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You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Anti-carcinogens are and explain in detail?
Carotenoids: The carotenoids are responsible for most of the yellow and red colours of fruits and flowers, and they provide the brilliance of fall when the chlorophyll molecules are degraded to reveal the carotenoids. In addition to their role in transferring energy to reaction centres, the carotenoids serve a safeguarding function. Carotenoids suppress damaging photochemical reactions, paicularly those including oxygen, that can be induced by bright sunlight. Indeed, plants lacking carotenoids are quickly killed on exposure to light and oxygenBeta-carotene and other provitamins A carotenoids are cleaved in the intestinal mucosa by carotene dioxygenase, yielding retinaldehyde, which is reduced to retinol, esterified, and secreted in chylomicrons
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Which is not a eugenol sealer? and explain in detail?
None
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Tyrosinemia type I and explain in detail?
Tyrosinemia type I is a genetic disorder that disrupts the metabolism of the amino acid tyrosine, resulting in damage primarily to the liver along with the kidneys and peripheral nerves. The inability of cells to process tyrosine can lead to chronic liver damage ending in liver failure, as well as renal disease and rickets. Symptoms such as poor growth and enlarged liver are associated with the clinical presentation of the disease. Clinical manifestation of disease occurs typically within the first two years of life. The severity of the disease is correlated with the timing of onset of symptoms, earlier being more severe.Tyrosinemia type I is an autosomal recessive disorder caused by mutations in both copies of the gene encoding the enzyme fumarylacetoacetate hydrolase (FAH). FAH is a metabolic enzyme that catalyzes the conversion of fumarylacetoacetate to fumarate and acetoacetate. It is expressed primarily in the liver and kidney. Loss of FAH activity results in the accumulation of certain metabolic intermediates in the tyrosine catabolic pathway. These compounds are toxic to cells and lead to differential gene expression and apoptosis in high concentrations. HT1 is diagnosed when elevated levels of succinylacetone (SA), one of the metabolites in this pathway, is detected in blood and urine samples.While there is no cure for tyrosinemia type I, management of the disease is possible utilizing dietary restrictions and medications. A diet low in tyrosine and phenylalanine is utilized indefinitely once a diagnosis is suspected or confirmed. Additionally, the drug nitisinone (brand name Orfadin) is prescribed and continued indefinitely in order to combat liver and kidney damage, promoting normal function of these organs. Prior to the development of nitisinone, dietary restrictions and liver transplantation were the only forms of treatment for HT1.Tyrosinemia type I is especially prevalent in the Saguenay-Lac Saint-Jean region of Quebec, where the prevalence is 1 in 1,850 births. It is most common among those with French-Canadian ancestry and this frequency of infliction has been attributed to the founder effect. There are five other known types of tyrosinemia, all of which derange the metabolism of tyrosine in the human body. They are distinguished by their symptoms and genetic cause. Signs and symptoms Type 1 tyrosinemia typically presents in infancy as failure to thrive and hepatomegaly. The primary effects are progressive liver and kidney dysfunction. The liver disease causes cirrhosis, conjugated hyperbilirubinemia, elevated AFP, hypoglycemia and coagulation abnormalities. This can lead to jaundice, ascites and hemorrhage. There is also an increased risk of hepatocellular carcinoma.The kidney dysfunction presents as Fanconi syndrome: Renal tubular acidosis, hypophosphatemia and aminoaciduria. Cardiomyopathy, neurologic and dermatologic manifestations are also possible. The urine has an odor of cabbage or rancid butter.The presentation of symptoms of tyrosinemia type 1 in terms of timing is broken into three categories: acute, sub-acute, and chronic.The acute classification typically is presented clinically between birth and 6 months of age. The common presentation in an acute case is synthetic liver failure, marked by the lack of formation of coagulation factors in blood. Patients are prone to infections at this stage accompanied by fever, vomiting, increased tendency to bleed, and diarrhea along with bloody feces as manifestations of sepsis. Other symptoms include enlarged liver, jaundice, and excess abdominal fluid.Sub-acute cases present between 6 months and the first year of life and the severity of liver disease is lessened to an extent. Again, synthetic function of the liver in terms of blood coagulation factors is impaired in addition to enlargement of the liver and spleen. The infant may also display a failure to thrive as their growth is limited by the disease. This growth impairment can manifest itself in rickets, which is the softening of bones.The final classification, chronic HT1, is detected with presentations occurring after one year of life. The course of the disease up to this point can lead to different ailments affecting the liver. Cirrhosis, liver failure, or cancer of the liver may present as a result of chronic liver disease. Additional symptoms common in this classification include cardiomyopathy, renal disease, and acute neurological crises. Liver The liver is the organ affected most by Tyrosinemia Type I due to the high level of expression of the gene for fumarylacetoacetate hydrolase (FAH) in liver cells. The production of blood coagulation factors by the liver is disrupted, causing hemophiliac-like symptoms. Acute liver failure is common, especially in early life. Additionally, the synthesis of albumin in the liver may be defective, therefore leading to hypoalbuminemia. As the disease progresses, cirrhosis is common. This can lead to a fatty liver and the development of tumors in areas affected by this scarring of liver tissue. These scars are known as nodules. There is a 37% chance of developing a hepatocellular carcinoma (HCC) for untreated patients. Renal and neurological manifestations Many patients display impaired kidney function and neurological symptoms. In addition to liver cells, kidney cell expression involves expression of the gene for FAH. Kidney failure is a potential result of impaired kidney function, but the most common symptom associated with renal dysfunction is hypophosphatemic rickets. Neurological manifestations are characterized by acute neurological crises due to overaccumulation of porphyrin. These crises are characterized by porphyria. They typically follow an infection. Patients can present with a variety of varied symptoms including paresthesias, abdominal pain, pain-induced seizures, and can result in self-mutilation in response to this pain. Episodes can last for 1–7 days and can lead to neuropathy. Genetics Tyrosinemia type I is an autosomal recessive inherited condition. Mutant alleles in the gene are inherited from both parents. The genetic mutation occurs to the fumarylacetoacetate hydrolase (FAH) enzyme gene, located on chromosome 15. The most common mutation is IVS12+5(G->A) which is a mutation in the splice site consensus sequence of intron 12, therefore affecting exon 12. A second allele is the IVS6-1(G-T) mutation. This mutation results in a nonfunctional enzyme.Type 1 tyrosinemia is inherited in an autosomal recessive pattern. Pathophysiology Fumarylacetoacetate hydrolase catalyzes the final step in the degradation of tyrosine - fumarylacetoacetate to fumarate, acetoacetate and succinate. Fumarylacetoacetate accumulates in hepatocytes and proximal renal tubal cells and causes oxidative damage and DNA damage leading to cell death and dysfunctional gene expression which alters metabolic processes like protein synthesis and gluconeogenesis. The increase in fumarylacetoacetate inhibits previous steps in tyrosine degradation leading to an accumulation of tyrosine in the body. Tyrosine is not directly toxic to the liver or kidneys but causes dermatologic and neurodevelopmental problems. Tyrosine metabolic pathway Fumarylacetoacetate hydrolase (FAH) is the final enzyme in the tyrosine metabolic pathway. The mutation of FAH enzyme results in nonfunctional FAH in all cells expressing this gene and thus metabolizing tyrosine is impaired. FAH catalyzes the conversion of fumarylacetoacetate to fumarate and acetoacetate. Loss of FAH results in the accumulation of upstream compounds in the catabolic pathway. These include maleylacetoacetate (MAA) and fumarylacetoacetate (FAA). MAA and FAA are converted to succinylacetoacetate (SAA) which is then catabolized to succinylacetone (SA).The accumulation of MAA, FAA, and SA in cells inhibits the breakdown of thiol derivatives, leading to post-translational modifications to the antioxidant glutathione. This inhibits the antioxidant activity of glutathione, leading to reactive oxygen species (ROS) damaging cell components. Over time, the combined effect of accumulation of toxic metabolic intermediates and elevated ROS levels in liver and kidney cells leads to apoptosis in these tissues which ultimately results in organ failure. Accumulated SA in liver and kidney cells results in its release into the bloodstream, which leads to secondary effects. SA inhibits the enzyme 5-ALA dehydratase which converts aminolevulinic acid (5-ALA) into porphobilinogen, a precursor to porphyrin. Consequently, porphyrin deposits form in the bloodstream and cause neuropathic pain, leading to the acute neurological crises experienced by some patients. Additionally. SA can function to inhibit renal tubular function, the synthesis of heme, and the immune system.The accumulation of unprocessed tyrosine itself in the blood stream as a consequence of deficient catabolism can also lead to disruption of hormonal signaling and neurotransmission. Tyrosine is a precursor molecule required for synthesis of several neurotransmitters and hormones, mainly Dopamine, norepinephrine, and thryoxine. Excessive synthesis of these molecules due to elevated tyrosine levels can impair physical growth, motor function, and speech development. Diagnosis Beyond the identification of physical clinical symptoms outlined above, the definitive criterion for diagnostic assessment of Tyrosinemia Type I is elevated succinylacetone (SA) in blood and urine. Elevated SA levels are not associated with any other known medical condition, so there is minimal risk of misdiagnosis. Quantitation of tyrosine levels is also used as a diagnostic but is less reliable due to high false positive and false negative rates. Newborns are not generally screened for HT1 due to rarity of the condition and lack of apparent symptoms at time of birth. However, prompt assessment upon the manifestation of physical symptoms such as fever, vomiting, increased tendency to bleed, diarrhea along with bloody feces, and jaundice is critical for improving long term prognosis. Management The primary treatment for type 1 tyrosinemia is nitisinone and restriction of tyrosine in the diet. Nitisinone inhibits the conversion of 4-OH phenylpyruvate to homogentisic acid by 4-Hydroxyphenylpyruvate dioxygenase, the second step in tyrosine degradation. By inhibiting this enzyme, the accumulation of the fumarylacetoacetate is prevented. Previously, liver transplantation was the primary treatment option and is still used in patients in whom nitisinone fails.Clinical treatment of HT1 relies on medications and strict regulation of diet. Nitisinone and dietary restrictions that decrease the amount of tyrosine and phenylalaine absorbed from the GI tract during protein digestion are used in combination as therapeutic measures that control the disease state if they are continued indefinitely. If not, there is a lack of control over the disease, resulting in continued liver and kidney damage, contributing to organ failure and death. In this case, a liver transplant may be required. Levels of SA are monitored throughout treatment in order to assess treatment effectiveness. Diet The prescribed diet for treatment of HT1 is low in protein. Patients received amino acid supplements lacking tyrosine and phenylalanine in order to acquire sufficient protein. It is recommended that tyrosine levels remain below 500 μmol/L. Phenylalnine is the precursor to tyrosine. The ideology behind maintaining low tyrosine levels is two-fold. Firstly, it prevents the toxic metabolic intermediates from accumulating as a result of the dysfunctional tyrosine metabolic pathway. Prior to the introduction of nitisinone, this was the main treatment measure. Secondly, the mechanism of action of nitisinone is prevention of any tyrosine metabolism, thus it is important to prevent tyrosine from accumulating. Dietary protein consumption while taking nitisinone can also lead to side effects affecting the ocular system, which are easily reversed by removing protein from the diet. Medication Nitisinone is prescribed ultimately to reduce the accumulation of toxic metabolic intermediates, such as succinylacetate, which are toxic to cells. It modifies the function of 4-hydrooxyphenylpyruvate dioxygenase by acting as a competitive inhibitor. 4-hydrooxyphenylpyruvate dioxygenase functions to convert 4-hydroxyphenylpyruvate to homogentisate as the second enzymatic reaction in the tyrosine catabolic pathway. This prevents the further catabolism of tyrosine. It is recommended that nitisinone treatment begins immediately following a confirmed or suspected case of HT1. It is supplied orally as a capsule or suspension in dose increments of 2 mg, 5 mg, 10 mg, or 20 mg or 4 mg/mL respectively. The starting dose is 1 mg/kg one time daily or 2 mg/kg one time daily for 48 hours if the patient is experiencing acute liver failure. Patient responsiveness to nitisinone is assessed by measuring blood coagulation activity and SA levels in blood and urine. Patients should display a positive response within 24–48 hours of first dose. Establishment of the long-term dosage will vary from patient to patient. It is recommended that nitisinone levels be maintained at 30-50 μM in the blood stream. Prognosis Prior to the development of nitisinone, dietary restrictions and liver transplantation were the only forms of treatment for HT1. A study regarding the efficacy of treatment with nitisinone and dietary restrictions found that 93% of people survived at two years, four years, and six years indicating the prognosis of stabilizing the HT1 disease state is positive. Epidemiology Tyrosinemia type I affects males and females in equal numbers. Its prevalence has been estimated to be 1 in 100,000 to 120,000 births worldwide. HT1 is especially prevalent in the Saguenay-Lac Saint-Jean region of Quebec is one in 1,850 births. The elevated frequency of this disorder within individuals of French-Canadian ancestry in Quebec is believed to be due to reduced genetic heterogeneity within the original founder population for the Saguenay-Lac Saint-Jean region. The initial settlement of Saguenay Lac-Saint-Jean (SLSJ) occurred between 1838 and 1911. From a total of 28,656 settlers, 75 percent originated from the neighboring Charlevoix region. The settling of the Charlevoix region itself started in 1675 when 599 founders of mostly French descent moved to this region from the Quebec City area.Worldwide, type I tyrosinemia affects about 1 person in 100,000. This type of tyrosinemia is much more common in Quebec, Canada. The overall incidence in Quebec is about 1 in 16,000 individuals. In the Saguenay-Lac-Saint-Jean region of Quebec, type 1 tyrosinemia affects 1 person in 1,846. The carrier rate has been estimated to be between 1 in 20 and 1 in 31. History Nitisinone was first used to clinically treat tyrosinemia type I in 1991. Nitisinone was approved by the European Medicine Agency (EMA) under exceptional circumstances in 2005. Originally, nitisinone was developed as a weed-killer by Zeneca Agrochemicals. It was epidemiologically observed that the growth of plants and weeds was inhibited under the bottlebrush plant (Callistemon citrinus). It became clear that neither the shade nor the litterfall of these plants was responsible for the suppression of plant and weed growth. Rather, a substance – which was identified as leptospermone – in the soil under the bottlebrush plant was shown to have bleaching activity on the emerging plants. The allelochemical leptospermone was extracted from the bottlebrush plant and chemically characterized. Leptospermone belongs to the triketone family and inhibits chloroplast development due to a lack of plastoquinone secondary to hepatic 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibition; thus, it served as a blueprint for the synthesis of nitisinone.In 1932, Grace Medes first described "a new disorder of tyrosine metabolism," She coined the condition "tyrosinosis" after observing 4-hydroxyphenylpyruvate in the urine of a 49-year-old man with myasthenia gravis. She proposed that the metabolic defect in this patient was a deficiency of 4-hydroxyphenylpyruvate dioxygenase, but her case remains puzzling and has since been assigned a separate OMIM number. The first typical patient with hepatorenal tyrosinemia was described in 1956 by Margaret D Baber at Edgware General Hospital in Middlesex, England. Starting the following year, Kiyoshi Sakai and colleagues, at the Jikei University School of Medicine in Tokyo, published 3 reports describing the clinical, biochemical, and pathological findings of a 2-year-old boy with hepatorenal tyrosinemia who was then thought to have an "atypical" case of tyrosinosis. Between 1963 and 1965, Swedish pediatrician Rolf Zetterström and colleagues at the Karolinska Institute in Sweden published the first detailed clinical account of hepatorenal tyrosinemia and its variants
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is A person is said to be mentally retarded when IQ is- and explain in detail?
Ans. is 'd' i.e., < 70 o Normal IQ- 90-109;o Borderline IQ- 70-89;o Mild mental retardation IQ- 50-69;o Moderate mental retardation IQ- 35-49;o Severe MR IQ- 20-34;o Profound MR IQ- 0-19.
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Fusion of the caudal portions of the kidneys during embryonic development is most likely to result in which of the following congenital conditions? and explain in detail?
During development, the kidneys typically "ascend" from a position in the pelvis to a position high on the posterior abdominal wall. Although the kidneys are bilateral structures, occasionally the inferior poles of the two kidneys fuse. When this happens, the "ascent" of the fused kidneys is arrested by the first midline structure they encounter, the inferior mesenteric artery. The incidence of horseshoe kidney is about 0.25% of the population.
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Down and out deviation of eyeball is due to Paralysis of which cranial nerve and explain in detail?
Down and out deviation is due to 3rd nerve palsy due to unopposed action of lateral rectus and superior oblique.
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Lewy bodies contain? and explain in detail?
Lews bodies are seen in parkinson disease.They certain α synuclein.
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What is Decrease in diffusion is diagnosed by: and explain in detail?
DLCO Stands for diffusion capacity for carbon monoxide It is used to estimate diffusion capacity of the lungs
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What is Mydriatic used in 3 years old child for refraction is and explain in detail?
B i.e. 1% Atropine ointment
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What is Subungual exostosis and explain in detail?
Subungual exostoses are a type of non-cancerous bone tumor of the chondrogenic type, and consists of bone and cartilage
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Which is true about stab wound : and explain in detail?
C i.e. Depth is maximum Punture (stab) wound is an injury caused by pointed weapon such as dagger, knife, needle, spear, arrow, scissor, bitchva, ice pick and its depth is greatest dimensionQ.
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Most common cause of dilated cardiomyopathy is? and explain in detail?
Ans. (a) AlocholRef: Braundwald's Heart Disease Ninth edition, Chapter 64
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Noonan syndrome and explain in detail?
Noonan syndrome (NS) is a genetic disorder that may present with mildly unusual facial features, short height, congenital heart disease, bleeding problems, and skeletal malformations. Facial features include widely spaced eyes, light-colored eyes, low-set ears, a short neck, and a small lower jaw. Heart problems may include pulmonary valve stenosis. The breast bone may either protrude or be sunken, while the spine may be abnormally curved. Intelligence in the syndrome is often normal. Complications of NS can include leukemia.A number of genetic mutations can result in Noonan syndrome. The condition may be inherited from a persons parents as an autosomal dominant condition or occur as a new mutation. Noonan syndrome is a type of RASopathy, the underlying mechanism for which involves overactivation within the RAS/MAPK cell signaling pathway. The diagnosis may be suspected based on symptoms, medical imaging, and blood tests. Confirmation may be achieved with genetic testing.No cure for NS is known. Treatment is based on the symptoms and underlying problems, and extra support in school may be required. Growth hormone therapy during childhood can increase an affected persons final height. Long-term outcomes typically depend on the severity of heart problems.An estimated 1 in 1000 people are mildly affected by NS, while about 1 in 2,000 have a more severe form of the condition. Males appear to be affected more often than females. The condition was first described in 1883 and was named after American pediatric cardiologist Jacqueline Noonan, who described further cases in 1963. Signs and symptoms The most common signs leading to the diagnosis of Noonan syndrome are unique facial characteristics and musculoskeletal features. The facial characteristics are most prominent in infancy, becoming less apparent with age in many people with Noonan syndrome. Head Some of the characteristic features of Noonan syndrome include a large head with excess skin on the back of the neck, low hairline at the nape of the neck, high hairline at the front of the head, triangular face shape, broad forehead, and a short, webbed neck. In the eyes, hypertelorism (widely set eyes) is a defining characteristic, present in 95% of people with Noonan syndrome. This may be accompanied by epicanthal folds (extra fold of skin at the inner corner of the eye), ptosis (drooping of the eyelids), proptosis (bulging eyes), strabismus (inward or outward turning of the eyes), nystagmus (jerking movement of the eyes) and refractive visual errors. The nose may be small, wide, and upturned. The development of the ears and auditory system may be affected in people with Noonans syndrome. This can result in low-set ears (in over 90%), backward-rotated ears (over 90%), thick helix (outer rim) of ear (over 90%), incomplete folding of ears, chronic otitis media (ear infections), and hearing loss. Development of the mouth may also be affected in Noonan syndrome. This can result in deeply grooved philtrum (top lip line) (over 90%), micrognathia (undersized lower jaw), high arched palate, articulation difficulties (teeth dont line up) which can lead to dental problems. Similar to the muscular manifestations above, in the mouth, poor tongue control may be observed. Skin Skin signs and symptoms in Noonan syndrome include lymphedema (lymph swelling of the extremities), keloid formation, excessive scar formation, hyperkeratosis (overdevelopment of outer skin layer), pigmented nevi (darkly pigmented skin spots), and connective tissue disease. Musculoskeletal Abnormalities in the limbs and extremities may occur in Noonan syndrome. This may manifest as bluntly ended fingers, extra padding on fingers and toes, edema of the back of hands and tops of feet, and cubitus valgus (wide carrying angle of the elbows). For short stature, growth hormone is sometimes combined with IGF-1 (or as an alternative, IGF-1 as a stand-alone) can be used to achieve an increased height/final height quicker. The final adult height of individuals with Noonan syndrome is about 161–167 cm in males and 150–155 cm in females, which approaches the lower limit of normal.Spinal abnormalities may be present up to 30% of the time and this may require surgery to correct in over 60% of these cases. Other musculoskeletal manifestations in Noonan syndrome are associated with undifferentiated connective-tissue disorders which can be associated with joint contractures (tightness) or joint hypermobility (looseness). Additional factors may present in the form of winging of the scapula, scoliosis, breast bone prominence (pectus carinatum), breast bone depression (pectus excavatum). Muscle abnormalities may present as hypotonia (low muscle tone), which may lead to lordosis (increased hollow in the back) due to poor abdominal muscle tone. Heart Noonan syndrome is the second most common syndromic cause of congenital heart disease. This includes pulmonary valvular stenosis (50–60%), atrial septal defects (10–25%), ventricular septal defects (5–20%) and hypertrophic cardiomyopathy (12–35%). Lungs Restrictive lung function has been reported in some people. Gastrointestinal A number of diverse gastrointestinal (GI) symptoms have been associated with Noonan syndrome. These include swallowing difficulties, low gut motility, gastroparesis (delayed gastric emptying), intestinal malrotation, and frequent or forceful vomiting. These digestive issues may lead to decreased appetite, failure to thrive from infancy to puberty (75%), and occasionally the need for a feeding tube. Genitourinary system In some males with Noonan syndrome, testicles do not descend (cryptorchidism). Circulation Lymphatic anomalies including Posterior cervical hygroma (webbed neck) and Lymphedema may present in people with Noonan syndrome. A number of bleeding disorders have been associated with Noonan syndrome, these include platelet dysfunction, Blood clotting disorders, partial deficiency of factor VIII:C, partial deficiency of factor XI:C, partial deficiency of factor XII:C, and an imbalance of plasminogen activator inhibitor type-1 (PAI-1) and tissue plasminogen activator (t-PA) activity. It has been associated with Von Willebrand disease, Amegakaryocytic thrombocytopenia (low platelet count), prolonged activated partial thromboplastin time, combined coagulation defects. When present, these Noonan-syndrome accompanying disorders can be associated with a predisposition to bruise easily, or hemorrhage. Neurological Occasionally, Chiari malformation (type 1), may occur, which can lead to hydrocephalus. Seizures have also been reported. Causes Recurrence in siblings and apparent transmission from parent to child has long suggested a genetic defect with autosomal dominant inheritance and variable expression. Mutations in the Ras/mitogen activated protein kinase signaling pathways are known to be responsible for about 70% of NS cases.Persons with NS have up to a 50% chance of transmitting it to their offspring. The fact that an affected parent is not always identified for children with NS suggests several possibilities: Manifestations could be so subtle as to go unrecognized (variable expressivity) NS is heterogeneous, comprising more than one similar condition of differing causes, and some of these may not be inherited. A high proportion of cases may represent new, sporadic mutations.Heterozygous mutations in NRAS, HRAS, BRAF, SHOC2, MAP2K1, MAP2K2, and CBL have also been associated with a smaller percentage of NS and related phenotypes.A condition known as "neurofibromatosis–Noonan syndrome" is associated with neurofibromin. Diagnosis NS can be confirmed genetically by the presence of any of the known mutations listed above. However, despite identification of 14 causative genes, the absence of a known mutation will not exclude the diagnosis, as more, as-yet-undiscovered genes can cause NS. Thus, the diagnosis of NS is still based on clinical features. In other words, it is made when a physician feels that a person has enough of the features to warrant the label. The principal values of making a genetic diagnosis are that it guides additional medical and developmental evaluations, it excludes other possible explanations for the features, and it allows more accurate recurrence risk estimates. With more genotype-phenotype correlation studies being performed, a positive genetic diagnosis will help the clinician to be aware of possible anomalies specific to that certain gene mutation. For example, an increase in hypertrophic cardiomyopathy is seen in people with a mutation of KRAS and an increased risk of juvenile myelomonocytic leukemia exists for a mutation of PTPN11. In the future, studies may lead to a targeted management of NS symptoms that depends on what genetic mutation a person has. Before birth Prenatal features that might lead physicians to consider a diagnosis of Noonan syndrome include cystic hygroma, increased nuchal translucency, pleural effusion, and edema. Differential diagnosis While Turner syndrome has similarities with renal anomalies and developmental delay, Turner syndrome is only found in females and often expresses differently. In Turner syndrome, there is a lower incidence of developmental delays, left-sided heart defects are constant and the occurrence of renal abnormalities is much lower.Other RASopathies Watson syndrome - Watson Syndrome has a number of similar characteristics with Noonans Syndrome such as short stature, pulmonary valve stenosis, variable intellectual development, and skin pigment changes. Cardiofaciocutaneous (CFC) syndrome - CFC syndrome is very similar to Noonans Syndrome due to similar cardiac and lymphatic features. However, In CFC syndrome intellectual disability and gastrointestinal problems are often more severe and pronounced. Costello syndrome - Like CFC syndrome, Costello syndrome has overlapping features with Noonans Syndrome. However, the conditions can be distinguished by their genetic cause. Neurofibromatosis 1 (NF1) Williams syndrome Management The treatment varies depending on complications but tend to be quite standard, reflecting the treatment of the general population. Management guidelines, divided by systems, including general, developmental, dental, growth and feeding, cardiovascular, audiological, haematological, renal and skeletal, that account for actions to be taken at diagnosis, after diagnosis and if symptomatic, have been published by an American consortium.Specifically, treatment of cardiovascular complications resemble that of the general population and treatment of bleeding diathesis is guided by the specific factor deficiency or platelet aggregation. Neuropsychological testing is recommended to find strengths and challenges to tailor support needed for school and career. Educational customization such as an individualized education program plan is sometimes needed for school-aged children. Speech therapy if speech and articulation issues present Physical therapy and occupational therapy for gross- and fine-motor delays Hypotonia and motor difficulties often impact handwriting. Accommodations for lessening handwriting demands will improve performance and save long-term hand function. Periodic follow up and lifelong monitoring of abnormalities found in any system, especially the cardiovascular system, is recommended. Anesthesia risk Although a few people with Noonan syndrome have been reported to develop malignant hyperthermia, the gene mutation of diseases known to be associated with malignant hyperthermia is different from that of Noonan syndrome. Prognosis The lifespan of people with Noonans syndrome can be similar to the general population, however, Noonan syndrome can be associated with several health conditions that can contribute to mortality. The greatest contributor to mortality in individuals with Noonan syndrome is complications of cardiovascular disease. Prognosis is therefore largely dependent on the presence or absence of cardiac disease, as well as the type and severity of the disease (if disease is present). Most notably, Noonan syndrome with hypertrophic cardiomyopathy is associated with increased mortality. History Jacqueline Noonan was practicing as a pediatric cardiologist at the University of Iowa when she noticed that children with a rare type of heart defect, valvular pulmonary stenosis, often had a characteristic physical appearance, with short stature, webbed neck, wide spaced eyes, and low-set ears
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What is Which of the following vasopressors woul be preferred in a patient with aortic stenosis and explain in detail?
None
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What is Most common site for bone metastasis in carcinoma of the breast in women is: and explain in detail?
(C) Spine > It is by this route that skeletal metastases occur, although the initial spread may be via the lymphatic system. In order of frequency the lumbar vertebrae, femur, thoracic vertebrae, rib and skull are affected and these deposits are generally osteolytic.> Metastases may also commonly occur in the liver, lungs and brain and, occasionally, the adrenal glands and ovaries; they have, in fact, been described in most body sites.
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What is In osteogenic sarcoma predominant histological finding is and explain in detail?
Histological appearance of osteosarcomaIt appears pale and extending through the coex on gross cut section examinationOn histological sections, it consists of malignant stromal tissue showing the osteoid formation (Refer: Mohindra's Fundamentals of Ohopedics, 2nd edition, pg no. 283)
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What is If a life time probability to develop a lung cancer is 25% than what are odds of deeveloping lung cancer in life time is - and explain in detail?
Ans. is 'b' i.e., 1 : 3 Odds It is another measure for the occurence of a outcome or event. It is the chance of frequency of occurrence of a characteristic relative to its non-occurrence, i.e., it is the ratio of occurrence. Odds Vs probability The probability is a propoion, i.e., it is the number of times a given outcome occurs divided by all the occurrences. If we take a sample of blood from a patient five times, and the sample is positive one time, then the probability is 1 in 5 or 0.20. On the other hand, the odds is a ratio, i.e., it is the number of times a given outcome occurs divided by the number of times that specific outcome does not occur. With same blood sample example, the odds of a positive sample is = No. of positive slide/No of negative slide = 1/4. Example If the probability of occurence of a cancer is 0.25 (25%). In otherword the nonoccurence of cancer will be = 1 - 0.25 = 0.75 (75%).
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What is Differentiating feature of Neisseria gonococcus from Neisseria meningitidis is ? and explain in detail?
None
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What is Dose of zinc used in acrodermatitis enteropathica is? and explain in detail?
Dose of zinc for acrodermatitis enteropathica is 2-3 mg/kg body weight
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What is All of the following are histological features of papillary carcinoma of thyroid, except: and explain in detail?
Histological features of Papillary thyroid carcinoma: Papillary carcinomas contain branching papillae having fibrovascular stalk covered by a single to multiple layers of cuboidal epithelial cells. Nuclei of papillary carcinoma cells contain finely dispersed chromatin, which impas an optically clear or empty appearance, giving rise to ground-glass appearance / Orphan Annie eye nuclei. Invaginations of cytoplasm often give appearance of intranuclear inclusions ("pseudo-inclusions") or intranuclear grooves. Concentrically calcified structures termed Psammoma bodies are often present within lesion, usually within cores of papillae Metastases to adjacent cervical lymph nodes occur in upto half of cases. Involvement of blood vessels is relatively uncommon, paicularly in smaller lesions. Amyloid deposits are found in medullary carcinoma of thyroid.
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What is Which of the following is not seen with SLE? and explain in detail?
Main lesion in SLE is synovitis and not monoahritis. SLEis assiciated with polyahritis but not monoahritis Alopecia, seizures & leucopenia- seen in SLE Note Most common cause of death in SLE : Lupus nephritis "Full house effect" and "Wireloop lesions" are seen in Lupus Nephritis Ahropathy associated with SLE : Jaccoud ahropathy Antibody responsible for CNS Lupus : Anti Ribosomal P
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What is Earliest light microscopic change in myocardial infarction is: and explain in detail?
When there is depletion of ATP, there is development of swelling in Myofibers leading to the haphazard arrangement of fibres causing waviness of the fibers. The typical changes of coagulative necrosis become detectable in the first 6 to 12 hours. "Wavy Fibers" may be present at the periphery of the infarct. These changes probably result from the forceful systolic tugs of the ble fibers on immediately adjacent, noncontractile dead fibers, causing stretching and folding.
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What is Shoest diameter of foetal skull is and explain in detail?
Bitemporal
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What is Most common cause of splenic rupture is - and explain in detail?
Most common cause of splenic rupture is Trauma. In the absence of trauma Spontaneous rupture of spleen occurs due to some minor physical insult to a spleen that has been rendered fragile by an underlying condition. The most common predisposing conditions are IMN, malaria, typhoid fever and lymphoid neoplasms.
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What is Single wavelength light is emitted by: and explain in detail?
Argon laser light has wavelength of 470 nm which is monochromatic (single wavelength or frequency) in nature.  It produces an intensity of 200 to 300 mW. ​Ref: Textbook of Operative Dentistry, Nisha and Amit Garg, 3rd edition, Pg no:277
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What is Ostium primum atrial septal defect and explain in detail?
The ostium primum atrial septal defect is a defect in the atrial septum at the level of the tricuspid and mitral valves. This is sometimes known as an endocardial cushion defect because it often involves the endocardial cushion, which is the portion of the heart where the atrial septum meets the ventricular septum and the mitral valve meets the tricuspid valve. Endocardial cushion defects are associated with abnormalities of the atrioventricular valves (the mitral valve and the tricuspid valve)
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What is Dissociative conversion disorder was previously described as - and explain in detail?
The term "hysteria" which was once prevalent is no more in use. Instead, these disorders are now called dissociation or conversion disorders.
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What is Leading questions are not asked in - and explain in detail?
None
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What is A 20-year old man has presented with increased alcohol consumption and sexual indulgence, irritability, lack of sleep, and not feeling fatigued even on prolonged periods of activity. All these changes have been present for 3 weeks. The most likely diagnosis is: and explain in detail?
C i.e. ManiaWhy Mania: The patient is irritable for 3 weeks (i.e. criteria A- abnormally & persistently elevated mood for atleast 1 week).There are 3 criteria B features i.e. increased sexual indulgence & alcohol consumption (excessive involvement in pleasureable activity) and decreased need for sleep.Q
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What is A 50-year-old presented to the ER with history of a road side accident. Patient was unconscious. e-Fast revealed fluid in the pelvis. Chest x-ray is given below. CT scan What is the most likely diagnosis in the above patient: - and explain in detail?
This is a case of diaphragmatic injury with herniation of bowel loops herniating into the thoracic cavity. Chest x-ray shows multiple air fluid levels in the right thoracic cavity - suggestive of bowel loops herniating into the thoracic cavity. CT scan shows discontinuity of diaphragm and herniation of bowel loops into the thoracic cavity. No hyperlucency with absence of bronchovascular markings seen in thorax - ruling out pneumothorax. No signs of pulmonary embolism seen. No opacification with detion of mediastinal structures to the ipsilateral side is seen - rules of collapse of lung.
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What is Which of the following is the likely organism causing ophthalmia neonatorum on the 3rd day of bih? and explain in detail?
The common causative organisms of ophthalmia neonatorum include Chlamydia trachomatis (most common), Neisseria gonorrhoeae (most threatening), Haemophilus species, Streptococcus species, Staphylococcus aureus, and viruses such as Herpes simplex (HSV). The "rule of fives" is a mnemonic for predicting the most likely bacterial etiology of the condition. However, there is considerable overlap in times to onset. 0 to 5 days: N gonorrhoeae 5 days to 5 weeks: Chlamydia 5 weeks to 5 years: Streptococcus or Haemophilus influenzae Ref: Levsky M.E., DeFlorio P. (2010). Chapter 2. Ophthalmologic Conditions. In K.J. Knoop, L.B. Stack, A.B. Storrow, R.J. Thurman (Eds), The Atlas of Emergency Medicine, 3e.
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What is Hereditary stomatocytosis and explain in detail?
Hereditary stomatocytosis describes a number of inherited, mostly autosomal dominant human conditions which affect the red blood cell and create the appearance of a slit-like area of central pallor (stomatocyte) among erythrocytes on peripheral blood smear. The erythrocytes cell membranes may abnormally leak sodium and/or potassium ions, causing abnormalities in cell volume. Hereditary stomatocytosis should be distinguished from acquired causes of stomatocytosis, including dilantin toxicity and alcoholism, as well as artifact from the process of preparing peripheral blood smears.: 237 Signs and symptoms Stomatocytosis may present with signs and symptoms consistent with hemolytic anemia as a result of extravascular hemolysis and often intravascular hemolysis. These include fatigue and pallor, as well as signs of jaundice, splenomegaly and gallstone formation from prolonged hemolysis. Certain cases of hereditary stomatocytosis associated with genetic syndromes have additional symptoms that are unrelated to the hemolytic anemia. Pathophysiology The two varieties of stomatocytosis classified with respect to cellular hydration status are overhydrated (hydrocytosis) and dehydrated (xerocytosis).: 225–226  Hereditary xerocytosis is characterized by autosomal dominant mutations in PIEZO1, which encodes a cation channel whose mechanosensitive properties enable erythrocytes to deform as they pass through narrow capillaries by decreasing their intracellular volume. More rarely, hereditary xerocytosis may be caused by mutations in KCNN4, which encodes a calcium ion-sensitive potassium channel that mediates the potassium efflux triggered by a rise in intracellular Ca2+ via activated PIEZO1 channels. Hereditary xerocytosis occurs more commonly in African populations, and it exhibits complex interactions with other hereditary alterations of red blood cells, including sickle cell disease and malaria resistance.Osmosis leads to the red blood cell having a constant tendency to swell and burst. This tendency is countered by manipulating the flow of sodium and potassium ions. A pump forces sodium out of the cell and potassium in, and this action is balanced by a process called the passive leak. In overhydrated hereditary stomatocytoses, the passive leak is increased and the erythrocyte becomes swamped with salt and water. The affected erythrocytes have increased osmotic fragility
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What is Severe thiamine deficiency is associated with: and explain in detail?
Ans. A Decreased RBC transketolase activity(Ref: Harper 31/e page 185)Thiamine is a coenzyme of Erythrocyte transketolase so its activity is decreased if Thiamine deficiency
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What is Adenomatoid odontogenic tumour is most commonly found in and explain in detail?
None
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What is Investigation of choice for diagnostic evaluation of hydrocephalus in one month old child : and explain in detail?
Investigation of choice for hydrocephalus in infant is USG.
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What is Mega voltage therapy consists of: and explain in detail?
Ans: A (Greater than 1000 k volts) Ref: Internet sourceExplanation:Megavoltage X-rays are produced by linear acceleratorsOperates at voltages in excess of 1000 kV (1 MV) range, and therefore have an energy in the MeV rangeBeams w ith the voltage range of 4-25 MV are used to treat patients because they penetrate w ell to deep sites within the body.
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What is Inhibition of glycolysis by increased supply of O2 is and explain in detail?
uCrab Tree Effect - Increasing concentrations of glucose accelerates glycolysis (the breakdown of glucose) which results in the production of appreciable amounts of ATP through substrate level phosphorylation. uPasteur effect - Under aerobic conditions, glycolysis is inhibited. This inhibitory effect of oxygen on glycolysis.uWarburg Effect - Most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells.Lehninger, Albe (2008). Principles of Biochemistry. 4th ed, p. 533.
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What is A 10 year old male patient complains of spacing between his upper front teeth. On clinical examination a midline diastema of 4 mm is seen. It is noted that the patient is in the mixed dentition period. Which of the following is the first line of treatment for this patient? and explain in detail?
Frenectomy before orthodontic space closure is contra-indicated due to the formation of scar tissue which may prevent the closure of space. As the age of the patient is 10 years, spontaneous correction could be an option due to the Broadbent phenomenon, however as a general guideline, diastema of more than 4mm is unlikely to resolve spontaneously.  Mesiodens is the most commonly seen supernumerary teeth and a diastema of more than 2 mm at the midline must always be inspected for the same.  A diastema of more than 2 mm should not be closed by tipping of the teeth, rather bodily repositioning is required.
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What is Which of the following surgical approach was first described by Orringer for the management of carcinoma esophagus- and explain in detail?
None
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What is A 35 years old, multigravida aboed 5 months back at 17 weeks of gestation. She has not got her periods yet. Urine pregnancy test is negative. Estrogen progesterone withdrawal test is negative. The likely diagnosis is: and explain in detail?
In Patient with secondary amenorrhea, after ruling out pregnancy progesterone challenge test is to be done. Patients with anovulation will get menses with progesterone. (Progesterone acts only on estrogen primed endometrium. In patients with anovulation, estrogen is present but progesterone is absent). Patients with both hypothalamo/ pituitary failure and ovarian failure will get menses with E + P. Absence of withdrawal by E + P indicates end organ failure. The Patient had a second-trimester aboion, following which a curettage may have been done to remove the retained products leading to Asherman syndrome The best diagnostic method is hysteroscopy and this is treated by Adhesiolysis
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What is Resolution provided by light microscope is: and explain in detail?
Resolving Power are : Light microscope – 0.25 um – 0.3 um – 200-300 nm Electron microscope – 2-10 A = 0.2 – 1 nm
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What is 1958. Most malignant form of NHL is - and explain in detail?
<p>Diffuse large B cell lymphoma comprises 31% of NHL.About half the cases have extranodal involvement at the time of presentation,paicularly in the bone marrow & alimentary tract.It is a high grade NHL & is very aggressive & disseminate widely.It has rapid proliferation rates,rapidly produces symptoms & is fatal if untreated.</p><p>Reference :Harsh mohan textbook of pathology sixth edition pg no 377</p>
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What is Which of the following types of mosquitos are now restricted to Andaman and Nicobar islands? and explain in detail?
Some points about Anopheles species given in Park 21th edition 1) Anopheles Culicifacies - Vector in rural and peri urban areas 2) Anopheles Stephensi - Vector in urban and industrial areas 3) Anopheles Flutilis - vector in hilly areas and forests of east 4) Anopheles Minimus - Vector in foot hills of Noh-Eastern states 5) Anopheles Dirus - Vector in forests of noh east 6) Anopheles Epiroticus - Vector in Andaman and Nicobar Islands Ref: Park, Edition 21, Page 232.
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What is Which one of the components of the TCR (T-cell receptor) is responsible for transmitting signals into the interior of the cell? and explain in detail?
The CD3 complex associated with the TCR receptor contains two zeta chains that function for transmitting intracellular signaling.
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What is Isotope used in myocardial perfusion scan is – a) Technetiumb) Thalliumc) Stannous pyrophosphated) Gallium and explain in detail?
Perfusion Scan   → Thallium (mc), technetium, MIBI. Infarct Scan       →  Technetium pyrophosphate.
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What is Objectives of National Mental Health Program include all except:- and explain in detail?
Objectives of National Mental Health Program - 1. To ensure availability & accessibility of minimum mental health care for all 2. To promote community paicipation in mental health services development 3. To encourage application of mental health knowledge in general health care Also remember, Aims of National Mental Health Program; Prevention & treatment of mental health disorders Use of mental health technology to improve health Application of mental health principles in development & to improve quality of life
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What is Creamy fishy odor is caused by : and explain in detail?
clinically creamy vaginal discharge with fishy odour without evidence of excessive inflammation Whiff test: Fishy odour when a drop of discharge is mixed with 10%KOH solution and is seen in bacterial vaginosis caused by Gardnerella vaginalis D.C.DUTTA'S TEXTBOOK OF GYNECOLOGY,Pg no:152,6th edition
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What is Women with vitamin B12 deficiency presents with dysphagia and anemia. What is the syndrome that describes this presentation? and explain in detail?
Classical features of Plummer-Vinson (Patterson Brown-kelly) Syndrome includes dysphagia, iron deficiency anemia, upper esophageal inflammation with web formation, angular stomatitis and gastritis. It usually affects females in their fouh or fifth decade. Esophageal webs are formed at the junction between squamous mucosa of esophagus and islands of gastric type mucosa in the upper esophagus. Barium swallow shows a web in the post-cricoid region and the same can be seen on oesophagoscopy. It is due to subepithelial fibrosis in this region. About 10% of the cases with this syndrome will develop post-cricoid carcinoma. Treatment: Primary treatment is to correct anemia by oral/parenteral iron. Associated B12 and B6 deficiency should also be corrected. Dilatation of the webbed area by esophageal bougies help to relieve dysphagia.
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What is Jamaican vomiting sickness cause by unripe apple fruit toxin? and explain in detail?
Ans. is 'd' i.e., Hypoglycin A Jamaican Vomiting Sickness Jamaican vomiting sickness is an acute illness caused by the toxin hypoglycin A, which is present in unripened fruit of the ackee tree. When ingested, hypoglycin A is metabolized to produce methylenecyclopropylacetic acid (MCPA). MCPA acts to inhibit the beta-oxidation of fatty acids. It is characterized by vomiting, coma, free fatty academia, dicarboxylicaciduria, depletion of liver glycogen, fatty degeneration of liver and death.
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What is Dental and periodontal infections can pose a severe risk to patients under and explain in detail?
None
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What is Which of the following drug belongs to antifolate group: September 2007 and explain in detail?
Ans. C: Pyrimethamine
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What is Inguinal ligament forms the boundaries of - and explain in detail?
Inguinal ligament forms the base of femoral triangle and also forms the inferior border of Hesselbach’s triangle.
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What is Stones are most commonly seen in which salivary gland: March 2005, 2007 and explain in detail?
Ans. A: Submandibular Sialolithiasis Most common disease of salivary glands Twice as common in males as females 80-95% occur in submandibular gland or duct ( because their secretion is highly viscous) Stones are most common cause of acute and chronic infection of salivary glands 80% of submandibular stones are opaque; 60% of parotid are opaque Consist of mainly calcium phosphate Not associated with systemic calcium abnormalities Very unusual for patients to have a combination of radio-opaque and non-opaque stones - Signs and symptoms Pain and swelling of involved gland Sialolithiasis causes pain and swelling of the involved salivary gland by obstructing the food-related flow of salivary secretions Calculi may cause stasis of saliva facilitating bacterial ascent into the gland and subsequent infection Some may be asymptomatic - Imaging Plain radiography Opaque stone in course of Whaon's (submandibular) or Stensen's (parotid) ducts CT Stone in duct Ductal dilatation
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What is Most abundant type of Crystalline protein in Lens is and explain in detail?
Among the Crystalline proteins, β Crystallin protein forms 55% of the total proteins.
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What is Morphine is used in the treatment of:- and explain in detail?
These are used as analgesic agents. Visceral, dull and constant pain is relieved more effectively than inflammatory pain. Opioids are however contraindicated in biliary colic. Morphine (i.v.) is useful in myocardial infarction as well as in pulmonary edema due to acute left ventricular failure.
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What is Epididymis is covered by: and explain in detail?
The epididymis is invested by tunica vaginalis, somewhat less closely applied than it is to the testis, except at its posterior margin. Ref: Gray's anatomy 40th edition, Chapter 97.
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What is Molluscum contagiosum is a ________: and explain in detail?
Ref: Textbook of Microbiology by Surinder Kumar, P 534* Molluscum contagiosum virus is a pox virus, which causes a contagious, benign epidermal tumor that occurs in humans only.* Lesion: small, pink, papular, warty, pearl-like benign tumors of the face, arm, back and buttocks.Poxviruses causing disease in humansGenusVirusPrimary hostDiseaseOrthopoxvirusVariolaHumansSmallpox (now eliminated)VacciniaHumansLocalized lesion; used for smallpox vaccinationBuffalopoxWater buffaloHuman infections rate; localized lesionMonkeypoxRodents, monkeysHuman infections rate; generalized diseaseCowpoxCowsHuman infections rare; localized ulcerating lesionParapoxvirusOrfSheepHuman infections rare; localized lesionPseudocowpoxCows Bovine popular stomatitisCows MollusapoxvirusMolluscum contagiosumHumansMany benign skin nodulesYatapoxvirusTanapoxMonkeysHuman infections rare; localized lesionYabapoxMonkeysHuman infections very rare and accidental; localized skin tumors
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What is Additional daily energy requirement during the first six months for a lactating woman is ? and explain in detail?
Ans. is 'None' Additional daily energy requirement during first six months of lactation is+- 600 Kcal/day.
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What is Sinus least involved in sinusitis is: and explain in detail?
Isolated involvement of sphenoid sinus is rare. It is often a pa of pansinusitis or is associated with infection of posterior ethmoidal sinus. The sphenoid sinus is rarely affected on its own --Turner 10th/ed p 48 The reason for sphenoid sinus to be least affected is that it opens high up in the sphero ethmoid recess which is not affected by most of the conditions of nose
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What is All of the following are advantages of laparoscope assisted vaginal hysterectomy (LAVH) over abdominal hysterectomy except: March 2011 and explain in detail?
Ans. D: Scope of wide exploration of the abdominal and pelvic organs Advantages of laparoscopy over laparotomy includes 1) reduced pain and quick recovery, 2) sho hospital stay and 3) less peritoneal adhesions postoperatively
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What is In a chronic alcoholic all the following may be seen in the liver except - and explain in detail?
Ans. is 'c' i.e., Granuloma formation
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What is Muller's muscle is supplied by: and explain in detail?
Each eyelid from anterior to posterior consists of thefollowing layers:1. Skin2. Subcutaneous areolar tissue3. Layer of striated muscle (orbicularis oculi andlevator palpebrae superioris in upper lid only)4. Submuscular areolar tissue5. Fibrous layer (tarsal) plate and septum orbitale6. Layer of non-striated muscle fibres (Muller'smuscle)7. Conjunctiva Layer of striated muscle. consists of orbicularis muscle which forms an oval sheet across the eyelids. It closes the eyelids and is supplied by zygomatic branch of the facial nerve. in paralysis of facial nerve there occurs lagophthalmos which may be complicated by exposure keratitis. Levator palpebrae superioris muscle (LPS).(main muscle ) It arises from the apex of the orbit and is inseed by three pas on the skin of lid, anterior surface of the tarsal plateand conjunctiva of superior fornix. It raises the upper lid. It is supplied by a branch of oculomotor nerve Layer of non-striated muscle fibres. It consists of the palpebral muscle of Muller (ascessory muscle)which lies deep to the septum orbitale in both the lids. In the upper lid it arises from the fibres of LPS muscle in the lower lid from prolongation of the inferior rectus muscle and is inseed on the peripheral margins of the tarsal plate. It is supplied by sympathetic fibres it helps in initial 15o opening of eye .
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What is Sensory supply to the posterior one third of tongue is: and explain in detail?
Parts of the Tongue
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What is Muscle relaxant associated with increased ICP is? and explain in detail?
Ans. is 'c' i.e., Suxamethoneum * Sch causes increases in all pressures - intraocular, intracranial, BP, and intrabdominalSuccinylcholine (Suxamethonium)* SCh is a depolarising skeletal muscle relaxant.* It causes sustained partial depolarization of muscle end plate - Initially produce twitching and fasciculation followed by flaccid paralysis.* It is the shortest and fastest acting skeletal muscle relaxant.* It is the only muscle relaxant which stimulate autonomic ganglia and vagus - Bradycardia occurs due to vagal stimulation.* SCh is the most commonly used muscle relaxant for passing endotracheal tube (rapacuronium and rocuronium are alternatives).* SCh is rapidly hydrolysed by plasma cholinersterase, some patients have genetically determined abnormality or deficiency of pseudocholinesterase, in them, SCh causes phase II block (dual block).* It can cause muscle fasiculations and soreness, change in BP and HR, arrhythmia, histamine release and K+ effux from muscles.* Post-operative muscle pain (myalgia, muscle soreness) is a very common problem.* It can accentuate malignant hyperthermia caused by halothane - Succinylcholine is the most common cause of malignant hyperthermia.* Succinylcholine can cause dangerous hyperkalemia in patients with: -# Burn# Massive trauma# Crush injury# Severe intra-abdominal infection# Spinal cord injury# Hemiplegia/Paraplegia# Muscular dystrophy# GB syndrome# Rhabdomyolysis# Severe Parkinsonism# Tetanus# Polyneuropathy# Closed head injury# Stroke# Encephalitis# Mysthenia gravis* SCh causes increases in all pressures -> intraocular, intracranial, BP, and intrabdominal.* SCh can cause Trismus (masseter spasm) especially in patients susceptible for malignant hyperthermia.
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What is External Cephalic Version (ECV) is contraindicated in all of the following , EXCEPT? and explain in detail?
ECV -Absolute contraindications : Placenta pre Multifetal gestation Severe contracted pelvis - Relative contraindications Early labor oligohydramnios or rupture of membranes structural uterine abnormalities fetal growth restriction prior abruption
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What is Commonest presentation of Hodgkin's lymphoma is - and explain in detail?
Most patients present with palpable lymphadenopathy that is nontender; in most patients, these lymph nodes are in the neck, supraclavicular area, and axilla. More than half the patients will have mediastinal adenopathy at diagnosis, and this is sometimes the initial manifestation. Subdiaphragmatic presentation of Hodgkin's disease is unusual and more common in older males." - Harrison
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What is A child presenting to the clinic is showing features of Down's syndrome. Which is the MOST common cardiac lesion in a child with Down's syndrome? and explain in detail?
The most common cardiac abnormality in children with Down's syndrome is atrioventricular septal defect which occur in 45% of cases. Isolated VSD occur in 35% cases, isolated secundum ASD is seen in 8% of cases and TOF is seen in 5% cases. Clinical manifestations of Down's syndrome are: Congenital anomalies of hea and GIT Epicanthal folds Flattened facial profile Small rounded ears Upslanted palpabral fissures Excess nuchal skin Brachycephaly Increased risk of leukemia Immune system defects Alzheimer like dementia Ref: Hurst's The Hea, 13e chapter 82.
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What is Akathisia is treated by all except: and explain in detail?
Ref: KDT 6/e p431 *Akathisia is a side effect of antipsychotic drugs like haloperidol: It is treated with - Central anticholinergics like Trihexyphenidyl - First generation antihistaminics like Promethazine *Propanolol *Diazepam
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What is Which of the following is the most radiosensitive ovarian tumors: and explain in detail?
“Below the age of 20 years 60% of the tumours are of germ cell origin and in girls under the age of 10 years almost 85% are of germ cell origin and are invariably malignant.” “Dysgerminoma is the most common malignant germ cell tumour accounting for about 40% of all ovarian cancers of germ cell origin.” “Dysgerminomas are the most common malignant germ cell tumours of the ovary and have been considered the female - equivalent of seminoma.” Most common germ cell tumour of ovary is dermoid cyst (mature teratoma). It is benign in nature. Remember: • Most common ovarian tumour (overall) – Epithelial cell tumour. • Most common tumour in young woman is – Germ cell tumour.  • Most common malignant tumour of ovary – Serous cystadenocarcinoma. • Most common benign tumour of ovary (overall) – Dermoid cyst.  • Most common benign epithelial tumor of ovary – Serous cystadenoma.  • Most common germ cell tumour – Mature teratoma (Dermoid cyst). • Most common malignant GCT – Dysgerminoma. • Most common ovarian tumour in pregnancy (but in remains undiagnosed) – Serous cystadenoma. • Most Common benign tumour diagnosed in pregnancy – Dermoid cyst. • Overall most common ovarian tumour diagnosed in pregnancy – Dermoid cyst. • Most common malignant ovarian tumor detected during pregnancy – Dysgerminoma. • Germ cell Tumor with best pregnosis Dyserminoma • Germ cell tumor with worst prognosis- endodermal sinus tumor • Germ cell tumor which has maximum bilaterality– Dysgerminoma • Germ cell tumor which presents as accute abdomen- Endodermal Sinus Tumor • Most common ovarian tumour to undergo torsion during pregnancy – Dermoid cyst. • Most common ovarian tumour to involve opposite ovary by metastasis – Granulosa cell tumour. • Most radiosensitive ovarian tumour – Dysgerminoma. • Most rapidly growing ovarian tumour – Yolk sac Tm- (Endodermal Sinus Tumor) • Most connective tissue tumour – Fibroma. Ovarian Tumour: Causing: • Pseudomyxoma peritonei – Mucinous cystadenoma. • Meig’s syndrome – Ovarian fibroma • Pseudomeig’s syndrome: – Brenner’s tumour – Granulosa cell tumour – Thecoma • Ovarian tumour associated with hyperpyrexia and hypercalcemia – Mesonephroid tumour. • Ovarian tumour arising from epithelium of urinary tract – Brenner Tm • Feminizing tumours: – Granulosa cell tumour – Theca cell tumour – Fibromas • Virilising tumour: – Androblastoma – Hilus cell Tm – Gynadroblastoma – Adrenal cortical tumour • Largest benign ovarian Tm – Mucinous cyst adenoma • Mucinous tumours are associated with: – Dermoid cyst (MBD) – Brenner’s tumour • Tumour with lymphocytic infilteration:
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What is Sulphasalazine is NOT used for the treatment of and explain in detail?
None
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What is Medicolegal autopsy requires the permission of -a) Policeb) Magistratec) Relatived) Medical superitendant and explain in detail?
Autopsy should,be done only after receiving written order from police officer or magistrate.
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What is Type of collagen present in the ovary? and explain in detail?
Type XXVI is distributed in Testis and ovary Reference: Harper; 30th edition; Page no: 628 Table no: 50-1
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What is A patient with acute psychosis, who is on haloperidol 20mg/day for last 2 days, has an episode characterized by tongue protrusion, oculogyric crisis, stiffness and abnormal posture of limbs and trunk without loss of consciousness for last 20 minutes before presenting to casualty. This improved within a few minutes after administration of diphenhydramine HCl. The most likely diagnosis is and explain in detail?
DOC for acute muscular dystonia is one of the central anticholinergic. Diphenhydramine has anticholinergic property, therefore the patient in question had improved after administration of diphenhydramine.
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What is Agents that block the differentiation or activity of osteoclasts are all except? and explain in detail?
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What is Largest pathogenic Bacillus organism is - and explain in detail?
The anthrax bacillus is one of the largest of pathogenic bacteria measuring 3-10 x 1-16 um. It resembles a Bamboo stick appearance Ref: Ananthanarayan & paniker's Textbook of Microbiology 9th edition pg no 244
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What is Characteristic of protective epithelium is- and explain in detail?
Ans. is 'a' i.e., Regeneration of membraneo The regeneration of epithelium is one of the protective mechnaism of epithelial cells, o There are three mechanism for healing:ResolutionIt is an ideal outcome of healing and occurs in acute inflammatory responses to minor injuriesRegenerationReplacement of lost parenchymal cells by division of adjacent surviving are parenchymal cells (Regeneration) can also restore injured tissue to normal.Whether regeneration occurs depends uponRegenerative capacity of the involved cell (i.e., their ability to divide)The no. of surviving viable cellsPresence of connective tissue framework that will provide the base for restoration ofnormal tissue structure.Repair by scar formation# A scar is a mass of collagen that is the end result of repair by organization and fibrosis. Repair by scar formation occurs when :o Resolution fails to occurs in an acute inflammatory responseo When there is ongoing tissue necrosis in chronic inflammation.o When parenchymal cells necrosis cannot be repaired by regeneration.
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What is Which one of the following conditions is associated with Kawasaki&;s syndrome? and explain in detail?
Kawasaki disease is an acute, febrile, multisystem disease of children. Although the disease is generally benign and self-limited, it is associated with coronary aery aneurysms in approximately 25% of cases.There is typical intimal proliferation and infiltration of the vessel wall with mononuclear cells. Beadlike aneurysms and thromboses may be seen along the aery. Other manifestations include pericarditis, myocarditis, myocardial ischemia and infarction, and cardiomegaly. High-dose IV g-globulin (2 g/kg as a single infusion over 10 h) together with aspirin (100 mg/kg per day for 14 days followed by 3-5 mg/kg per day for several weeks) have been shown to be effective in reducing the prevalence of coronary aery abnormalities when administered early in the course of the disease. Surgery may be necessary for Kawasaki disease patients who have giant coronary aery aneurysms or other coronary complications. Surgical treatment most commonly includes thromboendaerectomy, thrombus clearing, aneurysmal reconstruction, and coronary aery bypass grafting.Ref: Harrison&;s Principles of Internal Medicine; 19th edition; Chapter 385 The Vasculitis Syndromes; Page no: 2193
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What is Composition of super EBA includes all except: and explain in detail?
None
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What is Thoracic duct opens into and explain in detail?
In the neck, it arches laterally at the level of the transverse process of seventh cervical veebra. Finally it descends in front of the first pa of the left subclan aery and ends by opening into the angle of junction between the left subclan and left internal jugular veins ( both these left subclan and left internal jugular vein drains into left brachiocephalic vein ) <img src=" /> Ref : B D Chaurasia's Human Anatomy , seventh edition , volume 1, pg. no. 302
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What is Oestrogen causes proliferation of and explain in detail?
Oestrogen causes proliferation of glycogen containing superficial cells and progesterone causes proliferation of intermediate cells.
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What is Which diuretic could be considered appropriate for combining with ACE inhibitors and explain in detail?
ACE inhibitors are contra-indicated in the presence of hyperkalemia.Aldosterone antagonists and epithelial sodium channel blockers are potassium sparing diuretics and should not be combined with ACE inhibitors. Thiazides on the other hand cause hypokalemia and can be combined with ACE inhibitors.
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What is Least concentration of human immunodeficiency virus is seen in and explain in detail?
Viral load of HIV is maximum in blood, genital secretions like semen, and CSF It also found in breast milk, saliva, lymphocytes, cell-free plasma, cervical secretions, saliva, tears, & minimal in urine Saliva can contain fibronectin & glycoproteins, which prevent transmission of the virus. A salivary protein called secretory leucocyte protease inhibitor also has anti-HIV activity
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What is Small intestinal biopsy is diagnostic in :a) Whipple's diseaseb) Abetalipoproteinemiac) Celiac diseased) Agammaglobulinemia and explain in detail?
None
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What is Most common complication of acute otitis media in children - and explain in detail?
Most common complication following ASOM is mastoiditis. Facial nerve palsy is an uncommon complication of ASOM.
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What is During root canal instrumentation, the apical constriction is violated and enlarged to a size no. 50 instrument, which of the following is appropriate treatment for this canal: and explain in detail?
None
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What is Fine voluntary movements are transmitted by and explain in detail?
(A) Lateral corticospinal tract > The nerve fibers that pass from the motor cortex to the cranial nerve nuclei form the corticobulbar tract. The nerve fibers that cross the midline in the medullary pyramids and form the lateral corticospinal tract make up about 80% of the fibers in the corticospinal pathway.> The remaining 20% make up the anterior or ventral corticospinal tract, which does not cross the midline until it reaches the level of the muscles it controls. At this point, its fibers end on interneurons that make contact with motor nerves on both sides of the body.> The lateral corticospinal tract is concerned with skilled movements, and in humans its fibers end directly on the motor neurons.
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What is Downward displacement of enlarged spleen is prevented by : and explain in detail?
B. i.e. Phrenicocolic ligament
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What is The earliest identifiable cells of T-Cell lineage during maturation are and explain in detail?
None
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What is First step in epidemic done by an epidemiologist? and explain in detail?
Ans. is 'b' i.e., Confirmation of diagnosis Steps for Investigation of Epidemic : Verification of diagnosis : Is the first step in investigation of an epidemic' Confirmation of existence of an epidemic: Compare with disease frequencies during same period in previous years Epidemic threshold: An arbitrary limit of '2 standard errors from the endemic occurrence' Defining the population at risk: Obtaining the map of the area Calculation of 'appropriate denominator of population at risk' Rapid search for all cases and their characteristics: Medical survey Epidemiological case sheet Searching for more cases: Search for new cases is carried out everyday, till the area is declared free of epidemic; this period is usually taken as 'twice the incubation period of the disease since the occurrence of last case' Data analysis: Formulation of hypothesis Testing of hypothesis Evaluation of ecological factors Fuher investigation of population at risk Writing the repo
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What is True regarding gypsum bonded investments is: and explain in detail?
After dehydration all forms of gypsum shrink between 200-400° C. Between 400 and 700° C, a slight expansion is noted. Lateral shrinkage in gypsum is caused due to the decomposition and the release of sulfur dioxide. It is imperative, that gypsum investment should not be heated above 700° C. Phillip’s 12th edition page 201
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What is Rifle Classification is for : and explain in detail?
RIFLE - AKI. KDIGO Classification - CKD.
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What is Pentose pathway produces and explain in detail?
The major purpose of the pentose phosphate pathway is generation of reduced NADPH and pentose phosphates for nucleotide synthesis.Ref: DM Vasudevan, 7th edition, page no: 130
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What is All the following are the indicators for single visit endodontics EXCEPT and explain in detail?
None
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What is Dysphagia lusoria is most commonly caused by- and explain in detail?
Ans. is 'b' i.e., Aberrant right subclavian artery o Has been explained in previous sessions.
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What is Leydig cells secrete and explain in detail?
Leydig cells are the cells between the seminiferous tubules of the testis that secrete testosterone.Ref: Ganong&;s review of medical physiology; 24th edition; page no:-394
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What is "L-form" phenomenon is most likely to occur in ? and explain in detail?
Ans. is 'd' i.e., Mycoplasma
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What is When deviation of the mandible is seen during opening and closing movements, zygomatic arch fracture should be suspected. Trismus or inability to close the mouth may be an indication of a condylar injury. and explain in detail?
You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is A Patient, who is on anti-hypertensive drug, develops dry cough. Which of the following drug might be responsible for the condition: and explain in detail?
Ref: KDT, 6th ed. pg. 484* Angiotensin converting enzyme normally helps in conversion of angiotensin I to angiotensin II, which acts as a vasoconstrictor in case of hypovolemia.* In addition to that, ACE also helps in breakdown of bradykinin.* When ACE inhibitors (captopril) are given, it inhibits ACE and in addition inhibits breakdown of bradykinin also, which leads to accumulation of bradykinin level in body.* This increased level of bradykinin presents with Dry cough, rashes, urticaria and angioedema.Other side effects of ACE inhibitorsContraindications of ACE (-)Safe alternative of ACE (-)HypotensionHyperkalemiaFetal growth retardationPregnancyBilateral Renal artery stenosisHyperkalemiaAngiotensin receptor blocker is a safe alternative in case of cough, angioedema.* Why ACEI is contraindicated in bilateral renal stenosis# Patients with B/L renal artery stenosis or patients with single kidney having renal artery stenosis will develop renal failure if treated with ACEI.# In stenosis there is reduced GFR, and body manage the adequate GFR by angiotensin II mediated efferent arteriole constriction to maintain the renal perfusion. In such patients, Inhibition of ACE can induce acute renal insufficiency.
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What is Which of the following would be the best morphological feature to distinguish ulcerative colitis from Crohn's disease? and explain in detail?
Pseudopolyps are more commonly found in ulcerative colitis than Crohn's disease. These are discrete areas resulting from surviving islands of mucosa or heaped up granulation tissue. Since in ulcerative colitis there is diffuse mucosal inflammation these pseudopolyps are diffusely distributed. Distinguishing features between Ulcerative colitis and Crohn's disease: Ulcerative colitis Crohn's disease Rectal involvement Yes Variable Distribution Diffuse Segmental or diffuse Terminal ileum Backwash ileitis Thickened and stenosis Serosa Normal Creeping fat Mucosa Hemorrhagic Cobblestone and linear ulcers Pseudopolyps Frequent Less common Strictures No Common Fistulas No Common Lymphoid hyperplasia Infrequent Common Crypt abscess Extensive Focal Ref: Pediatric Inflammatory Bowel Disease By Petar Mamula page 227.
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What is Active principle of Oleander is? and explain in detail?