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Path - Cell Injury + Cell Death (ii) (Apoptosis (physiological causes…
Path - Cell Injury + Cell Death (ii)
Morphological changes to reversible injury
cellular swelling (aka hydronic change/vaculoar degeneration)
ultrastructural changes (seen with election microscopy)
protrusions in plamsa membrane (blebbing)
loss of microvilli
mt swelling
dilation of ER with ribosomal detachment
nuclear alterations
enzymes released (e.g. troponin in heart, amylase in pancreas)
Necrosis
morphological changes following cell death in living tissues
enzymatic digestion (autolysis + heterolysis)
irreversible
never physiological
always inflamm in surrounding tissue
cytoplasmic eosinophilia (damaged protein causes cytoplasts to pick up even more pink eosin stain than normal)
nuclear changes
1) pyknosis (nuclear condensation/shrinking, chromatin clumping)
2) karyorrhexis (nuclear fragmentation + breakdown)
3) karyolysis (pallor + dissolution)
types
1) coagulative
specific morphological pattern
structure outlines (cell shape) preserved
most common
hypoxic cell death everywhere EXCEPT BRAIN
e.g. due to infarction
nuclei disappear
2) liquefactive
transformation of solid tissue to liquid mass
complete digestion (enzymatic lysis) of dead cells - tissue structure destroyed
due to bacterial/fungal infections, abscesses, hypoxic cell death in CNS
3) Caseous
distinctively characteristic of mycobacterium TB (confirm with Ziehl-Neelson stain)
cheesy, crumbly, white gross appearance
granular debris surrounded by a ring of granulomatous inflamm
4) fat
mimics carcinoma but NOT related to neoplasia (dystrophic calcification - ca2+ deposits)
FAs complex with Ca2+ to form calcium soaps
caused by trauma + pancreatitis
5) fibrinoid
necrotic damage to blood vessel wall
associated with malignant hypertension (extremely high BP, develops rapidly, emergency, causes organ damage) + vasculitis
6) gangrenous
NOT a distintive type (clinical term only)
dry gangrene = coagulative (e.g. ischaemia of LL)
wet gangrene = liquefactive (ischaemia + secondary bacterial infection)
gas gangrene = clostridium infection
Apoptosis
programmed cell death
occurs in single cells or small clusters
physiological causes
embryogenesis
hormonal (involution of breast, endometrial shrinking)
death of post-infection inflamm cells
deletion of auto reactive T cells in thymus
failure to do so = autoimmunity
deletion in proliferating pops (e.g. intestinal epithelium)
pathological causes
virus infection (e.g. T cells apoptose in HIV/AIDS)
DNA damage
tumour cells
energy dependent
not associated with inflamm
membrane remains intact
proapoptotic gene - Bax
antiapoptotic gene = BCL2
triggered by int (mt/DNA damage, decreased hormone stim) or ext (stim of fas suicide R or TNF R) signals
cysteine protease cascade activated - protein cleavage
endonuclease activated - stepwise DNA fragmentation
apoptotic bodies form - rapidly phagocytosed/degraded
cells shrink rapidly (chromatin condensation + cytoplasmic eosinophilia)
increased in NDDs, decreased in neoplasia + autoimmunity