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Causes of<unk> can be categorized into three groups: congenital<unk> , acquired clonal<unk> , and acquired reversible<unk> . All cases involve dysfunctional heme synthesis or processing. This leads to granular deposition of iron in the mitochondria that form a ring around the nucleus of the developing red blood cell. Congenital forms often present with normocytic or microcytic anemia while acquired forms of<unk> are often normocytic or macrocytic. * Congenital<unk> * X-linked<unk> : This is the most common congenital cause of<unk> and involves a defect in ALAS2, which is involved in the first step of heme synthesis. Although X-linked, approximately one third of patients are women due to skewed X-inactivation (lyonizations). * Autosomal recessive<unk> involves mutations in the SLC25A38 gene. The function of this protein is not fully understood, but it is involved in mitochondrial transport of glycine. Glycine is a substrate for ALAS2 and necessary for heme synthesis. The autosomal recessive form is typically severe in presentation. * Genetic syndromes: Rarely,<unk> may be part of a congenital syndrome and present with associated findings, such as ataxia, myopathy, and pancreatic insufficiency. * Acquired clonal<unk> * Clonal<unk> s fall under the broader category of myelodysplastic syndromes (MDS). Three forms exist and include refractory anemia with ringed sideroblasts (RARS), refractory anemia with ringed sideroblasts and thrombocytosis (RARS-T), and refractory cytopenia with multilineage dysplasia and ringed sideroblasts (RCMD-RS). These anemias are associated with increased risk for leukemic evolution. * Acquired reversible<unk> * Causes include excessive alcohol use (the most common cause of<unk> , pyridoxine deficiency (vitamin B6 is the cofactor in the first step of heme synthesis), lead poisoning and copper deficiency. Excess zinc can indirectly cause<unk> by decreasing absorption and increasing excretion of copper. Antimicrobials that may lead to<unk> include isoniazid (which interferes with pyridoxine metabolism), chloramphenicol (which, by inhibiting the synthesis of mitochondrial membrane protein, impairs mitochondrial respiration), cycloserine, and linezolid. | Sideroblastic anemia | Refractory anemia with ring sideroblasts | Myelophthisic anemia | Myomatous erythrocytosis syndrome | Refractory anemia with excess of blasts | Congenital hypoplastic anemia | Hereditary spherocytosis | Thiamine responsive megaloblastic anemia syndrome | 00
| 29,368 |
<unk> in indicated for the treatment of people aged 12 years and older with chronic graft-versus-host disease (chronic GVHD) after failure of at least two prior lines of systemic therapy. | Belumosudil | Nicogel | Lesinurad | Vagisil | Degmacyte | Ladostigil | Lazaretto | Brodifacoum | 00
| 71,491 |
As<unk> , generally, is not considered a pathology, treatment is not always necessary. However the treatment of other problems caused by this condition, such as ovarian cysts, chocolate cysts, fertility, pelvic pain, adhesions, dyspareunia may need to be addressed depending on the case. Similar to endometriosis, cases of<unk> that cause significant amounts of pain can be treated with excision surgery by a specialist, though this is not a cure. Removal of the tissues, cysts, and adhesions can help to greatly reduce symptoms. Some surgeons believe add-back therapy with progesterone to also be helpful in reducing symptoms. Taking progesterone continuously keeps a woman at a specific time in her menstrual cycle. This prevents the body from reaching high levels of estrogen found in ovulation and further aggravating the condition. Dietary estrogen can wreak havoc in highly sensitive cases, and similar to endometriosis women are encouraged to eat diets low in estrogens. This means avoiding foods like soy, black liquorice, and tofu, to name a few. | Endosalpingiosis | Salpingitis | Oophoritis | Endometritis | Hematospermia | Vaginal stenosis | Pyometra | Autoimmune oophoritis | 00
| 59,108 |
<unk> , commercially known as QazVac, is a COVID-19 vaccine developed by the Research Institute for Biological Safety Problems in Kazakhstan. QazCoVac-P is a second COVID-19 vaccine developed by the Kazakh Biosafety Research Institute and in clinical trials. | QazCovid-in | Cephem | Azficel-T | Prosultiamine | Chloroquine | K-Quarantine | MedMagLabs | Crisaborole | 00
| 74,275 |
<unk> expiratory positive airway pressure<unk> is a treatment for obstructive sleep apnea (OSA) and snoring. Contemporary<unk> devices have two small valves that allow air to be drawn in through each nostril, but not exhaled; the valves are held in place by adhesive tabs on the outside of the nose. The mechanism by which<unk> may work is not clear; it may be that the resistance to<unk> exhalation leads to a buildup in CO2 which in turn increases respiratory drive, or that resistance to exhalation generates pressure that forces the upper airway to open wider. In OSA it appears to be effective to reduce but not eliminate apnea for people with mild to moderate OSA (Apnea–hypopnea index < 30) and for people who cannot tolerate CPAP, but within those groups it is not clear why some respond and others do not, and the evidence consists of small clinical trials with follow-up no longer than one year. As of 2015 there was evidence from one small trial that it may be useful in children with OSA. It has shown evidence of reducing snoring as well.<unk> is unlikely to be effective in people with significant<unk> obstruction. Side effects that emerged during clinical trials included difficulty breathing, difficulty falling or staying asleep, dry mouth,<unk> congestion, headache, difficulty putting on or removing the device, and anxiety. Ventus Medical received FDA 510K clearance for marketing the Provent<unk> device for OSA in 2009. Ventus received 510K clearance for an<unk> device to treat snoring in June 2012. Ventus was acquired by Theravent Inc. in 2013. | Nasal EPAP | Thorpe tube flowmeter | Real ear measurement | Nasal provocation test | Thermoacoustic imaging | Rhinoscope | Simple face mask | Acoustic angiography | 00
| 62,346 |
Etymologically, the word covers any substance that reduces pain, but doctors used it more narrowly. Some definitions restrict the term to topical medications, including herbal simples such as onion, lily, root of mallows, leaves of violet, and elderberry. Other definitions include ingested narcotics, hypnotics, and opioids. In the 19th century, the primary<unk> s were opium, henbane, hemlock, tobacco, nightshade (stramonium), and chloroform. Certain compound medicines were also called by this name, such as<unk> balsam, made of castile soap, camphor, saffron, and spirit of wine, and digested in a sand heat. It was recommended not only for easing extreme pain, but also for assisting in discharging the diseased tissue that caused or occurred with the pain. In literary usage, the word has escaped its strictly medical meaning to convey anything "soothing or relaxing" (since the 18th century) or even anything "non-contentious", "blandly agreeable", or unlikely to cause offence or debate. | Anodyne | Apyrexy | Baffle | Biorisk | OrthoCor | Aneugen | Protomap | Horopter | 00
| 13,853 |
<unk> , also known as estradiol benzoate<unk> /dihydroxyprogesterone acetophenide (EBB/DHPA) and sold under the brand names Neolutin N, Redimen, Soluna, and Unijab, is a form of combined injectable birth control which is used in Peru and Singapore. It contains estradiol benzoate<unk> (EBB), an estrogen, and algestone acetophenide (dihydroxyprogesterone acetophenide; DHPA), a progestin. The medication is given once per month by injection into muscle. | Estradiol benzoate butyrate/algestone acetophenide | Estradiol enantate/algestone acetophenide | Estradiol benzoate/estradiol dienanthate/testosterone enanthate benzilic acid hydrazone | Testosterone propionate/testosterone cypionate/prasterone | Testosterone propionate/testosterone enanthate | Estradiol benzoate/progesterone/testosterone propionate | Testosterone propionate/testosterone ketolaurate | Testosterone propionate/testosterone enanthate/testosterone undecylenate | 00
| 71,637 |
<unk> refers to 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<unk> . 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<unk> (also known as "isolated congenital nail clubbing") may be associated with HPGD. | Acropachy | Amastia | Hypertrichosis | Hamartia | Macrodontia | Hemifacial hypertrophy | Auricular hypertrichosis | Macrotia | 00
| 48,299 |
<unk> (E-EPA) is an<unk> ester of<unk> acid, which is an omega-3 fatty acid. | Ethyl eicosapentaenoic acid | Ellagic acid | Fish oil | Fish oil | Soybean oil | Etiocholanolone | Conjugated linoleic acid | Retinyl palmitate | 00
| 53,482 |
<unk> has many features in common with Dubin–Johnson syndrome, an exception being that the liver cells are not pigmented. The main symptom is a non-itching jaundice. There is a rise in bilirubin in the patient's serum, mainly of the conjugated type. It can be differentiated from Dubin–Johnson syndrome in the following ways:<unk> Dubin–Johnson syndrome appearance of liver normal histology and appearance liver has black pigmentation gallbladder visualization gallbladder can be visualized by oral cholecystogram gallbladder cannot be visualized total urine coproporphyrin content high with 80% being isomer 1 (normal urine contains more of isomer 3 than isomer 1)<unk> may exacerbate toxic side effects of the medication irinotecan. | Rotor syndrome | Gilbert's syndrome Gilbert's syndrome 1 | GRACILE syndrome | ZTTK syndrome | LIG4 syndrome | ATR-16 syndrome | MEDNIK syndrome | GAPO syndrome | 00
| 36,767 |
The molecular arrangement of BCL-2 protein, a potential cause to the development of the<unk> . The protein can inhibit the process of apoptosis when at a high abundance. The<unk> can arise through a number of causes: The origin of the<unk> can be understood through its biological and histochemistry foundations. It has been suggested that<unk> can be a result of a traumatic event. The occurrence of<unk> may be from a mutated cell from "the oral mucosa and the dental follicle" origin. Another probable cause is from pre-existing cysts or cancerous constituents. A potential biological origin of<unk> is a cyst developed at a salivary gland or simple epithelium, which undergoes maturation at the<unk> . Another origin is a primordial cyst that infiltrates the<unk> epithelial tissue through a highly organised cellular differentiation. Pathologists discovered a BCL-2 protein, commonly present in neoplasms, to exist in the tissue layers of the<unk> . The protein is capable of disrupting normal cell death function at the odontogenic region. The analysis of PTCH, a gene that specialises in neoplasm inhibition, was carried out to determine if any existing mutations played a role in the initiation of the<unk> . It is confirmed that the gene had no assistance in triggering cystic advancement. | Glandular odontogenic cyst | Calcifying odontogenic cyst | Paradental cyst | Dentigerous cyst | Odontogenic cyst | Ganglion cyst | Tornwaldt cyst | Gingival cyst | 00
| 41,266 |
The<unk> (SFAF) is a nonprofit organization dedicated to providing services for people with HIV/AIDS, with a mission to end the AIDS epidemic in the United States. They were founded in 1982, at the beginning of the AIDS epidemic. SFAF is one of the largest and oldest community-based AIDS service organizations in the United States. SFAF has an 87.67% overall rating, and a 97% accountability & transparency rating, at Charity Navigator. | San Francisco AIDS Foundation | AIDS Services of Austin | Uganda AIDS Commission | Canadian Foundation for AIDS Research | Medicines Control Authority of Zimbabwe | AIDS Education and Training Centers | President's Commission on the HIV Epidemic | Harvard AIDS Initiative | 00
| 66,468 |
<unk> accumulates mainly in the heart, where it causes stiffness and often thickening of its walls, leading consequently to shortness of breath and intolerance to exercise, called diastolic dysfunction. Excessively slow heart rate can also occur, such as in sick sinus syndrome, with ensuing fatigue and dizziness.<unk> -type<unk> deposition is also a common cause of carpal tunnel syndrome in elderly men, which may cause pain, tingling and loss of sensation in the hands. Some patients may develop carpal tunnel syndrome as an initial symptom of<unk> . There appears to be an increase in the risk for developing hematuria or blood in the urine due to urological lesions. | Wild-type transthyretin amyloid | Alpha-synuclein | Amyloid beta | Immunoreactive trypsinogen | Anti-gliadin antibodies | Keratic precipitate | Kamino bodies | Anchoring fibrils | 00
| 67,630 |
The mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most people affected by the condition are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important risk factors are diet (particularly sugar-sweetened beverage consumption), genetics, aging, sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use. The pathogenic role played in the syndrome by the excessive expansion of adipose tissue occurring under sustained overeating, and its resulting lipotoxicity was reviewed by Vidal-Puig. There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. Markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose. Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans. Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance. The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand, creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance. Stress Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis). A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis. HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke. Psychosocial stress is also linked to heart disease. Obesity Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waist circumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, affected people who are of normal weight may also be insulin-resistant and have the syndrome. Sedentary lifestyle Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a two fold increased risk of metabolic syndrome. Aging Metabolic syndrome affects 60% of the U.S. population older than age 50. With respect to that demographic, the percentage of women having the syndrome is higher than that of men. The age dependency of the syndrome's prevalence is seen in most populations around the world. Diabetes mellitus type 2 The metabolic syndrome quintuples the risk of type 2 diabetes mellitus. Type 2 diabetes is considered a complication of metabolic syndrome. In people with impaired glucose tolerance or impaired fasting glucose, presence of metabolic syndrome doubles the risk of developing type 2 diabetes. It is likely that prediabetes and metabolic syndrome denote the same disorder, defining it by the different sets of biological markers. The presence of metabolic syndrome is associated with a higher prevalence of CVD than found in people with type 2 diabetes or impaired glucose tolerance without the syndrome. Hypoadiponectinemia has been shown to increase insulin resistance and is considered to be a risk factor for developing metabolic syndrome. Coronary heart disease The approximate prevalence of the metabolic syndrome in people with coronary artery disease (CAD) is 50%, with a prevalence of 37% in people with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced. Lipodystrophy Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in people treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components. Rheumatic diseases There is research that associates comorbidity with rheumatic diseases. Both psoriasis and psoriatic arthritis have been found to be associated with metabolic syndrome. Chronic obstructive pulmonary disease Metabolic syndrome is seen to be a comorbidity in up to 50 percent of those with chronic obstructive pulmonary disease (COPD). It may pre-exist or may be a consequence of the lung pathology of COPD. | risks of Hypertriglyceridemia | risks of Atrial fibrillation | risks of Coronary artery disease | risks of Myocardial infarction | risks of Peripheral artery disease | risks of Subarachnoid hemorrhage | risks of Erectile dysfunction | risks of Stevens–Johnson syndrome | 00
| 3,799 |
subdivision = See text }}<unk> is a genus of positive-strand RNA viruses in the family Flaviviridae. The genus includes the West Nile virus, dengue virus, tick-borne encephalitis virus, yellow fever virus, Zika virus and several other viruses which may cause encephalitis, as well as insect-specific<unk> es (ISFs) such as cell fusing agent virus (CFAV), Palm Creek virus (PCV), and Parramatta River virus (PaRV). While dual-host<unk> es can infect vertebrates as well as arthropods, insect-specific<unk> es are restricted to their competent arthropods. The means by which<unk> es establish persistent infection in their competent vectors and cause disease in humans depends upon several virus-host interactions, including the intricate interplay between<unk> -encoded immune antagonists and the host antiviral innate immune effector molecules.<unk> es are named for the yellow fever virus; the word flavus means 'yellow' in Latin, and yellow fever in turn is named from its propensity to cause yellow jaundice in victims.<unk> es share several common aspects: common size (40–65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single-stranded RNA around 10,000–11,000 bases), and appearance under the electron microscope. Most of these viruses are primarily transmitted by the bite from an infected arthropod (mosquito or tick), and hence are classified as arboviruses. Human infections with most of these arboviruses are incidental, as humans are unable to replicate the virus to high enough titers to reinfect the arthropods needed to continue the virus life-cycle – humans are then a dead end host. The exceptions to this are the yellow fever virus, dengue virus and zika virus. These three viruses still require mosquito vectors but are well-enough adapted to humans as to not necessarily depend upon animal hosts (although they continue to have important animal transmission routes, as well). Other virus transmission routes for arboviruses include handling infected animal carcasses, blood transfusion, sex, child birth and consumption of unpasteurised milk products. Transmission from nonhuman vertebrates to humans without an intermediate vector arthropod however mostly occurs with low probability. For example, early tests with yellow fever showed that the disease is not contagious. The known non-arboviruses of the<unk> family reproduce in either arthropods or vertebrates, but not both, with one odd member of the genus affecting a nematode. | Flavivirus | Lentivirus | Pandoravirus | Arbovirus | Coronavirus | Coronavirus | Oncolytic virus | Henipavirus | 00
| 12,750 |
Type I This is a very rare disease (estimated at 0.6–1.0 per million live births), and consanguinity increases the risk of this condition (other rare diseases may be present). Inheritance is autosomal recessive. Intense jaundice appears in the first days of life and persists thereafter. Type 1 is characterised by a serum bilirubin usually above 345 μmol/L 20 mg/dL (range 310–755 μmol/L 18–44 mg/dL) (whereas the reference range for total bilirubin is 2–14 μmol/L 0.1–0.8 mg/dL). No UDP glucuronosyltransferase 1-A1 expression can be detected in the liver tissue. Hence, there is no response to treatment with phenobarbital, which causes CYP450 enzyme induction. Most patients (type IA) have a mutation in one of the common exons (2 to 5), and have difficulties conjugating several additional substrates (several drugs and xenobiotics). A smaller percentage of patients (type IB) have mutations limited to the bilirubin-specific A1 exon; their conjugation defect is mostly restricted to bilirubin itself. Before the availability of phototherapy, these children died of kernicterus (bilirubin encephalopathy) or survived until early adulthood with clear neurological impairment. Today, therapy includes * exchange transfusions in the immediate neonatal period * 12 hours/day phototherapy * heme oxygenase inhibitors to reduce transient worsening of hyperbilirubinemia (although the effect of the drug decreases over time) * oral calcium phosphate and carbonate to form complexes with bilirubin in the gut * liver transplantation before the onset of brain damage and before phototherapy becomes ineffective at later age Type II The inheritance patterns of both<unk> types I and II are autosomal recessive. However, type II differs from type I in a number of different aspects: * Bilirubin levels are generally below 345 μmol/L 20 mg/dL (range 100–430 μmol/L 6–24 mg/dL; thus, overlap may sometimes occur), and some cases are only detected later in life. * Because of lower serum bilirubin, kernicterus is rare in type II. * Bile is pigmented, instead of pale in type I or dark as normal, and monoconjugates constitute the largest fraction of bile conjugates. * UGT1A1 is present at reduced but detectable levels (typically <10% of normal), because of single base pair mutations. * Therefore, treatment with phenobarbital is effective, generally with a decrease of at least 25% in serum bilirubin. In fact, this can be used, along with these other factors, to differentiate type I and II. Differential diagnosis Neonatal jaundice may develop in the presence of sepsis, hypoxia, hypoglycemia, hypothyroidism, hypertrophic pyloric stenosis, galactosemia, fructosemia, etc. Hyperbilirubinemia of the unconjugated type may be caused by: * increased production * hemolysis (e.g., hemolytic disease of the newborn, hereditary spherocytosis, sickle cell disease) * ineffective erythropoiesis * massive tissue necrosis or large hematomas * decreased clearance * drug-induced * physiological neonatal jaundice and prematurity * liver diseases such as advanced hepatitis or cirrhosis * breast milk jaundice and Lucey–Driscoll syndrome *<unk> and Gilbert syndrome In<unk> and Gilbert syndrome, routine liver function tests are normal, and hepatic histology usually is normal, too. No evidence for hemolysis is seen. Drug-induced cases typically regress after discontinuation of the substance. Physiological neonatal jaundice may peak at 85–170 μmol/l and decline to normal adult concentrations within two weeks. Prematurity results in higher levels. | Crigler–Najjar syndrome | Gilbert's syndrome Gilbert's syndrome 1 | GRACILE syndrome | Baggio–Yoshinari syndrome | CLOVES syndrome | Hajdu–Cheney syndrome | DeSanto-Shinawi syndrome | Van Gogh syndrome | 00
| 31,580 |
<unk> contains different types of lipid storage disorders caused by the accumulation of lipids known as gangliosides. There are two distinct genetic causes of the disease. Both are autosomal recessive and affect males and females equally. | Gangliosidosis | Galactosialidosis | Glycogen storage disease | Beta-mannosidosis | Mucopolysaccharidosis | Sphingolipidoses | Sialidosis | GM1 gangliosidoses | 00
| 31,431 |
<unk> can be classified as a form of spondylolisthesis, since spondylolisthesis is often defined in the literature as displacement in any direction. Yet, medical dictionaries usually define spondylolisthesis specifically as the forward or anterior displacement of a vertebra over the vertebra inferior to it (or the sacrum).<unk> is also called retrospondylolisthesis. | Retrolisthesis | Spondylolisthesis | Disc protrusion | Back strain | Facet syndrome | Vertebral compression fracture | Discitis | Coccyx fracture | 00
| 22,729 |
Many different diseases can cause melanin pigmented lesions in the mouth through # Increase in the number of melanocytes or melanocytosis # Increased melanin production with or without melanocytosis Melanin is an endogenous pigment synthesized by melanocytes that are located in the basal layer of epithelium. Melanin is then transferred to keratinocytes in melanosomes. Nevus cells in the skin and<unk> mucosa also produce melanin.<unk> melanosis can present as black, gray, blue or brown lesions depending on the site and amount of melanin deposition in tissues. Physiological Increased melanin production without increase in melanocytes Peutz-Jeghers syndrome Increased production of melanin without increase in number of melanocytes Addison’s disease Decrease in blood adrenocortical hormone level causes increased levels of adrenocorticotropic hormone secreted by anterior pituitary gland. As a result, melanocyte-stimulating hormone is induced which causes<unk> melanosis Smoker’s melanosis Increased melanin production to defend against damage from tobacco smoke<unk> melanoacanthoma Increased number of dendritic melanocytes Melanocytic nevi Accumulation of nevus cells at the basal layer of the epithelium or in the connective tissue or both<unk> melanoma Increased number of malignant melanocytes | Oral pigmentation | Nipple pigmentation | Breast hypertrophy | Hypopigmentation | Trichomegaly | Blue nails | Tooth discoloration | Green nails | 00
| 56,187 |
<unk> is over-expressed in a number of cancers, and forced over-expression of<unk> in human cancer cells lines accelerates proliferation and protects cells against apoptosis. HETEs and EETs derived from<unk> have also been shown to contribute to the proper functioning of the cardiovascular system and the regulation of the renal and pulmonary systems in humans.<unk> is readily expressed in the cardiac myocytes and endothelial cells of the coronary artery where various EETs are produced. The presence of EETs relaxes vascular smooth muscle cells by hyperpolarizing the cell membrane, thus highlighting the protective anti-inflammatory function of<unk> in the circulatory system. There is still conflict in studies on the effects of EETs in relation to the cardiovascular system. P450 enzymes have shown both positive and negative effects in the heart, and the production of EETs has been shown to produce vascular protective and vascular depressive mechanisms. The over-expression of<unk> enhances the activation of mitoKATP, and is believed to confer a physiological benefit by altering the production of reactive oxygen species. | CYP2J2 | CYP1A2 | CYP2C19 | CYP2D6 | CYP3A5 | CYP2C8 | CYP3A4 | CYP2C9 | 00
| 48,387 |
<unk> procedure<unk> is the use of ultrasound to enhance the delivery of topically applied drugs.<unk> has been used in an effort to enhance the absorption of topically applied analgesics and anti-inflammatory agents through the therapeutic application of ultrasound.<unk> has been shown to be ineffective for some treatments, where it did not increase the efficacy of absorption of drugs, or did not improve the outcome more than the use of ultrasound alone. | Phonophoresis | Iontophoresis | Cynanthropy | Oscillopsia | Mydriasis | Facial toning | Carotidynia | Hypertonia | 00
| 46,016 |
Vacuoles are demonstrated in the<unk> parts of the cornea. The vesicles are located on the endothelial surface. The corneal endothelium is normally a single layer of cells that lose their mitotic potential after development is complete. In<unk> , the endothelium is often multilayered and has several other characteristics of an epithelium, including the presence of desmosomes, tonofilaments, and microvilli. These abnormal cells retain their ability to divide and extend onto the trabecular meshwork to cause glaucoma in up to 40% of cases. | Posterior polymorphous corneal dystrophy | Granular corneal dystrophy | Lattice corneal dystrophy | Subepithelial mucinous corneal dystrophy | Macular corneal dystrophy | Schnyder crystalline corneal dystrophy | Meesmann corneal dystrophy | Neurotrophic keratitis | 00
| 56,256 |
<unk> is a rotator cuff denervation syndrome in which the axillary nerve is compressed at the<unk><unk> of the rotator cuff. | Quadrilateral space syndrome | Sixth nerve palsy | Fourth nerve palsy | Posterior ramus syndrome | Occipital horn syndrome | Cauda equina syndrome | Median nerve palsy | Bulbar palsy | 00
| 67,707 |
<unk> is an alteration in the perception of the external world, causing sufferers to perceive it as unreal, distant, distorted or falsified. Other symptoms include feeling as if one's environment is lacking in spontaneity, emotional coloring, and depth. It is a dissociative symptom that may appear in moments of severe stress.<unk> is a subjective experience pertaining to a person's perception of the outside world, while depersonalization is a related symptom characterized by dissociation towards one's own body and mental processes. The two are commonly experienced in conjunction with one another, but are also known to occur independently. Chronic<unk> is fairly rare, and may be caused by occipital–temporal dysfunction. Experiencing<unk> for long periods of time or having recurring episodes can be indicative of many psychological disorders, and can cause significant distress among sufferers. However, temporary<unk> symptoms are commonly experienced by the general population a few times throughout their lives, with a lifetime prevalence of up to 26-74% and a prevalence of 31–66% at the time of a traumatic event. | Derealization | Body substance isolation | Rejuvenation | Jactitation | Depurination | Semantic satiation | Disinhibition | Marsupialization | 00
| 51,771 |
Topical steroid-induced rosacea (left); after steroid withdrawal and photobiomodulation therapy (right) The exact cause of rosacea is unknown. Triggers that cause episodes of flushing and blushing play a part in its development. Exposure to temperature extremes, strenuous exercise, heat from sunlight, severe sunburn, stress, anxiety, cold wind, and moving to a warm or hot environment from a cold one, such as heated shops and offices during the winter, can each cause the face to become flushed. Certain foods and drinks can also trigger flushing, such as alcohol, foods and beverages containing caffeine (especially hot tea and coffee), foods high in histamines, and spicy foods. Medications and topical irritants have also been known to trigger rosacea flares. 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. This suggests that the B. oleronius bacteria found in the mites could be responsible for the inflammation associated with the condition." Intestinal bacteria Small intestinal bacterial overgrowth (SIBO) was demonstrated to have greater prevalence in rosacea patients and treating it with locally acting antibiotics led to rosacea lesion improvement in two studies. Conversely in rosacea patients who were SIBO negative, antibiotic therapy had no effect. The effectiveness of treating SIBO in rosacea patients may suggest that gut bacteria play a role in the pathogenesis of rosacea lesions. | symptoms of Mucosal melanoma | symptom of Mucosal melanoma | symptom of Basal-cell carcinoma | symptom of Melanoma | symptom of Skin cancer | medical cause of Mucosal melanoma | symptom of Hodgkin lymphoma | symptom of Herpes labialis | 00
| 17,532 |
<unk> , sold under the brand name Zepzelca, is a medication for the treatment of adults with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy. The most common side effects include leukopenia, lymphopenia, fatigue, anemia, neutropenia, increased creatinine, increased alanine aminotransferase, increased glucose, thrombocytopenia, nausea, decreased appetite, musculoskeletal pain, decreased albumin, constipation, dyspnea, decreased sodium, increased aspartate aminotransferase, vomiting, cough, decreased magnesium and diarrhea.<unk> is a synthetic tetrahydropyrrolo 4,3,2-dequinolin-8(1H)-one alkaloid analogue with potential antineoplastic activity.<unk> covalently binds to residues lying in the minor groove of DNA, which may result in delayed progression through S phase, cell cycle arrest in the G2/M phase and cell death.<unk> was approved for medical use in the United States in June 2020. | Lurbinectedin | Paclitaxel | Doxorubicin | Busulfan | Lipoplatin | Cabazitaxel | Irinotecan | Capecitabine | 00
| 73,521 |
A 2006 review stated that RS often leads<unk> cancer between ages 30-50.<unk> cancer kills about 1 in 3 people, but 5-year survival rates improved between 1974-1976 and 1995-2000, from 52% to 64%. | Hereditary leiomyomatosis and renal cell cancer syndrome | Menke-Hennekam syndrome | Hereditary leiomyomatosis and renal cell carcinoma | Fryns syndrome | Heerfordt syndrome | Serrated polyposis syndrome | Hereditary breast–ovarian cancer syndrome | Ehlers–Danlos syndromes | 00
| 62,789 |
Some causes of<unk> may resolve spontaneously; many require operative treatment. In adults, frequently the surgical intervention and the treatment of the causative lesion are required. In malignant large<unk> , endoscopically placed self-expanding metal stents may be used to temporarily relieve the<unk> as a bridge to surgery, or as palliation. Diagnosis of the type of<unk> is normally conducted through initial plain radiograph of the abdomen, luminal contrast studies, computed tomography scan, or ultrasonography prior to determining the best type of treatment. Further research is needed to find out if parenteral nutrition is of benefit to people with an inoperable blockage of the bowel caused by advanced cancer. Small<unk> In the management of small<unk> s, a commonly quoted surgical aphorism is: "never let the sun rise or set on small-bowel<unk> " because about 5.5% of small<unk> s are ultimately fatal if treatment is delayed. Improvements in radiological imaging of small<unk> s allow for confident distinction between simple<unk> s, that can be treated conservatively, and<unk> s that are surgical emergencies (volvulus, closed-loop<unk> s, ischemic bowel, incarcerated hernias, etc.). A small flexible tube (nasogastric tube) may be inserted through the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but relieves the abdominal cramps, distention, and vomiting. Intravenous therapy is utilized and the urine output is monitored with a catheter in the bladder. Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the<unk> resolves. The patient is examined several times a day, and X-ray images are made to ensure he or she is not getting clinically worse. Conservative treatment involves insertion of a nasogastric tube, correction of dehydration and electrolyte abnormalities. Opioid pain relievers may be used for patients with severe pain. Antiemetics may be administered if the patient is vomiting. Adhesive<unk> s often settle without surgery. If the<unk> is complete surgery is usually required. Most patients improve with conservative care in 2–5 days. When the<unk> is cancer, surgery is the only treatment. Those with bowel resection or lysis of adhesions usually stay in the hospital a few more days until they can eat and walk. Small<unk> caused by Crohn's disease, peritoneal carcinomatosis, sclerosing peritonitis, radiation enteritis, and postpartum<unk> are typically treated conservatively, i.e. without surgery. | Bowel obstruction | Intestinal pseudo-obstruction | Intestinal ischemia | Hereditary angioedema | Splenic infarction | Spontaneous bacterial peritonitis | Bowel infarction | Gallstone ileus | 00
| 10,925 |
Depressed mood may not require professional treatment, and may be a normal temporary reaction to life events, a symptom of some medical condition, or a side effect of some drugs or medical treatments. A prolonged depressed mood, especially in combination with other symptoms, may lead to a diagnosis of a psychiatric or medical condition which may benefit from treatment. The UK National Institute for Health and Care Excellence (NICE) 2009 guidelines indicate that antidepressants should not be routinely used for the initial treatment of mild depression, because the risk-benefit ratio is poor. Physical activity can have a protective effect against the emergence of depression. Physical activity can also decrease depressive symptoms due to the release of neurotrophic proteins in the brain that can help to rebuild the hippocampus that may be reduced due to depression. Also yoga could be considered an ancillary treatment option for patients with depressive disorders and individuals with elevated levels of depression. Reminiscence of old and fond memories is another alternative form of treatment, especially for the elderly who have lived longer and have more experiences in life. It is a method that causes a person to recollect memories of their own life, leading to a process of self-recognition and identifying familiar stimuli. By maintaining one's personal past and identity, it is a technique that stimulates people to view their lives in a more objective and balanced way, causing them to pay attention to positive information in their life stories, which would successfully reduce depressive mood levels. Self-help books are a growing form of treatment for peoples physiological distress. There may be a possible connection between consumers of unguided self-help books and higher levels of stress and depressive symptoms. Researchers took many factors into consideration to find a difference in consumers and nonconsumers of self-help books. The study recruited 32 people between the ages of 18 and 65; 18 consumers and 14 nonconsumers, in both groups 75% of them were female. Then they broke the consumers into 11 who preferred problem-focused and 7 preferred growth-oriented. Those groups were tested for many things including cortisol levels, depressive symptomatology, and stress reactivity levels. There were no large differences between consumers of self-help books and nonconsumers when it comes to diurnal cortisol level, there was a large difference in depressive symptomatology with consumers having a higher mean score. The growth-oriented group has higher stress reactivity levels than the problem-focused group. However, the problem-focused group shows higher depressive symptomatology. There is limited evidence that continuing antidepressant medication for one year reduces the risk of depression recurrence with no additional harm. Recommendations for psychological treatments or combination treatments in preventing recurrence are not clear. There are empirical evidences of a connection between the type of stress management techniques and the level of daily depressive mood. | complications of Concussion | complications of Motion sickness | complications of Coma | complications of Hearing loss | medical cause of Hearing loss | complications of Stroke | medical cause of Lightheadedness | symptoms of Vertebral artery dissection | 00
| 17,805 |
<unk> (PPS) is a psychosomatic illness in humans brought on by mass hysteria. The syndrome is thought to be localized in villages in several states of India, including West Bengal, Assam, Bihar, Jharkhand, Orissa, and Chhattisgarh, and has been reported by tens of thousands of individuals. It is far more prevalent in areas with little access to education. People suffering from PPS believe that shortly after being bitten by a dog,<unk> es are conceived within their abdomen. This is said to be especially likely if the dog is sexually excited at the time of the attack. Victims are said to bark like dogs and have reported being able to see the<unk> es inside them when looking at water or hear them growling in their abdomen. It is believed that the victims will eventually die – especially men, who will give birth to their<unk> es through the penis. Witch doctors offer oral cures, which they claim will dissolve the<unk> es, allowing them to pass through the digestive system and be excreted "without the knowledge of the patient". Doctors in India have tried to educate the public about the dangers of believing in this condition. Most sufferers are referred to psychiatric services, but in some instances patients fail to take anti-rabies medication before symptom onset, thinking that they are pregnant with a<unk> and that folk medicine will cure them. This misbelief is further compounded by witch doctors who state that their medicine will fail if sufferers seek standard treatment. Some psychiatrists believe that PPS meets the criteria for a culture-bound disorder. | Puppy pregnancy syndrome | Molar pregnancy | Cryptic pregnancy | Ovarian hyperstimulation syndrome | complications of Pregnancy | Gestational trophoblastic disease | Postpartum physiological changes | Breus' mole | 00
| 64,381 |
Traditional Classification Combing early studies, the traditional symptoms of CWS centered on visual irreminiscence, prosopagnosia, and topographic agnosia. However, due to significant differences in the observations of<unk> and<unk> 's case work, this syndrome bridged the entire loss of dreaming, whether it be due to the isolated inability of the brain to produce images while asleep as<unk> had dictated, or the complete loss of dreaming all together as with<unk> . This has led to the terming of<unk> and<unk> variants, which corresponded to either the loss of dream imagery and visual irreminisence or the complete ceasing of dream experience often coupled with agnosia. Modern Classification There is new focus on the type of injury and analysis of REM sleep pertaining to CWS. A more current medical definition lists CWS as “the association of loss of the ability to conjure up visual images or memories and the loss of dreaming”. A 2004 case-evaluation of a 74-year-old woman who had experienced an acute, bilateral occipital artery infarction which rendered her dreamless for a 3-month period was to perform polysomnography testing in combination with patient dream reporting to determine both her sleep architecture or pattern of sleep stages, and subsequent dream recollection. Such techniques allow for associations between the physiological timetable of dreaming during REM sleep and the patient's ability to recall dreams to be compared closely. | Charcot–Wilbrand syndrome | Taussig–Bing syndrome | SACRAL syndrome | Michels syndrome | Bing–Neel syndrome | VEXAS syndrome | Char syndrome | Kearns–Sayre syndrome | 00
| 53,921 |
<unk> <unk> is the practice of recording electroencephalographic signals via depth electrodes (electrodes surgically implanted into the brain tissue). It may be used in patients with epilepsy not responding to medical treatment, and who are potential candidates to receive brain surgery in order to control seizures. This technique was introduced in the diagnostic work up of patients with epilepsy by the group of the S. Anne Hospital, Paris, France, in the second half of the 20th century. Intracerebral electrodes are placed within the desired brain areas to record the electrical activity during epileptic seizures, thus contributing to define with accuracy the boundaries of the "epileptogenic zone", i.e. the area of brain generating the seizures which should be eventually surgically resected to achieve freedom from epileptic seizures. Potential risks of the procedure, accounting for less than 1% of cases, include brain hemorrhage and infection, which can lead to permanent neurological impairment or death. For this reason,<unk> is reserved to selected and particularly complicated epilepsy cases. | Stereoelectroencephalography | Quantitative electroencephalography | Viral neuronal tracing | Magnetoencephalography | Echoencephalography | Electroencephalography | Brainstem auditory evoked potential | Steady state visually evoked potential | 00
| 40,355 |
Age Age is the most common cause of<unk> s. Lens proteins denature and degrade over time, and this process is accelerated by diseases such as diabetes mellitus and hypertension. Environmental factors, including toxins, radiation, and ultraviolet light have cumulative effects which are worsened by the loss of protective and restorative mechanisms due to alterations in gene expression and chemical processes within the eye. Trauma Post traumatic rosette<unk> of a 60-year-old male Blunt trauma causes swelling, thickening, and whitening of the lens fibers. While the swelling normally resolves with time, the white color may remain. In severe blunt trauma, or in injuries that penetrate the eye, the capsule in which the lens sits can be damaged. This damage allows fluid from other parts of the eye to rapidly enter the lens leading to swelling and then whitening, obstructing light from reaching the retina at the back of the eye.<unk> s may develop in 0.7 to 8.0% of cases following electrical injuries. Blunt trauma can also result in star- (stellate) or petal-shaped<unk> s. Radiation<unk> s can arise as an effect of exposure to various types of radiation. X-rays, one form of ionizing radiation, may damage the DNA of lens cells. Ultraviolet light, specifically UVB, has also been shown to cause<unk> s, and some evidence indicates sunglasses worn at an early age can slow its development in later life. Microwaves, a type of nonionizing radiation, may cause harm by denaturing protective enzymes (e.g., glutathione peroxidase), by oxidizing protein thiol groups (causing protein aggregation), or by damaging lens cells via thermoelastic expansion. The protein coagulation caused by electric and heat injuries whitens the lens. This same process is what makes the clear albumen of an egg become white and opaque during cooking. Genetics Christmas tree<unk> (Diffuse illumination) The genetic component is strong in the development of<unk> s, most commonly through mechanisms that protect and maintain the lens. The presence of<unk> s in childhood or early life can occasionally be due to a particular syndrome. Examples of chromosome abnormalities associated with<unk> s include 1q21.1 deletion syndrome, cri-du-chat syndrome, Down syndrome, Patau's syndrome, trisomy 18 (Edward's syndrome), and Turner's syndrome, and in the case of neurofibromatosis type 2, juvenile<unk> on one or both sides may be noted. Examples of single-gene disorder include Alport's syndrome, Conradi's syndrome, cerebrotendineous xanthomatosis, myotonic dystrophy, and oculocerebrorenal syndrome or Lowe syndrome. Skin diseases The skin and the lens have the same embryological origin and so can be affected by similar diseases. Those with atopic dermatitis and eczema occasionally develop shield ulcer<unk> s. Ichthyosis is an autosomal recessive disorder associated with cuneiform<unk> s and nuclear sclerosis. Basal-cell nevus and pemphigus have similar associations. Smoking and alcohol Cigarette smoking has been shown to double the rate of nuclear sclerotic<unk> s and triple the rate of posterior subcapsular<unk> s. Evidence is conflicting over the effect of alcohol. Some surveys have shown a link, but others which followed people over longer terms have not. Inadequate vitamin C Low vitamin C intake and serum levels have been associated with greater<unk> rates. However, use of supplements of vitamin C has not demonstrated benefit. Medications Some medications, such as systemic, topical, or inhaled corticosteroids, may increase the risk of<unk> development. Corticosteroids most commonly cause posterior subcapsular<unk> s. People with schizophrenia often have risk factors for lens opacities (such as diabetes, hypertension, and poor nutrition) but antipsychotic medications are unlikely to contribute to<unk> formation. Miotics and triparanol may increase the risk. Post-operative Nearly every person who undergoes a vitrectomy—without ever having had<unk> surgery—will experience progression of nuclear sclerosis after the operation. This may be because the native vitreous humor is different from the solutions used to replace the vitreous (vitreous substitutes), such as BSS Plus. This may also be because the native vitreous humour contains ascorbic acid which helps neutralize oxidative damage to the lens and because conventional vitreous substitutes do not contain ascorbic acid. Accordingly, for phakic patients requiring a vitrectomy it is becoming increasingly common for ophthalmologists to offer the vitrectomy combined with prophylactic<unk> surgery to prevent<unk> formation. Other diseases *Metabolic and nutritional diseases *Aminoaciduria or Lowe's syndrome *Cerebrotendineous xanthomatosis *Diabetes mellitus *Fabry's disease *Galactosemia / galactosemic<unk> *Homocystinuria *Hyperparathyroidism *Hypoparathyroidism *Hypervitaminosis D *Hypothyroidism *Hypocalcaemia *Mucopolysaccharidoses *Wilson's disease *Congenital *Congenital syphilis *Cytomegalic inclusion disease *Rubella *Cockayne syndrome *Genetic syndromes *Down syndrome *Patau syndrome *Edwards syndrome *Infections: *Cysticercosis *Leprosy *Onchocerciasis *Toxoplasmosis *Varicella *Secondary to other eye diseases: *Retinopathy of prematurity *Aniridia *Uveitis *Retinal detachment *Retinitis pigmentosa Sunflower<unk> of a forty-year-old male with Wilson's disease and decompensated chronic liver disease | Cataract | Ocular hypertension | Glaucoma | Refractive error | Vitreoretinopathy | Oculomotor nerve palsy | Auditory neuropathy | Aberrations of the eye | 00
| 5,601 |
The lymph nodes where lymphoma most commonly develops Lymphoma and lymphatic system Lymphoma may present with certain nonspecific symptoms; if the symptoms are persistent, an evaluation to determine their cause, including possible lymphoma, should be undertaken. * Lymphadenopathy or swelling of lymph nodes, is the primary presentation in lymphoma. It is generally painless. * B symptoms (systemic symptoms) – can be associated with both Hodgkin lymphoma and non-Hodgkin lymphoma. They consist of: * Fever * Night sweats * Weight loss * Other symptoms: * Anemia, bleeding, increased susceptibility to infections * Loss of appetite or anorexia * Fatigue * Respiratory distress or dyspnea * Itching Mouth Asymptomatic soft swelling, which may or may not be ulcerated, is primarily seen on the tonsils, buccal mucosa, palate, gums, salivary glands, tongue, the floor of the mouth, and retromolar region. | complications of Sjögren syndrome | complications of Behçet's disease | complications of Cat-scratch disease | symptom of Behçet's disease | complications of Rosacea | complications of Rheumatic fever | complications of Xeroderma pigmentosum | symptom of Chilaiditi syndrome | 00
| 5,073 |
People with SCAD may develop left lower quadrant abdominal cramping, intermittent rectal bleeding, and chronic diarrhea. Rectal bleeding (hematochezia) is the most common symptom, and is the presenting complaint in more than 70% of individuals with SCAD. | Segmental colitis associated with diverticulosis | Collagenous colitis | Chemical colitis | Diversion colitis | Microscopic colitis | Lymphocytic colitis | Fibrosing colonopathy | Cytomegalovirus colitis | 00
| 73,597 |
The 10th version of the International Classification of Diseases (ICD-10) classifies social anxiety as a mental and behavioral disorder. Cognitive aspects In cognitive models of social anxiety disorder, those with social phobias experience dread over how they will present to others. They may feel overly self-conscious, pay high self-attention after the activity, or have high performance standards for themselves. According to the social psychology theory of self-presentation, a sufferer attempts to create a well-mannered impression towards others but believes they are unable to do so. Many times, before the potentially anxiety-provoking social situation, sufferers may deliberately review what could go wrong and how to deal with each unexpected case. After the event, they may have the perception that they performed unsatisfactorily. Consequently, they will perceive anything that may have possibly been abnormal as embarrassing. These thoughts may extend for weeks or longer. Cognitive distortions are a hallmark and are learned about in CBT (cognitive-behavioral therapy). Thoughts are often self-defeating and inaccurate. Those with social phobia tend to interpret neutral or ambiguous conversations with a negative outlook and many studies suggest that socially anxious individuals remember more negative memories than those less distressed. An example of an instance may be that of an employee presenting to their co-workers. During the presentation, the person may stutter a word, upon which they may worry that other people significantly noticed and think that their perceptions of them as a presenter have been tarnished. This cognitive thought propels further anxiety which compounds further stuttering, sweating, and, potentially, a<unk> attack. Behavioural aspects Social anxiety disorder is a persistent fear of one or more situations in which the person is exposed to possible scrutiny by others and fears that they may do something or act in a way that will be humiliating or embarrassing. It exceeds normal "shyness" as it leads to excessive social avoidance and substantial social or occupational impairment. Feared activities may include almost any type of social interaction, especially small groups, dating, parties, talking to strangers, restaurants, interviews, etc. Those who have social anxiety disorder fear being judged by others in society. In particular, individuals with social anxiety are nervous in the presence of people with authority and feel uncomfortable during physical examinations. People who have this disorder may behave a certain way or say something and then feel embarrassed or humiliated after. As a result, they often choose to isolate themselves from society to avoid such situations. They may also feel uncomfortable meeting people they do not know and act distant when they are with large groups of people. In some cases, they may show evidence of this disorder by avoiding eye contact, or blushing when someone is talking to them. According to psychologist B. F. Skinner, phobias are controlled by escape and avoidance behaviors. For instance, a student may leave the room when talking in front of the class (escape) and refrain from doing verbal presentations because of the previously encountered anxiety attack (avoid). Major avoidance behaviors could include an almost pathological or compulsive lying behavior to preserve self-image and avoid judgment in front of others. Minor avoidance behaviors are exposed when a person avoids eye contact and crosses his/her arms to conceal recognizable shaking. A fight-or-flight response is then triggered in such events. Physiological aspects Physiological effects, similar to those in other anxiety disorders, are present in social phobias. In adults, it may cause tears as well as excessive sweating, nausea, difficulty breathing, shaking, and palpitations as a result of the fight-or-flight response. The walk disturbance (where a person is so worried about how they walk that they may lose balance) may appear, especially when passing a group of people. Blushing is commonly exhibited by individuals suffering from social phobia. These visible symptoms further reinforce the anxiety in the presence of others. A 2006 study found that the area of the brain called the amygdala, part of the limbic system, is hyperactive when patients are shown threatening faces or confronted with frightening situations. They found that patients with more severe social phobia showed a correlation with increased response in their amygdalae. People with SAD may avoid looking at other people, and even their surroundings, to a greater extent than their peers, possibly to decrease the risk of eye contact, which can be interpreted as a nonverbal signal of openness to social interaction. Social aspects People with SAD avoid situations that most people consider "normal". They may have a hard time understanding how others can handle these situations so easily. People with SAD avoid all or most social situations and hide from others, which can affect their personal relationships. Social phobia can completely remove people from social situations due to the irrational fear of these situations. People with SAD may be addicted to social media networks, have sleep deprivation, and feel good when they avoid human interactions. SAD can also lead to low self-esteem, negative thoughts, major depressive disorder, sensitivity to criticism, and poor social skills that don't improve. People with SAD experience anxiety in a variety of social situations, from important, meaningful encounters, to everyday trivial ones. These people may feel more nervous in job interviews, dates, interactions with authority, or at work. Comorbidity SAD shows a high degree of co-occurrence with other psychiatric disorders. In fact, a population-based study found that 66% of those with SAD had one or more additional mental health disorders. SAD often occurs alongside low self-esteem and most commonly clinical depression, perhaps due to a lack of personal relationships and long periods of isolation related to social avoidance. Clinical depression is 1.49 to 3.5 times more likely to occur in those with SAD. Research also indicates that the presence of certain social fears (e.g., avoidance of participating in small groups, avoidance of going to a party) are more likely to trigger comorbid depressive symptoms than other social fears, and thus deserve a very careful audit during clinical assessment among patients with SAD. Anxiety disorders other than SAD are also very common in patients with SAD, in particular generalized anxiety disorder. Avoidant personality disorder is likewise highly correlated with SAD, with comorbidity rates ranging from 25% to 89%. To try to reduce their anxiety and alleviate depression, people with social phobia may use alcohol or other drugs, which can lead to substance use disorders. It is estimated that one-fifth of patients with social anxiety disorder also have alcohol use disorder. However, some research suggests SAD is unrelated to, or even protective against alcohol-related problems. Those who have both alcohol use disorder and social anxiety disorder are more likely to avoid group-based treatments and to relapse compared to people who do not have this combination. | medical cause of Panic attack | complications of Panic attack | medical cause of Insomnia | symptom of Panic attack | medical cause of Lightheadedness | symptom of Narcolepsy | symptom of Delirium tremens | medical cause of Seizure | 00
| 56,259 |
<unk> is a disease caused by the parasitic roundworm Ascaris lumbricoides. Infections have no symptoms in more than 85% of cases, especially if the number of worms is small. Symptoms increase with the number of worms present and may include shortness of breath and fever in the beginning of the disease. These may be followed by symptoms of abdominal swelling, abdominal pain, and diarrhea. Children are most commonly affected, and in this age group the infection may also cause poor weight gain, malnutrition, and learning problems. Infection occurs by eating food or drink contaminated with Ascaris eggs from feces. The eggs hatch in the intestines, the larvae burrow through the gut wall, and migrate to the lungs via the blood. There they break into the alveoli and pass up the trachea, where they are coughed up and may be swallowed. The larvae then pass through the stomach for a second time into the intestine, where they become adult worms. It is a type of soil-transmitted helminthiasis and part of a group of diseases called helminthiases. Prevention is by improved sanitation, which includes improving access to toilets and proper disposal of feces. Handwashing with soap appears protective. In areas where more than 20% of the population is affected, treating everyone at regular intervals is recommended. Reoccurring infections are common. There is no vaccine. Treatments recommended by the World Health Organization are the medications albendazole, mebendazole, levamisole, or pyrantel pamoate. Other effective agents include tribendimidine and nitazoxanide. About 0.8 to 1.2 billion people globally have<unk> , with the most heavily affected populations being in sub-Saharan Africa, Latin America, and Asia. This makes<unk> the most common form of soil-transmitted helminthiasis. As of 2010 it caused about 2,700 deaths a year, down from 3,400 in 1990. Another type of Ascaris infects pigs.<unk> is classified as a neglected tropical disease. | Ascariasis | Toxocariasis | Acariasis | Schistosomiasis | Strongyloidiasis | Myiasis | Monorchism | Intestinal capillariasis | 00
| 12,229 |
Stone size influences the rate of spontaneous stone passage. For example, up to 98% of small stones (less than in diameter) may pass spontaneously through urination within four weeks of the onset of symptoms, but for larger stones ( in diameter), the rate of spontaneous passage decreases to less than 53%. Initial stone location also influences the likelihood of spontaneous stone passage. Rates increase from 48% for stones located in the proximal ureter to 79% for stones located at the vesicoureteric junction, regardless of stone size. Assuming no high-grade obstruction or associated infection is found in the urinary tract, and symptoms are relatively mild, various nonsurgical measures can be used to encourage the passage of a stone. Repeat stone formers benefit from more intense management, including proper fluid intake and use of certain medications, as well as careful monitoring. Pain management Management of pain often requires intravenous administration of NSAIDs or opioids. NSAIDs appear somewhat better than opioids or paracetamol in those with normal kidney function. Medications by mouth are often effective for less severe discomfort. The use of antispasmodics does not have further benefit. Medical expulsive therapy The use of medications to speed the spontaneous passage of stones in the ureter is referred to as medical expulsive therapy. Several agents, including alpha adrenergic blockers (such as tamsulosin) and calcium channel blockers (such as nifedipine), may be effective. Alpha-blockers likely result in more people passing their stones, and they may pass their stones in a shorter time. People taking alpha-blockers may also use less pain medication and may not need to visit the hospital. Alpha-blockers appear to be more effective for larger stones (over 5 mm in size) than smaller stones. However, use of alpha-blockers may be associated with a slight increase in serious, unwanted effects from this medication. A combination of tamsulosin and a corticosteroid may be better than tamsulosin alone. These treatments also appear to be useful in addition to lithotripsy. Lithotripsy lithotriptor machine with a mobile fluoroscopic system ("C-arm") is seen in an operating room; other equipment is seen in the background including an anesthesia machine. Extracorporeal shock wave lithotripsy (ESWL) is a noninvasive technique for the removal of kidney stones. Most ESWL is carried out when the stone is present near the renal pelvis. ESWL involves the use of a lithotriptor machine to deliver externally applied, focused, high-intensity pulses of ultrasonic energy to cause fragmentation of a stone over a period of around 30–60 minutes. Following its introduction in the United States in February 1984, ESWL was rapidly and widely accepted as a treatment alternative for renal and ureteral stones. It is currently used in the treatment of uncomplicated stones located in the kidney and upper ureter, provided the aggregate stone burden (stone size and number) is less than and the anatomy of the involved kidney is normal. For a stone greater than , ESWL may not help break the stone in one treatment; instead, two or three treatments may be needed. Some 80-85% of simple renal calculi can be effectively treated with ESWL. A number of factors can influence its efficacy, including chemical composition of the stone, presence of anomalous renal anatomy and the specific location of the stone within the kidney, presence of hydronephrosis, body mass index, and distance of the stone from the surface of the skin. Common adverse effects of ESWL include acute trauma, such as bruising at the site of shock administration, and damage to blood vessels of the kidney. In fact, the vast majority of people who are treated with a typical dose of shock waves using currently accepted treatment settings are likely to experience some degree of acute kidney injury. ESWL-induced acute kidney injury is dose-dependent (increases with the total number of shock waves administered and with the power setting of the lithotriptor) and can be severe, including internal bleeding and subcapsular hematomas. On rare occasions, such cases may require blood transfusion and even lead to acute kidney failure. Hematoma rates may be related to the type of lithotriptor used; hematoma rates of less than 1% and up to 13% have been reported for different lithotriptor machines. Recent studies show reduced acute tissue injury when the treatment protocol includes a brief pause following the initiation of treatment, and both improved stone breakage and a reduction in injury when ESWL is carried out at slow shock wave rate. In addition to the aforementioned potential for acute kidney injury, animal studies suggest these acute injuries may progress to scar formation, resulting in loss of functional renal volume. Recent prospective studies also indicate elderly people are at increased risk of developing new-onset hypertension following ESWL. In addition, a retrospective case-control study published by researchers from the Mayo Clinic in 2006 has found an increased risk of developing diabetes mellitus and hypertension in people who had undergone ESWL, compared with age and gender-matched people who had undergone nonsurgical treatment. Whether or not acute trauma progresses to long-term effects probably depends on multiple factors that include the shock wave dose (i.e., the number of shock waves delivered, rate of delivery, power setting, acoustic characteristics of the particular lithotriptor, and frequency of retreatment), as well as certain intrinsic predisposing pathophysiologic risk factors. To address these concerns, the American Urological Association established the Shock Wave Lithotripsy Task Force to provide an expert opinion on the safety and risk-benefit ratio of ESWL. The task force published a white paper outlining their conclusions in 2009. They concluded the risk-benefit ratio remains favorable for many people. The advantages of ESWL include its noninvasive nature, the fact that it is technically easy to treat most upper urinary tract calculi, and that, at least acutely, it is a well-tolerated, low-morbidity treatment for the vast majority of people. However, they recommended slowing the shock wave firing rate from 120 pulses per minute to 60 pulses per minute to reduce the risk of renal injury and increase the degree of stone fragmentation. Alpha-blockers are sometimes prescribed after shock wave lithotripsy to help the pieces of the stone leave the person's body. By relaxing muscles and helping to keep blood vessels open, alpha blockers may relax the ureter muscles to allow the kidney stone fragments to pass. When compared to usual care or placebo treatment, alpha blockers may lead to faster clearing of stones, a reduced need for extra treatment and fewer unwanted effects. They may also clear kidney stones in more adults than the standard shock wave lithotripsy procedure. The unwanted effects associated with alpha blockers are hospital emergency visits and return to hospital for stone-related issues, but these effects were more common in adults who did not receive alpha-blockers as a part of their treatment. Surgery Most stones under pass spontaneously. Prompt surgery may, nonetheless, be required in persons with only one working kidney, bilateral obstructing stones, a urinary tract infection and thus, it is presumed, an infected kidney, or intractable pain. Beginning in the mid-1980s, less invasive treatments such as extracorporeal shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy began to replace open surgery as the modalities of choice for the surgical management of urolithiasis. More recently, flexible ureteroscopy has been adapted to facilitate retrograde nephrostomy creation for percutaneous nephrolithotomy. This approach is still under investigation, though early results are favorable. Percutaneous nephrolithotomy or, rarely, anatrophic nephrolithotomy, is the treatment of choice for large or complicated stones (such as calyceal staghorn calculi) or stones that cannot be extracted using less invasive procedures. Ureteroscopic surgery Ureteroscopy has become increasingly popular as flexible and rigid fiberoptic ureteroscopes have become smaller. One ureteroscopic technique involves the placement of a ureteral stent (a small tube extending from the bladder, up the ureter and into the kidney) to provide immediate relief of an obstructed kidney. Stent placement can be useful for saving a kidney at risk for postrenal acute kidney failure due to the increased hydrostatic pressure, swelling and infection (pyelonephritis and pyonephrosis) caused by an obstructing stone. Ureteral stents vary in length from and most have a shape commonly referred to as a "double-J" or "double pigtail", because of the curl at both ends. They are designed to allow urine to flow past an obstruction in the ureter. They may be retained in the ureter for days to weeks as infections resolve and as stones are dissolved or fragmented by ESWL or by some other treatment. The stents dilate the ureters, which can facilitate instrumentation, and they also provide a clear landmark to aid in the visualization of the ureters and any associated stones on radiographic examinations. The presence of indwelling ureteral stents may cause minimal to moderate discomfort, frequency or urgency incontinence, and infection, which in general resolves on removal. Most ureteral stents can be removed cystoscopically during an office visit under topical anesthesia after resolution of urolithiasis. Research is currently uncertain if placing a temporary stent during ureteroscopy leads to different outcomes than not placing a stent in terms of number of hospital visits for post operative problems, short or long term pain, need | complications of Hypercalcaemia | medical cause of Hypercalcaemia | complications of Hyperkalemia | complications of Hypophosphatemia | medical cause of Hyperphosphatemia | medical cause of Hyperkalemia | complications of Osteoporosis | complications of Hyperparathyroidism | 00
| 2,727 |
An<unk> (from Latin , "to hear"; and from Italian -metria, “to measure” ) or Audiometric Officer, is a health-care professional technician who has received special training in the use of Pure tone audiometry equipment. An<unk> conducts hearing tests, or "audiometric screening", with an Audiometer to establish hearing levels. The results are represented by an audiogram, and are usually interpreted by an audiologist, or a registered Medical Officer, unless the<unk> is also an audiologist, with the aim of diagnosing hearing loss. There are currently some misconceptions regarding the definition of<unk> and Audiologist, which vary from country to country. These misconceptions continue to grow, in Australia in particular, which leads to the need for greater communication, less segregation of each other's role within the community and a broader understanding of each other's qualifications. | Audiometrist | Podiatrist | Pedorthist | Ophthalmic technician | Gnathology | Orthotist | Psychiatrist | SpyCatcher | 00
| 29,635 |
Peripheral edema and hypoalbuminemia<unk> is a form of protein deficiency, which can result in both osmotic imbalances and irregularities in the lymphatic system.<unk> is most notable for peripheral edema. The presence of edema in<unk> is correlated with very low albumin concentration (hypoalbuminemia). Edema results from a loss of fluid balance between the hydrostatic and oncotic pressures across the capillary blood vessel walls due to the lack of protein which affects the body's ability to draw fluid from the tissues into the bloodstream. Low albumin concentration influences negatively the strength of oncotic pressure. Failure leads to the fluid buildup in the abdomen, resulting in edema and belly distension. Furthermore, the release of antidiuretic hormone is stimulated by hypovolemia, also leading to the development of peripheral edema. Plasma renin is also stimulated, promoting sodium retention. It is important to distinguish the pathophysiology of marasmus and<unk> when it comes to treating malnourished children who may have hypovolemic shock that is cause by an acute loss of salt and water. Children with severe albumin deficiency struggle physiologically to maintain their blood volume. Low glutathione levels<unk> is also marked by low glutathione levels. Glutathione is used in many of the body processes on a molecule level. It is believed to be related to high oxidant levels commonly seen in people who suffer from starvation and rarely in chronic inflammation. Glutathione serves vital functions including management of oxidative stress which is an imbalance that plays a key role in the pathogenesis of many diseases. Cysteine is an essential amino acid that acts as the limiting amino acid for glutathione synthesis in humans. Factors that stimulate cysteine uptake by cells will increase glutathione levels and prevent glutathione deficiency in humans under various conditions including protein malnutrition. Evidence indicates that dietary amino acids balance has an important effect on protein nutrition and therefore on glutathione homeostasis. Others A proposed experimental theory suggests that alterations in the microbiome/virone contributes to edematous malnutrition, but further studies are required to understand the mechanism. | Kwashiorkor | Pellagra | Albinism | Pediatric end-stage liver disease | Philadelphia basement kidnapping | Uddanam nephropathy | Cystic kidney disease | Type 3c diabetes | 00
| 1,221 |
Mechanism of action Enkephalins are peptides produced by the body that act on opioid receptors with preference for the δ subtype. Activation of δ receptors inhibits the enzyme adenylyl cyclase, decreasing intracellular levels of the messenger molecule cAMP. The active metabolite of<unk> , thiorphan, inhibits enkephalinase enzymes in the intestinal epithelium with an IC50 of 6.1 nM, protecting enkephalins from being broken down by these enzymes.<unk> itself is much less potent at 4500 nM.) This reduces diarrhea related hypersecretion in the small intestine without influencing basal secretion.<unk> also has no influence on the time substances, bacteria or virus particles stay in the intestine. Pharmacokinetics Some metabolites of<unk> .top left: precursor to the active metabolitetop right: active metabolitebottom row: inactive metabolites<unk> is rapidly absorbed after oral administration and reaches Cmax within 60 minutes. Food delays Cmax by 60 to 90 minutes but does not affect the overall bioavailability.<unk> is rapidly and effectively metabolized to the moderately active S-acetylthiorphan the main active metabolite thiorphan, of which 90% are bound to blood plasma proteins. In therapeutic doses,<unk> does not pass the blood–brain barrier. Inhibition of enkephalinases starts 30 minutes after administration, reaches its maximum (75–90% inhibition with a therapeutic dose) two hours after administration, and lasts for eight hours. The elimination half-life, measured from enkephalinase inhibition, is three hours. Thiorphan is further metabolized to inactive metabolites such as the methyl thioether and the methyl sulfoxide. Both active and inactive metabolites are excreted, mostly via the kidney (81.4%), and to a lesser extent via the feces (8%). | Racecadotril | Moexipril | Spirapril | Ramipril | Macitentan | Methallenestril | Ambrisentan | Oprelvekin | 00
| 48,677 |
Technique for<unk> depends on which tissue is being targeted and what the overall objective of the treatment is. For example, one of the most common treatment objectives for<unk> , myofascial trigger points (TrPs), differs physiologically from treatments for scar tissue, connective tissue issues, and other medical issues. In the treatment of trigger points for persons with myofascial pain syndrome,<unk> is an invasive procedure in which a filiform needle is inserted into the skin and muscle directly at a myofascial trigger point. A myofascial trigger point consists of multiple, hyperirritable contraction knots related to the production and maintenance of the pain cycle; essentially, myofascial trigger points will generate much local pain upon stimulation or irritation. Deep<unk> for treating trigger points was first introduced by Czech physician Karel Lewit in 1979. Lewit had noticed that the success of injections into trigger points in relieving pain was apparently unconnected to the analgesic used.<unk> can be divided into categories in terms of depth of penetration: deep and superficial<unk> . Deep<unk> will inactivate myofascial triggers points by provoking a local twitch response (LTR), which is an involuntary spinal cord reflex in which the muscle fibers in the taut band of muscle contract. The LTR indicates the proper placement of the needle in a trigger point.<unk> that elicits LTRs improves treatment outcomes, and may work by activating endogenous opioids. The activation of the endogenous opioids is for an analgesic effect using the Gate Control Theory of Pain. In addition to relieving myofascial trigger points, deep<unk> is also identified to decreases pain, increase range of motion, and minimize myofascial trigger point irritability. In regards to the factor of pain reduction, relief occurs at four central levels: local pain, spinal pain through nerves, brain stem pain, and higher brain center pain. The relief of myofascial trigger points has been more highly researched than relief of connective tissues, muscle fascia, muscle tension, and scar tissue; however, the American Physical Therapy Association claims that there potentially may be some benefits of<unk> on these ailments according to some available evidence. The APTA also disclaims that<unk> should not be used as a standalone procedure, but should be used in conjunction with other treatment methods, including manual soft tissue mobilization, neuromuscular re-education, functional retraining, and therapeutic exercises. Once the needle is inserted, one can manually or electrically stimulate the filiform needle depending for the desired effect of treatment. | Dry needling | Acupuncture | Mustard bath | Premedication | Warm compress | Depot injection | Orthokeratology | Moxibustion | 00
| 40,859 |
Stem cell pluripotency LIF (Leukemia inhibitory factor) signaling, which maintains pluripotency in mouse embryonic stem cells, activates<unk> downstream of the JAK-STAT signaling pathway and subsequent activation of Klf4 (a member of the family of Kruppel-like factors). Oct-4,<unk> and Nanog positively regulate transcription of all pluripotency circuitry proteins in the LIF pathway. NPM1, a transcriptional regulator involved in cell proliferation, individually forms complexes with<unk> , Oct4 and Nanog in embryonic stem cells. These three pluripotency factors contribute to a complex molecular network that regulates a number of genes controlling pluripotency.<unk> binds to DNA cooperatively with Oct4 at non-palindromic sequences to activate transcription of key pluripotency factors. Surprisingly, regulation of Oct4-Sox2 enhancers can occur without<unk> , likely due to expression of other Sox proteins. However, a group of researchers concluded that the primary role of<unk> in embryonic stem cells is controlling Oct4 expression, and they both perpetuate their own expression when expressed concurrently. In an experiment involving mouse embryonic stem cells, it was discovered that<unk> in conjunction with Oct4, c-Myc and Klf4 were sufficient for producing induced pluripotent stem cells. The discovery that expression of only four transcription factors was necessary to induce pluripotency allowed future regenerative medicine research to be conducted considering minor manipulations. Loss of pluripotency is regulated by hypermethylation of some<unk> and Oct4 binding sites in male germ cells and post-transcriptional suppression of<unk> by miR134. Varying levels of<unk> affect embryonic stem cells' fate of differentiation.<unk> inhibits differentiation into the mesendoderm germ layer and promotes differentiation into neural ectoderm germ layer. Npm1/Sox2 complexes are sustained when differentiation is induced along the ectodermal lineage, emphasizing an important functional role for<unk> in ectodermal differentiation. A study conducted in Milano, Italy showed, through the development of a knockout model, that deficiency of<unk> results in neural malformities and eventually fetal death, further underlining<unk> 's vital role in embryonic development. Neural stem cells In neurogenesis,<unk> is expressed throughout developing cells in the neural tube as well as in proliferating central nervous system progenitors. However,<unk> is downregulated during progenitors' final cell cycle during differentiation when they become post mitotic. Cells expressing<unk> are capable of both producing cells identical to themselves and differentiated neural cell types, two necessary hallmarks of stem cells. Thus signals controlling<unk> expression in the presumptive neuronal compartment, like Notch signaling, control what size the neuronal compartment finally reaches. Proliferation of<unk> + neural stem cells can generate neural precursors as well as<unk> + neural stem cell population. Differences in brain size between the species thus relate to the capacity of different species to maintain<unk> expression in the developing neural systems. The difference in brain size between humans and apes, for instance, has been linked to mutations in the gene Asb11, which is an upstream activator of<unk> in the developing neural system. Induced pluripotency is possible using adult neural stem cells, which express higher levels of<unk> and c-Myc than embryonic stem cells. Therefore, only two exogenous factors, one of which is necessarily Oct4, are sufficient for inducing pluripotent cells from neural stem cells, lessening the complications and risks associated with introducing multiple factors to induce pluripotency. Eye deformities Mutations in this gene have been linked with bilateral anophthalmia, a severe structural eye deformity. Cancer In lung development,<unk> controls the branching morphogenesis of the bronchial tree and differentiation of the epithelium of airways. Overexpression causes an increase in neuroendocrine, gastric/intestinal and basal cells. Under normal conditions,<unk> is critical for maintaining self-renewal and appropriate proportion of basal cells in adult tracheal epithelium. However, its overexpression gives rise to extensive epithelial hyperplasia and eventually carcinoma in both developing and adult mouse lungs. In squamous cell carcinoma, gene amplifications frequently target the 3q26.3 region. The gene for<unk> lies within this region, which effectively characterizes<unk> as an oncogene, although in adenocarcinoma of the esophagus loss of<unk> is strongly associated with worse prognosis, effectively characterising<unk> as a tumor suppressor. It thus fair to say that the function of<unk> in cancer is pleiotropic.<unk> is a key upregulated factor in lung squamous cell carcinoma, directing many genes involved in tumor progression.<unk> overexpression cooperates with loss of Lkb1 expression to promote squamous cell lung cancer in mice. Its overexpression also activates cellular migration and anchorage-independent growth.<unk> expression is also found in high gleason grade prostate cancer, and promotes castration-resistant prostate cancer growth. The ectopic expression of<unk> may be related to abnormal differentiation of colorectal cancer cells.<unk> has been shown to be relevant in the development of Tamoxifen resistance in breast cancer. In Glioblastoma multiforme,<unk> is a well-established stem cell transcription factor needed to induce and maintain stemness properties of glioblastoma cancer cells. | SOX2 | TFM-4AS-1 | CDK13 | FOXP3 | SPATA16 | CoWIN | ERCC2 | WRAP53 | 00
| 47,704 |
The infection is caused by inhaling yeasts or spores. The fungus is not transmitted from person to person or from animal to person. A person with cryptococcal disease is not contagious. | Cryptococcus gattii | Cryptococcus neoformans | Aspergillus tubingensis | Paracoccidioides brasiliensis | Talaromyces marneffei | Candida parapsilosis | Mycobacterium canetti | Mycoplasma incognitus | 00
| 43,530 |
<unk> is a form of<unk> anemia. Non-immune drug<unk> hemolysis can occur via oxidative mechanisms. This is particularly likely to occur when there is an enzyme deficiency in the antioxidant defense system of the red blood cells. An example is where antimalarial oxidant drugs like primaquine damage red blood cells in Glucose-6-phosphate dehydrogenase deficiency in which the red blood cells are more susceptible to oxidative stress due to reduced NADPH production consequent to the enzyme deficiency. Some drugs cause RBC (red blood cell) lysis even in normal individuals. These include dapsone and sulfasalazine. Non-immune drug-induced hemolysis can also arise from drug-induced damage to cell volume control mechanisms; for example drugs can directly or indirectly impair regulatory volume decrease mechanisms, which become activated during hypotonic RBC swelling to return the cell to a normal volume. The consequence of the drugs actions are irreversible cell swelling and lysis (e.g. ouabain at very high doses). | Drug-induced nonautoimmune hemolytic anemia | Drug-induced autoimmune hemolytic anemia | Acquired hemolytic anemia | Mixed autoimmune hemolytic anemia | Cold autoimmune hemolytic anemia | Refractory anemia with excess of blasts | Warm antibody autoimmune hemolytic anemia | Autoimmune hemolytic anemia | 00
| 54,148 |
<unk> (Cal/BD) is a topical medication for the treatment of trunk, limb, and scalp plaque psoriasis. This medication is available in ointment, gel, aerosol, or foam, formulations. The ointment formulation was FDA approved in 2004, and is indicated for the once daily topical treatment of plaque-type psoriasis vulgaris amenable to topical therapy. The foam formulation was approved by the FDA in 2015, and is indicated for the topical treatment of plaque psoriasis in patients twelve years of age and older. In all pivotal trials of<unk> ointment, topical suspension, or foam, treatment success or achievement of 'clear' or 'almost clear' disease was defined by Investigator's Global Assessment, an alternative to the Psoriasis Area and Severity Index (PASI) score. ;Ointment In an international, double-blind, parallel group study of 1603 participants with psoriasis (affecting at least 10% of one or more body regions), more patients on once-daily<unk> ointment had controlled disease, defined as having absence or very mild disease at 4 weeks (56.3%) compared with Cal 50 μg/g (22.3%). In addition, a retrospective analysis of data from six phase 3, double-blind studies found that more patients treated with<unk> ointment achieved PASI 75 than patients treated with individual components, regardless of baseline disease severity. ;Foam The foam formulation has been studied in two pivotal, randomized, double-blind trials in patients with mild to severe plaque psoriasis. In the first study (randomized, phase 2) of 302 patients with body and scalp psoriasis, more patients treated with<unk> (Cal/BD) foam achieved 'clear' or ' almost clear' disease (45%) according to the IGA by 4 weeks compared with Cal 50 mcg/g or BD 0.5 mg/g (15% and 31%, respectively). In a second study (randomized, phase 3) of patients with psoriasis on the body (N=426), a significantly greater proportion of patients treated with once-daily Cal/BD foam achieved 'clear' or 'almost clear' disease (53.3%) vs. those receiving the vehicle control (4.8%). Mean modified PASI score was also significantly lower for patients treated with Cal/BD foam compared with vehicle (2.0 vs 5.5, respectively, at week 4), and itch relief was significantly greater in patients using the Cal/BD foam beginning at day 3. A recent study compared the Cal/BD foam formulation with the ointment formulation in patients with mild to severe psoriasis. At 4 weeks, significantly more patients achieved treatment success, defined as 'clear' or 'almost clear' disease according to the IGA with Cal/BD foam (54.6%) versus the ointment (43.0%). However, pronounced itch relief occurred quickly and was maintained throughout the 4-week study duration with both formulations. | Calcipotriol/betamethasone dipropionate | Triamcinolone benetonide | Clotrimazole/betamethasone dipropionate | Tretinoin/benzoyl peroxide | Triamcinolone acetonide | Fluocinolone acetonide | Hydrocortisone/miconazole | Olopatadine/mometasone | 00
| 68,204 |
<unk> s are mainly produced for use as fertilizers in agriculture because of their high solubility and biodegradability. The main<unk> fertilizers are ammonium, sodium, potassium, calcium, and magnesium salts. Several million kilograms are produced annually for this purpose. The second major application of<unk> s is as oxidizing agents, most notably in explosives where the rapid oxidation of carbon compounds liberates large volumes of gases (see gunpowder for an example). Sodium<unk> is used to remove air bubbles from molten glass and some ceramics. Mixtures of the molten salt are used to harden some metals.<unk> was also used as a film stock through nitrocellulose. Due to its high combustibility, the studios swapped to acetate safety film in 1950. | Nitrate | Bromide | Haloalkane | Phosphine | Saline | Alcohols | Phosphate | Gluten | 00
| 1,534 |
In all causes, the mechanism of<unk> is the formation of a fibrin mesh due to increased activation of the system of coagulation. The red blood cells are physically cut by these protein networks. The resulting fragments are the schistocytes observed in light m Schistocytes or helmet cells | Microangiopathic hemolytic anemia | Mixed autoimmune hemolytic anemia | Myomatous erythrocytosis syndrome | Acquired hemolytic anemia | Autoimmune hemolytic anemia | Mechanical hemolytic anemia | Refractory anemia with excess of blasts | Drug-induced nonautoimmune hemolytic anemia | 00
| 13,151 |
Migration routes and season may affect quail risk. Quail are never poisonous outside the migration season nor are the vast majority poisonous while migrating. European common quail migrate along three different flyways, each with different poisoning characteristics, at least in 20th-century records. The western flyway across Algeria to France is associated with poisonings only on the spring migration and not on the autumn return. The eastern flyway, which funnels down the Nile Valley, is the reverse. Poisonings were only reported in the autumn migration before the quail had crossed the Mediterranean. The central flyway across Italy had no associated poisonings. Migrating quail used to be caught and eaten in prodigious numbers (150,000 quail exported from Capri in 1850) but modern farming and droughts in the Sahel have led to a vast reduction in the size of the migrations. Conservation efforts and the availability of farmed quail have also reduced the consumption of these wild birds. | Coturnism | Crepitus | Oral galvanism | Pruritus ani | Varicose veins | Petechia | Wrinkly skin syndrome | Orthostatic purpura | 00
| 49,203 |
Goiter A low amount of thyroxine (one of the two thyroid hormones) in the blood, due to lack of dietary<unk> to make it, gives rise to high levels of thyroid stimulating hormone (TSH), which stimulates the thyroid gland to increase many biochemical processes; the cellular growth and proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland, or goiter. In mild<unk> , levels of triiodothyronine (T3) may be elevated in the presence of low levels of levothyroxine, as the body converts more of the levothyroxine to triiodothyronine as a compensation. Some such patients may have a goiter, without an elevated TSH. The introduction of<unk> d salt since the early 1900s has eliminated this condition in many affluent countries; however, in Australia, New Zealand, and several European countries,<unk> is a significant public health problem. It is more common in developing countries. Public health initiatives to lower the risk of cardiovascular disease have resulted in lower discretionary salt use at the table. Additionally, there is a trend towards consuming more processed foods in western countries. The noniodized salt used in these foods means that people are less likely to obtain<unk> from adding salt during cooking. Goiter is said to be endemic when the prevalence in a population is > 5%, and in most cases goiter can be treated with<unk> supplementation. If goiter is untreated for around five years, however,<unk> supplementation or thyroxine treatment may not reduce the size of the thyroid gland because the thyroid is permanently damaged. Congenital<unk> syndrome Congenital<unk> syndrome, previously known as cretinism, is a condition associated with<unk> and goiter, commonly characterised by mental deficiency, deafness, squint, disorders of stance and gait and stunted growth due to hypothyroidism. Paracelsus was the first to point out the relation between goitrous parents and their mentally disabled children. As a result of restricted diet, isolation, intermarriage, etc., as well as low<unk> content in their food, children often had peculiar stunted bodies and retarded mental faculties, a condition later known to be associated with thyroid hormone deficiency. Diderot, in his 1754 Encyclopédie, described these patients as "crétins". In French, the term "crétin des Alpes" also became current, since the condition was observed in remote valleys of the Alps in particular. The word cretin appeared in English in 1779. While reporting recent progress towards overcoming<unk> disorders worldwide, The Lancet noted: "According to World Health Organization, in 2007, nearly 2 billion individuals had insufficient<unk> intake, a third being of school age." A conclusion was made that the single most preventable cause of intellectual disability is that of<unk> . Fibrocystic breast changes There is preliminary evidence that<unk> enhances the sensitivity of breast tissue to estrogen. In rats treated with estradiol,<unk> has been shown to lead to changes similar to benign breast changes that are reversible by increased<unk> in the diet. In a few studies,<unk> supplementation had beneficial effects (such as reducing the presence of breast cyst, fibrous tissue plaques and breast pain) in women with fibrocystic breast changes. Protective effects of<unk> on breast cancer have been postulated from epidemiologic evidence and described in animal models. In view of the antiproliferative properties of<unk> in breast tissue, molecular<unk> supplementation has been suggested as an adjuvant in breast cancer therapy. | Iodine deficiency | Growth hormone deficiency | Thyroid dyshormonogenesis | Isolated growth hormone deficiency | Congenital hypothyroidism | Constitutional growth delay | Adrenocorticotropic hormone deficiency | Congenital iodine deficiency syndrome | 00
| 26,280 |
There is no cure for congenital<unk> , and in general, the approach to management is proactive, with the aim of preventing emerging complications. After a full physical examination, physicians should focus on the known complications of<unk> , such as hydrocephalus, otitis media, hearing loss, dental caries, joint symptoms, kyphoscoliosis, and mental state. Treatment is often limited to reducing or controlling the symptoms of the condition by, for example, medications to control seizures, hearing aids to ameliorate hearing loss, and routine physical therapy to assist with muscular pain and weakness. In some cases, a wheelchair may be appropriate if muscle or spinal impairments immobilize the individual affected. Hematopoietic stem cell transplantation (HSCT) can be a treatment option for some patients, however the risk-benefit profile is more favourable in younger patients, therefore ensuring an early diagnosis is critical for this to be a viable option. The rationale is that enzyme-producing donor cells repopulate the host tissue and transfer enzyme to nearby enzyme-deficient host cells. Despite early reports to the contrary, The possible benefits of HSCT must be weighed against the overall risk of procedure related morbidity and mortality. The benefits are greater in younger patients before complications have developed, and also transplant related complications are more frequent and severe in older patients. Enzyme replacement therapy (ERT) is a therapeutic alternative in a number of lysosomal storage diseases. The overall principle of ERT is that a recombinantly produced version of the deficient enzyme is introduced into the blood stream, from where it is internalised by the cells and reaches the lysosomes by mannose-6-phosphate receptor mediated uptake, thus replacing the missing endogenous enzyme. An ERT is approved for use in the European Union. | Alpha-mannosidosis | Beta-mannosidosis | Galactosialidosis | Aspartylglucosaminuria | Essential fructosuria | Alkaptonuria | Hawkinsinuria | Glycosuria | 00
| 19,353 |
<unk> (BIE), also known as benign infantile seizures (BIS), is an epilepsy syndrome of which several forms have been described. The International League Against Epilepsy (ILAE) classify two main forms of the syndrome (familial and nonfamilial) though several other forms have been described in the academic literature. Affected children, who have no other health or developmental problems, develop seizures during infancy. These seizures have focal origin within the brain but may then spread to become generalised seizures. The seizures may occur several times a day, often grouped in clusters over one to three days followed by a gap of one to three months. Treatment with anticonvulsant drugs is not necessary but they are often prescribed and are effective at controlling the seizures. This form of epilepsy resolves after one or two years, and appears to be completely benign. The EEG of these children, between seizures, is normal. The brain appears normal on MRI scan. The familial and nonfamilial forms have overlapping features and the presence of a family history of infantile seizures may be the only distinguishing criterion. The nonfamiliar form has a larger range of the onset of seizures: from three to twenty months with most occurring between five and six months. There is no difference between the sexes. With benign familial infantile epilepsy, the seizures onset from four to eight months of age. Some cases of nonfamilial benign infantile seizures occur during a case of mild gastroenteritis. Called benign infantile seizures associated with mild gastroenteritis (BIS with MG), the seizures only occur during this illness and no not recur. Infection with rotavirus is the most common cause. Although children with<unk> typically have a normal EEG between seizures, some infants have been found to have a characteristic abnormal EEG during sleep. Called benign infantile focal epilepsy with midline spikes and waves during sleep, these infants have few seizures and there may often be a family history. | Benign infantile epilepsy | Benign familial infantile epilepsy | Benign neonatal seizures | Benign familial neonatal seizures | Childhood absence epilepsy | Benign neonatal sleep myoclonus | Juvenile myoclonic epilepsy | Idiopathic childhood occipital epilepsy of Gastaut | 00
| 62,642 |
The most common adverse effects are headache, which occurs in 4–11% of patients, and constipation in up to 6% of patients. In less than 1% of patients, other gastrointestinal disorders occur, as well as sleeplessness, first- and second-degree atrioventricular block, muscle pain and shortness of breath.<unk> is similarly well tolerated as other 5-HT3 antagonists, and slightly less than placebo. | Palonosetron | Tropisetron | Alosetron | Granisetron | Cilansetron | Avacopan | Romidepsin | Tripelennamine | 00
| 45,191 |
<unk> is a genus of gram-negative, fermentative bacteria of the family Hafniaceae. It was first discovered in snakes in 1962. | Edwardsiella | Salmonella | Vibrio cholerae | Shigella | Kingella kingae | Escherichia coli | Listeria monocytogenes | Bacillus cereus | 00
| 56,205 |
<unk> is a skin condition caused by fibroblasts producing abnormally large amounts of mucopolysaccharides characterized by the occurrence of waxy, flesh-colored papules. | Discrete papular lichen myxedematosus | Localized lichen myxedematosus | Subcutaneous granuloma annulare | Nodular lichen myxedematosus | Localized granuloma annulare | Ichthyosis bullosa of Siemens | Acne keloidalis nuchae | Linear verrucous epidermal nevus | 00
| 54,868 |
The most common adverse effects (occurring in at least 1% of those taking the drug) include agitation, anxiety, confusion, dizziness, irritability, abnormal sensations, like pins and needles, without a physical cause, sleep disturbances (e.g. sleeplessness) and a drop in blood pressure upon standing up. Less frequent side effects include movement disorders (like tremors), precipitation of angle closure glaucoma and the potentially fatal side effects paralytic ileus and neuroleptic malignant syndrome. Dropout incidence due to side effects is about 20%. Side effects with unknown frequency include (but are not limited to): * Digestive effects: * Constipation * Diarrhoea * Dry mouth * Nausea * Taste disturbances * Vomiting * Effects on the heart: * Arrhythmia * ECG changes * Abnormal heart rhythm * Heart block * Sudden cardiac death * High heart rate * Blood abnormalities: * Abnormal blood cell counts * Blood sugar changes * Low blood sodium levels * Breast effects: * Breast enlargement, including in males. * Spontaneous breast milk secretion that is unrelated to breastfeeding or pregnancy * Effects on the skin: * Abnormal sweating * Hair loss * Hives * Increased light sensitivity * Itching * Rash * Mental / neurologic effects: * Delusions * Hallucinations * Headache * Hypomania/mania * Seizures * Suicidal behaviour * Other effects: * Appetite changes * Blurred vision * Difficulty emptying the bladder * Difficulty talking due to difficulties in moving the required muscles * Liver problems * Ringing in the ears * Sexual dysfunction, such as impotence * Swelling * Weight changes Withdrawal If abruptly stopped after regular use it can cause withdrawal effects such as sleeplessness, irritability and excessive sweating. | Lofepramine | Diphenhydramine | Sibutramine | Dezocine | Palonosetron | Zotepine | Avacopan | Quinupramine | 00
| 38,594 |
left<unk> is a selective, competitive angiotensin II receptor type 1 (AT1) antagonist, reducing the end organ responses to angiotensin II.<unk> administration results in a decrease in total peripheral resistance (afterload) and cardiac venous return (preload). All of the physiological effects of angiotensin II, including release of aldosterone, are antagonized in the presence of<unk> . Reduction in blood pressure occurs independently of the status of the renin–angiotensin system. As a result of<unk> dosing, plasma renin activity increases due to removal of the angiotensin II feedback. Renin is released from the kidneys when there is reduced renal arterial pressure, sympathetic activation, or increased sodium delivery to the distal renal tubule. Renin then acts by converting angiotensinogen to angiotensin I; angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II; angiotensin II causes vasoconstriction and aldosterone release. Aldosterone serves to retain sodium from the distal renal tubule. Sodium retention ultimately results in increased blood pressure. Therefore, the use of angiotensin II receptor antagonists like<unk> result in blocking the downstream effect of renin, angiotensin II, and ultimately decreasing blood pressure. Angiotensin II receptor antagonists include<unk> , valsartan, azilsartan, candesartan, eprosartan, irbesartan, olmesartan, and telmisartan. They all have the same mechanism of action and potentially inhibit the actions of angiotensin better than ACE inhibitors, such as lisinopril, because there are other enzymes than ACE that have the capability of producing angiotensin II.<unk> is a uricosuric. As a specific inhibitor of the urate transporter 1 (SLC22A12, URAT1),<unk> blocks the uptake of uric acid into cells, thus leaving more available in the bloodstream to be filtered and excreted by the kidneys. Because<unk> can cause hyperkalemia, individuals should not use potassium supplements or salt substitutes containing potassium without appropriate monitoring by a physician. | Losartan | Olmesartan | Valsartan | Irbesartan | Azilsartan | Telmisartan | Cyclothiazide | Candesartan | 00
| 27,765 |
The combination is an effective and well-tolerated malaria treatment, providing high cure rates even in areas of multi-drug resistance. | Artemether/lumefantrine | Artesunate/amodiaquine | Artesunate/mefloquine | Piperaquine/dihydroartemisinin | Artesunate/pyronaridine | Nifurtimox/eflornithine | Avermectin | Artesunate | 00
| 36,399 |
Solutions that have a<unk> approaching 1.000 are referred to as isobaric, as the density of the cerebrospinal fluid is approximately 1.0003+/- 0.0003. Solutions with a<unk> less than 0.999 are termed hypobaric, and are usually created by mixing the local anesthetic with distilled water. Hyperbaric solutions are created by mixing dextrose 5-8% with the desired local anesthetic. Hyperbaric solutions will flow in the direction of gravity and settle in the most dependent areas of the intrathecal space. Conversely, hypobaric mixtures will rise in relation to gravitational pull. These properties allow the anesthesia provider to preferentially control the spread of the block by choice of mixture and patient positioning. | Baricity | Pain out of proportion | Hyperintensity | Tenderness | Lusitropy | Acelity | Weakness | Pain asymbolia | 00
| 35,679 |
While typical drug side effects reactions are mild to moderate, sometimes serious adverse effects occur. Boxed warnings In 2008, the U.S. FDA added black box warnings on all fluoroquinolones, advising of the increased risk of tendon damage. In 2016, the FDA found that systemic use (by mouth or injection) of fluoroquinolones was associated with "disabling and potentially permanent serious side effects" involving the tendons, muscles, joints, nerves, and central nervous system, concluding that these side effects generally outweigh the benefits for people with acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections when other treatment options are available. Concerns regarding low blood sugar and mental health problems were added in 2018. Tendons<unk> s are associated with a small risk of tendonitis and tendon rupture; a 2013 review found the incidence of tendon injury among those taking fluoroquinolones to be between 0.08 and 0.20%. The risk appears to be higher among people older than 60 and those also taking corticosteroids; the risk also may be higher among people who are male, have a pre-existing joint or tendon issue, have kidney disease, or are highly active. Some experts have advised avoidance of fluoroquinolones in athletes. If tendonitis occurs, it generally appears within one month, and the most common tendon injured appears to be the Achilles tendon. The cause is not well understood. Nervous system Nervous-system effects include insomnia, restlessness, and rarely, seizure, convulsions, and psychosis. Other rare and serious adverse events have been observed with varying degrees of evidence for causation. Aortic dissection Fluoroquinolones can increase the rate of rare but serious tears in the aorta by 31% compared to other antibiotics. People at increased risk include those with aortic aneurysm, hypertension, certain genetic conditions such as Marfan syndrome and Ehlers-Danlos syndrome, and the elderly. For these people, fluoroquinolones should be used only when no other treatment options are available. Colitis Clostridium difficile colitis may occur in connection with the use of any antibacterial drug, especially those with a broad spectrum of activity such as clindamycin, cephalosporins, and fluoroquinolones. Fluoroquinoline treatment is associated with risk that is similar to or less than that associated with broad spectrum cephalosporins. Fluoroquinoline administration may be associated with the acquisition and outgrowth of a particularly virulent Clostridium strain. Other More generally, fluoroquinolones are tolerated, with typical drug side effects being mild to moderate. Common side effects include gastrointestinal effects such as nausea, vomiting, and diarrhea, as well as headache and insomnia. Postmarketing surveillance has revealed a variety of relatively rare but serious adverse effects associated with all members of the fluoroquinolone antibacterial class. Among these, tendon problems and exacerbation of the symptoms of the neurological disorder myasthenia gravis are the subject of "black box" warnings in the United States. A 2018 EU-wide review of fluoroquinolones concluded that they are associated with serious side effects including tendonitis, tendon rupture, arthralgia, pain in extremities, gait disturbance, neuropathies associated with paraesthesia, depression, fatigue, memory impairment, sleep disorders, and impaired hearing, vision, taste and smell. Tendon damage (especially to Achilles tendon but also other tendons) can occur within 48 hours of starting fluoroquinolone treatment but the damage may be delayed several months after stopping treatment. The overall rate of adverse events in people treated with fluoroquinolones is roughly similar to that seen in people treated with other antibiotic classes. A U.S. Centers for Disease Control and Prevention study found people treated with fluoroquinolones experienced adverse events severe enough to lead to an emergency department visit more frequently than those treated with cephalosporins or macrolides, but less frequently than those treated with penicillins, clindamycin, sulfonamides, or vancomycin. Fluoroquinolones prolong the heart's QT interval by blocking voltage-gated potassium channels. Prolongation of the QT interval can lead to torsades de pointes, a life-threatening arrhythmia, but in practice, this appears relatively uncommon in part because the most widely prescribed fluoroquinolones (ciprofloxacin and levofloxacin) only minimally prolong the QT interval. In 2019 study by Journal of the American College of Cardiology it was discovered that fluoroquinolones could increase the risk for heart valve diseases. Events that may occur in acute overdose are rare, and include kidney failure and seizure. Susceptible groups of patients, such as children and the elderly, are at greater risk of adverse reactions during therapeutic use. Mechanism of toxicity The mechanisms of the toxicity of fluoroquinolones have been attributed to their interactions with different receptor complexes, such as blockade of the GABAa receptor complex within the central nervous system, leading to excitotoxic type effects and oxidative stress. | Quinolone antibiotic | Polypeptide antibiotic | Beta-lactam antibiotics | Lipase inhibitors | Nonsteroidal anti-inflammatory drug | Antiviral drug | Protease inhibitor | Antibiotic | 00
| 60,985 |
If patients with HSAN I receive appropriate treatment and counseling, the prognosis is good. Early treatment of foot infections may avoid serious complications. Nevertheless, the complications are manageable, thus allowing an acceptable quality of life. The disease progresses slowly and does not influence the life expectancy if signs and symptoms are properly treated. | Hereditary sensory and autonomic neuropathy type I | Distal hereditary motor neuropathy type V | Familial amyloid neuropathy | Congenital myasthenic syndrome | Familial amyloid polyneuropathy | Hereditary motor and sensory neuropathy | Lambert–Eaton myasthenic syndrome | MGUS polyneuropathy | 00
| 64,827 |
Signs of<unk><unk> can include nipple retraction, inversion, pain, and classic green-brown discharge. | Duct ectasia of breast | Papillomatosis of breasts | Breast cyst | Adenomyoepithelioma of the breast | Breast eczema | Mucinous carcinoma of the breast | Keratin implantation cyst | Solitary cutaneous leiomyoma | 00
| 51,061 |
<unk> may be diagnosed with a test called a blood smear. During a blood smear, a medical technologist spreads a thin layer of blood on a microscope slide and stains the blood to help differentiate the cells. The technologist then views the blood under a microscope, where the sizes and shapes of the red blood cells can be seen. | Poikilocytosis | Anisocytosis | Macrocytosis | Anisopoikilocytosis | Monocytosis | Neuroacanthocytosis | Spherocytosis | Binucleated cells | 00
| 28,051 |
<unk> , also known as<unk> , or colorectal cancer suppressor is a protein which in humans is encoded by the<unk> gene.<unk> has long been implicated in colorectal cancer and its previous name was Deleted in colorectal carcinoma.<unk> is a single transmembrane<unk> . Since it was first discovered in a colorectal cancer study in 1990,<unk> has been the focus of a significant amount of research.<unk> held a controversial place as a tumour suppressor gene for many years, and is well known as an axon guidance<unk> that responds to<unk> -1. More recently<unk> has been characterized as a dependence<unk> , and many hypotheses have been put forward that have revived interest in<unk> s candidacy as a tumour suppressor gene, as it may be a ligand-dependent suppressor that is frequently epigenetically silenced. | Netrin receptor DCC | Thromboxane receptor | Fibroblast growth factor receptor 3 | VCAM-1 | Type II cytokine receptor | Type I cytokine receptor | Growth hormone secretagogue receptor | Low-density lipoprotein receptor gene family | 00
| 40,206 |
<unk> is a cutaneous condition, one of the rarest forms of urticaria, where within minutes of<unk> with<unk> from any source, itching and whealing occur at the precise site of<unk> , lasting up to 1 hour. | Localized heat contact urticaria | Delayed pressure urticaria | Physical urticaria | Dermatographic urticaria | Cold urticaria | Aquagenic urticaria | Pressure urticaria | Heat urticaria | 00
| 56,945 |
There are different ways to treat<unk> . Some doctors recommend special eye drops and taking care of your hygiene, while eye exercises and healthy diet is also vital for good eyesight. There are no surgical treatment. If<unk> is not treated at its early stages, it may lead to myopia. | Cyclospasm | Laryngospasm | Vasospasm | Bronchospasm | Eupnea | Cardiovascular drift | Mydriasis | Venospasm | 00
| 24,382 |
Deficiencies in<unk> s result in decreased ability to oxidize fatty acids, thereby signifying metabolic dysfunction. Medium-chain<unk> deficiencies (MCADD) are well known and characterized because they occur most commonly among<unk> s, leading to fatty acid oxidation disorders and the potential of life-threatening metabolic diseases. Some symptoms of medium-chain<unk> deficiency include intolerance to fasting, hypoglycemia, and sudden infant death syndrome. These symptoms are seen as directly connected to the inability to metabolize fats. Intolerance to fasting and hypoglycemia result from the inability to gain energy and make sugar from fat stores, which is how most of humans' excess energy is stored. Also, fatty acids can begin to accumulate in the blood, lowering the blood's pH and causing acidosis. MCAD is related to / has an association with Sudden Infant Death. Approximately 90% of cases of MCAD are due to a single point mutation where the Lysine at position 304 (Lys304)is replaced by a Glutamate residue and this prevents the enzyme from properly functioning. It is reported that, every year, 1 in 20,000 infants is born with a deficiency in his/her medium-chain<unk> s that is caused by a mutation. The mutation is recessive, and often parents of children who suffer from the deficiency can be diagnosed afterward as carriers. In humans the most common naturally occurring mutation in MCAD is located at amino acid residue Lys-304. The altered residue occurs as a result of a single-point mutation in which the lysine side chain is replaced by a glutamate. Lys-304 typically interacts with surrounding amino acid residues by forming hydrogen bonds with Gln-342, Asp-300, and Asp-346. When a mutation causes glutamate to take the place of lysine, an additional negative charge is introduced at that site, which disrupts the normally occurring H-bonding. Such a disruption alters the folding pattern of the enzyme, ultimately compromising its stability and inhibiting its function in fatty acid oxidation. The efficiency of the mutated protein is about 10 times lower than that of the natural protein. This can lead to the symptoms of the deficiency listed above. | Acyl-CoA dehydrogenase | Pyruvate carboxylase | Phenylalanine hydroxylase | Aldehyde dehydrogenase | Glutamate dehydrogenase | Butyrate esterase | Glycogen phosphorylase isoenzyme BB | Monoamine oxidase B | 00
| 37,951 |
<unk> also known as acne mallorca, is a special kind of polymorphous light eruption induced by ultra violet A radiation. This condition is said to be seasonal, usually affecting people in springtime and goes away in autumn when there is less sun light. This photo induced skin reaction leads to a monomorphous eruption that consists of multiple, uniform, red, papular lesions. This skin reaction is classified as a delayed-type hypersensitivity because the onset is 24–72 hours after sun exposure. The condition equally affects men and women between the ages of 20–40 years old with no prior history of acne vulgaris. The eruption is unusual because it spares the face but it affects the lateral aspects of the upper arms, shoulder girdle, back, and chest. This condition’s pathogenesis is not very well understood but scientists believe it an unfortunate side effect that results from a strong immune response to potentially cancer-causing cell damage. | Acne aestivalis | Corpora arenacea | Acne conglobata | Anagen effluvium | Aromaticum rosatum | Ichthyosis hystrix | Tinea imbricata | Steatocystoma simplex | 00
| 52,872 |
Some 125,000 cases a year have been reported in the United States, but actual incidence of spontaneous thrombophlebitis is unknown. A fourfold increased incidence from the third to the eight decade in men and a preponderance among women of approximately 55-70%. The average mean age of affected patients is 60 years. Thrombophlebitis can develop along the arm, back, or neck veins, the leg is by far the most common site. When it occurs in the leg, the great saphenous vein is usually involved, although other locations are possible. | Superficial thrombophlebitis | Pseudothrombophlebitis | Septic thrombophlebitis | Superficial vein thrombosis | Varicose veins | Thrombophlebitis | Trombiculosis | Venous ulcer | 00
| 55,138 |
Intellectual disability (ID), also known as general learning disability in the United Kingdom and formerly mental retardation (MR), is a generalized neurodevelopmental disorder characterized by significantly impaired intellectual and adaptive functioning. It is defined by an IQ under 70, in addition to deficits in two or more adaptive behaviors that affect everyday, general living. Intellectual functions are defined under DSM-V as reasoning, problem‑solving, planning, abstract thinking, judgment, academic learning, and learning from instruction and experience, and practical understanding confirmed by both clinical assessment and standardized tests. Adaptive behavior is defined in terms of conceptual, social, and practical skills involving tasks performed by people in their everyday lives. Intellectual disability is subdivided into syndromic intellectual disability, in which intellectual deficits associated with other medical and behavioral signs and symptoms are present, and non-syndromic intellectual disability, in which intellectual deficits appear without other abnormalities. Down syndrome and fragile X syndrome are examples of syndromic intellectual disabilities. Intellectual disability affects about 2 to 3% of the general population. Seventy-five to ninety percent of the affected people have mild intellectual disability. Non-syndromic, or idiopathic cases account for 30 to 50% of these cases. About a quarter of cases are caused by a genetic disorder, and about 5% of cases are inherited from a person's parents. Cases of unknown cause affect about 95 million people . | symptom of Birth defect | symptoms of Birth defect | symptom of Congenital heart defect | symptom of Stillbirth | types of Head injury | symptom of Nuchal cord | symptom of Achondroplasia | symptom of Arrhythmia | 00
| 50,921 |
<unk> (FFL) is<unk> ised or patchy process of lipid accumulation in the liver. It is likely to have different pathogenesis than non-alcoholic steatohepatitis which is a diffuse process. FFL may result from altered venous flow to liver, tissue hypoxia and malabsorption of lipoproteins. The condition has been increasingly recognised as sensitivity of abdominal imaging studies continues to improve. A fine needle biopsy is often performed to differentiate it from malignancy. | Focal fatty liver | Polycystic liver disease | Ischemic hepatitis | Alcoholic hepatitis | Autoimmune hepatitis | Non-alcoholic fatty liver disease | Adams–Oliver syndrome | Fatty liver disease | 00
| 45,285 |
It is through upper frontal chest discomfort (also known as cervical angina) and scapular pains which signs of<unk> s are shown. In 1937 a man named Oille was the first to state that these chest pains originated from the cervical nerve root. This new outlook helped shed light on exactly what signs indicated the beginning of these ailments for those suffering from<unk> s. It is now recognized that these patients feel pain, numbness, discomfort, and weakness along with neurological symptoms. *Numbness Numbness occurs when one develops a “pinched” nerve not allowing for the flow of electrical charges, which may result in the death of the nerve fiber. *Weakness An individual becomes weak due to the compression of nerves encompassing<unk> s, thus resulting in the inability to move or use arms. Those who suffer from such symptoms should seek medical treatment as soon as possible. Complications If not treated right away, there are many consequences and pains various<unk> s can cause. Brachial plexus *Neck pains Pains in the neck area tend to be tenacious and persistent and most muscles in the cervical<unk> l region tighten causing for discomfort. *Headaches Headaches are further triggered through the stiffness of neck muscles, which pull at their attachment to the skull. These headaches are recurrent in nature and start from the base of the skull and emanate upwards; they can be painful or mild. *Arm pains Muscular spasms within the arm are further common symptoms in which such spasms are seen right above the collarbones and pressure is placed on the Brachial plexus causing arms to feel heavy and ache. *Difficulty walking Hardships arise with cervical<unk> l injuries when issues with walking, balancing, and posture are affected all due to the<unk> l cord being compressed resulting in Myelopathy. *Those with extremely severe outcomes may result in:Impairment | Cervical spine disorder | Cervical spinal stenosis | Spinal disease | Spinal stenosis | Spinal tumor | Lumbar spinal stenosis | Spinal disc herniation | Spinal fracture | 00
| 16,706 |
<unk> results from coal<unk> , creosote, crude coal<unk> , or pitch, in conjunction with sunlight exposure, which induces a sunburn reaction associated with severe burning sensation. | Phototoxic tar dermatitis | Abietic acid dermatitis | Lacquer dermatitis | Blister beetle dermatitis | Rodent mite dermatitis | Autosensitization dermatitis | Phytophotodermatitis | Nummular dermatitis | 00
| 55,185 |
<unk> <unk> refers to a test that measures the urine urea to assess nitrogen balance. | Urine urea nitrogen | Urine osmolality | Urine protein/creatinine ratio | BUN-to-creatinine ratio | Microalbuminuria | Urine sodium | Blood urea nitrogen | Aldosterone-to-renin ratio | 00
| 66,194 |
A simple definition of the syndrome is "limited elevation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye. Harold W.<unk> characterized the syndrome in many ways such as: * Limited elevation in the eye when head is straight up * Eyes point out in a straight up gaze (divergence in up gaze) * Widening of the eyelids in the affected eye on adduction * Head tilts backwards (compensatory chin elevation to avoid double vision) * Near normal elevation in abduction He concluded that all of these features of<unk> syndrome were due to the shortening or tightening of the anterior superior oblique tendon. Because this syndrome can be acquired or occur at random and has spontaneous resolution,<unk> hypothesized one major truth for this disorder — that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral (on the same side) inferior oblique muscle and secondary to a permanent shortening. After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of<unk> . The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic. | Brown's syndrome | Horner's syndrome | Shone's syndrome | Seaver Cassidy syndrome | Nance–Horan syndrome | Pilotto syndrome | Weaver syndrome | Brown-Séquard syndrome | 00
| 45,387 |
The incubation period – the time between when infection occurs and when symptoms appear – varies from virus to virus, but is usually limited between 2 and 15 days for<unk> es. The majority of infections, however, are asymptomatic. Among cases in which symptoms do appear, symptoms tend to be non-specific, resembling a flu-like illness, and are not indicative of a specific causative agent. These symptoms include fever, headache, malaise, rash and fatigue. Rarely, vomiting and hemorrhagic fever may occur. The central nervous system can also be affected by infection, as encephalitis and meningitis are sometimes observed. Prognosis is good for most people, but is poor in those who develop severe symptoms, with up to a 20% mortality rate in this population depending on the virus. The very young, elderly, pregnant women, and people with immune deficiencies are more likely to develop severe symptoms.<unk> Disease(s) Incubation period Symptoms Duration of symptoms Complications Case fatality rate Vector(s) Primary host(s) Geographic distribution Does infection provide lifelong immunity? Dengue virus Dengue fever 3–14 days Asymptomatic in most cases; fever, headache, rash, muscle, and joint pains 7–10 days Shock, internal bleeding, and organ damage <1% with treatment, 1–5% without; about 25% in severe cases Aedes mosquitoes, especially Aedes aegypti Humans Near the equator globally Varies Japanese encephalitis virus Japanese encephalitis 5–15 days Asymptomatic in most cases; fever, headache, fatigue, nausea, and vomiting Encephalitis, seizures, paralysis, coma, and long-term brain damage 20–30% in encephalitis cases Culex mosquitoes, especially Culex tritaeniorhynchus Domestic pigs and wading birds Southeast and East Asia Yes Rift Valley fever virus Rift Valley fever 2–6 days Fever, headache, myalgia and liver abnormalities 4–7 days Hemorrhagic fever, meningoencephalitis 1% in humans; in pregnant livestock, 100% fatality rate for fetuses Culex tritaeniorhynchus and Aedes vexans Micropteropus pusillus and Hipposideros abae Eastern, Southern, and Western Africa Yes Tick-borne encephalitis virus Tick-borne encephalitis 7–14 days Fever, headache, muscle pain, nausea, vomiting, meningitis, and encephalitis Paralysis and long-term brain damage 1–2% Ixodes scapularis, Ixodes ricinus, and Ixodes persulcatus Small rodents Eastern Europe and Southern Russia Yes West Nile virus West Nile fever, encephalitis 2–15 days Asymptomatic in most cases; fever, headache, fatigue, nausea, vomiting, rash 3–6 days Swollen lymph nodes, meningitis, encephalitis, acute flaccid paralysis 3–15% in severe cases Culex mosquitoes Passerine birds North America, Europe, West and Central Asia, Oceania, and Africa Yes Yellow fever virus Yellow fever 3–6 days Fever, headache, back pain, loss of appetite, nausea, and vomiting 3–4 days Jaundice, liver damage, gastrointestinal bleeding, recurring fever 3% in general; 20% in cases with severe complications Aedes mosquitoes, especially Aedes aegypti Primates Tropical and subtropical regions of South America and Africa Yes | Arbovirus | Oncovirus | Coronavirus | Coronavirus | Echovirus | Senecavirus | Orthohantavirus | Pandoravirus | 00
| 12,840 |
Medication-induced +Medication related causes of<unk> Category Examples Antipsychotics Haloperidol, amisulpride, risperidone, aripiprazole, lurasidone, ziprasidone SSRIs Fluoxetine, paroxetine, citalopram, sertraline Antidepressants Venlafaxine, tricyclics, trazodone, and mirtazapine Antiemetics Metoclopramide, prochlorperazine, and promethazine Drug withdrawal Antipsychotic withdrawal Serotonin syndrome Harmful combinations of psychotropic drugs Medication-induced<unk> is termed acute<unk> and is frequently associated with the use of antipsychotics. Antipsychotics block dopamine receptors, but the pathophysiology is poorly understood. Additionally, drugs with successful therapeutic effects in the treatment of medication-induced<unk> have provided additional insight into the involvement of other transmitter systems. These include benzodiazepines, β-adrenergic blockers, and serotonin antagonists. Another major cause of the syndrome is the withdrawal observed in drug-dependent individuals. Since dopamine deficiency (or disruptions in dopamine signalling) appears to play an important role in the development of RLS, a form of<unk> focused in the legs, the sudden withdrawal or rapidly decreased dosage of drugs which increase dopamine signalling may create similar deficits of the chemical which mimic dopamine antagonism and thus can precipitate RLS. This is why sudden cessation of opioids, cocaine, serotonergics, and other euphoria-inducing substances commonly produce RLS as a side-effect.<unk> involves increased levels of the neurotransmitter norepinephrine, which is associated with mechanisms that regulate aggression, alertness, and arousal. It has been correlated with Parkinson's disease and related syndromes, and descriptions of<unk> predate the existence of pharmacologic agents.<unk> can be miscoded in side effect reports from antidepressant clinical trials as "agitation, emotional lability, and hyperkinesis (overactivity)"; misdiagnosis of<unk> as simple motor restlessness occurred, but was more properly classed as dyskinesia. | Akathisia | Restless legs syndrome | Tardive dyskinesia | Paroxysmal dyskinesia | Dystonia | Pseudoathetosis | Anxiety | Paroxysmal nonkinesigenic dyskinesia | 00
| 8,225 |
<unk> (also known as "hairy elbow syndrome") is a cutaneous condition characterized by multiple terminal hairs on both elbows in children. | Hypertrichosis cubiti | Woolly hair nevus | Onychophosis | Onychogryphosis | Auricular hypertrichosis | Xanthelasma | Dermatosis papulosa nigra | Granulomatous slack skin | 00
| 60,379 |
On the nasal surface of the body of the maxilla, in front of the opening of the sinus is a deep<unk> , the<unk> (or<unk> sulcus), which is converted into the nasolacrimal canal, by the<unk> bone and inferior nasal concha; this canal opens into the inferior meatus of the nose and transmits the nasolacrimal duct. | Lacrimal groove | Lacrimal sac | Optic recess | Orbital septum | Optic pit | Ateronon | Corneal button | Central canal | 00
| 36,574 |
Chlamydia trachomatis and Neisseria gonorrhoeae are usually the main cause of PID. Data suggest that PID is often polymicrobial. Isolated anaerobes and facultative microorganisms have been obtained from the upper genital tract. N. gonorrhoeae has been isolated from fallopian tubes, facultative and anaerobic organisms were recovered from endometrial tissues. The anatomical structure of the internal organs and tissues of the female reproductive tract provides a pathway for pathogens to ascend from the vagina to the pelvic cavity thorough the infundibulum. The disturbance of the naturally occurring vaginal microbiota associated with bacterial vaginosis increases the risk of PID. N. gonorrhoea and C. trachomatis are the most common organisms. The least common were infections caused exclusively by anaerobes and facultative organisms. Anaerobes and facultative bacteria were also isolated from 50 percent of the patients from whom Chlamydia and Neisseria were recovered; thus, anaerobes and facultative bacteria were present in the upper genital tract of nearly two-thirds of the PID patients. PCR and serological tests have associated extremely fastidious organism with endometritis, PID, and tubal factor infertility. Microorganisms associated with PID are listed below. Rarely cases of PID have developed in people who have stated they have never had sex. Bacteria *Chlamydia trachomatis *Neisseria gonorrhoeae *Prevotella spp. *Streptococcus pyogenes *Prevotella bivia *Prevotella disiens *Bacteroides spp. *Peptostreptococcus asaccharolyticus *Peptostreptococcus anaerobius *Gardnerella vaginalis *Escherichia coli *Group B streptococcus *α-hemolytic streptococcus *Coagulase-negative staphylococcus *Atopobium vaginae *Acinetobacter spp. *Dialister spp. *Fusobacterium gonidiaformans *Gemella spp. *Leptotrichia spp. *Mogibacterium spp. *Porphyromonas spp. *Sphingomonas spp. *Veillonella spp. *Cutibacterium acnes *Mycoplasma genitalium *Mycoplasma hominis *Ureaplasma spp. | complications of Chlamydia | symptom of Chlamydia | complications of Gonorrhea | complications of Trichinosis | medical cause of Dysmenorrhea | medical cause of Vaginitis | medical cause of Taeniasis | symptom of Bacterial vaginosis | 00
| 1,768 |
To date there is no treatment for<unk> albinism, probably because little is known about the receptor function and its role in the pathophysiology of the condition. Though surgery for strabismus is sometimes helpful, there does not seem to be a sure remedy for it until the cause of<unk> albinism is well established. However, with the recent discovery of the upstream ligand (L-DOPA) and the discovery of<unk> 's possible downstream G alpha partner (Gai3) the<unk> pathway is becoming clearer and future of<unk> research looks promising. Touloukian et al. have characterized<unk> immunologically as a melanoma/melanocyte differentiation antigen. Flow cytometry data suggests that<unk> -specific T cells are all CD8+. This indicates that<unk> peptide is processed and presented on the surface of melanoma cells to be recognized by antigen-specific T cells. Moreover, recognition of<unk> by T cells induces cytokine production by the<unk> -specific T cells. This means that<unk> is a potential target for melanoma vaccines. | Ocular albinism type 1 | Oculocutaneous albinism type I | Oculocutaneous albinism | Retinoschisis | Lafora disease | Leber congenital amaurosis | Bayoud disease | Tangier disease | 00
| 52,159 |
Itch can originate in the peripheral nervous system (dermal or neuropathic) or in the central nervous system (neuropathic, neurogenic, or psychogenic). Dermal/pruritoceptive A chipmunk scratching itself. Itch originating in the skin is known as pruritoceptive, and can be induced by a variety of stimuli, including mechanical, chemical, thermal, and electrical stimulation. The primary afferent neurons responsible for histamine-induced itch are unmyelinated C-fibres. Two major classes of human C-fibre nociceptors exist: mechano-responsive nociceptors and mechano-insensitive nociceptors. Mechano-responsive nociceptors have been shown in studies to respond to mostly pain, and mechano-insensitive receptors respond mostly to itch induced by histamine. However, it does not explain mechanically induced itch or itch produced without a flare reaction that involves no histamine. Therefore, it is possible that pruritoceptive nerve fibres have different classes of fibres, which is unclear in current research. Studies have been done to show that itch receptors are found only on the top two skin layers, the epidermis and the epidermal/dermal transition layers. Shelley and Arthur verified the depth by injecting individual itch powder (Mucuna pruriens) spicules and noting that maximal sensitivity occurred at the basal cell layer or the innermost layer of the epidermis. Surgical removal of those skin layers removed the ability for a patient to perceive itch. Itch is never felt in muscle or joints, which strongly suggests that deep tissue probably does not contain itch signaling apparatuses. Itch is often classified as that which is histamine mediated (histaminergic) and nonhistaminergic. Sensitivity to pruritic stimuli is evenly distributed across the skin and has a clear spot distribution with similar density to that of pain. The different substances that elicit itch upon intracutaneous injection (injection within the skin) elicit only pain when injected subcutaneously (beneath the skin). Itch is readily abolished in skin areas treated with nociceptor excitotoxin capsaicin but remains unchanged in skin areas rendered touch insensitive by pretreatment with anti-inflammatory saponins. Although experimentally induced itch can still be perceived under a complete A-fiber conduction block, it is significantly diminished. Overall, itch sensation is mediated by A-delta and C nociceptors located in the uppermost layer of the skin. Molecular diversity of itch transmitting primary afferents Using single-cell mRNA sequencing, sensory-modality specific primary afferent have been molecularly defined into clusters based on gene expression patterns. Here, 11 sub clusters were detected; NF1-3, transmitting innocuous nociceptive information; NF4-5, which transmit proprioceptive information; NP1-3, transmitting itch information; PEP1-2, nociceptive information and TH, which is involved in pleasant touch, The pruriceptive NP1-3 were shown to express genes related to histaminergic and non-histaminergic signaling, where NF1 expresses genes responding to lysophosphatidic acid (Lpar3 and Lpar5), NP2 chloroquine-responsive genes (Mrgpra3 and Mrgprx1), whereas NP3 expresses neuropeptides Nppb and Sst as well as genes involved in inflammatory itch (Il31ra, Osmr and Crystrl2). The histamine receptor gene Hrh1 was found in NP2 and NP3, suggesting that histaminergic itch is transmitted by both these pruriceptive sub clusters. The spinal itch pathway After the pruriceptive primary afferent has been activated, the signal is transmitted from the skin into the spinal dorsal horn. In this area, a number of interneurons will either be inhibited or activated to promote activation of projection neurons, mediating the puriceptive signal to the brain. The GRP-GRPR interneuron system has been found to be important for mediating both histaminergic and non-histaminergic itch, where the GRP neurons activate GRPR neurons to promote itch Neuropathic Neuropathic itch can originate at any point along the afferent pathway as a result of damage of the nervous system. They could include diseases or disorders in the central nervous system or peripheral nervous system. Examples of neuropathic itch in origin are notalgia paresthetica, brachioradial pruritus, brain tumors, multiple sclerosis, peripheral neuropathy, and nerve irritation. Neurogenic Neurogenic itch, which is itch induced centrally but with no neural damage, is mostly associated with increased accumulation of exogenous opioids and possibly synthetic opioids. Psychogenic Itch is also associated with some<unk> s of psychiatric disorders such as tactile hallucinations, delusions of parasitosis, or obsessive-compulsive disorders (as in OCD-related neurotic scratching). Peripheral sensitization Inflammatory mediators—such as bradykinin, serotonin (5-HT) and prostaglandins—released during a painful or pruritic inflammatory condition not only activate pruriceptors but also cause acute sensitization of the nociceptors. In addition, expression of neuro growth factors (NGF) can cause structural changes in nociceptors, such as sprouting. NGF is high in injured or inflamed tissue. Increased NGF is also found in atopic dermatitis, a hereditary and non-contagious skin disease with chronic inflammation. NGF is known to up-regulate neuropeptides, especially substance P. Substance P has been found to have an important role in inducing pain; however, there is no confirmation that substance P directly causes acute sensitization. Instead, substance P may contribute to itch by increasing neuronal sensitization and may affect release of mast cells, which contain many granules rich in histamine, during long-term interaction. Central sensitization Noxious input to the spinal cord is known to produce central sensitization, which consists of allodynia, exaggeration of pain, and punctuate hyperalgesia, extreme sensitivity to pain. Two types of mechanical hyperalgesia can occur: 1) touch that is normally painless in the uninjured surroundings of a cut or tear can trigger painful sensations (touch-evoked hyperalgesia), and 2) a slightly painful pin prick stimulation is perceived as more painful around a focused area of inflammation (punctuate hyperalgesia). Touch-evoked hyperalgesia requires continuous firing of primary afferent nociceptors, and punctuate hyperalgesia does not require continuous firing which means it can persist for hours after a trauma and can be stronger than normally experienced. In addition, it was found that patients with neuropathic pain, histamine ionophoresis resulted in a sensation of burning pain rather than itch, which would be induced in normal healthy patients. This shows that there is spinal hypersensitivity to C-fiber input in chronic pain. | symptom of Athlete's foot | symptom of Chemical burn | symptom of Sciatica | symptom of Legius syndrome | symptom of Burn | symptom of Peripheral artery disease | symptom of Deep vein thrombosis | symptom of Gout | 00
| 12,498 |
<unk> is a pyrrolodiazepine benzodiazepine and acts as a partial agonist at benzodiazepine receptors. The mean time taken to reach peak plasma levels is 2 hours and the mean half life of<unk> in humans is 11.5 hours. About 90% of the drug is excreted in unchanged form. Of the remaining 10% of the drug none of the metabolites showed any pharmacological activity. Thus<unk> produces no active metabolites in humans. | Premazepam | Halazepam | Medazepam | Oxazepam | Diclazepam | Camazepam | Cinolazepam | Temazepam | 00
| 50,018 |
Meningoencephalitis (; from Greek μῆνιγξ meninx, "membrane", ἐγκέφαλος, enképhalos "brain", and the medical suffix -itis, "inflammation"), also known as herpes meningoencephalitis, is a medical condition that simultaneously resembles both meningitis, which is an infection or inflammation of the meninges, and encephalitis, which is an infection or inflammation of the brain. | medical cause of General paresis of the insane | medical cause of Lightheadedness | complications of Heat stroke | symptom of Intracerebral hemorrhage | symptom of Stroke | complications of Coma | symptom of Vertebral artery dissection | medical cause of Conversion disorder | 00
| 33,341 |
Symptoms may include visible discoloring (ecchymosis), breast pain, and swelling. The symptoms may be similar to those of fibrocystic breast changes. | Breast hematoma | Breast cyst | Pelvis justo major | Hematocele | Ovarian cyst | Papillomatosis of breasts | Hematoma | Pelvic lipomatosis | 00
| 66,587 |
Arsenic compounds are highly toxic, and AsCl3 especially so because of its volatility and solubility. It is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act (42 U.S.C. 11002), and is subject to strict reporting requirements by facilities which produce, store, or use it in significant quantities. | Arsenic trichloride | Arsenic trioxide | Carbon tetrachloride | Desmethylchlorotrianisene | Tetrachlorodecaoxide | Butylated hydroxytoluene | Coal tar | Triphenylchloroethylene | 00
| 36,637 |
Locally produced<unk> in the vessel wall contributes to the development and progression of atherosclerosis.<unk> has been described to play a role in renal pathology including acute kidney injury and chronic kidney failure. The chronic activation of monocytes can lead to multiple metabolic, hematologic and immunologic abnormalities in patients with chronic kidney failure. In the context of acute kidney injury,<unk> has been implicated in promoting repair following injury, but also been described in an opposing role, driving proliferation of a pro-inflammatory<unk> phenotype. | Macrophage colony-stimulating factor | Macrophage-activating factor | Leukemia inhibitory factor | Hemopoietic growth factor | Thymic stromal lymphopoietin | Interleukin | Major basic protein | Tumor necrosis factor | 00
| 38,154 |
*Type 1 diabetes *Hypersensitivity to sulfonylureas *Severe renal or hepatic failure (But relatively useful in mild renal impairment e.g. CKD stage 3) *Pregnancy and lactation | Gliclazide | Glibenclamide | Linaclotide | Liranaftate | Lobeglitazone | Miglitol | Linagliptin | Saxagliptin | 00
| 37,417 |
Risk factors for incidentally discovered<unk> s are mainly: * General risk factors of lung cancer such as exposure to tobacco smoking or other carcinogens such as asbestos and previously diagnosed cancer, respiratory infections, or chronic obstructive pulmonary disease. * Size: larger size confers a higher risk of cancer subpleural<unk> . * Location: Upper lobe location is a risk factor for cancer, while a location close to a fissure or the pleura indicates a benign lymph node, especially if having a triangular shape. * Margin morphology: a spiculated margin is a risk factor for cancer. Benign causes tend to have a well defined border, whereas lobulated lesions or those with an irregular margin extending into the neighbouring tissue tend to be malignant. In particular, spiculations are highly predictive of malignancy with a positive predictive value up to 90%. Also, a "notch sign", which is an abrupt indentation of the<unk> , increases the risk of cancer, but may also be found in granulomatous diseases. File:CT of a round well-delineated solid<unk> with smooth border.Round well-delineated solid<unk> with smooth border. File:CT of a lobulated<unk> .Lobulated<unk> . File:CT of a spiculated<unk> .Spiculated<unk> . File:CT of a<unk> with a notch sign.A "notch sign". File:CT of perifissural<unk> .A triangular perifissural node can be diagnosed as a benign lymph node. * Multiplicity: Where the presence of up to an additional 3<unk> s has been found to increase the risk of cancer, but decrease in case of 4 or more additional ones, likely because it indicates a previous granulomatous infection rather than cancer. * Growth rate: solid cancers generally doubles in volume over between 100 and 400 days, while subsolid cancers (generally representing adenocarcinomas) generally doubles in volume over 3 to 5 years. One volume doubling equals approximately a 26% increase in diameter. * Presence of emphysema and/or fibrosis is a risk factor for cancer. In comparison, the typical size doubling are less than 20 days for infections, and more than 400 days for benign<unk> s. * Enhancement: If the exam is done as a combined non-contrast and contrast CT, a solitary<unk> with an enhancement off less than 15 Hounsfield units (HU), whereas a higher enhancement indicates a malignant tumor (with a sensitivity estimated at 98%). * Areas of fatty tissue (−40 to −120 HU) indicates a hamartoma. However, only about 50% of hamartomas are fat containing. * If there is a central cavity, then a thin wall points to a benign cause whereas a thick wall is associated with malignancy (especially 4 mm or less versus 16 mm or more). File:CT of a fat containing hamartoma.Low attenuating<unk> (in this case a fat containing hamartoma). File:CT of an aspergilloma.Cavitation with relatively thick wall, in this case aspergilloma). Calcifications and popcorn-like appearance, conferring a diagnosis of hamartoma. * In case of calcifications, a popcorn-like appearance indicates a hamartoma, which is benign. * In case of subsolid<unk> s, being part solid has a higher risk of cancer than being purely ground glass opacity. File:CT of part solid<unk> .Part solid<unk> . File:CT of ground glass<unk> .Ground glass opacity<unk> . * Pleural retraction is far more common in cancers. It is the pulling of visceral pleura towards the<unk> . File:CT of a<unk> with pleural retraction.Nodule with pleural retraction. File:CT of a subpleural<unk> with pleural retraction.In this case, pleural retraction is seen as a triangular fat component.<unk> abutting a pulmonary cyst. * A<unk> abutting a pulmonary cyst is a rare finding, yet indicating cancer. * Bubble-like lucencies in the<unk> indicate cancer: File:CT of spiculated<unk> with bubble-like lucencies.png File:CT of<unk> with bubble-like lucencies.png Thin slice and maximal intensity projection of a<unk> , the latter better visualizing vascular convergence. * Vascular convergence is where vessels converge to a<unk> without adjoining or contacting the edge of the<unk> , and is mainly seen in peripheral subsolid lung cancers. It reflects angiogenesis. Air bronchograms is defined as a pattern of air-filled bronchi on a background of airless lung, and may be seen in both benign and malignant<unk> s, but certain patterns thereof may help in risk stratification. CT densitometry, measuring absolute attenuation on the Hounsfield scale, has low sensitivity and specificity and is not routinely employed, apart from helping to distinguish solid from ground glass lesions, and to confirm visible fatty areas or calcifications. | Lung nodule | Lung abscess | Pulmonary consolidation | Lung tumor | Pleural disease | Mediastinal tumors | Pulmonary infiltrate | Malignant pleural effusion | 00
| 50,609 |
Diagnosis for genetic or rare diseases are often challenging. As such, diagnosis includes a combination of genetic testing, followed by a thorough examination of a person’s medical history, symptoms, a physical exam, and laboratory tests. In addition, a diagnosis may also include a biopsy of the affected muscle tissue. For example, the diagnosis of Pompe disease presents a serious diagnostic dilemma as a result of the rarity and nonspecific phenotypic features of Pompe disease. In other words, the overlapping signs and symptoms that Pompe disease shares with other neuromuscular diseases, such as muscle weakness and even cardiovascular diseases, create significant challenges for diagnosis. Muscle biopsy is often used as an early diagnostic tool in the diagnosis of all muscular diseases. However, it has been discovered that the use of muscle biopsies alone tends to result in false-negative results and subsequent delays in identifying and treating Pompe disease. Therefore, a combination of several tests is typically used in conjunction to confirm whether a patient is suffering from Pompe disease. As mentioned, the signs and symptoms of Pompe disease, such as poor muscle tone and an enlarged heart, are typical to other conditions too. As such, a thorough and differential diagnosis by specialists can help to distinguish Pompe from other diseases with similar symptoms. Supposing the differential diagnosis concludes that Pompe disease is indeed present, further testing such as enzyme activity tests to measure the levels and activity of the acid alpha-glucosidase enzyme, or genetic testing to examine the GAA gene to determine mutations, should be performed for confirmation. In addition, chest x-rays to check for an enlarged heart, electrocardiograms (ECG) to detect abnormal heartbeat patterns, and electromyograms (EMG) to assess for the presence of muscle injury and dysfunction, are additional tests that are performed to diagnosis Pompe disease. | Autophagic vacuolar myopathy | Centronuclear myopathy | Hereditary inclusion body myopathy | Brody myopathy | Nemaline myopathy | Mitochondrial myopathy | X-linked myotubular myopathy | Metabolic myopathy | 00
| 73,203 |
<unk> is a bacterium from the genus of<unk> which has been isolated from human infections. | Peptoniphilus coxii | Helicobacter bizzozeronii | Bacteroides caccae | Cheyletiella blakei | Madurella grisea | Pseudallescheria boydii | Bacteroides dorei | Bartonella rochalimae | 00
| 72,295 |
Affected individuals may present with hypoglycaemia during the neonatal period, or with growth retardation during childhood (those diagnosed in the neonatal period appear to be affected by a particularly severe form of the disorder).<unk> is a common cause of congenital hypopituitarism, and causes a permanent growth hormone deficit. Some<unk> -affected individuals may also present with adrenal hypoplasia (5-29%), diabetes insipidus (5-29%), primary amenorrhea (5-29%), hypothyroidism (30-79%), failure to thrive (80-99%), septooptic dysplasia (5-29%), and Fanconi anaemia.<unk> may be isolated, or, commonly, present with extra-pituitary malformations.<unk> features in neonates (may) include: * hypoglycaemia (30-79%) * (prolonged) jaundice * micropenis (30-79%) * cryptorchidism (5-29%) * delayed intellectual development * death in infancy (5-29%) * congenital abnormalities<unk> features in later childhood (may) include: * short stature (80-99%) * seizures (5-29%) * hypotension * delayed intellectual development * delayed puberty (30-79%)<unk> is associated with a higher frequency of breech presentation, Caeserian section, and/or low Apgar score, though these are likely consequences rather than causes. | Pituitary stalk interruption syndrome | Kallmann syndrome | Persistent adrenarche syndrome | Lipoid congenital adrenal hyperplasia | Hypopituitarism | Karak syndrome | Young's syndrome | Waldmann disease | 00
| 71,552 |
ECM biomaterials are used to promote healing in a number of tissues, especially the skin and tendons. Surgimend, a collagen matrix derived from fetal bovine<unk> , can trigger the healing of tendons (which do not heal spontaneously) in the ankle. This intervention can shorten healing time by almost half and allows the patient to return to full activity much sooner. Open wounds, like tendons, do not spontaneously heal and can persist for long stretches of time. When ECM biomaterials are added in multiple layers to the ulcer, the wound begins to close quickly and generates host tissue. Although preliminary studies seem promising, little information is available on the success of and direct comparisons between different ECM biomaterial devices in human trials. Alloderm, an<unk> derived from the skin of donated cadavers, is used in reconstructive and dental surgeries. In gingival grafts, the<unk> is an alternative to tissue cut from the palate of the patient's mouth. It has also been used for abdominal hernia repair, and to rebuild resected turbinates in the treatment of empty nose syndrome. Alloderm and other<unk> dermal matrices are used routinely in implant based breast reconstruction after mastectomy for improved soft tissue coverage and thus decrease the risk of visible rippling, capsular contraction, implant malposition, bottoming out and implant exposure. | Acellular dermis | Granulation tissue | Dermoepidermal junction | Neointima | Granulation | Moist desquamation | Keratin pearl | Stratum corneum | 00
| 57,057 |
<unk> is a description of the<unk> diseases that affect women; it seems that these diseases are much more prominent in women than they are in men. The root of such conditions are not exactly clear, but may in part, involve an extra copy of the X chromosome that females have compared to the single copy found in males. The elevated risk factor of<unk> conditions in women are thought to be associated with physiological changes; for example, hormonal shifts, sex chromosomes, stress, genetics or a variety of different factors. Some of these differences are unique to women, such as the effects during pregnancy. It is possible that this immune reaction could be heightened through pregnancy, as the mother's immune system works to protect both her and her infant. Women with<unk> diseases can safely have children. There are some risks for the mother or baby, depending on the disease and how severe it is. For some women, symptoms tend to improve during pregnancy, while others find that their symptoms flare up. Also, some medicines used to treat<unk> diseases might not be safe to use during pregnancy. Importantly, there are other methods for mediating these diseases, such as lifestyle changes to help control the over-active immune system. | Autoimmune disease in women | Thyroid disease in women | Cardiovascular disease in women | Risk factors for breast cancer | High-risk pregnancy | Dermatoses of pregnancy | Ergogenic use of anabolic steroids | complications of Sexually transmitted infection | 00
| 70,319 |
<unk> , sold under the brand name Treximet, is a combination medication used to treat migraines attacks. It is taken through oral route. | Sumatriptan/naproxen sodium | Naproxen/diphenhydramine | Phenylephrine/ketorolac | Hydrocodone/aspirin | Celecoxib/tramadol | Butalbital/acetaminophen | Amlodipine/celecoxib | Ibuprofen/paracetamol | 00
| 51,975 |
<unk> , known medically as tinea pedis, is a common skin infection of the feet caused by fungus. Signs and symptoms often include itching, scaling, cracking and redness. In rare cases the skin may blister.<unk> fungus may infect any part of the foot, but most often grows between the toes. The next most common area is the bottom of the foot. The same fungus may also affect the nails or the hands. It is a member of the group of diseases known as tinea.<unk> is caused by a number of different fungi, including species of Trichophyton, Epidermophyton, and Microsporum. The condition is typically acquired by coming into contact with infected skin, or fungus in the environment. Common places where the fungi can survive are around swimming pools and in locker rooms. They may also be spread from other animals. Usually diagnosis is made based on signs and symptoms; however, it can be confirmed either by culture or seeing hyphae using a microscope. Regardless of the name,<unk> can affect anyone. Some methods of prevention include: not going barefoot in public showers, keeping the toenails short, wearing big enough shoes, and changing socks daily. When infected, the feet should be kept dry and clean and wearing sandals may help. Treatment can be either with antifungal medication applied to the skin such as clotrimazole or, for persistent infections, antifungal medications that are taken by mouth such as terbinafine. The use of the cream is typically recommended for four weeks.<unk> was first medically described in 1908. Globally,<unk> affects about 15% of the population. Males are more often affected than females. It occurs most frequently in older children or younger adults. Historically it is believed to have been a rare condition that became more frequent in the 1900s due to the greater use of shoes, health clubs, war, and travel. | Athlete's foot | Pitted keratolysis | Trench foot | Heel stick wound | Daniel Sickles's leg | Butcher's wart | Bednar's aphthae | Diabetic sock | 00
| 18,596 |
Pathophysiology of hypovolemia The signs and symptoms of hypovolemia are primarily due to the consequences of decreased circulating volume and a subsequent reduction in the amount of blood reaching the tissues of the body. In order to properly perform their functions, tissues require the oxygen transported in the blood. A decrease in circulating volume can lead to a decrease in bloodflow to the brain, resulting in headache and dizziness. Baroreceptors in the body (primarily those located in the carotid sinuses and aortic arch) sense the reduction of circulating fluid and send signals to the brain to increase sympathetic response (see also: baroreflex). This sympathetic response is to release epinephrine and norepinephrine, which results in peripheral vasoconstriction (reducing size of blood vessels) in order to conserve the circulating fluids for organs vital to survival (i.e. brain and heart). Peripheral vasoconstriction accounts for the cold extremities (hands and feet), increased heart rate, increased cardiac output (and associated chest pain). Eventually, there will be less perfusion to the kidneys, resulting in decreased urine output. | complications of Hypoalbuminemia | complications of Acute liver failure | complications of Kidney disease | complications of Hemolytic–uremic syndrome | complications of HELLP syndrome | medical cause of Hyperphosphatemia | complications of Rhabdomyolysis | complications of Vasculitis | 00
| 13,352 |
<unk> is the mind's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. There are two models that can be used when exploring the concept of<unk> ": brain<unk> and<unk> . These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy brain<unk> can be seen as hardware and<unk> as software. All these factors are currently believed to contribute to global<unk> .<unk> is commonly used to refer to both brain and<unk> s in the literature. In 1988 a study published in Annals of Neurology reporting findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer's disease neuropathology and the clinical manifestations of the disease: some participants whose brains had extensive Alzheimer's disease pathology, had no or very few clinical manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater<unk> ". This is the first time this term has been used in the literature in this context. The study sparked off interest in this area, and to try to confirm these initial findings further studies were done. Higher<unk> was found to provide a greater threshold before clinical deficit appears. Furthermore, those with higher capacity once they become clinically impaired show more rapid decline, probably indicating a failure of all compensatory systems and strategies put in place by the individual with greater<unk> to cope with the increasing neuropathological damage. | Cognitive reserve | Psychological resilience | Biology of depression | Physiological functional capacity | Impact of health on intelligence | Psychological resistance | Lateralization of brain function | Homeostasis | 00
| 35,619 |
The condition gradually improves over a period of time which can range from six months to several years in more severe cases. People with longer term and heavier substance use have caused damage to the nervous system, where, after cessation of the primary addictive substance, the opioid receptors may become favorable to any potential agonist. This places people with longer term and heavier substance use at risk of becoming addicted to any other agonist with very little use of the secondary agonist. Abstinence from all agonists, sometimes taking multiple years, is required for full recovery. Flumazenil was found to be more effective than placebo in reducing feelings of hostility and aggression in patients who had been free of benzodiazepines for 4 to 266 weeks. This may suggest a role for flumazenil in treating protracted benzodiazepine withdrawal symptoms. Acamprosate has been found to be effective in alleviating some of the<unk><unk> withdrawal symptoms of alcohol withdrawal. Carbamazepine or trazodone may also be effective in the treatment of<unk><unk> withdrawal<unk> in regards to alcohol use. Cognitive behavioral therapy can also help the<unk><unk> withdrawal<unk> especially when cravings are a prominent feature. | Post-acute-withdrawal syndrome | Benzodiazepine withdrawal syndrome | Alcohol withdrawal syndrome | Nicotine withdrawal | Secondary poisoning | Drug withdrawal | Opioid withdrawal | Antidepressant discontinuation syndrome | 00
| 48,103 |
Treatment depends substantially on the type of<unk> . Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery. * Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction. * IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids. Medication * One review found that antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes. Other reviews found an unclear difference between intensive and less intensive blood pressure control. The American Heart Association and American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg. However, the evidence finds tentative usefulness as of 2015. * Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism. It thus overall does not result in better outcomes in those without hemophilia. * Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy. Platelets however appear to worsen outcomes in those with spontaneous<unk> bleeding on antiplatelet medication. * Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage. * H2 antagonists or proton pump inhibitors are commonly given for to try to prevent stress ulcers, a condition linked with<unk> . * Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended. Surgery Surgery is required if the hematoma is greater than , if there is a structural vascular lesion or lobar hemorrhage in a young patient. * A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures. * Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited. * A craniectomy may take place, where part of the skull is removed to allow a swelling brain room to expand without being squeezed. | Intracerebral hemorrhage | Stroke | Subarachnoid hemorrhage | Cerebral edema Cerebral edema 1 | Epidural hematoma | Intracranial hemorrhage | Subdural empyema | Brain herniation | 00
| 30,400 |