Part 5.1-BLOOD-COAGULATION DISORDER

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

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

b. balance

The vascular event in hemostasis is ________.

a. vasodilation
b. vasoconstriction

b. vasoconstriction

The cellular event in hemostasis involves platelet migration and ________.

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

d. aggregation

The protein event in hemostasis is the coagulation factor ________.

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

b. cascade

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

e. All of the above

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

h. b and c

• 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

g. a and d

• Arterial clots: platelet-rich "white thrombi"

• Venous clots: fibrin-rich "red thrombi"

Coagulation Cascade

after discussion nalang to

Intrinsic pathway:

a. XII

b. XI

c. IX

d. X

e. III

f. VII

g. X

a. XII

b. XI

c. IX

d. X

Extrinsic pathway:

a. XII

b. XI

c. IX

d. X

e. III

f. VII

g. X

e. III

f. VII

g. X

[Anti-platelet Aggregants]

Thromboxane synthesis inhibitor:

a. Clopidogrel

b. Warfarin

c. Heparin

d. Aspirin

d. Aspirin

[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

b. Inhibits COX of platelets, decreasing TXA₂ levels

[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

c. Irreversibly acetylating COX of platelets

[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

a. Acute myocardial infarction

• 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

b. Stroke

• primary and secondary = acute MI

• secondary = stroke

[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?

Bleeding

GI intolerance

Ulcer

Bronchospasm

Hypersensitivity

Salicylism

[Anti-platelet Aggregants]

Thienopyridines and Non-Thienopyridines

a. GIIb / IIIa inhibitors

b. Thromboxane synthesis inhibitor

c. Adenosine and Phosphodiesterase inhibitor

d. ADP inhibitor

d. ADP inhibitor

[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

a. Thienopyridines

[Anti-platelet Aggregants]

Ticagrelor

a. Thienopyridines

b. Non-Thienopyridines

b. Non-Thienopyridines

[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

c. Irreversible P2Y12 receptor inhibition

[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

a. Thienopyridines

[Anti-platelet Aggregants]

Given post- angioplasty

a. Thienopyridines

b. Non-Thienopyridines

both

[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)

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

[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

c. Blocking GPIIb/IIIa receptor to prevent platelet 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. Preventing platelet cross-linking (aggregation)

[Anti-platelet Aggregants]

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

b. Abciximab

[Anti-platelet Aggregants]

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

d. Eptifibatide

[Anti-platelet Aggregants]

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

a. Tirofiban

[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

c. Post-angioplasty prevention of acute thrombosis

-Given as IV infusion

[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. Inhibiting adenosine uptake and phosphodiesterase enzymes

[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

b. Inhibition of adenosine uptake

[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

d. Inhibition of cGMP and cAMP phosphodiesterase

[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

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

b. Combined with other antiplatelet or anticoagulant drugs

[Anti-platelet Aggregants]

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

d. Coronary steal phenomenon

[Anti-platelet Aggregants]

Cilostazol
a. A vasodilator
b. A vasoconstrictor

a. A vasodilator

[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

a. A phosphodiesterase inhibitor

[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. Intermittent claudication

[Anticoagulant]

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

b. Directly inhibiting factor IIa (thrombin)

[Anticoagulant]

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

d. Interfere the coagulation cascade

[Anticoagulant]

Parenteral Direct thrombin inhibitor except:

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Dabigatran

e. Argatroban

d. Dabigatran- oral

[Anticoagulant]

natural product from Leeches

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

a. Hirudin

[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

b. Lepirudin

[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

c. Bivalirudin

[Anticoagulant]

Alternative in the management of HIT

a. Hirudin

b. Lepirudin

c. Bivalirudin

d. Argatroban

d. Argatroban

[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

b. Direct inhibition of thrombin (factor IIa)

[Anticoagulant]

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

c. Prophylaxis of venous thromboembolism (VTE)

[Anticoagulant]

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

c. Warfarin

[Anticoagulant]

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

a. Bleeding

[Anticoagulant]

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

a. CYP3A4 inhibitors

[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

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

[Anticoagulant]

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

b. Parenteral indirect thrombin inhibitor

[Anticoagulant]

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

c. Sulfated mucopolysaccharide

[Anticoagulant]

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

d. Released by platelets

[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

b. Regular or high 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

a. Low molecular weight heparin

[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

d. Binding and forming a complex with antithrombin III

[Anticoagulant]

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

c. aPTT / PTT

[Anticoagulant]

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

b. Enoxaparin, dalteparin, tinzaparin

[Anticoagulant]

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

a. Synthetic polysaccharide indirect anticoagulant

[Anticoagulant]

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

b. Acute coronary syndrome

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

b. Acute coronary syndrome and venous thromboembolism

[Anticoagulant]

preferred in pregnancy

a. HMWH

b. LMWH

b. LMWH

[Anticoagulant]

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

anticoagulant

[Anticoagulant]

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

b. Bleeding

[Anticoagulant]

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

b. Protamine sulfate

[Anticoagulant]

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

d. HIT

-treated with Lepirudin

[Anticoagulant]

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

a. Osteoporosis

[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

b. Inhibiting factor Xa

[Anticoagulant]

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

c. Direct oral factor Xa inhibitor

[Anticoagulant]

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

b. Venous thromboembolism (VTE)

[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. Inhibiting formation of active vitamin K

[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

[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

-Phenindione, Anisindiones

[Anticoagulant]

Warfarin

a. Direct factor Xa inhibitor

b. LMWH

c. HMWH

d. VKORC (vitamin K epoxide reductase) inhibitor

d. VKORC (vitamin K epoxide reductase) inhibitor

[Anticoagulant]

VKORC Adverse effects

Bleeding or Clotting?

Intracerebral hemorrhage or Cerebral edema?

Arthritis or Abnormal bone development?

Dermatitis or Cutaneous necrosis?

Bleeding

Intracerebral hemorrhage

Abnormal bone development

Cutaneous necrosis

[Anticoagulant]

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

c. PT-INR

[Anticoagulant]

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

b. Underdose

[Anticoagulant]

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

a. Overdose

[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

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]

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

d. Streptokinase

[Fibrinolytic]

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

c. Bleeding and hypersensitivity

[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. Antihistamines and glucocorticoids

[Fibrinolytic]

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

a. Hypersensitivity reaction

[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

d. Aminosylated plasminogen streptokinase activator complex

[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

b. Alteplase, Tenecteplase, Reteplase

[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

a. Acute venous thromboembolism

[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

c. 3 hours

• 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

a. 30 minutes

• 3 hrs= acute ischemic stroke

• 30 min= STEMI

[Pro Coagulant]

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

b. Vitamin K

[Pro Coagulant]

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

a. Vitamin K1

[Pro Coagulant]

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

b. Vitamin K2

[Pro Coagulant]

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

c. Vitamin K3

[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

a. Bleeding secondary to vitamin K deficiency