NBME11 ANSWERS医学资料.docxVIP

Q 1 ans is F since TB is a reportable disease 2.CCWhen blood sugar is low, glucagon signals the adipocytes to activate hormone-sensitive lipase, and to convert triglycerides into free fatty acids3.EENinety percent of patients with gout develop excess urate stores due to an inability to excrete sufficient amounts of normally produced uric acid in the urine (underexcretion). The remaining patients either overconsume purines or produce excessive amounts of uric acid endogenously (overproduction).?In rare cases, overproduction of uric acid is primary, due to a genetic disorder. These disorders include hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome), glucose-6-phosphatase deficiency (von Gierke disease), fructose 1-phosphate aldolase deficiency, and PP-ribose-P synthetase variants. ?Overproduction of uric acid may also occur in disorders that cause high cell turnover with release of purines, such as meat intake and seafood intake. These disorders include myeloproliferative and lymphoproliferative disorders, psoriasis, chemotherapy (tissue lysis), hemolytic anemias, pernicious anemia, ineffective erythropoiesis (as in B-12 deficiency), excessive exercise, and obesity. ?Overproduction of uric acid can occur from overconsumption of foods high in purines.?Common causes of secondary gout due to underexcretion of uric acid include renal insufficiency, lead nephropathy (saturnine gout), starvation or dehydration, hypothyroidism, hyperparathyroidism, drugs (including loop and thiazide diuretics and cyclosporine A), low-dose aspirin, and chronic ethanol (especially beer and hard liquor) abuse. These disorders should be identified and corrected, if possible. ?Comorbidities, including hypertension, diabetes, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, diabetes, obesity, and early menopause, are associated with a higher incidence of gout. ?Consumption of fructose-rich foods and beverages are associated with an increased risk of g