Cell Injury Flashcards
what are some responses to cellular response to stress and injury
atrophy
hypertrophy
hyperplasia
metaplasia
what is atrophy?
decrease in the size of cells due to loss of cell substance
either physiological or pathological
- decreased workload
- loss of innervation
- diminished blood supply
- inadequate nutrition
- loss of endocrine stimulation
what is hypertrophy?
increase in the size of the cells resulting in an increase in the size of an organ
reflects increased production of cellular protein
occurs in cells incapable of division
physiological: skeletal muscle in exercise, uterus in pregnancy
pathological: left ventricular hypertrophy in hypertension
what is hyperplasia?
increase in the number of cells - usually also the size of the organ
physiologically: breast during pregnancy, after a partial hepatectomy
pathologically: excessive hormonal/growth factor
controlled process but fertile soil for cancer
columnar epithleium is better for what?
it is more adapt for acid, bile etc - contains goblet cells which produce mucous
squamus cell epithelium is better adapt for
physical strenghth, like skin, doesn’t produce mucous
what is the greatest factor of malnutrition in our country?
obesity
cellular response depends on …?
on the injury
- type
- severity
- duration
consequences of cellular injury depends on …?
The cell
- type
- state
- adaptability
which cell systems are most vulnerable to injuries?
- mitochondria
- cell membrane- requires energy to maintain
- synthetic apparatus - proteins and enzymes
- cytoskeleton
- genetic apparatus (DNA)
what mechanisms occur with cell injury?
- inhibition of aerobic respiration = ATP depletion
- generation of oxygen species (free radicals)
- defects in membrane permeability (ion depletion)
- disruption of calcium homeostasis (calcium influx)
PET scan detects what?i
it shows the activity of cells
describe what occurs when there is a decreased oxidative phosphorylation within the mitochondria?
- decreaed ATP
- increased anaerobic glycolysis
- reduced activity of sodium pump
- increased cytosolic free calcium - activates enzymes
- ATPase- decreased ATP
- phospholipase - decreased phospholipids
- endonuclease - nuclear chromatin damage
- protease- disruption of membrane and cytoskeletal proteins
normal function of lysozomes?
degradation of proteins
what ion, in high concentration, leads to necrosis?
calcium
How are free radicals degraded?
- spontaneous decay
- inactivation by enzymes
- antioxidants
how do free radicals cause cell injury?
- lipid peroxidation of membranes - react with membrane to produce highly reactive lipid peroxide
- oxidative modification of proteins
- react with DNA and cause mutation
- generally cells irreversibly damaged by free radicals are deleted by apoptosis (by gaurdian of the genome = P53)
what are the morphological changes associated with reversible cell injury?
cellular swelling (liver swells up after a three day drinking binge)
ultrastructural changes: plasma membrane alteration, mitochondrial swelling, dilation of ER with retachment of ribosomes, nuclear alterations
what is the definition of necrosis?
a live organism experiencing tissue death
so you couldn’t find necrosis on a dead person… becuase all of their tissue is dead
this is important b/c it generates an infection in the surrounding tissues
what nuclear changes are associated with necrosis?
- nucleus becomes pale = karyolysis
- nucleus become small and dense= pyknosis
- fragment/breakdown of the nucleus = karyorrhexis
what is coagulative necrosis?
preservation of the structural outlines, with necrosis
characteristic of hypoxic cell death except in the brain
what is liquefactive necrosis?
transformation of solid tissue into a liquid mass
- complete digestion of the dead cells leads to a complete loss of the tissue
characteristic of bacterial and some fungal infection , and hypoxic cell death in the CNS and the brain due to very little connective tissue stroma
what is fat necrosis?
necrosis due to lipases = common in breast
creates a hard mass and is a symptom of malignancy
what is gangrenous necrosis?
not a distinctive pattern of cell death - but infective in nature
ischaemia with secondary bacterial infection
- wet gangrene
- gas gangrene
- dry gangrene
what are some physiological reasons for apoptosis?
- thymus gland after infanthood
- endometrial shedding with menstrual cycle
- death of inflammatory cells after inflamation
- deletion of autoreactive T cells in thymus
what is the mechanism of apoptosis?
energy dependent
using various genes to regulate
plasma membrane remains intact, therefore inflammation is not induced
involved in morphogenesis and control of organ size
What are the controlling factors of apoptosis?
inhibitors = growth factrs, cell matrix, sex steroids etc
inducers = growth factor withdrawal, loss of matrix attachment, glucocorticoids, some viruses, free radicals etc
what internal signal leads to apoptosis?
mitochondrial damage
what external signal leads to apoptosis?
surface suicide receptor ( FAS CD95) is stimulated
dystrophic calcificaiton is what?
calcium level is normal in blood but the tissue is abnormal
ex) in cardiology= calcification of coronary arteries, breast calcificaiton due to breast carcinoma
