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Review of Pharmacology - 9E (2015)

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

126. Ans. (c) Breakdown <strong>of</strong> Gtp to Gdp (Ref: KDT 7/e p46)<br />

Alpha subunit <strong>of</strong> G protein contains GTPase activity and thus dissociates GTP to form GDP. This result in re-uniting <br />

subunit with β and g subunit<br />

127. Ans. (b) Guanylyl Cyclase (Ref: KDT 7/e p47-48)<br />

Remember that guanylyl cyclase is an enzyme while cGMP is a secondary messenger<br />

Types <strong>of</strong> second messengers<br />

There are three basic types <strong>of</strong> secondary messenger molecules:<br />

Note: Calcium in the setting <strong>of</strong> G proteins is considered as the third messenger whereas the drug itself is considered as the first messenger.<br />

128. Ans. (c) Decreases V max<br />

(Ref: KDT 7/e p39)<br />

• Competitive inhibitors increase K m<br />

value whereas non-competitive inhibitors decreases V max<br />

<strong>of</strong> an enzyme<br />

129. Ans. (c) Activation <strong>of</strong> protein kinase (Ref: KDT 7/e p46)<br />

• Cyclic AMP exerts most <strong>of</strong> its effects by stimulating cAMP-dependent protein kinases. These phosphorylate enzymes<br />

resulting in their activation or inhibition.<br />

130. Ans. (d) Pyrimethamine (Ref: KDT 7/e p66)<br />

• Important drugs causing hemolysis in G-6-PD deficiency are<br />

– Primaquine – Dapsone – Sulfonamides<br />

– Nitr<strong>of</strong>urantoin – Aspirin – Menadione<br />

– Chloroquine – Quinine – Nalidixic acid<br />

• Sulfonamides can cause hemolysis in patients with G-6-PD deficiency and not pyrimethamine.<br />

131. Ans. (c) Insulin (Ref: Katzung 11/e p730)<br />

For Details, see text.<br />

132. Ans. (c) ED 50<br />

<strong>of</strong> the drug corresponds to the efficacy (Ref: Katzung 11/e p30-31)<br />

ED 50<br />

corresponds to potency <strong>of</strong> a drug, not its efficacy. All other statements are true.<br />

133. Ans. (b) Binds to the receptor and causes opposite action (Ref: KDT 7/e p40)<br />

134. Ans. (a) Adenosine deaminase deficiency (Ref: KDT 7/e p66)<br />

135. Ans. (a) High affinity (Ref: KDT 6/e p42)<br />

136. Ans. (d) Ceftriaxone (Ref: KDT 7/e p66)<br />

137. Ans. (c) The substrate concentration at half maximal velocity (Ref: KDT 7/e p38)<br />

K m<br />

<strong>of</strong> an enzyme is similar to potency <strong>of</strong> a drug. It is the substrate concentration at which the velocity reaches half <strong>of</strong> the maximum<br />

known as V max.<br />

(similar to efficacy <strong>of</strong> a drug).Higher is the Km, lesser is the speed <strong>of</strong> the reaction.<br />

138. Ans. (d) Adrenaline and histamine; (e) Salbutamol and leukotrienes (Ref: Katzung 12/e p20)<br />

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

• Physiological antagonists are those drugs that produce opposite action by acting on different receptors.<br />

• Adrenaline reverses the bronchoconstrictor action <strong>of</strong> histamine (via. H 1<br />

receptors) by causing bronchodilation<br />

(through β 2<br />

receptors). Therefore, these are physiological antagonists.<br />

• Salbutamol reverses the bronchoconstrictor action <strong>of</strong> leukotrienes (via cysteinyl leukotriene receptors) through its<br />

action on β 2<br />

receptors. Therefore, it is also a physiological antagonism.<br />

• Isoprenaline (β 1<br />

and β 2<br />

agonist) and propranolol (β 1<br />

and β 2<br />

antagonist) are pharmacological antagonists because<br />

they are acting on same receptors.<br />

• Isoprenaline and salbutamol or adrenaline are not antagonists at all.<br />

47<br />

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