Cellular Adaption Flashcards
4 mechanisms of cell injury
ATP depletion - hypoxia, toxins
permeabilisation of cell membranes - toxins, hypoxia, reactive oxygen species
disruption of protein synthesis - hypoxia, reactive oxygen species
DNA damage - reactive oxygen species, replication errors or exogenous causes (radiation, toxins, viruses)
hallmarks of reversible cell injury
cell swelling
cytoplasmic vacuoles
hypereosinophilia
hydropic degeneration
acute swelling
especially hepatocytes and renal tubular cells
fatty change
accumulation of triglycerides in liver
energy imbalance
outcomes of cell injury
normal -
repair
adapt
senescence
death
abnormal - dysplasia –> neoplasia
hypertrophy
increased cell size
HCM in cats
response to increased workload in hypoxia
reversible if due to treatable disease
hyperplasia
increased cell number
goitre - thyroid hyperplasia due to iodine deficiency
response to increased stimulus, usually hormonal
atrophy
decrease in cell size
small liver from portosystemic chunt
response to lack of use or innervation
metaplasia
changes to a different cell type of same germ layer
squamous metaplasia in parrots with vitamina A deficiency - hyperkeratosis of oral cavity, conjunctiva and nasolacrimal duct
usually from a fragile type to more protective type
dysplasua
abnormal differentiation, can develop to neoplasia
actinic keratosis on white cat ears
show vaired size and shape, hyperchromatic nuclei, large nuclei, increased size and number of nucleoli and mitotic features
senescence
somatic cells that stop dividing but are still metabolically active
due to DNA damage or tumour suppressor genes
lipofuscin
normal feature of long lived post mitotic cells due to wear and tear - accumulation of lipoprotein in secondary lysosomes
excessive accumulation - disease - phalaris poisoning in ruminants
looks similar to ceroid - accumulated in dogs with vitamin E deficiency - brown gut
lysosomal storage disease
accumulation of waste products in cell
metastatic and dystrophic calcification
metastatic - due to increased circulating calcium
dystrophic - secondary to necrosis
necrosis - morphological features
swelling
hypereosinophilia
shrinking nucleus
fragmented nucleus
dissolution of nucleus
inflammation
apoptosis - morphological features
shrinkage
minimal inflammation
chromatin condensation around nuclear periphery
cytoplasmic blebs - apoptotic bodies
causes of necrosis
anoxia - lack of ATP production - can’t work pumps
membrane damage - pore forming agents, toxins, reactive oxygen species, enzyme activation
free radicals - reactive oxygen or nitrogen species - damage mitochondria (neutralised by vitamin e and selenium)
process of apoptosis
extrinsic - death ligand binds to receptor on cell, activated second messenger system
intrinsic - damage to DNA or cytocavity network, formation of apoptosome
caspase
liquefactive/lytic necrosis
liquefactive/lytic -
bacteria or fungi
CNS
hypoxia
pus
histo - cell debris, messy, eosinophilic
coagulative necrosis
hypoxic injury, bacterial or chemical toxins
tissue outline maintained
well demarcated with rim of inflammation
histo - tissue architecture preserved, inflammation, early attempts at healing
caseous necrosis
body trying to remove intracellular bacteria
common in birds and reptiles
cheese like
abscess, granuloma
histo - loss of architecture, central lysed leukocytes, border of granulomatous inflammation, dystophic calcification
gangrenous necrosis
sequel to coagulative
3 types -
wet - sloughing tissue, further degraded by bacteria
gaseous - bacteria proliferate and produce toxins in necrotic tissue - eg clostrium perfringens
dry - secondary to infarction by dehydration, lower end of an extremity, shivelled, no bacteria
fat necrosis
nutritional, enzymatic, traumatic or idiotpathic
focal areas of fat destruction
nutritional - steatitis - diet high in unsaturated fats and low vitamin e
enzymatic - pancreatitis
traumatic - crushing injury
firm, white, chalky
histo - large blobs of fat, eosinophilic/basophilic
fibroid necrosis
associated with inflammation in blood vessels - vasculitis
antigen-antibody complexes deposited in walls
fibrin leakage
histo - bright pink, amorphous hyaline, thrombosis
