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EMS MOD > atheroma, thrombosis and embolism > Flashcards

atheroma, thrombosis and embolism Flashcards

1
Q

what is the significance of this?

A

major cause of mortality and morbidity

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2
Q

what conditions do these include?

A

myocardial and cerebral infarction and pulmonary embolism

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3
Q

what is an atheroma?

A

it is a intimal (innermost) lesions that protrudes into a vessel wall. it consists of a raised lesion with a soft core of lipid and a fibrous cap.

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4
Q

what forms the soft core of lipids?

A

cholesterol and cholesterol esters

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5
Q

what is the function of the IEL?

A

the internal elastic lamina separates the media from the intima

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6
Q

what is in the fibrous cap?

A

foam cells, macrophages, elastin, collagen, lymphocytes, soft muscle cells

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7
Q

what is in the necrotic core?

A

cell debris, foam cells, cholesterol crystals and calcium

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8
Q

what are foam cells?

A

they are macrophages or smooth muscle cells that have migrated from the media and engulfed lipids

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9
Q

how is the necrotic core formed?

A

cells die, and lipid escapes from them

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10
Q

what do macrophages and SMCs do?

A

they produce collagen and elastin - these are the ECM proteins that form the fibrous cap of atheroma / top of lesion

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11
Q

how can atheroma form?

A

chronic inflammation within the intima

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12
Q

how can thrombosis form?

A

processes damaging the media

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13
Q

what are commonly affected vessels?

A 
sites of bifurcation - turbulent slow - occurs at ostia 
carotid vessels 
abdominal aorta 
circle of willis 
popliteal arteries 
coronary arteries
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14
Q

why does atherosclerosis occur?

A

it is a response to injury to the overlying endothelium - triggers a cascade of events leading to atherosclerosis

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15
Q

how does oestrogen link with MI?

A

prior to menopause men are more likely to have MI, post menopause women are due to levels of oestrogen

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16
Q

how can abnormalities in the transport of cholesterol impact these conditions?

A

LDL transports cholesterol to site of atherosclerosis and HDL away - abnormalities can change this and therefore mean more cholesterol is taken to the site

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17
Q

what are modifiable risk factors for atheroma and thrombosis?

A

cigarette smoking, CRP, diabetes, hyperlipidaemia and hypertension

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18
Q

what are non-modifiable risk factors?

A

gender, age, family history and genetic abnormalities

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19
Q

what is atherosclerosis?

A

chronic inflammatory response to injury to the endothelium

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20
Q

how does progression of lesion occur?

A

interaction between normal cellular constituents of the arterial wall, T lymphocytes, monocyte derived macrophages and modified lipoproteins

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21
Q

what is the response to endothelial injury?

A

increased permeability, leukocytes adhere to endothelium and emigrate through into intima. Cyto and chemokines cause the smooth muscle cells to emigrate from media to intima and activate macrophages - try to engulf the lipids. SMCs help engulf and produce ECM proteins for a fibrous plaque - cells start to die resulting in necrotic core and neovascularisation - small vessels form at edges of lesion

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22
Q

what is the fatty streak?

A

it is the earliest lesion in atherosclerosis, composed of lipid filled foamy macrophages, begining as multiple minute flat yellow spots and then coalescing into streaks - not significantly raised and do not cause disturbance to flow

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23
Q

what is an atherosclerotic plaque?

A

consists of lipid accumulation and intimal thickening
appear white yellow and superimposed thrombus on plaque is red
plaque will impinge on the vessel lumen

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24
Q

what are ostia and what are the complications here?

A

ostia are holes where branching arteries come off the aorta. Streaks form around the ostia, which sometimes contain calcium, and as lesion progresses, it becomes more severe. If lesion ruptures can cause blood clots here.

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25
Q

what can result in thrombosis?

A

increase in pressure or overlying turbulence, athero-embolisms, aneurysms and haemorrhages

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26
Q

what is an embolus?

A

when part of the plaque dislodges

27
Q

how do thrombi form?

A

when there is rupture, ulceration or erosion of the intimal surface then the blood is exposed to the highly thrombogenic core which induces thrombosis - lumen occlusion - ischaemia

28
Q

what is a thrombus?

A

it is a solid mass of blood constituents formed in the vascular system in vivo

29
Q

what is the most common cause of arterial thrombosis?

A

to be superimposed on an atheroma - the lesion causes turbulent blood flow and exposes to thrombogenic substances - rupture of plaque

30
Q

what is the most common cause of venous thrombosis?

A

stasis of blood making it sluggish - combination from virchows triad

31
Q

what is virchows triad composed of?

A

it is composed of abnormal blood floe, hypercoagulability and endothelial injury - changes to any one of these can result in a predisposition to thrombus formation

32
Q

why does changes to hypercoagulability result in thrombosis?

A

reduces the fibrinolytic cascade, increase the coagulation cascade

33
Q

how does changes to endothelium result in thrombosis?

A

the platelets adhere and activate, meaning that the coagulation cascade is triggered

34
Q

how do changes to blood flow affect thrombosis?

A

there is stasis or turbulence - affect the natural protective mechanisms within the blood and draw the platelets into contact with the endothelium resulting in thrombosis

35
Q

how does AF result in thrombosis?

A

pooling and stasis of blood

36
Q

what is PVD?

A

peripheral vascular disease - pain on walking due to reduced blood flow through arteries and can lead to ulcers

37
Q

where do heparin and warfarin work?

A

work on the coagulation cascade

38
Q

what predisposes us to thrombosis?

A

anything that tips the balance between fibrinolytic and pro-coagulative state

39
Q

what does a mutation in factor V mean?

A

it is resistance to breakdown from protein C and S and therefore more coagulative

40
Q

what will a mutated prothrombin gene result in?

A

more prothrombin to turn into thrombin and therefore more coagulation

41
Q

what is HIT?

A

heparin induced thrombocytopenia - when someone taking heparin produces antibodies against it and therefore activates platelets

42
Q

what is polycythaemia?

A

when there are more RBC in blood than required meaning that the blood is more viscous and volumous

43
Q

where do arterial thrombosis and venous typically occur?

A

arterial in the left heart chambers and venous in the venous sinusoids of muscles and valves of veins

44
Q

what conditions are associated with arterial?

A

acute coronary syndrome and ischaemic stroke claudication

45
Q

what conditions are associated with VTE?

A

DVT and PE

46
Q

what is the composition of VTE compared to arterial?

A

arterial is mainly platelets whereas venous is mainly fibrin

47
Q

what is the treatment for VTE compared to arterial?

A

anticoagulants for venous - warfarin or heparin

for arterial antiplatelets - clopidogrel

48
Q

what are the red and white parts in a thrombus?

A

red is RBCs

white is platelets and fibrin

49
Q

why are there no layers in clots?

A

there is no activation of platelets

50
Q

what are the major differences between clots of thrombi?

A 
clot:
red
no platelets involved 
gelatinous 
not attached to vessel wall 
can occur inside or outside vessel 
thrombus:
red and white 
platelets involved 
firm 
attached to vessel wall 
only occurs inside vessel
51
Q

what is the sequelae of thrombi?

A

occlusion of vessel, dissolution, incorporation into vessel wall, recanalisation and embolisation

52
Q

what is occlusion of vessel?

A

thrombin converts fibrinogen to fibrin in a mesh, if the body cannot remove platelets and therefore cannot remove clot due to the balance tipping then the clot becomes larger. Tissue dies and infarction due to inadequate blood supply through arteries. If it is in a vein then will appear hot and swollen.

53
Q

what is dissolution?

A

when the thrombus is broke down and dissolved

54
Q

what is incorporation into the vessel wall?

A

when the thrombus is gradually absorbed into the wall resulting in narrowing of the lumen

55
Q

what is recanalisation?

A

when macrophages and smooth muscle cells, followed by capillaries grow into the thrombus and form new blood vessels. The capillaries will connect and form channels. There is organisation through deposition of collagen

56
Q

what is an embolus?

A

it is a mass of material lodged in vascular system that blocks the lumen. Most are originating from a thrombi - most commonly PE from DVT

57
Q

what is a thrombus derived emboli made of?

A

atheromatous plaque material

58
Q

what are other sources of emboli?

A

when there is vegetation on the heart valves in infective carditis - can break off and travel in blood stream
fragments of tumour - metastasis
amniotic fluid - rare complication in vessels of mother
gas - pressure difference in deep sea diving
fat - long bone trauma - fat from bone marrow escapes lodges and blocks

59
Q

what are the effects of PE?

A

acute respiratory and cardiac problems, sudden death but effects depend on size of embolus

60
Q

what is a saddle embolus?

A

large embolus that blocks all blood from heart into lungs - heart cannot pump against, acute problems

61
Q

what is the result of a smaller embolus?

A

travels further down the arterial tree and lodges there, increased resistance and pulmonary hypertension

62
Q

where do systemic emboli typically originate?

A

from the heart or an atheromatous plaque

63
Q

what conditions can cause systemic emboli?

A

MI, AF, infective endocarditis

64
Q

what are other conditions systemic emboli can cause?

A

CVA, TIA, gangrene and bowel necrosis

EMS MOD (28 decks)

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