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General Pathology > Cellular Adaptations and Death > Flashcards

Cellular Adaptations and Death Flashcards

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
Q

Necrosis - mitochondria

A

Large, amorphous densities

26
Q

Necrosis - lysosomes

A

rupture, release of enzymes

27
Q

Necrosis - nuclei

A

Pyknosis, karyorrhexis, karyolysis

28
Q

Pyknosis:

A

Nucleus is small and dense

29
Q

Karyorrhexis

A

Nucleus is in little fragments

30
Q

Karyolysis

A

Nucleus fades and disappears

31
Q

What are the main necrosis morphologies

A

Coagulative
Liquefactive
Caseous

32
Q

Coagulative necrosis - what happens

A

Enzymes denature tissues
Structural outline is preserved

33
Q

coagulative necrosis - where does it happen

A

Any tissue except the brain

34
Q

coagulative necrosis - causes

A

Hypoxia, ischemia, acute toxicity, thermal injuries

35
Q

coagulative necrosis - gross

A

grey, white, yellow, or red
Depressed
Soft

36
Q

coagulative necrosis - histo

A

Tissue architecture preserved
Homogenous eosinophilic area
Nuclear change may or may not be present

37
Q

Liquefactive necrosis - what happens

A

Enzymatic or cellular degradation of cellular components
Tissue architecture is not preserved

38
Q

Liquefactive necrosis - where does it happen

A

Any tissue
ONLY type that occurs in the brain

39
Q

Liquefactive necrosis - causes

A

Bacterial or fungal infection, severe burns, chemical injuries

40
Q

Liquefactive necrosis - gross

A

Creamy, opaque material oozes from tissue
May or may not be encapsulated
Can be hard to distinguish from inflammation

41
Q

Liquefactive necrosis - histo

A

Loss of recognizable tissue architecture and cellular details
Eosinophilic proteinaceous material
Cellular debris
Variabel amounts of inflammation (depends on cause)

42
Q

Caseous necrosis - what is it

A

used to denote specific pathology
Pathogens induce a specific response in tissue

43
Q

Caseous necrosis - gross

A

White, gray, yellow material
Thick, pasty, cheese-like
Dry, slightly greasy, firm
May be lamellated
May have areas of mineralization

44
Q

Caseous necrosis - histo

A

Loss of recognizable tissue architecture and cellular details
Granulomatous and lymphocytic inflammation
Giant cells
May have mineralization

45
Q

Malacia:

A

Necrosis of the CNS
Remember - brains only do liquefactive necrosis

46
Q

What is another term for fat necrosis

A

Saponification

47
Q

Main categories of saponification

A

Enzymatic
Non-enzymatic (trauma)

48
Q

Dry gangrene:

A

Coagulative necrosis of an extremity

49
Q

Dry gangrene - gross

A

Shrunken and leathery
Necrotic material may slough

50
Q

Dry gangrene - clinically

A

Cold and dark color

51
Q

Dry gangrene - histo

A

Coagulative necrosis
Small numbers of bacteria

52
Q

Wet gangrene:

A

Liquefactive necrosis
Happens when necrotic tissue retains moisture and warmth
Superimposed bacterial infection

53
Q

wet gangrene - gross

A

Wet, dark, may contain gas pockets

54
Q

wet gangrene - histo

A

Liquifactive and coagulative necrosis, bacteria, gas bubbles

55
Q

Apoptosis - overall cell morphology

A

Shrunken and convoluted

56
Q

Necrosis - overall cell morphology

A

Swollen and disrupted

General Pathology (19 decks)

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