Cardiac Pathology

Outline the structure of the heart muscle

Atria, ventricles, muscle made up of myocardium (sensitive to low oxygen conditions/requires high demand of oxygen)

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Outline the progression of CVD

Risk factors, arteriosclerosis, coronary artery disease, ischaemia, plaque rupture and thrombosis, infarction, loss of contractibility, dilatation and remodelling, heart failure and end stage heart failure

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Outline features of circulation

Atherosclerosis (build up of plaques), stenosis, turbulent and laminar flow. Branching in vascular tree prone to clot formations (bifurcations)

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Describe features of atherosclerosis (1)

Fatty streaks in arteries, build up of cholesterol in lining of artery, narrow lumen of artery, plaque has lipid core, grows a fibrous cap (attempt to contain core), inflammatory problem (inflammatory cells invade plate)

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Describe features of atherosclerosis (2)

(platelet activation/thrombosis occurs due to rupture of plaque). Atherosclerosis can occur throughout vascular tree (range of issues - ischaemic limb/amputation, MI in coronary arteries)

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Describe features of atherosclerosis (3)

Changes in endothelial layer increases expression of molecules to allow monocyte/macrophage adhesion to endothelium. Migrate into internal layer of blood vessel (cytokines - caused by cholesterol build up), differentiate into macrophages

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Describe features of atherosclerosis (4)

Engulf cholesterol particles. Become very large cells with lipid droplets in cytoplasm. Become foam cells. If cells die by apoptosis, lipids can be released, large lipid core within plaque, smooth muscles can be activated by inflammation

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Describe features of atherosclerosis (5)

Differentiate into fibroblasts, migrate to internal layer/under endothelial layer, form fibrous caps (fibrous synthetic) for collagen. If endothelium is damaged/collagen exposed (platelet activation/thrombosis)

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Describe features of atherosclerosis (6)

Fibrous cap being damaged or thrombosis ruptured leads to formation of a clot downstream

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Describe features of cardiac myocyte-fibroblast interactions

Fibroblasts in between layers of cardiac myocyte. Homeostatic role - maintain extracellular matrix (gives heart structure/shape)

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What happens during a myocardial infarction? (1)

Myocytes damaged by lack of O2/ischaemia, terminally differentiated cells cannot regenerate, lose myocytes/muscle/function/contraction of cardiac muscle. Fibroblasts migrate into infarct (produce collagen/forms scar/stiff) - inflammatory response

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What happens during a myocardial infarction? (2)

Large areas of myocardium are akinetic. LV compromised. Not much change in diameter/thickness of ventricle during contraction (dilated/scar stretched/high pre-load/end diastolic volume increases). Work hard against preload. Heart failing.

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Describe features of calcification (1)

Elastin fibres in blood vessels calcified. Age dependent phenomenon. Artery becomes stiffer in older people (pulse pressure will be larger due to deposits of calcium in artery - graph). Veins are very compliant

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Describe features of calcification (2)

Can be independent to linked to atherosclerosis. Interconversion between cell types e.g. muscle to myofibroblasts (synthetic) or stem cells or osteoblasts (secrete Ca/phosphates) in vessel wall, deposits, stiffen artery

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Describe features of calcification (3)

Different types of calcification e.g. atherosclerotic (complete occlusion of lumen in vessel), on surface of endothelium, in vessel wall etc. Medial calcification (more stiff compared to artery, calcified in medial area)

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Describe features of the heart muscle structure

Myofilaments parallel in arrangement, densely packed mitochondria (high oxygen demand). Electromechanical conduction between myocytes, normal Ca regulation (E-C coupling)

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What is hypertrophic cardiomyopathy (form of heart failure)?

Disease of heart muscle, could be genetic cause, due to mutations in contractile proteins. Enlargement of heart muscle, structure disrupted, mitochondria more scattered/swollen, inefficient contraction, mitochondrial defect in generating ATP

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What is the main source of calcium for the contraction of cardiac muscle?

Calcium induced calcium release mechanism

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Describe features of hypertrophic remodelling (1)

In response to stretch/hypertension/genetics/release neurohormonal modulators (angiotension), activate signalling pathways, induction of hypertrophic gene programme, alter cell properties, induces hypertrophic growth (proteins change), hypertrophy

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Describe features of hypertrophic remodelling (2)

Increase in size of myocytes (in response to e.g. stress), cannot make more myocytes (terminally differentiated) to make bigger myocardium. Fibroblasts, produce collagen, increase density in intracellular matrix, compromises function of myocardium

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Describe features of hypertrophic remodelling (3)

Fibrosis occurs where there is cardiac myocyte drop out. Could get focal necrosis/fibrosis, results in deterioration of pump function

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Describe the different types of hypertrophy - physiological

e.g. exercise, increase demand for CO, heart gets bigger, pregnancy, additional circulation to support. It is reversible e.g. detrain. Change in length/width balanced, not linked to fibrosis. Ratio fibrosis/myocytes not different

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Describe the different types of hypertrophy - pathological

Thickening of ventricle muscle, reduction in size of ventricular cavity, myocyte width:length higher (thicker), pressure overload (increased afterload, thicker muscle, work harder)

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Describe the different types of hypertrophy - cardiac dilatation

Large increase in size of ventricular cavity, thinning of wall, myocyte length increases more than myocyte width. Extensive fibrosis. Irreversible (lead to heart failure). Can lead to decompensation (contractile function uncoupled from CO). MI

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What is concentric hypertrophy?

Thickening of muscle, reduction in size of cavity

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What is eccentric hypertrophy?

Increase in diameter of cavity in relation to wall thickness

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What are the common causes of cardiac hypertrophy?

High BP, pressure overload, heart valve stenosis (can be linked to calcification)

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Cardiac pathologies can affect which type of relationship?

Pressure volume relationship, PV loops

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Describe features of heart failure (1)

Right/left ventricle. Different types/classification (HFPEF or HFREF), heart failure to produce adequate CO. Increased CVP favours right atrial filling (and right ventricular filling)

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Describe features of heart failure (2)

Normally venous return is increased by CVP. In heart failure venous return is reduced by increased central venous pressure (blood in lower limbs). CVP takes value where venous return/right atrial filling are in balance

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Describe features of heart failure (3)

Central venous pressure is normally 3-7 mmHg. Often it is reported in cm H2O (6-10 cm). If CO fails, compensatory mechanisms may cause CVP to rise to favour ventricular filling and increase inotropy (Frank-Starling)

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Describe features of heart failure (4)

Can lead to a dilated heart and raised peripheral capillary pressure, can lead to oedema, nature of effects depend on which side of the heart e.g. pulmonary oedema due to right said

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What are the signs of heart failure?

SOB, coughing, increased jugular vein pressure distension, oedema of lower limbs, dilated left ventricle (Kerley lines caused by interstitial oedema)

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What is congestive heart failure associated with?

Large changes in blood flow to different organs, could get organ failure due to heart failure e.g. under perfusion of gut, kidney function, cold clammy skin/difficult to keep warm etc.

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Which factors are associated with chronic heart failure?

Fall in CO, fall in arterial pressure, long term increase in blood volume, increased central venous pressure, oedema, pulmonary congestion

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Describe features of axis deviations

Deviations of the axis can result from hypertrophy of part of the muscle from a physical displacement of the heat and from conduction defects but quite a wide range of deviations are consistent with a healthy heart (changes in ECG, defection in lead)

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Describe features of sinus arrhythmia (1)

Sinus rhythm but HR varies in cyclical pattern (increases/decreases), related to breathing cycle, affects filling volume and CO, frequency of HR. Progressive beat to beat change in R-R interval. Found more in young people (normal)

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Describe features of sinus arrhythmia (2)

Interaction between cardiovascular and respiratory control in brainstem is mediated by variation in parasympathetic drive

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What is AV block? (1)

Electrical impulses not getting into AV node in 1:1 ratio. Disease in AV node, not conducting properly, not conducting into ventricles. E.g. first degree AV block (change in distance between T wave - P wave/contraction of atria, QT interval increases

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What is AV block? (2)

Second degree AV block (no QTS interval, no ventricular depolarisation 2:1 ratio). Third degree AV block (3:1, 3 P waves for every ventricular contraction)

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Describe features of ventricular tachycardia and fibrillation

No CO, fatal (need to go back into sinus rhythm). VT (rapid series of depolarisation), abnormal ECG, VF (disorganised contraction of ventricles - lethal)

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What can lead to an electrical destabilisation of the heart? (1)

Hyperkalemia (K+ increase in plasma) - can present AP generation, heart could stop beating. (Nernst equation, equilibrium potential, depolarisation of Vm, no AP - lethal). depolarises myocytes/interferes with generation/propagation of AP

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What can lead to an electrical destabilisation of the heart? (2)

Hyperkalemia is a common problem for patients in hospitals. Also one of the three components of the lethal injection is KCl to induce hyperkalemia and stop the heart

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Cardiac Pathology

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