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ACEM Viva > Pathology - Cardiac > Flashcards

Pathology - Cardiac Flashcards

1
Q

What are the major causes of heart failure

A 
Ischaemic heart disease
Valvular heart disease
HTN
Cardiomyopathy
Fluid overload
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2
Q

What pathological processes occur in the myocardium and liver in heart failure

A

Heart:
- infarction
- ischaemia of myocardium
- calcification
- interstitial fibrosis
- eccentric or concentric remodelling
- hypertrophy of cardiac myocytes

Liver:
- nutmeg liver (mottled appearance due to hepatic congestion)
- centrilobular necrosis
- centrilobular fibrosis

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3
Q

What is heart failure and what are the types

A

when cardiac function is impaired and the heart is unable to maintain sufficient cardiac output to meet needs

types:

1) Systolic dysfunction = deterioration of myocardial contractile function
- causes: ischaemia, pressure or volume overload, primary myocardial failure

2) Diastolic dysfunction = inability of heart to relax and fill during diastole
- causes: HTN, hypertrophy, amyloid, constrictive pericarditis

also divided into:
1) Left sided heart failure = due to systolic failure or diastolic dysfunction
- causes: IHD, HTN, aortic or mitral valve disease

2) Right sided heart failure
- causes: left sided heart failure, tricuspid or pulmonary valve disease

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4
Q

What are the clinical feature of heart disease

A
  • cardiac: 3rd heart sound, displaced apex beat, AF, murmur, elevated JVP
  • lung: SOB, orthopnea, APO, pleural effusions
  • renal: AKI, pedal edema
  • hepatic: engorgement, ascites, cirrhosis
  • brain: confusion secondary to hypoxia
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5
Q

What is an acute coronary syndrome

A

clinical manifestation of IHD, and can represent unstable angina, acute MI or sudden cardiac death

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6
Q

What is the pathogenesis of myocardial infarction due to atherosclerosis

A

1) acute plaque change: rupture, fissuring, erosion, ulceration, haemorrhage
2) thrombosis: platelet adhesion, aggregation and activation of coagulation pathways leading to thrombus
3) vasoconstriction: stimulated by platelet contents and other circulating mediators (adrenergic agonists)
4) vessel occlusion: leading to decreased myocardial blood flow and myocyte necrosis

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7
Q

Describe the time course post myocardial infarction

A

1) reversible
- onset of ATP depletion (seconds)
- loss of contractility (<2 minutes)
- ATP 50% of normal (10 minutes)
- ATP 10% of normal (40 minutes)

2) irreversible
- irreversible cell injury (30 minutes)
- microvascular injury (>1 hour)
- necrosis (complete within 6 hours)

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8
Q

What are the consequences of re-perfusion post myocardial infarction

A
  • may restore viability but leave cells poorly contractile (stunned) for 1-2 days
  • re-perfused cells are usually haemorrhagic due to ischaemic vascular injury
  • irreversibly injured cells that are re-perfused show contraction band necrosis
  • may cause additional injury by recruitment of inflammatory cells
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9
Q

What are the complications of acute myocardial infarction

A

contractile dysfunction leading to cardiogenic shock
arrhythmia
thromboembolism
wall/papillary muscle rupture

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10
Q

What changes occur in ventricular remodelling post myocardial infarction

A

hypertrophy and dilatation

may lead to aneurysm and arrhythmia

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11
Q

What are the main cardiac rupture syndromes post myocardial infarction

A

free wall rupture leading to tamponade
septum rupture leading to VSD and left to right shunt
papillary muscle rupture leading to severe mitral regurgitation

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12
Q

What systemic features affect infarct healing

A

nutrition (protein, vitamin c)
metabolic (diabetes)
circulatory (arterial or venous)
hormonal (glucocorticoids)

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13
Q

What are the causes and clinical consequences of aortic stenosis

A 
cause: 
degeneration
men > 70
HTN, hyperlipidaemia
inflammation (rheumatic fever)
congenital bicuspid valve

effect:
concentric left ventricular hypertrophy due to chronic pressure overload
myocardial ischaemia
syncope
intravascular haemopysis

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14
Q

What are the complications of a congenital bicuspid aortic valve

A 
calcification
stenosis
regurgitation
infective endocarditis
aortic dilatation
dissection
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15
Q

What factors predispose to endocarditis, what organisms cause endocarditis and what are the complications

A

predisposition:

  • cardiac factors = mitral valve prolapse, calcific aortic stenosis, bicuspid aortic valve, prosthetic valve
  • host factors = bacteraemia, dental procedure, IVDU, immunodeficiency, diabetes

causes: strep viridans (most common), staph epidermidis (prosthetic valve), staph aureus (IVDU), candida (fungal)

complications: injury to valve, emboli (spleen, kidney, brain), renal failure, nephrotic syndrome, splenic infarction

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16
Q

What is cardiomyopathy, what are the types and give a cause for each (what type is alcohol related)

A
  • group of diseases of the myocardium associated with cardiac dysfunction (mechanical or electrical)
  • primary cardiomyopathy is congenital or acquired
  • secondary cardiomyopathy have myocardial involvement as a component of a systemic disorder

1) dilated cardiomyopathy: most common, 4 chamber hypertrophy and dilation, systolic dysfunction
- causes: genetic links, alcohol, pregnancy, myocarditis

2) hypertrophic (obstructed) cardiomyopathy: heavy muscular poorly compliant heart, diastolic dysfunction
- causes: mostly genetic

3) restrictive cardiomyopathy: restrictive ventricular filling leading to decreased CO, diastolic dysfunction
- causes: amyloidosis, sarcoidosis, scleroderma

17
Q

What are the potential pathological consequences of dilated cardiomyopathy

A

valve dysfunction
mural thrombi and embolization
arrhythmia
death

18
Q

What are the causes of acquired cardiomyopathy

A 
infection (viral, bacterial, fungal)
metabolic (hyperthyroidism, nutritional)
infiltrative (sarcoid)
immune (autoimmune myocarditis)
drugs/toxins (alcohol, chemotherapy)
ischaemia
hypertensive
valvular
19
Q

How does dilated and hypertrophic cardiomyopathy differ

A
  • dilated: poor LVEF <40%, impaired contractility (systolic dysfunction)
  • hypertrophic: normal LVEF 50-80%, impaired compliance (diastolic dysfunction)
20
Q

What are the characteristics and complications of hypertrophic cardiomyopathy

A

characteristics: heavy, muscular, hypercontractile, poorly compliant heart, poor diastolic relaxation
hypertrophy without dilation, asymmetrical IV septum thickening, decreased LV outflow

complications: SOB, angina, syncope, MI, arrhythmia, endocarditis, death

21
Q

Describe the clinical features and causes of pericarditis

A

features: pleuritic chest pain, pericardial friction rub, muffled heart sounds, elevated JVP, peripheral edema
causes: post MI, uraemia, infection (viral, bacterial, fungal), trauma, malignant

22
Q

What types of pericardial fluid exudate occur

A
  • serous: non-bacterial, may be viral, uraemia or tumours
  • fibrinous/serofibrinous: most common and usually post MI
  • purulent: almost always bacterial
  • haemorrhagic: post trauma
  • caseous: usually Tb
23
Q

What is cor pulmonale, causes and morphological features

A
  • right sided heart failure that is not secondary to left sided heart failure
    causes: COPD, bronchiectasis, pulmonary embolism, primary pulmonary HTN

morphology:

  • pulmonary congestion is minimal but engorgement of systemic and portal veins may be pronounced
  • right ventricular hypertrophy and dilatation with leftward bulging of septum
  • congestive hepatomegaly, centrilobular necrosis, splenomegaly
  • pleural and pericardial effusions and subcutaneous edema

ACEM Viva (39 decks)

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