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What is the morphologic hallmark of cell death?

loss of nucleus via: pyknosis (shrinking down of nucleus), karyorrhexis (breaking up into pieces), and karyolysis (breaking down into smaller parts)


What should I know about the process of necrosis?

death of lots of cells followed by acute inflammation


What is coagulative necrosis?

necrotic tissue that remains firm. cells are present, but the nuclei have disappeared. seen in ischemic infarction for every organ except the brain.
usually area of infarction is wedge-shaped and pale. wedge points to the area of occlusion


What is red infarction?

blood must reenter the tissue in a loosely organized tissue: classically, a testicle after a vein has collapsed.


What is liquefactive necrosis?

necrotic tissue that becomes liquefied via enzymatic lysis of the cells. seen in brain infarction (d/t microglia cells), abscess (d/t lytic enzymes from neutrophils), and pancreatitis (necrosis of the pancreas itself)


What is gangrenous necrosis?

coagulative necrosis that resembles mummified tissue. seen in ischemia of the lower limb and GI tract. If a superimposed infection occurs, then liquefactive necrosis occurs.


What is caseous necrosis?

soft friable necrotic tissue with a cottage cheese appearance:
combo of coagulative and liquefactive necrosis.
characteristic of granulomatous inflammation d/t TB or fungal infection


What is fat necrosis?

necrotic adipose tissue with chalky-white appearnce d/t deposition of calcium (saponification: binding of fat and calcium)
may be seen in the peripancreatic fat in pancreatitis
may also be caused by trauma to fat, esp. the breast. Also mediated by giant cells. Can present as a mass.


What is saponification>

fatty acids are released by trauma or lipase join with calcium.
this is an example of dystrophic calcification: dead or dying tissue allows calcium to deposit on the tissue. Also seen in semomma bodies. serum calcium is normal


What is metastatic calcification?

calcium or phosphate is elevated- forces calcium onto the tissues of the body.


What is fibrinoid necrosis?

necrotic damage to the blood vessel wall
leaking of proteins into the blood vessel that causes bright pink staining.
characteristic of malignant hypertension or vasculitis.


What are examples of physiologic apoptosis?

menstrual periods, CD8+ T cell mediated killing of virally infected cells, removal of skin between fingers during fetal development


Morphology of apoptosis

dying cell shrinks and become eosinophilic
nucleus condenses and fragments
apoptotic bodies fall from the cell and are removed by macrophages
no acute inflammation follows


What mediates apoptosis?

Caspases are activated, and they:
activate proteases, which break down the cytoskeleton, and activate endonucleases, which break down DNA


By what pathways do we activate caspases?

1. intrinsic mitochondrial pathway: caused by cellular injury, DNA damage (incr. BAX or BAF), or decr. hormonal stimulation that inactivates Bcl2. In this pathway, cytochrome c leaks out. Bcl2 guards the mitochondrial membrane and prevents cytochrome c from leaking out (Bcl2 binds to Apaf-1)
2. extrinsic receptor-ligand pathway: FAS ligand binds FAS death receptor on the target cell. Important for preventing self-recognition in T cells (negative selection). Also, TNF binding TNF receptor can do this.
3. Cytotoxic CD8+ T cell pathway: perforin from the T cell makes a hole in the target cell. granzyme enters the pore and activates caspases.

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