Cardiology Pathology Flashcards
what factors determines whether one has ischaemia or infarction?
the nature of the blood supply
the rate of development of the occlusion
vulnerability to the effects of hypoxia; neurones, myocardium vs CT, skeletal muscle
oxygen content of the blood; anaemia, hypoxic conditions
describe a red infarct
seen in the lung
because there are two blood supplies in the lung
bleeding into the tissues and it appears red
usually occur with venous occlusion; loose tissue
usually occur in dual circulation
describe a pale infarct
seen in the spleen because there is no blood there a single vascular channel has been occluded usually occur in solid organs usually occur in a single blood supply
what are the most common causes of ischaemia and infarction?
thrombosis embolism atheroma hyper viscosity vasculitis
describe the formation of a thrombus from an atheroma
atheromatous plaque causes turbulence in the blood flow
loss of endothelial cells
collagen exposure
platelet activation
clotting cascade activation
deposition of a thrombus
propagation; thrombus grows in the direction of flow
what are the clinical effects of an arterial thrombus?
limb; pale, cold, pulseless, ultimately undergoes infarction
coronary artery; MI
what are the clinical effects of a venous thrombosis?
leg; tissues become swollen, reddened, tender
what are the outcomes of thrombi?
full lysis and resolution
organisation; scar formation, vessel occlusion
slow recanalisation; leave a scar a residual thrombus
break off; embolism, may occlude another vascular system,
what are the types of emboli?
thromboembolism; 90% fragments of atheroma amniotic fluid gas embolism; trauma fat embolism; trauma, particularly fracture of long bones metastasis foreign material infective agents
define an atheroma
a deposition of material in the intimal layers of the tissues of the vascular tree
what are the components of atheroma?
fat macrophages
inflammatory cells
fibrovascular CT
what are the risk factors for developing atheroma?
age; older gender; male, frequent in women post-menopause HTN DM hyperlipidaemia smoking sedentary lifestyle obesity soft water ingestion high intake of complex carbohydrates hyperuricaemia
name the types of atheromatous lesions
fatty streaks
fibrolipid plaque
complicated lesions
describe fatty streaks
linear elevation in the intima
composed of lipid-laden macrophages
younger patients
describe fibrolipid plaques
further deposition of fat, fibroblasts and collagen
fibrosis formation
describe complication atheromatous lesions
narrow the lumen causing vascular insufficiency erosion of endothelium causing thrombosis haemorrhage into the plaque aneurysm formation
what sites are commonly affected by atheroma?
lower abdominal vessels aorta iliac arteries coronary arteries popliteal vessels descending thoracic aorta internal carotid vessels circle of willis
what are the complications of atheroma?
narrowing thrombus on a plaque fissuring cracking bleeding in a plaque aneurysm formation
what are the causes of ischaemic heart disease?
atheroma
vascular spasm
anaemia
what are the risk factors of ischaemic heart disease?
smoking race; black age men obesity DM; uncontrolled HTN hyperlipidaemia stress
describe the pathogenesis of ischaemic heart disease
the blood supply is insufficient for the metabolic demands of the heart
due to reduced blood supply, muscle hypertrophy, reduced oxygen carriage
what are the most common arteries to be affected by a MI?
LCA anterior descending branch
RCA
LCA circumflex branch
describe the occlusion of the LAD artery
most common
“artery of sudden death”
anterior infarct
describe the occlusion of the circumflex branch of the LCA
lateral infarction
1/5 of cases
describe occlusion of the LCA proximal to bifurcation
occluded all territory supplied by the circumflex and LAD
devastating event
describe coronary artery obstruction in the right side
ECG changes in leads 2, 3 and aVF; inferior
can involve the posterior septum
describe the changing of features of transmural MI over time
6hrs; ECG changes, electron microscopy shows swollen mitochondria
after 24hrs; region of infarction is pale, myocytes lose their typical striations
days-weeks; dead myocytes removed by macrophages
weeks; healing by repair, organisation, progressive fibrosis
months; fibrous scar matures and akinetic segment formed
what are the complications of MI?
sudden death; often due to VF arrhythmias angina HF mitral incompetence pericarditis cardiac rupture; 3-5 days post MI ventricular aneurysm autoimmune conditions; dresslers syndrome, rare
describe the pathogenesis of cardiac rupture
tissue weakening as damaged material is removed by macrophages
muscle necrosis and inflammation
rupture occurs at the point of weakest heart material; myomalacia cordis
ventricular septum; left to right ventricular shunt
papillary muscle damage; mitral incompetence
what are the symptoms and signs of Dressler’s syndrome?
chest pain
fever
pericardial effusion
describe the pathogenesis of ventricular aneurysm
dilatation of a fibrous scar
usually leads to dyskinetic segment, HF neural thrombosis
what does the prognosis of ischaemic heart disease depend on?
age extent of CAD live of myocardial damage symptom severity pumping ability of the heart
what are the risk factors for primary hypertension?
old age FHx african/caribbean origin high salt diet lack of exercise overnight smoking excess alcohol stress urban dwelling
what are the causes of secondary hypertension?
renal; parenchymal and renovascular disease
endocrine; pheochromocytoma, cushing’s, hyperaldosteronism
coarctation of the aorta
drugs; NSAIDs, OCP, steroids
pregnancy
name some renal parenchymal diseases
diabetes
chronic glomerulonephritis
polycystic kidney disease
chronic tubulointerstitial nephritis
what are the types of renovascular disease?
atherosclerosis fibromuscular dysplasia (FMD)
describe atherosclerosis in renovascular disease
primarily in male patients >50yrs
usually affects the aortic orifice or proximal segment of the renal artery
after 30yrs, causes renal atrophy and CKD
describe fibromuscular dysplasia in renovascular disease
primarily younger, female patients
pathologic thickening of the arterial wall. mostly the distal main renal artery or the intrarenal branches
describe the endocrine causes of secondary hypertension
aldosteronoma; benign tumour of the adrenal gland
pheochromocytoma; secretes nor/adrenaline
Cushing’s syndrome
describe the cardiovascular manifestations of hypertension
symmetrical LVH
atherosclerosis
arteriolosclerosis
define atherosclerosis
asymmetrical narrowing the lumen of larger vessels by lipid accumulation within the intima
define atheriolosclerosis
symmetrical narrowing of the lumen of the smaller vessels by deposition of protein within the walls of the blood vessels
how does hypertension cause haemorrhagic stroke?
rupture of small micro aneurysms within the brain tissue which have been weakened by chronic hypertension
describe hypertensive nephrosclerosis
progressive renal impairment caused by chronic, poorly controlled hypertension
this can damage small blood vessels, glomeruli and interstitial tissues causing benign hypertensive arteriolar nephrosclerosis
describe hypertensive retinopathy
long history/severe hypertension
thickened blood vessel walls leads to a reduction in blood flow, resulting in ischaemia and infarction
bleeding
loss of vision
what are the major and minor criteria required to rheumatic fever diagnosis?
carditis polyarthritis syndenham's chorea erythema marginatum subcutaneous nodules
fever arthralgia lab abnormalities; raised CRP ECG abnormalities; prolonged PR evidence of streptococcal infection; rising antistreptolysin O titre
what are the features of rheumatic fever?
pancarditis
pleural effusion
fibrinous pericarditis; audible rub
myocarditis; peculiar lesion known as the Aschoff body
swollen valves
small vegetations on the valve leaflets
valve disruption; fibrotic healing response
describe Aschoff bodies
central core of collagen
surrounded by small Aschoff giant cells
bordered by anitschkow cells; long bar of central chromatin
what are the causes and complications of aortic stenosis?
calcific degeneration
rheumatic fever
LVH angina syncope LV failure sudden death
what are the causes of aortic incompetence?
aortic root dilatation
rheumatic valve disease
inflammatory diseases; aortitis
what are the causes and complications of mitral stenosis?
rheumatic fever
pulmonary hypertension
LA and RV hypertrophy
what are the causes and complications of mitral incompetence?
floppy valve
rheumatic fever
dilated mitral valve annulus
papillary muscle dysfunction; myxoid degeneration
AF
describe infective endocarditis
a bacterium, fungi sor ricketsial organism invade the bloodstream and settles on a mass of thrombus on the valve leaflet
may occur on the endocardial surface of a chamber, intimal surface of the aorta
classified due to the nature of the causative organism
describe the types of organisms in infective endocarditis and how they enter the blood
mouth; viridian’s group of streptococci
skin; coagulase negative staphylococci
GI/urogenital tract; gram negative organisms and enterococci
IV drug users; pseudomonas aeruginosa, fungi
describe the histology of vegetations in infective endocarditis
a mass of fibrin, platelets, inflammatory cells and bacterial colonies
usually contain the relative organisms
what are the risk factors for developing infective endocarditis?
structural cardiac abnormalities; regurgitant flow prosthetic valves indwelling catheters IV drug use septic focus elsewhere chronic gingivitis immune suppression diabetes chronic alcoholism
what are the complications of infective endocarditis?
cusp/chordae rupture valvular incompetence; acute HF myocarditis AV block; infection extends into neighbouring myocardial tissue fever weight loss malaise necrosis of cerebral circulation, kidneys, lungs
what are the signs of infective endocarditis?
finger clubbing splinter haemorrhages laneway lesions roth spots glomerulonephritis
describe ejection fraction
SV/EDV
>50%; normal
<40%; reduced
what are the causes of HF?
myocardial abnormality IHD; most common valve disease pericardial endocardial heart rhythm conduction
describe the pathophysiology of HF
increase in the volume of blood remaining after systole
increased diastolic volume
myocardial stretch; enhances contractility and SV
myocyte size increase
size and weight of the heart increases
supply and demand mismatch; vulnerable to ischaemia
remodelling continues after initial insult
this impairs the function of the heart as a pump
circulating level of endothelin increase
ADH is raised; precipitates hyponatraemia
describe cardiac remodelling in HF
myocyte apoptosis
alteration of intracellular handling of calcium ions
reprogramming of gene expression
what neurohumeral systems are activated in HF?
RAAS
sympathetic nervous system
natriuretic peptide release
describe the sympathetic nervous system contribution in HF
reduction in stroke vuole causes an increase in heart rate
sinus tachycardia
chronic sympathetic activation; myocyte apoptosis
describe the actions of natriuretic peptides in HF
counter-regulatory system for RAAS
reduction in blood volume, arterial pressure, central venous pressure
describe LSHF
stasis of blood in the left chambers
inadequate perfusion of the downstream tissues; organ dysfunction
dilatation of the LA increases the risk of AF and thrombus; stroke risk
pulmonary congestion and oedema; haemosiderin -laden macrophages may be seen in the alveoli
elevated capillary pressure; pleural effusion
kidney hypo perfusion; impaired excretion of nitrogenous products, pre-renal azotaemia
cerebral hypo perfusion; hypoxic-ischaemic encephalopathy
what are the causes of RSHF?
commonly LSHF pulmonary hypertension RV infarction RV cardiomyopathy adult congenital heart disease
cor pulmonale; typically occurs in patients with a variety of lung disorders
describe the pathologies of RSHF
minimal pulmonary congestion
congestion of the systemic and portal venous systems
hepatic necrosis; perfusion failure
portal venous HTN; splenomegaly, platelet sequestration, chronic congestion and oedema of the bowel wall
systemic venous congestion; pleural, pericardial or peritoneal fluid accumulation
anasarca
backward failure; kidney and brain
describe false aneurysms
haematomas which lie alongside a blood vessel
often enveloped by a thin rim of adventitial tissue
communicate with the vascular lumen via a narrow defect in the media
what are the causes and the typical locations of aneurysms?
trauma atherosclerosis inflammatory disorders marfan's syndrome HTN pericyte loss in diabetes infection septic emboli
femoral artery
abdominal/thoracic aorta
cerebral artery or capillaries
retinal capillaries
what are the consequences of aneurysms?
rupture; haemorrhage
compress adjacent structures; ureter, causing hydronephrosis, cranial nerve
thrombus due to stasis
embolisation; ischaemia or infarction
what are the causes of myocarditis?
viral; coxsackie, ECHO, adenoviruses bacterial; meningococcus, diphtheria parasites; trypanosomiasis, chaga's disease ionising radiation drugs; adriamycin
what are the histological features of myocarditis?
inflammatory cell infiltrate; mostly T lymphocytes in the interstitial spaces
myocyte death
dallas criteria
what are the causes of pericarditis?
viral bacterial TB post-MI post-surgical autoimmune; dressler's syndrome carcinomatous uraemic
describe serous pericarditis
clear
straw coloured
high specific gravity
high protein content
describe serofibrinous pericarditis
clumps of fibrin within the fluid
describe purulent/suppurative pericarditis
frank pus may form in the pericardial sac
describe blood stained pericardial effusions
highly suspicious of malignancy
describe caseous pericarditis
fungi and mycobacterial organisms invade the pericardial space
may lead to fibrotic obliteration
known as constrictive pericarditis
what are the end results of shock?
hypotension
impaired tissue perfusion
cellular hypoxia
what are the effects of shock?
neuronal necrosis focal/widespread necrosis of the heart acute tubular necrosis diffuse alveolar damage fatty change of the liver, zone 3 necrosis haemorrhagic enteropathy of the bowel
