Weekly Endocrine Pathophysiology Poll Question #5 Subscribe Which statement is true regarding acromegaly? Elevated serum IGF-1 promotes hyperglycemia Growth hormone increases hepatic glucose output Reduction in lipolysis accounts for hyperglycemia in acromegaly Hyperglycemia associated with acromegaly responds easily to anti-hyperglycemic medicationsSubmit Your Response Weekly Endocrine Pathophysiology Poll Question #1 Newsletter What is the mechanism of pseudohyperaldosteronism in apparent mineralocorticoid excess Gain of function mutation (amiloride-sensitive sodium chloride transporter) Gain of function mutation of the thiazide-sensitive sodium-chloride co-transporter in the distal nephron Inhibition of 11beta-hydroxysteroid dehydrogenase 2 An autosomal recessive inactivating mutation of the 11beta-hydroxysteroid dehydrogenase 2 enzyme Deficiency of 11beta-hydroxylase enzymeSubmit Your Response Weekly Endocrine Pathophysiology Poll Question #2 Newsletter How does estrogen resistance contribute to tall stature in affected persons? Delays initial pubertal growth spurt Early closure of the epiphysis Testosterone directly delays growth plate senescence Delayed growth plate senescence due to estrogen insensitivitySubmit Your Response Weekly Endocrine Pathophysiology Poll Question #4 Contact Which of these proposed mechanisms central to our understanding of the pathophysiologic basis of type two diabetes mellitus is incorrect? Insulin resistance at the liver contributes to postprandial hyperglycemia Beta-cell dysfunction and insulin resistance at the level of skeletal muscle promotes hyperglycemia in the post-absorptive state Resistance of fat cells to the anti-lipolytic effects of insulin Pancreatic alpha cell dysfunction leads to significant hyperglucagonemia in the fasting stateSubmit Your Response Weekly Endocrine Pathophysiology Poll Question #4 Updates Which of these proposed mechanisms central to our understanding of the pathophysiologic basis of type two diabetes mellitus is incorrect? Insulin resistance at the liver contributes to postprandial hyperglycemia Beta-cell dysfunction and insulin resistance at the level of skeletal muscle promotes hyperglycemia in the post-absorptive state Resistance of fat cells to the anti-lipolytic effects of insulin Pancreatic alpha cell dysfunction leads to significant hyperglucagonemia in the fasting stateSubmit Your Response Leave a commentRegister / Login using your social network account Your email address will not be published. Required fields are marked *Comment *Name * Email * Website
