Thrombosis - PowerPoint by akashyap

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									Definition:  Formation of solid mass of blood constituents (blood clot) in an intact blood vessel or heart, in a living person  The solid mass is called a „thrombus”

Regulated by 3 components
 Endothelium  Platelets  Coagulation

cascade

Endothelium

Subendothelial collagen

Laminar flow

Site of injury

Exposure of subendothelial collagen (ECM)

Adhesion of platelets to ECM via vWF

vWF

Activation & shape change of platelets

Granules release ADP and Thromoboxane A2

Further aggregation of platelets Primary hemostatic plug

Activation of coagulation cascade by:

Tissue factor (by injured endothelium) Platelet factors

Fibrinogen

Fibrin



`bjhash





Haemostatic Plug

PATHOGENESIS OF THROMBOSIS:

“VIRCHOW TRIAD’’

 

Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability

ENDOTHELIAL INJURY

THROMBOSIS

ABNORMAL BLOOD FLOW

HYPERCOAGULABLITY



Important in thrombus formation within the cardiac chambers and arteries

Causes:
 ulcerated

arteries  Myocardial infarction  Inflammation of blood vessels (vasculitis)

plaques in atherosclerotic

Endothelial dysfunction
Hypertension  Cigarette smoking  Bacterial endotoxins  Hemodynamic stress


Imbalance between thrombotic and antithrombotic factors

Prothrombotic
Anti thrombotic

Platelet adhesion molecules-vWF Tissue factors

Thrombomodulin PGI 2 Tissue Plasminogen Activator ( t-PA)

Plasminogen activator inhibitor

 Turbulence  Stasis

How do Turbulence and Stasis predispose to thrombosis?
TURBULENCE Disturbs the laminar flow Endothelial injury STASIS Prevent dilution of activated clotting factors by fresh blood Retard the flow of clotting factor inhibitors

Ulcerated atherosclerotic plaques – turbulence Aneurysms-stasis Myocardial infarction-stasis Mitral Stenosis – left atrial dilatationstasis

HYPERCOAGULABLE STATES
Alteration in the coagulation pathways that predispose to thrombosis Primary

Secondary

Mutation in Factor V (Leiden mutation) Antithrombin III deficiency

High Risk
Prolonged bed rest Tissue damage Cancer

Low risk
Oral Contraceptives Smoking

May develop anywhere in the CVS - within the cardiac chambers - valve cusps -arteries -veins -capillaries They are variable in size & shape


In heart,aorta and arteriesEndothelial Injury or turbulence

In venous system
Stasis

Morphology of thrombus

In heart and major vessels Called Mural thrombi

b) Arteries

Most common sites- coronaries, cerebral and femoral arteries - are



occlusive

In arteries tend to grow in retrograde direction

In veins the propagation occurs in the direction of the flow

Thrombus is firmly adherent to the vessel wall Thrombus in heart, aorta and arteries shows prominent Lines of Zahn – Lines of Zahn alternate layers of pale area(platelets and fibrin) and dark area(RBCs)





most common in veins of lower extremities (90%) In order of frequency – deep calf veins, femoral, popliteal and iliac veins

Occurs due to stasis or hypercoagulable states
Because of the sluggish flow- more enmeshed RBCs-no lines of Zahn “Red or stasis thrombi

Fate of a thrombus

FATE OF THRMOBUS

RESOLUTION

EMBOLISATION

ORGANISATION RECANALISATION

RESOLUTION
Fibrinolysis by plasmin

Complete resolution may take place

Ingrowth of smooth muscle cells, fibroblasts and endothelial cells Incorporation into the wall

ORGANISATION

RECANALISATION
New capillary channels are formed Anastomosis of the capillary channels

Re-establishment of continuity of the lumen to a limited extent

EMBOLISATION

A portion of a thrombus dislodges and lodges at a new site

Dissolution – by fibrinolytic activity Organization and Recanalization Propagation – eventually resulting in obstruction of vessels  Embolization – part of the thrombus may be detached and carried along the blood stream to impact in a distant vessel  Central digestion with Infection  Calcification
  

1)Obstruction to the arteries and veins Arterial thrombi- Infarction Venous thrombi- congestion of tissue or organ

2) Source of emboli


								
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