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CELL DEATH - Simple Notes 🧬
What is Cell Death?
When a cell is badly injured, it may not be able to fix itself. When damage becomes too much to repair, the cell dies. There are two types of cell death:
- Apoptosis (controlled/planned death)
- Necrosis (uncontrolled/accidental death)
1. APOPTOSIS (Programmed Cell Death)
Think of it as "cell suicide" - the cell kills itself in an organized way.
Why does it happen?
- Some cells are no longer needed (like removing webbing between fingers in a baby)
- The cell has been badly damaged (e.g., by radiation)
- To stop damaged cells from becoming cancer
What happens to the dying cell?
- It swells up and then shrinks
- The nucleus breaks apart
- DNA gets chopped up
- The cell breaks into small pieces
How is apoptosis triggered?
From outside the cell:
- Withdrawal of growth hormones
- Signals via FAS receptors (TNF-R family)
From inside the cell:
- Heat, radiation, low oxygen (hypoxia)
Steps of apoptosis:
- Caspases get activated - these are proteins that destroy the cell from inside
- Death receptors activate - FAS receptors get switched on
- Control genes kick in - BCL-2 (can stop or allow apoptosis), p53 (promotes apoptosis)
- Cell dies - nucleus clumps up, organelles get damaged, cell membrane breaks down
- Phagocytosis - dead cell pieces get eaten up by nearby cells. Importantly, no inflammation occurs
2. NECROSIS (Uncontrolled Cell Death)
Think of it as "cell murder" - cells die from outside damage, and the body reacts with inflammation.
Causes:
- Low oxygen (hypoxia)
- Chemicals, heat, physical injury
- Bacterial infection
- Immune attack
Key signs of necrosis:
- Lytic enzymes digest the cell - cytoplasm becomes pink and homogeneous
- Proteins break down - nucleus shrinks (pyknosis), dissolves (karyolysis), or fragments (karyorrhexis)
- Always causes inflammation (unlike apoptosis)
Types of Necrosis (5 Types)
| Type | Simple Meaning | Where it happens |
|---|---|---|
| Coagulative | Cell shape preserved but contents dead | Heart, kidney, spleen (due to blocked blood supply) |
| Liquefactive (Colliquative) | Tissue melts into liquid pus | Brain (ischemia), Abscess (bacterial infection) |
| Caseous | Looks like crumbly dry cheese | TB (tuberculosis) infection |
| Fat | Chalky white deposits form | Pancreas, Breast tissue |
| Fibrinoid | Fibrin-like material deposited in vessel walls | Autoimmune diseases, hypertension, peptic ulcer |
Quick Memory Trick:
"Can Lose Cash For Fun" Coagulative, Liquefactive, Caseous, Fat, Fibrinoid
Apoptosis vs Necrosis - Quick Comparison
| Feature | Apoptosis | Necrosis |
|---|---|---|
| Type | Planned/controlled | Accidental/uncontrolled |
| Inflammation | ❌ No | ✅ Yes |
| Cell size | Shrinks | Swells |
| Cause | Natural signals or mild injury | Severe injury |
| Energy needed | Yes (active process) | No |
Anuswer for bams examination
CELL DEATH - BAMS Exam Answer Format 📝
Q. Write a note on Cell Death. / Explain Apoptosis and Necrosis.
INTRODUCTION
When a cell suffers acute or persistent injury, it loses its ability to maintain normal function (homeostasis). If the damage is irreversible, the cell dies. There are two main forms of cell death:
- Apoptosis
- Necrosis
APOPTOSIS
Definition:
Apoptosis is derived from the Greek word meaning "falling off." It is defined as controlled (programmed) cell death in multicellular organisms.
Features:
- Cell swells until it bursts
- Involves blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation and chromosomal DNA fragmentation
- It is a regulated process driven by signalling pathways
Importance of Apoptosis:
- Removes cells that are no longer needed during growth and development
- Prevents unrestrained cell growth (which can lead to cancer)
- Destroys irreparably damaged cells (e.g., after radiation)
- Removes cells deprived of hormonal stimulation
MECHANISM OF APOPTOSIS
Step 1 - Initiators of Apoptosis:
Triggers act at the cell membrane, intracellularly or extracellularly
- Extracellular: Withdrawal of growth hormones, cytokines; activation of FAS receptors (TNF-R family)
- Intracellular: Heat, radiation, hypoxia
Step 2 - Process of Programmed Cell Death:
(a) Activation of Caspases:
- Caspases act on nuclear proteins and organelles
- Activated by cell injury agents or unknown mechanisms
(b) Activation of Death Receptors:
- Activated caspases stimulate FAS receptors on T cells
- The receptor activates growth-controlling genes - BCL-2 and p53
(c) Activation of Growth Controlling Genes:
- BCL-2 gene - regulates apoptosis by either promoting or inhibiting it
- p53 molecule - promotes apoptosis
(d) Cell Death:
- Proteolytic actions on nucleus
- Chromatin clumping
- Cytoskeletal damage
- Mitochondrial damage
- Disruption of endoplasmic reticulum
- Cell membrane damage → Cell dies
Step 3 - Phagocytosis (Final Step):
- Dead cells undergo membrane changes that promote phagocytosis
- Phosphatidylserine and thrombospondin molecules (normally inside) appear on outer surface
- Dead cells are eaten up
- ⚠️ No inflammatory reaction occurs
NECROSIS
Definition:
Necrosis is the uncontrolled death of cells involving a localized area of tissue death, followed by tissue degradation by hydrolytic enzymes released from dead cells, always accompanied by inflammatory reaction.
Causes:
- Hypoxia
- Chemical and physical agents
- Microbial agents
- Immunological injury
Two Key Changes in Necrosis:
(a) Cell digestion by lytic enzymes:
- Seen as homogeneous, intensely eosinophilic cytoplasm
- May show cytoplasmic vacuolation or dystrophic calcification
(b) Denaturation of proteins:
- Nuclear changes:
- Pyknosis - condensation/shrinkage of nucleus
- Karyolysis - dissolution of nucleus
- Karyorrhexis - fragmentation into granular clumps
TYPES OF NECROSIS
There are 5 types based on morphology:
1. Coagulative Necrosis
- Most common type
- Caused by sudden stoppage of blood flow (ischemia)
- Organs affected: Heart, Kidney, Spleen
- Appears pale, firm, and shrunken initially
- Under microscope: Cell outline preserved but cytoplasmic and nuclear details are lost
- Dead cells look like "tombstones"
- Phagocytosis of dead cells occurs later
2. Liquefaction (Colliquative) Necrosis
- Tissue melts into liquid
- Due to ischemic injury and bacterial/fungal infections
- Example: Infarct brain or abscess cavity
- Affected area has a liquefied center filled with dead tissue
- Under microscope: Dead cell debris, macrophages, cyst wall with capillaries and inflammatory cells
3. Caseous Necrosis
- Found in tuberculosis (TB) infections
- Combines features of coagulative + liquefactive necrosis
- Looks like soft, granular, yellowish dry cheese
- Due to lipopolysaccharides in Mycobacterium tuberculosis
- Under microscope: Structureless, eosinophilic foci surrounded by granulomatous inflammation (epithelioid cells, giant cells, lymphocytes)
4. Fat Necrosis
- Occurs at two anatomically different locations with similar lesions:
- Acute pancreatitis (enzymatic)
- Traumatic fat necrosis in breasts
- Characterized by firm, yellowish-white deposits
- Calcium soaps form → chalky white appearance under microscope
5. Fibrinoid Necrosis
- Deposition of fibrin-like material in vessel walls
- Seen in:
- Immunologic tissue injury
- Immune complex vasculitis
- Autoimmune diseases
- Hypertension
- Peptic ulcer
- Under microscope: Brightly eosinophilic, hyaline-like deposition in vessel wall
- Surrounded by nuclear debris of neutrophils
- May cause local hemorrhage due to vessel rupture
APOPTOSIS vs NECROSIS (Comparison Table)
| Feature | Apoptosis | Necrosis |
|---|---|---|
| Type of death | Programmed/controlled | Uncontrolled/accidental |
| Cause | Physiological or mild injury | Severe irreversible injury |
| Inflammation | Absent | Present |
| Cell size | Shrinks | Swells |
| DNA | Fragmented in pattern | Random breakdown |
| Membrane integrity | Maintained initially | Lost early |
| Energy required | Yes (active) | No (passive) |
| Affect on neighbours | Single cell | Group of cells |
MEMORY AIDS 🧠
Types of Necrosis → "Can Liquify Caseous Fat Fibres"
Coagulative - Liquefactive - Caseous - Fat - Fibrinoid
Nuclear changes in Necrosis → "PKR"
Pyknosis → Karyolysis → Karyorrhexis
Source: Roga Nidana and Vikrti Vijñana, Volume-1
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