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Veterinary Pathology > Unit 2 Necrosis (2.5-2.6) > Flashcards

Unit 2 Necrosis (2.5-2.6) Flashcards

1
Q

What are four causes of coagulative necrosis?

A
  1. local heat
  2. local chemicals
  3. ischemia
  4. certain bacterial toxins
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2
Q

List 4 outcomes of coagulative necrosis:

A
  1. removal through slow digestion
  2. progression to liquefactive necrosis
  3. mineralization
  4. sequestration
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3
Q

A type of coagulative necrosis specific to striated muscle (skeletal or cardiac):

A

Zenker’s necrosis

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4
Q

What can give necrosis a putrid odor?

A

exposure to bacteria producing of H2S and methyl mercaptan

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5
Q

Pyknosis -

A

condensed, solid very basophilic chromatin

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6
Q

Karyorrhexis -

A

fragmented (may resemble bacteria or other infectious agents)

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7
Q

Karyolysis -

A

extremely pale nucleus due to dissolution of chromatin

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8
Q

How long after the cell has died before you can see microscopic morphological alterations?

A

6-8 hours

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9
Q

Why can cytoplasm become eosinophilic (acidophilic)?

A

due to loss of ribosomal RNA

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10
Q

Why can cytoplasm become basophilic?

A

chromatolysis of nucleus and diffusion of nuclear DNA

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11
Q

What are the gross characteristics of coagulative necrosis?

A

characterized by a yellow to grey color (unless filled with blood), firm, friable, and may either bulge or be depressed

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12
Q

What are the microscopic characteristics of coagulative necrosis?

A

cellular outline discernible, but nuclei in various stages of decomp.; generally stains more acidophilic

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13
Q

What is one of the major take-home points of processes such as vacuolar degeneration, fatty change, or mucoid generation?

A

reversible and sublethal cell injury

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14
Q

death of living cells in an animal

A

necrosis

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15
Q

How does necrosis differ from degeneration?

A

both are the result of cell injury, but the degenerations generally are a stage of change in which there is still some possibility of recuperation

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16
Q

List the order of change seen in a cell following injury:

A
  1. biochemical change
  2. functional change
  3. morphologic change
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17
Q

What are some of the common causes of necrosis (3)?

A

hypoxia, ischemia, membrane injury

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18
Q

The heart is a vital organ. So what would you see in a lesion to determine it to be non-fatal (not the true cause of death)?

A

there was time for morphologic evidence of necrosis to occur (6-8 hours)

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19
Q

Can you see structural change in coagulative necrosis?

A

not much; can still recognize what tissue it is microscopically

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20
Q

What morphologic changes of the nucleus would you expect to see in coagulative necrosis?

A

karyolysis, karyorrhexis, pyknosis

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21
Q

Why is calcium important in the final demise of injured cells?

A

b/c of its role as both an intracellular messenger and enzyme activator

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22
Q

Irreversible cell injury has been simplified into two important features:

A

failure to restore mitochondrial function and cellular membrane damage

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23
Q

Why is it important that calcium can activate phospholipase A?

A

destroys cell membranes including the inner mitochondrial membrane

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24
Q

Activation of any other phospholipase as opposed to phospholipase A generates?

A

arachidonic acid

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25
Q

Substrate for inflammatory mediators which is inhibited by NSAIDs:

A

arachidonic acid

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26
Q

tissue damage caused when blood supply returns to the tissue after a period of ischemia or hypoxia:

A

reperfusion injury

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27
Q

includes any molecule with an unpaired electron

A

free radical

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28
Q

Focal areas of coagulative necrosis due to ischemia:

A

infarcts

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29
Q

Infarcts most commonly occur secondary to:

A

thrombosis or thrombeembolism

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30
Q

Loss of adhesion of cell to the extracellular matrix, BM, and neighboring cells by integrins is a common feature of:

A

necrosis (and is seen to some advantage in coagulative necrosis)

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31
Q

Which part of the hepatic lobule receives blood last?

A

centrilobular or periacinar region of the lobule

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32
Q

What is the number one reason for passive congestion?

A

cardiac dysfunction or heart failure

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33
Q

What is the most common pattern of acute liver toxicity?

A

centrilobular coagulative necrosis

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34
Q

What is an important structure that occurs on the anti-mesenteric surface of the ileum?

A

Peyer’s patches

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35
Q

Cheese-like, granular, yellow to white mass on gross appearance. It is often well-encapsulated.

A

Caseous necrosis

36
Q

On microscopic appearance, it has a loss of cellular outline, only nuclear fragments remain producing an amorphous mass. There is a loss of staining affinity with a tendency toward purplish staining.

A

Caseous necrosis

37
Q

An irregular cavity filled with a cloudy to clear fluid. There is no evidence of a formed lining in the cavity or of a fibrous capsule.

A

Liquefactive necrosis

38
Q

On microscopic appearance it is usually only an empty space or a light pink staining proteinaceous residue. An irregular border demarcates the extent of the lesion.

A

Liquefactive necrosis

39
Q

Becomes opaque, chalky, granular, and firm on gross appearance.

A

Fat Necrosis

40
Q

What are the two liquefactive fates of necrosis?

A
  1. reabsorbed via lymph and blood stream OR

2. with abscess formation - rupture of abscess

41
Q

What are the four mechanisms and major inducers of apoptosis?

A
  1. injurious agents (radiation, toxins, free radicals)
  2. Withdrawal of growth factors or hormones
  3. Initiation by inflammatory mediators (i.e. TNF)
  4. Immunologic damage by T lymphocytes
42
Q

What are the 5 histopathologic signs of apoptosis?

A
  1. shrunken cells
  2. condensed chromatin
  3. fragmented cytoplasm
  4. cytoplasmic buds (that may separate or occur in adjacent cells or in macrophages as apoptotic bodies)
  5. No inflammation
43
Q

List the four types of necrosis:

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. fat
44
Q

In this type of necrosis all cellular detail is lost and, in addition, the tissue pattern is also totally destroyed

45
Q

Calcification occurring in necrotic tissue is referred to as:

A

dystrophic calcification

46
Q

What disease is the poster child for caseous necrosis with foci of mineralization, historically often seen on radiographs?

A

tuberculosis

47
Q

3 generic differential diagnoses of nodules:

A

abscess, granuloma, neoplasia

48
Q

Coagulative necrosis can progress to what type of necrosis is resolution is delayed?

A

caseous necrosis

49
Q

This lesion is seen mostly in nervous tissue where there is a high lipid and water content and no connective tissue stroma.

A

liquefactive necrosis

50
Q

softening of the brain

A

encephalomalacia

51
Q

softening of the spinal cord

A

myelomalacia

52
Q

Common in cows at peak lactation:

53
Q

death of cells and tissues while the body is whole (still living)

54
Q

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

A

Necrobiosis

55
Q

Programmed cell death, requiring energy and certain enzymes (active process)

56
Q

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

A

Autolysis (also called self-digestion)

57
Q

List some of the causes of cell death (7):

A
  1. ischemia
  2. loss of nerve supply
  3. loss of endocrine stimulation
  4. endotoxins
  5. mechanical/thermal injury
  6. chemical injury
  7. pressure
58
Q

Why does necrotic tissue tend to be lighter in color?

A

due to denaturing of proteins including cytochrome oxidases

59
Q

Cytoplasm broken up and gone (cell is basically gone)

A

cytoplasmolysis

60
Q

cytoplasm denser and stains more pink than before

A

coagulation

61
Q

2 cytoplasmic changes leading to increased eosinophilia:

A

cytoplasmolysis, coagulation

62
Q

seen with complete loss of blood supply (ischemia)

A

coagulative necrosis

63
Q

associated with granulomatous inflammation

A

caseous necrosis

64
Q

abscess with neutrophils that come in and form pus

A

liquefactive necrosis

65
Q

What level of protein breakdown occurs during coagulative necrosis?

A

tertiary and quaternary

66
Q

Why is it important that tertiary and quaternary protein structure gets broken down by coagulative necrosis?

A

changes proteins in ways that makes them no longer susceptible to enzymatic breakdown

67
Q

Significance of coagulative necrosis:

A

specific diagnostic lesion

68
Q

Typical microscopic appearance of coagulative necrosis:

A

hypereosinophilia, loss of cellular detail, karyorrhexis, karyolysis

69
Q

List the 3 causes of Zenker’s Necrosis:

A
  1. vitamin E deficiency
  2. Ischemic necrosis (MI and myocardium)
  3. Certain bacterial toxins (Clostridium, Blackleg)
70
Q

What is the gross appearance of Zenker’s necrosis (4)?

A
  1. original outline persists
  2. muscle slightly swollen
  3. waxy appearance
  4. light in color
71
Q

What is the microscopic appearance of Zenker’s necrosis?

A

preservation of tissue organization and cell outlines

72
Q

Saponification

A

fat and glycerine combine with metallic ions to form soap

73
Q

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

A

pancreatic fat necrosis

74
Q

manifested as steatitis leading to fat necrosis; cats eating a diet high in rancid oxidized fats

A

vitamin E deficiency

75
Q

due to lying on a hard surface (large animals); presents as firm tissue beneath the skin

A

traumatic fat necrosis

76
Q

mesenteric and omental fat become firm (necrotic) around the viscera; can cause obstructions (esp. bovine abdominal cavity)

A

metabolic fat necrosis

77
Q

Gross appearance of fat necrosis:

A

loss of shine, dull/opaque, firm soap-like consistency

78
Q

Microscopic appearance of fat necrosis:

A

cell outline remains, cytoplasm replaced by pale blue (soap) material; solid to stippled

79
Q

What are the 4 potential causes of fat necrosis?

A
  1. pancreatic fat necrosis
  2. vitamin E deficiency
  3. traumatic fat necrosis
  4. metabolic fat necrosis
80
Q

What are some of the causes of caseous necrosis?

A

bacterial infection, some chemicals

81
Q

Often infiltrated with macrophages (multinucleuated giant cells):

A

caseous necrosis

82
Q

Three main outomes of caseous necrosis?

A

encapsulation, liquefaction, mineralization

83
Q

What disease features of the CNS can lead to liquefactive necrosis?

A
  1. low amounts of coagulative protein
  2. high amounts of lipids
    (Together this creates a low pH)
84
Q

Why is an abscess considered liquefactive necrosis?

A

bacteria and neutrophils release proteolytic enzymes that liquefy tissue

85
Q

What are some of the outcomes of liquefactive necrosis (4)?

A

walled off, remain as fluid, resorbed, replaced by scar tissue

86
Q

Hallmarks of Necrosis:

A

swollen cell, hypereosinophilia, nuclear change (karylysis, karyorhexis, karyloysis), loss of nucleus and cellular detail

Veterinary Pathology (14 decks)

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