SP3: Pathology of Heart Diseases Flashcards
What is ischaemic heart disease
Spectrum of disorders resulting from an imbalance between myocardial need for oxygen and adequacy of supply
What are the causes of ischaemic heart disease
Caused by atheroma of the coronary arteries which narrows the lumen due to lipid build up
By vasculitides and arterial vasospasm
What is atheroma/atherosclerosis
The is a disease of large and medium sized arteries where there is a build up of lipid and formation of atheromatous plaques
Children = fatty streaks Adults = atheromatous plaques
What are the risk factors of ischaemic heart disease
- hypertension
- hyperlipidaemia
- smoking
- diabetes mellitus
- older age
- males
- familial predispositions
- obesity
- insufficient excercise
What is encrustation
When platelet thrombi over injured endothelium
What is imbibition
When there is low grade inflammation leading to increased plasma filtration which means lipids flow into the subendothelial layer and accumilates
Outline the stages of atherosclerosis
- Turbulence (eddies in blood flow) causes platelets to adhere and dislodge endothelial cells. This increased exposure causes low grade inflammation with oedema.
- The fluid builds up in the internal elastic lamina and ruptures the internal elastic lamina
- Platelets aggregate and smooth muscle cells from the tunica media migrate through breaks in the internal elastic lamina, proliferate and produce collagen
- Smooth muscle cells take up fat and store it as droplets
- Smooth muscle cells overloaded with fat burst and release fat droplets
- Macrophages take up the fat droplets by phagocytosis
- Collagen increases and cellularity decreases this reduces the elasticity of the blood vessel wall (forms a relatively acellular plaque abundant in collagen)
- The centre becomes necrotic and calcified and this is the atherosclerotic plaque (vessels from vasa forum grow into this calcified region)
- Plaque eventually ruptures - risk of massive thrombus formation due to collagen exposure and stimulation of coagulation factors
- Eddies downstream from a plaque stenosis causes platelet thrombus formation and growth causing occlusion of the lumen leaned to a HEART ATTACK
What are the clinical syndromes of IHD
- sudden death due to arrhythmias
- myocardial infarction
- angina
- chronic IHD
- cardiomegaly leads to heart failure due to accumulated myocardial damage
What is stable angina
Crushing central chest pain occurring after exercise relieved by vasodilators caused by low flow in coronary arteries
- may result in minor patchy fibrosis
- usually a stable plaque present
What is unstable angina
This has a sudden onset and increasing intensity which can also be unresponsive to drugs. It is associated with dynamic type 2 plaque; this could progress to MI or sudden death
What is an acute myocardial infarct
Heart attack resulting from acute thromboses due to plaque disruption and has the following patterns of infarction
- regional transmural
- regional subendocardial
- circumferential subendocardial
What causes a regional transmural infarct
Whole thickness of myocardium Type 2 plaque with thrombosis - most patients have arterial occlusion - flow can be re-established - persistent occlusion causes fatal outcome - STEMI
What is a regional subendocardial infarct
Inner third of the venticle, well defined area
Rapid lysis of occlusive thrombus
Significant collateral supply to outer ventricle
- NSTEMI
What is a circumferential subendocardial infarct
General uderperfusion due to moderate hypotension with vessel disease or severe hypotension and normal vessels
- severe anaemia can also contribute
What are the short term complications of MI
- Dysrhythmias/arhythmia (sudden death)
- Cardiogenic shock (cannot perfuse peripheral organs)
- Left ventricular failure
- Cardiac rupture - haemopericardium (blood in pericardial sac of heart)
- Septal rupture (IV communication impaired)
- Papillary muscle failure = incompetence of mitrial and tricuspid valves causing regurgitation
- Pericarditis
- Mural thrombosis
- Deep vein thrombosis
What are the long term complications of MI
- Left ventricular failure
- Aneurysm
- Dressler’s syndrome (late onset of autoimmune pericarditis presenting with chest pain)
- Recurrent infarction
- Sudden death/ arrhythmia
What is stenosis
Failure of valve to open fully preventing forward flow - this is due to chronic cusp abnormality
What is regurgitation
Failure of valve to close allowing backflow - this is due to abnormality of cusp or supporting structures; acute or chronic
What is infective endocarditis
Colonisation of heart valves by infectious agent
- requires bacteraemia/septicaemia - relevant in periodontitis because dental treatments causing injury to gums can allow bacteria to enter into bloodstream
- it is predisposed by immunosuppression
What increases the risk of infective endocarditis
Congential heart disease Rheumatic heart disease Artificial valves Floppy mitrial valve/calcified aortic valve Neutropenia Immunodeficiency Immunosupression IV drug abuse
What are the features of subacute IE
Has a background of valvular/congenital heart disease
- insidious onset (gradual)
- may recover with treatment (antibiotics)
- low virulence organisms (strep. viridian’s)
- vegetations are less bulky and inflammation is less destructive in the heart valves
What are the features of acute IE
This usually occurs with a previously normal healthy heart in the elderly and IVDUs
- virulent organisms (staph aureus, fungi)
- high mortality
- mitrial > aortic»_space; tricuspid
- bulky vegetations with severe necrotising inflammation
What are the cardiac complications with IE
valvular insufficiency valvular stenosis (not closing) myocardial abcess suppurative pericarditis dehiscence of artificial valve emboli to coronary arteries
What are the systemic embolic complications of IE to the left side of the heart
Affects the
- brain
- spleen
- kidneys
What are the systemic embolic complications of IE to the right side of the heart
Affects the
- lungs
- possibly with secondary abscess formation
What are the renal complications of IE
- embolic infarction
- embolic infection (secondary abscesses)
- focal glomerulonephritis (blood in urine)
- diffuse glomerulonephritis (blood in urine)
What is acute rheumatic fever
A recurrent inflammatory disease in childhood following pharyngeal infection by group A streptococcus
- immunologically mediated (host response)
- usually resolves but can lead to chronic valve disease
- small friable vegetations on valves
More common in underdeveloped countries
What are aschoff bodies
result from inflammation in the heart muscle and are characteristic of rheumatic heart disease; they have many T-lymphocytes, plasma cells, activated macrophages = mini-granulomas; this leads to fibrosis due to thickened valvular tissue
What are the symptoms of rheumatic fever
- fever
- migratory polyarthritis (in large joints)
- pancarditis
- subcutaneous nodules
- erythema marginatum = rash on trunk (upper arms and lips showing red marks)
- sydenhams chorea = (disorder of nervous systems causing rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles)
What is chronic rheumatic fever
10< years with acute
- caused by organisation of endocardial inflammation
- stenosis via fibrous scarring or calcification of valves with bridges between commissures
- regurgitation via fibrous scarring of chordae tendinae
What is a ventricular septal defect (and atrial)
When the left and right ventricles are connected by a hole (same for atrium)
Leads to shunts, obstruction or failure
Risk for infective endocarditis
Outline pathogenesis of ischaemic heart disease
- Encrustation = formation of platelet thrombi over injured endothelium
- Imbibition = low grade inflammation leading to increased plasma filtration thus lipid flows into the sub endothelial layer and accumulates
- Reaction to injury = increased permeability and smooth muscle accumulation
- Monoclonal hypothesis = smooth muscle cels are genetically transformed and undergo proliferation, differentiating into a plaque
What are the complications of atheroma formation
- Calcification
- Ulceration
- Fissuring
- Haemorrhage
- Thrombosis
- Aneurysm
What are the different types of atheromatous plaques
Type 1 = static
Type 2 = dynamic
Concentric
Eccentric
What happens when the following is the site of infarct:
Left main coronary artery
Massive anterolateral MI
What happens when the following is the site of infarct:
Left anterior descending
Anteroseptal MI
What happens when the following is the site of infarct:
Left circumflex
Lateral LV MI
What happens when the following is the site of infarct:
Right coronary artery
Posterior/Inferior MI
What macroscopic changes occur in ischaemic heart disease
6-12 hrs = unapparent 12-24 hrs = pallor > 24 hrs = defined yellow softened area 5-7 days = red rim > 7 days = scar tissue
What does the left main coronary artery branch into
- Left anterior descending (LAD) / Anterior inter ventricular artery (AIV)
- Left circumflex
What does the left anterior descending / anterior inter-ventricular artery supply
Anterior left ventricular wall
Anterior right ventricular wall
Anterior 2/3 inter ventricular septum
What does the left circumflex artery supply
Left atrium
Lateral walls of left ventricle
What does the right coronary artery branch into
- Posterior descending (PDA) / Posterior inter ventricular artery (PIV)
- Acute marginal branch
What does the posterior descending artery / posterior inter ventricular artery supply
Posterior ventricular walls
What does the acute marginal branch supply
Myocardium of the right side of heart
Two types of infective endocarditis
Acute and Subacute
Outline morphology of infective endocarditis
Friable, bulky, bacteria-laden vegetations
Single/ multiple upto several cm big
May perforate or erode leaflet
Outline pathology rheumatic heart disease
Small friable vegetations on valves (endocardium)
Aschoff bodies in myo- and pericardium
