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2C week 1 - acute coronary syndrome > CAD > Flashcards

CAD Flashcards

1
Q

what is coronary artery disease

A

the narrowing of coronary arteries due to atherosclerosis (lipid deposition, inflammation, thrombosis)

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2
Q

chronic and acute coronary syndrome (4)

A

STEMI, NSTEMI, unstable angina, chronic angina

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3
Q

atherosclerotic plaque development steps

A
  1. fatty streak - endothelial dysfunction allows cholesterol to enter the bv wall, it is recognised as a foreign body which drives leukocyte modification and recruitment, foam cells form;
  2. plaque progression - smooth muscle cells migrate and there is altered matrix synthesis and degradation, due to inflammation and cholesterol levels driving it;
  3. plaque disruption - disturbed plaque integrity due to unstable/thin surface, thrombus forms due to rupture into bv which can occlude the artery
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4
Q

why is smoking a risk factor for CAD

A

the toxins damage the bv wall

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5
Q

main trigger factors for bv wall inflammation (4)

A

cholesterol crystals; neutrophil extracellular traps; atheroprone flow (turbulent); hypoxia

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6
Q

risk factors for atherothrombosis (12)

A

hypertension; hypercholesterolemia; diabetes; smoking; FH; obesity/metabolic syndrome; male; old age; ethnicity; socio-economic status; genetic profile; inflammatory markers

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7
Q

what is used to calculate the future risk of CVD event

A

QRISK2 - increased by 10% indicates treatment for cholesterol should be given

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8
Q

what areas of arteries are at particular risk from atherosclerosis

A

branch points and bifurcations due to turbulent flow

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9
Q

what areas of arteries are at a particularly high risk of atherosclerosis

A

branches and bifurcations due to turbulent flow

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10
Q

what is ischaemia due to

A

fixed vessel narrowing and abnormal vascular tone

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11
Q

what determines myocardial O2 supply (7)

A

coronary blood flow; coronary perfusion pressure; coronary vascular resistance; external compression; intrinsic regulation; local metabolites; endothelial factors; neural innervation

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12
Q

what determines myocardial O2 demand (3)

A

wall stress (Pr/2h); heart rate; contractility

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13
Q

what determines the effect n blood flow of stenosis (2)

A

the degree of narrowing; the amount of compensatory vasodilation the arterioles can achieve

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14
Q

what can abnormal vascular tone result in? (2)

A

inappropriate vasoconstriction of coronary arteries; loss of normal antithrombotic properties

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15
Q

why does angina occur

A

metabolic hyperaemia can no longer match myocardial perfusion to myocardial oxygen demand in exercise due to restricted blood flow

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16
Q

4 characteristics of angina (location, character, relieving/exacerbating factors, duration)

A

location - retrosternal, diffuse, may involve both sides + chest;
character - pressure, tightness, heaviness, occasionally burning sensation or chocking if in the neck, toothache if in jaw;
relieving/precipitating - provoked by exertion, more easily provoked after a heavy meal or cold weather, rapid relief w GTN;
duration - attacks last a few minutes only

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17
Q

features of a normal lumen (3)

A

patent lumen; normal endothelial function; platelet aggregation inhibited

18
Q

features of stable angina lumen (2)

A

lumen narrowed by plaque; inappropriate vasoconstriction

19
Q

features of unstable angina (4)

A

plaque rupture; platelet aggregation; thrombus formation; unopposed vasoconstriction

20
Q

features of variant angina (2)

A

no overt plaques; intense vasospazam

21
Q

chest pain differentials (11)

A

cardiac - angina, pericarditis;
GI - reflux(GORD), peptic ulcer, oesophageal spasm, biliary colic;
msk - costochondral syndrome (sharp pain, rib fractures, cervical radiculitis
other - pneumonia, PE (stabbing pain), anxiety, aortic dissection

22
Q

symptoms of PE

A

sudden SOB; chest pain; anxiety; palpitations

23
Q

diagnostic tests for CAD (4)

A

stress ECG; myocardial perfusion imaging, stress echo; stress MRI

24
Q

imaging for CAD (2)

A

CT coronary angiogram; coronary angiogram

25
Q

what does a depressed ST segment in an ECG stress test indicate

A

ischaemia

26
Q

shape of RCA on angiogram

A

‘c’ shaped

27
Q

4 main coronary arteries

A

right coronary; left anterior descending; circumflex; left coronary

28
Q

what is the first region to be damaged by ischemia

A

subendothelial region as it is furthest from blood supply

29
Q

subendothelial vs transmural ischaemia ECG

A

subendothelial - ST depression
transmural - ST lelevation

30
Q

stable vs vulnerable plaques

A

stable - thick fibrous cap, small lipid pool
vulnerable - think fibrous cap, large lipid pool, many inflammatory cells

31
Q

what happens to a ruptured plaque

A

thrombogenic extracellular matrix exposed to lumen, thrombus formed; this can either be reabsorbed resulting in a narrower lumen and fibrous intima or in occlusion of the lumen

32
Q

what marker is key in identifying if an MI has occured

A

troponin - cardiac specific troponin can be identified, this elevates if the heart is damaged

33
Q

what can raised troponin indicate other than ACS

A

exercise; renal failure/other severe illness

34
Q

what is a pathological Q wave

A

a Q wave that is >3mm, it often appears post MI due to wall damage, it persists in the ECG after other changes have reverted

35
Q

NSTEMI ECG appearance

A

ST depression or T wave inversion; no pathological Q wave

36
Q

post MI complications (7)

A

A -arrythmia
C-congestive HF/cardiogenic shock
T- thromboembolism
R - rupture (V free wall, papillary muscle, septum)
A - aneuyrsm
P - pericarditis
I - ischaemia
D - dresslers syndrome/detah

37
Q

what is Dressler’s syndrome

A

inflammation of the sac surrounding the heart (pericarditis); the immune system responding to damage to heart tissue or damage to the pericardium

38
Q

how does endothelial dysfunction contribute to ACS

A

reduced vasodilator and antithrombotic effect

39
Q

dressler’s syndrome symptoms

A

fatigue; weakness; pain worse on lying down; pleural effusion; increased WCC

40
Q

what is pericardial friction rub (what does it sound like and why)

A

occurs due to the inflammation of the pericardium post MI and so the two layers rub against each other; grating, scratching, or rasping sound systolic and diastolic; best heard between the apex and sternum but may be widespread

2C week 1 - acute coronary syndrome (7 decks)

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