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Veterinary Pathology > Unit 3 - Chronic Inflammation & Hypersensitivity > Flashcards

Unit 3 - Chronic Inflammation & Hypersensitivity Flashcards

1
Q

Why is a persistence of antigens important in chronic inflammation?

A

antigens constantly call in more macrophages

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2
Q

When do you get an abscess?

A

acute inflammation fails to eliminate the stimulus

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3
Q

What causes the liquefaction seen with abscesses?

A

due to neutrophil enzymes

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4
Q

What is the role of fibroblasts in the formation of an abscess?

A

produce collagen and form a thin CT around the exudate

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5
Q

What is the name of the enzyme that liquefacts neutrophils?

A

myeloperoxidase

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6
Q

What is inside the pyogenic membrane?

A

vessels to allow continual recruitment of neutrophils

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7
Q

the inner wall of an abscess that is made up of granulation tissue:

A

pyogenic membrane

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8
Q

A track made by the body to drain pus:

A

fistulas

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9
Q

Why don’t bird liquefy purulent material?

A

don’t have the enzymes to support it

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10
Q

Granulomatous means:

A

MACROPHAGES

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11
Q

What is the gross appearance of granulomatous inflammation?

A

Diffuse: tissue appears thickened
Nodules: firm, various sizes

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12
Q

Microscopically, granulomatous inflammation should have:

A
  • LOTS of macrophages

- accompanied by lymphocytes, CT, plasma cells

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13
Q

More secretory and less phagocytic than typical macrophages:

A

epithelioid macrophages

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14
Q

Large, multinucleated cells that arise from the fusion of macrophages:

A

giant cells

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15
Q

Which cell looks like a fried egg?

A

plasma cell

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16
Q

When macrophages are in aggregates, they are referred to as:

A

granulomas

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17
Q

What is the characteristic look of classic granulomas?

A
  • central core of caseous necrosis
  • zone of epithelioid macrophages and giant cells
  • zone of lymphocytes
  • outer zone of fibroblasts and fibrosis
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18
Q

Th2 –>

A

diffuse granulomatous inflammation

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19
Q

Th1 –>

A

nodular granulomas

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20
Q

Johne’s is caused by:

A

Mycobacterium paratuberculosis

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21
Q

John’s is characterized by:

A

no well defined nodules

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22
Q

Grossly, lymphocytic inflammation is:

A

difficult to determine

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23
Q

Microscopically, lymphocytic inflammation should have:

A

lymphocytes (that can be mixed with plasma cells)

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24
Q

If extensive infiltrates are present in lymphocytic inflammation, it may affect the tissue by:

A

giving it a white/tan color

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25
Q

When do lymphocytes enter unresolved areas of acute inflammation?

A

24-48 hours

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26
Q

Plasma cells secrete:

A

antibody

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27
Q

Dense infiltrate of eosinophils with macrophages, varying numbers of lymphocytes, and plasma cells:

A

eosinophilic granulomas

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28
Q

Eosinophils are recruited into and stimulated to proliferate by:

A

IL-5, eotaxin

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29
Q

Green coloration to a mass often indicates:

A

eosinophils

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30
Q

Contribute to the structural integrity of tissue:

A

fibroblasts

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31
Q

synthesis of collagen and extracellular matrix proteins:

A

fibroblasts

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32
Q

What do fibroblastic growth factors signal?

A

proliferation (can lead to extensive fibrosis)

33
Q

Dense accumulation of fibroblasts and collagen =

A

fibrous CT

34
Q

What are the four phases of wound healing?

A
  1. hemostasis
  2. inflammation
  3. proliferation
  4. remodeling
35
Q

Can lead to a hypertrophic scar (aka proud flesh):

A

excessive granulation

36
Q

Seen when fibroblasts and endothelial cells have proliferated to fill in tissue defects:

A

granulation tissue

37
Q

Often will look granular on gross surface, but often bleeds:

A

granulation tissue

38
Q

Seen when edges of the wound are directly apposed. Heals rapidly with little trace of wound:

A

1st intention healing

39
Q

Seen when the wound is gaping or infected. Has disorganized CT:

A

2nd intention healing

40
Q

Epithelial cells at the periphery proliferate:

A

epithelialization

41
Q

For epithelialization to properly occur, what must the epithelial cells move along?

A

the BM

42
Q

List the three most common types of diseases where the response to foreign or self antigens is abnormal or inappropriate:

A
  1. hypersensitivity reactions
  2. autoimmunity
  3. immunodeficiency
43
Q

immediate hypersensitivity

A

type 1

44
Q

cytotoxic hypersensitivty

A

type 2

45
Q

immune complex hypersensitivity

A

type 3

46
Q

delayed hypersensitivity

A

type 4

47
Q

an inappropriate or exaggerated response to certain antigens:

A

hypersensitivty

48
Q

develops rapidly (within minutes) following exposure to an antigen binding to IgE:

A

type 1 hypersensitivity

49
Q

In antigen processing, if IL-4 predominates then Th2 lymphocytes will:

A

induce B cells to produce IgE

50
Q

What other substances (aside from IgE) can activate mast cells?

A
  • cytokines
  • complement
  • drugs
  • physical stimuli
51
Q

When mast cells are activated by something other than IgE, it is called an:

A

anaphylactoid reaction

52
Q

What are some of the generalized systemic effects of type 1 hypersensitivity?

A
  • drop in bp
  • bronchoconstriction
  • laryngeal edema
  • pulmonary congestion
53
Q

When type 1 hypersensitivities are localized:

A

the clinical signs and pathology are restricted to a specific tissue (commonly epithelial surfaces)

54
Q

What are some of the routes of exposure for allergic dermatitis (type 1)?

A
  • inhalation
  • ingestion
  • percutaneous absorption
55
Q

A genetic predisposition of allergic dermatitis is referred to as:

A

atopic dermatitis

56
Q

Red raised areas associated with allergic dermatitis are most often:

A

around the muzzle, periocular area, conjunctiva, and interdigital areas

57
Q

swelling of the skin and mucous membranes:

A

angioedema

58
Q

cell destruction mediated by the presence of antibodies directed against cell surface antigens:

A

type 2 hypersensitivity

59
Q

What are the three mechanisms of type 2 hypersensitivty?

A
  1. complement mediated
  2. leukocyte mediated
  3. antibody against cell surface receptor
60
Q

What are the clinical signs of transfusion reactions (type 2)?

A

acute hemolytic anemia

61
Q

What are gross/histo lesions associated with transfusion reactions?

A

splenomegaly and hemosiderosis of various tissues

62
Q

What is the pathogenesis of neonatal isoerythrolysis?

A
  1. mother develops antibodies against fetal erythrocytes
  2. leakage of fetal erythrocytes across the placenta
  3. antibodies to fetal erythrocytes are concentrated in the colostrum
  4. absorption of colostrum results in acute hemolytic crisis in the newborn
63
Q

What are some of the clinical signs associated with thrombocytopenia (type 2)?

A

petechiae and purpuric hemorrhage

64
Q

Antigen antibody complexes which form in the circulation or in tissues that become “stuck” or lodged in tissue:

A

type 3 hypersensitivity

65
Q

Size of the immune complex associated with type 3 hypersensitivity determines:

A

pathogenicity

66
Q

What systems cause damage to the vessels in type 3 hypersensitivities?

A

complement and neutrophils

67
Q

What type 3 hypersensitivities are localized:

A

an area of tissue necrosis forms from acute necrotizing vasculitis (arthus reaction)

68
Q

The amount of tissue damage seen with type 3 hypersensitivity is dependent on:

A

quantity of complexes formed

69
Q

Systemic type 3 hypersensitivities are the result of:

A

persistent infections, autoimmune diseases, or inhalation of foreign antigens

70
Q

a delayed hypersensitivity mediated by specific T-lymphocytes following exposure to antigen

A

type 4

71
Q

Which type of hypersensitivity is chronic and antibody independent?

A

type 4

72
Q

In delayed hypersensitivity, what stimulates the infiltration of lymphocytes and macrophages to the site?

A

persistent antigen

73
Q

persistent antigen that results in granulomatous and lymphocytic inflammation:

A

granulomatous hypersensitivity (type 4)

74
Q

What is the most important thing to keep in mind about hypersensitivities?

A
  • categories can overlap

- strict categorization of hypersensitivity reactions is an oversimplification

75
Q

What are the mechanisms of autioimmunity (3)?

A
  • release of sequestered antigens
  • alteration of self antigens
  • alteration of immune reactivity
76
Q

Many autoimmune diseases are:

A

type 2 or 3

77
Q

Which gender has a higher prevalence of autoimmunity?

A

females

78
Q

What are some of the genetic susceptibilities of autoimmunity?

A

species and breed predilections

Veterinary Pathology (14 decks)

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