irreversible cell injury and its phenomenon

1. IRREVERSIBLE
CELL INJURY

2. INTRODUCTION
“All organ injuries start with
structural or molecular
alterations in cells” concept
began by Virchow in 1800's
•modern study of disease
attempts to understand how cells
react to injury, often at the
subcellular or molecular level,
and how this is manifested in the
whole animal.

3. CLASSES OF CELL INJURY
Irreversible --> cell
death. Types:
Necrosis: pathological
 (dissolution of dead
cells by its own
digestive enzymes)
Apoptosis:
 PROGRAMMED cell
death
Reversible
 If stressor removed, and
 If cell damage mild: cells
survive

4. PROBABLE CAUSES
 The first is the inability to reverse mitochondrial
dysfunction (lack of oxidative phosphorylation and ATP
generation) even after resolution of the original injury.
 The second is the development of profound disturbances
in membrane function.

5. NECROSIS

6. NECROSIS
 DEFINITION:
 Death of a group of contiguous
cells within a living tissue or organ
 Affect both nucleus and cytoplasm
 Unregulated cell death with
inflammation

7. MORPHOLOGICAL CHANGES
DURING NECROSIS
 Cytoplasmic
 Nuclear
 Cytoplasmic changes :
 Cytoplasmic eosinophilia due to loss of normal
basophilia& increased binding of eosin to denaturated
proteins
 (Granular or homogenous glassy)
 Nuclear changes:
 Pyknosis: shrinkage-increased staining with
haematoxylin
 Karyorrhexis: fragmentation
 Karyolysis: total disappearance

8. TYPES: NECROSIS
Coagulative
Liquefactive
Caseation
Fat Necrosis
Fibrinoid Necrosis

9. COAGULATIVE NECROSIS
In: infarcts of kidney, heart, spleen
Gross: pale , yellow, opaque, firm
Mic.: All cellular details are lost but general
architecture of the tissue is preserved
Surrounding tissue----acute inflammation
Ex: Infarction - heart
Infarction - kidney

10. LIQUEFACTIVE NECROSIS
In: centers of pyogenic abscess
amoebiasis
infarcts of C.N.S.
Necrotic tissue---completely liquified---turbid
fluid----absorbed----space
Ex: Brain - infarction
Amoebiasis ---liver

11. CASEATION NECROSIS
 In: Tuberculosis
 Necrotic tissue is partially liquefied---cheesy material (caseation)
 Mic: Both cellular details & general architecture of dead tissue are
lost---structureless eosinophilic material

12. FAT NECROSIS
Traumatic: in female breast
Enzymatic: in acute hemorrhagic
pancreatitis
Gross: opaque & white
fat cells appear cloudy, surrounded by
chronic inflammatory cells, histiocytes,
foreign body giant cells

13. FIBRINOID NECROSIS
Fibrinoid necrosis is a
form of necrosis, or tissue
death, in which there is
accumulation of
amorphous, basic,
proteinaceous material in
the tissue matrix with a
staining pattern
reminiscent of fibrin.

14. APOPTOSIS

15. APOPTOSIS
(programmed cell death)
 Definition: death of individual cells
surrounded by viable cells
 when a cell dies through activation of an
internally suicide program
 It is an active process—energy
dependent
 Does not elicit inflammatory response
 May be physiologic or pathologic

16. APOPTOSIS CAUSES
PHYSIOLOGIC
 During embryogenesis e.g. removal of
interdigital webs during embryonic
development of toes and fingers
 Hormone-dependent e.g.
endometrial cellloss in menstruation
PATHOLOGIC
 Irradiated tissues
 Cell death induced by cytotoxic T-
lymphocytes
 Viral infections e.g. viral hepatitis
 Cell death in tumours

17. DIFFERENCES BETWEEN
NECROSIS AND APOPTOSIS
 Necrosis
 Death of groups of cells
 A passive process—not energy-dependent
 Elicits inflammatory response
 Always pathologic
 Apoptosis
 Death of individual cells
 Active process—energy-dependent
 Does not elicit inflammatory response
 May be pathologic or physiologic

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