Pathophysiology of atheroma, thrombosis and embolism, ischaemia and infarction Flashcards

1
Q

what is atheroma made up of?

A

fibrous cap

lipid core

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2
Q

what is the difference between atherosclerosis and arteriosclerosis?

A

atherosclerosis - atheroma formation in endothelium

arteriosclerosis - fibrosis of tissue with age

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3
Q

what is contained within the fibrous cap of atheroma?

A

collagen

inflammatory cells

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4
Q

what is the collagen in the fibrous cap of atheroma produced by and how?

A

smooth muscle cells, platelets, macrophages

through secretion of PDGF - platelet derived growth factor

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5
Q

which arteries are more likely to be affected?

A

muscular arteries

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6
Q

what are the chronological stages of an atheroma plaque, and when do they occur?

A

fatty streak (childhood)
early atheromatous plaque (young adult)
fully developed atheromatous plaque (30+ years)

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7
Q

what is the main culprit for developing atherosclerosis?

A

hypercholesterolaemia

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8
Q

what are possible signs of hypercholesterolaemia?

A
high LDL/total cholesterol in blood
genetically low LDL receptors
tendon xanthomata
xanthalasma
corneal arcus
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9
Q

what are the main risk factors for developing atherosclerosis?

A
hypertension
smoking
diabetes
age
male
(obesity)
(sedentary lifestyle)
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10
Q

what does a complicated atheroma mean and what are its consequences?

A

the rupture/fissure of a plaque, exposing its contents to the lumen –> trigger inflammatory reaction, thrombosis/embolism

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11
Q

what are the main features of a vulnerable atheroma plaque?

A

thin fibrous cap
large lipid core
active visible inflammation

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12
Q

what are the main non-drug prevention mechanisms for atherosclerosis?

A

stop smoking
weight loss
exercise
diet changes

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13
Q

what are the main drug prevention mechanisms for atherosclerosis and how do they affect atherosclerosis?

A

ACEI - reduce blood pressure (reduce risk of plaque rupturing)
statins - stabilise fibrous plaque and reduce cholesterol production
aspirin - antiplatelet (reduce risk of thrombosis on plaques)

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14
Q

what are the four main types of hypoxia?

A

hypoxic
anaemic
stagnant
cytotoxic

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15
Q

what are the six main factors affecting oxygen supply?

A
inspired O2
lung function
blood components (Hb)
blood flow
vasculature
tissue mechanisms
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16
Q

what are the two main factors affecting oxygen demand?

A

tissue specific demands

level of tissue activity above normal threshold

17
Q

what are the different types of necrosis which can happen post-infarction, and where do they occur?

A

coagulative - heart, lung, kidneys

colliquative/liquefactive - brain

18
Q

why are some tissues more sensitive to ischaemia than others?

A

because of different cell/tissue metabolism (some fast metabolism, some slow)

19
Q

what is a biochemical and cellular result of infarction?

A

anaerobic metabolism –> cell death –> necrosis

20
Q

what are the effects of infarction?

A

acute/chronic reduction in O2 supply
loss of function/dysfunction/pain
anaerobic metabolism –> cell death –> necrosis
effects depend on metabolism of affected cells

21
Q

what are the two different appearances of infarctions, how and when do they occur?

A

pale (anemic) infarct (arterial occlusion) - solid tissue (heart, kidney)
red (hemorragic) infarct (venous congestion) - loose tissue (liver, lungs, GI)

22
Q

what is the endstage of infarction in tissue appearance?

A

scar formation

23
Q

what are possible types of embolus?

A
thrombus (arterial or venous)
gas embolus (nitrogen)
mural embolus (ventricle dilation, AF)
air embolus
fat embolus (fat embolism syndrome)
placental/amniotic fluid embolus
tumour embolus
septic embolus
foreign object embolus
bone marrow embolus
24
Q

how does rheumatic fever cause emboli?

A

inflammation in endocardium/valves can cause thrombi forming on top of inflamed area and dislodge

25
Q

what is a typical hystological feature of rheumatic heart disease?

A

presence of aschoff bodies (containing anitschkow cells)

26
Q

what are lines of Zahn and how are they formed?

A

it’s alternation of RBC and fibrin deposition in thrombus formation, due to the inflammatory/clotting process involved

27
Q

how can rheumatic fever lead to rheumatic heart disease?

A

fever causes inflammation of joints and heart (pancarditis)

acute pancarditis can progress into rheumatic heart disease

28
Q

what is the most common effect of rheumatic heart disease?

A

mitral valve dysfunction

29
Q

other than lung cancer, what are some lung conditions for which surgery is sometimes required?

A
lung transplants (CF, emphysema, IPF)
lung abscess
empyema
thymus tumours
benign lung tumours
tracheal surgery
pneumothorax
bullous disease
bronchogenic cysts
30
Q

what are the stages of surgical removal of empyema called?

A

parietal pleural layer - pleurectomy

visceral pleural layer - decortication