Cellular Adaption

Question 1

4 mechanisms of cell injury

Answer 1

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)

Question 2

hallmarks of reversible cell injury

Answer 2

cell swelling
cytoplasmic vacuoles
hypereosinophilia

Question 3

hydropic degeneration

Answer 3

acute swelling
especially hepatocytes and renal tubular cells

Question 4

fatty change

Answer 4

accumulation of triglycerides in liver
energy imbalance

Question 5

outcomes of cell injury

Answer 5

normal -
repair
adapt
senescence
death

abnormal - dysplasia –> neoplasia

Question 6

hypertrophy

Answer 6

increased cell size

HCM in cats
response to increased workload in hypoxia

reversible if due to treatable disease

Question 7

hyperplasia

Answer 7

increased cell number

goitre - thyroid hyperplasia due to iodine deficiency

response to increased stimulus, usually hormonal

Question 8

atrophy

Answer 8

decrease in cell size

small liver from portosystemic chunt

response to lack of use or innervation

Question 9

metaplasia

Answer 9

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

Question 10

dysplasua

Answer 10

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

Question 11

senescence

Answer 11

somatic cells that stop dividing but are still metabolically active
due to DNA damage or tumour suppressor genes

Question 12

lipofuscin

Answer 12

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

Question 13

lysosomal storage disease

Answer 13

accumulation of waste products in cell

Question 14

metastatic and dystrophic calcification

Answer 14

metastatic - due to increased circulating calcium

dystrophic - secondary to necrosis

Question 15

necrosis - morphological features

Answer 15

swelling
hypereosinophilia
shrinking nucleus
fragmented nucleus
dissolution of nucleus
inflammation

Question 16

apoptosis - morphological features

Answer 16

shrinkage
minimal inflammation
chromatin condensation around nuclear periphery
cytoplasmic blebs - apoptotic bodies

Question 17

causes of necrosis

Answer 17

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)

Question 18

process of apoptosis

Answer 18

extrinsic - death ligand binds to receptor on cell, activated second messenger system
intrinsic - damage to DNA or cytocavity network, formation of apoptosome

caspase

Question 19

liquefactive/lytic necrosis

Answer 19

liquefactive/lytic -
bacteria or fungi
CNS
hypoxia
pus

histo - cell debris, messy, eosinophilic

Question 20

coagulative necrosis

Answer 20

hypoxic injury, bacterial or chemical toxins
tissue outline maintained
well demarcated with rim of inflammation

histo - tissue architecture preserved, inflammation, early attempts at healing

Question 21

caseous necrosis

Answer 21

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

Question 22

gangrenous necrosis

Answer 22

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

Question 23

fat necrosis

Answer 23

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

Question 24

fibroid necrosis

Answer 24

associated with inflammation in blood vessels - vasculitis
antigen-antibody complexes deposited in walls
fibrin leakage

histo - bright pink, amorphous hyaline, thrombosis