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L14 Consequences of vascular disease (+Shock)

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a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
vascular occlusion
consequence of impaction of an embolus in vessel whose calibre is too small to allow it to pass
state of reduced tissue oxygen availability
_________ hypoxia: whole body (e.g. due to altitude or anaemia)
_________ hypoxia: specific tissues affected
clinical measure of low blood PaO2
pathological reduction in blood flow to tissues; reduced metabolites including glucose; usually due to obstruction
non-ischaemic hypoxia
impaired oxygen supply only; other metabolites still supplied
glycolytic anaerobic respiration
in ischaema, fails due to lack of glucose and build up of metabolites
ischaema _____ tissues faster/more severely than hypoxia
limited or short duration ischaemia causes ________ cell injury
prolonged or sustained ischaemia causes _________ cell damage (necrosis)
ischaemic necrosis caused by occlusion of the arterial supply or venous drainage in a tissue
an area of infarction in a tissue
Ischaemia-reperfusion injury
generation of reactive oxygen species by repercussion of ischaemic tissues; ROS generated by inflammatory cells cause further cell damage
atherosclerotic plaque
rupture / thrombosis of an ____________ ________ causes the majority of infarctions; commonly arterial
cause of infarction: local coagulation of blood in part of the circulatory system
cause of infarction: contractile narrowing of blood vessel lumen
cause of infarction: ________ expansion, extending into vessel lumen
cause of infarction: extrinsic ___________, e.g. by tumour
cause of infarction: inflammation of blood vessel wall
cause of infarction: twisting of vessel roots
cause of infarction: ________ of vascular supply, e.g. AAA
venous occlusion
also causes infarction but is common; more common in organs with single outflow (e.g. testis, ovary)
morphological classification of infarction by _______
red infarction
dual blood supply / venous infarction (haemorrhagic)
white infarction
single blood supply hence totally cut off (anaemic)
most infarctions are _______-shaped due to obstruction of proximal vascular supply before vascular branches
coagulative necrosis
normal histological characteristic of infarction
colliquative necrosis
histological characteristic of brain infarction
low flow infarction
infarction in areas of diminished blood flow in vulnerable anatomical regions
portal vasculature
blood supplied via other parenchymal capillary beds - e.g. anterior pituitary (via hypothalamus), renal tubules (via glomeruli)
watershed region
point of anatomises between two vascular supplies - e.g. splenic flexure of colon (SMA, IMA), myocardium (ventricles & coronary arteries), regions of brain
pathophysiological state of reduced perfusion resulting in decreased oxygen delivery to the tissues
Mean Arterial Pressure
Shock can be explained as a decrease in this - comprises Cardiac Output & Total Peripheral Resistance
Hypovolaemic Shock
Intravascular fluid loss; ↓ venous return (pre-load), ↓stroke volume, ↓cardiac output
Cause of hypovolaemic shock: trauma, GI bleed, ruptured haematoma, pancreatitis complication, fractures, ruptured aortic, abdominal or left ventricular free wall aneurysm
non-haemorrhagic fluid loss
Cause of hypovolaemic shock: diarrhoea, vomiting, heat stroke, burns
Third spacing
Acute loss of fluid into non-functional interstitium; common postoperatively and in intestinal obstruction, pancreatitis or cirrhosis
Cardiogenic Shock
Cardiac pump failure; ↓CO
compensatory mechanism for hypovolaemic & cardiogenic shock; sympathetic - cold, clammy, "shut down"
Category of cariogenic shock: heart muscle failure, e.g. MI, cardiomyopathy, "stunned myocardium"
Category of cariogenic shock: ________-related: abnormal electrical activity; impaired ventricular contraction or filling
Category of cariogenic shock: defect in blood flow through heart; valvular defects (e.g. prolapse), VSDs, atrial myxomas, ruptured ventricular free wall aneurysm
Category of cariogenic shock: obstruction to blood flow outside the heart, e.g. massive PE, tension pneumothorax, constrictive pericarditis, pericardiac tamponade
Distributive Shock
Due to severe vasodilation reduces TPR; ⬆CO to compensate (flushed, warm, palpitations) - includes septic, anaphylactic, neurogenic and toxic shock syndrome
Septic Shock
Distributive shock: severe, over-whelming systemic infections; ⬆cytokines causes vasodilation; pro-coagulation (DIC) causes ischaemia
Anaphylactic Shock
Distributive shock: severe type I hypersensitivity reaction; sensitised individuals; small doses of allergen → IgE cross-linking; massive mast cell degranulation → vasodilation; circulatory collapse & respiratory distress
Neurogenic Shock
Distributive shock: spinal injury / anaesthetic accidents; loss of sympathetic vascular tone; vasodilation → shock
Toxic Shock Syndrome
Distributive shock: NOT the same as septic shock; S.aureus / S.pyogenes produce exotoxins ("super antigens"); non-specific binding of class II MHC to T cell receptors (no APC processing required); widespread release of massive amounts of cytokines
mixed shock
different types of shock co-existing - e.g. in septic shock: primary distributive component + hypovolaemic component + cariogenic component