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Review of Pharmacology - 9E (2015)

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Endocrinology<br />

Drugs causing Addison’s disease are:<br />

• Metyrapone<br />

• Ketoconazole<br />

• Aminoglutethimide<br />

• Mitotane<br />

108. Ans. (a) Chemotherapy induced vomiting (Ref: KDT 6/e p647)<br />

109. Ans. (c) Collecting ducts (Ref: Katzung 10/e p240)<br />

• Aldosterone is the principal mineralocorticoid. It stimulates the reabsorption <strong>of</strong> Na + and excretion <strong>of</strong> K + and H + by its<br />

action on late distal tubules and collecting ducts.<br />

110. Ans. (b) Acidosis (Ref: KDT 6/e p277)<br />

111. Ans. (c) Phospholipase A (Ref: KDT 6/e p279)<br />

112. Ans. (d) Lipocortin (Ref: KDT 6/e p279)<br />

Corticosteroids induce the synthesis <strong>of</strong> lipocortins that inhibit the enzyme phospholipase A2.<br />

113. Ans. (d) Methylprednisolone (Ref: KDT 6/e p281)<br />

114. Ans. (a) Prednisolone 20 mg/day oral for one year (Ref: KDT 6/e p286)<br />

• If used for more than two weeks, corticosteroids can lead to HPA-axis suppession. If discontinued abruptly, precipitation<br />

<strong>of</strong> acute adrenal insufficiency can result. This is the most serious adverse effect seen with the use <strong>of</strong> corticosteroids<br />

that can cause death <strong>of</strong> the patient.<br />

115. Ans. (a) Congenital adrenal hyperplasia (Ref: KDT 6/e p283)<br />

• Corticosteroids are used for the management <strong>of</strong> congenital adrenal hyperplasia.<br />

• Corticosteroids can result in hyperglycemia and thus may vitigate the control <strong>of</strong> blood glucose in diabetics.<br />

• Due to retention <strong>of</strong> Na + and water, corticosteroids can worsen the hypertension.<br />

• By inhibiting the production <strong>of</strong> gastroprotective prostaglandins, corticosteroids increase the risk <strong>of</strong> peptic ulcer<br />

disease.<br />

116. Ans . (d) Suppression <strong>of</strong> ACTH secretion (Ref: KDT 6/e p283)<br />

In congenital adrenal hyperplasia, due to decreased formation <strong>of</strong> steroids, there is decreased feedback inhibition <strong>of</strong> ACTH.<br />

Thus more ACTH is formed which leads to adrenal hyperplasia. Thus exogenous steroids are given to suppress ACTH<br />

secretion.<br />

117. Ans (b) Osteoporosis (Ref: KDT 6/e p286)<br />

Glucocorticoids have lot <strong>of</strong> adverse effects on long term use. These can lead to Cushing syndrome, hyperglycemia, osteoporosis,<br />

delayed wound healing, increased susceptibility to infections, cataract, glaucoma and many other adverse effects.<br />

118. Ans. (c) No change/increase in prednisolone dose (Ref: KDT 6/e p283)<br />

• During conditions <strong>of</strong> stress or infection, dose <strong>of</strong> steroids should not be decreased. Rather, increase in dose may be<br />

required.<br />

119. Ans. (a) They do not cause Na + and water retention (Ref: KDT 6/e p285)<br />

• Triamcinolone, betamethasone, dexamethasone and paramethasone are selective glucocorticoids (have zero mineralocorticoid<br />

action).<br />

• These are preferred for cerebral edema because they lack salt and water retaining potential (mineralocorticoid action).<br />

120. Ans. (c) Cortisol and fludrocortisone (Ref: KDT 6/e p282)<br />

Patient should be given both mineralocorticoids as will as glucocorticoid.<br />

Max. mineralocorticoid activity – Aldosterone<br />

Max. glucocorticoid activity – Dexamethasone<br />

121. Ans. (c) Betamethasone (Ref: KDT 6/e p282, 287)<br />

Steroids with long half life like betamethasone and dexamethasone cannot be used for alternate day therapy because even<br />

in alternate day therapy there will be sufficient blood levels <strong>of</strong> these steroids to cause suppression <strong>of</strong> HPA axis.<br />

General Endocrinology <strong>Pharmacology</strong><br />

297<br />

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