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Veterinary Pathology > Unit 2 - 2.8-2.9 > Flashcards

Unit 2 - 2.8-2.9 Flashcards

1
Q

In a nutshell: Necrotic tissue in a live animal can be modified by environmental effects, allowing it to decompose in particular ways

A

gangrene

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2
Q

Where does dry gangrene occur?

A

in tissues that have a relatively limited amount of blood and fluids

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3
Q

Give some examples of where you’d see dry gangrene (5):

A

extremities, feet, ear, tail, wattles, comb

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4
Q

What is the gross appearance of dry gangrene?

A

dry, shriveled, and leathery with a sharp line of demarcation

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5
Q

What causes dry gangrene?

A

interference of blood supply (ischemia)

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6
Q

List some examples of things that can cause dry gangrene (3):

A

freezing, vascular constriction, thrombosis

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7
Q

Where does moist gangrene occur?

A

in tissues that are rich in blood and fluids (lung, intestine, mammary gland, and muscle masses)

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8
Q

What bacterial process is favored in moist gangrene?

A

digestion of tissues

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9
Q

Describe the appearance of moist gangrene:

A

appears flabby, swollen, and soft, usually has a strong putrefactive odor, and may be pale, red or blackened

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10
Q

In life, gangrene is:

A

painless and cool to the touch

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11
Q

Gas gangrene is:

A

a form a moist gangrene caused by the invasion of gas-producing bacteria of the genus Clostridium

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12
Q

Why specifically Clostridium when dealing with gas gangrene?

A

have the ability to induce necrosis then live as saprophytes in the dead tissue

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13
Q

Name 2 disease examples where gas gangrene is a prominent feature:

A

blackleg, malignant edema

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14
Q

Which lymphocyte is present at the borders of gangrenous tissue?

A

neutrophils

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15
Q

Effects of dry gangrene:

A

sloughing of the involved portion of the extremity (animal may live)

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16
Q

Effects of moist/gas gangrene:

A

absorption of toxic materials and bacteria from the putrefaction (sapremia - can lead to fatal toxemia and sepsis)

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17
Q

Once cells die, three dynamic changes occur over the next hours/days:

A
  1. calcium salts accumulate
  2. cholesterol from membranes crystallizes
  3. phosopholipids from membranes form myelin figures
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18
Q

Gangrene is a follow up process to:

A

necrosis

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19
Q

Why can freezing lead to necrosis?

A

excessive vasoconstriction can lead to devitalization/necrosis; ice crystal formation can lead to vascular rupture

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20
Q

Why would there be tan coloration along the line of demarcation for gangrene?

A

live epidermis is dying, drying out, and lifting away from the dead tissues

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21
Q

The line of demarcation in gangrene denotes:

A

where the vasoconstriction occured

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22
Q

the degree to which a substance can cause harm

A

toxicity

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23
Q

the actual disease condition of an animal due to poisoning

A

toxicosis

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24
Q

Which type of gangrene has no significant effect on the animal’s long term health?

A

dry gangrene

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25
Q

What is the only real difference between dry and moist gangrene?

A

relative amount of moisture in the tissue involved

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26
Q

bacteria that feed on dead material - whether from within the body from outside

A

saprophytic bacteria

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27
Q

a medical condition in which a part of the intestine folds into the section next to it

A

intussesception

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28
Q

How can intussesception lead to gangrene?

A

static blood flow leads to hypoxia and eventually to anoxia; cellular degeneration is initiated and eventually progresses to necrosis

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29
Q

Where do saprophytic bacteria in an intussesception come from?

A

lumen of the intestine

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30
Q

Why are the results of moist gangrene so serious?

A

toxins from both the breakdown of putrefying tissue and from the bacteria are readily absorbed into the circulation

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31
Q

What can cause a green coloration to tissues (4)?

A
  1. eosinophil inflammation
  2. algae infection
  3. green jaundice (never really seen)
  4. sulfhemoglobin
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32
Q

disease caused by feed-borne toxin that damages the type 1 pneumocytes that line alveoli

A

acute (atypical) interstitial pneumonia

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33
Q

What happens if gastric fluid (hydrochloric acid and pepsin) is accidentally aspirated?

A

causes tremendous pulmonary damage (necrosis) and open the door bacterial invasion

34
Q

What happens to cause the green coloration in lungs when gastric acid is aspirated?

A

anaerobic environment is produced - H2S and hemoglobin combine, forming sulfhemoglobin and bilirubin

35
Q

On microscopic view, if you can still recognize the general tissue outlines, you might be looking at what type of necrosis?

A

coagulative

36
Q

What happens when Fusobacterium necrophorum becomes established in an injured tissue?

A

creates its own ideal environment for proliferation and causes severe progressive necrosis

37
Q

Algor mortis

A

cooling of body after death; highly variable

38
Q

What are some of the variables of algor mortis?

A

body temperature at time of death, ambient temperature, fat covering, wool or hair covering, etc.

39
Q

Rigor mortis

A

rigidity of skeletal and cardiac muscles after death

40
Q

Where does rigor mortis begin? Where does it progress to?

A

anterior muscles first and progresses posteriorly

41
Q

How long does it take for the beginning stages of rigor mortis to set in?

A

1-6 hours

42
Q

How long until rigor mortis disappears and why?

A

18-24 hours (but may persist for several days); beginning of autolysis

43
Q

Give the pathologic reasoning for rigor mortis:

A

due to loss of ATP production by the muscle cells when blood flow stops and all muscle glycogen is exhausted

44
Q

Why does loss of ATP cause rigor mortis?

A

actin and myosin of muscles cannot work without it

45
Q

Liver mortis

A

postmortem hypostatic congestion

46
Q

When does liver mortis begin?

A

within an hour or so after death

47
Q

When does liver mortis reach its peak?

A

within a few hours

48
Q

As postmortem lysis of blood occurs (usually after 10-18 hours), the freed hemoglobin escapes into the adjacent tissues giving them a homogeneous red coloration

A

hemoglobin imbibition

49
Q

Autolysis:

A

softening of tissues due to release of proteolytic enzymes within the cell

50
Q

List some of the tissues that autolyze faster than others (5):

A

brain, liver, kidney, lining of GI, adrenal medulla, gall bladder epithelium

51
Q

The accumulation of gas in the GI tract due to continued fermentation and progressing putrefaction

A

postmortem bloat

52
Q

How do you differentiate postmortem bloat from antemortem bloat?

A

Antemortem bloat has evidence of cyanosis in the cervical and head tissues

53
Q

Postmortem emphysema

A

the accumulation of gas in tissues other than the GI tract (caused by saprophytes)

54
Q

What organs are most commonly involved in postmortem emphysema?

A

lungs, liver

55
Q

Postmortem digestion of tissues by bacteria, fungi:

A

putrefaction

56
Q

Where are the most common places to see Pseudomelanosis?

A

GI tract, abdominal viscera

57
Q

Pseudomelanosis

A

postmortem blackening of the tissues

58
Q

H2S (from putrefaction) + Fe (from blood) –>

A

Fe2S3 (iron sulfide - which is black; pseudomelanosis)

59
Q

Hemoglobin comining with acid in putrefyng tissues produces:

A

hematin crystals, an artifact of autolysis

60
Q

Seeping of bile pigments through the gall bladder and bile duct into adjacent tissues giving them a greenish-yellow hue

A

bile imbibition

61
Q

What two imbibition processes occur at about the same rate as each other?

A

bile, blood

62
Q

What is the primary difference between autolysis and necrosis?

A

autolysis is diffuse, necrosis is a focal/multifocal process

63
Q

Why is evidence of inflammation indicative of necrosis?

A

because there is a tissue rxn (dead tissues do not exhibit inflammation)

64
Q

Decomposition of protein under aerobic conditions - utilized as a food source by microbes:

A

decay

65
Q

settling of blood to the most ventral portions of the body immediately after death before clotting occurs

A

liver mortis (hypostatic congestion)

66
Q

When glycogen and ATP in the myocytes become depleted, the muscle fibers:

A

remain in a state of sustained contraction (rigor mortis)

67
Q

What 2 things antemortem can accelerate the onset of rigor?

A

intense muscular activity, high temperature

68
Q

The tan foci sometimes left behind by putrefaction (bacterial colonies), can look like what previous module we learned about? How do you tell the difference?

A

foci of necrosis; histopath

69
Q

How do we distinguish nuclei in autolysis vs. necrosis?

A

autolysis - stain weakly and fade out gradually (karyloysis)

necrosis - undergo predictable changes

70
Q

Saprophytic bacteria can be a feature of (2):

A

decomposition (dead animal); gangrene (dead tissue in a live animal)

71
Q

A common change associated with autolysis (micrscopically):

A

separation of epithelial cells from the lamina propria or submucosa

72
Q

Very common in sheep:

A

copper toxicity

73
Q

What does PAS stain?

A

glycogen

74
Q

What is the name for a yellow coloration?

A

icterus

75
Q

Tubules of the kidney are lined by:

A

cuboidal epithelial

76
Q

Normally, the lumens of the kidney tubules should be:

A

clear

77
Q

Why do we use congo red for staining?

A

taken up by amyloid

78
Q

What are the ultrastructure features of cell injury (5)?

A
  1. detachment of ribosomes from RER
  2. Formation of “blebs”
  3. Swelling of mitochondria
  4. ER dilation
  5. Cell swelling
79
Q

What is a critical step in a cell transitioning from reversible to irreversible cell damage?

A

membrane damage

80
Q

What is an important mediator of many biochemical and morphologic alterations leading to cell death?

A

calcium

81
Q

What would you call a lesion affecting the white matter of the brain?

A

leukoencephalomalacia

Veterinary Pathology (14 decks)

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