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WEEK 21:
Vascular Disease - Infarction:
| Question | Answer |
|---|---|
| infarct meaning | area of ischemic necrosis (death of tissue due to lack of oxygen) due to abrupt cessation of arterial supply (arterial infarction)/ venous drainage (venous infarction) |
| infarction meaning | process of formation of an infarct |
| how does blockage lead to infarction | obstruction in vessel eg arterial embolus or thrombus |
| how does compression lead to infarction | by something outside vessel causing it to compress eg tumour/ hernia |
| how does torsion lead to infarction | twisting of an organ obstructing blood flow eg testicular torsion |
| how does rupture lead to infarction | trauma from rupture leads to loss of blood pressure downstream the rupture |
| how does vasoconstriction lead to infarction | narrowing of blood vessel leads to less blood flow |
| causes of infarction (5) | blockage, compression, torsion, rupture, and vasoconstriction |
| examples of infarction (6) | MI, cerebral infarction, pulmonary infarction, bowel infarction, testicular infarction, and gangrene |
| gangrene | life threatening condition which arises when a considerable mass of living healthy tissue dies |
| types of infarction/ infarction classified depending on (3) | colour (based on amount of haemorrhage), age, and infection |
| colour in infarction | pale/ white (in solid organs eg heart) and red/ haemorrhagic (in loose spongy tissue rich in blood supply of has dual blood eg lungs) |
| pale/ white infarct seen where | solid organs eg heart |
| red/haemorrhagic infarct seen where | in loose spongy tissue rich in blood supply or has dual blood eg lungs |
| age in infarction can be (2) | fresh or old |
| infection in infarction can refer to (2) | infection (septic) or no infection (bland) |
| features of infarction | usually wedge shaped with occluded artery at apex and base at periphery |
| margins of infarction | early poorly defined slightly haemorrhagic but later well defined |
| early margins of infarction | poorly defined, slightly haemorrhagic |
| later margins of infarction | well defined |
| outcomes of MI (3) | sudden death, survival with infarct replaced by granulation tissue and fibrous scar, and death due to complications during infarct healing process |
| stages of infarction (6) | 0-12 hours, 12-24 hours, 24-72 hours, 3-14 days, 14-21 days, and 21-56 days |
| 00-12 hours of infarction | early stages of cell death, loss of oxidative enzymes eg TTC |
| 12-24 hours of infarction | necrotic muscle fibres apparent microscopically (coagulative necrosis- tissues proteins are denatured by underlying structure of the tissue is preserved occurring because of denaturation of proteins causing albumin to change state- jelly) |
| 24-72 hours of infarction | acute inflammatory reaction to dead muscle to remove cell debris from the MI area where neutrophils undergo karyorrhexis |
| 3-14 days of infarction | macrophagic removal of debris and vascular granulation tissue formation (reparative phase) where macrophage goes from promoting inflammation to repair for healing |
| 14-21 days of infarction | fibrous granulation tissue formation |
| 21-56 days of infarction | scar formation and cicatrisation (healing by scar formation) |
| coagulative necrosis | form of necrosis where tissue proteins are denatured by underlying structure of tissue is preserved and this occurs at 12-24 hours of infarction because the denaturation causes albumin to change state (jelly) |
| during 3-14 days in infarction, healing of inflammation involves | ingrowth of capillaries filled with RBCs and fibroblasts producing collagen to form granulation tissue |
| how is granulation tissue formed | during 3-14 days of infarction, there is an ingrowth of capillaries filled with RBC and fibroblasts producing collagen |
| summary of stages of infarction | early cell death and tissue necrosis -> acute inflammatory reaction -> removal of debris and healing -> fibrous granulation tissue formation -> scar formation (healing) |
| sudden death in MI is due to (2) | cardiac dysrhytmia and acute left ventricular failure |
| rupture of myocardium in MI leads to | haemopericardium |
| rupture of papillary muscle leads to | acute valve failure -> LVF, mitral valve regurgitation and potentially fatal (subsequent acute life-threatening cardiogenic shock and pulmonary oedema) |
| mural thrombus on infarct leads to | embolism -> stroke and others |
| early complications of MI (5) | sudden death, rupture of myocardium, rupture of papillary muscle, mural thrombus on infarct, and fibrinous pericarditis and extension of MI |
| haemopericardium refers to | presence of blood within pericardial cavity |
| cause of haemopericardium | full thickness necrosis of myocardium after MI |
| haemopericardium can lead to | increased pressure in pericardial sac- if pressure becomes greater than intracardiac pressure then compression of adjacent cardiac chambers can occur, restricting cardiac filling and decreasing cardiac output |
| cardiac tamponade | compression of adjacent cardiac chambers (leading to decreased cardiac filling and cardiac output) due to pressure greater than intracardiac pressure |
| pericarditis | inflammation of pericardium |
| outer layer of pericardium | fibrous pericardium |
| injury to pericardium leads to release of (3) | release of inflammatory cells, fibrin and fluid |
| fibrinous pericarditis features | pericardial texture is rough, granular and has many fibrous adhesions |
| what is mural thrombus | thrombi which attach to wall of a blood vessel and occur in large vessels eg heart and aorta and can restrict blood flow (not entirely though) |
| major risk of left ventricular thrombus is | subsequent embolisation |
| late complications of MI (3) | chronic LVF, ventricular aneurysm, and swelling of a weakened area in the muscular wall of the heart |
| venous infarction | occurs when entire venous drainage from organ/ tissue remains completely obstructed |
| sequence of events leading to venous infarction | veins obstructed (by extrinsic pressure) -> tissues, capillaries + venules become congested with blood-> pressure in capillaries + venules rises so high leading to rupture with leakage of blood/ arterial blood cant enter leading to hypoxia |
| volvulus | when loop of intestine twists around itself and the mesentery, resulting in bowel obstruction - where delay in diagnosis and treatment is associated with high morbidity/ mortality |
| torsion of testes | occurs when testis twists and rotates trapping the spermatic cord, cutting off blood supply to testes and blood cannot drain out leading to venous infarction |
| ovarian torsion | occurs in ovaries around its ligamentous supports resulting in blood loss to ovaries and fallopian tube |
| factors affecting development of infarction | nature of vascular supply (end artery v dual blood supply), rate of development of occlusion (abrupt v gradual), and type of tissue (eg vulnerability to hypoxia, if its a neuron compared to myocardium etc) |
| how long does it take for infarction to occur in neurons | 2-3 minutes |
| how long does it take for infarction to occur in myocardium | 20-40 minutes |
| how long does it take for infarction to occur in fibroblasts | many hours |
Created by:
kablooey
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