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It became available in 1972 and was the second aminopenicillin to reach the market (after ampicillin in 1961). Co-amoxiclav became available in 1981. Society and culture
Economics
Amoxicillin is relatively inexpensive. Modes of delivery
Pharmaceutical manufacturers make amoxicillin in trihydrate form, for oral use available as capsules, regular, chewable and dispersible tablets, syrup and pediatric suspension for oral use, and as the sodium salt for intravenous administration.An extended-release is available. The intravenous form of amoxicillin is not sold in the United States. When an intravenous aminopenicillin is required in the United States, ampicillin is typically used. When there is an adequate response to ampicillin, the course of antibiotic therapy may often be completed with oral amoxicillin.Research with mice indicated successful delivery using intraperitoneally injected amoxicillin-bearing microparticles. Names
"Amoxicillin" is the International Nonproprietary Name (INN), British Approved Name (BAN), and United States Adopted Name (USAN), while "amoxycillin" is the Australian Approved Name (AAN).Amoxicillin is one of the semisynthetic penicillins discovered by Beecham scientists. The patent for amoxicillin has expired, thus amoxicillin and co-amoxiclav preparations are marketed under various brand names across the world. Veterinary uses
Amoxicillin is also sometimes used as an antibiotic for animals. The use of amoxicillin for animals intended for human consumption (chickens, cattle, and swine for example) has been approved. References
Further reading
Neal MJ (2002). Medical Pharmacology at a Glance (4th ed.). Oxford: Blackwell Science. ISBN 978-0-632-05244-8. External links
"Amoxicillin". Drug Information Portal. U.S. National Library of Medicine. | Cerebellar degeneration is a condition in which cerebellar cells, otherwise known as neurons, become damaged and progressively weaken in the cerebellum. There are two types of cerebellar degeneration; paraneoplastic cerebellar degeneration, and alcoholic or nutritional cerebellar degeneration. As the cerebellum contributes to the coordination and regulation of motor activities, as well as controlling equilibrium of the human body, any degeneration to this part of the organ can be life-threatening. Cerebellar degeneration can result in disorders in fine movement, posture, and motor learning in humans, due to a disturbance of the vestibular system. This condition may not only cause cerebellar damage on a temporary or permanent basis, but can also affect other tissues of the central nervous system, those including the cerebral cortex, spinal cord and the brainstem (made up of the medulla oblongata, midbrain, and pons).Cerebellar degeneration can be attributed to a plethora of hereditary and non-hereditary conditions. More commonly, cerebellar degeneration can also be classified according to conditions that an individual may acquire during their lifetime, including infectious, metabolic, autoimmune, paraneoplastic, nutritional or toxic triggers. Signs and symptoms
Patients with cerebellar degeneration experience a progressive loss of nerve cells (Purkinje cells) throughout the cerebellum. As well as this, it is common to incur an elevated blood protein level and a high volume of lymph cells within the cerebrospinal fluid, resulting in swelling and enlargement of the brain. | 0-1
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In double-blind, placebo-controlled trials other SSRIs like fluvoxamine, escitalopram and sertraline showed reduction of social anxiety symptoms, including anxiety, sensitivity to rejection and hostility.Citalopram also appears to be effective.General side-effects are common during the first weeks while the body adjusts to the drug. Symptoms may include headaches, nausea, insomnia and changes in sexual behavior. Treatment safety during pregnancy has not been established. In late 2004 much media attention was given to a proposed link between SSRI use and suicidality [a term that encompasses suicidal ideation and attempts at suicide as well as suicide]. For this reason, [although evidential causality between SSRI use and actual suicide has not been demonstrated] the use of SSRIs in pediatric cases of depression is now recognized by the Food and Drug Administration as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor. Recent studies have shown no increase in rates of suicide. These tests, however, represent those diagnosed with depression, not necessarily with social anxiety disorder. In addition, studies show that more socially phobic patients treated with anti-depressant medication develop hypomania than non-phobic controls. The hypomania can be seen as the medication creating a new problem. Other drugs
Other prescription drugs are also used, if other methods are not effective. Before the introduction of SSRIs, monoamine oxidase inhibitors (MAOIs) such as phenelzine were frequently used in the treatment of social anxiety. | CODEs are rare genetic changes to a single gene that affects the lining of the intestine or changes to the immune system that also affects the cell function of important nutrient and electrolyte transporters in the intestine such as Cl−/HCO3− mutation.Otherwise, socioeconomic factors and access to treatment/healthcare play a significant part in developing chronic diarrhea as an infant. For instance, leading causes of chronic diarrhea in developing countries are infections of the intestine. In developed countries, chronic diarrhea has a diverse range of causes such as chronic infection of the intestines, autoimmune enteropathy, and inability to absorb nutrients via celiac disease, food sensitivities, etc.From age 0–30 days, typical causes are:
Abetalipoproteinemia, a condition caused by a genetic mutation that creates abnormal absorption of fats and some vitamins. Acrodermatitis enteropathica, a condition in which the intestine cannot absorb zinc. Autoimmune enteropathy, a rare condition in which the intestines are perceived as a foreign threat by the immune system and are attacked leading to irritation and inflammation. Microvillous inclusion disease, a condition caused by a genetic mutation leading to severe diarrhea because intestinal cells did not have normal development and thus the intestines are not able to absorb nutrients properly. Congenital chloride diarrhea, a lifelong condition caused by a genetic mutation that leads to diarrhea with a high concentration of chloride. Congenital sodium diarrhea, a genetic disorder caused by mutations in electrolyte transporters that disrupt the transport of Na+ across the intestine and results in high levels of Na+ greater than 145 mM in the stool. | 0-1
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Lorlatinib, sold under the brand name Lorbrena in the United States, Canada, and Japan, and Lorviqua in the European Union, is an anti-cancer drug developed by Pfizer. It is an orally administered inhibitor of ALK and ROS1, two enzymes that play a role in the development of cancer. Medical uses
Lorlatinib is approved in the US and in Europe for the second- or third-line treatment of ALK-positive metastatic non-small-cell lung cancer (NSCLC). It is the only ALK inhibitor with meaningful activity against ALK G1202R mutation in lung cancer. Contraindications
Lorlatinib must not be combined with strong inducers (i.e. activators) of the liver enzymes CYP3A4/5 if it can be avoided, as serious cases of liver toxicity have been observed under combination with the CYP3A4/5 inducer rifampicin. Side effects
The most common side effects in studies were high blood cholesterol (84% of patients), high blood triglycerides (67%), edema (55%), peripheral neuropathy (48%), cognitive effects (29%), fatigue (28%), weight gain (26%), and mood effects (23%). Serious side effects led to dose reduction in 23% of patients and in termination of lorlatinib treatment in 3% of patients. Interactions
Lorlatinib is metabolized by the enzymes CYP3A4/5. Therefore, CYP3A4/5 inducers such as rifampicin, carbamazepine or St Johns wort decrease its concentrations in the blood plasma and can reduce its effectiveness. Additionally, the combination of lorlatinib with rifampicin showed liver toxicity in studies. Inhibitors of these enzymes such as ketoconazole or grapefruit juice increase lorlatinib plasma concentrations, leading to higher toxicity. | Lorbrena was analyzed in a clinical trial of 296 patients with ALK+ NSCLC whose cancer had migrated to multiple parts of the body including the brain. A trial comparing lorlatinib with crizotinib was conducted, with a primary endpoint of "progression-free survival", which is the period of time a patient is in remission (the tumor ceases growth). Preclinical studies are investigating lorlatinib for treatment of neuroblastoma. In 2017, Pfizer announced that lorlatinib was shown to have activity against lung and brain tumors in people with ALK or ROS1 positive advanced non-small-cell lung cancer. Approval
In 2015, FDA granted Pfizer orphan drug status for lorlatinib for the treatment of NSCLC. In 2018, the FDA approved lortalinib for second- or third-line treatment of ALK-positive metastatic NSCLC. In February 2019, the European CHMP of EMA recommended the granting of a conditional marketing authorisation. In May 2019 the European Commission approved lorlatinib for the 28 countries of the EU, also as a second- or third-line treatment. References
External links
"Lorlatinib". Drug Information Portal. U.S. National Library of Medicine. | 11
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38 (38): 6047–6056. doi:10.1016/j.vaccine.2020.06.021. PMID 32600916. External links
Inactivated Influenza Vaccine Information Statement, US Centers for Disease Control and Prevention (CDC)
Live, Intranasal Influenza Vaccine Information Statement, US Centers for Disease Control and Prevention (CDC)
Seasonal Influenza (Flu) Vaccination and Preventable Disease, US Centers for Disease Control and Prevention (CDC)
Misconceptions about Seasonal Flu and Flu Vaccines, US Centers for Disease Control and Prevention (CDC)
"Influenza Vaccine". Drug Information Portal. U.S. National Library of Medicine. Influenza Vaccines at the US National Library of Medicine Medical Subject Headings (MeSH) | It has been arbitrarily assumed that a number of over 4-5 leukocytes in the field of vision of the microscope indicates leukocyturia.At the moment, there are also quick test strips available, allowing after wetting a special diagnostic bar, the detection of granulocytes in the urine, as evidenced by the color change of the test strip. The principle of their operation is based on the detection of granulocytes esterases, including leukocytes. This method, however, is burdened with a large number of false positive results (use of antibiotics, such as imipenem, meropenem, clavulanic acid, which is sometimes combined with penicillin derivatives) or false negative (gentamicin, cefalexin, glycosuria, proteinuria).Leukocyturia is a laboratory symptom of many diseases like glomerulonephritis or pyelonephritis. It may occur in the case of diseases of the urinary tract, reproductive system and diseases of the abdominal organs. Leukocyturia is mostly a sign of urinary tract infection, especially if significant bacteriuria is found (for most people, the number of bacteria in a culture is > 10^5) and other symptoms associated with passing urine. The presence of leukocyturia does not indicate the need for antimicrobial therapy yet. Additional images
See also
Urinalysis
Bacteriuria
References
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The relief of pressure and the release of endorphins into the bloodstream after the expulsion causes the vomiter to feel better. Contents
Gastric secretions and likewise vomit are highly acidic. Recent food intake appears in the gastric vomit. Irrespective of the content, vomit tends to be malodorous.The content of the vomitus (vomit) may be of medical interest. Fresh blood in the vomit is termed hematemesis ("blood vomiting"). Altered blood bears resemblance to coffee grounds (as the iron in the blood is oxidized) and, when this matter is identified, the term coffee-ground vomiting is used. Bile can enter the vomit during subsequent heaves due to duodenal contraction if the vomiting is severe. Fecal vomiting is often a consequence of intestinal obstruction or a gastrocolic fistula and is treated as a warning sign of this potentially serious problem (signum mali ominis).If the vomiting reflex continues for an extended period with no appreciable vomitus, the condition is known as non-productive emesis or "dry heaves", which can be painful and debilitating. | The body takes a deep breath to avoid aspirating vomit. Retroperistalsis starts from the middle of the small intestine and sweeps up digestive tract contents into the stomach, through the relaxed pyloric sphincter. Intrathoracic pressure lowers (by inspiration against a closed glottis), coupled with an increase in abdominal pressure as the abdominal muscles contract, propels stomach contents into the esophagus as the lower esophageal sphincter relaxes. The stomach itself does not contract in the process of vomiting except for at the angular notch, nor is there any retroperistalsis in the esophagus. Vomiting is ordinarily preceded by retching. Vomiting also initiates an SNS response causing both sweating and increased heart rate. Phases
The vomiting act has two phases. In the retching phase, the abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. For this reason, an individual may confuse this phase with an episode of violent hiccups. In this retching phase, nothing has yet been expelled. In the next phase, also termed the expulsive phase, intense pressure is formed in the stomach brought about by enormous shifts in both the diaphragm and the abdomen. These shifts are, in essence, vigorous contractions of these muscles that last for extended periods of time—much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. Individuals who do not regularly exercise their abdominal muscles may experience pain in those muscles for a few days. | 11
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The companys own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high to bring about serious environmental degradation, including lead, mercury, manganese, arsenic, thallium, and copper, plus the chalcogen selenium. Identifying which particular poison was responsible for the disease proved to be extremely difficult and time-consuming. During 1957 and 1958, many different theories were proposed by different researchers. At first, manganese was thought to be the causal substance due to the high concentrations found in fish and the organs of the deceased. Thallium, selenium, and a multiple contaminant theory were also proposed, but in March 1958, visiting British neurologist Douglas McAlpine suggested that Minamata symptoms resembled those of organic mercury poisoning, so the focus of the investigation centered on mercury. In February 1959, the mercury distribution in Minamata Bay was investigated. The results shocked the researchers involved. Large quantities of mercury were detected in fish, shellfish, and sludge from the bay. The highest concentrations centred around the Chisso factory wastewater canal in Hyakken Harbour and decreased going out to sea, clearly identifying the plant as the source of contamination. Pollution was so heavy at the mouth of the wastewater canal, a figure of 2 kg of mercury per ton of sediment was measured: a level that would be economically viable to mine. Indeed, Chisso did later set up a subsidiary to reclaim and sell the mercury recovered from the sludge.Hair samples were taken from the individuals with the disease and also from the Minamata population in general. | Focal cortical dysplasia (FCD) is a congenital abnormality of brain development where the neurons in an area of the brain failed to migrate in the proper formation in utero. Focal means that it is limited to a focal zone in any lobe. Focal cortical dysplasia is a common cause of intractable epilepsy in children and is a frequent cause of epilepsy in adults. There are three types of FCD with subtypes, including type 1a, 1b, 1c, 2a, 2b, 3a, 3b, 3c, and 3d, each with distinct histopathological features. All forms of focal cortical dysplasia lead to disorganization of the normal structure of the cerebral cortex :
Type 1 FCD exhibits subtle alterations in cortical lamination. Type 2a FCD exhibits neurons that are larger than normal that are called dysmorphic neurons (DN). FCD type 2b exhibits complete loss of laminar structure, and the presence of DN and enlarged cells are called balloon cells (BC) for their large elliptical cell body shape, laterally displaced nucleus, and lack of dendrites or axons. The developmental origin of balloon cells is currently believed to be derived from neuronal or glial progenitor cells. Balloon cells are similar in structure to giant cells in the disorder tuberous sclerosis complex. Type 3 FCDs are cortical disorganisation associated with other lesions such as hippocampal sclerosis (type 3a), long-term epilepsy-associated tumors (3b), vascular malformations (3c) or scar/hypoxic damages (3d).Recent studies have demonstrated that FCD types 2a and 2b result from somatic mutations in genes that encode components of the mammalian target of rapamycin (mTOR) pathway. | 0-1
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Intracerebral implants: A neurosurgeon creates a cavity within a tumor to allow the placement of dime-sized chemotherapy wafers, such as Gliadel wafers. Several of these wafers can be placed at the time of surgery and will release the chemotherapy agent carmustine slowly over time. This provides a much higher concentration of chemotherapy in the brain than can be obtained with intravenous administration, and it causes fewer systemic side effects. However, it is an option only for patients with surgically resectable tumours; it cannot be used to treat DIPG. Osmotic blood–brain barrier disruption (BBBD): The cells of the blood–brain barrier are shrunk by a concentrated sugar solution (mannitol). This opens the barrier and allows 10 to 100 times more chemotherapy to enter the brain. A catheter is placed into a large artery (usually the one in the groin called the femoral artery) and threaded up to the carotid or vertebral artery. The hypertonic mannitol is injected, followed by a chemotherapeutic agent. Patients spend a few days in the hospital for each administration. This has been attempted with DIPG tumours. Convection-enhanced delivery: Chemotherapy is delivered to the tumour by a surgically implanted catheter under a pressure gradient to achieve more distribution than with diffusion alone. Limited experiments have been conducted with brain tumors, including one with a DIPG. Drug carriers: Carriers such as "Trojan horse" molecules, liposomes, and nanoparticles might theoretically allow a therapeutic drug to enter the brain. Such tactics are mostly in the investigatory stages and are not yet clinically relevant to brain tumour treatment. | Osteopoikilosis is a benign, autosomal dominant sclerosing dysplasia of bone characterized by the presence of numerous bone islands in the skeleton. Presentation
The radiographic appearance of osteopoikilosis on an X-ray is characterized by a pattern of numerous white densities of similar size spread throughout all the bones. This is a systemic condition. It must be differentiated from blastic metastasis, which can also present radiographically as white densities interspersed throughout bone. Blastic metastasis tends to present with larger and more irregular densities in less of a uniform pattern. Another differentiating factor is age, with blastic metastasis mostly affecting older people, and osteopoikilosis being found in people 20 years of age and younger. The distribution is variable, though it does not tend to affect the ribs, spine, or skull. Cause
Epidemiology
Men and women are affected in equal number, reflecting the fact that osteopoikilosis attacks indiscriminately. Additionally, the disease is often associated with melorheostosis, despite the apparent lack of correlation between melorheostosis and genetic heritability. It has been tied to LEMD3. Buschke–Ollendorff syndrome is a similar condition, which is also associated with LEMD3. See also
List of radiographic findings associated with cutaneous conditions
References
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Fryns syndrome is an autosomal recessive multiple congenital anomaly syndrome that is usually lethal in the neonatal period. Fryns (1987) reviewed the syndrome. Presentation
Usually associated with diaphragmatic hernia,
pulmonary hypoplasia,
imperforate anus,
micropenis,
bilateral cryptorchidism,
cerebral ventricular dilation,
camptodactyly,
agenesis of sacrum,
low-set ear. Cytogenetics
In a newborn boy thought to have Fryns syndrome, Clark and Fenner-Gonzales (1989) found mosaicism for a tandem duplication of 1q24-q31.2. They suggested that the gene for this disorder is located in that region. However, de Jong et al. (1989), Krassikoff and Sekhon (1990), and Dean et al. (1991) found possible Fryns syndrome associated with anomalies of chromosome 15, chromosome 6, chromosome 8 and chromosome 22, respectively. Thus, these cases may all represent mimics of the mendelian syndrome and have no significance as to the location of the gene for the recessive disorder.By array CGH, Slavotinek et al. (2005) screened patients with DIH and additional phenotypic anomalies consistent with Fryns syndrome for cryptic chromosomal aberrations. They identified submicroscopic chromosome deletions in 3 probands who had previously been diagnosed with Fryns syndrome and had normal karyotyping with G-banded chromosome analysis. Two female infants were found to have microdeletions involving 15q26.2 (see 142340), and 1 male infant had a deletion in band 8p23.1 (see 222400). Diagnosis
Prenatal Diagnosis:
Aymé, et al. (1989) reported prenatal diagnosis of Fryns syndrome by sonography between 24 and 27 weeks. Manouvrier-Hanu et al. (1996) described the prenatal diagnosis of Fryns syndrome by ultrasonographic detection of diaphragmatic hernia and cystic hygroma. The diagnosis was confirmed after termination of the pregnancy. | Most patients also had hypoplastic external genitalia and anomalies of internal genitalia, including bifid or hypoplastic uterus or immature testes. The digestive tract was also often abnormal; duodenal atresia, pyloric hyperplasia, malrotation and common mesentery were present in about half of the patients. When the brain was examined, more than half were found to have Dandy–Walker anomaly and/or agenesis of the corpus callosum. A few patients demonstrated cloudy cornea. Histologically, 2 of 3 patients showed retinal dysplasia with rosettes and gliosis of the retina, thickness of the posterior capsule of the lens, and irregularities of Bowman membrane. Alessandri et al. (2005) reported a newborn from the Comores Islands with clinical features of Fryns syndrome without diaphragmatic hernia. They noted that diaphragmatic hernia is found in more than 80% of cases and that at least 13 other cases had been reported with an intact diaphragm. In a postneonatal survivor of Fryns syndrome, Riela et al. (1995) described myoclonus appearing shortly after birth, which was well controlled on valproate. Progressive cerebral and brainstem atrophy was noted on serial MRIs made at 3 months and after 6 months of age. Van Hove et al. (1995) described a boy with Fryns syndrome who survived to age 3 years and reviewed the outcome of other reported survivors (approximately 14% of reported cases). Survivors tended to have less frequent diaphragmatic hernia, milder lung hypoplasia, absence of complex cardiac malformation, and severe neurologic impairment. | 11
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These abnormalities can lead to intellectual problems, seizures, vision problems, hearing problems, problems feeding and slow development.Whether the stage of pregnancy at which the mother becomes infected affects the risk to the fetus is not well understood, nor is whether other risk factors affect outcomes. One group has estimated the risk of a baby developing microcephaly at about 1% when the mother is infected during the first trimester, with the risk of developing microcephaly becoming uncertain beyond the first trimester. Affected babies might appear normal but actually have brain abnormalities; infection in newborns could also lead to brain damage. Cause
Reservoir
Zika virus is a mosquito-borne flavivirus closely related to the dengue and yellow fever viruses. While mosquitoes are the vector, the main reservoir species remains unknown, though serological evidence has been found in both West African monkeys and rodents. Transmission
Transmission is via the bite of mosquitoes from the genus Aedes, primarily Aedes aegypti in tropical regions. It has also been isolated from Ae. africanus, Ae. apicoargenteus, Ae. luteocephalus, Ae. albopictus, Ae. vittatus and Ae. furcifer. During the 2007 outbreak on Yap Island in the South Pacific, Aedes hensilli was the vector, while Aedes polynesiensis spread the virus in French Polynesia in 2013.Zika virus can also spread by sexual transmission from infected men to their partners. Zika virus has been isolated from semen samples, with one person having 100,000 times more virus in semen than blood or urine, two weeks after being infected. | Laboratory analysis found Zika infections in some patients with GBS in Brazil, El Salvador, Suriname and Venezuela, and the WHO declared on 22 March 2016 that Zika appeared to be "implicated" in GBS infection and that if the pattern was confirmed it would represent a global public health crisis. Research
Mechanism
Research has been ongoing to better understand how Zika virus causes microcephaly and other neurological disorders.It may involve infection of the primary neural stem cells of the fetal brain, known as neural progenitor cells. The main roles of brain stem cells are to proliferate until the correct number is achieved, and then to produce neurons through the process of neurogenesis. Zika proteins NS4A and NS4B have also been shown to directly suppress neurogenesis. Infection of brain stem cells can cause cell death, which reduces the production of future neurons and leads to a smaller brain. Zika also appears to have an equal tropism for cells of the developing eye, leading to high rates of eye abnormalities as well.In addition to inducing cell death, infection of neural progenitor cells may alter the process of cell proliferation, causing a depletion in the pool of progenitor cells. A large number of cases of microcephaly have been associated with inherited gene mutations, and specifically with mutations that lead to dysfunction of the mitotic spindle. | 11
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In turn, immune function decreases and infection opportunities increase. One of the most common mutations deletes 28 DNA nucleotides from the C2 gene. Therefore, no C2 protein which can help make C3-convertase is produced. Ultimately, this delays/decreases immune response. C3: In terms of deficiency of C3, it has been found that 17 mutations in the C3 gene cause problems with C3. This rare condition mutates or prevents C3 protein from forming, lowering the immune systems ability to protect. C4: C4 deficiency is highly associated with systemic lupus erythematosus. Aβ42, a protein involved in Alzheimers disease, can cause activation of C4 (even in plasma deficient of C1q). At least one study indicates that the genetic variation of C4 plays a role in schizophrenia. Diagnosis
The diagnostic tests used to diagnose a complement deficiency include:
CH50 measurement
Immunochemical methods/test
C3 deficiency screening
Mannose-binding lectin (lab study)
Plasma levels/regulatory proteins (lab study)
Types
Disorders of the proteins that act to inhibit the complement system (such as C1-inhibitor) can lead to an overactive response, causing conditions such as hereditary angioedema. Disorders of the proteins that act to activate the complement system (such as C3) can lead to an underactive response, causing greater susceptibility to infections. Treatment
In terms of management for complement deficiency, immunosuppressive therapy should be used depending on the disease presented. A C1-INH concentrate can be used for angio-oedema (C1-INH deficiency).Pneumococcus and Haemophilus infections can be prevented via immunization. Epsilon-aminocaproic acid could be used to treat hereditary C1-INH deficiency, though the possible side effect of intravascular thrombosis should be weighed. | In February 2018, the funding was approved for people under 18 years old.In August 2018, the National Institute for Health and Care Excellence (NICE), which weighs the cost-effectiveness of therapies for the NHS in England and Wales, recommended against offering nusinersen to people with SMA. Children with SMA type 1 were treated in the UK under a Biogen-funded expanded access programme; after enrolling 80 children, the scheme closed to new people in November 2018. In May 2019, however, NICE reversed its stance and announced its decision to recommend nusinersen for use across a wide spectrum of SMA for a 5-year period.The Irish Health Service Executive decided in February 2019 that nusinersen was too expensive to fund, saying the cost would be about €600,000 per patient in the first year and around €380,000 a year thereafter "with an estimated budget impact in excess of €20 million over a five-year period" for the 25 children with SMA living in Ireland. Both the manufacturer and patient groups disputed the numbers and pointed out that actual pricing arrangements for Ireland are in line with the negotiated price for the BeneluxA initiative which Ireland has been a member of since June 2018.As of May 2019, nusinersen was available in public healthcare in more than 40 countries.In December 2021, nusinersen was included in the extended insurance coverage of China, and the price was reduced from ¥697,000 per vial to around ¥33,000 (~US$5,100) per vial. References
Further reading
External links
"Cut and Paste: Treating Spinal Muscular Atrophy with Nusinersen". Youreka Science. Retrieved 2019-05-28. | 0-1
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Congenital dyserythropoietic anemia type IV (CDA IV) has been described with typical morphologic features of CDA II but a negative acidified-serum test. Presentation
CDA type IV is characterized by mild to moderate splenomegaly. Hemoglobin is very low and patients are transfusion dependent. MCV is normal or mildly elevated. Erythropoiesis is normoblastic or mildly to moderately megaloblastic. Nonspecific erythroblast dysplasia is present. Genetics
Congenital dyserythropoietic anemia type IV is an autosomal dominant inherited red blood cell disorder characterized by ineffective erythropoiesis and hemolysis resulting in anemia. Circulating erythroblasts and erythroblasts in the bone marrow show various morphologic abnormalities. Affected individuals with CDAN4 also have increased levels of fetal hemoglobin. Diagnosis
Treatment
Treatment consists of frequent blood transfusions and chelation therapy. Potential cures include bone marrow transplantation and gene therapy. See also
Congenital dyserythropoietic anemia
Thalassemia
Hemoglobinopathy
List of hematologic conditions
References
Further reading
Congenital dyserythropoietic anemia at the US National Institutes of Health Home Genetic Reference]
== External links == | An abscess of the thymus (also known as "Dubois abscesses") is a condition that is one of many possible causes of cysts in the mediastinum. It can present with chest pain behind the sternum.It can be associated with congenital syphilis.Although the thymus is usually classified with the immune system, thymic diseases are classified with endocrine disorders in ICD-9 and ICD-10. References
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In 2017, azithromycin was the second most prescribed antibiotic for outpatients in the United States. Research
COVID-19
Despite early evidence showing azithromycin slowed down coronavirus multiplication in laboratory settings, further research indicates it to be ineffective as a treatment for COVID-19 in humans. After a large-scale trial showed no benefit of using azithromycin in treating COVID-19, the UKs National Institute for Health and Care Excellence (NICE) updated its guidance and no longer recommends the medication for COVID-19. References
External links
"Azithromycin". Drug Information Portal. U.S. National Library of Medicine. | Etravirine (ETR, brand name Intelence, formerly known as TMC125) is a drug used for the treatment of HIV. Etravirine is a non-nucleoside reverse transcriptase inhibitor (NNRTI). Unlike the currently available agents in the class, resistance to other NNRTIs does not seem to confer resistance to etravirine. Etravirine is marketed by Janssen, a subsidiary of Johnson & Johnson. In January 2008, the Food and Drug Administration approved its use for patients with established resistance to other drugs, making it the 30th anti-HIV drug approved in the United States and the first to be approved in 2008. It was also approved for use in Canada on April 1, 2008.Etravirine is licensed in the United States, Canada, Israel, Russia, Australia and the European Union, and is under regulatory review in Switzerland. Indications and dosage
Etravirine, in combination with other anti-retrovirals, is indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in antiretroviral treatment-experienced adult patients, who have evidence of viral replication and HIV-1 strains resistant to a non-nucleoside reverse transcriptase inhibitor (NNRTI) and other antiretroviral agents. The recommended dose of etravirine is 200 mg (2 x 100 mg tablets, or 1 x 200 mg tablet as of 03/18/2011) taken twice daily following a meal. The type of food does not affect the exposure to etravirine. Contraindication
Each 100 mg etravirine tablet contains 160 mg of lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine. | 0-1
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Transient, stress-related paranoid or severe dissociative symptoms.Overall, the most distinguishing symptoms of BPD are pervasive patterns of instability in interpersonal relationships and self-image, alternating between extremes of idealization and devaluation of others, along with varying moods and difficulty regulating strong emotional reactions. Dangerous or impulsive behavior is also correlated with the disorder. Other symptoms may include feeling unsure of ones identity, morals, and values; having paranoid thoughts when feeling stressed; depersonalization; and, in moderate to severe cases, stress-induced breaks with reality or psychotic episodes. Individuals with BPD often have comorbid conditions, such as depressive and bipolar disorders, substance use disorders, eating disorders, post-traumatic stress disorder, and attention-deficit/hyperactivity disorder. Emotions
People with BPD may feel emotions with greater ease and depth and for a longer time than others do. A core characteristic of BPD is affective instability, which generally manifests as unusually intense emotional responses to environmental triggers, with a slower return to a baseline emotional state. According to Marsha Linehan, the sensitivity, intensity, and duration with which people with BPD feel emotions have both positive and negative effects. People with BPD are often exceptionally enthusiastic, idealistic, joyful, and loving, but may feel overwhelmed by negative emotions (anxiety, depression, guilt/shame, worry, anger, etc. ), experiencing intense grief instead of sadness, shame and humiliation instead of mild embarrassment, rage instead of annoyance, and panic instead of nervousness. Studies have shown that borderline patients experience chronic and significant emotional suffering and mental agony.People with BPD are also especially sensitive to feelings of rejection, criticism, isolation, and perceived failure. | Necrotizing bronchiolitis is an acute inflammatory lesion of the lower airway, a potential complication of mechanical ventilation. == References == | 0-1
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Research has demonstrated that by training the muscles around the knee appropriately through exercise treatment, the body can learn to control the knee again, and despite extra movement inside the knee, the knee can feel strong and able to withstand force.Typically, this approach involves visiting a physical therapist or sports medicine professional soon after injury to oversee an intensive, structured program of exercises. Other treatments may be used initially such as hands-on therapies in order to reduce pain. The physiotherapist will act as a coach through rehabilitation, usually by setting goals for recovery and giving feedback on progress. Estimated non-surgical recovery timeframe is 3–6 months and depends on the extent of the original injury, pre-existing fitness and commitment to the rehabilitation and sporting goals. Some may not be satisfied with the outcome of non-surgical management and may opt for surgery later. Surgery
ACL reconstruction surgery involves replacing the torn ACL with a "graft," which is a tendon taken from another source. Grafts can be taken from the patellar tendon, hamstring tendon, quadriceps tendon from either the person undergoing the procedure ("autograft") or a cadaver ("allograft"). The graft serves as scaffolding upon which new ligament tissue will grow.The surgery is done with an arthroscope or tiny camera inserted inside the knee, with additional small incisions made around the knee to insert surgical instruments. | Among high school girls in the US, the sport with the highest risk of ACL tear is soccer, followed by basketball and lacrosse. In the US womens basketball and soccer experience the most ACL tears then all other sports. The highest risk sport for high school boys in the US was basketball, followed by lacrosse and soccer. In basketball, women are 5-8 times more likely to experience an ACL tear then men. Dogs
Cruciate ligament rupture is a common orthopedic disorder in dogs. A study of insurance data showed the majority of the breeds with increased risk of cruciate ligament rupture were large or giant. References
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Parentheses indicate location in body
LigamentsAnterior cruciate ligament (knee), medial collateral ligament (knee), ulnar collateral ligaments (wrist/hand), interspinous ligaments (vertebrae)MusclesBiceps brachii (upper arm), rectus femoris (thigh), transverse abdominis (abdominals)TendonsPatellar tendon (knee), calcaneal/Achilles tendon (foot/lower leg), biceps tendon (shoulder/elbow)NervesBrachial plexus (shoulder), ulnar nerve (elbow/hand), peroneal nerve (ankle/foot), cranial nerves I-XII(head)BonesFemur (leg), humerus (arm), ribs (torso), metatarsals I-VI (foot), metacarpals I-VI (hand)CartilageMenisci (knee), intervertebral discs (spine), acetabulum (hip)
Management
RICE method
The RICE method is an effective procedure used in the initial treatment of a soft tissue injury. Rest
It is suggested that the patient take a break from the activity that caused the injury in order to give the injury time to heal. Ice
The injury should be iced on and off in 20 minute intervals, avoiding direct contact of the ice with the skin. Compression
Bandaging the injury will compress it, and prevent any further bleeding or swelling from occurring. Elevation
Elevating the injury above the heart while resting will aid in the reduction of swelling. No HARM protocol
This mnemonic indicates what not to do within the first 48–72 hours after the injury in order to speed up the recovery process. Heat
Applying heat to the injured area can cause blood flow and swelling to increase. Alcohol
Alcohol can inhibit the ability to feel if the injury is becoming more aggravated, as well as increasing blood flow and swelling. Re-injury
Avoid any activities that could aggravate the injury and cause further damage. Massage
Massaging an injured area can promote blood flow and swelling, and potentially cause more damage if done too early. | "Fountains syndrome: mental retardation, sensorineural deafness, skeletal abnormalities, and coarse face with full lips". J Med Genet. 26 (11): 722–724. doi:10.1136/jmg.26.11.722. PMC 1015742. PMID 2585470. Fryns JP, Dereymaeker A, Hoefnagels M, Van den Berghe H (1987). "Mental retardation, deafness, skeletal abnormalities, and coarse face with full lips: confirmation of the Fountain syndrome". Am J Med Genet. 26 (3): 551–555. doi:10.1002/ajmg.1320260307. PMID 3565469. Dunkle Mary (1996). "Fountain Syndrome". NORD. Retrieved 26 April 2012. "Fountain syndrome". Ailments.com. 2000. Retrieved 29 April 2012. "Childrens Health:Fountain syndrome". WebMD. 2011. Retrieved 30 April 2012. External links
Online Mendelian Inheritance in Man (OMIM): 229120 | 0-1
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The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes. UK
In the UK, the Herpes Association (now the Herpes Viruses Association) was started in 1982, becoming a registered charity with a Dept of Health grant in 1985. The charity started as a string of local group meetings before acquiring an office and a national spread. Research
Research has gone into vaccines for both prevention and treatment of herpes infections. Unsuccessful clinical trials have been conducted for some glycoprotein subunit vaccines. As of 2017, the future pipeline includes several promising replication-incompetent vaccine proposals while two replication-competent (live-attenuated) HSV vaccine are undergoing human testing.A genomic study of the herpes simplex type 1 virus confirmed the human migration pattern theory known as the out-of-Africa hypothesis. References
External links
Herpes simplex at Curlie | Sensory neurons lose the ability to transmit signals, while motor neurons has reduced ability to transmit signals.Genes related to Hereditary sensory and autonomic neuropathy Type 1:
Mutations in the SPTLC1 gene cause hereditary sensory neuropathy type 1. The SPTLC1 gene provides instructions for making one part (subunit) of an enzyme called serine palmitoyltransferase (SPT). The SPT enzyme is involved in making certain fats called sphingolipids. Sphingolipids are important components of cell membranes and play a role in many cell functions. SPTLC1 gene mutations reduce the amount of SPTLC1 subunit that is produced and result in an SPT enzyme with decreased function. A lack of functional SPT enzyme leads to a decrease in sphingolipid production and a harmful buildup of certain byproducts. Sphingolipids are found in myelin, which is the covering that protects nerves and promotes the efficient transmission of nerve impulses. A decrease in sphingolipids disrupts the formation of myelin, causing nerve cells to become less efficient and eventually die. When sphingolipids are not made, an accumulation of toxic byproducts can also lead to nerve cell death. This gradual destruction of nerve cells results in loss of sensation and muscle weakness in people with hereditary sensory neuropathy type 1. Type 2, Congenital sensory neuropathy
Hereditary sensory and autonomic neuropathy type II (HSAN2) is a condition that primarily affects the sensory nerve cells (sensory neurons) which transmit information about sensations such as pain, temperature, and touch. These sensations are impaired in people with HSAN2. | 0-1
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Acute erythrocyte leukemia is a rare form of acute myeloid leukemia (less than 5% of AML cases) where the myeloproliferation is of erythrocytic precursors. It is defined as type "M6" under the FAB classification. Signs and symptoms
The most common symptoms of AEL are related to pancytopenia (a shortage of all types of blood cells), including fatigue, infections, and mucocutaneous bleeding. Almost half of people with AEL exhibit weight loss, fever and night sweats at the time of diagnosis. Almost all people with AEL are anemic, and 77% have a hemoglobin level under 10.0 g/dl. Signs of thrombocytopenia are found in about half of people with AEL. Causes
The causes of AEL are unknown. Prior to a 2008 reclassification by the World Health Organization, cases that evolved from myelodysplastic syndromes, myeloproliferative neoplasms, chemotherapy for other cancers or exposure to toxins were defined as secondary AEL. These cases are now likely to instead be classified as acute myeloid leukemia with myelodysplasia-related changes or therapy-related AML. +
Diagnosis
Acute erythroid leukemias can be classified as follows:
M6a (Erythroleukemia)
50% or more of all nucleated bone marrow cells are erythroblasts, dyserythropoiesis is prominent and 20% or more of the remaining cells (non- erythroid) are myeloblasts. M6b (Pure erythroid leukemia)
In rare cases the erythroid lineage is the only obvious component of an acute leukemia; a myeloblast component is not apparent. The erythroid component consists predominantly or exclusively of proerythroblasts and early basophilic erythroblasts. These cells may constitute 90% or more of the marrow elements. | Chorditis is the inflammation of vocal cords (vocal folds) usually as a result of voice abuse but sometimes because of cancer. Types
Chorditis fibrinosa
Chorditis nodosa
Chorditis tuberosa
See also
Vocal fold nodule
References
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Copper toxicity (or Copperiedus) is a type of metal poisoning caused by an excess of copper in the body. Copperiedus could occur from consuming excess copper salts, but most commonly it is the result of the genetic condition Wilsons disease and Menkes disease, which are associated with mismanaged transport and storage of copper ions. Copper is essential to human health as it is a component of many proteins. Chronic toxicity by copper is "rare". The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 1.3 mg/L. So rare is the toxicity of copper that copper(II) sulfate is a routine reagent in undergraduate chemistry laboratories. Signs and symptoms
Acute symptoms of copper poisoning by ingestion include vomiting, hematemesis (vomiting of blood), hypotension (low blood pressure), melena (black "tarry" feces), coma, jaundice (yellowish pigmentation of the skin), and gastrointestinal distress. Individuals with glucose-6-phosphate dehydrogenase deficiency may be at increased risk of hematologic effects of copper. Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent.Chronic (long-term) copper exposure can damage the liver and kidneys. Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels.Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research on the function of the Cu/Zn ratio in neurological, endocrinological, and psychological conditions. | Acropachy is a dermopathy associated with Graves disease. It is characterized by soft-tissue swelling of the hands and clubbing of the fingers. Radiographic imaging of affected extremities typically demonstrates periostitis, most commonly the metacarpal bones. The exact cause is unknown, but it is thought to be caused by stimulating auto-antibodies that are implicated in the pathophysiology of Graves thyrotoxicosis. There is no effective treatment for acropachy. Since it is closely associated with Graves disease, it is associated with other manifestations of Graves disease, such as Graves ophthalmopathy and thyroid dermopathy.Hereditary acropachy (also known as "isolated congenital nail clubbing") may be associated with HPGD. See also
Periosteal reaction
References
External links
Radiopaedia.org: Thyroid acropachy | 0-1
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Ranolazine, sold under the brand name Ranexa among others, is a medication used to treat heart related chest pain. Typically it is used together with other medications when those are insufficient. Benefits appear smaller in women than men. It is taken by mouth.Common side effects include constipation, headache, nausea, and dizziness. Serious side effects may include QT prolongation. Use is not recommended in those with liver cirrhosis. How it works is not clear but may involve adenosine triphosphate.Ranolazine was approved for medical use in the United States in 2006. In 2019, it was the 211th most commonly prescribed medication in the United States, with more than 2 million prescriptions. Medical uses
Ranolazine is used to treat chronic angina. It may be used concomitantly with β blockers, nitrates, calcium channel blockers, antiplatelet therapy, lipid-lowering therapy, ACE inhibitors, and angiotensin receptor blockers. It is also effective at preventing atrial fibrillation, and has been studied as monotherapy as well as in combination with other medications used to treat irregular heartbeat.Its use is not recommended in Scotland as of 2019. Contraindications
Some contraindications for ranolazine are related to its metabolism and are described under Drug Interactions. Additionally, in clinical trials ranolazine slightly increased QT interval in some patients and the FDA label contains a warning for doctors to beware of this effect in their patients. The drugs effect on the QT interval is increased in the setting of liver dysfunction; thus it is contraindicated in persons with mild to severe liver disease. | Physical abuse can be detected by visible signs on the body including bruises, scratches, scars, sprains, or broken bones. More subtle indications of physical abuse include signs of restraint such as rope marks on the wrist or broken eyeglasses. Emotional abuse often accompanies the other types of abuse and can usually be detected by changes in the persons personality or behavior. The elder may also exhibit behavior mimicking dementia, such as rocking or mumbling. Emotional abuse is the most under reported abuse of elder abuse. Elder abuse occurs when a person fails to treat an elder with respect and includes verbal abuse. The elder experiences social isolation or lack of acknowledgement in this type of abuse. Some indicators of the emotional effects of elder abuse is the elder adult being unresponsive or uncommunicative. Also they can be unreasonably suspicious or fearful, more isolated, and not wanting to be as social as they may have been before. Emotional abuse is under reported but can have the most damaging effects because it leads to more physical and mental health problems. Financial exploitation is a more subtle form of abuse, in comparison to other types, and may be more challenging to notice. Signs of financial exploitation include significant withdrawals from accounts, belongings or money missing from the home, unpaid bills, and unnecessary goods or services. Sexual abuse, like physical abuse, can be detected by visible signs on the body, especially around the breasts or genital area. Other signs include inexplicable infections, bleeding, and torn underclothing. | 0-1
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Altitude sickness, the mildest form being acute mountain sickness (AMS), is the harmful effect of high altitude, caused by rapid exposure to low amounts of oxygen at high elevation. People can respond to high altitude in different ways. Symptoms may include headaches, vomiting, tiredness, confusion, trouble sleeping, and dizziness. Acute mountain sickness can progress to high-altitude pulmonary edema (HAPE) with associated shortness of breath or high-altitude cerebral edema (HACE) with associated confusion. Chronic mountain sickness may occur after long-term exposure to high altitude.Altitude sickness typically occurs only above 2,500 metres (8,000 ft), though some are affected at lower altitudes. Risk factors include a prior episode of altitude sickness, a high degree of activity, and a rapid increase in elevation. Diagnosis is based on symptoms and is supported in those who have more than a minor reduction in activities. It is recommended that at high altitude any symptoms of headache, nausea, shortness of breath, or vomiting be assumed to be altitude sickness.Prevention is by gradually increasing elevation by no more than 300 metres (1,000 ft) per day. Being physically fit does not decrease the risk. Treatment is generally by descending and sufficient fluids. Mild cases may be helped by ibuprofen, acetazolamide, or dexamethasone. Severe cases may benefit from oxygen therapy and a portable hyperbaric bag may be used if descent is not possible. Treatment efforts, however, have not been well studied.AMS occurs in about 20% of people after rapidly going to 2,500 metres (8,000 ft) and 40% of people going to 3,000 metres (10,000 ft). | History
The original name of dimercaprol reflects its origins as a compound secretly developed by British biochemists at Oxford University during World War II as an antidote for lewisite, a now-obsolete arsenic-based chemical warfare agent. See also
EDTA
2,3-Dimercapto-1-propanesulfonic acid
Dimercaptosuccinic acid
DMSA scan
Penicillamine
Heavy metal poisoning
References
External links
"Dimercaprol". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Pregnancy and breast feeding
Its use during pregnancy is contraindicated, although it has been placed in Australian pregnancy category C. Its use during the first trimester (during organogenesis) and 12 weeks prior to pregnancy has been associated with an increased risk of congenital malformations, especially malformations associated with maternal folic acid deficiency (which is most likely related to the mechanism of action of co-trimoxazole) such as neural tube defects such as spina bifida, cardiovascular malformations (e.g. Ebsteins anomaly), urinary tract defects, oral clefts, and club foot in epidemiological studies. Its use later on during pregnancy also increases the risk of preterm labour (odds ratio: 1.51) and low birth weight (odds ratio: 1.67). Animal studies have yielded similarly discouraging results.It appears to be safe for use during breastfeeding as long as the baby is healthy. Babies
Its use in those less than 2 months of age is not recommended due to the risk of adverse side effects. Adverse effects
Common side effects include nausea, vomiting, rash, and diarrhea. Severe allergic reactions and Clostridium difficile infection may occasionally occur. Its use in pregnancy is not recommended. It appears to be safe for use during breastfeeding as long as the baby is healthy. Trimethoprim/sulfamethoxazole generally results in bacterial death. It works by blocking the making and use of folate by the microorganisms. Contraindications
Contraindications include the following:
Interactions
Its use is advised against in people being concomitantly treated with:
Overdose
Likely signs of toxicity include:
The recommended treatment for overdose includes:
Administration of activated charcoal
Stomach pumping
General supportive measures
Haemodialysis, which is moderately effective in clearing co-trimoxazole from the plasma. | Trimethoprim/sulfamethoxazole, sold under the brand name Bactrim among others, is a fixed-dose combination antibiotic medication used to treat a variety of bacterial infections. It consists of one part trimethoprim to five parts sulfamethoxazole. It is used to treat urinary tract infections, methicillin-resistant Staphylococcus aureus (MRSA) skin infections, travelers diarrhea, respiratory tract infections, and cholera, among others. It is used both to treat and prevent pneumocystis pneumonia and toxoplasmosis in people with HIV/AIDS and other causes of immunosuppression. It can be given by mouth or intravenously.Trimethoprim/sulfamethoxazole is on the World Health Organizations List of Essential Medicines and is also available as a generic medication. In 2019, it was the 100th most commonly prescribed medication in the United States, with more than 6 million prescriptions. Medical uses
Pneumocystis jirovecii pneumonia
Trimethoprim/sulfamethoxazole (TMP/SMX) is the medicine most commonly used to prevent Pneumocystis jirovecii pneumonia (PCP) People who get Pneumocystis pneumonia have a medical condition that weakens their immune system, like HIV/AIDS, or take medicines (such as corticosteroids) that reduce the bodys ability to fight bacterial and viral infections. People with HIV/AIDS are less likely to get Pneumocystis pneumonia as a result of antiretroviral therapy (ART). However, Pneumocystis pneumonia is still a substantial public health problem. Most of what is scientifically known about Pneumocystis pneumonia and its treatment comes from studying people with HIV/AIDS. Susceptibility
Organisms against which trimethoprim/sulfamethoxazole can be effective include:
The only notable nonsusceptible organisms are Pseudomonas aeruginosa, the mycoplasmae and Francisella tularensis (the causative organism of tularaemia). | 11
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Side effects
At oral doses of 400 mg per day or higher, amiodarone can have serious, varied side effects, including toxicity to thyroid, liver, lung, and retinal functions, requiring clinical surveillance and regular laboratory testing. Allergic reactions to amiodarone may occur. Most individuals administered amiodarone on a chronic basis will experience at least one side effect. In some people, daily use of amiodarone at 100 mg oral doses can be effective for arrhythmia control with no or minimal side effects. Lung
Side effects of oral amiodarone at doses of 400 mg or higher include various pulmonary effects. The most serious reaction is interstitial lung disease. Risk factors include high cumulative dose, more than 400 milligrams per day, duration over two months, increased age, and preexisting pulmonary disease. Some individuals were noted to develop pulmonary fibrosis after a week of treatment, while others did not develop it after years of continuous use. Common practice is to avoid the agent if possible in individuals with decreased lung function. The most specific test of pulmonary toxicity due to amiodarone is a dramatically decreased DLCO noted on pulmonary function testing. Thyroid
Induced abnormalities in thyroid function are common. Both under- and overactivity of the thyroid may occur. Amiodarone is structurally similar to thyroxine and also contains iodine. Both of these contribute to the effects of amiodarone on thyroid function. | Congenital megaesophagus is usually identified when a foal begins to eat solid food from the ground; prior to this, as the foal nurses milk from its mother, the milk passes easily down into the stomach. The most common signs are difficulty swallowing (dysphagia) and inhalational pneumonia. References
External links
Canine megaesophagus | 0-1
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An antacid is a substance which neutralizes stomach acidity and is used to relieve heartburn, indigestion or an upset stomach. Some antacids have been used in the treatment of constipation and diarrhea. Marketed antacids contain salts of aluminum, calcium, magnesium, or sodium. Some preparations contain a combination of two salts, such as magnesium carbonate and aluminium hydroxide (e.g. hydrotalcite). Medical uses
Antacids are available over the counter and are taken by mouth to quickly relieve occasional heartburn, the major symptom of gastroesophageal reflux disease and indigestion. Treatment with antacids alone is symptomatic and only justified for minor symptoms. Alternative uses for antacids include constipation, diarrhea, hyperphosphatemia, and urinary alkalization. Some antacids are also used as an adjunct to pancreatic enzyme replacement therapy in the treatment of pancreatic insufficiency.Non-particulate antacids (sodium citrate, magnesium trisilicate) increase gastric pH with little or no effect on gastric volume, and therefore may see some limited use in pre-operative procedures. Sodium citrate should be given within 1 hour of surgery to be the most effective. Side effects
Conventional effervescent tablets contain a significant amount of sodium and are associated with increased odds of adverse cardiovascular events according to an 2013 study. Alternative sodium-free formulations containing magnesium salts may cause diarrhea, whereas those containing calcium or aluminum may cause constipation. Rarely, long-term use of calcium carbonate may cause kidney stones. Long-term use of antacids containing aluminum may increase the risk of developing osteoporosis. | In vitro studies have found a potential for acid rebound to occur due to antacid overuse, however the significance of this finding has been called into question. Properties of antacids
When an excess amount of acid is produced in the stomach, the natural mucous barrier that protects the lining of the stomach can degrade, leading to pain and irritation. There is also potential for the development of acid reflux, which can cause pain and damage to the esophagus. Antacids contain alkaline ions that chemically neutralize stomach gastric acid, reducing damage to the stomach lining and esophagus, and relieving pain. Some antacids also inhibit pepsin, an enzyme that can damage the esophagus in acid reflux.Antacids do not directly inhibit acid secretion, and thus are distinct from acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors. Antacids do not kill the bacteria Helicobacter pylori, which causes most ulcers. Interactions
Antacids are known to interact with several oral medications, including fluoroquinolone and tetracycline antibiotics, iron, itraconazole, and prednisone. Metal chelation is responsible for some of these interactions (e.g. fluoroquinolones, tetracyclines), leading to decreased absorption of the chelated drug. Some interactions may be due to the pH increase observed in the stomach following antacid ingestion, leading to increased absorption of weak acids, and decreased absorption of weak bases. | 11
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Thus, non secretive adenomas may be either null cell adenomas or a more specific adenoma that, however, remains non-secretive. Any type of pituitary adenocarcinoma listed in the table below may cause compressive symptoms due to local expansion in addition to the systemic effects of secreted hormones listed in the pathology column. Null cell adenomas by definition do not secrete hormones, but they commonly cause compressive effects on the pituitary stalk (stalk effect). This leads to decreased levels of dopamine from the hypothalamus reaching the anterior pituitary gland. Dopamine exerts an inhibitory effect on prolactin secretion. With the absence of this inhibitory effect, prolactin levels increase and are often increased in null cell adenomas. This leads to symptoms of hypogonadism. Pituitary incidentalomas
Pituitary incidentalomas are pituitary tumors that are characterized as an incidental finding. They are often discovered by computed tomography (CT) or magnetic resonance imaging (MRI), performed in the evaluation of unrelated medical conditions such as suspected head trauma, in cancer staging or in the evaluation of nonspecific symptoms such as dizziness and headache. It is not uncommon for them to be discovered at autopsy. In a meta-analysis, adenomas were found in an average of 16.7% in postmortem studies, with most being microadenomas (<10mm); macrodenomas accounted for only 0.16% to 0.2% of the decedents. | Pituitary adenomas are benign tumors that occur in the pituitary gland. Most pituitary tumors are benign, approximately 35% are invasive and just 0.1% to 0.2% are carcinomas. Pituitary adenomas represent from 10% to 25% of all intracranial neoplasms and the estimated prevalence rate in the general population is approximately 17%.Non-invasive and non-secreting pituitary adenomas are considered to be benign in the literal as well as the clinical sense; however a recent meta-analysis (Fernández-Balsells, et al. 2011) of available research has shown there are to date scant studies – of poor quality – to either support or refute this assumption. Adenomas exceeding 10 mm (0.39 in) in size are defined as macroadenomas, with those smaller than 10 mm (0.39 in) referred to as microadenomas. Most pituitary adenomas are microadenomas and have an estimated prevalence of 16.7% (14.4% in autopsy studies and 22.5% in radiologic studies). A majority of pituitary microadenomas often remain undiagnosed, and those that are diagnosed are often found as an incidental finding and are referred to as incidentalomas. Pituitary macroadenomas are the most common cause of hypopituitarism.While pituitary adenomas are common, affecting approximately one in 6 of the general population, clinically active pituitary adenomas that require surgical treatment are more rare, affecting approximately one in 1,000 of the general population. Signs and symptoms
Physical
Hormone secreting pituitary adenomas cause one of several forms of hyperpituitarism. The specifics depend on the type of hormone. | 11
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A positron emission tomography (PET) study found that brain occupancy of the H1 receptor was 12.6% for 10 mg cetirizine, 25.2% for 20 mg cetirizine, and 67.6% for 30 mg hydroxyzine. (A 10 mg dose of cetirizine equals about a 30 mg dose of hydroxyzine in terms of peripheral antihistamine effect.) PET studies with antihistamines have found that brain H1 receptor occupancy of more than 50% is associated with a high prevalence of somnolence and cognitive decline, whereas brain H1 receptor occupancy of less than 20% is considered to be non-sedative. In accordance, H1 receptor occupancy correlated well with subjective sleepiness for 30 mg hydroxyzine but there was no correlation for 10 or 20 mg cetirizine. As such, brain penetration and brain H1 receptor occupancy by cetirizine are dose-dependent, and in accordance, while cetirizine at doses of 5 to 10 mg have been reported to be non-sedating or mildly sedating, a higher dose of 20 mg has been found to induce significant drowsiness in other studies.Cetirizine also shows anti-inflammatory properties independent of H1 receptors. The effect is exhibited through suppression of the NF-κB pathway, and by regulating the release of cytokines and chemokines, thereby regulating the recruitment of inflammatory cells. It has been shown to inhibit eosinophil chemotaxis and LTB4 release. At a dosage of 20 mg, Boone et al. found that it inhibited the expression of VCAM-1 in patients with atopic dermatitis. Pharmacokinetics
Absorption
Cetirizine is rapidly and extensively absorbed upon oral administration in tablet or syrup form. | Some acne and wrinkle treatments reported to cause rosacea include microdermabrasion and chemical peels, as well as high dosages of isotretinoin, benzoyl peroxide, and tretinoin. Steroid-induced rosacea is caused by the use of topical steroids. These steroids are often prescribed for seborrheic dermatitis. Dosage should be slowly decreased and not immediately stopped to avoid a flare-up. Cathelicidins
In 2007, Richard Gallo and colleagues noticed that patients with rosacea had high levels of the antimicrobial peptide cathelicidin and elevated levels of stratum corneum tryptic enzymes (SCTEs). Antibiotics have been used in the past to treat rosacea, but they may only work because they inhibit some SCTEs. Demodex folliculitis and Demodex mites
Studies of rosacea and Demodex mites have revealed that some people with rosacea have increased numbers of the mite, especially those with steroid-induced rosacea. Demodex folliculitis (demodicidosis, also known as "mange" in animals) is a condition that may have a "rosacea-like" appearance.A 2007, National Rosacea Society-funded study demonstrated that Demodex folliculorum mites may be a cause or exacerbating factor in rosacea. The researchers identified Bacillus oleronius as distinct bacterium associated with Demodex mites. When analyzing blood samples using a peripheral blood mononuclear cell proliferation assay, they discovered that B. oleronius stimulated an immune system response in 79 percent of 22 patients with subtype 2 (papulopustular) rosacea, compared with only 29% of 17 subjects without the disorder. They concluded, "The immune response results in inflammation, as evident in the papules (bumps) and pustules (pimples) of subtype 2 rosacea. | 0-1
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Midodrine is a vasopressor/antihypotensive agent (it raises the blood pressure). Midodrine was approved in the United States by the Food and Drug Administration (FDA) in 1996 for the treatment of dysautonomia and orthostatic hypotension. In August 2010, the FDA proposed withdrawing this approval because the manufacturer, Shire plc, failed to complete required studies after the medicine reached the market. In September 2010, the FDA reversed its decision to remove midodrine from the market and allowed it to remain available to patients while Shire plc collected further data regarding the efficacy and safety of the drug. Shire announced on September 22, 2011, that it was withdrawing completely from supplying midodrine and leaving it to several generics to supply the drug. Medical uses
Midodrine is indicated for the treatment of symptomatic orthostatic hypotension. It can reduce dizziness and faints by about a third, but can be limited by troublesome goose bumps, skin itch, gastrointestinal discomfort, chills, elevated blood pressure while lying down, and urinary retention. A meta-analysis of clinical trials of midodrine or droxidopa in patients with low blood pressure when standing found that midodrine increased standing blood pressure more than droxidopa but that midodrine but not droxidopa increased the risk of high blood pressure when lying down. Small studies have also shown that midodrine can be used to prevent excessive drops in blood pressure in people requiring dialysis.Midodrine has been used in the complications of cirrhosis. | Stereochemistry
Midodrine contains a stereocenter and consists of two enantiomers, making it a racemate; i.e., a 1:1 mixture of (R)- and (S)-forms:
Synthesis
Acylation of 1,4-dimethoxybenzene with chloroacetyl chloride gives the chloroketone 2. The halogen is then converted to the amine 3 by any set of standard schemes, and the ketone reduced to an alcohol with borohydride (4). Acylation of the amino group in this last intermediate with chloroacetyl chloride affords the amide 5. The halogen is then displaced with azide and the resulting product 6 reduced catalytically to the glycinamide, midodrine (7). References
External links
Media related to Midodrine at Wikimedia Commons
"Midodrine". Drug Information Portal. U.S. National Library of Medicine. | 11
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In addition to winds, tornadoes also exhibit changes in atmospheric variables such as temperature, moisture, and pressure. For example, on June 24, 2003, near Manchester, South Dakota, a probe measured a 100-millibar (100 hPa; 3.0 inHg) pressure decrease. The pressure dropped gradually as the vortex approached then dropped extremely rapidly to 850 mbar (850 hPa; 25 inHg) in the core of the violent tornado before rising rapidly as the vortex moved away, resulting in a V-shape pressure trace. Temperature tends to decrease and moisture content to increase in the immediate vicinity of a tornado. Life cycle
Supercell relationship
Tornadoes often develop from a class of thunderstorms known as supercells. Supercells contain mesocyclones, an area of organized rotation a few kilometers/miles up in the atmosphere, usually 1.6–9.7 km (1–6 miles) across. Most intense tornadoes (EF3 to EF5 on the Enhanced Fujita Scale) develop from supercells. In addition to tornadoes, very heavy rain, frequent lightning, strong wind gusts, and hail are common in such storms.Most tornadoes from supercells follow a recognizable life cycle which begins when increasing rainfall drags with it an area of quickly descending air known as the rear flank downdraft (RFD). This downdraft accelerates as it approaches the ground, and drags the supercells rotating mesocyclone towards the ground with it. Formation
As the mesocyclone lowers below the cloud base, it begins to take in cool, moist air from the downdraft region of the storm. The convergence of warm air in the updraft and cool air causes a rotating wall cloud to form. | Roflumilast, sold under the trade name Daxas among others, is a drug that acts as a selective, long-acting inhibitor of the enzyme phosphodiesterase-4 (PDE-4). It has anti-inflammatory effects and is used as an orally administered drug for the treatment of inflammatory conditions of the lungs such as chronic obstructive pulmonary disease (COPD).In June 2010, it was approved in the European Union for severe COPD associated with chronic bronchitis. In February 2011, it gained FDA approval in the United States for reducing COPD exacerbations. Medical uses
Roflumilast is indicated for the treatment of severe chronic obstructive pulmonary disease (COPD) and for the treatment of plaque psoriasis.It is used in the prevention of exacerbations (lung attacks) in severe chronic obstructive pulmonary disease (COPD).A topical formulation of Rolflumilast was recently approved by the U.S. Food and Drug Administration for plaque psoriasis. Adverse effects
Common (1–10% incidence) adverse effects include:
Diarrhea
Weight loss
Nausea
Headache
Insomnia
Decreased appetite
Abdominal pain
Rhinitis
Sinusitis
Urinary tract infection
Depression
References
External links
"Roflumilast". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Their prolonged healthcare imposes a significant cost to the healthcare system and deprives others from receiving their timely healthcare. Studies show that preventive and primary care (which homeless people are not receiving) substantially lower the overall healthcare costs. Unfortunately, in terms of providing adequate treatment to homeless people with respect to their mental illness, the healthcare system’s performance has not been promising, either. It is apparent that a comprehensive solution to homelessness must include an effective approach to providing healthcare to homeless people. Disabilities, especially where disability services are non-existent, inconvenient, or poorly performing can impact a persons ability to support house payments, mortgages, or rent, especially if they are unable to work. Traumatic brain injury is one main disability that can account for homelessness. According to a Canadian survey, traumatic brain injury is widespread among homeless people and, for around 70% of respondents, can be attributed to a time "before the onset of homelessness"Being afflicted with a mental disorder, including substance use disorders, where mental health services are unavailable or difficult to access can also drive homelessness for the same reasons as disabilities. A United States federal survey done in 2005 indicated that at least one-third of homeless men and women have serious psychiatric disorders or problems. Autism spectrum disorders and schizophrenia are the top two common mental disabilities among the U.S. homeless. Personality disorders are also very prevalent, especially Cluster A. | There has been ongoing concern and studies about the health and wellness of the older homeless population, typically ages 50 to 64 and older, as to whether they are significantly more sickly than their younger counterparts, and if they are under-served.A 2011 study led by Dr. Rebecca T. Brown in Boston, conducted by the Institute for Aging Research (an affiliate of Harvard Medical School), Beth Israel Deaconess Medical Center, and the Boston Health Care for the Homeless Program found the elderly homeless population had "higher rates of geriatric syndromes, including functional decline, falls, frailty, and depression than seniors in the general population, and that many of these conditions may be easily treated if detected". The report was published in the Journal of Geriatric Internal Medicine. There are government avenues which provide resources for the development of healthcare for homeless people. In the United States, the Bureau of Primary Health Care has a program that provides grants to fund the delivery of healthcare to homeless people. According to 2011 UDS, data community health centers were able to provide service to 1,087,431 homeless individuals. There are also many nonprofit and religious organizations which provide healthcare services to homeless people. These organizations help meet the large need which exists for expanding healthcare for homeless people. There have been significant numbers of unsheltered persons dying of hypothermia, adding impetus to the trend of establishing warming centers, as well as extending enumeration surveys with vulnerability indexes. | 11
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See also
Germinal center B-cell like diffuse large B-cell lymphoma
References
Sources
Swerdlow SH, Campo E, Jaffe ES, Pileri SA, eds. (2008). WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC. ISBN 978-92-832-2431-0. Goldman L, Schafer AI (2012). Goldmans Cecil Medicine (24th ed.). ISBN 978-1-4377-1604-7. Turgeon ML (2005). Clinical hematology: theory and procedures. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-5007-3. == External links == | The first occurrence of a clinical event characteristic of MS in nearly half of the children examined was 2 years, though in a majority of cases, radiologic evolution, i.e. the increase in the number of size of lesions as detected in subsequent MRI, developed after one year. The presence of oligoclonal bands in the CSF and spinal cord lesions were associated with an increased risk of a first clinical event characteristic of MS. It was found that children with RIS had a substantial risk of subsequent clinical symptoms and/or radiologic evolution. Research directions
Calls have been made for longer prospective studies, tracking the development of potential disease progression over a longer period of time are warranted. This would ensure criteria in RIS is satisfactory and whether consideration should be given to treating individuals with RIS on current MS medication.RIS has been linked to prodromal multiple sclerosis. Etymology
The acronym RIS was coined in 2009 by Okuda and colleagues. Siva and colleagues suggested an alternate name, radiologically uncovered asymptomatic possible inflammatory-demyelinating disease (RAPIDD). == References == | 0-1
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patients on dialysis)
Sleep apnea
Severe depression, particularly when accompanied by suicidal tendencies
Acute intoxication with alcohol, narcotics, or other psychoactive substances
Myasthenia gravis (autoimmune disorder causing muscle weakness)
Hypersensitivity or allergy to any drug in the benzodiazepine class
Special caution needed
Temazepam should not be used in pregnancy, as it may cause harm to the fetus. The safety and effectiveness of temazepam has not been established in children; therefore, temazepam should generally not be given to individuals under 18 years of age, and should not be used at all in children under six months old. Benzodiazepines also require special caution if used in the elderly, alcohol- or drug-dependent individuals, and individuals with comorbid psychiatric disorders.Temazepam, similar to other benzodiazepines and nonbenzodiazepine hypnotic drugs, causes impairments in body balance and standing steadiness in individuals who wake up at night or the next morning. Falls and hip fractures are frequently reported. The combination with alcohol increases these impairments. Partial but incomplete tolerance develops to these impairments. The smallest possible effective dose should be used in elderly or very ill patients, as a risk of apnea and/or cardiac arrest exists. This risk is increased when temazepam is given concomitantly with other drugs that depress the central nervous system (CNS). Misuse and dependence
Because benzodiazepines can be abused and lead to dependence, their use should be avoided in people in certain particularly high-risk groups. These groups include people with a history of alcohol or drug dependence, people significantly struggling with their mood or people with longstanding mental health difficulties. | In the United States, Temazepam is currently a Schedule IV drug under the international Convention on Psychotropic Substances of 1971 and is only available by prescription. Specially coded prescriptions may be required in certain states. References
External links
"Temazepam". Drug Information Portal. U.S. National Library of Medicine. Temazepam | Inchem
Panorama document - 1995 - YouTube video | 11
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The second-generation vaccines are also administered through scarification with a bifurcated needle, and they carry the same side effects as the first-generation vaccinia strain that was cloned. However, the use of eggs or cell culture allows for vaccine production in a sterile environment, while first-generation vaccine contains skin bacteria from the animal that the vaccine was grown on.Ernest William Goodpasture, Alice Miles Woodruff, and G. John Buddingh grew vaccinia virus on the chorioallantoic membrane of chicken embryos in 1932. The Texas Department of Health began producing egg-based vaccine in 1939 and started using it in vaccination campaigns in 1948.: 588 Lederle Laboratories began selling its Avianized smallpox vaccine in the United States in 1959. Egg-based vaccine was also used widely in Brazil, New Zealand, and Sweden, and on a smaller scale in many other countries. Concerns about temperature stability and avian sarcoma leukosis virus prevented it from being used more widely during the eradication campaign, although no increase in leukemia was seen in Brazil and Sweden despite the presence of ASLV in the chickens. : 588 Vaccinia was first grown in cell culture in 1931 by Thomas Milton Rivers. The WHO funded work in the 1960s at the Dutch National Institute for Public Health and the Environment (RVIM) on growing the Lister/Elstree strain in rabbit kidney cells and tested it in 45,443 Indonesian children in 1973, with comparable results to the same strain of calf lymph vaccine. | Case 21 included several children and adults. Crucially all of at least four whom Jenner deliberately inoculated with smallpox virus resisted it. These included the first and last patients in a series of arm-to-arm transfers. He concluded that cowpox inoculation was a safe alternative to smallpox inoculation, but rashly claimed that the protective effect was lifelong. This last proved to be incorrect. Jenner also tried to distinguish between True cowpox which produced the desired result and Spurious cowpox which was ineffective and/or produced severe reaction. Modern research suggests Jenner was trying to distinguish between effects caused by what would now be recognised as non-infectious vaccine, a different virus (e.g. paravaccinia/milkers nodes), or contaminating bacterial pathogens. This caused confusion at the time, but would become important criteria in vaccine development. A further source of confusion was Jenners belief that fully effective vaccine obtained from cows originated in an equine disease, which he mistakenly referred to as grease. This was criticised at the time but vaccines derived from horsepox were soon introduced and later contributed to the complicated problem of the origin of vaccinia virus, the virus in present-day vaccine. : 165–78 The introduction of the vaccine to the New World took place in Trinity, Newfoundland, in 1798 by Dr. John Clinch, boyhood friend and medical colleague of Jenner. The first smallpox vaccine in the United States was administered in 1799. The physician Valentine Seaman gave his children a smallpox vaccination using a serum acquired from Jenner. | 11
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Premature separation of placenta
Placental insufficiency
Intra partum causes
Inadequate relaxation of uterus due to excess oxytocin
Prolonged delivery
Knotting of umbilical cord around the neck of infant
Risk factors
Elderly or young mothers
Prolonged rupture of membranes
Meconium-stained fluid
Multiple births
Lack of antenatal care
Low birth weight infants
Malpresentation
Augmentation of labour with oxytocin
Antepartum hemorrhage
Severe eclampsia and pre-eclampsia
Antepartum and intrapartum anemia
Treatment
A= Establish open airway: Suctioning, if necessary endotracheal intubation
B= Breathing: Through tactile stimulation, PPV, bag and mask, or through endotracheal tube
C= Circulation: Through chest compressions and medications if needed
D= Drugs: Adrenaline .01 of .1 solution
Hypothermia treatment to reduce the extent of brain injury
Epinephrine 1:10000 (0.1-0.3ml/kg) IV
Saline solution for hypovolemia
Epidemiology
A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death. Medicolegal aspects
There is current controversy regarding the medicolegal definitions and impacts of birth asphyxia. Plaintiffs attorneys often take the position that birth asphyxia is often preventable, and is often due to substandard care and human error. They have utilized some studies in their favor that have demonstrated that, "... although other potential causes exist, asphyxia and hypoxic-ihy affect a substantial number of babies, and they are preventable causes of cerebral palsy." The American Congress of Obstetricians and Gynecologists disputes that conditions such as cerebral palsy are usually attributable to preventable causes, instead associating them with circumstances arising prior to birth and delivery. References
== External links == | Tar melanosis is an occupational dermatosis that occurs among tar handlers after several years of exposure, characterized by a severe widespread itching that is soon followed by the appearance of reticular pigmentation, telangiectases, and a shiny appearance of the skin. : 858
See also
Skin lesion
== References == | 0-1
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According to this concept, testicular descent status is "set" during the period from eight to 14 weeks of gestation in humans. Undescended testis is a result of disruption in androgen levels only during this programming window. Mechanism
Normal development
The testes begin as an immigration of primordial germ cells into testicular cords along the gonadal ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the third to fifth months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-Müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia develops during the third and fourth months of gestation and the fetus continues to grow, develop, and differentiate. The testes remain high in the abdomen until the seventh month of gestation when they move from the abdomen through the inguinal canals into the two sides of the scrotum. Movement has been proposed to occur in two phases, under the control of somewhat different factors. The first phase, movement across the abdomen to the entrance of the inguinal canal, appears controlled (or at least greatly influenced) by anti-Müllerian hormone (AMH). The second phase, in which the testes move through the inguinal canal into the scrotum, is dependent on androgens (most importantly testosterone). | Cancer risk
One of the strongest arguments for early orchiopexy is reducing the risk of testicular cancer. About one in 500 men born with one or both testes undescended develops testicular cancer, roughly a four- to 40-fold increased risk. The peak incidence occurs in the third and fourth decades of life. The risk is higher for intra-abdominal testes and somewhat lower for inguinal testes, but even the normally descended testis of a man whose other testis was undescended has about a 20% higher cancer risk than those of other men.The most common type of testicular cancer occurring in undescended testes is seminoma. It is usually treatable if caught early, so urologists often recommend that boys who had orchiopexy as infants be taught testicular self-examination, to recognize testicular masses and seek early medical care for them. Cancer developing in an intra-abdominal testis would be unlikely to be recognized before considerable growth and spread, and one of the advantages of orchiopexy is that a mass developing in a scrotal testis is far easier to recognize than an intra-abdominal mass. Orchidopexy was originally thought to result in easier detection of testicular cancer, but did not lower the risk of actually developing cancer. However, recent data have shown a paradigm shift. | 11
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Parasomnias are a category of sleep disorders that involve abnormal movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or during arousal from sleep. Parasomnias are dissociated sleep states which are partial arousals during the transitions between wakefulness, NREM sleep, and REM sleep, and their combinations. Classification
The newest version of the International Classification of Sleep Disorders (ICSD, 3rd. Ed.) uses State Dissociation as the paradigm for parasomnias. Unlike before, where wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep were considered exclusive states, research has shown that combinations of these states are possible and thus, may result in unusual unstable states that could eventually manifest as parasomnias or as altered levels of awareness.Although the previous definition is technically correct, it contains flaws. The consideration of the State Dissociation paradigm facilitates the understanding of the sleep disorder and provides a classification of 10 core categories. Non-rapid eye movement (NREM)-related parasomnias
NREM parasomnias are arousal disorders that occur during stage 3 (or 4 by the R&K standardization) of NREM sleep—also known as slow wave sleep (SWS). They are caused by a physiological activation in which the patients brain exits from SWS and is caught in between a sleeping and waking state. In particular, these disorders involve activation of the autonomic nervous system, motor system, or cognitive processes during sleep or sleep-wake transitions.Some NREM parasomnias (sleep-walking, night-terrors, and confusional arousal) are common during childhood but decrease in frequency with increasing age. | It can include such acts as masturbation, inappropriate fondling themselves or others, having sex with another person; and in more extreme cases, sexual assault. These behaviors are unconscious, occur frequently without dreaming, and bring along clinical, social, and legal implications. It has a lifetime prevalence of 7.1% and an annual prevalence of 2.7%. Sleepwalking (somnambulism)
Sleepwalking has a prevalence of 1–17% in childhood, with the most frequent occurrences around the age of eleven to twelve. About 4% of adults experience somnambulism. Normal sleep cycles include states varying from drowsiness all the way to deep sleep. Every time an individual sleeps, he or she goes through various sequences of non-REM and REM sleep. Anxiety and fatigue are often connected with sleepwalking. For adults, alcohol, sedatives, medications, medical conditions and mental disorders are all associated with sleepwalking. Sleep walking may involve sitting up and looking awake when the individual is actually asleep, and getting up and walking around, moving items or undressing themselves. They will also be confused when waking up or opening their eyes during sleep. Sleep walking can be associated with sleeptalking. Sleep terrors (night terrors/ pavor nocturnus)
Sleep terror is the most disruptive arousal disorder since it may involve loud screams and panic; in extreme cases, it may result in bodily harm or property damage by running about or hitting walls. All attempts to console the individual are futile and may prolong or intensify their confused state. Usually they experience amnesia after the event but it may not be complete amnesia. | 11
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Prevalence
FGM is mostly found in what Gerry Mackie called an "intriguingly contiguous" zone in Africa—east to west from Somalia to Senegal, and north to south from Egypt to Tanzania. Nationally representative figures are available for 27 countries in Africa, as well as Indonesia, Iraqi Kurdistan and Yemen. Over 200 million women and girls are thought to be living with FGM in those 30 countries.The highest concentrations among the 15–49 age group are in Somalia (98 percent), Guinea (97 percent), Djibouti (93 percent), Egypt (91 percent), and Sierra Leone (90 percent). As of 2013, 27.2 million women had undergone FGM in Egypt, 23.8 million in Ethiopia, and 19.9 million in Nigeria. There is a high concentration in Indonesia, where according to UNICEF Type I (clitoridectomy) and Type IV (symbolic nicking) are practised; the Indonesian Ministry of Health and Indonesian Ulema Council both say the clitoris should not be cut. The prevalence rate for the 0–11 group in Indonesia is 49 percent (13.4 million). : 2 Smaller studies or anecdotal reports suggest that various types of FGM are also practised in various circumstances in Colombia, Jordan, Oman, Saudi Arabia, Malaysia, the United Arab Emirates, and India, but there are no representative data on the prevalence in these countries.Prevalence figures for the 15–19 age group and younger show a downward trend. For example, Burkina Faso fell from 89 percent (1980) to 58 percent (2010); Egypt from 97 percent (1985) to 70 percent (2015); and Kenya from 41 percent (1984) to 11 percent (2014). | Due to the abundance of readily-bound erythrocytes and minimal known metabolism, Brinzolamides whole blood half-life is very long (111 days). Metabolism
While definitive sites of metabolism have not been firmly established, there are several metabolites worthy of note. N-Desethylbrinzolamide is an active metabolite of the parent compound, and thus exhibits carbonic anhydrase inhibitory activity (largely carbonic anhydrase-I, when in the presence of Brinzolamide) and also accumulates in the erythrocytes. However, Brinzolamides other known metabolites (N-Desmethoxypropylbrinzolamide and O-Desmethylbrinzolamide) either have no activity or their activity is currently unknown. Excretion
Brinzolamide is excreted primarily unchanged (60%) in the urine, although the renal clearance rate has not been definitively determined. N-Desethylbrinzolamide is also found in the urine along with lower concentrations of the inactive metabolites, N-Desmethoxypropylbrinzolamide and O-Desmethylbrinzolamide; exact levels have not been definitively determined. Cautions
Side effects
Common, but mild: blurred vision; bitter, sour, or unusual taste; itching, pain, watering, or dryness of the eyes; feeling that something is in the eye; headache; runny nose
Rare, but serious: fast or irregular heartbeat; fainting; skin rash, hives, or itching; severe eye irritation, redness, or swelling; swelling in the face, lips, or throat; wheezing or trouble breathing
Precautions
Hypersensitivity to other sulfonamides
Acute angle-closure glaucoma
Concomitant administration of oral carbonic anhydrase inhibitors
Moderate-to-severe chronic kidney disease or liver disease
Combinations
With timolol
The combination of brinzolamide with timolol is marketed under the trade name Azarga. This combination may be more effective than either medication alone. With brimonidine
The combination of brinzolamide with brimonidine is marketed under the trade name Simbrinza. This combination may be more effective than either medication alone. References
Further reading
External links
"Brinzolamide". | 0-1
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Chiari 1.5 is a term used when both brainstem and tonsillar herniation through the foramen magnum are present.The diagnosis of a Chiari II malformation can be made prenatally, through ultrasound. Classification
In the late 19th century, Austrian pathologist Hans Chiari described seemingly related anomalies of the hindbrain, the so-called Chiari malformations I, II and III. Later, other investigators added a fourth (Chiari IV) malformation. The scale of severity is rated I – IV, with IV being the most severe. Types III and IV are very rare. Since Dr. Chiaris original descriptions Chiari 0, 1.5, 3.5, and 5 have been described in the medical literature. Types of Chiari malformation
Other conditions sometimes causally associated with Chiari malformation include hydrocephalus, syringomyelia, spinal curvature, tethered spinal cord syndrome, and connective tissue disorders such as Ehlers-Danlos syndrome and Marfan syndrome. Chiari malformation is the most frequently used term for this set of conditions. The use of the term "Arnold–Chiari malformation" has fallen somewhat out of favor over time, although it is used to refer to the type II malformation. Current sources use "Chiari malformation" to describe its four specific types, reserving the term "Arnold-Chiari" for type II only. Some sources still use "Arnold-Chiari" for all four types.Chiari malformation or Arnold–Chiari malformation should not be confused with Budd-Chiari syndrome, a hepatic condition also named for Hans Chiari. In Pseudo-Chiari Malformation, leaking of CSF may cause displacement of the cerebellar tonsils and similar symptoms sufficient to be mistaken for a Chiari I malformation. | Valrubicin (N-trifluoroacetyladriamycin-14-valerate, trade name Valstar) is a chemotherapy drug used to treat bladder cancer. Valrubicin is a semisynthetic analog of the anthracycline doxorubicin, and is administered by infusion directly into the bladder. It was originally launched as Valstar in the U.S. in 1999 for intravesical therapy of Bacille Calmette-Guérin (BCG)-refractory carcinoma in situ of the urinary bladder in patients in whom cystectomy would be associated with unacceptable morbidity or mortality; however, it was voluntarily withdrawn in 2002 due to manufacturing issues. Valstar was relaunched on September 3, 2009. Side effects
Blood in urine
Incontinence
painful or difficult urination
Unusually frequent urination
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These problems are alleviated by a change of gender role and/or physical characteristics.Many transgender and transsexual activists, and many caregivers, note that these problems are not usually related to the gender identity issues themselves, but the social and cultural responses to gender-variant individuals. Some transsexual people reject the counseling that is recommended by the Standards of Care because they do not consider their gender identity to be a cause of psychological problems. Brown and Rounsley noted that "some transsexual people acquiesce to legal and medical expectations in order to gain rights granted through the medical/psychological hierarchy." Legal needs, such as a change of sex on legal documents, and medical needs, such as sex reassignment surgery, are usually difficult to obtain without a doctor or therapists approval. Because of this, some transsexual people feel coerced into affirming outdated concepts of gender to overcome simple legal and medical hurdles. Regrets and detransitions
People who undergo sex reassignment surgery can develop regret for the procedure later in life, largely predicted by a lack of support from family or peers, with data from the 1990s suggesting a rate of 3.8%. In a 2001 study of 232 MTF patients who underwent GRS, none of the patients reported complete regret and only 6% reported partial or occasional regrets. | One person rejected treatment and died because he couldnt afford to pay for it. Boyer collected data on the cost of production and marketing, and found that the largest true cost to payers, $4100/vial, was that of the legal, regulatory and hospital activities involved in selling the drug. Clinical trials contributed $300/vial, and 25% of that had been paid for by government grants. Other costs were the same as in Mexico. References
External links
RxList: Crotalidae Polyvalent Immune Fab (Ovine) | 0-1
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Persistent bacteremia is characterized by the continuous presence of bacteria in the bloodstream. It is usually the result of an infected heart valve, a central line-associated bloodstream infection (CLABSI), an infected blood clot (suppurative thrombophlebitis), or an infected blood vessel graft. Persistent bacteremia can also occur as part of the infection process of typhoid fever, brucellosis, and bacterial meningitis. Left untreated, conditions causing persistent bacteremia can be potentially fatal.Bacteremia is clinically distinct from sepsis, which is a condition where the blood stream infection is associated with an inflammatory response from the body, often causing abnormalities in body temperature, heart rate, breathing rate, blood pressure, and white blood cell count. Treatment
The presence of bacteria in the blood almost always requires treatment with antibiotics. This is because there are high mortality rates from progression to sepsis if antibiotics are delayed.The treatment of bacteremia should begin with empiric antibiotic coverage. Any patient presenting with signs or symptoms of bacteremia or a positive blood culture should be started on intravenous antibiotics. The choice of antibiotic is determined by the most likely source of infection and by the characteristic organisms that typically cause that infection. Other important considerations include the patients history of antibiotic use, the severity of the presenting symptoms, and any allergies to antibiotics. Empiric antibiotics should be narrowed, preferably to a single antibiotic, once the blood culture returns with a particular bacteria that has been isolated. | Finally, Streptococcus bovis is a common cause of bacteremia in patients with colon cancer.Enterococci are an important cause of healthcare-associated bacteremia. These bacteria commonly live in the gastrointestinal tract and female genital tract. Intravenous catheters, urinary tract infections and surgical wounds are all risk factors for developing bacteremia from enterococcal species. Resistant enterococcal species can cause bacteremia in patients who have had long hospital stays or frequent antibiotic use in the past (see antibiotic misuse). Gram negative bacteremia
Gram negative bacterial species are responsible for approximately 24% of all cases of healthcare-associated bacteremia and 45% of all cases of community-acquired bacteremia. In general, gram negative bacteria enter the bloodstream from infections in the respiratory tract, genitourinary tract, gastrointestinal tract, or hepatobiliary system. Gram-negative bacteremia occurs more frequently in elderly populations (65 years or older) and is associated with higher morbidity and mortality in this population.E.coli is the most common cause of community-acquired bacteremia accounting for approximately 75% of cases. E.coli bacteremia is usually the result of a urinary tract infection. Other organisms that can cause community-acquired bacteremia include Pseudomonas aeruginosa, Klebsiella pneumoniae, and Proteus mirabilis. Salmonella infection, despite mainly only resulting in gastroenteritis in the developed world, is a common cause of bacteremia in Africa. It principally affects children who lack antibodies to Salmonella and HIV+ patients of all ages.Among healthcare-associated cases of bacteremia, gram negative organisms are an important cause of bacteremia in the ICU. Catheters in the veins, arteries, or urinary tract can all create a way for gram negative bacteria to enter the bloodstream. | 11
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Spontaneous coronary artery dissection (SCAD) is an uncommon but dangerous condition in which one of the arteries that supply the heart spontaneously develops a blood collection, or hematoma, within the artery wall. This leads to a separation and weakening of the walls of the artery. SCAD is a major cause of heart attacks in young, otherwise healthy women without known risk factors. While the exact cause is not yet known, SCAD is likely related to changes that occur during and after pregnancy, as well as other diseases. These changes lead to the dissection of the wall which restricts blood flow to the heart and causes symptoms. SCAD is often diagnosed in the cath lab with angiography, though more advanced confirmatory tests exist. While the risk of death due to SCAD is low, it has a relatively high rate of recurrence leading to further heart attack-like symptoms in the future. It was first described in 1931. Signs and symptoms
SCAD often presents like a heart attack in young to middle-aged, healthy women. This pattern usually includes chest pain, rapid heartbeat, shortness of breath, sweating, extreme tiredness, nausea, and dizziness. A minority of people with SCAD may also present in cardiogenic shock (2-5%), ventricular arrhythmias (3-11%), or after sudden cardiac death. Pregnancy- and postpartum-associated SCAD generally have worse outcomes compared to other cases. Causes
Risk factors include pregnancy and the postpartum period. Evidence suggests that estrogen- and progesterone-related vascular changes affect the coronary arteries during this period, contributing to SCAD. | Hay fever in Japan is caused primarily by sugi (Cryptomeria japonica) and hinoki (Chamaecyparis obtusa) tree pollen. "Allergy friendly" trees include: female ash, red maple, yellow poplar, dogwood, magnolia, double-flowered cherry, fir, spruce, and flowering plum. Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum pratense). An estimated 90% of people with hay fever are allergic to grass pollen. Weeds: ragweed (Ambrosia), plantain (Plantago), nettle/parietaria (Urticaceae), mugwort (Artemisia Vulgaris), Fat hen (Chenopodium), and sorrel/dock (Rumex)Allergic rhinitis may also be caused by allergy to Balsam of Peru, which is in various fragrances and other products. Genetic factors
The causes and pathogenesis of allergic rhinitis are hypothesized to be affected by both genetic and environmental factors, with many recent studies focusing on specific loci that could be potential therapeutic targets for the disease. Genome-wide association studies (GWAS) have identified a number of different loci and genetic pathways that seem to mediate the bodys response to allergens and promote the development of allergic rhinitis, with some of the most promising results coming from studies involving single-nucleotide polymorphisms (SNPs) in the interleukin-33 (IL-33) gene. The IL-33 protein that is encoded by the IL-33 gene is part of the interleukin family of cytokines that interact with T-helper 2 (Th2) cells, a specific type of T cell. Th2 cells contribute to the bodys inflammatory response to allergens, and specific ST2 receptors, also known as IL1RL1, on these cells bind to the ligand IL-33 protein. | 0-1
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The elemental diet demonstrates a high rate of response (almost 90% in children, 70% in adults), with a rapid relief of symptoms associated with histological remission. This diet involves using amino-acid based liquid formulas for 4-6 wk, followed by the histological evaluation of response. If remission is achieved, foods are slowly reintroduced. Pharmacologic treatment
In patients diagnosed with EoE, a trial of proton-pump inhibitors (PPI), such as esomeprazole 20 mg to 40 mg oral daily or twice daily as a first line therapy is a reasonable option. Nexium®, brand name esomeprazole, may be preferred as these tablets can be dispersed in half a glass of water and drank for those with difficulty swallowing pills. Those who respond to PPI therapy with symptomatic improvement, should have endoscopy with esophageal biopsy should be repeated. If no eosinophils are present in the repeat biopsy, the diagnosis is either acid mediated GERD with eosinophilia or non GERD PPI responsive EoE with unknown mechanism. If both symptoms and eosinophils persists after treatment with PPI, the diagnosis is immune mediated EoE.Medical therapy for immune mediated EoE primarily involves using corticosteroids. Systemic (oral) corticosteroids were one of the first treatment options shown to be effective in patients with EoE. Both clinical and histologic improvement have been noted in approximately 95% of EoE patients using systemic corticosteroids. However, upon discontinuation of therapy, 90% of patients using corticosteroids experience a recurrence in symptoms. | For mild acidosis, an effective fluid is 10% dextrose in ½ normal saline with 20 mEq/L KCl, but if acidosis is severe, 75–100 mEq/L NaHCO3 and 20 mEq/L of K acetate can be substituted for the NaCl and KCl. Metabolic control
Metabolic control often diminishes during and after puberty, as a result of a patient outgrowing their dietary treatment plan. Prognosis
Without adequate metabolic treatment, patients with GSD I have died in infancy or childhood of overwhelming hypoglycemia and acidosis. Those who survived were stunted in physical growth and delayed in puberty because of chronically low insulin levels. Intellectual disability resulting from recurrent, severe hypoglycemia is considered preventable with appropriate treatment. Liver complications have been serious in some patients. Adenomas of the liver can develop in the second decade or later, with a small chance of later malignant transformation to hepatoma or hepatic carcinomas (detectable by alpha-fetoprotein screening). Several children with advanced hepatic complications have improved after liver transplantation. Additional problems reported in adolescents and adults with GSD I have included hyperuricemic gout, pancreatitis, and chronic kidney failure. Despite hyperlipidemia, atherosclerotic complications are uncommon. With diagnosis before serious harm occurs, prompt reversal of acidotic episodes, and appropriate long-term treatment, most children will be healthy. With exceptions and qualifications, adult health and life span may also be fairly good, although lack of effective treatment before the mid-1970s means information on long-term efficacy is limited. Epidemiology
In the United States, GSD I has an incidence of approximately 1 in 50,000 to 100,000 births. | 0-1
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For example, the fermented bean product miso is less likely to produce as much intestinal gas. Some legumes also stand up to prolonged cooking, which can help break down the oligosaccharides into simple sugars. Fermentative lactic acid bacteria such as Lactobacillus casei and Lactobacillus plantarum reduce flatulence in the human intestinal tract.Probiotics (live yogurt, kefir, etc.) are reputed to reduce flatulence when used to restore balance to the normal intestinal flora. Live (bioactive) yogurt contains, among other lactic bacteria, Lactobacillus acidophilus, which may be useful in reducing flatulence. L. acidophilus may make the intestinal environment more acidic, supporting a natural balance of the fermentative processes. L. acidophilus is available in supplements. Prebiotics, which generally are non-digestible oligosaccharides, such as fructooligosaccharide, generally increase flatulence in a similar way as described for lactose intolerance. Digestive enzyme supplements may significantly reduce the amount of flatulence caused by some components of foods not being digested by the body and thereby promoting the action of microbes in the small and large intestines. It has been suggested that alpha-galactosidase enzymes, which can digest certain complex sugars, are effective in reducing the volume and frequency of flatus. The enzymes alpha-galactosidase, lactase, amylase, lipase, protease, cellulase, glucoamylase, invertase, malt diastase, pectinase, and bromelain are available, either individually or in combination blends, in commercial products. The antibiotic rifaximin, often used to treat diarrhea caused by the microorganism E. coli, may reduce both the production of intestinal gas and the frequency of flatus events. | It is now known that gas is moved along the gut independently of solids and liquids, and this transit is more efficient in the erect position compared to when supine. It is thought that large volumes of intestinal gas present low resistance, and can be propelled by subtle changes in gut tone, capacitance and proximal contraction and distal relaxation. This process is thought not to affect solid and liquid intra-lumenal contents.Researchers investigating the role of sensory nerve endings in the anal canal did not find them to be essential for retaining fluids in the anus, and instead speculate that their role may be to distinguish between flatus and faeces, thereby helping detect a need to defecate or to signal the end of defecation.The sound varies depending on the tightness of the sphincter muscle and velocity of the gas being propelled, as well as other factors, such as water and body fat. The auditory pitch (sound) of the flatulence outburst can also be affected by the anal embouchure. Among humans, flatulence occasionally happens accidentally, such as incidentally to coughing or sneezing or during orgasm; on other occasions, flatulence can be voluntarily elicited by tensing the rectum or "bearing down" on stomach or bowel muscles and subsequently relaxing the anal sphincter, resulting in the expulsion of flatus. Management
Since problems involving intestinal gas present as different (but sometimes combined) complaints, the management is cause-related. | 11
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However, there are instances where monitoring may be beneficial for special populations, for example individuals with kidney insufficiency or those that are obese. In this case, anti-Xa units can be measured and dosing adjusted accordingly. Reversal agent
Protamine sulfate is less effective at reversing enoxaparin compared to heparin, with a maximum neutralization of approximately 60% of the anti-factor Xa effect. Pregnancy
Enoxaparin is a FDA pregnancy category B drug which means enoxaparin is not expected to cause harm to an unborn baby when used during pregnancy. This statement is based on reproductive studies involving pregnant rats and rabbits. No birth defects or toxic effects to an unborn fetus due to enoxaparin were observed during these animals studies. However a humans response to enoxaparin might be different from that of a small animal, therefore enoxaparin should be used during pregnancy only if there is a definite need. Enoxaparin does not cross the placenta therefore it is unlikely an unborn baby would be exposed to it. Some fetal deaths have been reported by women who used enoxaparin during pregnancy, but it is unclear if enoxaparin caused these deaths. Pregnant woman on enoxaparin should be monitored on a regular basis for bleeding and/or "excessive anticoagulation" especially when the delivery date is approaching. The risk of hemorrhage is higher during delivery if the person is still using enoxaparin and this could endanger the life of the baby and/or the mother. The multiple-dose vials of the brand name enoxaparin (Lovenox) contain 15 mg benzyl alcohol per 1 mL as a preservative. | Enoxaparin sodium, sold under the brand name Lovenox among others, is an anticoagulant medication (blood thinner). It is used to treat and prevent deep vein thrombosis (DVT) and pulmonary embolism (PE) including during pregnancy and following certain types of surgery. It is also used in those with acute coronary syndrome (ACS) and heart attacks. It is given by injection just under the skin or into a vein. It is also used during hemodialysis.Common side effects include bleeding, fever, and swelling of the legs. Bleeding may be serious especially in those who are undergoing a spinal tap. Use during pregnancy appears to be safe for the baby. Enoxaparin is in the low molecular weight heparin family of medications.Enoxaparin was first made in 1981 and approved for medical use in 1993. It is on the World Health Organizations List of Essential Medicines. Enoxaparin is sold under several brand names and is available as a generic medication. Enoxaparin is made from heparin. In 2017, it was the 299th most commonly prescribed medication in the United States, with more than one million prescriptions. Medical uses
Treatment of unstable angina (UA) and non-Q-wave myocardial infarction (NQMI), administered concurrently with aspirin
DVT and pulmonary embolism prophylaxis in bed-ridden patients
DVT prophylaxis in knee replacement surgery
DVT prophylaxis in hip replacement surgery
DVT prophylaxis in abdominal surgery
Treatment of DVT with or without pulmonary embolism
Treatment of DVT inpatient, with ST-segment elevation myocardial infarction (STEMI)
Bridging treatment for those with INR below therapeutic range
Monitoring
Enoxaparin has predictable absorption, bioavailability, and distribution therefore monitoring is not typically done. | 11
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", states as follows:
Whoever, with the intention of wounding the feelings of any person, or of insulting the religion of any person, or with the knowledge that the feelings of any person are likely to be wounded, or that the religion of any person is likely to be insulted thereby,
commits any trespass in any place of worship or on any place of sculpture, or any place set apart from the performance of funeral rites or as a depository for the remains of the dead, or offers any indignity to any human corpse, or causes disturbance to any persons assembled for the performance of funeral ceremonies, shall be punished with imprisonment of either description for a term which may extend to one year, or with fine, or with both. Although sex with a corpse is not explicitly mentioned, a person who has sex with a corpse may be convicted under the above section. Section 377 of the Indian Penal Code can also be invoked. Philippines
There are no laws which explicitly prohibit sexual acts on corpses. The closest applicable law is the provision in the Revised Penal Code which only criminalizes "defamation to blacken the memory of one who is dead". There were at least efforts to introduce bills criminalizing sexual acts on corpses during the 15th Congress; one by which penalizes sexual acts of males of corpses of women, and another which covers sexual intercourse, anal sex, and oral sex done on corpses. Both proposals penalizes the act with fine and imprisonment. | Copulation with a dead female pilot whale by a captive male pilot whale has been observed, and possible sexual behaviour between two male humpback whales, one dead, has also been reported.In 1983, a male rock dove was observed to be copulating with the corpse of a dove that shortly before had its head crushed by a car. In 2001, a researcher laid out sand martin corpses to attract flocks of other sand martins. In each of six trials, 1–5 individuals from flocks of 50–500 were observed attempting to copulate with the dead sand martins. This occurred one to two months after the breeding season; since copulation outside the breeding season is uncommon among birds, the researcher speculated that the lack of resistance by the corpses stimulated the behaviour. Charles Brown observed at least ten cliff swallows attempt to copulate with a road-killed cliff swallow in the space of 15 minutes. He commented, "This isnt the first time Ive seen cliff swallows do this; the bright orange rump sticking up seems to be all the stimulus these birds need." Necrophilia has also been reported in the European swallow, grey-backed sparrow-lark, Starks lark, and the snow goose. A Norwegian television report showed a male hybrid between a black grouse and western capercaillie kill a male black grouse before attempting to copulate with it. In 2015, due to work done by the University of Washington, it was found that crows would commit necrophilia on dead crow corpses in about 4% of encounters with corpses. | 11
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These idioms reflect the emphasis that collectivist cultures place on healing trauma through familial, cultural and religious activities while avoiding the stigma that accompanies a mind-body approach. Prescribing PTSD diagnostics within these communities is ineffective and often detrimental. For trauma that extends beyond the individual such as the effects of war, anthropologists believe applying the term “social suffering” or “cultural bereavement” to be more beneficial.Every facet of society is affected by conflict; the prolonged exposure to mass violence can lead to a ‘continuous suffering’ among civilians, soldiers, and bordering countries. Entered into the DSM in 1980, clinicians and psychiatrists based the diagnostic criteria for PTSD around American veterans of the Vietnam war. Though the DSM (in its fifth edition at the time of writing) gets reviewed and updated regularly, it is unable to fully encompass the disorder due to its Americanization (or Westernization). That is, what may be considered characteristics of PTSD in western society, may not directly translate across to other cultures around the world. Displaced people of the African country Burundi experienced symptoms of depression and anxiety, though little symptoms of PTSD were noted. In a similar review, Sudanese refugees relocated in Uganda were ‘concerned with material [effects]’ (lack of food, shelter, and healthcare), rather than psychological distress. In this case, many refugees didn’t present symptoms at all, with a minor few developing anxiety and depression. | Tricyclic antidepressants are equally effective but are less well tolerated. Evidence provides support for a small or modest improvement with sertraline, fluoxetine, paroxetine, and venlafaxine. Thus, these four medications are considered to be first-line medications for PTSD. Benzodiazepines
Benzodiazepines are not recommended for the treatment of PTSD due to a lack of evidence of benefit and risk of worsening PTSD symptoms. Some authors believe that the use of benzodiazepines is contraindicated for acute stress, as this group of drugs can cause dissociation. Nevertheless, some use benzodiazepines with caution for short-term anxiety and insomnia. While benzodiazepines can alleviate acute anxiety, there is no consistent evidence that they can stop the development of PTSD and may actually increase the risk of developing PTSD 2–5 times. Additionally, benzodiazepines may reduce the effectiveness of psychotherapeutic interventions, and there is some evidence that benzodiazepines may actually contribute to the development and chronification of PTSD. For those who already have PTSD, benzodiazepines may worsen and prolong the course of illness, by worsening psychotherapy outcomes, and causing or exacerbating aggression, depression (including suicidality), and substance use. Drawbacks include the risk of developing a benzodiazepine dependence, tolerance (i.e., short-term benefits wearing off with time), and withdrawal syndrome; additionally, individuals with PTSD (even those without a history of alcohol or drug misuse) are at an increased risk of abusing benzodiazepines. | 11
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Cerebellar circuitry has capacities to compensate and restore function thanks to cerebellar reserve, gathering multiple forms of plasticity. LTDpathies gather immune disorders targeting long-term depression (LTD), a form of plasticity. Diagnosis
Imaging studies - A CT scan or MRI of the brain might help determine potential causes. An MRI can sometimes show shrinkage of the cerebellum and other brain structures in people with ataxia. It may also show other treatable findings, such as a blood clot or benign tumour, that could be pressing on the cerebellum. Lumbar puncture (spinal tap) - A needle is inserted into the lower back (lumbar region) between two lumbar vertebrae to obtain a sample of cerebrospinal fluid for testing. Genetic testing - Determines whether the mutation that causes one of the hereditary ataxic conditions is present. Tests are available for many but not all of the hereditary ataxias. Treatment
The treatment of ataxia and its effectiveness depend on the underlying cause. Treatment may limit or reduce the effects of ataxia, but it is unlikely to eliminate them entirely. Recovery tends to be better in individuals with a single focal injury (such as stroke or a benign tumour), compared to those who have a neurological degenerative condition. A review of the management of degenerative ataxia was published in 2009. A small number of rare conditions presenting with prominent cerebellar ataxia are amenable to specific treatment and recognition of these disorders is critical. | Teduglutide (brand names Gattex in the US and Revestive in Europe) is a 33-membered polypeptide and glucagon-like peptide-2 (GLP-2) analog that is used for the treatment of short bowel syndrome. It works by promoting mucosal growth and possibly restoring gastric emptying and secretion. In Europe it has been granted orphan drug status and is marketed under the brand Revestive by Nycomed. It was approved by the United States under the name Gattex on 21 December 2012, where it was given status as an orphan drug. Medical uses
Up to a certain point, the gut can adapt to partial resections that result in short bowel syndrome. Still, parenteral substitution of water, minerals and vitamins (depending on which part of the gut has been removed) is often necessary. Teduglutide may reduce or shorten the necessity of such infusions by improving the intestinal mucosa and possibly by other mechanisms. Adverse effects
Common adverse effects in clinical studies included abdominal discomfort (49% of patients), respiratory infections (28%), nausea (27%) and vomiting (14%), local reactions at the injection site (21%), and headache (17%). Chemistry and mechanism of action
Teduglutide differs from natural GLP-2 by a single amino acid: an alanine is replaced with a glycine. This blocks breaking down of the molecule by dipeptidyl peptidase and increases its half-life from seven minutes (GLP-2) to about two hours, while retaining its biological actions. These include maintenance of the intestinal mucosa, increasing intestinal blood flow, reducing gastrointestinal motility and secretion of gastric acid. == References == | 0-1
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Another possible option is splinting, to secure the elbow, a conservative procedure endorsed by some. In cases where surgery is needed, cubital tunnel release, where the ligament of the cubital tunnel is cut, thereby alleviating pressure on nerve can be performed.Treatment for the common occurrence of ulnar neuropathy resulting from overuse, with no fractures or structural abnormalities, is treatment massage, ice, and anti-inflammatories. Specifically, deep tissue massage to the triceps, myofascial release for the upper arm connective tissue, and cross-fiber friction to the triceps tendon. Prognosis
In terms of the prognosis of ulnar neuropathy early decompression of the nerve sees a return to normal ability (function), which should be immediate. Severe cubital tunnel syndrome tends to have a faster recovery process in individuals below the age of 70, as opposed to those above such an age. Finally, revisional surgery for cubital tunnel syndrome does not result well for those individuals over 50 years of age. References
Further reading
"NIOSHTIC-2 Publications Search - 20045060 - Do comorbid ulnar symptoms or ulnar neuropathy affect the prognosis of workers with carpal tunnel syndrome?". www.cdc.gov. Retrieved 2016-07-22. Yoon, Joon Shik; Walker, Francis O.; Cartwright, Michael S. (1 February 2010). "Ulnar Neuropathy With Normal Electrodiagnosis and Abnormal Nerve Ultrasound". Archives of Physical Medicine and Rehabilitation. 91 (2): 318–320. doi:10.1016/j.apmr.2009.10.010. ISSN 0003-9993. PMC 2892824. PMID 20159139. Warner, Mark A.; Warner, David O.; Matsumoto, Joseph Y.; Harper, Michel C.; Schroeder, Darrell R.; Maxson, Pamela M. (1 January 1999). "Ulnar Neuropathy in Surgical Patients". The Journal of the American Society of Anesthesiologists. 90 (1): 54–59. doi:10.1097/00000542-199901000-00009. | Elective right hemicolectomy may be used to prevent recurrence but is generally not recommended"...The authors have found nonoperative treatment highly effective in patients who do not manifest signs of peritonitis, perforation, gastrointestinal hemorrhage, or clinical deterioration. Recurrent typhlitis was frequent after conservative therapy (recurrence rate, 67 percent), however," as based on studies from the 1980s
Prognosis
Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death
. See also
Colitis
References
== External links == | 0-1
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Diagnosis
The diagnosis of DS-AMKL in young children is indicated by: a history of TMD; findings of increased presence of blast cells (e.g. ≥20% of nucleated cells) that have the megakaryoblast phenotype in blood and/or bone marrow as defined by the morphology of these cells in blood or bone marrow smears; failure to obtain a bone marrow aspirate because of marrow fibrosis; and immunophenotyping analyses of platelet precursor cells lineage as determined by flow cytometry and immunohistochemistry. Malignant megakaryoblasts are usually medium-sized to large cells with a high nuclear-cytoplasmic ratio. Nuclear chromatin is dense and homogeneous. There is scanty, variable basophilic cytoplasm which may be excessively vacuolated. An irregular cytoplasmic border is often noted in some of the megakaryoblasts and occasionally projections resembling budding atypical platelets are present. Megakaryoblasts lack myeloperoxidase (MPO) activity and stain negatively with Sudan Black B. They are alpha naphthyl butyrate esterase negative and manifest variable alpha naphthyl acetate esterase activity usually in scattered clumps or granules in the cytoplasm. PAS diastase staining varies from negative to focal or granular positivity to strongly positive. | Immunochemical analyses, often conducted by flow cytometry, of the surface antigens on leukemic blast cells are positive for CD41, CD42b, CD51, and Von Willebrand factor in AMKL but not leukemia involving non-platelet malignant cells.Where indicated and available, the diagnosis of DS-AMKL is further supported by; immunophenotyping analysis using monoclonal antibody directed against megakaryocyte restricted antigen (CD41 and CD61) and DNA sequencing to detect GATA1 mutations that are projected to cause the gene to make GATA1-S but not GATA1 transcription factors. Treatment
The chemotherapy regimens used for all types of AMKL are similar to those used for AML. A final confirmation of safety and efficacy phase 3 study consisted of 4 cycles of induction therapy with cytarabine and daunorubicin followed by a single course of intensification therapy consisting of cytarabine and L-asparaginase, and concluded with a central nervous system consolidation course of 3 additional doses of intrathecal cytarabine. The dosages of cytarabine in this study were kept low because DS-AMKL patients proved highly susceptible to the toxic effects of the regimen which used a higher cytarabine dosage to treat AML. The low-dose cytarabine regimen achieved excellent results in DS-AMKL with relatively reduced overall toxicity and is currently recommended as a preferred treatment regimen for the disease.Autologous hematopoietic stem cell transplantation (i.e. transplantation of stem cells derived from the individual being transplanted) did not improve relapse-free survival in one large study of DS-AMKL. Allogenic hematopoietic stem cell transplantation (i.e. | 11
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These adverse effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohol on aberrant neuronal plasticity and cortical damage. Repeated periods of acute intoxication followed by acute detoxification has profound effects on the brain and is associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics who have detoxified repeatedly but not as severe as in alcoholics who have no history of prior detox. Thus, the acute withdrawal syndrome appears to be the most important factor in causing damage or impairment to brain function. The brain regions most sensitive to harm from binge drinking are the amygdala and prefrontal cortex.People in adolescence who experience repeated withdrawals from binge drinking show impairments of long-term nonverbal memory. Alcoholics who have had two or more alcohol withdrawals show more frontal lobe cognitive dysfunction than those who have experienced one or no prior withdrawals. Kindling of neurons is the proposed cause of withdrawal-related cognitive damage. Kindling from repeated withdrawals leads to accumulating neuroadaptive changes. Kindling may also be the reason for cognitive damage seen in binge drinkers. Diagnosis
Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol in order to assess the level of withdrawal present and therefore the amount of medication needed. When overuse of alcohol is suspected but drinking history is unclear, testing for elevated values of carbohydrate-deficient transferrin or gammaglutamyl transferase can help make the diagnosis of alcohol overuse and dependence more clear. | Limited evidence supports the use of gabapentin or carbamazepine for the treatment of mild or moderate alcohol withdrawal as the sole treatment or as combination therapy with other medications; however, gabapentin does not appear to be effective for treatment of severe alcohol withdrawal and is therefore not recommended for use in this setting. A 2010 Cochrane review similarly reported that the evidence to support the role of anticonvulsants over benzodiazepines in the treatment of alcohol withdrawal is not supported. Paraldehyde combined with chloral hydrate showed superiority over chlordiazepoxide with regard to life-threatening side effects and carbamazepine may have advantages for certain symptoms. Long term anticonvulsant medications are not usually recommended in those who have had prior seizures due to withdrawal. Prevention of further drinking
There are three medications used to help prevent a return to drinking: naltrexone, acamprosate, and disulfiram. They are used after withdrawal has occurred. Other
Clonidine may be used in combination with benzodiazepines to help some of the symptoms. No conclusions can be drawn concerning the efficacy or safety of baclofen for alcohol withdrawal syndrome due to the insufficiency and low quality of the evidence.Antipsychotics, such as haloperidol, are sometimes used in addition to benzodiazepines to control agitation or psychosis. Antipsychotics may potentially worsen alcohol withdrawal as they lower the seizure threshold. Clozapine, olanzapine, or low-potency phenothiazines (such as chlorpromazine) are particularly risky; if used, extreme caution is required.While intravenous ethanol could theoretically be used, evidence to support this use, at least in those who are very sick, is insufficient. | 11
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Hyperestrogenism, hyperestrogenic state, or estrogen excess, is a medical condition characterized by an excessive amount of estrogenic activity in the body. Signs and symptoms
Signs of hyperestrogenism may include heightened levels of one or more of the estrogen sex hormones (usually estradiol and/or estrone), lowered levels of follicle-stimulating hormone and/or luteinizing hormone (due to suppression of the hypothalamic–pituitary–gonadal axis by estrogen), and lowered levels of androgens such as testosterone (generally only relevant to males). Symptoms of the condition in women may consist of menstrual irregularities, amenorrhea, abnormal vaginal bleeding, and enlargement of the uterus and breasts. It may also present as isosexual precocity in children and as hypogonadism, gynecomastia, feminization, impotence, and loss of libido in males. If left untreated, hyperestrogenism may increase the risk of estrogen-sensitive cancers such as breast cancer later in life. Causes
Hyperestrogenism can be caused by ovarian tumors, genetic conditions such as aromatase excess syndrome (also known as familial hyperestrogenism), or overconsumption of exogenous sources of estrogen, including medications used in hormone replacement therapy and hormonal contraception. Liver cirrhosis is another cause, though through lowered metabolism of estrogen, not oversecretion or overconsumption like the aforementioned. Its necessary to know there exist two kinds of hyperestrogenism: Absolute (more concentration than usual of estrogen) and relative (a normal concentration of estrogen, higher with respect to progesterone). An example of absolute hyperestrogenism could be: persistent follicles that later undergo atresia without ovulating; and the example of relative hyperestrogenism: luteal insufficiency. | The Attitude Towards Heights Questionnaires (ATHQ) and Behavioural Avoidance Tests (BAT) are also used.However, acrophobic individuals tend to have biases in self-reporting. They often overestimate the danger and question their abilities of addressing height relevant issues. A Height Interpretation Questionnaire (HIQ) is a self-report to measure these height relevant judgements and interpretations. The Depression Scale of the Depression Anxiety Stress Scales short form (DASS21-DS) is a self report used to examine validity of the HIQ. Treatment
Traditional treatment of phobias is still in use today. Its underlying theory states that phobic anxiety is conditioned and triggered by a conditional stimulus. By avoiding phobic situations, anxiety is reduced. However, avoidance behaviour is reinforced through negative reinforcement. Wolpe developed a technique called systematic desensitization to help participants avoid "avoidance". Research results have suggested that even with a decrease in therapeutic contact, densensitization is still very effective. However, other studies have shown that therapists play an essential role in acrophobia treatment. Treatments like reinforced practice and self-efficacy treatments also emerged.There have been a number of studies into using virtual reality therapy for acrophobia. Botella and colleagues and Schneider were the first to use VR in treatment. Specifically, Schneider utilised inverted lenses in binoculars to "alter" the reality. Later in the mid-1990s, VR became computer-based and was widely available for therapists. A cheap VR equipment uses a normal PC with head-mounted display (HMD). In contrast, VRET uses an advanced computer automatic virtual environment (CAVE). | 0-1
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Article 12.2d of the ICESCR stipulates the need for "the creation of conditions which would assure to all medical service and medical attention in the event of sickness", and is interpreted in the 2000 comment to include timely access to "basic preventative, curative services… for appropriate treatment of injury and disability.". Obstetric care shares close ties with reproductive rights, which includes access to reproductive health.Surgeons and public health advocates, such as Kelly McQueen, have described surgery as "Integral to the right to health". This is reflected in the establishment of the WHO Global Initiative for Emergency and Essential Surgical Care in 2005, the 2013 formation of the Lancet Commission for Global Surgery, the 2015 World Bank Publication of Volume 1 of its Disease Control Priorities Project "Essential Surgery", and the 2015 World Health Assembly 68.15 passing of the Resolution for Strengthening Emergency and Essential Surgical Care and Anesthesia as a Component of Universal Health Coverage. The Lancet Commission for Global Surgery outlined the need for access to "available, affordable, timely and safe" surgical and anesthesia care; dimensions paralleled in ICESCR General Comment No. 14, which similarly outlines need for available, accessible, affordable and timely healthcare. History
Trepanation
Surgical treatments date back to the prehistoric era. The oldest for which there is evidence is trepanation, in which a hole is drilled or scraped into the skull, thus exposing the dura mater in order to treat health problems related to intracranial pressure and other diseases. | As the first two methods suggested by Pasteur were inappropriate for the treatment of human tissue, Lister experimented with the third, spraying carbolic acid on his instruments. He found that this remarkably reduced the incidence of gangrene and he published his results in The Lancet. Later, on 9 August 1867, he read a paper before the British Medical Association in Dublin, on the Antiseptic Principle of the Practice of Surgery, which was reprinted in the British Medical Journal. His work was groundbreaking and laid the foundations for a rapid advance in infection control that saw modern antiseptic operating theatres widely used within 50 years. Lister continued to develop improved methods of antisepsis and asepsis when he realised that infection could be better avoided by preventing bacteria from getting into wounds in the first place. This led to the rise of sterile surgery. Lister introduced the Steam Steriliser to sterilize equipment, instituted rigorous hand washing and later implemented the wearing of rubber gloves. These three crucial advances – the adoption of a scientific methodology toward surgical operations, the use of anaesthetic and the introduction of sterilised equipment – laid the groundwork for the modern invasive surgical techniques of today. The use of X-rays as an important medical diagnostic tool began with their discovery in 1895 by German physicist Wilhelm Röntgen. He noticed that these rays could penetrate the skin, allowing the skeletal structure to be captured on a specially treated photographic plate. | 11
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The trait is now extinct and was never fully characterized.Diplopodia-3
This is an autosomal trait that may be the least severe of the five. Diplopodia-4
This sex-linked mutation is similar to the previous mutations, but causes the embryo to grow thicker wing bones.Diplopodia-5
This is an autosomal mutation that gives embryos webbing between the inner two front toes on each foot, in addition to the usual characteristics of diplopodia. Almost all of the embryos survive to the end of incubation, but they are unable to clear the fluid from their lungs or absorb the blood from their extraembryonic vessels. These problems always prevent them from hatching. Almost all diplopodia-5 embryos have only one or two extra toes on each foot, so this mutation causes the least extreme foot malformation. See also
Limb development
Congenital abnormality
Dysmelia
Sonic hedgehog
Polydactyly
== References == | Paleness may refer to:
Pallor, a medical condition
Paleness (color)
See also
Pale (disambiguation) | 0-1
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Édouard Séguin described it as separate from cretinism in 1844. By the 20th century, Down syndrome had become the most recognizable form of mental disability. In antiquity, many infants with disabilities were either killed or abandoned. In June 2020, the earliest incidence of Down syndrome was found in genomic evidence from an infant that was buried before 3200 BC at Poulnabrone dolmen in Ireland. Researchers believe that a number of historical pieces of art portray Down syndrome, including pottery from the pre-Columbian Tumaco-La Tolita culture in present-day Colombia and Ecuador, and the 16th-century painting The Adoration of the Christ Child.In the 20th century, many individuals with Down syndrome were institutionalized, few of the associated medical problems were treated, and most people died in infancy or early adulthood. With the rise of the eugenics movement, 33 of the then 48 U.S. states and several countries began programs of forced sterilization of individuals with Down syndrome and comparable degrees of disability. Action T4 in Nazi Germany made public policy of a program of systematic involuntary euthanization.With the discovery of karyotype techniques in the 1950s it became possible to identify abnormalities of chromosomal number or shape. In 1959 Jérôme Lejeune reported the discovery that Down syndrome resulted from an extra chromosome. However, Lejeunes claim to the discovery has been disputed, and in 2014 the Scientific Council of the French Federation of Human Genetics unanimously awarded its Grand Prize to his colleague Marthe Gautier for her role in this discovery. | Pilomatricoma, is a benign skin tumor derived from the hair matrix. These neoplasms are relatively uncommon and typically occur on the scalp, face, and upper extremities. Clinically, pilomatricomas present as a subcutaneous nodule or cyst with unremarkable overlying epidermis that can range in size from 0.5 to 3.0 cm, but the largest reported case was 24 cm. Presentation
Associations
Pilomatricomas have been observed in a variety of genetic disorders including Turner syndrome, myotonic dystrophy, Rubinstein-Taybi syndrome, Trisomy 9, and Gardner syndrome. It has been reported that the prevalence of pilomatricomas in Turner syndrome is 2.6%.Hybrid cysts that are composed of epidermal inclusion cysts and pilomatricoma-like changes have been repeatedly observed in Gardner syndrome. This association has prognostic import, since cutaneous findings in children with Gardner Syndrome generally precede colonic polyposis. Histologic features
The characteristic components of a pilomatricoma include a stroma of fibrovascular connective tissue
surrounding irregularly shaped, lobulated islands containing basaloid cells (being darkly stained, round or elongated, with indistinct cell borders and minimal cytoplasm, with nuclei being round to ovoid, deeply basophilic and generally prominent nucleoli), which abruptly or gradually transitions into ghost cells (having abundant, pale, eosinophilic cytoplasm, well defined cell borders and a central clear area, but only faint traces of nuclear material), which in turn may transition into keratinaceous to amorphous necrosis.The presence of calcifications with foreign body giant cells is common within the tumors. Pathogenesis
Pilomatricoma is associated with high levels of beta-catenin caused by either a mutation in the APC gene or a stabilizing mutation in the beta-catenin gene, CTNNB1. | 0-1
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These contain additional material from chromosome 21 and occur in about 2.5% of cases. An isochromosome results when the two long arms of a chromosome separate together rather than the long and short arm separating together during egg or sperm development. Trisomy 21
Trisomy 21 (also known by the karyotype 47,XX,+21 for females and 47,XY,+21 for males) is caused by a failure of the 21st chromosome to separate during egg or sperm development (nondisjunction). As a result, a sperm or egg cell is produced with an extra copy of chromosome 21; this cell thus has 24 chromosomes. When combined with a normal cell from the other parent, the baby has 47 chromosomes, with three copies of chromosome 21. About 88% of cases of trisomy 21 result from nonseparation of the chromosomes in the mother, 8% from nonseparation in the father, and 3% after the egg and sperm have merged. Mosaicism
Mosaicism is diagnosed when there is a mixture of two types of cells: some cells have three copies of chromosome 21 but some cells have the typical two copies of chromosome 21. Mosaicism is the least common form of Down syndrome and accounts for only about 1% of all cases of Down syndrome. Children with mosaic Down syndrome may have the same features as other children with Down syndrome. However, they may have fewer characteristics of the condition due to the presence of some (or many) cells with a typical number of chromosomes. | Other common features include: a flat and wide face, a short neck, excessive joint flexibility, extra space between big toe and second toe, abnormal patterns on the fingertips and short fingers. Instability of the atlantoaxial joint occurs in about 20% and may lead to spinal cord injury in 1–2%. Hip dislocations may occur without trauma in up to a third of people with Down syndrome.Growth in height is slower, resulting in adults who tend to have short stature—the average height for men is 154 cm (5 ft 1 in) and for women is 142 cm (4 ft 8 in). Individuals with Down syndrome are at increased risk for obesity as they age. Growth charts have been developed specifically for children with Down syndrome. Neurological
This syndrome causes about a third of cases of intellectual disability. Many developmental milestones are delayed with the ability to crawl typically occurring around 8 months rather than 5 months and the ability to walk independently typically occurring around 21 months rather than 14 months.Most individuals with Down syndrome have mild (IQ: 50–69) or moderate (IQ: 35–50) intellectual disability with some cases having severe (IQ: 20–35) difficulties. Those with mosaic Down syndrome typically have IQ scores 10–30 points higher than that. As they age, people with Down syndrome typically perform worse than their same-age peers.Commonly, individuals with Down syndrome have better language understanding than ability to speak. Between 10 and 45% have either a stutter or rapid and irregular speech, making it difficult to understand them. | 11
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In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression. Antidepressants
Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that SSRIs, such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo on achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression. Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo. Antidepressants work less well for the elderly than for younger individuals with depression.To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement. Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence, and even up to one year of continuation is recommended. | SERKAL syndrome (SEx Reversion, Kidneys, Adrenal and Lung dysgenesis) is an autosomal recessive disorder in XX humans. It is caused by loss of function in WNT4, a protein involved in sex development. The main outcome is female to male sex reversal. Other names include sex reversion-kidneys and adrenal and lung dysgenesis syndrome. The conditions prevalence is lower than 1 in 1,000,000. Presentation
The effect of the disorder is female to male sex reversal. Patients also exhibit renal, adrenal, and lung dysgenesis. One indicator is low levels of unconjugated estriol in maternal serum, because this denotes adrenal hypoplasia. Genetics
The disorder is linked to a mutation in the Wnt4 gene. There is an intraexonic homozygous C to T transition at cDNA position 341. This leads to an alanine to valine residue substitution at amino acid position 114, a location highly conserved in all organisms, including zebrafish and Drosophila. A subsequent influence on mRNA stability leads to protein loss of function. WNT4 usually represses male sex development. Diagnosis
References
External links
SERKAL syndrome (The Monarch Initiative) | 0-1
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Gonococcal arthritis – Neisseria gonorrhoeae is a common cause of septic arthritis in people who are sexually active and under 40 years old. The bacteria is spread through the blood to the joint following sexual transmission. Other symptoms of disseminated gonococcal infection can include migration of joint pain, tenosynovitis and dermatitis. Synovial fluid cultures are positive in 25 to 70% of the cases while blood cultures are seldom positive. Apart from blood and joint cultures, swabs from urethra, rectum, pharynx, and cervix should also be taken. Polymerase chain reaction (PCR) is another useful way of identifying gonococcal infections if diagnosis is difficult and clinical presentation is similar to reactive arthritis. Others – Fungal and mycobacterial infections are rare causes of septic arthritis and usually have a slow onset of joint symptoms. Mycobacterial joint infection most commonly affects hip and knee joints, caused by reactivation of past mycobacterial infections, with or without signs and symptoms of tuberculosis in lungs. Synovial fluid cultures will be positive in 80% of the cases. However, acid fast smears are not useful. Histology is not specific to myocobacterial infection as there are other granulomatous diseases that can show similar histology. Borrelia burgdorferi, a bacterium that causes lyme disease, can affect multiple large joints such as the knee. Confirmation of Lyme disease is done through enzyme-linked immunosorbent assay (ELISA) followed by confirmation using Western Blot test. It cannot be cultured from synovial fluid. However, PCR testing yields 85% positive result from synovial fluid. | The use of prophylactic antibiotics before dental, genitourinary, gastrointestinal procedures to prevent infection of the implant is controversial.Low-quality evidence suggests that the use of corticosteroids may reduce pain and the number of days of antibiotic treatment in children. Outcomes
Risk of permanent impairment of the joint varies greatly. This usually depends on how quickly treatment is started after symptoms occur as longer lasting infections cause more destruction to the joint. The involved organism, age, preexisting arthritis, and other comorbidities can also increase this risk. Gonococcal arthritis generally does not cause long term impairment. For those with Staphylococcus aureus septic arthritis, 46 to 50% of the joint function returns after completing antibiotic treatment. In pneumococcal septic arthritis, 95% of the joint function will return if the person survives. One-third of people are at risk of functional impairment (due to amputation, arthrodesis, prosthetic surgery, and deteriorating joint function) if they have an underlying joint disease or a synthetic joint implant. Mortality rates generally range from 10 to 20%. These rates increase depending on the offending organism, advanced age, and comorbidities such as rheumatoid arthritis. Epidemiology
In children and adolescence septic arthritis and acute hematogenous osteomyelitis occurs in about 1.34 to 82 per 100,000 per annual hospitalization rates. In adults septic arthritis occurs in about 5 people per 100,000 each year. It occurs more commonly in older people. With treatment, about 15% of people die, while without treatment 66% die. References
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The National Institutes of Health Stroke Scale (NIHSS) is a standardized method for quantifiable assessment of stroke symptoms. It is the preferred scoring system, and scores range from 0 to 42. A patient with a higher score on this scale is more likely to be considered disabled; however, the definition of "disabling" depends on age, occupation, underlying life-limiting comorbidities, advance directives. The crucial step in the evaluation of stroke patients is to obtain brain imaging to ascertain the type and characteristics of the stroke. In this regard, non-contrast CT of the head is the imaging modality of choice. Ischemic changes may classify as acute, subacute, and chronic, depending on the time in which they present after the onset of stroke. CT scan can also rule out intracranial hemorrhage. [18] If an intracranial hemorrhage is present, aneurysmal rupture should be investigated given its association with arterial vasospasm resulting in stroke. [3] Anterior cerebral artery strokes could be missed on imaging studies depending on their location or size. One case series found that 37.5% (6 of 16) of ACA infarcts evaluated by CT were identifiable only after using contrast injection or angiography. If the area of hypodensity is small and localized over a sulcus, the infarct could be overlooked. [1] [13] Noncontrast head CT should be quickly followed by CT angiography of the head and neck to expedite identification of intracranial large vessel occlusion. | Chattem, Inc. is an American, Chattanooga, Tennessee-based, producer and marketer of over-the-counter healthcare products, toiletries, dietary supplements, topical analgesics, and medicated skin care products. Originally named the Chattanooga Medicine Company, the company’s brand portfolio holds twenty-two brands including Allegra, Gold Bond, Flexall, IcyHot, Rolaids, Sun-In, Pamprin, Dexatrim, Aspercreme, and Selsun Blue. The company produces two-thirds of its products at its Chattanooga production facilities with the remaining produced by third-party producers. The company is a subsidiary of the French multinational pharmaceutical company Sanofi. The company’s brands are sold nationally through mass merchandiser, drug and food retailers. In 2005, 70% of the firms sales were made through its top ten customers, which include Wal-Mart, Walgreens, and Kroger. Sales to Wal-Mart constituted 36% of Chattem’s total sales in 2005. Chattem supports these sales with a forty-five-person sales force and broadcast media advertising. Chattem has market penetration in the United States, Europe, Canada, Latin America, and the Caribbean. History
Chattem was founded by Zeboim Cartter Patten as the Chattanooga Medicine Company in 1879. The company incorporated in 1909 and has remained in Chattanooga, Tennessee, to this day. During World War II, the Chattanooga Medicine Company turned into a major supplier of K-Rations to the US Army, producing 34 million rations from 1942 to 1945, earning 5 "E" Awards for support of war efforts. The firm adopted Chattem as its name and went public in 1969. Chattem’s top and bottom lines grew significantly from 1989 through 1992. | 0-1
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Her husband custom-made a special bra to support her breasts.In 2007, a Chilean TV station covered the story of 32-year-old Yasna Galleguillos from Antofagasta, who experienced ongoing back pain, making everyday tasks very difficult to perform. She underwent breast reduction surgery to relieve her pain. Surgeons removed 4.25 kilograms (9.4 lb) from one breast and 3.33 kilograms (7.3 lb) from the other breast.On October 29, 2009, the Philippine television network GMA News and Public Affairs, producers of Wish Ko Lang ("Just My Wish") hosted by Vicky Morales, profiled the story of Pilma Cabrijas, a 30-year-old woman affected by gigantomastia. The woman was told by a folk healer that her condition may have been caused by a curse. The measured bust circumference without appropriate bra support was 160 cm (63 in). The weight of her breasts was not reported in detail, but seemed to weigh "as much as two children." She had breast reduction surgery performed, but her breasts regrew. The producers of Wish Ko Lang paid for additional surgery. Virginal breast hypertrophy
In 1993, the Japanese journal Surgery Today reported on the case of a 12-year-old girl. Only 152 centimetres (60 in) tall and weighing 43 kilograms (95 lb), her breasts began to develop at age 11 before the onset of menstruation. Over the next eight months, both breasts grew abnormally large, and physicians treating her found that her physiological development was normal except for her breasts. The weight produced by their symmetrical and massive enlargement resulted in marked curvature of the spine. | In severe cases of VBH, hypertrophy of the clitoris occurs.At the onset of puberty, some females with who have experienced little or no breast development can reportedly reach three or more cup sizes within a few days (see below).As of 1992, 70 cases of virginal breast hypertrophy had been reported. Gestational breast hypertrophy
This same effect can also occur at the onset of pregnancy or between the 16th to 20th week of gestation. When the swelling in the connective tissue occurs after birth, it can negatively impact long term milk supply. The swelling increases with each subsequent pregnancy. The extremely rapid growth of the breasts can result in intense heat. The womans breasts can generate extraordinary discomfort, turning feverish, red, itchy, and even causing the skin to peel. The swelling can suppress the milk supply, pinching off the milk ducts, and leading to mastitis.Gestational gigantomastia is estimated to in 1 out of every 28,000 to 100,000 pregnancies.Breast size in women with gestational breast hypertrophy typically reverts to approximately pre-pregnancy size or near it after pregnancy and cessation of breastfeeding. This is not always the case however and in some only partial reduction in breast size may occur, necessitating surgical breast reduction. Other types of breast hypertrophy
Only 15% of cases of breast hypertrophy are unrelated to puberty or pregnancy. Other types and causes of breast hypertrophy include idiopathic, drug-induced (e.g., penicillamine, cyclosporine, bucillamine), autoimmunity-associated, tumors, and syndromes. Two case reports of prepubertal breast hypertrophy, both in infants, have been reported. | 11
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Following treatment with Preotact, patients can be treated with a bisphosphonate to further increase bone mineral density
Contraindications for use
Parathyroid hormone treatment should not be initiated in patients:
with hypersensitivity to PTH or excipients
who have received radiation therapy to the skeleton
with pre-existing hypercalcemia and other disturbances in the metabolism of phosphate or calcium
with metabolic bone diseases other than primary osteoporosis (including hyperparathyroidism and Pagets disease
with unexplained elevations of bone-specific alkaline phosphatase
with severe chronic kidney disease
with severe liver impairment
Interactions
Parathyroid hormone is a natural peptide that is not metabolised in the liver. It is not protein bound and has a low volume of distribution, therefore no specific drug-drug interactions are suspected. From the knowledge of the mechanism of action, combined use of Preotact and cardiac glycosides may predispose patients to digitalis toxicity if hypercalcemia develops. Undesirable effects
Hypercalcemia and/or hypercalciuria reflect the known pharmacodynamic actions of parathyroid hormone in the gastrointestinal tract, the kidney and the skeleton, and is therefore an expected undesirable effect. Nausea is another commonly reported adverse reaction to the use of parathyroid hormone. Pharmacodynamic properties
Mechanism of action
Preotact contains recombinant human parathyroid hormone which is identical to the full-length native 84-amino acid polypeptide. Physiological actions of parathyroid hormone include stimulation of bone formation by direct effects on bone forming cells (osteoblasts) indirectly increasing the intestinal absorption of calcium and increasing the tubular reabsorption of calcium and excretion of phosphate by the kidney. Pharmacodynamic effects
The skeletal effects of parathyroid hormone depend upon the pattern of systemic exposure. | Transient elevations in parathyroid hormone levels after subcutaneous injection of Preotact stimulates new bone formation on trabecular and cortical bone surfaces by preferential stimulation of osteoblastic activity over osteoclastic activity. Effects on serum calcium concentrations
Parathyroid hormone is the principal regulator of serum calcium hemostasis. In response to subcutaneous doses of Preotact (100 micrograms), serum total calcium levels increase gradually and reach peak concentration at approximately 6 to 8 hours after dosing. In general, serum calcium levels return to normal within 24 hours. Clinical efficacy
In an 18-month double-blind, placebo controlled study, the effects of Preotact on the fracture incidence in 2532 women with postmenopausal osteoporosis was studied. Approximately 19% of patients had a prevalent vertebral fracture at baseline and the mean lumbar T-score of -3.0 in both active and placebo arm. Compared to the placebo group, there was a 61% relative risk reduction of a new vertebral fracture at month 18 for the women in the Preotact group. To prevent one or more new vertebral fractures, 48 women had to be treated for a median of 18 months for the total population. For patients who were already fractured, the number needed to treat was 21. Effect on bone mineral density
In the same study mentioned above, Preotact increased bone mineral density in the lumbar spine after 18 months treatment by 6.5% compared with a reduction by 0.3% in the placebo group. The difference was statistically significant. | 11
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Some cultures try hard to restrain sexual desire. Others try to excite it. Concepts of "normal" levels of sexual desire are culturally dependent and rarely value-neutral. In the 1970s, there were strong cultural messages that sex is good for you and "the more the better". Within this context, people who were habitually uninterested in sex, who in previous times may not have seen this as a problem, were more likely to feel that this was a situation that needed to be fixed. They may have felt alienated by dominant messages about sexuality and increasingly people went to sex-therapists complaining of low sexual desire. It was within this context that the diagnosis of ISD was created.In the revision of the DSM-III, published in 1987 (DSM-III-R), ISD was subdivided into two categories: Hypoactive Sexual Desire Disorder and Sexual Aversion Disorder (SAD). The former is a lack of interest in sex and the latter is a phobic aversion to sex. In addition to this subdivision, one reason for the change is that the committee involved in revising the psychosexual disorders for the DSM-III-R thought that the term "inhibited" suggests psychodynamic cause (i.e., that the conditions for sexual desire are present, but the person is, for some reason, inhibiting their own sexual interest). The term "hypoactive sexual desire" is more awkward, but more neutral with respect to the cause. The DSM-III-R estimated that about 20% of the population had HSDD. | Causes
Low sexual desire alone is not equivalent to HSDD because of the requirement in HSDD that the low sexual desire causes marked distress and interpersonal difficulty and because of the requirement that the low desire is not better accounted for by another disorder in the DSM or by a general medical problem. It is therefore difficult to say exactly what causes HSDD. It is easier to describe, instead, some of the causes of low sexual desire.In men, though there are theoretically more types of HSDD/low sexual desire, typically men are only diagnosed with one of three subtypes. Lifelong/generalised: The man has little or no desire for sexual stimulation (with a partner or alone) and never had. Acquired/generalised: The man previously had sexual interest in his present partner, but lacks interest in sexual activity, partnered or solitary. Acquired/situational: The man was previously sexually interested in his present partner but now lacks sexual interest in this partner but has desire for sexual stimulation (i.e. alone or with someone other than his present partner. )Though it can sometimes be difficult to distinguish between these types, they do not necessarily have the same cause. The cause of lifelong/generalized HSDD is unknown. In the case of acquired/generalized low sexual desire, possible causes include various medical/health problems, psychiatric problems, low levels of testosterone or high levels of prolactin. One theory suggests that sexual desire is controlled by a balance between inhibitory and excitatory factors. This is thought to be expressed via neurotransmitters in selective brain areas. | 11
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Beta blockers, also spelled β-blockers, are a class of medications that are predominantly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack after a first heart attack (secondary prevention). They are also widely used to treat high blood pressure, although they are no longer the first choice for initial treatment of most patients.Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response. Some block activation of all types of β-adrenergic receptors and others are selective for one of the three known types of beta receptors, designated β1, β2 and β3 receptors. β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-adrenergic receptors are located in fat cells.Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine (adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones and weaken the effects of stress hormones. | The physiological symptoms of the fight-or-flight response (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand. Musicians, public speakers, actors, and professional dancers have been known to use beta blockers to avoid performance anxiety, stage fright, and tremor during both auditions and public performances. The application to stage fright was first recognized in The Lancet in 1976, and by 1987, a survey conducted by the International Conference of Symphony Orchestra Musicians, representing the 51 largest orchestras in the United States, revealed 27% of its musicians had used beta blockers and 70% obtained them from friends, not physicians. Beta blockers are inexpensive, said to be relatively safe, and on one hand, seem to improve musicians performances on a technical level, while some, such as Barry Green, the author of "The Inner Game of Music" and Don Greene, a former Olympic diving coach who teaches Juilliard students to overcome their stage fright naturally, say the performances may be perceived as "soulless and inauthentic". Surgery
Low certainty evidence indicates that the use of beta blockers around the time of cardiac surgery may decrease the risk of heart dysrhythmias and atrial fibrillation. Starting them around the time of other types of surgery, however, may worsen outcomes. For non-cardiac surgery, the use of beta blockers to prevent adverse effects may reduce the risk of atrial fibrillation and myocardial infarctions (very low certainty evidence), however, there is moderate certainty evidence that this approach may increase the risk of hypotension. | 11
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Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them. Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability. Causes
The most common causes of TBI in the U.S. include violence, transportation accidents, construction site mishaps, and sports. Motor bikes are major causes, increasing in significance in developing countries as other causes reduce. The estimates that between 1.6 and 3.8 million traumatic brain injuries each year are a result of sports and recreation activities in the US. In children aged two to four, falls are the most common cause of TBI, while in older children traffic accidents compete with falls for this position. TBI is the third most common injury to result from child abuse. Abuse causes 19% of cases of pediatric brain trauma, and the death rate is higher among these cases. Although men are twice as likely to have a TBI. Domestic violence is another cause of TBI, as are work-related and industrial accidents. Firearms and blast injuries from explosions are other causes of TBI, which is the leading cause of death and disability in war zones. According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan." | Pre-existing or emerging mutations that contribute to rod photoreceptor degeneration in retinitis pigmentosa are passed down through familial lines; thus, allowing certain RP cases to be concentrated to specific geographical regions with an ancestral history of the disease. Several hereditary studies have been performed to determine the varying prevalence rates in Maine (USA), Birmingham (England), Switzerland (affects 1/7000), Denmark (affects 1/2500), and Norway. Navajo Indians display an elevated rate of RP inheritance as well, which is estimated as affecting 1 in 1878 individuals. Despite the increased frequency of RP within specific familial lines, the disease is considered non-discriminatory and tends to equally affect all world populations. Research
Future treatments may involve retinal transplants, artificial retinal implants, gene therapy, stem cells, nutritional supplements, and/or drug therapies. 2012: Scientists at the University of Miami Bascom Palmer Eye Institute presented data showing protection of photoreceptors in an animal model when eyes were injected with mesencephalic astrocyte-derived neurotrophic factor (MANF). Researchers at the University of California, Berkeley were able to restore vision to blind mice by exploiting a "photoswitch" that activates retinal ganglion cells in animals with damaged rod and cone cells.2015: A study by Bakondi et al. at Cedars-Sinai Medical Center showed that CRISPR/Cas9 can be used to treat rats with the autosomal dominant form of retinitis pigmentosa. | 0-1
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: 142 In 1982, Quinton together with Dr Sakharam Mahurkar, a nephrologist at County Cook Hospital in Chicago, developed dual-lumen catheter which became the standard for haemodialysis and apheresis.Sheridan was dubbed the "Catheter King" by Forbes magazine in 1988. He also invented the modern "disposable" plastic endotracheal tube now used routinely in surgery. Materials
Urinary catheters
A range of polymers are used for the construction of catheters, including silicone rubber, nylon, polyurethane, polyethylene terephthalate (PET), latex, and thermoplastic elastomers. Silicone is one of the most common implantable choice because it is inert and unreactive to body fluids and a range of medical fluids with which it might come into contact. On the other hand, the polymer is weak mechanically, and a number of serious fractures have occurred in catheters. For example, silicone is used in Foley catheters where fractures have been reported, often requiring surgery to remove the tip left in the bladder. There are many different types of catheters for bladder problems. A typical modern intermittent catheter is made from polyurethane and comes in different lengths and sizes for men, women and children.Some catheters are packed in a sterile saline solution. | Extending his inventiveness to his familys medical problems, Benjamin Franklin invented the flexible catheter in 1752 when his brother John suffered from bladder stones. Franklins catheter was made of metal with segments hinged together with a wire enclosed to provide rigidity during insertion.According to a footnote in his letter in Volume 4 of the Papers of Benjamin Franklin (1959), Franklin credits Francesco Roncelli-Pardino from 1720 as the inventor of a flexible catheter. In fact, Franklin claims the flexible catheter may have been designed even earlier.An early modern application of the catheter was employed by Claude Bernard for the purpose of cardiac catheterization in 1844. The procedure involved entering a horses ventricles via the jugular vein and carotid artery. This appears to be an earlier and modern application of the catheter because this catheter approach technique is still performed by neurosurgeons, cardiologists, and cardiothoracic surgeons.David S. Sheridan invented the modern disposable catheter in the 1940s. Prior to this, some reusable catheters consisted of braided cotton tubes, which were varnished, heat-treated and polished. As these were primarily produced in France, the advent of World War II threatened the supply chain.In 1959, Teschan first described central venous catheter as means of blood vessel access for haemodialysis.Other reusable catheters consisted of red rubber tubes. Although sterilized prior to reuse, they still posed a high risk of infection and often led to the spread of disease. | 11
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Most swine flu vaccines include an H1N1 and an H3N2 strain. Swine influenza has been recognized as a major problem since the outbreak in 1976. Evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the problem when the virus strains match enough to have significant cross-protection. Customised (autogenous) vaccines made from the specific viruses isolated, are made and used in the more difficult cases. The vaccine manufacturer Novartis claims that the H3N2 strain (first identified in 1998) has brought major losses to pig farmers. Abortion storms are a common sign and sows stop eating for a few days and run a high fever. The mortality rate can be as high as fifteen percent. Dogs
In 2004, influenza A virus subtype H3N8 was discovered to cause canine influenza. Because of the lack of previous exposure to this virus, dogs have no natural immunity to this virus. However, a vaccine was found in 2004. Annual reformulation
Each year, three strains are chosen for selection in that years flu vaccination by the WHO Global Influenza Surveillance and Response System. The chosen strains are the H1N1, H3N2, and Type-B strains thought most likely to cause significant human suffering in the coming season. Starting with the 2012–2013 Northern Hemisphere influenza season (coincident with the approval of quadrivalent influenza vaccines), the WHO has also recommended a 2nd B-strain for use in quadrivalent vaccines. | Periodontosis is an obsolete term that was used to describe what was once thought to be certain type of unique and distinguishable chronic periodontal disease that manifested as degenerative bony changes without concomitant inflammation. Although utilized for more than 50 years, the term has since been dropped in favor of a more contemporary disease classification for periodontal disease. Described by Gottlieb as a "diffuse atrophy of the alveolar bone," the term periodontosis was later applied and it gained acceptance as a disease entity, being defined as:
"a degenerative, noninflammatory destruction of the periodontium, originating in one or more of the periodontal structures and characterized by migrating and loosening of the teeth in the presence or absence of secondary epithelial proliferation and pocket formation or secondary gingival disease. "Noted as a rare disease, periodontosis was said to have been seen primarily in young patients. And despite being defined as being a "noninflammatory destruction of the periodontium," almost all cases did exhibit varying degrees of gingival inflammation. References
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The distal phalanges, as compared with the distal phalanges of the finger, are smaller and are flattened from above downward; each presents a broad base for articulation with the corresponding bone of the second row, and an expanded distal extremity for the support of the nail and end of the toe. Distal phalanx
In the hand, the distal phalanges are flat on their palmar surface, small, and with a roughened, elevated surface of horseshoe form on the palmar surface, supporting the finger pulp.: 6b. 3. The Phalanges of the Hand The flat, wide expansions found at the tips of the distal phalanges are called apical tufts. They support the fingertip pads and nails. The phalanx of the thumb has a pronounced insertion for the flexor pollicis longus (asymmetric towards the radial side), an ungual fossa, and a pair of unequal ungual spines (the ulnar being more prominent). This asymmetry is necessary to ensure that the thumb pulp is always facing the pulps of the other digits, an osteological configuration which provides the maximum contact surface with held objects.In the foot, the distal phalanges are flat on their dorsal surface. It is largest proximally and tapers to the distal end. The proximal part of the phalanx presents a broad base for articulation with the middle phalanx, and an expanded distal extremity for the support of the nail and end of the toe.: 6b. 3. | The arboreal specialization of these terminal phalanges makes it impossible for the sloth to walk on the ground where the animal has to drag its body with its claws. Additional images
See also
Hand
Foot
References
External links
MedTerms.com Medical Dictionary | 11
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Treatment
Historically, acute MS was a fatal disease, with death occurring within a year of onset, often secondary to extensive brain stem demyelination. Treatment recommendations, based on anecdotes, include plasma exchange in conjunction with high-dose glucocorticoids(e.g., 1 to 2 g/day of methylprednisolone for 10 days followed by a slow taper). For patients who survive the acute attack, follow-up treatments include immunosuppression (monthly mitoxantrone or cyclophosphamide) either alone or in combination with IFN beta or GA (glatiramer acetate). Prognosis
Marburg variant of MS is an acute fulminant demyelinating process which in most cases progresses inexorably to death within 1–2 years. However, there are some reports of Marburg MS reaching stability by three years. See also
Malignant multiple sclerosis
Tumefactive multiple sclerosis
References
== External links == | In a marathon, several percent of runners may be affected. Wearing footwear which fits helps prevent runners toe.If the shoe is too loose on the midfoot, the foot can slide forwards in the shoe, especially when going downhill. This may jam the toes into the end of the toebox. If the foot is sliding forwards because the shoe is too loose around the midfoot, it may be restrained by lacing the shoe carefully, or placing bulky padding between the tongue and the lacing, or by wrapping a strap in a figure-eight around the foot and ankle (image). : 86–87, 128, 142 Excessively tight or uneven fit around the midfoot may, however, cause tendon problems. : 125 Separately, if there is not enough space around the toes, the toes will also hit the toebox repeatedly. Feet become longer and wider when weight is put on them, because the arches flatten, and the toes also splay and bend. : p15, 18, 72–73 At the end of a long journey on foot, the arches flatten, the metatarsals spread, and the foot swells more than after a short one. : 52 The toes also need vertical space; a toe cap which is low enough to press on the top of the toe may also cause bruising under the nail, especially if the toe cap is stiff. If the toebox is pointed, the toes may be wedged forwards into the area with inadequate height. : 52–53, 135 Toenails which protrude unevenly may concentrate force on the toenail; properly-cut nails are therefore also important.Some susceptible runners may also have Mortons toe. | 0-1
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Despite these reductions, several women with Bloom syndrome have had children, and there is a single report of a male with Bloom syndrome bearing children.Although some persons with Bloom syndrome can struggle in school with subjects that require abstract thought, there is no evidence that intellectual disability is more common in Bloom syndrome than in other people.The most serious and frequent complication of Bloom syndrome is cancer. In the 281 persons followed by the Bloom Syndrome Registry, 145 persons (51.6%) have been diagnosed with a malignant neoplasm, and there have been 227 malignancies. The types of cancer and the anatomic sites at which they develop resemble the cancers that affect persons in the general population. The age of diagnosis for these cancers is earlier than for the same cancer in normal persons. And many persons with Bloom syndrome have been diagnosed with multiple cancers. The average life span is approximately 27 years. The most common cause of death in Bloom syndrome is from cancer. Other complications of the disorder include chronic obstructive lung disease and type 2 diabetes.There are a variety of excellent sources for more detailed clinical information about Bloom syndrome.There is a closely related entity that is now referred to as Bloom-syndrome-like disorder (BSLD) which is caused by mutations in components of the same protein complex to which the BLM gene product belongs, including TOP3A, which encodes the type I topoisomerase, topoisomerase 3 alpha, RMI1, and RMI2. | The features of BSLD include small size and dermatologic findings, such as cafe-au-lait spots, and the presence of the once pathognomonic elevated SCEs is reported for persons with mutations in TOP3A and RMI1.Bloom syndrome shares some features with Fanconi anemia possibly because there is overlap in the function of the proteins mutated in this related disorder. Genetics
Bloom syndrome is an autosomal recessive disorder, caused by mutations in the maternally- and paternally-derived copies of the gene BLM. As in other autosomal recessive conditions, the parents of an individual with Bloom syndrome do not necessarily exhibit any features of the syndrome. The mutations in BLM associated with Bloom syndrome are nulls and missense mutations that are catalytically inactive. The cells from persons with Bloom syndrome exhibit a striking genomic instability that is characterized by hyper-recombination and hyper-mutation. Human BLM cells are sensitive to DNA damaging agents such as UV and methyl methanesulfonate, indicating deficient repair capability. At the level of the chromosomes, the rate of sister chromatid exchange in Blooms syndrome is approximately 10 fold higher than normal and quadriradial figures, which are the cytologic manifestations of crossing-over between homologous chromosome, are highly elevated. Other chromosome manifestations include chromatid breaks and gaps, telomere associations, and fragmented chromosomes. The hyper-recombination can also be detected by molecular assays The BLM gene is a member of the protein family referred to as RecQ helicases. | 11
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Rectal or mouth swabs are required to diagnose infections in those areas.Prevention is by not having sex, the use of condoms, or having sex with only one other person, who is not infected. Chlamydia can be cured by antibiotics with typically either azithromycin or doxycycline being used. Erythromycin or azithromycin is recommended in babies and during pregnancy. Sexual partners should also be treated, and infected people should be advised not to have sex for seven days and until symptom free. Gonorrhea, syphilis, and HIV should be tested for in those who have been infected. Following treatment people should be tested again after three months.Chlamydia is one of the most common sexually transmitted infections, affecting about 4.2% of women and 2.7% of men worldwide. In 2015, about 61 million new cases occurred globally. In the United States about 1.4 million cases were reported in 2014. Infections are most common among those between the ages of 15 and 25 and are more common in women than men. In 2015 infections resulted in about 200 deaths. The word chlamydia is from the Greek χλαμύδα, meaning "cloak". Signs and symptoms
Genital disease
Women
Chlamydial infection of the cervix (neck of the womb) is a sexually transmitted infection which has no symptoms for around 70% of women infected. The infection can be passed through vaginal, anal, or oral sex. Of those who have an asymptomatic infection that is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. | PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy. Chlamydia is known as the "silent epidemic", as at least 70% of genital C. trachomatis infections in women (and 50% in men) are asymptomatic at the time of diagnosis, and can linger for months or years before being discovered. Signs and symptoms may include abnormal vaginal bleeding or discharge, abdominal pain, painful sexual intercourse, fever, painful urination or the urge to urinate more often than usual (urinary urgency). For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection. Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use. Guidelines recommend all women attending for emergency contraceptive are offered chlamydia testing, with studies showing up to 9% of women aged <25 years had chlamydia. Men
In men, those with a chlamydial infection show symptoms of infectious inflammation of the urethra in about 50% of cases. Symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, testicular pain or swelling, or fever. If left untreated, chlamydia in men can spread to the testicles causing epididymitis, which in rare cases can lead to sterility if not treated. | 11
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During an acute illness, especially in children, nutritional problems may first present or can exacerbate an existing problem (example: aspiration) as well as cause other health issues such as electrolyte and blood sugar disturbances. Orthopaedics
Skeletal problems associated with weak muscles in SMA include tight joints with limited range of movement, hip dislocations, spinal deformity, osteopenia, an increase risk of fractures and pain. Weak muscles that normally stabilize joints such as the vertebral column lead to development of kyphosis and/or scoliosis and joint contracture. Spine fusion is sometimes performed in people with SMA I/II once they reach the age of 8–10 to relieve the pressure of a deformed spine on the lungs. Furthermore, immobile individuals, posture and position on mobility devices as well as range of motion exercises, and bone strengthening can be important to prevent complications. People with SMA might also benefit greatly from various forms of physiotherapy, occupational therapy and physical therapy.Orthotic devices can be used to support the body and to aid walking. For example, orthotics such as AFOs (ankle foot orthoses) are used to stabilise the foot and to aid gait, TLSOs (thoracic lumbar sacral orthoses) are used to stabilise the torso. Assistive technologies may help in managing movement and daily activity and greatly increase the quality of life. | Side effects
As with other opioid analgesics, central nervous system effects (such as sedation, confusion, and dizziness) are considerations with butorphanol. Nausea and vomiting are common. Less common are the gastrointestinal effects of other opioids (mostly constipation). Another side effect experienced by people taking the medication is increased perspiration. Name
Within the INN, USAN, BAN, and AAN naming systems this drug is known as butorphanol, while within JAN it is named torbugesic. As the tartrate salt, butorphanol is known as butorphanol tartrate (USAN, BAN).Its tradename Stadol was recently discontinued by the manufacturer. It is now only available in its generic formulations manufactured by Apotex, Mylan, Novex and Ben Venue Laboratories. Availability
Butorphanol is available in the U.S. as a generic drug; it is available in various nations under one of any number of trade names, including Moradol and Beforal (Brand name Stadol no longer available in the US); veterinary trade names include Butorphic, Dolorex, Morphasol, Torbugesic, and Torbutrol. Legality
Butorphanol is listed under the Single Convention on Narcotic Drugs 1961 and in the United States is a Schedule IV Narcotic controlled substance with a DEA ACSCN of 9720; being in Schedule IV it is not subject to annual aggregate manufacturing quotas. The free base conversion ratio of the hydrochloride is 0.69. Butorphanol was originally in Schedule II and at one point it was decontrolled. Veterinary use
In veterinary anesthesia, butorphanol (trade name: Torbugesic) is widely used as a sedative and analgesic in dogs, cats and horses. | 0-1
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Schizoaffective disorder is more likely to occur in women and symptoms begin manifesting at a young age. Therapy
Psychosocial treatments have been found to improve outcomes related to schizoaffective disorder. Supportive psychotherapy and cognitive behavioral therapy are both helpful. Intensive case management (ICM) has been shown to reduce hospitalizations, improve adherence to treatment, and improve social functioning. With ICM, clients are assigned a case manager responsible for coordination of care and assisting clients to access supports to address needs in multiple areas related to well-being, including housing. Psychiatric/psychosocial rehabilitation is often a component of schizoaffective disorder treatment. This rehabilitation method focuses on solving community integration problems such as obtaining and keeping housing and increasing involvement in positive social groups. It also focuses on improving and increasing activities of daily living; increasing daily healthy habits and decreasing unhealthy behaviors, thereby significantly improving quality of life. Psychiatric rehabilitation may also focus on vocational rehabilitation. Evidence suggests that cognition-based approaches may be able to improve work and social functioning.Psychiatric rehabilitation consists of eight main areas:
Psychiatric (symptom reduction and management)
Health and Medical (maintaining consistency of care)
Housing (safe environments)
Basic living skills (hygiene, meals [including increasing healthy food intake and reducing processed food intake], safety, planning and chores)
Social (relationships, family boundaries, communication and integration of client into the community)
Education and vocation (coping skills, motivation and suitable goals chosen by client)
Finance (personal budget)
Community and legal (resources)
Medication
Antipsychotic medication is usually required both for acute treatment and the prevention of relapse. | Familial dysalbuminemic hyperthyroxinemia is a type of hyperthyroxinemia associated with mutations in the human serum albumin gene. The term was introduced in 1982. References
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Methotrexate is teratogenic and hence is not advised for either the prospective father to take it before or for the mother to take it before or during pregnancy (pregnancy category X) and for a period after birth. Methotrexate can also cause mucositis.Central nervous system reactions to methotrexate have been reported, especially when given via the intrathecal route (directly into the cerebrospinal fluid), which include myelopathies and leukoencephalopathies. It has a variety of cutaneous side effects, particularly when administered in high doses.Another little understood but serious possible adverse effect of methotrexate is neurological damage and memory loss. Neurotoxicity may result from the drug crossing the blood–brain barrier and damaging neurons in the cerebral cortex. People with cancer who receive the medication often nickname these effects "chemo brain" or "chemo fog". Drug interactions
Penicillins may decrease the elimination of methotrexate, so increase the risk of toxicity. While they may be used together, increased monitoring is recommended. The aminoglycosides, neomycin and paromomycin, have been found to reduce gastrointestinal (GI) absorption of methotrexate. Probenecid inhibits methotrexate excretion, which increases the risk of methotrexate toxicity. Likewise, retinoids and trimethoprim have been known to interact with methotrexate to produce additive hepatotoxicity and haematotoxicity, respectively. Other immunosuppressants like cyclosporins may potentiate methotrexates haematologic effects, hence potentially leading to toxicity. NSAIDs have also been found to fatally interact with methotrexate in numerous case reports. Nitrous oxide potentiating the haematological toxicity of methotrexate has also been documented. | Methotrexate (MTX), formerly known as amethopterin, is a chemotherapy agent and immune-system suppressant. It is used to treat cancer, autoimmune diseases, and ectopic pregnancies. Types of cancers it is used for include breast cancer, leukemia, lung cancer, lymphoma, gestational trophoblastic disease, and osteosarcoma. Types of autoimmune diseases it is used for include psoriasis, rheumatoid arthritis, and Crohns disease. It can be given by mouth or by injection.Common side effects include nausea, feeling tired, fever, increased risk of infection, low white blood cell counts, and breakdown of the skin inside the mouth. Other side effects may include liver disease, lung disease, lymphoma, and severe skin rashes. People on long-term treatment should be regularly checked for side effects. It is not safe during breastfeeding. In those with kidney problems, lower doses may be needed. It acts by blocking the bodys use of folic acid.Methotrexate was first made in 1947 and initially was used to treat cancer, as it was less toxic than the then current treatments. In 1956 it provided the first cures of a metastatic cancer. It is on the World Health Organizations List of Essential Medicines. Methotrexate is available as a generic medication. In 2019, it was the 111th most commonly prescribed medication in the United States, with more than 5 million prescriptions. Medical uses
Chemotherapy
Methotrexate was originally developed and continues to be used for chemotherapy, either alone or in combination with other agents. | 11
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It is believed that the U.S. ban on lead paint in buildings in the late 1970s, as well as the phaseout of leaded gasoline in the 1970s and 1980s, partially helped contribute to the decline of violent crime in the United States since the early 1990s. Exposure routes
Lead is a common environmental pollutant. Causes of environmental contamination include industrial use of lead, such as found in facilities that process lead-acid batteries or produce lead wire or pipes, and metal recycling and foundries. Storage batteries and ammunition are made with the largest amounts of lead consumed in the economy each year, in the US as of 2013. Children living near facilities that process lead, such as lead smelters, have been found to have unusually high blood lead levels. In August 2009, parents rioted in China after lead poisoning was found in nearly 2000 children living near zinc and manganese smelters. Lead exposure can occur from contact with lead in air, household dust, soil, water, and commercial products. Leaded gasoline has also been linked to increases in lead pollution. Some research has suggested a link between leaded gasoline and crime rates. Man made lead pollution has been elevated in the air for the past 2000 years. Lead pollution in the air is entirely due to human activity (mining and smelting, as well as in gasoline). Occupational exposure
In adults, occupational exposure is the main cause of lead poisoning. | A carotid-cavernous fistula results from an abnormal communication between the arterial and venous systems within the cavernous sinus in the skull. It is a type of arteriovenous fistula. As arterial blood under high pressure enters the cavernous sinus, the normal venous return to the cavernous sinus is impeded and this causes engorgement of the draining veins, manifesting most dramatically as a sudden engorgement and redness of the eye of the same side. Presentation
CCF symptoms include bruit (a humming sound within the skull due to high blood flow through the arteriovenous fistula), progressive visual loss, and pulsatile proptosis or progressive bulging of the eye due to dilatation of the veins draining the eye. Pain is the symptom that patients often find the most difficult to tolerate.Patients usually present with sudden or insidious onset of redness in one eye, associated with progressive proptosis or bulging.They may have a history of similar episodes in the past. Causes
Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas. Diagnosis
This is based on MRI scan, magnetic resonance angiography and CT scan. A cerebral digital subtraction angiography (DSA) enhances visualization of the fistula. CT scans classically show an enlarged superior ophthalmic vein, cavernous sinus enlargement ipsilateral (same side) as the abnormality and possibly diffuse enlargement of all the extraocular muscles resulting from venous engorgement. Selective arteriography is used to evaluate arteriovenous fistulas. | 0-1
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However, only about 0.4–0.5% of breastfeeding mothers develop an abscess.Some predisposing factors are known but their predictive value is minimal. It appears that proper breastfeeding technique, frequent breastfeeding and avoidance of stress are the most important factors that can be influenced. Light cases of mastitis are often called breast engorgement; the distinction is overlapping and possibly arbitrary or subject to regional variations. Non pregnancy related
The term nonpuerperal mastitis describes inflammatory lesions of the breast occurring unrelated to pregnancy and breastfeeding. This article includes description of mastitis as well as various kinds of mammary abscesses. Skin related conditions like dermatitis and foliculitis are a separate entity. Names for non-puerperal mastitis are not used very consistently and include mastitis, subareolar abscess, duct ectasia, periductal inflammation, Zuskas disease and others. Periductal mastitis is a form of nonlactational mastitis, and is characterized by inflammation of the subareolar ducts. Although the cause of periductal mastitis is currently unknown, it is predicted that smoking may be related. This condition is mainly seen in young women but can also be seen in men. Signs and symptoms
Lactation mastitis usually affects only one breast and the symptoms can develop quickly. It develops into three stages, from the initial stage, the pus formation stage, to the restoration stage. | There is a possibility that infants carrying infectious pathogens in their noses can infect their mothers; the clinical significance of this finding is still unknown. Mastitis and breast abscesses can also be caused by direct trauma to the breast. Such injury can occur for example during sports activities or due to seat belt injury. Mastitis can also develop due to contamination of a breast implant or any other foreign body, for example after nipple piercing. In such cases, the removal of the foreign body is indicated.Women who are breastfeeding are at risk for developing mastitis especially if they have sore or cracked nipples or have had mastitis before while breastfeeding another baby. Also, the chances of getting mastitis increases if women use only one position to breastfeed or wear a tight-fitting bra, which may restrict milk flow Difficulties in getting a nursing infant to latch on to the breast can also increase the risk for mastitis.Women with diabetes, chronic illness, AIDS, or an impaired immune system may be more susceptible to the development of mastitis. Infection
Some women (approximately 15%) will require antibiotic treatment for infection which is usually caused by bacteria from the skin or the babys mouth entering the milk ducts through skin lesions of the nipple or through the opening of the nipple. Infection is usually caused by Staphylococcus aureus. Infectious pathogens commonly associated with mastitis are Staphylococcus aureus, Streptococcus spp. and Gram-negative bacilli such as Escherichia coli. | 11
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Within the cataract removal procedures which take place a variety of complications may occur including;
chronic inflammation inside the eye
retinal detachment
infection
Rehabilitation
There are several medications which need to be consumed in order to treat phacolytic glaucoma. The medicines induced ensure the management of glaucoma and reduce inflammation. These medications consist of: Aqueous suppressants, anti-inflammatory drugs, hyper-osmotic agents, cycloplegics, anti-glaucoma medications. Medical therapy, however, is only a temporary treatment until cataract surgery can take place.The use of an eyepatch for a certain amount of time, as well as a contact lens to protect the eye which dissolves releasing antibiotics, must be incorporated in the rehabilitation process to reduce the risk of infection of the eye and to allow for an effective healing process. Additionally, the patient must consistently visit the specialist in order to ensure a successful removal of phacolytic glaucoma. There may be a need for medical therapies which treat arising issues for the eye such as inflammation. These medical therapy procedures for phacolysis consist of controlling the intraocular pressure which may include the use of topical steroids in order to decrease inflammation in the eye, and mydriatics in order to prevent the formation of synechiae. Medication
It is found that with most cases, of phacolytic glaucoma post surgery patients are not exposed to many further obstacles in the healing process which therefore avoids the need for medication. Although, it is mostly encouraged that patients take antiglaucoma medication in order to deter the possibility of glaucoma and inflammation implicating the eye. | Diflorasone diacetate is a topical steroid that comes in the form of a cream. It is manufactured by E. Fougera & Co. and is used as an anti-inflammatory and anti-itching agent, like other topical corticosteroids. It is prescribed for psoriasis and atopic dermatitis, among other conditions. With respect to potency, it is regarded as a Class I corticosteroid [of classes I – VII] in the United States.No long-term animal studies have been done to determine whether diflorasone diacetate could have carcinogenic properties.Little data is available regarding whether diflorasone diacetate would be present in great enough quantities to cause harm to an infant. References
External links
"Diflorasone diacetate". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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In general, surgery is not recommended, as Kaposi sarcoma can appear in wound edges. In general, more widespread disease, or disease affecting internal organs, is treated with systemic therapy with interferon alpha, liposomal anthracyclines (such as liposomal doxorubicin or daunorubicin), thalidomide, or paclitaxel.Alitretinoin, applied to the lesion, may be used when the lesion is not getting better with standard treatment of HIV/AIDS and chemotherapy or radiation therapy cannot be used. Epidemiology
With the decrease in the death rate among people with HIV/AIDS receiving new treatments in the 1990s, the rates and severity of epidemic KS also decreased. However, the number of people living with HIV/AIDS is increasing in the United States, and it is possible that the number of people with AIDS-associated Kaposi sarcoma will again rise as these people live longer with HIV infection. Society
Because of their highly visible nature, external lesions are sometimes the presenting symptom of AIDS. Kaposi sarcoma entered the awareness of the general public with the release of the film Philadelphia, in which the main character was fired after his employers found out he was HIV-positive due to visible lesions. By the time KS lesions appear, likely, the immune system has already been severely weakened. It has been reported that only 6% of men who have sex with men are aware that KS is caused by a virus different from HIV. Thus, there is little community effort to prevent KSHV infection. Likewise, no systematic screening of organ donations is in place. | Prudent advice is to use commercial lubricants when needed and avoid deep kissing with partners with KSHV infection or whose status is unknown.KSHV is also transmissible via organ transplantation and blood transfusion. Testing for the virus before these procedures is likely to effectively limit iatrogenic transmission. Pathology
Despite its name, in general it is not considered a true sarcoma, which is a tumor arising from mesenchymal tissue. The histogenesis of KS remains controversial. KS may arise as a cancer of lymphatic endothelium and forms vascular channels that fill with blood cells, giving the tumor its characteristic bruise-like appearance. KSHV proteins are uniformly detected in KS cancer cells.KS lesions contain tumor cells with a characteristic abnormal elongated shape, called spindle cells. The most typical feature of Kaposi sarcoma is the presence of spindle cells forming slits containing red blood cells. Mitotic activity is only moderate and pleomorphism is usually absent. The tumor is highly vascular, containing abnormally dense and irregular blood vessels, which leak red blood cells into the surrounding tissue and give the tumor its dark color. Inflammation around the tumor may produce swelling and pain. Variously sized PAS positive hyaline bodies are often seen in the cytoplasm or sometimes extracellularly.The spindle cells of Kaposi sarcoma differentiate toward endothelial cells, probably of lymph vessel rather than blood vessel origin. The consistent immunoreactivity for podoplanin supports the lymphatic nature of the lesion. | 11
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A craniopharyngioma is a rare type of brain tumor derived from pituitary gland embryonic tissue that occurs most commonly in children, but also affects adults. It may present at any age, even in the prenatal and neonatal periods, but peak incidence rates are childhood-onset at 5–14 years and adult-onset at 50–74 years. People may present with bitemporal inferior quadrantanopia leading to bitemporal hemianopsia, as the tumor may compress the optic chiasm. It has a point prevalence around two per 1,000,000. Craniopharyngiomas are distinct from Rathkes cleft tumours and intrasellar arachnoid cysts. Symptoms and signs
Craniopharyngiomas are almost always benign. However, as with many brain tumors, their treatment can be difficult, and significant morbidities are associated with both the tumor and treatment. Headache (obstructive hydrocephalus)
Hypersomnia
Myxedema
Postsurgical weight gain
Polydipsia
Polyuria (diabetes insipidus)
Vision loss (bitemporal hemianopia)
VomitingOften occurs after treatment
Growth hormone (GH) insufficiency, caused by the reduction in GH production - symptoms include:
Stunted growth and delayed puberty (in children)
General fatigue, loss of muscle mass and tone (in adults)
Pituitary insufficiency
Often occurs to some degree because craniopharyngiomas develop in the area of the pituitary stalk, which can affect the function of the pituitary gland and many other hormones
Reduction in prolactin production is very uncommon and occurs with severe pituitary insufficiency. Large pituitary tumors can paradoxically elevate blood prolactin levels due to the "stalk effect". This elevation occurs as a result of the compression of the pituitary stalk, which interferes with the brains control of prolactin production. | A computed tomography (CT) scan is also a good diagnostic tool, as it detects calcification in the tumor.Two distinct types are recognized:
Adamantinomatous craniopharyngiomas, which resemble ameloblastomas (the most common type of odontogenic tumor), are characterized by activating CTNNB1 mutations. Papillary craniopharyngiomas are characterized by BRAFv600E mutations.In the adamantinomatous type, calcifications are visible on neuroimaging and are helpful in diagnosis. The papillary type rarely calcifies. A vast majority of craniopharyngiomas in children are adamantiomatous, whereas both subtypes are common in adults. Mixed-type tumors also occur.On macroscopic examination, craniopharyngiomas are cystic or partially cystic with solid areas. On light microscopy, the cysts are seen to be lined by stratified squamous epithelium. Keratin pearls may also be seen. The cysts are usually filled with a yellow, viscous fluid rich in cholesterol crystals. Of a long list of possible symptoms, the most common presentations include headaches, growth failure, and bitemporal hemianopsia. Malignant craniopharyngioma
Craniopharyngiomas are usually successfully managed with a combination of adjuvant chemotherapy and neurosurgery. Recent research describes the rare occurrence of malignant transformations of these normally benign tumors. | 11
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Medications
The primary medications used for GERD are proton-pump inhibitors, H2 receptor blockers and antacids with or without alginic acid. The use of acid suppression therapy is a common response to GERD symptoms and many people get more of this kind of treatment than their case merits. The overuse of acid suppression is a problem because of the side effects and costs. Proton-pump inhibitors
Proton-pump inhibitors (PPIs), such as omeprazole, are the most effective, followed by H2 receptor blockers, such as ranitidine. If a once-daily PPI is only partially effective they may be used twice a day. They should be taken one half to one hour before a meal. There is no significant difference between PPIs. When these medications are used long term, the lowest effective dose should be taken. They may also be taken only when symptoms occur in those with frequent problems. H2 receptor blockers lead to roughly a 40% improvement. Antacids
The evidence for antacids is weaker with a benefit of about 10% (NNT=13) while a combination of an antacid and alginic acid (such as Gaviscon) may improve symptoms by 60% (NNT=4). Metoclopramide (a prokinetic) is not recommended either alone or in combination with other treatments due to concerns around adverse effects. The benefit of the prokinetic mosapride is modest. Other agents
Sucralfate has similar effectiveness to H2 receptor blockers; however, sucralfate needs to be taken multiple times a day, thus limiting its use. | PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin. PTH was one of the first hormones to be shown to use the G-protein adenylyl cyclase second messenger system. Regulation of serum phosphate
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine. However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, absorption of both calcium and phosphate is mediated by an increase in activated vitamin D. The absorption of phosphate is not as dependent on vitamin D as is that of calcium. The end result of PTH release is a small net drop in the serum concentration of phosphate. Vitamin D synthesis
PTH upregulates the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol, the major circulating form of inactive vitamin D, into 1,25-dihydroxycholecalciferol, the active form of vitamin D, in the kidney. Interactive pathway map
Regulation of PTH secretion
Secretion of parathyroid hormone is determined chiefly by serum ionized calcium concentration through negative feedback. Parathyroid cells express calcium-sensing receptors on the cell surface. PTH is secreted when [Ca2+] is decreased (calcitonin is secreted when serum calcium levels are elevated). | 0-1
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Chicken Pox)
Contraceptive sponges
History of a recent birth, miscarriage, or abortion
Using super-absorbent tampons
Previously having TSS
Diagnosis
For staphylococcal toxic shock syndrome, the diagnosis is based upon CDC criteria defined in 2011, as follows:
Body temperature > 38.9 °C (102.02 °F)
Systolic blood pressure < 90 mmHg
Diffuse macular erythroderma
Desquamation (especially of the palms and soles) 1–2 weeks after onset
Involvement of three or more organ systems:
Gastrointestinal (vomiting, diarrhea)
Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal for laboratory
Mucous membrane hyperemia (vaginal, oral, conjunctival)
Kidney failure (serum creatinine > 2 times normal)
Liver inflammation (bilirubin, AST, or ALT > 2 times normal)
Low platelet count (platelet count < 100,000 / mm3)
Central nervous system involvement (confusion without any focal neurological findings)
Negative results of:
Blood, throat, and CSF cultures for other bacteria (besides S. aureus)
Negative serology for Rickettsia infection, leptospirosis, and measlesCases are classified as confirmed or probable as follows:
Confirmed: All six of the criteria above are met (unless the patient dies before desquamation can occur)
Probable: Five of the six criteria above are met
Treatment
The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure. Treatment includes removal or draining of the source of infection—often a tampon—and draining of abscesses. Outcomes are poorer in patients who do not have the source of infection removed.Antibiotic treatment should cover both S. pyogenes and S. aureus. This may include a combination of cephalosporins, penicillins or vancomycin. | She did not recover, and died sixteen days later on April 22 from toxic shock poisoning at the age of 42. Mike Von Erich, d. 1987, developed the syndrome after shoulder surgery: he made an apparent recovery but experienced brain damage and weight loss as a result of the condition; he died by suicide later. References
External links
Stevens DL (1995). "Streptococcal toxic-shock syndrome: spectrum of disease, pathogenesis, and new concepts in treatment". Emerging Infectious Diseases. 1 (3): 69–78. doi:10.3201/eid0103.950301. PMC 2626872. PMID 8903167. "Toxic Shock Syndrome (TSS): The Facts". Toxic Shock Syndrome information service. tssis.com. | 11
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Long-term studies of adults with post-surgical clubfeet, especially those needing multiple surgeries, show that they may not fare as well in the long term. Some people may require additional surgeries as they age, though there is some dispute as to the effectiveness of such surgeries, in light of the prevalence of scar tissue present from earlier surgeries. Developing world
Despite effective treatments, children in LMICs face many barriers such as limited access to equipment (specifically casting materials and abduction braces), shortages of healthcare professionals, and low education levels and socioeconomic status amongst caregivers and families. These factors make it difficult to detect and diagnose children with clubfoot, connect them to care, and train their caregivers to follow the proper treatment and return for follow-up visits. It is estimated that only 15% of those diagnosed with clubfoot receive treatment.In an effort to reduce the burden of clubfoot in LMICs, there have been initiatives to improve early diagnosis, organize high-volume Ponseti casting centers, utilize mid-level practitioners and non-physician health workers, engage families in care, and provide local follow-up in the persons community. Cultural references
Hippolyte Tautain, the stableman at the Lion DOr public house in the 1856 novel Madame Bovary by Gustave Flaubert, has clubfoot. Charles Bovary tries to correct it, but the procedure is unsuccessful, and Tautain must have an amputation. Philip Carey, the main character of the 1915 novel Of Human Bondage by W. Somerset Maugham, has clubfoot. It is a central theme of the work. Velma, a character in the 1941 film High Sierra, has clubfoot. | Loose anagen syndrome hairs at the occipital scalp can be knotted easily when theres movement of those hairs against the pillow at night.There are 3 different types of loose anagen hair syndrome. Loose anagen syndrome type A is when the hair of the patient appears to be fine and thinly distributed. Patients with type A loose anagen syndrome experience a decrease in the density of their hairs. Patients diagnosed with type B loose anagen hair syndrome tend to have hair that is difficult to manage and has a disordered, unruly appearance. Type C loose anagen syndrome is when the hair sheds but the appearance of their hair appears to be normal. Loose anagen syndrome type A and B are more prevalent in children. Loose anagen hair syndrome type C is most frequently seen in adults. There is not specific treatment for each type of loose anagen syndrome. It is also unknown as to how each type is developed. Differential diagnosis
Loose Anagen Syndrome can commonly be misdiagnosed for other skin and hair disorders such as short anagen syndrome, alopecia areata, telogen effluvium, trichotillomania and toxic ingestion. Similar symptoms and signs appear in these conditions, however there are different aspects that distinguish each one from another. Short anagen syndrome and loose anagen syndrome are similar as both conditions lead to the inability to grow long hair and patients rarely need to get their hair cut. | 0-1
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Roughly 50-75% of all pregnant women are immune to parvovirus B19 while the remainder of women are susceptible to mild illness. A majority of fetuses who do contract parvovirus B19 show either no significant symptoms or complete resolution of the virus. However, the following serious complications are rare but possible: miscarriage, stillbirth, fetal anemia, hepatic failure, and abnormal neurodevelopment outcome. In some cases, fetuses would develop hydrops fetalis due to congenital parvovirus B19. This condition was studied as a determinant of later fetal outcomes, such as miscarriage or perinatal death, in 2016 systematic review. The review showed that those born with parvovirus B19 that caused hydrops fetalis did have an association with higher mortality risk and higher risk of complications. While the potential consequences of erythema infectiosum can be quite serious in pregnancy, mothers can be tested for immunity via the presence of IgG and IgM antibodies.In addition to fetuses, parvovirus B19 infection and its effects has been studied in adults as well. The virus has also been associated with the development of neurological complications, as identified in a systematic review in 2014. This analysis included a total of 89 studies covering complications in both the central and nervous system such as encephalitis, meningitis, and peripheral neuropathy. However, the specific pathophysiology of these complications has yet to be discovered but the review does encourage the use of antibody testing to determine a patients risk. Infection of this virus is not limited to the nervous system. | It manifests in painful swelling of the joints that feels similar to arthritis. Older children and adults with fifth disease may have difficulty in walking and in bending joints such as wrists, knees, ankles, fingers, and shoulders.The disease is usually mild, but in certain risk groups and rare circumstances, it can have serious consequences:
In pregnant women, infection in the first trimester has been linked to hydrops fetalis, causing spontaneous miscarriage. In people with sickle-cell disease or other forms of chronic hemolytic anemia such as hereditary spherocytosis, infection can precipitate an aplastic crisis. Those who are immunocompromised (HIV/AIDS, chemotherapy) may be at risk for complications if exposed. In less than 5% of women with parvovirus B19 infection, a baby may develop severe anemia leading to miscarriage. This occurs most often during the first half of pregnancy. Causes
Fifth disease, also known as erythema infectiosum, is caused by parvovirus B19, which only infects humans. Infection by parvovirus B19 can lead to multiple clinical manifestations, but the most common is fifth disease.Parvovirus B19 (B19V) is a small, single-stranded, non-enveloped DNA virus. Binding of B19V capsid to the cellular receptor globoside (Gb4Cer) results in a cascade of structural changes and subsequent signal transduction processes facilitating the entry of parvovirus B19 into the host cell. After gaining access to the host cell, BV19 binds to glycosphingolipid globoside (blood group P antigen) targeting erythroid lineage in the bone marrow. | 11
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A mastocytoma or mast cell tumor is a type of round-cell tumor consisting of mast cells. It is found in humans and many animal species; it also can refer to an accumulation or nodule of mast cells that resembles a tumor. Mast cells originate from the bone marrow and are normally found throughout the connective tissue of the body as normal components of the immune system. As they release histamine, they are associated with allergic reactions. Mast cells also respond to tissue trauma. Mast cell granules contain histamine, heparin, platelet-activating factor, and other substances. Disseminated mastocytosis is rarely seen in young dogs and cats, while mast cell tumors are usually skin tumors in older dogs and cats. Although not always malignant, they do have the potential to be. Up to 25 percent of skin tumors in dogs are mast cell tumors, with a similar number in cats. Signs and symptoms
Humans
When mastocytomas affect humans, they are typically found in skin. They usually occur as a single lesion on the trunk or wrist. Although it is rare, mastocytomas are sometimes found in the lung. It can also affect children. Other animals
Mast cell tumors are known among veterinary oncologists as the great pretenders because their appearance can be varied, from a wart-like nodule to a soft subcutaneous lump (similar on palpation to a benign lipoma) to an ulcerated skin mass. Most mast cell tumors are small, raised lumps on the skin. They may be hairless, ulcerated, or itchy. | Mineralization of the tumor is common. In pigs and cattle, mast cell tumors are rare. They tend to be solitary and benign in pigs and multiple and malignant in cattle. Mast cell tumors are found in the skin of cattle most commonly, but these may be metastases from tumors of the viscera. Other sites in cattle include the spleen, muscle, gastrointestinal tract, omentum, and uterus. Dogs
Mast cell tumors mainly occur in older adult dogs, but have been known to occur on rare occasions in puppies. The following breeds are commonly affected by mast cell tumors:
Boxer
Staffordshire bull terrier
Bulldog
Basset hound
Weimaraner
Boston terrier
Great Dane
Golden retriever
Labrador retriever
Beagle
German shorthaired pointer
Scottish terrier
Pug
Shar pei
Rhodesian ridgeback
Cats
Two types of mast cell tumors have been identified in cats, a mast cell type similar to dogs and a histiocytic type that appears as subcutaneous nodules and may resolve spontaneously. Young Siamese cats are at an increased risk for the histiocytic type, although the mast cell type is the most common in all cats and is considered to be benign when confined to the skin.Mast cell tumors of the skin are usually located on the head or trunk. Gastrointestinal and splenic involvement is more common in cats than in dogs; 50 percent of cases in dogs primarily involved the spleen or intestines. Gastrointestinal mast cell tumors are most commonly found in the muscularis layer of the small intestine, but can also be found in the large intestine. | 11
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In the bloodstream, the bacteria can infect both phagocytes and non-phagocytes. B. pseudomallei use their flagella to move near host cells, then attach to the cells using various adhesion proteins, including the type IV pilus protein PilA as well as adhesion proteins BoaA and BoaB. Additionally, adhesion of the bacteria partially depends on the presence of the host protein Protease-activated receptor-1 which is present on the surface of endothelial cells, platelets, and monocytes. Once bound, the bacteria enter host cells through endocytosis, ending up inside an endocytic vesicle. As the vesicle acidifies, B. pseudomallei uses its Type 3 secretion system (T3SS) to inject effector proteins into the host cell, disrupting the vesicle and allowing the bacteria to escape into the host cytoplasm. Within the host cytoplasm, the bacteria evade being killed by the host autophagy using various T3SS effector proteins. The bacteria replicate in the host cytoplasm.Inside the host cell, the bacteria move by inducing the polymerization of the host actin behind them, propelling the bacteria forward. This actin-mediated motility is accomplished with the autotransporter BimA which interacts with actin at the tail-end of the bacterium. The bacteria that has BimABm allele has higher possibility of causing neurological melioidosis, thus higher chance of death and residual disability to the host when compared to the bacteria that has BimABp variant. Propelled by actin, the bacteria push against the host membrane, creating protrusions that extend into neighbouring cells. These protrusions cause neighboring cells to fuse, leading to the formation of multinucleated giant cells (MNGCs). | The clinical manifestation of the disease can range from simple skin changes such as abscesses or ulcerations to severe organ problems. The commonest organs affected are liver, spleen, lungs, prostate, and kidneys. Among the most common features are bacteremia (in 40 to 60% of cases), pneumonia (50%), and septic shock (20%). People with only pneumonia may have a prominent cough with sputum and shortness of breath. However, those with septic shock together with pneumonia may have minimal coughing. Results of a chest X-ray can range from diffuse nodular infiltrates in those with septic shock to progressive consolidation located most commonly in the upper lobes for those with pneumonia only. Pleural effusion and empyema are more common for melioidosis affecting lower lobes of the lungs. In 10% of cases, people develop secondary pneumonia caused by other bacteria after the primary infection. In northern Australia, 60% of the infected children presented with only skin lesions, while 20% presented with pneumonia.Depending on the course of infection, other severe manifestations develop. Approximately 1 to 5% of those infected develop inflammation of the brain and brain covering or brain abscess; 14 to 28% develop pyelonephritis, kidney abscess or prostatic abscesses; 0 to 30% develop neck or salivary gland abscesses; 10 to 33% develop liver, spleen, or paraintestinal abscesses; and 4 to 14% develop septic arthritis and osteomyelitis. Rare manifestations include lymph node disease resembling tuberculosis, mediastinal masses, pericardial effusion, mycotic aneurysm, and inflammation of the pancreas. | 11
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A brachial plexus injury (BPI), also known as brachial plexus lesion, is an injury to the brachial plexus, the network of nerves that conducts signals from the spinal cord to the shoulder, arm and hand. These nerves originate in the fifth, sixth, seventh and eighth cervical (C5–C8), and first thoracic (T1) spinal nerves, and innervate the muscles and skin of the chest, shoulder, arm and hand.Brachial plexus injuries can occur as a result of shoulder trauma, tumours, or inflammation, or obstetric. Obstetric injuries may occur from mechanical injury involving shoulder dystocia during difficult childbirth, with a prevalence of 1 in 1000 births. "The brachial plexus may be injured by falls from a height on to the side of the head and shoulder, whereby the nerves of the plexus are violently stretched. The brachial plexus may also be injured by direct violence or gunshot wounds, by violent traction on the arm, or by efforts at reducing a dislocation of the shoulder joint".The rare Parsonage–Turner syndrome causes brachial plexus inflammation without obvious injury, but with nevertheless disabling symptoms. Signs and symptoms
Signs and symptoms may include a limp or paralyzed arm, lack of muscle control in the arm, hand, or wrist, and lack of feeling or sensation in the arm or hand. Although several mechanisms account for brachial plexus injuries, the most common is nerve compression or stretch. Infants, in particular, may experience brachial plexus injuries during delivery and these present with typical patterns of weakness, depending on which portion of the brachial plexus is involved. | Periodic fever syndromes are a set of disorders characterized by recurrent episodes of systemic and organ-specific inflammation. Unlike autoimmune disorders such as systemic lupus erythematosus, in which the disease is caused by abnormalities of the adaptive immune system, people with autoinflammatory diseases do not produce autoantibodies or antigen-specific T or B cells. Instead, the autoinflammatory diseases are characterized by errors in the innate immune system.The syndromes are diverse, but tend to cause episodes of fever, joint pains, skin rashes, abdominal pains and may lead to chronic complications such as amyloidosis.Most autoinflammatory diseases are genetic and present during childhood. The most common genetic autoinflammatory syndrome is familial Mediterranean fever, which causes short episodes of fever, abdominal pain, serositis, lasting less than 72 hours. It is caused by mutations in the MEFV gene, which codes for the protein pyrin.Pyrin is a protein normally present in the inflammasome. The mutated pyrin protein is thought to cause inappropriate activation of the inflammasome, leading to release of the pro-inflammatory cytokine IL-1β. Most other autoinflammatory diseases also cause disease by inappropriate release of IL-1β. Thus, IL-1β has become a common therapeutic target, and medications such as anakinra, rilonacept, and canakinumab have revolutionized the treatment of autoinflammatory diseases.However, there are some autoinflammatory diseases that are not known to have a clear genetic cause. This includes PFAPA, which is the most common autoinflammatory disease seen in children, characterized by episodes of fever, aphthous stomatitis, pharyngitis, and cervical adenitis. | 0-1
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Pain can also occur due to bursal inflammation, swelling or fracture at the base of the tumor stalk. Some of the clinical signs and symptoms of malignant osteochondroma are pain, swelling, and mass enlargement. Mechanism
Osteochondromas are long and slender, pedunculated on a stalk often taking the shape of a cauliflower. The cartilage cap is covered by fibrous perichondrium and continues with the periosteum of the underlying bone. The cartilage cap is less than 2 cm thick and the thickness decreases with age. A cap more than 2 cm thick, indicates malignant transformation of a tumor. The cartilage cap merges with the epiphyseal area of the long bones called spongiosa. In the spongiosa, the chondrocytes are arranged in accordance with the epiphyseal growth plate. The spongiosa of the stalk continues with the underlying cancellous bone. Fractures within the stalk causes fibroblastic proliferation and formation of a new bone. Development of bursa takes place over the osteochondroma, which is attached to the perichondrium of the cap. Inflammation of the bone is indicated by the bursal wall lined by the synovium. As a result, patients may have swelling for years related to the location and site of the lesion indicative of mechanical obstruction, nerve impingement, pseudoaneurysm of the overlying vessel, fracture at the stalk of the lesion, or formation of bursa over the osteochondroma. Heparan sulphate (HS) are glycosaminoglycans which are involved in the formation of proteoglycans. | The biosynthesis of HS takes place in the Golgi apparatus and endoplasmic reticulum, where glycosaminoglycans chains are maintained by type II glycosyltransferases encoded by EXOSTOSIN genes EXT1 and EXT2. Decreased levels of HS leads to mutations in EXT1 or EXT2 causing skeletal abnormality. The underlying mechanism for solitary and multiple osteochondromas have been associated with genetic alterations in EXT1 or EXT2 genes located on chromosomes 8 and 11. Approximately 65% of osteochondromas arise in the EXT1 gene loci on chromosome 8 and 35% arise in EXT2 gene loci on chromosome 11. About 70–75% of multiple osteochondromas are caused by point mutations, often involving deletion of single or multiple axons as found in 10% of all hereditary cases. In about 10–15% of all cases no genomic alterations are detected. The mechanism behind the formation of multiple osteochondroma is large genomic deletions of EXT1 and EXT2 genes. The identified mechanism behind solitary osteochondromas is the homozygous deletions of the EXT1 gene. However, the exact cause of osteochondroma is unknown. Additionally, the molecular basis of genetics and clinical variability of multiple osteochondroma as well as the underlying causes for the malignant transformation and the onset of osteochondroma in EXT negative patients is also currently unknown. Diagnosis
Osteochondromas are often asymptomatic and may not cause any kind of discomfort. They are often found accidentally when an X-ray is done for an unrelated reason. X-rays are the first tests performed that characterize a lesion. | 11
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Metoclopramide is a medication used for stomach and esophageal problems. It is commonly used to treat and prevent nausea and vomiting, to help with emptying of the stomach in people with delayed stomach emptying, and to help with gastroesophageal reflux disease. It is also used to treat migraine headaches.Common side effects include: feeling tired, diarrhea, and feeling restless. More serious side effects include: movement disorder like tardive dyskinesia, a condition called neuroleptic malignant syndrome, and depression. It is thus rarely recommended that people take the medication for longer than twelve weeks. No evidence of harm has been found after being taken by many pregnant women. It belongs to the group of medications known as dopamine-receptor antagonists and works as a prokinetic.In 2012, metoclopramide was one of the top 100 most prescribed medications in the United States. It is available as a generic medication. It is on the World Health Organizations List of Essential Medicines. In 2017, it was the 253rd most commonly prescribed medication in the United States, with more than one million prescriptions. Medical uses
Nausea
Metoclopramide is commonly used to treat nausea and vomiting associated with conditions such as uremia, radiation sickness, cancer and the effects of chemotherapy, labor, infection, and emetogenic drugs. As a perioperative anti-emetic, the effective dose is usually 25 to 50 mg (compared to the usual 10 mg dose). | The litigation was complicated since there was a lack of clarity in jurisdiction between state laws, where product liability is determined, and federal law, which determines how drugs are labelled, as well as between generics companies, which had no control over labelling, and the originator company, which did. The litigation yielded at least two important cases. In Conte v. Wyeth in the California state courts, the claims of the plaintiff against the generic companies Pliva, Teva, and Purepac that had sold the drugs that the plaintiff actually took, and the claims against Wyeth, whose product the plaintiff never took, were all dismissed by the trial court, but the case was appealed, and in 2008 the appellate court upheld the dismissal of the cases against the generic companies, but reversed on Wyeth, allowing the case against Wyeth to proceed. This established an "innovator liability" or "pioneer liability" for pharmaceutical companies. The precedent was not widely followed in California nor in other states. Litigation over the same issues related to metoclopramide also reached the US Supreme Court in PLIVA, Inc. v. Mensing, in which the court held in 2011 that generic companies cannot be held liable for information, or the lack of information, on the originators label. | 11
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In physiology, dehydration is a lack of total body water, with an accompanying disruption of metabolic processes. It occurs when free water loss exceeds free water intake, usually due to exercise, disease, or high environmental temperature. Mild dehydration can also be caused by immersion diuresis, which may increase risk of decompression sickness in divers. Most people can tolerate a 3-4% decrease in total body water without difficulty or adverse health effects. A 5-8% decrease can cause fatigue and dizziness. Loss of over ten percent of total body water can cause physical and mental deterioration, accompanied by severe thirst. Death occurs at a loss of between fifteen and twenty-five percent of the body water. Mild dehydration is characterized by thirst and general discomfort and is usually resolved with oral rehydration. Dehydration can cause hypernatremia (high levels of sodium ions in the blood) and is distinct from hypovolemia (loss of blood volume, particularly blood plasma). Signs and symptoms
The hallmarks of dehydration include thirst and neurological changes such as headaches, general discomfort, loss of appetite, decreased urine volume (unless polyuria is the cause of dehydration), confusion, unexplained tiredness, purple fingernails, and seizures. The symptoms of dehydration become increasingly severe with greater total body water loss. A body water loss of 1-2%, considered mild dehydration, is shown to impair cognitive performance. While in people over age 50, the bodys thirst sensation diminishes with age, a study found that there was no difference in fluid intake between young and old people. Many older people have symptoms of dehydration. | at sea or in a desert), seawater or drinks with significant alcohol concentration will worsen dehydration. Urine contains a lower solute concentration than seawater; this requires the kidneys to create more urine to remove the excess salt, causing more water to be lost than was consumed from seawater. If a person is dehydrated and taken to a medical facility, IVs can also be used.For severe cases of dehydration where fainting, unconsciousness, or other severely inhibiting symptoms are present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids containing a proper balance of replacement electrolytes are given orally or intravenously with continuing assessment of electrolyte status; complete resolution is normal in all but the most extreme cases. See also
Hydrational fluids
Terminal dehydration
Dryness (medical)
Hypernatremia
References
Further reading
External links
Definition of dehydration by the U.S. National Institutes of Healths MedlinePlus medical encyclopedia | 11
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However, there is ongoing debate over the active mechanisms, including whether the main cause is the direct toxic effect of alcohol itself or whether the disease is a result of alcoholism-related malnutrition. A 2019 metastudy found that the relationship between ethanol toxicity and neuropathy remained unproven. Effects due to nutritional deficiency
Frequently alcoholics have disrupted social links in their lives and have an irregular lifestyle. This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance. Alcoholism may also result in loss of appetite, alcoholic gastritis, and vomiting, which decrease food intake. Alcohol abuse damages the lining of the gastrointestinal system and reduces absorption of nutrients that are taken in. The combination of all of them may result in a nutritional deficiency that is linked to the development of alcoholic polyneuropathy.There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, indicating that vitamin deficiency may be a major factor in the development and progression of alcoholic polyneuropathy. In experimental models of alcoholic polyneuropathy utilizing rats and monkeys no convincing evidence was found that proper nutritional intake along with alcohol results in polyneuropathy. In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, a carbohydrate, increases the metabolic demand for thiamine (vitamin B1) because of its role in the metabolism of glucose. Thiamine levels are usually low in alcoholics due to their decreased nutritional intake. | Palifermin (trade name Kepivance, marketed by Biovitrum) is a truncated human recombinant keratinocyte growth factor (KGF) produced in Escherichia coli. KGF stimulates the growth of cells that line the surface of the mouth and intestinal tract. Therapeutic use(s)
When patients with blood cancers (leukemia and lymphoma) receive high dose chemotherapy and radiation therapy to undergo bone marrow transplantation, they usually get severe oral mucositis. Palifermin reduces the incidence and duration of severe oral mucositis by protecting those cells and stimulating the growth of new epithelial cells to build up the mucosal barrier. Palifermin is also being studied in the prevention and treatment of oral mucositis and dysphagia (difficulty swallowing) in other types of cancer. Drug target and mechanism of action
Keratinocyte growth factor (KGF) resides in the family of fibroblast growth factor (FGF). The drugs target is the KGF receptor. Through the binding of this drug to the aforementioned receptor, Palifermin stimulates epithelial cell proliferation, differentiation, and upregulation of cytoprotective mechanisms to reduce the symptoms of oral mucositis. Side effects
Common side effects often seen in conjunction with the use of Palifermin include, but are not limited to:
Some of the more serious side effects can be seen below:
Administration
Palifermin is administered via intravenous bolus injection. The drug comes as a lyophilized powder that must be reconstituted with sterile water for injection before it may be administered. It is given for three days before, and three days after chemotherapy is undergone. However, it is important that the drug is not administered within 24 hours of the actual chemotherapy process. | 0-1
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Immediate early genes, which encode proteins for example ICP22 that regulate the expression of early and late viral genes, are the first to be expressed following infection. Early gene expression follows, to allow the synthesis of enzymes involved in DNA replication and the production of certain envelope glycoproteins. Expression of late genes occurs last; this group of genes predominantly encode proteins that form the virion particle.Five proteins from (UL) form the viral capsid - UL6, UL18, UL35, UL38, and the major capsid protein UL19. Cellular Entry
Entry of HSV into a host cell involves several glycoproteins on the surface of the enveloped virus binding to their transmembrane receptors on the cell surface. Many of these receptors are then pulled inwards by the cell, which is thought to open a ring of three gHgL heterodimers stabilizing a compact conformation of the gB glycoprotein, so that it springs out and punctures the cell membrane. The envelope covering the virus particle then fuses with the cell membrane, creating a pore through which the contents of the viral envelope enters the host cell.The sequential stages of HSV entry are analogous to those of other viruses. At first, complementary receptors on the virus and the cell surface bring the viral and cell membranes into proximity. Interactions of these molecules then form a stable entry pore through which the viral envelope contents are introduced to the host cell. The virus can also be endocytosed after binding to the receptors, and the fusion could occur at the endosome. | Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known by their taxonomical names Human alphaherpesvirus 1 and Human alphaherpesvirus 2, are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of humans. Both HSV-1 and HSV-2 are very common and contagious. They can be spread when an infected person begins shedding the virus. As of 2016, about 67% of the world population under the age of 50 had HSV-1. In the United States, about 47.8% and 11.9% are estimated to have HSV-1 and HSV-2, respectively, though actual prevalence may be much higher. Because it can be transmitted through any intimate contact, it is one of the most common sexually transmitted infections. Symptoms
Many of those who are infected never develop symptoms. Symptoms, when they occur, may include watery blisters in the skin or mucous membranes of the mouth, lips, nose, genitals, or eyes (herpes simplex keratitis). Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause mild or atypical symptoms during outbreaks. However, they can also cause more troublesome forms of herpes simplex. As neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by hiding from the immune system in the cell bodies of neurons, particularly in sensory ganglia. After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. | 11
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In the past, the Kveim test was used to diagnose sarcoidosis. This now obsolete test had a high (85 percent) sensitivity, but required spleen tissue of a known sarcoidosis patient, an extract of which was injected into the skin of a suspected case.Only biopsy of suspicious lesions in the brain or elsewhere is considered useful for a definitive diagnosis of neurosarcoid. This would demonstrate granulomas (collections of inflammatory cells) rich in epithelioid cells and surrounded by other immune system cells (e.g. plasma cells, mast cells). Biopsy may be performed to distinguish mass lesions from tumours (e.g. gliomas).MRI with gadolinium enhancement is the most useful neuroimaging test. This may show enhancement of the pia mater or white matter lesions that may resemble the lesions seen in multiple sclerosis.Lumbar puncture may demonstrate raised protein level, pleiocytosis (i.e. increased presence of both lymphocytes and neutrophil granulocytes) and oligoclonal bands. Various other tests (e.g. ACE level in CSF) have little added value. Criteria
Some recent papers propose to classify neurosarcoidosis by likelihood:
Definite neurosarcoidosis can only be diagnosed by plausible symptoms, a positive biopsy and no other possible causes for the symptoms
Probable neurosarcoidosis can be diagnosed if the symptoms are suggestive, there is evidence of central nervous system inflammation (e.g. CSF and MRI), and other diagnoses have been excluded. A diagnosis of systemic sarcoidosis is not essential. Possible neurosarcoidosis may be diagnosed if there are symptoms not due to other conditions but other criteria are not fulfilled. Treatment
Neurosarcoidosis, once confirmed, is generally treated with glucocorticoids such as prednisolone. | Char syndrome is an autosomal dominant congenital disease caused by mutations in TFAP2B gene which affects the development of the bones of the face as well as the heart and limbs. During embryo development, TFAP2B regulates the production of the protein AP-2β, a transcription factor that is active in the neural crest and helps regulate genes that control cell division and apoptosis. There are at least 10 mutations of this gene that have been identified in people presenting Char syndrome, which alters specific regions of the gene preventing production of the transcription factor and disrupting normal development of embryo structures. People with this condition present a very distinct facial appearance with flattened cheek bones, flat and broad tip nose, shortened distance between the nose and upper lip, triangular-shaped mouth with tick lips and strabismus. It is also characterized by a patent ductus arteriosus, which is the failure to close the ductus that connects the aorta and pulmonary artery during pre-birth life and may cause many symptoms including breathing issues and heart failure. Abnormalities of hand and finger development have also been reported in people with this condition, including short or absent fifth finger. Other abnormal findings include supernumerary nipples. These conditions often affect multiple members of a family and there are no reports of non-genetic factors that might be related with incidence of this syndrome. It was first described by Florence Char in 1978. == References == | 0-1
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Spinal Cord Injury
When myelomalacia occurs, the damage done to the spinal cord may range from minimal to extensive. The spinal cord and the brain work together, making them the key components of the central nervous system. Damage to this system affects specific functions of the body, primarily relating to the function of muscles. The areas most commonly injured include the cervical vertebrae (C1-C7), and the lumbar spine (L1-L5). Symptoms
The onset of myelomalacia may be so subtle that it is overlooked. Depending on the extent of the spinal cord injury, the symptoms may vary. In some cases, the symptom may be as common as hypertension. Though every case is different, several cases reported loss of motor functions in the extremities, areflexia or sudden jerks of the limbs, loss of pain perception, or even paralysis; all of which are possible indicators of a damaged and softened spinal cord. In the most severe cases, paralysis of the respiratory system manifests in death. Cause
The most common way the disorder occurs is from a result of hemorrhaging (bleeding within) or inadequate blood supply to the spinal cord, making it weak and susceptible to damage.Because myelomalacia involves a damaged spinal cord, it may occur in any individual. Those most at risk are the geriatric population due to weaker bone density. Once the spinal injury has occurred, one of two things may happen. Firstly, hemorrhaging within the spinal cord may cause compression, which damages the spinal cord even further. | Myelomalacia is a pathological term referring to the softening of the spinal cord. Possible causes of myelomalacia include cervical myelopathy, hemorrhagic infarction, or acute injury, such as that caused by intervertebral disc extrusion.In advanced stages, this disorder causes flaccid paraplegia (impairment of motor function in lower extremities), total areflexia (below normal or absence of reflexes) of the pelvic limbs and anus, loss of deep pain perception caudal (toward the coccyx, or tail) to the site of spinal cord injury, muscular atrophy (wasting away of muscle tissue), depressed mental state, and respiratory difficulty due to intercostal (muscles that run between the ribs) and diaphragmatic paralysis. Gradual cranial migration of the neurological deficits (problems relating to the nervous system), is known as ascending syndrome and is said to be a typical feature of diffuse myelomalacia. Although clinical signs of myelomalacia are observed within the onset (start) of paraplegia, sometimes they may become evident only in the post-operative period, or even days after the onset of paraplegia. Death from myelomalacia may occur as a result of respiratory paralysis when the ascending lesion (abnormal damaged tissue) reaches the motor nuclei of the phrenic nerves (nerves between the C3-C5 region of the spine) in the cervical (neck) region. Classification
Myelomalacia affects the neurological functions in the spinal cord. Once breached, the ramification of the damage directly affects the motor functions of the body. Because the central nervous system is affected, the condition is classified under the neurological field of study. | 11
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Signs and symptoms
Risk factors
Condition follows an autosomal recessive patternThe mutated gene must be inherited from both the mother and father
Both males and females must have an equal frequency of inheritance
Diagnosis
Health professionals must look at a persons history, symptoms, physical exam and laboratory test in order to make a diagnosis. If the results show patients with low levels of lymphocytes, absence of granulocytes or absence of thymus then the patient may be suspected to have RD. Treatment
RD can only be treated temporarily through hematopoietic stem cell transplantation (HSCT) and cytokine therapy. Hematopoietic stem cell transplantation
Transplantation of stem cells are taken from the bone marrow, peripheral blood or umbilical cord of healthy, matched donors. Hematopoietic stem cell transplantation (HSCT) involves intravenous infusion of stem cells to those who have either a damaged bone marrow or defective immune system. Transplantation is a simple process. Bone marrow product is infused through a central vein over a period of several hours. The hematopoietic cells are able to go to the bone marrow through tracking mechanisms. Patients who suffer from RD will now have more stem cells that can differentiate into immune cells. Cytokine Therapy
Recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) can be used as a temporary cure. GM-CSF stimulates production of white blood cells. This cure is commonly used in patients who are awaiting bone marrow transplantation. Response to this cure can vary. Those with a more severe combined immunodeficiency may have no response to this therapy. Prognosis
The survival range is estimated to be 3 days to 17 weeks without treatment. | Sodium calcium edetate (sodium calcium EDTA), also known as edetate calcium disodium among other names, is a medication primarily used to treat lead poisoning, including both short-term and long-term lead poisoning. Sodium calcium edetate came into medical use in the United States in 1953. Chelation agent
Sodium calcium edetate is in the chelating agent family of medication. It is a salt of edetate with two sodium and one calcium atoms. It works by binding to a number of heavy metals, which renders them almost inert and allows them to leave the body in the urine.Edetate disodium is a different formulation which does not have the same effects. Medical use
Sodium calcium edetates primary use is to treat lead poisoning,
for which it is an alternative to succimer. It is given by slow injection into a vein or into a muscle.For lead encephalopathy sodium calcium edetate is typically used together with dimercaprol. It may also be used to treat plutonium poisoning. It does not appear to be useful for poisoning by tetra-ethyl lead. Side effects
Common side effects include pain at the site of injection. Other side effects may include kidney problems, diarrhea, fever, muscle pains, and low blood pressure. Benefits when needed in pregnancy are likely greater than the risks. History
Sodium calcium edetate came into medical use in the United States in 1953. It is on the World Health Organizations List of Essential Medicines. References
External links
"Sodium calcium edetate". U.S. National Library of Medicine. Drug Information Portal. U.S. National Institutes of Health. | 0-1
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Gonadotropin therapy in HH men usually is able to generate enough sperm for fertility to occur, however sperm count is still lower than normal.In the female, the goal for gonadotropin therapy is to obtain ovulation. This is obtained with FSH treatment followed by hCG or LH to trigger ovulation. FSH will stimulate granulosa cells for follicular maturation while LH will act on luteal cells to produce steroids aiding follicular maturation and preparing the endometrium for pregnancy.For hyperprolactinaemia-caused AHH, dopamine agonists are used to improve GnRH secretion. Dopamine binds to D2 receptors on lactotrophs within the anterior pituitary. This results in the inhibition of secretion of prolactin resulting in less direct and indirect inhibition of GnRH secretion.In up to 10–20% of cases, patients can exhibit sustained fertility and steroid production after therapy, resulting in hypogonadotropic hypogonadism reversal. The mechanism for this reversal is unknown but there is believed to be some neuronal plasticity within GnRH releasing cells. See also
Androgens and estrogens
GnRH and gonadotropins (FSH and LH)
Hypergonadotropic hypogonadism
Hypothalamic–pituitary–gonadal axis
Isolated hypogonadotropic hypogonadism
References
== External links == | The 2011-12 NHANES figures documented another 31% overall increase among American teens since the previous decade, with a total adolescent population impact of 61% afflicted. More than one in five American teens (23%) have moderate to severe dental fluorosis on at least two teeth. Mechanism
Teeth are the most studied body tissues to examine the impact of fluoride to human health. There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiates the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluoride interacts with mineralising tissues.In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins (amelogenin) are enzymatically broken down and the rate at which the subsequent breakdown products are removed. Fluoride may also indirectly alter the action of protease via a decrease in the availability of free calcium ions in the mineralization environment. This results in the formation of enamel with less mineralization. | 0-1
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Usually, a red color indicates a flow toward the ultrasound transducer, while blue indicates a flow away from the transducer. Based on the display, doctors can evaluate blood flow to the umbilical arteries, umbilical veins, or other organs such as heart and brain. Nonstress test
Nonstress test (NST) is a type of electronic fetal monitoring that uses a cardiotocograph to monitor fetal heartbeat, fetal movement and mothers contraction. NST is typically monitored for at least 20 minutes. Signs of a reactive (normal) NST include a baseline fetal heart rate (FHR) between 110 and 160 beats per minute (bpm) and 2 accelerations of FHR of at least 15 bpm above baseline for over 15 seconds. Vibroacoustic stimulation and longer monitoring may be needed if NST is non-reactive. Biophysical profile
A biophysical profile is a noninvasive procedure that uses the ultrasound to evaluate the fetal health based on NST and four ultrasound parameters: fetal movement, fetal breathing, fetal muscle tone, and the amount of amniotic fluid surrounding the fetus. A score of 2 points is given for each category that meets the criteria or 0 points if the criteria are not met (no 1 point). Sometimes, the NST is omitted, making the highest score 8/8 instead of 10/10. Generally, a score of 8/10 or 10/10 is considered a normal test result, unless 0 points is given for amniotic fluid. A score of 6/10 with normal amniotic fluid is considered equivocal, and a repeated test within 24 hours may be needed. | The four most common are stripping the membranes, breaking the mothers water, giving the hormone prostaglandin, and giving the synthetic hormone pitocin. Stripping the membranes does not work for all women, but can for most. A doctor inserts a finger into the mothers cervix and moves it around to separate the membrane connecting the amniotic sac, which houses the baby, from the walls of the uterus. Once this membrane is stripped, the hormone prostaglandin is naturally released into the mothers body and initiates contractions. Most of the time doing this only once will not immediately start labor. It may have to be done several times before the stimulant hormone is released, and contractions start. The next method is breaking the mothers water, which is also referred to as an amniotomy. The doctor uses a plastic hook to break the membrane and rupture the amniotic sac. Within a few hours labor usually begins. Giving the hormone prostaglandin ripens the cervix, meaning the cervix softens, thins out, or dilates. The drug Cervidil is administered by mouth in tablet form or in gel form as an insert. This is most often done in the hospital overnight. The hormone oxytocin is usually given in the synthetic form of Pitocin. It is administered through an IV throughout the labor process. This hormone stimulates contractions. Pitocin is also used to "restart" labor when it is lagging.The use of misoprostol is also allowed, but close monitoring of the mother is required. | 11
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Once these joints can be aligned, thin wires are usually placed across these joints to hold them in the corrected position. These wires are temporary and left out through the skin for removal after 3–4 weeks. Once the joints are aligned, tendons (typically the Achilles, posterior tibialis, and flexor halluces longus) are repaired at an appropriate length. The incision (or incisions) are closed with dissolvable sutures. The foot is then casted in the corrected position for 6–8 weeks. It is common to do a cast change with anesthesia after 3–4 weeks, so that pins can be removed and a mold can be made to fabricate a custom AFO brace. The new cast is left in place until the AFO is available. When the cast is removed, the AFO is worn to prevent the foot from returning to the old position.For feet with partial correction of deformity with non-operative treatment, surgery may be less extensive and may involve only the posterior part of the foot and ankle. This might be called a posterior release. This is done through a smaller incision and may involve releasing only the posterior capsule of the ankle and subtalar joints, along with lengthening the Achilles tendon. Surgery leaves residual scar tissue and typically there is more stiffness and weakness than with nonsurgical treatment. As the foot grows, there is potential for asymmetric growth that can result in recurrence of foot deformity that can affect the forefoot, midfoot, or hindfoot. Many patients do fine, but some require orthotics or additional surgeries. | Clubfoot is a birth defect where one or both feet are rotated inward and downward. Congenital clubfoot, is the most common congenital malformation of the foot with an incidence of 1 per 1000 births. In approximately 50% of cases, clubfoot affects both feet, but it can present unilaterally causing one leg or foot to be shorter than the other. Most of the time, it is not associated with other problems. Without appropriate treatment, the foot deformity will persist and lead to pain and impaired ability to walk, which can have a dramatic impact on the quality of life.The exact cause is usually not identified. Both genetic and environmental factors are believed to be involved. There are two main types of congenital clubfoot: idiopathic (80% of cases) and secondary clubfoot (20% of cases). The idiopathic congenital clubfoot is a multifactorial condition that includes environmental, vascular, positional, and genetic factors. There appears to be hereditary component for this birth defect given that the risk of developing congenital clubfoot is 25% when a first-degree relative is affected. In addition, if one identical twin is affected, there is a 33% chance the other one will be as well. The underlying mechanism involves disruption of the muscles or connective tissue of the lower leg, leading to joint contracture. Other abnormalities are associated 20% of the time, with the most common being distal arthrogryposis and myelomeningocele. | 11
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These groups include:
Those who have used topical corticosteroids over a prolonged period of time
Those who have used corticosteroids to cover a large surface area
Those with broken skin barrier or extensive abrasions
Those who have recently undergone stress (such as illness, trauma, surgery)
Children under the age of 12HPA axis suppression is preventable by supplementation with glucocorticosteroids. If HPA axis suppression occurs, it is often reversed shortly after discontinuation of treatment. Pharmacology
Mechanism of action
Pharmacokinetics
Absorption of topical corticosteroids depends on several factors such as the vehicle, or delivery system used by the drug, the integrity of the epidermal barrier, and whether or not an occlusive bandage is used in combination with the drug.The absorption of topical betamethasone dipropionate is theoretically minuscule; however, if absorbed it follows the same pharmacokinetic profile that is typical of systemic corticosteroids. It is metabolized primarily by the liver by hydrolysis to its metabolites B17P (primary) and betamethasone and the 6β-hydroxy derivatives of those metabolites, and it is excreted primarily by the kidneys. Chemistry
Betamethasone dipropionate is a white to almost white crystalline powder. Regulation
Betamethasone dipropionate was patented by Merck in 1987, as an augmented cream/lotion, Diprolene in the U.S., and Disprosone in Europe. These patents expired in 2003 and 2007 respectively leading to generic production of betamethasone dipropionate. During this time other topical corticosteroids such as triamcinolone acetonide and clobetasol propionate also became available as generic creams. | Betamethasone dipropionate is a glucocorticoid steroid with anti-inflammatory and immunosuppressive abilities. It is applied as a topical cream, ointment, lotion or gel (Diprolene) to treat itching and other minor skin conditions such as eczema. Minor side effects include dry skin and mild, temporary stinging when applied. Betamethasone dipropionate is a "super high potency" corticosteroid used to treat inflammatory skin conditions such as dermatitis, eczema and psoriasis. It is a synthetic analog of the adrenal corticosteroids. Although its exact mechanism of action is not known, it is effective when applied topically to cortico-responsive inflammatory dermatoses. It is available as a generic medication. Adverse effects
Although the absorption of betamethasone dipropionate is small, when used for prolonged periods of time (periods exceeding two weeks), or across a large surface area (total use greater than 50 grams per week), it can have adverse effects. One such effect is the ability of the corticosteroid to suppress the hypothalamic–pituitary–adrenal axis. This can lead to a depression in the release of adrenal hormones such as cortisol and adrenocorticotropic hormone, or ACTH. Symptoms of HPA axis suppression are often subtle and variable, but can often be detected using simple blood or urine tests such at ACTH stimulation test or urinary free cortisol. Those at increased risk for HPA axis suppression are those who are more likely to absorb more of the steroid through the skin. | 11
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The RFD also focuses the mesocyclones base, causing it to draw air from a smaller and smaller area on the ground. As the updraft intensifies, it creates an area of low pressure at the surface. This pulls the focused mesocyclone down, in the form of a visible condensation funnel. As the funnel descends, the RFD also reaches the ground, fanning outward and creating a gust front that can cause severe damage a considerable distance from the tornado. Usually, the funnel cloud begins causing damage on the ground (becoming a tornado) within a few minutes of the RFD reaching the ground. Maturity
Initially, the tornado has a good source of warm, moist air flowing inward to power it, and it grows until it reaches the "mature stage". This can last from a few minutes to more than an hour, and during that time a tornado often causes the most damage, and in rare cases can be more than 1.6 km (1 mile) across. The low pressured atmosphere at the base of the tornado is essential to the endurance of the system. Meanwhile, the RFD, now an area of cool surface winds, begins to wrap around the tornado, cutting off the inflow of warm air which previously fed the tornado. The flow inside the funnel of the tornado is downward, supplying water vapor from the cloud above. This is contrary to the upward flow inside hurricanes, supplying water vapor from the warm ocean below. Therefore, the energy of the tornado is supplied from the cloud above. | If its effects are severely disabling, resulting in very little physical activity for the person, social elements can also suffer. Workplace environments can also be limited, since most labor-intensive work requires basic physical agility that spastic diplegics may not possess. However, the degree of variability among individuals with spastic diplegia means that no greater or lesser degree of stigma or real-world limitation is standard. Lesser effects usually mean fewer physical limitations, better-quality exercise, and more real-world flexibility, but the person is still in general seen as different from the norm. How such a person chooses to react to outside opinion is of paramount importance when social factors are considered. Mechanism
Spastic diplegias particular type of brain damage inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma amino butyric acid (GABA), the amino acid that regulates muscle tone in humans. | 0-1
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The intracranial pressure can be elevated if cysts develop in the brain. Migraine-like headaches can occur. Eyes
Smaller blood vessels of the retina are abnormally developed and appear tortuous and dilated to a variable extent, typically in one sector and mainly in the peripheral and temporal portions of the retina. This is known as telangiectasia. The vessel walls are weak and leak blood plasma and lipid within and underneath the retina. This leakage can lead to exudative retinal detachment, also known as exudative retinopathy in this context. The detachment typically has a yellowish tint because the fluid under the retina contains lipid. These findings mimic Coats disease. Characteristically, the abnormal vessels are localized and the retinal blood vessels peripheral to the abnormal ones seemingly have failed to develop and are thus not seen. In some eyes, retinal vessels form small nodules on the surface of the retina, known as angiomas. These can bleed and be attached to the vitreous humour. The attachment can cause traction retinal detachment. Gastrointestinal tract
Recurrent intestinal bleeding is fairly common. It originates from telangiectatic small blood vessels in the intestinal mucosa. Additional findings in some individuals are portal hypertension and liver failure. Blood
Many affected children develop anemia, which may be macrocytic in type. Some also develop thrombocytopenia. Bone marrow examinations may show megaloblasts and increased erythropoiesis or bone marrow suppression. Bones
The long bones show osteopenia and pathologic fractures can occur. Skin, nails and hair
Some children have sparse and greying hair, café au lait spots and nail dystrophy. | Imaging findings
The most consistent finding are widespread calcifications, which involve
the white matter of the cerebrum mostly adjacent to the junction with the grey matter, the thalami, the basal ganglia and the brainstem. The white matter of the cerebellum and the dentate nuclei are less often involved. However, the brain may appear normal in the neonatal period. The calcifications are visible both with computed tomography and with magnetic resonance imaging. Magnetic resonance imaging shows additionally diffuse or patchy white matter changes, especially in the periventricular region, the thalami and the internal capsule. Cerebellar and brainstem lesions are less common. Imaging also uncovers parenchymal cysts situated mainly in the thalamic region and more rarely in the brainstem, the parietal lobe and the frontal lobe. The long bones may be osteopenic and various skeletal changes are found in several patients, such as metaphyseal sclerosis and mild flaring, which is most pronounced in the femur and tibia. Laboratory findings
The cerebrospinal fluid and blood tests are typically normal, except for anemia and thrombocytopenia in some children. Screening
Because of the rarity of the syndrome, it is not routinely screened before birth. Prenatal diagnosis is possible in families in which a prior child has been diagnosed, because the responsible gene CTC1is known. Management
Seizures are managed with anticonvulsive medications. Laser coagulation or cryoablation (freezing) of the retina can be used to destroy the abnormal blood vessels. Retinal detachment is repaired with a scleral buckle or with vitrectomy. | 11
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In 1973, Ruth Bishop and colleagues described related viruses found in children with gastroenteritis.In 1974, Thomas Henry Flewett suggested the name rotavirus after observing that, when viewed through an electron microscope, a rotavirus particle looks like a wheel (rota in Latin); the name was officially recognised by the International Committee on Taxonomy of Viruses four years later. In 1976, related viruses were described in several other species of animals. These viruses, all causing acute gastroenteritis, were recognised as a collective pathogen affecting humans and animals worldwide. Rotavirus serotypes were first described in 1980, and in the following year, rotavirus from humans was first grown in cell cultures derived from monkey kidneys, by adding trypsin (an enzyme found in the duodenum of mammals and now known to be essential for rotavirus to replicate) to the culture medium. The ability to grow rotavirus in culture accelerated the pace of research, and by the mid-1980s the first candidate vaccines were being evaluated.In 1998, a rotavirus vaccine was licensed for use in the United States. Clinical trials in the United States, Finland, and Venezuela had found it to be 80 to 100% effective at preventing severe diarrhoea caused by rotavirus A, and researchers had detected no statistically significant serious adverse effects. The manufacturer, however, withdrew it from the market in 1999, after it was discovered that the vaccine may have contributed to an increased risk for intussusception, a type of bowel obstruction, in one of every 12,000 vaccinated infants. | In the United States, before initiation of the rotavirus vaccination programme, rotavirus caused about 2.7 million cases of severe gastroenteritis in children, almost 60,000 hospitalisations, and around 37 deaths each year. Public health campaigns to combat rotavirus focus on providing oral rehydration therapy for infected children and vaccination to prevent the disease. The incidence and severity of rotavirus infections has declined significantly in countries that have added rotavirus vaccine to their routine childhood immunisation policies. Signs and symptoms
Rotavirus gastroenteritis is a mild to severe disease characterised by vomiting, watery diarrhoea, and low-grade fever. Once a child is infected by the virus, there is an incubation period of about two days before symptoms appear. Symptoms often start with vomiting followed by profuse diarrhoea after at least four days. Dehydration is more common in rotavirus infection than in most of those caused by bacterial pathogens, and is the most common cause of death related to rotavirus infection.Rotavirus A infections can occur throughout life: the first usually produces symptoms, but subsequent infections are typically mild or asymptomatic, as the immune system provides some protection. : 106–124 Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age. Infection in newborn children, although common, is often associated with mild or asymptomatic disease; the most severe symptoms tend to occur in children six months to two years of age, the elderly, and those with compromised or absent immune system functions. | 11
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Pattern hair loss by age 50 affects about half of men and a quarter of women. About 2% of people develop alopecia areata at some point in time. Terminology
Baldness is the partial or complete lack of hair growth, and part of the wider topic of "hair thinning". The degree and pattern of baldness varies, but its most common cause is androgenic hair loss, alopecia androgenetica, or alopecia seborrheica, with the last term primarily used in Europe. Hypotrichosis
Hypotrichosis is a condition of abnormal hair patterns, predominantly loss or reduction. It occurs, most frequently, by the growth of vellus hair in areas of the body that normally produce terminal hair. Typically, the individuals hair growth is normal after birth, but shortly thereafter the hair is shed and replaced with sparse, abnormal hair growth. The new hair is typically fine, short and brittle, and may lack pigmentation. Baldness may be present by the time the subject is 25 years old. Signs and symptoms
Symptoms of hair loss include hair loss in patches usually in circular patterns, dandruff, skin lesions, and scarring. Alopecia areata (mild – medium level) usually shows in unusual hair loss areas, e.g., eyebrows, backside of the head or above the ears, areas the male pattern baldness usually does not affect. In male-pattern hair loss, loss and thinning begin at the temples and the crown and hair either thins out or falls out. Female-pattern hair loss occurs at the frontal and parietal. People have between 100,000 and 150,000 hairs on their head. | The work of Joaquin Farias has shown that sensorimotor retraining activities and proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost due to blepharospasm.Developed by The Eye Research Group Oxford, PressOp™ is a new ethically approved spectacle mounted device that arose after studying individuals with Blepharospasm who regularly use “sensory tricks”. By applying pressure to the temple region of their forehead patients found this helped to enable eye opening. The device is particularly helpful controlling an episode of severe spasm when the carrying out of specific tasks is necessary. Blepharospasm sufferers may find continuity in their quality of life by using the device while effectiveness of treatment is not at its peak. See also
Levator palpebrae superioris muscle
Myokymia
Fasciculation
References
External links
Blepharospasm – Resource Guide from the National Eye Institute (NEI) | 0-1
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Acral persistent papular mucinosis
Atypical lichen myxedematosus (intermediate lichen myxedematosus)
Atypical tuberous myxedema (Jadassohn–Dosseker syndrome)
Cutaneous focal mucinosis
Cutaneous lupus mucinosis (papular and nodular mucinosis in lupus erythematosus, papular and nodular mucinosis of Gold, papulonodular mucinosis in lupus erythematosus)
Discrete papular lichen myxedematosus
Eccrine mucinosis
Follicular mucinosis (alopecia mucinosa, mucinosis follicularis, Pinkus follicular mucinosis, Pinkus follicular mucinosis–benign primary form)
Localized lichen myxedematosus
Myxoid cyst (digital mucous cyst, mucous cyst)
Myxoid lipoblastoma
Neuropathia mucinosa cutanea
Nodular lichen myxedematosus
Papular mucinosis (generalized lichen myxedematosus, sclerodermoid lichen myxedematosus, scleromyxedema)
Papular mucinosis of infancy (cutaneous mucinosis of infancy)
Perifollicular mucinosis
Reticular erythematous mucinosis (midline mucinosis, plaque-like cutaneous mucinosis, REM syndrome)
Scleroderma
Self-healing juvenile cutaneous mucinosis
Self-healing papular mucinosis
Stiff skin syndrome (congenital fascial dystrophy)
Neurocutaneous
Neurocutaneous conditions are due organic nervous system disease or are psychiatric in etiology. Atypical chronic pain syndrome
Body dysmorphic disorder (dysmorphic syndrome, dysmorphophobia)
Brachioradial pruritus
Bromidrosiphobia
Complex regional pain syndrome (reflex sympathetic dystrophy)
Congenital insensitivity to pain with anhidrosis
Delusional parasitosis (delusions of parasitosis, Ekbom syndrome, monosymptomatic hypochondriacal psychosis)
Dermatothlasia
Factitious dermatitis (dermatitis artefacta, factitial dermatitis)
Glossodynia (burning mouth syndrome, burning tongue, orodynia)
Levator ani syndrome
Malum perforans pedis (neurotrophic ulcer, perforating ulcer of the foot)
Meralgia paresthetica (Roth–Bernhardt disease)
Neurotic excoriations
Notalgia paresthetica (hereditary localized pruritus, posterior pigmented pruritic patch, subscapular pruritus)
Postencephalitic trophic ulcer
Psychogenic pruritus
Riley–Day syndrome (familial dysautonomia)
Scalp dysesthesia
Sciatic nerve injury
Scrotodynia
Syringomyelia (Morvans disease)
Traumatic neuroma (amputation neuroma)
Trichotillomania (trichotillosis)
Trigeminal neuralgia (tic douloureux)
Trigeminal trophic lesion (trigeminal trophic syndrome)
Vulvodynia (vestibulodynia)
Noninfectious immunodeficiency-related
Noninfectious immunodeficiency-related cutaneous conditions are caused by T-cell or B-cell dysfunction. | Acute radiodermatitis
Chronic radiation keratosis
Chronic radiodermatitis
Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy
Fluoroscopy burn
Radiation acne
Radiation cancer
Radiation dermatitis (radiodermatitis)
Radiation recall reaction
Radiation-induced erythema multiforme
Radiation-induced hypertrophic scar
Radiation-induced keloid
Radiation-induced morphea
Urticaria and angioedema
Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swellings of the skin. Angioedema, which can occur alone or with
urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, or upper airway. Acquired C1 esterase inhibitor deficiency
Acute urticaria
Adrenergic urticaria
Anaphylaxis
Aquagenic urticaria
Cholinergic urticaria
Chronic urticaria (ordinary urticaria)
Cold urticaria
Dermatographism (dermographism)
Episodic angioedema with eosinophilia (Gleichs syndrome)
Exercise urticaria (exercise-induced urticaria)
Galvanic urticaria
Heat urticaria
Hereditary angioedema (Quinckes edema)
Localized heat contact urticaria
Mast cell-independent urticaria
Physical urticaria
Primary cold contact urticaria
Pressure urticaria (delayed pressure urticaria)
Reflex cold urticaria
Schnitzler syndrome
Secondary cold contact urticaria
Solar urticaria
Systemic capillary leak syndrome
Urticarial allergic eruption
Urticaria-like follicular mucinosis
Vibratory angioedema
Vascular-related
Vascular-related cutaneous conditions result from dysfunction of the blood or blood vessels in the dermis, or lymphatics in the subcutaneous tissues. | 11
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Conversely, the absence of a milky appearance does not mean a chylothorax is not present as they may instead appear serous or bloody. Treatment
The treatment for chylothorax depends on the underlying cause but may include dietary modification, medication to prevent chyle formation including somatostatin/octreotide, midodrine and sirolimus, pleurodesis, and surgical treatment including ligation of the thoracic duct, pleurovenous or pleuroperitoneal shunting or thoracic duct embolization. Initial
The initial treatment of a chylothorax is usually drainage of the fluid from the pleural space. This may be necessary to restore lung function compromised by the pressure exerted by the chyle on the lungs. Those with large chylothoraces may need nutritional support due to the nutrients lost, primarily to correct protein and electrolyte losses. Once the affected person is hemodynamically and nutritionally stable, then specific treatment can begin. Conservative
A conservative treatment is changing diet to include fewer long-chain fatty acids, in particular free fatty acids. Since chyle is formed from these acids, chyle formation will reduce, allowing the defects to heal spontaneously. However, this can lead to fat deficiency and malnutrition over time. A possible response to this drawback is a venous fat hemorrhage, in which small and medium-chain fatty acids are given by diet, and long-chain fatty acids are given intravenously. Thoracentesis and an indwelling catheter for use at home is generally used to drain the chylothorax. If a malignant neoplastic chylothorax is present, then treatment with radiotherapy and/or chemotherapy is warranted. | It has no gender or age predisposition. A chylothorax occurs in 0.2-1% of cardiothoracic surgeries, 5-10% of esophagostomies, and 3-7% of lung resections. Other animals
Horses
Chylothorax is uncommon in horses. Clinical signs and symptoms in foals include difficulty breathing, fast breathing, cough, fever, and lethargy. The fluid generally appears opalescent and milky without any odor. A line of fluid is observed on percussion and there are reduced lung sounds. To differentiate between chyle is pseudochyle, which does not clear after centrifugation. There is not much information on the treatment of chylothorax in horses. Supportive care, antimicrobials, drainage of the thorax, and dietary management have been used with success. Surgery has been done in other animals with limited success, but has not yet been reported in horses. Although success has been reported, the prognosis is relatively unknown due to the lack of data. References
== External links == | 11
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