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Medicine Cardiovascular > Coronary Artery Disease > Flashcards

Coronary Artery Disease Flashcards

1
Q

Risk factors for atherosclerosis

A

Smoking, hypertension, hyperlipidaemia, diabetes, age, sex (male), genetics

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2
Q

Pathogenesis of atherosclerosis

A

Primary endothelial injury → accumulation of lipids and macrophages → migration of smooth muscle cells → increase in size

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3
Q

What do atheromas look like?

A

Pale, yellow, porridge like sludge in the artery walls

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4
Q

Earliest sign of accumulation of atheromatous plaques

A

Fatty streaks

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5
Q

Progression of atheromatous plaques

A

Fatty streaks, fibrofatty plaque, complicated plaque

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6
Q

When is atheromatous narrowing of an artery likely to produce critical disease? (3)

A
  • If it is the only artery supplying an organ or tissue
  • If the artery diameter is very small
  • Overall blood flow is reduced
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7
Q

Complications of atheroma (5)

A

Arterial stenosis, thrombosis, aneurysm, dissection, embolism

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8
Q

Aneurysm definition

A

Abnormal and persistent dilatation of an artery due to a weakness in its wall

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9
Q

Most common site for aneurysm

A

Abdominal aorta

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10
Q

Types of aneurysm

A

Mycotic, atherosclerotic, dissecting, congenital, arteriovenous, traumatic, syphilitic

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11
Q

Complications of aneurysm

A

Rupture, thrombosis, embolism, pressure erosion of adjacent structures, infection

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12
Q

Dissection definition

A

Splitting within the media by flowing blood (artery splits in 2 with normal in the middle and another lumen all the way round)

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13
Q

Risk factors for and associations with dissection

A

Middle age +/- atheroma

Atheroma, hypertension, trauma, coarctation, marfan’s, pregnancy

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14
Q

Usual targets for embolism

A

Cerebral infarct, renal infarct and renal failure, lower limb infarction

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15
Q

Clinical effects of cardiac ischaemia

A

Reduced exercise intolerance, angina (stable and unstable), myocardial infarction, cardiac failure

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16
Q

What does cardiac fibrosis result from?

A

Loss of cardiac myocytes and replacement by fibrous tissue

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17
Q

Complications of arterial stenosis in the carotid artery

A

TIA, stroke, vascular dementia

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18
Q

Complications of arterial stenosis in the renal arteries

A

Hypertension and renal failure

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19
Q

Complications of arterial stenosis in the peripheral arteries

A

Claudication and foot/leg ischaemia

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20
Q

Clinical effects of thrombosis

A

MI, cerebral infarction, renal infarction, intestinal infarction

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21
Q

Chronic stable angina

A

Fixed stenosis within a coronary artery. There is demand led ischaemia, it is predictable and causes safe symptoms. Patients advised to stop, rest, and use GTN spray

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22
Q

Cardiac chest pain

A

Nature of heavy feeling, weight on the chest, pressure, tightness. Centre of the chest radiating into the jaw and into the left arm.

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23
Q

Continuum of acute coronary syndrome

A

Asymptomatic → stable angina → unstable angina → acute non STEMI and non-Q wave, sub-endocardial MI → STEMI and AMI Q wave MI

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24
Q

What is the hallmark of coronary syndromes

A

Going from stable to unstable

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25
Q

Factors affecting plaque rupture/fissure

A

Lipid content of plaque, thickness of fibrous cap, sudden changes in intraluminal pressure or tone, bending and twisting of an artery during each heart contraction, plaque shape, mechanical injury

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26
Q

3 steps in the platelet cascade

A

Initiation, adhesion, activation

27
Q

What happens in the initiation stage of the platelet cascade?

A

Vascular damage causes exposed tissue elements, including subendothelial collagen

28
Q

What happens in the adhesion stage of the platelet cascade?

A

Platelet recruitment and adhesion at the site of injury forming a monolayer

29
Q

What happens in the activation stage of the platelet cascade?

A

There is a release of activators through degranulation (e.g. ADP), which bind to surface receptors, affecting circulating platelets. Platelet activation accelerates and results in platelet aggregation. Activation of platelets also triggers the inflammatory cascade and an organised fibrin-rich thrombus forms

30
Q

ECG changes in acute STEMI

A

≥ 1mm ST elevation in 2 adjacent limb leads or ≥ 2mm ST elevation in at least 2 continuous precordial leads, T wave inversion sometimes, Q waves sometimes

31
Q

Evolving ECG changes of acute MI

A

ST elevation – first few hours
Q wave formation and T wave inversion – first day
Q waves +/- inverted T waves – ‘old MI’

32
Q

Protein marker used in MI

A

Troponin - highly specific for cardiac muscle damage

33
Q

Differentiation of angina attack vs acute MI:

  • Duration
  • Onset
  • Severity
  • GTN
  • Associated symptoms
A
  • Duration - angina = 10 mins, MI = 30 mins or longer
  • Onset - angina = on exertion, MI = at rest
  • Severity - angina = usual pain, MI = severe
  • GTN - angina = relief, MI = no effect
  • Symptoms - angina = usually none, MI = sweating, nausea and vomiting
34
Q

Early treatment in STEMI

A 
M - morphine (with anti-emetic)
O - oxygen if hypoxic
N - nitrates
A - aspirin (300mg and chewed to increase surface area)
T - ticagrelor or clopidogrel
35
Q

Indications for reperfusion therapy (thrombolysis or PCI)

A

Chest pain suggestive of MI that has been going on for > 20 mins but <12 hours, ECG changes relating to MI, no contraindications

36
Q

Risks of thrombolysis therapy

A

Failure to reperfuse, haemorrhage, hypersensitivity

37
Q

When is PCI used to treat MI

A

Better to treat MI but must be given within 120 minutes

38
Q

Complications of acute MI

A 
D - death
A - arrhythmia 
R - rupture
T - tamponade
H - heart failure
V - valve disease
A - aneurysm of ventricle
D - Dressler's syndrome/depression
E - embolism
R - mitral regurgitation
39
Q

Non ST elevated myocardial infarction

A

Unstable coronary syndrome caused by dynamic narrowing of the artery

40
Q

Pathogenic trigger for NSTEMI

A

Spontaneous platelet rupture

41
Q

Score for identifying high risk patients suffering from NSTEMI

A

GRACE score

42
Q

Coronary revascularisation technique

A

Advance a guidewire past the blockage, the balloon is passed over and is inflated which breaks up the plaques, the stent is embedded into the vessel wall and this plasters down the plaque and increases blood supply and makes stasis and clotting less likely.

43
Q

Troponin-itis

A

A condition leading to a misdiagnosis of acute coronary syndrome based only on a troponin elevation

44
Q

Conditions other than MI where troponin is elevated

A

Heart failure, hypertensive crisis, renal failure, PE, sepsis, stroke, pericarditis, post arrhythmia

45
Q

Factors relating to type II myocardial infarction

A

Secondary to ischaemic imbalance, increased myocardial oxygen demand, decreased myocardial oxygen/blood flow

46
Q

Type I vs type II MI:

  • Chest pain
  • ECG changes
  • Cause
  • Troponin
  • Coronary artery disease
A
  • Chest pain - Type I = sudden symptoms, Type II = less chest pain
  • ECG changes - Type I = major ECG changes, Type II = minor ECG changes
  • Cause - Type I = no obvious cause, Type II = tachycardia/low BP/illness
  • Troponin - Type 1 = higher trop with rise then fall, Type II = smaller more static trop
  • CAD - Type I = severe CAD, Type II = mild to moderate CAD
47
Q

Conditions associated with non-ischaemic myocardial injury with necrosis

A

Cardiac contusion, ablation, pacing, AICD shocks, myocarditis, cardiotoxic chemotherapy, severe sepsis or respiratory failure, PE, pulmonary hypertension, chronic severe heart failure, chronic renal failure, severe acute neurological diseases e.g. stroke, exercise, burns, stress cardiomyopathy

48
Q

Secondary prevention for MI

A

Healthy lifestyle, smoking cessation, good control of BP, cholesterol and diabetes

49
Q

4 phases of cardiac rehab

A

Phase 1 = inpatient
Phase 2 = early post discharge period
Phase 3 = structured exercise programme
Phase 4 = long-term maintenance of physical activity and lifestyle change

50
Q

Drugs given in the Cath lab to treat MI

A

Heparin intra-arterially, atropine if bradycardic, adrenaline if things not going right, nitrate, verapamil, group IIb/IIIa inhibitors

51
Q

Why is heparin given in the Cath lab?

A

To prevent clots from forming around the equipment

52
Q

Dose of heparin given in Cath lab

A

100mg/kg

53
Q

Why are nitrates given in the Cath lab?

A

To vasodilate the arteries, and radially to prevent spasm of radial artery

54
Q

Why is verapamil given in the Cath lab?

A

Causes relaxation of the radial artery to prevent spasm

55
Q

Drug treatment in thrombolysis

A

Tenecteplase (usually used), alteplase, reteplase, aspirin and clopidogrel, exoxaparin

56
Q

Absolute contraindications for thrombolysis

A

Previous intracranial haemorrhage or unknown stroke, ischaemic stroke <6 months, CNS damage, arteriovenous malformation, major trauma/head injury/surgery

57
Q

Relative contraindications for thrombolysis

A

TIA <6 months, oral anticoagulant therapy, pregnancy or 1 week postpartum, refractory hypertension, advanced liver disease, infective endocarditis, active peptic ulcer, prolonged or traumatic resuscitation

58
Q

Risks for hazards in thrombolysis

A

Female, advanced age, lower weight, previous cerebrovascular disease, systolic and diastolic hypertension

59
Q

Immediate management of NSTEMI

A

Morphine + anti-emetic, oxygen , nitrates, aspirin

60
Q

Drugs given on admission with NSTEMI

A

Ticagrelor/clopidogrel, beta blocker if haemodynamically unstable, fondaparinux

61
Q

Medications on discharge for people suffered MI

A

Aspirin, clopidogrel/ticagrelor/prasugrel, bisoprolol, ramipril or ACE inhibitor, eplerenone, statin (usually atorvastatin)

62
Q

Risks with prescribing aspirin

A

Can cause stomach ulcers, people are allergic

63
Q

Side effect of ticagrelor

A

Dyspnoea

64
Q

When is prasugrel contraindicated?

A

Previous stroke/TIA, not recommended in >75 years or low weight

Medicine Cardiovascular (24 decks)

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