1. CLS 223

2. Lecture #2
Cellular response to stress
(continue)

3. Cellular response to stress
Cellular response to stress may be adaptive or non adaptive.
Adaptive
Non-adaptive (cell injury-----cell death)
hypertrophy
Dysplasia
hyperplasia
Neoplasia
Atrophy
Degeneration
Metaplasia
Necrosis, apoptosis & gangrene
Reversible
Reversible* / Irreversible
*to a certain limit

4. Overview of cell injury and death
Cell injury results when cells are stressed so severely that they are no longer able to adapt. Injury may progress through a reversible stage and reach cell death (irreversible stage).
Reversible cell injury: in mild injury or injury of short duration the changes the cell go through are reversible if the damaging stimulus is removed. At this stage, the injury has not progressed to severe membrane damage and nuclear dissolution.
Cell death: with severe injury or injury of long duration the changes and damage become irreversible, the cell can’t recover and dies
(Necrosis, apoptosis & gangrene)
Dissolution (decompose)
From Reversible cell injury-----irreversible cell injury (cell death)

5. Reversible cell injury
E.g.: Degeneration
Cellular swelling (hydropic changes, vacuolar degeneration):
The first manifestation of almost all forms of injury to cells.
It is the result of failure of energy dependent ion pumps in the plasma membrane, leading to an inability to maintain ionic and fluid homeostasis.
Microscopic examination reveal clear vacuoles within the cytoplasm

6. B) Fatty changes:
Occurs in hypoxic injury and is manifested by the appearance of lipid vacuoles in the cytoplasm, it occurs mainly in cells involved in fat metabolism, such as hepatocytes and myocardial cells.
Microscopic examination reveal lipid vacuoles in the cytoplasm

7. Irreversible cell injury
Necrosis:
When damage to the membrane is severe, enzymes leak out of lysosomes, enter the cytoplasm, and digest the cell, resulting in necrosis.
Necrosis is the major pathway of cell death in many common injuries such as ischemia, toxins, infections, and trauma.
Necrosis is always a pathological process.

8. B) Apoptosis: When the cell is deprived of growth factors or the cell’s DNA or proteins are damaged beyond repair, the cell kills itself by apoptosis (programmed cell death) which is characterized by nuclear dissolution without complete loss of membrane integrity. It is an active, energy dependent, tightly regulated type of cell death. Apoptosis serve many normal functions and is not necessarily associated with pathologic cell injury. E.g.: ?
Embryonic development.

9. necrosis apoptosis necrosis apoptosis
Necrosis
Apoptosis

10. Types of necrosis Coagulative Necrosis:
E.g.: Infarction: Occurs when the artery that supplies the organ becomes obstructed (ischemic necrosis)
2) Liquifactive Necrosis:
E.g.: Abcess.
Infarction -----the affected tissue takes on a firm texture
liquifactive necrosis: bacterial or fungal infection----inzymes of luecocytes digest the tissue (inflammatory response)

11. Traumatic fat necrosis occurs in breast.
Enzymatic fat necrosis occurs in pancreas.
3) Caseous Necrosis:
E.g.: Tuberculosis infection
Caseous (cheese like): yellow whit appearance

12. C) Gangrene: Necrosis + Putrifaction Types of gangrene: 1)Dry or senile gangrene: Gradual arterial occlusion, usually affect the extreities. the skin is dry, dark brown or black in color. There is a line of demarcation between the gangrenous area and the healthy tissue e.g.: Senile gangrene of the lower limb
Putrifaction: the decomposition of organic matter

13. E.g.: Strangulated hernia.
2) Moist gangrene:
Sudden arterial and venous occlusion, usaully affect the internal organs or exteremeties. Bacterial invasion plays an important role. The skin is black, moist, and of foul odor. The symptoms are severe and may lead to death. No line of demarcation.
E.g.: Strangulated hernia.
foul odor (by the bacteria)

14. 3) Gas gangrene:
Due to infection with gas producing organism such as Clostridia species.