Path 12: Thrombosis, embolism, and infracion Flashcards
Thrombosis is described as?
Pathologic formation of a blood clot. Solid structure formed by components of the blood within the circulatory system
What can form thrombosis?
platelets
fibrin
leucocytes
What are the necessary conditions for the Virchow triad?
Endothelial damage
Alteration of blood flow
Alteration of blood composition
you just need one to have thrombosis
What are the requirements for thrombosis?
Blood must flow (stagnant blood clots, but do not form thrombi)
Decreased flow rate (permits contact of thrombocytes with endothelium)
Once attached to the endothelium, thrombocytes resist blood flow and current by forming “eddies” which allows more thrombocytes to adhere ad form a mass -> Thrombus
Analyze this image
Endothelial damage
Endothelial damage leading to platelet activation almost inevitably underlies thrombus formation in the heart and arterial circulation, where the high rates of blood flow impedes clot formation.
Endothelial damage or change to prothrombotic status (endothelial activation) > exposure of vWF and TF.
Endothelial activation: Physical injuries, infectious agents, abnormal blood flow, inflammatory mediators, metabolic abnormalities (hypercholesterolemia), toxins > prothrombotic state
Endothelial damage: Most important factor. Endothelium must be damaged, physically ruptured, or dysfunctional to contribute to the development of thrombosis. Dysfunction eg: produce more clotting factors and less anticoagulants (hypertension, turbulent flow, endotoxins, radiation, hypercholesterolemia
Alterations of the normal blood flow
Turbulence > endothelial injury or dysfunction and countercuurents, contributing to local formation of stasis
-Promotes endothelial activation (shift in genetic expression)
-Breaks laminar flow (platelets touch the endothelium)
-Promotes «washing» of activated clotting factors.
Stasis: major contributor to formation of venous thrombus
Hypercoagubility
aka thrombophilia
Any disorder of the blood that predisposed to thrombosis
Important role in venous thrombosis
Primary (gnetic) and seconday (acquired)
P: factor V mutation, prothrombin mutation
S: prolonged immolization, myocardial infraction, atrial fibrillation, tissue injury, cancer, prosthetic cardiac valves, DIC, cardiomyopathy, nephrotic syndrome, Hyper-estrogenic states, others)
mass tissue destruction > release of large amounts of tissue thromboplastin
Thrombi can develop where?
Anywhere in the cardiovasular system. Focally attached to underlying vascular surface
-arterial or cardiac: sites of turbulence or endothelial injury, tend to grow downstream from the site of attachment
-venous: characteristically occur at sites of statsis, tend to extend upstream from their point of origin
BOTH GROW AWAY FROM THE HEART
Arterial or cardiac thrombi
Usually at sites of endothelial injury (atheroscerotic plaques) or turbulence (vessel bifurcation)
Tend to grow in downstream from point of attachment
Tend to be *occlusive**
Thrombi development on heart valves
- infective endocarditis: bacterial/ fungal infection
- sterile endocarditis: hyper coagulable states
Analyze the photo
Spirocerca lupi
Venous thrombi
Typically at sites of STASIS: contain more RBCs
Tend to grow against the direction of blood flow
Tend to be occlusive
May be confused with postmortem clots
More frequent than arterial thrombi. Hepatic abscesses >Thrombosis of caudal vena cava > pulmonary emboli.
look at bottom of image
Abscess
-green
Happened from the outlined red line which is a venous thrombus
Fate of thrombi?
If patient survives immediate effects of thrombotic vascular obstruction, thrombi may under one or more events
Propagation
Embolization
Dissolution
Organization & Recanalization