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Choose the correct answer:
1. In the fasting state, cortisol promotes hepatic gluconeogenesis by:
A. increasing the breakdown of muscle protein.
B. decreasing the release of glycerol from adipose tissue.
C. suppressing gluconeogenic enzymes in other tissues.
D. increasing hepatic production of beta-hydroxybutyrate.
E. decreasing hepatic production of beta-hydroxybutyrate.
2. When TRH is administered to an individual with hypothyroidism:
A. TSH levels will increase if there is a pituitary defect.
B. TSH levels will remain unchanged, but T3 and T4 levels will increase.
C. no change in circulating T3 and T4 concentrations will be seen if there is a defect at the level of the thyroid.
D. measurements of circulating TSH and thyroid hormone concentrations will not distinguish between a defect at the level of the pituitary versus the hypothalamus.
E. negative feedback on the pituitary will be relieved.
3. Transcortin (CBG):
A. levels in the blood are decreased in pregnancy.
B. increases the solubility of cortisol.
C. binds glucocorticoids and mineralocorticoids.
D. increases the excretion of cortisol by the kidneys.
E. stimulates cyclic AMP production by the transcortex.
4. A patient who has many symptoms of corticoid excess is noted as having excessive skin pigmentation. This individual probably has:
A. secondary hypercortisolism.
B. increased numbers of circulating lymphocytes.
C. severe allergy problems that are being treated.
D. low levels of circulating ACTH.
E. atrophied adrenal cortices.
5. The thyroid:
A. stores several months supply of thyroid hormone.
B. produces more T3 than T4.
C. is required for the maintenance of calcium homeostasis.
D. produces thyroxine binding globulin.
E. does not have any developmental effects.
6. In humans, total adrenalectomy is invariably fatal without replacement therapy, whereas hypophysectomy is not. Which of the following best explains this observation?
A. The adrenal cortex undergoes compensatory hypertrophy after hypophysectomy.
B. Aldosterone secretion is not markedly decreased after hypophysectomy.
C. Hypophysectomy reduces the glomerular filtration rate, thus preventing sodium loss.
D. The kidney secretes ACTH after hypophysectomy.
E. Tissue requirements for cortisol decrease to low levels after hypophysectomy.
7. A patient has increased plasma concentrations of ACTH, transcortin (cortisol-binding globulin), and total cortisol, but a normal concentration of free cortisol. These findings are most consistent with:
A. adrenocortical insufficiency.
B. hepatic failure.
C. pregnancy.
D. primary hyperadrenocorticism.
E. Cushing's syndrome.
8. Removal of one adrenal gland leads to an acute decrease in ___________________, which ultimately directly produces an increase in ______________________ in the remaining adrenal.
A. aldosterone secretion; ACTH secretion
B. anterior pituitary weight; weight
C. ACTH secretion; CRH secretion
D. sleep-mediated cortisol release; aldosterone secretion
E. blood cortisol levels; cortisol secretion
9. Angiotensin II
A. stimulates aldosterone secretion from the zona reticularis.
B. is a vasoactive molecule formed from angiotensin I in the liver.
C. levels increase in the blood following renal artery stenosis.
D. acts on renal cells of the distal tubule to increase Na+ reabsorption.
E. stimulates glucocorticoid secretion from the zona fasciculata.
10. Triiodothyronine, T3
A. is the predominant secretory product of the thyroid.
B. has higher affinity for TBG than does thyroxine.
C. is elevated in persons suffering from starvation.
D. is the major form of the thyroid hormone bound to receptors in the nucleus of target cells.
E. is the primary inactive metabolite of thyroxine.
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1-a?
2C
3B?
4E
5A?
6B
7C
8E
9C
10D
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ANSWERS:
Q1: In the fasting state, cortisol promotes hepatic gluconeogenesis by:
Correct answer: A.) increasing the breakdown of muscle protein.
Reasoning: The primary role of cortisol is long term maintenance of glucose mobilization. This is from stimulation of gluconeogenic enzymes and of gluconeogenesis (primarily in the liver). Amino acids from muscle protein breakdown (also stimulated by cortisol) serve as substrates for gluconeogenesis.
Q2: When TRH is administered to an individual with hypothyroidism:
Correct answer: C.) no change in circulating T3 and T4 concentrations will be seen if there is a defect at the level of the thyroid.
Reasoning: TRH given to a patient with a hypothalamic dysfunction in the thyroid axis of regulation will produce an increase in TSH and T3/T4. No response will be seen with TSH and T3/T4 if the defect is at the level of the pituitary, or with T3/T4 if the defect is at the level of the thyroid. This test will not affect feedback regulation, but can distinguish a pituitary from an hypothalamic defect.
Q3: Transcortin (CBG):
Correct answer: B.) increases the solubility of cortisol.
Reasoning: CBG is the serum binding protein for cortisol and progesterone, not aldosterone. It increases solubility and half-life of these hormones in the circulation. As a result of the binding, renal excretion is reduced. It's levels are increased in pregnancy due to enhanced synthesis of CBG in the liver caused by elevated estradiol levels.
Additional question: What is the transcortex?
Q4: A patient who has many symptoms of corticoid excess is noted as having excessive skin pigmentation. This individual probably has:
Correct answer: A.) secondary hypercortisolism.
Reasoning: The excessive pigmentation is likely due to increased ACTH (the MSH-like activity contained therein). Since cortisol levels are also probably elevated, this suggests a pituitary (secondary) defect. As a result, the adrenal cortices would be hypertrophied (increased ACTH), and circulating lymphocytes would be reduced (anti-inflammatory action of cortisol). If the patient were being treated for allergies with cortisol, ACTH would be reduced due to negative feedback on the pituitary.
Q5: The thyroid:
Correct answer: A.) stores several months supply of thyroid hormone.
Reasoning: Thyroid hormone is stored in the follicular colloid for about three months attached to thyroglobulin. The thyroid gland produces more T4 than T3, and produces calcitonin which is not directly required for calcium homeostasis. Thyroxine binding globulin is produced in the liver, and T3/T4 are profoundly involved in development and growth.
Q6: In humans, total adrenalectomy is invariably fatal without replacement therapy, whereas hypophysectomy is not. Which of the following best explains this observation?
Correct answer: B.) Aldosterone secretion is not markedly decreased after hypophysectomy.
Reasoning: Aldosterone depletion causes the death associated with adrenalectomy. Hypophysectomy does not deplete aldosterone because ACTH is not the main regulator of aldosterone secretion. The primary regulator is the renin-angiotensin system.
Q7: A patient has increased plasma concentrations of ACTH, transcortin (cortisol-binding globulin), and total cortisol, but a normal concentration of free cortisol. These findings are most consistent with:
Correct answer: C.) pregnancy.
Reasoning: CBG (transcortin) synthesis in the liver is elevated in response to high estrogen concentrations during pregnancy. As a result, ACTH and total cortisol will increase to maintain normal free cortisol blood levels. This is because it is the free levels of steroid hormones that provide feedback signals for regulation of the hypothalamic-pituitary-target gland loops.
Q8: Correct answer E. Removal of one adrenal gland leads to an acute decrease in blood cortisol levels, which ultimately directly produces an increase in cortisol secretion in the remaining adrenal.
Reasoning: Removal of one adrenal would initially decrease cortisol (half the source), followed by an increase in ACTH which would eventually produce compensatory hypertrophy of the remaining adrenal (due to its trophic action). This would restore normal cortisol levels by increasing its production in the remaining adrenal. Aldosterone does not regulate ACTH release. Sleep-mediated cortisol secretion is entrained to a circadian rhythm.
Q9: Angiotensin II:
Correct answer: C.) levels increase in the blood following renal artery stenosis.
Reasoning: Angiotensin II is formed from Angiotensin I in the blood stream and stimulates aldosterone secretion in the zona glomerulosa of the adrenal cortex. The production of Ag II is initiated by release of renin from the juxtaglomerular apparatus in the kidney (in response to reductions in renal blood flow as with renal artery stenosis). AgII does not directly regulate renal reabsorption of Na+ or glucocorticoid secretion.
Q10: Triiodothyronine, T3:
Correct answer: D.) is the major form of the thyroid hormone bound to receptors in the nucleus of target cells.
Reasoning: T3 is the primary active metabolite of thyroxine (T4) and binds more tightly to the nuclear receptor in target cells than does T4. On the other hand, T4 is predominantly produced in the thyroid and has a higher affinity for TBG. In starvation, conversion of T4 to rT3 (inactive metabolite) is increased, this effectively conserves fuel by decreasing T3, hence decreasing the basal metabolic rate.
