Endocrinology poll questions

Weekly Endocrine Pathophysiology Poll Question #5

Updates

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 medications

Weekly Endocrine Pathophysiology Poll Question #1

Updates

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 enzyme

Weekly Endocrine Pathophysiology Poll Question #2

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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 insensitivity

Weekly Endocrine Pathophysiology Poll Question #4

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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