Pathology 1.1 Flashcards
causes of cell injury and death
physical, hypoxia, toxins, infection, inflammation, genetics, nutrition
which are cells most prone to injury
high metabolic activity, rapidly proliferating
free radicals
major cause of cell damage.
ACE vitamins protect from them
degrees of cell injury
reversible- not enough to kill cell
Mild ATN, toxic liver injury, severe exercisee
irreversible- cell death
holes in membrane, long Ca++ influx, mitochondrial loss
apoptosis
programmed cell death
energy requiring
one cell @ a time, no inflammation
completely normal, happens in embryology down to regular cell turnover.
viral infections can induce it
necrosis
uncontrolled cell death
cell membrane disruption
inflammation
cell clusters
*gangrene.
hypoxia
loss of ATP, anaerobic glycolysis with lactate and acidosis.
cell swells and ER vacuoles, fatty change
Apoptosis mechanisms
intrinsic pathway- dominant, based on mitochondria. BCL2 and Bax.
Caspase cascade
apoptptic cell
condensed cell body, nucleus is shriveled up. DNA gets degraded. TdT stains for free ends of DNA
too much apoptosis
neurodegenerative disease, ischemic diseases (MI, Stroke)
too little apoptosis
neoplasms (p53 mutations common)
viral infections. immune induced apoptosis
cellular changes in necrosis
deep red cytoplasm swollen cells nuclei not basiphilic hemorrhage acute inflammation fibrosis
pyknosis
shriveled dark nucleus
karyolysis
digested, pale nucleus. no longer blue
Karyorrhexis
nuclear fragmentation
patterns of necrosis
coagulative- with ischemia. makes infarct. lose myocardium.
liquefactive- loss of substance, in brain or accesses
fat necrosis- necrosis in fat
caseous necrosis- necrotizing granulomas combination of liquefactive and coagulative. fungal or TB infection
gangrenous necrosis- necrosis of whole anatomic area
firinoid necrosis-
coagulative necrosis stages
1 day normal
3 days neutrophils
1 week lymph’s mostly present
2 weeks macros
caseous necrosis
multicellular giant bunches. pale cheesy look to it.
fibronoid necrosis
really fibrin deposition + necrosis
myelin figure
opening in the cells membrane
lipofuscin
degraded lipid in lysosomes, free radical damdge
bilirubin
hemoglobin breakdown product
normally present in bile
jaundice
hemosiderin
iron containing pigment
excessive iron absorption, bleeding into tissues.
looks like brown stuff in tissues.
found by iron stain, turn blue.
Melanin
brown pigment, made in melanocytes
intracellular protein storage
alpha 1 antitrypsin deficiency- looks like blood clumps.
can end up with emphysema.
Russel bodies in plasma cells- antibody accumulation.
extracellular protein storage
amyloid.
fibrosis
Anthracosis
carbon pigment
mostly in lungs- coal workers.
calcification
Hydroxyapatite
Dystrofic- into damaged tissue
metastatic- into normal tissue.
