vascular disease pathology 2 Flashcards
how does a thrombus form
damage to blood vessel
endothelial cells lifted up
platelets are attracted to collagen found underneath endothelial cells
platelets then gather
positive feedback loop leading to platelet aggregation
also blood clotting occurs- fibrinogen to fibrin
factors which can precipitate thrombosis in blood vessesl
change in vessel wall
change in blood flow (change in laminar flow)
change in blood constituents (e.g. platelet numbers)
causes of ischaemic disease
atheroslerosis
myocaridal hypertrophy
small vessel disease
athersclerosis
disease of arterial blood vessesl
myocardial hypertrophy
increase in heart muscle due to increase in cell size
athersclerosis
plaque has reduced the lumen size
risk factors for athlesclerosis
- industrial deprived areas
- cigarette smoking (nicotine damages endothelial cells, can lead to atherosclerotic plaque formation)
- Hypertension (HBP, due to endothelial cells being damaged)
- uncontrolled diabetes mellitus
- hyperlipidaemia
what can left ventricular hypertrophy lead to
ischemic heart pathology
blood low is the same but more muscle needs blood supply
what can cause hypertrophy of the heart
calcified valves
heart has to work harder to move blood through, hypertrophy will occur
more hypertrophic more blood requried
what keeps vessels open
nitric oxide
types of ischaemic heart disease
regional transmural myocardial infarction
subendocardial infarction
chronic ischaemia
regional transmural myocardial infarction
death of heart muscle due to lack of blood
blockage in one of the main coronary artery
lack of collateral circulation from other vessels
subendocardial infarction
inner part of ventricle dies
sever coronar artery atherosclerosis in all 3 coronary arteries
sudden reduction in blood flow
chronic ischaemia
fixed atqheroscleroci lesions
angina, myocardial fibrosis, hibernating myocardium
some heart muscle die over time, but there is still some heart muscle alive
complications of myocardial infarction
- sudden death
- arrhythmias (particularly atrial fibrillation)
- cardiac failure
- mitral incompetence
- pericarditis
- cardiac rupture
- mural thrombosis
- ventricular aneurysm
- pulmonary emboli
cardiac rupture
weakening of the wall due to muscle necrosis and acute inflammation
rupture into pericardial sac
rupture into interventriclar septum
mural thrombosis
thrombosis on the abnormal endothelial surface following infarction
embolisation to any arterial site, causes further infarcts in the rest of the body
what is hypertenion
high BP
over 140 systolic
- can have later in life due to aorta being less elastic
primary vs secondary hypertension
primary - no cause
secondary - identifiable cause
secondary causes of hypertension
secondary means identifiable cause
renal
- salt and water overload
endocrine
- cushings, adrenal gland
coarctation of aorta
- stenosis in aorta
blood pressure higher in upper body
clinicopathological classification of hypertension
benigin
- long asymptomatic period
increased frequency of complications later
Malignant
- raised diastolic
symptomatic
effects of hypertension
- accelerated atherosclerosis
- sclerosis of smaller vessels (particularly in the kidney so can lead to kidney failure)
- microaneurysms and haemorrhages
- kidney/heart failure
- cerebral haemorrhages = strokes
