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Cells to systems > Lecture 14 > Flashcards

Lecture 14 Flashcards

1
Q

What happens right before cell death

A 
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
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2
Q

What happen to eosinophilia in cytoplasm during oncotic necrosis

A

– loss of cytoplasmic RNA; denatured cytoplasmic proteins

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3
Q

What happen to Vacuolation in cytoplasm during oncotic necrosis

A

– digestion of cytoplasmic organelles by liberated enzymes

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4
Q

What happen to Mineralization in cytoplasm during oncotic necrosis

A

degradation of membrane phospholipids > FA accumulation

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5
Q

What happen to the nucleus during oncotic necrosis

A

Pyknosis (shrinkage) > Karyorrhexis (fragmentation) > Karyorrlysis (fading

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6
Q

When will evidence of necrosis be detectable

A
  1. Serum biochemistry (< 1/2hour)
  2. Ultrastructural changes (1/2 - 4hours)
  3. Light microscopic changes (4 – 12hours)
  4. Gross changes (12 – 24 hours)
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7
Q

What is the formation of degeneration during early/reversible cell

A

Early/Reversible
Cell swelling
Surface blebs
Cytoplasmic eosinophilia

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8
Q

What is the formation of necrosis during ongoing/irreversible cell

A

Cell loss
Cell fragmentation
Pyknosis
Karyorrlysis

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9
Q

What are necrosis cells caused by viral injury in spleen

A 
Lymphocytes
Necrosis
pyknosis
karyorrhexis (arrow)
karyorrlysis
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10
Q

What kind of necrosis happens during toxic injury in renal tubules

A 
Kidney - Chloroform toxicity
Tubular epithelial cells demonstrating
Hydropic degeneration
Necrosis
pyknosis (arrow)
karyorrlysis (arrowhead)
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11
Q

What is coagulative necrosis

A

Denaturation of cellular proteins including lysosomal enzymes
> retention of tissue architecture

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12
Q

What are the cause of coagulative necrosis

A

Hypoxia, ischemia, toxins

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13
Q

What are the infarction in coagulative necrosis

A

reflects obstruction of blood supply to a region of an organ

> coagulative necrosis of affected region

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14
Q

What happens when there is subacute to chronic infarcts

A

loss of tissue/ fibrous scarring

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15
Q

What is caseous necrosis

A
  • Caseous = Cheese-like
  • Chronic form of necrosis
  • Loss of tissue architecture
  • Loss of cellular detail
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16
Q

Is caseous infectious

A

yes, • eg. Corynebacterium pseudotuberculosis = Cheesy gland = Caseous lymphadenitis

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17
Q

What causes caseous necrosis

A

Mycobacteriosis - Mycobacterium spp

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18
Q

What are prone to caseous necrosis

A

Avians and reptiles

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19
Q

What is liquefactive necrosis

A

• Cells are lysed and the necrotic tissue is converted to a liquid phase

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20
Q

What infection is cause liquefactive necrosis

A

Common in pyogenic bacterial infections – eg. cat bite abscess

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21
Q

What is Oncotic necrosis in the brain and spinal cord manifests as

A

liquefactive necrosis

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22
Q

Why does liquefective necrosis happen

A

• Lack of a fibrous interstitium to uphold tissue
structure
• Cells of the CNS tend to be rich in lipids and lytic
enzymes

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23
Q

What is the malacia

A

• Gross appearance of softened, necrotic tissue in

the CNS is malacia

24
Q

What animal are susceptible to Polioencephalomalacia

A

• Adult doe (goat)

25
What are some symptoms of Polioencephalomalacia
Recumbency, inability to stand, abnormal limb movement, non-responsive, star-gazing (opisthotonos)
26
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
27
What is gangrenous necrosis
• Gangrene is a relatively old term = tissue necrosis
28
What are the three main types of gangrene
* Dry gangrene * Wet gangrene * Gas gangrene
29
What is dry gangrene
``` • Coagulative necrosis which develops in tissue with impaired blood supply (ischemia) ```
30
What is wet gangrene
• Necrotic tissue is infected by bacteria – hemorrhage, oedema
31
What is gas gangrene
• Bacterial infection in tissues producing gas – Clostridium spp
32
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
33
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
34
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
35
which tissue is most vulnerable for autolysis
• Tissues most vulnerable – GIT, pancreas, liver, kidney vs muscle
36
putrefaction
the process of decay or rotting in a body or other organic matter after death. With proliferation of bacteria
37
What is Bile imbibition
``` Leakage of bile into the surrounding parenchyma after death ```
38
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 ```
39
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 ```
40
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 ```
41
What happen during apoptosis
Cellular fragments are extruded as plasma membrane-bound bodies > recognized by phagocytes
42
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 ```
43
What is the intrinsic pathway of apoptosis
``` Growth factor withdrawal DNA damage - ROS, radiation, toxins Misfolded proteins damage from inside of the cell ```
44
What are thhe pathologic apoptosis
Immune mediated disease Canine - Skin - Erythema multiforme, TEN Viral infection Murine – Liver – Mouse hepatitis virus – Necrosis and apoptosis
45
Does virus always cause necrosis
Virus causes hepatocellular death, typically by oncotic necrosis, but sometimes by apoptosis
46
What does hepato mean
liver related
47
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
48
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
49
What is metastatic mineralization
• Metastatic = soft tissue calcification as the result of elevated serum calcium concentration (Ca/Phos imbalance) v
50
Where are mineral deposited in during metastatc mineralization
blood vessels - lungs, pleura, endocardium, | kidneys, and stomach
51
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
52
What is pyknosis
shrinkage
53
What is kayorrhexis
fragmentation
54
what is karyorrlysis
fading
55
What is congenital syndactyly
failure of proper apoptosis

Cells to systems (25 decks)

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