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Pathology > Exam 2: Necrosis, Apoptosis, and Autolysis > Flashcards

Exam 2: Necrosis, Apoptosis, and Autolysis Flashcards

1
Q

What is necrosis?

A

Death of cells and tissues while the body is whole (still living)
Some cells and tissues are dead

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2
Q

What is necrobiosis?

A

The natural death of cells of tissues through aging, as distinguished from necrosis or pathological death

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3
Q

What are examples of necrobiosis?

A

Enterocytes forming crypts
Keratinocytes in the skin
These cells are constantly dying a being replaced

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4
Q

What is apoptosis?

A

Programmed cell death, requiring energy and certain enzymes

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5
Q

When is apoptosis commonly seen?

A

Following DNA damage

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6
Q

What is apoptosis a safeguard against?

A

Neoplasia following DNA damage

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7
Q

What happens during apoptosis?

A

The cell breaks up into small pieces surrounded by the cytoplasmic membrane

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8
Q

What is autolysis?

A

The destruction of tissues or cells of an organism by the action of substances, such as enzymes, that are produced within the organism
AKA self-digestion

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9
Q

When does death occur?

A

At the point at which a cell, even given proper substrates, can no longer resume the biochemical processes necessary for normal homeostasis

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10
Q

What are causes of cell death?

A 
Loss of blood supply (ischemia)
Loss of nerve supply
Loss of endocrine stimulation
Endotoxins
Mechanical/thermal injury
Chemical injury
Pressure
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11
Q

What is seen grossly in the morphologic changes of cells as it dies?

A

Necrotic tissue tends to be lighter in color due to denaturing of proteins including cytochrome oxidases

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12
Q

What is seen histologically in the morphologic changes of cells as it dies?

A 
Nuclear changes (pyknosis, karyorrhexis, karyolysis)
Cytoplasmic changes (increased eosinophilia, cytoplasmolysis, coagulation)
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13
Q

What is pyknosis?

A

Shrunken, dense nucleus

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14
Q

What is karyorrhexis?

A

Fragmentation of the nucleus

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15
Q

What is karyolysis?

A

Loss of the nucleus

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16
Q

What is cytoplasmolysis?

A

Cytoplasm broken up and gone

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17
Q

What is coagulation?

A

Cytoplasm denser and stains more pink than before

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18
Q

What are the types of necrosis?

A

Coagulative
Caseous
Liquefactive
Gangrenous

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19
Q

Describe coagulative necrosis

A

Complete loss of blood supply
Fat necrosis
Zenker’s necrosis

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20
Q

Describe caseous necrosis

A

Associated with granulomatous inflammation

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21
Q

Describe liquefactive necrosis

A

Enzymatic breakdown of tissue

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22
Q

Describe gangrenous necrosis

A

Archaic term applied to necrosis caused by loss of blood supply
Dry and wet gangrene

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23
Q

What happens as coagulative necrosis occurs?

A

Coagulation of proteins in the tissue

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24
Q

What are causes of coagulative necrosis?

A

Local heat
Local chemicals
Ischemia
Certain bacterial toxins

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25
Q

What is the significance of coagulative necrosis?

A

Specific diagnostic lesion

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26
Q

What do you see grossly with coagulative necrosis?

A

Tissue retains original form and coherent strength
Firm, pale, dry
Will eventually become friable
Often surrounded by a reddened area or hyperemia

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27
Q

What do you see microscopically with coagulative necrosis?

A

Tissue organization remains
Cell outline remains with loss of cellular detail
Nuclear changes
Cytoplasmic coagulation and hypereosinophilia

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28
Q

What is the outcome of coagulative necrosis?

A

Removal through slow digestion
Progression to liquefactive necrosis
Mineralization
Sequestration

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29
Q

What is Zenker’s necrosis?

A

A type of coagulative necrosis is specific to striated muscle

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30
Q

What are causes of Zenker’s necrosis?

A

Vitamin E deficiency
Ischemic necrosis
Certain bacterial toxins

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31
Q

What is seen grossly with Zenker’s necrosis?

A

Original outline persists
Muscle slightly swollen
Waxy appearance
Light in color

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32
Q

What is seen microscopically with Zenker’s necrosis?

A

Preservation of tissue organization and cell outlines

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33
Q

What is fat necrosis?

A

Fat and glycerine combine with metallic ions to form soap (saponification)

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34
Q

What are the causes of fat necrosis?

A

Pancreatic fat necrosis
Vitamin E deficiency
Traumatic fat necrosis
Metabolic fat necrosis

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35
Q

How does pancreatic fat necrosis occur?

A

Secondary to pancreatic disease with release of lipase and other enzymes that break down fat

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36
Q

How does vitamin E deficiency cause fat necrosis?

A

Manifested as steatitis leading to fat necrosis

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37
Q

How does traumatic fat necrosis occur?

A

Due to lying on a hard surface

Presents as firm tissue beneath the skin

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38
Q

How does metabolic fat necrosis occur?

A

Mesenteric and omental fat become firm around the viscera

Can cause obstructions

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39
Q

What is seen grossly with fat necrosis?

A

Loss of shine
Dull, opaque
Firm, soap-like consistency

40
Q

What is seen microscopically with fat necrosis?

A

Cell outline remains

Cytoplasm replace by pale blue material (soap); solid to stippled

41
Q

What is the outcome of fat necrosis?

A

Saponified fat remains in the abdominal cavity

It may have no effect or can cause mechanical effects

42
Q

What are causes of caseous necrosis?

A 
Bacterial infection
Some chemicals (turpentine)
43
Q

What is seen grossly with caseous necrosis?

A

Dry but slightly greasy
Firm, but no cohesive strength, usually pale to white
Easily separated with a blunt instrument

44
Q

What is seen microscopically with caseous necrosis?

A

Loss of all tissue outline
Amorphous, granular debris, mass
Infiltrated with mΦ, multinucleated giant cells
Often surrounded by fibrous connective tissue capsule

45
Q

What is the outcome of caseous necrosis?

A

Encapsulation
Liquefaction
Mineralization

46
Q

What are causes of liquefactive necrosis in the CNS?

A

Necrosis in the CNS almost always results in liquefactive necrosis (malacia)
Low amounts of coagulative protein
High amounts of lipids (tends to liquefy)
Create a low pH

47
Q

Describe liquefactive necrosis as an abscess

A

A liquid center
A focus of liquefactive necrosis that is surrounded by a connective tissue capsule
Bacteria and neutrophils release proteolytic enzymes that liquefy tissue

48
Q

What is seen grossly with liquefactive necrosis?

A

A fluid filled cavity in a tissue
White to pale tan, brown, red, green liquid
Consistency of cream or pudding
Frequently more foul smelling than coagulative or caseous necrosis
Frequently surrounded by fibrous conenctive tissue capsule

49
Q

What is seen microscopically liquefactive necrosis?

A

Pink, proteinacious fluid

Edges made up of frayed tissue

50
Q

What is the outcome of liquefactive necrosis?

A

Walled off
Remain as fluid
Resorbed
Replaced by scar tissue

51
Q

What is gangrenous necrosis?

A

Necrotic tissue invaded by saprophytic bacteria

52
Q

What are causes of moist gangrene?

A

Twisted intestine; devitalized intestine
Lung due to aspiration
Anywhere else conditions are right

53
Q

What is seen grossly with moist gangrene?

A

Swollen, soft, pulpy, dark in color with putrefactive smell

In vivo- insensitive; cold

54
Q

What are causes of dry gangrene?

A

Seen in extremities due to vascular compromise or ischemia; ergot
Not as many bacteria proliferating

55
Q

What is seen grossly dry gangrene?

A

Tissue is shrunken, wrinkled, leathery, often firm
Can be pale or darker than normal
Marginal hyperemia

56
Q

What are results of necrosis?

A 
Consequences if the animal survives
Calcification of dead tissue
Liquefaction and removal
Liquefaction and encapsulation
Replacement with fibrous connective tissue
Liquefaction and migration
Desquamation
57
Q

What are the consequences of necrosis if the animal survives?

A

Organ dysfunction
Necrotic tissue removed
Defect filled by fibrous connective tissue

58
Q

Describe calcification of dead tissue

A

A way to neutralize the effects of necrotic tissue
Can have mechanical effects depending on where
Dystrophic mineralization

59
Q

Describe liquefaction and removal

A

Slow and imperceptible

Removed by mΦ and lymph drainage

60
Q

Describe liquefaction and migration

A

Migration of liquid along any plane of least resistance

Pressure builds up due to influx of cells, which causes migration

61
Q

Describe encapsulation with sequestration

A

Isolation by encapsulation

Commonly seen with necrosis of bone

62
Q

What is desquamation?

A

Shedding of dead tissue from a surface

63
Q

What are types of desquamation?

A

Erosion
Ulceration
Slough

64
Q

What is erosion?

A

Loss of epithelium with an intact basement membrane

65
Q

How does erosion heal?

A

Cells will regenerate with an intact basement membrane

Heals by regeneration (no scar)

66
Q

What is ulceration?

A

Destruction of the basement membrane

67
Q

How does ulceration heal?

A

Always heals by scarring (connective tissue)

68
Q

What is slough?

A

Shedding of a large amount of tissue (second and third degree burns)

69
Q

What does necrosis occur in the absence of?

A

Energy. It does not require metabolism to complete

70
Q

What is the mechanism of necrosis?

A

Mitochondrial ATP production stops
Plasma membrane energy-dependent Na pumps shut down
Na/H2O enter cell
Cell swelling/membrane stretching
Glycolysis allows cell to function at a decreased level
Failure of Ca pumps— Ca enters the cell— many effects
Ca activation of enzyme systems
Unfolded protein response (attempt to prevent protein denaturation)
Protein denaturation starts
Damage to all membranes of all organelles
ER and other organelles swell
More changes in membrane permeability with massive influx of Ca

71
Q

What are results of the mechanisms of necrosis?

A

Mitochondria are often damaged
Inner membrane permeability is increased
Loss of proton motive force leads to deathblow for the cells
Leakage of cytochrome c

72
Q

What is apoptosis?

A

Programmed cell death

73
Q

What happens during apoptosis?

A 
Deletion of un-needed cells during embryogenesis
Normal involution
Regression of hyperplasia
Deletion of genetically unstable cells
Activation of viruses
Activation by immune cells
74
Q

Does apoptosis elicit inflammation?

A

No

75
Q

What does apoptosis require?

A

Energy

76
Q

What is apoptosis mediated by?

A

Caspases

77
Q

At what level does apoptosis act?

A

The individual cell level

78
Q

What are features of apoptosis?

A

Cells shrink, round up, become more dense, and detach from neighbors
Chromatin becomes very dense and separates into homogeneous, frequently semi-lunar or sickle shaped mass adjacent to the nuclear membrane
Budding and blebbing
Phagocytosis by macrophages and surrounding cells
Characteristic DNA ladder formation

79
Q

Is death by apoptosis normal?

A

Yes, it serves to eliminate cells that are no longer needed

80
Q

What are physiologic situations where apoptosis occurs?

A 
Embryogenesis
Hormone dependent involution
Cell deletion in proliferating pools
Death of senile cells (neutrophils)
Elimination of self reactive lymphocytes
Cells death induced by cytotoxic T cells
81
Q

What are events that are caused by hormone dependent involution?

A

Post partum endometrial cell breakdown
Regression of the lactating mammary glands after weaning
Prostatic atrophy castration

82
Q

What are pathologic situations where apoptosis occurs?

A

Cell death following injury
Cell injury in some viral diseases
Pathogenic atrophy in some organs
Cell death in some tumors

83
Q

What are biochemical features of apoptosis?

A

Apoptotic cells usually exhibit a distinctive constellation of biochemical modifications that underlie the structural changes in cells
Protein cleavage
DNA breakdown
Phagocytic recognition

84
Q

How does protein cleavage occur?

A

Via activation of several members of a cysteine protease family called caspases

85
Q

What are the mechanisms of apoptosis?

A

Extrinsic (death receptor-initiated pathway)
Intrinsic (mitochondrial pathway)
Cytotoxic T cell method

86
Q

What is the extrinsic pathway of apoptosis initiated by?

A

Engagement of cell surface death receptors

87
Q

What is the intrinsic pathway of apoptosis a result of?

A

Increased mitochondrial permeability and release of pro-apoptotic molecules into the cytoplasm

88
Q

Read about the extrinsic and intrinsic pathways of apoptosis

A

Read about the extrinsic and intrinsic pathways of apoptosis

89
Q

Describe the cytotoxic T cell method

A

Cytotoxic t lymphocytes recognize foreign Ag present on infected cell membranes
On recognition, CTLs release perforins
Granzyme B cleaves proteins at aspartate residues and activates several caspases

90
Q

What is the cytotoxic T cell method used as?

A

A bypass mechanism for cells that refuse suicide via extrinsic or intrinsic pathways

91
Q

Describe somatic death

A

Like cell death, often difficult to pinpoint the exact time
In humans, considered to be cessation of EEG activity
Not all tissues die at the same time

92
Q

How long can neurons survive?

A

3 minutes

93
Q

How long can cardiac muscle survive?

A

20 minutes

94
Q

How long can parenchymal cells survive?

A

1 hour

95
Q

How long can chondrocytes survive?

A

Several days

Pathology (16 decks)

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