. The curve for the no-shirking condition (labelled NSC) thus goes to infinity at full employment. The inflation-fighting benefits to the entire economy arising from a presumed optimum level of unemployment have been studied extensively. The Shapiro–Stiglitz model suggests that wages never bid down sufficiently to reach 0% unemployment. | 11
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This bill would put in place the system of "presumed consent".The Mental Capacity Act is another legal policy in place for organ donation in the UK. The act is used by medical professionals to declare a patients mental capacity. The act claims that medical professionals are to "act in a patients best interest", when the patient is unable to do so. India
India has a fairly well developed corneal donation programme; however, donation after brain death has been relatively slow to take off. Most of the transplants done in India are living related or unrelated transplants. To curb organ commerce and promote donation after brain death the government enacted a law called "The Transplantation of Human Organs Act" in 1994 that brought about a significant change in the organ donation and transplantation scene in India. Many Indian states have adopted the law and in 2011 further amendment of the law took place. Despite the law there have been stray instances of organ trade in India and these have been widely reported in the press. This resulted in the amendment of the law further in 2011. Deceased donation after brain death have slowly started happening in India and 2012 was the best year for the programme. Source the Indian Transplant News Letter of the MOHAN FoundationThe year 2013 has been the best yet for deceased organ donation in India. A total of 845 organs were retrieved from 310 multi-organ donors resulting in a national organ donation rate of 0.26 per million population(Table 2). | * ODR (pmp) – Organ Donation Rate (per million population)
In the year 2000 through the efforts of an NGO called MOHAN Foundation state of Tamil Nadu started an organ sharing network between a few hospitals. This NGO also set up similar sharing network in the state of Andhra Pradesh and these two states were at the forefront of deceased donation and transplantation programme for many years. As a result, retrieval of 1,033 organs and tissues were facilitated in these two states by the NGO.Similar sharing networks came up in the states of Maharashtra and Karnataka; however, the numbers of deceased donation happening in these states were not sufficient to make much impact. In 2008, the Government of Tamil Nadu put together government orders laying down procedures and guidelines for deceased organ donation and transplantation in the state. These brought in almost thirty hospitals in the programme and has resulted in significant increase in the donation rate in the state. With an organ donation rate of 1.15 per million population, Tamil Nadu is the leader in deceased organ donation in the country. The small success of Tamil Nadu model has been possible due to the coming together of both government and private hospitals, NGOs and the State Health department. Most of the deceased donation programmes have been developed in southern states of India. The various such programmes are as follows:
In the year 2012 besides Tamil Nadu other southern states too did deceased donation transplants more frequently. | 11
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The United States Presidents Council on Bioethics made it clear, for example, in its White Paper of December 2008, that the British concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States. Evolution of diagnostic criteria
The United Kingdom (UK) criteria were first published by the Conference of Medical Royal Colleges (with advice from the Transplant Advisory Panel) in 1976, as prognostic guidelines. They were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought "to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery". The published criteria – negative responses to bedside tests of some reflexes with pathways through the brainstem and a specified challenge to the brainstem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects – were held to be "sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists". | A small minority of medical practitioners working in the UK have argued that neither requirement of the UK Health Departments Code of Practice basis for the equation of brainstem death with death is satisfied by its current diagnostic protocol and that in terms of its ability to diagnose de facto brainstem death it falls far short. Most of these criticisms overlook the fact that in practice brainstem death testing would not be conducted in isolation. In most cases this is only performed after running a series of CT and MRI scans to look at brain and brainstem health. References
External links
Great Ormond Street Hospital for Children | 11
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The observable clinical manifestations may consist of rapid, hyperkinetic movements as well as tonic/dystonic posturing of the limbs. Other potential manifestations include brief arousals from sleep or wandering ambulatory behavior. Non-motor manifestations (such as sensory or emotional phenomenon) are common and retained awareness during seizures may occur. Seizures usually occur during non-REM sleep. The frequency of seizures can be very high and as many as dozens may occur every night which results in poor sleep quality. In addition, many patients with SHE suffer from cognitive impairment and have behavioral/psychological problems. There are many risks associated with nocturnal seizures including concussion, suffocation and sudden unexpected death (SUDEP). Cause
Approximately 86% of SHE cases are sporadic, 14% of patients have a family history of epilepsy and 5% are inherited in an autosomal dominant manner (i.e. autosomal dominant sleep-related hypermotor epilepsy). Both genetic, structural and multifactorial etiologies can occur. In structural cases, the most common pathology is focal cortical dysplasia.The first described mutation in SHE was found in genes coding for the neuronal nicotinic acetylcholine receptor. Since then multiple other genes have been identified including KCNT1, DEPDC5, NPRL2, NPRL3, PRIMA1, CABP4, CRH and others. In some cases, structural and genetic etiologies can coexist such as with mutations in DEPDC5. Diagnosis
The condition may be difficult to diagnose and misdiagnosis is common. The subject may be unaware they have a seizure disorder. To others, the involuntary movements made during sleep may appear no different from those typical of normal sleep. | Hematemesis is the vomiting of blood. It is always an important sign. It can be confused with hemoptysis (coughing up blood) or epistaxis (nosebleed), which are more common. The source is generally the upper gastrointestinal tract, typically above the suspensory muscle of duodenum. It may be caused by ulcers, tumors of the stomach or esophagus, varices, prolonged and vigorous retching, gastroenteritis, ingested blood (from bleeding in the mouth, nose, or throat), or certain drugs.Hematemesis is treated as a medical emergency, with treatments based on the amount of blood loss. Investigations include endoscopy. Any blood loss may be corrected with intravenous fluids and blood transfusions. Patients may need to avoid taking anything by mouth. Definition
Hematemesis is the vomiting of blood. This is usually vomit that contains bright red blood. Coffee ground vomiting is similar to hematemesis, but is distinct in not involving bright red blood.Hematemesis is always an important sign. It must be differentiated from hemoptysis (coughing up blood) and epistaxis (nosebleed). Both of these are more common conditions. These may be difficult to distinguish. Differential diagnosis
Hematemesis may be caused by:
Peptic ulcer. This may be related to Zollinger–Ellison syndrome, which causes severe disease. Vascular malfunctions of the gastrointestinal tract, such as bleeding gastric varices or intestinal varices. Mallory-Weiss syndrome: bleeding tears in the esophagal mucosa, usually caused by prolonged and vigorous retching. Vomiting of ingested blood after bleeding in the mouth, nose, or throat. Tumors of the stomach or esophagus. Irritation or erosion of the lining of the esophagus or stomach. Radiation poisoning. Viral hemorrhagic fevers. | 0-1
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A study in 2017 correlated several inflammatory diseases of the respiration tract with objective evidence of damp-caused damage in homes.The WHO has classified the reported symptoms into broad categories, including: mucous membrane irritation (eye, nose, and throat irritation), neurotoxic effects (headaches, fatigue, and irritability), asthma and asthma-like symptoms (chest tightness and wheezing), skin dryness and irritation, gastrointestinal complaints and more.Several sick occupants may report individual symptoms which do not appear to be connected. The key to discovery is the increased incidence of illnesses in general with onset or exacerbation within a fairly close time frame – usually within a period of weeks. In most cases, SBS symptoms will be relieved soon after the occupants leave the particular room or zone. However, there can be lingering effects of various neurotoxins, which may not clear up when the occupant leaves the building. In some cases – particularly in sensitive individuals – there can be long-term health effects. Cause
ASHRAE has recognized that polluted urban air, designated within the United States Environmental Protection Agency (EPA)s air quality ratings as unacceptable, requires the installation of treatment such as filtration for which the HVAC practitioners generally apply carbon-impregnated filters and their likes. Different toxins will aggravate the human body in different ways. Some people are more allergic to mold, while others are highly sensitive to dust. Inadequate ventilation will exaggerate small problems (such as deteriorating fiberglass insulation or cooking fumes) into a much more serious indoor air quality problem. | Pyknoachondrogenesis is a very rare, fatal, presumably autosomal recessive genetic disorder characterized by symptoms similar to those shown by patients with achondrogenesis alongside severely osteoclerotic bones and early death. The findings that can be seen in patients with this condition include hydrops fetalis, palpebral edemas, low-set ears, abdomen prominence, short neck, large head, depressed nasal bridge, shortening and widening of the trunk, severe short-limbed dwarfism, craniofacial hyperostosis, agenesis of the pubic bones, hypoplasia of the pelvic bones and ischium, poor (sometimes absent) ossification of the vertebrae and sacrum, webbing of the neck, and shortening of a long bone and the ribs. Pregnancies of babies with this condition generally arent compatible with life and they end up in miscarriage, stillbirth, or in neonatal death (that is, death soon after birth). Only 5 cases from Italy and the United States, respectively, have been described in medical literature. == References == | 0-1
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Its distribution resembles to that of the distribution of median nerve in the hand. Its muscular branches supply the abductor hallucis, the flexor digitorum brevis, the flexor hallucis brevis and the first lumbrical. Cutaneous distribution of the medial plantar nerve supplies the medial sole and medial three and one half toes through four digital branches. Each digital branch give off a dorsal branch to supply the nail beds on the dorsum. This nerve also gives off articular branches to supply the bones of the tarsus and metatarsus. Lateral plantar nerve - It is the smaller terminal branch of the tibial nerve. It courses laterally and forward until the base of fifth metatarsal bone, where it divides into superficial and deep branches. Its distribution resembles to the distribution of ulnar nerve in the hand. The main trunk of the nerve supplies two muscles: flexor digitorum accessorius and abductor digiti minimi. This nerve also supplies the skin of the sole. The superficial branch is divided into medial and lateral branches. The lateral branch supplies three muscles: flexor digiti minimi, 3rd and 4th interossei, and the skin over the lateral side of the toe. The medial branch communicates with the medial plantar nerve and supplies the skin over the fourth interdigital cleft. The deep branch supplies the 2nd, 3rd, and 4th lumbricals, first and second plantar interossei and adductor hallucis. Clinical Significance
Damage to the tibial nerve is rare, and is often a result of direct trauma, entrapment through narrow space or compression for long period of time. | Articular branches - There are three articular branches arises from the upper part of the fossa: superior medial genicular nerve (located on the surface of medial condyle of femur, middle genicular nerve (pierces the posterior capsule of the knee joint to supply the structures located in the intercondylar notch of the femur, and inferior genicular nerve (runs along the upper border of the popliteus to reach the medial condyle of tibia). Back of the leg
At the inferior angle of the popliteal fossa, tibial nerve passes deep to the tendinous arch of soleus to enter the back of the leg. In the leg, it runs downwards and medially to reach the posteromedial side of the ankle, midway between the medial malleolus and medial tubercle of the calcaneum. It terminates deep to the flexor retinaculum at the origin of the abductor hallucis by dividing into medial and lateral plantar nerves to supply the foot. The tibial nerve gives off several branches to supply the back of the leg:
Muscular branches - Supplies tibialis posterior, flexor digitorum longus, flexor hallucis longus, and deep part of soleus. Cutaneus branches - The medial calcaneal nerve pierces the flexor retinaculum to supply the skin of the back and lower surface of the heel. Articular branches - Supplies the ankle joint
Foot
In the foot, the nerve terminates by dividing into medial and lateral plantar branches. Medial plantar nerve - It is the larger terminal branch of the tibial nerve. It passes between the abductor hallucis and flexor digitorum brevis to divide further into branches. | 11
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In contrast to most other AAS, 17α-alkylated testosterone derivatives show resistance to metabolism due to steric hindrance and are orally active, though they may be esterified and administered via intramuscular injection as well.In addition to oral activity, 17α-alkylation also confers a high potential for hepatotoxicity, and all 17α-alkylated AAS have been associated, albeit uncommonly and only after prolonged use (different estimates between 1 and 17%), with hepatotoxicity. In contrast, testosterone esters have only extremely rarely or never been associated with hepatotoxicity, and other non-17α-alkylated AAS only rarely, although long-term use may reportedly still increase the risk of hepatic changes (but at a much lower rate than 17α-alkylated AAS and reportedly not at replacement dosages). In accordance, D-ring glucuronides of testosterone and DHT have been found to be cholestatic.Aside from prohormones and testosterone undecanoate, almost all orally active AAS are 17α-alkylated. A few AAS that are not 17α-alkylated are orally active. Some examples include the testosterone 17-ethers cloxotestosterone, quinbolone, and silandrone, which are prodrugs (to testosterone, boldenone (Δ1-testosterone), and testosterone, respectively), the DHT 17-ethers mepitiostane, mesabolone, and prostanozol (which are also prodrugs), the 1-methylated DHT derivatives mesterolone and metenolone (although these are relatively weak AAS), and the 19-nortestosterone derivatives dimethandrolone and 11β-MNT, which have improved resistance to first-pass hepatic metabolism due to their 11β-methyl groups (in contrast to them, the related AAS trestolone (7α-methyl-19-nortestosterone) is not orally active). As these AAS are not 17α-alkylated, they show minimal potential for hepatotoxicity. | It was approved for medical use in Australia in March 2021.Bemfola was approved for medical use in the European Union in March 2014. Side effects of FSH preparations
Side effects of FSH preparations include:
Local irritation at the injection site
Feeling of fullness, bloating, and tenderness in the lower abdomen due to increasing size of the ovaries. Mood swings
Fatigue
FSH analogues
Corifollitropin alfa
Merck received approval on February 15, 2010, from the European Commission for ELONVA (corifollitropin alfa) a long lasting single injection fusion protein lacking LH activity. Only one injection is required for the first seven days, replacing the first seven daily injections of conventional FSH. Initial results demonstrates similar pregnancy rates as daily recombinant FSH injections. LH (Luteinizing hormone) preparations
Prepared from recombinant DNA. Generic
lutropin alfa for injection
Brands
Luveris
hCG preparations
Human chorionic gonadotropin (hCG) can be recovered from the urine of pregnant women or be produced from recombinant DNA. It acts similarly to LH, but the larger supply makes it less costly; it also has a longer half-life. In veterinary medicine, equine chorionic gonadotropin (eCG) extracted from pregnant mare serum is used instead on a variety of mammals, sometimes eliciting an immune response in non-horse species.In Women:
Used to induce final maturation of follicle and subsequent ovulation. Also used for luteal phase support. Typically a single injection of 10,000 international units is used to induce ovulation. In men:
Used to treat select cases of Hypogonadotropic Hypogonadism in adult males. | 0-1
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CRPS typically develops after an injury, surgery, heart attack, or stroke. Investigators estimate that 2–5% of those with peripheral nerve injury, and 13-70% of those with hemiplegia (paralysis of one side of the body) will develop CRPS. In addition, some studies have indicated that cigarette smoking was strikingly present in patients and is statistically linked to RSD. This may be involved in its pathology by enhancing sympathetic activity, vasoconstriction, or by some other unknown neurotransmitter-related mechanism. This hypothesis was based on a retrospective analysis of 53 patients with RSD, which showed that 68% of patients and only 37% of controls were smokers. The results are preliminary and are limited by their retrospective nature. 7% of people who have CRPS in one limb later develop it in another limb. Pathophysiology
Inflammation and alteration of pain perception in the central nervous system are proposed to play important roles. The persistent pain and the perception of nonpainful stimuli as painful are thought to be caused by inflammatory molecules (IL-1, IL2, TNF-alpha) and neuropeptides (substance P) released from peripheral nerves. This release may be caused by inappropriate cross-talk between sensory and motor fibers at the affected site. CRPS is not a psychological illness, yet pain can cause psychological problems, such as anxiety and depression. | See also
Handedness
Laterality
Orthodox stance
Southpaw stance
Surefootedness
== References == | 0-1
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It typically involves the bulbar conjunctivae, is not accompanied by suppuration, and is not painful. This usually begins shortly after the onset of fever during the acute stage of the disease. Anterior uveitis may be present under slit-lamp examination. Iritis can occur, too. Keratic precipitates are another eye manifestation (detectable by a slit lamp, but are usually too small to be seen by the unaided eye).Kawasaki disease also presents with a set of mouth symptoms, the most characteristic of which are a red tongue, swollen lips with vertical cracking, and bleeding. The mucosa of the mouth and throat may be bright red, and the tongue may have a typical "strawberry tongue" appearance (marked redness with prominent gustative papillae). These mouth symptoms are caused by necrotizing microvasculitis with fibrinoid necrosis.Cervical lymphadenopathy is seen in 50% to 75% of children, whereas the other features are estimated to occur in 90%, but sometimes it can be the dominant presenting symptom. According to the diagnostic criteria, at least one impaired lymph node ≥ 15 mm in diameter should be involved. Affected lymph nodes are painless or minimally painful, nonfluctuant, and nonsuppurative; erythema of the neighboring skin may occur. Children with fever and neck adenitis who do not respond to antibiotics should have Kawasaki disease considered as part of the differential diagnoses. | Myocarditis, diarrhea, pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues. If left untreated, some symptoms will eventually relent, but coronary artery aneurysms will not improve, resulting in a significant risk of death or disability due to myocardial infarction. If treated quickly, this risk can be mostly avoided and the course of illness cut short. Other reported nonspecific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.The course of the disease can be divided into three clinical phases. The acute febrile phase, which usually lasts for one to two weeks, is characterized by fever, conjunctival injection, erythema of the oral mucosa, erythema and swelling of the hands and feet, rash, cervical adenopathy, aseptic meningitis, diarrhea, and hepatic dysfunction. Myocarditis is common during this time, and a pericardial effusion may be present. Coronary arteritis may be present, but aneurysms are generally not yet visible by echocardiography. The subacute phase begins when fever, rash, and lymphadenopathy resolve at about one to two weeks after the onset of fever, but irritability, anorexia, and conjunctival injection persist. Desquamation of the fingers and toes and thrombocytosis are seen during this stage, which generally lasts until about four weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest. | 11
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It has since been marketed under more than 100 trade names, from Amepromat through Quivet to Zirpon.A December 1955 study of 101 patients at the Mississippi State Hospital in Whitfield, Rankin County, Mississippi, found meprobamate useful in the alleviation of "mental symptoms": 3% of patients made a complete recovery, 29% were greatly improved, 50% were somewhat better, while 18% realized little change. Self-destructive patients became cooperative and calmer, and experienced a resumption of logical thinking. In 50% of the cases, relaxation brought about more favorable sleep habits. Following the trial, hydrotherapy and all types of shock treatment were subsequently halted. Meprobamate was found to help in the treatment of alcoholics by 1956. By 1957, over 36 million prescriptions had been filled for meprobamate in the US alone, a billion pills had been manufactured, and it accounted for fully a third of all prescriptions written. Berger, clinical director of Wallace Laboratories, described it as a relaxant of the central nervous system, whereas other tranquilizers suppressed it. A University of Michigan study found that meprobamate affected driving skills. Though patients reported being able to relax more easily, meprobamate did not completely alleviate their tense feelings. The disclosures came at a special scientific meeting at the Barbizon Plaza Hotel in New York City, at which Aldous Huxley addressed an evening session. | Dietary copper can be found in whole grain cereals, legumes, oysters, organ meats (particularly liver), cherries, dark chocolate, fruits, leafy green vegetables, nuts, poultry, prunes, and soybean products like tofu.Copper deficiency can have many hematological consequences, such as myelodysplasia, anemia, low white blood cell count, and low count of neutrophils (a type of white blood cell that is often called "the first line of defense" of the immune system). Copper deficiency has long been known as a cause of myelodysplasia (when a blood profile has indicators of possible future leukemia development), but it was not until 2001 that copper deficiency was associated with neurological manifestations like sensory ataxia (irregular coordination due to proprioceptive loss), spasticity, muscle weakness, and more rarely visual loss due to damage in the peripheral nerves, myelopathy (disease of the spinal cord), and rarely optic neuropathy. Signs and symptoms
Blood symptoms
The characteristic hematological (blood) effects of copper deficiency are anemia (which may be microcytic, normocytic or macrocytic) and neutropenia. Thrombocytopenia (low blood platelets) is unusual.The peripheral blood and bone marrow aspirate findings in copper deficiency can mimic myelodysplastic syndrome. Bone marrow aspirate in both conditions may show dysplasia of blood cell precursors and the presence of ring sideroblasts (erythroblasts containing multiple iron granules around the nucleus). | 0-1
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PMID 19579890. Alkatib AA, Cosma M, Elamin MB, Erickson D, Swiglo BA, Erwin PJ, Montori VM (October 2009). "A systematic review and meta-analysis of randomized placebo-controlled trials of DHEA treatment effects on quality of life in women with adrenal insufficiency". J. Clin. Endocrinol. Metab. 94 (10): 3676–81. doi:10.1210/jc.2009-0672. PMID 19773400. Panjari M, Davis SR (June 2010). "DHEA for postmenopausal women: a review of the evidence". Maturitas. 66 (2): 172–9. doi:10.1016/j.maturitas.2009.12.017. PMID 20089375. Oberbeck R, Kobbe P (2010). "Dehydroepiandrosterone (DHEA): a steroid with multiple effects. Is there any possible option in the treatment of critical illness?". Curr. Med. Chem. 17 (11): 1039–47. doi:10.2174/092986710790820570. PMID 20156161. Prati A, Santagni S, Rattighieri E, Campedelli A, Ricchieri F, Chierchia E, Despini G, Genazzani AR, Genazzani AD (June 2014). "[The putative role and use of DHEA and its association with the hormone replacement therapy]". Minerva Ginecol (in Italian). 66 (3): 313–24. PMID 24971788. Genazzani AR, Pluchino N (August 2010). "DHEA therapy in postmenopausal women: the need to move forward beyond the lack of evidence". Climacteric. 13 (4): 314–6. doi:10.3109/13697137.2010.492496. PMID 20540592. S2CID 5578070. Luci M, Valenti G, Maggio M (September 2010). "[Dehydroepiandrosterone [DHEA(S)]: anabolic hormone?]". Recenti Prog Med (in Italian). 101 (9): 333–44. hdl:11381/2436727. PMID 21268370. Gleicher N, Barad DH (May 2011). "Dehydroepiandrosterone (DHEA) supplementation in diminished ovarian reserve (DOR)". Reprod. Biol. Endocrinol. 9: 67. doi:10.1186/1477-7827-9-67. PMC 3112409. PMID 21586137. Davis SR, Panjari M, Stanczyk FZ (June 2011). "Clinical review: DHEA replacement for postmenopausal women". J. Clin. Endocrinol. Metab. 96 (6): 1642–53. doi:10.1210/jc.2010-2888. PMID 21411558. Panjari M, Davis SR (September 2011). | From its discovery in 1934 until 1959, DHEA was referred to by a number of different names in the literature, including dehydroandrosterone, transdehydroandrosterone, dehydroisoandrosterone, and androstenolone. The name dehydroepiandrosterone, also known as DHEA, was first proposed by Fieser in 1949, and subsequently became the most commonly used name of the hormone. For decades after its discovery, DHEA was considered to be an inactive compound that served mainly as an intermediate in the production of androgens and estrogens from cholesterol. In 1965, an association between DHEA sulfate levels and aging was reported by De Nee and Vermeulen. Following this, DHEA became of interest to the scientific community, and numerous studies assessing the relationship between DHEA and DHEA sulfate levels and aging were conducted.Prasterone, the proposed INN and recommended INN of DHEA and the term used when referring to the compound as a medication, were published in 1970 and 1978, respectively. The combination of 4 mg estradiol valerate and 200 mg prasterone enanthate in an oil solution was introduced for use in menopausal hormone therapy by intramuscular injection under the brand name Gynodian Depot in Europe by 1978. In the early 1980s, prasterone became available and was widely sold over-the-counter as a non-prescription supplement in the United States, primarily as a weight loss aid. It was described as a "miracle drug", with supposed anti-aging, anti-obesity, and anti-cancer benefits. | 11
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Both are primarily caused by the polymerization of sickle cells in the kidney microvasculature due to the low O2 tension, high osmolarity, and low acidity. This polymerization fills and occludes blood vessels such as the vasa recta in the kidneys leading to microinfarctions, leakage into surrounding tissues and potentially papillary necrosis and renal infarcts. Renal papillae are especially susceptible to damage eventually causing papillary necrosis since these vessels are only supplied with blood by the vasa recta. The sickling of the cells also contribute to two other mechanisms which are chronic hypoxia and chronic hemolysis. Hypoxia is caused from both the insufficient ability for the red blood cells to transport oxygen alongside blood vessel occlusions promoting the activation of Hypoxia Inducible Factor-1𝛂. The hypoxia also causes the over expression of endothelin-1 and functional nitric oxide deficiency and due to the chronic hemolysis, reactive oxygen species are produced leading to vasoconstriction and further medullary hypoxia. This nitric oxide deficiency alongside endothelin-1 overproduction leads to the inability to properly respond to stress and hemodynamic changes which increases the likelihood of experiencing acute kidney injury.The hyperfiltration has multiple contributing factors such as the increased cardiac output caused by the normal physiological response to anemia leading to greater renal blood flow and an increase in glomerular filtration rate (GFR). This is not the only factor because having multiple blood transfusions does not reverse this effect. | Thalassemias are inherited blood disorders characterized by decreased hemoglobin production. Symptoms depend on the type and can vary from none to severe. Often there is mild to severe anemia (low red blood cells or hemoglobin). Anemia can result in feeling tired and pale skin. There may also be bone problems, an enlarged spleen, yellowish skin, and dark urine. Slow growth may occur in children.Thalassemias are genetic disorders inherited from a persons parents. There are two main types, alpha thalassemia and beta thalassemia. The severity of alpha and beta thalassemia depends on how many of the four genes for alpha globin or two genes for beta globin are missing. Diagnosis is typically by blood tests including a complete blood count, special hemoglobin tests, and genetic tests. Diagnosis may occur before birth through prenatal testing.Treatment depends on the type and severity. Treatment for those with more severe disease often includes regular blood transfusions, iron chelation, and folic acid. Iron chelation may be done with deferoxamine, deferasirox or deferiprone. Occasionally, a bone marrow transplant may be an option. Complications may include iron overload from the transfusions with resulting heart or liver disease, infections, and osteoporosis. If the spleen becomes overly enlarged, surgical removal may be required. Thalassemia patients who do not respond well to blood transfusions can take hydroxyurea or thalidomide, and sometimes a combination of both. Hydroxyurea is the only FDA approved drug for thalassemia. | 0-1
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Polycephaly is the condition of having more than one head. The term is derived from the Greek stems poly (Greek: "πολύ") meaning "many" and kephalē (Greek: "κεφαλή") meaning "head". A polycephalic organism may be thought of as one being with a supernumerary body part, or as two or more beings with a shared body. Two-headed animals (called bicephalic or dicephalic) and three-headed (tricephalic) animals are the only type of multi-headed creatures seen in the real world, and form by the same process as conjoined twins from monozygotic twin embryos.In humans, there are two forms of twinning that can lead to two heads being supported by a single torso. In dicephalus parapagus dipus, the two heads are side by side. In craniopagus parasiticus, the two heads are joined directly to each other, but only one head has a functional torso. Survival to adulthood is rare, but does occur in some forms of dicephalus parapagus dipus. There are many occurrences of multi-headed animals in mythology. In heraldry and vexillology, the double-headed eagle is a common symbol, though no such animal is known to have ever existed. Occurrences
Two-headed people and animals, though rare, have long been known to exist and documented. Occurrence in humans
In humans, as in other animals, partial twinning can result in formation of two heads supported by a single torso. Two ways this can happen are dicephalus parapagus, where there are two heads side by side, and craniopagus parasiticus, where the heads are joined directly. | Kinneret is the Hebrew name of the Sea of Galilee, the largest freshwater lake in Israel. Other meanings of Kinneret and Kineret include:
Places
Camp Kinneret, a summer camp of Canadian Young Judaea
Kinneret (archaeological site), biblical city which gave the Sea of Galilee its Hebrew name; now Tell el-Oreimeh or Tel Kinrot on the northwestern coast of the lake
Kinneret College, college south of the Sea of Galilee
Kinneret Farm, experimental training farm (1908-1949), now museum
Kinneret Subdistrict, Israel
Kvutzat Kinneret, kibbutz southwest of the Sea of Galilee
Moshavat Kinneret, village (moshava) southwest of the Sea of Galilee
People
Kineret (singer), an Orthodox Jewish recording artist
Kinneret Shiryon (born 1955), Reform rabbi, the first female rabbi in Israel
Other
Kineret (medication), brand name of anakinra; no direct relation to the lake
Kinneret, Israeli song based on Rachel Bluwsteins poem "Perhaps" ("VeUlai")
Kinneret bream or Kinneret bleak, Acanthobrama terraesanctae, fish endemic to the Sea of Galilee and a second lake in Syria
Kinneret Zmora-Bitan Dvir, publishing company, Israel
Operation Kinneret, another name of the Israeli military Operation Olive Leaves
See also
All pages with titles containing Kinneret
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A 2017 meta-analysis found a benefit of preventative antibiotics for recurrent cellulitis in the lower limbs, but the preventative effects appear to diminish after stopping antibiotic therapy. Treatment
Antibiotics are usually prescribed, with the agent selected based on suspected organism and presence or absence of purulence, although the best treatment choice is unclear. If an abscess is also present, surgical drainage is usually indicated, with antibiotics often prescribed for co-existent cellulitis, especially if extensive. Pain relief is also often prescribed, but excessive pain should always be investigated, as it is a symptom of necrotizing fasciitis. Elevation of the affected area is often recommended.Steroids may speed recovery in those on antibiotics. Antibiotics
Antibiotics choices depend on regional availability, but a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin is currently recommended for cellulitis without abscess. A course of antibiotics is not effective in between 6 and 37% of cases. Epidemiology
Cellulitis in 2015 resulted in about 16,900 deaths worldwide, up from 12,600 in 2005.Cellulitis is a common global health burden, with more than 650,000 admissions per year in the United States alone. In the United States, an estimated 14.5 million cases annually of cellulitis account for $3.7 billion in ambulatory care costs alone. The majority of cases of cellulitis are nonculturable and therefore the causative bacteria are unknown. In the 15% of cellulitis cases in which organisms are identified, most are due to β-hemolytic Streptococcus and Staphylococcus aureus. | Treatment
Treatments for CPVT aim to prevent lethal abnormal heart rhythms from occurring, and to rapidly restore a normal rhythm if they do occur. As the arrhythmias in CPVT generally occur at times when the heart is exposed to high levels of adrenaline or other similar chemical messengers (catecholamines), many treatments for CPVT aim to lower the levels of catecholamines the heart is exposed to or block their effects on the heart.The first-line treatment for those with CPVT involves lifestyle advice. This includes avoiding competitive sports, very strenuous exercise and highly stressful environments, as high levels of adrenaline can occur in these settings, which can provoke arrhythmias. Medication
Several medications can be useful for those with CPVT. The mainstays of treatment are beta blockers, which block the effects of adrenaline and other catecholamines on the heart, reducing the chance of abnormal heart rhythms developing. Of all the beta blockers, nadolol has been proven to be the most effective for treating CPVT. This drug lowers the heart rate to a greater extent than other beta blockers and only needs to be taken once daily, reducing the risk of missed doses. Nadolol may be difficult to obtain and is not available in all countries, and an alternative beta blocker suitable for use in CPVT may be propranolol, which however has a more complex dosing regimen. | 0-1
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WHO Drug Information advises against its use in primary sclerosing cholangitis in unapproved doses beyond 13–15 mg/kg/day.UDCA in a dose of 28-30mg/kg/day increases risk of death and need for liver transplant by 2.3 folds among those with primary sclerosing cholangitis, despite decrease in liver enzymes. Intrahepatic cholestasis of pregnancy
UDCA has been used for intrahepatic cholestasis of pregnancy. UDCA lessens itching in the mother and may reduce the number of preterm births. Effects on fetal distress and other adverse outcomes are unlikely to be great. Cholestasis
UDCA use is not licensed in children, as its safety and effectiveness have not been established. Evidence is accumulating that ursodeoxycholic acid is ineffective, unsafe and its use is associated with significant risk of morbidity and mortality in neonatal hepatitis and neonatal cholestasis. Other conditions
UDCA has been suggested to be an adequate treatment of bile reflux gastritis.In cystic fibrosis there is insufficient evidence to justify routine use of UDCA, especially as there is a lack of available data for long-term outcomes such as death or need for liver transplantation.UDCA has also been in effective in non-alcoholic fatty liver disease, in liver bile duct-paucity syndromes. It is contraindicated in obstruction of biliary tracts such as biliary atresia. Its not effective in liver allograft rejection, and in Graft-versus-host disease involving the liver. Adverse effects
Diarrhea was the most frequent adverse event seen in trial of UDCA in gallstone dissolution, occurring in 2 to 9%, which is less frequent than with chenodeoxycholic acid therapy. | Dissociation, in the wide sense of the word, is an act of disuniting or separating a complex object into parts. Dissociation may also refer to:
Dissociation (chemistry), general process in which molecules or ionic compounds (complexes, or salts) split into smaller particles, usually in a reversible manner
Dissociation (neuropsychology), identification of the neural substrate of a particular brain function through various methods
Dissociation (psychology), an experience of having ones attention and emotions detached from the environment
Dissociation (rhetoric), a rhetorical device in which the speaker separates a notion considered to form a unitary concept into two new notions to affect an audience in some way
Dissociation (album), by the Dillinger Escape Plan, 2016
See also
Dissociation: Progress in the Dissociative Disorders (1988-1997) published by International Society for the Study of Trauma and Dissociation
"Disassociation", a 2021 song by the Rions
Dissociative, a class of hallucinogen
All pages with titles beginning with Dissociation
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History
Tisotumab was developed by Genmab in Utrecht, the Netherlands, and Copenhagen, Denmark, with the code name TF-011-MMAE. It is marketed in a 50/50 partnership between Genmab and Seagen, which developed and owns the intellectual property for vedotin technology (monoclonal antibody–MMAE conjugates). References
External links
"Tisotumab vedotin". Drug Information Portal. U.S. National Library of Medicine. Clinical trial number NCT03438396 for "A Trial of Tisotumab Vedotin in Cervical Cancer" at ClinicalTrials.gov
Clinical trial number NCT03245736 for "Tisotumab Vedotin Continued Treatment in Patients With Solid Tumors" at ClinicalTrials.gov
Clinical trial number NCT02001623 for "Tisotumab Vedotin (HuMax-TF-ADC) Safety Study in Patients With Solid Tumors" at ClinicalTrials.gov
Clinical trial number NCT02552121 for "Tisotumab Vedotin (HuMax-TF-ADC) Safety Study in Patients With Solid Tumors" at ClinicalTrials.gov | Pemphigus herpetiformis is a cutaneous condition, a clinical variant of pemphigus that combines the clinical features of dermatitis herpetiformis with the immunopathologic features of pemphigus. Pathophysiology
Pemphigus Herpetiformis is an IGg mediated autoantibodies that affect the epidermal layer of the skin. Diagnosis
See also
Adult linear IgA disease
List of cutaneous conditions
== References == | 0-1
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Singing
Children are able to sing in the same octave as women. When the voices of male teenagers break, they are no longer able to sing in the same octave. For music sung in the same key as women, they can sing in falsetto or drop an octave. See also
Puberty
Voice masculinization and feminization
== References == | If a trauma case or chronic tracheal illnesses were the cause, the first steps of treatment would be to address these underlying issues. If the cause is genetic or the previous underlying issues could not be fixed, other treatments would be assessed. More severe treatments include silicone stenting to prevent tracheal constriction, surgery to strengthen or attempt to rebuild the walls, continuous positive airway pressure that has a machine blow small amounts of air into the trachea to keep it open (mainly at night), or a tracheostomy, which is surgically inserted into the patients neck that leads to the trachea to help with breathing. Another form of treatment may include a tracheobronchoplasty which is a specific surgical procedure that helps control the airway by splinting the trachea. The splint helps strengthen the trachea with the hopes that the symptoms improve. People with tracheobronchomalacia who do not experience symptoms do not need treatment and are often undiagnosed.On 28 May 2013, it was reported that a cure had been developed via a 3D printed windpipe. This cure has currently saved the lives of at least 3 infants. See also
Bronchomalacia
Tracheomalacia
References
External links
Tracheobronchomalacia in Children on Medscape
Tracheobronchomalacia on Genetic and Rare Diseases Information Center (GARD)
CureTBM Foundation on CureTBM.org | 0-1
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Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. People with polio that develop equinus foot cannot walk properly because they cannot put their heels on the ground. A similar situation can develop if the arms become paralyzed.In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis). Osteoporosis and increased likelihood of bone fractures may occur. An intervention to prevent or lessen length disparity can be to perform an epiphysiodesis on the distal femoral and proximal tibial/fibular condyles, so that limbs growth is artificially stunted, and by the time of epiphyseal (growth) plate closure, the legs are more equal in length. Alternatively, a person can be fitted with custom-made footwear which corrects the difference in leg lengths. Other surgery to re-balance muscular agonist/antagonist imbalances may also be helpful. | The two can be differentiated as follows: a hamartoma is an excess of normal tissue in a normal situation (e.g., a birthmark on the skin), while a choristoma is an excess of tissue in an abnormal situation (e.g., pancreatic tissue in the duodenum). The term hamartoma is from the Greek ἁμαρτία, hamartia ("error"), and was introduced by D.P.G. Albrecht in 1904. Causes
Hamartomas result from an abnormal formation of normal tissue, although the underlying reasons for the abnormality are not fully understood. They grow along with, and at the same rate as, the organ from whose tissue they are made, and, unlike cancerous tumors, only rarely invade or compress surrounding structures significantly. Diagnosis
Types
Lung
About 5–8% of all solitary lung nodules and about 75% of all benign lung tumors, are hamartomas. They almost always arise from connective tissue and are generally formed of cartilage, connective tissue, and fat cells, although they may include many other types of cells. The great majority of them form in the connective tissue on the outside of the lungs, although about 10% form deep in the linings of the bronchi. They can be worrisome, especially if situated deep in the lung, as it is sometimes difficult to make the important distinction between a hamartoma and a lung malignancy. An X-ray will often not provide a definitive diagnosis, and even a CT scan may be insufficient if the hamartoma lacks the typical cartilage and fat cells. Lung hamartomas may have popcorn-like calcifications on chest xray or computed tomography (CT scan). | 0-1
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If AKI develops after major abdominal surgery (13.4% of all people who have undergone major abdominal surgery) the risk of death is markedly increased (over 12-fold). Kidney function
Depending on the cause, a proportion of patients (5–10%) will never regain full kidney function, thus entering end-stage kidney failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after being discharged from hospital, even if their kidney function has recovered.The risk of developing chronic kidney disease is increased (8.8-fold). Epidemiology
New cases of AKI are unusual but not rare, affecting approximately 0.1% of the UK population per year (2000 ppm/year), 20x incidence of new ESKD (end-stage kidney disease). AKI requiring dialysis (10% of these) is rare (200 ppm/year), 2x incidence of new ESKD.There is an increased incidence of AKI in agricultural workers because of occupational hazards such as dehydration and heat illness. No other traditional risk factors, including age, BMI, diabetes, or hypertension, were associated with incident AKI. Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.Acute kidney injury was one of the most expensive conditions seen in U.S. hospitals in 2011, with an aggregated cost of nearly $4.7 billion for approximately 498,000 hospital stays. This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute kidney injury stays. | Acute kidney injury (AKI), previously called acute renal failure (ARF), is a sudden decrease in kidney function that develops within 7 days, as shown by an increase in serum creatinine or a decrease in urine output, or both.Causes of AKI are classified as either prerenal (due to decreased blood flow to the kidney), intrinsic renal (due to damage to the kidney itself), or postrenal (due to blockage of urine flow). Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications like ACE inhibitors or NSAIDs. Intrinsic renal causes of AKI include glomerulonephritis, lupus nephritis, acute tubular necrosis, certain antibiotics, and chemotherapeutic agents. Postrenal causes of AKI include kidney stones, bladder cancer, neurogenic bladder, enlargement of the prostate, narrowing of the urethra, and certain medications like anticholinergics.The diagnosis of AKI is made based on a persons signs and symptoms, along with lab tests for serum creatinine and measurement of urine output. Other tests include urine microscopy and urine electrolytes. Renal ultrasound can be obtained when a postrenal cause is suspected. A kidney biopsy may be obtained when intrinsic renal AKI is suspected and the cause is unclear.AKI is seen in 10-15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit (ICU). AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, effects on other organ systems, and death. | 11
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Fidaxomicin, sold under the brand name Dificid among others, is the first member of a class of narrow spectrum macrocyclic antibiotic drugs called tiacumicins. It is a fermentation product obtained from the actinomycete Dactylosporangium aurantiacum subspecies hamdenesis. Fidaxomicin is minimally absorbed into the bloodstream when taken orally, is bactericidal, and selectively eradicates pathogenic Clostridioides difficile with relatively little disruption to the multiple species of bacteria that make up the normal, healthy intestinal microbiota. The maintenance of normal physiological conditions in the colon may reduce the probability of recurrence of Clostridioides difficile infection.It is marketed by Merck, which acquired Cubist Pharmaceuticals in 2015, and had in turn bought the originating company, Optimer Pharmaceuticals. It is used for the treatment of Clostridioides difficile infection, which is also known as Clostridioides difficile-associated diarrhea or Clostridioides difficile-associated illness (CDI), and can develop into Clostridioides difficile colitis and pseudomembranous colitis. Fidaxomicin is available in a 200 mg tablet that is administered every 12 hours for a recommended duration of 10 days. Total duration of therapy should be determined by the patients clinical status. It is currently one of the most expensive antibiotics approved for use. A standard course costs upwards of £1350. Mechanism
Fidaxomicin binds to and prevents movement of the "switch regions" of bacterial RNA polymerase. Switch motion occurs during the opening and closing of the DNA:RNA clamp, a process that occurs throughout RNA transcription but is especially important in the opening of double-stranded DNA during the initiation of transcription. | It has minimal systemic absorption and a narrow spectrum of activity; it is active against Gram positive bacteria, especially clostridia. The minimal inhibitory concentration (MIC) range for C. difficile (ATCC 700057) is 0.03–0.25 μg/mL. Clinical trials
Good results were reported by the company in 2009, from a North American Phase III clinical trial comparing it with oral vancomycin for the treatment of Clostridioides difficile infection. The study met its primary endpoint of clinical cure, showing that fidaxomicin was non-inferior to oral vancomycin (92.1% vs. 89.8%). In addition, the study met its secondary endpoint of recurrence: 13.3% of the subjects had a recurrence with fidaxomicin vs. 24.0% with oral vancomycin. The study also met its exploratory endpoint of global cure (77.7% for fidaxomicin vs. 67.1% for vancomycin). Clinical cure was defined as patients requiring no further therapy for the treatment of Clostridioides difficile infection two days after completion of study medication. Global cure was defined as patients who were cured at the end of therapy and did not have a recurrence in the next four weeks. Fidaxomicin was shown to be as good as the standard-of-care, vancomycin, for treating Clostridioides difficile infection in a Phase III clinical trial published in February 2011. The authors also reported significantly fewer recurrences of infection, a frequent problem with C. difficile, and similar drug side effects. | 11
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Research shows at least 10 differences in MC1R between African and chimpanzee samples and that the gene has probably undergone a strong positive selection (a selective sweep) in early Hominins around 1.2 million years ago. This is consistent with positive selection for the high-eumelanin phenotype seen in Africa and other environments with high UV exposure. Light skin
For the most part, the evolution of light skin has followed different genetic paths in European and East Asian populations. Two genes, however, KITLG and ASIP, have mutations associated with lighter skin that have high frequencies in both European and East Asian populations. They are thought to have originated after humans spread out of Africa but before the divergence of the European and Asian lineages around 30,000 years ago. Two subsequent genome-wide association studies found no significant correlation between these genes and skin color, and suggest that the earlier findings may have been the result of incorrect correction methods and small panel sizes, or that the genes have an effect too small to be detected by the larger studies. KITLG
The KIT ligand (KITLG) gene is involved in the permanent survival, proliferation and migration of melanocytes. A mutation in this gene, A326G (rs642742), has been positively associated with variations of skin color in African-Americans of mixed West African and European descent and is estimated to account for 15–20% of the melanin difference between African and European populations. | The babys weight is an indicator of the mother and babys health. In 2013, 22 million newborns had low birth weight, around 16 percent of all babies globally. Data on low birth weight is adjusted to account for under reporting. South Asia has the highest rate of babies not weighed at birth with 66 percent, but also have the highest low birth weight at 28 percent worldwide. West and Central Africa and least developed countries are next with 14 percent low birth weight worldwide.More than 96.5% of low birth weight babies are born in developing countries around the world. Because low birth weight babies can require more extensive care, it places a financial burden on communities. Prevention
The World Health Organization (WHO) recently announced an initiative to have a thirty percent reduction in low birth weight worldwide. This is public health priority, as birth weight can have short and long term effects. WHO estimates that worldwide, 15-20 % of all births each year are considered low birth weight, which is about 20 million births.The start of prenatal care is very important to help prevent low birth weight and early medical problems. Going to regular doctors visits is very important for the health of the mother and the baby. At the visits the OB/GYN will be checking maternal nutrition and weight gain because that is linked with the babys weight gain. The mother having a healthy diet is essential for the baby. | 0-1
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Alcoholism is, broadly, any drinking of alcohol that results in significant mental or physical health problems. Because there is disagreement on the definition of the word alcoholism, it is not a recognized diagnostic entity. Predominant diagnostic classifications are alcohol use disorder (DSM-5) or alcohol dependence (ICD-11); these are defined in their respective sources.Excessive alcohol use can damage all organ systems, but it particularly affects the brain, heart, liver, pancreas and immune system. Alcoholism can result in mental illness, delirium tremens, Wernicke–Korsakoff syndrome, irregular heartbeat, an impaired immune response, liver cirrhosis and increased cancer risk. Drinking during pregnancy can result in fetal alcohol spectrum disorders. Women are generally more sensitive than men to the harmful effects of alcohol, primarily due to their smaller body weight, lower capacity to metabolize alcohol, and higher proportion of body fat. In a small number of individuals, prolonged, severe alcohol misuse ultimately leads to cognitive impairment and frank dementia. Environment and genetics are two factors in the risk of development of alcoholism, with about half the risk attributed to each. Stress and associated disorders, including anxiety, are key factors in the development of alcoholism as alcohol consumption can temporarily reduce dysphoria. Someone with a parent or sibling with an alcohol use disorder is three to four times more likely to develop an alcohol use disorder themselves, but only a minority of them do. Environmental factors include social, cultural and behavioral influences. High stress levels and anxiety, as well as alcohols inexpensive cost and easy accessibility, increase the risk. | Clomipramine, sold under the brand name Anafranil among others, is a tricyclic antidepressant (TCA). It is used for the treatment of obsessive–compulsive disorder, panic disorder, major depressive disorder, and chronic pain. It may increase the risk of suicide in those under the age of 25. It is taken by mouth. It has also been used to treat premature ejaculation.Common side effects include dry mouth, constipation, loss of appetite, sleepiness, weight gain, sexual dysfunction, and trouble urinating. Serious side effects include an increased risk of suicidal behavior in those under the age of 25, seizures, mania, and liver problems. If stopped suddenly a withdrawal syndrome may occur with headaches, sweating, and dizziness. It is unclear if it is safe for use in pregnancy. Its mechanism of action is not entirely clear but is believed to involve increased levels of serotonin.Clomipramine was discovered in 1964 by the Swiss drug manufacturer Ciba-Geigy. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. Medical uses
Clomipramine has a number of uses in medicine including in the treatment of:
Obsessive–compulsive disorder (OCD) which is its only U.S. FDA-labeled indication. Other regulatory agencies (such as the TGA of Australia and the MHRA of the UK) have also approved clomipramine for this indication. Major depressive disorder (MDD) a popular off-label use in the US. It is approved by the Australian TGA and the United Kingdom MHRA for this indication. | 0-1
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Other methods of manufacture
Methods of vaccine generation that bypass the need for eggs include the construction of influenza virus-like particles (VLP). VLP resemble viruses, but there is no need for inactivation, as they do not include viral coding elements, but merely present antigens in a similar manner to a virion. Some methods of producing VLP include cultures of Spodoptera frugiperda Sf9 insect cells and plant-based vaccine production (e.g., production in Nicotiana benthamiana). There is evidence that some VLPs elicit antibodies that recognize a broader panel of antigenically distinct viral isolates compared to other vaccines in the hemagglutination-inhibition assay (HIA).A gene-based DNA vaccine, used to prime the immune system after boosting with an inactivated H5N1 vaccine, underwent clinical trials in 2011.On November 20, 2012, Novartis received FDA approval for the first cell-culture vaccine. In 2013, the recombinant influenza vaccine, Flublok, was approved for use in the United States.On September 17, 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for Supemtek, a quadrivalent influenza vaccine (recombinant, prepared in cell culture). The applicant for this medicinal product is Sanofi Pasteur. Supemtek was approved for medical use in the European Union in November 2020.Australia authorised its first and cell-based vaccine in March 2021, based on an "eternal cell line" of a dog kidney. Because of the way it is produced, it produces better-matched vaccine (to the flu strains). | The frequency of schizophrenia varies across the world, within countries, and at the local and neighborhood level; this variation in prevalence between studies over time, across geographical locations, and by gender is as high as fivefold.Schizophrenia causes approximately one percent of worldwide disability adjusted life years and resulted in 17,000 deaths in 2015.In 2000, WHO found the percentage of people affected and the number of new cases that develop each year is roughly similar around the world, with age-standardized prevalence per 100,000 ranging from 343 in Africa to 544 in Japan and Oceania for men, and from 378 in Africa to 527 in Southeastern Europe for women. History
Conceptual development
Accounts of a schizophrenia-like syndrome are rare in records before the 19th century; the earliest case reports were in 1797 and 1809. Dementia praecox, meaning premature dementia, was used by German psychiatrist Heinrich Schüle in 1886, and then in 1891 by Arnold Pick in a case report of hebephrenia. In 1893 Emil Kraepelin used the term in making a distinction, known as the Kraepelinian dichotomy, between the two psychoses – dementia praecox, and manic depression (now called bipolar disorder). | 0-1
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sequenced the coding regions of the OXT gene in other genera in new world primates and identified the following variants in addition to Leu8- and Pro8-OT: Ala8-OT, Thr8-OT, and Val3/Pro8-OT. Ren et al. identified a variant further, Phe2-OT in howler monkeys.The biologically active form of oxytocin, commonly measured by RIA and/or HPLC techniques, is the oxidized octapeptide oxytocin disulfide, but oxytocin also exists as a reduced straight-chain (non-cyclic) dithiol nonapeptide called oxytoceine. It has been theorized that oxytoceine may act as a free radical scavenger, as donating an electron to a free radical allows oxytoceine to be re-oxidized to oxytocin via the dehydroascorbate / ascorbate redox couple.Recent advances in analytical instrumental techniques highlighted the importance of liquid chromatography (LC) coupled with mass spectrometry (MS) for measuring oxytocin levels in various samples derived from biological sources. Most of these studies optimized the oxytocin quantification in electrospray ionization (ESI) positive mode, using [M+H]+ as the parent ion at mass-to-charge ratio (m/z) 1007.4 and the fragment ions as diagnostic peaks at m/z 991.0, m/z 723.2 and m/z 504.2. These important ion selections paved the way for the development of current methods of oxytocin quantification using MS instrumentation. The structure of oxytocin is very similar to that of vasopressin. Both are nonapeptides with a single disulfide bridge, differing only by two substitutions in the amino acid sequence (differences from oxytocin bolded for clarity): Cys – Tyr – Phe – Gln – Asn – Cys – Pro – Arg – Gly – NH2. | Rhinophyma is a condition causing development of a large, bulbous nose associated with granulomatous infiltration, commonly due to untreated rosacea. The condition is most common in older white males.Colloquial terms for the rhinophyma include "whiskey nose", "gin blossom", "toros nose", and "potato nose". Signs and symptoms
Rhinophyma is characterised by prominent pores and a fibrous thickening of the nose, sometimes with papules. It is associated with the common skin condition rosacea and it can be classified clinically into 5 grades of increasing severity. Complications
Tissue thickening may come to cause airway obstruction and impede breathing.Rhynophyma cause psychological distress due to its effect on ones personal appearance and social perceptions of a link with alcoholism. Causes
Rhinophyma develops in certain individuals with an unknown predisposition from long-standing rosacea which has progressed to a severe form.Although rhinophyma has been commonly presumed to be linked to alcoholism, a direct causal relationship between the condition and excessive alcohol consumption has not been substantiated. Alcohol may cause increased flushing in those affected. Pathophysiology
Rhinophyma develops in some individuals after long-standing rosacea that has progressed to acne rosacea.Rosacea usually commences in people between the age of 20-30 years. Rosacea begins with facial flushing (pre-rosacea). The nasal skin then thickens and hypervascularises, leading to persistent erythema (vascular rosacea). Papules and pustules then develop, marking the beginning of acne (inflammatory) rosacea. A subset of those affected by acne rosacea go on to develop rhinophyma. | 0-1
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In case of minor thrombosis, there are some chances of survival using cadaveric liver transplant. Causes
Causes of high serum-ascites albumin gradient (SAAG or transudate) are
Cirrhosis – 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
Heart failure – 3%
Hepatic venous occlusion: Budd–Chiari syndrome or veno-occlusive disease
Constrictive pericarditis
Kwashiorkor (childhood protein-energy malnutrition)Causes of low SAAG ("exudate") areCancer (metastasis and primary peritoneal carcinomatosis) – 10%
Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis
Pancreatitis – 1%
Serositis
Nephrotic syndrome
Hereditary angioedemaOther rare causesMeigs syndrome
Vasculitis
Hypothyroidism
Renal dialysis
Peritoneum mesothelioma
Abdominal tuberculosis
Mastocytosis
Diagnosis
Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the person with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. | Caplacizumab (INN; trade name Cablivi) is a bivalent single-domain antibody (VHH) designed for the treatment of thrombotic thrombocytopenic purpura and thrombosis.This drug was developed by Ablynx NV. On 30 August 2018, it was approved in the European Union for the "treatment of adults experiencing an episode of acquired thrombotic thrombocytopenic purpura (aTTP), in conjunction with plasma exchange and immunosuppression".It is an anti-von Willebrand factor humanized immunoglobulin. It acts by blocking platelet aggregation to reduce organ injury due to ischemia. Results of the phase II TITAN trial have been reported.In February 2019, caplacizumab-yhdp (Cablivi, Ablynx NV) was approved in the United States for the treatment of adults with acquired thrombotic thrombocytopenic purpura (aTTP). The drug is used in combination with plasma exchange and immunosuppressive therapy. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication. References
External links
"Caplacizumab". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Genetics
Genetic factors can cause pretesticular, testicular, and post-testicular azoospermia (or oligospermia) and include the following situations: The frequency of chromosomal abnormalities is inversely proportional to the semen count, thus males with azoospermia are at risk to have a 10–15% (other sources citing 15–20% incidence) abnormalities on karyotyping versus about <1 % in the fertile male population.Pretesticular azoospermia may be caused by congential hypopituitarism, Kallmann syndrome, Prader-Willi syndrome and other genetic conditions that lead to GnRH or gonadotropin deficiency. Testicular azoospermia is seen in Klinefelter syndrome (XXY) and the XX male syndrome. In addition, 13% of men with azoospermia have a defective spermatogenesis that is linked to defects of the Y chromosome. Such defects tend to be de novo micro-deletions and affect usually the long arm of the chromosome. A section of the long arm of the Y chromosome has been termed Azoospermia Factor (AZF) at Yq11 and subdivided into AZFa, AZFb, AZFc and possibly more subsections. Defects in this area can lead to oligospermia or azoospermia, however, a tight genotype-phenotype correlation has not been achieved. Spermatogenesis is defective with gene defects for the androgen receptor.Post-testicular azoospermia can be seen with certain point mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene commonly associated with congenital vas deferens abnormalities.Genetic counselling is indicated for men with genetic causes of azoospermia. In terms of reproduction, it needs to be considered if the genetic defect could be transmitted to the offspring. BRD7
BRD7, a transcription regulatory protein, is normally highly expressed in the testis. | History
The disease was first noted by German pathologist Karl Theodor Fahr in 1930. A less common name for the condition is Chavany-Brunhes syndrome and Fritsches syndrome, the former named after Jacques Brunhes, Jean Alfred Émile Chavany, while the later named after R. Fritsche.Fewer than 20 families had been reported in the literature up to 1997. In literature
Fahrs syndrome features in Norwegian Jo Nesbøs crime fiction novel "The Snowman" (the seventh novel in the Harry Hole detective series). See also
Primrose syndrome
References
External links
Fahr Syndrome Images (MedPix)
National Organization for Rare Disorders (NORD)
National Institute on Aging (NIA)
National Institute of Mental Health (NIMH) | 0-1
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Avapritinib, sold under the brand name Ayvakit among others, is a medication used for the treatment of advanced systemic mastocytosis and for the treatment of tumors due to one specific rare mutation: it is specifically intended for adults with unresectable or metastatic gastrointestinal stromal tumor (GIST) that harbor a platelet-derived growth factor receptor alpha (PDGFRA) exon 18 mutation.Common side effects include edema (swelling), nausea, fatigue/asthenia (abnormal physical weakness or lack of energy), cognitive impairment, vomiting, decreased appetite, diarrhea, hair color changes, increased lacrimation (secretion of tears), abdominal pain, constipation, rash and dizziness.Avapritinib is a kinase inhibitor. Medical uses
Avapritinib is indicated for the treatment of adults with unresectable or metastatic gastrointestinal stromal tumors (GIST) harboring the platelet-derived growth factor receptor alpha (PDGFRA) exon 18 mutation, including PDGFRA D842V mutations.Avapritinib is also indicated for the treatment of adults with advanced systemic mastocytosis, aggressive systemic mastocytosis, systemic mastocytosis with an associated hematological neoplasm, and mast cell leukemia (MCL). History
The U.S. Food and Drug Administration (FDA) approved avapritinib in January 2020. The application for avapritinib was granted fast track designation, breakthrough therapy designation, and orphan drug designation. The FDA granted approval of Ayvakit to Blueprint Medicines Corporation.Avapritinib was approved based on the results from the Phase I NAVIGATOR clinical trial involving 43 subjects with GIST harboring a PDGFRA exon 18 mutation, including 38 subjects with PDGFRA D842V mutation. Subjects received avapritinib 300 mg or 400 mg orally once daily until disease progression or they experienced unacceptable toxicity. The recommended dose was determined to be 300 mg once daily. | Sular may refer to:
Nisoldipine, a pharmaceutical
Sular, Iran, a village | 0-1
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As of July 2019, both girls remain healthy and the family planned to return to their home in Pakistan in 2020. History
The Moche culture of ancient Peru depicted conjoined twins in their ceramics dating back to 300 CE. Writing around 415 CE, St. Augustine of Hippo, in his book, City of God, refers to a man "double in his upper, but single in his lower half—having two heads, two chests, four hands, but one body and two feet like an ordinary man. "According to Theophanes the Confessor, a Byzantine historian of the 9th century, around 385/386 CE, "in the village of Emmaus in Palestine, a child was born perfectly normal below the navel but divided above it, so that it had two chests and two heads, each possessing the senses. One would eat and drink but the other did not eat; one would sleep but the other stayed awake. There were times when they played with each other, when both cried and hit each other. They lived for a little over two years. One died while the other lived for another four days and it, too, died. "In Arabia, the twin brothers Hashim ibn Abd Manaf and Abd Shams were born with Hashims leg attached to his twin brothers head. | The thickness of the meniscus, its diminished vascular blood supply, and in some instances, weak capsular attachment, makes it more prone to tears compared to a normal meniscus. The anomaly in itself is asymptomatic; however, a tear of the meniscus can result in pain, swelling, and snapping in the affected knee. The orthopedic classification of discoid menisci includes: complete, incomplete or Wrisberg-ligament types as depicted here. Coverage of the lateral tibial plateau determines the designation of complete or incomplete. The Wrisberg-ligament type has an abnormal posterior attachment by attaching to part of the posterior cruciate ligament. Symptoms
Symptom is usually pain in the knee. And when the knee is bent or stretched it makes the sound of bouncing bones. Diagnosis
The transverse diameter of a normal meniscus is approximately 10 to 11 mm; therefore a normal meniscus body will be visible on only 2 slices of a MR with 4-5-mm sagittal slices. A discoid meniscus should be considered if more than two contiguous body segments are present. However, this method may lead to a false negative when evaluating people with the Wrisberg variant of discoid meniscus since it maintains a narrow crescent shape. Coronal and radial images of the meniscus are useful to demonstrate the extension of the aberrant meniscus into the joint as seen here. On coronal images, it is diagnosed when the horizontal measurement between the free margin and the periphery of the body is more than 1.4 cm. | 0-1
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On occasion, neck tenderness or a sore throat may become apparent after a few days, if moderate inflammation in the thyroid develops and produces discomfort in the neck or throat area. This is usually transient, and not associated with a fever, etc.It is recommended that breastfeeding be stopped at least six weeks before radioactive iodine treatment and that it not be resumed, although it can be done in future pregnancies. It also shouldnt be done during pregnancy, and pregnancy should be put off until at least 6–12 months after treatment.A common outcome following radioiodine is a swing from hyperthyroidism to the easily treatable hypothyroidism, which occurs in 78% of those treated for Graves thyrotoxicosis and in 40% of those with toxic multinodular goiter or solitary toxic adenoma. Use of higher doses of radioiodine reduces the number of cases of treatment failure, with penalty for higher response to treatment consisting mostly of higher rates of eventual hypothyroidism which requires hormone treatment for life.There is increased sensitivity to radioiodine therapy in thyroids appearing on ultrasound scans as more uniform (hypoechogenic), due to densely packed large cells, with 81% later becoming hypothyroid, compared to just 37% in those with more normal scan appearances (normoechogenic). Thyroid storm
Thyroid storm presents with extreme symptoms of hyperthyroidism. | Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. It is noted that thyrotoxicosis is related to hyper-kinetic movement disorders including chorea and myoclonus. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature and often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.Graves disease is the cause of about 50% to 80% of the cases of hyperthyroidism in the United States. Other causes include multinodular goiter, toxic adenoma, inflammation of the thyroid, eating too much iodine, and too much synthetic thyroid hormone. A less common cause is a pituitary adenoma. The diagnosis may be suspected based on signs and symptoms and then confirmed with blood tests. Typically blood tests show a low thyroid stimulating hormone (TSH) and raised T3 or T4. Radioiodine uptake by the thyroid, thyroid scan, and TSI antibodies may help determine the cause.Treatment depends partly on the cause and severity of disease. There are three main treatment options: radioiodine therapy, medications, and thyroid surgery. | 11
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Any individual histrionic may exhibit one or more of the following:
Treatment
Treatment is often prompted by depression associated with dissolved romantic relationships. Medication does little to affect the personality disorder, but may be helpful with symptoms such as depression. Treatment for HPD itself involves psychotherapy, including cognitive therapy. Interviews and self-report methods
In general clinical practice with assessment of personality disorders, one form of interview is the most popular: an unstructured interview. The actual preferred method is a semi-structured interview but there is reluctance to use this type of interview because they can seem impractical or superficial. The reason that a semi-structured interview is preferred over an unstructured interview is that semi-structured interviews tend to be more objective, systematic, replicable, and comprehensive. Unstructured interviews, despite their popularity, tend to have problems with unreliability and are susceptible to errors leading to false assumptions of the patient.One of the single most successful methods for assessing personality disorders by researchers of normal personality functioning is the self-report inventory following up with a semi-structured interview. There are some disadvantages with the self-report inventory method that with histrionic personality disorder there is a distortion in character, self-presentation, and self-image. This cannot be assessed simply by asking most clients if they match the criteria for the disorder. Most projective testing depend less on the ability or willingness of the person to provide an accurate description of the self, but there is currently limited empirical evidence on projective testing to assess histrionic personality disorder. | Eosinopenia is a form of agranulocytosis where the number of eosinophil granulocytes is lower than expected. Leukocytosis with eosinopenia can be a predictor of bacterial infection. It can be induced by stress reactions, Cushings syndrome, or the use of steroids. Pathological causes include burns and acute infections. See also
Eosinophilia
Hypereosinophilia
References
Further reading
Krause JR, Boggs DR (1987). "Search for eosinopenia in hospitalized patients with normal blood leukocyte concentration". Am. J. Hematol. 24 (1): 55–63. doi:10.1002/ajh.2830240108. PMID 3799595. S2CID 20021710. == External links == | 0-1
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Adenoma of the adrenal gland
Adrenal adenomas are benign tumors of the adrenal gland. In most cases, the tumors display no symptoms and require no treatment. In rare cases, however, some adrenal adenomas may become activated. When activated, the adenoma begins to produce hormones in much larger quantities than what the adrenal glands would normally produce, leading to health complications including primary aldosteronism and hyperandrogenism. Arrhenoblastoma
Arrhenoblastoma is an uncommon tumor of the ovary. It is composed of sterol cells, Leydig cells, or some combination of the two. The tumor can produce male or female hormones and may cause masculinization. In a prepubescent child, a tumor may cause precocious puberty. Malignant arrhenoblastoma accounts for 30% of cases of arrhenoblastoma, the other 70% being largely benign and curable with surgery. Hilar cell tumor
A hilar cell tumor is an androgen-producing ovarian tumor that is most commonly found in older women and often leads to the development of male sex characteristics. The tumor tends to occur around the region of the ovary where the blood vessels enter the organ, known as the hilum. This type of tumor tends to be small in size and in most cases can be entirely removed and its symptoms reversed through surgery. Krukenberg tumor
A Krukenberg tumor is a quickly developing malignant tumor found in one or both ovaries. In most cases, the tumor primarily originates from tissues in the stomach, pancreas, gallbladder, colon, or breast. It colonized the ovary by spreading through the peritoneal cavity. These tumors cause virilization. | Heredity
Hyperandrogenism can appear as a symptom of many different genetic and medical conditions. Some of the conditions with hyperandrogenic symptoms, including PCOS, may sometimes be hereditary. Additionally, it is thought that epigenetics may contribute to the pathogenesis of polycystic ovary syndrome.One potential cause of PCOS is maternal hyperandrogenism, whereby hormonal irregularities in the mother can affect the development of the child during gestation, resulting in the passing of polycystic ovary syndrome from mother to child. However, no androgen elevations in were found in the umbilical cord blood of children born to mothers with PCOS. Diagnosis
Diagnosing hyperandrogenism can be complex due to the wide variety and severity of signs and symptoms that may present. It is most often diagnosed by checking for signs of hirsutism according to a standardized method that scores the range of excess hair growth.Girls may show symptoms of hyperandrogenism early in life, but physicians become more concerned when the patient is in her late teens or older.Checking medical history and a physical examination of symptoms are used for an initial diagnosis. Patient history assessed includes age at thelarche, adrenarche, and menarche; patterns of menstruation; obesity; reproductive history; and the start and advancement of hyperandrogenism symptoms. Patterns of menstruation are examined since irregular patterns may accompany hyperandrogenism. Other conditions that may present alongside hirsutism that can contribute to diagnosis include androgenic alopecia and acne. | 11
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A 2002 editorial in the British Medical Journal warned of inappropriate medicalization leading to disease mongering, where the boundaries of the definition of illnesses are expanded to include personal problems as medical problems or risks of diseases are emphasized to broaden the market for medications.Gary Greenberg, a psychoanalyst, in his book "the Book of Woe", argues that mental illness is really about suffering and how the DSM creates diagnostic labels to categorize peoples suffering. Indeed, the psychiatrist Thomas Szasz, in his book "the Medicalization of Everyday Life", also argues that what is psychiatric illness, is not always biological in nature (i.e. social problems, poverty, etc. ), and may even be a part of the human condition. Potential routine use of MRI/fMRI in diagnosis
in 2018 the American Psychological Association commissioned a review to reach a consensus on whether modern clinical MRI/fMRI will be able to be used in the diagnosis of mental health disorders. the criteria presented by the APA stated that the Biomarkers used in diagnosis should:
"have a sensitivity of at least 80% for detecting a particular psychiatric disorder"
should "have a specificity of at least 80% for distinguishing this disorder from other psychiatric or medical disorders"
"should be reliable, reproducible, and ideally be noninvasive, simple to perform, and inexpensive"
proposed biomarkers should be verified by 2 independent studies each by a different investigator and different population samples and published in a peer-reviewed journal.the review concluded that although neuroimaging diagnosis may technically be feasible, very large studies are needed to evaluate specific biomarkers which were not available. | Pralidoxime has an important role in reversing paralysis of the respiratory muscles but due to its poor blood–brain barrier penetration, it has little effect on centrally-mediated respiratory depression. Atropine, which is choice of drug to antagonise the muscarinic effects of organophosphates, is administered even before pralidoxime during the treatment of organophosphate poisoning. While the efficacy of atropine has been well-established, clinical experience with pralidoxime has led to widespread doubt about its efficacy in treatment of organophosphorus poisoning. Dosage
Adults: 30 mg/kg (typically 1–2 g), administered by intravenous therapy over 15–30 minutes, repeated 60 minutes later. It can also be given as a 500 mg/h continuous IV infusion. Children: 20–50 mg/kg followed by a maintenance infusion at 5–10 mg/kg/h.Intravenous infusions can lead to respiratory or cardiac arrest if given too quickly. Interactions
When atropine and pralidoxime are used together, the signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be expected when atropine is used alone. This is especially true if the total dose of atropine has been large and the administration of pralidoxime has been delayed. The following precautions should be kept in mind in the treatment of anticholinesterase poisoning, although they do not bear directly on the use of pralidoxime: since barbiturates are potentiated by the anticholinesterases, they should be used cautiously in the treatment of convulsions; morphine, theophylline, aminophylline, succinylcholine, reserpine, and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning. Contraindications
There are no known absolute contraindications for the use of pralidoxime. | 0-1
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With spastic hemiplegia, one upper extremity and one lower extremity is affected, so cervical, lumbar and sacral segments of the spinal column can be affected. Diagnosis
Infants with spastic hemiplegia may develop a hand preference earlier than is typical. Treatment
There is no known cure for cerebral palsy, however, there is a large array of treatments proven effective at improving quality of life and relieving some of the symptoms associated with CP, especially SHCP. Some treatments are aimed at improving mobility, strengthening muscle and improving coordination. Although CP is due to permanent damage and is not progressive in nature, without treatment the symptoms can become worse, intensifying in pain and severity, and create complications that were not initially present. Some treatments are preventative measures to help prevent further complications, such as complete paralysis of the arm due to non-use and subsequent worsening hypertonia and joint contracture. Others forms of treatment are corrective in nature. Many treatments target symptoms that are indirectly related to or caused by the SHCP. Many of these treatments are common for other forms of CP as well. Treatment is individualized based on each case and the specific needs of the patient. Treatments are often combined with other forms of treatment and a long-term treatment plan is created and continuously evaluated. Treatment can include the following:
Physical therapy – Physical therapy is the most common form of treatment (source needed). It may include sensory stimulation, stretching, strengthening and positioning. | The frequency of medullary sponge kidney has been reported by various authors to be 12 – 21% in patients with kidney stones. The disease is bilateral in 70% of cases. References
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sidewise curvature of the spine), or other structural disfigurements that result from compensatory mechanisms. Presentation
FMC tumors most commonly present as slow-growing, firm, mobile, nontender, spindle-shaped masses in the lower two-thirds of the sternocleidomastoid muscle of infants within 8 weeks (average: 24 days) of delivery. At diagnosis, these infants heads may tilt toward the side with the mass while their chins tilt to the opposite, uninvolved side. This tilting is due to sternocleidomastoid muscle contracture. FMC tumors are more common in males and the right sternocleidomastoid muscle although very rare cases present with bilateral tumors. Untreated, the masses may continue to grow for weeks after birth but then stabilize, start regressing after 4–8 months of life, and over the ensuing 1–2 years typically fully resolve. In three studies, >25%, >50% and >80% of these infants have had difficult deliveries such as a breech birth, delivery requiring forceps, primigravida birth (i.e. mothers first child), prolonged, difficult labor, or delivery by Caesarean section. From 6-20% of newborns with fibromatosis colli also present with other congenital lesions such as hip dysplasia or, less commonly, facial asymmetry. Pathology
Microscopic histopathological analyses of biopsied FMC tumor tissues typically find benign-appearing, spindle-shaped fibroblasts, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers in a collagen fiber-containing background. If necessary, these tumors are typically diagnosed by microscopic examination of fine-needle aspiration samples rather than the more invasive approach of tumor biopsy sampling. The asperates show scant to moderately cellular, scattered, oval-shaped to spindle-shaped fibroblasts, naked nuclei (i.e. | Fibromatosis colli (FMC), also termed sternocleidomastoid tumor of infancy, pseudotumor of infancy, and infancy sternocleidomastoid pseudotumor, is an uncommon (incidence: 0.4%-1.3% of live births), congenital tumor in one of the two sternocleidomastoid neck muscles although rare cases have presented with a FMC tumor in both sternocleidomastoid muscles. A tumor is here defined as a growth of tissue that is not coordinated with the normal surrounding tissue and persists in growing even if the original trigger for its growth is removed. FMC tumors are benign growths that may cause disfigurements but are not cancers and do not metastasize (i.e. spread) to distant tissues.As judged by microscopic cytology analyses, fibromatosis colli tumors consist of spindle-shaped fibroblasts (i.e. the most common cell type in connective tissue) located in a background of collagen fibers, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers. The fibroblasts have a completely normal appearance with no evidence suggesting that they are malignant. The World Health Organization, 2020, classified fibromatosis colli as in the category of benign fibroblastic and myofibroblastic tumors.In the majority of cases, FMC tumors decrease in size and completely resolve by the newborns second year. If left untreated, however, a significant percentage of cases progress to, and are the most frequent cause of, congenital muscular torticollis, i.e. an abnormal, asymmetrical head or neck position commonly called wry neck. Untreated FMC tumors may also progress to facial asymmetry, plagiocephaly (i.e. flattened head), permanent loss of neck mobility, scoliosis (i.e. | 11
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Zinc sulfide (ZnS) is used in luminescent pigments such as on the hands of clocks, X-ray and television screens, and luminous paints. Crystals of ZnS are used in lasers that operate in the mid-infrared part of the spectrum. Zinc sulfate is a chemical in dyes and pigments. Zinc pyrithione is used in antifouling paints.Zinc powder is sometimes used as a propellant in model rockets. When a compressed mixture of 70% zinc and 30% sulfur powder is ignited there is a violent chemical reaction. This produces zinc sulfide, together with large amounts of hot gas, heat, and light.Zinc sheet metal is used to make zinc bars.64Zn, the most abundant isotope of zinc, is very susceptible to neutron activation, being transmuted into the highly radioactive 65Zn, which has a half-life of 244 days and produces intense gamma radiation. Because of this, zinc oxide used in nuclear reactors as an anti-corrosion agent is depleted of 64Zn before use, this is called depleted zinc oxide. For the same reason, zinc has been proposed as a salting material for nuclear weapons (cobalt is another, better-known salting material). A jacket of isotopically enriched 64Zn would be irradiated by the intense high-energy neutron flux from an exploding thermonuclear weapon, forming a large amount of 65Zn significantly increasing the radioactivity of the weapons fallout. | 2
ZnSO
4
+
2
H
2
O
⟶
2
Zn
+
O
2
+
2
H
2
SO
4
{\displaystyle {\ce {2ZnSO4 + 2H2O -> 2Zn + O2 + 2H2SO4}}}
The sulfuric acid is regenerated and recycled to the leaching step. | 11
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Diagnosis of Behçets disease is based on clinical findings including oral and genital ulcers, skin lesions such as erythema nodosum, acne, or folliculitis, ocular inflammatory findings and a pathergy reaction. Inflammatory markers such ESR, and CRP may be elevated. A complete ophthalmic examination may include a slit lamp examination, optical coherence tomography to detect nerve loss, visual field examinations, fundoscopic examination to assess optic disc atrophy and retinal disease, fundoscopic angiography, and visual evoked potentials, which may demonstrate increased latency. Optic nerve enhancement may be identified on Magnetic Resonance Imaging (MRI) in some patients with acute optic neuropathy. However, a normal study does not rule out optic neuropathy. Cerebrospinal fluid (CSF) analysis may demonstrate elevated protein level with or without pleocytosis. Imaging including angiography may be indicated to identify dural venous sinus thrombosis as a cause of intracranial hypertension and optic atrophy. Diagnostic guidelines
According to the International Study Group guidelines, for a patient to be diagnosed with Behçets disease, the patient must have oral (aphthous) ulcers (any shape, size, or number at least 3 times in any 12 months period) along with 2 out of the following 4 "hallmark" symptoms:
eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous)
genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men)
pathergy reaction (papule >2 mm dia. 24–48 hrs or more after needle-prick). | Atovaquone, sold under the brand name Mepron, is a quinone antimicrobial medication for the prevention and treatment of Pneumocystis jirovecii pneumonia (PCP).Atovaquone is a chemical compound that belongs to the class of naphthoquinones. Atovaquone is a hydroxy-1,4-naphthoquinone, an analog of both ubiquinone and lawsone, with antipneumocystic activity. Medical uses
Atovaquone is a medication used to treat or prevent:
For pneumocystis pneumonia (PCP), it is used in mild cases, although it is not approved for treatment of severe cases. For toxoplasmosis, the medication has antiparasitic and therapeutic effects. For malaria, it is one of the two components (along with proguanil) in the drug Malarone. Malarone has fewer side effects and is more expensive than mefloquine. Resistance has been observed. For babesia, it is often used in conjunction with oral azithromycin.Trimethoprim/sulfamethoxazole (TMP-SMX, Bactrim) is generally considered first-line therapy for PCP (not to be confused with sulfadiazine and pyrimethamine, which is first line for toxoplasmosis). However, atovaquone may be used in patients who cannot tolerate, or are allergic to, sulfonamide medications such as TMP-SMX. In addition, atovaquone has the advantage of not causing myelosuppression, which is an important issue in patients who have undergone bone marrow transplantation. Atovaquone is given prophylactically to kidney transplant patients to prevent PCP in cases where Bactrim is contraindicated for the patient. Malaria
Atovaquone, as a combination preparation with proguanil, has been commercially available from GlaxoSmithKline since 2000 as Malarone for the treatment and prevention of malaria. Research
COVID-19
Preliminary research found that atovaquone could inhibit the replication of SARS-CoV-2 in vitro. | 0-1
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American Journal of Human Genetics. 46 (3): 533–8. PMC 1683634. PMID 2309703. == External links == | Eszopiclone, sold under the brand-name Lunesta among others such as Night Calm in Egypt, is a medication used in the treatment of insomnia. Evidence supports slight to moderate benefit up to six months. It is taken orally.Common side effects include headache, dry mouth, nausea, and dizziness. Severe side effects may include suicidal thoughts, unhealthy non-medical use, hallucinations, and angioedema. Greater care is recommended in those with liver problems and older people. Rapid decreasing of the dose may result in withdrawal. Eszopiclone is classified as a nonbenzodiazepine sedative hypnotic and as a cyclopyrrolone. It is the S-stereoisomer of zopiclone. It works by interacting with the GABA receptors.Approved for medical use in the United States in 2004, eszopiclone is available as generic medication. In 2019, it was the 223rd most commonly prescribed medication in the United States, with more than 2 million prescriptions. Eszopiclone is not sold in the European Union, as in 2009 the European Medicines Agency (EMA) ruled that it was too similar to zopiclone to be considered a new patentable product. Medical uses
A 2018 Cochrane review found that it produced moderate improvement in sleep onset and maintenance. The authors suggest that where preferred non-pharmacological treatment strategies have been exhausted, eszopiclone provides an efficient treatment for insomnia. | 0-1
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Clobetasol propionate is a corticosteroid used to treat skin conditions such as eczema, contact dermatitis, seborrheic dermatitis, and psoriasis. It is applied to the skin as a cream, ointment, or shampoo. Use should be short term and only if other weaker corticosteroids are not effective. Use is not recommended in rosacea or perioral dermatitis.Common side effects include skin irritation, dry skin, redness, pimples, and telangiectasia. Serious side effects may include adrenal suppression, allergic reactions, cellulitis, and Cushings syndrome. Use in pregnancy and breastfeeding is of unclear safety. Clobetasol is believed to work by activating steroid receptors. It is a US Class I (Europe: class IV) corticosteroid, making it one of the strongest available. Clobetasol propionate was patented in 1968 and came into medical use in 1978. It is available as a generic medication. In 2019, it was the 180th most commonly prescribed medication in the United States, with more than 3 million prescriptions. Medical uses
Clobetasol propionate is used for the treatment of various skin disorders including eczema, herpes labialis, psoriasis, and lichen sclerosus. It is also used to treat several auto-immune diseases including alopecia areata, lichen planus (auto immune skin nodules), and mycosis fungoides (T-cell skin lymphoma). It is used as first-line treatment for both acute and chronic GVHD of the skin.Clobetasol propionate is used cosmetically for skin whitening, although this use is controversial. The U.S. Food and Drug Administration has not approved it for that purpose, and sales without a prescription are illegal in the U.S. | Clinical significance
Infection of the urethra is urethritis, which often causes purulent urethral discharge. It is most often due to a sexually transmitted infection such as gonorrhoea or chlamydia, and less commonly due to other bacteria such as ureaplasma or mycoplasma; trichomonas vaginalis; or the viruses herpes simplex virus and adenovirus. Investigations such as a gram stain of the discharge might reveal the cause; nucleic acid testing based on the first urine sample passed in a day, or a swab of the urethra sent for bacterial culture and sensitivity may also be used. Treatment usually involves antibiotics that treat both gonorrhoea and chlamydia, as these often occur together. A person being treated for urethritis should not have sex until the infection is treated, so that they do not spread the infection to others. Because of this spread, which may occur during an incubation period before a person gets symptoms, there is often contact tracing so that sexual partners of an affected person can be found and treatment offered.Cancer can also develop in the lining of the urethra. When cancer is present, the most common symptom in an affected person is blood in the urine; a physical medical examination may be otherwise normal, except in late disease. Cancer of the urethra is most often due to cancer of the cells lining the urethra, called transitional cell carcinoma, although it can more rarely occur as a squamous cell carcinoma if the type of cells lining the urethra have changed, such as due to a chronic schistosomiasis infection. | 0-1
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It comes in single-use filled syringe similar to law enforcement kits. A single dose costs AU$20; for those with a prescription, five doses can bought for AU$40, amounting to a rate of eight dollars per dose (2019).In Alberta, in addition to pharmacy distribution, take-home naloxone kits are available and commonly distributed in most drug treatment or rehabilitation centres.In Europe, take home naloxone pilots were launched in the Channel Islands and in Berlin in the late 1990s. In 2008 the Welsh Assembly government announced its intention to establish demonstration sites for take-home naloxone, and in 2010 Scotland instituted a national naloxone program. Inspired by North American and European efforts, non-governmental organizations running programs to train drug users as overdose responders and supply them with naloxone are now operational in Russia, Ukraine, Georgia, Kazakhstan, Tajikistan, Afghanistan, China, Vietnam, and Thailand. | The influence of 20 or 50 μg/day oral ethinylestradiol on coagulation factors and HDL cholesterol is markedly greater than that of 2 mg/day oral estradiol valerate.Estradiol-containing birth control pills, which contain 1 to 3 mg/day estradiol or estradiol valerate, have been found to increase sex hormone-binding globulin (SHBG) levels by 1.5-fold. Oral estradiol valerate at 6 mg/day has been found to increase SHBG levels by 2.5- to 3-fold in transgender women. For comparison, combined birth control pills containing ethinylestradiol and a progestin with minimal androgenic or antiandrogenic activity have been found to increase SHBG levels by about 3- to 4-fold. Pharmacokinetics
Regardless of the route of administration, estradiol valerate behaves as a prodrug of estradiol via cleavage by esterases into estradiol and the natural fatty acid valeric acid. This cleavage occurs not only in the liver, but also in the blood and in tissues, and the hydrolysis of estradiol valerate into estradiol and valeric acid is complete regardless of whether the medication is administered orally or parenterally. High levels of circulating estradiol are found after an intravenous injection of estradiol valerate, and this indicates very rapid cleavage of the medication upon entering circulation. Oral administration
Esterification of the C17β position of estradiol as in estradiol valerate reduces the metabolism of estradiol valerate by 17β-hydroxysteroid dehydrogenase (17β-HSD). As approximately 80% of estradiol is metabolized into estrone (and estrone sulfate) by 17β-HSD during first-pass metabolism, this improves the metabolic stability and hence bioavailability of estradiol valerate. | 0-1
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Worth syndrome, also known as benign form of Worth hyperostosis corticalis generalisata with torus platinus, autosomal dominant osteosclerosis, autosomal dominant endosteal hyperostosis or Worth disease, is a rare autosomal dominant congenital disorder that is caused by a mutation in the LRP5 gene. It is characterized by increased bone density and benign bony structures on the palate. Causes
Worth syndrome is caused by a mutation in the LRP5 gene, located on human chromosome 11q13.4. The disorder is inherited in an autosomal dominant fashion. This indicates that the defective gene responsible for a disorder is located on an autosome (chromosome 11 is an autosome), and only one copy of the defective gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. Diagnosis
Treatment
History
The condition was first reported by H. M. Worth in 1966. In 1977, two doctors, R.J. Gorlin and L. Glass, distinguished the syndrome from van Buchem disease. In 1987 a group of Spanish doctors pointed out that the condition may not be benign, and may sometimes cause nerve damage. References
== External links == | Treatment
Non-surgical
Early treatment for mild cases of hallux rigidus may include prescription foot orthotics, shoe modifications (such as a pad under the joint, and/or a deeper toe box to take the pressure off the toe and/or facilitate walking), specialized footwear (rocker-sole shoes), medications (anti-inflammatory drugs) or injection therapy (corticosteroids to reduce inflammation and pain). Physical therapy programs may be recommended, although there is very limited evidence that they provide benefit for reducing pain and improving function of the joint. Surgical
The goal of surgery is to eliminate or reduce pain. There are several types of surgery for treatment of hallux rigidus. The type of surgery is based on the stage of hallux rigidus. According to the Coughlin and Shurnas Clinical Radiographic Scale:Stage 1 hallux rigidus involves some loss of range of motion of the big toe joint or first MTP joint and is often treated conservatively with prescription foot orthotics. Stage 2 hallux rigidus involves greater loss of range of motion and cartilage and may be treated via cheilectomy in which the metatarsal head is reshaped and bone spurs reduced. Stage 3 hallux rigidus often involves significant cartilage loss and may be treated by an osteotomy in which cartilage on the first metatarsal head is repositioned, possibly coupled with a hemi-implant in which the base of the proximal phalanx (base of the big toe) is resurfaced. Stage 4 hallux rigidus, also known as end stage hallux rigidus, involves severe loss of range of motion of the big toe joint and cartilage loss. | 0-1
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If it has not been adequately purified during manufacture it can degrade over time to even more unstable forms. This makes nitroglycerin highly dangerous to transport or use. In its undiluted form, it is one of the worlds most powerful explosives, comparable to the more recently developed RDX and PETN. Early in its history, liquid nitroglycerin was found to be "desensitized" by freezing it at a temperature below 45 to 55 °F (7 to 13 °C) depending on its purity. Its sensitivity to shock while frozen is somewhat unpredictable: "It is more insensitive to the shock from a fulminate cap or a rifle ball when in that condition but on the other hand it appears to be more liable to explode on breaking, crushing, tamping, etc." Frozen nitroglycerine is much less energetic than liquid, and so must be thawed before use. Thawing it out can be extremely sensitizing, especially if impurities are present or the warming is too rapid. Ethylene glycol dinitrate or another polynitrate may be added to lower the melting point and thereby avoid the necessity of thawing frozen explosive.Chemically "desensitizing" nitroglycerin is possible to a point where it can be considered about as "safe" as modern high explosives, such as by the addition of ethanol, acetone, or dinitrotoluene. The nitroglycerin may have to be extracted from the desensitizer chemical to restore its effectiveness before use, for example by adding water to draw off ethanol used as a desensitizer. Detonation
Nitroglycerin and any diluents can deflagrate (burn). | The explosive power of nitroglycerin derives from detonation: energy from the initial decomposition causes a strong pressure wave that detonates the surrounding fuel. This is a self-sustained shock wave that propagates through the explosive medium at 30 times the speed of sound as a near-instantaneous pressure-induced decomposition of the fuel into a white-hot gas. Detonation of nitroglycerin generates gases that would occupy more than 1,200 times the original volume at ordinary room temperature and pressure. The heat liberated raises the temperature to about 5,000 °C (9,000 °F). This is entirely different from deflagration, which depends solely upon available fuel regardless of pressure or shock. The decomposition results in a much higher ratio of energy to gas moles released compared to other explosives, making it one of the hottest detonating high explosives. Manufacturing
Nitroglycerin can be produced by acid-catalyzed nitration of glycerol (glycerin). The industrial manufacturing process often reacts glycerol with a nearly 1:1 mixture of concentrated sulfuric acid and concentrated nitric acid. This can be produced by mixing white fuming nitric acid—a quite expensive pure nitric acid in which the oxides of nitrogen have been removed, as opposed to red fuming nitric acid, which contains nitrogen oxides—and concentrated sulfuric acid. More often, this mixture is attained by the cheaper method of mixing fuming sulfuric acid, also known as oleum—sulfuric acid containing excess sulfur trioxide—and azeotropic nitric acid (consisting of about 70% nitric acid, with the rest being water). The sulfuric acid produces protonated nitric acid species, which are attacked by glycerols nucleophilic oxygen atoms. | 11
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Cancer
WHO organization International Agency for Research on Cancer (IARC) list AAS under Group 2A: Probably carcinogenic to humans. Cardiovascular
Other side-effects can include alterations in the structure of the heart, such as enlargement and thickening of the left ventricle, which impairs its contraction and relaxation, and therefore reducing ejected blood volume. Possible effects of these alterations in the heart are hypertension, cardiac arrhythmias, congestive heart failure, heart attacks, and sudden cardiac death. These changes are also seen in non-drug-using athletes, but steroid use may accelerate this process. However, both the connection between changes in the structure of the left ventricle and decreased cardiac function, as well as the connection to steroid use have been disputed.AAS use can cause harmful changes in cholesterol levels: Some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol. Growth defects
AAS use in adolescents quickens bone maturation and may reduce adult height in high doses. Low doses of AAS such as oxandrolone are used in the treatment of idiopathic short stature, but this may only quicken maturation rather than increasing adult height. Feminization
There are also sex-specific side effects of AAS. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase. Reduced sexual function and temporary infertility can also occur in males. | Anabolic steroids, also known more properly as anabolic–androgenic steroids (AAS), are steroidal androgens that include natural androgens like testosterone as well as synthetic androgens that are structurally related and have similar effects to testosterone. They increase protein within cells, especially in skeletal muscles, and also have varying degrees of virilizing effects, including induction of the development and maintenance of masculine secondary sexual characteristics such as the growth of facial and body hair. The word anabolic, referring to anabolism, comes from the Greek ἀναβολή anabole, "that which is thrown up, mound". Androgens or AAS are one of three types of sex hormone agonists, the others being estrogens like estradiol and progestogens like progesterone. AAS were synthesized in the 1930s, and are now used therapeutically in medicine to stimulate muscle growth and appetite, induce male puberty and treat chronic wasting conditions, such as cancer and AIDS. The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases and that the gains in muscular strength achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.Health risks can be produced by long-term use or excessive doses of AAS. These effects include harmful changes in cholesterol levels (increased low-density lipoprotein and decreased high-density lipoprotein), acne, high blood pressure, liver damage (mainly with most oral AAS), and dangerous changes in the structure of the left ventricle of the heart. | 11
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Formulations
Fenofibrate is available in several formulations and is sold under several brand names, including:
Tricor by AbbVie
Lipofen by Kowa Pharmaceuticals America Inc
Lofibra by Teva
Lipanthyl, Lipidil, Lipantil micro and Supralip by Abbott Laboratories
Fenocor-67 by Ordain Health Care
Fibractiv 105/35 by Cogentrix Pharma (India)
Fenogal by SMB Laboratories
Antara by Oscient Pharmaceuticals
Tricheck by Zydus (CND)
Atorva TG by Zydus Medica
Golip by GolgiUSA
Stanlip by Ranbaxy (India)The formulations may differ in terms of pharmacokinetic properties, particularly bioavailability; some must be taken with meals, whereas others may be taken without regard to food.The choline salt of fenofibrate is available in the United States, sold as Trilipix, and may be taken without regard to meals. Environmental presence
Fenofibric acid was one of the 12 compounds identified in sludge samples taken from 12 wastewater treatment plants in California that were associated with estrogenic activity in in vitro. History
Fenofibrate was first synthesized in 1974, as a derivative of clofibrate, and was initially offered in France. It was initially known as procetofen, and was later renamed fenofibrate to comply with World Health Organization International Nonproprietary Name guidelines.Fenofibrate was developed by Groupe Fournier SA of France. In the United States, Tricor was reformulated in 2005. This reformulation was controversial, seen as an attempt to stifle competition from generic equivalents, and was the subject of antitrust litigation by Teva. References
External links
"Fenofibrate". Drug Information Portal. U.S. National Library of Medicine. | The defense mechanisms of the body present as cold and flu-like symptoms that occur in individuals who experience either acute or chronic reactions.The mold spores are inhaled and provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly Saccharopolyspora rectivirgula), which generate IgG-type antibodies. Following a subsequent exposure, IgG antibodies combined with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs. This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung. After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung. Prevention
Farmers lung disease (FLD) is permanent and cannot be reversed, therefore in order to prevent the onset of further stages, farmers should inform their doctor of their occupation and if they have mold in their work environment. Prevention of this respiratory illness can be facilitated through the ventilation of work areas, drying of materials, and the use of a mask when working in confined areas with moldy hay or crops. Diagnosis
Diagnoses of Farmers lung is difficult due to its similarity to cold and flu-like symptoms. Doctors diagnose patients with Farmers lung under the following conditions:
A clinical history of symptoms such as cough, fever, and labored breathing when exposed to mold in work environment. The presence of diffuse lung disease in chronic cases. | 0-1
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For patients, this has the major benefit that they can take less saquinavir, while maintaining sufficient saquinavir blood plasma levels to efficiently suppress the replication of HIV.The mechanism behind this welcome observation was not directly known, but later it was determined that ritonavir inhibits the cytochrome P450 3A4 isozyme. Normally, this enzyme metabolizes saquinavir to an inactive form, but with the ritonavir inhibiting this enzyme, the saquinavir blood plasma levels increased considerably. Additionally, ritonavir also inhibits multidrug transporters, although to a much lower extent.Unlike other protease inhibitors, the absorption of saquinavir seems to be improved by omeprazole. Mechanism of action
Saquinavir is a protease inhibitor. Proteases are enzymes that cleave protein molecules into smaller fragments. HIV protease is vital for both viral replication within the cell and release of mature viral particles from an infected cell. Saquinavir binds to the active site of the viral protease and prevents cleavage of viral polyproteins, preventing maturation of the virus. Saquinavir inhibits both HIV-1 and HIV-2 proteases. History
Saquinavir was developed by the pharmaceutical company Roche. Saquinavir was the sixth antiretroviral and the first protease inhibitor approved by the US Food and Drug Administration (FDA), leading ritonavir and indinavir by a few months. | Saquinavir (SQV), sold under the brand names Invirase and Fortovase, is an antiretroviral drug used together with other medications to treat or prevent HIV/AIDS. Typically it is used with ritonavir or lopinavir/ritonavir to increase its effect. It is taken by mouth.Common side effects include nausea, vomiting, diarrhea, and feeling tired. More serious side effects include problems with QT prolongation, heart block, high blood lipids, and liver problems. It appears to be safe in pregnancy. It is in the protease inhibitor class and works by blocking the HIV protease.Saquinavir was patented in 1988 and first sold in 1995. Medical uses
Saquinavir is used together with other medications to treat or prevent HIV/AIDS. Typically it is used with ritonavir or lopinavir/ritonavir to increase its effect. Side effects
The most frequent adverse events with saquinavir in either formulation are mild gastrointestinal symptoms, including diarrhoea, nausea, loose stools and abdominal discomfort. Invirase is better tolerated than Fortovase. Bioavailability and drug interactions
Saquinavir, in the Invirase formulation, has a low and variable oral bioavailability, when given alone. The Fortovase formulation at the standard dosage delivers approximately eightfold more active drug than Invirase, also at the standard dosage.In the clinic, it was found that the oral bioavailability of saquinavir in both formulations significantly increases when patients also receive the PI ritonavir. | 11
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Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period. "The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as high risk and some risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting. Unknown exposure
For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels. Confirmed absence of exposure
Confirmed absence of exposure would apply to planned pregnancies in which no alcohol was used or pregnancies of women who do not use alcohol or report no use during the pregnancy. This designation is relatively rare, as most people presenting for an FASD evaluation are at least suspected to have had a prenatal alcohol exposure due to presence of other key features of FASD. | Persistent polyclonal B-cell lymphocytosis (PPBL) is an anomaly of the human immune system characterized by mildly elevated levels of white blood cells (called leukocytosis), chronic, stable absolute polyclonal B-cell lymphocytosis, elevated polyclonal IgM and binucleated cells. Although cases of non-smoking women or men have been reported, patients are predominantly young smoking women. Signs and symptoms
Ten percent of patients present with splenomegaly and lymphadenopathy. Some patients report a varying degree of fatigue, consistent with a chronic fatigue syndrome, or postviral fatigue as seen in EBV infections while others remain asymptomatic. Genetics
Genetically, PPBL has been associated with a few unusual genetic characteristics. Among them, it is associated with a particular genetic variant of the human leukocyte antigen called HLA-DR7. This variant is normally present in 26% in the Caucasian population. Chromosome analysis has detected an isochromosome +i(3q), with or without premature chromosome condensation. Also, a t(14;18)(q22;21) bcl-2/IgH rearrangement has been described, as usually seen in follicular lymphoma. Immunologically, peripheral B-cells show more functional IgD+ positive CD27 cells than usual. Prognosis
In the followup of 111 patients, most remained stable and event free. However, two patients developed IgM gammopathy 2 lung cancer; one developed cervical cancer and three developed non-Hodgkins lymphoma. The possibility of developing a clonal proliferation, malignant lymphoma or secondary solid cancer led the authors to conclude not to classify PPBL as a benign pathology, as has been previously postulated but rather to recommend a careful and continued clinical and biological longterm follow-up. == References == | 0-1
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If the adrenal glands appear not to be working then tetracosactide injection can be given to check whether the problem is due to diseased or damaged adrenals or due to lack of pituitary ACTH. Tetracosactide stimulates the release of corticosteroids such as cortisol from the adrenal glands, and is used for the ACTH stimulation test to assess adrenal gland function. : 271
Chemistry
The synthetic form consists of the first 24 (of a total of 39) amino acids of ACTH and retains full function of the parent peptide. : 1165
Manufacturing
History
Society and culture
Approved forms
In the US, available forms of animal-derived corticotrophin have included:
Cortiocotrophin derived from pituitary glands from pigs, in a gel formulation as well as in a zinc hydrochloride formulation, each first approved in the US in 1955 and subsequently discontinued. In September 2015 ANI Pharmaceuticals and Merck & Co. agreed that ANI would purchase NDA 009854 and NDA 008975 and related trademarks and other assets related to these two versions of corticotrophin from Merck for $75M and ongoing royalties; the transaction closed in January 2016. As of November 2016 ANI was preparing its supplemental NDA to get approval to re-introduce this formulation; in 2015 ANI estimated that the US market for these products was about $1 billion per year, based on sales of Acthar gel. Corticotrophin, first approved in 1952 and subsequently discontinued; as of January 2017 this NDA was under control of Parkedale, a subsidiary of King Pharmaceuticals which is in turn a subsidiary of Pfizer. | The Federal Trade Commission and attorneys general from five states sued Mallinckrodt for anti-competitive behavior with regard to the acquisition of Synacthen Depot and the monopolistic pricing of Acthar, and in January 2017 the company settled, agreeing to pay $100 million and to license Synacthen Depot to a competitor. According to Kaiser Health News, Mallinckrodt responded by increasing its Congressional lobbying to $610,000, and its contributions to Congress members to $44,000, in the first quarter of 2017.In Canada, Synacthen Depots pricing increased by 2000% in 2015, causing some provincial single payer authorities to delist the drug from funded medications. The increase in the drugs price came after Mallinckrodt acquired Questcor and its drug portfolio, which included the worldwide rights to Synacthen Depot. Prior to the price increase, Mallinckrodt claims that the drug was manufactured at a loss. Some have claimed that the price increase is abusive. The drug had been priced at $33 but rose to $680 per vial. As an off-patent pharmaceutical, a similar drug, differing in formulation, available in Europe, made by a different manufacturer, sells for $8 per vial. Research
Acthar gel has been proposed as a therapy to treat refractory autoimmune diseases and refractory nephrotic syndrome due to a variety of glomerular diseases. Veterinary medicine
Both versions of the hormone are also used to perform the ACTH stimulation test to diagnose hypoadrenocorticism in dogs and sometimes cats. References
External links
Adrenocorticotropic+Hormone at the US National Library of Medicine Medical Subject Headings (MeSH)
Cosyntropin at the US National Library of Medicine Medical Subject Headings (MeSH) | 11
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This test will reproduce vertigo and nystagmus characteristic of posterior canal BPPV.When performing the Dix–Hallpike test, people are lowered quickly to a supine position, with the neck extended by the person performing the maneuver. For some people, this maneuver may not be indicated, and a modification may be needed that also targets the posterior semicircular canal. Such people include those who are too anxious about eliciting the uncomfortable symptoms of vertigo, and those who may not have the range of motion necessary to comfortably be in a supine position. The modification involves the person moving from a seated position to side-lying without their head extending off the examination table, such as with Dix–Hallpike. The head is rotated 45 degrees away from the side being tested, and the eyes are examined for nystagmus. A positive test is indicated by the patient report of a reproduction of vertigo and clinician observation of nystagmus. Both the Dix–Hallpike and the side-lying testing position have yielded similar results, and as such the side-lying position can be used if the Dix–Hallpike cannot be performed easily.The roll test can determine whether the horizontal semicircular canal is involved. The roll test requires the person to be in a supine position with their head in 30° of cervical flexion. Then the examiner quickly rotates the head 90° to the left side, and checks for vertigo and nystagmus. This is followed by gently bringing the head back to the starting position. | A specific antibody and epitope binding that shows the highest affinity and is pathogenic occurs between GPA antibodies and the anti-GBM epitope region, designated EA, which is residues 17-31 of the alpha 3 subunit of non-collagenous domain of type IV collagen. T cells are also implicated, though it is generally considered a type II hypersensitivity reaction. Diagnosis
The diagnosis of GPS is often difficult, as numerous other diseases can cause the various manifestations of the condition and the condition itself is rare. The most accurate means of achieving the diagnosis is testing the affected tissues by means of a biopsy, especially the kidney, as it is the best-studied organ for obtaining a sample for the presence of anti-GBM antibodies. On top of the anti-GBM antibodies implicated in the disease, about one in three of those affected also has cytoplasmic antineutrophilic antibodies in their bloodstream, which often predates the anti-GBM antibodies by about a few months or even years. The later the disease is diagnosed, the worse the outcome is for the affected person.In addition, if there is substantial suspicion of the disease, seralogic testing for ELISA assay is usually done by looking for alpha3 NC1 domain area of collagen IV in order to avoid false positives. Treatment
The major mainstay of treatment for GPS is plasmapheresis, a procedure in which the affected persons blood is sent through a centrifuge and the various components separated based on weight. The plasma contains the anti-GBM antibodies that attack the affected persons lungs and kidneys, and is filtered out. | 0-1
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The renin–angiotensin system may be subsequently activated, because of the decrease in perfusion of juxtaglomerular apparatus, which may result in hypertension. : 554
Nonproliferative
This is characterised by forms of glomerulonephritis in which the number of cells is not changed. These forms usually result in the nephrotic syndrome. Causes include:
Minimal change disease
Minimal change disease is characterised as a cause of nephrotic syndrome without visible changes in the glomerulus on microscopy. Minimal change disease typically presents with edema, an increase in proteins passed from urine and decrease in blood protein levels, and an increase in circulating lipids (i.e., nephrotic syndrome) and is the most common cause of the nephrotic syndrome in children. Although no changes may be visible by light microscopy, changes on electron microscopy within the glomeruli may show a fusion of the foot processes of the podocytes (cells lining the basement membrane of the capillaries of glomerulus). It is typically managed with corticosteroids and does not progress to chronic kidney disease. : 500 : 550
Focal segmental glomerulosclerosis
Focal segmental glomerulosclerosis is characterised by a sclerosis of segments of some glomeruli. It is likely to present as a nephrotic syndrome. This form of glomerulonephritis may be associated with conditions such as HIV and heroin abuse, or inherited as Alport syndrome. The cause of about 20–30% of focal-segmental glomerulosclerosis is unknown. On microscopy, affected glomeruli may show an increase in hyalin, a pink and homogenous material, fat cells, an increase in the mesangial matrix and collagen. | See also
Methylmalonic acidemia
Organic acidemia
Notes
The term combined malonic and methylmalonic aciduria with the suffix -uria (from Greek ouron, urine) has become established in the scientific literature in contrast to the other term combined malonic and methylmalonic acedemia with the suffix -emia (from Greek aima, blood). However, in the context of CMAMMA, no clear distinction is made, since malonic acid and methylmalonic acid are elevated in both blood and urine. References
External links
Combined malonic and methylmalonic acidemia at Orphanet | 0-1
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: 61–9 Mirror box therapy produces the illusion of movement and touch in a phantom limb which in turn may cause a reduction in pain.Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief. : 61–9
Breakthrough
Breakthrough pain is transitory pain that comes on suddenly and is not alleviated by the patients regular pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl. Asymbolia and insensitivity
The ability to experience pain is essential for protection from injury, and recognition of the presence of injury. | In severe cases of thiamine deficiency, a few of the positive symptoms (including neuropathic pain) may persist indefinitely. Even after the restoration of a balanced nutritional intake, those patients with severe or chronic polyneuropathy may experience lifelong residual symptoms. Epidemiology
In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy. The rate of incidence of alcoholic polyneuropathy involving sensory and motor polyneuropathy has been stated as from 10% to 50% of alcoholics depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria are used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed.The distribution and severity of the disease depends on regional dietary habits, individual drinking habits, as well as an individuals genetics. Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees. For unknown reasons, alcoholic polyneuropathy has a high incidence in women.Certain alcoholic beverages can also contain congeners that may also be bioactive; therefore, the consumption of varying alcohol beverages may result in different health consequences. An individuals nutritional intake also plays a role in the development of this disease. | 0-1
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Either of these pathways will result in decreased endothelial thromboresistance, leukocyte adhesion to damaged endothelium, complement consumption, enhanced vascular shear stress, and abnormal vWF fragmentation. The central and primary event in this progression is injury to the endothelial cells, which reduces the production of prostaglandin and prostacyclin, ultimately resulting in the loss of physiological thromboresistance, or high thrombus formation rate in blood vessels. Leukocyte adhesion to the damaged endothelial wall and abnormal von Willebrand factor (or vWF) release can also contribute to the increase in thrombus formation. More recently, researchers have attributed both TTP and HUS to targeted agents, such as targeted cancer therapies, immunotoxins, and anti-VEGF therapy.Bacterial toxins are the primary cause of one category of thrombotic microangiopathy known as HUS or hemolytic uremic syndrome. HUS can be divided into two main categories: Shiga-toxin-associated HUS (STx-HUS), which normally presents with diarrhea, and atypical HUS. The Shiga-toxin inhibits the binding of eEF-1-dependent binding of aminoacyl tRNA to the 60S subunit of the ribosome, thus inhibiting protein synthesis. The cytotoxicity from the lack of protein damages glomerular endothelial cells by creating voids in the endothelial wall and detaching the basement membrane of the endothelial layer, activating the coagulation cascade. Atypical HUS may be caused by an infection or diarrheal illness or it may be genetically transmitted. This category of TMA encompasses all forms that do not have obvious etiologies. Mutations in three of the proteins in the complement cascade have been identified in patients with atypical HUS. | Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension,
antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity. Signs and symptoms
The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), kidney failure, thrombocytopenia and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs. Cause
The specific cause is dependent of the type of TMA that is presented, but the two main pathways that lead to TMA are external triggers of vascular injury, such as viruses, bacterial Shiga toxins or endotoxins, antibodies, and drugs; and congenital predisposing conditions, including decreased levels of tissue factors necessary for the coagulation cascade. | 11
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Zoons balanitis has been successfully treated with the carbon dioxide laser; and more recently, Albertini and colleagues report the avoidance of circumcision and successful treatment of Zoons balanitis with an Er:YAG laser. Another study, by Retamar and colleagues, found that 40 percent of those treated with CO2 laser relapsed. Circinate balanitis, also known as balanitis circinata, is a serpiginous annular dermatitis associated with reactive arthritis. Pseudoepitheliomatous keratotic and micaceous balanitis
Treatment
Initial treatment in adults often involves simply pulling back the foreskin and cleaning the penis. However, some topical antibiotic and fungal ointments may be used for treatment for mild cases. Depending upon severity, hydrocortisone and other steroidal creams may be used upon consultation. Epidemiology
Balanitis "is a common condition affecting 11% of adult men seen in urology clinics and 3% of children" in the United States; globally, balanitis "may occur in up to 3% of uncircumcised males". Other animals
In dogs, balanoposthitis is caused by a disruption in the integumentary system, such as a wound or intrusion of a foreign body. A dog with this condition behaves normally, with the exception of excessive licking at the prepuce, and a yellow green, pus-like discharge is usually present. In sheep (rams/wethers), ulcerative enzootic balanoposthitis is caused by the Corynebacterium renale group (C. renale, C. pilosum & C. cystidis). For the condition in bulls, caused by a virus see Bovine herpesvirus 1. Balanoposthitis is believed to have contributed to the decline to near-extinction of Gilberts potoroo. References
Further reading
Edwards S. (for the Clinical Effectiveness Group) National guideline on the management of balanitis. | However, in some cases, including double X-deficiency, the ratio can be much more than half, making the individual almost as sensitive as males.Red blood cell breakdown (also known as hemolysis) in G6PD deficiency can manifest in a number of ways, including the following:
Prolonged neonatal jaundice, possibly leading to kernicterus (arguably the most serious complication of G6PD deficiency)
Hemolytic crises in response to:
Illness (especially infections)
Certain drugs (see below)
Certain foods, most notably broad beans, from which the word favism derives
Certain chemicals
Diabetic ketoacidosis
Hemoglobinuria (red or brown urine)
Very severe crisis can cause acute kidney injuryFavism is a hemolytic response to the consumption of fava beans, also known as broad beans. Though all individuals with favism show G6PD deficiency, not all individuals with G6PD deficiency show favism. The condition is known to be more prevalent in infants and children, and G6PD genetic variant can influence chemical sensitivity. Other than this, the specifics of the chemical relationship between favism and G6PD are not well understood. Cause
G6PD deficiency results from mutations in the G6PD gene. G6PD gene contributes to the production of glucose-6-phosphate dehydrogenase. Chemical reactions involving glucose-6-phosphate dehydrogenase produce compounds that prevent reactive oxygen species from building up to toxic levels within red blood cells. If reduction in the amount of glucose-6-phosphate dehydrogenase or alteration of structure occurs due to the mutations of G6PD gene, the enzyme loses it protective role and leads to the accumulation of reactive oxygen species and thus damage of red blood cells. | 0-1
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In 2013, a man in Taiwan died 25 days after being infected by Naegleria fowleri.It affects healthy children or young adults who have recently been exposed to bodies of fresh water. Some people have presented with a clinical triad of edematous brain lesions, immune suppression and fever. Scientists speculate that lower age groups are at a higher risk of contracting the disease because adolescents have a more underdeveloped and porous cribriform plate, through which the amoeba travels to reach the brain. Cause
N. fowleri invades the central nervous system via the nose, specifically through the olfactory mucosa of the nasal tissues. This usually occurs as the result of the introduction of water that has been contaminated with N. fowleri into the nose during activities such as swimming, bathing or nasal irrigation.The amoeba follows the olfactory nerve fibers through the cribriform plate of the ethmoid bone into the skull. There, it migrates to the olfactory bulbs and subsequently other regions of the brain, where it feeds on the nerve tissue. The organism then begins to consume cells of the brain, piecemeal through trogocytosis, by means of an amoebostome, a unique actin-rich sucking apparatus extended from its cell surface. It then becomes pathogenic, causing primary amoebic meningoencephalitis (PAM or PAME).Primary amoebic meningoencephalitis presents symptoms similar to those of bacterial and viral meningitis. Upon abrupt disease onset, a plethora of problems arise. Endogenous cytokines, which release in response to pathogens, affect the hypothalamus thermoregulatory neurons and cause a rise in body temperature. | In cases of saccular type of cyst, excision and placement of T-shaped tube is done.Currently, there is no accepted indication for fetal intervention in the management of prenatally suspected choledochal cysts. References
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Imaginary time is not real or unreal, it is something that is hard to visualize. Philosophers can agree that physical time exists outside of the human mind and is objective, and psychological time is mind-dependent and subjective. Unreality
In 5th century BC Greece, Antiphon the Sophist, in a fragment preserved from his chief work On Truth, held that: "Time is not a reality (hypostasis), but a concept (noêma) or a measure (metron)." Parmenides went further, maintaining that time, motion, and change were illusions, leading to the paradoxes of his follower Zeno. Time as an illusion is also a common theme in Buddhist thought.J. M. E. McTaggarts 1908 The Unreality of Time argues that, since every event has the characteristic of being both present and not present (i.e., future or past), that time is a self-contradictory idea (see also The flow of time). These arguments often center on what it means for something to be unreal. Modern physicists generally believe that time is as real as space – though others, such as Julian Barbour in his book The End of Time, argue that quantum equations of the universe take their true form when expressed in the timeless realm containing every possible now or momentary configuration of the universe, called "platonia" by Barbour.A modern philosophical theory called presentism views the past and the future as human-mind interpretations of movement instead of real parts of time (or "dimensions") which coexist with the present. | Dundar and coworkers found that the LMBR1 gene links to pre axial polydactyly. This gene encodes for a new transmembrane receptor and it is proposed that this receptor is an upstream regulator of SHH. Diagnosis
Management
Society
Three main support groups of this syndrome are the ASGA in Australia, The Association for Children with Genetic Disorders in Poland, and the Association of People of Genetic Disorders in Greece. References
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This tends to occur in the farsighted, who have smaller anterior chambers, making physical contact between the iris and trabecular meshwork more likely. A variety of tests may be performed to detect those at risk of angle-closure glaucoma.Normal-tension glaucoma (NTG, also called low-tension or normal-pressure glaucoma) is a condition in which the optic nerve is damaged although intraocular pressure (IOP) is in the normal range (12 to 22 mmHg (1.6 to 2.9 kPa)). Individuals with a family history of NTG, those of Japanese ancestry, those with a history of systemic heart disease and those with Flammer syndrome are at an elevated risk of developing NTG. The cause of NTG is unknown. Secondary glaucoma refers to any case in which another disease, trauma, drug or procedure causes increased eye pressure, resulting in optic nerve damage and vision loss, which may be mild or severe. This may be the result of an eye injury, inflammation, a tumor or advanced cases of cataracts or diabetes. It can also be caused by certain drugs such as steroids. Treatment depends on whether the condition is identified as open-angle or angle-closure glaucoma. With pseudoexfoliation glaucoma (also known as PEX or exfoliation glaucoma) the pressure results from the accumulation of microscopic granular protein fibers, which can block normal drainage of the aqueous humor. PEX is prevalent in Scandinavia, primarily in those over 70, and more commonly in women. | Dolichocephaly (derived from the Ancient Greek δολιχός long and κεφαλή head) is a condition where the head is longer than would be expected, relative to its width. In humans, scaphocephaly is a form of dolichocephaly. Dolichocephalic dogs (such as German Shepherds) have elongated noses. This makes them vulnerable to fungal diseases of the nose such as aspergillosis. In humans the anterior–posterior diameter (length) of dolichocephaly head is more than the transverse diameter (width).It can be present in cases of Sensenbrenner syndrome, Crouzon syndrome, Sotos syndrome, CMFTD as well as Marfan syndrome. See also
Brachycephaly
Cephalic index
Plagiocephaly
References
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Triamterene (trade name Dyrenium among others) is a potassium-sparing diuretic often used in combination with thiazide diuretics for the treatment of high blood pressure or swelling. The combination with hydrochlorothiazide, is known as hydrochlorothiazide/triamterene. Side effects
Common side effects may include a depletion of sodium, folic acid, and calcium, nausea, vomiting, diarrhea, headache, dizziness, fatigue, and dry mouth. Serious side effects may include heart palpitations, tingling/numbness, fever, chills, sore throat, rash, and back pain. Triamterene can also cause kidney stones through direct crystallization or by seeding calcium oxalate stones. Triamterene is best avoided in patients with chronic kidney disease due to the possibility of hyperkalemia. People using this drug should use salt substitute cautiously.Triamterene may impart a blue fluorescent color to the urine. Caution with certain disease states
Diabetes: Use with caution in people with prediabetes or diabetes mellitus as there may be a change in glucose control. Liver impairment: Use with caution in people with severe liver dysfunction; in cirrhosis, avoid electrolyte and acid/base imbalances that might lead to hepatic encephalopathy. Kidney failure: combined triamterene and indomethacin therapy caused reversible acute kidney injury in some people.Kidney stones: Use with caution in people with kidney stones. Use should be avoided if the creatinine clearance is less than 10 ml/minute. Mechanism of action
Triamterene directly blocks the epithelial sodium channel (ENaC) on the lumen side of the kidney collecting tubule. | Specific tests are needed to confirm that these properties are in fact due to excessive levels of fat. Fats in feces can be measured over a defined time (often five days). Other tests include the (13)C-mixed triglycerides test and fecal elastase, to detect possible fat maldigestion due to exocrine pancreatic insufficiency, or various specific tests to detect other causes of malabsorption such as celiac disease. Treatment
Treatments are mainly correction of the underlying cause, as well as digestive enzyme supplements. See also
Rectal discharge
Keriorrhea
Fecal leakage
Steatocrit
References
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Social anxiety in individuals with FXS is related to challenges with face encoding, the ability to recognize a face that one has seen before.It appears that individuals with FXS are interested in social interaction and display greater empathy than groups with other causes of intellectual disability, but display anxiety and withdrawal when placed in unfamiliar situations with unfamiliar people. This may range from mild social withdrawal, which is predominantly associated with shyness, to severe social withdrawal, which may be associated with co-existing autism spectrum disorder.Females with FXS frequently display shyness, social anxiety and social avoidance or withdrawal. In addition, premutation in females has been found to be associated with social anxiety. Female individuals with FXS show decreased activation in the prefrontal regions of the brain. Mental health
Attention deficit hyperactivity disorder (ADHD) is found in the majority of males with FXS and 30% of females, making it the most common psychiatric diagnosis in those with FXS. Children with fragile X have very short attention spans, are hyperactive, and show hypersensitivity to visual, auditory, tactile, and olfactory stimuli. These children have difficulty in large crowds due to the loud noises and this can lead to tantrums due to hyperarousal. Hyperactivity and disruptive behavior peak in the preschool years and then gradually decline with age, although inattentive symptoms are generally lifelong.Aside from the characteristic social phobia features, a range of other anxiety symptoms are very commonly associated with FXS, with symptoms typically spanning a number of psychiatric diagnoses but not fulfilling any of the criteria in full. | Fragile X syndrome (FXS) is a genetic disorder characterized by mild-to-moderate intellectual disability. The average IQ in males with FXS is under 55, while about two thirds of affected females are intellectually disabled. Physical features may include a long and narrow face, large ears, flexible fingers, and large testicles. About a third of those affected have features of autism such as problems with social interactions and delayed speech. Hyperactivity is common, and seizures occur in about 10%. Males are usually more affected than females.This disorder and finding of Fragile X syndrome has an X-linked dominant inheritance. It is typically caused by an expansion of the CGG triplet repeat within the FMR1 (fragile X messenger ribonucleoprotein 1) gene on the X chromosome. This results in silencing (methylation) of this part of the gene and a deficiency of the resultant protein (FMRP), which is required for the normal development of connections between neurons. Diagnosis requires genetic testing to determine the number of CGG repeats in the FMR1 gene. Normally, there are between 5 and 40 repeats; fragile X syndrome occurs with more than 200. A premutation is said to be present when the gene has between 55 and 200 repeats; women with a premutation have an increased risk of having an affected child. Testing for premutation carriers may allow for genetic counseling.There is no cure. Early intervention is recommended, as it provides the most opportunity for developing a full range of skills. These interventions may include special education, speech therapy, physical therapy, or behavioral therapy. | 11
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As no drugs or poison were found in her system, her death remains a mystery. Fulfilling their pact, June proceeded to live an otherwise-normal life. The Burari Deaths, wherein a family of 11 members was found hanging in their home in Delhi, was ruled as a case of "Shared Psychosis," led by the youngest son of the matriarch. In popular culture
In Folie à Deux (The X-Files) Season 5, Episode 19 (1998), Mulder is taken hostage by an employee who believes his boss is turning his coworkers into zombies. Bug (2006) is a film that depicts a couple with a shared delusion that aphids are living under their skin. In Season 2, Episode 3 of Criminal Minds, "The Perfect Storm" (2006), Dr. Reid mentions that the rapists had this condition. Folie à Deux (2008) is an album by American rock band Fall Out Boy
The independent film Apart (2011) depicts two lovers affected and diagnosed with induced delusional disorder, trying to uncover a mysterious and tragic past they share. In a 2011 interview, director Aaron Rottinghaus stated the film was based on research from actual case studies. Nine Perfect Strangers shows a couple who lost one of their two children. The couple and the surviving child have shared hallucinations of the dead child. | A tufted angioma (also known as an "Acquired tufted angioma," "Angioblastoma," "Angioblastoma of Nakagawa," "Hypertrophic hemangioma," "Progressive capillary hemangioma," and "Tufted hemangioma") usually develops in infancy or early childhood on the neck and upper trunk, and is an ill-defined, dull red macule with a mottled appearance, varying from 2 to 5 cm in diameter. : 596
See also
List of cutaneous conditions
Skin lesion
References
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Those with white matter injury often exhibit "tight coupling" of leg joints (all extending or all flexing) much longer than other infants (premature and full-term). Additionally, infants with PVL may not be able to assume the same positions for sleeping, playing, and feeding as premature or full-term children of the same age. These developmental delays can continue throughout infancy, childhood, and adulthood. Vision deficits
Premature infants often exhibit visual impairment and motor deficits in eye control immediately after birth. However, the correction of these deficits occurs "in a predictable pattern" in healthy premature infants, and infants have vision comparable to full-term infants by 36 to 40 weeks after conception. Infants with PVL often exhibit decreased abilities to maintain a steady gaze on a fixed object and create coordinated eye movements. Additionally, children with PVL often exhibit nystagmus, strabismus, and refractive error. Seizures
Occurrence of seizures is often reported in children with PVL. In an Israel-based study of infants born between 1995 and 2002, seizures occurred in 102 of 541, or 18.7%, of PVL patients. Seizures are typically seen in more severe cases of PVL, affecting patients with greater amounts of lesions and those born at lower gestational ages and birth weights. Causes
Predisposing factors
Those generally considered to be at greatest risk for PVL are premature, very low birth-weight infants. It is estimated that approximately 3-4% of infants who weigh less than 1,500 g (3.3 lb) have PVL, and 4-10% of those born prior to 33 weeks of gestation (but who survive more than three days postpartum) have the disorder. | Glibenclamide, also known as glyburide, is an antidiabetic medication used to treat type 2 diabetes. It is recommended that it be taken together with diet and exercise. It may be used with other antidiabetic medication. It is not recommended for use by itself in type 1 diabetes. It is taken by mouth.Common side effects include nausea and heartburn. Serious side effects may include angioedema and low blood sugar. It is generally not recommended during pregnancy but can be used during breastfeeding. It is in the sulfonylureas class of medications and works by increasing the release of insulin from the pancreas.Glibenclamide was discovered in 1969 and approved for medical use in the United States in 1984. It is available as a generic medication. In 2019, it was the 254th most commonly prescribed medication in the United States, with more than 1 million prescriptions. Medical uses
Glibenclamide is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes.It is not as good as either metformin or insulin in those who have gestational diabetes. Side effects
Frequently reported side effects include: nausea, heartburn, weight gain, and bloating. The medication is also a major cause of medication-induced hypoglycemia. The risk is greater than with other sulfonylureas.Glibenclamide may be not recommended in those with G6PD deficiency, as it may cause acute hemolysis. Pregnancy and breastfeeding
It is generally not recommended during pregnancy but can be used during breastfeeding. | 0-1
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If the reconstruction is ultimately successful, it is easy to remove the percutaneous BAHA abutment. If the surgery is unsuccessful, the abutment can be replaced and the implant re-activated to restore hearing. External ear
The age when outer ear surgery can be attempted depends upon the technique chosen. The earliest is 7 for Rib Cartilage Grafts. However, some surgeons recommend waiting until a later age, such as 8–10 when the ear is closer to adult size. External ear prostheses have been made for children as young as 5. For auricular reconstruction, there are several different options:
Rib Cartilage Graft Reconstruction: This surgery may be performed by specialists in the technique. It involves sculpting the patients own rib cartilage into the form of an ear. Because the cartilage is the patients own living tissue, the reconstructed ear continues to grow as the child does. In order to be sure that the rib cage is large enough to provide the necessary donor tissue, some surgeons wait until the patient is 8 years of age; however, some surgeons with more experience with this technique may begin the surgery on a child aged six. The major advantage of this surgery is that the patients own tissue is used for the reconstruction. This surgery varies from two to four stages depending on the surgeons preferred method. A novel one stage ear reconstruction technique is performed by a few select surgeons. One team is able to reconstruct the entire external ear and ear canal in one operation. | Reconstruct the ear using a polyethylene plastic implant (also called Medpor): This is a 1–2 stage surgery that can start at age 3 and can be done as an outpatient without hospitalization. Using the porous framework, which allows the patients tissue to grow into the material and the patients own tissue flap, a new ear is constructed in a single surgery. A small second surgery is performed in 3–6 months if needed for minor adjustments. Medpor was developed by John Reinisch. This surgery should only be performed by experts in the techniques involved. The use of porous polyethylene implants for ear reconstruction was initiated in the 1980s by Alexander Berghaus. Ear Prosthesis: An auricular (ear) prosthesis is custom made by an anaplastologist to mirror the other ear. Prosthetic ears can appear very realistic. They require a few minutes of daily care. They are typically made of silicone, which is colored to match the surrounding skin and can be attached using either adhesive or with titanium screws inserted into the skull to which the prosthetic is attached with a magnetic or bar/clip type system. These screws are the same as the BAHA (bone anchored hearing aid) screws and can be placed simultaneously. The biggest advantage over any surgery is having a prosthetic ear that allows the affected ear to appear as normal as possible to the natural ear. The biggest disadvantage is the daily care involved and knowing that the prosthesis is not real. | 11
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A CT scan is also not typically recommended in children.Otherwise a noncontrast helical CT scan with 5 millimeters (0.2 in) sections is the diagnostic method to use to detect kidney stones and confirm the diagnosis of kidney stone disease. Near all stones are detectable on CT scans with the exception of those composed of certain drug residues in the urine, such as from indinavir. Where a CT scan is unavailable, an intravenous pyelogram may be performed to help confirm the diagnosis of urolithiasis. This involves intravenous injection of a contrast agent followed by a KUB film. Uroliths present in the kidneys, ureters, or bladder may be better defined by the use of this contrast agent. Stones can also be detected by a retrograde pyelogram, where a similar contrast agent is injected directly into the distal ostium of the ureter (where the ureter terminates as it enters the bladder).Renal ultrasonography can sometimes be useful, because it gives details about the presence of hydronephrosis, suggesting that the stone is blocking the outflow of urine. Radiolucent stones, which do not appear on KUB, may show up on ultrasound imaging studies. Other advantages of renal ultrasonography include its low cost and absence of radiation exposure. Ultrasound imaging is useful for detecting stones in situations where X-rays or CT scans are discouraged, such as in children or pregnant women. Despite these advantages, renal ultrasonography in 2009 was not considered a substitute for noncontrast helical CT scan in the initial diagnostic evaluation of urolithiasis. | Chromosome duplication can found by that technique also. Diagnostic Test of NDM
Fasting plasma glucose test: measures a diabetics blood glucose after he or she has gone 8 hours without eat. This test is used to detect diabetes or pre-diabetes
Oral glucose tolerance test- measures an individuals blood glucose after he or she have gone at least 8 hours without eating and two hours after the diabetic individual have drunk a glucose-containing beverage. This test can be used to diagnose diabetes or pre-diabetes
Random plasma glucose test-the doctor checks ones blood glucose without regard to when an individual may have eaten his or her last meal. This test, along with an evaluation of symptoms, are used to diagnose diabetes but not pre-diabetes. Genetic Testing of NDM
Uniparental Disomy Test:Samples from fetus or child and both parents are needed for analysis. Chromosome of interest must be specified on request form. For prenatal samples (only): if the amniotic fluid (non-confluent culture cells) are provided. Amniotic fluid is added and charged separately. Also, if chorionic villus sample is provided, a genetic test will be added and charged separately. Microsatellites markers and polymerase chain reaction are used on the chromosomes of interest to test the DNA of the parent and child to identify the presence of uniparental disomy. Treatment
Neonates with diabetes are initially treated by intravenous infusion of insulin, with a dose of 0.05 units/kilogram/hour commonly used.Treatment options depend on the underlying genetic variations of each person with neonatal diabetes. | 0-1
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As is the case with all pervasive developmental disorder categories, there is considerable controversy about the right treatment for CDD. Signs and symptoms
CDD is a rare condition, with only 1.7 cases per 100,000.A child affected with childhood disintegrative disorder shows normal development. Up until this point, the child has developed normally in the areas of language skills, social skills, comprehension skills, and has maintained those skills for about two years. However, between the ages of two and 10, skills acquired are lost almost completely in at least two of the following six functional areas:
Expressive language skills (being able to produce speech and communicate a message)
Receptive language skills (comprehension of language – listening and understanding what is communicated)
Social skills and self care skills
Control over bowel and bladder
Play skills
Motor skillsLack of normal function or impairment also occurs in at least two of the following three areas:
Social interaction
Communication
Repetitive behavior and interest patternsIn her book, Thinking in Pictures, Temple Grandin argues that compared to "Kanners classic autism" and to Asperger syndrome, CDD is characterized with more severe sensory processing disorder but less severe cognitive problems. She also argues that compared to most autistic individuals, persons with CDD have more severe speech pathology and they usually do not respond well to stimulants. Causes
All of the causes of childhood disintegrative disorder are still unknown. Sometimes CDD surfaces abruptly within days or weeks, while in other cases it develops over a longer period of time. | Childhood disintegrative disorder (CDD), also known as Hellers syndrome and disintegrative psychosis, is a rare condition characterized by late onset of developmental delays—or severe and sudden reversals—in language, social function, and motor skills. Researchers have not been successful in finding a cause for the disorder. CDD has some similarity to autism and is sometimes considered a low-functioning form of it. In May 2013, CDD, along with other sub-types of PDD (Aspergers syndrome, autism, and PDD-NOS), was fused into a single diagnostic term called "autism spectrum disorder" under the new DSM-5 manual.CDD was originally described by Austrian educator Theodor Heller (1869–1938) in 1908, 35 years before Leo Kanner and Hans Asperger described autism. Heller had previously used the name dementia infantilis for the syndrome.An apparent period of fairly normal development is often noted before a regression in skills or a series of regressions in skills. The age at which this regression can occur varies, after three years of normal development is typical. The regression, known as a ‘prodrome,’ can be so dramatic that the child may be aware of it, and may in its beginning even ask, vocally, what is happening to them. Some children describe or appear to be reacting to hallucinations, but the most obvious symptom is that skills apparently attained are lost.Many children are already somewhat delayed when the disorder becomes apparent, but these delays are not always obvious in young children. This has been described by many writers as a devastating condition, affecting both the family and the individuals future. | 11
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But there are also small-subgroups of people with autism that commit crimes because they lack understanding of the laws they have broken. Misunderstandings are especially common regarding autism and sex offenses, since many people with autism do not receive sex education. Cause
Although little is known about the biological basis of autism, studies have revealed structural abnormalities in specific brain regions. Regions identified in the "social" brain include the amygdala, superior temporal sulcus, fusiform gyrus area and orbitofrontal cortex. Further abnormalities have been observed in the caudate nucleus, believed to be involved in restrictive behaviors, as well as in a significant increase in the amount of cortical grey matter and atypical connectivity between brain regions. Diagnosis and IQ
HFA is not a recognised diagnosis by the American Psychological Association (DSM-5) or the World Health Organization (ICD-10). HFA is often, however, used in clinical settings to describe a set of symptoms related to an autism spectrum disorder whereby they exhibit standard autism indicators although have an intelligence quotient (IQ) of 70 or greater.For modern IQ tests, the raw score is transformed to a normal distribution with mean 100 and standard deviation 15. This results in approximately two-thirds of the population scoring between IQ 85 and IQ 115 and about 2.5 percent each above 130 and below 70.IQ scales are ordinally scaled. The raw score of the norming sample is usually (rank order) transformed to a normal distribution with mean 100 and standard deviation 15. | Relapsing linear acantholytic dermatosis is a cutaneous condition characterized by relapsing linear erosions and crusting, histologically identical to Hailey–Hailey disease. : 849 It is not to be confused with transient acantholytic dermatosis. See also
Linear porokeratosis
List of cutaneous conditions
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Medical uses
Furosemide is primarily used for the treatment of edema, but also in some cases of hypertension (where there is also kidney or heart impairment). It is often viewed as a first-line agent in most people with edema caused by congestive heart failure because of its anti-vasoconstrictor and diuretic effects. Compared with furosemide, however, torasemide (aka "torsemide") has been demonstrated to show improvements to heart failure symptoms, possibly lowering the rates of rehospitalisation associated with heart failure, with no difference in risk of death. Torsemide may also be safer than furosemide.Furosemide is also used for liver cirrhosis, kidney impairment, nephrotic syndrome, in adjunct therapy for swelling of the brain or lungs where rapid diuresis is required (IV injection), and in the management of severe hypercalcemia in combination with adequate rehydration. Kidney disease
In chronic kidney diseases with hypoalbuminemia, furosemide is used along with albumin to increase diuresis. It is also used along with albumin in nephrotic syndrome to reduce edema. Other information
Furosemide is mainly excreted by tubular secretion in the kidney. In kidney impairment, clearance is reduced, increasing the risk of adverse effects. Lower initial doses are recommended in older patients (to minimize side-effects) and high doses may be needed in kidney failure. It can also cause kidney damage; this is mainly by loss of excessive fluid (i.e., dehydration), and is usually reversible.Furosemide acts within 1 hour of oral administration (after IV injection, the peak effect is within 30 minutes). | Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is in addition to those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring benign moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever ones shadow is shorter than ones height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses. Diagnosis
Clinical diagnosis can be made with the naked eye using the ABCD guideline or by using dermatoscopy. An online-screening test is also available to help screen out benign moles. Classification
Melanocytic nevi can mainly be classified by depth, being congenital versus acquired, and/or specific dermatoscopy or histopathology patterns:
Depth
Congenital versus acquired
Congenital nevus: Small to large nevus present at or near time of birth. Small ones have low potential for forming melanomas, however the risk increases with size, as in the giant pigmented nevus. Acquired nevus: Any melanocytic nevus that is not a congenital nevus or not present at birth or near birth.Specific dermatoscopy or histopathology patterns
Recurrence
Recurrent nevus: Any incompletely removed nevus with residual melanocytes left in the surgical wound. | 0-1
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Despite the high plasma protein binding, sertraline and its metabolite desmethylsertraline at respective tested concentrations of 300 ng/mL and 200 ng/mL were found not to interfere with the plasma protein binding of warfarin and propranolol, two other highly plasma protein-bound drugs. Metabolism
Sertraline is subject to extensive first-pass metabolism, as indicated by a small study of radiolabeled sertraline in which less than 5% of plasma radioactivity was unchanged sertraline in two males. The principal metabolic pathway for sertraline is N-demethylation into desmethylsertraline (N-desmethylsertraline) mainly by CYP2B6. Reduction, hydroxylation, and glucuronide conjugation of both sertraline and desmethylsertraline also occur. Desmethylsertraline, while pharmacologically active, is substantially (50-fold) weaker than sertraline as a serotonin reuptake inhibitor and its influence on the clinical effects of sertraline is thought to be negligible. Based on in vitro studies, sertraline is metabolized by multiple cytochrome 450 isoforms; however, it appears that in the human body CYP2C19 plays the most important role, followed by CYP2B6. In addition to the cytochrome P450 system, sertraline can be oxidatively deaminated in vitro by monoamine oxidases; however, this metabolic pathway has never been studied in vivo. Elimination
The elimination half-life of sertraline is on average 26 hours, with a range of 13 to 45 hours. The half-life of sertraline is longer in women (32 hours) than in men (22 hours), which leads to 1.5-fold higher exposure to sertraline in women compared to men. | The effect of this drug in emptying psychiatric hospitals has been compared to that of penicillin and infectious diseases. But the popularity of the drug fell from the late 1960s as newer drugs came on the scene. From chlorpromazine a number of other similar antipsychotics were developed. It also led to the discovery of antidepressants.Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy, psychosurgery, and insulin shock therapy. By 1964, about 50 million people worldwide had taken it. Chlorpromazine, in widespread use for 50 years, remains a "benchmark" drug in the treatment of schizophrenia, an effective drug although not a perfect one. The relative strengths or potencies of other antipsychotics are often ranked or measured against chlorpromazine in aliquots of 100 mg, termed chlorpromazine equivalents or CPZE.In the movie: "Shutter Island", chlorpromazine is presented as being the new medicament for psychosis treatment however with adverse effects like tremors or abstinence syndrome. Society and culture
Names
Brand names include Thorazine, Largactil, Hibernal, and Megaphen (sold by Bayer in West-Germany since July 1953).) Research
Chlorpromazine has tentative benefit in animals infected with Naegleria fowleri, and shows antifungal and antibacterial activity in vitro. Veterinary use
The veterinary use of chlorpromazine has generally been superseded by use of acepromazine.Chlorpromazine may be used as an antiemetic in dogs and cats, or, less often, as sedative before anesthesia. In horses, it often causes ataxia and lethargy, and is therefore seldom used.It is commonly used to decrease nausea in animals that are too young for other common anti-emetics. | 0-1
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It may be that manipulation can cause dissection, or it may be that the dissection is already present in some people who seek manipulative treatment. At this time, conclusive evidence does not exist to support either a strong association between neck manipulation and stroke, or no association. However, the two most authoritative articles on the subject, recent literature reviews and analyses, conclude that although there exists an association between stroke from vertebral artery dissection and chiropractic adjustment, there is insufficient evidence to indicate that the adjustment caused the dissection. A recent meta-analysis of the published data on the topic also looked to apply Hills criteria for assigning causation in biological systems to the relationship between chiropractic adjustment and cervical artery dissection, finding that the relationship did not fulfill the required criteria for causality. Mechanism
The vertebral arteries arise from the subclavian artery, and run through the transverse foramen of the upper six vertebrae of the neck. After exiting at the level of the first cervical vertebra, its course changes from vertical to horizontal, and then enters the skull through the foramen magnum. Inside the skull, the arteries merge to form the basilar artery, which joins the circle of Willis. In total, three quarters of the artery are outside the skull; it has a high mobility in this area due to rotational movement in the neck and is therefore vulnerable to trauma. Most dissections happen at the level of the first and second vertebrae. | Anticoagulation may be relatively unsafe if a large stroke has already occurred, as hemorrhagic transformation is relatively common, and if the dissection extends into V4 (carrying a risk of subarachnoid hemorrhage). Anticoagulation may be appropriate if there is rapid blood flow (through a severely narrowed vessel) on transcranial doppler despite the use of aspirin, if there is a completely occluded vessel, if there are recurrent stroke-like episodes, or if free-floating blood clot is visible on scans. Warfarin is typically continued for 3–6 months, as during this time the flow through the artery usually improves, and most strokes happen within the first 6 months after the development of the dissection. Some regard 3 months as sufficient.Professional guidelines in the UK recommend that patients with VA dissection should be enrolled in a clinical trial comparing aspirin and anticoagulation if possible. American guidelines state that the benefit of anticoagulation is not currently established. Thrombolysis, stenting and surgery
Thrombolysis, stenting and surgery are not used as widely as anticoagulation or antiplatelet drugs. These treatments are invasive, and are typically reserved for situations where symptoms worsen despite medical treatment, or where medical treatment may be unsafe (e.g. an unacceptable bleeding tendency).Thrombolysis is enzymatic destruction of blood clots. This is achieved by the administration of a drug (such as urokinase or alteplase) that activates plasmin, an enzyme that occurs naturally in the body and digests clots when activated. Thrombolysis is an accepted treatment for heart attacks and stroke unrelated to dissection. In cervical artery dissection, only small case series are available. | 11
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The FDA said its approval of Zarxio is based on review of evidence that included structural and functional characterization, animal study data, human pharmacokinetic and pharmacodynamics data, clinical immunogenicity data and other clinical safety and effectiveness data that demonstrates Zarxio is biosimilar to Neupogen.In 2018, filgrastim-aafi (trade name Nivestym) was approved for use in the United States.In September 2008, Ratiograstim, Tevagrastim, Biograstim, and Filgrastim ratiopharm were approved for use in the European Union. Filgrastim ratiopharm was withdrawn in July 2011 and Biograstim was withdrawn in December 2016. In February 2009, Filgrastim Hexal and Zarzio were approved for use in the European Union.In June 2010, Nivestim was approved for use in the European Union.In October 2013, Grastofil was approved for use in the European Union.In September 2014, Accofil was approved for use in the European Union.In 2016, Fraven was approved for use by Republic of Turkey ministry of health.Nivestym was approved for medical use in Canada in April 2020.In October 2021, Nypozi was approved for medical use in Canada. Economics
Shortly after it was introduced, analyses of whether filgrastim is a cost-effective way of preventing febrile neutropenia depended upon the clinical situation and the financial model used to pay for treatment. The longer-acting pegfilgrastim may in some cases be more cost-effective. The introduction of biosimilars into the market resulted in a price reduction for the original, patent-protected product and increased use. References
Further reading
Santoso B, van Boxtel CJ, Edwards RI, eds. (2001). Drug benefits and risks: international textbook of clinical pharmacology. New York: Wiley. ISBN 0-471-89927-5. External links
"Filgrastim". | Trichorrhexis nodosa is a defect in the hair shaft characterized by thickening or weak points (nodes) that cause the hair to break off easily. : 766 : 636 This group of conditions contributes to the appearance of hair loss, lack of growth, and damaged-looking hair. Symptoms
Among the symptoms (and signs) for this condition are the following:
lack of apparent hair growth
hair appears patchy
hair breaks easily close to scalp
hair may have thickenings or nodes in the shaft
ends of hair thinned or split
whitish discoloration of hair tips
hair breaks easily at tips
Complications
This condition is not dangerous but may affect self-esteem. Causes
Trichorrhexis may have a genetic basis but appears to be precipitated by environmental factors. Among Caucasians the defect often appears at the ends of the hair shaft with splitting of the ends, thinning and whitish discoloration. These conditions are directly related to environmental causes such as "perming", blow drying, aggressive hair brushing, and excessive chemical exposure. In some cases, trichorrhexis nodosa may be caused by an underlying disorder such as argininosuccinic aciduria, Menkes kinky hair syndrome, Nethertons syndrome, hypothyroidism, or trichothiodystrophy. Diagnosis
Examination of the hair shafts with a microscope may reveal changes of trichorrhexis nodosa. Prevention
Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits. Treatment
Improving environmental factors will reduce damage to the hair. Gentle brushing with a soft brush should replace more aggressive brushing, ratting, or other procedures. Harsh chemicals such as hair straightening compounds and permanents should be avoided. The hair should not be ironed. Excessively harsh shampoo should be avoided. Hair conditioners should be used. | 0-1
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An injection is given every 3–5 minutes. If priapism is not resolved in one hour, another form of therapy is considered. Side effects
Phenylephrine may cause side effects such as headache, reflex bradycardia, excitability, restlessness and cardiac arrhythmias. Phenylephrine is not suggested for use in people with hypertension. Heart
The primary side effect of phenylephrine is high blood pressure. People with high blood pressure are typically advised to avoid products containing it. Because this medication is a sympathomimetic amine without beta-adrenergic activity, it does not increase contractility force and output of the cardiac muscle. It may increase blood pressure resulting in a slow heart rate through stimulation of vascular (likely carotid) baroreceptors. A common side effect during IV administration is reflex bradycardia. The low concentration eye drops do not cause blood pressure changes and the changes with the higher dose drops do not last long. Other
Prostatic hyperplasia can also be worsened by use, and chronic use can lead to rebound hyperemia. People with a history of anxiety or panic disorders, or on anticonvulsant medication for epilepsy should not take this substance. The drug interaction might produce seizures. Some patients have been shown to have an upset stomach, severe abdominal cramping, and vomiting issues connected to taking this drug.Phenylephrine is pregnancy category C. Due to the lack of studies done in animals and in humans, it is not known whether there is harm to the fetus. | Because having a sibling with schizencephaly has been statistically shown to increase risk of the disorder, it is possible that there is a heritable genetic component to the disease. References
9.^ Herrera Ortiz, A., & Ortiz Sandoval, H. (2021). Open Lip Schizencephaly: A Case Report. Revista Cuarzo, 26(2), 27-29. https://doi.org/10.26752/cuarzo.v26.n2.510
External links
Schizencephaly at NINDS
OMIM entries on Familial Schizencephaly, SIX3-Related | 0-1
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In addition it has now been documented in the medical literature that one of the major metabolites of quazepam, N-desalkyl-2-oxoquazepam (N-desalkylflurazepam), which is long-acting and prone to accumulation, binds unselectively to benzodiazepine receptors, thus quazepam may not differ all that much pharmacologically from other benzodiazepines. Special precautions
Benzodiazepines require special precaution if used in the during pregnancy, in children, alcohol or drug-dependent individuals and individuals with comorbid psychiatric disorders.Quazepam and its active metabolites are excreted into breast milk.Accumulation of one of the active metabolites of quazepam, N-desalkylflurazepam, may occur in the elderly. A lower dose may be required in the elderly. Elderly
Quazepam is more tolerable for elderly patients compared to flurazepam due to its reduced next day impairments. However, another study showed marked next day impairments after repeated administration due to accumulation of quazepam and its long-acting metabolites. Thus the medical literature shows conflicts on quazepams side effect profile. A further study showed significant balance impairments combined with an unstable posture after administration of quazepam in test subjects. An extensive review of the medical literature regarding the management of insomnia and the elderly found that there is considerable evidence of the effectiveness and durability of non-drug treatments for insomnia in adults of all ages and that these interventions are underutilized. Compared with the benzodiazepines including quazepam, the nonbenzodiazepine sedative/hypnotics appeared to offer few, if any, significant clinical advantages in efficacy or tolerability in elderly persons. | One such organism is Micrococcus luteus (American Type Culture Collection strain number ATCC 49442), which develops a yellow color due to production of riboflavin while growing on pyridine, but not when grown on other substrates, such as succinic acid. Laboratory synthesis
The first total synthesis of riboflavin was carried out by Richard Kuhns group. A substituted aniline, produced by reductive amination using D-ribose, was condensed with alloxan in the final step:
Uses
Treatment of corneal thinning
Keratoconus is the most common form of corneal ectasia, a progressive thinning of the cornea. The condition is treated by corneal collagen cross-linking, which increases corneal stiffness. Cross-linking is achieved by applying a topical riboflavin solution to the cornea, which is then exposed to ultraviolet A light. Migraine prevention
In its 2012 guidelines, the American Academy of Neurology stated that high-dose riboflavin (400 mg) is "probably effective and should be considered for migraine prevention," a recommendation also provided by the UK National Migraine Centre. A 2017 review reported that daily riboflavin taken at 400 mg per day for at least three months may reduce the frequency of migraine headaches in adults. Research on high-dose riboflavin for migraine prevention or treatment in children and adolescents is inconclusive, and so supplements are not recommended. Food coloring
Riboflavin is used as a food coloring (yellow-orange crystalline powder), and is designated with the E number, E101, in Europe for use as a food additive. Dietary recommendations
The National Academy of Medicine updated the Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for riboflavin in 1998. | 0-1
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A Cochrane review found that there is no evidence of a difference between oral DTIs (dabigatran, rivaroxaban, edoxaban, apixaban) and standard anticoagulation in the prevention of recurrent pulmonary embolism.In people with cancer who develop pulmonary embolism, therapy with a course of LMWH is favored over warfarin or other oral anticoagulants. Similarly, pregnant women are treated with low molecular weight heparin until after delivery to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy, but it can be used while breastfeeding.Anticoagulation therapy is usually continued for 3–6 months, or "lifelong" if there have been previous DVTs or PEs, or none of the usual transient risk factors is present. In those without a known cause that can be reversed 2 years of treatment may be better than 6 months. For those with small PEs (known as subsegmental PEs) the effects of anticoagulation is unknown as it has not been properly studied as of 2020. Thrombolysis
Massive PE causing hemodynamic instability (shock and/or low blood pressure, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. In this situation, it is the best available treatment in those without contraindications and is supported by clinical guidelines. It is also recommended in those in cardiac arrest with a known PE. Catheter-directed thrombolysis (CDT) is a new technique found to be relatively safe and effective for massive PEs. | Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion. Dressler syndrome is also known as postmyocardial infarction syndrome and the term is sometimes used to refer to post-pericardiotomy pericarditis. It was first characterized by William Dressler at Maimonides Medical Center in 1956.It should not be confused with the Dresslers syndrome of haemoglobinuria named for Lucas Dressler, who characterized it in 1854. Presentation
Dressler syndrome was historically a phenomenon complicating about 7% of myocardial infarctions, but in the era of percutaneous coronary intervention, it is very uncommon. The disease consists of a persistent low-grade fever, chest pain (usually pleuritic), pericarditis (usually evidenced by a pericardial friction rub, chest pain worsening when recumbent, and diffuse ST elevation with PR segment depression), and/or a pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction but can also be delayed a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade. Elevated ESR is an objective but nonspecific laboratory finding. Causes
It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI. A similar pericarditis can be associated with any pericardiotomy or trauma to the pericardium or heart surgery which is called postcardiotomy syndrome. | 0-1
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The FDA also awarded the manufacturer a rare pediatric disease priority review voucher, and granted the approval of Zolgensma to AveXis Inc.In June 2015, the European Commission granted orphan designation for the drug. In July 2019, the drug was removed from the Committee for Medicinal Products for Human Use (CHMP) accelerated assessment program.In May 2019, onasemnogene abeparvovec received US FDA approval as a treatment for children less than two years old. Since 2019, the treatment has been reimbursed in Israel and Qatar. In March 2020, onasemnogene abeparvovec was granted regulatory approval in Japan with the label identical to the US one. Also in March 2020, the European Medicines Agency recommended a conditional marketing authorization for use in people with SMA type 1 or with any SMA type and having no more than three copies of the SMN2 gene. In May 2020, Onasemnogene abeparvovec was conditionally approved in Europe.In August 2020, onasemnogene abeparvovec was granted regulatory approval in Brazil by the Brazilian Health Regulatory Agency (ANVISA).In December 2020, onasemnogene abeparvovec was approved for medical use in Canada.Onasemnogene abeparvovec was approved for medical use in Australia in February 2021.An official approval in Russia was granted in December 2021. Society and culture
Economics
The drug carries a list price of US$2.125 million per treatment, making it the most expensive medication in the world as of 2019. | Adverse effects
Common adverse reactions may include nausea and elevated liver enzymes. Serious adverse reactions may include liver problems and low platelets. Transient elevated levels of cardiac troponin‑I were observed in clinical trials; the clinical importance of these findings is not known. However, cardiac toxicity was seen in studies of other animals.As the medication may reduce the platelet count, platelets may need to be checked before the medication is started, then weekly for the first month and every two weeks for the next two months until the level is back to baseline. Liver function should be monitored for three months after administration. Mechanism of action
SMA is a neuromuscular disorder caused by a mutation in the SMN1 gene, which leads to a decrease in SMN protein, a protein necessary for survival of motor neurons. Onasemnogene abeparvovec is a biologic drug consisting of AAV9 virus capsids that contains a SMN1 transgene along with synthetic promoters. Upon administration, the AAV9 viral vector delivers the SMN1 transgene to the affected motor neurons, where it leads to an increase in SMN protein. History
Onasemnogene abeparvovec was developed by the US biotechnology startup AveXis, which was acquired by Novartis in 2018, based on the work at the Institut de Myologie in France.The U.S. Food and Drug Administration (FDA) granted the application for onasemnogene abeparvovec-xioi fast track, breakthrough therapy, priority review, and orphan drug designations. | 11
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This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computed axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the surrounding brain tissue and can affect various aspects of a persons mood, personality, and cognitive functioning. A SLI or any type of silent stroke places an individual at greater risk for future major stroke. Pathophysiology
According to Koffler et al., lacunes are derived from an "occlusion of a single deep penetrating artery that arises directly from the constituents of the circle of Willis, cerebellar arteries, and basilar artery". Other lesions that are associated with lacunes appear in the "deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)". These lesions are less common within other brain regions such as the cerebellum, cerebral white matter and anterior limb of the internal capsule.The two proposed mechanisms are microatheroma and lipohyalinosis. At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). | Furthermore, splints and braces can be used to support limbs and joints to prevent or treat complications such as contractures and spasticity. The rehabilitation healthcare team should also educate the patient and their family on common stroke symptoms and how to manage an onset of stroke. Continuing follow-up with a physician is essential so that the physician may monitor medication dosage and risk factors. Epidemiology
It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual incidence of approximately 15 per 100,000 people. They may be more frequent in men and in people of African, Mexican, and Hong Kong Chinese descent. References
== External links == | 11
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Types of collision include head-on, road departure, rear-end, side collisions, and rollovers. Many different terms are commonly used to describe vehicle collisions. The World Health Organization uses the term road traffic injury, while the U.S. Census Bureau uses the term motor vehicle accidents (MVA), and Transport Canada uses the term "motor vehicle traffic collision" (MVTC). Other common terms include auto accident, car accident, car crash, car smash, car wreck, motor vehicle collision (MVC), personal injury collision (PIC), road accident, road traffic accident (RTA), road traffic collision (RTC), and road traffic incident (RTI) as well as more unofficial terms including smash-up, pile-up, and fender bender. Some organizations have begun to avoid the term accident, instead preferring terms such as collision, crash or incident. This is because the term accident implies that there is no one to blame, whereas most traffic collisions are the result of driving under the influence, excessive speed, distractions such as mobile phones or other risky behavior.Historically, in the United States, the use of terms other than accident had been criticized for holding back safety improvements, based on the idea that a culture of blame may discourage the involved parties from fully disclosing the facts, and thus frustrate attempts to address the real root causes. Health effects
Physical
A number of physical injuries can commonly result from the blunt force trauma caused by a collision, ranging from bruising and contusions to catastrophic physical injury (e.g., paralysis), traumatic or non-traumatic cardiac arrest and death. Psychological
Following collisions, long-lasting psychological trauma may occur. | Four driver behaviors (speed, stopping at intersections when the control light was amber, turning left in front of oncoming traffic, and gaps in following distance) were measured at various sites before and after the law. Changes in these behaviors in Newfoundland were similar to those in Nova Scotia, except that drivers in Newfoundland drove slower on expressways after the law, contrary to the risk compensation theory. MaintenanceA well-designed and well-maintained vehicle, with good brakes, tires and well-adjusted suspension will be more controllable in an emergency and thus be better equipped to avoid collisions. Some mandatory vehicle inspection schemes include tests for some aspects of roadworthiness, such as the UKs MOT test or German TÜV conformance inspection. The design of vehicles has also evolved to improve protection after collision, both for vehicle occupants and for those outside of the vehicle. Much of this work was led by automotive industry competition and technological innovation, leading to measures such as Saabs safety cage and reinforced roof pillars of 1946, Fords 1956 Lifeguard safety package, and Saab and Volvos introduction of standard fit seatbelts in 1959. Other initiatives were accelerated as a reaction to consumer pressure, after publications such as Ralph Naders 1965 book Unsafe at Any Speed accused motor manufacturers of indifference towards safety. | 11
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It is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility, which could be the result of either organic heart disease or cardiac surgical procedures. Higher doses are not useful with history of recent ischemic heart disease because it increases heart rate and thus increases myocardial oxygen demand.The drug is also commonly used in the hospital setting as a pharmacologic stress testing agent to identify coronary artery disease. Adverse effects
Primary side effects include those commonly seen for β1 active sympathomimetics, such as hypertension, angina, arrhythmia, and tachycardia. Used with caution in atrial fibrillation as it has the effect of increasing the atrioventricular (AV) conduction.The most dangerous side effect of dobutamine is increased risk of arrhythmia, including fatal arrhythmias. Overall, dobutamine tends to produce less tachycardia and peripheral vascular effects than agents such as epinephrine and isoproterenol. Pharmacology
Dobutamine is a direct-acting agent whose primary activity results from stimulation of the β1-adrenoceptors of the heart, increasing contractility and cardiac output. Since it does not act on dopamine receptors to inhibit the release of norepinephrine (another α1 agonist), dobutamine is less prone to induce hypertension than is dopamine. Dobutamine is predominantly a β1-adrenergic agonist, with weak β2 activity, and α1 selective activity, although it is used clinically in cases of cardiogenic shock for its β1 inotropic effect in increasing heart contractility and cardiac output. | Oral iron should thus be also considered. Parenteral iron therapy is an option as it accelerated recovery. Most women with mild to moderate anemia, however, resolve the anemia sufficiently rapidly with oral iron alone and do not need parenteral iron. Prognosis
Women with a history of PPH have a 2 to 3 times higher risk of PPH in their following pregnancies. References
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Treatment of porphyria of the skin generally involves the avoidance of sunlight, while treatment for acute porphyria may involve giving intravenous heme or a glucose solution. Rarely, a liver transplant may be carried out.The precise prevalence of porphyria is unclear, but it is estimated to affect between 1 and 100 per 50,000 people. Rates are different around the world. Porphyria cutanea tarda is believed to be the most common type. The disease was described as early as 370 BC by Hippocrates. The underlying mechanism was first described by German physiologist and chemist Felix Hoppe-Seyler in 1871. The name porphyria is from the Greek πορφύρα, porphyra, meaning "purple", a reference to the color of the urine that may be present during an attack. Signs and symptoms
Acute porphyrias
Acute intermittent porphyria (AIP), variegate porphyria (VP), aminolevulinic acid dehydratase deficiency porphyria (ALAD) and hereditary coproporphyria (HCP). These diseases primarily affect the nervous system, resulting in episodic crises known as acute attacks. The major symptom of an acute attack is abdominal pain, often accompanied by vomiting, hypertension (elevated blood pressure), and tachycardia (an abnormally rapid heart rate).The most severe episodes may involve neurological complications: typically motor neuropathy (severe dysfunction of the peripheral nerves that innervate muscle), which leads to muscle weakness and potentially to quadriplegia (paralysis of all four limbs) and central nervous system symptoms such as seizures and coma. Occasionally, there may be short-lived psychiatric symptoms such as anxiety, confusion, hallucinations, and, very rarely, overt psychosis. | The enzyme (hematin) necessary to alleviate symptoms is not absorbed intact on oral ingestion, and drinking blood would have no beneficial effect on the sufferer. Finally, and most important, the fact that vampire reports were literally rampant in the 18th century, and that congenital erythropoietic porphyria is an extremely rare manifestation of a rare disease, makes it an unlikely explanation of the folkloric vampire. Notable cases
King George III. The mental illness exhibited by George III in the regency crisis of 1788 has inspired several attempts at retrospective diagnosis. The first, written in 1855, thirty-five years after his death, concluded that he had acute mania. M. Guttmacher, in 1941, suggested manic-depressive psychosis as a more likely diagnosis. The first suggestion that a physical illness was the cause of King Georges mental derangement came in 1966, in a paper called "The Insanity of King George III: A Classic Case of Porphyria", with a follow-up in 1968, "Porphyria in the Royal Houses of Stuart, Hanover and Prussia". The papers, by a mother/son psychiatrist team, were written as though the case for porphyria had been proven, but the response demonstrated that many experts, including those more intimately familiar with the manifestations of porphyria, were unconvinced. Many psychiatrists disagreed with the diagnosis, suggesting bipolar disorder as far more probable. The theory is treated in Purple Secret, which documents the ultimately unsuccessful search for genetic evidence of porphyria in the remains of royals suspected to have had it. | 11
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Marcus Gunn phenomenon is an autosomal dominant condition with incomplete penetrance, in which nursing infants will have rhythmic upward jerking of their upper eyelid. This condition is characterized as a synkinesis: when two or more muscles that are independently innervated have either simultaneous or coordinated movements.Common physiologic examples of synkineses occur during sucking, chewing, or conjugate eye movements. There are also several abnormal cranial nerve synkineses, both acquired and congenital. Marcus Gunn jaw-winking is an example of a pathologic congenital synkinesis. First described by the ophthalmologist Marcus Gunn in 1883, this condition presents in approximately 5% of neonates with congenital ptosis. This condition has been associated with amblyopia (in 54% of cases), anisometropia (26%), and strabismus (56%). Presentation
Behavioral and social implications
Although treatment may be unnecessary, there may be social implications, especially in young children when venturing from a supportive home environment to a public environment (e.g., starting school). Continued support, including monitoring behavior and educating the child about his or her appearance as seen by others, is encouraged. Gradual or sudden withdrawal from interaction with others is a sign that may or may not be related to such behavior. Studies are being conducted to elucidate these implications. | Pathophysiology
It has been postulated that the synkinesis is due to damage to cranial nerve nuclei, caused by peripheral nerve injury and the nuclear lesion releases evolutionarily older [neural] mechanisms with their tendency toward associated movements, and so primitive reflexes are not inhibited.Marcus Gunn jaw-winking is an exaggeration of a very weak physiologic co-contraction that has been disinhibited secondary to a congenital brain stem lesion. The stimulation of the trigeminal nerve by contraction of the pterygoid muscles of jaw results in the excitation of the branch of the oculomotor nerve that innervates the levator palpebrae superioris ipsilaterally (on the same side of the face), so the patient will have rhythmic upward jerking of their upper eyelid.There are two major groups of trigemino-oculomotor synkineses:
1) External pterygoid-levator synkinesis is when the eyelid raises upon:
Jaw thrust to opposite side (homolateral external pterygoid)
Jaw is projected forward (bilateral external pterygoid)
Mouth is opened widely2) Internal pterygoid-levator synkinesis is when the eyelid raises upon teeth clenching
External pterygoid-levator synkinesis is the more common group. Treatment
Treatment is usually unnecessary. In severe cases, surgery with a bilateral levator excision and frontalis brow suspension may be used. Inverse Marcus Gunn phenomenon
Inverse Marcus Gunn phenomenon is a rare condition that causes the eyelid to fall upon opening of the mouth. In this case, trigeminal innervation to the pterygoid muscles of the jaw is associated with an inhibition of the branch of the oculomotor nerve to the levator palpebrae superioris, as opposed to stimulation in Marcus Gunn jaw-winking. References
== External links == | 11
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Vogel CL, Johnston MA, Capers C, Braccia D (2014). "Toremifene for breast cancer: a review of 20 years of data". Clin. Breast Cancer. 14 (1): 1–9. doi:10.1016/j.clbc.2013.10.014. PMID 24439786. Mustonen MV, Pyrhönen S, Kellokumpu-Lehtinen PL (2014). "Toremifene in the treatment of breast cancer". World J Clin Oncol. 5 (3): 393–405. doi:10.5306/wjco.v5.i3.393. PMC 4127610. PMID 25114854. External links
Toremifene - AdisInsight | Choreoathetosis is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing). It is caused by many different diseases and agents. It is a symptom of several diseases, including Lesch–Nyhan syndrome, phenylketonuria, and Huntington disease and can be a feature of kernicterus (rapidly increasing unconjugated bilirubin that cross the blood-brain-barrier in infants). Choreoathetosis is also a common presentation of dyskinesia as a side effect of levodopa-carbidopa in the treatment of Parkinson disease.The use of crack cocaine or amphetamines can result in conditions nicknamed crack dancing, or tweaking respectively, described as choreathetoid. See also
Ulegyria
References
== External links == | 0-1
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Southern tick-associated rash illness (STARI) is an emerging infectious disease related to Lyme disease that occurs in southeastern and south-central United States. It is spread by tick bites and it was hypothesized that the illness was caused by the bacteria Borrelia lonestari. However, there is insufficient evidence to declare this Borrelia strain as a causative agent. Symptoms
Diagnosis is based on a circular "bulls-eye" rash at the site of infection called erythema chronicum migrans, which is very similar to that seen in Lyme disease. However, the symptoms of STARI are mild, and resemble influenza, with fatigue, muscle pains, and headache. Fever is sometimes seen, but is not characteristic. Causes
This illness is a tick-borne disease carried by the lone star tick Amblyomma americanum. This tick was first proposed as a possible vector of disease in 1984, and the illnesses associated with the tick called "Lyme-like disease", but it was not recognized to be distinct from Lyme disease until the late 1990s.Several studies have failed to detect Borrelia burgdorferi, which is the causative agent of Lyme disease, in patients from the southern United States. This disease may be caused by the related bacterium Borrelia lonestari, which is a spirochete first isolated in culture in 2004. However, this conclusion is controversial since the spirochete is not detected in all cases of the syndrome, which has led some authors to argue that the illness is not caused by a bacterial pathogen. Treatment
Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs. | Prognosis
No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease. See also
Borrelia
Zoonosis
References
External links
Southern Tick-Associated Rash Illness (STARI) Home Page Centers for Disease Control
STARI Fact Sheet Florida Department of Health
Southern Tick-Associated Rash Illness (STARI) SCWDS Briefs, January 2003, Vol.18, No.4 | 11
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There is some enterohepatic recirculation of CEEs. Following a single oral dose of 0.625 CEEs, the biological half-life of estrone was 26.7 hours, of baseline-adjusted estrone was 14.8 hours, and of equilin was 11.4 hours. Chemistry
CEEs are naturally occurring estrane steroids. They are in conjugate form, as the sodium salts of the C17β sulfate esters. The estrogens in CEEs, in their unconjugated active forms, include bioidentical human estrogens like estradiol and estrone as well as equine-specific estrogens such as equilin and 17β-dihydroequilin. The equine estrogens differ from human estrogens in that they have additional double bonds in the B ring of the steroid nucleus. CEEs contain both 17β-estrogens like estradiol and 17β-dihydroequilin and the C17α epimers like 17α-estradiol and 17α-dihydroequilin. History
Conjugated estriol, an extract of the urine of pregnant women and sold under the brand names Progynon and Emmenin in the 1930s, was the predecessor of Premarin. Both of these products contained conjugated estrogens similarly to Premarin, but the estrogens were human estrogens as opposed to equine estrogens and the composition differed. The major active ingredient in Progynon and Emmenin was estriol glucuronide. Estrone sulfate was first isolated from the urine of pregnant mares in the late 1930s by researchers in the Department of Biochemistry at University of Toronto. Premarin was first introduced in 1941 by Wyeth Ayerst as a treatment for hot flashes and other symptoms of menopause; at that time, Wyeth Ayerst only had to prove its safety, and not its efficacy. | Society and culture
Legal status
In November 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 under exceptional circumstances for the medicinal product Voraxaze, intended to reduce toxic plasma methotrexate concentration. The applicant for this medicinal product is SERB SAS. Glucarpidase was approved for medical use in the European Union in January 2022. References
External links
"Glucarpidase". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Upon hydrolysis using an alcoholic solution of potassium hydroxide forms a dipotassium salt, chlorazepate. Legal status
In the United States, clorazepate is listed under Schedule IV of the Controlled Substances Act. References
External links
Rx-List.com - Clorazepate
Inchem.org - Clorazepate | The United States Presidents Council on Bioethics made it clear, for example, in its White Paper of December 2008, that the British concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States. Evolution of diagnostic criteria
The United Kingdom (UK) criteria were first published by the Conference of Medical Royal Colleges (with advice from the Transplant Advisory Panel) in 1976, as prognostic guidelines. They were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought "to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery". The published criteria – negative responses to bedside tests of some reflexes with pathways through the brainstem and a specified challenge to the brainstem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects – were held to be "sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists". | 0-1
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In normal subjects, increases in growth hormone occurs, whereas, in benzodiazepine-tolerant individuals, this effect is blunted.Animal studies have shown that repeated withdrawal from benzodiazepines leads to increasingly severe withdrawal symptoms, including an increased risk of seizures; this phenomenon is known as kindling. Kindling phenomena are well established for repeated ethanol (alcohol) withdrawal; alcohol has a very similar mechanism of tolerance and withdrawal to benzodiazepines, involving the GABAA, NMDA, and AMPA receptors.The shift of benzodiazepine receptors to an inverse agonist state after chronic treatment leads the brain to be more sensitive to excitatory drugs or stimuli. Excessive glutamate activity can result in excitotoxicity, which may result in neurodegeneration. The glutamate receptor subtype NMDA is well known for its role in causing excito-neurotoxicity. The glutamate receptor subtype AMPA is believed to play an important role in neuronal kindling as well as excitotoxicity during withdrawal from alcohol as well as benzodiazepines. It is highly possible that NMDA receptors are involved in the tolerance to some effects of benzodiazepines.Animal studies have found that glutamergic changes as a result of benzodiazepine use are responsible for a delayed withdrawal syndrome, which in mice peaks 3 days after cessation of benzodiazepines. This was demonstrated by the ability to avoid the withdrawal syndrome by the administration of AMPA antagonists. It is believed that different glutamate subreceptors, e.g., NMDA and AMPA, are responsible for different stages/time points of the withdrawal syndrome. NMDA receptors are upregulated in the brain as a result of benzodiazepine tolerance. AMPA receptors are also involved in benzodiazepine tolerance and withdrawal. | Apraclonidine (INN), also known under the brand name Iopidine, is a sympathomimetic used in glaucoma therapy. It is an α2 adrenergic receptor agonist and a weak α1 adrenergic receptor agonist.Topical apraclonidine is administered at a concentration of 1% for the prevention and treatment of post-surgical intraocular pressure (IOP) elevation and 0.5% for short-term adjunctive therapy in patients on maximally tolerated medical therapy who require additional reduction of IOP. One drop is usually added one hour prior to laser eye surgery and another drop is given after the procedure is complete. Clinical uses
Apraclonidine is indicated for the short-term adjunctive treatment of glaucoma for patients on maximally tolerated medical therapy who require additional reduction of IOP. These patients, who are treated with apraclonidine to delay surgery, should have frequent follow-up examinations and treatment should be discontinued if the intraocular pressure rises significantly. Apraclonidine may be useful in the diagnosis of Horners syndrome. In Horners syndrome, the sympathetic innervation to the pupillary dilator muscle is lost. The affected pupil is thus miotic and the pupillary dilator responds to denervation by increasing α1 receptors. Apraclonidine is useful in this case due to its weak α1-adrenergic properties. When applied to the denervated (and thus hyper-sensitive) pupillary dilator muscle, a super-normal dilatory response is generated in which the pupil dilates to a degree greater than that which would be seen in a non-denervated muscle. This causes the reversal of anisocoria that is characteristic of Horners. | 0-1
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Specific symptoms attributable to early hypercapnia are dyspnea (breathlessness), headache, confusion and lethargy. Clinical signs include flushed skin, full pulse (bounding pulse), rapid breathing, premature heart beats, muscle twitches, and hand flaps (asterixis). The risk of dangerous irregularities of the heart beat is increased. | Increased work of breathing accounted for most of the elevation of
P
a
C
O
2
{\displaystyle {P_{a_{CO_{2}}}}}
(alveolar gas equation) in exposures above 1 atm (100 kPa), as indicated by the results when helium was substituted for nitrogen at 4 atm (400 kPa). | 11
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Congenital hemangioma
Congenital hemangiomas are present and fully formed at birth, and only account for 2% of the hemangiomas. They do not have the postnatal phase of proliferation common to infantile hemangiomas. There are two main variants of congenital hemangioma: non-involuting, and rapidly involuting (beginning in the first year of life). A third variant is also recognised as partially involuting. Congenital hemangiomas can also be distinguished from infantile hemangiomas in that neither variant of congenital hemangioma expresses the glucose transporter GLUT 1.Some cases have been associated with a mild form of thrombocytopenia. Rare cases have been associated with heart failure. Hemangioblastoma
Hemangioblastomas are vascular tumors of the central nervous system. Pyogenic granuloma
A range of benign vascular tumors are described as reactive proliferative lesions that grow in response to a stimulus, such as trauma, or a local thrombosis. They can also form infrequently during pregnancy as a hormonal reaction affecting the gums.The most common type of reactive proliferative tumors are pyogenic granulomas also known as lobular capillary hemangiomas, that are more often found in children and young adults. These granulomas are well defined growths of less than a centimetre across. They are bright red due to being highly vascularised, and bleed and ulcerate easily. Their colouring fades with age. Tufted angioma
Tufted angiomas are hereditary hemangiomas found in infants from birth to five years of age, however they may occur in adults. They are found on the neck, shoulders, and trunk as rounded nodules. Tufted angiomas are usually poorly defined lesions of purple colouration. | Pathophysiology
The hemisection of the cord results in a lesion of each of the three main neural systems:
the principal upper motor neuron pathway of the corticospinal tract
one or both dorsal columns
the spinothalamic tractAs a result of the injury to these three main brain pathways the patient will present with three lesions:
The corticospinal lesion produces spastic paralysis on the same side of the body below the level of the lesion (due to loss of moderation by the UMN). At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion). The lesion to fasciculus gracilis or fasciculus cuneatus (dorsal column) results in ipsilateral loss of vibration and proprioception (position sense) as well as loss of all sensation of fine touch. The loss of the spinothalamic tract leads to pain and temperature sensation being lost from the contralateral side beginning one or two segments below the lesion.In addition, if the lesion occurs above T1 of the spinal cord it will produce ipsilateral Horners syndrome with involvement of the oculosympathetic pathway. Diagnosis
Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions.Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). | 0-1
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Mifepristone is contraindicated in the presence of adrenal failure, long-term oral corticosteroid therapy (although inhaled and topical steroids are fine), hemorrhagic disorders, inherited porphyria, and hemophilia or anticoagulant use. Women with an intrauterine device in their uterus should remove the IUD prior to medication abortion to avoid unnecessary cramping. Mifepristone is not effective in treating ectopic pregnancy. A postmarketing summary found, of about 1.52 million women who had received mifepristone until April 2011 in the United States, 14 were reported to have died after application. Eight of these cases were associated with sepsis; the other six had various causes such as drug abuse and suspected murder. Other incidents reported to the FDA included 612 nonlethal hospitalizations, 339 blood transfusions, 48 severe infections, and 2,207 (0.15%) adverse events altogether. Cancer
No long-term studies to evaluate the carcinogenic potential of mifepristone have been performed. This is in accord with ICH guidelines, which do not require carcinogenicity testing in nongenotoxic drugs intended for administration for less than six months. Pregnancy
Mifepristone alone results in abortion within 1–2 weeks in 54% to 92% of pregnancies. The effectiveness increases to greater than 90% if misoprostol is given after the mifepristone. There is no evidence that the effects of mifepristone can be reversed, although some anti-abortion groups claim that it can be reversed by giving progesterone. Researchers in the United States initiated a trial of the so-called "reversal" regimen in 2019, but stopped prematurely due to serious safety concerns about using mifepristone without follow-up misoprostol. | Bardet–Biedl syndrome (BBS) is a ciliopathic human genetic disorder that produces many effects and affects many body systems. It is characterized by rod/cone dystrophy, polydactyly, central obesity, hypogonadism, and kidney dysfunction in some cases. Historically, slower mental processing has also been considered a principal symptom but is now not regarded as such. Signs and symptoms
Bardet–Biedl syndrome is a pleiotropic disorder with variable expressivity and a wide range of clinical variability observed both within and between families. The most common clinical features are rod–cone dystrophy, with childhood-onset night-blindness followed by increasing visual loss; postaxial polydactyly; truncal obesity that manifests during infancy and remains problematic throughout adulthood; varying degrees of learning disabilities; male hypogenitalism and complex female genitourinary malformations; and renal dysfunction, a major cause of morbidity and mortality.There is a wide range of secondary features that are sometimes associated with BBS: 147–148 including: 153–154
Strabismus, cataracts, astigmatism, pigmentary retinopathy, poor visual acuity, low vision, and/or blindness caused by an impaired photoreceptor transport mechanism in the retina. "Brachydactyly, syndactyly of both the hands and feet is common, as is partial syndactyl (most usually between the second and third toes)"
Polyuria/polydipsia (nephrogenic diabetes insipidus)
Ataxia/poor coordination/imbalance
Mild hypertonia (especially lower limbs)
Diabetes mellitus
Hepatic involvement
Anosmia
Auditory deficiencies
Hirschsprung disease and subsequent bowel obstruction has been described. Hypertrophy of interventricular septum and left ventricle and dilated cardiomyopathy. | 0-1
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Nystagmus is a condition of involuntary (or voluntary, in some cases) eye movement. Infants can be born with it but more commonly acquire it in infancy or later in life. In many cases it may result in reduced or limited vision. Due to the involuntary movement of the eye, it has been called "dancing eyes".In normal eyesight, while the head rotates about an axis, distant visual images are sustained by rotating eyes in the opposite direction of the respective axis. The semicircular canals in the vestibule of the ear sense angular acceleration, and send signals to the nuclei for eye movement in the brain. From here, a signal is relayed to the extraocular muscles to allow ones gaze to fix on an object as the head moves. Nystagmus occurs when the semicircular canals are stimulated (e.g., by means of the caloric test, or by disease) while the head is stationary. The direction of ocular movement is related to the semicircular canal that is being stimulated.There are two key forms of nystagmus: pathological and physiological, with variations within each type. Nystagmus may be caused by congenital disorder or sleep deprivation, acquired or central nervous system disorders, toxicity, pharmaceutical drugs, alcohol, or rotational movement. Previously considered untreatable, in recent years several drugs have been identified for treatment of nystagmus. Nystagmus is also occasionally associated with vertigo. Causes
The cause of pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder. | Treatment consists of learning strategies to compensate for the impaired system.A Cochrane Review on interventions for eye movement disorders due to acquired brain injury, updated in June 2017, identified three studies of pharmacological interventions for acquired nystagmus but concluded that these studies provided insufficient evidence to guide treatment choices. Epidemiology
Nystagmus is a relatively common clinical condition, affecting one in several thousand people. A survey conducted in Oxfordshire, United Kingdom found that by the age of two, one in every 670 children had manifested nystagmus. Authors of another study in the United Kingdom estimated an incidence of 24 in 10,000 (c. 0.240%), noting an apparently higher rate amongst white Europeans than in individuals of Asian origin. Law enforcement
In the United States, testing for horizontal gaze nystagmus is one of a battery of field sobriety tests used by police officers to determine whether a suspect is driving under the influence of alcohol. The test involves observation of the suspects pupil as it follows a moving object, noting
lack of smooth pursuit,
distinct and sustained nystagmus at maximum deviation, and
the onset of nystagmus prior to 45 degrees.The horizontal gaze nystagmus test has been highly criticized and major errors in the testing methodology and analysis found. However, the validity of the horizontal gaze nystagmus test for use as a field sobriety test for persons with a blood alcohol level between 0.04 and 0.08 is supported by peer reviewed studies and has been found to be a more accurate indication of blood alcohol content than other standard field sobriety tests. | 11
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The fibrotic form is typically characterized by irregular linear opacities/coarse reticulations, traction bronchiectasis, and honeycombing, patchy ground-glass attenuation, centrilobular nodules, and mosaic attenuation. Three-density pattern (head cheese sign) is radiological sign which shows a region of the lung with three or more different types of attenuation which can be typical for the fibrotic type. Histopathology
The acute form can be characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells. The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis. Much like the pathogenesis of idiopathic pulmonary fibrosis (IPF), chronic HP is related to increased expression of Fas antigen and Fas ligand, leading to increased epithelial apoptosis activation in the alveoli. Cholesterol clefts or asteroid bodies are present within or outside granulomas. Pulmonary Function Testing
Pulmonary function tests (PFTs) can generally reveal a restrictive pattern however, either a restrictive or obstructive pattern (or both) may emerge on PFTs. PFTs, therefore, are less useful in making a diagnosis but rather tracking improvement or deterioration in lung function following removal or addition of suspected antigens. They may also demonstrate reduced diffusion capacity of lungs for carbon monoxide (DLCO). Bronchoscopy
Bronchoalveolar lavage (BAL) is a reliable way to detect inflammation in the lung airways. Fluid analysis from the lavage extracted from the airways on bronchoscopy often reveals a total elevation in cell count in addition to an elevation in the percentage of T lymphocytes. | Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis (EAA) is a syndrome caused by the repetitive inhalation of antigens from the environment in susceptible or sensitized people. Common antigens include molds, bacteria, bird droppings, bird feathers, agricultural dusts, bioaerosols and chemicals from paints or plastics. People affected by this type of lung inflammation (pneumonitis) are commonly exposed to the antigens by their occupations, hobbies, the environment and animals. The inhaled antigens produce a hypersensitivity immune reaction causing inflammation of the airspaces (alveoli) and small airways (bronchioles) within the lung. Hypersensitivity pneumonitis may eventually lead to interstitial lung disease. Signs and symptoms
Hypersensitivity pneumonitis (HP) can be categorized as acute, subacute, and chronic based on the duration of the illness. Acute
In the acute form of HP dose of antigen exposure tends to be very high but only for a short duration. Symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure. Subacute
Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. Findings may be present in patients who have experienced repeated acute attacks. Chronic
In chronic HP, dose of the antigen tends to be low volume but for a longer duration. Patients often lack a history of acute episodes. | 11
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Rosman and Resnick concluded that their data challenged the conventional view of necrophiliacs as generally psychotic, mentally deficient, or unable to obtain a consenting partner. Other animals
Necrophilia has been observed in mammals, birds, reptiles and frogs. In 1960, Robert Dickerman described necrophilia in ground squirrels, which he termed "Davian behaviour" in reference to a limerick about a necrophiliac miner named Dave. The label is still used for necrophilia in animals. Certain species of arachnids and insects practice sexual cannibalism, where the female cannibalises her male mate before, during, or after copulation. Kees Moeliker made an observation while he was sitting in his office at the Natural History Museum Rotterdam, when he heard the distinctive thud of a bird hitting the glass facade of the building. Upon inspection, he discovered a drake (male) mallard lying dead outside the building. Next to the downed bird, a second drake mallard was standing close by. As Moeliker observed the couple, the living drake pecked at the corpse of the dead one for a few minutes then mounted the corpse and began copulating with it. The act of necrophilia lasted for about 75 minutes, in which time, according to Moeliker, the living drake took two short breaks before resuming with copulating behaviour. Moeliker surmised that at the time of the collision with the window the two mallards were engaged in a common pattern in duck behaviour called "attempted rape flight". | In unguarded, taped interviews with his defense attorney, Wendy Patrickus, Jeffrey Dahmer explicitly stated that he had sex with his victims before and after their deaths. He explained that he wanted to remain with the person as long as possible, preserving some of his victims selected organs, skeletal tissue and bones. Ted Bundy
Ted Bundy (1946–1989) was an American serial killer who raped and murdered at least 30 young women during the 1970s. He also confessed to participating in necrophilic acts, claiming to have chosen secluded disposal sites for his victims bodies specifically for post-mortem sexual intercourse. Karen Greenlee
In 1987, Karen Greenlee gave a detailed interview called “The Unrepentant Necrophile” for Jim Mortons (edited by Adam Parafrey) book Apocalypse Culture. In this interview, she stated that she had a preference for younger men and was attracted to the smell of blood and death. She considered necrophilia an addiction. The interview was held in her apartment, which was apparently a small studio filled with books, necrophilic drawings, and satanic adornments. She also had written a confession letter in which she claimed to have abused 20–40 male corpses. Dennis Nilsen
Dennis Nilsen (1945–2018) was a Scottish serial killer who had developed an association between death and intimacy, later finding posing as a corpse a source of sexual arousal. In 1978, Nilsen committed his first murder and had intercourse with the victims corpse, keeping the body for months before disposal. Nilsen was reported to have sexually abused the corpses of various victims until his arrest. | 11
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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. | Esophageal cancer, a meta-analysis concluded that bisphosphonate treatment is NOT associated with excess risk of esophageal cancer. General: infrequent cases of skin rash, rarely manifesting as Stevens–Johnson syndrome and toxic epidermal necrolysis, eye problems (uveitis, scleritis) and generalized muscle, joint, and bone pain (rarely severe) have been reported. In laboratory tests, decreased calcium and phosphate values may be seen but reflect expected action of the drug and are almost always not clinically relevant. Osteonecrosis of the jaw may occur while on this drug, if dental work of any kind is carried out. The risk is considerably higher for extractions in the mandible (lower jaw) than other areas of the mouth, and the risk increases if you have been taking it for four or more years Although this side effect is uncommon (0.4-1.6% for oral alendronic acid), it occurs primarily in patients being administered intravenous bisphosphonates, with most cases being reported in cancer patients. Bone: alendronate has been linked in long-term users to the development of low-impact femoral fractures. Further, studies suggest that users of alendronate have an increase in the numbers of osteoclasts and develop giant, more multinucleated osteoclasts; the significance of this development is unclear. Fosamax has been linked to a rare type of leg fracture that cuts straight across the upper thigh bone after little or no trauma (subtrochanteric fractures). Interactions
Food and drugs containing large amounts of calcium, magnesium or aluminium (antacids) decrease the absorption of alendronate. | 0-1
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WFH as % of median reference value is calculated this way:
W
F
H
=
weight of a given child
median weight for a given child of that height
×
100
{\displaystyle \mathrm {WFH} ={\frac {\mbox{weight of a given child}}{\mbox{median weight for a given child of that height}}}\times 100}
Cutoff points may vary, but <80% (close to −2 Z-score) is often used. | Research advancements in the field
While it has been commonly known that the influenza virus increases ones chances of contracting pneumonia or meningitis caused by the streptococcus pneumonaie bacteria, new medical research in mice indicates that the flu is actually a necessary component for the transmission of the disease. Researcher Dimitri Diavatopoulo from the Radboud University Nijmegen Medical Centre in the Netherlands describes his observations in mice, stating that in these animals, the spread of the bacteria only occurs between animals already infected with the influenza virus, not between those without it. He says that these findings have only been inclusive in mice, however, he believes that the same could be true for humans. Mechanism of disease manifestation
Three stages can be used to categorize the infection process of pneumococcal pneumonia: transmission, colonization, and invasion. The Streptococcus pneumoniae (S. pneumoniae) leave the colonized host via shedding in order to be transmissible to new hosts, and must survive in the environment until infection of a new host (unless direct transmission occurs). Animal models have allowed scientists to have an increased understanding of these stages of infection. Transmission
In order for transmission to occur, there must be close contact with a carrier or amongst carriers. The likelihood of this increases during colder, dryer months of the year. The probability of transmission is shown to proliferate in coordination with other upper respiratory tract (URT) infections. Animal models have allowed for an increased understanding of the transmission stage during infection. | 0-1
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Pathophysiology
The cause of takotsubo cardiomyopathy is not fully understood, but several mechanisms have been proposed. It is well documented that elevated catecholamine levels have been implicated in the vast majority of TTS cases. Theories suggest a link between brain activation of stress-related biochemicals and the effects these chemicals have on areas of the heart. More specifically, adrenal stimulation by the sympathetic nervous system has been noted in cases ranging from physical events such as ischemic stroke, to emotional events such as depression or loss of a loved-one. How these increased levels of catecholamines act in the body to produce the changes seen with TTS is not clearly understood. Research supports the widely-held understanding that microvascular dysfunction and coronary vasospasm caused by a rapid influx of catecholamines to cardiac myocytes results in apical stunning and transient cardiomyopathy. Microvascular dysfunction/Transient vasospasm: Some of the original researchers of takotsubo suggested that multiple simultaneous spasms of coronary arteries could cause enough loss of blood flow to cause transient stunning of the myocardium. Other researchers have shown that vasospasm is much less common than initially thought. It has been noted that when there are vasospasms, even in multiple arteries, that they do not correlate with the areas of myocardium that are not contracting. However, the idea of coronary artery vasospasm is still believed to contribute to the TTS disease process. The theory of vasospasm is not easily separated from that of microvascular dysfunction and in fact, microvascular dysfunction could explain vasospasticity. | In anagen effluvium, histopathologic evaluation of a punch biopsy of the scalp will exhibit a normal anagen-to-telogen ratio, which is less than 15% telogen hair follicles. If greater than 15% of the hair follicles are in the telogen phase, this more supports a diagnosis of telogen effluvium. Treatment
The management of anagen effluvium should be aimed at limiting the amount of time the patient has alopecia. To date, several agents have been studied; unfortunately, no treatment appears to be effective in preventing or stopping the hair loss. Although the results have not been impressive in stopping or preventing hair loss, it has been postulated that topical minoxidil is effective in reducing the period of baldness by an average of fifty days. Several studies have described limiting drug delivery to the scalp by using a scalp tourniquet during chemotherapy. If scalp or brain metastases are a possibility, this method should not be used to allow penetration of the chemotherapeutic agent. Another method that has shown success is inducing scalp hypothermia (by keeping ice over the scalp) to a scalp temperature of fewer than 24° Celsius during chemotherapy with daunorubicin, doxorubicin, paclitaxel, vincristine, vinblastine, mechlorethamine, actinomycin D, and epirubicin.As pharmacologic agents successful in treating and preventing anagen effluvium have not been found, patient education and aesthetic advice on managing hair loss are fundamental to managing androgen effluvium. | 0-1
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The goal is to induce a brisk diuresis to prevent myoglobin precipitation and deposition, which can cause acute kidney injury. Mannitol can be added to assist with diuresis. Adding sodium bicarbonate to the IV fluids will cause alkalinization of the urine, believed to reduce the breakdown of myoglobin into its nephrotoxic metabolites, thus preventing renal damage. Often, IV normal saline is all that is needed to induce diuresis and alkalinize the urine. Epidemiology
See also
Pigmenturia
References
Further reading
Pedley, edited by Lewis P. Rowland, Timothy A. (2010). Merritts neurology (12th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 885. ISBN 978-0781791861. Retrieved 10 September 2015. {{cite book}}: |first1= has generic name (help)
Nyhan, edited by Georg F. Hoffmann, Johannes Zschocke, William L. (2010). Inherited metabolic diseases : a clinical approach. Heidelberg: Springer. p. 165. ISBN 978-3-540-74722-2. Retrieved 10 September 2015. {{cite book}}: |first1= has generic name (help)
External links
Overview on the Neuromuscular disease center website. | Megaduodenum is a congenital or acquired dilation and elongation of the duodenum with hypertrophy of all layers that presents as a feeling of gastric fullness, abdominal pain, belching, heartburn, and nausea with vomiting sometimes of food eaten 24 hours prior.Megaduodenum does not let the muscles of the duodenum function properly, the movement of waste material in the intestines gets impaired, which in turn affects digestion and nutrition.This condition is a rare entity in adults, because it may be either primary idiopathic or secondary. The secondary causes include Chagas disease, systematic sclerosis, duodenal stenosis, and visceral myopathy. Signs and Symptoms
The signs of duodenum can vary amongst patients. A high rate of chromosomal damage found in blood lymphocytes can indicate the presence of megaduodenum.Symptoms include:
Dilated Duodenum
Abdominal distention
Nausea
Vomiting and diarrhea
Severe digestive pseudo-obstruction
Recurrent urinary retention
Vacuolar degeneration and fibrosis of the longitudinal layer of gastrointestinal muscle.It is possible that this disease can be misdiagnosed and mimic other intestinal disorders, or later increase the chances of becoming a tumor. Causes
Although environmental factors can play a role in the development of Megaduodenum, genetic factors are responsible for creating tumors. Therefore, many complications of chromosomal damage in the blood lymphocytes can be possible causes. However, the main causes are:
Annular pancreas
Adhesions
Systemic sclerosis
Superior mesenteric artery syndrome
Aneurysm. Duodenal atresiaMegaduodenum due to its duodenal ganglionitis is an unusual condition, Megaduodenums similarity to megacolon and megaesophagus diseases can better explain the most plausible causes of it. In addition, some theories state that megaduodenum can be associated with the following causes: post-vagotomy, vitamin deficiency, and collagen diseases. | 0-1
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Subcutaneous allergen immunotherapy adverse events vary significantly depending on different allergenic extracts and the application of different allergen immunotherapy schedules.Allergen immunotherapy schedules include the "cluster" approach, which involves administering several doses sequentially in a single day; a "conventional" approach, which involves incrementally increasing the dose over approximately 15 weeks; and the "rush" approach, which involves administering incremental doses at intervals of 15–60 minutes over 1–3 days).It is challenging to perform an adequate risk assessment on the use of subcutaneous allergen immunotherapy compared to other forms of allergen immunotherapy administration due to the variability of immunotherapy schedules and further research is required. Sublingual
Sublingual immunotherapy involves putting drops or a tablet of allergen extracts under the tongue, which are then absorbed through the lining of the mouth. Sublingual immunotherapy has been demonstrated to be effective against rhinoconjuctivitis and asthma symptoms. This effectiveness, however, varies depending on the type of allergen. The strongest evidence for the efficacy of sublingual immunotherapy comes from studies that used grass allergens or mite allergens to alleviate allergic rhinitis symptoms; the evidence shows modest improvement.Sublingual immunotherapy is used to treat allergic rhinitis, often from seasonal allergies, and is typically given in several doses over a 12-week period. It works best when given 12 weeks before the start of the pollen season. The first dose is given by a physician to monitor for any rare reactions or anaphylaxis. Subsequent doses can be taken at home which makes this a convenient alternative to subcutaneous immunotherapy. | Mutations in the genes AGXT and GRHPR cause PH1 and PH2, respectively, through decreased production or activity of the proteins they make, which stops the normal breakdown of glyoxylate. Similarly, mutations in the gene HOGA1 cause PH3 due to loss-of-function mutations resulting in impaired protein function.PH1 is considered to be the most common and rapidly progressing form, accounting for about 80% of all currently diagnosed cases and PH2 and PH3 accounting for approximately 10% each of the current cases. However, recent evidence has suggested that PH2 and PH3 are not as benign as previously thought, with up to 50% of patients with PH2 developing kidney failure (chronic kidney disease [CKD] stage 5). While current estimates indicate that kidney failure is rarer in patients with PH3 compared to PH1 and PH2, CKD has been reported in patients with PH3. Moreover, the genetic prevalence based on known PH3 variants is much higher than the diagnosed prevalence of the disease, which could mean either incomplete penetrance (i.e. variant present with no clinical symptoms) or underdiagnosis (i.e. variant present with clinical symptoms but not diagnosed). Treatment
Increased water intake and alkalinization of urine is advised to prevent oxalate precipitation in urinary tract. In addition, Vitamin B6 (pyridoxine) is used to treat PH1 because alanine glyoxylate transaminase requires pyridoxine as cofactor. In approximately one third of patients with PH1, pyridoxine treatment decreases oxalate excretion and prevent kidney stone formation. | 0-1
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Long-term steroids are avoided if possible because of potential side-effects that include osteoporosis, diabetes and cataracts. Anti-D
Another option, suitable for Rh-positive patients with functional spleens is intravenous administration of Rho(D) immune globulin [Human; Anti-D]. The mechanism of action of anti-D is not fully understood. However, following administration, anti-D-coated red blood cell complexes saturate Fcγ receptor sites on macrophages, resulting in preferential destruction of red blood cells (RBCs), therefore sparing antibody-coated platelets. There are two anti-D products indicated for use in patients with ITP: WinRho SDF and Rhophylac. The most common adverse reactions are headache (15%), nausea/vomiting (12%) chills (<2%) and fever (1%). Steroid-sparing agents
There is increasing use of immunosuppressants such as mycophenolate mofetil and azathioprine because of their effectiveness. In chronic refractory cases, where immune pathogenesis has been confirmed, the off-label use of the vinca alkaloid and chemotherapy agent vincristine may be attempted. However, vincristine has significant side effects and its use in treating ITP must be approached with caution, especially in children. Intravenous immunoglobulin
Intravenous immunoglobulin (IVIg) may be infused in some cases in order to decrease the rate at which macrophages consume antibody-tagged platelets. However, while sometimes effective, it is costly and produces improvement that generally lasts less than a month. Nevertheless, in the case of an ITP patient already scheduled for surgery who has a dangerously low platelet count and has experienced a poor response to other treatments, IVIg can rapidly increase platelet counts, and can also help reduce the risk of major bleeding by transiently increasing platelet counts. | A detailed report of its development and properties appeared in 1975 in a paper authored by Richard Wallin, Bernard Regan, Martha Napoli and Ivan Stern. It was introduced into clinical practice initially in Japan in 1990 by Maruishi Pharmaceutical Co., Ltd. Osaka, Japan. The rights for sevoflurane worldwide were held by AbbVie. It is now available as a generic drug. Sevoflurane is an inhaled anaesthetic that is often used to put children asleep for surgery. During the process of waking up from the medication, it has been known to cause agitation and delirium. It is not clear if this can be prevented. | 0-1
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The extent of repetition in itself might serve as an additional contextualization or paralinguistic cue, to "extend the lexical meaning of the words, add character to the sentences, and allow fine-tuning and personalisation of the message". Computer representations
In computing, several ellipsis characters have been codified, depending on the system used. In the Unicode standard, there are the following characters:
Unicode recognizes a series of three period characters (U+002E) as compatibility equivalent (though not canonical) to the horizontal ellipsis character.In HTML, the horizontal ellipsis character may be represented by the entity reference … (since HTML 4.0), and the vertical ellipsis character by the entity reference ⋮ (since HTML 5.0). Alternatively, in HTML, XML, and SGML, a numeric character reference such as … or … can be used. In the TeX typesetting system, the following types of ellipsis are available:
In LaTeX, note that the reverse orientation of \ddots can be achieved with \reflectbox provided by the graphicx package: \reflectbox{\ddots} yields . With the amsmath package from AMS-LaTeX, more specific ellipses are provided for math mode. The horizontal ellipsis character also appears in the following older character maps:
in Windows-1250—Windows-1258 and in IBM/MS-DOS Code page 874, at code 85 (hexadecimal)
in Mac-Roman, Mac-CentEuro and several other Macintosh encodings, at code C9 (hexadecimal)
in Ventura International encoding at code C1 (hexadecimal)Note that ISO/IEC 8859 encoding series provides no code point for ellipsis. | In 2012, crofelemer completed a Phase III trial, and it was approved in December 2012 by the FDA for the indication "symptomatic relief of non-infectious diarrhea in patients with HIV/AIDS on anti-retroviral therapy".The drug substance is manufactured by Glenmark Pharmaceuticals, and is manufactured as 125 mg delayed-release tablets by Patheon Pharmaceuticals Inc. for Napo Pharmaceuticals. References
External links
"Crofelemer". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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The symptoms may include frequency, suprapubic pain (pain felt above the pubis), hematuria (blood in the urine), dysuria (difficult urination or pain during urination), urgency, and urge incontinence. The white lesion may be seen during cystoscopy, where it appears as a whitish-gray or yellow lesion, on a background of inflamed urothelium and there may be floating debris in the bladder. Leukoplakia of the bladder may undergo cancerous changes, so biopsy and long term follow up are usually indicated. Anal canal
Leukoplakia of the anal canal is rare. It may extend up to the anorectal junction. On digital examination it feels hard and granular, and at proctoscopy, it appears as white plaques which may be diffuse, circumferential, or circumscribed. The histologic appearance is similar to oral leukoplakia, with hyperkeratosis and acanthosis. It may be asymptomatic, with symptoms due to other lesions such as hemorrhoids or fissures. Progression to anal stenosis has been described. The malignant potential is seemingly low, and few cases of anal carcinoma have been reported associated with anal leukoplaka. Signs and symptoms
Most cases of leukoplakia cause no symptoms, but infrequently there may be discomfort or pain. The exact appearance of the lesion is variable. Leukoplakia may be white, whitish yellow or grey. The size can range from a small area to much larger lesions. The most common sites affected are the buccal mucosa, the labial mucosa and the alveolar mucosa, although any mucosal surface in the mouth may be involved. | The degree of hyperkeratosis, epithelial thickness (acanthosis/atrophy), dysplasia and inflammatory cell infiltration in the underlying lamina propria are variable. In mucous membranes, hyperkeratosis can be defined as "an increase in the thickness of the keratin layer of the epithelium, or the presence of such a layer in a site where none would normally be expected." In leukoplakia, the hyperkeratosis varies in thickness and may be either ortho- or para-keratosis, (depending upon whether cell nuclei are lost or retained in the superficial layers respectively), or a mixture of both in different areas of the lesion.The epithelium may show hypertrophy (e.g. acanthosis) or atrophy. Red areas within leukoplakia represent atrophic or immature epithelium which has lost the ability to keratinize. The transition between the lesion and normal surrounding mucosa may be well-demarcated, or poorly defined. Melanin, a pigment naturally produced in oral mucosa, can leak from cells and give a grey color to some leukoplakia lesions.Hyperkeratosis and altered epithelial thickness may be the only histologic features of a leukoplakia lesion, but some show dysplasia. The word "dysplasia" generally means "abnormal growth", and specifically, in the context of oral red or white lesions, refers to microscopic changes ("cellular atypia") in the mucosa that indicate a risk of malignant transformation. When dysplasia is present, there is generally an inflammatory cell infiltration in the lamina propria. The following are commonly cited as being possible features of epithelial dysplasia in leukoplakia specimens:
Cellular pleomorphism, in which cells are of abnormal and different shapes. | 11
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Pharmacokinetics
Brivaracetam exhibits linear pharmacokinetics over a wide dose range, is rapidly and completely absorbed after oral administration, has an elimination half-life of seven to eight hours, and has plasma protein binding of less than 20%. It is extensively metabolized (>90%), primarily via hydrolysis of the acetamide group, and secondarily through hydroxylation mediated by the liver enzyme CYP2C19. The three major metabolites (hydroxy, acid, and hydroxyacid) are pharmacologically inactive. Brivaracetam is eliminated as urinary metabolites, with over 95% of a radioactive test dose recovered in the urine within 72 hours, including only 8.6% as unchanged brivaracetam. Pharmacogenetics
As noted above, brivaracetam is primarily metabolized by hydrolysis, via amidase enzymes, to an inactive metabolite. To a lesser extent, it is also metabolized by a minor metabolic pathway via CYP2C19-dependent hydroxylation. Individuals who have no CYP2C19 enzyme activity, "CYP2C19 poor metabolizers", will have a greater exposure to standard doses of brivaracetam. Because they are less able to metabolize the drug to its inactive form for excretion, they may have an increased risk of adverse effects. The most common adverse effects of brivaracetam therapy include sedation, fatigue, dizziness, and nausea. The FDA-approved drug label for brivaracetam states that patients who are CYPC19 poor metabolizers, or are taking medicines that inhibit CYP2C19, may require a dose reduction. Chemical and physical properties
Brivaracetam is the 4R-propyl analogue of the anticonvulsant levetiracetam. | The Gothenburg criterion consists of the presence of peristaltic contractions, with an amplitude of 180 mm Hg at any place in the esophagus. The Richter criterion involves the presence of peristaltic contractions with an amplitude of greater than 180 mm Hg from an average of measurements taken 3 and 8 cm above the lower esophageal sphincter. It has been incorporated into a number of clinical guidelines for the evaluation of dysphagia. The Achem criteria are more stringent, and are an extension of the study of 93 patients used by Richter and Castell in the development of their criteria, and require amplitudes of greater than 199 mm Hg at 3 cm above the lower esophageal sphincter (LES), greater than 172 mm Hg at 8 cm above the LES, or greater than 102 mm Hg at 13 cm above the LES. Treatment
People are usually reassured that the disease is unlikely to worsen. However, the symptoms of chest pain and trouble swallowing may be severe enough to require treatment with medications, and rarely, surgery. The initial step of treatment focuses on reducing risk factors. While weight reduction may be useful in reducing symptoms, the role of acid suppression therapy to reduce esophageal reflux is still uncertain. Very cold and very hot beverages may trigger esophageal spasms. Medications
Medications for nutcracker esophagus includes the use of calcium-channel blockers, which relax the lower esophageal sphincter (LES) and palliate the dysphagia symptoms. Diltiazem, a calcium-channel blocker, has been used in randomized control studies with good effect. | 0-1
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If overdose of opium tincture is suspected, rapid professional intervention is required. The primary concern is re-establishing a viable airway and institution of assisted or controlled ventilation if the patient is unable to breathe on their own. Other supportive measures such as the use of vasopressors and oxygen may be indicated to treat cardiac and/or pulmonary failure. Cardiac arrhythmias or arrest will require advanced life-saving measures. Intravenous naloxone or nalmefene, quick-acting opioid antagonists, are the first-line treatment to reverse respiratory depression caused by an overdose of opium tincture. Gastric lavage may be of some use in certain cases. In fiction
In Mary Shelleys novel Frankenstein (1818), Victor Frankenstein takes laudanum as his only means of sleeping and thus preserving his life while in recovery from months of fever and a series of horrible events. In Charles Dickenss novel Oliver Twist (1837), Nancy gave William "Bill" Sikes laudanum to keep him asleep while she ran away to meet Rose Maylie. In Uncle Toms Cabin (1852), an anti-slavery novel by Harriet Beecher Stowe, an enslaved woman named Cassy talks about how she killed her newborn by laudanum overdose to spare him from experiencing the horrors of slavery. In the novel Silas Marner: The Weaver of Raveloe by George Eliot (Mary Ann Evans) (1861), Silas finds and adopts a two-year old girl who had wandered into his house. The girl had been abandoned while walking with her opium-addicted mother, Molly Farren, who had fallen asleep in the snow and died. | Glaucoma is an umbrella term indicating ailments which damage the neural cable from the eye to the brain called the optic nerve, and which can lead to a loss of vision. In most cases of glaucoma, typically called primary open-angle glaucoma, the outflow does not happen normally but doctors can not see what is causing the blockage; with PEX, however, the flakes are believed to be a cause of the blockage. PEX flakes by themselves do not directly cause glaucoma, but can cause glaucoma indirectly by blocking the outflow of aqueous humor, which leads to higher intraocular pressure, and this can cause glaucoma. PEX has been known to cause a weakening of structures within the eye which help hold the eyes lens in place, called lens zonules. Causes
The cause of pseudoexfoliation glaucoma is generally unknown.PEX is generally believed to be a systemic disorder, possibly of the basement membrane of the eye. Researchers have noticed deposits of PEX material in various parts of the body, including in the skin, heart, lungs, liver, kidneys, and elsewhere. Nevertheless, what is puzzling is that PEX tends to happen in only one eye first, which scientists call unilaterality, and in some cases, gradually affects the other eye, which is termed bilaterality. According to this reasoning, if PEX were a systemic disorder, then both eyes should be affected at the same time, but they are not. There are contrasting reports about the extent and speed with which PEX moves from one eye to both eyes. | 0-1
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This piece labeled PNP as a "multiorgan disease characterized by antibodies against plakins, desmogleins and the α2-macroglobulin-like-1 (A2ML1) protein, in association with an underlying neoplasm".A study concluded in 2009, summarized in 2010, surrounded the surgical removal of the associated tumor as a means to treat PNP. While 7/22 of the subjects perished due to resulting infection from the bodys inability to heal itself after surgery, the other 15 cases survived. This study outlined the importance of early detection and prompt treatment as of utmost important in the treatment of PNP.In 2011, a case study of a woman with ulcers on the back of her leg reported as being diagnosed with PNP. The underlying tumors are almost exclusively of B-cell lineage. However, T-cells and CD56+ Natural Killer cells have also been postulated to be associated effectors of paraneoplastic pemphigus. This case demonstrated the rare association between Natural Killer cell lymphoma and PNP, suggesting that Natural Killer cells could be involved in the pathogenesis of PNP. The article warned clinicians to be alert to the possibility that paraneoplastic pemphigus in lymphomas not of B-cell lineage. This added to the already complex, not fully understood pathogenesis of PNP.A study in 2013 outlined the effectiveness of plasma exchange in PNP patients with benign tumors.The University of Toronto has been working to develop a form of treatment that improves the patients overall quality of life while remaining economically achievable. They believe they have achieved this through fixed-dose rituximab. | For people who are critically ill that require a feeding tube, there is evidence suggesting that the risk of aspiration pneumonia may be reduced by inserting the feeding tube into the duodenum or the jejunum (post-pyloric feeding), when compared to inserting the feeding tube into the stomach (gastric feeding). Enhanced swallow
Many people at risk for aspiration pneumonia have an impaired swallowing mechanism, which may increase the chance of aspiration of food particles with meals. There is some evidence to indicate that training of various parts of the body involved in the act of swallowing, including the tongue and lips, may reduce episodes of aspiration and aspiration pneumonia; however, further research is required to confirm this benefit. Other simple actions during feeding can improve the swallowing capability of a person and thus reduce the risk of aspiration, including changes in position and feeding assistance. After surgery
Many instances of aspiration occur during surgical operations, especially during anesthesia induction. The administration of anesthesia causes suppression of protective reflexes, most importantly the gag reflex. As a result, stomach particles can easily enter the lungs. Certain risk factors predispose individuals to aspiration, especially conditions causing dysfunction of the upper gastrointestinal system. Identifying these conditions before the operation begins is essential for proper preparation during the procedure. It is recommended that patients fast prior to procedures as well. Other practices that may be beneficial but have not been well-studied include medication that reduce the acidity of gastric contents and rapid sequence induction. | 0-1
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Medical uses
Cefiderocol is used to treat adults with complicated urinary tract infections, including kidney infections caused by susceptible Gram-negative microorganisms, who have limited or no alternative treatment options.In the United States, cefiderocol is indicated in adults 18 years of age or older who have limited or no alternative treatment options for the treatment of complicated urinary tract infections (cUTIs), including pyelonephritis caused by the following susceptible Gram-negative microorganisms: Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, and Enterobacter cloacae complex.For the treatment of severe pneumonia (HABP and VABP), it is indicated in patients 18 years of age and older whose pneumonia is not responding to other, more commonly used antibiotics and is confirmed to be caused by one of the following Gram-negative organisms:
Acinetobacter baumannii complex
Escherichia coli
Enterobacter cloacae complex
Klebsiella pneumoniae
Pseudomonas aeruginosa
Serratia marcescensThis indication is supported by the 2018 APEKS-NP study, where cefiderocol was compared in nosocomial pneumonia caused by Gram-Negative bacteria to meropenem, where it was shown not to be inferior to meropenem. The primary endpoint of the study was all-cause mortality at day 14, where both antibiotics were shown to be almost equally effective. As of 2020, cefiderocol is indicated in the European Union for the treatment of infections due to aerobic Gram-negative bacteria in adults with limited treatment options. | It bypasses the bacterial porin channels by using the bacterias own iron-transport system for being transported in. History
Cefiderocol received a Qualified Infectious Disease Product designation from the U.S. Food and Drug Administration (FDA) and was granted priority review. In November 2019, the FDA granted approval of cefiderocol to Shionogi & Co. as an antibacterial drug for treatment of adults 18 years of age or older with complicated urinary tract infections (cUTI), including kidney infections caused by susceptible Gram-negative microorganisms, who have limited or no alternative treatment options.The safety and effectiveness of cefiderocol was demonstrated in a study (NCT02321800) of 448 participants with cUTIs. Of the participants who were administered cefiderocol, 72.6% had resolution of symptoms and eradication of the bacteria approximately seven days after completing treatment, compared with 54.6% in participants who received an alternative antibiotic. The clinical response rates were similar between the two treatment groups. The trial included participants from Europe, United States and Mexico.In the clinical trial, participants with cUTI were chosen at random to receive cefiderocol, or another antibacterial drug called imipenem/cilastatin. Both treatments were given intravenously for 7–14 days and neither the participants nor the health care professionals knew which drugs were given until after the trial was complete. | 11
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