Review of Pharmacology - 9E (2015)

Autacoids
85. Ans. (b) Aspirin suppresses flushing associated with large dose of nicotinic acid (Ref: KDT 6/e p191)
Nicotinic acid can cause flushing due to release of PGs. Premeditation with aspirin decreases this complication. Aspirin
can cause hyperthermia in overdose. It decreases the risk of developing colon cancer.
86. Ans. (d) Antiplatelet aggregatory (Ref: KDT 6/e p191)
87. Ans. (b) Its potential to cause agranulocytosis (Ref: KDT 6/e p195)
88. Ans. (a) Indomethacin (Ref: KDT 6/e p195)
89. Ans. (b) Indomethacin (Ref: KDT 6/e p195)
Sedation caused by indomethacin can interfere with driving.
90. Ans. (a) Less likely to cause gastric ulcer and their complications (Ref: KDT 6/e p197)
Selective COX-2 inhibitors are less likely to cause GI complications like PUD. However as COX-2 is also present constitutively
in the kidney, chances of renal complications are similar. These drugs have similar or less efficacy than non-selective
COX inhibitors.
91. Ans. (b) Paracetamol (Ref: KDT 6/e p198)
92. Ans. (b) Ibuprofen (Ref: KDT 6/e p190, 193)
93. Ans. (a) Irreversibly inhibits its target enzyme (Ref: KDT 6/e p185)
94. Ans. (b) Inhibition of cyclooxygenase (Ref: KDT 6/e p191)
Aspirin acts as an antiplatelet drug in MI. It inhibits cox enzyme and thus reduces the synthesis of TXA 2
. However it has
no effect on the enzyme, thromboxane synthetase. Therefore, answer here is the inhibition of cox.
95. Ans. (a) Inhibition of thromboxane synthesis (Ref: KDT 6/e p191)
See the difference from the above question. Here in the question, it is written thromboxane synthesis and not synthetase.
Aspirin inhibits TX synthesis via inhibiting cox and thus this is more specific explanation of its antiplatelet action.
96. Ans. (a) Leukotrienes (See below)
Aspirin inhibits cox enzyme and results in the diversion of AA pathway towards LT synthesis. As LTs are powerful bronchoconstrictor
agents, these may result in the shortness of breath in patients who are susceptible. Aspirin acetylated cox
starts producing lipoxins (known as aspirin triggered lipoxins) that also have bronchoconstrictor properties.
97. Ans. (d) Reye’s syndrome (Ref: KDT 6/e p189)
Aspirin can increase the risk of Reye’s syndrome, if used in children with viral diseases.
98. Ans. (d) Treatment with acetylcysteine (Ref: KDT 6/e p189, 190)
General Autacoids Pharmacology
This patient is a case of salicylate poisoning. Gastric lavage is done to remove unabsorbed poison. Metabolic acidosis
must be corrected by sodium bicarbonate. Alkalization of urine will increase the excretion of this weakly acidic
drug. Treatment with acetylcysteine has no role in salicylate poisoning. It is the antidote of choice for paracetamol
poisoning.
99. Ans. (b) Decreased hepatocellular stores of glutathione (Ref: KDT 6/e p198, 199)
Chronic alcohol intake results in liver dysfunction and decreased glutathione stores. Deficiency of this compound increases
the toxicity of acetaminophen because NAPQ, a metabolite of this compound, can now react easily with sulfhydryl
groups of the biomolecules. Alcohol also induces the enzymes responsible for conversion of acetaminophen to NAPQ.
100. Ans. (c) Alprostadil (Ref: KDT 6/e p182)
Prostaglandins (like alprostadil) are used to keep ductus arteriosus patent whereas aspirin or indomethacin are used for
the treatment (closure) of PDA.
101. Ans. (c) N-acetylcysteine (Ref: KDT 6/e p199)
102. Ans. (b) Misoprostol (Ref: KDT 6/e p634)
103. Ans. (c) Uricosuria (Ref: KDT 6/e p188)
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