Adaptasi sel

dr. Emika Prastyan

Patterns of cells in persistent

sublethal injury
Major ADAPTIVE respons
Atrophy
Hypertrophy
Hyperplasia
Metaplasia

Atrophy
Decrease in size & function of a cell(organ)
Physiological / pathological
Decreased workload (disuse)
Loss of innervation
Inadequate supply of oxygen
Nutrient insufficiency
Aging
Likely due to imbalance between protein
synthesis & degradation

Atrophy of the brain

Mechanism of hypertrophy
& hyperplasia
Only labile / stable cells
Non dividing cells(myocard,skeletal
muscle)do not
Activation of cell signalling pathways
induce transcription of genes
involved in proliferation(hyperplasia)
& / growth related
protein(hypertrophy)

hypertrophy
Increase cell size organ
Increase synthesis of more structural
protein and organelle
Physiologic or pathologic
Cause by increase functional
demand/hormonal stimulation

Myocardial/heart
hypertrophy

hyperplasia
Increase the number of cells in
organ/tissue
Often develop concurrently with
hypertrophy
Physiologic or pathologic

Hyperplasia
Physiologic
Proliferation of glandular epithelium of
female breast at puberty/pregnancy
Pathology
Endometrial hyperplasia,benign
prostate hyperplasia

Epidermal hyperplasia in
psoriasis

Metaplasia
Reversible change from one adult cell
type to another adult cell type
(cell sensitive to a particular stress
replaced by other cell type better
able to withstand the adverse
environment)
Response to chronic irritation

Mechanism of metaplasia
Due to reprogramming of stem
cells/undifferentiated mesenchymal
cells to different cell type
Both extra & intracellular signals
induce transcription of genes
controlling differentiation along new
pathway

metaplasia

Fatty change
Vacuolation due to lipid droplets
accumulation
Result of disturbance to ribosomal
function& uncoupling lipid from
protein metabolism
Commonly affected: liver (in
hypoxia,alcoholic,diabetes)
Large vacuole displacing nucleus

Fatty liver