hypersensitivity Flashcards

1
Q

immune response that causes disease

A

hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

subtype of hypersensitivity

A

allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

first contact with antigen

A

sensitizes (generation of immune response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

second contact =

A

hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

sxs are from

A

overreaction of immune sys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

type 1

A

immediate reactions to antigen due to preformed IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

in type 1, antibodies are bound to mast cells then antigen binds are cross links IgE leading to

A

mast cell degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

key cytokine for IgE production

A

IL-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IgE does not activate

A

complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

type I sxs

A

urticaria (hives)
runny nose
wheezing
conjunctivitis
diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

anaphylaxis is a

A

type I hypersensitivity rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

genetic predisposition to localized hypersensitivity

A

atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

type 1 examples

A

asthma
penicillin drug allergy
seasonal allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

type I early sxs

A

occur in mins
degranulation
edema, redness, itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

type I late sxs

A

around 6hrs
synthesis/ release of cytokines
influx of inflammatory cells
induration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

histamine role

A

vasodilation
increased permeability
smooth m contraction

17
Q

PGE2 role

A

vasodilation
edema
fever
pain

18
Q

PGD2 role

A

bronchoconstriction
eosinophil infiltration

19
Q

LTC4/LTD4

A

vasoconstriction
bronchoconstriction

20
Q

LTB4

A

neurotrophic/eosinophil chemotaxis

21
Q

serotonin causes

A

vasodilation

22
Q

platelet activating factor causes

A

bronchoconstriction

23
Q

ECF-A attracts

A

eosinophils

24
Q

desensitization changes IgE to

25
type II
antibodies directed against tissue antigens
26
3 mechs of tissue damage in type II
1. phagocytosis 2. complement mediated lysis 3. antibody-dependent cytotoxicity
27
antibody dependent cell mediated cytoxicity =
natural killer cells bind Fc portion of IgG
28
type II examples
rheumatic fever, exposure to wrong blood type, autoimmune hemolytic anemia, myasthenia gravis
29
type III hypersensitivity
antigen-antibody (IgG) complex form and activate complement
30
2 types of type III
1. serum sickness 2. arthus reaction
31
serum sickness =
immune complexes in plasma deposit in various tissues and trigger immune response
32
serum sickness sxs
palpable purpura low serum complement levels elevated sedimentation rate diffuse lymphadenopathy
33
classic serum sickness examples
rabies anti toxin monoclonal antibodies SLE
34
Arthur reaction
local tissue reaction due to injection of antigen, preformed antibodies in plasma/tissue bind antigen and form immune complexes
35
Arthur reaction leads to
complement activation, edema, necrosis
36
Arthur reaction examples
tetanus booster, insulin
37
type IV
cell mediated reaction from memory T cells initiating immune response