Review of Pharmacology - 9E (2015)

Review of Pharmacology
67. Ans. (a) Aspirin; (c) Indomethacin; (e) Rofecoxib (Ref: KDT 6/e p184)
68. Ans. (a) It is PGF 2α
derivative used in glaucoma (Ref: KDT 6/e p147)
69. Ans. (b) Essential hypertension (Ref: KDT 6/e p190, 191)
70. Ans. (c) Ibuprofen (Ref: KDT 6/e p185)
Alprostadil (PGE 1
) and prednisolone do not inhibit cox enzyme whereas aspirin is an irreversible inhibitor of this enzyme.
71. Ans. (a) LTC 4
(Ref: KDT 6/e p175)
LTC 4
, D 4
and E 4
are known as slow reacting substance of anaphylaxis as these can cause bronchoconstriction.
72. Ans. (d) Prednisolone (Ref: KDT 6/e p279)
It is a powerful anti-inflammatory agent. It acts by inhibiting the synthesis of PG, TX and LT via the inhibition of phospholipase
A 2
enzyme. However, its most important mechanism of anti-inflammatory action is the inhibition of chemotaxis.
73. Ans. (c) Is available in a parenteral formulation that can be used intramuscularly or intravenously (Ref: KDT 6/e p194,
195)
Keterolac is the only NSAID that can be administered intravenously.
74. Ans. (c) History of peptic ulcer disease (Ref: KDT 6/e p197)
Non-selective COX inhibitors on long term use are associated with peptic ulcer disease. These should be avoided in the
patients having history of PUD. Selective COX-2 inhibitors like celecoxib are safe in this regard.
75. Ans. (a) Aspirin (Ref: KDT 6/e p185)
76. Ans. (a) Treatment of patent ductus arteriosus (Ref: KDT 6/e p181, 191)
Autacoids
142
• PGE 2
analogues are used to maintain the patency of ductus arteriosus whereas aspirin or indomethacin are
used for the treatment of PDA.
• PGE 2
is a bronchodilator and can be used to treat bronchial asthma via inhalational route.
• Cervical priming and NSAID induced PUD are other indications of this agent.
77. Ans. (b) Platelet cannot synthesize fresh COX molecules (Ref: KDT 6/e p185)
Aspirin in low doses irreversibly inhibits COX enzyme in platelets and the endothelium. Platelets lack nucleus and thus
cannot regenerate COX whereas endothelium can synthesize fresh enzyme. Net effect of this process is the inhibition of
platelet cox and thus, TXA 2
synthesis. Low TXA 2
level results in the anti-aggregation of platelets.
78. Ans. (d) Leuktoriene C 4/
D 4
(Ref: KDT 6/e p222)
79. Ans. (a) Paracetamol (Ref: KDT 6/e p198)
80. Ans. (b) It is inducible (Ref: KDT 6/e p185)
COX-1 is a house-keeping enzyme that is responsible for the generation of gastroprotective PGs. COX-2 is an inducible
enzyme whose production is markedly increased at inflammatory sites. Indomethacin is a non-selective inhibitor of both
isoforms of cox.
81. Ans. (b) Prolongation of prothrombin time (Ref: KDT 6/e p186)
Prothrombin time is increased by the drugs interfering with the coagulation pathway (e.g. warfarin). As cox has no role in
coagulation, inhibitors of PG synthesis do not prolong PT. However, bleeding time (BT) is prolonged by the drugs interfering
with platelet function. Aspirin increases BT by acting as an antiplatelet agent.
82. Ans. (c) Hyperventilation (Ref: KDT 6/e p186, 188)
• All other actions are mediated via inhibition of PG synthesis whereas hyperventilation caused by aspirin is due to
respiratory stimulation.
83. Ans. (b) Hypoglycemia (Ref: KDT 6/e p188)
84. Ans. (b) Is longer for anti-inflammatory doses compared to that for analgesic dose (Ref: KDT 6/e p189)
• Aspirin and other salicylates show saturation kinetics (zero order) and thus, their half life is not constant. Clearance
at high doses (anti-inflamatory) is lesser than at low (analgesic) doses. Thus t 1/2
is more for anti-inflammatory dose
than for analgesic dose.
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