Summary: Episode 48: In this episode, you’ll learn about cell death, types of necrosis and lots of examples of pathophysiologic states that exemplify each condition.<br> Listen to the podcast here…<br> Apoptosis – Programmed cell death<br> Normal functions of apoptotic genes – “programmed to die” (theory).<br> (1) embryo – small bowel got lumens from apoptosis.<br> (2) King of the body – Y c’some (for men); MIF very imp b/c all mullarian structures (uterus, cervix, upper 1/3 of vagina) are gone, therefore, no mullarian structures. MIF is a signal working with apoptosis, via caspasases. They destroy everything, then wrap everything in apoptotic bodies to be destroyed, and lipofuscin is left over.<br> (3)For woman – X c’some; only have one functioning one b/c the other is a barr body. Absence of y c’some caused germinal ridge to go the ovarian route, therefore apoptosis knocked off the wolfian structures (epidydymis, seminal vesicles, and vas deferens).<br> (4) Thymus in anterior mediastinum – large in kids; if absent, it is DiGeorge syndrome (absent thymic shadow), and would also have tetany; cause of thymus to involute is apoptosis.<br> (5) Apoptosis is the major cancer killing mechanism.<br> (6) Process of atrophy and reduced cell or tissue mass is due to apoptosis. Ex. Hepatitis – councilman body (looks like eosinophilic cell without apoptosis) of apoptosis (individual cell death with inflammation around it). Just needs a signal (hormone or chemical) which activate the caspases, and no inflammation is around it. Apoptosis of neurons – loss brain mass and brain atrophy, and leads to ischemia. Red cytoplasm, and pycnotic nucleas.<br> Atherosclerotic plaque. Therefore, apoptosis is involved in embryo, pathology, and knocking off cancer cells.<br> <br> IV. Types of necrosis – manifestations of tissue damage.<br> <br> A. Coagulation Necrosis:<br> Results often from a sudden cutoff of blood supply to an organ i.e. Ischemia (definition of ischemia = decrease in arterial blood flow). In ischemia, there is no oxygen therefore lactic acid builds up, and leads to coagulation necrosis. Gross manifestation of coagulation necrosis is infarction. Under microscope, looks like cardiac muscle but there are no striations, no nuclei, bright red, no inflammatory infiltrate, all due to lactic acid that has denatured and destroyed all the enzymes (cannot be broken down – neutrophils need to come in from the outside to breakdown). Therefore, vague outlines = coagulation necrosis (see color change in heart).<br> Pale vs hemorrhagic infarctions: look at consistency of tissue. Good consistency = grossly look pale: infarct: heart, kidney, spleen, liver (rarest of the organ to infarct b/c dual blood supply); ie coagulation necrosis. Example of a pale infarction of the spleen, most likely due to emboli from left side of heart; causes of emboli: vegetations (rarely embolize in acute rheumatic endocarditis); infective endocarditis; mitral stenosis (heart is repeatedly attacked by group A beta hemolytic streptococcus); and clots/thrombi.<br> The worst arrhythmia associated with embolization in the systemic circulation is atrial fib b/c there is stasis in the atria, clot formation, then it vibrates (lil pieces of clot embolize).<br> <br> B. Gangrenous Necrosis: dry and wet gangrene: <br> Picture of a dry gangrene – not wet/no pus. This commonly occurs in diabetic’s with atherosclerosis of popliteal artery and possible thrombosis; (dry gangrene related to coagulation necrosis related with ischemia (definition of ischemia = decrease in arterial blood flow), which is due to atherosclerosis of the popliteal artery. Pathogenesis of MI: coronary thrombosis overlying the atheromatous plaque, leading to ischemia, and lumen is blocked due to thrombosis. MCC nontraumatic amputation = diabetes b/c enhanced atherosclerosis (popliteal artery = dangerous artery).<br> Coronary is also dangerous b/c small lumen.
