Exam 3: Hypersensitivity Type II and III Flashcards

(57 cards)

1
Q

what type of immune response is type II hypersensitivity

A

humoral immune response

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2
Q

type II hypersensitivity characteristics

A

RBC antigens

blood transfusion between genetically different individuals, the red cell antigens will stimulate an antibody response in the recipient

Antibody + complement = RBC destruction

animals may have antibodies against foreign blood group antigens even without previous exposure

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3
Q

how do you know if you can perform a blood transfusion

A

absence of agglutination

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4
Q

what is the antibody that produces agglutination in blood

A

IgM

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5
Q

possible blood types

A
A+
A-
B+
B-
AB+
AB-
O+
O-
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6
Q

is there an immune response if animal donor = animal recipient

A

no immune response

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7
Q

is there an immune response if animal donor does not equal animal recipient

A

yes immune response

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8
Q

what is the 1st stage?

A

hypotension
bradycardia
apnea

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9
Q

what is the 2nd stage

A

hypertension
cardiac arrhythmia
increased HR
increased respiratory rate

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10
Q

hemolytic disease of the newborn (HDN) neonatal isoerythrolysis

A
  1. newborn with different blood type than mother
    ex - mom is Aa- and baby is Aa+
  2. mother must be sensitized to this red cell antigen
  3. mother’s response must to be boosted to transplacental hemorrhage or repeated pregnancies
  4. newborn animal must ingest colostrum with high antibodies against its red cells

foal ingests antibodies against its RBC and will produce hemolytic disease

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11
Q

type II hypersensitivity to drugs

A

drugs + antibodies + complement –> bystander effect on RBC

drugs attached to RBC membrane + antibodies + complement on RBC

drugs that modify RBC membrane + antibodies = phagocytosis

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12
Q

type II hypersensitivity in infectious diseases

A

equine infectious anemia, anaplasmosis, trypanosomiasis, babesiosis –> severe anemia

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13
Q

why is there a yellow pigmentation with type II hypersensitivity

A

due to release of immunoglobulins

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14
Q

what do you use to treat type II hypersensitivity

A

has to be treated with a blood transfusion

make sure foal does not drink any more of the mother’s colostrum

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15
Q

what is needed to produce immune complex in type III hypersensitivity

A

antigen + antibody
complement

animal must have high amounts of antigens or high levels of antibodies to produce immune complex

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16
Q

what type of immune response is type III hypersensitivity associated with

A

humoral immune response

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17
Q

what is the main cell type in type III hypersensitivity

A

neutrophils

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18
Q

what do neutrophils do in type III hypersensitivity

A

release enzymes to promote inflammation

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19
Q

what do immune complexes lead to when they are deposited in tissues

A

chemotactic peptides

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20
Q

type III hypersensitivity - local type - where are IC formed

A

immune complexes are formed within the tissue

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21
Q

type III hypersensitivity - generalized type - where are IC formed

A

immune complexes are formed within the blood stream

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22
Q

type III hypersensitivity - generalized type - where are IC deposited

A

within the glomeruli in the kidney

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23
Q

local type III hypersensitivity important complement component

A

C5a

C5a is chemotactic for neutrophils

24
Q

local type III hypersensitivity - arthus reaction

A

high level of antibodies in bloodstream, antigen injected SQ

red edematous swelling, local hemorrhage, thrombosis, tissue destruction

6-8 hours reaction

first neutrophils, then macrophages = nitric oxide, chemokines, leukotrienes, cytokines

25
local type III hypersensitivity - reversed arthus reaction
high levels of antigens, antibodies injected SQ
26
what complement component attracts neutrophils
C5a
27
pathogenesis of arthus reaction - macrophages
produce nitric oxides --> proteases and oxidants --> tissue destruction produce proinflammatory cytokines (IL-1, TNF-a) --> enhanced selectin expression --> neutrophil emigration --> neutrophil accumulation --> degranulation --> proteases and oxidants --> tissue destruction
28
pathogenesis of arthus reaction - neutrophils
phagocytosis --> neutrophil accumulation --> degranulation --> proteases and oxidants --> tissue destruction
29
pathogenesis of arthus reaction - mast cells
degranulation --> proteases and oxidants --> tissue destruction
30
pathogenesis of arthus reaction - activated complement
C5a --> neutrophil chemotaxis --> neutrophil accumulation --> degranulation --> proteases and oxidants --> tissue destruction
31
local type III hypersensitivity - blue eye
canine adenovirus type-1 produced in response to vaccination when the dog has high levels of antibodies against canine adenovirus inflammation of fungus of the eye accumulation of immune complexes and neutrophils in cornea after a few days goes back to normal
32
local type III hypersensitivity - hypersensitivity pneumonitis
Saccharopolyspora rectivirgula fungus in hay --> animals in contact with hay and get fungus hypersensitivity produced animals develop pneumonia due to constant contact with antigen nasal secretions
33
local type III hypersensitivity - staphylococcal hypersensitivity
chronic infection of skin causes chronic lesions from chronic exposure to antigen
34
what happens to IC under normal circumstances
IC are removed by erythrocytes and macrophages
35
what happens in generalized type II hypersensitivity where there is production of high amount of IC
IC get deposited in blood vessels where there is a physiological outflow of fluid glomeruli in kidney choroid plexus in brain synovial membranes in joints
36
Generalized type III hypersensitivity steps?
1. IV antigen + circulating antibodies 2. Immune complex (IC) 3. Production of high amounts of IC leads to deposition on blood vessels with physiological outflow of fluid
37
how are IC removed in primates
binding to complement receptors of RBC carried to liver where they are transferred to Kupffer cells for phagocytosis
38
what happens to IC in type III generalized in absence of complement components
significant accumulation of IC occurs in tissues IC bind to receptors on platelets
39
serum sickness
generalized type III thrombosis, inflammation of kidney and joints once IC eliminated, everything goes back to normal
40
Generalized type III - high IC accumulate in arteries
neutrophil accumulation leads to arteritis
41
Generalized type III - high IC accumulate in kidney
proliferation response leads to glomerulonephritis
42
Generalized type III - high IC accumulate in synovial membranes
neutrophil accumulation leads to arthritis
43
two types of IC
soluble complexes insoluble complexes
44
what happens to soluble IC
get deposited in blood vessels walls sometimes bound to red cells and are removed by mononuclear phagocytic cells in liver
45
what happens to insoluble IC
removed by mononuclear phagocytic cells in liver
46
glomerulus general function
where blood filtration occurs
47
where are IC deposited in glomerulus
on either side of on within the basement membrane
48
type I glomerulonephritis
mesangioproliferative glomerulonephritis --> capillary endothelial proliferation, mesangial proliferation, capillary wall thickening --> immune complexes contain IgG, IgM, IgA, C3 --> in mesangial and subendothelial regions --> type I glomerulonephritis
49
type III glomerulonephritis
mesangioproliferative glomerulonephritis --> capillary endothelial proliferation, mesangial proliferation, capillary wall thickening --> immune complexes contain IgG, IgM, IgA, C3 --> in subepithelial region --> type III glomerulonephritis
50
type II glomerulonephritis
mesangioproliferative glomerulonephritis --> capillary endothelial proliferation, mesangial proliferation, capillary wall thickening --> dense deposits within glomerular basement membrane, do not contain Ig, but do contain C3 --> type II glomerulonephritis
51
where are type I, II, and III, glomerulonephritis located in glomerulus
type I --> mesangial cells, capillary endothelial cells type II --> basement membrane type III --> epithelial cells
52
what do IgG, IgM, IgA, and C3 do in glomerulonephritis
these can accumulate and produce inflammation complement activation and attraction of neutrophils
53
fibrosis
avoid normal filtration of blood
54
large immune complexes
type I MPGN --> mesangial and endothelial cell proliferation (IL-6) --> TGF-B --> fibrosis
55
small immune complexes
Type III MPGN --> epithelial cell proliferation
56
glomerulonephritis - chronic diseases
viruses, bacterial infections, tumors equine infectious anemia, infectious canine hepatitis, African swine fever, leishmaniasis, Lyme disease, pyometra, chronic pneumonia, bacterial endocarditis, tumors (lymphosarcoma, osteosarcomas, mastocytomas)
57
infectious diseases with a significant type III hypersensitivity component and what are the major lesions
bacteria, viruses, parasites Major lesions: glomerulonephritis arthritis arteritis