Cell Injury, Apoptosis, Necrosis Content

Hypertrophy

increase in size

example of hypertophy

Cardiac hypertrophy, enlarged heart, S4 heart sounds,

physiological reason for hypertrophy

uterus in pregnancy

hyperplasia

increase in cell number not size

Clinical example of Hyperplasia

endomentrial , abnormal uterine bleeding, progesterone therapy

atrophy

lower in cell size example is muscle

Metaplasia

change in phenotype of differentiated cells, caused by chronic irritation,

Clinical Corrilate for metaplasia

epthelia meta columnar trachea to squamaus , and barett esophagus squamous to columnar

R or I lower atp equals swelling

R

Ribosomal detachment R or I

R

blebbing R or I

R

nuclear Changes R or I

R

myelin figures R or I

R

break down of troponin R or I

I

michondrial damage R or I

I

rupture of lysosome R or I

I

nuclear degradation pykosis

I

heart attack check what levels

troponin

Liver damage check what

ALT and AST

muscle levels to check

Creatine Kinas

coagulative

not in brain, caused by blood lost,

liquefactive necrosis

digestino of dead cells, brain and lungs,

caseous

cheese like, TB,

Fbrinoid necrosis

protein leaking of wall, immune response complexes, malignant hypertension

Fat necrosis

pancrease and breast, activated lipase,

Gangernous necrosis Dry

promiment inflamatory, low blood supply,

Gangrenous Necrosis Wet

Bacteria Infections, blood supply, organs, lunchs no inflamantory zone

Initiator caspases

start process 8,9,10

Executioner Caspases

3,6,7

BAX and BAK

proapoptotic ( BAD for survival)

BCl-2 BCL-xl

antiapoptotic

BAX and BAK

form pores in mitochondrial membrane releases cytochrome C activates Caspases

BCL2

lowers capsases activation

extrinstic pathway is started by what

FasL or Tnf alpha, or perfornin and granzyme B release, Fas- Fas L needed for negative selection