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f. All
Drugs for coagulation disorders.
a. Antithrombotics
b. Fibrinolytics
c. Pro-thrombotics
d. a and b
e. b and c
f. All
c. Both
Antithrombotics
a. Anticoagulants
b. Antiplatelets
c. Both
d. None
f. All
Anticoagulants.
a. Interfere with blood coagulation cascade by acting on different clotting factors such as IIa and Xa
b. Target blood coagulation cascade inhibiting Ia (Fibrin) Formation resulting to bleeding
c. Can be indirect thrombin inhibitors or direct thrombin inhibitors
d. a and b
e. b and c
f. All
d. a and b
Clotting factors inhibited by anticoagulants.
a. IIa
b. Xa
c. VIIa
d. a and b
e. b and c
f. All
b. Direct thrombin inhibitors
Blocks IIa directly.
a. Indirect thrombin inhibitors
b. Direct thrombin inhibitors
HBAD
Hirudin, Lepirudin
Bivalirudin
Argatroban
Dabigatran
Direct thrombin inhibitors.
e. Dabigatran
Parenteral direct thrombin inhibitors except:
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
f. None
d. Hirudin
Natural from Hirudo medicinalis.
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
b. Lepirudin
Recombinant; 1st line for Heparin induced thrombocytopenia (HIT).
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
a. Bivalirudin
Mgt of post-Percutaneous transluminal coronary angioplasty (PTCA).
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
c. Argatroban
Alternative for HIT.
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
Dabigatran
Oral direct thrombin inhibitor.
e. Dabigatran
Mgt of thrombo embolism usually as an alternative to warfarin.
a. Bivalirudin
b. Lepirudin
c. Argatroban
d. Hirudin
e. Dabigatran
b. Prothrombin
Clotting factor II.
a. Fibrinogen
b. Prothrombin
c. Tissue thromboplastin or tissue factor)
d. Ionized calcium
e. Labile factor or proaccelerin
f. All
coumarin derivatives → warfarin
Indirect anticoagulant/thrombin inhibitors.
a. Unfractionated Heparin
b. LMW Heparin
c. Coumarin derivatives
d. a and b
e. b and c
f. All
d. a and b
Parenteral indirect anticoagulant/thrombin inhibitors.
a. Unfractionated Heparin
b. LMW Heparin
c. Coumarin derivatives
d. a and b
e. b and c
f. All
e. None
True about Heparin except:
a. Polymeric mixture of sulfated mucopolysaccharides indicating that it is a carbohydrate
b. Macromolecule
c. Targets Anti-thrombin forming a active complex
d. Increases the activity of antithrombin by 1000-fold
e. None
a. Regular Heparin
Unfractionated heparin.
a. Regular Heparin
b. Enoxaparin
c. Dalteparin
d. Tinzaparin
e. a and b
f. b, c, and d
f. All
LMW Heparins.
a. Enoxaparin
b. Dalteparin
c. Tinzaparin
d. a and b
e. b and c
f. All
a. Regular Heparin
Target clotting factor II and and Xa.
a. Regular Heparin
b. Enoxaparin
c. Dalteparin
d. Tinzaparin
e. a and b
f. b, c, and d
b. Xa - LMWHs act mainly via antithrombin to inhibit factor Xa; they have little effect on inhibition of thrombin
LMWH target
a. IIa
b. Xa
c. Both
d. None
e. None
Uses of heparins except:
a. Preoperative prophylaxis against Deep Vein Thrombosis (DVT)
b. Administered following acute MI or pulmonary embolism
c. Reduces pulmonary embolism in patients with established thrombosis
d. Prevents clotting in extracorporeal circulation devices
e. None
f. All
Contraindications of heparin:
a. Bleeding
b. Aspirin (ASA) therapy
c. Thrombocytopenia
d. a and b
e. b and c
f. All
c. Coumarin derivatives
Oral indirect anticoagulant/thrombin inhibitors.
a. Unfractionated Heparin
b. LMW Heparin
c. Coumarin derivatives
d. a and b
e. b and c
f. All
f. All
Coumarin Derivatives.
a. Orally administered
b. Derived from 4-hydroxycoumarin
c. Include dicumarol, warfarin sodium, and phenprocoumon
d. a and b
e. b and c
f. All
f. All
Coumarin derivatives.
a. Dicumarol
b. Warfarin sodium
c. Phenprocoumon
d. a and b
e. b and c
f. All
f. All
Warfarin
a. Has the best bioavailability
b. The least severe adverse effects
c. Has narrow therapeutic index thus toxic
d. a and b
e. b and c
f. All
c. VIII
Warfarin inhibits synthesis of Vitamin K-dependent clotting factors which include the following except:
a. II
b. VII
c. VIII
d. IX
e. X
f. None
c. Both
Warfarin inhibits synthesis of Vitamin K-dependent clotting factors by inhibiting VKERC (Epoxide Reductase Complex) which results to
a. Reduce Vit K
b. Inhibition of formation Ia (Fibrin)
c. Both
d. None
e. None
Uses of warfarin except:
a. Treatment and prophylaxis of Ventricular Tachycardia (VT) and Pulmonary embolism (PE)
b. Mgt of Atrial Fibrillation
c. Mgt of thromboembolism in patients with mechanical heart valves
d. Mgt of Rheumatic heart disease (RHD)
e. None
d. Warfarin
Causes purple toe syndrome.
a. UF Heparin
b. Enoxaparin
c. Dabigatran
d. Warfarin
b. 2-3
Normal PT-INR.
a. 1-2
b. 2-3
c. 3-4
d. 4-5
e. a and c
Above normal PT-INR.
a. Risk of Hemorrhage
b. Thrombosis
c. Overdose of warfarin
d. Underdose of warfarin
e. a and c
f. b and d
f. b and d
Below normal PT-INR.
a. Risk of Hemorrhage
b. Thrombosis
c. Overdose of warfarin
d. Underdose of warfarin
e. a and c
f. b and d
f. All
Can increase PT-INR; increase risk of bleeding.
a. Amiodarone and Sulfinpyrazone
b. ASA and Salicylates
c. Antibiotics
d. a and b
e. b and c
f. All
d. a and b
Can decrease PT-INR; increase risk of thrombosis.
a. Barbiturates and Rifampin
b. OCPs
c. Antibiotics
d. a and b
e. b and c
f. All
f. None
True about newer anticoagulant agents except:
a. Xa inhibitors
b. Orally administered
c. No monitoring required
d. Safer than warfarin
e. Include the "-xabans"
f. None
c. Both
Newer anticoagulant agents:
a. Apixaban
b. Rivaroxaban
c. Both
d. None
a. Heparin
Inhibitor of action of clotting factors.
a. Heparin
b. Warfarin
b. Warfarin
Inhibitor of the synthesis of clotting factors.
a. Heparin
b. Warfarin
e. None
Mechanisms of anti-platelets except:
a. Inhibition of COX
b. Inhibition of Adenosine diphosphate (ADP)
c. Inhibition of Phosphodiesterase enzyme (PDE)
d. Inhibition of Glycoprotein IIb/IIIa
e. None
a. Inhibition of COX
Results to inhibition of Thromboxane A2 (TXA2) Synthesis.
a. Inhibition of COX
b. Inhibition of Adenosine diphosphate (ADP)
c. Inhibition of Phosphodiesterase enzyme (PDE)
d. Inhibition of Glycoprotein IIb/IIIa
e. None
c. Inhibition of Phosphodiesterase enzyme (PDE)
Results to increase cAMP levels in endothelial cell that can cause antiplatelet effect.
a. Inhibition of COX
b. Inhibition of Adenosine diphosphate (ADP)
c. Inhibition of Phosphodiesterase enzyme (PDE)
d. Inhibition of Glycoprotein IIb/IIIa
e. None
f. I, II, III, IV, V, VI, VII, VIII
Antiplatelet agents.
I. Aspirin
II. Clopidogrel
III. Ticlopidine
IV. Dipyridamole
V. Cilostazol
VI. Eptifibatide
VII. Abciximab
VIII. Tirofiban
a. I, II, III
b. I
c. II, III
d. IV, V
e. VI, VII, VIII
f. I, II, III, IV, V, VI, VII, VIII
b. I
COX inhibitor antiplatelet agents.
I. Aspirin
II. Clopidogrel
III. Ticlopidine
IV. Dipyridamole
V. Cilostazol
VI. Eptifibatide
VII. Abciximab
VIII. Tirofiban
a. I, II, III
b. I
c. II, III
d. IV, V
e. VI, VII, VIII
f. I, II, III, IV, V, VI, VII, VIII
c. II, III
Thienopyridines or ADP inhibitor anntiplatelet agents.
I. Aspirin
II. Clopidogrel
III. Ticlopidine
IV. Dipyridamole
V. Cilostazol
VI. Eptifibatide
VII. Abciximab
VIII. Tirofiban
a. I, II, III
b. I
c. II, III
d. IV, V
e. VI, VII, VIII
f. I, II, III, IV, V, VI, VII, VIII
d. IV, V
PDE inhibitors antiplatelet agents.
I. Aspirin
II. Clopidogrel
III. Ticlopidine
IV. Dipyridamole
V. Cilostazol
VI. Eptifibatide
VII. Abciximab
VIII. Tirofiban
a. I, II, III
b. I
c. II, III
d. IV, V
e. VI, VII, VIII
f. I, II, III, IV, V, VI, VII, VIII
e. VI, VII, VIII
GP IIb/IIIa inhibitor Antiplatelet agents.
I. Aspirin
II. Clopidogrel
III. Ticlopidine
IV. Dipyridamole
V. Cilostazol
VI. Eptifibatide
VII. Abciximab
VIII. Tirofiban
a. I, II, III
b. I
c. II, III
d. IV, V
e. VI, VII, VIII
f. I, II, III, IV, V, VI, VII, VIII
f. All
Fibrinolytics.
a. Also known as Plasminogen Activators
b. Target pathway is in the activation of plasminogen
c. Enhance/accelerate plasmin that can destroy the clot
d. a and b
e. b and c
f. All
a. True
Plasminogen is an inactive protein that is activated into plasmin by the tissue plasminogen activator
a. True
b. False
f. None
Fibrinolytics except:
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
f. None
e. Urokinase
Produce in the kidneys; activates plasminogen.
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
d. Streptokinase
Bacterial glycoprotein: activates plasminogen.
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
c. Duteplase
Recombinant human tPA with a single amino acid change.
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
b. Reteplase
Recombinant fragment of human tPA.
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
a. Alteplase
Recombinant natural human tPA.
a. Alteplase
b. Reteplase
c. Duteplase
d. Streptokinase
e. Urokinase
d. Urokinase
Recombinant fibrinolytics except:
a. Alteplase
b. Reteplase
c. Duteplase
d. Urokinase
e. None
f. All
Prothrombotics.
a. Actions is by causing clot formation
b. Increase Clotting Factors X, IX, VII, II
c. Increase Ia (Fibrin) Formation resulting to clotting
d. a and b
e. b and c
f. All
f. All
Prothrombotics.
a. Vitamin K
b. Tranexamic acid
c. Aprotonin
d. a and b
e. b and c
f. All
d. a and b - Vitamin K
Required for translational modification of clotting factors II, VII, IX, and X.
a. Phytonadione
b. Menaquinone
c. Tranexamic acid
d. a and b
e. b and c
f. All
c. Tranexamic acid
Inhibitor of plasminogen activation.
a. Phytonadione
b. Menaquinone
c. Tranexamic acid
d. a and b
e. b and c
f. All
a. Phytonadione
Vitamin K:
Vitamin K1
Clinically useful
Found in food and is available for oral or parenteral use
a. Phytonadione
b. Menaquinone
c. Both
d. None
b. Menaquinone
Vitamin K:
Vitamin K2
Found in human tissues and is the form synthesized by intestinal bacteria
a. Phytonadione
b. Menaquinone
c. Both
d. None
e. None
Tranexamic acid except:
a. Hemostan
b. A potent analogue of aminocaproic acid
c. Inhibit plasminogen activation; Inhibits fibrinolysis
d. Used in the Mgt of post-procedural bleeding
e. None
c. Aminocaproic acid
Tranexamic acid is potent analogue of
a. Nitrocaproic acid
b. Nitrocaprylic acid
c. Aminocaproic acid
d. Aminocaprylic acid
c. Tranexamic acid
Used in the Mgt of post-procedural bleeding.
a. Phytonadione
b. Menaquinone
c. Tranexamic acid
d. a and b
e. b and c
f. All
A. Endothelin release inducing reflex vasoconstriction
What immediate vascular reaction follows Step 1 endothelial injury in primary hemostasis?
A. Endothelin release inducing reflex vasoconstriction
B. Nitric oxide release inducing rapid vasodilation
C. Histamine release causing vascular permeability
D. Prostacyclin release inhibiting platelet activation
B. Collagen is exposed and binds to von Willebrand Factor
In Step 2 of primary hemostasis, what subendothelial structure is exposed upon injury, and what factor binds to it?
A. Fibrinogen binds directly to endothelial cell membranes
B. Collagen is exposed and binds to von Willebrand Factor
C. Tissue factor is exposed and binds to Factor VIII
D. Antithrombin III binds to exposed smooth muscle cells
B. Glycoprotein Ib
In Step 3 of primary hemostasis, through which surface glycoprotein receptor do platelets adhere to bound von Willebrand Factor?
A. Glycoprotein IIb/IIIa
B. Glycoprotein Ib
C. Glycoprotein VI
D. Glycoprotein Ia/IIa
B. Glycoprotein IIb/IIIa receptor forming a white thrombus primary platelet plug
In Step 5 of primary hemostasis, which receptor mediates interplatelet binding, and what structure is formed?
A. Glycoprotein Ib receptor forming a red thrombus
B. Glycoprotein IIb/IIIa receptor forming a white thrombus primary platelet plug
C. Tissue factor receptor forming a fibrin clot
D. Antithrombin III receptor forming a secondary platelet plug
C. Factors X, V, II, and I
Which clotting factors form the Common Pathway of the coagulation cascade?
A. Factors XII, XI, IX, VIII
B. Factors III and VII
C. Factors X, V, II, and I
D. Factors XIII, Protein C, and Protein S
C. Antithrombin III, Protein C, and Protein S
Which endogenous anticoagulants inhibit active thrombin and coagulation factors in the blood?
A. Tissue Factor and Factor VIIa
B. Thromboxane A2 and ADP
C. Antithrombin III, Protein C, and Protein S
D. Tissue Plasminogen Activator and Plasmin
A. Endothelial injury, Stasis, and Hypercoagulation state
What three pathologic features comprise Virchow's Triad in thrombosis formation?
A. Endothelial injury, Stasis, and Hypercoagulation state
B. Vasoconstriction, Platelet adhesion, and Fibrin degradation
C. Hemophilia, Thrombocytopenia, and Anemia
D. Hypertension, Hyperglycemia, and Hyperlipidemia