Day 1: (TEXT) Flashcards
Difference between ischemia and anoxia?
Ischemia is insufficient blood flow to provide adequate oxygenation. this leads to absence of oxygen, or anoxia.
What are consequences of anoxia, intracellularly and cellularly?
Lower oxidative phosphorylation means less ATP. Lowers Na+ pump. This increases influx of calcium, water, and sodium, and increases efflux of potassium. This results in cellular swelling. Furthermore, we see anaerobic glycolysis and detachment of ribosomes (lowering protein synthesis).
What is sublethal injury? What morphological changes occur?
Reversible cell injury: stage at which deranged function and morphology can return to normal without injurious agent, typically with mild/transient injury.
CYTPOPLASM: changes-> cellular swelling
NUCLEUS: stays the same
fatty change!
What is the difference between necrosis and apoptosis?
Necrosis: cell dies because of severe attack (anoxia or toxin exposure): accidental, unregulated death
includes swelling of endoplasmic reticulum and mitochondria
Apoptosis: purposeful cell death because of steps involving protein synthesis and enzyme activation, called cell suicide. might happen in physiological steps like embryogenesis.
What happens to cell size for necrosis v. apoptosis?
Necrosis: enlarged (swelling)
Apoptosis: reduced (shrinkage)
What happens to plasma membrane for necrosis v. apoptosis?
Necrosis: disrupted plasma membrane
Apoptosis: intact, altered structure, orientation of lipids change.
Cellular contents in necrosis v. apoptosis?
necrosis: enzymatic digestion, may leak out of cell
apoptosis: intact, may be released in apoptotic bodies
Adjacent inflammation in necrosis v. apoptosis?
frequent inflammation around necrotic cells, not around apoptotic cells
Name the five morphologic forms of necrosis.
Coagulative, liquefactive, caseous, fat, and fibrinoid
What can cause coagulative necrosis? How does it look histologically?
ischemia due to sudden arterial occlusion by a thrombus. in solid tissues like heart, kidney, and spleen.
you see neutrophils (inflammatory response after ruptured cell membrane after ruptured lysosomes)
and intensely eosinophilic cells because of loss of RER and associated mRNA
What causes liquefactive necrosis? How does it look histologically?
Unlike coagulative, you see digestion of dead cells so tissue architect ure is lost.
Occurs when focal bacterial infections caused by microbes that stimulate rapid neutrophil and tissue digestion bc of lysosomes. also always a consequence of hypoxic death of nervous system cells.
the liquefied tissue is pus, and it’s removed by macrophages.
What causes caseous necrosis? What does it look like?
occurs because of tuberculosis.
grossly appears as cheesy, granular semi liquid material, . typically a focus of caseous necrosis is surrounded by macrophages and lymphocytes forming a granuloma.
foci of caseous necrosis may have calcium deposits from the blood, such tissue deposition of calcium is called dystrophic calcification.
What causes fat necrosis? How do you detect? What does it look like?
activated lipases are released from acute pancreatitis, go into peritoneal cavity.
this is an emergency! you can detect by finding amylases in the blood.
fat necrosis appears as foci of chalky gritty deposits in mesenteric fat, dead fat cells seen with deposition of bluish staining calcium.
What causes fibrinoid necrosis? What does it look like?
deposition of antigen-antibody complexes in vessel walls, then blood vessels undergo necrosis.
immune complexes and fibrin leaks out of the damaged vessels into the vessel wall stain bright pink in H adn E stained tissue sections, as does fibrin.
pink amorphous granular material along with necrosis of the vessel wall.
What causes hyaline change? What does it look like?
not cell injury, but rather it’s just an appearance that you see in chemically diverse substances.
microscopically, appears as homogenous, glassy, pink material in routine H and E stains.
