book- general pathology Flashcards
(13 cards)
hypertrophy vs hyperplasia
increased cell size usually via increased hormones or functional demand
increased number of cells usually from hormones, functional demand, and persistent cell injury
metaplasia
conversion of one type of tissue to another due to persistent injury
epithelial changes in GERD
stratified squamous –> simple columnar
mechanisms of reversible cell injurt
reduced ATP
increased anaerobic respiration (glycolysis) causing a build up of lactate and decrease in pH
failure of Na/K pump
failure of ATP-depednet calcium pump; increases intracellular calcium
decreased pH activates cell lysosomal enzyme and contribute to mitochondrial damage
fatty changes via ethanol, protein and iron malnutrition, diabetes –> mobilize FFA and have more triglycerides in liveri
irreversible changes to cells
necrosis
coagulative necrosis; esp if no collateral flow (in organs with end arteries), from ischemia
liquefactive necrosis; destroy tissue by lysosomal enzymes i.e. from bacterial infection
caseous necrosis; coagulation plus liquefaction necrosis i.e. in TB granulomas (soft and cheese like tissue)
gangrenous necrosis; ischemia to lower extremity or bowel
enzymatic fat necrosis; complication of pancreatitis- enzymes activated too quick and digest pancreas; liberate fatty acids which combine with Ca2+ and makes soaps
fibrinoid necrosis: autoimmune like SLE- get deposits in tunica media of medium and small arteries of fibrinogen, complement, Igs, proteins that get calcified and impact blood flow
gene in cancers that blocks apoptosis and immortalizes affected cells
bcl-2 gene
also no more p53 tumor suppressor gene
infiltration
excess calcium, amyloid or fat
amyloid- protein depositions especially Igs (antibodies); stain in Congo red dye
calcium: necrotic tissues when cancer cells die, hyperparathyroid, excess vitamin D intake etc
hemosiderin
yellow brown granules if iron bound to ferritin; in cytoplasm of macrophages. from transfusions, hemochromatosis, internal bleeds
melanin
from oxidation products of tyrosine in melanosomes; sun exposure
lipofuscin
yellow brown granules with lipid residues from lysosomal digestion
bilirubin
yellow bile pigment; sodium billirubinate (soluble) or insoluble calcium salt gallstones. formed by hemoglobin in destruction of ertythrocytes. associated with jaundice
cells and findings in acute vs chronic inflammation
acute: neutrophils, swelling, edema
chronic: macrophages, lymphocytes, plasma cells, fibroblasts, new blood vessels, systemic sx, granulomas