Vascular Pathology 2 - Thrombosis, Embolism, Ischaemia, Infarction Flashcards

1
Q

What is ischaemia?

A

A deficiency, real or relative, of oxygenated blood in a tissue causing a shortage of oxygen and impaired aerobic respiration

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2
Q

What is ischaemia due to?

A

Either increased demand for oxygen that is not met, local vascular narrowing or occlusion, or a systemic reduction in tissue perfusion

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3
Q

What happens in chronic ischaemia?

A

The decreased oxygen lasts for months to years and results in cell and tissues atrophying and dying - often results in fibrosis and extra collagen deposition and healing will be impaired due to lack of good blood supply

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4
Q

Where does chronic ischaemia commonly occur?

A

In the kidney due to arteriolosclerosis, in the heart, in the legs due to peripheral vascular disease

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5
Q

What happens in acute ischaemia?

A

The decreased oxygen lasts for minutes to hours - will lead to impaired function and may cause pain - often occurs due to increased demand

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6
Q

Where does acute ischaemia commonly occur?

A

The heart (angina), the legs (claudication), the brain (TIA)

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7
Q

What is angina?

A

Pain in the chest associated with poor blood supply to the heart

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8
Q

What is claudication?

A

Pain in the skeletal muscles with increased exertion causing an increased oxygen demand so causes acute ischaemia - similar to angina

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9
Q

What is a TIA?

A

A transiet ischaemic attack - generally due to an embolism occlusion that is not long enough to cause infarction

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10
Q

What is an infarction?

A

An area of necrosis caused by acute ischaemia

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11
Q

What are the causes of infarction?

A

thrombotic arterial occlusion, embolic arterial occlusion, external compression of artery in dissection, vasospasm of artery, venous occlusion, systemic reduction in tissue perfusion, compartment syndrome

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12
Q

What are the two types of infarction?

A

Pale (anaemic) or red (haemorrhagic)

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13
Q

What type of necrosis occurs in infarction?

A

Coagulative necrosis

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14
Q

How do infarcts heal?

A

By organisation (except in the brain)

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15
Q

What does the size of the infarct from arterial occlusion depend on?

A

The size of the artery occluded, the duration of the occlusion, the vulnerability of the cells to occlusion, whether the artery is carrying oxygenated or deoxygenated blood, the nature of the arterial supply, the oxygen content of the blood, the state of systemic circulation

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16
Q

When does a pale infarct occur?

A

Due to the blockage of an end artery

17
Q

Where do pale infarcts occur?

A

In the spleen, kidney and the heart mostly and the brain

18
Q

What is the shape of a pale infarct?

A

Wedge shaped with the base of the wedge along the outer part of the organ

19
Q

When do haemorrhagic infarcts occur?

A

Usually related to dual circulation, reperfusion, venous occlusion - when blood comes in to dead area

20
Q

Where do haemorrhagic infarcts occur?

A

In the lung, in the bowel, in the brain

21
Q

What is the shape of haemorrhagic infarcts?

A

Wedge shaped

22
Q

What does an infarction look like histologically?

A

Initally (6-12 hours), cells become hypereosinophilic and can just see the cell outline - after time there is acute inflammation and lots of neutrophils come in and then after 1-2 weeks there is granulation tissue and then scarring

23
Q

Why do abnormalities of haemostasis occur?

A

Because of problems with platelets, the coagulation cascade or vessel walls

24
Q

What is the role of the endothelium in inhibiting thrombosis?

A
  • prostacyclin and NO impede platelet adhesion and vasodilate
    • adenosine diphosphatase - degrades ADP to inhibit platelet aggregation
    • heparin like molecules - cofactors that enhance inactivation of thrombin
    • thrombomodulin - binds to thrombin and converts it to an anticoagulant
    • tissue factor pathway inhibitor - inhibits tissue factor
    • tissue type plasminogen activator (tPA) - cleaves plasminogen to form plasmin which cleaves fibrin to degrade thrombi
25
Q

What are the three causes of thrombosis in Virchow’s triad?

A

Endothelial dysfunction or injury, hypercoagulability of blood, changes in blood flow

26
Q

How does endothelial dysfunction lead to thrombosis?

A

Expsoure of collagen, exposure of tissue factor, disruption of balance of production of pro and anti thrombotic factors

27
Q

What are some causes of endothelial dysfunction?

A

direct trauma, atherosclerosis, infection

28
Q

What are some causes of hypercoagulability?

A

post operative state, post traumatic state, factor V leiden mutation, prothrombin mutation, malignancies, high oestrogen levels, antiphospholipid antibody syndrome, obesity, post MI

29
Q

How do changes in blood flow lead to thrombosis?

A

More platelets come in to contact with epithelium, either by turbulence or slowing

30
Q

What are some causes of change in blood flow?

A

aneurysms, poor muscle pumps, atrial fibrillation

31
Q

What will happen to a thrombus?

A

Embolism, spontaneously lyse, organisation, remain in one spot

32
Q

What are the lines of Zahn?

A

Characteristic thrombi that occur in atrial fibrillation

33
Q

What are the different types of emboli?

A

thombo-emboli, athero-emboli, septic emboli, tumor emboli, air emboli, gaseous nitrogen bubbles, fat and marrow emboli, amniotic fluid

34
Q

What is gangrene?

A

Necrosis that is complicated by saprophytic bacterial infection - makes the tissue black

35
Q

What is primary gangrene?

A

gas gangrene - caused by clostridium usually due to infection after trauma

36
Q

What is secondary gangrene?

A

Infection after the tissue is already necrotic

37
Q

What are the two types of secondary gangrene?

A

Dry gangrene and wet gangrene

38
Q

What is dry gangrene?

A

Peripheral vascular disease causes necrosis in the toes/feet/legs and then get a saprophytic infection

39
Q

What is wet gangrene?

A

Occurs in the internal organs - e.g. complicating acute appendicitis or cholecystitis or infarction of small bowel