Thrombosis, embolism, infarction and shock Flashcards
Haemostasis
He maintenance of blood levels - preventing bleeding and blood clot formation in normal circulation
What are the three components involved in haemostasis?
Vascular wall, platelets and coagulation cascade
Importance of vascular wall in haemostasis
Provides contraction and a small cat to close the gap on the broken side and prevent blood from leaking out
Importance of platelets in haemostasis
Form small plaques that cover holes in blood vessels to prevent bleeding
Importance of coagulation cascade in haemostasis
Activated when the cut is too large or severe and involves a variety of enzymes that cause a clot to form
Thrombosis
A solid mass formed within the vascular system usually due to overactive haemostatic processes. Prone to fragmentation
What are the three predisposing factors of thrombosis?
Endothelial injury (most important), stasis and turbulence of bloodflow and blood hypercoagulability (thrombophilia)
Endothelial injury
Exposes the extracellular matrix due to a loss of cell integrity. Collagen and tissue factors are then able to activate platelets and clotting factors to cause adhesion
Stasis of blood flow
Stagnant bloodflow leads to accumulation of clotting factors and platelets promotes coagulation. Contribute to venous thrombosis
Turbulence of bloodflow
Causes damage to endothelial cells which then promotes thrombosis. Contributes to arterial and cardiac thrombosis
Stages of arterial thrombosis
Atheroma, ulceration, platelet adherence and thrombus formation
Atheroma
A bulge filled with lipids forms in the collagen layer underneath epithelial cells. A plaque forms on top of the epithelial cells. Causes mechanical disruption and damage
Ulceration
Loss of endothelial cells which exposes collagen
Platelet adherence
Clotting factors and platelets are activated I did hear to the blood vessel wall where the endothelial cells were lost
Thrombus formation
Alternating layers of fibrin, platelets and red blood cells that forms a platform for other clotting factors to cause hypercoagulation
Risk factors for thrombosis
Prolonged bedrest or immobilisation, myocardial infarction, arterial fibrillation, prosthetic cardiac valves, tissue injury, cancer and increased age
Common sites of arterial thrombosis
Coronary, cerebral and femoral arteries. Due to turbulence
Common sites of Venous thrombosis
Superficially on deep veins of the leg. Due to stasis at valves. Causes pulmonary infarction after metastasis
Embolisation
A solid mass travelling in the bloodstream often due to dislodging of the thrombus
What are the fates of a thrombus?
Propagation (growing bigger), embolisation, dissolution and organisation/recanalisation
Dissolution
Result of fibrinolysis (breakdown of fibrin)
Recanalisation
Blood vessel Newmans are restored by forming new channels after occlusion
Organisation of thrombuses
Formation of scar and connective tissue by the invasion of macrophages. Prevents risk of embolism but bloodflow is now lost
Complications of venous thrombosis
Blood and extracellular fluid accumulates locally causing oedema due to impaired drainage. Embolism after better stasis and dislodging. Pulmonary embolism and infarction due to less bloodflow to the left ventricle of the heart
Sources of emboli
Dislodged thrombus or blood clot, infected lesions, gas bubbles (oxygen or nitrogen, from injections or divers moving from high to low pressures), fat deposits, bone marrow and fractions, tumour cells and amniotic fluid during labour
Complications of pulmonary embolism
Most are clinically silent but symptoms can be right heart failure, cardiovascular collapse or even sudden death
Gangrene
Dead and necrotic tissue turned black due to ischaemia
Infarct
An area of ischaemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a tissue. Only arises if the cause is blood vessel occlusions – otherwise simply called necrosis
Other causes of infarction
Vasospasms, haemorrhage into plaques, vessel compression by tumours and traumatic rupture due to hyperoxia
Shape of infarcts
Wedge - in lungs, triangular - in kidney, scarred - in spleen
How are infarcts classified?
Based on their colour (reflects haemorrhage) and any microbial infection
White infarcts
Anaemic. In solid organ is with end arterial circulation
Red infarcts
Haemorrhagic. Mainly in the brain
Septic infarcts
Infected
Bland infarcts
Non-infected
Factors that influence infarction outcomes
Availability of alternative blood supply, rates of occlusion development, vulnerability to hyperoxia and is normal oxygen content of the blood
What and when are the first visible signs of infarction?
After 24hrs, pallor seen and inflammation at the edge
Shock
Inadequate tissue perfusion
What is shock characterised by?
Systemic hypotension due to reduced cardiac output and circulating blood flow
Cardiogenic shock
Results from low cardiac output due to heart failure and poor myocardial contractility
Extravasation
Blood leaking out into the tissues
Hypovolaemic shock
Results from low cardiac output due to the loss of blood plasma volume
Causes of blood loss
Haemorrhage, vomiting and diarrhoea, increased diuresis, burns and diabetes insipidus
Septic shock
Results from vasodilation and peripheral pooling of blood as part of a systemic immune reaction to infection
Symptoms of shock
Confusion, restlessness, excessive thirst, weak and rapid pulse, pale cool moist skin
