Necrosis
A lung abscess is a localised area of necrosis of lung parenchyma with a cavity (usually 2 cm or more) containing pus or necrotic debris, caused by infection.
What our notes say
- A lung abscess is a localised area of necrosis of lung parenchyma with a cavity (usually 2 cm or more) containing pus or necrotic debris, caused by infection. (Lung Abscess)
- The diarrhoea is attributed to massive ischaemic necrosis of the intestinal villi by the enterotoxin (Paediatrics end of 2nd semester exam (MBPE 4300): 5 October 2021, 50 MCQs)
- In hospital, acute tubular necrosis (an intrinsic injury) is the leading cause. (Internal Medicine (MBIM 4100) special/supplementary exam, Paper Two: 14 August 2)
- | Renal (intrinsic) | The kidney itself is damaged | Acute tubular necrosis (ATN) from ischaemia or toxins (aminoglycosides, contrast, herbal remedies); glomerulonephritis; interstitial nephritis (drugs, infection); blackwater fever in malaria; rhabdomyolysis | (Acute kidney injury)
- Obstetric fistula (VVF/RVF) from pressure necrosis, and neonatal infection (Reproductive Health End of Trimester 2 CAT (MBOG 4223): labour and cord prolapse)
- Obstetric (the commonest cause in developing countries): prolonged obstructed labour with pressure necrosis of the bladder and vagina, uterine rupture, and injury during instrumental delivery, caesarean section or symphysiotomy. (Junior Clerkship in Reproductive Health (MBOG 4200): end of year examination, 4 )
Study material on Necrosis
- General Pathology MCQs: Fixatives, FNA, Endocrine & ARDS
- Liver Histology & Physiology
- renal pathology
- Liver Histology & Physiology
- CARDIOVASCULAR PATHOLOGY
- Lung Pathology — Must-Know
- Gastrointestinal and liver
- Pathology CAT 1: Cell Injury, Metaplasia & Hypoxia Q&A
- Pathology Spot Exam Revision: Lymphoma, Adenoma, Appendicitis, FISH
- Acute Tubular Injury (ATI): AKI Causes, Pathology & Prognosis
- 50 Multiple Choice Questions
- Cell Injury, Adaptation & Death.
- Cell Injury & Adaptation
- Pathology MCQs: Cell Injury, Cell Death, and Adaptations
- PATHOLOGY MCQs: CELL INJURY, DEATH, AND ADAPTATIONS
- Weekly Pathology Exam - June 19, 2026 (Section A: MCQs)
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Practice questions on Necrosis
Caseous necrosis differs from coagulative necrosis in that it:
- Occurs only in viral infections
- Shows complete preservation of cellular architecture
- Appears as structureless granular debris with granulomatous inflammation
- Results from direct enzymatic fat digestion
Answer: C. Caseous necrosis (characteristic of tuberculosis) shows loss of architecture with amorphous debris and distinctive granulomatous inflammation. Coagulative necrosis preserves architecture. This is not enzymatic fat necrosis and occurs in bacterial (mycobacterial) not viral infections. The gross "cheese-like" appearance gives it its name. ---
A patient develops acute pancreatitis. Areas of fat necrosis in the peritoneum appear as chalky-white deposits. This appearance is due to:
- Deposition of fibrin from vascular injury
- Accumulation of cholesterol crystals
- Formation of calcium soaps (saponification)
- Infiltration by neutrophils with myeloperoxidase
Answer: C. In fat necrosis, pancreatic lipases break down triglycerides to fatty acids, which combine with calcium to form calcium soaps—visible as chalky-white areas. This is saponification. This type of necrosis is specific to enzymatic fat breakdown, distinguishing it from other forms. ---
Fibrinoid necrosis is MOST commonly associated with:
- Ischemic injury to parenchymal organs
- Immune complex deposition in blood vessels
- Bacterial infections of the skin
- Chronic alcohol-induced liver damage
Answer: B. Fibrinoid necrosis is a special form of vascular damage seen when immune complexes deposit in vessel walls, combined with leakage of plasma proteins, creating a bright pink "fibrin-like" appearance. It's characteristic of vasculitis syndromes, not ischemia or infections. ---
Which feature would BEST distinguish apoptosis from necrosis in tissue sections?
- Presence of eosinophilic cytoplasm
- Lack of adjacent inflammatory response
- Evidence of DNA fragmentation
- Cell membrane disruption
Answer: B. While both may show DNA fragmentation and eosinophilia, the ABSENCE of inflammation is the most reliable distinguishing feature of apoptosis in routine sections. Apoptotic cells maintain membrane integrity and are rapidly phagocytosed without eliciting inflammation, whereas necrosis causes membrane rupture and inflammation. ---
Necroptosis differs from necrosis primarily in that:
- It does not involve plasma membrane rupture
- It is triggered by genetically regulated signaling pathways
- It requires caspase activation
- It occurs only in neuronal tissue
Answer: B. Necroptosis is "programmed necrosis"—genetically regulated via RIPK1/RIPK3/MLKL signaling. Morphologically it resembles necrosis (membrane rupture, inflammation). It is CASPASE-INDEPENDENT, distinguishing it from apoptosis. It can occur in many tissues, not just neurons. ---
A research study examines cellular responses to tissue necrosis from various causes including ischemia, trauma, and chemical injury. Which sensor mechanism is responsible for detecting damaged cells regardless of the cause of injury?
- Mannose-binding lectin recognizing microbial sugars
- TLR-4 detecting lipopolysaccharide
- NOD-like receptors detecting uric acid and ATP
- Complement C3b opsonizing cellular debris
- Scavenger receptors binding oxidized LDL
Answer: C. NOD-like receptors (NLRs) are cytosolic receptors that recognize diverse molecules released from damaged cells, making them the universal sensors of cell damage. These include uric acid (DNA breakdown product), ATP (from damaged mitochondria), reduced intracellular K+ (from membrane injury), and cytoplasmic DNA. NLRs activate the inflammasome, which produces IL-1, triggering inflammation. The other options are more s