Review of Pharmacology - 9E (2015)

Hematology
71. Ans. (c) Warfarin (Ref: KDT 6/e p602)
Oral anticoagulants inhibit the activation of several clotting factors (II, VII, IX and X) as well as anti-clotting proteins (protein
C and S). First to disappear is protein C that can result in hypercoagulation resulting in dermal vascular necrosis.
72. Ans. (d) All of these (Ref: KDT 6/e p597)
73. Ans. (a) Higher efficacy in arterial thrombosis (Ref: KDT 6/e p603)
Anticoagulants are mainly effective for venous thrombosis (like in DVT).
74. Ans. (a) They interfere with an early step in the synthesis of clotting factors (Ref: KDT 6/e p600, 601)
Oral anticoagulants inhibit the activation of factor II, VII, IX and X. These do not affect the synthesis of these factors.
75. Ans. (d) Oral contraceptives (Ref: KDT 6/e p603)
Estrogen increases the synthesis of various clotting factors and produce a hypercoagulable state. Thus OCP containing
estrogen decrease the effectiveness of warfarin and other oral anticoagulants.
76. Ans. (b) Prevention of venous thrombosis and pulmonary embolism (Ref: KDT 6/e p603)
• Anticoagulants are mainly used for prophylaxis of venous thrombosis (DVT and pulmonary embolism)
• Antiplatelet drugs are used to prevent arterial thrombosis (MI and stroke).
77. Ans. (b) Protein C (Ref: KDT 6/e p602)
78. Ans. (c) PTTK (Ref: KDT 6/e p598, 599)
79. Ans. (a) Antithrombin III (Ref: KDT 6/e p597)
80. Ans. (a) Heparin (Ref: KDT 6/e p598)
81. Ans. (a) Heparin (Ref: KDT 6/e p598,601)
82. Ans. (a) Phytonadione (Ref: KDT 6/e p593)
83. Ans. (b) Ximelgatran (Ref: Katzung 11/e p514)
84. Ans. (b) Factor V inhibition (Ref: KDT 6/e p599)
85. Ans. (a) Skin necrosis (Ref KDT 6/e p599)
86. Ans (c) Hypokalemia (Ref: KDT 6/e p599)
87. Ans. (b) Most common sites are toes and tips of fingers (Ref: Harrison 18/e p433)
Common sites of warfarin-induced skin necrosis are breasts, thighs and buttocks.
88. Ans. (c) Prothrombin time (PT) (Ref: K.D.T. 6/e p602)
89. Ans. (b) Heteropolysaccharide (Ref: Katzung 11/e p591)
90. Ans. (c) Xa (Ref: KDT 6/e p599)
91. Ans. (b) 12 hours (Ref: Harrison 18/e p2027)
General Hematology Pharmacology
• Fibrinolytic therapy can reduce the relative risk of in-hospital death by up to 50% when administered within
the first hour of the onset of symptoms of STEMI, and much of this benefit is maintained for at least 10 years.
• Since myocardium can be salvaged only before it has been irreversibly injured, the timing of reperfusion therapy,
by fibrinolysis or a catheter-based approach, is of extreme importance in achieving maximum benefit.
• The patients treated within 1–3 h of the onset of symptoms generally benefit most. Although reduction of the
mortality rate is more modest, the therapy remains of benefit for many patients seen 3–6 h after the onset of
infarction, and some benefit appears to be possible up to 12 h, especially if chest discomfort is still present
and ST segments remain elevated.
• Compared with PCI for STEMI (primary PCI), fibrinolysis is generally the preferred reperfusion strategy for
patients presenting in the first hour of symptoms, if there are logistical concerns about transportation of the
patient to a suitable PCI center (experienced operator and team with a track record for a “door-to-balloon”
time of