Part 5.1-BLOOD-COAGULATION DISORDER

Proverbs 16:3

b. balance

Hemostasis refers to the ________ that maintains normal blood clotting and bleeding.

a. imbalance
b. balance
c. infection
d. inflammation

b. vasoconstriction

The vascular event in hemostasis is ________.

a. vasodilation
b. vasoconstriction

d. aggregation

The cellular event in hemostasis involves platelet migration and ________.

a. destruction
b. synthesis
c. inhibition
d. aggregation

b. cascade

The protein event in hemostasis is the coagulation factor ________.

a. inhibition
b. cascade
c. breakdown
d. transport

e. All of the above

Stimuli for coagulation and clot formation include:

a. Endothelial injury

b. Presence of foreign bodies

c. Stasis of blood

d. a and b

e. All of the above

h. b and c

• Arterial clots: platelet-rich "white thrombi"

• Venous clots: fibrin-rich "red thrombi"

Arterial clots are predominantly:

a. Fibrin-rich

b. Platelet-rich

c. White thrombi

d. Red thrombi

e. a and c

f. b and d

g. a and d

h. b and c

g. a and d

• Arterial clots: platelet-rich "white thrombi"

• Venous clots: fibrin-rich "red thrombi"

Venous clots are predominantly:

a. Fibrin-rich

b. Platelet-rich

c. White thrombi

d. Red thrombi

e. a and c

f. b and d

g. a and d

h. b and c

after discussion nalang to

Coagulation Cascade

a. XII

b. XI

c. IX

d. X

Intrinsic pathway:

a. XII

b. XI

c. IX

d. X

e. III

f. VII

g. X

e. III

f. VII

g. X

Extrinsic pathway:

a. XII

b. XI

c. IX

d. X

e. III

f. VII

g. X

d. Aspirin

[Anti-platelet Aggregants]

Thromboxane synthesis inhibitor:

a. Clopidogrel

b. Warfarin

c. Heparin

d. Aspirin

b. Inhibits COX of platelets, decreasing TXA₂ levels

[Anti-platelet Aggregants]

Mechanism of action (MOA) of aspirin:

a. Stimulates platelet aggregation

b. Inhibits COX of platelets, decreasing TXA₂ levels

c. Activates fibrin formation

d. Increases thromboxane production

c. Irreversibly acetylating COX of platelets

[Anti-platelet Aggregants]

Aspirin acts on platelets by:

a. Reversibly inhibiting COX

b. Blocking calcium channels

c. Irreversibly acetylating COX of platelets

d. Stimulating platelet receptors

a. Acute myocardial infarction

• primary and secondary = acute MI

• secondary = stroke

[Anti-platelet Aggregants]

Aspirin is used for primary and secondary prevention of:

a. Acute myocardial infarction

b. Asthma

c. Diabetes mellitus

d. Peptic ulcer disease

b. Stroke

• primary and secondary = acute MI

• secondary = stroke

[Anti-platelet Aggregants]

Aspirin is commonly used for secondary prevention of:

a. Pneumonia

b. Stroke

c. Renal failure

d. Epilepsy

Bleeding

GI intolerance

Ulcer

Bronchospasm

Hypersensitivity

Salicylism

[Anti-platelet Aggregants]

Adverse effects of Aspirin:

Bleeding or Clotting?

GI indigestion or GI intolerance?

Gastritis or Ulcer?

Bronchospasm or Bronchodilation?

Agitation or Hypersensitivity?

Salicylism or Metabolic disturbances?

d. ADP inhibitor

[Anti-platelet Aggregants]

Thienopyridines and Non-Thienopyridines

a. GIIb / IIIa inhibitors

b. Thromboxane synthesis inhibitor

c. Adenosine and Phosphodiesterase inhibitor

d. ADP inhibitor

a. Thienopyridines

[Anti-platelet Aggregants]

Ticlopidine

a. Thienopyridines

b. Non-Thienopyridines

a. Thienopyridines

[Anti-platelet Aggregants]

Clopidogrel

a. Thienopyridines

b. Non-Thienopyridines

a. Thienopyridines

[Anti-platelet Aggregants]

Prasugrel

a. Thienopyridines

b. Non-Thienopyridines

b. Non-Thienopyridines

[Anti-platelet Aggregants]

Ticagrelor

a. Thienopyridines

b. Non-Thienopyridines

c. Irreversible P2Y12 receptor inhibition

[Anti-platelet Aggregants]

The mechanism of thienopyridines is best described as:
a. Reversible COX-1 inhibition
b. Reversible P2Y12 receptor blockade
c. Irreversible P2Y12 receptor inhibition
d. Direct thrombin inhibition

a. Thienopyridines

[Anti-platelet Aggregants]

Given in for primary and secondary prevention of acute myocardial infarction (given at least 9 months after ACS)

a. Thienopyridines

b. Non-Thienopyridines

both

[Anti-platelet Aggregants]

Given post- angioplasty

a. Thienopyridines

b. Non-Thienopyridines

a. Given for post angioplasty (to prevent acute thrombosis)

[Anti-platelet Aggregants]

Ticagrelor

a. Given post- angioplasty (to prevent acute thrombosis)

b. Given in for primary and secondary prevention of acute myocardial infarction (given at least 9 months after ACS)

c. Blocking GPIIb/IIIa receptor to prevent platelet aggregation

[Anti-platelet Aggregants]

Glycoprotein IIb/IIIa inhibitors act by:
a. Blocking thromboxane A2 synthesis
b. Activating P2Y12 receptor
c. Blocking GPIIb/IIIa receptor to prevent platelet aggregation
d. Inhibiting fibrin formation directly

b. Preventing platelet cross-linking (aggregation)

[Anti-platelet Aggregants]

The main effect of GPIIb/IIIa inhibitors is:
a. Increasing platelet adhesion
b. Preventing platelet cross-linking (aggregation)
c. Enhancing coagulation cascade
d. Promoting fibrinolysis

b. Abciximab

[Anti-platelet Aggregants]

GPIIb/IIIa inhibitor
a. Clopidogrel
b. Abciximab
c. Warfarin
d. Heparin

d. Eptifibatide

[Anti-platelet Aggregants]

GPIIb/IIIa inhibitor
a. Clopidogrel
b. Ticagrelor
c. Warfarin
d. Eptifibatide

a. Tirofiban

[Anti-platelet Aggregants]

GPIIb/IIIa inhibitor
a. Tirofiban
b. Prasugrel
c. Warfarin
d. Heparin

c. Post-angioplasty prevention of acute thrombosis

-Given as IV infusion

[Anti-platelet Aggregants]

The primary clinical use of GPIIb/IIIa inhibitors is:
a. Long-term prevention of stroke
b. Treatment of hypertension
c. Post-angioplasty prevention of acute thrombosis
d. Treatment of anemia

b. Inhibiting adenosine uptake and phosphodiesterase enzymes

[Anti-platelet Aggregants]

Adenosine and phosphodiesterase inhibitors work by:
a. Blocking thromboxane A2 synthesis
b. Inhibiting adenosine uptake and phosphodiesterase enzymes
c. Activating platelet aggregation
d. Blocking vitamin K recycling

b. Inhibition of adenosine uptake

[Anti-platelet Aggregants]

Dipyridamole’s mechanism of action includes:
a. Irreversible P2Y12 receptor blockade
b. Inhibition of adenosine uptake
c. Direct thrombin inhibition
d. COX-1 activation

d. Inhibition of cGMP and cAMP phosphodiesterase

[Anti-platelet Aggregants]

Dipyridamole’s mechanism of action includes:
a. Irreversible P2Y12 receptor blockade
b. COX-1 activation
c. Direct thrombin inhibition
d. Inhibition of cGMP and cAMP phosphodiesterase

a. Primary and secondary prevention of acute myocardial infarction (with other antiplatelet/anticoagulant drugs)

[Anti-platelet Aggregants]

Dipyridamole is clinically used for:
a. Primary and secondary prevention of acute myocardial infarction
b. Treatment of asthma
c. Hypertension monotherapy
d. Acute pain relief

b. Combined with other antiplatelet or anticoagulant drugs

[Anti-platelet Aggregants]

Dipyridamole is most effective when:
a. Used alone as monotherapy
b. Combined with other antiplatelet or anticoagulant drugs
c. Given only in emergency stroke treatment
d. Used only in pediatric patients

d. Coronary steal phenomenon

[Anti-platelet Aggregants]

A key adverse effect of dipyridamole is:
a. Hepatotoxicity
b. Bone marrow suppression
c. Nephrotoxicity
d. Coronary steal phenomenon

a. A vasodilator

[Anti-platelet Aggregants]

Cilostazol
a. A vasodilator
b. A vasoconstrictor

a. A phosphodiesterase inhibitor

[Anti-platelet Aggregants]

Cilostazol is best described as:
a. A phosphodiesterase inhibitor
b. A vitamin K antagonist
c. A thrombin activator
d. A COX-2 inhibitor

b. Intermittent claudication

[Anti-platelet Aggregants]

The primary use of cilostazol is:
a. Treatment of hypertension
b. Intermittent claudication
c. Acute myocardial infarction reversal
d. Prevention of infection

b. Directly inhibiting factor IIa (thrombin)

[Anticoagulant]

Direct thrombin inhibitors MOA
a. Blocking factor Xa
b. Directly inhibiting factor IIa (thrombin)
c. Inhibiting vitamin K epoxide reductase
d. Activating plasminogen

d. Interfere the coagulation cascade

[Anticoagulant]

Direct thrombin inhibitors MOA
a. Blocking factor Xa
b. Activating plasminogen
c. Inhibiting vitamin K epoxide reductase
d. Interfere the coagulation cascade

d. Dabigatran- oral

[Anticoagulant]

Parenteral Direct thrombin inhibitor except:

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Dabigatran

e. Argatroban

a. Hirudin

[Anticoagulant]

natural product from Leeches

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

b. Lepirudin

[Anticoagulant]

Recombinant form

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

b. Lepirudin

[Anticoagulant]

Clinically used

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

b. Lepirudin

[Anticoagulant]

DOC for HIT or Heparin induced thrombocytopenia

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

c. Bivalirudin

[Anticoagulant]

Small molecule that inactivates factor II-a

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

c. Bivalirudin

[Anticoagulant]

Used as a antithrombotic post angioplasty

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

d. Argatroban

[Anticoagulant]

Alternative in the management of HIT

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

b. Direct inhibition of thrombin (factor IIa)

[Anticoagulant]

The mechanism of action of dabigatran is:
a. Irreversible inhibition of P2Y12 receptor
b. Direct inhibition of thrombin (factor IIa)
c. Inhibition of vitamin K recycling
d. Activation of plasmin

c. Prophylaxis of venous thromboembolism (VTE)

[Anticoagulant]

Dabigatran is primarily used for:
a. Treatment of asthma
b. Treatment of hypertension
c. Prophylaxis of venous thromboembolism (VTE)
d. Pain management

c. Warfarin

[Anticoagulant]

Dabigatran is best described as an alternative to:
a. Aspirin
b. Heparin only
c. Warfarin
d. Clopidogrel

a. Bleeding

[Anticoagulant]

A major adverse effect of dabigatran is:
a. Bleeding
b. Hypoglycemia
c. Hypertension
d. Neutropenia

a. CYP3A4 inhibitors

[Anticoagulant]

Drug interactions with dabigatran involve mainly:
a. CYP3A4 inhibitors
b. MAO inhibitors
c. Beta blockers
d. Calcium channel blockers

a. Inhibit synthesis or formation of active clotting factors (factor II-a)

[Anticoagulant]

Indirect thrombin inhibitors are best described as drugs that:
a. Inhibit synthesis or formation of active clotting factors (factor II-a)
b. Directly inhibit factor IIa
c. Activate thrombin
d. Inhibit platelet adhesion only

b. Parenteral indirect thrombin inhibitor

[Anticoagulant]

Heparin is classified as:
a. Oral anticoagulant
b. Parenteral indirect thrombin inhibitor
c. Direct factor Xa inhibitor
d. Antiplatelet drug

c. Sulfated mucopolysaccharide

[Anticoagulant]

The chemical nature of heparin is:
a. Protein hormone
b. Lipid compound
c. Sulfated mucopolysaccharide
d. Steroid derivative

d. Released by platelets

[Anticoagulant]

Heparin is naturally:
a. Synthesized in liver
b. Derived from plasma albumin
c. Produced in kidney
d. Released by platelets

b. Regular or high molecular weight heparin

[Anticoagulant]

Unfractionated heparin (UFH) is also known as:
a. Low molecular weight heparin
b. Regular or high molecular weight heparin
c. Synthetic anticoagulant
d. Oral anticoagulant

a. Low molecular weight heparin

[Anticoagulant]

Fractionated heparin is also known as:
a. Low molecular weight heparin
b. Regular or high molecular weight heparin
c. Synthetic anticoagulant
d. Oral anticoagulant

d. Binding and forming a complex with antithrombin III

[Anticoagulant]

The mechanism of unfractionated heparin is:
a. Direct inhibition of thrombin
b. Blocking platelet P2Y12 receptor
c. Inhibition of vitamin K epoxide reductase
d. Binding and forming a complex with antithrombin III

c. aPTT / PTT

[Anticoagulant]

The key monitoring parameter for UFH therapy is:
a. INR
b. Bleeding time
c. aPTT / PTT
d. Platelet count only

b. Enoxaparin, dalteparin, tinzaparin

[Anticoagulant]

Low molecular weight heparin (LMWH) includes:
a. Warfarin, dabigatran
b. Enoxaparin, dalteparin, tinzaparin
c. Aspirin, clopidogrel
d. Heparin only

a. Synthetic polysaccharide indirect anticoagulant

[Anticoagulant]

Fondaparinux is classified as:
a. Synthetic polysaccharide indirect anticoagulant
b. Vitamin K antagonist
c. Direct thrombin inhibitor
d. Antiplatelet drug

b. Acute coronary syndrome

[Anticoagulant]

LMWH is the drug of choice (DOC) in:
a. Asthma
b. Acute coronary syndrome
c. Epilepsy
d. Hypertension

b. Acute coronary syndrome and venous thromboembolism

LMWH and HMWH are used in the management of:
a. Asthma
b. Acute coronary syndrome and venous thromboembolism
c. Epilepsy
d. Hypertension

b. LMWH

[Anticoagulant]

preferred in pregnancy

a. HMWH

b. LMWH

anticoagulant

[Anticoagulant]

HMWH and LMWH are used when initiating [anticoagulant/coagulant] therapy

b. Bleeding

[Anticoagulant]

Major adverse effect of heparin is:
a. Hypertension
b. Bleeding
c. Hypoglycemia
d. Hypercalcemia

b. Protamine sulfate

[Anticoagulant]

Antidote for heparin overdose is:
a. Vitamin K
b. Protamine sulfate
c. Naloxone
d. Atropine

d. HIT

-treated with Lepirudin

[Anticoagulant]

A/E of heparin therapy:
a. Cataracts
b. Diabetes
c. Lung fibrosis
d. HIT

a. Osteoporosis

[Anticoagulant]

A long-term adverse effect of heparin therapy is:
a. Osteoporosis
b. Diabetes
c. Lung fibrosis
d. Cataracts

b. Inhibiting factor Xa

[Anticoagulant]

Oral anti–factor Xa inhibitors act primarily by:
a. Directly inhibiting thrombin (factor IIa)
b. Inhibiting factor Xa
c. Activating vitamin K
d. Blocking platelet receptors

c. Direct oral factor Xa inhibitor

[Anticoagulant]

Rivaroxaban and Apixaban are classified as:
a. Vitamin K antagonists
b. Antiplatelet drugs
c. Direct oral factor Xa inhibitor
d. Heparin derivatives

b. Venous thromboembolism (VTE)

[Anticoagulant]

Direct factor Xa inhibitors are mainly used in the management of:
a. Asthma
b. Venous thromboembolism (VTE)
c. Epilepsy
d. Diabetes mellitus

d. Inhibiting formation of active vitamin K

[Anticoagulant]

Vitamin K epoxide reductase (VKORC) inhibitors act by:
a. Activating thrombin
b. Increasing platelet aggregation
c. Blocking factor Xa directly
d. Inhibiting formation of active vitamin K

d. VKORC (vitamin K epoxide reductase) inhibitor

[Anticoagulant]

Dicumarol

a. Direct factor Xa inhibitor

b. LMWH

c. HMWH

d. VKORC (vitamin K epoxide reductase) inhibitor

d. VKORC (vitamin K epoxide reductase) inhibitor

[Anticoagulant]

Phenprocoumon

a. Direct factor Xa inhibitor

b. LMWH

c. HMWH

d. VKORC (vitamin K epoxide reductase) inhibitor

d. VKORC (vitamin K epoxide reductase) inhibitor

-Phenindione, Anisindiones

[Anticoagulant]

Indanedione

a. Direct factor Xa inhibitor

b. LMWH

c. HMWH

d. VKORC (vitamin K epoxide reductase) inhibitor

d. VKORC (vitamin K epoxide reductase) inhibitor

[Anticoagulant]

Warfarin

a. Direct factor Xa inhibitor

b. LMWH

c. HMWH

d. VKORC (vitamin K epoxide reductase) inhibitor

Bleeding

Intracerebral hemorrhage

Abnormal bone development

Cutaneous necrosis

[Anticoagulant]

VKORC Adverse effects

Bleeding or Clotting?

Intracerebral hemorrhage or Cerebral edema?

Arthritis or Abnormal bone development?

Dermatitis or Cutaneous necrosis?

c. PT-INR

[Anticoagulant]

Warfarin monitoring is best assessed using:
a. aPTT
b. Bleeding time
c. PT-INR
d. Platelet count

b. Underdose

[Anticoagulant]

In PT-INR monitoring, an INR of <2 indicates:
a. Overdose
b. Underdose

a. Overdose

[Anticoagulant]

In PT-INR monitoring, an INR of >3 indicates:
a. Overdose
b. Underdose

a. Conversion of inactive plasminogen into active plasmin

Activation of Fibrinolytic System

↓

Inactive proenzyme (Plasminogen)

↓ (conversion/activation)

Active enzyme (Plasmin)

↓ (enzymatic degradation)

Breakdown of Fibrin

[Fibrinolytic]

Fibrinolytics MOA

a. Conversion of inactive plasminogen into active plasmin
b. Conversion of plasmin to plasminogen
c. Direct inhibition of thrombin
d. Activation of platelet adhesion

d. Streptokinase

[Fibrinolytic]

Derived from Beta-hemolytic streptococci
a. Alterplase
b. Reteplase
c. APSAC
d. Streptokinase

c. Bleeding and hypersensitivity

[Fibrinolytic]

Major adverse effects of streptokinase include:
a. Hypertension and constipation
b. Hyperglycemia and fever
c. Bleeding and hypersensitivity
d. Kidney failure and anemia

a. Antihistamines and glucocorticoids

[Fibrinolytic]

Premedications commonly given before streptokinase infusion are:
a. Antihistamines and glucocorticoids
b. Antibiotics and antivirals
c. Diuretics and beta blockers
d. NSAIDs and opioids

a. Hypersensitivity reaction

[Fibrinolytic]

Subsequent exposure to streptokinase should be avoided because of risk of:
a. Hypersensitivity reaction
b. Renal toxicity
c. Hyperkalemia
d. Hypertension

d. Aminosylated plasminogen streptokinase activator complex

[Fibrinolytic]

APSAC stands for:
a. Activated plasmin synthetic anticoagulant complex
b. Activated streptokinase protein complex
c. Anti-plasmin streptococcal activator complex
d. Aminosylated plasminogen streptokinase activator complex

b. Alteplase, Tenecteplase, Reteplase

[Fibrinolytic]

Which of the following are recombinant t-PA agents?
a. Warfarin, heparin, dabigatran
b. Alteplase, Tenecteplase, Reteplase
c. Clopidogrel, prasugrel, ticagrelor
d. Enoxaparin, dalteparin, tinzaparin

a. Acute venous thromboembolism

[Fibrinolytic]

Recombinant t-PA agents are used in the management of:
a. Acute venous thromboembolism
b. Diabetes mellitus
c. Asthma exacerbation
d. Chronic kidney disease

c. 3 hours

• 3 hrs= acute ischemic stroke

• 30 min= STEMI

[Fibrinolytic]

Recombinant t-PA for acute ischemic stroke is most effective when given within:
a. 12 hours
b. 6 hours
c. 3 hours
d. 24 hours

a. 30 minutes

• 3 hrs= acute ischemic stroke

• 30 min= STEMI

[Fibrinolytic]

Recombinant t-PA for ST-segment elevation myocardial infarction (STEMI) should ideally be given within:
a. 30 minutes
b. 6 hours
c. 12 hours
d. 24 hours

b. Vitamin K

[Pro Coagulant]

Which of the following is classified as a procoagulant?
a. Heparin
b. Vitamin K
c. Streptokinase
d. Dabigatran

a. Vitamin K1

[Pro Coagulant]

Which vitamin K form is also called phylloquinone or phytonadione?
a. Vitamin K1
b. Vitamin K2
c. Vitamin K3
d. Vitamin B12

b. Vitamin K2

[Pro Coagulant]

Menaquinone is another name for:
a. Vitamin K1
b. Vitamin K2
c. Vitamin K3

c. Vitamin K3

[Pro Coagulant]

Menadione refers to:
a. Vitamin K1
b. Vitamin K2
c. Vitamin K3

a. Bleeding secondary to vitamin K deficiency

[Pro Coagulant]

Vitamin K is mainly used in the management of:
a. Bleeding secondary to vitamin K deficiency
b. Asthma exacerbation
c. Acute myocardial infarction
d. Diabetes mellitus