1. Outcomes of necrosis:-
1.Inflammation & resolution
occurs if the injury is mild & the tissue has the
power to proliferate.
2.Inflammation & organization (fibrosis).
occurs if the injury is severe &/or the tissue
do
not have the power to proliferate.
3. Dystrophic calcification- deposition of Ca++
salts in necrotic tissue.

2. Myocardial infarction (Posterolateral pale infarct)
2

3. Inflammation
& fibrosis of
severe burn
3

4. Aortic valve , gross , (calcified aortic stenosis).
4

5. APOPTOSIS
Apoptosis come from the Greek word which means
“falling off”.

6. Apoptosis
• “A programmed active single cell death”
that is induced by a tightly regulated
intracellular program.Cells actually expend
energy in order to die.
• Causes of Apoptosis
- Physiologic situations
- Pathologic conditions

7. APOPTOSIS
• NORMAL
(preprogrammed)
• PATHOLOGIC
(associated with
Necrosis)

8. Apoptosis in Physiologic Situations
• Programmed destruction of cell during
embryogenesis & development
• Hormone-dependent tissue involution
- endometrial cells (menstrual cycle)
• Cell deletion in proliferating cell population e.g skin
• Post-inflammatory clean up- neutrophils.
• Cell death induced by cytotoxic T-cells to eliminate
harmful cells
- viral infected or tumor cells

9. Apoptosis in Pathologic Conditions
• Cell death produced by injurious stimuli –
radiation, cytotoxic drug
• Cell injury in certain viral diseases – viral
hepatitis
• Pathologic atrophy
• Cell death in tumors .

10. MORPHOLOGICAL
FEATURES OF APOPTOSIS
• Cell shrinkage
• Chromatin condensation and fragmentation.
• Formation of cytoplasmic blebs and apoptotic
bodies.
• Phagocytosis of apoptotic bodies by adjacent
healthy cells or macrophages.
• Lack of inflammation.

11. Morphology of
Apoptosis
Cell shrinkage
Chromosome
condensation
Formation of
cytoplasmic blebs
and apoptotic bodies
Phagocytosis of
apoptotic cells or cell
bodies

12. Cellular swelling, Membrane
normalcell chromatin cluping damage
The sequential ultrastructual changes in necrosis and
apoptosis
Nuclear chromatin
Cytoplasmic budding and Phagocytosisi of
condensation and
apoptosisi body apoptosis body
fragmentation

13. Apotosis of hepatocytes

14. • Fig 1-18

15. SHRINKAGE/HYPERCHROMASIA

16. PHAGOCYTOSIS

17. APOPTOSIS
BIOCHEMISTRY
• Protein Digestion
(Caspases)
• DNAbreakdown
(endonucleases)
• Phagocytic Recognition

18. Comparison of cell death by apoptosis and necrosis

19. Comparison of cell death by apoptosis
and necrosis
Feature Necrosis Apoptosis
Mechanism injurious programmed
passive cell death active cell death
Cell size Enlarged Reduced
Extent single cell group of cells
Nucleus Pyknosis / karyorrhexis / karyolysis condensation &
Fragmentation
(Apoptotic bodies)
Plasma membrane Disrupted Intact
Cellular contents swell& Enzymatic digestion Intact

20. Comparison of cell death by apoptosis
and necrosis
Biochemistry impairment & cessation of ion homeostasis' Active DNA digestion
lysosomes leak lytic enzymes by endonuclease
lysosomes intact
Inflammation usual None
Fate of dead cells phagocytosed by inflammatory phagocytose by
cells ( neutrophils & macrophages) macrophages
Cause induced by pathologic stimuli induced by
physiologic &
pathologic
stimuli