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Pathology > Necrosis, Apoptosis, Autolysis > Flashcards

Necrosis, Apoptosis, Autolysis Flashcards

1
Q

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

Necrobiosis

A

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

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3
Q

What are 2 examples of necrobiosis?

A
  • enterocytes forming the crypts

- keratinocytes in the skin (slough)

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4
Q

Apoptosis

A

Programmed cell death, requiring energy and certain enzymes

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5
Q

Is apoptosis active or passive?

A

Active!

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6
Q

When does apoptosis commonly occur?

A

Following DNA damage, is a safeguard against neoplasia

  • repaired –> mitosis
  • no appropriate repair possible –> apoptosis
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7
Q

Process of apoptosis

A

Cell breaks up into small pieces surrounded by the cytoplasmic membrane

  • no inflammatory response!!!
  • quick, easy, unobtrusive
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8
Q

Autolysis

A

Destruction of tissues or cells of an organism by the action of substances (enzymes) that are produced within the organism

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9
Q

What is autolysis also known as?

A

Self digestion

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10
Q

At what point does death occur?

A

When a cell, even given the proper substrates, can no longer resume the biochemical processes necessary for normal homeostasis

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11
Q

Post mortem rot is an example of _______

A

Autolysis

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12
Q

What are common 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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13
Q

Gross changes of cells

A

Necrotic tissue tends to be lighter in color (unless filled with blood, then darker) due to denaturing of proteins including cytochrome oxidases

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14
Q

Pyknosis

A

Shrunken, dense nucleus

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15
Q

Karyorrhexis

A

Fragmentation of the nucleus

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16
Q

Karyolysis

A

Loss of the nucleus

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17
Q

Cytoplasmolysis

A

Cytoplasm broken up and gone

- cell is basically gone

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18
Q

Coagulation

A

Cytoplasm denser and stains more pink than before

- hypereosinophilia

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19
Q

Coagulative necrosis - common causes

A
  • complete loss of blood supply
  • fat necrosis
  • Zenker’s necrosis
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20
Q

Caseous necrosis

A

Associated with granulomatous inflammation

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21
Q

Liquifactive necrosis

A

Enzymatic breakdown of tissue

  • ex: abscesses
  • common in CNS due to high fat content
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22
Q

Gangrenous necrosis

A

Archaic term applied to necrosis causes by loss of blood supply

  • dry and wet
  • also implies the body part has saprophytic bacterial infection
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23
Q

Coagulative necrosis - overview

A

Coagulation of proteins in the tissue (breakdown of 3 and 4 structures)

  • causes: local heat, local chemicals, ischemia, certain bacterial toxins
  • significance: specific diagnostic lesion
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24
Q

Gross characteristics of coagulative necrosis

A

Tissue retains original form and coherent strength!

  • firm, pale, dry
  • will eventually become friable
  • surrounded by a reddened area (hyperemia)
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25
Q

Microscopic characteristics of coagulative necrosis

A

Tissue organization remains

  • cell outline remains with loss of cellular detail
  • nuclear changes
  • cytoplasmic coagulation and hypereosinophilia
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26
Q

What are 4 causes of coagulative necrosis?

A
  • local heat
  • local chemicals
  • ischemia
  • certain bacterial toxins
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27
Q

Outcome of coagulative necrosis

A
  • removal through slow digestion
  • progression to liquefactive necrosis
  • mineralization
  • sequestration
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28
Q

Zenker’s necrosis

A

Type of coagulative necrosis specific to striated muscle (skeletal, cardiac)
- causes: vitamin E deficiency, ischemic necrosis, certain bacterial toxins (Clostridium, Blackleg)

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29
Q

Gross appearance of Zenker’s necrosis

A
  • original outline persists
  • muscle slightly swollen
  • waxy appearance
  • light in color
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30
Q

Microscopic appearance of Zenker’s necrosis

A

Preservation of tissue organization and cell outlines

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31
Q

Saponification

A

Fat and glycerine combine with metallic ions (Na, K, Ca) to form soap
- fat necrosis

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32
Q

What are 4 common causes of fat necrosis?

A
  • pancreatic fat necrosis
  • vitamin E deficiency
  • traumatic fat necrosis
  • metabolic fat necrosis
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33
Q

Pancreatic fat necrosis

A

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

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34
Q

Vitamin E deficiency

A

Manifested as steatitis leading to fat necrosis

- cats eating a diet high in rancid oxidized fats

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35
Q

Traumatic fat necrosis

A

Due to lying on a hard surface (large animals)

- presents as firm tissue beneath the skin

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36
Q

Metabolic fat necrosis

A

Mesenteric and omental fat become firm (necrotic) around the viscera
- causes obstructions (bovine abdominal cavity)

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37
Q

Gross appearance of fat necrosis

A

Loss of shine

  • dull, opaque
  • firm, soap like consistency
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38
Q

Micro appearance of fat necrosis

A

Cell outlines remain

  • cytoplasm replaced by pale blue soap material (solid to stippled)
  • soap will remain thru the staining process
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39
Q

Outcome of fat necrosis

A

Saponified fat remains in the abdominal cavity

- may have no effect or can cause mechanical effects (stops peristalsis)

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40
Q

What substance is present within adipose cells of fat necrosis?

A

Soap

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41
Q

Causes of caseous necrosis

A 
Bacterial infection (bacterial proteases and neutrophil proteases cause tissue breakdown)
- or caused by some chemicals (turpentine)
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42
Q

Gross appearance of caseous necrosis

A
  • dry but slightly greasy
  • firm, no cohesive strength, usually pale to white
  • easily separated with a blunt instrument (finger)
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43
Q

Micro appearance of caseous necrosis

A
  • loss of all tissue outline (no discernible tissue)
  • amorphous, granular debris, mass
  • infiltrated with multinucleated giant cells
  • often surrounded by fibrous connective tissue capsule
44
Q

What is typical of caseous necrosis?

A

Granular tissue with loss of all tissue architecture

45
Q

Outcome of caseous necrosis?

A
  • encapsulation
  • liquefaction
  • mineralization
46
Q

Causes of liquefactive necrosis in the CNS

A
  • low amounts of coagulative protein
  • high amounts of lipids (tends to liquefy)
  • creates a low pH
47
Q

Malacia

A

Abnormal softening of tissues

- used to describe liquefactive necrosis in the CNS

48
Q

Abscess

A

Liquid center (pus)

  • focus of liquefactive necrosis that is surrounded by a connective tissue capsule
  • bacteria and neutrophils release proteolytic enzymes that liquefy tissue
49
Q

Gross appearance of liquefactive necrosis

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 other necrosis
  • surrounded by fibrous connective tissue capsule
50
Q

Micro appearance of liquefactive necrosis

A

Pink, proteinacious fluid (or hole)

- edges made up of frayed tissue

51
Q

How would you describe the gross appearance of liquefactive necrosis lesions?

A

Discrete, fluid-filled cavities, containing white to pale tan creamy liquid

52
Q

Why is liquefactive necrosis expected in the CNS?

A

Low amounts of coagulative protein and high amounts of lipids, which tend to liquefy

53
Q

Outcome of liquefactive necrosis

A
  • walled off
  • remain as fluid
  • resorbed
  • replaced by scar tissue
54
Q

Putrefactive

A

Necrotic tissue invaded by saprophytic bacteria

55
Q

Causes of moist gangrene

A
  • twisted intestine (gangrenous enteritis), devitalized intestine
  • lung due to aspiration (gangrenous pneumonia)
  • anywhere where conditions are right
56
Q

Gross appearance of moist gangrene

A

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

- in vivo: insensitive (no viable blood supply), cold (no body head)

57
Q

Causes of dry gangrene

A

Seen in extremities due to vascular compromise or ischemia (tail, ears, toes)

  • ergot
  • not as many bacteria proliferating
58
Q

Gross appearance of dry gangrene

A
  • tissue is shrunken, wrinkled, leathery, often firm
  • can be pale or darker than normal
  • marginal hyperemia
59
Q

Consequences of necrosis, assuming animal survives

A
  • organ dysfunction (especially conducting organs)
  • necrotic tissue removed
  • defect filled by fibrous connective tissue (scar formation, contracture)
60
Q

Calcification of dead tissue

A

Way to neutralize the effects of necrotic tissue

  • can have mechanical effects depending on organ
  • dystrophic mineralization
61
Q

Liquefaction and removal

A

Slow and imperceptible

- removed by lymph drainage

62
Q

Abscess formation is a result of

A

Liquefaction and encapsulation

63
Q

Liquefaction and migration

A

Migration of liquid along any plane of least resistance

  • pressure builds up due to influx of cells, which causes migration
  • migratory tracts (fistulas, phlegmon)
64
Q

Encapsulation with sequestration

A

Isolated by encapsulation

- commonly seen with necrosis of bone (bone sequestra) and muscle

65
Q

Involucrum

A

Connective tissue capsule around a sequestrum

66
Q

Desquamation

A

Shedding of dead tissue from a surface

67
Q

Erosion

A

Loss of epithelium with an intact basement membrane

  • cells will regenerate with an intact BM
  • heals by regeneration (no scar)
68
Q

Ulceration

A

Destruction of the basement membrane

- always heals by scarring (connective tissue)

69
Q

Slough

A

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

70
Q

Necrosis is a ____ form of cell death

A

Passive

  • occurs in the absence of energy, does not require metabolism
  • frequently affects large numbers of cells (infarct)
  • associated with injurious insults
71
Q

What are the 4 common results after an injurious stimulus to a cell?

A
  • decrease in ATP
  • membrane damage
  • increase intracellular Ca
  • reactive oxygen species
72
Q

What are the 7 mechanisms 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 allowing Ca to enter cells
  • Ca activation of enyzme systems
73
Q

What happens when mitochondrial ATP production stops?

A

ATP depletion and decreased ATP synthesis are associated with hypoxic and chemical injury
- ATP depletion to <5% to 10% of normal levels has widespread effects

74
Q

What happens during glycolysis?

A
  • glycogen stores are depleted
  • lactic acid accumulates
  • cell pH drops –> induction of Heat Shock Response
75
Q

Effects of increased intracellular Ca

A
  • disruption of protein synthetic apparatus
  • detachment of ribosomes
  • decreased protein synthesis
76
Q

What damages mitochondria?

A

Increases in cytosolic Ca

77
Q

What is considered to be a “deathblow” for the cell?

A

Loss of proton motive force due to increase in permeability of the inner mito membrane

78
Q

What triggers apoptotic death pathways in the cytoplasm?

A

Leakage of cytochrome c

79
Q

Unfolded protein response

A

Attempt to prevent protein denaturation

  • protein denaturation starts
  • damage to all membranes of organelles
  • ER and other organelles swell
  • more changes in membrane permeability with massive influx of Ca
80
Q

Scenarios of 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
81
Q

Does apoptosis elicit inflammation?

A

No

82
Q

Can cells undergo necrosis without apoptosis?

A

Yes, if the injury is so severe and rapid

83
Q

Process of apoptosis

A

Cell contracts –> broken off fragments have a plasma membrane that does not elicit inflammation –> phagocytosis of apoptotic cells and fragments

84
Q

Does the cell swell during necrosis or apoptosis?

A

Necrosis

85
Q

Necrosis or apoptosis: fragmentation of the nucleus into nucleosome size fragments

A

Apoptosis

86
Q

Necrosis or apoptosis: disruption of plasma membrane

A

Necrosis

87
Q

Necrosis or apoptosis: cellular contents intact, may be released in apoptotic bodies

A

Apoptosis

88
Q

Necrosis or apoptosis: adjacent inflammation

A

Necrosis

89
Q

Necrosis: physiologic or pathologic role

A

Invariably pathologic (culmination of irreversible cell injury)

90
Q

Apoptosis: physiologic or pathologic role

A

Physiologic, means of eliminating unwanted cells

- may be pathologic after some form of cell injury (especially DNA damage)

91
Q

Active form of cell death

A

Apoptosis

  • mediated by caspases
  • does not elicit inflammation
  • acts at the individual cell level
  • balance to mitosis
  • uses highly conserved cellular machinery
92
Q

Characteristic DNA ladder formation occurs with ______

A

Apoptosis

93
Q

What happens to cells that have apoptosed?

A

Phagocytosis by macrophages and surrounding cells

94
Q

Embryogenesis

A

Physiologic situations of apoptosis

- implantation, organogenesis, developmental involution, metamorphosis

95
Q

Hormone dependent involution

A

Physiologic situation of apoptosis

  • post partum endometrial cell breakdown
  • regression of the lactating mammary glands after weaning
  • prostatic atrophy after castration
96
Q

Death of senile cells

A

Cells that have served their purpose (neutrophils)

- often deprived of normal survival signals

97
Q

Cell death induced by cytotoxic T cells

A

Form of physiologic apoptosis

  • defense mechanism against viruses and tumors
  • same mechanism acts in rejection of transplants
98
Q

Pathologic situations of apoptosis

A
  • cell death following injury
  • cell injury in some viral disease
  • pathogenic atrophy in some organs
  • cell death in some tumors
99
Q

Biochemical features of apoptosis - protein cleavage

A

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

  • present as proenzymes that must be activated to induce apoptosis
  • break up nuclear scaffold and cytoskeleton
  • also activate DNAses
100
Q

Biochemical features of apoptosis - DNA breakdown

A

Apoptotic cells exhibit characteristic breakdown of DNA into 50-300 kb pieces

  • intranucleosomal cleavage into multiple 180-200 bp fragments by Ca and Mg dependent endonucleases (ladders on a gel)
  • necrotic cells develop a smear on gel
101
Q

Biochemical features of apoptosis - phagocytic recognition

A

Apoptotic cells express phosphatidylserine in outer layer of membrane

  • allows for early recognition, resulting in phagocytosis without the release of proinflammatory cellular components
  • disposes of cells with minimal compromise to surrounding tissue
102
Q

Mechanisms of apoptosis

A
  • extrinsic (death receptor-initiated pathway)
  • intrinsic (mitochondrial pathway)
  • cytotoxic T cell (bypass) method
  • ligands for phagocytic cell receptors
103
Q

Extrinsic (death receptor) pathway

A

Initiated by engagement of cell surface death receptors

  • Fas cross linked by a ligand (FasL)
  • 3 or more FasL molecules come together to form a binding site for FADD
  • FADD binds to pro-caspase 8 which cleave each other to become active
  • initiation of caspase cascade
  • apoptosis
104
Q

Intrinsic (mitochondrial) pathway

A

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

  • withdrawal of growth factors or cell stress –> leakage of cytochrome c
  • cytochrome c binds to Apaf-1 in the cytoplasm
  • caspase 9 is activated
  • caspase cascade
  • apoptosis
105
Q

Cytotoxic T cell (bypass) method

A

Cytotoxic T-lymphocytes recognize foreign Ag present on infected cell membranes

  • CTLs release perforins (allowing entry of granyzme B)
  • granzyme B cleaves proteins at aspartate residues and activates several caspases
  • method used by immune privileged sites (brain, cornea, gonads)
106
Q

Bypass mechanism for cells that refuse suicide via extrinsic or intrinsic pathways

A

Bypasses upstream signaling events

- directly induces the effector phase of apoptosis

107
Q

Somatic death

A

Difficult to pinpoint the exact time

  • not all tissues die at the same time!
  • neurons: 3 minutes
  • cardiac muscle: 20 min
  • parenchymal cells: 1 hour
  • chondrocytes: several days

Pathology (19 decks)

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