Pathology Flashcards
What happens during ischemia
Na pump slows.
In flux calcium, efflux of potassium.
Anerobic increase
low glycogen ,increase. lactic acid, low pH
Mechanisms of irreversible injury
Low ATP
Mitochondrial damage
Membrane damage (calcium influx)
Increased ROS damage to lipids , proteins, and NA
Reversable vs irreversible
Reverse: swelling of ER and mitochondria, goes back down.
Irr: Breakage of PM , organelles , and nucleus leakage.
Morphology of irreversible damage
Hypereosinophilia (RNA loss-pink)
Mitochondrial swelling nad amorphous densities.
Nuclear pynknosis (chromatin condensation), fragmentation, and dissolution.
Intracytopladmic myelin figures.
Loss of O2 in cell
decrease in phospholipids
Effect of increased cytosolic calcium
Lipid break down (due to phospholipase and protease activation).
Examples of liquefaction
brain infarct , abscess
Examples of fat necrosis
pancreatitis , pancreatic trauma
Example of caseous necrosis
TB, histoplasmosis.
Example of fibrinoid necrosis
nectorotic tissue due to immunological reaction.
Usually seen in blood vessels with deposition of complement and antibodies in vessels wall.
Physiological apoptosis
embryogenesis , menstrual cycle, lactating breast
Pathologic apoptosis
viral, injuring agents, anticancer drugs, radiation.
Apoptosis mechanisms
Endonuclease activation
Cytoskeleton disruption by protease
Cytoplasmic protein cross linking by transglutaminase
Cell surface changes leading to phagocytosis
Apoptotic morphology
shinrkage
chromatin condense
bleb (apoptotic bodies)
phagocytosis
lack of inflammatory reaction
Intrinsic pathway (mitochondrial)
**cytochrome C
Due to DNA damage or protein misfolding
Extrinsic pathway
Receptor ligand interaction
Fas , TNF receptor
caspase activation
Intrinsic pathway
cytochrome C
caspase -9 activated,
process inhibited by BCL2
Extrinsic pathway
occurs in special cases
remove self reactive T-cells and kill infected cells, etc
also lead to caspase activity that breaks nucleus and cytoplasmic structure
Hyperplasia
Physiologic: hormone induce
Pathologic: viral, papillomavirus. BPH -excessive stimulation.
Hypertrophy
Physiologic: hormonal stimulaiton.
Pathologic: LVH, due to HTN, or valve stenosis-heart works very hard. The myocytes cannot divide, so only option is to increase in size.
Metaplasia
Reversible change
One type to another
-ciliated columnar to squamous (which is not functional in bronchi) can lead to squamous cell carcinoma.
If stimulus such as smoking persist, it can progress to displasia (cancer growth).
Hemosiderosis
iron overload in phagocytic cells (WBCs) no tissue damage
Hemochromatosis
iron overload in parenchymal cells
there is tissue damage
Causes of metastatic calcification
hyperparathyroidism
bone breakdown (cancer)
Increased vitamin D or sarcoidosis
Renal failure