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Pathology > Thrombosis, embolism, infarction and shock > Flashcards

Thrombosis, embolism, infarction and shock Flashcards

1
Q

Haemostasis

A

He maintenance of blood levels - preventing bleeding and blood clot formation in normal circulation

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2
Q

What are the three components involved in haemostasis?

A

Vascular wall, platelets and coagulation cascade

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3
Q

Importance of vascular wall in haemostasis

A

Provides contraction and a small cat to close the gap on the broken side and prevent blood from leaking out

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4
Q

Importance of platelets in haemostasis

A

Form small plaques that cover holes in blood vessels to prevent bleeding

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5
Q

Importance of coagulation cascade in haemostasis

A

Activated when the cut is too large or severe and involves a variety of enzymes that cause a clot to form

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6
Q

Thrombosis

A

A solid mass formed within the vascular system usually due to overactive haemostatic processes. Prone to fragmentation

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7
Q

What are the three predisposing factors of thrombosis?

A

Endothelial injury (most important), stasis and turbulence of bloodflow and blood hypercoagulability (thrombophilia)

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8
Q

Endothelial injury

A

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

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9
Q

Stasis of blood flow

A

Stagnant bloodflow leads to accumulation of clotting factors and platelets promotes coagulation. Contribute to venous thrombosis

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10
Q

Turbulence of bloodflow

A

Causes damage to endothelial cells which then promotes thrombosis. Contributes to arterial and cardiac thrombosis

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11
Q

Stages of arterial thrombosis

A

Atheroma, ulceration, platelet adherence and thrombus formation

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12
Q

Atheroma

A

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

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13
Q

Ulceration

A

Loss of endothelial cells which exposes collagen

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14
Q

Platelet adherence

A

Clotting factors and platelets are activated I did hear to the blood vessel wall where the endothelial cells were lost

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15
Q

Thrombus formation

A

Alternating layers of fibrin, platelets and red blood cells that forms a platform for other clotting factors to cause hypercoagulation

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16
Q

Risk factors for thrombosis

A

Prolonged bedrest or immobilisation, myocardial infarction, arterial fibrillation, prosthetic cardiac valves, tissue injury, cancer and increased age

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17
Q

Common sites of arterial thrombosis

A

Coronary, cerebral and femoral arteries. Due to turbulence

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18
Q

Common sites of Venous thrombosis

A

Superficially on deep veins of the leg. Due to stasis at valves. Causes pulmonary infarction after metastasis

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19
Q

Embolisation

A

A solid mass travelling in the bloodstream often due to dislodging of the thrombus

20
Q

What are the fates of a thrombus?

A

Propagation (growing bigger), embolisation, dissolution and organisation/recanalisation

21
Q

Dissolution

A

Result of fibrinolysis (breakdown of fibrin)

22
Q

Recanalisation

A

Blood vessel Newmans are restored by forming new channels after occlusion

23
Q

Organisation of thrombuses

A

Formation of scar and connective tissue by the invasion of macrophages. Prevents risk of embolism but bloodflow is now lost

24
Q

Complications of venous thrombosis

A

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

25
Q

Sources of emboli

A

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

26
Q

Complications of pulmonary embolism

A

Most are clinically silent but symptoms can be right heart failure, cardiovascular collapse or even sudden death

27
Q

Gangrene

A

Dead and necrotic tissue turned black due to ischaemia

28
Q

Infarct

A

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

29
Q

Other causes of infarction

A

Vasospasms, haemorrhage into plaques, vessel compression by tumours and traumatic rupture due to hyperoxia

30
Q

Shape of infarcts

A

Wedge - in lungs, triangular - in kidney, scarred - in spleen

31
Q

How are infarcts classified?

A

Based on their colour (reflects haemorrhage) and any microbial infection

32
Q

White infarcts

A

Anaemic. In solid organ is with end arterial circulation

33
Q

Red infarcts

A

Haemorrhagic. Mainly in the brain

34
Q

Septic infarcts

A

Infected

35
Q

Bland infarcts

A

Non-infected

36
Q

Factors that influence infarction outcomes

A

Availability of alternative blood supply, rates of occlusion development, vulnerability to hyperoxia and is normal oxygen content of the blood

37
Q

What and when are the first visible signs of infarction?

A

After 24hrs, pallor seen and inflammation at the edge

38
Q

Shock

A

Inadequate tissue perfusion

39
Q

What is shock characterised by?

A

Systemic hypotension due to reduced cardiac output and circulating blood flow

40
Q

Cardiogenic shock

A

Results from low cardiac output due to heart failure and poor myocardial contractility

41
Q

Extravasation

A

Blood leaking out into the tissues

42
Q

Hypovolaemic shock

A

Results from low cardiac output due to the loss of blood plasma volume

43
Q

Causes of blood loss

A

Haemorrhage, vomiting and diarrhoea, increased diuresis, burns and diabetes insipidus

44
Q

Septic shock

A

Results from vasodilation and peripheral pooling of blood as part of a systemic immune reaction to infection

45
Q

Symptoms of shock

A

Confusion, restlessness, excessive thirst, weak and rapid pulse, pale cool moist skin

Pathology (8 decks)

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