Block 5 Parthyroid Phys Pharm MCQ's

5a-reductase is an enzyme that converts testosterone into dihydrotestosterone (DHT), which is a more potent androgen. This conversion is important for the normal development of male sexual characteristics during puberty. In the case of 5a-reductase deficiency, the patient may experience abnormal sexual development due to the reduced production of DHT.

Activation of beta-1 and beta-2 receptors by catecholamines released from the adrenal medulla will result in increased cardiac output (CO) due to increased contractility and heart rate (HR) mediated by beta-1 receptors. This is accompanied by decreased total peripheral resistance (TPR) due to vasodilation mediated by beta-2 receptors. Therefore, the correct answer is Increased CO, decreased TPR, increased HR.

Hyperparathyroidism is a condition where the parathyroid glands produce too much parathyroid hormone (PTH), which regulates the levels of calcium and phosphate in the body. In this condition, the increased PTH levels cause the kidneys to excrete more phosphate, leading to a decrease in the plasma level of phosphate. Therefore, the correct answer is phosphate.

PTH, or parathyroid hormone, stimulates bone resorption, which is the process of breaking down bone tissue. This increases the release of calcium from the bone into the bloodstream. On the other hand, calcitonin inhibits bone resorption, preventing the breakdown of bone tissue and reducing the release of calcium into the bloodstream. Therefore, PTH increases bone resorption, while calcitonin inhibits bone resorption.

Parathyroid hormone is the most likely hormone to account for the findings of a modest increase in plasma calcium and a substantial decrease in urine calcium. Parathyroid hormone is responsible for regulating calcium levels in the body. It acts on the bones, kidneys, and intestines to increase calcium levels in the blood. In this case, the increase in plasma calcium suggests that parathyroid hormone is stimulating the release of calcium from the bones. The decrease in urine calcium indicates that the kidneys are reabsorbing more calcium, which is also regulated by parathyroid hormone.

Both thyroid hormone and steroid hormones are highly bound to plasma proteins. This means that only a small fraction of the hormones are free and available for action. The majority of the hormones are bound to proteins such as albumin, which serves as a reservoir for the hormones and helps to regulate their availability and distribution in the body. This binding also affects the half-life of the hormones, as it slows down their metabolism and clearance from the circulation. Therefore, the high binding to plasma proteins is a common aspect of both thyroid hormone and steroid hormone storage, transport, and action.

When plasma calcium levels are high, the body's response is to decrease the synthesis of 1,25 dihydroxy vitamin D3. This is because 1,25 dihydroxy vitamin D3 helps increase the absorption of calcium from the intestine, and when plasma calcium levels are already high, there is no need for further absorption. By decreasing the synthesis of 1,25 dihydroxy vitamin D3, the body can help regulate calcium levels and prevent them from becoming too elevated.

The most likely combination of hyper and/or hyposecretion for these hormones would be hypersecretion of CRH and ACTH, and hyposecretion of cortisol. This is because the patient is experiencing symptoms of adrenal insufficiency, such as fatigue and lightheadedness, which can be caused by a deficiency in cortisol production. The darker-than-usual complexion and hyponatremia are also consistent with adrenal insufficiency. The hypersecretion of CRH and ACTH can be a compensatory mechanism due to the low levels of cortisol.

Calcium's influx is an absolute requirement for epinephrine secretion in the chromaffin cells of the adrenal medulla. This is because calcium plays a crucial role in the process of exocytosis, which is the release of secretory vesicles containing epinephrine into the bloodstream. When calcium enters the chromaffin cells, it triggers the fusion of these vesicles with the cell membrane, allowing the release of epinephrine. Without calcium influx, the secretion of epinephrine cannot occur.

Diabetes mellitus is the most likely clinical condition to produce these six findings. Polyuria and polydipsia are common symptoms of diabetes mellitus, as the high levels of glucose in the blood cause increased urine production and excessive thirst. Weakness and fatigue can also be attributed to the body's inability to properly use glucose for energy. The presence of peripheral neuropathy and visual changes further support the diagnosis of diabetes mellitus, as these are common complications associated with the disease.

The patient's symptoms of lethargy, nausea, and muscle weakness, along with the abnormal levels of plasma corticotropin, cortisol, renin, aldosterone, and adrenal androgens, are consistent with Addison's Disease. This condition is characterized by the adrenal glands not producing enough cortisol and aldosterone. The elevated levels of plasma corticotropin suggest a primary defect in the adrenal glands, ruling out secondary renal insufficiency. Cushing's Disease and ectopic corticotropin-producing tumors would result in elevated cortisol levels, which is not seen in this patient. Congenital adrenal hyperplasia would typically present with elevated levels of adrenal androgens, which is not the case here.

Prednisone is a glucocorticoid medication that can cause osteoporosis and bone loss. Inhibition of intestinal calcium absorption is a known side effect of prednisone, which can lead to decreased bone density and increased risk of fractures. This can result in lower back pain, especially in individuals with pre-existing conditions such as rheumatoid arthritis.

Teriparatide is a drug that stimulates new bone formation. It is used in the treatment of osteoporosis by promoting the production of new bone cells. Teriparatide is a synthetic form of parathyroid hormone, which helps to increase bone density and reduce the risk of fractures. It works by stimulating the activity of osteoblasts, the cells responsible for bone formation. This drug is particularly effective in individuals with severe osteoporosis or those who have not responded well to other treatments.

The most likely explanation for this patient's endocrine problem is insufficient production of CRF by hypothalamic neurons. This is supported by the undetectable levels of plasma ACTH and very low plasma cortisol. CRF is responsible for stimulating the release of ACTH, which in turn stimulates the production and release of cortisol by the adrenal cortex. Therefore, if there is insufficient production of CRF, it would result in low levels of ACTH and cortisol. The fact that exogenous CRF increases plasma cortisol further supports this explanation, as it suggests that the patient's adrenal cortex is still capable of producing cortisol when stimulated.

1,25-dihydroxycholecalciferol, also known as active vitamin D, is the most important hormone in maintaining plasma calcium levels. When calcium levels drop, the parathyroid glands release parathyroid hormone (PTH), which stimulates the production of 1,25-dihydroxycholecalciferol in the kidneys. 1,25-dihydroxycholecalciferol then acts on the intestines, kidneys, and bones to increase calcium absorption from the diet, reabsorption from the kidneys, and release from the bones. This helps to restore and maintain normal plasma calcium levels.

PNMT (phenylethanolamine-N-methyl transferase) is the correct answer because it is the enzyme responsible for the synthesis of epinephrine from norepinephrine. In situations of stress and anxiety, cortisol stimulates the production of norepinephrine, and then PNMT converts norepinephrine into epinephrine. This increase in epinephrine synthesis helps the body respond to stress by increasing heart rate, blood pressure, and energy availability.

The expected outcome of 11-deoxycorticosterone-induced hypervolemia and hypertension on the renin-angiotensin-aldosterone system would be a decrease in renin, angiotensin II, and aldosterone levels. This is because 11-deoxycorticosterone is a mineralocorticoid hormone that acts similarly to aldosterone, causing sodium and water retention. This increased blood volume and pressure would lead to a negative feedback loop, suppressing the release of renin from the kidneys and subsequently decreasing the production of angiotensin II and aldosterone.

The correct answer is E. The sympathetic branch of the autonomic nervous system elicits catecholamine release from the adrenal medulla. The neurotransmitter responsible for increased epinephrine release from adrenal medullary chromaffin cells is acetylcholine, and the receptor involved is nicotinic.

A pheochromocytoma is a tumor of the adrenal gland that causes excessive production of catecholamines, such as epinephrine and norepinephrine. These catecholamines are synthesized from the amino acid tyrosine by the enzyme tyrosine hydroxylase. By inhibiting tyrosine hydroxylase, the production of catecholamines can be reduced, which can help in the treatment of pheochromocytoma. Therefore, a tyrosine hydroxylase inhibitor would be the best-suited drug for this condition.

The dietary supplements providing 1000 mg of elemental calcium per day will not have any effect on hormone levels in the woman's plasma. Calcium supplementation does not directly affect hormone levels such as PTH, CT, vitamin D, or thyroid hormones. Therefore, there will be no change in hormone levels due to the calcium supplements.

Tricyclic antidepressants are known to inhibit the reuptake of norepinephrine, increasing its availability in the synaptic cleft. This increased concentration of norepinephrine would lead to an increased breakdown of norepinephrine, resulting in higher levels of 3-methoxy-4-hydroxymandelic acid. Thus, the presence of a tricyclic antidepressant would slow down the formation of this metabolite in pheochromocytoma.

Cortisol stimulates the conversion of epinephrine to norepinephrine in the synthesis of adrenal medullary hormones.