Table of Contents · 6 sections
Necrosis is the death of cells and tissues in a living organism followed by enzymatic degradation. This is one of the core sections of pathological anatomy, essential for understanding myocardial infarctions, gangrene, abscesses, and numerous other pathological processes. This article covers classification, morphology, differences from apoptosis, and clinical correlations.
Definition and causes of necrosis
Necrosis is pathological (unregulated) cell death accompanied by an inflammatory response. Causes:
- Ischemia — impaired blood supply (myocardial infarction, stroke, gangrene)
- Toxins — poisons, medications (paracetamol → hepatocyte necrosis)
- Infection — bacterial toxins, direct viral damage
- Physical factors — trauma, thermal burns, frostbite, radiation
- Immune mechanisms — autoimmune, allergic (Arthus phenomenon)
Morphological signs of necrosis
Nuclear changes (crucial for diagnostics)
| Sign | Description |
|---|---|
| Karyopyknosis | Nuclear shrinkage, chromatin condensation |
| Karyorrhexis | Fragmentation of the nucleus into clumps |
| Karyolysis | Dissolution of the nucleus (terminal stage) |
Cytoplasmic changes
- Mitochondrial swelling, membrane rupture
- Cytoplasmic eosinophilia (loss of RNA → loss of basophilia)
- Release of intracellular enzymes into the blood (troponins, AST, ALT, LDH, CPK) — the basis of laboratory diagnostics
Types of necrosis
| Type | Mechanism | Macroscopy | Common location |
|---|---|---|---|
| Coagulative | Protein denaturation > autolysis | Firm, pale focus with preserved outlines | Infarction of the myocardium, kidney, spleen |
| Liquefactive (wet) | Autolysis > denaturation (high water content) | Softening, fluid-filled cavity | Brain, abscesses |
| Caseous | Combination of coagulation and liquefaction | Friable «cheesy» masses | Tuberculosis, syphilis, fungal infections |
| Fat (steatonecrosis) | Lipases break down fat → soaps (Ca²⁺ + fatty acids) | White «chalky» spots | Acute pancreatitis |
| Fibrinoid | Infiltration of the vessel wall with fibrin | Microscopic (eosinophilic masses) | Vasculitis, malignant hypertension, rheumatic fever |
| Gangrene | Necrosis complicated by putrefactive infection (wet) or desiccation (dry) | Black/dark color (iron sulfide) | Limbs, intestines, lungs |
Necrosis vs apoptosis: key differences
| Sign | Necrosis | Apoptosis |
|---|---|---|
| Regulation | Unregulated (pathological) | Genetically programmed |
| Cause | Damage (ischemia, toxins) | Physiological signals or pathology |
| Extent of damage | Groups of cells, entire tissue areas | Single cells |
| Membrane | Ruptured → leakage of contents | Intact, apoptotic bodies form |
| Inflammation | Yes (pronounced) | No (phagocytosis without inflammation) |
| Energy | Not required (passive process) | ATP-dependent (caspases) |
| DNA | Random fragmentation | Internucleosomal fragmentation ("ladder" pattern on electrophoresis) |
Outcomes of necrosis
- Organization — replacement of necrosis by scar (connective) tissue. The most common outcome. Example: post-infarction cardiosclerosis
- Encapsulation — formation of a connective tissue capsule around the focus (caseous necrosis in TB)
- Petrification — deposition of calcium salts (dystrophic calcification)
- Ossification — bone formation within the focus of necrosis (rare)
- Suppuration — secondary pyogenic infection → abscess
- Sequestration — rejection of necrotic masses (bone sequestrum in osteomyelitis)
Frequently asked questions
Why does liquefactive (colliquative) rather than coagulative necrosis develop in the brain?
The brain contains a lot of water and lipids, but little protein — autolysis (dissolution) prevails over denaturation (coagulation). A fluid-filled cavity (cyst) forms. Other organs (heart, kidneys) are rich in protein → denaturation prevails → coagulative necrosis with preservation of outlines.
How to distinguish caseous necrosis in tuberculosis from ordinary necrosis?
Caseous necrosis is a crumbly, white "cheesy" mass. Microscopically: homogeneous eosinophilic masses without preservation of cellular outlines (unlike coagulative necrosis), surrounded by granulomatous inflammation (epithelioid cells + Langhans cells + lymphocytes). Ziehl-Neelsen stain reveals acid-fast bacilli.
Study pathological anatomy through interactive lessons on the platform. Related topics: inflammation, epithelial tissue, acute abdomen. Use clinical calculators for morphological scales.