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400. C) he variation in proteins expressed by each cell re- lects cell-speciic expression and repression of speciic genes. Each cell contains the same DNA in the nucleus and the same number of genes, and thus diferentiation results not from diferences in the genes but from selective repression and/or activation of diferent gene promoter Join @Superspeciality for more questions and detailed explanation For all recent updates, join https://t.me/DocopsyPoint_Superspeciality

399. Explanation A) (B) Hemochromatosis is defined as a disorder in iron metabolism that is characterized by excess iron absorption, saturation of iron-binding proteins, and deposition of hemosiderin in the tissues. The primary affected tissues are the liver, pancreas, and skin. Iron deposition in the liver leads to cirrhosis and in the pancreas causes diabetes. The excess iron deposition leads to bronze pigmentation of the organs and skin. In fact, the bronze skin pigmentation seen in hemochromatosis, coupled with the resulatant diabetes lead to the designation of this condition as bronze diabetes. The primary cause of hemochromatosis is the inheritance of an autosomal recessive allele. The locus causing hemochromatosis has been designated HFE and is a major histocompatibility complex (MHC) class-1 gene. The gene encodes an alpha-chain protein with three immunoglobulin- like domains. This alpha-chain protein associates with beta-2-microglobulin. Normal HFE has been shown to form a complex with the transferrin receptor and in so doing is thought to regulate the rate of iron transfer into cells. A mutation in HFE will therefore, lead to increased iron uptake and storage. The majority of hereditary hemochromatosis patients harbor a mutation in HFE that results in the substitution of Cys 282 for a Tyr. This mutation causes loss of conformation of one of the immunoglobulin domains in HFE. Another mutation found in HFE causes a change of His 68 to Asp. DMT1 (choice A) is responsible for the intestinal absorption of dietary iron and thus, a deficiency in this protein would lead to reduced total body iron, not excess. Ferritin (choice C) is the intracellular iron binding and storage protein. A deficiency in ferritin would lead to less iron deposition, not excess. Ferroportin (choice D) is the iron transport protein that moves dietary iron from within intestinal enterocytes across the basolateral membrane to the circulation, therefore, a deficiency in this protein would have consequences similar to deficiencies in DMT1. Transferrin (choice E) is the iron transport protein of the blood that binds to the trasferrin receptor on cell surfaces, allowing cellular uptake of circulating iron. A deficiency in this protein would lead to less iron deposition not more. @Superspeciality

399. Explanation A) (B) Hemochromatosis is defined as a disorder in iron metabolism that is characterized by excess iron absorption, saturation of iron-binding proteins, and deposition of hemosiderin in the tissues. The primary affected tissues are the liver, pancreas, and skin. Iron deposition in the liver leads to cirrhosis and in the pancreas causes diabetes. The excess iron deposition leads to bronze pigmentation of the organs and skin. In fact, the bronze skin pigmentation seen in hemochromatosis, coupled with the resulatant diabetes lead to the designation of this condition as bronze diabetes. The primary cause of hemochromatosis is the inheritance of an autosomal recessive allele. The locus causing hemochromatosis has been designated HFE and is a major histocompatibility complex (MHC) class-1 gene. The gene encodes an alpha-chain protein with three immunoglobulin- like domains. This alpha-chain protein associates with beta-2-microglobulin. Normal HFE has been shown to form a complex with the transferrin receptor and in so doing is thought to regulate the rate of iron transfer into cells. A mutation in HFE will therefore, lead to increased iron uptake and storage. The majority of hereditary hemochromatosis patients harbor a mutation in HFE that results in the substitution of Cys 282 for a Tyr. This mutation causes loss of conformation of one of the immunoglobulin domains in HFE. Another mutation found in HFE causes a change of His 68 to Asp. DMT1 (choice A) is responsible for the intestinal absorption of dietary iron and thus, a deficiency in this protein would lead to reduced total body iron, not excess. Ferritin (choice C) is the intracellular iron binding and storage protein. A deficiency in ferritin would lead to less iron deposition, not excess. Ferroportin (choice D) is the iron transport protein that moves dietary iron from within intestinal enterocytes across the basolateral membrane to the circulation, therefore, a deficiency in this protein would have consequences similar to deficiencies in DMT1. Transferrin (choice E) is the iron transport protein of the blood that binds to the trasferrin receptor on cell surfaces, allowing cellular uptake of circulating iron. A deficiency in this protein would lead to less iron deposition not more. @Superspeciality

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Medicine Q Q) pt has level of leison at umbilicus, what is the vertebral leison - T7- T9 Q) one from onco, CKD 20 + CDK 7-, not seen on PET scan - ovarian - breast - lung - colon Q) mean>median > mode( values were given) - positively skewed - negatively skewed - no change - Q) pt with steatorrhoea schillings positive, d xylose normal, duodenal biopsy normal - ileal disease - intestinal lymphangectasia - UC - celiac disease Q) elderly patient with MI 6 months back require add on therapy to metformin, - SGLT2 - voglibose - - Q) In CLD pt Not useful in MRSA Meropenam Linezolid Daptomycin Teicoplanin Q) One hyponatremia correction, S Na 110 Body weight 75 How much ml of 3percent saline will increase sodium by 8 meq: 800ml 400ml 200ml 100ml Q) clinically homocyteinuria, which one will u add in diet - pyridoxine - carbo - protein - lipid Q) something on body packing/cocaine/heroin Q) which is used in Hairy cell leukemia recently treated with Fludaribine, requires blood transfusion - leukoreduced RBCS - irradiated RBCS - whole blood - Q) patient with 2 spon abortions in past, travelled for 8 hrs, Now has DVT, Aptt 3 time ULN Treatment - warf then aspirain - LMWH f/b warf with inr target 2.5-3.5 for life long - LMWH f/b warf with INr target 2-3 for 12 months - Q) which is not a/ with hep C - FSGS -PAN - MN -MPGN Q) which is not seen in amyloid - stroke - sensory neuropathy - lumbisacral radiculopathy - autonomic neuropathy Q) which one is not used in fluid resuscitation - IVC collapsiblity - SV with passive SLR - USG of lung - Q) which is not used as initial inv for secondary ammenorrhea -FSH/LH - USG abdo - testosterone - prolactin Q) which is not included in clinical pulmonary infection score - BP - fever - CXR - Q) which is not a feature of seronegative spA - strongly associated with HLA B27 - Rf negative - uveitis - symmetrical polyarthritis Q) Elderly male with hyponatremia ,which of the test is not useful as first line investigation: -ONDST -ACTH stimulation -TSH -Urine sodium Q) diff SIADH vs CSW - extravasc volume status - serun uric acid levels - high urine Na - high urine osm Q) On routine examination patient found to have LVH, systolic ejection murmur, ( sounded like HOCM) Performs valsalva, what will happen to his murmur - increase - decrease - no change - Q) one patient sudden collapses while playing basketball, found to have VT, which electrolytes will u ask - ca, k, Mg -na, k, ca - na, ca, mg - Q) In relation to SACD which is false - always corealtes with anemia - inv of lateral and dorsal colums - cu def has similar manifestation - Q) patient of DM on triple drugs- Metformin, dapagliflozim and ? Has acidosis . What is the cause - metformin induced lactic acidosis - euglycemia ketoacidosis - - Q) which is not useful in ICH scoring - age - volume kf bleed - location of bleed - delay in presentation Q)regarding covid vaccine which is incorrect - VITT is an indiosyncratic reaction - chadox is adenovirus vector - mrna vaccines rarely causes myocarditis in males - Q) which is false about tocilizumab In a patient who has presented with ARDS and is planed to get intubated - subcut is inferior to iv - used when CRP>60 - given as single dose - Q) patient on treatment of depression, one ECG was given ( looked like TCA toxicity) Which is false statement - this ia a case of BZD poisoning - QRS> 100 increases risk of seizures - ? Gastric decontamination Q) patient with oligouria, u output of 10ml/hr is started on furosemide infusion of 0.3mg/hr Which is false - furosemide increases risk of ATn in sepsis - Furosemide delays Need of dialysis -at this dose it wont cause ototoxicity - @superspeciality

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399. Explanation A) (B) Hemochromatosis is defined as a disorder in iron metabolism that is characterized by excess iron absorption, saturation of iron-binding proteins, and deposition of hemosiderin in the tissues. The primary affected tissues are the liver, pancreas, and skin. Iron deposition in the liver leads to cirrhosis and in the pancreas causes diabetes. The excess iron deposition leads to bronze pigmentation of the organs and skin. In fact, the bronze skin pigmentation seen in hemochromatosis, coupled with the resulatant diabetes lead to the designation of this condition as bronze diabetes. The primary cause of hemochromatosis is the inheritance of an autosomal recessive allele. The locus causing hemochromatosis has been designated HFE and is a major histocompatibility complex (MHC) class-1 gene. The gene encodes an alpha-chain protein with three immunoglobulin- like domains. This alpha-chain protein associates with beta-2-microglobulin. Normal HFE has been shown to form a complex with the transferrin receptor and in so doing is thought to regulate the rate of iron transfer into cells. A mutation in HFE will therefore, lead to increased iron uptake and storage. The majority of hereditary hemochromatosis patients harbor a mutation in HFE that results in the substitution of Cys 282 for a Tyr. This mutation causes loss of conformation of one of the immunoglobulin domains in HFE. Another mutation found in HFE causes a change of His 68 to Asp. DMT1 (choice A) is responsible for the intestinal absorption of dietary iron and thus, a deficiency in this protein would lead to reduced total body iron, not excess. Ferritin (choice C) is the intracellular iron binding and storage protein. A deficiency in ferritin would lead to less iron deposition, not excess. Ferroportin (choice D) is the iron transport protein that moves dietary iron from within intestinal enterocytes across the basolateral membrane to the circulation, therefore, a deficiency in this protein would have consequences similar to deficiencies in DMT1. Transferrin (choice E) is the iron transport protein of the blood that binds to the trasferrin receptor on cell surfaces, allowing cellular uptake of circulating iron. A deficiency in this protein would lead to less iron deposition not more. @Superspeciality

398. Explanation A) (A) Pityriasis rosea is a papulosquamous eruption consisting of multiple oval-shaped scaling lesions which are truncal in distribution. This eruption resembles the papulosquamous eruption of secondary syphilis, although the rash of secondary syphilis often involves the palms and soles. The etiology of pityriasis rosea is unknown, but is felt to be viral. It is a self-limiting illness lasting several weeks to a few months, and there is no adequate treatment other than symptomatic treatment of pruritus, when necessary @Superspeciality