0630- histology of MI- CG Flashcards
by Alex
Define ischaemia and describe its consequences Also define ischaemic heart diease
Inadequate supply of blood to body part May be due to impeded arterial flow or reduced venous drainage (build up of pressure that impedes arterial flow- block) Compromises O2 and metabolic subtrate supply Ischaemic heart diseases- group of syndromes arising due to myocardial ischaemia
Define infarction and and compare arterial with venous
sufficient ischaemia to cause tissue necrosis Arterial- complete block by thrombosis or embolisms ( WHITE , less blood), (heart, wedged shaped, why??) Venous infaction- mechanical compression of the vascular supply, usually RED - haemorrhagic Also strokes, result of hernia
What is necrosis
morphologic changes that follow (unregulated) cell death in living tissue (micro and macroscopic) Due to denaturation of intracellular proteins, enzymatic degradation of cell
Types of necrosis- Histology= NO NUCLEI, PINK PORRIDGE
Coagulative ischaemia, MI - denaturation of protein, cell outlines, ghost cells (blue nuclei disappears) Liquefactive- abscess, cerebral infarct - mostly enzyme digestion- cyst, macrophages eat tissue Caseous necrosis- ( TB ), distinctive, cheesy- can be found in genitourinary tract, lung apex (oxygen) Fat necrosis- fat destruction, ( pancreatitis , due to leaking enzymes) –> saponification
Coronary artery blood supply
Right coronary artery supplies posterior and right lateral walls Circumflex- left lateral section Left anterior descending- anterior middle wall
Clinical manifestations of CVD
Angina- pain due to cardiac ischaemia- atypical/silent- mostly in diabetes and women Stable - goes away with rest, predictable- affixed plaque with fibrous cap Unstable - worsening, unpredictable, doesn’t go away with rest- RISK OF HR Prinzmetal - spasm of coronary artery heart failure, sudden cardiac death, arrhythmias can develop from MI due to hypertrophy and scarring
KNOW MORHPOLOGICAL DEVELOPMENT AT VARIOUS TIME POINTS AFTERWARDS PUT THIS SHIT INTO A TABLE
1 HOUR??? 4 hour- wavy fibres 1 day- macro- subtle softening of tissue, dark mottling micro- coagulation, necrosis, haemorrhage from reperfusion, scant neutrophils 2 days- mottled appearance 1 week-
Determinants of IHD
Number , distribution and structure of athermatous plaques, degree of narrowing they cause How quickly the plaque evolve Sudden is bad- unstable, no chance to compensate (collateral vessels- diabetics bad at making collaterals) Slower plaques with more narrowing and big fibrous cap better than smaller ones that rupture (stable angina, but no ‘acute coronary syndrome’) Risk factors- male, family history, age, HTN, hypercholesterolaemia, DM, cigarette
Pathogenesis of IHD/MI- CORONARY ARTERIAL OCCLUSION,
- fatty streak and atherosclerosis- plaque cause narrowing of coronary vessels 2. stable plaque becomes unstable- leading to acute coronary syndrome (unstable angina, sudden cardiac death, MI) Trigger- intrinsic (plaque structure/composition), extrinsic (mechanical stress, platelets reactivity) 3. fissuring, ulceration, haemorrhage 4. vasospasm, platelet AAA, extrinsic coag pathway 5. THROMOGENIC PLAQUE EXPOSURE - THROMBUS AND ARTERIAL OCCLUSION-
Non-atherosclerosis causes of MI
10% Vasospasm, emboli (ie AF), vasculitis, haemoglobinopathies (increased thrombosis ie EPO), amyloid, vascular dissection
Myocardial response and consequences of infarction
Ischaemia via loss of blood supply to myocardium functional, biochemical, morphological Timeframe seconds- cessation of aerobic glycolysis, minute- loss of contractility 30min- necrosis of myocytes 6hr- complete necrosis Factors- location, severity,- transmural or sub-endocardial?, rate, duration, metabolic needs, collaterals, BP, HR, rhythm
Complications of MI- morphological changes
4 hours- wavy fibres, contraction bands 1 day- mottling, softening of walls (macro), coagulation necrosis, haemorrhage (micro) 2 days- mottled with yellow/tan infarct centre, micro- neutrophils 1 week- hyperaemic border, disintegration of necrotic myofibres, dying neurphils 2 weeks- soft yellow, depressed infarct borders, phagocytosis, granulation tissue and fibrosis
Complications of MI
50% die before hospital, 75% have complications Outside –> inside contractile dysfunction- LV fail- cardiogenic shock arrhythmia- sudden cardiac death (his) pericarditis (if transmural) cardiac tamponade/haemopericadium, myocardial rupture, infarct extension/expansion, ventricular aneurysm, mural thrombus, papillary muscle dysfunction- can scar
Timeline of complications
• Arrhythmia – Immediate leading to sudden death – Early – Ongoing i.e. bundle branch block • Contractile dysfunction – Immediate, within 60 seconds – Cardiogenic shock – Chronic left ventricular failure • Pericarditis – 2-3 days usual – May appear weeks after MI = Dressler’s syndrome • Myocardial rupture – 3-7 days when necrotic myocardium at it’s weakness • Mural thrombosis with risk of embolism – Highest risk at 10 days, lasting for 3 mths • Aneurysm – late complication
