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

Unit 3 - Chronic Inflammation & Hypersensitivity Flashcards

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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
When do lymphocytes enter unresolved areas of acute inflammation?
24-48 hours
26
Plasma cells secrete:
antibody
27
Dense infiltrate of eosinophils with macrophages, varying numbers of lymphocytes, and plasma cells:
eosinophilic granulomas
28
Eosinophils are recruited into and stimulated to proliferate by:
IL-5, eotaxin
29
Green coloration to a mass often indicates:
eosinophils
30
Contribute to the structural integrity of tissue:
fibroblasts
31
synthesis of collagen and extracellular matrix proteins:
fibroblasts
32
What do fibroblastic growth factors signal?
proliferation (can lead to extensive fibrosis)
33
Dense accumulation of fibroblasts and collagen =
fibrous CT
34
What are the four phases of wound healing?
1. hemostasis 2. inflammation 3. proliferation 4. remodeling
35
Can lead to a hypertrophic scar (aka proud flesh):
excessive granulation
36
Seen when fibroblasts and endothelial cells have proliferated to fill in tissue defects:
granulation tissue
37
Often will look granular on gross surface, but often bleeds:
granulation tissue
38
Seen when edges of the wound are directly apposed. Heals rapidly with little trace of wound:
1st intention healing
39
Seen when the wound is gaping or infected. Has disorganized CT:
2nd intention healing
40
Epithelial cells at the periphery proliferate:
epithelialization
41
For epithelialization to properly occur, what must the epithelial cells move along?
the BM
42
List the three most common types of diseases where the response to foreign or self antigens is abnormal or inappropriate:
1. hypersensitivity reactions 2. autoimmunity 3. immunodeficiency
43
immediate hypersensitivity
type 1
44
cytotoxic hypersensitivty
type 2
45
immune complex hypersensitivity
type 3
46
delayed hypersensitivity
type 4
47
an inappropriate or exaggerated response to certain antigens:
hypersensitivty
48
develops rapidly (within minutes) following exposure to an antigen binding to IgE:
type 1 hypersensitivity
49
In antigen processing, if IL-4 predominates then Th2 lymphocytes will:
induce B cells to produce IgE
50
What other substances (aside from IgE) can activate mast cells?
- cytokines - complement - drugs - physical stimuli
51
When mast cells are activated by something other than IgE, it is called an:
anaphylactoid reaction
52
What are some of the generalized systemic effects of type 1 hypersensitivity?
- drop in bp - bronchoconstriction - laryngeal edema - pulmonary congestion
53
When type 1 hypersensitivities are localized:
the clinical signs and pathology are restricted to a specific tissue (commonly epithelial surfaces)
54
What are some of the routes of exposure for allergic dermatitis (type 1)?
- inhalation - ingestion - percutaneous absorption
55
A genetic predisposition of allergic dermatitis is referred to as:
atopic dermatitis
56
Red raised areas associated with allergic dermatitis are most often:
around the muzzle, periocular area, conjunctiva, and interdigital areas
57
swelling of the skin and mucous membranes:
angioedema
58
cell destruction mediated by the presence of antibodies directed against cell surface antigens:
type 2 hypersensitivity
59
What are the three mechanisms of type 2 hypersensitivty?
1. complement mediated 2. leukocyte mediated 3. antibody against cell surface receptor
60
What are the clinical signs of transfusion reactions (type 2)?
acute hemolytic anemia
61
What are gross/histo lesions associated with transfusion reactions?
splenomegaly and hemosiderosis of various tissues
62
What is the pathogenesis of neonatal isoerythrolysis?
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
What are some of the clinical signs associated with thrombocytopenia (type 2)?
petechiae and purpuric hemorrhage
64
Antigen antibody complexes which form in the circulation or in tissues that become "stuck" or lodged in tissue:
type 3 hypersensitivity
65
Size of the immune complex associated with type 3 hypersensitivity determines:
pathogenicity
66
What systems cause damage to the vessels in type 3 hypersensitivities?
complement and neutrophils
67
What type 3 hypersensitivities are localized:
an area of tissue necrosis forms from acute necrotizing vasculitis (arthus reaction)
68
The amount of tissue damage seen with type 3 hypersensitivity is dependent on:
quantity of complexes formed
69
Systemic type 3 hypersensitivities are the result of:
persistent infections, autoimmune diseases, or inhalation of foreign antigens
70
a delayed hypersensitivity mediated by specific T-lymphocytes following exposure to antigen
type 4
71
Which type of hypersensitivity is chronic and antibody independent?
type 4
72
In delayed hypersensitivity, what stimulates the infiltration of lymphocytes and macrophages to the site?
persistent antigen
73
persistent antigen that results in granulomatous and lymphocytic inflammation:
granulomatous hypersensitivity (type 4)
74
What is the most important thing to keep in mind about hypersensitivities?
- categories can overlap | - strict categorization of hypersensitivity reactions is an oversimplification
75
What are the mechanisms of autioimmunity (3)?
- release of sequestered antigens - alteration of self antigens - alteration of immune reactivity
76
Many autoimmune diseases are:
type 2 or 3
77
Which gender has a higher prevalence of autoimmunity?
females
78
What are some of the genetic susceptibilities of autoimmunity?
species and breed predilections

Veterinary Pathology (14 decks)

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