BIOM3002 Lecture Notes - Lecture 2: Valvular Heart Disease, Thrombophilia, Thrombosis
26 May 2018
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HISTOPHATHOLOGY LECTURE TWO
Cardiovascular pathology:
o Links to other diseases [CKD, stroke, retinopathy]
o Diabetes and CVD = close links
o Risk of death from MI increases in diabetes
Changes that occur in heart and vascular disease include:
o Atherosclerosis and aortic aneurisms
o Thrombosis and Virchow's Triad; thrombus and embolus
o Ischaemia and infarction
o Cardiac hypertrophy and valvular diseases, left vs right
heart failure
Atherosclerosis: process of changes [lipid, carbohydrate,
calcium etc] in intima of artery
o Stimulated by endothelial damage when lipids build-up
o Can cause reaction 'platelet' aggregation and RBC and fibrin
aggregation = blood clot [thrombus]
o Process = thrombosis
Atheroma: Atherosclerotic plaque in an artery. Reversible
accumulation of degenerative material in the intimal layer of
artery wall. Material consists mostly of macrophage cells and
debris containing lipids, Ca2+ and variable amounts fibrous
CT.
Aneurism: abnormal widening or ballooning in an artery wall =
weakening and rupture -> aneurism/clot = weak walls =
ballooning = rupture
Saccular: balls [e.g. genetic in Circle of Willis]
Fusiform: ballooning
Dissecting: vessel wall splits
Thrombus and blood flow: may allow small amount or completely
occlude vessel
Thrombosis: process or presence of a blood clot in a vein or
artery
DVT symptoms:
1. Pain and tenderness in leg
2. Pain on extending foot
3. Swelling over lower leg, ankle and foot
4. Skin is red and warm
VIRCHOW'S TRIAD: Endothelial injury + hypercoagulability +
abnormal blood flow [stasis or turbulence] = THROMBOSIS
find more resources at oneclass.com
find more resources at oneclass.com
Thrombus: clot of blood, formed during life within heart or
BVs
Embolus: bit of foreign matter in bloodstream – thrombus,
cancer cells, fat, cardiac vegetations, air bubble
Venous thrombus and embolus:
o Thrombi form anywhere in CVS
o Common outcome is pulmonary embolism [surrounding infarction
lung tissue]
o Thrombus = RBCs with fibrin binding together
Outcomes of thrombus:
1. Lysis and vessel returns to normal
2. Scarring of vessel walls and complete blockage of blood-flow
[organisation]
3. Re-cannularisation thrombus [blood-flow re-established]
4. Embolism e.g. kidney infarct
Ischemia: inadequate blood supply to an organ or part of the
body, especially heart muscles
Infarct: small, localised area of necrosis usually resulting
from failure of blood supply
o Blockage blood flow not necessarily infarct
o Immediate re-flow blood = sub-lethal injury
o No re-flow/large blockage = necrosis = cohesive areas and
inflammation [helps repair] -> fibrosis and granulation
tissue
Most commonly occluded BV in heart: left anterior descending
Process: 0hr, 2hr, 24hr:
0hr = zone of perfusion [at risk]
2hr = zone of necrosis [small]
24hr = zone of necrosis [whole wall]
Re-perfusion:
o Delay = substantial infarct and partial salvage
o Possible to salvage tissue
o Oxidative stress: when BV is re-perfused; typically
apoptotic cell death therefore less inflamed
Histopathology myocardial infarction: infarcted necrotic area
surrounded by cardiac muscle fibres that are stained intensely
by easin [easinophilic] when compared to normal myocardial
fibres; separation myocytes by oedema; heavy infiltration
damaged myocardium by neutrophils – at this stage no
granulation tissue formation [would have come after had
patient survived]
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Cardiovascular pathology: links to other diseases [ckd, stroke, retinopathy, diabetes and cvd = close links, risk of death from mi increases in diabetes. Changes that occur in heart and vascular disease include: atherosclerosis and aortic aneurisms, thrombosis and virchow"s triad; thrombus and embolus, ischaemia and infarction, cardiac hypertrophy and valvular diseases, left vs right heart failure. Atherosclerosis: process of changes [lipid, carbohydrate, calcium etc] in intima of artery: stimulated by endothelial damage when lipids build-up, can cause reaction "platelet" aggregation and rbc and fibrin aggregation = blood clot [thrombus, process = thrombosis. Reversible accumulation of degenerative material in the intimal layer of artery wall. Material consists mostly of macrophage cells and debris containing lipids, ca2+ and variable amounts fibrous. Aneurism: abnormal widening or ballooning in an artery wall = weakening and rupture -> aneurism/clot = weak walls = ballooning = rupture. Saccular: balls [e. g. genetic in circle of willis]
