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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

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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
label the diagram of the coronary arteries (E)
done
26
right coronary artery arises from
anterior aortic sinus
27
right coronary artery supplies (2)
RV, inferior wall
28
left coronary artery arises from
aortic sinus
29
left coronary artery supplies
LAD ventricle walls, left circumflex LV and LA
30
if the infarction is in the inferior wall, i.e. right coronary artery the ECG changes will be in leads (3)
II, III, aVF
31
if the infarction is in the anterior wall, i.e. LAD artery, the ECG changes will be (2)
ST elevation, V1-V6
32
if the infarction is in the lateral wall, i.e. left circumflex artery the ECG changes will be in leads (3)
V5, V6, aVL
33
look at the diagrams that show where different wall infarctions will show in the ECF (F)
done
34
label the leads on the chest diagram (G)
done
35
look at the diagrams and explanations of the different types of MI (H)
done
36
drug treatments for MI (4)
anti-platelets, LMWH, statin, anti-ischaemic
37
anti-platelets used in MI
aspirin + one of clopidogrel, ticagrelor, prasugrel
38
why do we give anti-platelets in MI?
reduce risk of thrombus growing
39
why do we give LMWH in MI?
targets thrombus
40
why do we give statins in MI? (2)
reduce cholesterol, stabilise plaque
41
anti-ischaemics used in MI
beta-blockers, nitrates
42
why are beta-blockers (anti-ischaemics) used in MI??
decrease heart rate and stress on plaque
43
in STEMI we may also treat using (2)
PCI, thrombolysis
44
marker we use in MI
troponin
45
how sensitive is troponin?
sensitive to myocardium damage
46
how specific is troponin?
not specific for MI
47
why else could troponin be raised? (6)
PE, pulmonary hypertension, septicaemia, subarachnoid haemorrhage, AF, aortic stenosis
48
to diagnose an MI there must be what in troponin? (2)
20% rise or fall, few hours apart
49
troponin physiology (6 steps)
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
label the diagrams of actin and myosin (I)
done
51
myocardial wall rupture
damaged myocardium next to healthy, contracting myocardium can rupture
52
myocardial wall rupture prognosis
unsurvivable
53
myocardial rupture of inter-ventricular septum diagram (J)
done
54
myocardial rupture develops at the margin of the
necrotic and non-necrotic myocardium (hinge point)
55
myocardial rupture of the interventricular septum causes
left to right shunting
56
myocardial rupture of interventricular septum prognosis
very bad, ~100% mortality
57
the papillary muscles hold the
2 cusps of mitral valve
58
posteromedial papillary muscle is supplied by
posterior descending artery
59
anterolateral papillary muscle is supplied by
LAD, LCx
60
which papillary muscles ruptures more frequently?
posteromedial
61
presentation of ruptured papillary muscle (3)
acute hypotension, pulmonary oedema, holosystolic murmur
62
left venrticular dysfunction (2)
long term problem with LV, acute/chronic heart failure
63
left ventricular dysfunction symptoms (4)
SOB, peripheral oedema, orthopnoea, PND
64
fill in the table of new york heart classification classes (K)
done
65
left ventricular aneurysm
infarction of inferior cardiac wall, not ruptured but aneurysm formed
66
cardiac arrest
sudden stop in effective blood flow due to failure of heart to contract
67
treatment for cardiac arrest (3)
AICD, bradycardia, ventricular tachycardia
68
stable angina pain character (2)
central, tight
69
stable angina radiation (3)
arm, jaw, teeth
70
stable angina aggravating factors (1)
exercise
71
stable angina relieving factors (2)
rest, nitrates
72
stress testing (3)
exercise ECG, stress ECHO, myocardial perfusion scan
73
exercise ECG at rest in stable angina
normal
74
exercise ECG with exercise in stable angina
depression of ST segment below isoelectric line
75
stress ECHO (2 steps)
1. patient exercises whilst having US of heart | 2. if function worsens may be issue with circulation
76
myocardial perfusion scan (3 steps)
1. myocardium takes up radioactive tracer 2. at rest lots of uptake 3. on exercise there are gaps in orange
77
aucte coronary syndrome is caused by (3)
STEMI, NSTEMI, unstable angina
78
STEMI (2)
ST elevation MI, completely occluded vessel
79
STEMI treatment (2)
clot busting drug, PCI
80
NSTEMI (2)
no ST elevation, partial occlusion
81
fill in the flow chart of acute chest pain (L)
done

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

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