Cell Injury 2 Free Radicals Tylenol toxic to liver causes fulminate Hepatitis No #1 acetylminophen impacts cytochrom P450 CP450

metabolizes Drugs changes drugs to free radicles Liver changes some drugs to active metabolyte (pheyltoin, ex). Target liver and kidneys Where in liver? around central bein treatment: ancylcysteine superoxide dismutiase neutralizes superoxide radicls Glutithione (G) hexose pentse shunts, generates nadph,for anabolic reactions G fx to neurt free radicls esp from peroxide like h2o2 used up with acetyllminophen Acetylcystein replenishes the Gl component Glut s made from acetylcystein keep glut levels up. like leukoverin rescue example Carbontetrachloride: not addresd as often drycleaning..free radicle...ccl3 also along with asprin- destroys kidney acetylminophen aniliates renal medula (free radicle damage) Renl meduula gets 10 % of blood flow already relatively hypoxic alreadly, free radicles knocks off renal tubules asa acts on pge2 (vasodilator) afferent alteriole, leaving vasotension 2 (vasoconstrictor) in charge of renal blood flow. slough renal medula or wipe out ability to concentrate in the loop analgesic nephropathy APOPTOSIS programed cell dath theory of aging has great embryology tie in many orgnns where solid and became hollow by apoptosis Maleness due to Y chromosome germinal ridge went the testicle route generated mullerian inhibitory factor all mullrian structures went through apoptosis (uterus,cervix, uppr 1/3 of vagina ) mullerian inhibitory factor was a signal , the capisisis,

wraps them up and destroys it..leaving lipofusion for parts not digested. female x chromosome one functional x chromosome other is a bar body germinal ridge goes ovarian route factor knocked off wolfian duct structures (eppipdymus, seminal vesicles, vas deferans) thymus is small in adult big in a kid laeral xray if absent= diGeorge syndrome tetany involved in cancer killing also atrophy reducing cell mass hepatitis coulcle mans body indiv cell death no inflam trigger t cell operations often kill by apopoptosis msg neurons in brain atherosclerotic plaques in brain ischem to brain loss of brain mass caspercises pix gross and microscopic necrosis (damage) ischemia- lactic acid denatures and has coagul necrosis heart pale gross is infarction, micro no striation, red, neur from outside vauge outlines of what used to be coagulation necosis pale and hemorrhagic depend on consistentcy good consistency when tissues die including bloood vesles red bloods cells not released from the vessles, take on a pale appearance ex: heart, kidney, spleen, liver, bowel is lose, testicle torsion, hemmorhagic, lungs are loose rbc trickle out to cause hemmorhagic appearance coagul necrosis spleen.pale (embolization) from left side of heart infective endocarditis, miral stenosis, repeatedly attcked by grp a beta streptococus. clots in left atrium, gets atrial fibrilation

arrhyhmia most associated with embolization is atrial fibrilation spaces, clot formation and clots, vegitation dry gangrene wet gangrene has pus oozing off foot-diabetic (from popliteal artery) will have atheroscleosis possible thrombos most common nontraumatic ambutation of lower limbs is diabetes popliteal artery is most dangerous next to cardiac artery (small lumen) dry gangrene is coagulation necrosis due to ischemia ischemia is decrease in arterial blood low pathogensis- atherosclerosis of popliteal arteery pathogenesis of cardiac infarction corronary thrombus over lying artheromatus plaque small bowel hemmrrhagic hemmorhagic infartion trapped into indirect hernia (2nd most comon cause of bowel infarction in small bowel) most coomon is adhesions incarcerated in inguinal hernia sac-hennrrhagic infacttion lung hemmorrhagic infartion of lung is wedgeshaped through the pleurosurface would hav an effusion exudate produced eneutrophils inflam pleua would have pleuritic chest pain, knofelke on inspiration embolis in pulmonary vessle produces hemmorh infarction exception to the rule brain when infarct brain, bruis, narrow lumnen thrombus blocks it and causes trans isch plaques motor /sensory abnl, resolved in 24 hours brain has little mesh work analogousto fibroblast is the astrocyte acting like fibroblast it liquifys no vauge outline liquifaction necrosis no structure, liquifys

cerebral abscess, and old infart-both are liquifative necrosis infection/ple,

liquification is related to neutrophiles purpose: act as host and liquify them most cases are due to infection acute on exception, related to infarct..noninflamatory either infarct/infection same process gram stain: gram positive in clusters (coagulase) forms abscess, converts to fibrin, localizes infction neur not get out stre[ relases hyline neuronidase breaks down gag (cellulitis) lung yellowish areas (gm tain shown gm pos dipplococcus strept pneumonia (most coomon) liq necrosis infartion would be wedged shape in perphery plae and round is abscess grm stain, fever night sweats and wt loss is tb granulomatous interleuk 1, helper t-cells, aslo caseous necrosis (cheesy) means mycobacterial infection or systemic fungal infection lipid in cell wall of the organisms cheesy sarcoidosis (yes, not caseous) not related to mycobactrium mycobacterium or systemic fungal infections oly cause casesous necrosis giant cells, pancrease, abnl pain radiating to the back is pancreatits not peptic ulcer dz (pancrease is retroperitoneal) enymatic fat necroisis fat necrosis related to enymes pendulous breats damaged from running (fat necrosis) traumatic fat necrosuis (can calcify)

lok like cancer painful in trauma, painless in cancer enz in uniue to pancrease, enymes bind calcium and form chalky areas white chalky areas, supponification-soap liek substance salt seen in xray if see xray of pt having pain penetrating his back rt upper quadrant, areas of calcium pancreatitis in pt who is a alcholic enymatic fat necrosis appearance bvlue color in coornary -always calcium dytrophic calcifiaction of damaged tissue calcium salt enzyme is elevated? amylase or lipase lipase more specific amylase is in parotid and sml bowel in fallopin tubes lipase only found in pancrease underlying cause is alcohol fibrinoid necrosis looks like fibrosis but not immunologic dz palpebral pupeba, small vessle vasculitis immuune complex type 3 sm vessle dz immune complex deposition pathogenesis antigen and ab circ in circulation depost in narrow ares, glumerulos, small vesle activates the complement system. alternative system which produces c5a cemotactic neutrophils type 3 hyperens neur does the damage henoch-schl peurpera cobble purpera type 3 vegitations of rheum fveralong the mitral valve sterile fibrinlike material

fibrinoid necrosis nodules on extensor surface with morning stiffness rheum arthritis, fibrinoid due to immonologic damage be anywhere will see it in lupus as well triad area