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MSS-IHL Final Exam > Hypersensitivities Type I-IV > Flashcards

Hypersensitivities Type I-IV Flashcards

1
Q

hypersensitive

A

above and beyond normal response

-causes pathology

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2
Q

how many types of hypersensitivities?

A

4 types

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3
Q

type IV hypersensitivity

A

T cell mediated diseases

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4
Q

type I hypersensitivity

A

aka immediate hypersensitivity

-atopic diseases

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5
Q

atopic diseases

A

caused by Type I hypersensitivity

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6
Q

IgE

A

big player in type I hypersensitivity**

extra constant region domain
-allows it to bind Fc on mast cells

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7
Q

three properties controlling IgE?

A

1 half life of IgE
2 T cell control (need isotype switching)
3 cross-linking of IgE on surface of mast cells and basophils

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8
Q

half life of IgE?

A

2 days in serum (very short)

produced in response to allergens

half life increased when binds to mast cells and basos

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9
Q

receptor for IgE on mast cells and basos?

A

FcERI

high affinity

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10
Q

half-life of IgG

A

3 weeks woah!

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11
Q

receptors for IgE on B cells?

A

FcERII

low affinity

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12
Q

Th1 activation leads to?

A

IFN-gamma and IL-12
no upregulation of IgE

**suppressive the atopic reaction

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13
Q

Th2 activation leads to?

A 
IL-4, IL-5 IL-13
leads to class switching (via IL-4) to IgE

**increases the atopic reaction

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14
Q

IL-5 activity?

A

stimulates maturation of eosinophils

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15
Q

allergen

A

antigen that gives rise to immediate hypersensitivity
-most are proteins

-usually taken in very small quantities that is sustained throughout life (ex/ dust)

food - large dose

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16
Q

mediators of IgE (intermediate) response in mast cells?

A

histamine, heparin, and tryptase (5 minutes)

also, newly generated (5-30 minutes)

  • arachidonic adic
  • leukotriene D4
  • prostaglandin D2

**vasoactive amines and lipid mediators

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17
Q

late phase reaction of mast cells immediate hypersensitivty?

A

2-10 hours later

-cyrokines, IL-4, TNF-alpha

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18
Q

released by eosinophils?

A

cationic granule proteins and eosinophil peroxidase

**to kill worms, but can kill self cells

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19
Q

what must occur for mast cell activation?

A

binding of IgE and must be CROSS-LINKED**

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20
Q

allergic rhinitis?

A

increased mucus secretion

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21
Q

wheal

A

extravasation of sera

22
Q

flare

A

axon reflex

23
Q

late phase reaction ?

A

4-6 hours after type I reaction
-can persist 1-2 days

infiltration of PMNs, eosinophils, macrophages, lymphocytes, basophils

occurs bc mast cells produce TNF-alpha and IL-1 which leads to increased extravasation

mast cells also produce neutrophil chemotactic factor

on-site release of IL-3, IL-5, IL-8, and GM-CSF

24
Q

normal function of IgE

A

protection against parasites

25
Q

Type II Hypersensitivity

A

antibody mediated
-IgG/IgM/FcR/C’
initiating antigen is a surface

antibodies bind FcR on tissue surface initiating effector cells

binding of C1 to IgG or IgM activates C’ cascade

damages target cells
-locallized to cells bearing antigens

26
Q

“fixed antigens”

A

antibodies against cell surfaces are usually pathogenic

antibodies against internal antigens are usually not pathogenic

27
Q

C3a and C5a?

A

chemotaxis of PMNs, basophils, and eosinophils

28
Q

normal phagocyte activation?

A

machophage binds Fc receptor and C3 receptor
-results in phagocytosis and lysosomal fusion

degrades cell

29
Q

frustrated phagocytosis

A

cannot internalize complex
instead, releases all of its enzymes to intravascular space and degrades tissue

**occurs in hypersensitivity type II

30
Q

hemolytic disease of the newborn (HDNB)

A

when mother Rh- and baby is Rh+
aka erythroblastosis fetalis

during birth, mother will make IgM antibodies against Rh+ (there is some blood exchange during birth)
-makes memory which will respond to next pregnancy if baby is Rh+

31
Q

how to avoid erythroblastosis fetalis?

A

use Rhogam

binds the Rh antigens and inhibits the mothers immune response from being exposed to it

32
Q

antigens involved in HDNB?

A 
Rhesus D most positive
also Kell (K) antigen
33
Q

using whole blood during transfusion?

A

giving someone serum (no good)

34
Q

donated blood is what?

A

separated to serum and cells first

35
Q

autoimmune hemolytic anemia

A

warm antibodies - different epitopes than transfusion rxn. (Rhesus)

cold antibodies - high titer IgM
-usually in old people during winter

can be spontaneous or drug caused

36
Q

myasthenia gravis

A

self-antibodies to AcH receptors

extreme muscle weakness**

37
Q

Type III Hypersensitivity

A

involve immune complexes

soluble antigen**

normally, taken care of by waste management
-if not, lead to pathology

can have interlacing collection with increased pathology

38
Q

three groups of type III hypersensitivity

A

persistent infection
autoimmune disease
inhalation of antigen

39
Q

normal waste management?

A

CR1 receptor on RBCs bind to immune complexes

taken to spleen and liver where they are degraded

40
Q

when immune complexes settle out?

A

in very small vessels
-bring in baspohils, mast cells, macrophages results in leakiness (great area for immune complex)

platelet aggregation occurs

increase in BP, vascular turbulence, and complex deposition

41
Q

arthus reaction

A

presensitized with IgG

allergy shots

so that it won’t bind IgE

get localized hemorrhage in 4-10 hours

can lead to allergic alveolitis

42
Q

serum sickness

A

induced by large injection of foreign antigen

complexes deposit in blood vessels and tissues

leads to arthritis and glomerulonephritis

complication of equine serum therapy (horse) or antigen excess (acute infectious disease)

43
Q

mechanisms of Type II and III

A

inflammatory pathways are identical
-difference is initiator

type II - fixed surface
type III - soluble

complement major mediator

44
Q

delayed type hypersensitivity?

A

Type IV hypersensitivity

T cells are mediator

  • effector T cells are stimulated
  • can lead to granulomas from macrophages
45
Q

three types of DTH?

A

contact
tuberculin (ex/ PPD test)
granulomatous (clinically most important)
-usually 28 days out

46
Q

contact sensitivity stages?

A

sensitization and elicitation

sensitization - 10-14 days in epidermis

  • ex/ poison oak/ivy (require haptens)
  • build memory cells

elicitation - recruit CD4 T cells to site of contact
pro-inflammatory cytokine driven
-monocytes, macrophages
-mainly CD4 T and small number of CD8

47
Q

tuberculin type DTH?

A

looking for a recall - to see if you have been sensitized to it

ex/ tuberculin skin test

48
Q

granulomatous DTH?

A

usually persistance of macrophages

  • microbes that can resist killing
  • other cells cell can’t destroy

occurs with Th1 response

49
Q

basis for classification of hypersensitivity?

A

Coombs and Gell

50
Q

what immune complexes deposited the most?

A

small positively-charged ones

51
Q

diseases assocaited with DTH?

A

tuberculosis, leprosy, schistosomiasis, sarcoidosis, Crohn’s disease

MSS-IHL Final Exam (15 decks)

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