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Endo, Cardio and Neuro > Coronary heart disease/athersclerosis > Flashcards

Coronary heart disease/athersclerosis Flashcards

1
Q

modifiable risk factors of coronary heart disease

A 
smoking
lipids
blood pressure
diabetes
obesity
sendentary lifestyle
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2
Q

non modifiable risk factors of coronary heart disease

A

age
sex
genetic background

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3
Q

what combination of risk factors has the greatest impact on coronary heart disease

A

hypertension
smoking
high cholesterol

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4
Q

where is athersclerosis most likely to develop

A

at branches of vessels

e.g carotid, coronary and iliac arteries

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5
Q

why is atherosclerosis more likely to develop at artery branches

A

turbulent flow causing inflammation

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6
Q

where does athersclerosis happen within a blood vessel

A

between endothelium and internal elastic layer (intima)

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7
Q

what do coronary arteries do at lesion prone locations

A

adaptive thickening of the smooth muscle - intima widens and is larger

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8
Q

what is a type II lesion

A

macrophage foam cells infiltrate intima

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9
Q

what is a type III lesion/preatheroma

A

small pools of extracellular lipid form around the macrophage foam cells

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10
Q

what is a type IV lesion/atheroma

A

a core of extracellular lipid forms (small pools have joined up) around macrophage foam cells

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11
Q

what is a type V lesion/fibroatheroma

A

fibrous thickening around core of extracellular lipid and macrophage foam cells, hardening of vessel constriction

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12
Q

what is a type VI or complicated lesion?

A

a rupture/surface defect caused by a haematoma and fissure within intima causes a thrombus to form on outer layer of intima/lumen

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13
Q

when is the best time to intervene with atherosclerosis

A

intermediate or advanced lesions

for primary prevention of rupture/stenosis - lifestyle changes and risk factor management

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14
Q

what interventions are needed for complicated lesions?

A

stenosis/plaque rupture treatment
catheter based interventions
revascularisation surgery
treatment of heart failure

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15
Q

what cells are involved in athersclerosis

A 
vascular endothelium
macrophages
vascular smooth muscle cells
T lymphocytes
platelets
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16
Q

how are vascular endothelial cells involved in athersclerosis

A

barrier function against athersclerosis

leukocyte recruitment

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17
Q

how are macrophages involved in athersclerosis

A

foam cell formation
major source of free radicals and metalloproteinases
cytokine and growth factor release

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18
Q

how are vascular smooth muscle cells involved in athersclerosis

A

migration and proliferation
collagen synthesis
remodelling, fibrous cap formation

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19
Q

how are t lymphocytes involved in athersclerosis

A

macrophage activation

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20
Q

how are platelets involved in athersclerosis

A

thrombus generation

cytokine/growth factor release

21
Q

what are the two main classes of macrophages

A

inflammatory macrophages - kill germs

resident macrophages - homeostasis e.g osteoclasts, alveolar macrophages, spleen macrophages

22
Q

what is low density lipoprotein

A

bad cholesterol synthesised in liver

carries cholesterol from liver to body tissues

23
Q

what is high density lipoprotein

A

good cholesterol

reverse cholesterol transport

24
Q

what are oxidised/modified LDLs

A

impact of free radicals on LDL

highly inflammatory and toxic forms of LDL in vessel walls

25
Q

structure of low density lipoprotein

A 
docking molecules for fat delivery
lipid monolayer (micelle)
cargo fat
26
Q

how do LDLs cause athersclerosis

A

lwak through endothelial barrier
binds to proteoglycans in sub-endothelial layer
oxidated by free radicals, phagocytosed by macrophages CREATES FOAM CELLS and stimulates chronic inflammation

27
Q

what is familial hypercholesterolaemia

A

autosomal genetic disease
elevated cholesterol
failure to clear LDL from blood
early athersclerosis - MI before 20

28
Q

what are statins

A

HMG-CoA reductase inhibitors

29
Q

how do macrophages impact atherosclerosis inflammation

A

generate free radicals to oxidise lipoproteins
phagocytose lipoproteins and become foam cells
express cytokines that recruit monocytes
express chemoattractants and growth factors for VSMC
generate proteinases to degrade tissue

30
Q

what free radicals do macrophages produce

A

NADPH oxidase

myeloperoxidase

31
Q

what cytokines do macrophages express to recruit monocytes

A

IL-1 upregulates VCAM-1

vicious cycle of self-perpetuating inflammation

32
Q

what chemoattractants do macrophages express

A

protein growth factors for vascular smooth muscle cells, stimulate them to proliferate and deposit ECM
platelet derived growth factor (PDGF) - VSMC chemotaxis, survival and cell division
transforming growth factor beta (TGFb) - increased collagen synthesis and matrix deposition

33
Q

what are metalloproteinases

A

degrade collagen by zinc based mechanism

34
Q

what is the fate of macrophages involved in athersclerosis

A

protective systems overwhelmed
die by apoptosis
release toxic lipids and tissue factors into lipid necrotic core
builds up until plaque ruptures and these are spilled out into the blood encouraging a clot

35
Q

what is nuclear factor kappa B

A

transcription factor
activated by scavenger receptors, cytokines etc
switch on inflammatory genes for metalloproteinases, nitric oxide synthase, IL-1

36
Q

what macrophage scavenger receptors bind to oxidised LDL

A

scavenger receptor A and B (CD204, CD36)

37
Q

first line management of a STEMI

A

antiplatelet and anti-ischaemic/coagulant treatment

then PCI/CABG

38
Q

long term management of STEMI

A 
antiplatelet therapy
statin
beta blocker
ACEi
cardiac rehabilitation + lifestyle changes
39
Q

pathophysiology of STEMI

A

nearly always coronary plaque rupture resulting in thrombosis formation, occluding a coronary artery

40
Q

pathophysiology of NSTEMI

A

incomplete thrombus formation, doesnt stop blood and oxygen completely but restrictio is great enough that oxygen is used up quickly. in distal arteries and arterioles, tissue death occurs due to oxygen starvation
affected area is small to not cause ST elevation but causes depression and Troponin elevation

41
Q

pathophysiology of unstable angina

A

plaque becomes unstable, fibrous cap disrupts and forms thrombus but enough for lumen to meet demand during rest

42
Q

clinical difference between unstable angina and NSTEMI

A

NSTEMI shows raised Troponin levels

43
Q

typical angina components

A

precipitated by physical exertion
retrosternal pain in chest
relieved by rest or glyceryl trinitrate (GTN)

44
Q

what do blood troponin levels indicate

A

elevated in heart damage, remain elevated for 2wk
normal levels = less likelihood of muscle damage, more likely angina
rise/fall in series of troponin results indicates heart attack

45
Q

treatment of unstable angina and NSTEMI first steps

A

risk assessment for future coronary events

46
Q

low risk NSTEMI and unstable angina patient management

A

conservative treatment aspirin, clopidogrel, heparin, nitrates, b blockers
stress test

47
Q

low risk patients NSTEMI and unstable angina stress test results mean

A

negative - discharge

positive - coronary angiography (PCI, CABG etc)

48
Q

high risk NSTEMI and unstable angina patients management

A

invasive management

coronary angiography - PCI, CABG

49
Q

assessment of patient who is at high risk of future coronary events

A

positive troponin, ST changes, patient generally unstable

Endo, Cardio and Neuro (22 decks)

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