Cell Injury & Adaptation Flashcards
Hypoxia, chem injury, microbial infection
Cell responds specifically to type
Cell injury: Acute & transient
Cell:
Reversible swelling,
fatty change
Progressive & severe (DNA damage) to cell
Cell responds:
irreversible injury so cell death
- necrosis
- apoptosis
Cell has metabolic alterations, genetic/acquired or chronic injury
Cell responds:
intracell accumulations of
- pigments
- proteins
- fats
- glycogen
- calcifcation
Cell has cumulative sublethal injury over long life span
cell responds by cellular aging
Cell Response to Injury and adaptation
Adaptation Mech
- depends on adaptation type
- induce fetal proteins
- increase GF
- increase protein syn
- Ubiq ligase proteasome pathway
- autophagy
- apoptosis
- reprogram stem cells- cytokines, GF, EC matrix
Hypertrophy
Increase in size of cell
Happens to terminally diff cells
Physiological:
- uterus in preg
- breast during lactation
- skeletal m. of body builders
Path:
- cardiac m. in long term hyperT
Muscular Hypertrophy mech
- Increase TGF-B syn, IGF-1 and FGF
- Increase fetal & contractile prot syn like ANF (not syn in adults unless patient has hyperT)
- vasoactive agents: a adrenergic agonits, endothelin -1, ANG II; GPCR [cardiac path]
- mech stretch R: PI3 kinase/Akt pathway [phys body building]
Subcellular Hypertrophy
- SER hypertrophy
- due to barbiturates which stim CP450 rxns
- also caused by alc
- Genetic polymorphism influence indiv’s responses
Hyperplasia
increase in cell number
Organ cannot be terminally diff; use stem cells
Phys:
- female breast during puberty & preg
- uterus in preg
Path:
- endometrial
- prostatic hyperplasia
- hyperplastic scar
- papilloma virus (warts)
Hyperplasia Mech
- from GF driven prolif of mature cells or stem cell increased output
- G0 cells enter G1 and multiply
- Estrogen & erythropoietin influence
- Due to increased demand ie high altitude, immune response
- chronic injury ie chronic cystitis, excess estrogen stim
- compensatory hyperplasia ie hepatectomy
Atrophy
shrinkage of size & loss of cell number
phys:
- thyroglossal duct, notochord
- breast, uterus in post menopausal women
- uterus after parturition
path:
- decreased work load
- loss of innervation
- diminished blood supply (pronounced sulci in brain)
- inadequate nutrition
- loss of endocrine stim (small testicles)
- P
Loss of Innervation
Broken bone
Pressure Atrophy
Due to neoplasm that enlarges and compresses surrounding tissue
Atrophy Mech
- Production & destruction changes ie skeletal m.
- prot syn decreases
- prot degrade- activate ubiq-ligase proteasome pathway
- increase autophagy
- change gene expression
- E utilization- decrese FFA as E source
- apoptosis
Metaplasia
One adult cell type replaced by another adult cell type
phys:
- squamous metaplasia in resp tract & cervix
path:
- columnar intestinal metaplasia in Barrett’s esophagus
Squamous metaplasia
columnar cells turn to squamous cells in cervical mucsa
Barrett’s Esophagus
Goblet cells found above G-E junction
From intestinal cells b/c stomach does not contain Goblet Cells
Important to recognize early b/c its reversible from metaplasia that keeps progressing, dysplasia (cancerous stage) evolves!
CT metaplasia
fat calcified in breast tissue
Metaplasia mech
- Reprogrammed stem cells that exist in normal tissues or undiff mesenchymal cells in CT
- diff of stem cells due to cytokines, GFs & EC matrix components that cause a change in gene expression
- Vit A def/poisoning leads to changes in gene transcription by influencing diff of progenitor cells.
