Thromboembolic Disease Flashcards
How can you differentiate between thrombus and post-mortem clot?
Thrombus:
- firm
- can be pale or red or laminated with lines of Zahn (characteristic feature of anti-mortem clot)
- adhered to vessel wall
Post-mortem
- gelatinous
- pale on top and dark red underneath
- not adhered to vessel wall
Where do pale platelets form? Why do they have pale colour?
High flow environment such as heart or arteries
Pale due to being formed from platelets because high flow environment leads to RBC being pushed past meshwork associated with the clot formation
What is the difference between a mural and occlusive clot? What type of clot are they both classified under?
Mural thrombi:
- decrease the blood flow through a vessel by adhering to 1 wall
- associated with large vessels
Occlusive thrombi
- lead to complete obstruction of blood flow
- associated with small/medium vessels
Pale thrombi= arterial thrombi specifically
What are examples of pale and red thrombi?
Pale:
- arterial
- cardiac
Red:
-venous
What are the causes of arterial thrombosis?
Atherosclerosis
Aneurysms
Inflammation + vasculitis
How are lines of Zahn formed and what is their significance?
Altering deposition of fibrin/platelets and erythrocytes leads to alternating pale and red layers forming
Evidence that thrombi was formed anti-mortem
What are the 3 locations of cardiac thrombi and what can cause each of them to form?
Atria
-HF and AF
Vales/vegitations
- rheumatic fever
- infective endocarditis
- non-bacterial thrombotic endocarditis
Ventricles:
-MI
-cardiomyopathy
I.e. both cause thinning of myocardium which predisposes to thrombus formation
How are red thrombi formed and what is the consequence of their formation?
Blood statis in veins leads to emeshing of erythrocytes to form clot
Thrombus propagates towards the heart
What type of thrombus is described as a red thrombi and what are the predisposing factors?
Venous thrombosis
Immobility Post-operative Severe trauma MI i.e. scarring weakens the ventricle and increase the risk of blood stasis Congestive HF Pelvic mass Thrombophlebitis= infection of the veins
What is 3 factors form Virchow’s triad? What does it relate to?
Endothelial injury
- hypocholesterolemia
- inflammation
Abnormal blood flow
- turbulence= atherosclerotic vessel narrowing
- stasis= AF + bed rest
Hyper-coagulability
- inherited E.g factor V Leiden
- Acquired e.g. disseminated cancer
The factors which promote thrombosis
How is thrombosis initiated? What are the initial stages?
Exaggeration of normal haemostatic mechanisms involving the coagulation cascade, platelets and vascular endothelium
Reflex vasoconstriction due to endothelin release from site of damage
Primary haemostasis:
-formation of primary platelet plug via platelet adhesion using adhesion proteins
Secondary haemostasis:
-cascade of reactions leading to conversion of fibrinogen to fibrin which forms mesh network around the platelet plug
Thrombus and antithrombus events
What are the 2 main fates of thrombus?
Resolved due to recanalisation
-endothelial cells penetrate the thrombus to form vascular channels which leads to blood flow and can cause thrombus to dissolve
Thrombus becomes fibrotic
-clot replaced by scar tissue and permanent vessel lesion forms
What are the possible consequences of thrombosis?
Embolism
Ischaemia
Infarction
What is an embolism?
Passage of insoluble mass in bloodstream and impaction in distant site
How does a PE form?
- Thrombotic embolus forms due to fragmentation of venous thrombus i.e. DVT -Carried into progressively larger veins until reaches RA
- embolus lodges in pulmonary arteries
NOTE: PE can arise from within R heart rather than embolus from DVT
How does a systemic embolus form? What is a paradoxical embolus?
Fragment from thrombus in left heart or aorta is carried into progressively smaller arteries until lodges in branch of aorta
Fragment from venous thrombi transverse cardiac defect to enter left side of heart and enter systemic circulation to give rise to systemic embolus
What is ischaemia? What causes ischaemia and what alters the severity?
Cell injury due to reduced BF to tissue or organ OR reduced venous drainage
Cause:
Intrinsic disease of vessels
Thrombi or emboli
External compression
Severity dependent on: Speed of onset Extent of obstruction Anatomy of local blood supply to organ/tissue Cardiac state + blood oxygenation Vulnerability of tissue
What anatomical difference in arterial supply can lead to variation in severity of ischaemia?
If end arteries to organ (i.e. renal arteries to kidney) there is not alternative blood supply
If parallel arteries are present to enable compensation
Interarterial branches
Collateral circulation
What is an infarction? What shape does infarction normally take?
Ischaemic necrosis causes by occlusion of arterial supply or venous damage
Wedge shaped
-occluded vessel at apex and periphery of organ at base
What are the 2 different types of infarct and how is their formation different?
White:
Lack of blood w/i infarct
Formed due to occlusion of arteries in organ with end arteries meaning tissue density limits blood seepage
Red:
Blood accumulates within infarct
Formed due to:
-loose spongy tissue enabling blood to leak out
-venous occlusion
-dual circulation meaning blood from collateral circulation pools in dead tissue
-previous congestion
-Re-established blood flow at site of previous arterial occlusion
Which organs are associated with red and white infarction?
Red:
Lung
SI
Testis
White:
Heart
Spleen
Kidney
What histological changes occur with an infarction and when does these changes occur?
< 6hrs= none
6-12hrs= coagultive necrosis
6hrs-7days= acute inflammation
3days-2weeks= organisation i.e. in growth of capillaries and macrophages and fibroblasts
2weeks-3months= scar formation due to deposition of collagen and polymerisation
