Types of Tissue Necrosis Flashcards
Coagulative Necrosis
=Form of necrosis in which the architecture of dead tissues is preserved for a span of at least a few days (preservation of basic cell outlines)
- Injury denatures structural proteins and enzymes
- Necrotic cells are removed by phagocytosis
- Can be classified as an acute process
- Most easily recognized in liver, kidney, myocardium, skeletal muscle
- An early response to acute anoxia (ex: ischemia), acute toxic injury, and certain bacterial and viral agents
- Sequelae: removal of debris with scarring or regeneration (ex: liver)
Examples of coagulative necrosis
- Thrombus –> hypoxia/anoxia –> myocardial infarct
- “Downer cow” –> necrosis of thigh muscles due to ischemia
- Anemia –> hypoxia –> coagulative hepatic necrosis (O2 is spent and cannot get to the tissues; affects central lobular part of the liver)
- Herpesvirus infection –> viral induced cytolysis –> multifocal hepatic necrosis
Gross coagulative necrosis
-Pale tan to pale gray
-Often sharply demarcated from the normal color of adjacent viable tissue
-Solid
(cells are swelling and lysing)
Histologic coagulative necrosis
- Cytoplasm is homogenous and eosinophilic (coagulation of cell proteins; losing RNA, proteins denaturing)
- Outline of cells and architecture remains
- Dead cells appear as “ghosts”
- Nuclei:
- -Pyknosis (looks similar to lymphocyte)
- -Karyolysis
- -Karyorrhexis
- -Absent
- Inflammation
Infarct
-Is NOT the same as ischemia
=A localized area of coagulative necrosis due to ischemia
-Ischemia caused by obstruction in a vessel may lead to coagulative necrosis of the supplied tissue in all organs except the brain (do not want inflammation in the brain)
-Sequelae: death due to organ dysfunction or scarring
Zencker’s necrosis
- Coagulative necrosis of striated muscle
- Causes:
- -Plant toxins (white snake root)
- -Bacteria (Clostridium chauvoei)
- -Vitamin E - Se deficiency (“white muscle disease;” common in fetal pigs)
- -Exertional (“capture”) myopathy
- -Ischemia
Liquefactive necrosis
- Characterized by tissue that has liquefied due to the action of hydrolytic enzymes (breakdown the tissue), primarily from neutrophils
- Occurrence
- -Abscess
- –Occurs anywhere
- –A localized collection of pus (liquid inflammatory debris)
- –Elicited by certain bacterial agents (pyogenic bacteria) that attract neutrophils
- -CNS
- –Characteristic pattern of ischemic necrosis in nervous tissue
- –Especially brain and spinal cord
- –See even without PMNs
CNS
- Abscess or suppurative inflammation (dense accumulation of neutrophils - release proteases and activated oxygen metabolites via autolysis of their own lysosomal enzymes)
- Ischemic necrosis in nervous tissue
Non-CNS
-Abscess or diffuse suppurative inflammation (no ischemic necrosis)
Leukoencephalomalacia
=White brain softening
- Disease of horses
- Caused by ingestion of Fumonisin B1 produced by the fungus Fusarium verticillioides on moldy corn
- 25% of exposed animals are affected and the death rate is high in affected horses
- There is no known treatment; prevention is key
- -Examine the corn for pink fungi
- White matter becomes gelatinous and yellowish
Leukoencephalomalacia pathogenesis
- Ingestion of moldy corn –> elevated levels of fumonisin B1 in the body
1. –> fumonisin B1 binds to sphingosine N-acetyltransferase –> inhibition of this enzyme –> blocking synthesis of sphingolipids –> increasing sphingosine in the nervous tissue –> necrosis of white matter in the brain
2. –> fumonisin B1 also induces micro-circulatory damage
Polioencephalomalacia
=Gray brain softening
- Disease of ruminants
- Cause is often not known
- -Deficiency of thiamine or a disturbance in its metabolism is implicated
- –Thiaminase-producing bacteria that proliferate after CHO ingestion can destroy thiamine
- –Thiaminase-producing plants, such as bracken fern
- –Ingestion of high sulfur-containing diets
- —Sulfite can cleave thiamine, rendering it inactive
- –Dietary deficiency in thiamine
- Treatment of early cases consists of administration of thiamine and can be quite successful
Polioencephalomalacia lesions
- Initial change is edema, as evidenced by swelling of gyri
- Cerebral laminar necrosis that gives a yellow color to the gray matter
- Microscopically:
- -Edema, necrosis of neuronal cell bodies, and endothelial cell swelling
- Undigested membrane debris remains within the macrophages as ceroid pigment, this pigment fluoresces under UV light
Polioencephalomalacia pathogenesis
- Thiamine is a cofactor in the hexose monophosphate shunt which is the major metabolic pathway for glucose in the brain
- Thiamine also serves as coenzymes in the Krebs Cycle
- Deficiency poof thiamine results in a reduction in Na/K pump and subsequent loss of osmotic control
- Thiamine deficiency –> decreased energy –> lack of ATP –> decreased use of Na/K pumps –> necrosis of neurons
Caseous necrosis
=Resembling coagulated protein or curds
- Characteristic of certain bacterial infections and has a distinct appearance
- More common in cows
