bbs ii slide cell injury death and adaption

Blok BBS 2

Departemen Patologi Anatomi Fakultas
Kedokteran Universitas Sumatera Utara
Medan - 2011

Stages in the cellular response to stress &
injurious stimuli

Table 1-1. Cellular Responses to Injury
Nature &Severity of Injurious Stimulus
Altered physiologic stimuli:
• demand, trophic stimulation (e.g. growth
factors, hormones)
•

Cellular Response
Cellular adaptations:

nutrients, stimulation

• Hyperplasia, hypertrophy
• Atrophy

• Chronic irritation (chemical /physical)
O2 supply; chemical injury; microbial
infection
• Acute & self-limited

• Metaplasia
Cell injury:
• Acute reversible injury

• Progessive & severe (including DNA damage) • Irreversible injury

➙ cell death

Necrosis
Apoptosis
• Mild chronic injury

• Subcellular alterations in various organelles

Metabolic alterations (genetic / acquired)

Intracellular accumulations; calcifications

Prolonged life span with cumulative
sublethal injury

Cellular aging

Stresses/pathologic stimuli the cell
Can undergo

Adaptation
•
•
•
•

Atrophy
Hypertrophy
Hyperplasia
Metaplasia

Irreversible injury & dies

Perubahan sel & jaringan
Agenesis

Hyperplasia

Aplasia

Metaplasia

Hypoplasia

Dysplasia

Atrophy

Anaplasia

Hypertrophy

Granuloma

Agenesis
• Complete absent of
organ
• e.g. :
– Renal agenesis
– Ovarial agenesis
– Tubal agenesis, etc.

Aplasia
• Is present
• But never develops
• e.g. :

– Lung aplasia with tissue
containing rudimentary
duct & connective tissue

Hypoplasia

• Developved incompletly
• But the tissue histhologicaly normal
• e.g. : microcephaly

Atrophy

• Decrease in the:
– Size
– Function of a cell

• But not dead

Causes of atrophy :
1.

2.
3.
4.

5.
6.

functional demand (immobilitation in fracture, prolonged
bed rest)
Inadequate supply O2 (ischemia)
Insufficient nutrients (starvation, inadequate nutrition,
chronic disease)
Interruption of trophic signals transmitted by chemical
mediators (endocrine system/neuromusculator transmission)
e.g. : thyroid, adrenal cortex, ovarium, testis.
Persistent cell injury by chronic inflamation
e.g. : chronic gastritis, prolonged pressure
Aging : brain, heart (Senile Atrophy)

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The mechanism of atrophy :
Synthesis
Catabolism
↑ Hormones
e.g. :
• Insulin
• Tyroid stimulating hormon
• Glucocorticoids

Hypertrophy
•

size of cell accompanied by ↑ functional
capacity

• Is a response to trophic signals
• Commonly a normal procesess

… hypertrophy
Physiological (hormonal) hypertrophy
• in puberty
• production of sex hormon
• Hypertrophy breast tissue
• Abnormal hormon production in cancer

Functional demands
• Exercise
• Pathological conditions (myocardial cell)
• Kidney hypertrophy on surgical removed

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Hyperplasia
the number of cells in an organ / tissue

Hyperplasia can be :
Physiologic hyperplasia

Pathologic hyperplasia

• Hormonal hyperplasia
• Compensatory
hyperplasia

• ↑ hormonal / growth
factor stimulation
• e.g. :
• Endometrial
hyperplasia

Metaplasia
1 adult cell type another adult cell type
(convertion of 1 differentiated cell type of another)
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• Squamous metaplasia of the bronchial epithelium to tobacco
• Lower oesophagus by reflux acidic gastric
• Endocervical metaplasia

Usually reversible if the stimulus is removed

Metaplasia of normal columnar (left) to squamous epithelium
(right) in a bronchus, (A) schematically and (B) histologically

Dysplasia
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