Cell Injury Flashcards
(20 cards)
what is steatosis? how does it occur?
fatty change in the liver; alcohol changes fat metabolism by decreasing fatty acid oxidation, decreasing lipoprotein synthesis and increasing triglyceride synthesis.
What is Mallory’s hyaline?
an example of permanent damage to a hepatocyte. abstinence from alcohol will still leave a damaged hepatocyte. dense pink rope like body in the cytoplasm of hepatocytes and is an accumulation of Cytokeratin filaments.
what is hemochromatosis?
a genetic disease that results in abnormal accumulation of iron in tissues. seen as rusty tan color in stain.
Burkitt lymphoma is an example of:
what histological pattern is associated with this:
macrophage phagocytosis of apoptotic B cells
“starry sky” – lightly stained macrophages with apoptotic bodies surrounded by the dense infiltrate of malignant lymphocytes
what is ischemia?
the effect of oxygen deprivation on cell morphology
what are some of the early, reversible effects of hypoxia on a cell?
a histologic example of early hypoxia would be:
increased cell volume as Na enters w/water, increased Ca influx causes damage to cell membrane
myocardial edema
what is necrosis?
cell death at tissue level.»_space; morphological changes of tissue due to enzymatic degradation of dead cells by lysosomal enzymes, and denaturation of proteins
The two types of necrosis are _____ and _____
coagulative and liquifactive
Coagulative necrosis results from:
denaturation of proteins (dominate picture). ex: mycoardial/renal/pulmonary infarction
Liquifactive necrosis results from:
extensive inflammation due to bacteria or fungus»_space; complete digestion of tissue. ex: abcess & cerebral infarction
what is caseous necrosis?
usually associated w/TB. combo of liquifactive and coagulative necrosis»_space; cheese like morphology
1) Distinguish reversible from irreversible cell injury.
reversible ex: steatosis. Liver hepatocyte–> steatosis (fatty change)»_space; abstinence»_space;healthy hepatocyte
permanent: ex: hepatocyte –> mallory’s hyaline (cytokeratin) –> abstinence –> damaged hepatocyte
reversible ex2: excess iron absorption»_space; hemosiderosis»_space; treatment»_space; normal hepatocyte
permant ex 2: hemosiderosis»_space; no treatment»_space; cirrhosis
2) Identify the cytological changes that are associated with irreversible injury.
Mitochondrial swelling, loss of nuclear envelope/cell membrane, invasion by keratin filaments
3) Explain how steatosis occurs due to alcohol ingestion.
Mobilizization of fatty acids from stores
Decreased fatty acid oxidation
Increased triglyceride synthesis
Increased lipoprotein synthesis
Decreased glycosylation & transport of VLDL = accumulation of tryglycerides in liver
4) Name and distinguish 4 types of pathological necrosis.
Liquifactive: necrosis w/significant inflammation often due to bacterial or fungal infection. ex: abcess or cerebral infarction
Coagulative: most common. denaturation of cellular proteins. ex: ischemic origin, “white necrosis”
Caseous: combo of L & C necrosis
Gangrenous: overlay of liquifactive on already necrosed tissue
5) Explain the relationship between hemochromatosis and cirrhosis.
Hemochromatosis (genetic increase in iron absorption) results in liver cirrhosis if untreated. Overaccumulation of iron»_space; scarring (cirrhosis)
6) Diagram the mechanisms active in cellular apoptosis.
1
7) Name four features of cellular injury that are reversible.
cellular swelling loss of microvilli Bleb myelin figures ER swelling
8) Describe the electrolyte shifts that occur in ischemic cell injury leading to cell death.
Cells lose ability to maintain Na/K gradient via ATPase (no O2 = no oxidative phosphorylation). Na and Ca enter the cell and result in additional injury to cytoskeletal and membrane integrity
9) Explain the role of Ca++ ions in irreversible cell injury.
Enters cell freely and causes release of phospholipases, proteases, endonucleases, and decreased ATPase activity. Mitochondria swell and Ca deposits are seen on EM.
