Hemodynamic Disorders L18,19 Flashcards
Hemostasis
The normal process of keeping blood in a fluid state while rapidly forming a clot at an injury site.
Thrombosis
A pathological condition where a solid blood clot forms within the circulatory system (unruptured vessels).
What are the three main abnormalities that can lead to thrombus formation?
Virchow’s triad:
1. Endothelial injury
2. Stasis or turbulence of blood flow
3. Blood hypercoagulability
Why is endothelial injury a risk factor for thrombosis, particularly in the heart and arteries?
*Normal high blood flow rates in these areas prevent clotting by minimizing platelet adhesion and diluting clotting factors.
*Endothelial damage exposes underlying tissue, which platelets can adhere to, and triggers clotting factor release.
How do turbulence and stasis contribute to thrombosis?
GDisrupt laminar flow, bringing platelets into contact with the endothelium.
*Prevent dilution of activated clotting factors by fresh blood flow.
*Hinder the arrival of clotting factor inhibitors.
*May promote endothelial injury, leading to platelet adhesion.
What are some causes of turbulence and stasis?
*Ulcerated atherosclerotic plaques (expose subendothelial tissue and cause turbulence).
*Abnormal heart or artery widening (aneurysms).
*Areas of non-contractile heart muscle (e.g., after a heart attack).
*Heart valve stenosis (e.g., mitral valve).
*Hyperviscosity syndromes (thick blood due to conditions like polycythemia).
*Sickle cell anemia (deformed red blood cells that obstruct vessels).
What is hypercoagulability?
An alteration in clotting pathways that increases the risk of thrombosis.
How does hypercoagulability differ in arterial/cardiac vs. venous thrombosis?
*Less frequent contributor to arterial/cardiac thrombosis.
*Important risk factor for venous thrombosis.
What are the two main categories of hypercoagulability disorders?
1.Primary (genetic) disorders (e.g., factor V or prothrombin gene mutations).
2.Secondary (acquired) disorders (caused by various factors).
What are some examples of secondary hypercoagulability disorders?
*Cardiac failure or trauma (stasis or injury may be the main cause).
*Oral contraceptives or pregnancy (increased clotting factor synthesis).
*Cancers (release of procoagulant substances by tumors).
*Aging (increased platelet aggregation).
*Smoking and obesity (unknown mechanisms).
What are these microscopic features seen in thrombi, and what do they indicate?
Lines of Zahn are alternating pale (platelet/fibrin) and dark (red blood cell) layers, suggesting antemortem (before death) thrombosis.
How can thrombi be distinguished based on lamination?
Postmortem clots typically lack lamination (lines) (bland, uniform).
Venous thrombi may show poorly defined laminations upon careful examination.
Types of Thrombi:
Mural Thrombi
Arterial Thrombi
Venous Thrombosis (Phlebothrombosis)
Vegetations
Where do mural thrombi form?
Heart chambers or aortic lumen.
What are some causes of mural thrombi?
*Abnormal heart contractions (arrhythmias, infarction).
*Endomyocardial injury.
What is the typical composition of arterial thrombi?
A loose network of platelets, fibrin, red blood cells, and degenerating white blood cells.
What are the common causes of arterial thrombi?
Atherosclerotic plaque buildup and vascular injury (vasculitis, trauma).
How do venous thrombi differ from arterial thrombi in composition and location?
*Nearly occlusive (can almost completely block the vein).
*More red blood cells due to slower venous blood flow (stasis thrombi).
*Develop most commonly in the lower leg veins.
*Platelets play a secondary role in their formation compared to the coagulation cascade.
What are vegetations, and how can they form?
Thrombi that develop on heart valves. Bacterial or fungal infections can damage heart valves, leading to the growth of large thrombotic masses (infective endocarditis).
What are the four main events that can happen to a thrombus after it forms?
1.Propagation: Grows larger with additional platelets and fibrin.
2.Embolization: Breaks off and travels through the bloodstream.
3.Dissolution: Gets broken down by fibrinolytic activity.
4.Organization and recanalization: Triggers inflammation and scarring, potentially reopening the blood vessel partially.
What are the four main events that can happen to a thrombus after it forms?
1.Propagation: Grows larger with additional platelets and fibrin.
2.Embolization: Breaks off and travels through the bloodstream.
3.Dissolution: Gets broken down by fibrinolytic activity.
4.Organization and recanalization: Triggers inflammation and scarring, potentially reopening the blood vessel partially.
What are the two main clinical effects of thrombi?
1.Obstruction of arteries and veins
2.Source of emboli (fragments that travel and cause blockages elsewhere)
How does the effect of a thrombus differ depending on its location (arterial vs. venous)?
*Venous thrombi: More likely to cause congestion and edema, but the biggest risk is pulmonary embolism (traveling to the lungs).
*Arterial thrombi: More likely to cause blockages in critical areas (e.g., heart, brain) leading to tissue death (infarction). They can also embolize.
Where do most venous thrombi occur?
Superficial or deep veins of the leg.
