01 cell growth, injury, death Flashcards
keratomalacia
stratified keratinizing squamous metaplasia of conjuctiva. Vitamin A deficiency. Normal = simple squamous.
hypoxemia values
PaO2 <60 mm SaO2 <90%
CO poisoning Sx
cherry red skin, headache
methemoglobinemia - phys, Sx, Tx
Fe3+ cannot bind O2; normal PaO2, low SaO2; drugs (sulfas, nitrates) or newborns; chocolate blood; methylene blue
why does hypoxemia damage cells
now ATP –> Na-K pump and Ca2+ fail –> water, Na+, and Ca2+ buildup INSIDE; lactic acid builds up, low pH
loss of nucleus - 3 stages
pyknosis (condensation, karyorrhexis (fragmentation), karyolysis (dissolution)
liquifactive necrosis - mechanism
proteolytic enzymes from microglia, neutrophils, or pancreas
gangrene necrosis - cause and locations
ischemia of lower limbs and GI tract
fat necrosis mechanism
saponification - fatty acids combine with calcium
fibrinoid necrosis
necrotic damage of blood vessels wall due to leakage of proteins - stains bright pink
intrinsic (mitochondrial) apoptosis
cell/DNA damage or loss of hormone signals –> Bcl2 turns OFF –> cytochrome C leaks from inner mitochondrial membrane –> activates caspases –> activate proteases and endonucleases
extrinsic apoptosis - 2 mechanisms
A. FAS ligand binds FAS death receptor (CD 95) - i.e. negative selection of T cells
B. TNF binds TNF receptor
most harmful free radical + 2 causes and mechanism of damage
hydroxyl (OH-)
ionizing radiation, metals (copper and iron)
peroxidation of lipids, oxidation of DNA and proteins
name 4 antioxidants
vitamins A,C,E and glutathione
3 enzymes that handle free radicals, their location, and mechanism
- SOD - mitochondria; makes H2O2
- Glutathione peroxidase - mitochrondria
- Catalase - peroxisomes; turns H2O2 into O2 and H2O