5 Pages
Unlock Document

University of Manitoba
Biochem. and Medical Genetics
BGEN 3020
Jason Leboe- Mcgowan

Apoptosis Programmed cell death. Apoptotic genes – “programmed to die” (theory). Normal functions: (1) embryo – small bowel got lumens from apoptosis. (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. (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). (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. (5) Apoptosis is the major cancer killing mechanism. (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 pynotic nucleas. Atherosclerotic plaque. Therefore, apoptosis is involved in embryo, pathology, and knocking off cancer cells. Types of necrosis – manifestations of tissue damage. A. Coagulation Necrosis: 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). 1. Pale vs hemorrhagic infarctions: look at consistency of tissue. (a) 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. 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). Gangrenous Necrosis: dry and wet gangrene: Picture of a dry gangrene – not wet gangrene b/c there’s no pus. 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). Coronary is also dangerous b/c small lumen. In wet gangrene, it’s complicated by infective heterolysis and consequent liquefactive necrosis. (b) Loose consistency of tissue= hemorrhagic infarct: bowel, testes (torsion of the testes), especially the lungs b/c is has a loose consistency and when the blood vessels rupture, the RBC’s will trickle out, leading to a hemorrhagic appearance. nd Example: hemorrhagic infarction of small bowel due to indirect hernia. 2 MCC of bowel infarction is getting a piece of small bowel trapped in indirect hernial sac. MCC of bowel infarction is adhesions from previous surgery. Example: In the Lung – hemorrhagic infarction, wedge shaped, went to pleural surface, therefore have effusion and exudates; neutrophils in it; have pleuritic chest pain (knife-like pain on inspiration). Pulmonary embolus leads to hemorrhagic infarction. B. Liquefactive Necrosis: Exception to rule of Coagulation necrosis seen with infarctions: brain. MC site of infarction from carotid artery – why we listen for a bruit (hearing for a noise that is going thru a vessel that has a narrow lumen – place with thrombus develops over atherosclerotic plaque and leads to stroke); leads to transient ischemic attacks is little atherosclerotic plaques going to little vessels of the brain, producing motor and sensory abnormalities, that go away in 24 hrs. Brain with ‘meshwork’ – in brain, astrocytes is analogous to the fibroblasts b/c of protoplasmic processes. Therefore, acting like fibroblast (can’t make collagen), but its protoplasmic processes gives some structure to the brain. Therefore, infarction of the brain basically liquefies it (has no struct), and you see a cyst space – liquefactive necrosis. Therefore, exception to the rule of infarctions not being coagulative necrosis is the brain and it undergoes liquefactive necrosis (no struc, therefore leaves a hole). Cerebral abscess and old atherosclerotic stroke -both are liquefactive necrosis. Liquefactive – liquefies; think neutrophil, b/c their job is to phagocytosis with their enzymes (to ‘liquefy’); liquefactive necrosis relates to an infection with neutrophils involved (usually acute infection – producing an abscess or an inflammatory condition, which liquefies tissue). Therefore, liquefactive necrosis usually applies to acute inflammation, related to neutrophils damaging the tissue. Exception to the rule: liquefactive necrosis related to infarct (not an inflammatory condition, it just liquefies) (slide shows liquefactive necrosis due to infection in the brain). So, if you infarct the brain, or have an infection, or have an abscess it is the same process – liquefactive necrosis. Example: Abscess – gram “+” cocci in clusters. Why are they in clusters? Coagulase, which leads to abscesses with staph aur. Coagulase converts fibrinogen into fibrin, so it localizes the infection, fibrin strands get out, resulting in an abscess. Strep: releases hyaluronidase, which breaks down GAG’s in tissue, and infection spreads through the tissue (cellulitis). From point of view of necrosis, neutrophils are involved, therefore it is liquefactive necrosis. Example: ABSCESS: Lung – yellowish areas, high fever and productive cough; gram stain showed gram “+” diplococcus, which is strep pneumoniae. (MCC of bronchopneumonia.). Not hemorrhagic b/c its pale, and wedged shaped necrosis at the periphery, which leads to pleuritic chest pain. Example: pt with fever, night sweats, wt loss – M tb, which has granulomatous (caseous) necrosis. Pathogenesis of granuloma (involves IL-12 and subset of helper T cells and “+” PPD). C. Caseous (cheesy consistency) Necrosis: – either have mycobacterial infection (any infections, including atypicals, or systemic fungal infection); these are the ONLY things that will produce caseation in a granuloma. It is the lipid in the cell wall of the organism’s leads to cheesy appearance. Sarcoidosis – get granulomas, but they are not caseous b/c they are not mybacterium or systemic fungi (hence ‘noncaseating’ granulomas) Crohn’s dz – get granulomas, but not caseous b/c not related to mycobacterium or systemic fungi. Fat Necrosis: 1. Enzymatic Fat Necrosis: unique to pancreas Example: pt with epigastric distress with pain radiating to the back – pancreatitis (cannot be Peptic Ulcer Dz b/c pancreas is retroperitoneal), therefore just have epigastric pain radiating to the back. A type of enzymati
More Less

Related notes for BGEN 3020

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.