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Phase 2a > Thrombosis and Infarction > Flashcards

Thrombosis and Infarction Flashcards

1
Q

What is the most common lesion which impedes vascular flow in arteries?

A

Atheroma

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2
Q

How do atheromatous plaques cause a) angina b) hypertension?

A

Stenosis of arteries

a) myocardial ischaemia
b) renal artery stenosis causes low perfusion to juxtaglomerular cells, kidney thinks body has low BP, activated RAS to increase BP

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3
Q

Arterial spasms which cause transient ischaemia can cause what apart from angina?

A

Raynaurds disease (small blood vessels in extremities are over sensitive to temperature)

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4
Q

What is steal syndrome?

A

Blood is diverted away from vital territory when an area proximal needs increased supply; if there is pre-existing narrowing then that area will undergo transient ischaemia

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5
Q

What can cause ischaemia at the arteriolar, capillary and venular level?

A

Hyper-viscosity of blood

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6
Q

How is a clot formed?

A
  1. Damage to blood vessel
  2. Platelet aggravation
  3. Platelet plug formed
  4. Clotting factors cause fibrin to stick together and create mesh
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7
Q

What is a thrombus?

A

A blood clot in the circulatory system.

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8
Q

How are platelets activated?

A

Contact with collagen

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9
Q

What are the 3 predisposing situations which may result in thrombus formation?

A
  1. Changes in intimal surface of vessel
  2. Changes in pattern of blood flow
  3. Changes in blood constituents
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10
Q

How does an atheromatous plaque form in an artery?

A
  1. Initial fatty streak on intimal surface
  2. Enlarges and protrudes causing turbulence
  3. Loss of intimal cells so plaque surface come into contact with platelets
  4. Fibrin deposition and clumping
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11
Q

What direction do thrombi grow in arteries?

A

In the direction of blood flow

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12
Q

What might you see in an arthero-thrombotic plaque?

A

Lines of Zahn - alternating layers (laminations) of platelets mixed with fibrin, which appear lighter, and darker layers of red blood cells

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13
Q

Why don’t artheromas form in veins?

A

Lower blood pressure

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14
Q

Where do most venous thrombi form and why?

A

Near valves because there is natural turbulance

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15
Q

In what fashion do thrombi for in veins?

A

Laminated/corallini growth

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16
Q

What is thrombophlebitis?

A

Thrombosed veins cause inflammation

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17
Q

What is seen in an arterial thrombosis?

A
  1. Loss of pulse distal to thrombus
  2. Area is cold, pale, painful
  3. May progress to necrosis/gangrene
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18
Q

What is seen in a venous thrombosis?

A

Area becomes red, tender and swollen

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19
Q

What can happen to a thrombus?

A
  1. Resolution and lysis
  2. Organisation into scar tissue (fibroblasts making collagen)
  3. Recanalistion
  4. Embolism
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20
Q

If a thrombus is reorganised into scar tissue in the heart what may it form?

A

Mural module

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21
Q

Name the types of embolism 9)

A
  1. Pulmonary
  2. Systemic
  3. Embolic atheroma
  4. Platelet emboli
  5. Infective emboli
  6. Fat embolus
  7. Gas embolus
  8. Amniotic embolism
  9. Tumour embolism
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22
Q

What is a saddle embolus?

A

Embolus across bifurcation of a major artery

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23
Q

Where do systems emboli originate?

A

Usually left side of heart

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24
Q

Where in the atria does blood tend to stagnate?

A

Appendages

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25
Q

What is a marantic vegetation?

A

Vegetation at valves consisting of platelets and fibrin

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26
Q

Where are embolic artheromas found?

A

Lower limbs of arteriopathic people

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27
Q

When might a fat embolus arise?

A

After trauma/surgery of long bone - fat released from the marrow

28
Q

When can a gas embolus form?

A

The bends

29
Q

Why are tumour embolisms important?

A

Mechanism of metastasis

30
Q

What are the 3 layers of arteries?

A
  1. Intima - single layer of endothelium with a thin supporting framework of connective tissue
  2. Media - mostly smooth muscle - more elastin in aorta
  3. Adventitia - fibrous connective tissue
31
Q

What separates the layers of the arteries?

A

Internal elastic lamina, external elastic lamina

32
Q

How do arteries receive oxygen?

A
  1. Intima - direct diffusion from blood in lumen

2. Media/adventia - vasa vesorum

33
Q

What is atherosclerosis?

A

Disease characterised by formation of focal elevated lesions in the intima of large and medium-sized arteries

34
Q

What general changes occur to the 3 layers of arteries in atherosclerosis?

A
  1. Intima - fibrous thickening of the intima
  2. Media - fibrosis and scarring of media
  3. Fragmentation of elastic laminae
35
Q

What is the earliest lesion seen in atherosclerosis?

A

Fatty streak

36
Q

What is an atherosclerotic plaque?

A

Lesion with a central lipid core with a cap of fibrous tissue covered by the arterial endothelium

37
Q

What cells/substances are found in an atherosclerotic plaque?

A

T-lymphocytes, SMC, collagen, macrophages, lipid deposits, fragmented internal elastic lamina, cholesterol

38
Q

What is the most important risk factor which leads to atherosclerosis?

A

Hypercholesterolaemia

39
Q

What are some other risk factors for developing atherosclerosis?

A

smoking, hypertension, diabetes, male gender, increasing age, obesity, sedentary lifestyle, low birth weight

40
Q

What are the 2 major steps in the development of an atherosclerotic plaque?

A
  1. Injury to the endothelium

2. Tissue response to injury

41
Q

How might the endothelium be damaged?

A

Stress caused by high BP, diabetes, cholesterol, free radicals (smoking)

42
Q

What is it about hypercholesterolaemia which encourages atherosclerosis?

A

LDLs can pass in/out of arterial wall where they accumulate causing damage to the endothelium

43
Q

What adhesion molecules do damaged endothelial cells release and what does this cause?

A

ICAM-1 and E-selectin; allows inflammatory cells and lipids to enter intimal layer

44
Q

What are foam cells?

A

Lipid-laden macrophages

45
Q

What forms the lipid core of a plaque?

A

LDLs; apoptosis of foam cells spill lipids into core

46
Q

What happens during the tissue response stage of plaque formation?

A

PDGF stimulates the proliferation of intimal smooth muscle cells which secrete collagen/elastin/mucopolyssccaride synthesis which forms a fibrous cap

47
Q

What other mechanism expands the volume of the plaque?

A

Haemorrhage due to rupture of micro vessels

48
Q

What may eventually happen to the collage/elastin cap which makes it more prone to rupture?

A

Calcification

49
Q

What are the processes in atherosclerosis which lead to clinical disease?

A
  1. Lumen narrowing due to high grade plaque stenosis
  2. Acute atherothrombotic occlusion (MI)
  3. Embolisation of the distal arterial bed
  4. Ruptured abdominal atherosclerotic aneurysm
50
Q

What is infarction?

A

Loss of blood supply to an area resulting in tissue death

51
Q

What is a repurfusion injury?

A

Reperfusion appears to trigger oxygen dependant free radical systems that begin to clear away dead cells

52
Q

How might infarcted tissues look after 24 hours?

A

Pale, striations disappear from cardiac myosotes, inflammation at edge

53
Q

How might infarcted tissues look after 6 hours?

A

No visible changes, swollen mitochondria, ECG changes

54
Q

How might infarcted tissue look after days-weeks later?

A

Dead myocytes removed by macrophages; replaced by fibrous tissue; amorphus/acellular; tissue at its weakest - prone to rupture

55
Q

How might infarcted tissues look after several months later?

A

Fibrous scar, grey collagenous tissue

56
Q

What shaped infarcts exist and where are they found?

A

Wedge shaped (lung), triangular/conical (kidney), irregular (spleen)

57
Q

Where does gangrene occur?

A

When mixed tissues die in bulk

58
Q

What are the 2 types of gangrene?

A

Dry and wet

59
Q

What happens in dry gangrene?

A

Tissues die and become mummified, healing occurs above it, dead area drops off, sterile process

60
Q

What happens in wet gangrene?

A

Bacterial infection as secondary complication; gangrene spreads proximally; death from sepsis

61
Q

What is gas gangrene?

A

Infection with gas producing anaerobic bacteria such as clostridium perfingens

62
Q

What is capillary ischaemia?

A

Capillary contraction followed by a fixed dilation, or can occur by blockage by parasites/sickled RBCs, includes DIC

63
Q

Which tissues are vunerable to low-perfusion infarction (rather than due to blockage)?

A

Watershed areas - interface between the adjacent territories of two arteries with no collateral circulation

64
Q

Give some examples of watershed areas

A

Splenic flexure of the colon (SMA/IMA); areas of cerebral cortex; area of heart between sub-endocardium and tissue perfused by coronaries

65
Q

What is a portal system? Why vunerable to infarction?

A

Tissues are perfused by blood that has already passed through one set of capillaries; blood has lower saturation

66
Q

Give 3 examples of portal circulation

A

Anterior pituitary; renal tubular epithelium; exocrine pancreas

67
Q

In what state do portal systems and watershed areas become infarcted?

A

Hypovolaemic shock

Phase 2a (3 decks)

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