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Cardiovascular system > Coronary syndromes > Flashcards

Coronary syndromes Flashcards

1
Q

How do plaques develop?

A

fatty streak - endothelial dysfunction, lipoprotein entry + modification, leukocyte recruitment, foam cell formation

plaque progression - smooth muscle cell migration, altered matrix synthesis and degradation

plaque disruption - disrupted plaque integrity, thrombus formation

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2
Q

CAD modifiable risk factors

A

smoking
hypertension
high cholesterol
diabetes

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3
Q

CAD non-modifiable risk factors

A

age
gender
family history
ethnicity

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4
Q

What calculator is used to assess cardiovascular disease risk?

A

QRISK2

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5
Q

What is atherosclerosis?

A

chronic disease characterised by inflammation and lipid deposition affecting the intima

affects large and medium sized muscular and elastic arteries

branch points and bifurcations are particularly at risk (due to more turbulent blood flow)

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6
Q

What 2 factors cause ischaemia in stable angina?

A

fixed vessel narrowing
abnormal vascular tone

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7
Q

What does the effect of a stenosis on blood flow depend on?

A

degree of narrowing of epicardial vessel

amount of compensatory vasodilation that the arterioles can achieve

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8
Q

What does abnormal vascular tone result in?

A

(endothelial dysfunction causes abnormal vascular tone)

results in:
- inappropriate vasoconstriction of coronary arteries
- loss of normal antithrombotic properties

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9
Q

What are 4 broad characteristics of angina?

A

location
character
precipitating and relieving factors
duration

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10
Q

Angina location

A

retrosternal
diffuse
may involve both sides of chest (L>R), arms (L>R), neck, lower jaw, upper abdomen

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11
Q

Angina character

A

pressure, tightness of heavy weight
sometimes burning

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12
Q

Angina precipitating and relieving factors

A

provoked by exertion (walking uphill)
more easily provoked after heavy meal/cold weather
rapid relief (2 mins) with GTN

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13
Q

Angina duration

A

attacks last a few minutes (not very brief or very prolonged)

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14
Q

Describe a stable angina artery

A

lumen narrowed by plaque
inappropriate vasoconstriction

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15
Q

Describe an unstable angina artery

A

plaque rupture
platelet aggregation
thrombus formation
unopposed vasoconstriction

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16
Q

Describe a variant angina artery

A

no overt plaques
intense vasospasm

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17
Q

Cardiac causes of recurrent chest pain

A

angina
pericarditis

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18
Q

GI causes of recurrent chest pain

A

reflux (GORD)
peptic ulcer
oesophageal spasm
biliary colic

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19
Q

MSK causes of recurrent chest pain

A

costochondral syndrome
cervical radiculitis

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20
Q

Diagnostic tests for coronary artery disease

A

ECG
Stress tests - exercise ECG, myocardial perfusion imaging, stress echocardiography, stress MRI
Imaging - Non-invasive = CT coronary angiogram, Invasive = coronary angiogram

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21
Q

Define myocardial ischaemia

A

reduced blood supply to the heart

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22
Q

Define myocardial infarction

A

necrosis of myocardial cells

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23
Q

What does transmural MI mean?

A

full thickness

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24
Q

What are acute coronary syndromes usually due to?

A

plaque rupture

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25
What are the 2 types of plaques?
stable vulnerable
26
Describe a stable plaque
thick fibrous cap, small lipid pool
27
Describe a vulnerable plaque
thin fibrous cap, large lipid pool
28
What does plaque rupture cause?
exposes thrombogenic extracellular matrix and lipid core to circulation --> platelet aggregation and thrombus formation
29
What are the 2 types of ACS?
ST elevation (STEMI) Non-ST elevation (NSTEMI)
30
How can an ECG appear in a STEMI? (and how does it change over time)
Acute = ST elevation hours = ST elevation, reduced R wave, Q wave begins days 1-2 = T wave inversion, Q wave deeper days later = ST normalises, T wave inverted weeks later = ST + T normal, Q wave persists
31
How can an ECG appear in an NSTEMI? (and how does it change over time)
Acute = T wave inversion or ST depression weeks later = ST + T normal, no Q waves
32
Post MI complications
ACT RAPID Arrhythmias Congestive cardiac failure/cardiogenic shock Thromboembolism Rupture (ventricular free wall, septum, papillary muscle) Aneurysm Pericarditis Ischaemia Death/Dressler's syndrome main late complications = arrhythmias and heart failure
33
If there is partial occlusion of a coronary artery, what is this called?
NSTEMI
34
If there if complete occlusion of a coronary artery, what is this called?
STEMI
35
Symptomatic treatment for stable coronary artery disease
lifestyle drugs - antianginals, nitrates revascularisation (eg. PCI)
36
Prognostic benefit treatment for stable coronary artery disease
lifestyle (stop smoking) drugs - statins, aspirin, beta blockers, ACE inhibitors revascularisation eg. CABG
37
Define ischaemia
inadequate oxygen supply to myocardial tissue
38
What factors could affect supply of oxygen to myocardial tissue?
coronary stenosis anaemia lung problems
39
What factors could affect demand of oxygen supply to myocardial tissue?
tachycardia preload (venous return) afterload (BP) muscle mass (eg. hypertrophy, infarcted) muscle contractility
40
What investigations can be done to confirm angina?
exercise stress test (low sensitivity and specificity) MIBI CTCA (anatomical test) stress MRI dobutamine stress echo coronary angiogram CTCA (CT coronary angiogram) = first line for most patients
41
What is PCI?
percutaneous coronary intervention
42
Indications for PCI
stable angina: - limiting symptoms despite 2 anti-anginals ACS: - NSTEMI = urgent - STEMI = emergency treatment
43
Indications for CABG
'surgical disease': - left main stem - LM equivalent - proximal 3 vessel disease especially if: - left ventricular dysfunction - diabetes - complex disease (high risk score - syntax score)
44
NSTEMI drugs
dual antiplatelet (aspirin, ticagrelor) anticoagulant beta blocker statin long term = consider ACE-i/ARB
45
What would the troponin be in unstable angina?
near normal
46
If chest pain radiates to back, what needs to be ruled out?
aortic dissection - tenni ball sign seen on CT
47
What can PE cause a rise in?
troponin (due to right heart strain)
48
What other events can cause ST elevation (other than STEMI)?
brain events (eg. subarachnoid haemorrhage)
49
Modifiable biomedical risk factors for coronary heart disease
diabetes high blood cholesterol hypertension
50
Lifestyle/behavioural risk factors for coronary heart disease
smoking sedentary lifestyle obesity diet alcohol stress
51
Non-modifiable risk factors for coronary heart disease
family history gender ethnicity age
52
What family history increases risk of coronary heart disease
1st degree female relative under 65 1st degree male relative under 55 risk increases 1.5x if one relative risk increases 1.5-2x if more than one relative familial hypercholesterolaemia
53
Secondary prevention of coronary heart disease
anti-platelets (aspirin, clopidogrel, ticagrelor) beta-blockers statin ACE-i lifestyle modification psychosocial factors cardiac rehabilitation
54
Lifestyle modifications to reduce blood pressure
weight loss mediterranean diet reduced salt intake physical activity moderate alcohol
55
HDLs function
(high density lipoproteins) carry cholesterol away from arteries and back to liver, then excreted from the body
56
LDLs function
(low density lipoproteins) build up in the walls of the arteries to form thick, hard deposits that narrow the arteries and make them less flexible
57
Triglycerides function
main storage form of LDL
58
What lifestyle modifications can improve lipid profile?
diet aerobic exercise resistance training
59
What is obesity associated with?
raised BP raised LDL and triglycerides low HDL impaired glucose tolerance increased insulin resistance
60
Diet modifications to reduce coronary heart disease risk
pile on fruit and vegetables choose healthy fats pick seeds, nuts and legumes focus on fish and chicken over red meat add herbs and spices rather than salt
61
What is cardiac rehabilitation?
comprehensive, long-term programs involving medical evaluation, prescribed exercise, cardiac risk factor modification, education and counselling designed to limit physiologic and psychological effects of cardiac illness, reduce the risk for sudden death or re-infarction, control cardiac symptoms, reverse/stabilise atherosclerotic process and enhance vocational status of patients
62
6 core components of BACPR
health behaviour change and education lifestyle risk factor management psychosocial health medical risk management long-term strategies audit and evaluation
63
What is the heart manual?
home based exercise program trained facilitators inclusion/exclusion criteria principles of self-management: - gain understanding and acceptance of condition - pace themselves - set short, medium and long-term goals - promote realistic exercise and activity - self monitor progress and condition - maintain behaviour change - deal with setbacks
64
What types of fat should you eat?
MUFA/PUFA (monounsaturated/polyunsaturated fatty acids) reduce amounts of saturated fat eaten

Cardiovascular system (33 decks)

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