CELL INJURY & ADAPTATIONS

1. CELL INJURY &
ADAPTATIONS

2. Contents:
• Causes of cell injury
• Pathogenesis and morphology of
cell injury.
• Cellular adaptation

3. 3
CELL INJURY
• Defined as variety of stresses a cell encounters
as a result of internal or external environmental
changes.
• Cell injury is common to all pathologic
processes.
• Cell injury results from a disruption of one
or more of the cellular components that
maintain cell viability.

4. CELL INJURY
Injury at one point induces a cascade of
effects.
• Cellular adaptation
• Reversible or irrversible cell injury
• Subcellular changes and intracellular accumlation
4

5. Etiology:
• Hypoxia and Ischamia:
• Physical agents
• Chemicals and drugs
• Microbial agents
• Immunologic agents
• Nutritional derangemtns
• Psychogenic diseases
• Iatrogenic causes
• Idiopathic diseases

6. HYPOXIC INJURY
Cerebral infarction Myocardial infarction
Renal atrophy 6

7. INFECTIOUS DISEASE
Primary Herpes
Candidiasis
Tuberculosis Actinomycosis
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8. PHYSICAL INJURY
Thermal Burn Traumatic ulcer
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9. CHEMICAL/DRUG INJURY
Asprin Burn
9

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Pathogenesis of cell injury
• General principles of pathogenesis
1. Type, duration and severity of injurious agents
2. Type, status and adaptability of target cell
3. Underlying intracellular phenomena
eg. Mitochondrial damage, cell wall damage, free
radicals
4. Morphological consequences
eg. Ultrastrucal changes, swelling

11. OUTCOMES OF CELL INJURY
REVERSIBLE CELL DEATH CELL
ADAPTATIONS
N ORMA L CELL
CELL INJURY / CELL S T R E S S
ACUTE CHRONIC
11

12. Cellular adaptation:
Classifcation:
a)Atrophy and Hypertrophy (↑or ↓in size)
b)Hyperplesia (↑number of cells)
c) Metaplasia(change from one type to another
type) and dysplasia (changed phenotypic
differentiation)

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a. Atrophy
1. Physiologic atrophy: Brain,Gonads,
2. Pathologic atrophy
a) Starvation atrophy
b) Ischaemic atrophy eg, atropic kidney
c) Disuse atrohy eg, atropy of pancreas
d)Neuropathic atrophy eg. Motor neuron
disease
e)Endocrine atrophy eg, atropy of thyroid
and adrenal

14. ATROPHY & ISCHEMIA
Renal atrophy
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15. ATROPHY & AGING
Normal Brain
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Atrophic Brain

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b. Hypertrophy
– Physiologic hypertrophy e g uterus in
pregnancy
– Pathologic hypertrophy
• Hypertrophy of cardiac muscle
• Hypertrophy of smooth muscle
– Cardiac achalasia
– Pyloric stenosis
– Intestinal strictures
– Muscular arteries in hypertension
• Hypertrophy of skeletal muscle
• Compensatory hypertrophy eg, nephrectomy of one
side, removal of one adrenal gland

17. HYPERTROPHY & INCREASED
FUNCTIONAL D E M A N D
A
A
A = Normal heart
B
B
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B = Hypertensive heart
C
C
C = Dilated heart

18. c. Hyperplasia:
• Temporary Increase in the number of the parenchymal
cells.
• Resulting in enlargement of organ.
• Often hypertrophy and hyperplasia occures
simultaneously
• Occures due to increased in mitosis of the resting cells.
• Neoplasia causes change in the genetic composition of
the cells.

19. CAUSES:
A. PHYSIOLOGICAL HYPERPLASIA:
I) Hormonal hyperplasia eg: ↑in size of breast during
pregnancy
and lactation. Pregnant uterus
ii) Compensatory hyperplasia: Eg: Regenration of liver cells
after hepatectomy,epidermis after skin abrasion.
B. PATHOLOGIC HYPERPLASIA:
I) Endometrial hyperplasia in excess oestrogen
In wound healing: proliferation of fibroblasts cells
Formation of skin warts: papilloma viral infection

20. d. Metaplasia:
• It is defined as a reversible change of one type of
epithelial or mesenchymal cells to another type of
adult epithelium or mesenchymal cells.
• long time metaplasia may result in cancer.

21. Divided in 2 types:
EPITHELIAL METAPLASIA:
• Squamous metaplasia:
Eg: In bronchus of chronic smokers Utreus
of old age
• Columnar metaplasia:
Eg: Intestinal metaplasia in healed chronic
gastric ulcer.
• MESENCHYMAL METAPLASIA:
Osseous metaplasia: Eg: arterial wall in old
age
Cartilaginous metaplasia: Eg; healing of
fractures

22. e. Dysplasia:
• Means 'disordered cellular development'.
• Often accompanied with metaplasia and hyperplasia.
• Often occurs in epithelial cells.
• Observed charactertics are
– Increased number of layers of epithelial cells
– Increased mitotic activity
– Disorderly arrangement of cells from basel layer to
surface layer.
– Cellular and nuclear pleomorphism (variability in the
size, shape and staining of cells and/or their nuclei.)

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Morphology of Reversible cell injury
1. Hydropic change-swelling-kidney, liver,pancreas
2.Hyaline change- glass like
3.Mucoid change- mucus
4.Fatty change- fat accumlation eg fatty liver

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Morphology of Irreversible cell
injury
a) Autolysis or self digestion
b) Necrosis
c) Apoptosis
d) Gangrene
e) Calcification

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CONCEPTS - CELL DEATH
• There is no singal biochemical event that
equates with cell death.
• Necrosis = “cell murder”
• Apoptosis = “programmed cell death or cell suicide”

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NECROSIS
• Morphologic types of necrosis
– Coagulative
– Liquifactive
– Caseous
– Enzymatic (fat)
• The type of necrosis is dependent upon patterns of
enzymatic degradation of cells and extracellular
matrix, the type of necrotic debris, and by
bacterial products when present.

28. Coagulative necrosis:
• Common type of necrosis
• caused by irreversible focal injury,ischemia.
• Foci are pale,firm and slightly swollen.
• Hall mark is presence of tombstones.
Liquefaction necrosis:
Caused due to ischaemic injury or bacterial
infection.
Eg: infarct brain.
Affected area is soft containing necrotic debris.
Caseous necrosis:
Found in foci of tuberclosis infection.
have the features of coagulative and liquefaction
necrosis.
Appears like dry cheese,soft, granular and yellowish.

29. Fat necrosis:
• Present at pancrease and breast.
• Yellowish white firm deposits.
• Fat cells have cloudy appearance and
surrounded by inflammatory reactions.
• Calcium soaps are present in the cells.
Fibrinoid necrosis:
• Deposition of fibrin like material.
• Present in immunological tissue injuries.
• Arterioles of hypertension,peptic ulcers.
• Appears like brightly eosinophillic in vessel
wall.

30. COAGULATIVE NECROSIS
• Cell outline
• Pink cytoplasm
• Anucleated cells
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31. COAGULATIVE NECROSIS
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32. CASEOUS NECROSIS
Tuberculosis
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33. Apoptosis:
In 2 process:
A. Physiological process:
1. During development of embryo
2. Cells of hormone dependent tissues eg: endometrial sheeding,
regression of lactating breast.
3. Involution of thymus gland in early age.
B. Pathological process:
1. Cell death in tumour exposed to chemotherapeutic agents
2. Cell death by cytotoxic T cells in graft rejection.
3. Progressive depletion of CD4 cells in AIDS.
4. Cell death in viral infection
5. Pathological atropy
6. Cell death after exposure of radiations, hypoxia etc
7. Degenerative diseases of CNS eg: Alzheimers disease etc
8. Heart diseases

34. MORPHOLOGY OF
APOPTOSIS
Chromatin condensation
Progressive cell shrinkage
Plasma membrane blebbing
Apoptotic bodies
Phagocytosis - no inflammation 34

35. M E C H A N I S M S OF APOPTOSIS
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