Chapter 2 Flashcards
hypertrophy
increased cell and organ size due to increased work load
stimulus - mechanical stress, agonists, GF leads to activation of signal transduction pathways
effects - induction of embryonic/fetal genes, increased synthesis of proteins, increased production of GF
occurs in - cardiac mm, skeletal mm, and nerves
hyperplasia
increased cell numbers in response to hormones and GF
mechanism - increased cell production from stem cells
physiologic - due to action of hormones, need to increase functional capacity of organs or compensatory increase after damage
pathologic - excessive or inappropriate actions of hormones of GF acting on target cells
atrophy
decrease in cell and organ size due to decreased nutrient supply or disuse
can be physiologic or pathologic
decreased cell number - apoptosis
decreased cell size - ubiquitin proteasomal pathway and increased autophagy
metaplasia
change in phenotype of epithelial or mesenchymal cells due to response to chronic irritation that makes cells better to withstand stress
mechanism - reprogramming of stem cells that are known to exist in normal tissues or undifferentiated mesenchymal cells present in CT
reversible cell injury
cellular swelling due to changes in ion concentrations and water influx
reduced oxidative phosphorylation w/ resultant depletion of ATP
irreversible cell injury
membrane damage
necrosis or apoptosis
necrosis
cell size - enlarged (swelling)
nucleus - pyknosis, karyorrhexis, karyolysis
plasma membrane - disrupted
cellular contents - enzymatic digestion, may leak out of cell
adjacent inflammation - frequent
physiologic or pathologic role - invariably pathologic
apoptosis
cell size - reduced (shrinkage)
nucleus - fragmentation into nucleosome-size fragments
plasma membrane - intact, altered structure, orientation of lipids
cellular contents - intact, may be released in apoptotic bodies
adjacent inflammation - no
physiologic or pathologic role- often physiologic, may be pathologic
karyolysis
basophilia of chromatin fade
due to loss of DNA by enzymatic degradation by endonucleases
pyknosis
nuclear shrinkage and increased basophilia
chromatin condense
karyorrhexis
fragmentation of pyknosis nucleus
coagulative necrosis
architecture of dead tissue is preserved
tissue has firm texture
nucleus not present
presence of phagocytosis and leukocytes through lysosomes
caused by ischemia causes by obstruction in vessel (infarct)
not seen in the brain
liquefactive necrosis
digestion of the dead cells leading to the tissues becoming a liquid viscous mass
seen in bacterial or fungal infections
creamy yellow due to leukocytes
caused by hypoxic death of cells w/in CNS
seen in brain, abscess, and pancreatitis
gangrenous necrosis
seen in limb that has undergone coagulative necrosis
liquefactive necrosis is also seen - wet gangrene
seen in lower limb and GI tract
caseous necrosis
friable and white cheese like
seen w/ tuberculous (fungal infection)
structure less collection of fragmented or lysed cells and amorphous granular debris enclosed w/in distinctive inflammatory border
fat necrosis
focal areas of fat destruction due to pancreatic lipase activity or trauma
chalky white appearance due to deposition of Ca
shadowy outlines of necrotic fat cells w/ basophilic Ca deposits surrounded by an inflammatory reaction
fibrinoid necrosis
abs and ags complexes are deposited in the walls of a along with fibrin
bright pink and amorphous
seen in blood vessels due to malignant hypertension or vasculitis
depletion of ATP
decrease in Na dependent pump - ion imbalance and cellular swelling
increase in anaerobic glycolysis - decrease in pH leads to clumping of nuclear chromatin
detachment of ribosomes - decrease protein synthesis
superoxide
due to incomplete reduction of oxygen
inactivated by SOD converting to H2O2 and O2
hydrogen peroxide
created by SOD and oxidases in peroxisomes
inactivated by catalase or glutathione peroxidase converting to H20 and O2
hydroxyl radical
created by hydrolysis of H20
inactivated by glutathione peroxidase converting to H20
ONOO
creased by superoxide and NO through NO synthase
inactivated by peroxiredoxins to HNO2
cystic fibrosis
affected protein - CFTR
pathogenesis - defects in Cl transport
familial hypercholesterolemia
affected protein - LDL R
pathogenesis - hypercholesterolemia
tay-sachs disease
affected protein - hexosaminidase beta subunit
pathogenesis - storage of GM2 gangliosides in neurons
alpha-1-antitrypsin deficiency
affected protein - alpha 1 antitrypsin
pathogenesis - apoptosis
creutzfeldt-jacob disease
affected protein - prions
pathogenesis - abnormal folidng of PrPsc leads to neuronal cell death
alzheimer disease
affected protein - A beta peptide
pathogenesis - aggregation w/in neurons and apoptosis
