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hypersensitivity Flashcards

1
Q

type 1/ immediate hyper

A

this is what you think of with allergies
-mediated by IgE
-immediate

worst point: anaphylactic shock

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2
Q

type 2 / cytotoxic

A

mediated by IgG or IgM and complement

ex. hemolysis of RBC

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3
Q

why is type 2 called cytotoxic

A

found on a cell surface so when you get an antigen-antibody response it destroys the cell

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4
Q

type 3 / complex mediated

A

mediated by IgG or IgM and complement

ex. SLE serum sickness

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5
Q

difference between type 2 and 3

A

antigen is not found on the cell surface, but is soluble in type 3

have aggregates of antigen-antibody complex that precipitate out of solution and fall onto solution= destruction

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6
Q

type 4 / delay hypersensitivity

A

no antibody involved; T cell mediated mainly through cytokine activation

-may take hours to days to develop

ex. PPD and poison ivy

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7
Q

main players in type 1

A

IgE, basophils, mast cells, eosinophils

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8
Q

what happens in type 1 when exposure to an allergen

A

T2 helper cells to release cytokines calling forth production of IgE

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9
Q

3 stages of type 1

A

1- sensitization
2-activation
3-effector

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10
Q

sensitization stage

A

-come in contact with allergen for the first time

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11
Q

in sensitization stage what is produced and attaches to what

A

IgE produced
-Fc portion attached to mast cell/basophil

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12
Q

every one baso can have how many receptors

A

20,000 for IgE

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13
Q

once IgE attaches half life goes from 2 days to

A

2 weeks

-once sit on cells now a receptor for that allergen

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14
Q

activation stage

A

antigen cross links 2 Fab regions

-need 2 IgE molecules close enough for antigen to straddle 2 regions

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15
Q

what happens in activation stage

A

-causes large number of chemical rxn and release mediators that are stored in mast cells and basophils

-degranulation of these cells and release of mediators associated with allergic reactions

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16
Q

ex of mediators released

A

histamine, heparin, eosinophil chemotactic factor, leukotrienes (slow histamine)

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17
Q

effector stage

A

-experience all the effects of release of these

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18
Q

histamine

A

increase vascular permeability and contraction of smooth muscle

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19
Q

Eosinophil chemotactic factor

A

call forth more EOS

-eos can call forth platelet which counter heparin– increase amount of histamine released

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20
Q

effects seen in allergic reactions – type 1

A
  • Watery eyes
    • Runny nose
    • Hives (urticaria)
    • Trouble breathing
    • Wheel and flare reaction - swelling and hardness of site
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21
Q

main sign of type 1 rxn

A

wheel and flare

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22
Q

late and slow reacting substance

A

leukotrienes

-cause allergic rxn to be prolonged for hours after exposure
-call forth platelets to site of rxn

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23
Q

why do we have allergies

A

-genetic inheritance
-decreased amount of IgA and absence of Ir gene
-environmental factors plat (gut flora)

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24
Q

what is given for topical allergies

A

corticosteroids

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25
why give anti-histamine
block receptor site for histamine and reduce the symptoms -also have anti-leukotrienes
26
only used in severe allergic reactions to help constrict dilated blood vessels and relax smooth muscles
epinephrine
27
bronchodilators
inhalers
28
fast acting bronchodilators
not interchangeable with regular bronchodilators
29
Anti-IgE monoclonal antibodies
instead of allergen attach to IgE, monoclonal antibody attaches to IgE
30
prevention of type 1
hyposensitivity therapy aka allergy shots -small doses of allergen over prolonged period of time
31
small introduction of allergen will produce
IgG and not IgE -then allergen will bind to IgG instead -chance of allergic rxn when doing this -not uncommon to have wheel and flare
32
anaphylaxis
extreme and life threatening reaction to allergen
33
where does anaphylaxis start
respiratory system, mucous membrane inflamed, serve build up of fluid (drown in own fluid), asthma attacks
34
in anaphylaxis patient can go into shock because of
dilation of blood vessels, getting massive amounts of fluid to that site ○ Drop in BP and go into cardiac arrest
35
most sensitive way to determine allergies
skin test/ prick -need to be off medication for 3-4 days
36
in skin prick test you measure
wheel and flare reaction you get if 3-4 ml or greater= allergic rxn
37
when do intradermal testing
○ Only done if get negative reaction on prick test and have high sus you have this allergy -under the skin and done on arm
38
if start to have bad reaction with intradermal
tie tourniquet to decrease blood flow -better for environmental allergies
39
blood testing con
not as sensitive and if not exposure to allergen in a while, blood test may not be positive
40
2 kinds of blood testing
total IgE antigen-specific IgE
41
total IgE known as
RIST- radio immunosorbent test
42
antigen-specific known as
RAST
43
type 2 also known as
cytotoxic mediated
44
type 2 mediated by
IgG and/or IgM and complement
45
where is antigen that causes reaction in type 2 located
on cell surface -causes cell damage
46
3 ways cell damage occurs in type 2
1- antigen-antibody response 2- ADCC 3- coating of cell
47
what is ADCC
antibody direct cytotoxicity -happens with NK or macrophages -antibody hooks up to receptor on either and cells release cytokine which pokes holes into target antigen
48
Complete coating of the cell with IgG to
increase opsonization and phagocytosis by a macrophage
49
examples of type 2 hyper sensitvity
ABO/Rh incompatibilty autoimmune hemolytic anemia goodpasture's syndrome
50
3 kinds of autoimmune anemia
warm autoimmune cold antibody drug-induced
51
warm autoimmune
IgG secondary: Lupus
52
cold antibody
IgM -paroxysmal hemoglobinuria -mycoplasma pneumonia (anti-I)
53
good pasture's syndrome
tissue and cellular death involves kidney and lungs autoantibody produced against an antigen on glomerular basement and particular antigen found in lungs
54
type 3 mediated by
both IgM and/or IgG and complement
55
type 3 aka
immune complex hypersensitivity
56
difference between type 3 and type 2
type 3 antigen is soluble -get formation of antigen-antibody complex that is insoluble and precipitates out of solution and falls on tissue
57
sizing of type 3 complexes
moderately sized that immune system can't destroy -mild antigen excess; post zone and body can't clear well happens with antigens of lower valence
58
classic type 3
arthus reaction serum sickness RA kidney damage done due to lupus
59
arthus reaction localized
tissue necrosis by immune complex
60
arthus reaction caused by
injecting antigen into the skin -repeated introduction of an antigen into same area -localized in small blood vessels right under skin and macrophages try to destroy antigen
61
main ex of arthus reaction
insulin injection lower molecule weight compound!!
62
serum sickness
-not only injecting antibodies, injecting horse antigen/protein -if at same sight= arthus reaction -semi-purified
63
Rheumatoid arthritis
○ Antigen-antibody reaction to certain peptides and cytokines fall on joints which causes damage
64
Kidney Damage done due to Lupus
Responses due to DNA do not get cleared completely by the kidney, but as try to pass through kidney get deposited on the glomerular membrane main cause of death of lupus patients!!
65
type 4 also called
delayed type hypersensitivity -may not see for 48-72 hours after coming in contact with offender
66
type 4 is mediated through
T cell mediated destruction
67
what in type 4 causes delay
Tumor necrosis factor and gamma interferon
68
localized example of type 4
contact dermatitis ex. poison ivy, hair dye, PPD
69
systemic type 4 example
intracellular pathogens -consistent introduction of an antigen ex. : mycobacterium leprae
70
Hypersensitivity pneumonitis
* Repeat introduction of inhaled antigen * Ex. Farmer lung - breath in mold * Chlamydia pneumonitis- from exocytic birds
71
how to prevent type 4
patch test -take some of product and introduce to a small area on the skin

immuno (5 decks)

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