Rosh Review – Metabolic ,Endocrine Questions And Answers Rated A+
- African-American male (X-linked) - hemolytic anemia after exposure to oxidative agent (fava beans, TMP-SMX, sulfa drugs, ASA, antimalarials, nitrofurantoin, methylene blue) - Heinz bodies (denatured Hgb) on smear - Coombs' negative - Answer-Classic G6PD presentation - Blurred vision, anorexia, abnormal skin pigmentation, loss of hair, dry skin, pruritus, long-bone pain, and an increased incidence of bone fractures - Massive doses --> idiopathic intracranial hypertension and hepatic failure. - Answer-Symptoms of Hypervitaminosis A - charcoal, dextrose, octreotide (somatostatin analogue) - Answer-Management of hypoyglycemia caused by sulfonylureas - Insulin - Things that increase endogenous insulin secretion: - Sulfonylureas (glyburide, glypizide) --> bind to ATP-sensitive K+ channels on pancreatic beta cells --> depolarization --> voltage gated Ca2+ channels open --> fusion of insulin vesicles w/membrane - Metiglinides (-glinides) --> same MOA same as sulfonylurea, but with weaker affinity - DPP-4 inhibitors (-liptins) --> increases incretin levels --> blocks glucacon release --> increases insulin secretion - Answer-Diabetic drugs that cause hypoglycemia (within 1 day of ingestion) Bones (fractures), stones (kidney stones), groans (abdominal cramping, ileus, nausea, constipation), psychiatric overtones (lethargy, depression, psychosis)Tx - 1st, IV NS; loop diuretics (after adequate rehydration), bisphosphonates, calcitonin, dialysis (for severe, >18) - Answer-HyperCa2+ - CP, tx Chloride - central access Gluconate - peripheral access - Answer-How do you administer calcium gluconate vs chloride? Destructive thyroiditis (majority) and iodine load (400 times daily requirement) - Answer-Two causes of amiodarone induced hyperthyroidism HHS - glucose > 600, bicarb > 15, +/- ketones, anion gap < 12 DKA - glucose > 250, bicarb < 18, many ketones, anion gap > 10 - Answer-Differentiate between hyperosmolar hyperglycemic state (HHS) and diabetic ketoacidosis (DKA) in lab values (plasma glucose, pH, bicarb, anion gap) Hypokalemia (2/2 low Mg2+ --> increased K+ excretion in the kidney) - Answer-What electrolyte imbalance is associated with hypomagnesium inpatient - cancer outpatient - 1' hyperPTH - Answer-Most common cause of inpatient and outpatient hyperCa2+ Membrane stabilization - Calcium: acts immediately, duration: 30-60 min Shifts K+ back into cell - Insulin: acts within 20-30 min, duration: 4-6 hrs - Albuterol: acts within 15-30 min, duration: 2-4 hrs - Sodium bicarb: acts within 5-10 min, duration: 1-2 hrsExcretion - Furosemide: acts within 15-30 min, duration: 2-3 hrs - Sodium polystyrene: acts within 1-4 hrs, duration: 4-6 hrs - Hemodialysis: acts immediately; duration: 2-6 hours - Answer-Treatment, onset, duration of hyperkalemia Neuromuscular: tremors, tetany, seizures, weakness, apathy, coma CV: prolonged QTc, widening of QRS, atrial and ventricular dysrhythmias Others: Hypokalemia. hypocalcemia, hypoPTH - Answer-What are the manifestations of hypomagnesemia? Precipitants: sepsis, MI, trauma, surgery and pregnancy CP - Autonomic instability - fever - Cardiac - tachycardia, atrial tachydysrhythmias, high-output heart failure - GI - CNS Treatment (in order of administration) 1) Block peripheral effects of hormone --> Propanolol (also blocks peripheral conversion) 2) Block hormone synthesis --> PTU (faster onset, OK in pregnancy, also blocks peripheral conversion) or methimazole (teratogenic) 3/4) Block peripheral conversion of T4 to T3 --> dexamethasone3/4) Block hormone release from the thyroid gland --> potassium iodide (administer 1 hr after PTU/methimazole, after synthetic pathway blocked) - Answer-Thyroid storm - precipitants, CP, treatment
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rosh metabolic endocrine
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