Physiology of Blood Clotting and Thrombosis

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Questions and Answers

What is the primary physiological mechanism activated to prevent blood loss from damaged vessels?

Vascular dilation

Blood filtration

Blood haemostasis (correct)

Coagulation cascade

What type of thrombosis is primarily associated with atherosclerosis?

Venous thrombosis

Capillary thrombosis

Microvascular thrombosis

Arterial thrombosis (correct)

Which component is primarily associated with venous thrombosis?

Increased platelet activation

Stasis of blood (correct)

Vasodilation

Large platelet component

What occurs immediately after a wound that aids in preventing blood loss?

Platelet aggregation and activation Signup and view all the answers

What is not a typical consequence of arterial thrombosis?

Large fibrin component Signup and view all the answers

What is the main purpose of antiplatelet agents?

To prevent arterial thrombogenesis Signup and view all the answers

Which mechanism is primarily associated with platelet adhesion and activation?

Fibrinogen bridging between GPIIb/IIIa receptors Signup and view all the answers

Which drug is primarily used to inhibit thromboxane 2 and has an antiplatelet effect?

Aspirin Signup and view all the answers

What can be a potential consequence of inappropriate platelet activation in diseased arteries?

Formation of a thrombus leading to thrombosis Signup and view all the answers

What role does COX1 play in platelet function?

It produces thromboxane 2 which promotes aggregation Signup and view all the answers

What is the primary mechanism of action of clopidogrel?

It is a prodrug that requires metabolic activation. Signup and view all the answers

In which scenario is clopidogrel primarily indicated?

For patients experiencing unstable coronary artery disease. Signup and view all the answers

Which statement is true regarding the use of prasugrel?

It may require dose adjustment in older or underweight patients. Signup and view all the answers

What is the role of abciximab in clinical settings?

It is a monoclonal antibody for use in high-risk patients undergoing coronary angioplasty. Signup and view all the answers

What are the adverse drug reactions (ADRs) associated with epoprostenol?

Flushing, headache, and hypotension. Signup and view all the answers

How is tirofiban administered in the clinical setting?

Intravenously as an adjunct to aspirin and heparin. Signup and view all the answers

What is the purpose of using epoprostenol during haemodialysis?

To prevent thrombosis in patients where heparin is contraindicated. Signup and view all the answers

Which medication should not be combined with clopidogrel due to interaction?

Cimetidine. Signup and view all the answers

What is the main mechanism by which low-dose aspirin achieves its antiplatelet effect?

Inhibition of thromboxane A2 (TXA2) synthesis Signup and view all the answers

What effect does dipyridamole have on intraplatelet levels of AMPc?

It decreases the degradation of AMPc Signup and view all the answers

What is an adverse drug reaction (ADR) associated with aspirin that particularly affects the gastrointestinal system?

Peptic ulcer Signup and view all the answers

Aspirin's antiplatelet effect is considered long-lasting because of what characteristic of platelets?

Platelet half-life is approximately 10 days. Signup and view all the answers

What distinguishes aspirin's antiplatelet effect from its anti-inflammatory effect?

100 mg more of aspirin provides an enhanced antiplatelet effect than its anti-inflammatory action. Signup and view all the answers

What is the final step in the process of platelet aggregation?

Expression of platelet GPIIb/IIIa receptors Signup and view all the answers

Which drug's mechanism includes increasing the synthesis of prostaglandin I2 (PGI2)?

Dipyridamole Signup and view all the answers

What is a potential complication of low-dose aspirin use in children?

Reye's syndrome Signup and view all the answers

Study Notes

Coagulation and Aggregation

Blood homeostasis is a physiological mechanism preventing blood loss from damaged vessels, essential for survival.
Following a wound, main processes include vasoconstriction, platelet adhesion/activation (including aggregation and Von Willebrand factor secretion), and blood coagulation (fibrin formation).

Thrombosis

Thrombosis is a pathological condition resulting from inappropriate activation of haemostatic mechanisms leading to a 'haemostatic' plug formation within the vasculature, without sufficient bleeding.
Arterial thrombosis often associates with atherosclerosis, featuring a large platelet component ("white coagulum"). This can disrupt blood flow, potentially causing ischaemia or infarction.
Venous thrombosis is frequently linked to blood stasis with small platelet and significant fibrin component ("red coagulum"), often treated with anticoagulant therapy. Thrombi can detach and circulate.

Coagulation Cascade

Homeostasis balances coagulation and anticoagulation mechanisms.
A cascade of events, starting from exposure of acidic phospholipids, involves platelet adhesion/activation, mediator secretion (e.g., ADP, TXA2, PAF), and further platelet aggregation, culminating in thrombin activation.
This process leads to fibrinogen conversion into fibrin, forming the clot (blood coagulation)

Predispositions: Thrombus Development vs. Haemorrhage

Thrombus development is opposed by haemostasis, requiring targeted drugs like platelet stimulants, anti-aggregants, anticoagulants, and thrombolytics.
Haemorrhage is opposed by coagulation, using coagulation stimulants and platelet stimulants.

Platelet Adhesion and Activation

Platelets maintain circulatory integrity through activation processes vital for homeostasis though pathologically triggered by diseased artery walls (atherosclerosis), leading to thrombosis.
Platelet aggregation involves fibrinogen binding and bridging between GPIIb/IIIa receptors on platelets.
Activated platelets become fibrin formation sites.

Antiplatelet Drugs

Aspirin irreversibly inhibits platelet COX1, reducing TXA2 formation and increasing PGI2 formation.
Dipyridamole inhibits phosphodiesterase, decreasing cAMP breakdown and increasing adenosine and PGI2 synthesis.
Glycoprotein IIb/IIIa receptor antagonists (e.g., abciximab, tirofiban) block fibrinogen binding.
Adenosine (P2Y12) receptor antagonists (e.g., clopidogrel, prasugrel, ticagrelor) interfere with ADP-mediated platelet activation.
Epoprostenol (PGI2) exhibits vasodilation and inhibits platelet aggregation. Epoprostenol is particularly useful during hemodialysis and in conditions where heparin use is contraindicated.

Specific Antiplatelet Drugs

Aspirin: Low doses inhibit TXA2 synthesis, crucial for chronic use in preventing cardiovascular events; has rapid effects with high doses for acute situations.
Clopidogrel: Blocks ADP receptors and is effective for urgent interventions but requires a loading dose initially or to address specific situations.
Abciximab/Tirofiban: Prevent fibrinogen binding within the GPIIb/IIIa receptor, used for high-risk procedures like coronary angioplasty. Given intravenously as an adjunct, these drugs have potent effects in preventing early events associated with acute coronary syndromes.
Epoprostenol: This drug's usefulness emerges for vasodilation and combating platelet aggregation, particularly in cases of thrombosis/haemodialysis/pulmonary hypertension.

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Description

This quiz covers essential concepts related to hemostasis and thrombosis, including physiological mechanisms that prevent blood loss and the role of various agents in platelet function. Test your knowledge on topics such as arterial and venous thrombosis, antiplatelet agents, and the impact of atherosclerosis on thrombosis.