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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
Q

What are some symptoms of Polioencephalomalacia

A

Recumbency, inability to stand, abnormal limb movement, non-responsive,
star-gazing (opisthotonos)

26
Q

Why does gross lesions of cortical necrosis autofluoresce under
ultraviolet light

A

presence of lipid metabolites in macrophages or of high-molecular-weight
collagen-like material

27
Q

What is gangrenous necrosis

A

• Gangrene is a relatively old term = tissue necrosis

28
Q

What are the three main types of gangrene

A
  • Dry gangrene
  • Wet gangrene
  • Gas gangrene
29
Q

What is dry gangrene

A 
• Coagulative necrosis which develops in tissue with impaired
blood supply (ischemia)
30
Q

What is wet gangrene

A

• Necrotic tissue is infected by bacteria – hemorrhage, oedema

31
Q

What is gas gangrene

A

• Bacterial infection in tissues producing gas – Clostridium spp

32
Q

What causes fat necrosis

A

• 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
Q

What are the impact of necrosis

A

• 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
Q

what is Autolysis

A

• 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
Q

which tissue is most vulnerable for autolysis

A

• Tissues most vulnerable – GIT, pancreas, liver, kidney vs muscle

36
Q

putrefaction

A

the process of decay or rotting in a body or other organic matter after death.
With proliferation of bacteria

37
Q

What is Bile imbibition

A 
Leakage of bile into
the
surrounding
parenchyma
after death
38
Q

What is Apoptosis

A 
• 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
Q

What are factors in Necrosis

A 
Response to irreversible injury
(pathologic)
Accidental and random process
Inactive process – ATP depletion
Involves groups of cells
Cell membranes disrupted
40
Q

What are the factor of apoptosis

A 
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
Q

What happen during apoptosis

A

Cellular fragments are
extruded as plasma
membrane-bound bodies >
recognized by phagocytes

42
Q

What is the extrinsic pathway of apoptosis

A 
‘Death’ ligands include
FAS – via Tc cells
TNF – cytokine
Also
Perforin, granzymes,
granulysin – via Tc cells
damage from outside of the cell
43
Q

What is the intrinsic pathway of apoptosis

A 
Growth factor withdrawal
DNA damage
- ROS, radiation, toxins
Misfolded proteins
damage from inside of the cell
44
Q

What are thhe pathologic apoptosis

A

Immune mediated disease
Canine - Skin - Erythema multiforme, TEN

Viral infection
Murine – Liver – Mouse hepatitis virus – Necrosis and apoptosis

45
Q

Does virus always cause necrosis

A

Virus causes hepatocellular death,
typically by oncotic necrosis, but
sometimes by apoptosis

46
Q

What does hepato mean

A

liver related

47
Q

What causes Dystrophic and Metastatic Mineralization

A
  • Deposition of calcium salts in soft tissues
  • Accummulation of hard, white, gritty mineral
  • Microscopically see granular basophilic (blue) material
48
Q

What is dystrophic

A

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
Q

What is metastatic mineralization

A

• Metastatic = soft tissue calcification as the result of
elevated serum calcium concentration (Ca/Phos imbalance)
v

50
Q

Where are mineral deposited in during metastatc mineralization

A

blood vessels - lungs, pleura, endocardium,

kidneys, and stomach

51
Q

What are some disease that cause metastatic mineralization

A

• 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
Q

What is pyknosis

A

shrinkage

53
Q

What is kayorrhexis

A

fragmentation

54
Q

what is karyorrlysis

A

fading

55
Q

What is congenital syndactyly

A

failure of proper apoptosis

Cells to systems (25 decks)

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