WorksheetsChapter 118 (51 to up)
Total questions: 100
Worksheet time: 50mins
Which anticoagulant is LEAST affected by plasma protein binding?
UFH
LMWH
Fondaparinux
Warfarin
Which anticoagulant has NO available reversal agent?
UFH
LMWH
Fondaparinux
Warfarin
Protamine sulfate completely reverses
UFH only
LMWH only
Fondaparinux
Warfarin
Which anticoagulant accumulates most in renal failure?
Argatroban
UFH
LMWH
Warfarin
Preferred anticoagulant in pregnancy
Warfarin
UFH
LMWH
Fondaparinux
Which drug prolongs INR but should NOT be monitored with INR?
Warfarin
Argatroban
Dabigatran
Heparin
The primary reason LMWH does not require routine aPTT monitoring
Short half-life
Weak thrombin inhibition
Minimal effect on aPTT reagents
Hepatic clearance
Which anticoagulant is contraindicated in mechanical heart valves?
UFH
LMWH
Warfarin
DOACs
The most common cause of heparin treatment failure
HIT
Heparin resistance
Inadequate dosing
Platelet activation
In extensive DVT with iliac vein involvement, an adjunctive option is
Aspirin
Systemic fibrinolysis
Catheter-directed thrombolysis
Oral warfarin monotherapy
The single most important determinant of arterial thrombosis is
Blood stasis
Endothelial denudation
High shear stress
Hypercoagulability
Venous thrombi are typically rich in
Platelets and VWF
Platelets and collagen
Fibrin and red blood cells
Tissue factor and platelets
The earliest platelet response after vascular injury is
Platelet aggregation
Platelet secretion
Platelet adhesion
Thrombin generation
Platelet adhesion to exposed collagen requires
GpIIb/IIIa
GpIa/IIa
P2Y₁₂
PAR-1
Binding of platelets to VWF occurs via
GpIb
GpIIb/IIIa
GpIa/IIa
Integrin αvβ3
Platelet aggregation is mediated by
VWF bridging GpIb
Fibrin bridging GpIa
Fibrinogen bridging GpIIb/IIIa
Collagen bridging GpIa
Thrombin amplifies coagulation by activating
Factors II and X
Factors V, VIII, and XI
Factors VII and IX
Protein C and S
Which drug blocks thromboxane A₂ synthesis?
Dipyridamole
Aspirin
Ticagrelor
Vorapaxar
Aspirin inhibits platelet function by
Reversibly inhibiting COX-1
Irreversibly inhibiting COX-1
Inhibiting COX-2 only
Blocking ADP receptors
At high doses, aspirin also inhibits
COX-1 selectively
COX-2 in endothelial cells
ADP-mediated aggregation
PAR-1 receptors
The main reason aspirin is no longer recommended for routine primary prevention
Poor efficacy
High cost
Bleeding risk outweighs benefit
Resistance is common
Which P2Y₁₂ inhibitor is a prodrug requiring CYP metabolism?
Ticagrelor
Cangrelor
Clopidogrel
Dipyridamole
Which genetic polymorphism explains clopidogrel resistance?
VKORC1
CYP2C9
CYP2C19
CYP3A4
Which P2Y₁₂ inhibitor is reversible and orally active?
Clopidogrel
Prasugrel
Ticagrelor
Cangrelor
Which antiplatelet agent is given IV with immediate onset and offset?
Prasugrel
Ticagrelor
Cangrelor
Abciximab
The final common pathway of platelet aggregation is blocked by
Aspirin
Clopidogrel
Abciximab
Vorapaxar
Abciximab differs from other Gp IIb/IIIa inhibitors because it
Is renally cleared
Has a very short platelet binding time
Is a monoclonal antibody fragment
Is orally active
The most serious adverse effect of Gp IIb/IIIa inhibitors
Hepatic failure
Immune thrombocytopenia
Hypertension
Bronchospasm
Dipyridamole is avoided in symptomatic coronary artery disease because
It increases thrombosis
It causes vasodilation
It causes severe hypertension
It blocks aspirin metabolism
Unfractionated heparin inhibits thrombin by
Direct binding to thrombin
Bridging thrombin and antithrombin
Inhibiting factor Xa only
Blocking tissue factor
The pentasaccharide sequence of heparin is required for
Platelet inhibition
Antithrombin activation
Thrombin binding
Protein C activation
LMWH differs from UFH because LMWH
Inhibits thrombin more strongly
Has dose-independent clearance
Preferentially inhibits factor Xa
Requires aPTT monitoring
Best laboratory test to monitor LMWH when needed
aPTT
INR
Anti-factor Xa level
Bleeding time
Fondaparinux inhibits
Thrombin directly
Thrombin via antithrombin
Factor Xa via antithrombin
Factors II and X
Fondaparinux does NOT
Bind antithrombin
Inhibit factor Xa
Cause HIT
Inhibit thrombin
Heparin-induced thrombocytopenia is mediated by
IgM antibodies
Platelet destruction
Antibodies to PF4–heparin complexes
Bone marrow suppression
The paradox of HIT is explained by
Low platelet count causing bleeding
Antibody-mediated platelet activation
Reduced fibrinolysis
Depletion of clotting factors
First management step in suspected HIT
Platelet transfusion
Stop heparin
Start warfarin
Increase LMWH dose
Preferred anticoagulant in HIT with renal failure
Fondaparinux
Enoxaparin
Argatroban
Dabigatran
Argatroban is cleared primarily by
Kidneys
Liver
Platelets
Endothelium
Warfarin exerts its effect by inhibiting
Thrombin directly
Factor Xa
Vitamin K epoxide reductase
Antithrombin
Warfarin causes initial hypercoagulability due to depletion of
Factor VII
Protein C
Factor X
Prothrombin
The clotting factor most closely associated with warfarin’s antithrombotic effect
Factor VII
Factor IX
Factor X
Factor II
Genetic polymorphism with greatest impact on warfarin dose
CYP2C19
CYP3A4
VKORC1
P-glycoprotein
Warfarin skin necrosis is most likely in patients with
Factor V Leiden
Protein C deficiency
HIT
Antithrombin deficiency
Why must warfarin overlap with heparin initially?
INR rises before anticoagulation
Protein C declines before clotting factors
Warfarin increases platelet activation
Warfarin has poor absorption
Which anticoagulant has no reliable reversal agent?
UFH
LMWH
Fondaparinux
Warfarin
Long-term unfractionated heparin is associated with
Renal failure
Osteoporosis
Hepatic necrosis
Myelosuppression
Preferred anticoagulant in pregnancy
Warfarin
DOACs
LMWH
Fondaparinux
Which cell type contributes to thrombosis by producing neutrophil extracellular traps (NETs)?
Monocytes
Neutrophils
Endothelial cells
Platelets
DNA released in NETs promotes thrombosis primarily by
Degrading fibrin
Activating factor XII
Inhibiting antithrombin
Increasing prostacyclin
Venous thrombi rarely form at sites of
Valve cusps
Sluggish blood flow
Endothelial activation
Atheroscle
Venous thrombi rarely form at sites of
Valve cusps
Sluggish blood flow
Endothelial activation
Atherosclerotic plaque rupture
Reduced clearance of activated clotting factors in veins is due to
Endothelial dysfunction
Platelet consumption
Impaired blood flow
Low oxygen tension
The color difference between arterial and venous thrombi is due to
Degree of endothelial injury
Platelet content
Trapped red blood cells
Thrombin concentration
The primary platelet agonists released from dense granules include
ADP and calcium
Thromboxane and serotonin
ADP and thromboxane A₂
Calcium and fibrinogen
Thromboxane A₂ synthesis occurs via
Lipoxygenase
Cyclooxygenase
Phosphodiesterase
Adenylate cyclase
Platelet shape change after adhesion is triggered by
Fibrin
ADP secretion
von Willebrand factor
Thrombin inhibition
Activated platelets potentiate coagulation primarily by
Secreting fibrinogen
Providing a phospholipid surface
Inhibiting fibrinolysis
Binding tissue plasminogen activator
Which factor converts fibrinogen to fibrin?
Factor Xa
Factor IXa
Thrombin
Factor XIII
Factor XIII activation results in
Platelet aggregation
Fibrin cross-linking
Thrombin amplification
Protein C activation
Aspirin doses >1 g/day reduce platelet inhibition because
COX-1 is saturated
COX-2 inhibition reduces prostacyclin
Platelet turnover increases
TXA₂ synthesis increases
Dual antiplatelet therapy increases major bleeding risk by approximately
5%
10%
20%
40%
Which antiplatelet agent has the longest half-life?
Aspirin
Ticagrelor
Clopidogrel
Vorapaxar
Vorapaxar blocks platelet activation by inhibiting
ADP signaling
Thromboxane synthesis
PAR-1 receptors
GpIIb/IIIa binding
The most important contraindication to vorapaxar use
Renal insufficiency
Prior intracranial hemorrhage
Peptic ulcer disease
Thrombocytopenia
Why is dipyridamole avoided in symptomatic coronary artery disease?
Platelet activation
Coronary steal phenomenon
Increased bleeding
Reduced aspirin efficacy
Dipyridamole increases local adenosine levels by
Enhancing synthesis
Blocking reuptake
Increasing degradation
Inhibiting receptors
Which Gp IIb/IIIa inhibitor is cleared by the kidneys?
Abciximab
Eptifibatide
Both B and C
None
The shortest plasma half-life among Gp IIb/IIIa inhibitors
Abciximab
Eptifibatide
Tirofiban
Vorapaxar
UFH clearance becomes slower at higher doses because
Renal saturation
Endothelial binding saturation
Platelet activation
Reduced antithrombin
Which heparin chain length is required to inhibit thrombin?
≥5 saccharide units
≥10 saccharide units
≥18 saccharide units
≥25 saccharide units
Anti-factor Xa levels are preferred over aPTT when
INR is elevated
Factor VIII is increased
Platelets are low
Warfarin is used
Heparin resistance is commonly due to elevated levels of
Antithrombin
Protein C
Acute-phase reactants
Vitamin K
Platelet factor 4 reduces heparin efficacy by
Increasing clearance
Neutralizing heparin
Inhibiting antithrombin
Activating fibrinolysis
HIT typically develops
Within 24 hours of heparin exposure
1–3 days after initiation
5–14 days after initiation
After 1 month
HIT is more common in
Medical patients
Surgical patients
Pediatric patients
Pregnant patients
The most specific diagnostic test for HIT
ELISA for PF4
Platelet count trend
Serotonin release assay
Bleeding time
Why is warfarin contraindicated in acute HIT?
INR is unreliable
Platelet count falls further
Rapid protein C depletion
Hepatic toxicity
Argatroban monitoring is performed using
INR
Anti-Xa level
aPTT
ACT
Which anticoagulant does NOT bind plasma proteins significantly?
UFH
LMWH
Fondaparinux
Warfarin
Warfarin effect is delayed because
Slow absorption
Delayed inhibition of VKOR
Existing clotting factors must degrade
Platelet turnover
Factor VII has the shortest half-life among vitamin K–dependent factors, making it useful for
Monitoring thrombosis risk
Monitoring early warfarin effect
Assessing bleeding risk
Guiding heparin dosing
Warfarin is highly protein bound; the active fraction is
Albumin-bound
Free drug
Hepatic metabolite
Renal metabolite
Which CYP enzyme metabolizes S-warfarin?
CYP3A4
CYP2D6
CYP2C9
CYP1A2
Patients with CYP2C9 variants have
Higher warfarin dose requirements
Lower bleeding risk
Reduced warfarin clearance
Faster onset of action
LMWH bioavailability after subcutaneous injection is approximately
50%
70%
90%
100%
LMWH accumulation is most likely in
Obesity
Hepatic failure
Renal insufficiency
Pregnancy
Protamine incompletely reverses LMWH because
It cannot bind LMWH
Short heparin chains remain active
LMWH inhibits factor Xa directly
Protamine is renally cleared
Fondaparinux is preferred over heparin in HIT because it
Is reversible
Does not bind PF4
Inhibits thrombin
Has hepatic clearance
Which physiologic anticoagulant is enhanced by heparin?
Protein C
Protein S
Antithrombin
Tissue factor pathway inhibitor
The anticoagulant effect of antithrombin is strongest against
Factor VIIa
Factor IXa
Factor Xa and thrombin
Factor XIIIa
Which coagulation factor is NOT vitamin K–dependent?
Factor II
Factor VII
Factor IX
Factor VIII
The INR primarily reflects the activity of
Intrinsic pathway
Common pathway only
Extrinsic pathway
Fibrinolytic system
Which clotting factor contributes MOST to INR prolongation early in warfarin therapy?
Factor II
Factor VII
Factor IX
Factor X
The half-life of platelets is approximately
24 hours
3 days
7–10 days
21 days
The duration of aspirin’s antiplatelet effect is determined by
Drug half-life
Platelet regeneration
Hepatic metabolism
Renal clearance
Which agent inhibits platelet aggregation by increasing prostacyclin effect indirectly?
Aspirin
Dipyridamole
Clopidogrel
Vorapaxar
Platelet granules that store fibrinogen are
Dense granules
Lysosomes
Alpha granules
Peroxisomes
Dense platelet granules contain
Fibrinogen
von Willebrand factor
ADP and calcium
Factor V
