Cellular Adaptation,

Cellular Injury & Cell Death

 Cellular Injury & Adaptation:
• Normal cell is in a steady state “homeostasis”
• Injury is any stimulus bringing changes in cell physiology and or
anatomy
• Injury can be : Reversible / Irreversible
• Adaptation is the changes in a cell due to reversible Injury,
including:
– Hyperplasia,
– Hypertropy,
– Atrophy,
– Metaplasia

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 Stages In the cellular response to stress and injurious stimuli

Normal Cell
(Homeostasis)

Stress, increased demand Injurious stimulus

Adaptation Cell Injury  Cell Death

Inability to adapt

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 Cell injury and cell death
• Reversible injury : Pathologic cell changes that can be restored to
normal if the stimulus is removed or if the cause of injury is mild

• Irreversible injury : Stressors exceed the capacity of the cell to

adapt and denotes permanent pathological changes that cause cell
death.

• The two morphologic and mechanism pattern of cell death are

necrosis and apoptosis

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 Response to Injury:
 Adaptations (reversible)
 Hydropic degeneration
 Hypertrophy, Hyperplasia, Atrophy

 Cell death / Necrosis (irreversible)

 Coagulative ex Infarction - Heart (sel nekrotik bentuknya
tetap, akibat sel litik dihambat kondisi lokal pada
jantung,ginjal,limpa)
 Liquifactive ex Brain, abscess (sel nekrotik mengalami
pencairan akibat kerja enzim pada otak dan medullla spinalis)
 Caseous ex Tuberculosis /nekrosis kaseosa : sel nekrotik
hancur tetapi pecahnya tetap berada disekitar paru.
 Gangrene ex With infection – limbs.
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 Hyperplasia

 Hyperplasia is on excess proliferation of cells.

 It should be distinguished from the normal proliferation of
cells which occurs in repair and in certain physiological states
e.g. pregnancy causing increase in breast tissue.

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  The main causes are :
(a) Chronic irritation e.g.
chronic inflammation
of skin.
(b) Imbalance of
hormonal activity e.g.
the irregular
enlargement of the
prostate in old age is
due to hyperplasia of
the component
tissues.

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  The main causes are :
(a) Chronic irritation e.g.
chronic inflammation
of skin.
(b) Imbalance of
hormonal activity e.g.
the irregular
enlargement of the
prostate in old age is
due to hyperplasia of
the component
tissues.

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 Hypertrophy

 Increase in the size of cells resulting in enlargement of a

tissue or organ without any change in the number of cells.
 It is the result of increased functional requirements e.g.
changes in myocardium in high blood pressure.

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 Hypertrophy

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 Hypertrophy
 Hypertrophy is increase in cell size

Left Ventricular Hypertrophy

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 Atrophy

 Reduction in size of individual cells resulting in a diminution

in size and function of an organ.
 Its main causes are lack of use and disturbances in nutrition.

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 Renal Artery stenosis - Atrophy

Nephrosclerosis Atrophic Kidney

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 Muscle - ischemic atrophy:

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 Hyperplasia
 Hyperplasia is increase in number of cells

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 Metaplasia

• Metaplasia is a change from one type of differentiated tissue

to another
• The change is commonly seen in lining epithelium but occurs
also in connective tissues and lining of serous cavities.

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 Metaplasia
e.g. (a) Change from mucus-secreting epithelium to stratified
squamous epithelium as in the bronchial irritation associated
with smoking.

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 Causes of cell Injury:
• Reduced oxygen - Ischemia, infarction
• Physical agents: Trauma, heat, cold, radiation, electric shock
• Chemical agents & drugs: Therapeutic drugs, poisons, environmental
pollutants, alcohol
• Toxins
• Biological agents :Viruses, Bacteria, fungi, parasites
• Immune reaction – autoimmune & hypersensitivity
• Nutritional deficiencies.

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 NECROSIS
 Morphologic changes that follow cell death in living tissue
or organs.
 Two processes underlie the basic morphologic changes:
1. Denaturation of proteins
2. Enzymatic digestion of organelles and other cytosolic
components

 Nuclear changes in necrosis including : Pyknosis, karyolysis

and karyorrhexis

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 Patterns of necrosis
 Coagulative necrosis which is predominate by protein
denaturation
 Liquefactive necrosis occurs when autolysis predominates
over protein denaturation
 Caseous necrosis is characteristic of tuberculous lesions
 Fat necrosis is seen in adipose tissue.(nekrosis akibat enzim
pankreas mengalir di luar duktus pada pankreas)

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 Renal Infarction - Coagulative

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Caseous necrosis
(Lung tuberculosis)

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 Stroke- Liquifactive necrosis

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 Gangren
 Definisi: kematian jaringan yang luas dan disertai invasi
kuman saprovit.
 Terjadi pada bagian-bagian yang telah nekrotik dan tempat
kuman dapat sampai

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 Gangren
 Terjadi pada alat yang berhubungan dengan dunia luar:
 Kulit
 Lambung
 Usus
 Mulut
 Paru-paru
 Cervix,dll
 Tidak terjadi pada jantung, limpa, dan hati

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 Gangren
1. Gangren basah
• Pada alat tubuh yang mengandung cairan, akibat obstruksi vena, pada
tempat-tempat yang tidak memungkinkan terjadinya penguapan.
• Contoh: lambung, paru-paru

2. Gangren kering
• Pada jaringan yang sedikit cairan dan mudah terjadi penguapan atau
drainase yang baik
• Contoh: Ekstremitas
• Contoh : pada aterosklerosis /penyumbatan lumen arteri

• Penyebab :
– Hilangnya perbekalan darah
– Terdapat infeksi bakteri

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 Gangrene Intestine - Thrombosis.

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 Gangrene - Diabetic foot

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 Gangrene - Amputated Diabetic foot

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 APOPTOSIS
 Programmed cell death occurs when a cell dies trough
activation of a tightly regulated internal “suicide program”
 Function of apoptosis is to eliminate unwanted cells
selectively with minimal disturbance to surrounding cells and
host

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 APOPTOSIS

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 APOPTOSIS
 Causes of apoptotic are physiologic and pathologic
 Physiologic causes:
 Programmed destruction of cells during embryogenesis
 Hormone-dependent involution of tissue in adult
 Death of cells that have served their useful purpose

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 APOPTOSIS
 Pathologic causes:
 Cell death by variety of injurious stimuli
 Cell death in certain viral infections ex. Hepatitis
 Pathologic atrophy in parenchymal organs after duct
obstruction ex pancreas
 Cell death in tumors

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