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

Unit 2 Necrosis (2.5-2.6) Flashcards

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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
Substrate for inflammatory mediators which is inhibited by NSAIDs:
arachidonic acid
26
tissue damage caused when blood supply returns to the tissue after a period of ischemia or hypoxia:
reperfusion injury
27
includes any molecule with an unpaired electron
free radical
28
Focal areas of coagulative necrosis due to ischemia:
infarcts
29
Infarcts most commonly occur secondary to:
thrombosis or thrombeembolism
30
Loss of adhesion of cell to the extracellular matrix, BM, and neighboring cells by integrins is a common feature of:
necrosis (and is seen to some advantage in coagulative necrosis)
31
Which part of the hepatic lobule receives blood last?
centrilobular or periacinar region of the lobule
32
What is the number one reason for passive congestion?
cardiac dysfunction or heart failure
33
What is the most common pattern of acute liver toxicity?
centrilobular coagulative necrosis
34
What is an important structure that occurs on the anti-mesenteric surface of the ileum?
Peyer's patches
35
Cheese-like, granular, yellow to white mass on gross appearance. It is often well-encapsulated.
Caseous necrosis
36
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.
Caseous necrosis
37
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.
Liquefactive necrosis
38
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.
Liquefactive necrosis
39
Becomes opaque, chalky, granular, and firm on gross appearance.
Fat Necrosis
40
What are the two liquefactive fates of necrosis?
1. reabsorbed via lymph and blood stream OR | 2. with abscess formation - rupture of abscess
41
What are the four mechanisms and major inducers of apoptosis?
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
What are the 5 histopathologic signs of apoptosis?
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
List the four types of necrosis:
1. coagulative 2. liquefactive 3. caseous 4. fat
44
In this type of necrosis all cellular detail is lost and, in addition, the tissue pattern is also totally destroyed
caseous
45
Calcification occurring in necrotic tissue is referred to as:
dystrophic calcification
46
What disease is the poster child for caseous necrosis with foci of mineralization, historically often seen on radiographs?
tuberculosis
47
3 generic differential diagnoses of nodules:
abscess, granuloma, neoplasia
48
Coagulative necrosis can progress to what type of necrosis is resolution is delayed?
caseous necrosis
49
This lesion is seen mostly in nervous tissue where there is a high lipid and water content and no connective tissue stroma.
liquefactive necrosis
50
softening of the brain
encephalomalacia
51
softening of the spinal cord
myelomalacia
52
Common in cows at peak lactation:
ketosis
53
death of cells and tissues while the body is whole (still living)
necrosis
54
The natural death of cells or tissues through aging, as distinguished from necrosis or pathological death
Necrobiosis
55
Programmed cell death, requiring energy and certain enzymes (active process)
apoptosis
56
The destruction of tissues or cells of an organism by the action of substances, such as enzymes, that are produced within the organism.
Autolysis (also called self-digestion)
57
List some of the causes of cell death (7):
1. ischemia 2. loss of nerve supply 3. loss of endocrine stimulation 4. endotoxins 5. mechanical/thermal injury 6. chemical injury 7. pressure
58
Why does necrotic tissue tend to be lighter in color?
due to denaturing of proteins including cytochrome oxidases
59
Cytoplasm broken up and gone (cell is basically gone)
cytoplasmolysis
60
cytoplasm denser and stains more pink than before
coagulation
61
2 cytoplasmic changes leading to increased eosinophilia:
cytoplasmolysis, coagulation
62
seen with complete loss of blood supply (ischemia)
coagulative necrosis
63
associated with granulomatous inflammation
caseous necrosis
64
abscess with neutrophils that come in and form pus
liquefactive necrosis
65
What level of protein breakdown occurs during coagulative necrosis?
tertiary and quaternary
66
Why is it important that tertiary and quaternary protein structure gets broken down by coagulative necrosis?
changes proteins in ways that makes them no longer susceptible to enzymatic breakdown
67
Significance of coagulative necrosis:
specific diagnostic lesion
68
Typical microscopic appearance of coagulative necrosis:
hypereosinophilia, loss of cellular detail, karyorrhexis, karyolysis
69
List the 3 causes of Zenker's Necrosis:
1. vitamin E deficiency 2. Ischemic necrosis (MI and myocardium) 3. Certain bacterial toxins (Clostridium, Blackleg)
70
What is the gross appearance of Zenker's necrosis (4)?
1. original outline persists 2. muscle slightly swollen 3. waxy appearance 4. light in color
71
What is the microscopic appearance of Zenker's necrosis?
preservation of tissue organization and cell outlines
72
Saponification
fat and glycerine combine with metallic ions to form soap
73
secondary to pancreatic disease with release of lipase and other enzymes that break down fat
pancreatic fat necrosis
74
manifested as steatitis leading to fat necrosis; cats eating a diet high in rancid oxidized fats
vitamin E deficiency
75
due to lying on a hard surface (large animals); presents as firm tissue beneath the skin
traumatic fat necrosis
76
mesenteric and omental fat become firm (necrotic) around the viscera; can cause obstructions (esp. bovine abdominal cavity)
metabolic fat necrosis
77
Gross appearance of fat necrosis:
loss of shine, dull/opaque, firm soap-like consistency
78
Microscopic appearance of fat necrosis:
cell outline remains, cytoplasm replaced by pale blue (soap) material; solid to stippled
79
What are the 4 potential causes of fat necrosis?
1. pancreatic fat necrosis 2. vitamin E deficiency 3. traumatic fat necrosis 4. metabolic fat necrosis
80
What are some of the causes of caseous necrosis?
bacterial infection, some chemicals
81
Often infiltrated with macrophages (multinucleuated giant cells):
caseous necrosis
82
Three main outomes of caseous necrosis?
encapsulation, liquefaction, mineralization
83
What disease features of the CNS can lead to liquefactive necrosis?
1. low amounts of coagulative protein 2. high amounts of lipids (Together this creates a low pH)
84
Why is an abscess considered liquefactive necrosis?
bacteria and neutrophils release proteolytic enzymes that liquefy tissue
85
What are some of the outcomes of liquefactive necrosis (4)?
walled off, remain as fluid, resorbed, replaced by scar tissue
86
Hallmarks of Necrosis:
swollen cell, hypereosinophilia, nuclear change (karylysis, karyorhexis, karyloysis), loss of nucleus and cellular detail

Veterinary Pathology (14 decks)

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