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3 Rs of success:

Respect for self,


Respect for others and
Responsibility for all your
actions

Cellular Injury

Departement of Pathology
Jember School of Medicine

Cell Injury:

Shashi Mar-00

Cell Injury:

Cellular Injury &


Adaptation:

Normal cell is in a steady state


Homeostasis
External stimuli bringing changes
in cell physiology and or anatomy
Injury Reversible / Irreversible
Adaptation / Injury / cell death /
autolysis
Shashi Mar-00

Cell Injury:

Cell Death

Necrosis: Morphologic changes seen


in dead cells within living tissue.
Autolysis: Dissolution of dead cells by
the cells own digestive enzymes. (not
seen)
Apoptosis: Programmed cell death.
Physiological, cell regulation.
Shashi Mar-00

Cell Injury:

Causes of cell Injury:

Reduced oxygen Hipoxia, Ishemia,


infarction
Physical agents
Chemical
Toxins
Biological agents - Viruses, Bacteria etc.
Immune reaction - Hypersensitivity
Nutritional deficiencies.
Genetic abnormalitiy - Sickle,
Hemophilia
Shashi Mar-00

Cell Injury:

Targets of cell Injury:

Respiration,
Integrity of cell membrane,
synthesis of proteins,
integrity of genetic apparatus.
Injury at one locus results in wide
ranging secondary effects.
Morphology becomes apparent late.
Shashi Mar-00

Cell Injury:

General Considerations:

Morphology becomes apparent late


in cell injury.
Reaction of cell to injury depends
on type of injury, duration and
severity.
Reaction of cell to injury also
depends on the type, state &
adaptability of the cell.
Shashi Mar-00

Cell Injury:

Response to Injury:
Adaptations (reversible)

Hydropic degeneration
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Accumulations - hyaline, fat, etc.

Necrosis (irreversible)..
Shashi Mar-00

Cell Injury:

Types of Necrosis:

Coagulative - Infarction
Liquifactive - Brain, abscess
Caseous - Bacterial / Tuberculosis
Fat Necrosis
Gangrene - With infection

Shashi Mar-00

Cell Injury:

Normal & Ischemic - kidney tubule

Microvilli

Shashi Mar-00

Cell Injury:

Infarct Adrenal gland:

Shashi Mar-00

Cell Injury:

Cerebral atrophy - Alzheimers:

Shashi Mar-00

Cell Injury:

Left ventricle hypertrophy :

Shashi Mar-00

Cell Injury:

Caseous
necrosis
Tuberculosis
hilar lymphnode

Shashi Mar-00

Cell Injury:

Extensive
Caseous
necrosis
Tuberculosis

Shashi Mar-00

Cell Injury:

Caseous necrosis - Tuberculosis

Shashi Mar-00

Cell Injury:

Muscle ischemic atrophy:

Shashi Mar-00

Cell Injury:

Cirrhosis - Healing by fibrosis:

Shashi Mar-00

Cell Injury:

Dystrophic calcification - Stomach.

Shashi Mar-00

Cell Injury:

Fat Necrosis - Peritoneum.

Shashi Mar-00

Cell Injury:

Fatty Liver - Alcoholism

Shashi Mar-00

Cell Injury:

Gangrene - Diabetic foot

Shashi Mar-00

Cell Injury:

BPH - Benign Prostatic Hyperplasia.

Shashi Mar-00

Cell Injury:

Gangrene Intestine - Thrombosis.

Shashi Mar-00

Cell Injury:

Lipofuscin - Wear & Tear pigment Age

Shashi Mar-00

Cell Injury:

Stroke- Liquifactive necrosis

Shashi Mar-00

Cell Injury:

Lung abscess:
Liquifactive
necrosis

Shashi Mar-00

Cell Injury:

Liver abscess: Liquifactive necrosis

Shashi Mar-00

Cell Injury:

Oesophagitis - Gastric metaplasia.

Shashi Mar-00

Cell Injury:

Myocardial Infarction- Necrosis

Shashi Mar-00

Cell Injury:

Renal Infarction - Coagulative

Shashi Mar-00

Cell Injury:

Renal Infarction - Coagulative


necrosis

Shashi Mar-00

Cell Injury:

Conclusions:
Cellular Injury - Various causes
Reversible Injury - Adaptations

Irreversible Injury - Necrosis

Hypertrophy, Hyperplasia, Atrophy


Accumulations - Hydropic, hyaline, fat..
Coagulative, Liquifactive, Caseous, fat

Aging - Lipofuscin
Apoptosis - Programmed cell death.
Shashi Mar-00

Thank you...

Departement of Pathology
Jember School of Medicine

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