Pathology - Cardiac Flashcards
What are the major causes of heart failure
Ischaemic heart disease Valvular heart disease HTN Cardiomyopathy Fluid overload
What pathological processes occur in the myocardium and liver in heart failure
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
What is heart failure and what are the types
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
What are the clinical feature of heart disease
- 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
What is an acute coronary syndrome
clinical manifestation of IHD, and can represent unstable angina, acute MI or sudden cardiac death
What is the pathogenesis of myocardial infarction due to atherosclerosis
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
Describe the time course post myocardial infarction
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)
What are the consequences of re-perfusion post myocardial infarction
- 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
What are the complications of acute myocardial infarction
contractile dysfunction leading to cardiogenic shock
arrhythmia
thromboembolism
wall/papillary muscle rupture
What changes occur in ventricular remodelling post myocardial infarction
hypertrophy and dilatation
may lead to aneurysm and arrhythmia
What are the main cardiac rupture syndromes post myocardial infarction
free wall rupture leading to tamponade
septum rupture leading to VSD and left to right shunt
papillary muscle rupture leading to severe mitral regurgitation
What systemic features affect infarct healing
nutrition (protein, vitamin c)
metabolic (diabetes)
circulatory (arterial or venous)
hormonal (glucocorticoids)
What are the causes and clinical consequences of aortic stenosis
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
What are the complications of a congenital bicuspid aortic valve
calcification stenosis regurgitation infective endocarditis aortic dilatation dissection
What factors predispose to endocarditis, what organisms cause endocarditis and what are the complications
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
What is cardiomyopathy, what are the types and give a cause for each (what type is alcohol related)
- 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
What are the potential pathological consequences of dilated cardiomyopathy
valve dysfunction
mural thrombi and embolization
arrhythmia
death
What are the causes of acquired cardiomyopathy
infection (viral, bacterial, fungal) metabolic (hyperthyroidism, nutritional) infiltrative (sarcoid) immune (autoimmune myocarditis) drugs/toxins (alcohol, chemotherapy) ischaemia hypertensive valvular
How does dilated and hypertrophic cardiomyopathy differ
- dilated: poor LVEF <40%, impaired contractility (systolic dysfunction)
- hypertrophic: normal LVEF 50-80%, impaired compliance (diastolic dysfunction)
What are the characteristics and complications of hypertrophic cardiomyopathy
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
Describe the clinical features and causes of pericarditis
features: pleuritic chest pain, pericardial friction rub, muffled heart sounds, elevated JVP, peripheral edema
causes: post MI, uraemia, infection (viral, bacterial, fungal), trauma, malignant
What types of pericardial fluid exudate occur
- 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
What is cor pulmonale, causes and morphological features
- 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
