Vascular Pathology II Flashcards
What are the differences between acute and chronic ischaemia?
- actue: seconds, minutes, hours, days
- can cause infarction
- chronic: weeks, months, years
- not typically associated with infarction
What are the causes of acute and chronic ischaemia?
deficiency of oxygenated blood in tissue, causing O2 shortage and impaired aerobic respiration due to:
- unmet increased O2 demand
- local vascular narrowing or occlusion
- systemic reduction in tissue perfusion
How can acute and chronic ischemia impact organs?
Acute
- infarction is acute cell death
- acute narrowing or occlusion of a vessel
- impairment of tissue (e.g. heart)
- pain
- sufficient duration (mins to hours, tissue dependent) leads to infarction
Chronic
- cellular and tissue atrophy, due to apoptosis, death
- cytokine release by local macrophages
- activation of fibroblasts –> fibrosis
- collagen deposition
- impaired healing (restricted blood supply)
What are the potential causes of infarction?
- arterial occlusion
- thrombosis, atherosclerosis, embolism
- external compression (dissection, vasospasm)
- venous occlusion
- thrombosis, twisting or compression
- systemic reduction in tissue perfusion
- shock, -O2 exchange
- compartment syndrome
What influences the development and size of an infarct?
- size of artery occluded
- duration of occlusion and vulnerability of cells to ischaemia
- neurons (4-5mins), cardiac muscle (10-20mins), skeletal muscle (several hours)
- glial cells, endothelial cells much more resistant to ischaemia
- whether the artery is carrying O2’d or deO2’d blood
- nature of the arterial supply
- e.g. LV arteries are end arteries
- some areas have dual supply that is anastamosed
- collateral circulation
- natural or developed as a result of chronic ischaemia (enlarged, can -size of infarct)
- O2 content of the blood
- state of systemic circulation
What is a pale infarct?
- anaemic
- result from blockage of end arteries
- mainly in spleen, kidney, and heart
- often wedge-shaped in spleen and kidney
- location in heart depends which artery is blocked (LAD, circumflex, right coronary)
- often get accompanying haemorrhage when vessels at edge leak
- causes acute inflammation
- red ring around, but still a pale infarct
What is a haemorrhagic infarct?
- red
- contain blood
- usually related to dual or collateral circulation, reperfusion, or venous occlusion
- occurs in:
- lung: pulmonary infarct due to thromboembolis from deep veins of legs, blocking venous blood (arterial blood still comes in through pulmonary veins)
- bowel: (usually) venous occlusion or twisting of bowel, significant congestion; bleeding from mesenteric arteries and collaterals
- brain: embolic/thrombic occlusions, reperfusion into dead vessels when it lyses
How do infarcts heal?
- by organization/scar tissue formation (except in brain)
- coagulative necrosis (6-12 hours post)
- infarcted cells become more eosinophilic, nuclei karyolyse/fade
- acute inflammation (1 day+)
- increase in neutrophils
- organization (1-2 weeks)
- granulation tissue @ edge of infarct
- dead muscle present, very eosinophilic
- macrophages, capillaries, fibroblasts, a few lymphocytes
- scar tissue formation
- mature scar
- few fibroblast nuclei, few capillaries
- some normal muscle may be present
What is the first stage of infarction healing?
coagulative necrosis (6-12 hours post)
infarcted cells become more eosinophilic, nuclei karyolyse/fade
What is the second stage of infarction healing?
acute inflammation (1 day+)
increase in neutrophils
What is the third stage of infarction healing?
organization (1-2 weeks)
granulation tissue @ edge of infarctdead muscle present, very eosinophilic
macrophages, capillaries, fibroblasts, a few lymphocytes
What is the fourth stage of infarction healing?
mature scar
few fibroblast nuclei, few capillaries
some normal muscle may be present
What distinguishes pale, haemorrhagic, and healed infarcts?
- pale infarcts are yellowish-white (6-12 hours)
- haemorrhagic infarcts are red
- healed infarcts are pale white (weeks)
Haemotoma
What are the predisposing factors of thrombus formation?
Virchow’s Triad
endothelial dysfunction or injury
- exposure of collagen and tissue factor, acivating platelets and the CC
- imbalance between production of antithromibic (NO, PGI2, andtithrombin) & prothrombitic factors
hypercoagulability of blood
- +pro/-anti coagulation factors
changes in blood flow
- turbulence, slowing
- +platelet contact with endothelium
- +platelet activation
What type of necrosis is demonstrated by infarction?
- coagulative
- can still see outlines of cells
- nuclei fading (karyolysis)
- appears normal for 6-12 hours
- then cells become hyper-eosinophilic
- neutrophils likely present after 1 day
How does the endothelium contribute to haemostasis?
- produces prostacyclin (PGI2), NO, antithrombin to inhibit platelet aggregation
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