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Cell death.
Cell death
| Question | Answer |
|---|---|
| what is cell death ? | The morphologic hallmark of cell death is loss of the nucleus, which occurs via nuclear condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis), B, The two mechanisms of cell death are necrosis and apoptosis. |
| What is (pyknosis? | nuclear condensation |
| What is (karyorrhexis)? | fragmentation of the nucleus |
| what is karyolysis)? | dissolution of the nucleus |
| what is necrosis? | Death of large groups of cells followed by acute inflammation(usually in infection and necrosis) Due to some underlying pathologic process; never physiologic Divided into several types based on gross features |
| What is coagulative necrosis? | tissue dies.. structure+ architecture remain firm(coagulation of protiens)... but NO NUCLEUS NOTE Characteristic of ischemic infarction of any organ except BRAIN!!!!!!! This ischemic infarction is of two kinds- pale and red. |
| Describe pale infarction in coagulative necrosis | Area of infarcted tissue is wedge-shaped (pointing to focus of vascular occlusion) & pale. When the artery is occluded, arterioles get no blood.this forms a triangle of dead pale necrotic tissue(no blood not red)(arterioles form arms of the triangle) |
| Describe red infarction in coagulative necrosis | Red infarction arises if blood re-enters a loosely organized tissue (e.g.testicular infarction) in testicles artery going in is thick keeps carrying blood.vien going out collapses... then there is an infarction with blood in it with necrosis |
| what is liquefactive necrosis? | 1. Necrotic tissue that becomes liquefied; enzymatic lysis of cells and protein results NOTE: BRAIN-no coagulative necrosis but liquifactive —Proteolytic enzymes from microglial cells(monophages of the brain) NOTE:Also infection of dead tissue |
| describe liquifactive necrosis in the brain and in abscess | BRAIN-no coagulative necrosis but liquifactive —Proteolytic enzymes from microglial cells(monophages of the brain) Abscess(walled of area)—Proteolytic enzymes from neutrophils |
| Describe liquifactive necrosis in pancreatitis? | Proteolytic enzymes from pancreas liquefy parenchyma(usually they get activated in the digestive tract). This kills the pancreas cells. Different that fat necrosis which is destructionof the fat surrounding the pancreas |
| What is gangrenous necrosis? | C. Gangrenous necrosis 1. Coagulative necrosis that resembles mummified tissue. 2. Characteristic of ischemia of lower limb and GI tract 3. If superimposed infection of dead tissues occurs, t h e n liquefactive necrosis ensues (wet gangrene). |
| What is caseous necrosis? | 1. Soft and friable necrotic tissue with "cottage cheese-like" appearance (Fig. 1.8) 2. Combination of coagulative and liquefactive necrosis 3. Characteristic of granulomatous inflammation due to tuberculous or fungal infection |
| What is fat necrosis? | chalky-white appearance due to calcium deposit in breast and pancreatic fat 3. Fatty acids released by trauma (e.g., to breast) or lipase [e.g., pancreatitis) join with calcium via a process called saponification. |
| What is dystrophic calcification? | When the membrane of a vesicle gets damaged, calcium binds to the phospholipid in the membrane. Phosphatases within the membrane add phosphate groups to the calcium, forming calcium phosphate Enough calcium phosphate, clumps together as a visible deposit |
| what is metastatic calcification? | high serum calcium or phosphate levels lead to calcium deposition in NORMAL TISSUES(e.g., hyperparathyroidism leading to nephrocalcinosis), |
| what is fibrinoid necrosis? | Necrotic damage to blood vessel wall 2, Leaking of proteins (including fibrin) into vessel wall results in bright pink staining of the wall microscopically. 3, Characteristic of malignant hypertension and vasculitis |
| What is apoptosis? | Energy (ATP)-dependent, genetically programmed cell death involving single cells or small groups of cells. |
| What does apoptosis look like? | 1. Dying cell shrinks, leading cytoplasm to become more eosinophilic 2. Nucleus condenses (pyknosis) and fragments (karyorrhexis). 3. Apoptotic bodies fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation. |
| How are caspases activated for apoptosis by intrinsic pathway? | i. Cellular injury, DNA damage, or loss of hormonal stimulation leads to inactivation of Bcl2. ii. Lack of Bel 2 allows cytochrome c to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases. |
| How are caspases activated for apoptosis by extrinsic pathway? | FAS ligand binds FAS death receptor (CD95) on the target cell, activating caspases Tumor necrosis factor (TNF) binds TNF receptor on the target ccll, activating caspases. |
| How are caspases activated for apoptosis by Cytotoxic CD8+ Tcell-mediated pathway? | i. Perforins secreted by CD8+ T cell create pores in membrane of target cell, ii. Granzyme from CD8+ T cell enters pores and activates caspases. |
| What do the ACTIVATED caspases do to allow for apoptosis? | Apoptosis is mediated by caspases that activate proteases and endonucleases, t. Proteases break down the cytoskeleton. 2. Endonucleases break down DNA, |
| What is free radical ? | Free radicals are chemical species with an unpaired electron in their outer orbit.these free radicals can cause injury within the cell when generated pathologically |
| How are free radicals generated physiologically? | during oxidative phosporylation...cytochrome C gives electrons which are picked up by oxygen to form water. Sometimes o2 accepts less than 4 electons and forms free radicals o2-->o2- --> H2o2-->OH-->H2o |
| How are free radicals generated pathologically in radiation? | ionization radiation= radiation hits water within tissue and then generates OH radicals MOST damaging. |
| How are free radicals generated pathologically in inflamation? | Inflammation= nuetrophils have two mechanism- o2 dependent --> oxygen is acted on by NADPH oxidase to make o2-(FREE RADICAL) which is acted on my sulphur oxygen dismutase to make H2o2 is acted on by miloperoxidase to make HOCL(bleach) |
| How are free radicals generated pathologically with metals? | Fe- in Fenton reaction. Fe left unbound in blood generates OH radicals Example HEmachromatosis- tissue damage from access Fe Copper built up in Wilsons disease |
| How are free radicals generated pathologically with drugs? | acetaminophen in the liver is converted into free radicals by the P450 pathway and causes liver necrosis |
| what is the mechanism behind damages by free radicals? | Free radicals cause cellular injury via peroxidation of lipids and oxidation of DNA and proteins which damages cells and DNA leading to mutationin DNA and possible cancers. |
| How to eliminate free radicals? | Antioxidants (glutathione and vitamins A , C, and E) Metal carrier proteins (e.g., transferrin and ceruloplasmin) for free Fe and Cu Enzymes->Superoxide dismuiase(o2- -->H2o2) Catalase-H202->H2o+02 TWO Glutathione peroxidase-> H2o2-->H2o |
| Destruction by CCL4 generated free radicals? | dry cleaning industry Converted to CC13, free radical by P450 system of hepatocytes Results in cell injury with swelling of RER; consequently, ribosomes detach, impairing protein synthesis. Decreased apolipoproteins lead to fatty change in the liver |
| Destruction by reperfusion of blood to cells? | L Return of blood to ischemic tissue results in production of O,-derived free radicals, which further damage tissue.(non functioning oxidative phosphorylation therefore less than 4 electorns are generated per oxygen molecule) Example myocardial infarcti |
| Difference between apoptosis and necrosis? | apoptosis is not followed by inflammation while necrosis is followed by inflammation |
Created by:
atayal
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