Myocardial Infarction (MI) Study Guide

Myscandid Infashion is a Coagulaty type of necross of candise husle 2 is due to prolonged severu ishemia. EAdogy →cound by an imbldonu belucon the demand & supply of oxygeneld blond to myocaretium. 1. Devrand I Impaired Coronary led dow. (0) Coronary atherosclerosis navrous one or mor epicential coronary anturies. dercars Coronary blood flow In about 90% Cases → Rish of IHD depends on - extend & severity of pre-castry athenslaas y sudden) dynamic charge in attusontos plegen extend & seusity of bed athaoscleroth ocaleses... ho affucked / inuched. stcture of plays. - Stable plaques desse collegesives & thick fibray Cops with mind inflematon →less Woly to ecuptor. + Vulnerable plaque core with wing foam cells, fibrous cap is thin. E incmend inffomenton. → likely so gempture. degen lestent of steness. feed whistention lus than 70%. asymptombe food obstruction of 75% or mae catial stenos precipitate istenia by exercise → Steble Ongine 4 food detenchor of 90%. & abwe Gods to inadequte blond ha angina. → Rate of deudop and of alumn 4 shas progresion develop collo feed circulates prevent infantis aule blockinge to fiue to defend low infarction. foctor which infleme consequences of coronary others sclerosis. Potent of information - shrambes developoul in disrupted pleque. Y coronary was constiden. dudde klanja in a theo tous plage (b) othe lours of Cowrnay anky occlusion. 4 Coronary vara sperm. Coronary emboli y diminished availability of blond & Oxygen 2. Inercand yo candid demand occu in with hyocardid hyperkupply. - incrand heart st eno tund shers ek. Pathogenesis of Hu Coronary arteries with fixed atherosclerste occluser indequus coronary prafusion superimpond performs Humbas/ Coronary vasspadm Thrombles anche in der to ante plege change. Lequer of eunts in a typical Ceau of Mi 9. Aeste plage change. → sudden change leunt occuring in atheromtoes plaqw. → convert pentially occlusive atheroscleroth pleque to pradne sudden istenia. a) Rupkin / Assuming of plaque →→Coupese highly throubogume pleque consthants Sidden theeambas fortes Sedden occlusion of lumen. b) Emons/ ulceration of plaque → expos highly thrombegure subendothelial bound whow. ↓ suden Strombie hauen oclion of Cu c) hamerikage into lental cas of plaqu increase plaque size. ↓ Sedden occlusion of lun 2. Fornton of miere thrombi Acute plaque charges expose throw bogenie sub endothebol collagen platilite asther to se ↓ formator of mices therubi on panted a complete occlurin of affrced coronay anhly. 3. Vauspasm Activated platelet, endothelial cells & inflamator cells. Julkan ruditas Coles vasospasm al sil atheromes further harming of us. 14. Activation of Congubilar pethuay 5. Mys canded hechesis complete occluses result in the ann ischen wagubite necrosis of Suppliced by particules courery artiny. Consequence of Myocandid Ischemia A. Reversible injury. Biochemical changes cerseton of cerche glycolyus deurwand production & AT accumulon of toxic hukbolha. Funchond charges loss of consulity ppt aut heart feker. - + prophologic chorps mitochonded swelling glycogen dylan mofibrilla subsector. B. Jeupeversible Irij wory → develops after pudorged ischemia of wore then 4 Biochemical changes. → leakage of cytoplasme predeins into blood due to breakdan of Sexedem heen beps. (hyoglobe, LDH, CK, kuponins). & Functional changes rythmias. Morphologe changes Coogulshe beclectis of Cardio muscles. Morphology. gross within fast 12 hows to identifiable gros changes sen Tripheryl telre adiom chlonde sidently informed 2-3 hours after anset (stain) Non-inforced hyprandium brich red. 4 Infprited area unstained pel - Old inforces whil & glistening. •By 12-24 hrs ple ndash fhe area → progressively sharply defined, yellow fan & soft. After 3-5 dap matted with contral pole, yellowish reache region. By 10 days to Iweeks appears seff & en hund by bypuremie zone of highly vascularised gumblin disse Ather diyechs lider Leded infarele appen firm, pale gray E Contructed develops into fibrous scar. • 1-8 weils praen of hesling stes from wengine. → bacblest peditus & collagen deposite/ 2-$ week increed collagen depositon & less cellebeing > Imeros dense collaginary scar. Enzyme changes for hyocardid infarction due to leakage of proteins. into blood Graubhar. from hevesh hyvcarded cells. 1. Cardias Jeronins →puture involved in heart much contreden →increased plesame levels establish diagnosis of Mi two typus Troponin (T) { Troponin (4) →hest sensitive & specific meerkers.. → Quels 2-4 hous peck at 48 hous -> elebaked levels rewin la 7-10 dep. 2. Cardier Ceactive plesphokinase ->Non specific enzyme worker MB Present in Cordics munde. →fensit but not speake. →CK-MB bed heist within 2-4 hous, peek at du haus to houd within 72 Lour. 3. LDH hot -> starts porsiy 24-48 han. lemons to nory days, homl 7-14 bys 2. Myoglobin Caulics meanter of MI → level gives within 1-3 hom peck of abal 8-12 haus. hind Ih-36 hours. Complictors of M . Loff verticular falon & Candiagem, shock 1 Me proderes controchle functional abnormalities of left ventricle paoplationik to the size of the infarct. 2. Araybhas →derclop abhand cardior togt rhythm by canalul evitability / Conduction disturborces arrty thawas. 3. Myocardial rupture → hebross & hendropile infiltration causes softening & weduring d myocardium lead to candier rupturs. L. Dilekton of verder wes chamber. Area of infared wood regions dispropaotchoutly Arakhed dilshun of infand reyn 5. Vente cular aneurysm. 6. Mured shrombus. Infpry Cool abnormality in Endocardil deminge. byocarded Controlling & → Hurd thecotubess.