Cellular Adaptation

Dr. Madeeha Rehan

Consultant Hematologist
Associate prof. Pathology
Medical Educationist
FUMC/FFH
Learning Objective
At the end of this lecture students will be
able to:
Identify normal adaptive processes of cells
Identify abnormal adaptive processes of
cells
Correlate clinical conditions associated
with adaptive processes
Describe Pathogenesis of adaptive cell
processes
Cellular Adaptation
Cells are able to adapt to increased
work demands or threats to survival
by changing their size(atrophy and
hypertrophy), number (hyperplasia),
and form (metaplasia).
Normal cellular adaptation occurs in
response to an appropriate stimulus
and ceases once the need for
adaptation has ceased.
 Cellular Adaptations

Hypertrophy

Atrophy

Hyperplasia

Metaplasia
 Hypertrophy

Types:
Physiologic
Pathologic
Usual stimulus:
Increased functional
demand or
Hormonal stimulation
 Hypertrophy
Increased demand
Exemplified by increased workload put
on the skeletal muscles of body builders
Cardiac muscle: chronic hemodynamic
overload, like in hypertension or
defective valves
Enlarged cell achieves a new equilibrium
permitting it to function at higher level of
activity
Hypertrophy

Hormone induced
Estrogen induced hyperplasia/hypertrophy
of uterus in pregnancy

Estrogen/prolactin induced changes in

lactating breast
 Normal
vs

Hypertrophied
 Atrophy
decrease in the size of the cells of an
organ /tissue
resulting in decreased size of the organ

Types:
Physiological: like uterus after parturition

Pathological: localized or generalized

Causes:
1.Disuse
2.Denervation
3.Lack of hormones
4.Nutritional deficiency
5.Ischemia
6.Senile
7.Pressure
Pathogenesis
• Increase work load
Decrease oxygen consumption and protein
synthesis decrease.
 Low insulin and IGF-1 levels/ catabolic
signals are present,
Reduced synthetic processes,
Increased proteolysis by the ubiquitin–
proteasome system,
Pathogenesis
Apoptosis or programmed cell death
 ubiquitin–proteasome system,-destruction
of protiens intracellular proteins
Ubiquitin- Small protein
 small cytoplasmic organelles- proteasomes
Metaplasia
Reversible change in which one adult cell type
(epithelial or mesenchyme) is replaced by
another adult cell

Characteristics:

1. Reprogramming of undifferentiated stem cells

2. New tissue is structurally normal

3. Cellular organization & primary boundaries are

maintained
Causes

Changed differentiation of stem cells

response to environmental change
occurrence/types
epithelial and connective tissue
Columnar to squamous
Epithelium

Respiratory tract: (trachea/bronchi)

Focal or widespread
Chronic irritation (smoking or environmental
pollution)
 Vitamin A deficiency
 Excretory
ducts of
Salivary glands
Pancreas

cause:

stones
Squamous metaplasia-endocervix
Transitional to squamous

Urinary bladder
Usual cause:
Infestation by Schistosoma
Squamous to columnar
Inlower part of esophagus
Cause: acid reflux
Mechanism

Phenotype of the cells does not change

Reprogramming of stem cells occurs due to
altered signals
Signals include the changed balance of
cytokines/growth factors & vitamin A
In mesenchyme metaplasia, certain drugs
also play role
Outcome of metaplasia

Advantages
More appropriate cells which can better
withstand the altered environment are
formed
Disadvantages
Specialized functions of the indigenous
cells are lost
Dysplasia
Deranged cell growth of a specific tissue
that results in cells that vary in size,
shape, and organization.
Chronic irritation or inflammation..
Although dysplasia is
Irreversible after the irritating cause has
been removed.
Pre-cancerous
Example
Preterm babies (prematurity and lack of
surfactant, & term infants (intubation
and ventilated oxygen) in the first month-
bronchopulmonary dysplasia (BPD)
Respiratory tract and the uterine cervix,
dysplastic changes