text1
stringlengths 11
17.4k
| text2
stringlengths 11
8.2k
| label
class label 2
classes |
|---|---|---|
The authors of the FDA analysis note that "given the large number of comparisons made in this review, chance is a very plausible explanation for this difference". The more complete data submitted later by the sertraline manufacturer Pfizer indicated increased suicidal behavior. Similarly, the analysis conducted by the UK MHRA found a 50% increase of odds of suicide-related events, not reaching statistical significance, in the patients on sertraline as compared to the ones on placebo. Overdose
Acute overdosage is often manifested by emesis, lethargy, ataxia, tachycardia and seizures. Plasma, serum or blood concentrations of sertraline and norsertraline, its major active metabolite, may be measured to confirm a diagnosis of poisoning in hospitalized patients or to aid in the medicolegal investigation of fatalities. As with most other SSRIs its toxicity in overdose is considered relatively low. Interactions
As with other SSRIs, sertraline may increase the risk of bleeding with NSAIDs (ibuprofen, naproxen, mefenamic acid), antiplatelet drugs, anticoagulants, omega-3 fatty acids, vitamin E, and garlic supplements due to sertralines inhibitory effects on platelet aggregation via blocking serotonin transporters on platelets. Sertraline, in particular, may potentially diminish the efficacy of levothyroxine.Sertraline is a moderate inhibitor of CYP2D6 and CYP2B6 in vitro. Accordingly, in human trials it caused increased blood levels of CYP2D6 substrates such as metoprolol, dextromethorphan, desipramine, imipramine and nortriptyline, as well as the CYP3A4/CYP2D6 substrate haloperidol. This effect is dose-dependent; for example, co-administration with 50 mg of sertraline resulted in 20% greater exposure to desipramine, while 150 mg of sertraline led to a 70% increase. | The drug should not be used in children under two years of age, people with kidney disease, or people who are allergic to aspirin.Side effects are primarily gastrointestinal but may also include headache; GI effects include nausea, diarrhea and abdominal pain. There have been scattered reports of various problems when the oral form is used, including: problems caused by myelosuppression (leukopenia, neutropenia, agranulocytosis, aplastic anaemia, and thrombocytopenia), as well as hair loss, peripheral neuropathy, pancreatitis, liver problems, myocarditis and pericarditis, allergic and fibrotic lung reactions, lupus erythematosus-like reactions and rash (including urticaria), drug fever, interstitial nephritis and nephrotic syndrome, usually reversible on withdrawal. Very rarely, use of mesalazine has been associated with an exacerbation of the symptoms of colitis, Stevens Johnson syndrome and erythema multiforme. Chemistry
Mesalazine is the active moiety of sulfasalazine, which is metabolized to sulfapyridine and mesalazine. It is also the active component of the prodrug balsalazide along with the inert carrier molecule 4-aminobenzoyl-beta-alanine. It is in the category of disease-modifying antirheumatic drugs (DMARDs) family of medications. It is unclear exactly how it works. Mechanism of action
Exact mechanism of mesalazine is unknown, but is speculated that mesalazine decreases synthesis of prostaglandin and leukotriene, modulating the inflammatory response derived from the cyclooxygenase and lipooxygenase pathways. It appears to act locally on colonic mucosa. Society and culture
Brand names
Mesalazine is sold under various names including Apriso, Asacol, Asacol HD, Canasa, Delzicol, Fivasa, Lialda, Pentasa, Rowasa, and Sfrowasa. References
External links
"Mesalamine". Drug Information Portal. U.S. National Library of Medicine. | 0-1
|
In 1986, Young helped found the Bridge School, an educational organization for children with severe verbal and physical disabilities, and its annual supporting Bridge School Benefit concerts, together with his wife Pegi. Nicolas Hamilton, a British racing driver competing in BTCC. He is the half-brother of Formula 1 driver Lewis Hamilton. Geri Jewell, who had a regular role in the prime-time series The Facts of Life. Josh Blue, winner of the fourth season of NBCs Last Comic Standing, whose act revolves around his CP. Blue was also on the 2004 U.S. Paralympic soccer team. Jason Benetti, play-by-play broadcaster for ESPN, Fox Sports, Westwood One, and Time Warner covering football, baseball, lacrosse, hockey, and basketball. Since 2016, he is also the television play-by-play announcer for Chicago White Sox home games. Jack Carroll, British comedian and runner-up in the seventh season of Britains Got Talent. Abbey Curran, an American beauty queen who represented Iowa at Miss USA 2008 and was the first contestant with a disability to compete. Francesca Martinez, British stand-up comedian and actress. Evan OHanlon, Australian Paralympian, the fastest athlete with cerebral palsy in the world. Arun Shouries son Aditya, about whom he has written a book Does He Know a Mothers Heart
Maysoon Zayid, the self-described "Palestinian Muslim virgin with cerebral palsy, from New Jersey", who is an actress, stand-up comedian, and activist. Zayid has been a resident of Cliffside Park, New Jersey. She is considered one of Americas first Muslim women comedians and the first person ever to perform standup in Palestine and Jordan. | Also, the terminology used to describe orthoses needs to be standardised to ensure studies can be reproduced and readily compared and evaluated. Surgical intervention in CP children mainly includes orthopaedic surgery and neurosurgery (selective dorsal rhizotomy). Orthotics in the concept of therapy
To improve the gait pattern, orthotics can be included in the therapy concept. An orthosis can support physiotherapeutic treatment in setting the right motor impulses in order to create new cerebral connections. The orthosis must meet the requirements of the medical prescription. In addition, the orthosis must be designed by the orthotist in such a way that it achieves the effectiveness of the necessary levers, matching the gait pattern, in order to support the proprioceptive approaches of physiotherapy. The characteristics of the stiffness of the orthosis shells and the adjustable dynamics in the ankle joint are important elements of the orthosis to be considered. Due to these requirements, the development of orthoses has changed significantly in recent years, especially since around 2010. At about the same time, care concepts were developed that deal intensively with the orthotic treatment of the lower extremities in cerebral palsy. Modern materials and new functional elements enable the rigidity to be specifically adapted to the requirements that fits to the gait pattern of the CP patient. The adjustment of the stiffness has a decisive influence on the gait pattern and on the energy cost of walking. | 11
|
"In the American literature, the terms long-face syndrome and short-face syndrome are often used." To be sure, there are reported "long and short face anomalies" and open bite cases. However, in the opinion of Hugo Obwegeser, there is no medical justification for naming them as a "syndrome"—the signs and symptoms do not meet the definitional threshold. : 22 There is controversy concerning the use of the descriptor "long-face syndrome." While increased anterior "total and lower face height" in many ages, combined with vertical maxillary excess in adults has been observed, the causes are controversial. Specifically, there is disagreement about possible potential environmental influences on genetic components.Anecdotally, it was said to be a genetic condition, which could only be corrected with "massive amounts" of debilitating, frequent and long dental and facial reconstructive surgery.In children, there is a concern that mouth breathing can contribute to the development of long face syndrome. A recent study finds that it is a growing problem which should be treated as "it wont just go away." In addition to mouth breathing, it may be associated with sleep apnea.Because of long face syndromes sometime association with pediatric obstructive sleep apnea (OSA) and allergic reactions, it is essential that treating physicians differentiate the conditions and the treatments; treating one may not cure the other. Notable people
Actor and screenwriter Craig Chester says he has had the condition. See also
Adenoid facies
Facies (medical)
Dolichocephaly
Notes
== References == | Fibrofolliculomas are 2 to 4 mm in diameter, dome-shaped, yellowish or skin-colored papules usually located on the head, neck, and upper trunk. They are characteristically seen in Birt–Hogg–Dubé syndrome. : 674
See also
List of cutaneous conditions
List of cutaneous neoplasms associated with systemic syndromes
Trichodiscoma
== References == | 0-1
|
By 1950 the work led to the knowledge that ethanol is oxidized to acetaldehyde by alcohol dehydrogenase and acetaldehyde is oxidized to acetic acid by aldehyde dehydrogenase (ALDH), and that disulfiram works by inhibiting ALDH, leading to a buildup of acetaldehyde, which is what causes the negative effects in the body.The drug was first marketed in Denmark and as of 2008, Denmark is the country where it is most widely prescribed. It was approved by the FDA in 1951. The FDA later approved other drugs for treatment of alcoholism, namely naltrexone in 1994 and acamprosate in 2004. Society and culture
Though the Occupational Safety and Health Administration (OSHA) in the US has not set a permissible exposure limit (PEL) for disulfiram in the workplace, the National Institute for Occupational Safety and Health has set a recommended exposure limit (REL) of 2 mg/m3 and recommended that workers avoid concurrent exposure to ethylene dibromide. Research
Disulfiram has been studied as a possible treatment for cancer, parasitic infections, anxiety disorder, and latent HIV infection.Disulfiram has shown reversing of retinitis pigmentosa in rats. Cancer
When disulfiram creates complexes with metals (dithiocarbamate complexes), it is a proteasome inhibitor and as of 2016 it had been studied in in vitro experiments, model animals, and small clinical trials as a possible treatment for liver metastasis, metastatic melanoma, glioblastoma, non-small cell lung cancer, and prostate cancer. Various clinical trials of copper depletion agents have been carried out. | Implants, made from hard metals or silicone, associated with anaplastic large cell lymphoma. Familial component
Familial lymphoid cancer is rare. The familial risk of lymphoma is elevated for multiple lymphoma subtypes, suggesting a shared genetic cause. However, a family history of a specific subtype is most strongly associated with risk for that subtype, indicating that these genetic factors are subtype-specific. Genome-wide association studies have successfully identified 67 single-nucleotide polymorphisms from 41 loci, most of which are subtype specific. HIV/AIDS
The Centers for Disease Control and Prevention (CDC) included certain types of non-Hodgkin lymphoma as AIDS-defining cancers in 1987. Immune suppression rather than HIV itself is implicated in the pathogenesis of this malignancy, with a clear correlation between the degree of immune suppression and the risk of developing NHL. Additionally, other retroviruses, such as HTLV, may be spread by the same mechanisms that spread HIV, leading to an increased rate of co-infection. The natural history of HIV infection has greatly changed over time. As a consequence, rates of non-Hodgkin lymphoma (NHL) in people infected with HIV has significantly declined in recent years. Treatment
The traditional treatment of NHL includes chemotherapy, radiotherapy, and stem-cell transplants. There have also been developments in immunotherapy used in the treatment of NHL. Chemotherapy
The most common chemotherapy used for B-cell non-Hodgkin lymphoma is R-CHOP, which is a regimen of four drugs (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus rituximab. Treatment complications
If participants receive stem-cell transplants, they can develop a graft-versus-host disease. | 0-1
|
Other signs of portal hypertension on ultrasound include a portal flow mean velocity of less than 12 cm/s, porto–systemic collateral veins (patent paraumbilical vein, spleno–renal collaterals and dilated left and short gastric veins), splenomegaly and signs of cirrhosis (including nodularity of the liver surface).The hepatic venous pressure gradient (HVPG) measurement has been accepted as the gold standard for assessing the severity of portal hypertension. Portal hypertension is defined as HVPG greater than or equal to 5 mm Hg and is considered to be clinically significant when HVPG exceeds 10 to 12 mm Hg. Treatment
The treatment of portal hypertension is divided into:
Portosystemic shunts
Selective shunts select non-intestinal flow to be shunted to the systemic venous drainage while leaving the intestinal venous drainage to continue to pass through the liver. The most well known of this type is the splenorenal. This connects the splenic vein to the left renal vein thus reducing portal system pressure while minimizing any encephalopathy. In an H-shunt, which could be mesocaval (from the superior mesenteric vein to the inferior vena cava) or could be, portocaval (from the portal vein to the inferior vena cava) a graft, either synthetic or the preferred vein harvested from elsewhere on the patients body, is connected between the superior mesenteric vein and the inferior vena cava. The size of this shunt will determine how selective it is.With the advent of transjugular intrahepatic portosystemic shunting (TIPS), portosystemic shunts are less performed. TIPS has the advantage of being easier to perform and doesnt disrupt the livers vascularity. | Prevention of bleeding
Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin such as terlipressin) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding.The management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide), endoscopic banding ligation, balloon tamponade and TIPS. Ascites
The management of ascites needs to be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, kidney failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, and transjugular intrahepatic portosystemic shunt (TIPS). Hepatic encephalopathy
A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated. References
Further reading
== External links == | 11
|
A sperm granuloma is a lump of leaked sperm that appears along the vasa deferentia or epididymides in vasectomized individuals. While majority of sperm granulomas are present along the vas deferens, the rest of them form at the epididymis. Sperm granulomas range in size, from one millimeter to one centimeter. They consist of a central mass of degenerating sperm surrounded by tissue containing blood vessels and immune system cells. Sperm granulomas may also have a yellow, white, or cream colored center when cut open. While some sperm granulomas can be painful, most of them are painless and asymptomatic. Sperm granulomas can appear as a result of surgery (such as a vasectomy), trauma, or an infection (such as sexually transmitted diseases). They can appear as early as four days after surgery and fully formed ones can appear as late as 208 days later.Sperm granulomas are a common complication of different types of vasectomy. In vasectomies, the vas deferens are cut and the two ends are tied to prevent sperm from passing. Sperm granuloma may then form at the point where the vas deferens were cut, due to the possibility of sperm leaking out at this site. History of trauma or inflammation of the epididymis can also lead to a sperm granuloma. Sperm granulomas are seen as the bodys immune response to sperm being outside of their normal location, and are therefore seen as a protective mechanism. Sperm granulomas are quite common after surgery, occurring in up to 40% of patients. | On the contrary, sperm granulomas comprise only 2.5% of the general population. Amongst adolescents and pediatric patients, sperm granulomas are considered a rare phenomenon as this population does not undergo vasectomy often. The most common cause of sperm granuloma in pediatric and adolescent patients is often attributed to tumor obstruction, injury, or infection to the area.While sperm granuloma is considered a complication in most cases, it allows decompression of the vas deferens and epididymis at the vasectomy site. This allows for successful future reversal of vasectomy given the good quality sperm in the vas fluid. Any surgery in the genital area can lead to castration anxiety (fear of loss or damage to the genital organ.) Diagnosis
Sperm granulomas are diagnosed using a microscope to examine tissues (histology) taken from the area, typically done with fine needle aspiration and occur within a few weeks of a vasectomy. An example of a histology based diagnosis supporting sperm granuloma would be a sperm core surrounded by inflammatory cells, apoptotic cells, and fibrous tissue. Often, there will be empty tubes with cellular debris near the granuloma. Additionally, physicians might use high frequency ultrasounds to aid in properly diagnosing epididymal conditions such as sperm granulomas. Using these ultrasounds provide a better view of the anatomy of the epididymis, which could prevent misdiagnosis of conditions such as testicular tumors or supernumerary testis (the presence of more than two testes). Signs and symptoms
Sperm granulomas appear as hard and firm nodules that do not exceed 1 cm in size. | 11
|
Other spinal abnormalities associated with DSS include widened intervertebral disks, small, dense vertebral bodies, irregular vertebral endplates, hypoplastic vertebral bodies, and pronounced vertebral anterior notches.More than 80% of patients also reported abnormalities of the skull. Common symptoms include craniofacial hyperostosis, which is the excessive growth of bone in the skull and face. Skull base sclerosis, periorbital sclerosis, hypoplastic mandibular condyle, and absent paranasal or frontal sinuses are present in rare cases.It is also reported that individuals may also have pelvic abnormalities. This includes the development of narrow iliac wings, as well as widened femoral necks. However, incidence of both symptoms are rare in patients with DSS, occurring in less than 30% of cases.The occurrence of DSS also leads to deformities of the limbs. 80% of patients reported with abnormalities of the metaphysis such as metaphyseal flaring, radiolucent metaphyses, abnormal metaphyseal trabeculation, which is abnormal trabecula patterns in the metaphyseal region, and epimetaphyseal sclerosis. Other limbic abnormalities include progressive bowing of long bones, which is present in rare cases. Physical abnormalities
In general, patients appear to be short statured. In addition, as a result of sclerosis of the frontal and parietal region of the calvarium, macrocephaly and square shaped heads are reported in more than 80% of patients.Abnormal skin conditions of red-violet macular mottled skins over the entire body are occasionally observed in patients. However it is unclear whether this clinical feature is relevant to diagnosis of DSS. Neurological abnormalities
Visual problems are often found in people with DSS. | Mutation of TCIRG1 gene may arise from deletion or gene splicing defects, leading to frame-shifts of the nucleotides of the gene.TCIRG1 mutations illustrate the heterogeneity of DSS through a case study where DSS occurred due to a frameshift mutation, in conjunction with a mutation at an intron located in the gene in one of the alleles of chromosome 11 resulting in a splice site mutation. Despite a frameshift mutation altering the C-terminal of the proton pump, due to increased remnant expression of the wild type transcript, it only resulted in intermediate autosomal recessive DSS due to the partial retainment of vacuolar proton pump function. TNFRSF11A mutation
The TNFRSF11A gene is present in chromosome locus 18q21.33, which encodes for the receptor activator of NF-κB (RANK). RANK is expressed in immature osteoclasts, which facilitates osteoclasts maturation upon binding of RANK ligand (RANKL). Binding of RANK ligand mediates the RANK/RANKL/OPG signalling pathway. The pathway mediates osteoclast differentiation and activation by promoting differentiation of precursors into multinucleated osteoclasts, and activating osteoclasts, thereby contributing to bone resorption and remodelling. Health conditions related to genetic changes in TNFRSF11A includes osteopetrosis, osteolysis, and Pagets disease of bone.Multiple reports of gene mutations exists underlining the mutation of the exons and introns leading to aberrant splicing. There are five variants to the TNFRSF11A gene which produces five unique protein iso-forms. The effects of alternative splicing on each variants are unclear. However, it is suggested that such changes lead to different expression patterns of the gene in both space and time. | 11
|
Apri (āprī) in Sanskrit means "conciliation, propitiation" and refers to special invocations spoken previous to the offering of oblations in an animal sacrifice. Some scholars have proposed however, that these hymns were originally meant for a family ritual centered around Agni, which was then later connected to the animal sacrifice. Aprisuktas
Of the ten Aprisuktas mentioned in Gargya Narayanas commentary, I.13 and I.142 both invoke the Narāśaṁsa and Tanūnapāt manifestations of Agni, I.188, III.4, IX.5 and X.110 invoke only the Tanūnapāt manifestation and II.3, V.5, VII.2 and X.70 invoke only the Narāśaṁsa manifestation. References
āprī in: Monier-Williams A Sanskrit Dictionary, 1899. R. Fick, "Gotra" in: ed. Hastings, Encyclopaedia of Religion and Ethics vol. 6, 1999, p. 355
Samir Nath, "Gotra-system" in: Dictionary Of Vedanta, 2002, p. 153. | This depends on the amount of water damage and mold that grows after an incident. Research suggests that there will be an increase of 30-50% in adverse respiratory health outcomes caused by dampness and mold exposure for those living in coastal and wetland areas. Fungal contamination in homes is associated with increased allergic rhinitis and asthma. Vector borne diseases increase as well due to the increase in still water after the floods have settled. The diseases that are vector borne are malaria, dengue, West Nile, and yellow fever. Floods have a huge impact on victims psychosocial integrity. People suffer from a wide variety of losses and stress. One of the most treated illness in long-term health problems are depression caused by the flood and all the tragedy that flows with one. Loss of life
Below is a list of the deadliest floods worldwide, showing events with death tolls at or above 100,000 individuals. Secondary and long-term effects
Economic hardship due to a temporary decline in tourism, rebuilding costs, or food shortages leading to price increases is a common after-effect of severe flooding. The impact on those affected may cause psychological damage to those affected, in particular where deaths, serious injuries and loss of property occur. Urban flooding also has significant economic implications for affected neighborhoods. In the United States, industry experts estimate that wet basements can lower property values by 10–25 percent and are cited among the top reasons for not purchasing a home. | 0-1
|
Penetrating trauma is an open wound injury that occurs when an object pierces the skin and enters a tissue of the body, creating a deep but relatively narrow entry wound. In contrast, a blunt or non-penetrating trauma may have some deep damage, but the overlying skin is not necessarily broken and the wound is still closed to the outside environment. The penetrating object may remain in the tissues, come back out the path it entered, or pass through the full thickness of the tissues and exit from another area.A penetrating injury in which an object enters the body or a structure and passes all the way through an exit wound is called a perforating trauma, while the term penetrating trauma implies that the object does not perforate wholly through. In gunshot wounds, perforating trauma is associated with an entrance wound and an often larger exit wound. Penetrating trauma can be caused by a foreign object or by fragments of a broken bone. Usually occurring in violent crime or armed combat, penetrating injuries are commonly caused by gunshots and stabbings.Penetrating trauma can be serious because it can damage internal organs and presents a risk of shock and infection. The severity of the injury varies widely depending on the body parts involved, the characteristics of the penetrating object, and the amount of energy transmitted to the tissues. Assessment may involve X-rays or CT scans, and treatment may involve surgery, for example to repair damaged structures or to remove foreign objects. | Bacillary peliosis is a form of peliosis hepatis that has been associated with bacteria in the genus Bartonella. == References == | 0-1
|
Surgical
Surgical methods range from the complete removal of the foreskin to more minor operations to relieve foreskin tightness:
Dorsal slit (superincision) is a single incision along the upper length of the foreskin from the tip to the corona, exposing the glans without removing any tissue. Ventral slit (subincision) is an incision along the lower length of the foreskin from the tip of the frenulum to the base of the glans, removing the frenulum in the process. Often used when frenulum breve occurs alongside the phimosis. Preputioplasty, in which a limited dorsal slit with transverse closure is made along the constricting band of skin, can be an effective alternative to circumcision. It has the advantage of only limited pain and a short healing duration relative to circumcision, while also avoiding cosmetic effects. Circumcision is sometimes performed for phimosis, and is an effective treatment; however, this method has become less common as of 2012.While circumcision prevents phimosis, studies of the incidence of healthy infants circumcised for each prevented case of phimosis are inconsistent. Prognosis
The most acute complication is paraphimosis. In this condition, the glans is swollen and painful, and the foreskin is immobilized by the swelling in a partially retracted position. The proximal penis is flaccid. Some studies found phimosis to be a risk factor for urinary retention and carcinoma of the penis. Epidemiology
A number of medical reports of phimosis incidence have been published over the years. | A potential complication of phimosis is paraphimosis, where the tight foreskin becomes trapped behind the glans. Signs and symptoms
At birth, the inner layer of the foreskin is sealed to the glans penis. The foreskin is usually non-retractable in early childhood, and some males may reach the age of 18 before their foreskin can be fully retracted.Medical associations advise not to retract the foreskin of an infant, in order to prevent scarring. Some argue that non-retractability may "be considered normal for males up to and including adolescence." Hill states that full retractability of the foreskin may not be achieved until late childhood or early adulthood. A Danish survey found that the mean age of first foreskin retraction is 10.4 years.Rickwood, as well as other authors, has suggested that true phimosis is over-diagnosed due to failure to distinguish between normal developmental non-retractability and a pathological condition. Some authors use the terms "physiologic" and "pathologic" to distinguish between these types of phimosis; others use the term "non-retractile foreskin" to distinguish this developmental condition from pathologic phimosis.In some cases a cause may not be clear, or it may be difficult to distinguish physiological phimosis from pathological phimosis if an infant appears to have discomfort while urinating or demonstrates obvious ballooning of the foreskin. However, ballooning does not indicate urinary obstruction.In women, a comparable condition is known as "clitoral phimosis", whereby the clitoral hood cannot be retracted, limiting exposure of the glans clitoridis. Severity
Score 1: full retraction of foreskin, tight behind the glans. | 11
|
MGUS is categorized into the following sub-types based upon the identity and levels of the myeloma proteins detected as well as the prognoses for progressive disease indicated by these myeloma protein findings. Non-IgM MGUS
Non-IgM MGUS, commonly termed MGUS, is diagnosed in individuals who exhibit a serum IgG, IgD, IgA, or IgE monoclonal protein with or without increased levels of blood and/or urine free κ or λ light chains. These patients typically also show small increases in bone marrow plasma cells. Further requirements for the diagnosis of non-IgM MGUS are: a) bone marrow clonal plasma cells <10% of total nucleated cells; b) absence of any of the four CRAB criteria (CRAB criteria are C = Calcium serum levels >1 milligram/deciliter above normal values and/or a serum level >11 milligram/deciliter; R = Renal insufficiency as defined by a glomerular filtration rate <40 milliliter/minute and/or a serum creatinine >2 gram/deciliter due to myeloma protein-induced kidney damaged; A = Anemia, as defined by a blood hemoglobin level >2 gram/deciliter below normal and/or <10 gram/deciliter due to the plasma cell dyscrasia rather than e.g. iron deficiency or blood loss; B = Bone lesions, i.e. ≥1 lytic (i.e. bone re-adsorbing) bone lesion due to a plasmacytoma as detected by skeletal radiography, computed tomography, or positron emission tomography-computed tomography); c) no evidence of a plasmacytoma in bone or soft tissues, of amyloidosis, or of another plasma cell disorder; d) a ratio of free serum light chains (i.e. | Human serum albumin is the serum albumin found in human blood. It is the most abundant protein in human blood plasma; it constitutes about half of serum protein. It is produced in the liver. It is soluble in water, and it is monomeric.Albumin transports hormones, fatty acids, and other compounds, buffers pH, and maintains oncotic pressure, among other functions. Albumin is synthesized in the liver as preproalbumin, which has an N-terminal peptide that is removed before the nascent protein is released from the rough endoplasmic reticulum. The product, proalbumin, is in turn cleaved in the Golgi apparatus to produce the secreted albumin. The reference range for albumin concentrations in serum is approximately 35–50 g/L (3.5–5.0 g/dL). It has a serum half-life of approximately 21 days. It has a molecular mass of 66.5 kDa. The gene for albumin is located on chromosome 4 in locus 4q13.3 and mutations in this gene can result in anomalous proteins. The human albumin gene is 16,961 nucleotides long from the putative cap site to the first poly(A) addition site. It is split into 15 exons that are symmetrically placed within the 3 domains thought to have arisen by triplication of a single primordial domain. Human serum albumin (HSA) is a highly water-soluble globular monomeric plasma protein with a relative molecular weight of 67 KDa, consisting of 585 amino acid residues, one sulfhydryl group and 17 disulfide bridges. | 0-1
|
Paralytic shellfish poisoning (PSP) is one of the four recognized syndromes of shellfish poisoning, which share some common features and are primarily associated with bivalve mollusks (such as mussels, clams, oysters and scallops). These shellfish are filter feeders and accumulate neurotoxins, chiefly saxitoxin, produced by microscopic algae, such as dinoflagellates, diatoms, and cyanobacteria. Dinoflagellates of the genus Alexandrium are the most numerous and widespread saxitoxin producers and are responsible for PSP blooms in subarctic, temperate, and tropical locations. The majority of toxic blooms have been caused by the morphospecies Alexandrium catenella, Alexandrium tamarense, Gonyaulax catenella and Alexandrium fundyense, which together comprise the A. tamarense species complex. In Asia, PSP is mostly associated with the occurrence of the species Pyrodinium bahamense.Some pufferfish, including the chamaeleon puffer, also contain saxitoxin, making their consumption hazardous. PSP and cyanobacteria
Saxitoxin can be produced in both eukaryotic dinoflagellates as well as prokaryotic cyanobacteria (usually referred to as blue-green algae). The biosynthesis pathway of this toxin within cyanobacteria is well defined, while the pathway within dinoflagellates is mostly unknown. Within cyanobacteria the saxitoxin pathway is complex with many steps, enzymes and chemical reactions. Using radioisotope tracing experiments scientists have determined how the initial reagent of the pathway, L-arginine (via acetyl-CoA), turns into this toxin. L-arginine goes through a rare reaction known as Claisen condensation forming four intermediates before turning into the final product of saxitoxin.Cyanobacteria is general responsible for the accumulation of PSP toxins, mainly being saxitoxin, within freshwater marine life. | In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes. Services should be carried out by behavior analysts, special education teachers, speech pathologists, and licensed psychologists. Intensive, sustained special education programs and behavior therapy early in life often improves functioning and decreases symptom severity and maladaptive behaviors; claims that intervention by around age three years is crucial are not substantiated.No known medication relieves autisms core symptoms of social and communication impairments. Education
Early, intensive ABA therapy has demonstrated effectiveness in enhancing communication and adaptive functioning in preschool children; it is also well-established for improving the intellectual performance of that age group. It is not known whether treatment programs for children lead to significant improvements after the children grow up, and the limited research on the effectiveness of adult residential programs shows mixed results. Alternative medicine
Although many alternative therapies and interventions were used, few are supported by scientific studies. Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance. Some alternative treatments placed autistic individuals at risk. For example, in 2005, a five-year-old child with autism was killed by botched chelation therapy (which is not recommended for autism as risks outweigh any potential benefits). Epidemiology
Globally, classic autism was understood to affect an estimated 24.8 million people as of 2015. | 0-1
|
An 8-ft-high fence may be added to keep deer away from the tick-safe zone. Occupational exposure
Outdoor workers are at risk of Lyme disease if they work at sites with infected ticks. This includes construction, landscaping, forestry, brush clearing, land surveying, farming, railroad work, oil field work, utility line work, park or wildlife management. U.S. workers in the northeastern and north-central states are at highest risk of exposure to infected ticks. Ticks may also transmit other tick-borne diseases to workers in these and other regions of the country. Worksites with woods, bushes, high grass or leaf litter are likely to have more ticks. Outdoor workers should be most careful to protect themselves in the late spring and summer when young ticks are most active. Host animals
Ticks can feed upon the blood of a wide array of possible host species, including lizards, birds, mice, cats, dogs, deer, cattle and humans. The extent to which a tick can feed, reproduce, and spread will depend on the type and availability of its hosts. Whether it will spread disease is also affected by its available hosts. Some species, such as lizards, are referred to as "dilution hosts" because they dont tend to support Lyme disease pathogens and so decrease the likelihood that the disease will be passed on by ticks feeding on them. White-tailed deer are both a food source and a "reproductive host", where ticks tend to mate. The white-footed mouse is a reservoir host in which the pathogen for Lyme disease can survive. | Injury of axillary nerve (axillary neuropathy) is a condition that can be associated with a surgical neck of the humerus fracture. It can also be associated with a dislocated shoulder or with traction injury to the nerve, which may be caused by over-aggressive stretching or blunt trauma that does not result in fracture or dislocation. One form of this injury is referred to as axillary nerve palsy. Injury most commonly occurs proximal to the quadrangular space.Injury in this nerve causes paralysis (as always) to the muscles innervated by it, most importantly deltoid muscle. This muscle is the main abductor of the shoulder joint from 18 to 90 degrees (from 0 to 18 by supraspinatus). Injury can result in a reduction in shoulder abduction. So a test can be applied to a patient with injury of axillary nerve by trying to abduct the injured shoulder against resistance.The pain from axillary neuropathy is usually dull and aching rather than sharp, and increases with increasing range of motion. Many people notice only mild pain but considerable weakness when they try to use the affected shoulder. References
== External links == | 0-1
|
Red blood cells may decrease the outflow of aqueous humor, therefore the eye pressure should be kept low by giving oral acetazolamide (a diuretic given to reduce intraoccular pressure). Accidental trauma during sleep should be prevented by patching with an eye shield during night time. Avoid giving aspirin, heparin/warfarin and observe daily for resolution or progression. A large hyphema may require careful anterior chamber washout. Rebleeds may require additional intervention and therapy. Later, surgical repair may be considered for larger avulsions causing significant double vision, cosmesis or glare symptoms. Surgical repair is usually done by 10-0 prolene suture taking the base of iris avulsion and suturing it to the scleral spur and ciliary body junction. See also
Eye injury
References
== External links == | Volkmanns contracture is a permanent flexion contracture of the hand at the wrist, resulting in a claw-like deformity of the hand and fingers. Passive extension of fingers is restricted and painful. Causes
Any fracture in the elbow region or upper arm may lead to Volkmanns ischemic contracture, but it is especially associated with supracondylar fracture of the humerus. It is also caused by fractures of the forearm bones if they cause bleeding from the major blood vessels of the forearm.The condition may be caused by obstruction on the brachial artery near the elbow, possibly from improper use of a tourniquet, improper use of a plaster cast, or compartment syndrome. Pathophysiology
Volkmanns contracture results from acute ischaemia and necrosis of the muscle fibres of the flexor group of muscles of the forearm, especially the flexor digitorum profundus and flexor pollicis longus. The muscles become fibrotic and shortened. Prevention
Prevention of the condition requires restoration of blood flow after injury and reduction of compartmental pressure on the muscles. Any splints, bandages, or other devices that might be obstructing circulation must be removed.A fasciotomy may be required to reduce pressure in the muscle compartment. Treatment
If contracture occurs, surgery to release the fixed tissues may help with the deformity and function of the hand. History
It is named after Richard von Volkmann (1830–1889), the 19th century German doctor who first described it, in a paper on "non-Infective Ischemic conditions of various fascial compartments in the extremities". | 0-1
|
Chronic pulmonary aspergillosis is a long-term fungal infection caused by members of the genus Aspergillus—most commonly Aspergillus fumigatus. The term describes several disease presentations with considerable overlap, ranging from an aspergilloma—a clump of Aspergillus mold in the lungs—through to a subacute, invasive form known as chronic necrotizing pulmonary aspergillosis which affects people whose immune system is weakened. Many people affected by chronic pulmonary aspergillosis have an underlying lung disease, most commonly tuberculosis, allergic bronchopulmonary aspergillosis, asthma, or lung cancer. Classification
Chronic pulmonary aspergillosis as a term encompasses a number of different presentations of varying severity. There is considerable overlap between disease forms which adds to confusion during diagnosis. The primary differentiation comes from radiological findings and serology. Aspergilloma
An aspergilloma is a fungus ball composed of Aspergillus hypha - the long filamentous strands which extend from the fungus to enable growth and reproduction. They can arise within any bodily cavity, though in chronic pulmonary aspergillosis they form within pulmonary cavities that have been colonized by Aspergillus spp. If there is a single, stable cavity that provides minimal symptoms, the term simple aspergilloma is commonly used to distinguish it from more severe forms of chronic pulmonary aspergillosis. Aspergillus nodule
Aspergillus can form single or multiple nodules which may or may not form a cavity. Whilst usually benign in nature, they can sometimes cause symptoms such as cough or an exacerbation of existing disease such as asthma. Histologically, there is necrosis surrounded by granulomatous inflammation with some multinucleated giant cells present. | Posaconazole or isavuconazole can be used as third-line agent for people with chronic pulmonary aspergillosis who are intolerant of or developed resistance to the first- and second-line agents. Regular chest X-rays, serological and mycological parameters, and quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these medications. Prognosis
References
== External links == | 11
|
People require double antiplatelet therapy for a period of up to 3 months after the procedure and aspirin therapy for up to 1 year. In a systematic analysis of 19 studies with 207 cases, there was an 87% improvement in overall symptom rate and 90% cure rate for treatment of papilledema. Major complications only occurred in 3/207 people (1.4%). In the largest single series of transverse sinus stenting there was an 11% rate of recurrence after one stent, requiring further stenting.Due to the permanence of the stent and small but definite risk of complications, most experts will recommend that person with IIH must have papilledema and have failed medical therapy or are intolerant to medication before stenting is undertaken. Surgery
Two main surgical procedures exist in the treatment of IIH: optic nerve sheath decompression and fenestration and shunting. Surgery would normally only be offered if medical therapy is either unsuccessful or not tolerated. The choice between these two procedures depends on the predominant problem in IIH. Neither procedure is perfect: both may cause significant complications, and both may eventually fail in controlling the symptoms. There are no randomized controlled trials to guide the decision as to which procedure is best.Optic nerve sheath fenestration is an operation that involves the making of an incision in the connective tissue lining of the optic nerve in its portion behind the eye. | Borderline lepromatous leprosy is a skin condition with numerous, symmetrical skin lesions. : 346
See also
Leprosy
Cutaneous conditions
References
== External links == | 0-1
|
Fostamatinib, sold under the brand names Tavalisse and Tavlesse, is a tyrosine kinase inhibitor medication for the treatment of chronic immune thrombocytopenia (ITP). The drug is administered by mouth.Fostamatinib blocks the activity of the enzyme spleen tyrosine kinase (SYK). This enzyme is involved in stimulating parts of the immune system. By blocking SYKs activity, fostamatinib reduces the immune systems destruction of platelets, so allowing the platelet count to rise, which reduces the likelihood of excessive bleeding.The most commonly reported side effects are diarrhea, high blood pressure, nausea, respiratory infection, dizziness, increased liver enzymes, rash, abdominal pain, fatigue, chest pain and decreased white blood cell count.The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication. Medical uses
Fostamatinib is a drug used to treat adults with low platelet count due to chronic immune thrombocytopenia (ITP) when a prior treatment for ITP has not worked well enough. Chronic immune thrombocytopenia is an autoimmune bleeding disorder where the blood doesnt clot as it should because of a low platelet count. Pharmacology
Mechanism of action
The tablets are formulated as fostamatinib disodium hexahydrate, a disodium hexahydrate salt, and is a prodrug of the active compound tamatinib (R-406), which is an inhibitor of the enzyme spleen tyrosine kinase (Syk), hence it is an syk inhibitor. Syk is a protein tyrosine kinase associated with various inflammatory cells, including macrophages, which are presumed to be the cells responsible for ITP platelet clearance. | Incidence
Seabathers eruption is common throughout the range of Linuche unguiculata in the Caribbean, Florida, Mexico, and Gulf States. Cases were first identified in Brazil in 2001. The closely related Linuche aquila, found anywhere between Malaysia, the Philippines and the east coast of Africa, is also known to cause the condition.Swimmers in Queensland, Australia, have reported seabathers eruption during the summer months of the year. Swimmers at the east-coast beaches of Auckland and the rest of the Hauraki Gulf in New Zealand can develop seabathers eruption, typically during summer. References
== External links == | 0-1
|
Epidemiology
Rotator cuff tears are among the most common conditions affecting the shoulder.A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear, with the overall frequency of tears increasing with age. By the age of 50 10% of people with normal shoulders have a rotator cuff tear.In an autopsy study of rotator cuff tears, the incidence of partial tears was 28%, and of complete rupture 30%. Frequently, tears occurred on both sides and occurred more often with females and with increasing age. Other cadaver studies have noted intratendinous tears to be more frequent (7.2%) than bursal-sided (2.4%) or articular-sided tears (3.6%). However, clinically, articular-sided tears are found to be 2 to 3 times more common than bursal-sided tears and among a population of young athletes, articular-sided tears constituted 91% of all partial-thickness tears. Rotator cuff tears may be more common in men between the ages of 50–60, though between 70 and 80 there is minimal difference across genders.In terms of the size of tears, a study compared the ages of patient to the size of tears. It was emphasized the older you are, the more massive of a tear you will have. It was found that mean age increased with larger tear sizes (small tears 59 years, medium tears 62 years, large tears 64 years, and massive tears 66 years). | In-office testing
As part of clinical decision-making, a simple, minimally invasive, in-office procedure may be performed, the rotator cuff impingement test. A small amount of a local anesthetic and an injectable corticosteroid are injected into the subacromial space to block pain and to provide anti-inflammatory relief. If pain disappears and shoulder function remains good, no further testing is pursued. The test helps to confirm that the pain arises from the shoulder primarily rather than referred from the neck, heart, or gut. If pain is relieved, the test is considered positive for rotator-cuff impingement, of which tendinitis and bursitis are major causes. However, partial rotator-cuff tears may also demonstrate good pain relief, so a positive response cannot rule out a partial rotator-cuff tear. However, with demonstration of good, pain-free function, treatment will not change, so the test is useful in helping to avoid overtesting or unnecessary surgery. Classification
Tears of the rotator cuff tendon are described as partial or full thickness, and full thickness with complete detachment of the tendons from bone. Partial-thickness tears often appear as fraying of an intact tendon. Full-thickness tears are "through-and-through". These tears can be small pinpoint, larger buttonhole, or involve the majority of the tendon where it still remains substantially attached to the humeral head and thus maintains function. Full-thickness tears may also involve complete detachment of the tendon(s) from the humeral head and may result in significantly impaired shoulder motion and function.Shoulder pain is variable and may not be proportional to the size of the tear. | 11
|
Several agents are used to temporarily lower K+ levels. The choice depends on the degree and cause of the hyperkalemia, and other aspects of the persons condition. Myocardial excitability
Calcium (calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. A standard ampule of 10% calcium chloride is 10 mL and contains 6.8 mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26 mmol of calcium. Clinical practice guidelines recommend giving 6.8 mmol for typical EKG findings of hyperkalemia. This is 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate. Though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line. Onset of action is less than one to three minutes and lasts about 30–60 minutes. The goal of treatment is to normalise the EKG and doses can be repeated if the EKG does not improve within a few minutes.Some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. Recent literature questions the validity of this concern. Temporary measures
Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. | Hyperglycemia can also contribute to hyperkalemia by causing hyperosmolality in extracellular fluid, increasing water diffusion out of the cells and causes potassium to move alongside water out of the cells also. The co-existence of insulin deficiency, hyperglycemia, and hyperosmolality is often seen in those affected by diabetic ketoacidosis. Apart from diabetic ketoacidosis, there are other causes that reduce insulin levels such as the use of the medication octreotide, and fasting which can also cause hyperkalemia. Increased tissue breakdown such as rhabdomyolysis, burns, or any cause of rapid tissue necrosis, including tumor lysis syndrome can cause the release of intracellular potassium into blood, causing hyperkalemia.Beta2-adrenergic agonists act on beta-2 receptors to drive potassium into the cells. Therefore, beta blockers can raise potassium levels by blocking beta-2 receptors. However, the rise in potassium levels is not marked unless there are other co-morbidities present. Examples of drugs that can raise the serum potassium are non-selective beta-blockers such as propranolol and labetalol. Beta-1 selective blockers such as metoprolol do not increase serum potassium levels.Exercise can cause a release of potassium into bloodstream by increasing the number of potassium channels in the cell membrane. The degree of potassium elevation varies with the degree of exercise, which range from 0.3 meq/L in light exercise to 2 meq/L in heavy exercise, with or without accompanying ECG changes or lactic acidosis. However, peak potassium levels can be reduced by prior physical conditioning and potassium levels are usually reversed several minutes after exercise. | 11
|
Though it was first described in 1575, there is evidence that the condition occurred in people more than 5,000 years ago. Signs and symptoms
Atherosclerosis is asymptomatic for decades because the arteries enlarge at all plaque locations, thus there is no effect on blood flow. Even most plaque ruptures do not produce symptoms until enough narrowing or closure of an artery, due to clots, occurs. Signs and symptoms only occur after severe narrowing or closure impedes blood flow to different organs enough to induce symptoms. Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack. These symptoms, however, still vary depending on which artery or organ is affected.Abnormalities associated with atherosclerosis begin in childhood. Fibrous and gelatinous lesions have been observed in the coronary arteries of children aged 6–10. Fatty streaks have been observed in the coronary arteries of juveniles aged 11–15, though they appear at a much younger age within the aorta.Clinically, given enlargement of the arteries for decades, symptomatic atherosclerosis is typically associated with men in their 40s and women in their 50s to 60s. Sub-clinically, the disease begins to appear in childhood and rarely is already present at birth. Noticeable signs can begin developing at puberty. Though symptoms are rarely exhibited in children, early screening of children for cardiovascular diseases could be beneficial to both the child and his/her relatives. | Both anatomic and physiologic methods allow early detection before symptoms show up, disease staging, and tracking of disease progression. Anatomic methods are more expensive and some of them are invasive in nature, such as IVUS. On the other hand, physiologic methods are often less expensive and safer. But they do not quantify the current state of the disease or directly track progression. In recent years, developments in nuclear imaging techniques such as PET and SPECT have provided ways of estimating the severity of atherosclerotic plaques. Prevention
Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Medical management of atherosclerosis first involves modification to risk factors–for example, via smoking cessation and diet restrictions. Prevention then is generally by eating a healthy diet, exercising, not smoking, and maintaining a normal weight. Diet
Changes in diet may help prevent the development of atherosclerosis. Tentative evidence suggests that a diet containing dairy products has no effect on or decreases the risk of cardiovascular disease.A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Evidence suggests that the Mediterranean diet may improve cardiovascular results. There is also evidence that a Mediterranean diet may be better than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure). Exercise
A controlled exercise program combats atherosclerosis by improving circulation and functionality of the vessels. Exercise is also used to manage weight in patients who are obese, lower blood pressure, and decrease cholesterol. | 11
|
Nonetheless, they are useful when used in adjunct with other voice assessment measures, or as a tool for monitoring therapeutic effects over time. Prevention
Given that certain occupations are more at risk for developing dysphonia (e.g. teachers) research into prevention studies have been conducted. Research into the effectiveness of prevention strategies for dysphonia have yet to produce definitive results, however, research is still ongoing. Primarily, there are two types of vocal training recognized by professionals to help with prevention: direct and indirect. Direct prevention describes efforts to reduce conditions that may serve to increase vocal strain (such as patient education, relaxation strategies, etc. ), while indirect prevention strategies refer to changes in the underlying physiological mechanism for voice production (e.g., adjustments to the manner in which vocal fold adduction occurs, respiratory training, shifting postural habits, etc.). Treatment
Although there is no universal classification of voice problems, voice disorders can be separated into certain categories: organic (structural or neurogenic), functional, neurological (psychogenic) or iatrogenic, for example. Depending on the diagnosis and severity of the voice problem, and depending on the category that the voice disorder falls into, there are various treatment methods that can be suggested to the patient. The professional has to keep in mind there is not one universal treatment, but rather the clinical approach must find what the optimal effective course of action for that particular patient is.There are three main type of treatments: medical treatments, voice therapy and surgical treatments. When necessary, certain voice disorders use a combination of treatment approaches. | In the brain, the dorsal striatum may be associated with physical (motor) but not affective withdrawal sign. Treatment
Gradually reducing nicotine intake causes less withdrawal than abruptly stopping. Another way to reduce nicotine withdrawal symptoms is to provide the body with an alternative source of nicotine (nicotine replacement therapy) for a temporary period and then taper this new nicotine intake. Other medication used for quitting smoking include bupropion, varenicline, cytisine, nortriptyline, and clonidine. Treatments other than medication, such as increased exercise, can also reduce nicotine withdrawal. Many behavior changes such as avoiding situations where one usually smoked, planning ahead to deal with temptations, and seeking the support of friends and family are effective in helping people quit smoking, but whether this is due to reduced withdrawal is unclear. Epidemiology
Most nicotine users have at least one of the above withdrawal symptoms when they try to stop. These effects are much milder to those who use isolated nicotine over tobacco. Withdrawal can occur in less frequent users, but heavier users and those with a past or current psychiatric disorder tend to have more severe withdrawal. Genetics also influence the severity of withdrawal. See also
Withdrawal
Smoking cessation
Nicotine dependence
References
== External links == | 0-1
|
A version of cosyntropin in solution (as opposed to powder) was developed by Sandoz/Novartis and was approved under the 505b(2) pathway in 2008; as of January 2017 it had been discontinued.In the UK, available forms of tetracosactide/cosyntropin, the synthetic form of corticotrophin, have been approved for both therapeutic and diagnostic uses, and have included:
A version branded Synacthen and provided in solution 250 mcg ampoules, for diagnostic uses, approved in 2008 and as of January 2017 controlled by Mallinckrodt. A version branded Synacthen, absorbed on to zinc phosphate, provided in milky white suspension, approved in 2008 and as of January 2017 controlled by Mallinckrodt. Doping
As of 2007, it was widely reported that tetracosactide had been used as an illegal performance-enhancing drug by professional cyclists. It is known to be used as a doping agent to increase the secretion of glucocorticoids by adrenal glands. Pricing
Mallinckrodt acquired the US rights to the animal-derived form via its acquisition of Questcor Pharmaceuticals in 2014. When Questcor acquired the drug in 2001 it sold for $40 a vial; within a year of the acquisition Questcor raised the price of the drug to $1,500 per vial and to $28,000 by 2013. In 2013, Questcor acquired the US rights to a competing product, Synacthen Depot, from Novartis. In 2014 Mallinckrodt raised the price of Acthar further to $34,000. | However, since anxiety and depression are also very common in persons with confirmed medical illnesses, it remains unproven whether such symptoms are a consequence of the physical impairment or a cause. Somatic symptom disorders are not the result of conscious malingering (fabricating or exaggerating symptoms for secondary motives) or factitious disorders (deliberately producing, feigning, or exaggerating symptoms). Somatic symptom disorder is difficult to diagnose and treat. Some advocates of the diagnosis believe this is because proper diagnosis and treatment requires psychiatrists to work with neurologists on patients with this disorder. History
Somitisation disorder was first described by Paul Briquet in 1859 and was subsequently known as Briquets syndrome. He described patients who had been sickly most of their lives and complained of multiple symptoms from different organ systems. Symptoms persist despite multiple consultations, hospitalisations and investigations. Definition
Somatic symptom disorders are a group of disorders, all of which fit the definition of physical symptoms similar to those observed in physical disease or injury for which there is no identifiable physical cause. As such, they are a diagnosis of exclusion. Somatic symptoms may be generalized in four major medical categories: neurological, cardiac, pain, and gastrointestinal somatic symptoms. Diagnostic and Statistical Manual of Mental Disorders
Somatic symptom disorders used to be recognized as Somatoform disorders in the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association. | 0-1
|
Cutaneous T-cell lymphoma (CTCL) is a class of non-Hodgkin lymphoma, which is a type of cancer of the immune system. Unlike most non-Hodgkin lymphomas (which are generally B-cell-related), CTCL is caused by a mutation of T cells. The cancerous T cells in the body initially migrate to the skin, causing various lesions to appear. These lesions change shape as the disease progresses, typically beginning as what appears to be a rash which can be very itchy and eventually forming plaques and tumors before spreading to other parts of the body. Signs and symptoms
The presentation depends if it is mycosis fungoides or Sézary syndrome, the most common, though not the only types. Among the symptoms for the aforementioned types are: enlarged lymph nodes, an enlarged liver and spleen, and non-specific dermatitis. Cause
The cause of CTCL is unknown. Diagnosis
A point-based algorithm for the diagnosis for early forms of cutaneous T-cell lymphoma was proposed by the International Society for Cutaneous Lymphomas in 2005. Classification
Cutaneous T-cell lymphoma may be divided into the several subtypes. : 727–740 Mycosis fungoides is the most common form of CTCL and is responsible for half of all cases. A WHO-EORTC classification has been developed. Treatment
There is no cure for CTCL, but there are a variety of treatment options available and some CTCL patients are able to live normal lives with this cancer, although symptoms can be debilitating and painful, even in earlier stages. | FDA approved treatments include the following:
(1999) Denileukin diftitox (Ontak)
(2000) Bexarotene (Targretin) a retinoid
(2006) Vorinostat (Zolinza) a hydroxymate histone deacetylase (HDAC) inhibitor
(2009) Romidepsin (Istodax) a cyclic peptide histone deacetylase (HDAC) inhibitor
(2018) Poteligeo (mogamulizumab-kpkc)Histone deacetylase (HDAC) inhibitors are shown to have antiproliferative and cytotoxic properties against CTCL.Other (off label) treatments include:
In 2010, the U.S. Food and Drug Administration granted orphan drug designation for naloxone lotion as a treatment for pruritus in cutaneous T-cell lymphoma to a pharmaceutical company called Elorac. Epidemiology
Of all cancers involving lymphocytes, 2% of cases are cutaneous T cell lymphomas. CTCL is more common in men and in African-American people. The incidence of CTCL in men is 1.6 times higher than in women.There is some evidence of a relationship with human T-lymphotropic virus (HTLV) with the adult T-cell leukemia/lymphoma subtype. No definitive link between any viral infection or environmental factor has been definitely shown with other CTCL subtypes. See also
Cutaneous B-cell lymphoma
List of cutaneous conditions
References
External links
DermNet dermal-infiltrative/cutaneous-t-cell-lymphoma | 11
|
A cholangiocarcinoma occurring at the junction where the left and right hepatic ducts meet to form the common hepatic duct may be referred to eponymously as a Klatskin tumor.Although cholangiocarcinoma is known to have the histological and molecular features of an adenocarcinoma of epithelial cells lining the biliary tract, the actual cell of origin is unknown. Recent evidence has suggested that the initial transformed cell that generates the primary tumor may arise from a pluripotent hepatic stem cell. Cholangiocarcinoma is thought to develop through a series of stages – from early hyperplasia and metaplasia, through dysplasia, to the development of frank carcinoma – in a process similar to that seen in the development of colon cancer. Chronic inflammation and obstruction of the bile ducts, and the resulting impaired bile flow, are thought to play a role in this progression.Histologically, cholangiocarcinomas may vary from undifferentiated to well-differentiated. They are often surrounded by a brisk fibrotic or desmoplastic tissue response; in the presence of extensive fibrosis, it can be difficult to distinguish well-differentiated cholangiocarcinoma from normal reactive epithelium. There is no entirely specific immunohistochemical stain that can distinguish malignant from benign biliary ductal tissue, although staining for cytokeratins, carcinoembryonic antigen, and mucins may aid in diagnosis. Most tumors (>90%) are adenocarcinomas. Diagnosis
Blood tests
There are no specific blood tests that can diagnose cholangiocarcinoma by themselves. Serum levels of carcinoembryonic antigen (CEA) and CA19-9 are often elevated, but are not sensitive or specific enough to be used as a general screening tool. | The prevalence of cholangiocarcinoma in people with primary sclerosing cholangitis may be as high as 30%, based on autopsy studies.Multiple studies have documented a steady increase in the incidence of intrahepatic cholangiocarcinoma; increases have been seen in North America, Europe, Asia, and Australia. The reasons for the increasing occurrence of cholangiocarcinoma are unclear; improved diagnostic methods may be partially responsible, but the prevalence of potential risk factors for cholangiocarcinoma, such as HIV infection, has also been increasing during this time frame. References
External links
American Cancer Society Detailed Guide to Bile Duct Cancer. Patient information on extrahepatic bile duct tumors, from the National Cancer Institute. Cancer.Net: Bile Duct Cancer
Cholangiocarcinoma Foundation
World Cholangiocarcinoma Day | 11
|
A melanocytic nevus (also known as nevocytic nevus, nevus-cell nevus and commonly as a mole) is a type of melanocytic tumor that contains nevus cells. Some sources equate the term mole with "melanocytic nevus", but there are also sources that equate the term mole with any nevus form.The majority of moles appear during the first two decades of a persons life, with about one in every 100 babies being born with moles. Acquired moles are a form of benign neoplasm, while congenital moles, or congenital nevi, are considered a minor malformation or hamartoma and may be at a higher risk for melanoma. A mole can be either subdermal (under the skin) or a pigmented growth on the skin, formed mostly of a type of cell known as a melanocyte. The high concentration of the bodys pigmenting agent, melanin, is responsible for their dark color. Moles are a member of the family of skin lesions known as nevi and can occur in all mammalian species, but have been documented most extensively in humans, dogs, and horses. Signs and symptoms
According to the American Academy of Dermatology, the most common types of moles are skin tags, raised moles and flat moles. Benign moles are usually brown, tan, pink or black (especially on dark-colored skin). They are circular or oval and are usually small (commonly between 1–3 mm), though some can be larger than the size of a typical pencil eraser (>5 mm). Some moles produce dark, coarse hair. | Article 12.2d of the ICESCR stipulates the need for "the creation of conditions which would assure to all medical service and medical attention in the event of sickness", and is interpreted in the 2000 comment to include timely access to "basic preventative, curative services… for appropriate treatment of injury and disability.". Obstetric care shares close ties with reproductive rights, which includes access to reproductive health.Surgeons and public health advocates, such as Kelly McQueen, have described surgery as "Integral to the right to health". This is reflected in the establishment of the WHO Global Initiative for Emergency and Essential Surgical Care in 2005, the 2013 formation of the Lancet Commission for Global Surgery, the 2015 World Bank Publication of Volume 1 of its Disease Control Priorities Project "Essential Surgery", and the 2015 World Health Assembly 68.15 passing of the Resolution for Strengthening Emergency and Essential Surgical Care and Anesthesia as a Component of Universal Health Coverage. The Lancet Commission for Global Surgery outlined the need for access to "available, affordable, timely and safe" surgical and anesthesia care; dimensions paralleled in ICESCR General Comment No. 14, which similarly outlines need for available, accessible, affordable and timely healthcare. History
Trepanation
Surgical treatments date back to the prehistoric era. The oldest for which there is evidence is trepanation, in which a hole is drilled or scraped into the skull, thus exposing the dura mater in order to treat health problems related to intracranial pressure and other diseases. | 0-1
|
At the level of homotopy and homology, the mapping class group can be identified as the action on the first homology (or equivalently, first cohomology, or on the fundamental group, as these are all naturally isomorphic; also the first cohomology group generates the cohomology algebra:
MCG
Ho
(
T
n
)
=
Aut
(
π
1
(
X
)
)
=
Aut
(
Z
n
)
=
GL
(
n
,
Z
)
. | They concluded that the environment influenced the development of children and that this was especially important for the development of social competence. According to them, infants needed to be in contact with their mothers to receive sufficient love and care for their development. In the 1940s, the idea that infections led to hospitalism was increasingly criticized, especially since hospitalized infants were often kept alone in small cubicles, without any contact with caregivers or external stimuli, to prevent cross-infections.In 1945, the psychoanalyst René Spitz redefined the term hospitalism by arguing that the mortality rate of infants was still high, despite the isolation in cubicles, because the lack of maternal care impaired their development. Spitz conducted research for his hypothesis by comparing infants in a foundling hospital in Mexico and in a prison nursery in New York with two control groups of children growing up with their families. With the help of Katherine Wolf, he assessed the development of the infants using the Viennese Baby Tests. Spitz concluded that the decline in development and the high susceptibility to diseases he discovered in institutionalized babies were not due to a lack of environmental stimuli, since the prison nursery infants actually had access to toys, but mostly due to emotional and social deprivation. According to Spitz, a stable and intimate mother-child relationship is critical for the healthy development of the child. In his short film, Grief: A Peril in Infancy, he demonstrated the consequences of hospitalism. | 0-1
|
"In 2017, the U.S. Department of Health and Human Services (HHS) announced a public health emergency due to an increase in the misuse of opioids. The administration introduced a strategic framework called the Five-Point Opioid Strategy, which includes providing access recovery services, increasing the availability of reversing agents for overdose, funding opioid misuse and pain research, changing treatments of people managing pain, and updating public health reports related to combating opioid drug misuse.The US epidemic in the 2000s is related to a number of factors. Rates of opioid use and dependency vary by age, sex, race, and socioeconomic status. With respect to race the discrepancy in deaths is thought to be due to an interplay between physician prescribing and lack of access to healthcare and certain prescription drugs. Men are at higher risk for opioid use and dependency than women, and men also account for more opioid overdoses than women, although this gap is closing. Women are more likely to be prescribed pain relievers, be given higher doses, use them for longer durations, and may become dependent upon them faster.Deaths due to opioid use also tend to skew at older ages than deaths from use of other illicit drugs. This does not reflect opioid use as a whole, which includes individuals in younger age demographics. Overdoses from opioids are highest among individuals who are between the ages of 40 and 50, in contrast to heroin overdoses, which are highest among individuals who are between the ages of 20 and 30. | Dysequilibrium syndrome may refer to:
Cerebellar ataxia, mental retardation, and dysequilibrium syndrome 1 (CAMRQ1), an autosomal recessive cerebellar ataxia associated with the VLDLR gene
Cerebellar ataxia, mental retardation, and dysequilibrium syndrome 2 (CAMRQ2), an autosomal recessive cerebellar ataxia associated with the WDR81 gene
Cerebellar ataxia, mental retardation, and dysequilibrium syndrome 3 (CAMRQ3), an autosomal recessive cerebellar ataxia associated with the CA8 gene
Cerebellar ataxia, mental retardation, and dysequilibrium syndrome 4 (CAMRQ4), an autosomal recessive cerebellar ataxia associated with the ATP8A2 gene | 0-1
|
Regarding the antigen property of the blood all human beings can be classified into four groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:
Antigen A with antibody B
Antigen B with antibody A
Antigen AB with neither antibody A nor B
Antigen null (group O) with both antibody A and BThere is an agglutination reaction between similar antigen and antibody (for example, antigen A agglutinates the antibody A and antigen B agglutinates the antibody B). Thus, transfusion can be considered safe as long as the serum of the recipient does not contain antibodies for the blood cell antigens of the donor.The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually immunoglobulin M, abbreviated IgM, antibodies. It has been hypothesized that ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses, although blood group compatibility rules are applied to newborn and infants as a matter of practice. The original terminology used by Karl Landsteiner in 1901 for the classification was A/B/C; in later publications "C" became "O". Type O is often called 0 (zero, or null) in other languages. Rh blood group system
The Rh system (Rh meaning Rhesus) is the second most significant blood-group system in human-blood transfusion with currently 50 antigens. | Blood Transfusion in Clinical Medicine (10th ed.). Oxford UK: Blackwell Science. ISBN 0-86542-881-6. External links
BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH has details of genes and proteins, and variations thereof, that are responsible for blood types
Online Mendelian Inheritance in Man (OMIM): ABO Glycosyltransferase; ABO - 110300
Online Mendelian Inheritance in Man (OMIM): Rhesus Blood Group, D Antigen; RHD - 111680
"Blood group test". Gentest.ch GmbH. Archived from the original on 2017-03-24. Retrieved 2017-03-23. "Blood Facts – Rare Traits". LifeShare Blood Centers. Archived from the original on September 26, 2006. Retrieved September 15, 2006. "Modern Human Variation: Distribution of Blood Types". Dr. Dennis ONeil, Behavioral Sciences Department, Palomar College, San Marcos, California. 2001-06-06. Archived from the original on 2001-06-06. Retrieved November 23, 2006. "Racial and Ethnic Distribution of ABO Blood Types – BloodBook.com, Blood Information for Life". bloodbook.com. Archived from the original on 2010-03-04. Retrieved September 15, 2006. "Molecular Genetic Basis of ABO". Retrieved July 31, 2008. | 11
|
Julian Nowak later proposed the name mycoplasma for certain filamentous microorganisms imagined to have both cellular and acellular stages in their lifecycles, which could explain how they were visible with a microscope, but passed through filters impermeable to other bacteria. Later, the name for these mycoplasmas was pleuropneumonia-like organisms (PPLO), broadly referring to organisms similar in colonial morphology and filterability to the causative agent (a Mycoplasma species) of contagious bovine pleuropneumonia. At present, all these organisms are classified as Mollicutes and the term Mycoplasma refers solely to the genus. Species that infect humans
Species of Mycoplasma, other than those listed below, have been recovered from humans, but are assumed to have been contracted from a non-human host. The following species use humans as the primary host:
Pathophysiology
Mycoplasma species have been isolated from women with bacterial vaginosis. M. genitalium is found in women with pelvic inflammatory disease. In addition, infection is associated with increased risk of cervicitis, infertility, preterm birth and spontaneous abortion. Mycoplasma genitalium has developed resistance to some antibiotics. Mycoplasma species are associated with infant respiratory distress syndrome, bronchopulmonary dysplasia, and intraventricular hemorrhage in preterm infants. Characteristics
Over 100 species have been included in the genus Mycoplasma, a member of the class Mollicutes. They are parasites or commensals of humans, animals, and plants. The genus Mycoplasma uses vertebrate and arthropod hosts. Dietary nitrogen availability has been shown to alter codon bias and genome evolution in Mycoplasma and Phytoplasma.Mycoplasma species are among the smallest free-living organisms (about 0.2 - 0.3 µm in diameter). | ciprofloxacin or Clarithromycin) before the irreversible stage, the infected cells should return to normal. Connections to cancer in vivo and future research
Epidemiologic, genetic, and molecular studies suggest infection and inflammation initiate certain cancers, including those of the prostate. M. genitalium and M. hyorhinis induce malignant phenotype in benign human prostate cells (BPH-1) that were not tumorigenic after 19 weeks of exposure. Types of cancer associated with Mycoplasma
Colon cancer: In a study to understand the effects of Mycoplasma contamination on the quality of cultured human colon cancer cells, a positive correlation was found between the number of M. hyorhinis cells present in the sample and the percentage of CD133-positive cells (a glycoprotein with an unknown function).Gastric cancer: Strong evidence indicates the infection of M. hyorhinis contributes to the development of cancer within the stomach and increases the likelihood of malignant cancer cell development.Lung cancer: Studies on lung cancer have supported the belief that more than a coincidental positive correlation exists between the appearance of Mycoplasma strains in patients and the infection with tumorigenesis.Prostate cancer: p37, a protein encoded for by M. hyorhinis, has been found to promote the invasiveness of prostate cancer cells. The protein also causes the growth, morphology, and gene expression of the cells to change, causing them to become a more aggressive phenotype.Renal cancer: Patients with renal cell carcinoma (RCC) exhibited a significantly high amount of Mycoplasma sp. compared with the healthy control group. This suggests Mycoplasma may play a role in the development of RCC. | 11
|
Beta thalassemia intermedia
Patients with beta thalassemia intermedia require no transfusions or may require episodic blood transfusions during certain circumstances (infection, pregnancy, surgery). Patients with frequent transfusions may develop iron overload and require chelation therapy. Transmission is autosomal recessive; however, dominant mutations and compound heterozygotes have been reported. Genetic counseling is recommended and prenatal diagnosis may be offered. Beta thalassemia minor
Patients with beta thalassemia minor are usually asymptomatic and are often monitored without treatment. Beta thalassemia minor may coexist with other conditions such as chronic hepatitis B, chronic hepatitis C, non-alcoholic fatty liver disease and alcoholic liver disease that, when combined or co-existing, may cause a person to have iron overload of the liver and more severe liver disease. Epidemiology
The beta form of thalassemia is particularly prevalent among the Mediterranean peoples and this geographical association is responsible for its naming: thalassa (θάλασσα) is the Greek word for sea and haima (αἷμα) is the Greek word for blood. In Europe, the highest concentrations of the disease are found in Greece and the Turkish coastal regions. The major Mediterranean islands (except the Balearics) such as Sicily, Sardinia, Corsica, Cyprus, Malta and Crete are heavily affected in particular. Other Mediterranean peoples, as well as those in the vicinity of the Mediterranean, also have high incidence rates, including people from West Asia and North Africa. The data indicate that 15% of the Greek and Turkish Cypriots are carriers of beta-thalassaemia genes, while 10% of the population carry alpha-thalassaemia genes. | Facial weakness is a medical sign associated with a variety of medical conditions.Some specific conditions associated with facial weakness include:
Stroke
Neurofibromatosis
Bells palsy
Ramsay Hunt syndrome
Spontaneous cerebrospinal fluid leak
Myasthenia gravis
See also
Acute facial nerve paralysis
Facioscapulohumeral muscular dystrophy
References
External links
Differential diagnosis
Diagram of appearance in stroke | 0-1
|
Pathogenesis
Inhaled conidia of Blastomyces are phagocytosed by neutrophils and macrophages in alveoli. Some of these escape phagocytosis and transform into yeast phase rapidly. Having thick walls, these are resistant to phagocytosis. Once they have transitioned to the yeast phase, the Blastomyces cells express the protein BAD-1, which helps the yeast cells attach to host cells, and also impairs activation of immune cells while inhibiting release of tumor necrosis factor. In lung tissue, the cells multiply and may also disseminate through blood and lymphatics to other organs, including the skin, bone, genitourinary tract, and brain. The incubation period for pulmonary blastomycosis is 3 to 15 weeks, although 30–50% of infections are asymptomatic. Diagnosis
Because the symptoms of blastomycosis resemble those of many other conditions, including tuberculosis and lung cancer, diagnosis is often delayed. In 40% of cases, the diagnosis takes more than a month. A rapid diagnosis can however be made based on microscopic examination of sputum samples or samples obtained from a tissue biopsy or bronchoalveolar lavage.Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic broad based budding organisms in sputum or tissues by KOH prep, cytology, or histology. Tissue biopsy of skin or other organs may be required in order to diagnose extra-pulmonary disease. Blastomycosis is histologically associated with granulomatous nodules. Commercially available urine antigen testing appears to be quite sensitive in suggesting the diagnosis in cases where the organism is not readily detected. | Peripheral collapses usually involve abnormally low blood pressure and result in collapsed arteries and/or veins, leading to oxygen deprivation to tissues, organs, and limbs.Acute collapse can result from heart failure causing the primary vessels of the heart to collapse, perhaps combined with cardiac arrest. Diagnosis
Treatment
References
== External links == | 0-1
|
Mothers with a history of mental health issues should also talk to their doctor about it early in the pregnancy to help with possible depressive symptoms. Signs and symptoms
Antenatal depression is classified based on a womans symptoms. During pregnancy, a lot of changes to mood, memory, eating habits, and sleep are common. When these common traits become severe, and begin to alter ones day-to-day life, that is when it is considered to be antenatal depression. Symptoms of antenatal depression are:
Inability to concentrate. Overwhelming anxiety and fear. Difficulty remembering. Feeling emotionally numb. Extreme irritability. Sleeping too much or not enough, or restless sleep. Extreme or unending fatigue. Desire to over eat, or not eat at all. Weight loss/gain unrelated to pregnancy. Loss of interest in sex. A sense of dread about everything, including the pregnancy. Feelings of failure, or guilt. Persistent sadness. Thoughts of suicide, or death.Other symptoms can include the inability to get excited about the pregnancy, and/or baby, a feeling of disconnection with the baby, and an inability to form/feel a bond with the developing baby. This can drastically affect the relationship between the mother and the baby, and can drastically affect the mothers capacity for self-care. Such inadequacies can lead to even greater risk factors for the mother. Antenatal depression can be triggered by various causes, including relationship problems, family or personal history of depression, infertility, previous pregnancy loss, complications in pregnancy, and a history of abuse or trauma. Onset and duration of symptoms
Antenatal depression can be caused by many factors. | Calan may refer to
Calan (band), a Welsh band
Calan, Morbihan, a town in Brittany, France
Calan, a trade name for the drug Verapamil
Călan, a town in Hunedoara County, Romania
Alline Calandrini (born 1988), known as Calan, a Brazilian footballer | 0-1
|
Since being in poverty from childhood is more harmful than it is for an adult, it is seen that children in poor households tend to fall behind in certain cognitive abilities compared to other average families.For a child to grow up emotionally healthy, the children under three need "A strong, reliable primary caregiver who provides consistent and unconditional love, guidance, and support. Safe, predictable, stable environments. Ten to 20 hours each week of harmonious, reciprocal interactions. This process, known as attunement, is most crucial during the first 6–24 months of infants lives and helps them develop a wider range of healthy emotions, including gratitude, forgiveness, and empathy. Enrichment through personalized, increasingly complex activities". In one survey, 67% of children from disadvantaged inner cities said they had witnessed a serious assault, and 33% reported witnessing a homicide. 51% of fifth graders from New Orleans (median income for a household: $27,133) have been found to be victims of violence, compared to 32% in Washington, DC (mean income for a household: $40,127). Studies have shown that poverty changes the personalities of children who live in it. The Great Smoky Mountains Study was a ten-year study that was able to demonstrate this. During the study, about one-quarter of the families saw a dramatic and unexpected increase in income. The study showed that among these children, instances of behavioral and emotional disorders decreased, and conscientiousness and agreeableness increased. Education
Research has found that there is a high risk of educational underachievement for children who are from low-income housing circumstances. | In countries with completion rates between 60% and 80%, gender disparity is generally smaller, but disparity at the expense of poor girls is especially marked in Cameroon, Nigeria and Yemen. Exceptions in the opposite direction are observed in countries with pastoralist economies that rely on boys labour, such as the Kingdom of Eswatini, Lesotho and Namibia. Shelter
The geographic concentration of poverty is argued to be a factor in entrenching poverty. William J. Wilsons "concentration and isolation" hypothesis states that the economic difficulties of the very poorest African Americans are compounded by the fact that as the better-off African Americans move out, the poorest are more and more concentrated, having only other very poor people as neighbors. This concentration causes social isolation, Wilson suggests, because the very poor are now isolated from access to the job networks, role models, institutions, and other connections that might help them escape poverty. Gentrification means converting an aging neighborhood into a more affluent one, as by remodeling homes. Landlords then increase rent on newly renovated real estate; the poor people cannot afford to pay high rent, and may need to leave their neighborhood to find affordable housing. The poor also get more access to income and services, while studies suggest poor residents living in gentrifying neighbourhoods are actually less likely to move than poor residents of non-gentrifying areas.Poverty increases the risk of homelessness. | 11
|
Orthorexia nervosa (also known as orthorexia) (ON) is a proposed eating disorder characterized by an excessive preoccupation with eating healthy food. The term was introduced in 1997 by American physician Steven Bratman, M.D. He suggested that some peoples dietary restrictions intended to promote health may paradoxically lead to unhealthy consequences, such as social isolation, anxiety, loss of ability to eat in a natural, intuitive manner, reduced interest in the full range of other healthy human activities, and, in rare cases, severe malnutrition or even death.In 2009, Ursula Philpot, chair of the British Dietetic Association and senior lecturer at Leeds Metropolitan University, described people with orthorexia nervosa as being "solely concerned with the quality of the food they put in their bodies, refining and restricting their diets according to their personal understanding of which foods are truly pure." This differs from other eating disorders, such as anorexia nervosa and bulimia nervosa, where those affected focus on the quantity of food eaten.Orthorexia nervosa also differs from anorexia nervosa in that it does not disproportionally affect one gender. Studies have found that orthorexia nervosa is equally found in both men and women with no significant gender differences at all. Furthermore, research has found significant positive correlations between ON and both narcissism and perfectionism, but no significant correlation between ON and self esteem. This shows that high-ON individuals likely take pride over their healthy eating habits over others and that is the driving force behind their orthorexia as opposed to body image like anorexia. | Micafungin, sold under the brand name Mycamine, is an echinochandin antifungal medication used to treat and prevent invasive fungal infections including candidemia, abscesses, and esophageal candidiasis. It inhibits the production of beta-1,3-glucan, an essential component of fungal cell walls that is not found in mammals. Micafungin is administered intravenously. It received final approval from the U.S. Food and Drug Administration (FDA) in March 2005, and gained approval in the European Union in April 2008. It is on the World Health Organizations List of Essential Medicines. Indications
Micafungin is indicated for the treatment of candidemia, acute disseminated candidiasis, Candida peritonitis, abscesses and esophageal candidiasis. Since January 23, 2008, micafungin has been approved for the prophylaxis of Candida infections in patients undergoing hematopoietic stem cell transplantation (HSCT). Micafungin works by way of concentration-dependent inhibition of 1,3-beta-D-glucan synthase resulting in reduced formation of 1,3-beta-D-glucan, which is an essential polysaccharide comprising one-third of the majority of Candida spp. cell walls. This decreased glucan production leads to osmotic instability and thus cellular lysis. Dosage
The metabolism of micafungin occurs hepatically via acryp sulfatase followed by secondary metabolism by a transferase. Precautions should be taken with regards to dosing, as micafungin weakly inhibits CYP3A4. Dosage forms
Micafungin is a natural antifungal product derived from other fungi as a defense mechanism for competition of nutrients, etc. To be specific, micafungin is derived from FR901379, and is produced by Coleophoma empetri. References
Further reading
External links
"Micafungin". Drug Information Portal. U.S. National Library of Medicine. | 0-1
|
In some regions of the UK, reduced used of fluoroquinolone antibiotics seems to lead to reduced rates of CDI. Probiotics
Some evidence indicates probiotics may be useful to prevent infection and recurrence. Treatment with Saccharomyces boulardii in those who are not immunocompromised with C. difficile also may be useful. Initially, in 2010, the Infectious Diseases Society of America recommended against their use due to the risk of complications. Subsequent reviews, however, did not find an increase in adverse effects with treatment, and overall treatment appears safe and moderately effective in preventing Clostridium difficile-associated diarrhea.One study in particular found that there does appear to be a "protective effect" of probiotics, specifically reducing the risk of antibiotic-associated diarrhea (AAD) by 51% in 3,631 outpatients, but it is important to note that the types of infections in the subjects were not specified. Yogurt, tablets, dietary supplements are just a few examples of probiotics available for people. Infection control
Rigorous infection protocols are required to minimize this risk of transmission. Infection control measures, such as wearing gloves and noncritical medical devices used for a single person with CDI, are effective at prevention. This works by limiting the spread of C. difficile in the hospital setting. In addition, washing with soap and water will wash away the spores from contaminated hands, but alcohol-based hand rubs are ineffective. These precautions should remain in place among those in hospital for at least 2 days after the diarrhea has stopped.Bleach wipes containing 0.55% sodium hypochlorite have been shown to kill the spores and prevent transmission. | Both sets of repeats share a region of a few hundred bps, the so-called "a sequence"; the other regions of the repeats are sometimes referred to as "b sequence" and "c sequence". Life cycle
Viral replication is nuclear and lysogenic. Entry into the host cell is achieved by attachment of the viral glycoproteins to host receptors, which mediates endocytosis. Replication follows the dsDNA bidirectional replication model. DNA templated transcription, with some alternative splicing mechanism is the method of transcription. Translation takes place by leaky scanning. The virus exits the host cell by nuclear egress, and budding. Humans and monkeys serve as the natural hosts. Transmission routes are dependent on coming into contact with bodily fluids (such as saliva, urine, and genital secretions) from an infected individual. All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals. Genetic engineering
The CMV promoter is commonly included in vectors used in genetic engineering work conducted in mammalian cells, as it is a strong promoter and drives constitutive expression of genes under its control. History
Cytomegalovirus was first observed by German pathologist Hugo Ribbert in 1881 when he noticed enlarged cells with enlarged nuclei present in the cells of an infant. Years later, between 1956 and 1957, Thomas Huckle Weller together with Smith and Rowe independently isolated the virus, known thereafter as "cytomegalovirus". | 0-1
|
In cats, it is the first line of treatment due to its efficacy and few side effects. Systemic hypertension in cats is usually secondary to another abnormality, such as chronic kidney disease, and so amlodipine is most often administered to cats with kidney disease. While amlodipine is used in dogs with systemic hypertension, it is not as efficacious. Amlodipine is also used to treat congestive heart failure due to mitral valve regurgitation in dogs. By decreasing resistance to forward flow in the systemic circulation it results in a decrease in regurgitant flow into the left atrium. Similarly, it can be used on dogs and cats with left-to-right shunting lesions such as ventricular septal defect to reduce the shunt. Side effects are rare in cats. In dogs, the primary side effect is gingival hyperplasia. References
External links
"Amlodipine". Drug Information Portal. U.S. National Library of Medicine. onog | Senna glycoside, also known as sennoside or senna, is a medication used to treat constipation and empty the large intestine before surgery. The medication is taken by mouth or via the rectum. It typically begins working in around 30 minutes when given by rectum and within twelve hours when given by mouth. It is a weaker laxative than bisacodyl or castor oil.Common side effects of senna glycoside include abdominal cramps. It is not recommended for long-term use, as it may result in poor bowel function or electrolyte problems. While no harm has been found to result from use while breastfeeding, such use is not typically recommended. It is not typically recommended in children. Senna may change urine to a somewhat reddish color. Senna derivatives are a type of stimulant laxative and are of the anthraquinone type. While its mechanism of action is not entirely clear, senna is thought to act by increasing fluid secretion within and contraction of the large intestine.It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. Sennosides come from the group of plants Senna. In plant form, it has been used at least since the 700s CE. In 2019, it was the 344th most commonly prescribed medication in the United States, with fewer than one million prescriptions. It is sold under a number of brand names including Ex-Lax and Senokot. | 0-1
|
Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about 5% of people evaluated for fainting. The tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). A number of factors make a heart related cause more likely including age over 35, prior atrial fibrillation, and turning blue during the event. Electrocardiogram
Electrocardiogram (ECG) finds that should be looked for include signs of heart ischemia, arrhythmias, atrioventricular blocks, a long QT, a short PR, Brugada syndrome, signs of hypertrophic obstructive cardiomyopathy (HOCM), and signs of arrhythmogenic right ventricular dysplasia (ARVD/C). Signs of HCM include large voltages in the precordial leads, repolarization abnormalities, and a wide QRS with a slurred upstroke. Signs of ARVD/C include T wave inversion and epsilon waves in lead V1 to V3.It is estimated that from 20 to 50% of people have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting. Sometimes, a Holter monitor may be used. | The FDA currently allows individual allergists to create the formula for each dosage, whereas the EMEA requires treatment extracts to be prepared at manufacturing sites. The FDA has approved sublingual therapy through the use of tablets, but has not approved specific formulation. The EMEA has also approved sublingual therapy through both tablets and solution, and this administration now accounts for 45% of immunotherapy treatments.The FDA advisory board has supported the use of AR101, an oral immunotherapy, for patients with peanut allergies in 2019. Science communication
Allergen immunotherapy is viewed as a beneficial way to curb allergies in the perspective of the media. It is seen where it can be covered by insurance and offer a more permanent solution than antihistamines or nasal steroids that treat symptoms, not the bodys reaction. Communication about allergen immunotherapy is not described very often in the news media; it is usually only communicated by the science community. The scientific community describes allergen immunotherapy as a scientific solution that helps not only patients with allergies but also positively impacts the quality of life of them and others around them. As temperatures increase due to changing climates, pollen levels also increase. Allergies are becoming a more common problem among the public, which is why the science community advocates for allergen immunotherapy. Subcutaneous allergen immunotherapy, according to the scientific community, is an effective solution to allergies due to numerous positive studies. Research
Oral immunotherapy
As of 2015, oral immunotherapys balance of risk to benefit for food allergies was not well studied. | 0-1
|
Possible explanations may include cold temperature-induced changes in the respiratory system, decreased immune response, and low humidity causing an increase in viral transmission rates, perhaps due to dry air allowing small viral droplets to disperse farther and stay in the air longer.The apparent seasonality may also be due to social factors, such as people spending more time indoors, near infected people, and specifically children at school. Although normal exposure to cold does not increase ones risk of infection, severe exposure leading to significant reduction of body temperature (hypothermia) may put one at a greater risk for the common cold; although controversial, the majority of evidence suggests that it may increase susceptibility to infection. Other
Herd immunity, generated from previous exposure to cold viruses, plays an important role in limiting viral spread, as seen with younger populations that have greater rates of respiratory infections. Poor immune function is a risk factor for disease. Insufficient sleep and malnutrition have been associated with a greater risk of developing infection following rhinovirus exposure; this is believed to be due to their effects on immune function. Breast feeding decreases the risk of acute otitis media and lower respiratory tract infections among other diseases, and it is recommended that breast feeding be continued when an infant has a cold. In the developed world breast feeding may not be protective against the common cold in and of itself. Pathophysiology
The symptoms of the common cold are believed to be primarily related to the immune response to the virus. | CA-125 is elevated. Clinical diagnosis can be made based on history and imaging, while the gold standard for definitive diagnosis remains Video-assisted thoracoscopic surgery, or VATS, which allows not only the visualization of the lesion, but also surgical treatment via cauterization of the ectopic endometrial tissue. Special staining under a microscope or utilizing a cell marker, such as PAX8, can be used to positively identify endometrial stroma. Classification
Catamenial pneumothorax is the most common form of thoracic endometriosis syndrome, which also includes
catamenial hemothorax, catamenial hemoptysis, catamenial hemothorax and endometriosis lung nodules, as well as some exceptional presentations. Treatment
Pneumothorax can be a medical emergency, as it can become associated with decreased lung function, and if progressed to tension pneumothorax, potentially fatal. In many cases, catamenial pneumothorax will resolve spontaneously and not require immediate intervention. In more severe cases, a chest tube may be required to release air and/or blood and to allow the lung to re-expand.Surgery, hormonal treatments and combined approaches have all been proposed, with variable results in terms of short and long term outcome. These have both been effective, separately and together. Both have been used to treat women with this condition, and specifics depend on each patient and each situation. Surgery may be used to excise endometrial tissue from the lungs and pleural space as well as repair damage and holes in the diaphragm. Surgery may also be used to remove blisters (blebs). | 0-1
|
Long-term health problems following acute Rocky Mountain spotted fever infection include partial paralysis of the lower extremities, gangrene requiring amputation of fingers, toes, or arms or legs, hearing loss, loss of bowel or bladder control, movement disorders, and language disorders. These complications are most frequent in persons recovering from severe, life-threatening disease, often following lengthy hospitalizations. Epidemiology
There are between 500 and 2500 cases of Rocky Mountain spotted fever reported in the United States per year, and in only about 20% can the tick be found.Host factors associated with severe or fatal Rocky Mountain spotted fever include advanced age, male sex, African or Caribbean background, long-term excessive alcohol use and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Deficiency of G6PD is a genetic condition affecting about 12 percent of the Afro-American male population. Deficiency in this enzyme is associated with a high proportion of severe cases of Rocky Mountain spotted fever. This is a rare clinical complication that is often fatal within five days of the onset of the disease. In the early 1940s, outbreaks were described in the Mexican states of Sinaloa, Sonora, Durango, and Coahuila driven by dogs and Rhipicephalus sanguineus sensu lato, the brown dog tick. Over the ensuing 100 years case fatality rates were 30%–80%. In 2015, there was an abrupt rise in Sonora cases with 80 fatal cases. From 2003 to 2016, cases increased to 1394 with 247 deaths. | Once the abdominal wall can no longer expand, any further fluid leaking into the tissue results in fairly rapid rises in the pressure within the closed space. Initially this increase in pressure does not cause organ failure but does prevent organs from working properly – this is called intra-abdominal hypertension and is defined as a pressure over 12 mmHg in adults. ACS is defined by a sustained IAP(intra-abdominal pressure) above 20 mmHg with new-onset or progressive organ failure. Severe organ dysfunctionent syndrome. These pressure measurements are relative. Small children get into trouble and develop compartment syndromes at much lower pressures while young previously healthy athletic individuals may tolerate an abdominal pressure of 20 mmHg very well. The underlying cause of the disease process is capillary permeability caused by the systemic inflammatory response syndrome (SIRS) that occurs in every critically ill patient. SIRS leads to leakage of fluid out of the capillary beds into the interstitial space in the entire body with a profound amount of this fluid leaking into the gut wall, mesentery and retroperitoneal tissue. Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremities. When increased compression occurs in such a hollow space, organs will begin to collapse under the pressure. As the pressure increases and reaches a point where the abdomen can no longer be distended it starts to affect the cardiovascular and pulmonary systems. When abdominal compartment syndrome reaches this point without surgery and help of a silo the patient will most likely die. | 0-1
|
Gingivitis is a non-destructive disease that causes inflammation of the gums. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that is attached to tooth surfaces, termed plaque-induced gingivitis. Most forms of gingivitis are plaque-induced.While some cases of gingivitis never progress to periodontitis, periodontitis is always preceded by gingivitis.Gingivitis is reversible with good oral hygiene; however, without treatment, gingivitis can progress to periodontitis, in which the inflammation of the gums results in tissue destruction and bone resorption around the teeth. Periodontitis can ultimately lead to tooth loss. Signs and symptoms
The symptoms of gingivitis are somewhat non-specific and manifest in the gum tissue as the classic signs of inflammation:
Swollen gums
Bright red or purple gums
Gums that are tender or painful to the touch
Bleeding gums or bleeding after brushing and/or flossing
Bad breath (halitosis)Additionally, the stippling that normally exists in the gum tissue of some individuals will often disappear and the gums may appear shiny when the gum tissue becomes swollen and stretched over the inflamed underlying connective tissue. The accumulation may also emit an unpleasant odor. When the gingiva are swollen, the epithelial lining of the gingival crevice becomes ulcerated and the gums will bleed more easily with even gentle brushing, and especially when flossing. | Either a registered dental hygienist or a dentist may perform the comprehensive periodontal exam but the data interpretation and diagnosis are done by the dentist. The comprehensive periodontal exam consists of a visual exam, a series of radiographs, probing of the gingiva, determining the extent of current or past damage to the periodontium and a comprehensive review of the medical and dental histories. Current research shows that activity levels of the following enzymes in saliva samples are associated with periodontal destruction: aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and acid phosphatase (ACP). Therefore, these enzyme biomarkers may be used to aid in the diagnosis and treatment of gingivitis and periodontitis. A dental hygienist or dentist will check for the symptoms of gingivitis, and may also examine the amount of plaque in the oral cavity. A dental hygienist or dentist will also look for signs of periodontitis using X-rays or periodontal probing as well as other methods. If gingivitis is not responsive to treatment, referral to a periodontist (a specialist in diseases of the gingiva and bone around teeth and dental implants) for further treatment may be necessary. Classification
1999 Classification
As defined by the 1999 World Workshop in Clinical Periodontics, there are two primary categories of gingival diseases, each with numerous subgroups:
Dental plaque-induced gingival diseases. | 11
|
Topical antibiotics such as metronidazole and erythromycin have been used for CGPD. Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. Trimethoprim/sulfamethoxazole has also been used. The use of oral systemic antibiotics is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children.The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others saw incomplete resolution or prolonged symptoms. Topical azelaic acid has been used successfully to treat CGPD. Immediate discontinuation of topical corticosteroids is recommended since corticosteroids are thought to worsen CGPD. Prognosis
CGPD is known to be a temporary skin disease with a benign course. The skin papules typically resolve after a few months to a few years. After CGPD resolves, the skin may return to normal without scarring or may have small atrophic depressions with collagen loss, milia, or small pit-like scars. Epidemiology
CGPD occurs most often in children of Afro-Caribbean descent before puberty though reports of this disease occurring in Asian and Caucasian children have also been described. Due to the limited number of reported cases, it remains controversial whether CGPD occurs more often in African children than in children of other races. | A vanishing twin, also known as twin resorption, is a fetus in a multigestation pregnancy that dies in utero and is then partially or completely reabsorbed. In some instances, the dead twin is compressed into a flattened, parchment-like state known as fetus papyraceus.Vanishing twins occur in up to one of every eight multifetus pregnancies and may not even be known in most cases. "High resorption rates, which cannot be explained on the basis of the expected abortion rate, suggest intense fetal competition for space, nutrition, or other factors during early gestation, with frequent loss or resorption of the other twin(s). "In pregnancies achieved by in vitro fertilization, "it frequently happens that more than one amniotic sac can be seen in early pregnancy, whereas a few weeks later there is only one to be seen and the other has vanished." See also
Chimera (genetics)
Mosaicism
Parasitic twin
References
Further reading
External links
Vanishing twin at eMedicine.com
50 articles about vanishing twin phenomenon in PubMed | 0-1
|
Attack rates are similar for men and women.The most important determinant of risk is the travelers destination. High-risk destinations include developing countries in Latin America, Africa, the Middle East, and Asia. Among backpackers, additional risk factors include drinking untreated surface water and failure to maintain personal hygiene practices and clean cookware. Campsites often have very primitive (if any) sanitation facilities, making them potentially as dangerous as any developing country.Although travelers diarrhea usually resolves within three to five days (mean duration: 3.6 days), in about 20% of cases, the illness is severe enough to require bedrest, and in 10%, the illness duration exceeds one week. For those prone to serious infections, such as bacillary dysentery, amoebic dysentery, and cholera, TD can occasionally be life-threatening. Others at higher-than-average risk include young adults, immunosuppressed persons, persons with inflammatory bowel disease or diabetes, and those taking H2 blockers or antacids. Immunity
Travelers often get diarrhea from eating and drinking foods and beverages that have no adverse effects on local residents. This is due to immunity that develops with constant, repeated exposure to pathogenic organisms. The extent and duration of exposure necessary to acquire immunity has not been determined; it may vary with each individual organism. A study among expatriates in Nepal suggests that immunity may take up to seven years to develop—presumably in adults who avoid deliberate pathogen exposure. Conversely, immunity acquired by American students while living in Mexico disappeared, in one study, as quickly as eight weeks after cessation of exposure. | However, it has been shown to have comparable affinity with calcitriol for the vitamin D receptor (VDR), while being less than 1% as active as the calcitriol in regulating calcium metabolism. The vitamin D receptor belongs to the steroid/thyroid receptor superfamily, and is found on the cells of many different tissues including the thyroid, bone, kidney, and T cells of the immune system. T cells are known to play a role in psoriasis, and it is thought that the binding of calcipotriol to the VDR modulates the T cells gene transcription of cell differentiation and proliferation related genes. In mouse studies, topical calcipotriol administration to the ear and dorsal skin led to a dose-dependent increase in the production of the epithelial cell-derived cytokine TSLP by keratinocytes, and triggered atopic dermatitis at high concentrations. This upregulation of TSLP production due to calcipotriol application is thought to be mediated through the coactivation of vitamin D receptor/RXRα and vitamin D receptor/RXRβ heterodimers. As psoriasis is typically thought to be partially driven by Th1/Th17 inflammatory cytokines, calcipotriol treatment at appropriate concentrations may alleviate psoriasis symptoms by repressing Th1/Th17 inflammation through TSLP production, which is linked to a Th2 response. However, it is important to note that this has not yet been confirmed. Pharmacokinetics
After application and systemic uptake, calcipotriol undergoes rapid hepatic metabolism. Calcipotriol is metabolized to MC1046 (the α,β−unsaturated ketone analog), which is subsequently metabolized to its primary metabolite, the saturated ketone analog MC1080. | 0-1
|
Treatment
Treatment can be either active or conservative. Active
Treatment options include surgery, laser and radiofrequency ablation, and ultrasound-guided foam sclerotherapy. Newer treatments include cyanoacrylate glue, mechanochemical ablation, and endovenous steam ablation. No real difference could be found between the treatments, except that radiofrequency ablation could have a better long-term benefit. Conservative
The National Institute for Health and Clinical Excellence (NICE) produced clinical guidelines in July 2013 recommending that all people with symptomatic varicose veins (C2S) and worse should be referred to a vascular service for treatment. Conservative treatments such as support stockings should not be used unless treatment was not possible. The symptoms of varicose veins can be controlled to an extent with the following:
Elevating the legs often provides temporary symptomatic relief. Advice about regular exercise sounds sensible but is not supported by any evidence. The wearing of graduated compression stockings with variable pressure gradients (Class II or III) has been shown to correct the swelling, nutritional exchange, and improve the microcirculation in legs affected by varicose veins. They also often provide relief from the discomfort associated with this disease. Caution should be exercised in their use in patients with concurrent peripheral arterial disease. The wearing of intermittent pneumatic compression devices have been shown to reduce swelling and pain. Diosmin/hesperidin and other flavonoids. Anti-inflammatory medication such as ibuprofen or aspirin can be used as part of treatment for superficial thrombophlebitis along with graduated compression hosiery – but there is a risk of intestinal bleeding. | Timolol can also lead to fainting, congestive heart failure, depression, confusion, worsening of Raynauds syndrome and impotence.Side effects when given in the eye include: burning sensation, eye redness, superficial punctate keratopathy, corneal numbness. Formulations
It is available in tablet and liquid formulations.For ophthalmic use, timolol is also available combined:
with carbonic anhydrase inhibitors:
timolol and brinzolamide
timolol and dorzolamide
with α2 agonists:
timolol and brimonidine
with prostaglandin analogs:
timolol and latanoprost
timolol and travoprost
Brand names
Timolol is marketed under many trade names worldwide. Timolol eye drops are marketed under the brand name Istalol among others. References
External links
"Timolol". Drug Information Portal. U.S. National Library of Medicine. "Timolol Ophthalmic". Drug Information Portal. U.S. National Library of Medicine. "Timolol maleate". Drug Information Portal. U.S. National Library of Medicine. "Timolol Ophthalmic". MedlinePlus. | 0-1
|
Type 2: Triangular or heart-shaped ossicle measuring up to 12 mm, which represents a secondary ossification center connected to the navicular tuberosity by a 1–2 mm layer of fibrocartilage or hyaline cartilage. Portions of the posterior tibialis tendon sometimes insert onto the accessory ossicle, which can cause dysfunction, and therefore, symptoms. Type 3: A cornuate navicular bone represents an enlarged navicular tuberosity, which may represent a fused Type 2 accessory bone. Occasionally symptomatic due to bunion formation. Os trigonum
The os trigonum or accessory talus represents a failure of fusion of the lateral tubercle of the posterior process of the talus bone. Is estimated to be present in 7–25% of adults. It can be mistaken for an avulsion fracture of lateral tubercle of talus (Shepherd fracture) or a fracture of the Stieda process. In most cases, Os Trigonum will go unnoticed, but with some ankle injuries it can get trapped between the heel and ankle bones which irritates the surrounding structures, leading to Os Trigonum Syndrome. Less common accessory bones
Other locations
Neck
Nodules in the posterior margin of the nuchal ligament form bone tissue in approximately 11% of males and 3–5% in females after the third decade of life, and may then be regarded to be sesamoid bones. Shoulder
An os acromiale forms when any of its four ossification centers fail to fuse. These four ossification centers are called (from tip to base) pre-acromion, meso-acromion, meta-acromion, and basi-acromion. | When bright red blood is vomited, it is termed hematemesis. Hematemesis, in contrast to coffee ground vomitus, suggests that upper gastrointestinal bleeding is more acute or more severe, for example due to a Mallory–Weiss tear, gastric ulcer or Dieulafoys lesion, or esophageal varices. This condition may be a medical emergency and urgent care may be required.Oxidized blood from an upper gastrointestinal bleed can also be excreted in stool. It produces blackened, "tarry" stools known as melena. References
External links
Coffee Ground Vomitus | 0-1
|
Mechanism of action
GTN is a prodrug which must be denitrated, with the nitrite anion or a related species further reduced to produce the active metabolite nitric oxide (NO). Organic nitrates that undergo these two steps within the body are called nitrovasodilators, and the denitration and reduction occur via a variety of mechanisms. The mechanism by which such nitrates produce NO is widely disputed. Some believe that organic nitrates produce NO by reacting with sulfhydryl groups, while others believe that enzymes such as glutathione S-transferases, cytochrome P450 (CYP), and xanthine oxidoreductase are the primary source of GTN bioactivation. In recent years, a great deal of evidence has been produced that supports the conclusion that GTNs clinically relevant denitration and reduction produce 1,2-glyceryl dinitrate (GDN) and NO, and that this reaction is catalysed by mitochondrial aldehyde dehydrogenase (ALDH2 or mtALDH). The NO produced by this process is a potent activator of guanylyl cyclase (GC) by heme-dependent mechanisms; this activation results in formation of cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). Among other roles, cGMP serves as a substrate for a cGMP-dependent protein kinase that activates myosin light chain phosphatase. Thus, production of NO from exogenous sources such as GTN increases the level of cGMP within the cell, and stimulates dephosphorylation of myosin, which initiates relaxation of smooth muscle cells in blood vessels. | Pacman dysplasia is a lethal autosomal recessive skeletal dysplasia. The dysplasia is present during fetal development. References
Wilcox WR, Wenger DA, Lachman RS, Rimoin DL (2005). "Distinguishing Pacman dysplasia from mucolipidosis II: comment on Saul et al. [2005]". Am J Med Genet A. 135 (3): 333. doi:10.1002/ajmg.a.30717. PMID 15887286. S2CID 38848656. Saul RA, Proud V, Taylor HA, Leroy JG, Spranger J (2005). "Prenatal mucolipidosis type II (I-cell disease) can present as Pacman dysplasia". Am J Med Genet A. 135 (3): 328–32. doi:10.1002/ajmg.a.30716. PMID 15887289. S2CID 2151584. Wilcox WR, Lucas BC, Loebel B, Bachman RP, Lachman RS, Rimoin DL (1998). "Pacman dysplasia: report of two affected sibs". Am J Med Genet. 77 (4): 272–6. doi:10.1002/(SICI)1096-8628(19980526)77:4<272::AID-AJMG4>3.0.CO;2-P. PMID 9600734. Shohat M, Rimoin DL, Gruber HE, Lachman R (1993). "New epiphyseal stippling syndrome with osteoclastic hyperplasia". Am J Med Genet. 45 (5): 558–61. doi:10.1002/ajmg.1320450506. PMID 8456823. Miller SF, Proud VK, Werner AL, Field FM, Wilcox WF, Lachman RS, Rimoin DL (2003). "Pacman dysplasia: a lethal skeletal dysplasia with variable radiographic features". Pediatr Radiol. 33 (4): 256–60. doi:10.1007/s00247-002-0859-4. PMID 12709756. S2CID 185059. External links
Online Mendelian Inheritance in Man (OMIM): 167220 | 0-1
|
Rheumatic fever (RF) is an inflammatory disease that can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves.Rheumatic fever may occur following an infection of the throat by the bacterium Streptococcus pyogenes. If the infection is left untreated, rheumatic fever occurs in up to three percent of people. The underlying mechanism is believed to involve the production of antibodies against a persons own tissues. Due to their genetics, some people are more likely to get the disease when exposed to the bacteria than others. Other risk factors include malnutrition and poverty. Diagnosis of RF is often based on the presence of signs and symptoms in combination with evidence of a recent streptococcal infection.Treating people who have strep throat with antibiotics, such as penicillin, decreases the risk of developing rheumatic fever. In order to avoid antibiotic misuse this often involves testing people with sore throats for the infection; however, testing might not be available in the developing world. Other preventive measures include improved sanitation. | The risks, benefits, and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Vaccine
No vaccines are currently available to protect against S. pyogenes infection, although research is underway to develop one. Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine. Infection
People with positive cultures for Streptococcus pyogenes should be treated with penicillin as long as allergy is not present. The use of antibiotics will not alter cardiac involvement in the development of rheumatic fever. Some suggest the use of benzathine benzylpenicillin.Monthly injections of long-acting penicillin must be given for a period of five years in patients having one attack of rheumatic fever. If there is evidence of carditis, the length of therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence. Inflammation
While corticosteroids are often used, evidence to support this is poor. Salicylates are useful for pain.Steroids are reserved for cases where there is evidence of an involvement of the heart. The use of steroids may prevent further scarring of tissue and may prevent the development of sequelae such as mitral stenosis. | 11
|
Leukemic cells may gather in the spleen and cause it to swell; this can have the side effect of making the person feel full even when he or she has not eaten much.Hairy cell leukemia is commonly diagnosed after a routine blood count shows unexpectedly low numbers of one or more kinds of normal blood cells, or after unexplained bruises or recurrent infections in an otherwise apparently healthy patient.Platelet function may be somewhat impaired in HCL patients, although this does not appear to have any significant practical effect. It may result in somewhat more mild bruises than would otherwise be expected for a given platelet count or a mildly increased bleeding time for a minor cut, likely the result of producing slightly abnormal platelets in the overstressed bone marrow tissue. Patients with a high tumor burden may also have somewhat reduced levels of cholesterol, especially in patients with an enlarged spleen. Cholesterol levels return to more normal values with successful treatment of HCL. Cause
As with many cancers, the cause of HCL is unknown. Exposure to tobacco smoke, ionizing radiation, or industrial chemicals (with the possible exception of diesel) does not appear to increase the risk of developing it. | About 10% of people with HCL have this variant form of the disease, representing about 60-75 new cases of HCL-V each year in the U.S. While classic HCL primarily affects men, HCL-V is more evenly divided between males and females. While the disease can appear at any age, the median age at diagnosis is over 70.Similar to B-cell prolymphocytic leukemia (B-PLL) in chronic lymphocytic leukemia, HCL-V is a more aggressive disease. Historically, it has been considered less likely to be treated successfully than is classic HCL, and remissions have tended to be shorter. The introduction of combination therapy with concurrent rituximab and cladribine therapy, though, has shown excellent results in early follow-up. As of 2016, this therapy is considered the first-line treatment of choice for many people with HCL-V.Many older treatment approaches, such as interferon-alpha, the combination chemotherapy regimen "CHOP", and common alkylating agents such as cyclophosphamide, showed very little benefit. Pentostatin and cladribine administered as monotherapy (without concurrent rituximab) provide some benefit to many people with HCL-V, but typically induce shorter remission periods and lower response rates than when they are used in classic HCL. More than half of people respond partially to splenectomy.In terms of B-cell development, the prolymphocytes are less developed than are lymphocytes or plasma cells, but are still more mature than their lymphoblastic precursors. | 11
|
Some salivary components are crucial for plaques ecosystem, such as salivary alpha-amylase which plays a role in binding and adhesion. Proline-rich proteins (PRP) and statherins are also involved in the formation of plaque. Supragingival biofilm
Supragingival biofilm is dental plaque that forms above the gums, and is the first kind of plaque to form after the brushing of the teeth. It commonly forms in between the teeth, in the pits and grooves of the teeth and along the gums. It is made up of mostly aerobic bacteria, meaning these bacteria need oxygen to survive. If plaque remains on the tooth for a longer period of time, anaerobic bacteria begin to grow in this plaque. Subgingival biofilm
Subgingival biofilm is plaque that is located under the gums. It occurs after the formation of the supragingival biofilm by a downward growth of the bacteria from above the gums to below. This plaque is mostly made up of anaerobic bacteria, meaning that these bacteria will only survive if there is no oxygen. As this plaque attaches in a pocket under the gums, they are not exposed to oxygen in the mouth and will therefore thrive if not removed.The extracellular matrix contains proteins, long-chain polysaccharides and lipids. The most common reasons for ecosystem disruption are the ecological factors discussed in the environment section. The bacteria that exhibit the most fit plasticity for the change in environment dominate the given environment. Often, this leads to opportunistic pathogens which may cause dental caries and periodontal disease. | Increased PTH levels trigger the release of stored calcium through the dissolution of old bone, as well as the conservation of serum calcium through a cessation in the production of new bone.Generally, the first bones to be affected are the fingers, facial bones, ribs, and pelvis. Long bones, which are longer than they are wide, are also among the first affected. As the disease progresses, any bone may be affected. Diagnosis
OFC may be diagnosed using a variety of techniques. Muscles in patients with OFC can either appear unaffected or "bulked up." If muscular symptoms appear upon the onset of hyperparathyroidism, they are generally sluggish contraction and relaxation of the muscles. Deviation of the trachea (a condition in which the trachea shifts from its position at the midline of the neck), in conjunction with other known symptoms of OFC can point to a diagnosis of parathyroid carcinoma.Blood tests on patients with OFC generally show high levels of calcium (normal levels are considered to range between 8.5 and 10.2 mg/dL, parathyroid hormone (levels generally above 250 pg/mL, as opposed to the "normal" upper-range value of 65 pg/mL), and alkaline phosphatase (normal range is 20 to 140 IU/L). X-rays may also be used to diagnose the disease. Usually, these X-rays will show extremely thin bones, which are often bowed or fractured. However, such symptoms are also associated with other bone diseases, such as osteopenia or osteoporosis. Generally, the first bones to show symptoms via X-ray are the fingers. | 0-1
|
One night he claimed to have been visited by the ghost of Schubert and wrote down the music that he was hearing. Thereafter, he began making claims that he could hear an angelic choir singing to him. As his condition worsened, the angelic voices developed into demonic ones.Brian Wilson, songwriter and co-founder of the Beach Boys, has schizoaffective disorder that presents itself in the form of disembodied voices. They formed a major component of Bill Pohlads Love & Mercy (2014), a biographical film which depicts Wilsons hallucinations as a source of musical inspiration, constructing songs that were partly designed to converse with them. Wilson has said of the voices: "Mostly [theyre] derogatory. Some of its cheerful. Most of it isnt." To combat them, his psychiatrist advised that he "talk humorously to them", which he says has helped "a little bit".The onset of delusional thinking is most often described as being gradual and insidious. Patients have described an interest in psychic phenomena progressing to increasingly unusual preoccupations and then to bizarre beliefs "in which I believed wholeheartedly". One author wrote of their hallucinations: "they deceive, derange and force me into a world of crippling paranoia". In many cases, the delusional beliefs could be seen as fairly rational explanations for abnormal experiences: "I increasingly heard voices (which Id always call loud thoughts)... I concluded that other people were putting these loud thoughts into my head". Some cases have been described as an "auditory ransom note". | The relationship between an individual and their hallucinations is personal, and everyone interacts with their troubles in different ways. There are those who hear solely malevolent voices, solely benevolent voices, those that hear a mix of the two, and those that see them as either malevolent or benevolent and not believing the voice. Mood disorders and dementias
Mood disorders such as bipolar disorder and major depression have also been known to correlate with auditory hallucinations, but tend to be milder than their psychosis-induced counterpart. Auditory hallucinations are a relatively common sequelae of major neurocognitive disorders (formerly dementia) such as Alzheimers disease. Transient causes
Auditory hallucinations have been known to manifest as a result of intense stress, sleep deprivation, and drug use. Auditory hallucinations can also occur in mentally healthy individuals during the altered state of consciousness while falling asleep (hypnagogic hallucinations) and waking up (hypnopompic hallucinations).High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon. Intoxication of psychoactive drugs such as PCP, amphetamines, cocaine, marijuana and other substances can produce hallucinations in general, especially in high doses. Withdrawal from certain drugs such as alcohol, sedatives, hypnotics, anxiolytics, and opioids can also produce hallucinations, including auditory. Pathophysiology
The following areas of the brain have been found to be active during auditory hallucinations, through the use of fMRIs. | 11
|
Blood is collected from volunteer donors who agree to let doctors draw blood stem cells from their blood or bone marrow for transplantation. Blood that is taken straight from collected blood stem cells is known as peripheral blood stem cell donation. A peripheral stem cell donor must have the same blood type as the patient receiving the blood cells. Once the stem cells are in the patients body through an IV, the cells mature and become blood cells. Before donation, a drug is injected into the donor, which increases the number of stem cells into their body. Feeling cold and lightheaded, having numbness around the mouth and cramping in the hands are common symptoms during the donation process. After the donation, the amount of time for recovery varies for every donor, "But most stem cell donors are able to return to their usual activities within a few days to a week after donation". Epidemiology
For those with severe bone marrow failure, the cumulative incidence of resulting stem cell transplantation or death was greater than 70% by individuals 60 years of age. The incidence of bone marrow failure is triphasic: one peak at two to five years during childhood (due to inherited causes), and two peaks in adulthood, between 20 and 25 years old and after 60 years old (from acquired causes).One in ten individuals with bone marrow failure have unsuspected Fanconi anemia (FA). FA is the most common inherited bone marrow failure with an incidence of one to five episodes per million individuals. | Bone marrow failure occurs in individuals who produce an insufficient amount of red blood cells, white blood cells or platelets. Red blood cells transport oxygen to be distributed throughout the bodys tissue. White blood cells fight off infections that enter the body. Bone marrow also contains platelets, which trigger clotting, and thus help stop the blood flow when a wound occurs. Signs and symptoms
The two most common signs and symptoms of bone marrow failure are bleeding and bruising. Blood may be seen throughout the gums, nose or the skin, and tend to last longer than normal. Children have a bigger chance of seeing blood in their urine or stools, which results in digestive problems with an unpleasant scent. Individuals with this condition may also encounter tooth loss or tooth decay. Chronic fatigue, shortness of breath, and recurrent colds can also be symptoms of bone marrow failure. Causes
Bone marrow failure in both children and adults can be either inherited or acquired. Inherited bone marrow failure is often the cause in young children, while older children and adults may acquire the disease later in life. A maturation defect in genes is a common cause of inherited bone marrow failure. The most common cause of acquired bone marrow failure is aplastic anemia. Working with chemicals such as benzene could be a factor in causing the illness. Other factors include radiation or chemotherapy treatments, and immune system problems. Diagnosis
Treatment
The type of treatment depends on the severity of the patients bone marrow failure disease. Blood transfusion is one treatment. | 11
|
Four of the following seven specific symptoms should be present:
Avoids occupational activities that involve significant interpersonal contact, because of fears of criticism, disapproval, or rejection
is unwilling to get involved with people unless certain of being liked
shows restraint within intimate relationships because of the fear of being shamed or ridiculed
is preoccupied with being criticized or rejected in social situations
is inhibited in new interpersonal situations because of feelings of inadequacy
views self as socially inept, personally unappealing, or inferior to others
is unusually reluctant to take personal risk or to engage in any new activities because they may prove embarrassing
Differential diagnosis
In contrast to social anxiety disorder, a diagnosis of avoidant personality disorder (AvPD) also requires that the general criteria for a personality disorder be met. According to the DSM-5, avoidant personality disorder must be differentiated from similar personality disorders such as dependent, paranoid, schizoid, and schizotypal. But these can also occur together; this is particularly likely for AvPD and dependent personality disorder. Thus, if criteria for more than one personality disorder are met, all can be diagnosed.There is also an overlap between avoidant and schizoid personality traits (see Schizoid avoidant behavior) and AvPD may have a relationship to the schizophrenia spectrum.Avoidant personality disorder must also be differentiated from the autism spectrum, specifically Asperger syndrome. | Levocardia is where the heart is on the normal side of the body (the left), as opposed to dextrocardia, in which the heart is in the right side of the thoracic cavity. This can be associated with situs solitus, where the remainder of the organs are on normal side as well; or situs inversus, in which the viscera (stomach, liver, intestines, lungs, etc.) on the opposite side as normal. The latter condition may or may not be associated with clinically relevant abnormalities. See also
Isolated levocardia
References
== External links == | 0-1
|
Early experiments suggested that tennis elbow was primarily caused by overexertion. However, studies show that trauma such as direct blows to the epicondyle, a sudden forceful pull, or forceful extension cause more than half of these injuries. Repeatedly mis-hitting a tennis ball in the early stages of learning the sport causes shock to the elbow joint and may contribute to contracting the condition. Pathophysiology
Histological findings include granulation tissue, micro-rupture, degenerative changes, and there is no traditional inflammation. Therefore, the disorder is more appropriately referred to as tendinosis or tendinopathy—more accurately an enthesopathy—rather than tendinitis. There is no evidence of inflammation or repair.The extensor digiti minimi also has a small origin site medial to the elbow that this condition can affect. The muscle involves the extension of the little finger and some extension of the wrist allowing for adaption to "snap" or flick the wrist—usually associated with a racquet swing. Most often, the extensor muscles become painful due to tendon breakdown from over-extension. Improper form or movement allows for power in a swing to rotate through and around the wrist—creating a moment on that joint instead of the elbow joint or rotator cuff. This moment causes pressure to build impact forces to act on the tendon causing irritation and inflammation.Other speculative risk factors for lateral epicondylitis include taking up tennis later in life, unaccustomed strenuous activity, decreased mental chronometry and speed and repetitive eccentric contraction of muscle (controlled lengthening of a muscle group). Diagnosis
Physical examination
Diagnosis is based on symptoms and clinical signs that are discrete and characteristic. | For example, extension of the elbow and flexion of the wrist cause outer elbow pain. There is point tenderness at the origin of the extensor carpi radialis brevis muscle from the lateral epicondyle (extensor carpi radialis brevis origin), 1 cm distal and slightly anterior to the lateral epicondyle. There is also pain with resisted wrist extension (Cozens test). Medical imaging
Medical imaging is not necessary or helpful.X-rays can confirm and distinguish possibilities of existing causes of pain that are unrelated to tennis elbow, such as fracture or arthritis. Rarely, calcification can be found where the extensor muscles attach to the lateral epicondyle. Medical ultrasonography and magnetic resonance imaging (MRI) are other valuable tools for diagnosis but are frequently avoided due to the high cost.Longitudinal sonogram of the lateral elbow displays thickening and heterogeneity of the common extensor tendon that is consistent with tendinosis, as the ultrasound reveals calcifications, intrasubstance tears, and marked irregularity of the lateral epicondyle. Although the term “epicondylitis” is frequently used to describe this disorder, most histopathologic findings of studies have displayed no evidence of an acute, or a chronic inflammatory process. Histologic studies have demonstrated that this condition is the result of tendon degeneration, which replaces normal tissue with a disorganized arrangement of collagen. Treatment
In some cases, severity of tennis elbow symptoms mend without any treatment, within six to 24 months. Tennis elbow left untreated can lead to chronic pain that degrades quality of daily living. | 11
|
The buffer reactions are:
H
+
+
HCO
3
−
↽
−
−
⇀
H
2
CO
3
↽
−
−
⇀
CO
2
+
H
2
O
{\displaystyle {\ce {H+ + HCO3- <=> H2CO3 <=> CO2 + H2O}}}
The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:
pH
=
pK
a
+
L
o
g
[
HCO
3
−
]
[
CO
2
]
{\displaystyle {\text{pH}}={\text{pK}}_{a}+\mathop {\mathrm {Log} } {\frac {\left[{\text{HCO}}_{3}^{-}\right]}{\left[{\text{CO}}_{2}\right]}}}
Using Henrys law, we can say that [CO2] = 0.03 × PaCO2
(PaCO2 is the pressure of CO2 in arterial blood)
Adding the other normal values, we get
pH
=
6.1
+
L
o
g
[
24
0.03
×
40
]
{\displaystyle {\text{pH}}=6.1+\mathop {\mathrm {Log} } \left[{\frac {24}{0.03\times 40}}\right]}
=
6.1
+
1.3
{\displaystyle =6.1+1.3}
=
7.4
{\displaystyle =7.4}
Consequences
Acute Metabolic Acidosis
Acute Metabolic Acidosis most often occurs during hospitalizations, and acute critical illnesses. | Increased anion gap
Causes of increased anion gap include:
Lactic acidosis
Ketoacidosis (e.g., Diabetic, alcoholic, or starvation)
Chronic kidney failure
Transient 5-oxoprolinemia due to long-term ingestion of high-doses of acetaminophen (often seen with sepsis, liver failure, kidney failure, or malnutrition)
Intoxication:
Salicylates, methanol, ethylene glycol
Organic acids, paraldehyde, ethanol, formaldehyde
Carbon monoxide, cyanide, ibuprofen, metformin
Propylene glycol (metabolized to L and D-lactate and is often found in infusions for certain intravenous medications used in the intensive care unit)
Massive rhabdomyolysis
Isoniazid, iron, phenelzine, tranylcypromine, valproic acid, verapamil
Topiramate
SulfatesNormal anion gap
Causes of normal anion gap include
Inorganic acid addition
Infusion/ingestion of HCl, NH4Cl
Gastrointestinal base loss
Diarrhea
Small bowel fistula/drainage
Surgical diversion of urine into gut loops
Renal base loss/acid retention:
Proximal renal tubular acidosis
Distal renal tubular acidosisHyperalimentation
Addison disease
Acetazolamide
Spironolactone
Saline infusionTo distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the sum of the chloride and bicarbonate levels from the sum of the sodium and potassium levels. As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8–16 mmol/L (12±4). An elevated anion gap (i.e. > 16 mmol/L) can indicate particular types of metabolic acidosis, such as types caused by certain poisons, lactate acidosis, and ketoacidosis. It is important to note that the anion gap can be spuriously normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can also be increased due to relatively low levels of cations other than sodium and potassium (e.g. | 11
|
The zero result indicates the image was uniform (non-changing) within this small patch. Negative or positive sums mean the image was varying (changing) within this small patch of nine photoreceptors. The above matrix is only an approximation to what really happens inside the retina. The differences are:
The above example is called "balanced". The term balanced means that the sum of the negative weights is equal to the sum of the positive weights so that they cancel out perfectly. Retinal ganglion cells are almost never perfectly balanced. The table is square while the centre–surround structures in the retina are circular. Neurons operate on spike trains traveling down nerve cell axons. Computers operate on a single floating-point number that is essentially constant from each input pixel. (The computer pixel is basically the equivalent of a biological photoreceptor.) The retina performs all these calculations in parallel while the computer operates on each pixel one at a time. The retina performs no repeated summations and shifting as would a computer. Finally, the horizontal and amacrine cells play a significant role in this process, but that is not represented here.Here is an example of an input image and how edge detection would modify it. Once the image is spatially encoded by the centre–surround structures, the signal is sent out along the optic nerve (via the axons of the ganglion cells) through the optic chiasm to the LGN (lateral geniculate nucleus). The exact function of the LGN is unknown at this time. | In ON cells, an increment in light intensity in the centre of the receptive field causes the firing rate to increase. In OFF cells, it makes it decrease. In a linear model, this response profile is well described by a difference of Gaussians and is the basis for edge detection algorithms. Beyond this simple difference, ganglion cells are also differentiated by chromatic sensitivity and the type of spatial summation. Cells showing linear spatial summation are termed X cells (also called parvocellular, P, or midget ganglion cells), and those showing non-linear summation are Y cells (also called magnocellular, M, or parasol retinal ganglion cells), although the correspondence between X and Y cells (in the cat retina) and P and M cells (in the primate retina) is not as simple as it once seemed. In the transfer of visual signals to the brain, the visual pathway, the retina is vertically divided in two, a temporal (nearer to the temple) half and a nasal (nearer to the nose) half. The axons from the nasal half cross the brain at the optic chiasma to join with axons from the temporal half of the other eye before passing into the lateral geniculate body. Although there are more than 130 million retinal receptors, there are only approximately 1.2 million fibres (axons) in the optic nerve. So, a large amount of pre-processing is performed within the retina. The fovea produces the most accurate information. | 11
|
The NPC1 gene encodes a protein that is located in membranes inside the cell and is involved in the movement of cholesterol and lipids within cells. A deficiency of this protein leads to the abnormal buildup of lipids and cholesterol within cell membranes. The NPC2 gene encodes a protein that binds and transports cholesterol. It has been shown to closely interact with NPC1. "Type D" variant
Type D Niemann–Pick has only been found in the French Canadian population of Yarmouth County, Nova Scotia, and is now known to be allelic with Niemann–Pick type C.
Genealogical research indicates that Joseph Muise (c. 1679–1729) and Marie Amirault (1684 – c. 1735) are common ancestors to all people with Type D. This couple is the most likely origin for the type D variant. Pathophysiology
Niemann–Pick type C is biochemically, genetically and clinically distinct from Niemann–Pick Types A or and B. In Types A and B, there is complete or partial deficiency of the lysosomal enzyme called acid sphingomyelinase. In Niemann–Pick type C, the protein product of the major mutated gene NPC1 is not an enzyme but appears to function as a transporter in the endosomal-lysosomal system, which moves large water-insoluble molecules through the cell. The protein coded by the NPC2 gene more closely resembles an enzyme structurally but seems to act in cooperation with the NPC1 protein in transporting molecules in the cell. The disruption of this transport system results in the accumulation of cholesterol and glycolipids in lysosomes.Cholesterol and glycolipids have varied roles in the cell. | The request was approved by the FDA on September 23, 2010, and bi-monthly intrathecal injections of HPbCD into the spine were administered starting in October 2010.On December 25, 2010, the FDA granted approval for HPbCD to be delivered via IV to an additional patient, Peyton Hadley, aged 13, under an IND through Rogue Regional Medical Center in Medford, Oregon. Soon after in March 2011, approval was sought for similar treatment of his sibling, Kayla, age 11, and infusions of HPbCD began shortly after. Both have since begun intrathecal treatments beginning in January 2012.In April 2011, the National Institutes of Health (NIH), in collaboration with the Therapeutics for Rare and Neglected Diseases Program (TRND), announced they were developing a clinical trial utilizing cyclodextrin for Niemann–Pick type C patients.On September 20, 2011, the European Medicines Agency (EMA) granted HPbCD orphan drug status and designated the compound as a potential treatment for Niemann–Pick type C disease.On December 31, 2011, the FDA granted approval for IV HPbCD infusions for a fifth child in the United States, Chase DiGiovanni, under a compassionate use protocol. The child was 29 months old at the time of his first intravenous infusion, which was started in January 2012.Due to unprecedented collaboration between individual physicians and parents of children affected by NPC, approximately 15 patients worldwide have received HPbCD cyclodextrin therapy under compassionate use treatment protocols. Treatment involves a combination of intravenous therapy (IV), intrathecal therapy (IT) and intracerebroventricular (ICV) cyclodextrin therapy. | 11
|
Absorption of the phosphate forms involves their dephosphorylation catalyzed by the enzyme alkaline phosphatase. Most of the vitamin is taken up by the liver. There, the dephosphorylated vitamins are converted to the phosphorylated PLP, PNP and PMP, with the two latter converted to PLP. In the liver, PLP is bound to proteins, primarily albumin. The PLP-albumin complex is what is released by the liver to circulate in plasma. Protein-binding capacity is the limiting factor for vitamin storage. Total body stores, the majority in muscle, with a lesser amount in liver, have been estimated to be in the range of 61 to 167 mg.Enzymatic processes utilize PLP as a phosphate-donating cofactor. PLP is restored via a salvage pathway that requires three key enzymes, pyridoxal kinase, pyridoxine 5-phosphate oxidase, and phosphatases. Inborn errors in the salvage enzymes are known to cause inadequate levels of PLP in the cell, particularly in neuronal cells. The resulting PLP deficiency is known to cause or implicated in several pathologies, most notably infant epileptic seizures.The end-product of vitamin B6 catabolism is 4-pyridoxic acid, which makes up about half of the B6 compounds in urine. 4-Pyridoxic acid is formed by the action of aldehyde oxidase in the liver. Amounts excreted increase within 1–2 weeks with vitamin supplementation and decrease as rapidly after supplementation ceases. Other vitamin forms excreted in the urine include pyridoxal, pyridoxamine and pyridoxine, and their phosphates. When large doses of pyridoxine are given orally, the proportion of these other forms increases. | In 2001, MHLW enacted a new regulatory system, Foods with Health Claims (保健機能食品; FHC), which consists of the existing FOSHU system and the newly established Foods with Nutrient Function Claims (栄養機能表示食品; FNFC), under which claims were approved for any product containing a specified amount per serving of 12 vitamins, including vitamin B6, and two minerals. To make a health claim based on a foods vitamin B6 content, the amount per serving must be in the range of 0.3–25 mg. The allowed claim is: "Vitamin B6 is a nutrient that helps produce energy from protein and helps maintain healthy skin and mucous membranes. "In 2010, the European Food Safety Authority (EFSA) published a review of proposed health claims for vitamin B6, disallowing claims for bone, teeth, hair skin and nails, and allowing claims that the vitamin provided for normal homocysteine metabolism, normal energy-yielding metabolism, normal psychological function, reduced tiredness and fatigue, and provided for normal cysteine synthesis.The US Food and Drug Administration (FDA) has several processes for permitting health claims on food and dietary supplement labels. There are no FDA-approved Health Claims or Qualified Health Claims for vitamin B6. Structure/Function Claims can be made without FDA review or approval as long as there is some credible supporting science. Examples for this vitamin are "Helps support nervous system function" and "Supports healthy homocysteine metabolism." Absorption, metabolism and excretion
Vitamin B6 is absorbed in the jejunum of the small intestine by passive diffusion. Even extremely large amounts are well absorbed. | 11
|
The level of organisation varies: sometimes games are part of an official league, sometimes only friendly matches. The standard of play is below that of club cricket and often includes beginners to the sport. W
Waft
A loose non-committal shot, usually played to a ball pitched short of length and well wide of the off stump. Wag
when the tail (the lower order of the batting line-up) scores more runs than it is expected to, it is said to have wagged (as an extension of the animal tail metaphor)
Wagon wheel
1. a graphic which divides the field into six sectors (looking like the spoked wheel of a wagon), indicating how many runs a batsman has scored with shots into each sector. 2. see spider graph
Wait
a call by a batsman which defers the decision for a few seconds, before being followed by a call of yes or no. Used when it is unclear whether a fielder will reach the ball before it passes them. The batting partner should not begin a run, but remain ready to do so (including backing up) until the follow-up call. Walk
of a batsman, to walk off the pitch, knowing or believing that they are out, rather than waiting for an umpire to give them out (the umpire is required to intervene if they were not about to give an out decision). Generally considered to be sportsmanlike behaviour, but rarer in international cricket than domestic cricket. | Drift
the slight lateral curved-path movement that a spinner extracts while the ball is in flight. Considered very good bowling as it increases the difficulty for a batsman to correctly judge the precise movement and path of the ball . Drinks
an agreed short break in play, generally taken in the middle of a session, when refreshments are brought out to the players and umpires by the twelfth men of each side. Drinks breaks do not always need to take place, but they are usual in test matches, particularly in hot countries. Drinks waiter
a jocular term for the twelfth man, referring to his job of bringing out drinks. Drive
a shot played with a straight bat on the front foot, aiming anywhere between point on the off side and mid-wicket on the leg side. The drive is the most common shot for scoring runs, and often considered the most aesthetically pleasing. Several sub-types are recognised depending on direction, including the square drive, cover drive, off drive, straight drive and on drive. Drop
1. the accidental "dropping" of a ball that was initially caught by a fielder, thus denying the dismissal of the batsman; when such an event occurs, the batsman is said to have been "dropped". 2. the number of dismissals which occur in a teams innings before a given batsman goes in to bat; a batsman batting at first drop is batting at number three in the batting order, going in after one wicket has fallen. | 11
|
Conservative treatments
Initial treatment may include physical therapy, bracing, anti-inflammatory drugs, or corticosteroid injections to increase flexibility, endurance, and strength.Common anti-inflammatory drugs and painkillers prescribed for meniscus tears include acetaminophen, non-steroidal inflammatory drugs, and corticosteroids.Exercises can strengthen the muscles around the knee, especially the quadriceps. Stronger and bigger muscles will protect the meniscus cartilage by absorbing a part of the weight. The patient may be given paracetamol or anti-inflammatory medications. For patients selecting non-surgical treatment, physical therapy may reduce symptoms of pain and swelling. This type of rehabilitation focuses on maintenance of full range of motion and functional progression without aggravating symptoms. Physical therapists can employ electric stimulation, cold therapy, and ultrasonography. Accelerated rehabilitation programs can be as successful as the conservative program. The program reduces the time the patient spends using crutches and allows weight bearing activities. The less conservative approach allows the patient to apply a small amount of stress while protecting range of motion. It is likely that a patient with a peripheral tear can pursue the accelerated program, while a patient with a larger tear adopts the conservative program. The use of platelet rich plasma (PRP) to aid in the healing process has become widely accepted among US athletes. Although the procedure has grown in popularity, studies assessing the efficacy of PRP treatment have yielded contradictory results. Surgery
Arthroscopy is a surgical technique in which a joint is operated on using an endoscopic camera as opposed to open surgery on the joint. The meniscus can either be repaired or completely removed. | BAFF stimulates and extends the life of B lymphocytes, which produce antibodies against foreign and self-protein. It was approved by the FDA in March 2011. Genetically engineered immune cells are also being studied in animal models of the disease as of 2019.In September 2022, researchers at the University of Erlangen-Nuremberg published promising results using genetically altered immune cells to treat severely ill patients. Four women and one man received transfusions of CAR T cells modified to attack their B cells, eliminating the aberrant ones. The therapy drove the disease into remission in all five patients, who have been off lupus medication for several months after the treatment ended. See also
Canine discoid lupus erythematosus in dogs
List of people with lupus
References
External links
Lupus at Curlie
Systemic Lupus Erythematosus at the National Institute of Arthritis and Musculoskeletal and Skin Diseases | 0-1
|
In addition to the obvious risks (e.g., known exposure to a patient with MDR-TB), risk factors for MDR-TB include male sex, HIV infection, previous incarceration, failed TB treatment, failure to respond to standard TB treatment, and relapse following standard TB treatment. A large proportion of people with MDR-TB are unable to access treatment due to what Paul Farmer describes as an "Outcome Gap". The majority of people struck with MDR-TB live in "resource-poor settings" and are denied treatment because international organizations have refused to make technologies available to countries who cannot afford to pay for treatment, the reason being that second line drugs are to expensive therefore treatment methods for MDR-TB are not sustainable in impoverished nations. Farmer argues that this is social injustice and we cannot allow people to die simply because they are faced with circumstances where they cannot afford "effective therapy".Treatment of MDR-TB must be done on the basis of sensitivity testing: it is impossible to treat such patients without this information. If treating a patient with suspected MDR-TB, the patient should be started on SHREZ+MXF+cycloserine pending the result of laboratory sensitivity testing. A gene probe for rpoB is available in some countries and this serves as a useful marker for MDR-TB, because isolated RMP resistance is rare (except when patients have a history of being treated with rifampicin alone). If the results of a gene probe (rpoB) are known to be positive, then it is reasonable to omit RMP and to use SHEZ+MXF+cycloserine. | Has 82% incidence in diagnosis cases)However, in actuality, only a small percentage of patients experience all three symptoms, and the full triad occurs more frequently among those who have overused alcohol. Also a much more diverse range of symptoms has been found in patients with this condition, including:
pupillary changes, retinal hemorrhage, papilledema, impaired vision and hearing, vision loss
hearing loss,
fatigability, apathy, irritability, drowsiness, psycho and/or motor slowing
dysphagia, blush, sleep apnea, epilepsy and stupor
lactic acidosis
memory impairment, amnesia, depression, psychosis
hypothermia, polyneuropathy, hyperhidrosis.Although hypothermia is usually diagnosed with a body temperature of 35 °C / 95° Fahrenheit, or less, incipient cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can promote the development of an infection. The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. The lack of thiamine sometimes affects other major energy consumers, the myocardium, and also patients may have developed cardiomegaly. Heart failure with lactic acidosis syndrome has been observed. Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach, and are not classified as a separate disease. Infections have been pointed out as one of the most frequent triggers of death in WE. | 0-1
|
Schistosoma mansoni is a water-borne parasite of humans, and belongs to the group of blood flukes (Schistosoma). The adult lives in the blood vessels (mesenteric veins) near the human intestine. It causes intestinal schistosomiasis (similar to S. japonicum, S. mekongi, S. guineensis, and S. intercalatum). Clinical symptoms are caused by the eggs. As the leading cause of schistosomiasis in the world, it is the most prevalent parasite in humans. It is classified as a neglected tropical disease. As of 2021, the World Health Organization reports that 236.6 million people have schistosomiasis and most of it is due to S. mansoni. It is found in Africa, the Middle East, the Caribbean, Brazil, Venezuela and Suriname.Unlike other flukes (trematodes) in which sexes are not separate (monoecious), schistosomes are unique in that adults are divided into males and females, thus, gonochoric. However, a permanent male-female pair, a condition called in copula, is required to become adults; for this, they are considered as hermaphrodites. The life cycle of schistosomes includes two hosts: humans as definitive hosts, where the parasite undergoes sexual reproduction, and snails as intermediate hosts, where a series of asexual reproduction takes place. S. mansoni is transmitted through water, where freshwater snails of the genus Biomphalaria act as intermediate hosts. The larvae are able to live in water and infect the hosts by directly penetrating the skin. Prevention of infection is done by improved sanitation and killing the snails. Infection is treated with praziquantel. | For the first few weeks, those affected are usually advised to rest, change their activities, take pain medications, and stretch. If this is not sufficient, physiotherapy, orthotics, splinting, or steroid injections may be options. If these measures are not effective, additional measures may include extracorporeal shockwave therapy or surgery.Between 4% and 7% of the general population has heel pain at any given time: about 80% of these are due to plantar fasciitis. Approximately 10% of people have the disorder at some point during their life. It becomes more common with age. It is unclear if one sex is more affected than the other. Signs and symptoms
When plantar fasciitis occurs, the pain is typically sharp and usually unilateral (70% of cases). Bearing weight on the heel after long periods of rest worsens heel pain in affected individuals. Individuals with plantar fasciitis often report their symptoms are most intense during their first steps after getting out of bed or after prolonged periods of sitting. Symptoms typically improve with continued walking. Rare, but reported symptoms include numbness, tingling, swelling, or radiating pain. Typically there are no fevers or night sweats.If the plantar fascia is overused in the setting of plantar fasciitis, the plantar fascia can rupture. Typical signs and symptoms of plantar fascia rupture include a clicking or snapping sound, significant local swelling, and acute pain in the bottom of the foot. | 0-1
|
Anemia of prematurity (AOP) refers to a form of anemia affecting preterm infants with decreased hematocrit. AOP is a normochromic, normocytic hypoproliferative anemia. The primary mechanism of AOP is a decrease in erythropoietin (EPO), a red blood cell growth factor. Pathophysiology
Preterm infants are often anemic and typically experience heavy blood losses from frequent laboratory testing in the first few weeks of life. Although their anemia is multifactorial, repeated blood sampling and reduced erythropoiesis with extremely low serum levels of erythropoietin (EPO) are major causative factors. Blood sampling done for laboratory testing can easily remove enough blood to produce anemia. Obladen, Sachsenweger and Stahnke (1987) studied 60 very low birth weight infants during the first 28 days of life. Infants were divided into 3 groups, group 1 (no ventilator support, 24 ml/kg blood loss), group 2(minor ventilated support, 60 ml/kg blood loss), and group 3(ventilated support for respiratory distress syndrome, 67 ml/kg blood loss). Infants were checked for clinical symptoms and laboratory signs of anemia 24 hours before and after the blood transfusion. The study found that groups 2 and 3 who had significant amount of blood loss, showed poor weight gain, pallor and distended abdomen. These reactions are the most frequent symptoms of anemia in very low birth weight infants.During the first weeks of life, all infants experience a decline in circulating red blood cell (RBC) volume generally expressed as blood hemoglobin concentration (Hb). As anemia develops, there is even more of a significant reduction in the concentration of hemoglobin. | Pharmacokinetics
Brivaracetam exhibits linear pharmacokinetics over a wide dose range, is rapidly and completely absorbed after oral administration, has an elimination half-life of seven to eight hours, and has plasma protein binding of less than 20%. It is extensively metabolized (>90%), primarily via hydrolysis of the acetamide group, and secondarily through hydroxylation mediated by the liver enzyme CYP2C19. The three major metabolites (hydroxy, acid, and hydroxyacid) are pharmacologically inactive. Brivaracetam is eliminated as urinary metabolites, with over 95% of a radioactive test dose recovered in the urine within 72 hours, including only 8.6% as unchanged brivaracetam. Pharmacogenetics
As noted above, brivaracetam is primarily metabolized by hydrolysis, via amidase enzymes, to an inactive metabolite. To a lesser extent, it is also metabolized by a minor metabolic pathway via CYP2C19-dependent hydroxylation. Individuals who have no CYP2C19 enzyme activity, "CYP2C19 poor metabolizers", will have a greater exposure to standard doses of brivaracetam. Because they are less able to metabolize the drug to its inactive form for excretion, they may have an increased risk of adverse effects. The most common adverse effects of brivaracetam therapy include sedation, fatigue, dizziness, and nausea. The FDA-approved drug label for brivaracetam states that patients who are CYPC19 poor metabolizers, or are taking medicines that inhibit CYP2C19, may require a dose reduction. Chemical and physical properties
Brivaracetam is the 4R-propyl analogue of the anticonvulsant levetiracetam. | 0-1
|
In addition, patients with camptocormia often experience low back pain as a result of the condition. BSS often appears in individuals with Parkinsons disease, muscular dystrophies, endocrine disorders, inflammatory conditions (myositis), or mitochondrial myopathies. As previously mentioned, the disease is more common in older individuals. Pathology
When initially identified, camptocormia was classified as a psychogenic disease. Although the condition is sometimes a psychogenic manifestation, camptocormia typically originates from either muscular or neurological diseases. However, due to the wide variety of pathologies resulting in camptocormia, there is no singular cause that is most influential for the condition. Muscular origin
Myopathic origin BSS can be secondary to various muscular disorders or occur as a primary idiopathy. These etiologies are termed secondary and primary BSS respectively. Idiopathic primary BSS is a late-onset myopathy with progressive muscular weakness that is detected on the spinal extensor muscles in elderly patients and is more predominant in females. The pathogenesis of primary BSS is typically related to fibrosis and fatty infiltration of muscular tissues and to mitochondrial changes due to the aging process. Specifically, weakening occurs in the paravertebral muscles of patients. | Wheal may refer to:
Wheals, a type of skin lesion
Brad Wheal (born 1996), British cricketer
Donald James Wheal (1931–2008), British British television writer, novelist and non-fiction writer
David John Wheal, Australian businessman
"The Wheal", a 1987 song by Coil
See also
All pages with titles containing Wheal
Mining in Cornwall and Devon, includes mines whose names include Wheal
Wheel (disambiguation) | 0-1
|
The greatest period of growth is during the end of the second trimester, between 20–26 weeks.A measure of mass volume divided by head circumference, termed cystic adenomatoid malformation volume ratio (CVR) has been developed to predict the risk of hydrops. The lung mass volume is determined using the formula (length × width × anteroposterior diameter ÷ 2), divided by head circumference. With a CVR greater than 1.6 being considered high risk. Fetuses with a CVR less than 1.6 and without a dominant cyst have less than a 3% risk of hydrops. After delivery, if the patient is symptomatic, resection is mandated. If the infant is asymptomatic, the need for resection is a subject of debate, though it is usually recommended. Development of recurrent infections, rhabdomyosarcoma, adenocarcinomas in situ within the lung malformation have been reported. Treatment
In most cases, a fetus with CPAM is closely monitored during pregnancy and the CPAM is removed via surgery after birth. Most babies with a CPAM are born without complication and are monitored during the first few months. Many patients have surgery, typically before their first birthday, because of the risk of recurrent lung infections associated with CPAMs. Some pediatric surgeons can safely remove these lesions using very tiny incisions using minimally invasive surgical techniques (thoracoscopy). However, some CPAM patients live a full life without any complication or incident. It is hypothesized that there are thousands of people living with an undetected CPAM. Through ultrasound testing employed in recent years, many more patients are aware that they live with this condition. | Identifying characteristics on the sonogram include: an echogenic (bright) mass appearing in the chest of the fetus, displacement of the heart from its normal position, a flat or everted (pushed downward) diaphragm, or the absence of visible lung tissue.CPAMs are classified into three different types based largely on their gross appearance. Type I has a large (>2 cm) multiloculated cysts. Type II has smaller uniform cysts. Type III is not grossly cystic, referred to as the "adenomatoid" type. Microscopically, the lesions are not true cysts, but communicate with the surrounding parenchyma. Some lesions have an abnormal connection to a blood vessel from an aorta and are referred to as "hybrid lesions." Imaging
The earliest point at which a CPAM can be detected is by prenatal ultrasound. The classic description is of an echogenic lung mass that gradually disappears over subsequent ultrasounds. The disappearance is due to the malformation becoming filled with fluid over the course of the gestation, allowing the ultrasound waves to penetrate it more easily and rendering it invisible on sonographic imaging. When a CPAM is rapidly growing, either solid or with a dominant cyst, they have a higher incidence of developing venous outflow obstruction, cardiac failure and ultimately hydrops fetalis. If hydrops is not present, the fetus has a 95% chance of survival. When hydrops is present, risk of fetal demise is much greater without in utero surgery to correct the pathophysiology. | 11
|
Mastitis is inflammation of the breast or udder, usually associated with breastfeeding. Symptoms typically include local pain and redness. There is often an associated fever and general soreness. Onset is typically fairly rapid and usually occurs within the first few months of delivery. Complications can include abscess formation.Risk factors include poor latch, cracked nipples, use of a breast pump, and weaning. The bacteria most commonly involved are Staphylococcus and Streptococci. Diagnosis is typically based on symptoms. Ultrasound may be useful for detecting a potential abscess.Prevention is by proper breastfeeding techniques. When infection is present, antibiotics such as cephalexin may be recommended. Breastfeeding should typically be continued, as emptying the breast is important for healing. Tentative evidence supports benefits from probiotics. About 10% of breastfeeding women are affected. Types
When it occurs in breastfeeding mothers, it is known as puerperal mastitis, lactation mastitis, or lactational mastitis. When it occurs in non breastfeeding women it is known as non-puerperal or nonlactational. Mastitis can, in rare cases, occur in men. Inflammatory breast cancer has symptoms very similar to mastitis and must be ruled out. The symptoms are similar for puerperal and nonpuerperal mastitis but predisposing factors and treatment can be very different. Pregnancy related
Puerperal mastitis is the inflammation of the breast in connection with pregnancy, breastfeeding or weaning. Since one of the most prominent symptoms is tension and engorgement of the breast, it is thought to be caused by blocked milk ducts or milk excess. It is relatively common; estimates range depending on methodology between 5–33%. | RLS occurs in 3% of individuals from the Mediterranean or Middle Eastern regions, and in 1–5% of those from East Asia, indicating that different genetic or environmental factors, including diet, may play a role in the prevalence of this syndrome. RLS diagnosed at an older age runs a more severe course. RLS is even more common in individuals with iron deficiency, pregnancy, or end-stage kidney disease. The National Sleep Foundations 1998 Sleep in America poll showed that up to 25 percent of pregnant women developed RLS during the third trimester. Poor general health is also linked.There are several risk factors for RLS, including old age, family history, and uremia. The prevalence of RLS tends to increase with age, as well as its severity and longer duration of symptoms. People with uremia receiving renal dialysis have a prevalence from 20% to 57%, while those having kidney transplant improve compared to those treated with dialysis.RLS can occur at all ages, although it typically begins in the third or fourth decade. Genome‐wide association studies have now identified 19 risk loci associated with RLS. Neurological conditions linked to RLS include Parkinsons disease, spinal cerebellar atrophy, spinal stenosis, lumbosacral radiculopathy and Charcot–Marie–Tooth disease type 2. History
The first known medical description of RLS was by Sir Thomas Willis in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS. | 0-1
|
Patients may have hypertrophy, particularly of the legs, and may have lower bone mineral content and density in the legs.GSD-V patients may experience myogenic hyperuricemia (exercise-induced accelerated breakdown of purine nucleotides in skeletal muscle). The Purine Nucleotide Cycle (PNC) is activated when the ATP (energy) reservoir in muscle cells runs low, and is a part of Protein Metabolism. Adenine (a purine) is converted into AMP (adenosine monophosphate), IMP (inosine monophosphate), and S-AMP (adenylosuccinate) in a circular fashion; the byproducts are fumarate (which goes on to produce ATP via oxidative phosphorylation), ammonia (from the conversion of AMP into IMP), and uric acid (from excess IMP). To avoid health complications, GSD-V patients need to get their ATP (energy) primarily from Free Fatty Acids (Lipid Metabolism) rather than Protein Metabolism. Over-reliance on protein metabolism can be best avoided by not depleting the ATP reservoir, such as by not pushing through the pain and by not going too fast, too soon. "Be wary of pushing on when you feel pain start. This pain is a result of damaging muscles, and repeated damage will cause problems in the long term. But also this is counterproductive--it will stop you from getting into second wind. By pressing on despite the pain, you start your protein metabolism which then effectively blocks your glucose and fat metabolism. If you ever get into this situation, you need to stop completely for 30 minutes or more and then start the whole process again. | Glycogen storage disease type V (GSD5, GSD-V), also known as McArdles disease, is a metabolic disorder, one of the metabolic myopathies, more specifically a muscle glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as one in 100,000, roughly the same as glycogen storage disease type I.The disease was first reported in 1951 by Dr. Brian McArdle of Guys Hospital, London. Signs and symptoms
The onset of this disease is usually noticed in childhood, but often not diagnosed until the third or fourth decade of life. Symptoms include exercise intolerance with muscle pain, early fatigue, painful cramps, inappropriate rapid heart rate response to exercise, and may include myoglobin in the urine (often provoked by a bout of exercise). "In McArdles, our heart rate tends to increase in what is called an inappropriate response. That is, after the start of exercise it increases much more quickly than would be expected in someone unaffected by McArdles." Myoglobinuria may be seen due to the breakdown of skeletal muscle known as rhabdomyolysis, a condition in which muscle cells breakdown, sending their contents into the bloodstream. | 11
|
Supplementation with Vitamin C and Vitamin E was shown in one study to reduce the amount of sunburn after a controlled amount of UV exposure. A review of scientific literature through 2007 found that beta carotene (Vitamin A) supplementation had a protective effect against sunburn, but that the effects were only evident in the long-term, with studies of supplementation for periods less than 10 weeks in duration failing to show any effects. There is also evidence that common foods may have some protective ability against sunburn if taken for a period before the exposure. Protecting children
Babies and children are particularly susceptible to UV damage which increases their risk of both melanoma and non-melanoma skin cancers later in life. Children should not sunburn at any age and protective measures can ensure their future risk of skin cancer is reduced. Infants 0–6 months: Children under 6mo generally have skin too sensitive for sunscreen and protective measures should focus on avoiding excessive UV exposure by using window mesh covers, wide brim hats, loose clothing that covers skin, and reducing UV exposure between the hours of 10am and 4pm. Infants 6–12 months: Sunscreen can safely be used on infants this age. It is recommended to apply a broad-spectrum, water-resistant SPF 30+ sunscreen to exposed areas as well as avoid excessive UV exposure by using wide-brim hats and protective clothing. Toddlers and Preschool-aged children: Apply a broad-spectrum, water-resistant SPF 30+ sunscreen to exposed areas, use wide-brim hats and sunglasses, avoid peak UV intensity hours of 10am-4pm and seek shade. | Necrolytic acral erythema is a cutaneous condition that is a manifestation of hepatitis C viral infection or zinc deficiency.It is a papulosquamous and sometimes vesiculobullous eruption bearing clinical and histologic similarity to other necrolytic erythemas such as necrolytic migratory erythema, pseudoglucagonoma and nutritional deficiency syndromes. See also
List of cutaneous conditions
References
== External links == | 0-1
|
Restricted emotions and interpersonal functioning
Individuals with this disorder may display little affection and warmth; their relationships and speech tend to have a formal and professional approach, and not much affection is expressed even to loved ones, such as greeting or hugging a significant other at an airport or train station.They are extremely careful in their interpersonal interactions. They have little spontaneity when interacting with others, and ensure that their speech follows rigid and austere standards by excessively scrutinising it. They filter their speech for embarrassing or imperfect articulation, and they have a low bar for what they consider to be such. They lower their bar even further when they are communicating with their superiors or with a person of high status. Communication becomes a time-consuming and exhausting effort, and they start avoiding it altogether. Others regard them as cold and detached as a result.Their need for restricting affection is a defense mechanism used to control their emotions. They may expunge emotions from their memories and organize them as a library of facts and data; the memories are intellectualized and rationalized, not experiences that they can feel. This helps them avoid unexpected emotions and feelings and allows them to remain in control. They view self-exploration as a waste of time and have a patronising attitude towards emotional people. Interpersonal control
Individuals with OCPD are at one extreme of the conscientiousness continuum. While conscientiousness is a desirable trait generally, its extreme presentation for those with OCPD leads to interpersonal problems. | Periungual warts are warts that cluster around the fingernail or toenail. They appear as thickened, fissured cauliflower-like skin around the nail plate. Periungual warts often cause loss of the cuticle and paronychia. Nail biting increases susceptibility to these warts.Warts of this kind often cause damage to the nail either by lifting the nail from the skin or causing the nail to partially detach. If they extend under the nail, then the patient may suffer pain as a result. Sometimes periungual wart infections resemble the changes that are found in onychomycosis. In worst cases, if the infection causes injury or damage to the nail matrix, deformity in the nail may become permanent. As with other wart types, a number of treatments are available, including laser therapy, cryotherapy, salicylic acid, and other topical treatments. == References == | 0-1
|
United Kingdom
In the United Kingdom 10 per 100,000 people newly develop the condition a year while the number of people affected is 243 per 100,000. Approximately 146,000 people in the United Kingdom have been diagnosed with UC. History
The first description of ulcerative colitis occurred around the 1850s. Research
Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in people with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of people in the developed world may lead to inflammation. Both helminthic therapy and fecal microbiota transplant induce a characteristic Th2 white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction.Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human ICAM-1 messenger RNA through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. ICAM-1 propagates an inflammatory response promoting the extravasation and activation of leukocytes (white blood cells) into inflamed tissue. Increased expression of ICAM-1 has been observed within the inflamed intestinal mucosa of ulcerative colitis patients, where ICAM-1 over production correlated with disease activity. | Infliximab, ustekinumab, or vedolizumab are recommended in those with moderate or severe disease.A formulation of budesonide was approved by the U.S. Food and Drug Administration (FDA) for treatment of active ulcerative colitis in January 2013. In 2018, tofacitinib was approved for treatment of moderately to severely active ulcerative colitis in the United States, the first oral medication indicated for long term use in this condition. The evidence on methotrexate does not show a benefit in producing remission in people with ulcerative colitis. Cyclosporine is effective for severe UC and tacrolimus has also shown benefits. Aminosalicylates
Sulfasalazine has been a major agent in the therapy of mild to moderate ulcerative colitis for over 50 years. In 1977, it was shown that 5-aminosalicylic acid (5-ASA, mesalazine/mesalamine) was the therapeutically active component in sulfasalazine. Many 5-ASA drugs have been developed with the aim of delivering the active compound to the large intestine to maintain therapeutic efficacy but with reduction of the side effects associated with the sulfapyridine moiety in sulfasalazine. Oral 5-ASA drugs are particularly effective in inducing and in maintaining remission in mild to moderate ulcerative colitis. Rectal suppository, foam or liquid enema formulations of 5-ASA are used for colitis affecting the rectum, sigmoid or descending colon, and have been shown to be effective especially when combined with oral treatment. Biologics
Biologic treatments such as the TNF inhibitors infliximab, adalimumab, and golimumab are commonly used to treat people with UC who are no longer responding to corticosteroids. | 11
|
This usually happens with chronic obstruction of the bladder outlet or with diseases damaging the nerves supplying the urinary bladder. The urine stretches the bladder without the person feeling the pressure, and eventually, it overwhelms the ability of the urethral sphincter to hold it back. Mixed incontinence contains symptoms of multiple other types of incontinence. It is not uncommon in the elderly female population and can sometimes be complicated by urinary retention. Other types
Functional incontinence occurs when a person recognizes the need to urinate but cannot make it to the bathroom. The loss of urine may be large. There are several causes of functional incontinence including confusion, dementia, poor eyesight, mobility or dexterity, unwillingness to the toilet because of depression or anxiety or inebriation due to alcohol. Functional incontinence can also occur in certain circumstances where no biological or medical problem is present. For example, a person may recognize the need to urinate but may be in a situation where there is no toilet nearby or access to a toilet is restricted. Structural incontinence: Rarely, structural problems can cause incontinence, usually diagnosed in childhood (for example, an ectopic ureter). Fistulas caused by obstetric and gynecologic trauma or injury are commonly known as obstetric fistulas and can lead to incontinence. These types of vaginal fistulas include, most commonly, vesicovaginal fistula and, more rarely, ureterovaginal fistula. These may be difficult to diagnose. The use of standard techniques along with a vaginogram or radiologically viewing the vaginal vault with instillation of contrast media. | CAT intended to file an Investigational New Drug (IND) application for GCR-8015 in various CD22 positive B-cell malignancies, including Non-Hodgkin lymphoma and chronic lymphocytic leukemia, following a period of manufacturing development which is expected to be complete by the end of 2006 and to support the NCIs ongoing development of GCR-3888 in Hairy cell leukemia (HCL) and pediatric acute lymphoblastic leukemia (pALL).CAT-8015 exhibited a greater affinity for CD22 than its predecessor, CAT-3888 and CATs language such as "CAT will support the NCIs ongoing development of CAT-3888..." suggested at the time that their focus was on the second generation candidate.CAT was acquired by AstraZeneca, who also acquired MedImmune, combining the two into a biologics division. MedImmune renamed CAT-8015 to moxetumomab pasudotox.On 16 May 2013, AstraZeneca announced that CAT-8015 had started Phase III clinical trials. History
On 5 December 2008, orphan designation (EU/3/08/592) was granted by the European Commission to Medimmune Limited, United Kingdom, for murine anti-CD22 antibody variable region fused to truncated Pseudomonas exotoxin 38 for the treatment of hairy cell leukaemia. It was renamed to Moxetumomab pasudotox. The sponsorship was transferred to AstraZeneca AB, Sweden, in January 2019.On 17 July 2013, orphan designation (EU/3/13/1150) was granted by the European Commission to MedImmune Ltd, United Kingdom, for moxetumomab pasudotox for the treatment of B-lymphoblastic leukaemia / lymphoma. | 0-1
|
There may be a reduced but moderate number of cells and ducts enveloped in fibrous sheaths, as well as fibrous proliferation of the glands septa. The cytologic findings by themselves may not be specific, and the diagnosis requires adjunct consideration of both the ultrasonogram and clinical presentation. Application of magnetic resonance imaging (MRI) has been tried to non-invasively examine the morphological variations in Küttners tumor and differentiate them from those seen in malignant tumors; while MRI findings of the affected tissue and the pattern of cellular infiltration may offer some diagnostic clues for this condition, so far the results have been inconclusive. Existing treatment
Standard, and most effective, therapy to date is glandular sialadenectomy, which is associated with fairly low operative morbidity; however, in recent times, the administration of steroid (which can shrink the inflammatory lesion and is known to reduce serum IgG4 values) has been considered favorably, and may be useful in younger patients or those who refuse surgery. See also
Sialadenitis
References
== External links == | The transverse nasal crease or groove is a usually white line between the upper two-thirds and the lower third of the human nose (slightly above the cartilage tip between the bridge and nostrils). It can occur as the result of heredity, accident, or the constant rubbing or wiping of the nose, commonly referred to as the allergic salute. Occurrence
In addition to cases caused by heredity, physical injury, the transverse nasal crease is common in children and adults with chronic nasal allergies. People with allergies often use their hands to remove mucus from a runny nose or rub an itchy nose. As the hand slides upward, the tip of the nose is pressed up, thus creating the crease. Appearance
The appearance of the line depends on skin pigmentation. On lighter-skinned people, the transverse nasal crease is lighter in color than the surrounding skin, and may appear white. This is due to hypopigmentation resulting from the low level of melanin present in the damaged skin. In darker-skinned people, the line may appear darker than the surrounding skin. == References == | 0-1
|
There is growing consensus in the pediatric community that this disorder should be renamed "medical abuse" to highlight the harm caused by the deception and to make it less likely that the sufferer can use a psychiatric defense when harm is done. Diagnosis
Due to the behaviors involved, diagnosing factitious disorder is very difficult. If the healthcare provider finds no physical reason for the symptoms, they may refer the person to a psychiatrist or psychologist (mental health professionals who are specially trained to diagnose and treat mental illnesses). Psychiatrists and psychologists use thorough history, physical examinations, laboratory tests, imagery, and psychological testing to evaluate a person for physical and mental conditions. Once the persons history has been thoroughly evaluated, diagnosing factitious disorder imposed on self requires a clinical assessment. Clinicians should be aware that those presenting with symptoms (or persons reporting for that person) may exaggerate, and caution should be taken to ensure there is evidence for a diagnosis. Lab tests may be required, including complete blood count (CBC), urine toxicology, drug levels from blood, cultures, coagulation tests, assays for thyroid function, or DNA typing. In some cases CT scan, magnetic resonance imaging, psychological testing, electroencephalography, or electrocardiography may also be employed. | Band keratopathy is a corneal disease derived from the appearance of calcium on the central cornea. This is an example of metastatic calcification, which by definition, occurs in the presence of hypercalcemia. Signs and symptoms
Signs and symptoms of band keratopathy include eye pain and decreased visual acuity. Causes
Band keratopathy has several causes. These causes include uveitis, interstitial keratitis, superficial keratitis, phthisis, sarcoidosis, trauma, intraocular silicone oil, systemic diseases (high levels of calcium in the blood, vitamin D intoxication, Fanconis Syndrome, low levels of phosphorus in the blood, gout, milk-alkali syndrome, myotonic dystrophy, and chronic mercury exposure). Pathology
Band keratopathy is seen when there is calcification of the epithelial basement membrane, Bowmans membrane, and the anterior stroma with destruction of Bowmans membrane. The calcium salts are intracellular when the process is due to alteration of systemic calcium metabolism, whereas they are extracellular when due to local disease. Diagnosis
Band keratopathy is diagnosed by slit lamp examination of the eye. Treatment
Treatment is indicated if vision is threatened or if the eye is uncomfortable. It is important to recognize and treat any underlying condition. Improvement of vision may be obtained by scraping off the opacity. Topical disodium EDTA can be used as a chelating agent. It can also be removed with the excimer laser (phototherapeutic keratectomy). Other modalities include diamond burr and lamellar keratoplasty. References
== External links == | 0-1
|
Current treatment standards include the starting of a bisphosphonate to reduce future fracture risk by up to 50%. Epidemiology
Hip fractures are seen globally and are a serious concern at the individual and population level. By 2050, it is estimated that there will be six million cases of hip fractures worldwide. One study published in 2001 found that in the US alone, 310,000 individuals were hospitalized due to hip fractures, which can account for 30% of Americans who were hospitalized that year. Another study found that in 2011, femur neck fractures were among the most expensive conditions seen in US hospitals, with an aggregated cost of nearly $4.9 billion for 316,000 inpatient hospitalizations. Rates of hip fractures are declining in the United States, possibly due to increased use of bisphosphonates and risk management. Falling, poor vision, weight, and height are all seen as risk factors. Falling is one of the most common risk factors for hip fractures. Approximately 90% of hip fractures are attributed to falls from standing height.Given the high morbidity and mortality associated with hip fractures and the cost to the health system, in England and Wales, the National Hip Fracture Database is a mandatory nationwide audit of care and treatment of all hip fractures. Population
All populations experience hip fractures but numbers vary with race, gender, and age. Women have three times as many hip fractures as men. In a lifetime, men have an estimated 6% risk whereas postmenopausal women have an estimated 14% risk of having a hip fracture. | 70% of cryptorchid testes can be felt and are unable to be pulled into the scrotum or retreats quickly after being pulled into a higher position. In 30% of cases the testes cannot be felt indicating an intra-abdominal location. The risk factors for Cryptorchidism are:
A family history of the condition
Low birth weight
Prematurity
Poor semen quality
Poor semen quality is measured not only by the number of sperm a man produces but also by how effective the sperm is at fertilising an egg. The motility and shape of the sperm are important for this role. A man with poor semen quality will often present with fertility problems which is defined as a couple trying to conceive for over 1 year with no success. Diagnosis can be made from semen analysis, taking a sample of the mans semen and running tests to count numbers and quality of the individual sperm. Testicular cancer
The most common presentation of testicular cancer is a hard, painless lump which can be felt on one of the testis. It is either noticed by a clinician during a routine examination, or the patient themselves. Risk factors for TC include:
Cryptorchidism
Family history
Previous testicular cancerThe diagnosis is confirmed in different ways. An ultrasound scan can be used to diagnose to a 90-95% accuracy. Bloods can also be taken to look for elevated tumour markers which is also used to analyse the patients response to treatment. 80% of testicular cancer cases are from the 20-34 year old age range
== References == | 0-1
|
For instance, one of the main predictors of a successful recovery is dependent on the number of continuous days a user is able to stay off of the substance. Alternative holistic treatments such as physical exercise and Meditation has been proven effective in reducing cocaine cravings. Other non-pharmacological treatments such as acupuncture and hypnosis have been explored, but without conclusive results. Medications
Numerous medications have been investigated for use in cocaine dependence, but as of 2015, none of them were considered to be effective. Anticonvulsants, such as carbamazepine, gabapentin, lamotrigine, and topiramate, do not appear to be effective as treatment. Limited evidence suggests that antipsychotics are also ineffective for treatment of cocaine dependence. Few studies have examined bupropion (a novel antidepressant) for cocaine dependence; however, trials performed thus far have not shown it to be an effective form of treatment for this purpose.The National Institute on Drug Abuse (NIDA) of the U.S. National Institutes of Health is researching modafinil, a narcolepsy drug and mild stimulant, as a potential cocaine treatment. Ibogaine has been under investigation as a treatment for cocaine dependency and is used in clinics in Mexico, the Netherlands and Canada. It was legal for a time in Costa Rica, but has been illegal since 2018. It is illegal to use in many countries, such as Sweden, Norway, the United Kingdom, and in the United States. Other medications that have been investigated for this purpose include acetylcysteine, baclofen, and vanoxerine. Medications such as phenelzine, have been used to cause an "aversion reaction" when administered with cocaine. | The second phase, or withdrawal phase occurs 1–10 weeks after cocaine users quit, symptoms include: lethargy, anxiety, erratic sleep, strong craving, emotional lability, irritability, depression, poor concentration, and bowel issues. Finally the last phase or the extinction phase occurs up to 28 weeks after discontinued use, symptoms include: episodic cravings and some dysphoria. Epidemiology and prevalence rates
In the United States, past year cocaine users in 2019 was 5.5 million for people aged 12 or older. When broken into age groups, ages 12–17 had 97,000 users; ages 18–25 had 1.8 million users and ages 26 or older had 3.6 million users.Past year cocaine users with a cocaine use disorder in 2019 was 1 million for people aged 12 or older. When broken into age groups, ages 12–17 had 5,000 people with a cocaine use disorder; ages 18–25 had 250,000 people with a cocaine use disorder and ages 26 or older had 756,000 people with a cocaine use disorderIn the United States, cocaine use overdose deaths have been on the rise and in 2019, the CDC reported over 16,000 deaths from cocaine overdose. Risk
A study consisting of 1,081 U.S. residents who had first used cocaine within the previous 24 months was conducted. It was found that the risk of becoming dependent on cocaine within two years of first use was 5–6%. The risk of becoming dependent within 10 years of first use increased to 15–16%. These were the aggregate rates for all types of use considered, such as smoking, snorting, and injecting. | 11
|
An osteoclast (from Ancient Greek ὀστέον (osteon) bone, and κλαστός (clastos) broken) is a type of bone cell that breaks down bone tissue. This function is critical in the maintenance, repair, and remodeling of bones of the vertebral skeleton. The osteoclast disassembles and digests the composite of hydrated protein and mineral at a molecular level by secreting acid and a collagenase, a process known as bone resorption. This process also helps regulate the level of blood calcium. Osteoclasts are found on those surfaces of bone which are undergoing resorption. On such surfaces, the osteoclasts are seen to be located in shallow depressions called resorption bays (Howships lacunae). The resorption bays are created by erosive action of osteoclasts on the underlying bone. The border of the lower part of an osteoclast exhibits finger-like processes due to presence of deep infoldings of the cell membrane; this border is called ruffled border. The ruffled border lies in contact with the bone surface within a resorption bay. The periphery of the ruffled border is surrounded by a ring-like zone of cytoplasm which is devoid of cell organelles but is rich in actin filaments. This zone is called clear zone or sealing zone. The actin filaments enable the cell membrane surrounding the sealing zone to be anchored firmly to the bony wall of Howships lacunae. In this way, a closed subosteoclastic compartment is created between the ruffled border and the bone that is undergoing resorption. | The positioning of this "sealing zone" appears to be mediated by integrins expressed on the osteoclast surface. With the sealing zone in place, the multinucleated osteoclast reorganizes itself. Developing the highly invaginated ruffled membrane apposing the resorption compartment allows massive secretory activity. In addition, it permits the vesicular transcytosis of the mineral and degraded collagen from the ruffled border to the free membrane of the cell, and its release into the extracellular compartment. This activity completes the bone resorption, and both the mineral components and collagen fragments are released to the general circulation. Regulation
Osteoclasts are regulated by several hormones, including parathyroid hormone (PTH) from the parathyroid gland, calcitonin from the thyroid gland, and growth factor interleukin 6 (IL-6). This last hormone, IL-6, is one of the factors in the disease osteoporosis. Osteoporosis occurs when there is an imbalance between the bone resorption activities of osteoclasts and the bone formation activities of osteoblasts.Osteoclast activity is also mediated by the interaction of two molecules produced by osteoblasts, namely osteoprotegerin and RANK ligand. Note that these molecules also regulate differentiation of the osteoclast. Odontoclast
An odontoclast (/odon·to·clast/; o-don´to-klast) is an osteoclast associated with absorption of the roots of deciduous teeth. Alternate use of term
An osteoclast can also be an instrument used to fracture and reset bones (the origin is Greek osteon: bone and klastos: broken). To avoid confusion, the cell was originally termed osotoclast. When the surgical instrument went out of use, the cell became known by its present name. | 11
|
Common variable immunodeficiency (CVID) is an immune disorder characterized by recurrent infections and low antibody levels, specifically in immunoglobulin (Ig) types IgG, IgM and IgA. Symptoms generally include high susceptibility to foreign invaders, chronic lung disease, and inflammation and infection of the gastrointestinal tract. CVID affects males and females equally. The condition can be found in children or teens but is generally not diagnosed or recognized until adulthood. The average age of diagnosis is between 20 and 50. However, symptoms vary greatly between people. "Variable" refers to the heterogeneous clinical manifestations of this disorder, which include recurrent bacterial infections, increased risk for autoimmune disease and lymphoma, as well as gastrointestinal disease. CVID is a lifelong disease. Signs and symptoms
The symptoms of CVID vary between those affected. Its main features are hypogammaglobulinemia and recurrent infections. Hypogammaglobulinemia manifests as a significant decrease in the levels of IgG antibodies, usually alongside IgA antibodies; IgM antibody levels are also decreased in about half of those affected. Infections are a direct result of the low antibody levels in the circulation, which do not adequately protect them against pathogens. The microorganisms that most frequently cause infections in CVID are bacteria Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus. Pathogens less often isolated from those affected include Neisseria meningitidis, Pseudomonas aeruginosa, and Giardia lamblia. Infections mostly affect the respiratory tract (nose, sinuses, bronchi, lungs) and the ears; they can also occur at other sites, such as the eyes, skin, and gastrointestinal tract. | Psychiatry
A 2015 Cochrane review found no evidence of benefit in anxiety disorders as of 2015. Another review found preliminary evidence of benefit. Evidence for use in addiction is tentative but also unclear. Mechanism of action
Cycloserine works as an antibiotic by inhibiting cell-wall biosynthesis in bacteria. As a cyclic analogue of D-alanine, cycloserine acts against two crucial enzymes important in the cytosolic stages of peptidoglycan synthesis: alanine racemase (Alr) and D-alanine:D-alanine ligase (Ddl). The first enzyme is a pyridoxal 5-phosphate-dependent enzyme which converts the L-alanine to the D-alanine form. The second enzyme is involved in joining two of these D-alanine residues together by catalyzing the formation of the ATP-dependent D-alanine-D-alanine dipeptide bond between the resulting D-alanine molecules. If both of these enzymes are inhibited, then D-alanine residues cannot form and previously formed D-alanine molecules cannot be joined together. This effectively leads to inhibition of peptidoglycan synthesis. Chemical properties
Under mildly acidic conditions, cycloserine hydrolyzes to give hydroxylamine and D-serine. Cycloserine can be conceptualized as a cyclized version of serine, with an oxidative loss of dihydrogen to form the nitrogen-oxygen bond.Cycloserine is stable under basic conditions, with the greatest stability at pH = 11.5. History
The compound was first isolated nearly simultaneously by two teams. Workers at Merck isolated the compound, which they called oxamycin, from a species of Streptomyces. The same team prepared the molecule synthetically. Workers at Eli Lilly isolated the compound from strains of Streptomyces orchidaceus. It was shown to hydrolyze to serine and hydroxylamine. | 0-1
|
Cardiac complications can be life-threatening, but the heart muscle generally improves with weight gain, and the heart normalizes in size over weeks to months, with recovery. Atrophy of the heart muscle is a marker of the severity of the disease, and while it is reversible with treatment and refeeding, it is possible that it may cause permanent, microscopic changes to the heart muscle that increase the risk of sudden cardiac death. Individuals with anorexia nervosa may experience chest pain or palpitations; these can be a result of mitral valve prolapse. Mitral valve prolapse occurs because the size of the heart muscle decreases while the tissue of the mitral valve remains the same size. Studies have shown rates of mitral valve prolapse of around 20 percent in those with anorexia nervosa, while the rate in the general population is estimated at 2–4 percent. It has been suggested that there is an association between mitral valve prolapse and sudden cardiac death, but it has not been proven to be causative, either in patients with anorexia nervosa or in the general population. Relapse
Rates of relapse after treatment range from 9–52% with many studies reporting a relapse rate of at least 25%. Relapse occurs in approximately a third of people in hospital, and is greatest in the first six to eighteen months after release from an institution. Epidemiology
Anorexia is estimated to occur in 0.9% to 4.3% of women and 0.2% to 0.3% of men in Western countries at some point in their life. | Ceresin
A wax derived from the purification of the natural wax ozokerite.Lanolin alcohol
A subfraction of lanolin (wool wax), a mixture of hydrocarbons that imparts emulsifying properties and provides emollient (skin smoothing) properties. Lanolin alcohol is composed of cholesterol, other sterols, and free fatty acids. Moisturizers containing Cholesterol and fatty acid mixtures have been shown to provide skin benefits. Since this ingredient is sourced from wool from animals, this product is not suitable for vegans. Glycerin
A moisturizing factor (NMF) and humectant that attracts and binds moisture in the stratum corneum (outer-most layer of epidermis), helping to keep it hydrated. It is commonly used as a moisturizing agent in lotions, creams, and cosmetics. Most glycerin used in products in the U.S. comes from animals. If it is natural glycerin, it will typically be labeled ‘plant derived’.Panthenol
Also known as pro- Vitamin B5, when applied topically, has humectant properties and conditions the skin.Bisabolol
Derived from the Chamomile plant, bisabolol can have anti-inflammatory, anti-pruritic and healing effects in-vivo. See also
Medicine portal
References
External links
Official website | 0-1
|
Right ventricular (RVH) is a condition defined by an abnormal enlargement of the cardiac muscle surrounding the right ventricle. The right ventricle is one of the four chambers of the heart. It is located towards the lower-end of the heart and it receives blood from the right atrium and pumps blood into the lungs. Since RVH is an enlargement of muscle it arises when the muscle is required to work harder. Therefore, the main causes of RVH are pathologies of systems related to the right ventricle such as the pulmonary artery, the tricuspid valve or the airways. RVH can be benign and have little impact on day-to-day life or it can lead to conditions such as heart failure, which has a poor prognosis. Signs and symptoms
Symptoms
Although presentations vary, individuals with right ventricular hypertrophy can experience symptoms that are associated with pulmonary hypertension, heart failure and/or a reduced cardiac output. These include:
Difficulty breathing on exertion
Chest pain (angina) on exertion
Fainting (syncope) on exertion
General fatigue/lethargy
Dizziness
Feeling of fullness in the upper abdominal area
Discomfort or pain in the right upper abdomen
Reduced appetite
Swelling (oedema) of the legs, ankles or feet
Racing heart beat (palpitations)People may rarely present with the symptoms of Ortners syndrome, which include cough, haemoptysis and hoarseness. Signs
On physical examination, the most prominent features are due to the development of right-sided heart failure. These can include a raised jugular venous pressure, ascites, left parasternal heave and a tender, enlarged liver on palpation. | In the sense that it is associated with irresistible urges to perform unwanted repetitive behavior, trichotillomania is akin to some of these conditions, and rates of trichotillomania among relatives of OCD patients is higher than expected by chance. However, differences between the disorder and OCD have been noted, including: differing peak ages at onset, rates of comorbidity, gender differences, and neural dysfunction and cognitive profile. When it occurs in early childhood, it can be regarded as a distinct clinical entity.Because trichotillomania can be present in multiple age groups, it is helpful in terms of prognosis and treatment to approach three distinct subgroups by age: preschool age children, preadolescents to young adults, and adults.In preschool age children, trichotillomania is considered benign. For these children, hair-pulling is considered either a means of exploration or something done subconsciously, similar to nail-biting and thumb-sucking, and almost never continues into further ages.The most common age of onset of trichotillomania is between ages 9 and 13. In this age range, trichotillomania is usually chronic, and continues into adulthood. Trichiotillomania that begins in adulthood most commonly arises from underlying psychiatric causes.Trichotillomania is often not a focused act, but rather hair pulling occurs in a "trance-like" state; hence, trichotillomania is subdivided into "automatic" versus "focused" hair pulling. Children are more often in the automatic, or unconscious, subtype and may not consciously remember pulling their hair. | 0-1
|
An early recipient of warfarin was US President Dwight Eisenhower, who was prescribed the drug after having a heart attack in 1955.The exact mechanism of action remained unknown until it was demonstrated, in 1978, that warfarin inhibits the enzyme vitamin K epoxide reductase, and hence interferes with vitamin K metabolism.Lavrenty Beria and I. V. Khrustalyov are thought to have conspired to use warfarin to poison Soviet leader Joseph Stalin. Warfarin is tasteless and colourless, and produces symptoms similar to those that Stalin exhibited. Pest control
Rodents
Coumarins (4-hydroxycoumarin derivatives) are used as rodenticides for controlling rats and mice in residential, industrial, and agricultural areas. Warfarin is both odorless and tasteless, and is effective when mixed with food bait, because the rodents will return to the bait and continue to feed over a period of days until a lethal dose is accumulated (considered to be 1 mg/kg/day over about six days). It may also be mixed with talc and used as a tracking powder, which accumulates on the animals skin and fur, and is subsequently consumed during grooming. The LD50 for warfarin is 50–100 mg/kg for a single dose, after 5–7 days. LD50 1 mg/kg for repeated daily doses for 5 days, after 5–8 days. The IDLH value is 100 mg/m3 (warfarin; various species).The use of warfarin itself as a rat poison is now declining, because many rat populations have developed resistance to it, and poisons of considerably greater potency are now available. Resistance is due to an autosomal dominant on chromosome 1 in Norway rats. | Embolization
A thrombus may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel, which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. Venous thrombosis can lead to pulmonary embolism when the migrated embolus becomes lodged in the lung. In people with a "shunt" (a connection between the pulmonary and systemic circulation), either in the heart or in the lung, a venous clot can also end up in the arteries and cause arterial embolism.Arterial embolism can lead to obstruction of blood flow through the blood vessel that is obstructed by it, and a lack of oxygen and nutrients (ischemia) of the downstream tissue. The tissue can become irreversibly damaged, a process known as necrosis. This can affect any organ; for instance, arterial embolism of the brain is one of the causes of stroke. Prevention
The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding. In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired. Hence thromboprophylaxis (prevention of thrombosis) is increasingly emphasized. | 0-1
|
Lactose is often used as the primary filler (main ingredient) in most prescription and non-prescription solid pill form medications, though product labeling seldom mentions the presence of lactose or milk, and neither do product monograms provided to pharmacists, and most pharmacists are unaware of the very wide scale yet common use of lactose in such medications until they contact the supplier or manufacturer for verification. Milk substitutes
Plant-based milks and derivatives such as soy milk, rice milk, almond milk, coconut milk, hazelnut milk, oat milk, hemp milk, macadamia nut milk, and peanut milk are inherently lactose-free. Low-lactose and lactose-free versions of foods are often available to replace dairy-based foods for those with lactose intolerance. Lactase supplements
When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, then enzymatic lactase supplements may be used.Lactase enzymes similar to those produced in the small intestines of humans are produced industrially by fungi of the genus Aspergillus. The enzyme, β-galactosidase, is available in tablet form in a variety of doses, in many countries without a prescription. It functions well only in high-acid environments, such as that found in the human gut due to the addition of gastric juices from the stomach. Unfortunately, too much acid can denature it, so it should not be taken on an empty stomach. Also, the enzyme is ineffective if it does not reach the small intestine by the time the problematic food does. Lactose-sensitive individuals can experiment with both timing and dosage to fit their particular needs. | Lactose intolerance is different from a milk allergy. Management is typically by decreasing the amount of lactose in the diet, taking lactase supplements, or treating the underlying disease. People are able to drink at least one cup of milk without developing symptoms, with greater amounts tolerated if drunk with a meal or throughout the day.Worldwide, around 65% of adults are affected by lactose malabsorption. Other mammals usually lose the ability to digest lactose after weaning and this was the ancestral state of all humans before the recent evolution of lactase persistence, which extends lactose tolerance into adulthood. Lactase persistence evolved in several populations independently, probably as an adaptation to the domestication of dairy animals around 10,000 years ago. Today the prevalence of lactose tolerance varies widely between regions and ethnic groups. The ability to digest lactose is most common in people of European descent, and to a lesser extent in parts of the Middle East and Africa. Traditional food cultures reflect local variations in tolerance and historically many societies have adapted to low levels of tolerance by making dairy products that contain less lactose than fresh milk. The medicalization of lactose intolerance as a disorder has been attributed to biases in research history, since most early studies were conducted amongst populations which are normally tolerant, as well as the cultural and economic importance of milk in countries such as the United States. Terminology
Lactose intolerance primarily refers to a syndrome with one or more symptoms upon the consumption of food substances containing lactose sugar. | 11
|
Rifapentine, sold under the brand name Priftin, is an antibiotic used in the treatment of tuberculosis. In active tuberculosis it is used together with other antituberculosis medications. In latent tuberculosis it is typically used with isoniazid. It is taken by mouth.Common side effects include low neutrophil counts in the blood, elevated liver enzymes, and white blood cells in the urine. Serious side effects may include liver problems or Clostridium difficile associated diarrhea. It is unclear if use during pregnancy is safe. Rifapentine is in the rifamycin family of medication and works by blocking DNA-dependent RNA polymerase.Rifapentine was approved for medical use in the United States in 1998. It is on the World Health Organizations List of Essential Medicines. In many areas of the world it is not easy to get as of 2015. Medical uses
A systematic review of regimens for prevention of active tuberculosis in HIV-negative individuals with latent TB found that a weekly, directly observed regimen of rifapentine with isoniazid for three months was as effective as a daily, self-administered regimen of isoniazid for nine months. The three-month rifapentine-isoniazid regimen had higher rates of treatment completion and lower rates of hepatotoxicity. However, the rate of treatment-limiting adverse events was higher in the rifapentine-isoniazid regimen compared to the nine-month isoniazid regimen. Pregnancy
Rifapentine has been assigned a pregnancy category C by the U.S. Food and Drug Administration (FDA). Rifapentine in pregnant women has not been studied, but animal reproduction studies have resulted in fetal harm and were teratogenic. | CPNP belongs to the nitrosamine class of compounds, some of which are classified as probable or possible human carcinogens (substances that could cause cancer), based on laboratory tests such as rodent carcinogenicity studies. Although there are no data available to directly evaluate the carcinogenic potential of CPNP, information available on closely related nitrosamine compounds was used to calculate lifetime exposure limits for CPNP.As of January 2021, the FDA continues to investigate the presence of 1-methyl-4-nitrosopiperazine (MNP) in rifampin or 1-cyclopentyl-4-nitrosopiperazine (CPNP) in rifapentine approved for sale in the US. See also
Rifampicin
Isoniazid
Rifamycin
Rifabutin
References
External links
"Rifapentine". Drug Information Portal. U.S. National Library of Medicine. | 11
|
Unfortunately, due to a lack of overall known neurological knowledge, Molaisons surgeons removed his bilateral medial temporal lobe, causing profound AA and RA. The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system. HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory. Patients who have RA due to surgery are "P.B." and "F.C." who had unilateral removal of the medial areas in the left temporal lobe. Controlled induction
Clinically induced RA has been achieved using different forms of electrical induction. Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory. Tests show that information from days and weeks before the ECT can be permanently lost. The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation). Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects. Researchers induce RA in rats, for example, by giving daily ECS treatments. This is done to further understand RA. Brain structures
The most commonly affected areas are associated with episodic and declarative memory such as the hippocampus, the diencephalon, and the temporal lobes. | The reminder effect consists of re-exposing the patient to past personal information, which cannot reverse RA. Thus, reminding the patient about details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity. Case studies
Since researchers are interested in examining the effects of disrupted brain areas and conducting experiments for further understanding of an unaffected, normal brain, many individuals with brain damage have volunteered to undergo countless tests to advance our scientific knowledge of the human brain. For example, Henry Molaison (HM) was someone with significant brain damage and participated in a lot of neurological research. Furthermore, he was also the most tested person in neuropsychology. All living people who participate are referred to in literature using only their initials to protect privacy. Each case of RA has led to different symptoms and durations, where some patients have exhibited an inability to describe future plans, whether in the near future (e.g., this afternoon) or in the distant future (e.g., next summer) because of their inability to consolidate memories. Furthermore, researchers have also found that some patients can identify themselves and loved ones in photographs, but cannot determine the time or place the photo was taken. It has also been found that patients with RA greatly differ from the general population in remembering past events.A few case examples are:
After a head injury, AB had to relearn personal information. Many of ABs habits had also changed. | 11
|
Past and future patterns
Climatology and the study of mosquito-borne disease have been developed only over the past 100 years. Historical records of weather patterns and distinct symptoms associated with mosquito-borne diseases can be utilized to trace the prevalence of these diseases in relation to the climate over longer time periods. Further, statistical models are being created to predict the impact of climate change on vector-borne diseases using these past records, and these models can be utilized in the field of public health in order to create interventions to reduce the impact of these predicted outcomes. Two types of models are used to predict mosquito-borne disease spread in relation to climate: correlative models and mechanistic models. Correlative models focus primarily on vector distribution, and generally function in 3 steps. First, data is collected regarding geographical location of a target mosquito species. Next, a multivariate regression model establishes the conditions under which the target species can survive. Finally, the model determines the likelihood of the mosquito species to become established in a new location based on similar living conditions. The model can further predict future distributions based on environmental emissions data. Mechanistic models tend to be broader and include the pathogens and hosts in the analysis. These models have been used to recreate past outbreaks as well as predict the potential risk of a vector-borne disease based on an areas forecasted climate.Mosquito-borne diseases are currently most prevalent in East Africa, Latin America, Southeast Asia, and India. An emergence in Europe was recently observed. | The hexagonal pattern will only become visible when the carapace of the stage with square eyes is molted.The head also has an elongated, forward-projecting, stinger-like proboscis used for feeding, and two sensory palps. The maxillary palps of the males are longer than their proboscises, whereas the females’ maxillary palps are much shorter. In typical bloodsucking species, the female has an elongated proboscis. The thorax is specialized for locomotion. Three pairs of legs and a pair of wings are attached to the thorax. The insect wing is an outgrowth of the exoskeleton. The Anopheles mosquito can fly for up to four hours continuously at 1 to 2 km/h (0.6–1 mph), traveling up to 12 km (7.5 mi) in a night. Males beat their wings between 450 and 600 times per second.The abdomen is specialized for food digestion and egg development; the abdomen of a mosquito can hold three times its own weight in blood. This segment expands considerably when a female takes a blood meal. The blood is digested over time, serving as a source of protein for the production of eggs, which gradually fill the abdomen. Feeding by adults
Typically, both male and female mosquitoes feed on nectar, aphid honeydew, and plant juices, but in many species the mouthparts of the females are adapted for piercing the skin of animal hosts and sucking their blood as ectoparasites. | 11
|
The $875 million settlement broke down to $290 million for violating the Prescription Drug Marketing Act, $559.5 million to settle federal fraud charges for overcharging Medicare, and $25.5 million reimbursement to 50 states and Washington, D.C., for filing false claims with the states Medicaid programs. The case arose under the False Claims Act with claims filed by Douglas Durand, a former TAP vice president of sales, and Joseph Gerstein, a doctor at Tufts Universitys HMO practice. Durand, Gerstein, and Tufts shared $95 million of the settlement.There have since been various suits concerning leuprorelin use, none successful. They either concern the oversubscription of the drug or undue warning about the side effects. Between 2010 and 2013, the FDA updated the Lupron drug label to include new safety information on the risk of thromboembolism, loss of bone density and convulsions. The FDA then asserted that the benefits of leuprorelin outweigh its risks when used according to its approved labeling. Since 2017, the FDA has been evaluating leuprorelins connection to pain and discomfort in musculoskeletal and connective tissue. "Lupron protocol"
A 2005 paper in the controversial and non-peer reviewed journal Medical Hypotheses suggested leuprorelin as a possible treatment for autism, the hypothetical method of action being the now defunct hypothesis that autism is caused by mercury, with the additional unfounded assumption that mercury binds irreversibly to testosterone and therefore leuprorelin can help cure autism by lowering the testosterone levels and thereby mercury levels. However, there is no scientifically valid or reliable research to show its effectiveness in treating autism. | Society and culture
Legal status
On 24 March 2022, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Camcevi, intended for the treatment of the cancer of the prostate in adult men when the cancer is "hormone-dependent", which means that it responds to treatments that reduce the levels of the hormone testosterone. The applicant for this medicinal product is Accord Healthcare S.L.U. Names
Leuprorelin is the generic name of the drug and its INN and BAN, while leuprorelin acetate is its BANM and JAN, leuprolide acetate is its USAN and USP, leuprorelina is its DCIT, and leuproréline is its DCF. It is also known by its developmental code names A-43818, Abbott-43818, DC-2-269, and TAP-144.Leuprorelin is marketed by Bayer AG under the brand name Viadur, by Tolmar under the brand names Eligard and Fensolvi, and by TAP Pharmaceuticals (1985–2008), by Varian Darou Pajooh under the brand name Leupromer and Abbott Laboratories (2008–present) under the brand name Lupron. Controversy
In October 2001, the US Department of Justice, states attorneys general, and TAP Pharmaceutical Products, a subsidiary of Abbott Laboratories, settled criminal and civil charges against TAP related to federal and state medicare fraud and illegal marketing of the drug leuprorelin. TAP paid a total of $875 million, which was a record high at the time. | 11
|
Biopsies for routine histologic examination and direct immunofluorescence are useful for distinguishing these disorders from oral LP. Graft-versus-host disease (GVHD)
Lacy, reticulated plaques or erosions that resemble oral LP may occur in GVHD. The histologic findings of these disorders are also similar. The patient history is useful for differentiating chronic GVHD from oral LP. Oral involvement in acute GVHD is less well characterized than chronic GVHD, but has been associated with erythematous, erosive, ulcerative, or lichenoid oral lesions. Leukoplakia
Leukoplakia is a manifestation of squamous epithelial hyperplasia that may be a precursor to oral squamous cell carcinoma. White patches or plaques usually appear on the oral mucosa. To rule out malignancy, a biopsy of leukoplakia is indicated. Oral squamous cell carcinoma
Oral squamous cell carcinoma (SCC) can present as erythematous or white patches, ulcers, or exophytic masses. The highest risk for oral SCC may occur in patients with erythematous or erosive oral LP. A biopsy is indicated. Leukoedema
Leukoedema is a common, benign finding in the oral cavity that presents as white-gray, somewhat translucent plaques on the mucosa. The buccal mucosa is the most common site for involvement. Symptoms are absent, and no treatment is necessary. Oropharyngeal candidiasis
Oropharyngeal candidiasis (also known as thrush) is a common infection that has a predilection for infants, older adults with dentures, immunosuppressed individuals, and individuals utilizing intraoral corticosteroid therapy. Patients present with white plaques or erythematous patches on the buccal mucosa, palate, tongue, or oropharynx that may be mistaken for reticular LP. | Mucosal forms are those affecting the lining of the gastrointestinal tract (mouth, pharynx, esophagus, stomach, anus), larynx, and other mucosal surfaces including the genitals, peritoneum, ears, nose, bladder and conjunctiva of the eyes. Pattern
Lichen planus lesions can occur in many different forms:
Overlap syndromes
Occasionally, lichen planus is known to occur with other conditions. For example:
Lupus erythematosus overlap syndrome. Lesions of this syndrome share features of both lupus erythematosus and lichen planus. Lesions are usually large and hypopigmented, atrophic, and with a red to blue colour and minimal scaling. Telangectasia may be present. Lichen sclerosus overlap syndrome, sharing features of lichen planus and lichen sclerosus. Signs and symptoms
Although lichen planus can present with a variety of lesions, the most common presentation is as a well defined area of purple-coloured, itchy, flat-topped papules with interspersed lacy white lines (Wickhams striae). This description is known as the characteristic "6 Ps" of lichen planus: planar (flat-topped), purple, polygonal, pruritic, papules, and plaques. This rash, after regressing, is likely to leave an area of hyperpigmentation that slowly fades. That said, a variety of other lesions can also occur. Skin
Variants of cutaneous lichen planus are distinguished based upon the appearance of the lesions and/or their distribution. Lesions can affect the:
Extremities (face, dorsal hands, arms, and nape of neck). This is more common in Middle Eastern countries in spring and summer, where sunlight appears to have a precipitating effect. Palms and soles
Intertriginous areas of the skin. This is also known as "inverse lichen planus." | 11
|
The unspoken assumption is that by the age of five, unusual behaviors will either resolve or develop into diagnosable autism. However, some parents view the PDD label as no more than a euphemism for autism spectrum disorders, problematic because this label makes it more difficult to receive aid for early childhood intervention. Classification
The pervasive developmental disorders were:
Pervasive developmental disorder not otherwise specified (PDD-NOS), which includes atypical autism, and is the most common (47% of autism diagnoses);
Typical autism, the best-known;
Asperger syndrome (9% of autism diagnoses);
Rett syndrome; and
Childhood disintegrative disorder (CDD).The first three of these disorders are commonly called the autism spectrum disorders; the last two disorders are much rarer, and are sometimes placed in the autism spectrum and sometimes not.In May 2013, the Diagnostic and Statistical Manual–5th Edition (DSM-V) was released, updating the classification for pervasive developmental disorders. The grouping of disorders, including PDD-NOS, Autism, Asperger Syndrome, Rett Syndrome, and CDD, has been removed and replaced with the general term of Autism Spectrum Disorders. The American Psychiatric Association has concluded that using the general diagnosis of ASD supports more accurate diagnoses. The combination of these disorders was also fueled by the standpoint that Autism is characterized by common symptoms and should therefore bear a single diagnostic term. In order to distinguish between the different disorders, the DSM-V employs severity levels. The severity levels take into account required support, restricted interests and repetitive behaviors, and deficits in social communication. PDD and PDD-NOS
There is a division among doctors on the use of the term PDD. | Treatment
Medications are used to address certain behavioral problems; therapy for children with PDD should be specialized according to the childs specific needs.Some children with PDD benefit from specialized classrooms in which the class size is small and instruction is given on a one-to-one basis. Others function well in standard special education classes or regular classes with support. Early intervention, including appropriate and specialized educational programs and support services, play a critical role in improving the outcome of individuals with PDD. See also
Infantile neuroaxonal dystrophy
Multiple complex developmental disorder
Multisystem developmental disorder
Overactive disorder associated with mental retardation and stereotyped movements
References
External links
CDCs "Learn the Signs. Act Early." campaign - Information for parents on early childhood development and developmental disabilities
NINFS Pervasive Developmental Disorders Information Page | 11
|
Lipedema is a condition that is almost exclusively found in women and results in enlargement of both legs due to deposits of fat under the skin. Women of any weight may develop lipedema and the fat associated with lipedema is resistant to traditional weight-loss methods. There is no cure and typically it gets worse over time, pain may be present, and patients bruise easily. Over time mobility may be reduced, and due to reduced quality of life, patients often experience depression. In severe cases the trunk and upper body may be involved. Lipedema is commonly misdiagnosed and is now becoming known as lipoalgia due to there being no oedema.The cause is unknown but is believed to involve genetics and hormonal factors. It often runs in families; having a family member with the condition is a risk factor for developing it. Other conditions that may present similarly include lipohypertrophy, chronic venous insufficiency, and lymphedema. It is estimated to affect up to 11% of women. Onset is typically during puberty, pregnancy, or menopause.The fat associated with lipedema is shown to be resistant to weight loss methods; however, unlike other fat, lipedema is not associated with increased risks of diabetes or cardiovascular disease. Physiotherapy may help to preserve mobility for a little longer than would otherwise be the case. Exercise, only as much as the patient is able to do without causing damage to the joints, may help with overall fitness but will not prevent progression of the disease. | Unlike lipedema, which occurs primarily in the trunk and legs, the fatty growths can occur anywhere on the body. Treatment
A number of treatments may be useful including physiotherapy and light exercise which does not put undue stress on the lymphatic system. The two most common conservative treatments are manual lymphatic drainage (MLD) where a therapist gently opens lymphatic channels and moves the lymphatic fluid using hands-on techniques, and compression garments that keep the fluid at bay and assist the sluggish lymphatic flow.The use of surgical techniques is not universal but research has shown positive results in both short-term and long-term studies regarding lymph-sparing liposuction and lipectomy.The studies of highest quality involve tumescent local anesthesia (TLA), often referred to as simply tumescent liposuction. This can be accomplished via both Suction-Assisted Liposuction (SAL) and Power-Assisted (vibrating) liposuction. The treatment of lipedema with tumescent liposuction may require multiple procedures. While many health insurance carriers in the United States do not reimburse for liposuction for lipedema, in 2020 several carriers regard the procedure as reconstructive and medically necessary and do reimburse. Water Assisted Liposuction (WAL) is technically not considered to be tumescent but achieves the same goal as the anesthetic solution is injected as part of the procedure rather than before-hand. Developed by Doctor Ziah Taufig from Germany, it is usually performed under general anesthesia and is also considered to be lymph-sparing and protective of other tissues such blood vessels. Prognosis
There is no cure. | 11
|
Blocking of the eustachian tube leads to decreased pressure in the middle ear relative to the external ear, and this causes decreased motion of both the ossicles and the tympanic membrane. Acute or Serous otitis media
Chronic suppurative otitis media (CSOM)
Perforated eardrum
Tympanosclerosis or scarring of the eardrum
Cholesteatoma
Eustachian Tube Dysfunction, inflammation or mass within the nasal cavity, middle ear, or eustachian tube itself
Otosclerosis, abnormal growth of bone in or near the middle ear
Middle ear tumour
Ossicular discontinuity as a consequence of infection or temporal bone trauma
Congenital malformation of the ossicles. This can be an isolated phenomenon or can occur as part of a syndrome where development of the 1st and 2nd branchial arches is seen such as in Goldenhar syndrome, Treacher Collins syndrome, branchio-oto-renal syndrome etc. Barotrauma unequal air pressures in the external and middle ear. This can temporarily occur, for example, by the environmental pressure changes as when shifting altitude, or inside a train going into a tunnel. It is managed by any of various methods of ear clearing manoeuvres to equalize the pressures, like swallowing, yawning, or the Valsalva manoeuvre. More severe barotrauma can lead to middle ear fluid or even permanent sensorineural hearing loss. Inner ear
Third window effect caused by:
Superior canal dehiscence – which may require surgical correction. Enlarged vestibular aqueduct
Labyrinthine fistula
Presentation
Conductive hearing loss makes all sounds seem faint or muffled. The hearing loss is usually worse in lower frequencies. Congenital conductive hearing loss is identified through newborn hearing screening or may be identified because the baby has microtia or other facial abnormalities. | On an audiogram, the "x" represents responses in the left ear at each frequency, while the "o" represents responses in right ear at each frequency. CT scan
Most causes of conductive hearing loss can be identified by examination but if it is important to image the bones of the middle ear or inner ear then a CT scan is required. CT scan is useful in cases of congenital conductive hearing loss, chronic suppurative otitis media or cholesteatoma, ossicular damage or discontinuity, otosclerosis and third window dehiscence. Specific MRI scans can be used to identify cholesteatoma. Pathophysiology
Management
Management falls into three modalities: surgical treatment, pharmaceutical treatment, and supportive, depending on the nature and location of the specific cause. In cases of infection, antibiotics or antifungal medications are an option. Some conditions are amenable to surgical intervention such as middle ear fluid, cholesteatoma, and otosclerosis. If conductive hearing loss is due to head trauma, surgical repair is an option. If absence or deformation of ear structures cannot be corrected, or if the patient declines surgery, hearing aids which amplify sounds are a possible treatment option. Bone conduction hearing aids are useful as these deliver sound directly, through bone, to the cochlea or organ of hearing bypassing the pathology. These can be on a soft or hard headband or can be inserted surgically, a bone anchored hearing aid, of which there are several types. Conventional air conduction hearing aids can also be used. See also
Hearing loss
Sensorineural hearing loss
References
== External links == | 11
|
They are usually organised in an orderly manner and densely compacted.Genetics is one of the causing factors of loose anagen syndrome. It has been studied that this hair condition is autosomal dominantly inherited. Diagnosis
Patients with loose anagen syndrome do not report the same hair abnormalities. Loose anagen syndrome is usually diagnosed after taking into consideration the physical examination, clinical history and a microscopic examination of the hairs of the patient. Some patients visit a dermatologist for diagnosis and to distinguish between loose anagen hair syndrome and other conditions that it can be misdiagnosed for.A pull test is performed in order to diagnose a patient with loose anagen hair syndrome as one of the characteristics of this hair condition is hair that is easily removed from the scalp. A group of around 40-60 hairs, that are attached to the scalp, is pulled in a clement manner. The patient will be diagnosed with loose anagen syndrome if great amounts of hair is detached from the head. If at least 50% of the hairs removed is at the anagen hair stage, the outcome of the pull test is positive. The detachment of only 4-6 hairs is considered a normal outcome, as approximately 10% of the hairs on the scalp are at the telogen stage. The removed loose anagen hairs are not fragile and are of normal tensile strength.In an electron microscope image of a loose anagen hair, deformities such as grooves, curls and ridges are visible in the hair shaft, which is made from keratin. | Aphonia is defined as the inability to produce voiced sound. Damage to the nerve may be the result of surgery (e.g., thyroidectomy) or a tumor.Aphonia means "no sound". In other words, a person with this disorder has lost their voice. Causes
Injuries are often the cause of aphonia. Minor injuries can affect the second and third dorsal area in such a manner that the lymph patches concerned with coordination become either atrophic or relatively nonfunctioning. Tracheotomy can also cause aphonia.Any injury or condition that prevents the vocal cords, the paired bands of muscle tissue positioned over the trachea, from coming together and vibrating will have the potential to make a person unable to speak. When a person prepares to speak, the vocal folds come together over the trachea and vibrate due to the airflow from the lungs. This mechanism produces the sound of the voice. If the vocal folds cannot meet together to vibrate, sound will not be produced. Aphonia can also be caused by and is often accompanied by fear. Psychogenic
Psychogenic aphonia is often seen in patients with underlying psychological problems. Laryngeal examination will usually show bowed vocal folds that fail to adduct to the midline during phonation. However, the vocal folds will adduct when the patient is asked to cough. Treatment should involve consultation and counseling with a speech pathologist and, if necessary, a psychologist.In this case, the patients history and the observed unilateral immobility rules out function aphonia. See also
Muteness
Lists of language disorders
References
External links
Muscle Tension Aphonia Video Example | 0-1
|
The arthritis may also involve the spine, leading to ankylosing spondylitis if the entire spine is involved, or simply sacroiliitis if only the sacroiliac joint is involved. The symptoms of arthritis include painful, warm, swollen, stiff joints, and loss of joint mobility or function.Crohns disease increases the risk of osteoporosis or thinning of the bones. Individuals with osteoporosis are at increased risk of bone fractures. Dermatological
Crohns disease may also involve the skin, blood, and endocrine system. Erythema nodosum is the most common type of skin problem, occurring in around 8% of people with Crohns disease, producing raised, tender red nodules usually appearing on the shins. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue, and is characterized by septal panniculitis.Pyoderma gangrenosum is a less common skin problem, occurring in under 2%, and is typically a painful ulcerating nodule.Clubbing, a deformity of the ends of the fingers, may also be a result of Crohns disease. Other very rare dermatological manifestations include: Pyostomatitis vegetans, Psoriasis, Erythema multiforme, Epidermolysis bullosa acquista (described in a case report), and Metastatic CD (the spread of Crohns inflammation to the skin). It is unknown if Sweets Syndrome is connected to Crohns disease.Neurological
Crohns disease can also cause neurological complications (reportedly in up to 15%). The most common of these are seizures, stroke, myopathy, peripheral neuropathy, headache, and depression.Central and peripheral neurological disorders are described in patients with IBD and include peripheral neuropathies, myopathies, focal central nervous system defects, convulsions, confusional episodes, meningitis, syncope, optic neuritis, and sensorineural loss. | All this new knowledge in the pathogenesis of Crohns disease allows us to put this multifactorial disease in the group of autoinflammatory syndromes.Some examples of how the innate immune system affects bowel inflammation have been described. A meta-analysis of CD genome-wide association studies revealed 71 distinct CD-susceptibility loci. Interestingly, three very important CD-susceptibility genes (the intracellular pathogen-recognition receptor, NOD2; the autophagy-related 16-like 1, ATG16L1 and the immunity-related GTPase M, IRGM) are involved in innate immune responses against gut microbiota, while one (the X-box binding protein 1) is involved in regulation of the [adaptive] immune pathway via MHC class II, resulting in autoinflammatory inflammation. Studies have also found that increased ILC3 can overexpress major histocompatibility complex (MHC) II. MHC class II can induce CD4+ T cell apoptosis, thus avoiding the T cell response to normal bowel micro bacteria. Further studies of IBD patients compared with non-IBD patients found that the expression of MHC II by ILC3 was significantly reduced in IBD patients, thus causing an immune reaction against intestinal cells or normal bowel bacteria and damaging the intestines. This can also make the intestines more susceptible to environmental factors, such as food or bacteria.The thinking is, that because Crohns disease has strong innate immune system involvement and has NOD2 mutations as a predisposition, Crohns disease is more likely an autoinflammatory disease than an autoimmune disease. Immunodeficiency theory
A substantial body of data has emerged in recent years to suggest that the primary defect in Crohns disease is actually one of relative immunodeficiency. | 11
|
Paraneoplastic pemphigus (PNP) is an autoimmune disorder stemming from an underlying tumor. It is hypothesized that antigens associated with the tumor trigger an immune response resulting in blistering of the skin and mucous membranes. While patients with malignant and benign tumors are both at risk, malignancy is associated with high mortality rates (near 90%). Current treatment focuses on general wound healing and administering corticosteroids, which has not demonstrated a high success rate. Recent research developments aim to treat the underlying tumor in order to alleviate the symptoms of PNP. Signs and symptoms
While the presence of lesions is the denominator among patients with PNP, the characteristics of the lesions differ. The five clinical presentations of lesions associated with PNP include:
"Pemphigus-like": Flaccid blister (discrete), crusts over the raw exuding skin lesions
"Pemphigoid-like": Tense blister(s) on brick red erythema
"Erythema multiforme-like": Severe polymorphic skin and/or mucous membrane lesions
"Graft-vs.-host disease-like": Widespread lichenoid eruption with severe mucous membrane involvement
"Lichen planus-like": Small red flat-topped scaly papulesIt is most common that mucous membrane lesions of the oral cavity are presented first. They can involve the oropharynx, nasopharynx, tongue, and vermilion (red portion) of the lips. They are also known to develop in the conjunctiva of the eye, anogenital (perineum) region, and esophagus. Cutaneous lesions tend to follow the onset of mucosal lesions. The blisters often erupt in waves, usually affecting the upper trunk, head, neck, and proximal extremities. Pemphigoid-like lesions are seen more often on the extremities. | It has proven to be effective among auto-immune diseases, but the correct administration process for treating PNP is yet to be defined. The results of the study demonstrated varying levels of remission. References
Notes
== External links == | 11
|
Propionic acidemia, also known as propionic aciduria or propionyl-CoA carboxylase deficiency (PCC deficiency), is a rare autosomal recessive metabolic disorder, classified as a branched-chain organic acidemia.The disorder presents in the early neonatal period with poor feeding, vomiting, lethargy, and lack of muscle tone. Without treatment, death can occur quickly, due to secondary hyperammonemia, infection, cardiomyopathy, or brain damage. Symptoms and signs
Propionic acidemia is characterized almost immediately in newborns. Symptoms include poor feeding, vomiting, dehydration, acidosis, low muscle tone (hypotonia), seizures, and lethargy. The effects of propionic acidemia quickly become life-threatening. Long-term complications can include chronic kidney disease, cardiomyopathy, and prolonged QTc interval. Pathophysiology
In healthy individuals, enzyme propionyl-CoA carboxylase converts propionyl-CoA to methylmalonyl-CoA. This is one of many steps in the process of converting certain amino acids and fats into energy. Individuals with propionic acidemia cannot perform this conversion because the enzyme propionyl-CoA carboxylase is nonfunctional. The essential amino acids valine, methionine, isoleucine, and threonine can not be converted and this leads to a buildup of propionyl-CoA. Instead of being converted to methylmalonyl-CoA, propionyl-CoA is then converted into propionic acid, which builds up in the bloodstream. This in turn causes an accumulation of dangerous acids and toxins, which can cause damage to the organs.In many cases, propionic acidemia can damage the brain, heart, kidney, liver, cause seizures and delays to normal development such as walking or talking. The patient may need to be hospitalized to prevent breakdown of proteins within the body. | These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states.Liver transplant is gaining a role in the management of these patients, with small series showing improved quality of life. Epidemiology
Propionic acidemia is inherited in an autosomal recessive pattern and is found in about 1 in 35,000 live births in the United States. The condition appears to be more common in Saudi Arabia, with a frequency of about 1 in 3,000. The condition also appears to be common in Amish, Mennonite and other populations with higher frequency of consanguinuity. History
In 1957, a male child was born with poor mental development, repeated attacks of acidosis, and high levels of ketones and glycine in the blood. Upon dietary testing, Dr. Barton Childs discovered that his symptoms worsened when given the amino acids leucine, isoleucine, valine, methionine, and threonine. In 1961, the medical team at Johns Hopkins Hospital in Baltimore, Maryland published the case, calling the disorder ketotic hyperglycinemia. In 1969, using data from the original patients sister, scientists established that propionic acidemia was a recessive disorder, and that propionic acidemia and methylmalonic acidemia are caused by deficiencies in the same enzyme pathway. See also
Methylmalonic acidemia
Isovaleric acidemia
Maple syrup urine disease
References
External links
Propionic acidemia at NLM Genetics Home Reference
Propionic acidemia at NIHs Office of Rare Diseases
"Propionic acidemia". Orphanet. | 11
|
Bevacizumab is an anti-VEGF drug used in intravitreal injection that is known to cause reversal of sea fan lesions and reduce the duration of vitreous hemorrhage. Intravitreal injection of anti-VEGF drugs can also be used prior to surgery to aid separation of tissues involved in the sea fan lesion and to reduce intraoperative and postoperative hemorrhage. It is useful in combination with photocoagulation. Laser
Indications for laser photocoagulation include
Peripheral neovascularization of upwards of 60° circumference
Sickle cell retinopathy affecting both eyes
Large elevated sea fans
Rapid progression of neovascularizationThere are two methods of photocoagulation mainly used; feeder vessel coagulation and scatter laser coagulation. The first method closes the vessels that supply the neovascularized areas using laser burns. Both the xenon arc and argon laser can be used however, the argon laser carries a reduced risk of complications. In comparison, scatter laser coagulation has an indirect effect. Ischemic retina produces vascular endothelial growth factor (VEGF) which promotes neovascularization. Scatter laser coagulation destroys this ischemic retina using laser burns thus preventing vitreous hemorrhage, retinal detachment and vision loss. Surgery
Surgical intervention is indicated for severely advanced disease that poses a threat to visual acuity. Indications include longstanding vitreous haemorrhage, vitreous haemorrhage in both eyes, vitreous haemorrhage in patients with only one eye, epiretinal membranes, macular holes and the various forms of retinal detachment. Scleral buckle was a previously popular surgical intervention however, its complications include anterior segment ischemia as a result of vascular occlusion. The vascular occlusion can in turn lead to phthisis bulbi. | Non-proliferative sickle cell retinopathy (NPSCR)
Non-proliferative sickle cell retinopathy (NPSCR) can feature the following retinal manifestations:
Venous tortuousity is commonly observed in patients with homozygous HbSS sickle cell disease. Numerous diseases that feature blood hyperviscosity similar to sickle cell disease can manifest as retinal venous tortuousity. Tortuosity is caused by arteriovenous shunting from the retinal periphery. It can feature small bleeds of the retina known as intra-retinal hemorrhages, due to blockage of blood vessels by the sickled blood cells, thus triggering vessel wall necrosis. The resulting hemorrhages are initially bright red and oval shaped. As the hemorrhage ages over a period of days to weeks, the color then changes to a salmon hue known as a salmon patch. They are usually seen adjacent to the retinal arteriole. Bleeding in the deeper layers of the retina leads to the appearance of dark lesions known as black sunburst spots. These oval or round shaped pigmented spots are formed due to RPE proliferation. As the haemoglobin within the hemorrhage breaks down over time, yellow spots known as iridescent bodies are formed within the layers of the sensory retina. Maculopathy occurs in a significant portion of patients affected by sickle cell retinopathy. It is more prevalent in homozygous HbSS type sickle cell disease. The fovea can be found within the macula and is known as the center of the visual field. Maculopathy in sickle cell retinopathy is due to long term changes of capillaries that interact at the fovea. | 11
|
Almost all multi-exon genes will produce incorrectly spliced transcripts but the frequency of this background noise will depend on the size of the genes, the number of introns, and the quality of the splice site sequences.In some cases, splice variants will be produced by mutations in the gene (DNA). These can be SNP polymorphisms that create a cryptic splice site or mutate a functional site. They can also be somatic cell mutations that affect splicing in a particular tissue or a cell line. When the mutant allele is in a heterozygous state this will result in production of two abundant splice variants; one functional and one non-functional. In the homozygous state the mutant alleles may cause a genetic disease such as the hemophilia found in descendants of Queen Victoria where a mutation in one of the introns in a blood clotting factor gene creates a cryptic 3 splice site resulting in aberrant splicing. A significant fraction of human deaths by disease may be caused by mutations that interfere with normal splicing; mostly by creating cryptic splice sites.Incorrectly spliced transcripts can easily be detected and their sequences entered into the online databases. They are usually described as "alternatively spliced" transcripts, which can be confusing because the term does not distinguish between real, biologically relevant, alternative splicing and processing noise due to splicing errors. One of the central issues in the field of alternative splicing is working out the differences between these two possibilities. | Cutaneous actinomycosis is a chronic disease that affects the deep subcutaneous tissue of the skin. Caused by an anaerobic, Gram-positive, filamentous type of bacteria in the genus Actinomyces,: 270 invasion of the soft tissue leads to the formation of abnormal channels leading to the skin surface (external sinus tracts) that discharge pale yellow sulfur granules.This disease is uncommon, and has non-specific clinical features, making it difficult to diagnose.Cervicofacial, pulmonary/thoracic and gastrointestinal forms exist, yet cervicofacial disease accounts for two-thirds of reported infections. See also
Skin lesion
== References == | 0-1
|
Babies with SUA may have a higher likelihood of having other congenital abnormalities, especially of the heart. However, additional testing (high level ultrasound scans) can rule out many of these abnormalities prior to birth and alleviate parental anxiety.It may be associated with Trisomy 18, also known as Edwards syndrome. Intrauterine growth restriction has been found to be associated. Diagnosis
It can be detected in the first trimester of pregnancy with the use of 2D ultrasound. The sonographer is able to identify a 2 vessel cord in an image with the bladder and color Doppler, which will show only one artery going around one side of the bladder. In a normal fetus, there would be 2 arteries (one on each side of the bladder). Echocardiograms of the fetus may be advised to ensure the heart is functioning properly. Genetic counseling may be useful, too, especially when weighing the pros and cons of more invasive procedures such as chorionic villus sampling and amniocentesis. These invasive procedures are usually performed when there is a suspected chromosomal abnormality or genetic defect and will confirm a diagnosis. Prognosis
Although the presence of an SUA is a risk factor for additional complications, most fetuses with the condition will not experience other problems, either in utero or after birth. Especially encouraging are cases in which no other soft markers for congenital abnormalities are visible via ultrasound. Given that, the vast majority of expectant mothers do not receive the kind of advanced ultrasound scanning required to confirm SUA in utero. | Brigatinib, sold under the brand name Alunbrig among others, is a small-molecule targeted cancer therapy being developed by Ariad Pharmaceuticals, Inc. Brigatinib acts as both an anaplastic lymphoma kinase (ALK) and epidermal growth factor receptor (EGFR) inhibitor.Brigatinib could overcome resistance to osimertinib conferred by the EGFR C797S mutation if it is combined with an anti-EGFR antibody such as cetuximab or panitumumab. Mechanism of action
Brigatinib is an inhibitor of ALK and mutated EGFR.ALK was first identified as a chromosomal rearrangement in anaplastic large cell lymphoma (ALCL). Genetic studies indicate that abnormal expression of ALK is a key driver of certain types of non-small cell lung cancer (NSCLC) and neuroblastomas, as well as ALCL. Since ALK is generally not expressed in normal adult tissues, it represents a highly promising molecular target for cancer therapy. Brigatinib inhibits ROS proto-oncogene-1 fusions and EGFR mutations and has a remarkable effect on the central nervous system.Epidermal growth factor receptor (EGFR) is another validated target in NSCLC. Additionally, the T790M "gatekeeper" mutation is linked in approximately 50 percent of patients who grow resistant to first-generation EGFR inhibitors. While second-generation EGFR inhibitors are in development, clinical efficacy has been limited due to toxicity thought to be associated with inhibiting the native (endogenous or unmutated) EGFR. A therapy designed to target EGFR, the T790M mutation but avoiding inhibition of native EGFR is another promising molecular target for cancer therapy. | 0-1
|
Medical uses
Senna is used for episodic and chronic constipation though there is a lack of high-quality evidence to support its use for these purposes. It may also be used to aid in the evacuation of the bowel prior to surgery or invasive rectal or colonic examinations. Administration
It should be taken once daily at bedtime. Oral senna products typically produce a bowel movement in 6 to 12 hours. Rectal suppositories can act within minutes or take up to two hours. Contraindications
According to Commission E, senna is contraindicated in cases of intestinal obstruction, acute intestinal inflammation (e.g., Crohns disease), ulcerative colitis, appendicitis, and abdominal pain of unknown origin.Senna is considered contraindicated in people with a documented allergy to anthraquinones. Such allergies are rare and typically limited to dermatological reactions of redness and itching. Adverse effects
Adverse effects are typically limited to gastrointestinal reactions and include abdominal pain or cramps, diarrhea, nausea, and vomiting. Regular use of senna products can lead to a characteristic brown pigmentation of the internal colonic wall seen on colonoscopy. This abnormal pigmentation is known as melanosis coli. Interactions
Senna glycosides can increase digoxin toxicity in patients taking digoxin by reducing serum potassium levels, thereby enhancing the effects of digoxin. Mechanism of action
The breakdown products of senna act directly as irritants on the colonic wall to induce fluid secretion and colonic motility. Pharmacology
They are anthraquinone derivatives and dimeric glycosides. Society and culture
Formulations
Senna is an over-the-counter medication available in multiple formulations, including oral formations (liquid, tablet, granular) and rectal suppositories. | Senna products are manufactured by multiple generic drug makers and sold under various brand names.Kayam churna is a traditional Indian laxative that contains senna leaves. Brand names
Ex-Lax, Geri-kot, Perdiem Overnight Relief, Senexon, Pursennid, Senna Smooth, Senna-Gen, Senna-GRX, Senna-Lax, Senna-Tabs, Senna-Time, SennaCon, Senno, Senokot. References
External links
"Senna". Drug Information Portal. U.S. National Library of Medicine. | 11
|
Exclude other diseases
If the echocardiogram is compatible with a diagnosis of pulmonary hypertension, common causes of pulmonary hypertension (left heart disease and lung disease) are considered and further tests are performed accordingly. These tests generally include electrocardiography (ECG), pulmonary function tests including lung diffusion capacity for carbon monoxide and arterial blood gas measurements, X-rays of the chest and high-resolution computed tomography (CT) scanning. Ventilation/perfusion scintigraphy
If heart disease and lung disease have been excluded, a ventilation/perfusion scan is performed to rule out CTEPH. If unmatched perfusion defects are found, further evaluation by CT pulmonary angiography, right heart catheterization, and selective pulmonary angiography is performed. CT scan
Signs of pulmonary hypertension on CT scan of the chest are:
Enlargement of the pulmonary trunk (measured at its bifurcation). It is, however, a poor predictor of pulmonary hypertension in patients with interstitial lung disease.A diameter of more than 27 mm for women and 29 mm for men is suggested as a cutoff. A cutoff of 31.6 mm may be a more statistically robust in individuals without interstitial lung disease.Increased ratio of the diameter of the main pulmonary artery (pulmonary trunk) to the ascending aorta (measured at its bifurcation).A ratio of 1.0 is suggested as a cutoff in adults. Cutoff ~1.09 in children.Increased diameter ratio of segmental arteries to bronchi. This finding in three or four lobes, in the presence of a dilated pulmonary trunk (≥29 mm), and absence of significant structural lung disease confers a specificity of 100% for pulmonary hypertension. | ECT in combination with benzodiazepines is used to treat malignant catatonia. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.Electroconvulsive therapy (ECT) is an effective treatment for catatonia that is well acknowledged. ECT has also shown favorable outcomes in patients with chronic catatonia. However, it has been pointed out that further high quality randomized controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.There is evidence clozapine works better than other antipsychotics to treat catatonia, following a recent systematic review.Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine may be used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors. Prognosis
Patients who experience an episode of catatonia are more likely to recur. | 0-1
|
Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies. Recent research has shown that some common parasites, such as intestinal worms (e.g., hookworms), secrete chemicals into the gut wall (and, hence, the bloodstream) that suppress the immune system and prevent the body from attacking the parasite. This gives rise to a new slant on the hygiene hypothesis theory—that co-evolution of humans and parasites has led to an immune system that functions correctly only in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive. In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants. However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms. Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies. It may be that the term parasite could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work. For more information on this topic, see Helminthic therapy. | Adhesive patches, usually treated with several common allergic chemicals or skin sensitizers, are applied to the back. The skin is then examined for possible local reactions at least twice, usually at 48 hours after application of the patch, and again two or three days later. Blood testing
An allergy blood test is quick and simple and can be ordered by a licensed health care provider (e.g., an allergy specialist) or general practitioner. Unlike skin-prick testing, a blood test can be performed irrespective of age, skin condition, medication, symptom, disease activity, and pregnancy. Adults and children of any age can get an allergy blood test. For babies and very young children, a single needle stick for allergy blood testing is often gentler than several skin pricks. An allergy blood test is available through most laboratories. A sample of the patients blood is sent to a laboratory for analysis, and the results are sent back a few days later. Multiple allergens can be detected with a single blood sample. Allergy blood tests are very safe since the person is not exposed to any allergens during the testing procedure. The test measures the concentration of specific IgE antibodies in the blood. Quantitative IgE test results increase the possibility of ranking how different substances may affect symptoms. A rule of thumb is that the higher the IgE antibody value, the greater the likelihood of symptoms. Allergens found at low levels that today do not result in symptoms cannot help predict future symptom development. | 11
|
References
Citations
Sources
External links
"Etomidate". Drug Information Portal. U.S. National Library of Medicine. | Physiology of death by decapitation
Decapitation is quickly fatal to humans and most animals. Unconsciousness occurs within 10 seconds without circulating oxygenated blood (brain ischemia). Cell death and irreversible brain damage occurs after 3–6 minutes with no oxygen, due to excitotoxicity. Some anecdotes suggest more extended persistence of human consciousness after decapitation, but most doctors consider this unlikely and consider such accounts to be misapprehensions of reflexive twitching rather than deliberate movement, since deprivation of oxygen must cause nearly immediate coma and death ("[Consciousness is] probably lost within 2–3 seconds, due to a rapid fall of intracranial perfusion of blood").A laboratory study testing for humane methods of euthanasia in awake animals used EEG monitoring to measure the time duration following decapitation for rats to become fully unconscious, unable to perceive distress and pain. It was estimated that this point was reached within 3–4 seconds, correlating closely with results found in other studies on rodents (2.7 seconds, and 3–6 seconds). The same study also suggested that the massive wave which can be recorded by EEG monitoring approximately one minute after decapitation ultimately reflects brain death. | 0-1
|
IDH1 and IDH2 mutations in gliomas, as well as deletion of chromosome arms 1p and 19q, generally indicate better prognosis. TP53, ATRX, EGFR, PTEN, and TERT mutations are also useful in determining prognosis. Glioblastoma multiforme
Glioblastoma multiforme (GBM) is the most aggressive (grade IV) and most common form of a malignant brain tumor. Even when aggressive multimodality therapy consisting of radiotherapy, chemotherapy, and surgical excision is used, median survival is only 12–17 months. Standard therapy for glioblastoma multiforme consists of maximal surgical resection of the tumor, followed by radiotherapy between two and four weeks after the surgical procedure to remove the cancer, then by chemotherapy, such as temozolomide. Most patients with glioblastoma take a corticosteroid, typically dexamethasone, during their illness to relieve symptoms. Experimental treatments include targeted therapy, gamma knife radiosurgery, boron neutron capture therapy, gene therapy also chemowafer implants. Oligodendrogliomas
Oligodendrogliomas are incurable but slowly progressive malignant brain tumors. They can be treated with surgical resection, chemotherapy, radiotherapy or a combination. For some suspected low-grade (grade II) tumors, only a course of watchful waiting and symptomatic therapy is opted for. These tumors show a high frequency of co-deletions of the p and q arms of chromosome 1 and chromosome 19 respectively (1p19q co-deletion) and have been found to be especially chemosensitive with one report claiming them to be one of the most chemosensitive tumors. A median survival of up to 16.7 years has been reported for grade II oligodendrogliomas. Acoustic neuroma
Acoustic neuromas are non-cancerous tumors. They can be treated with surgery, radiation therapy, or observation. | Retained placenta is a condition in which all or part of the placenta or membranes remain in the uterus during the third stage of labour. Retained placenta can be broadly divided into:
failed separation of the placenta from the uterine lining
placenta separated from the uterine lining but retained within the uterusA retained placenta is commonly a cause of postpartum haemorrhage, both primary and secondary.Retained placenta is generally defined as a placenta that has not undergone placental expulsion within 30 minutes of the baby’s birth where the third stage of labor has been managed actively. Signs and symptoms
Risks of retained placenta include hemorrhage and infection. After the placenta is delivered, the uterus should contract down to close off all the blood vessels inside the uterus. If the placenta only partially separates, the uterus cannot contract properly, so the blood vessels inside will continue to bleed. A retained placenta thereby leads to hemorrhage. Management
Drugs, such as intraumbilical or intravenous oxytocin, are often used in the management of placental retention. It is useful ensuring the bladder is empty. However, ergometrine should not be given as it causes tonic uterine contractions which may delay placental expulsion. Controlled cord traction has been recommended as a second alternative after more than 30 minutes have passed after stimulation of uterine contractions, provided the uterus is contracted. Manual extraction may be required if cord traction also fails, or if heavy ongoing bleeding occurs. | 0-1
|
Neurobiologist Jan Vodka emphasizes that, for those purposes, "violent behavior is defined as overt and intentional physically aggressive behavior against another person. "Based on the idea of human nature, scientists do agree violence is inherent in humans. Among prehistoric humans, there is archaeological evidence for both contentions of violence and peacefulness as primary characteristics.Since violence is a matter of perception as well as a measurable phenomenon, psychologists have found variability in whether people perceive certain physical acts as "violent". For example, in a state where execution is a legalized punishment we do not typically perceive the executioner as "violent", though we may talk, in a more metaphorical way, of the state acting violently. Likewise, understandings of violence are linked to a perceived aggressor-victim relationship: hence psychologists have shown that people may not recognise defensive use of force as violent, even in cases where the amount of force used is significantly greater than in the original aggression.The concept of violence normalization is known as socially sanctioned, or structural violence and is a topic of increasing interest to researchers trying to understand violent behavior. It has been discussed at length by researchers in sociology, medical anthropology, psychology, psychiatry, philosophy, and bioarchaeology.Evolutionary psychology offers several explanations for human violence in various contexts, such as sexual jealousy in humans, child abuse, and homicide. Goetz (2010) argues that humans are similar to most mammal species and use violence in specific situations. | The following should be considered prior to carrying out any dental treatment:
Size of the antrum and proximity to teeth – this can be assessed radiographically
Shape and size of teeth and roots – this can be assessed radiographically
Presence of periapical pathology – this can be assessed radiographically
The age of the patient
The patient’s past dental historyIf the above factors are assessed as increasing the risk of OAC development, the clinician should take appropriate steps to carefully remove the tooth in question, possibly carrying out a surgical extraction and in an appropriate setting. Hence, in such cases:
Avoid using too much of apical pressure during tooth extraction
Perform surgical extraction with roots sectioning
Consider referral to OMFS at local hospital
Treatment
The primary aim of treatment of a newly formed oroantral communication is to prevent the development of an oroantral fistula as well as chronic sinusitis. The decision on how to treat OAC/OAF depends on various factors. Small size communications between 1 and 2 mm in diameter, if uninfected, are likely to form a clot and heal by itself later. Communications larger than this require treatments to close the defect and these interventions can be categorised into 3 types: surgical, non-surgical and pharmacological. Surgery
Surgical methods are required if a large defect is present or if a defect persists. Surgery involves creating a flap utilising local tissue to close the communication. There are a number of different flaps that can be used such as the buccal advancement flap, the buccal fat pad flap, a combination of the two and a palatal flap. | 0-1
|