Lecture 14 Flashcards
What happens right before cell death
Cell membrane damage → swelling mitochondria, ER, lysosomes, PM Cytoskeletal damage swelling, dissociation Mitochondrial dysfunction amorphous densities Release of lysosomal enzymes cell damage Nuclear changes condensation/ fragmentation
What happen to eosinophilia in cytoplasm during oncotic necrosis
– loss of cytoplasmic RNA; denatured cytoplasmic proteins
What happen to Vacuolation in cytoplasm during oncotic necrosis
– digestion of cytoplasmic organelles by liberated enzymes
What happen to Mineralization in cytoplasm during oncotic necrosis
degradation of membrane phospholipids > FA accumulation
What happen to the nucleus during oncotic necrosis
Pyknosis (shrinkage) > Karyorrhexis (fragmentation) > Karyorrlysis (fading
When will evidence of necrosis be detectable
- Serum biochemistry (< 1/2hour)
- Ultrastructural changes (1/2 - 4hours)
- Light microscopic changes (4 – 12hours)
- Gross changes (12 – 24 hours)
What is the formation of degeneration during early/reversible cell
Early/Reversible
Cell swelling
Surface blebs
Cytoplasmic eosinophilia
What is the formation of necrosis during ongoing/irreversible cell
Cell loss
Cell fragmentation
Pyknosis
Karyorrlysis
What are necrosis cells caused by viral injury in spleen
Lymphocytes Necrosis pyknosis karyorrhexis (arrow) karyorrlysis
What kind of necrosis happens during toxic injury in renal tubules
Kidney - Chloroform toxicity Tubular epithelial cells demonstrating Hydropic degeneration Necrosis pyknosis (arrow) karyorrlysis (arrowhead)
What is coagulative necrosis
Denaturation of cellular proteins including lysosomal enzymes
> retention of tissue architecture
What are the cause of coagulative necrosis
Hypoxia, ischemia, toxins
What are the infarction in coagulative necrosis
reflects obstruction of blood supply to a region of an organ
> coagulative necrosis of affected region
What happens when there is subacute to chronic infarcts
loss of tissue/ fibrous scarring
What is caseous necrosis
- Caseous = Cheese-like
- Chronic form of necrosis
- Loss of tissue architecture
- Loss of cellular detail
Is caseous infectious
yes, • eg. Corynebacterium pseudotuberculosis = Cheesy gland = Caseous lymphadenitis
What causes caseous necrosis
Mycobacteriosis - Mycobacterium spp
What are prone to caseous necrosis
Avians and reptiles
What is liquefactive necrosis
• Cells are lysed and the necrotic tissue is converted to a liquid phase
What infection is cause liquefactive necrosis
Common in pyogenic bacterial infections – eg. cat bite abscess
What is Oncotic necrosis in the brain and spinal cord manifests as
liquefactive necrosis
Why does liquefective necrosis happen
• Lack of a fibrous interstitium to uphold tissue
structure
• Cells of the CNS tend to be rich in lipids and lytic
enzymes
What is the malacia
• Gross appearance of softened, necrotic tissue in
the CNS is malacia
What animal are susceptible to Polioencephalomalacia
• Adult doe (goat)
What are some symptoms of Polioencephalomalacia
Recumbency, inability to stand, abnormal limb movement, non-responsive,
star-gazing (opisthotonos)
Why does gross lesions of cortical necrosis autofluoresce under
ultraviolet light
presence of lipid metabolites in macrophages or of high-molecular-weight
collagen-like material
What is gangrenous necrosis
• Gangrene is a relatively old term = tissue necrosis
What are the three main types of gangrene
- Dry gangrene
- Wet gangrene
- Gas gangrene
What is dry gangrene
• Coagulative necrosis which develops in tissue with impaired blood supply (ischemia)
What is wet gangrene
• Necrotic tissue is infected by bacteria – hemorrhage, oedema
What is gas gangrene
• Bacterial infection in tissues producing gas – Clostridium spp
What causes fat necrosis
• Nutritional
• diet high in unsaturated fatty acids and low in vitamin E or other antioxidants
> ROS synthesis
• Enzymatic
• Peripancreatic – release of lipases from
damaged pancreas
• Traumatic – vascular
• Idiopathic – retroperitoneal fat in ruminants
What are the impact of necrosis
• Location of the injury within the affected tissue
• Extent of the injury
• Retention of the supporting tissue architecture
eg. kidney tubular damage and retention/loss of tubular basement membrane
• Regenerative capacity of the injured tissue
liver versus brain
what is Autolysis
• Self digestion of tissues due to the release of enzymes
into the cytoplasm of the cells after death
• Variation in tissues – content of proteolytic enzymes
> variation in rate and degree of autolysis
which tissue is most vulnerable for autolysis
• Tissues most vulnerable – GIT, pancreas, liver, kidney vs muscle
putrefaction
the process of decay or rotting in a body or other organic matter after death.
With proliferation of bacteria
What is Bile imbibition
Leakage of bile into the surrounding parenchyma after death
What is Apoptosis
• Regulated form of cell death • Programmed or directed process doi: 10.1242/dev.127878 DOI: 10.1177/0300985814537530 • Important in Embryologic development Homeostasis Involution of tissues – hormone or growth factor removal Response to certain types of injury – immune-mediated disease - cytotoxic T cells Oncology – cancer avoidance of apoptosis
What are factors in Necrosis
Response to irreversible injury (pathologic) Accidental and random process Inactive process – ATP depletion Involves groups of cells Cell membranes disrupted
What are the factor of apoptosis
Removal of excess cells (physiologic) but can be a response to injury Regulated and programmed process Active – requires energy/ATP Involves individual cells Cell membranes intact
What happen during apoptosis
Cellular fragments are
extruded as plasma
membrane-bound bodies >
recognized by phagocytes
What is the extrinsic pathway of apoptosis
‘Death’ ligands include FAS – via Tc cells TNF – cytokine Also Perforin, granzymes, granulysin – via Tc cells damage from outside of the cell
What is the intrinsic pathway of apoptosis
Growth factor withdrawal DNA damage - ROS, radiation, toxins Misfolded proteins damage from inside of the cell
What are thhe pathologic apoptosis
Immune mediated disease
Canine - Skin - Erythema multiforme, TEN
Viral infection
Murine – Liver – Mouse hepatitis virus – Necrosis and apoptosis
Does virus always cause necrosis
Virus causes hepatocellular death,
typically by oncotic necrosis, but
sometimes by apoptosis
What does hepato mean
liver related
What causes Dystrophic and Metastatic Mineralization
- Deposition of calcium salts in soft tissues
- Accummulation of hard, white, gritty mineral
- Microscopically see granular basophilic (blue) material
What is dystrophic
calcification of necrotic tissue
• Normal serum calcium and phosphate levels
• Failure to regulate energy dependent intracellular calcium balance
• Association of calcium with lipid deposits from degenerate cell
membranes (phospholipids) - extracellular
What is metastatic mineralization
• Metastatic = soft tissue calcification as the result of
elevated serum calcium concentration (Ca/Phos imbalance)
v
Where are mineral deposited in during metastatc mineralization
blood vessels - lungs, pleura, endocardium,
kidneys, and stomach
What are some disease that cause metastatic mineralization
• Renal disease - phosphate retention > calcium-phosphate imbalance
• Vitamin D toxicosis – rodenticide ingestion, toxic plants (vit D-like)
• Neoplasia – excess synthesis of parathyroid hormone or PTH-like hormones
> lymphoma in dogs – PTH-like compound
What is pyknosis
shrinkage
What is kayorrhexis
fragmentation
what is karyorrlysis
fading
What is congenital syndactyly
failure of proper apoptosis
