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Cellular

Adaptations
SUBMITTED TO : DR.RIMPALJEET KAUR
SUBMITTED BY : ASHISH
DR.MAHESH THAKUR
ROLL NO.165
Overview & Introduction
Cellular Adaptations are :
 Functional & Structural
 Reversible adjustments
 An altered steady state is achieved
 Due to stress, stimuli or changing environment

Reversible changes in size,number,metabolic activity phenotype or


functions of cells in response to stimulus or stresses or any other
change in their environment.
Hypertrophy
 Increase in size of cell
 Resulting in enlargement of organ, tissue
 No change in number of cells in pure hypertrophy
 Due to increased functional demand or by hormonal
stimulation
 In non dividing cell, only hypertrophy occurs
Physiologic hypertrophy :
 Enlargement of size of uterus in pregnancy
 Hypertrophy of skeletal muscles as in athletes

Pathologic hypertrophy :
 Hypertrophy of cardiac muscles in cardiovascular diseases.
 Hypertrophy of smooth muscles in pyloric stenosis.
Mechanism of hypertrophy
Cardiac hypertrophy
Atrophy
 Reduction of cell growth & number

Due to
 Decreased work load
 Lose of innervation
 Diminished blood supply
 Inadequate nutrition
 Aging
 Loss of hormone stimulation
Physiologic atrophy :
 Atrophy of lymphoid tissue with age
 Atrophy of thymus with age
 Atrophy of gonads after menopause
 Atrophy of brain with aging

Pathologic atrophy :
 Atrophy of kidney in atherosclerosis of renal artery
 Atrophy of brain in cerebral atherosclerosis
 Wasting of muscles immobilised in cast
 Starvation atrophy leads to general weakness & anaemia
 Atrophy of pancreas in obstruction of pancreatic duct
Mechanism of atrophy :
 Decreased protein synthesis
 Increased protein degradation
Hyperplasia
 Increase in number of cells
 Resulting in enlargement of tissue or organ
 Only occurs in cells capable of dividing
 All body cells do not posses hyperplasia

 Neoplasms loss growth regulatory mechanism


while hyperplasia persists as long as stimulus
presents.
Physiologic hyperplasia :
 Hyperplasia of female breast at puberty
 Hyperplasia of pregnant uterus
 Proliferation of endometrium after
normal menstrual cycle
 Regeneration of liver

Pathologic hyperplasia :
 Endometrial Hyperplasia due to oestrogen excess
 Benign prostatic hyperplasia in old age
 Skin warts
Mechanism of hyperplasia
 Growth factor driven
proliferation of cells
 Increased output of new cells
from tissue stem cells
Metaplasia
 Reversible change
 One type of cell to another type of cell
 Due to abnormal stimuli

Reverts back to normal on removal of stimulus but if


stimulus persists for long time, metaplasia may progess to
dysplasia & further cancer.
Divided in two types :
I) Epithelial metaplasia (Squamous & Columnar)
II) Mesenchymal metaplasia

Squamous Metaplasia :
Squamous metaplastic change due to chronic
may be mechanical, chemical or infective.
In bronchus in heavy smokers (normally pseudo stratified columnar)
In stones in ducts at different locations
Columnar Metaplasia :
Transformation to Columnar epithelium
• Intestinal Metaplasia in healed chronic ulcers
• In Barrett’s oesophagus change of squamous to columnar in lower oesophagus

: Mesenchymal Metaplasia
transformation of one type of mesenchymal
tissue to another
• In arterial wall in old age
• In cartilage of larynx and bronchi in elderly people
Mechanism of Metaplasia
 Reprogramming of stem cells
 Triggered by exogenous stimuli

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