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Block 13 - The Development of Cardiorespiratory Disease > ALS Lecture 9 - The Cardiac Consequences of Atheroma DONE > Flashcards

ALS Lecture 9 - The Cardiac Consequences of Atheroma DONE Flashcards

1
Q

what is the most serious thing caused by atheroma? (2)

A

ventricular fibrillation, sudden death

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2
Q

what percentage of patients who have an MI die before they get to hospital?

A

50%

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3
Q

look at the graphs on cardiovascular disease (A)

A

done

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4
Q

atheroma

A

nodular accumulation of degenerative material in the tunica intima of artery wall

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5
Q

what do atheromas consist of? (4)

A

macrophages, lipids, calcium, fibrous connective tissue

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6
Q

modifiable risk factors for developing heart disease (7)

A

smoking, diet, obesity, lipids, hypertension, stress, lack of exercise

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7
Q

non-modifiable risk factors for developing heart disease (4)

A

fh, age, gender, ethnicity

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8
Q

spectrum of coronary disease (1-5)

A
  1. asymptomatic
  2. unstable angina
  3. acute coronary syndrome
  4. heart failure
  5. sudden death
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9
Q

give the 5 steps of atherosclerosis development

A
  1. fatty streak forms
  2. fibrous cap forms over fat deposits
  3. inside cap becomes necrotic
  4. fibrous cap ruptures
  5. thrombus formation leads to arterial occlusion
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10
Q

label the diagram of sequences in progression of atherosclerosis (B)

A

done

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11
Q

common sites of atheromas (5)

A

aorta (especially abdominal), coronary, carotid, cerebral, leg arteries

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12
Q

look at the pictures of plaque rupture/fibrous tissue (C)

A

done

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13
Q

myocardial infarction (MI) occurs when

A

blood flow stops to part of heart, so lack of oxygen and muscle death

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14
Q

2 types of MI

A

full thickness (transmural), partial thickness (subendocardial)

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15
Q

full thickness MI involves the

A

entire thickness of LV wall

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16
Q

example of blocked artery that would cause a full thickness MI

A

left anterior descending (LAD) artery that supplies left heart

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17
Q

partial thickness MI involves

A

multi-focal necrosis of inner 1/3 to 1/2 of LV wall

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18
Q

partial thickness MI are caused by blocks of

A

smaller arteries

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19
Q

other 2 classifications of MI

A

STEMI, NSTEMI

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20
Q

MI causes (3)

A

occlusive intracoronary thrombus, vasospasm, emboli

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21
Q

MI pathophysiology steps (5)

A
  1. thrombus over atheroma blocks blood flow
  2. lack of O2 to myocytes
  3. adrenaline in blood so heart beats faster
  4. myocytes stop, rest of heart works harder
  5. myocyte walls break down, leak troponin
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22
Q

label the diagram of a normal 12 lead ECG (C)

A

done

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23
Q

with acute coronary syndromes, what are we interested in on ECG? (2)

A

ST elevation, deviation from isometric line

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24
Q

label the diagram of STEMI ECG (D)

A

done

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25
Q

label the diagram of the coronary arteries (E)

A

done

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26
Q

right coronary artery arises from

A

anterior aortic sinus

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27
Q

right coronary artery supplies (2)

A

RV, inferior wall

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28
Q

left coronary artery arises from

A

aortic sinus

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29
Q

left coronary artery supplies

A

LAD ventricle walls, left circumflex LV and LA

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30
Q

if the infarction is in the inferior wall, i.e. right coronary artery the ECG changes will be in leads (3)

A

II, III, aVF

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31
Q

if the infarction is in the anterior wall, i.e. LAD artery, the ECG changes will be (2)

A

ST elevation, V1-V6

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32
Q

if the infarction is in the lateral wall, i.e. left circumflex artery the ECG changes will be in leads (3)

A

V5, V6, aVL

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33
Q

look at the diagrams that show where different wall infarctions will show in the ECF (F)

A

done

34
Q

label the leads on the chest diagram (G)

A

done

35
Q

look at the diagrams and explanations of the different types of MI (H)

A

done

36
Q

drug treatments for MI (4)

A

anti-platelets, LMWH, statin, anti-ischaemic

37
Q

anti-platelets used in MI

A

aspirin + one of clopidogrel, ticagrelor, prasugrel

38
Q

why do we give anti-platelets in MI?

A

reduce risk of thrombus growing

39
Q

why do we give LMWH in MI?

A

targets thrombus

40
Q

why do we give statins in MI? (2)

A

reduce cholesterol, stabilise plaque

41
Q

anti-ischaemics used in MI

A

beta-blockers, nitrates

42
Q

why are beta-blockers (anti-ischaemics) used in MI??

A

decrease heart rate and stress on plaque

43
Q

in STEMI we may also treat using (2)

A

PCI, thrombolysis

44
Q

marker we use in MI

A

troponin

45
Q

how sensitive is troponin?

A

sensitive to myocardium damage

46
Q

how specific is troponin?

A

not specific for MI

47
Q

why else could troponin be raised? (6)

A

PE, pulmonary hypertension, septicaemia, subarachnoid haemorrhage, AF, aortic stenosis

48
Q

to diagnose an MI there must be what in troponin? (2)

A

20% rise or fall, few hours apart

49
Q

troponin physiology (6 steps)

A
  1. attached to tropomyosin
  2. when muscle cell stimulated, calcium attaches to troponin
  3. troponin causes tropomyosin to move from binding site
  4. exposes myosin binding sites on actin filaments
  5. myosin binds to actin
  6. cross-bridge formation and muscle contraction
50
Q

label the diagrams of actin and myosin (I)

A

done

51
Q

myocardial wall rupture

A

damaged myocardium next to healthy, contracting myocardium can rupture

52
Q

myocardial wall rupture prognosis

A

unsurvivable

53
Q

myocardial rupture of inter-ventricular septum diagram (J)

A

done

54
Q

myocardial rupture develops at the margin of the

A

necrotic and non-necrotic myocardium (hinge point)

55
Q

myocardial rupture of the interventricular septum causes

A

left to right shunting

56
Q

myocardial rupture of interventricular septum prognosis

A

very bad, ~100% mortality

57
Q

the papillary muscles hold the

A

2 cusps of mitral valve

58
Q

posteromedial papillary muscle is supplied by

A

posterior descending artery

59
Q

anterolateral papillary muscle is supplied by

A

LAD, LCx

60
Q

which papillary muscles ruptures more frequently?

A

posteromedial

61
Q

presentation of ruptured papillary muscle (3)

A

acute hypotension, pulmonary oedema, holosystolic murmur

62
Q

left venrticular dysfunction (2)

A

long term problem with LV, acute/chronic heart failure

63
Q

left ventricular dysfunction symptoms (4)

A

SOB, peripheral oedema, orthopnoea, PND

64
Q

fill in the table of new york heart classification classes (K)

A

done

65
Q

left ventricular aneurysm

A

infarction of inferior cardiac wall, not ruptured but aneurysm formed

66
Q

cardiac arrest

A

sudden stop in effective blood flow due to failure of heart to contract

67
Q

treatment for cardiac arrest (3)

A

AICD, bradycardia, ventricular tachycardia

68
Q

stable angina pain character (2)

A

central, tight

69
Q

stable angina radiation (3)

A

arm, jaw, teeth

70
Q

stable angina aggravating factors (1)

A

exercise

71
Q

stable angina relieving factors (2)

A

rest, nitrates

72
Q

stress testing (3)

A

exercise ECG, stress ECHO, myocardial perfusion scan

73
Q

exercise ECG at rest in stable angina

A

normal

74
Q

exercise ECG with exercise in stable angina

A

depression of ST segment below isoelectric line

75
Q

stress ECHO (2 steps)

A
  1. patient exercises whilst having US of heart

2. if function worsens may be issue with circulation

76
Q

myocardial perfusion scan (3 steps)

A
  1. myocardium takes up radioactive tracer
  2. at rest lots of uptake
  3. on exercise there are gaps in orange
77
Q

aucte coronary syndrome is caused by (3)

A

STEMI, NSTEMI, unstable angina

78
Q

STEMI (2)

A

ST elevation MI, completely occluded vessel

79
Q

STEMI treatment (2)

A

clot busting drug, PCI

80
Q

NSTEMI (2)

A

no ST elevation, partial occlusion

81
Q

fill in the flow chart of acute chest pain (L)

A

done

Block 13 - The Development of Cardiorespiratory Disease (14 decks)

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