atherosclerosis etc Flashcards
what is ischaemia
loss of blood supply to tissue bc blocked bv mostly arteries impaired aerobic resp acut or chronic can result in coagulative necrosis
what is infarction
area of ischaemic necrosis within tissue or organ
caused by blockage eg aretieral thrombosis/embolism
heals by organisation and fibrosis
what is white infarction (cause, shape, look like)
arterial sudden obstruction shaped according to territory of vessel supply pale with red border late stage scarring
describe red infarction (causes and patho))
sudden obstruction to venous drainage or occlusion of arterial supply to tissue with dual blood supply
congestion -> inc pressure -> rupture small vessels -> blood enters tissues
reperfusion of white infarct
what is thrombosis and thrombus
interaction of bv walls, platelets, plasma proteins
balance b/thrombogenesis + thrombolysis
thrombus = clotted mass blood within cardiovascular system
what are the functions of the endothelium
barrier b/blood + tissue normally antithrombotic (surface molecules + blood molecules inhibit platelet aggregation) can be prothombotic secrete vasodilators/constrictors normally resistant to leukocyte adhesion
describe function of platelets (where do they flow, adhere, activated by, release what)
flow in centre of stream
dont adhere to endothelium unless injury
activated by collagen exposed after vessel injury
release chemicals to attract more platelets
what does virchows triad describe
3 categories that contribute to thrombosis
alterations in blood flow, endothelial wall injury, hypercoaguability
what happens in blood flow stasis and why
disruption of laminar flow (bc aneurysms, over-atherosclerotic plaques, atrial fibrilation prolonged immobility (bc old, post-surgical, unconscious)
what contributes to hypercoagulability of blood
post-operative, genetic, malignancies, high oestrogens, sepsis, obesity, dehydration
what causes endothelial wall injury
injury, trauamainjury, direct trauma, inflammation, infection, indwelling catheters smoking, atherosclerosis
what are the 3 types of thrombi and their associations
arterial = atherosclerosis/anuerysm venous = slow blood + hypercoag cardiac = left V bc MI/aneurysm or left A bc fibrilation
what are the possible fates of a thrombus and its complications
embolisation, fibrinolysis (breakdown), organisation (replace w/scar tissue) persistence
complications = obstruct blood flow + embolism
what is embolism and embolus
embolism = lodging of blockage-causing piece of material inside BV
embolus = intravacular solid, liquid, gaseous mass carried into bloodstream to some site remote from origin
can be athero-emboli, septic, gaseous, fat
risk factors for dvt using virchows triad
alterations in blood flow = immobilisation + cardiac failure
endothelial wall injury = trauma, surgical injury, smoking
hypercoagulability = post-op, jigh oestrogen, malignancies…..
what is the pathway of pulmonary embolism
dvt forms in lower limb -> travels towards heart -> IVC -> RA -> RV -? PA -> lungs
large emboli = lodge in PA and prevent blood from travelling to lungs
consequences of pulmonary embolism
pulmonary infarct (rare bc dual lung blood supply) pulmonary hypertension => reduction size functional pulmonary vascular bed sudden death => inc in burden RHS heart => right ventricular failure
what is atherosclerosis and its consequences
accumulation plaque on walls of medium + large arteries (tunica intima)
plaques = central lipid core + fibrous cap
consequences = narrowed vessels = ischaemia,
plaque + acute plaque event = inc ischaemia
plaque + thrombus = infarction
risk factors for atherosclerosis
smoking, hypertension, diabetes, dyslipidaemia, age, male, genetics, obesity, lack of exercise, stress
7 steps to atherosclerosis pathogenesis
`1. chronic endo injury inc vascular perm with leuk adhesion + thrombotic potential
- accumulate LDL in intima
- monocytes migrate -> macs -> engulf lipids -> foam cells
- platelets adhere
- release cytokines and growth factor to smooth muscle cells enter intima from media
- smooth muscle proliferate + produce ECM
- more accumulation
morphological characteristics of atherosclerosis
fat streaks, fibrous plaques, plaque rupture
atherosclerosis site of occurrence
elastic arteries (aorta, carotid + iliac arteries) large + medium muscular arteries (coronary + popliteal + cerebral arteries)
consequences of atherosclerosis
thombosis on fibrous plaque, bleeding into plaque, weakening of vessel wall
myocardial + cerebral infarction, aortic aneurysm, preipheral vascular disease
what is an aneurysm, causes _ consequences
abnormal focal dilation in wall of vessel or cardiac chamber
bc weajening media (eg bc atherosclerosis)
consequence = thrombosis + rupture
prevention and treatment of atherosclerosis
prevention = reduce risk factors, prophylatic medication (aspirin + statins) treatments = statins = regression of atherosclerotic plaque, stents (inc lumen size), bypass surgery (HDL levels improve and inc removal of bad cholesterol
