histo cardio Flashcards
atherosclerosis definition
an srteriosclerosis characterised by atheromatous deposits and fibrosis in the inner lining of arteries tunica intima but protrude into vessel lumen
stages of atherosclerosis
- damage to endothelium 2. platelet deposition on damaged tissue 3. endothelial proliferation 4. fibrous cap 5. cholesterol deposits in core 6. plaque enlarges blocking artery
macroscopic description of a atherosclerotic plaque
raised lesion lipid core white fibrous cap
major RF for atherosclerosis
age gender genetics HTN hyperlipidaemia DM smoking
how does multiplicitive effect in atheroclerosis work
2RF- 4x risk 3RF-7x risk
murmer in mitral prolapse
late systolic murmer and mid systolic click
most significant independent RF in atherosclerosis
genetics
how does DM increase atherosclerosis risk
induces hypercholesterolaemia
injury hypothesis of atherosclerosis
Endothelial injury Lipoprotien accumulation (LDL) Monocyte adhesion to endothelium Monocyte migration into intima -> macrophages & foam cells Platelet adhesion Factor release Smooth muscle cell recruitment Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells chronic inflammation and atherosclerosis e.g. metabolic stress
two complications of atheromatous plaque
rupture obstruction
at what point does stenosis cause symptoms
70% occlusion causes stable angina
changes seen in acute plaque change
erosion haemmorhage rupture
effect of a haemmorage into atheroscerotic plaque
increase in plaque size
effect of atherosclerotic plaque rupture
exposure of prothrombotic plaque contents
effect of atherosclerotic plaque erosiion
exposure of prothrombotic sub-endothelial basement membrane
characteristics of a avulnerable atherosclerotic plaque
thin cap many foam cells few smooth muscle cells many inflammatory cell clusters
how does vasoconstriction increase risk of plaque rupture
smaller lumen so greater local mechanical forces
factors increasing risk of plaque rupture by vasoconstriction
adrenergic agonists reduced endothelial relaxins platelet contents
what causes prinzmetal angina
coronary artery vasospasm
what is seen in the first 6 hours after an MI
no histological change
what is seen between 6 and 24 hours after MI
loss of nuclei homogeneous cytoplasm necrosis
what is seen 1-4 days after MI
invasion of polymorphs then macropahges
what is seen 5-10 days post MI
clearing up debris
what is seen 1-2 weeks post MI
granulation tissue restructuring new blood vessels, collagen synthesis
what is seen weeks and months after MI
decellularising the scar strengthening tissue
when may ST changes not be seen on ECG in an MI
subendocardial infarct
what happens in reperfusion injury
arrythmia
what causes reperfusion injury
ca overload oxiadative stress and inflammation
what is hibernating myocardium
chronic sub threshold ischaemia lower rate of metabolism in myocytes
how to reverse hibernating myocardium
revascularisation
complications of MI
Pericarditis (Dressler’s syndrome) mural thrombosis infarct expansion RV infarction ventricular aneurysm papilliary muscle rupture
definition of sudden cardiac death
“Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1hr) after onset of symptoms
symptoms of left sided heart failure
SOB pulmonary oedema
symptoms of right sided heart failure
peripheral oedema
CAUSES of heart failure
Ischaemic heart disease Valve disease Hypertension Myocarditis Cardiomyopathy Left sided heart failure (Right)
complications of heart failure
pulmonary emboli arrythmia sudden death
macroscopic findings of heart failure
dilated heart scarring and thinning of walls
microscopic findings of heart failure
fibrosis and replacment of ventricular myocardium
three types of cardiomyopathy
restrictive dilated hypertrophic
toxin driven causes of DCM
toxins: alcohol, iron, cobalt, chemo
infective causes of DCM
infection: viral myocarditis i
immunological causes of DCM
mmunological: myocarditis
hormonal causes of DCM
hormonal: diabetes, hyper/ hypothyroidism post partum
genetic causes of DCM
genetic Fabry’s, McArdles, haemochromotosis
pathology in HOCM
beta myosin heavy chain defect
inheritance of HOCM
autosomal dominant
consequences of HOCM
thickening of septum narrow left ventricular outflow
macroscopic findings on restrictive cardiomayopathy
large atria
causes of restrictive cardiomyopathy
secondary to myocardial disease such as amyloidosis or sarcoid
pathology of restrictive cardiomyopathy
reduced ventricular compliance
valves commonly affected by valvular disease
M>A>T>P
pathology of valvular disease
secondary to rheumatic fever thickening of valve leaflets fusuion of commisures
causes of aortic regurgitation
rigidity: rheumatic disease, degeneration destruction: microbial endocarditis marfan’s syphilitic aortitis ank spond dissecting aneurusm
difference between a true and false aneurysm
true aneurysm: involves all layer of vessel wall false: extravascular haematoma
causes of aneurysm
marfans atherosclerosis HTN
causes of DCM
idiopathic alcohol, peripartum sarcoidosis, amyloidosis
how does DCM cause heart failure
systolic dysfunction
how does hypertrophic cardiac myopathy cause heart failure
diastolic dysfunction
how does restrictive cardiomyopathy cause heart failure
diastolic dysfunction
causes of restrictive cardiomyopathy
amyloidosism sarcoidosis, radiation induced fibrosis
genetic defect in HCM
autosomal dominant inheritance of mutated betaMHC gene 403arg-glycine
histological appearance of HCM
myocyte disarray
mutations in HCM
bMHC troponin T (Sudden death) MYBP-C
what is ARVC
arrythmyogenic righ ventricular cardiomyopathy replacement of myocytes with fibrofatty tissue in the right ventricle
organism responsible for acute rheumatic fever
group A beta haemolytic strep
symptoms of rheumatic fever
skin: erythema marginatum, subcutaneous nodules heart: endocarditis, myocarditis, pericarditis joint: arthritis, synovitis cns: encephalitis, sydenhams chorea
what are the major jones criteria for rheumatic heart disease
Carditis Arthritis Sydenham’s chorea Erythema marginatum Subcutaneous nodules
what are minor jones criteria for rheumatic heart disease
fever raised ESR/ CRP prolonged PR interval tachycardia migratory arthralgia malaise previous rheumatic fever
how to diagnoses rheumatic heart disease
group A beta haemolytic strep infection + 1 major criterion 1 major and 2 minor criteria
which valve does rheumatic heart disease tend to affect and what is the consequence
mitral valve and MR/ MS due to scarring
what valve is affected in 25% of cases of rheumatic heart disease
aortic
causes of aneurysm
marfans atherosclerosis HTN
causes of DCM
idiopathic alcohol, peripartum sarcoidosis, amyloidosis
how does DCM cause heart failure
systolic dysfunction
how does hypertrophic cardiac myopathy cause heart failure
diastolic dysfunction
how does restrictive cardiomyopathy cause heart failure
diastolic dysfunction
causes of restrictive cardiomyopathy
amyloidosism sarcoidosis, radiation induced fibrosis
genetic defect in HCM
autosomal dominant inheritance of mutated betaMHC gene 403arg-glycine
histological appearance of HCM
myocyte disarray
mutations in HCM
bMHC troponin T (Sudden death) MYBP-C
what is ARVC
arrythmyogenic righ ventricular cardiomyopathy replacement of myocytes with fibrofatty tissue in the right ventricle
organism responsible for acute rheumatic fever
group A beta haemolytic strep
symptoms of rheumatic fever
skin: erythema marginatum, subcutaneous nodules heart: endocarditis, myocarditis, pericarditis joint: arthritis, synovitis cns: encephalitis, sydenhams chorea
what are the major jones criteria for rheumatic heart disease
Carditis Arthritis Sydenham’s chorea Erythema marginatum Subcutaneous nodules
what are minor jones criteria for rheumatic heart disease
fever raised ESR/ CRP prolonged PR interval tachycardia migratory arthralgia malaise previous rheumatic fever
how to diagnoses rheumatic heart disease
group A beta haemolytic strep infection + 1 major criterion 1 major and 2 minor criteria
which valve does rheumatic heart disease tend to affect and what is the consequence
mitral valve and MR/ MS due to scarring
what valve is affected in 25% of cases of rheumatic heart disease
aortic
what is the eponymous name of the organism responsible for rheumatic heart disease
lancefield group A strep
what is the pathology of rheumatic heart disease
antigen mimcry, cell mediated immunity to strep antigens where antibodies cross react with myocardial antigens
3 histological findings of rheumatic heart disease
Aschoff bodies beady fibrous vegetations Anitschkov myocytes
what are aschoff bodies
small giant cell granulomas
what are anitschkov myocytes
regenerating myocytes
what is the term for the fibrous vegetations in rheumatic heart diease
verrucae
treatment of rheumatic heart disease
benzylpenicillin or erythromycin if allergic
appearance of verrucae of rheumatic heart disease
small warty vegetations along the lines of closure of the valve leaflet
pathology of infective endocarditis
colonisation of heart valve/ mural endocardium with microbe
appearance of infective endocarditis vegetations
large irregular mass on valve cusps that extends into the chordae
vegetations seen in non-bacterial thrombotic endocarditis
small bland vegetations formed of thrombi along the lines of closure
what is libman-sacks endocarditis associated with
SLE anti-phopholipid syndorme
appearance of libman sacks endocarditis vegetaions
sterile platelet rich vegetations up to 2mm
organisims causing acute infective endocarditis
staph aureaus strep pyogenes
organisms causing subacute infective endocarditis
strep viridans staph epidermis HACEK coxiella mycoplsma candida
HACEK organisms
gram negative bacteria haemophilus aggregatibacter cardiobacterium eikenella kingella
difference in location of masses between acute and subacute IE
acute: large masses on aorta subacute: small friable masses on chordae
features of IE
immune: oslers nodes, roth spots, haematuria due to glomerulonephritis thrombotic: janeway lesions, splinter haemmorgages, splenomegaly, microemboli and septic abscesses
which valves are affected in IE
mitral/ aortic unless IVDU when RHS valves
criteria for IE
Dukes criteria
major dukes criteria
culture of a typical IE causing organism 2 positive cultures taken 12 hours apart evidence of vegetation on echo/ new murmur
minor dukes criteria
risk factor e.g. prothestic valve fever >38 immune phenomena thrombotic phenomena positive blood cultures not meeting major criteria
what dukes criteria is diagnostic of IE
2 major 1 major and 3 minor 5 minor
treatment of MSSA IE
flucloxacillin
treatment of MRSA IE
vancomycin + gentamicin + rifampicin
treatmetn of subacute IE
benzylpenicillin + gentamicin for 4 weeks /vancomycin for 4 weeks
causes of aortic stenosis
age congenital bicuspid valve
pathology of aortic stenosis
high velocitity high pressure flow
murmer for aortic stenosis
mid systolic ejection murmer over aortic area
murmer for aortic regurgitation
diastolic descrendo murmer
causes of aortic regurgitation
IE LV dilation, dissecting aortic aneurysm marfans, ank spond
mitral stenosis murmer
diastolic descrescendo murmer with opening snap
pathology of mitral stenosis
backpressure into left atrium high pressure flow through narrowed mitral valve
cause of mitral stenosis
rheumatic fever
cause of mitral regurgitaion
IE, connective tissue disease post MI, LV dilatation
mitral regurgitation murmer
pansystolic murmer
what is chronic rheumatic heart disease
thickening along the commisures/ lines of closure of valve leaflets usually left sides/ mitral valve
causes of pericarditis
uraemia, viral, TB
5 types of pericarditis
fibrous granulomatous- TB haemorrhagic- TB, uraemia purulent- staph fibrinous- MI, uraemia
what is pericardial effusion
serous fluid in pericardial sac
cause of pericardial effusion
chronic heart failure
what is haemopericardium
myocardial rupture due to trauma or infarction
