Cellular Adaptations and Death Flashcards

(56 cards)

1
Q

What are the mechanisms that can cause atrophy

A

Decreased protein synthesis
Increased protein degradation

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2
Q

What is the most common cause for hypertrophy

A

Increased workload
(skeletal muscles, uterus, heart)

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3
Q

What causes an increase in the production of cellular proteins

A

mechanical stretch (more work)
Agonists (hormones, enzymes)
GFs

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4
Q

What causes differentiation in metaplasia

A

Cytokines, GF, ECM signaling alter gene expression and lead to differentiation

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5
Q

What are the general causes of cell injury

A

Hypoxia
Physical damage
Chemical damage
Infection
Immune reactions
Genetic derangement
Nutritional imbalances

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6
Q

What does the response to cell unjury depend on

A

The nature, duration, and severity of the injury

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7
Q

reversible injury - cell membrane

A

Blebbing
Distirtion

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8
Q

reversible injury - ER

A

detachment of ribosomes

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9
Q

reversible injury - mitochondria

A

amorphous densities

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10
Q

reversible injury - lysozomes

A

Autophagy

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11
Q

reversible injury - nuclei

A

chromatin clumping

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12
Q

reversible injury - gross appearance

A

Pallor
Swelling
Increased weight
organ-opathy

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13
Q

reversible injury - histo

A

Hydropic degeneration
Increased cell volume
Cytoplasm vacuolization
Peripheral nuclei

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14
Q

Apoptsis:

A

Carefully regulated cell death

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15
Q

What are the apoptotic pathways

A

Intrinsic and extrinsic

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16
Q

What triggers the intrinsic pathway

A

Loss of stimulation or GFs

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17
Q

What triggers the extrinsic pathway

A

Death receptors

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18
Q

What do both apoptotic pathways result in (not the end result - where the pathways merge)

A

Executioner caspase activation

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19
Q

Apoptosis - ultrastructure

A

Cell shrinkage
Condensation of nuclear chromatin and cytoplasm
Cytoplasmic blebs
Apoptotic bodies

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20
Q

Apoptosis - histo

A

Single cells or small clusters
Round or oval, intensely eosinophilic cytoplasm
Dense nuclear chromatin
Minimal inflammation

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21
Q

Can necrosis be physiologic

A

No

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22
Q

Necrosis - mechanism

A

Permanent mitochondrial damage
Severe disturbance in membrane function
Ca influx –> activates phospholipase A

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23
Q

Necrosis - cell membrane

A

Defects, myelin figures

24
Q

Necrosis - ER

A

Lysis, loss of ribosomes

25
Necrosis - mitochondria
Large, amorphous densities
26
Necrosis - lysosomes
rupture, release of enzymes
27
Necrosis - nuclei
Pyknosis, karyorrhexis, karyolysis
28
Pyknosis:
Nucleus is small and dense
29
Karyorrhexis
Nucleus is in little fragments
30
Karyolysis
Nucleus fades and disappears
31
What are the main necrosis morphologies
Coagulative Liquefactive Caseous
32
Coagulative necrosis - what happens
Enzymes denature tissues Structural outline is preserved
33
coagulative necrosis - where does it happen
Any tissue except the brain
34
coagulative necrosis - causes
Hypoxia, ischemia, acute toxicity, thermal injuries
35
coagulative necrosis - gross
grey, white, yellow, or red Depressed Soft
36
coagulative necrosis - histo
Tissue architecture preserved Homogenous eosinophilic area Nuclear change may or may not be present
37
Liquefactive necrosis - what happens
Enzymatic or cellular degradation of cellular components Tissue architecture is not preserved
38
Liquefactive necrosis - where does it happen
Any tissue ***ONLY type that occurs in the brain***
39
Liquefactive necrosis - causes
Bacterial or fungal infection, severe burns, chemical injuries
40
Liquefactive necrosis - gross
Creamy, opaque material oozes from tissue May or may not be encapsulated Can be hard to distinguish from inflammation
41
Liquefactive necrosis - histo
Loss of recognizable tissue architecture and cellular details Eosinophilic proteinaceous material Cellular debris Variabel amounts of inflammation (depends on cause)
42
Caseous necrosis - what is it
used to denote specific pathology Pathogens induce a specific response in tissue
43
Caseous necrosis - gross
White, gray, yellow material Thick, pasty, cheese-like Dry, slightly greasy, firm May be lamellated May have areas of mineralization
44
Caseous necrosis - histo
Loss of recognizable tissue architecture and cellular details Granulomatous and lymphocytic inflammation Giant cells May have mineralization
45
Malacia:
Necrosis of the CNS Remember - brains only do liquefactive necrosis
46
What is another term for fat necrosis
Saponification
47
Main categories of saponification
Enzymatic Non-enzymatic (trauma)
48
Dry gangrene:
Coagulative necrosis of an extremity
49
Dry gangrene - gross
Shrunken and leathery Necrotic material may slough
50
Dry gangrene - clinically
Cold and dark color
51
Dry gangrene - histo
Coagulative necrosis Small numbers of bacteria
52
Wet gangrene:
Liquefactive necrosis Happens when necrotic tissue retains moisture and warmth Superimposed bacterial infection
53
wet gangrene - gross
Wet, dark, may contain gas pockets
54
wet gangrene - histo
Liquifactive and coagulative necrosis, bacteria, gas bubbles
55
Apoptosis - overall cell morphology
Shrunken and convoluted
56
Necrosis - overall cell morphology
Swollen and disrupted