Growth Adaptations, Cell Death, Free Radical Injury Flashcards
3 permanent tissues
nerves
cardiac myocytes
sk muscle
Which hyperplastic conditions does not carry with it an increased risk of cancer
BPH-benign prostatic hyperplasia
Cell type switch in Barrett’s esophagus
non-keratinizing stratified squamous –>
non-ciliated columnar with mucin glands
Skin appearance of CO poisoning
cherry-red skin
but they are hypoxic
Iron in which oxidative state binds oxygen
Fe2+
Fe2+ binds O2
Hallmark findings of:
reversible injury
irreversible injury
reversible: cellular swelling
irreversible: membrane damage
Morphologic hallmark of cell death
loss of nucleus
Necrosis basics
pathologic dying of large groups of cells
followed by acute inflammation
Coagulative necrosis
gross pattern
usually wedge-shaped
because due to occlusion of blood vessel
vessels usually supply a wedge-shaped area
Coagulative necrosis due to
ischemic injury in all organs except the brain
Ischemic injury to brain causes
liquifactive necrosis
due to cleanup via microglial cells
Brain infarction
Abscess
Pancreatitis
necrosis type
liquifactive necrosis
brain infarction: microglial cells
pancreatitis: proteolytic enzymes
abscess: proteolytic enzymes from neutrophils
Caseous necrosis
examples
fungal infection
Tb
Fat necrosis
classically seen in
leads to
fat necrosis of peripancreatic fat
leads to soapinification, deposition of Ca on necrotic tissues
Fat necrosis
non-pancreatitis example
trauma to fat
ie breast trauma
causes giant cell reaction with fat present
Fibroid necrosis
2 etiologies
malignant hypertension
vasculitis
A young woman with malignant hypertension
etiology may be
pre-eclampsia
causes fibrinoid necrosis of placenta
These proteins regulate apoptosis
caspaces
Activation of intrinsic apoptotic pathway
cytochrome c leaking
- Bcl2 inactivation
- normally Bcl2 blocks cytochrome c leak from mitochondria
- cytochrome c leaks to activate caspaces
Activation of extrinsic apoptotic pathway
FAS (CD95)-FAS ligand
negative selection of thymocytes in thymus
Cytotoxic CD8 killing mechanism
perforins open cell up a little
granzymes released into target cell
granzymes activate caspaces in cell
apoptosis
Reperfusion injury
carry O2 and WBC back into tissue
causes further damage after reperfusion of tissue
troponin may go up still even after reperfusion due to this mechanism
