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ED Primary Exam > Week 11 Pathology - The Heart > Flashcards

Week 11 Pathology - The Heart Flashcards

1
Q

What are the three types of cardiomyopathy?

A
  1. Dilated cardiomyoptathy
  2. Hypertrophic cardiomyopathy
  3. Restrictive cardiomyopathy
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2
Q

What is the difference between primary and secondary cardiomyopathy?

A

Primary = confined to myocardium
Secondary = cardiac manifestation of systemic disease (i.e. sarcoidosis, chronic anaemia)

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3
Q

What is the epidemiology and causes of DCM?

A

20-50 years

Alcohol, genetic, peripartum, sarcoid, haemachromatosis, myocarditis, IHD, HTN

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4
Q

What is the mechanism of HF and morphology associated with DCM?

A

HFrEF, EF <40%
Dilated/floppy chambers with variable wall thickness, non specific histologic changes

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5
Q

What is the cause of HCM?

A

Genetic, disorder of sarcomeric proteins, Beta myosin heavy chain most commonly affected –> hypertrophy –> can cause ventricular outflow obstruction in 1/3 cases (where septum bulges and obstructs the aortic valve)

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6
Q

What is the mechanism of HF in HCM?

A

Impaired compliance of stiff/hypertrophied ventricle –> “diastolic dysfunction/HFpEF

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7
Q

What are the histological features of HCM?

A

Myocyte hypertrophy
Disorganised arrangement of myocytes
Interstitial fibrosis

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8
Q
A
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9
Q

What is the cause of restrictive cardiomyopathy?

A

Wall stiffness caused by myocardial deposition disease (amyloidosis, radiation induced fibrosis, idiopathic)

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10
Q
A
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11
Q
A
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12
Q

What are the 3 classifications of cardiomyopathy?

A

Dilated
Hypertrophic
Restrictive

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13
Q

What are the causes of DCM, and what is the mechanism of heart failure?

A

IHD, HTN, thyrotoxicosis, anaemia, alcohol, sarcoid

Systolic dysfunction, HFrEF, EF < 40%

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14
Q

What is the cause of HCM?

A

Sarcomeric protein dysfunction, most commonly Beta myosin heavy chain. Causes haphazard arrangement of myocytes and asymmetrical septal hypertrophy

Causes restrictive cardiomyopathy –> HFpEF

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15
Q

What are the complications of HCM?

A

Ischaemic: Angina, ACS in absence of CAD
Arrhythmic: AF, VT, Sudden cardiac death
Structural: CHF, mural thrombus, IE of mitral valve

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16
Q

What are the morphological and histological features of HCM?

A

Morph: asymmetric septal hypertrophy, decreased ventricular chamber size
Histo: hypertrophied myocytes, haphazard arrangement, interstitial fibrosis

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17
Q

What are the causes of restrictive cardiomyopathy?

A

Cardiac deposition disease –> amyloidosis, radiation induced, idiopathic –> causes stiff, poorly compliant muscle, HFpEF with diastolic dysfunction

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18
Q

What is the morphology of RCM?

A

Normal ventricular size, non dilated cavities, firm myocardium, but with dilated atria

19
Q

What is serous pericarditis?

A

Inflammatory exudate
Causes including viral, ARF, uraemia, SLE

20
Q

What is fibrinous pericarditis commonly caused by?

A

Dressler’s syndrome (post MI)

21
Q

What is suppurative pericarditis caused by?

A

Bacterial, parasitic, fungal

22
Q

What is Haemorrhagic pericarditis caused by?

A

Cardiac surgery, TB, malignancy

23
Q

What is constrictive pericarditis?

A

Restricted diastolic dysfunction due to pericardial effusion, commonly associated with post-suppurative or TB pericarditis

24
Q

What are the most common causes of secondary pericarditis?

A

MI, cardiac surgery, uraemia

25
Q

What is Beck’s Triad?

A
  1. Hypotension with narrow pulse pressure
  2. Distended neck veins
  3. Muffled heart sounds
26
Q

What is acute rheumatic fever?

A

Acute, immunologically mediated, multi system disease that occurs post Group A Haemolytic streptococcus infection (pharyngitis, skin)

27
Q

What is the pathogenesis?

A

Hypersensitivity reaction caused by antibodies that )(via incidence of molecular mimicry) mistake proteins in myocardium and cardiac valves for strep antigens (M proteins) –> injury mediated by complement, macrophages and T cells

28
Q

What eponymous term is pathognomonic for ARF?

A

Aschoff bodies –> aggregates of inflammatory cell in heart muscle

29
Q

What are the cardiac manifestations of ARF?

A

Pancarditis
Fibrinous pericardial exudate
Fibrinoid necrosis and fibrin deposition forming valvular vegetations, commonly mitral valve

30
Q

When does ARF present?

A

2-3 weeks post strep infection

31
Q

What is the most common presentation of ARF?

A

Fevers and migratory polyarthritis

32
Q

What is the biochemical inclusion criteria required for a diagnosis of ARF?

A

Serological evidence of previous GAS infection

33
Q

What mix of criteria are required for meeting threshold of diagnosis?

A

2 major OR 1 major and 2 minor

34
Q

What are the major elements of Jones criteria?

A
  1. Carditis (clinical or echo)
  2. Migratory polyarthritis or polyarthralgia
  3. Subcutaneous nodules
  4. Erythema marginatum
  5. Sydenham chorea
35
Q

What are the minor criteria for ARF?

A

Fever
Elevated inflammatory markers
Prolonged PR on ECG

36
Q

What is heart failure?

A

Inability of the heart to supply adequate blood flow to match metabolic demands of peripheral tissues/organs

37
Q

List common causes of heart failure?

A

CAD
IHD
Cardiomyopathy
Chronic HTN
Sepsis
Valvular disease

38
Q

What is the most common clinical classification of heart failure?

A

HFrEF
HFpEF

39
Q

What single change in terms of heart function triggers the compensatory mechanisms associated with heart failure?

A

Decreased stroke volume

40
Q

How does the Frank-Starling mechanism relate to heart failure compensation?

A

Decreased stroke volume –> decreased cardiac output.

Heart utilised Frank-Starling mechanism to increase cardiac output by increasing end-diastolic volume.

41
Q

What are compensatory neurohumoral changes in the setting of heart failure?

A

Activation of RAAS
Increased circulating catecholamines
Vasopressin/ADH
Natriuretic peptides

42
Q

How does heart failure lead to increased blood volume?

A
  1. Decreased renal perfusion –> increased renin secretion
  2. Decreased baroreceptor stretch –> ADH secretion
43
Q

How does increased blood volume cause problems in heart failure?

A

Reliance on increased volume to increase preload and therefore CO –> also increased afterload and venous pressures, leading to pulmonary and peripheral oedema.

ED Primary Exam (46 decks)

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