Anesthesia Pharmacology Chapter 22: Adrenocorticosteroid Pharmacology Practice Questions

Natural adrenocortical hormones are produced in released by:
1. pituitary
2. hypothalamus
3. adrenal cortex
4. liver
5. all the above
Natural and synthetic corticosteroids are mainly used for:
1. diagnosis of adrenal function disorders
2. treatment of adrenal function disorders
3. treatment of inflammatory/immunologic disorders
Adrenocortical steroid secretion is mainly controlled by:
1. angiotensin release
2. renin
3. calcitonin
4. corticotropin
5. vasopressin
Hormonal steroids most influential on intermediary metabolism:
1. mineralocorticoids
2. glucocorticoids
Quantitatively, the major human androgen:
1. testosterone
2. dehydroepiandrosterone (DHEA)
3. androstenedione
4. A & C
5. none of the above
Cortisol:
1. major human glucocorticoid
2. synthesized by zona fasciculata and zona reticularis cells
3. released into the circulation under the control of ACTH
4. mostly bound to corticosteroid-binding globulin (CBG)
5. all the above
Factor(s) that increase(s) corticosteroid-binding globulin (CBG)
1. pregnancy
2. decreased estrogen levels
3. hypothyroidism
4. A & B
5. A, B & C
Mediators of glucocorticoid action:
1. proteins synthesized due to RNA transcribed by glucocorticoid target genes
2. paracrine effects of hormone-regulated cytokines
3. both
4. neither
Examples of "permissive" glucocorticoid effects:
1. diminished vascular smooth muscle response to catecholamines in the absence of cortisol
2. reduced lipolytic response of adipocytes to epinephrine
3. major metabolic effects of glucocorticoid secretion
4. A & B
5. A, B & C
Glucocorticoid metabolic effects:
1. gluconeogenesis in diabetics
2. decreased amino acid uptake in the liver
3. decreased amino acid uptake in the kidney
4. decreased glycogen synthase activity in the liver
5. decreased glucose production for protein
Physiological consequences of supraphysiologic glucocorticoid levels:
1. weakness
2. decreased muscle mass
3. growth reduction in children
4. osteoporosis in Cushing's syndrome
5. all the above
Mechanism(s) those glucocorticoid anti-inflammatory effects
1. reduce prostaglandin synthesis
2. increase leukotriene synthesis (resulting from phospholipase A-2 activation)
3. reduction in circulating lymphocytes
4. A & C
5. A, B & C
Mechanism(s) those glucocorticoid anti-inflammatory/anti-immune effects
1. inhibition of COX-II expression
2. inhibition of kinin and bacterial endotoxin activity
3. decreased leukocyte responsiveness to mitogens/antigens
4. decreased macrophage phagocytotic action
5. all of the above
Glucocorticoid effect(s):
1. suppression of pituitary beta-lipotropin release
2. large doses decrease stomach acid production
3. increased erythrocytes and platelets by enhancing hematopoiesis
4. A & C
5. A, B & C
Example of short-to medium-acting glucocorticoid
1. triamcinolone (Aristocort)
2. fluprednisolone
3. prednisolone (Prelone)
4. fludrocortisone (Florinef)
5. dexamethasone (Decadron)
Long-acting glucocorticoid
1. cortisone
2. fluprednisolone
3. triamcinolone (Aristocort)
4. betamethasone (Celestone)
5. desoxycorticosterone acetate
inhibition of 11 beta-hydroxylase activity (P450c11) would reduce formation of:
1. aldosterone
2. cortisol
3. progesterone
4. A & B
5. A,B & C
inhibition of 21 beta-hydroxylase activity (P450c21) would reduce formation of:
1. testosterone
2. estradiol
3. corticosterone
4. A & B
5. A, B & C