Types of Necrosis
How does fat necrosis appear microscopically?
-outline of adipocytes is obscured -fatty acid and cholesterol crystals may be present due to breakdown of stored triglycerides -inflammation
What are the microscopic characteristics of coagulative necrosis?
-outline of cells and architecture remains -hypereosinophilia -nuclear changes: pyknosis, karyorrhexis, karyolysis, absence -dead cells appear as ghost cells -inflammatory changes around the periphery of the necrosis
What are gross characteristics of coagulative necrosis?
-pale tan to white to yellow -firm tissue -friable
what are causes of zencker's necrosis?
-plant toxins: white snake root in ruminants -bacteria: Clostridium chauvoei -Vitamin E-Selenium deficiency: white muscle disease -exertional myopathy: seen in game capture -ischemia
what causes coagulative necrosis?
1) acute ischemia 2)acute toxic injury 3) certain bacterial or viral agents
What is the sequalae to caseous necrosis?
1) can become encapsulated and persist for a long time 2) heal by scarring
What are the 3 things that can happen to an abscess?
1) septicemia: can arise if bacteria alone enters the bloodstream - a piece of the abscess can break off and enter into the blood stream 2) pyemia: dead leukocytes and bacteria in the bloodstream 3)abscess can wall-off with the fibrous capsule and the debris can be resorbed - a scar will form in the area of the necrotic parenchyma
what are common bacterial species that cause abscesses?
1) staphylococcus 2) streptococcus 3) corynebacterium
What are characteristics of moist gangrene?
commonly involves internal organs & mammary gland grossly: appears like liquefactive necrosis -dark red to black -soft -moist -friable microscopically: appears as coagulative necrosis with liquefactive necrosis superimposed sharp line of demarcation between necrotic and unaffected tissue
what are ghost cells?
dead cells as a result of coagulative necrosis appear as shadows or ghosts due to losing their nuclei
what are other causes of fat necrosis?
diets high in polyunsaturated fats leads to increases in ROS nutritional deficiency in antioxidants -> free radical damage -> fat necrosis pressure to the subcutis of a down cow's sternum -> occludes blood vessels -> ischemia -> fat necrosis ergot and fescue toxicosis
what are the two types of gangrenous necrosis?
dry gangrene: necrosis that is modified by varying air exposure wet gangrene: necrosis that is modified by the liquefactive action of bacteria
what is fat necrosis?
necrosis of adipose tissue due to the action of lipases commonly occurs in SQ and mesenteric fat common initial finding in autopsy
What is the pathogenesis of fat necrosis in pancreatitis?
necrosis of pancreatic acinar cells -> release of digestive enzymes into adjacent tissue -> action of lipases and lecithinases -> fat necrosis of peripancreatic fat
how does malacia present histologicially?
nervous tissue has: -decreased density -pale eosinophilia
how does malacia present grossly?
nervous tissue is: -depressed -yellow to brown in color
What are the characteristics of dry gangrene?
occurs in external locations with limited circulation common in areas where moisture from necrotic tissue can evaporate lesion: dry, shriveled, dark red to black, cold microscopically: appears as coagulative necrosis
How does fat necrosis appear grossly?
opaque, white firm to hard gritty
What is gliosis?
proliferation of several different types of glial cells following liquefactive necrosis
coagulative necrosis
represents cell death in which the gross and microscopic architecture of the tissue is still recognizable
What is malacia?
softening of CNS tissue due to liquefactive necrosis
what happens to old abscesses?
the fibrous capsule will remain and the necrotic material can mineralize
what is an abscess?
the most common form of liquefactive necrosis microscopic to large well-circumscribed encircled by a fibrous capsule filled with pus
what is pus
the necrotic material arising from digestion creamy yellow - due to the presence of dead leukocytes liquid-viscous-semisolid
what is the pathogenesis of polioencephalomalacia?
thiamine deficiency thiamine is an important co-factor in the hexose monophosphate shunt --important for glucose metabolism for the brain deficiency of thiamine results in reduction in the Na+/K+ pump subsequent loss of osmotic control cell swelling necrosis of neurons
what are some causes of polioencephalomalacia?
thiamine deficiency (Vitamin B1) thiamine-producing bacteria can be destroyed by thiaminase-producing bacteria that proliferate after ingestion of excessive CHO ingesting thiaminase-containing plants such as bracken fern ingestion of high-sulfur diets
what is liquefactive necrosis?
tissue that has liqueifed due to the action of hydrolytic enzymes from neutrophils lysing
How does caseous necrosis appear grossly?
well-demarcated, localized lesion soft, friable with gray to white material resembling cheese dry and crumbly or soft and pasty mineralization is common in bovine
What is leukoencephalomalacia?
white-brain-softening liquefactive necrosis that happens in horses Cause: ingestion of a toxin produced by the fungus, Fusarium verticillioides, which is found on corn "moldy corn disease"
What is an infarct?
a localized area of ischemia that has resulted in coagulative necrosis due to the obstruction of a vessel
How does leukoencephalomalacia manifest?
clinical signs appear one week to 2 months after ingestion clinical signs: -inappetence -weakness -behavioral changes -impaired vision -circling -ataxia -paralysis of pharyngeal muscles disease progresses in 1-10 days after 1st signs appear -recumbency -convulsions -coma -death
what is zencker's necrosis?
coagulative necrosis of striated muscle
what is the possible cause of polioencephalomalacia in calves?
ingestion of high sulfur containing diets
What infections have caseous necrosis?
-Mycobacterium bovis (TB) -Corynebacterium pseudotuberculosis (ovine caseous lymphadenitis) - appears as a layered apperance
what are gitter cells?
activated phagocytic cells of the CNS that may populate the necrotic tissue phagocytizing the lipid-laden debris
what are the clinical signs of polioencephalomalacia?
anorexia staggering apparent blindness head-pressing opisthotonos dorsomedial strabismus repetitive chewing facial twitching if not treated, in 3-4 days: -recumbency -convulsions -death
what are the causes of gangrenous necrosis?
anything that impacts blood supply to an area resulting in ischemia -thrombus -vascular occlusion due to mechanical compression (torsion, vovulus) -vasocontriction due to spasms or cold temps -aspiration of gastric contents into lungs some specific bacteria like Salmonella, Clostridium, Mannhemia, can all lead to vascular compromise - gangrene
what is the MOA of liquefactive necrosis
bacteria stimulate the accumulation of leukocytes and the liberation of enzymes from these inflammatory cells that act to digest the dead cells
What is caseous necrosis?
caseous: resembles coagulated protein or curds classified by its gross appearance as a combination between coagulative necrosis and liquefactive necrosis
what is the saponification of fat?
fat hydrolysis occurs in fat necrosis common with pancreatitis microscopically: amorphous granular material replacing fat. stains pink, blue or purple
what happens in the CNS following necrosis instead of fibrosis?
fibrillary astrocytes can proliferate and fill a void of lost tissue
what is the lesion in leukoencephalomalacia?
focal necrosis of white matter of cerebral hemispheres appear: -yellow -soft -hemorrhagic -cavitated with gelatinous fluid in spaces
What is a common cause of dry gangrene?
frost-bite ingestion of toxic alkaloids produced by the fungus Claviceps purpurea toxic alkaloid ergotamine, stimulates the arteriolar smooth muscle to vasoconstrict -- ischemic necrosis
what is the pathogenesis of leukoencephalomalacia?
fumonisin B1 interferes with sphingolipid synthesis sphinosine is produced - which is involved in cell signaling of necrosis, inflammation and apoptosis also induces micro-circulatory damage
what is polioencephalomalacia?
gray-brain-softening a CNS disease in ruminants that is caused by a deficiency of thiamine or a disturbance in thiamine metabolism
what is the lesion of polioencephalomalacia?
grossly: -edema (swelling of gyri) -cerebral laminar necrosis -gray matter becomes yellow microscopically: -edema -necrosis of neuronal cell bodies -endothelial cell swelling -loss of neurons and vacuolation of CNS after 7-10 days, gitter cells invade and ingest myelin and cell debris undigested membrane remains within the macrophages - fluoresces under UV light
What are the inflammatory changes that are seen with coagulative necrosis?
hyperemia leukocyte infiltration edema
what is Gangrenous necrosis
ischemic injury modified to varying degrees by exposure to air or by the liquefactive action of bacteria usually associated with necrosis of extremities like limbs, ears, combs OR lungs/ intestine
what is pus comprised of?
large number of polymorphonuclear cells necrosis of parenchyma
What happens when the CNS experiences hypoxia?
liquefactive necrosis
How does caseous necrosis appear microscopically?
loss of tissue architecture replaced with granular to eosinophilic debris - sometimes basophilic nuclear remnants and mineral the periphery of caseous necrosis is populated with macrophages and other inflammatory cells bovine TB caseous necrosis has multinucleated giant cells around the periphery
what is the sequale of liquefactive necrosis in CNS?
loss of vital CNS function - death - usually doesn't get a chance to heal
