coags

Question 1

What initiates thrombogenesis?

Answer 1

Vascular injury exposing collagen and von Willebrand factor (vWF).

Question 2

What platelet receptors bind to collagen and vWF?

Answer 2

GP Ia binds collagen; GP Ib binds vWF.

Question 3

What happens when platelets adhere during thrombogenesis?

Answer 3

Platelets activate and release ADP, TXA₂, and 5-HT.

Question 4

What is the role of ADP in thrombogenesis?

Answer 4

ADP enhances platelet aggregation.

Question 5

What is the role of TXA₂ in thrombogenesis?

Answer 5

TXA₂ enhances platelet aggregation.

Question 6

How does serotonin (5-HT) aid thrombogenesis?

Answer 6

It promotes vasoconstriction, reducing blood flow.

Question 7

How do platelets form a plug in thrombogenesis?

Answer 7

Fibrinogen binds to GP IIb/IIIa receptors on platelets.

Question 8

What stabilizes the platelet plug in thrombogenesis?

Answer 8

Thrombin converts fibrinogen to fibrin.

Question 9

What is the role of prostacyclin (PGI₂) in thrombogenesis?

Answer 9

It inhibits platelet aggregation in uninjured areas.

Question 10

What activates the intrinsic coagulation pathway?

Answer 10

Collagen exposure.

Question 11

Outline the steps in the intrinsic coagulation pathway.

Answer 11

Factor XII → XIIa → XI → XIa → IX → IXa (+ Factor VIII and Ca²⁺) → X.

Question 12

What activates the extrinsic coagulation pathway?

Answer 12

Tissue damage.

Question 13

Outline the steps in the extrinsic coagulation pathway.

Answer 13

Tissue factor (TF) + Factor VII → VIIa → Factor X.

Question 14

What are the steps in the common coagulation pathway?

Answer 14

Factor X → Xa (+ Factor V and Ca²⁺) → Prothrombin → Thrombin → Fibrinogen → Fibrin (+ Factor XIII) → Stable clot.

Question 15

What are the causes of DVT?

Answer 15

Stasis (immobility), hypercoagulability, and endothelial injury.

Question 16

How do white thrombi form?

Answer 16

In high-pressure arteries, mainly composed of platelets and fibrin.

Question 17

How do red thrombi form?

Answer 17

In low-pressure veins, with red cells around a fibrin-platelet core.

Question 18

What is the danger of red thrombi?

Answer 18

Their ‘tail’ can detach and cause embolism.

Question 19

What are the inherited risk factors for DVT?

Answer 19

Antithrombin III deficiency, protein C/S deficiency, sickle cell anemia, activated protein C resistance.

Question 20

What are acquired risk factors for DVT?

Answer 20

Bedridden, surgery/trauma, obesity, estrogen use, malignancies, chronic venous insufficiency.

Question 21

What is DIC?

Answer 21

Disseminated intravascular coagulation involves overstimulation of clotting, leading to excessive clot formation and bleeding.

Question 22

What causes DIC?

Answer 22

Massive tissue injury, malignancy, and sepsis.

Question 23

How is DIC treated?

Answer 23

Plasma transfusion and addressing the underlying cause.

Question 24

What is HIT?

Answer 24

Heparin-induced thrombocytopenia, an immune response to heparin causing low platelets.

Question 25

How is HIT treated?

Answer 25

Discontinuing heparin and possibly using alternative anticoagulants.

Question 26

What is TTP?

Answer 26

Thrombotic thrombocytopenic purpura, involving widespread platelet aggregation and microvascular clots.

Question 27

How is TTP treated?

Answer 27

Plasma exchange therapy.

Question 28

Outline the steps in fibrinolysis.

Answer 28

t-PA, urokinase, or streptokinase bind plasminogen → convert to plasmin → break fibrin into degradation products (e.g., D-dimers).

Question 29

What are examples of anticoagulants?

Answer 29

Warfarin, heparin, hirrudin, argatroban, apixoban

Question 30

What are examples of antiplatelet drugs?

Answer 30

Aspirin, clopidogrel, abcuximab

Question 31

What are examples of thrombolytics?

Answer 31

Streptokinase, urokinase.

Question 32

What are examples of hemostatic/antifibrinolytic drugs?

Answer 32

Aminocaproic acid, tranexamic acid.

Question 33

How do indirect thrombin inhibitors work?

Answer 33

Heparin and LMWH enhance antithrombin activity, inactivating thrombin and Factor Xa.

Question 34

How do direct thrombin inhibitors work?

Answer 34

Bind directly to thrombin’s active sites, inhibiting thrombin without needing antithrombin.

Question 35

What are the differences between HMW, LMW, and fondaparinux heparins?

Answer 35

HMW: Broad activity, less specific for Factor Xa. LMW: More specific for Factor Xa, fewer side effects. Fondaparinux: Synthetic, selectively inhibits Factor Xa, useful in HIT patients.

Question 36

What are the toxicities of HMW heparin?

Answer 36

Bleeding and thrombocytopenia.

Question 37

What are contraindications for HMW heparin use?

Answer 37

Active bleeding, hemophilia, severe hypertension, intracranial hemorrhage, TB, hepatic disease.

Question 38

How is HMW heparin toxicity treated?

Answer 38

Discontinue heparin and use protamine sulfate for reversal. Protamine is a positive charge and heparin is negative so it binds to it and inactivates it.

Question 39

What does prothrombin time (PT) assess?

Answer 39

The extrinsic and common coagulation pathways.

Question 40

What is the normal INR range?

Answer 40

0.8–1.2.

Question 41

What does aPTT assess?

Answer 41

The intrinsic and common coagulation pathways.

Question 42

What is the normal aPTT range?

Answer 42

35–45 seconds.

Question 43

How does warfarin work?

Answer 43

It blocks vitamin K recycling, reducing clotting factor synthesis.

Question 44

What are treatment considerations for warfarin?

Answer 44

Monitor INR and adjust dose to balance efficacy and bleeding risk.

Question 45

What are some non-warfarin anticoagulants?

Answer 45

Factor Xa inhibitors: Apixaban, rivaroxaban. Direct thrombin inhibitors: Dabigatran.

Question 46

What are fibrinolytic drugs, and how do they work?

Answer 46

Streptokinase, urokinase, and tPA activate plasminogen to plasmin, breaking down fibrin clots.