Flashcards in Cell Injury 3 Deck (18)
Morphologic features of necrosis- CYTOPLASMIC CHANGES
-EARLY PHASE: Cytoplasm becomes homogenous pink in HE staining. Increased eosinophilia.
Loss of RNA causes cytoplasmic basophilia.
Consolidation of cytoplasmic components on cell collapse.
Degradation of cytoplasmic proteins gives a 'ghost like' appearance to the cell.
Necrotic cells become INDIVIDUALISED- Lose adherence to basement membranes and adjacent cells- Are found free in tubules, alveoli, follicles and other lumens or surfaces.
-LATE PHASE- Cell rupture with loss of integrity and release of cell contents.
Morphologic features of necrosis- NUCLEAR CHANGES
Nucleus is shrunken, dark, homogeneous and round.
Nuclear membrane is ruptured, dark fragments of the nucleus are released in to the cytoplasm.
The nuclear outline is extremely pale due to dissolution of the chromatin caused by the action of DNAases.
Swelling/pressure necrosis. 5 types:
1. COAGULATION NECROSIS eg. Ischaemic or toxin induced necrosis in liver/heart/kidneys
2. CASEATION/CASEOUS NECROSIS- Associated with mycobacterial infections.
3. LIQUEFACTIVE NECROSIS eg. Ischaemic or toxin induced necrosis in CNS
4. GANGRENOUS NECROSIS- Gas/moist/dry gangrene caused by bacterial toxins, other toxic agents, ischaemia.
5. ENZYMATIC NECROSIS- Typically of adipose tissue by leakage of pancreatic enzymes (lipases) subsequent to exocrine acinar tissue injury.
Preservation of basic outline of necrotic cells.
Cytoplasm has homogenous eosinophilic appearance due to coagulation of cellular proteins.
Delayed proteolysis due to denaturing of structural proteins/enzymes.
Occurs in any tissue, EXCEPT BRAIN PARENCHYMA.
Common in kidney, liver, muscle.
Commonly caused by loss of blood supply/hypoxia (leads to infarcts), bacterial toxins, chemical toxins.
Necrotic cells and tissues form granular, friable material. Necrotic focus (centre) is coagulum of nuclear and cytoplasmic debris. Surrounded by granulomatous inflammation. Mainly from dead leukocytes.
Typically seen in TB (M. bovis) and Corynebacterium pseudotuberculosis.
Seen throughout body.
Dystrophic calcification commonly occurs at later stages.
"Compared with coagulation necrosis, caseation is an older (chronic) lesion often associated with poorly degradable lipid substances of bacterial origin"
CENTRAL NERVOUS SYSTEM.
Initially individual neurones show coagulative necrosis, then a liquefactive process affects the neuroparenchyma- Enzymatic.
Hypoxia or toxin induced.
Due to little fibrous connective tissue in the CNS, there is no fibrotic reaction to replace lost/necrosed tissue.
The resulting cavity fills with fluid and neuronal lipid membrane debris.
Debris will be cleared up by macrophages (Gitter cells)
Can occur in tissues other than CNS- Abscess formation following destruction of pyogenic bacteria by neutrophils.
If dehydration occurs, pus inspissates, turning liquefaction in to caseation.
Spinal Cord Compression
Can cause haemorrhage and necrosis.
HISTOLOGICALLY- Malacia of white and grey matter.
-Pallor (rarefaction of neutrophil)
Starts as coagulation necrosis, which progresses with specific mechanisms and morphologic patterns.
Three types- Dry/Moist/Gas.
Seen in fact necrosis- SAPONIFICATION is caused by leakage of enzymes.
Appears as white spots of fat on surface of tissue.
eg.. Mesenteric fat necrosis.
Traumatic- Crushed fat eg. Pelvic fat in calf dystocia, sternal fat of recumbent animals.
Abdominal fat necrosis in cattle- Necrosis is seen in fat of mesentery, omentum and retroperitoneum.
Thick plaques of fibrinonecrotic exudate, seen for example in Infectious Bovine Rhinotracheitis.
Covers laryngeal and tracheal mucosae.
Produced due to secondary bacterial infection.
Canine Parvovirus Enteritis
An important disease condition that is also characterised by necrosis.
MULTIFOCAL/SEGMENTAL NECROSIS seen in GI tract.
Flaccid, dilated, segmentally reddened intestine
Histologically- Hyperplastic crypt epithelial cells
Squamoid crypt epithelial cells
GALT responds to infection with CPV-2 virus.
CPV-2 INFECTION- Initial infection and multiplication in lymphoid tissues
-> dissemination of virus to GI tract (+ other areas)
-> necrosis of crypt epithelial cells
-> crypt dilation
-> villus atrophy due to inability to replace enterocytes from crypts
Canine Infectious Hepatitis
Caused by Canine Adenovirus 1 (CAV-1)
Enlarged, friable liver, fibrin tags often visible on capsular surface.
Thickened gall bladder wall due to oedema.
Serosa has granular appearance.
Histologically- Necrosis and loss of hepatocytes
- Large amphophilic/basophilic intranuclear inclusions visible in hepatocytes (may also be visible in endothelial cells)
SEQUELAE TO ONCOTIC NECROSIS
Inflammatory reaction seen in viable tissue (band of white blood cells, hyperaemia)
Digestion and liquefaction of necrotic tissue. Macrophage phagocytosis, drainage/diffusion by blood or lymphatic vessels.
Regeneration of normal tissue or formation of fibrous scar tissue.