This document outlines different types of cell injury and death. It begins by defining cell injury as occurring when stress exceeds a cell's ability to adapt. Reversible cell injury involves swelling while irreversible injury involves membrane damage, ultimately leading to cell death via either necrosis or apoptosis. Necrosis is unprogrammed cell death from pathology, resulting in inflammation, while apoptosis is genetically programmed single-cell death without inflammation. Various patterns of necrosis are described, including coagulative, liquefactive, and caseous necrosis. Apoptosis involves cell and nuclear shrinkage followed by organized nuclear fragmentation and removal of apoptotic bodies by macrophages.

1. By Dr. Amnah Shaukat

2. OUTLINE:
1. Introduction
2. Causes of Cell Injury
3. Reversible & Irreversible Cell Injury
4. Cell Death
a. Necrosis
b. Apoptosis

3. 1. INTRODUCTION:
Cellular injury occurs when a stress exceeds the
cell’s ability to adapt.
The extent of injury depends upon type of
stress, severity of stress and the type of cell
affected.
For example neurons suffer cell injury by
ischemic(shortage of blood) stress while skeletal
muscles may adapt & survive.

4. 1. INTRODUCTION:
Similarly slow developing ischemia may cause
atrophy while acute(sudden) ischemia results
in cell injury.
Causes of cell injury:
1. Inflammation
2. Nutritional deficiency
3. Hypoxia
4. Trauma
5. Genetic mutations

5. 2. Causes of
Cell Injury
1. Hypoxia
2. Inflammation
3.
4. Trauma
5. Gene Mutations

6. HYPOXIA:
Low oxygen delivery to tissues.
Causes of hypoxia are;
1. Ischemia(decreased blood supply to
tissues)
2. Hypoxemia(low partial pressure of oxygen
in blood; on high altitude areas)
3. Decreased Oxygen carrying capacity of
blood; Anaemia(low Hb levels) or Carbon
monoxide poisoning.

7. 3. REVERSIBLE & IRREVERSIBLE CELL
INJURY:
Process of cell injury
1. Hypoxia impairs the oxidative phosphorylation
in the cell which leads to decreased ATP
production
2. ATP deficiency disrupts cell functions like Na+
K+ pump and aerobic glycolysis(use of
glucose and oxygen to make energy/ATP).
3. Cells switch to anaerobic glycolysis
(anaerobic: in the absence of oxygen).

8. 3. REVERSIBLE & IRREVERSIBLE CELL
INJURY:
4. At first the injury is reversible. Hallmark of
reversible injury is Cellular Swelling
5. Eventually the injury becomes irreversible. The
hall mark of irreversible injury is Membrane
Damage.
6. The end result of irreversible injury is Cell Death.

10. 4. CELL DEATH:
The morphological hall mark of cell death is
loss of Nucleus.
Nucleus is lost by;
Pyknosis (nuclear condensation)
+
Karyorrhesis (nuclear fragmentation)
+
Karyolysis (dissolution of nucleus)

12. 4. CELL DEATH:
There are two mechanisms of cell death;
a. Necrosis (defined as death of large group
of cells followed by acute inflammation.
Due to some underlying pathology, never
physiological).
b. Apoptosis (energy dependent, genetically
programmed cell death involving single
cell of small group of cells).

14. 4(A). NECROSIS:

15. 4(A). NECROSIS:
Gross patterns of necrosis include;
1. Coagulative Necrosis
2. Liquefactive Necrosis
3. Gangrenous Necrosis
4. Caseous Necrosis
5. Fat Necrosis
6. Fibrinoid Necrosis

16. 1. Coagulative necrosis:
A type of necrosis in which the basic
architecture of the cell and organ remains
intact.
The structure of organ is preserved by
coagulation of proteins but the Nuclei
disappear.
Seen in ischemic infarction of organs except
brain.
A. Necrosis

17. Coagulative necrosis in kidney
Wedge shaped infarction pointing
to the area of occlusion of artery
A. Necrosis

18. 2. Liquefactive Necrosis:
Type of necrosis in which the necrotic tissue
become liquefied.
Enzymatic degradation of proteins results in
liquefaction.
Infarction of brain, abscess formation and
pancreatitis are examples of liquefactive
necrosis.
A. Necrosis

19. Liquefactive Necrosis in brain
Area of ischemic infarction is liquefied
A. Necrosis

20. 3. Gangrenous Necrosis:
Ischemia of lower limb and GIT shows this
pattern of necrosis.
Dry gangrene: coagulative necrosis that
resembles mummified tissue.
Wet gangrene: infection of necrotic tissue
causes liquefactive necrosis.
A. Necrosis

21. A. Necrosis

22. 4. Caseous Necrosis:
Soft and friable necrotic tissue with cottage
cheese like appearance.
It is a combination of coagulative and
liquefactive necrosis.
Examples are granulomatous inflammation
in Tb and Fungal infection.
A. Necrosis

23. Caseous Necrosis in Lung
A. Necrosis

24. 5. Fat Necrosis:
Necrosis of adipose tissue with chalky-white
appearance due to calcium deposition.
Seen in trauma to fat tissue. For example
breast tissue and peri-pancreatic fat.
A. Necrosis

25. 6. Fibrinoid Necrosis:
Necrotic damage to blood vessel wall.
Leakage of proteins(including fibrin) into the
vessel wall results in bright pink staining on
microscopy.
Seen in malignant hypertension and
vasculitis.
A. Necrosis

26. Fibrinoid Necrosis
A. Necrosis

27. B. APOPTOSIS:
Energy(ATP) dependent, genetically
programmed cell death involving single cell
or small groups of cells.
Examples include;
Removal of cells during embryogenesis
Killing of virally infected cells by immune
system.
Morphology includes;
1. Dying cells shrink in size and cytoplasm
becomes more eosinophilic(pink).

28. B. APOPTOSIS:
2. Nucleus condenses and fragments in an
organized manner.
3. Apoptotic bodies are formed from the cell
and are eaten up by macrophages.
4. There is no inflammation after apoptosis.