Pathophysiology of atheroma, thrombosis and embolism, ischaemia and infarction Flashcards
what is atheroma made up of?
fibrous cap
lipid core
what is the difference between atherosclerosis and arteriosclerosis?
atherosclerosis - atheroma formation in endothelium
arteriosclerosis - fibrosis of tissue with age
what is contained within the fibrous cap of atheroma?
collagen
inflammatory cells
what is the collagen in the fibrous cap of atheroma produced by and how?
smooth muscle cells, platelets, macrophages
through secretion of PDGF - platelet derived growth factor
which arteries are more likely to be affected?
muscular arteries
what are the chronological stages of an atheroma plaque, and when do they occur?
fatty streak (childhood)
early atheromatous plaque (young adult)
fully developed atheromatous plaque (30+ years)
what is the main culprit for developing atherosclerosis?
hypercholesterolaemia
what are possible signs of hypercholesterolaemia?
high LDL/total cholesterol in blood genetically low LDL receptors tendon xanthomata xanthalasma corneal arcus
what are the main risk factors for developing atherosclerosis?
hypertension smoking diabetes age male (obesity) (sedentary lifestyle)
what does a complicated atheroma mean and what are its consequences?
the rupture/fissure of a plaque, exposing its contents to the lumen –> trigger inflammatory reaction, thrombosis/embolism
what are the main features of a vulnerable atheroma plaque?
thin fibrous cap
large lipid core
active visible inflammation
what are the main non-drug prevention mechanisms for atherosclerosis?
stop smoking
weight loss
exercise
diet changes
what are the main drug prevention mechanisms for atherosclerosis and how do they affect atherosclerosis?
ACEI - reduce blood pressure (reduce risk of plaque rupturing)
statins - stabilise fibrous plaque and reduce cholesterol production
aspirin - antiplatelet (reduce risk of thrombosis on plaques)
what are the four main types of hypoxia?
hypoxic
anaemic
stagnant
cytotoxic
what are the six main factors affecting oxygen supply?
inspired O2 lung function blood components (Hb) blood flow vasculature tissue mechanisms
what are the two main factors affecting oxygen demand?
tissue specific demands
level of tissue activity above normal threshold
what are the different types of necrosis which can happen post-infarction, and where do they occur?
coagulative - heart, lung, kidneys
colliquative/liquefactive - brain
why are some tissues more sensitive to ischaemia than others?
because of different cell/tissue metabolism (some fast metabolism, some slow)
what is a biochemical and cellular result of infarction?
anaerobic metabolism –> cell death –> necrosis
what are the effects of infarction?
acute/chronic reduction in O2 supply
loss of function/dysfunction/pain
anaerobic metabolism –> cell death –> necrosis
effects depend on metabolism of affected cells
what are the two different appearances of infarctions, how and when do they occur?
pale (anemic) infarct (arterial occlusion) - solid tissue (heart, kidney)
red (hemorragic) infarct (venous congestion) - loose tissue (liver, lungs, GI)
what is the endstage of infarction in tissue appearance?
scar formation
what are possible types of embolus?
thrombus (arterial or venous) gas embolus (nitrogen) mural embolus (ventricle dilation, AF) air embolus fat embolus (fat embolism syndrome) placental/amniotic fluid embolus tumour embolus septic embolus foreign object embolus bone marrow embolus
how does rheumatic fever cause emboli?
inflammation in endocardium/valves can cause thrombi forming on top of inflamed area and dislodge
