Histopath - Cardio Flashcards

1
Q

Causes of death after MI

A

Arrythmia –> cardiac arrest
Cardiogenic shock
Rupture

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2
Q

Causes of LV hypertrophy

A

HTN
Aortic stenosis
Ischaemia may contribute

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3
Q

ECG lead & corresponding vessels

A

II, III, aVF = right coronary artery (inferior)

V1 - V4 = left anterior descending (anterior)

1, V5, V6 = circumflex (lateral)

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4
Q

Diagnostic criteria for STEMI

A

> 2mm ST elevation in 2 leads?

>1mm ST elevation in 2 consecutive chest leads

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5
Q

Blockage of which cardiac vessel is more likely to cause arrhythmia?

A

Right coronary (vs LAD)

Supplies SA & AV nodes

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6
Q

ECG evidence of old MI

A

Deep Q waves

T wave inversion?

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7
Q

RF for atherosclerosis

A
Family Hx - most significant independent RF
Age
Sex - male
Hyperlipidaemia
HTN
Smoking
DM
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7
Q

RF for atherosclerosis

A
Family Hx - most significant independent RF
Age
Sex - male
Hyperlipidaemia
HTN
Smoking
DM
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8
Q

How do risk factors interact in atherosclerosis

A

Multiplicative effect

2 RF = 4 fold increased risk
3 RF = 7 fold

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9
Q

Pathogenesis of atherosclerosis - process

A

Endothelial damage

Lipoprotein accumulation (LDL)

Monocyte adhesion to endothelium + migration into intima

Monocytes –> macrophages + foam cells (ingest fat)

Platelet adhesion

Release of various pro-inflammatory factors

Smooth muscle cell recruitment –> endothelial proliferation

Lipid accumulation - extracellular + intracellular

Atheroma

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10
Q

Earliest atherosclerotic lesion seen

A

Fatty streaks - lipid filled foam cells / macrophages

present in virtually all children >10yo

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11
Q

Macroscopic features of atherosclerotic plaque

A

Raised lesion
Soft lipid core
White fibrous cap
Appear eccentric

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12
Q

Critical stenosis threshold

A

~70% occlusion OR (lumen) diameter <1mm

When demand > supply

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13
Q

Forms of acute atherosclerotic plaque change

A

Rupture - exposes pro-thrombogenic contents

Erosion - exposed pro-thrombogenic sub endothelial basement membrane

Haemorrhage into plaque - increases size

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14
Q

Criteria for increased risk of atherosclerotic plaque rupture

A

Lots of foam cells or extracellular lipid

Thin fibrous cap

Few smooth muscle cells

Clusters of inflammatory cells

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15
Q

Pathogenesis of ischaemic heart disease

A

Insufficient coronary perfusion
(imbalance of supply vs demand for oxygenated blood)

+ less removal of waste –> less well tolerated than pure hypoxia

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16
Q

Plaque distribution in IHD

A

First few cm of LAD or LCX

or entire length of RCA

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17
Q

Threshold for pain at rest

A

90% stenosis

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18
Q

Definition of angina pectoris

A

Transient ischaemia NOT resulting in myocyte necrosis

19
Q

Definition of myocardial infarction

A

Death of cardiac muscle due to prolonged ischaemia

20
Q

Timing of MI reversibility

A

Irreversible after 20-30 mins

21
Q

Most common MI locations

A

LAD - 50%, anterior wall of left ventricle, anterior septum, apex

RCA - 40%, posterior wall of left ventricle, posterior septum, posterior right ventricle

LCX - 20%, lateral left ventricle (not apex)

22
Q

Timeline of MI changes

A

<6h = none

6-24h = Macro: none. Micro: loss of nuclei, homogenous cytoplasm, necrotic cell death.

24h = Macro: pale, oedema. Micro: oedema, inflammation (neutrophils)

3-4 days = Macro: haemorrhage. Micro: coagulative necrosis, granulation, infiltration of polymorphs THEN macrophages

1-3 weeks = Macro: thin, yellow. Micro: granulation tissue, new vessels, myofibroblasts, collagen synthesis.

> 3-6 weeks = Macro: tough white. Micro: dense fibrosis, decellularising scar

23
Q

Mechanism of re-perfusion injury

A

Oxidative stress + Ca overload + inflammation

Arrhythmias common

24
Q

Macroscopic features of chronic IHD

A

Enlarged, heavy heart

Hypertrophied, dilated LV

Atherosclerosis

+/- mural thrombi

25
Q

Microscopic feature of chronic IHD

A

Fibrosis

26
Q

Definition of sudden cardiac death

A

Unexpected death from cardiac cause in individuals without symptomatic heart disease OR early (1 hr) after onset of Sx

27
Q

Most common cause of sudden cardiac death

A

Lethal arrhythmia

Acute MI –> electrical instability at site distant from conduction system

28
Q

Macroscopic features of cardiac failure

A

Dilated heart

Scarring/thinning of walls

29
Q

Microscopic features of cardiac failure

A

Fibrosis

Replacement of ventricular myocardium

30
Q

Causes of dilated cardiomyopathy

A

Idiopathic

Infection - viral myocarditis

Toxic - EtOH, chemotherapy, cobalt, iron

Hormonal - hyper/hypothyroid, diabetes, peri-partum?

Genetic - haemochromatosis, Fabry’s, McArdle’s

Immuno - myocarditis

31
Q

Causes of hypertrophic cardiomyopathy

A

Familial in 50% - autosomal dominant, variable penetrance

Beta-myosin heavy chain?

32
Q

Causes of restrictive cardiomyopathy

A

Idiopathic

2ndary to myocardial disease - amyloid, sarcoid

33
Q

Order of valves affected by chronic rheumatic valve disease

A

Mitral > aortic > tricuspid > pulmonary

34
Q

Most common cause of aortic stenosis

A

Calcified aortic stenosis

Affects 70-80yo
Calcium deposits in outflow side of cusp –> impaired opening

35
Q

Causes of aortic regurgitation

A

Rigidity - rheumatic disease, degenerative

Microbial endocarditis

Dilatation - valve insufficient to cover increased area e.g. Marfan’s, dissecting aneurysm, Ank Spond

36
Q

Duke’ criteria for IE

A

Major:

  • bacteraemia (2 cultures, 12 hours apart)
  • echo findings: vegetation

Minor:

  • Fever 38+
  • Echo findings (not meeting major criteria)
  • Vascular phenomenon: Embolisation, splinter haemorrhage, Janeway lesions
  • Immuno phenomenon: Osler’s nodes, Roth spots, GN, Rh factor
  • Microbiological: 1 culture +ve
  • Risk factor: IVDU, predisposing heart disease
37
Q

Interpretation of Duke’s criteria for IE

A

Diagnosed if:

2 major
OR 1 major + 3 minor
OR 5 minor

38
Q

Tx of IE

A

Strep viridans = Benzylpenicillin + gentamicin

MSSA = flucloxacillin

MRSA - Vancomycin

Prosthetic valve = vancomycin + gentamicin + rifampicin

39
Q

Features of Ventricular aneurysm

A

Post MI

ECG changes - ST elevation in V2-5

No chest pain, SOB or other Sx

40
Q

Most common cause of constrictive pericarditis in ‘developing’ world

A

Tuberculosis

41
Q

Effects of amyloidosis in the heart?

A

Restrictive cardiomyopathy

Arrhythmia

42
Q

Clinical features of heart failure

A

Left = pulmonary oedema, SOB

Right (cor pulmonale) = peripheral oedema

43
Q

Effect of mycobacteria in the heart

A

Calcifying pericarditis

44
Q

Takotsubo’s cardiomyopathy - key features

A

‘Broken heart syndrome’

Develops in response to intensive physical or emotional experience

ECG changes + apical akinesia + interventricular septum hypertrophy

Cardiac enzymes, CXR, percutaneous coronary intervention NAD.