Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMMUNO > Hypersensitivity Type I > Flashcards

Hypersensitivity Type I Flashcards

1
Q

characterize type I-IV hypersensitivities by:

  • name
  • basic immunologic mechanism
  • identify any immediate vs delayed types
A
  • Type I - allergic/anaphylactic hypersensitivity
    • IgE mediates mast cell degranulation → histamine release
    • immediate onset
  • Type II - cytotoxic type
    • complement binds IgG / IgM bound to surface antigen → complement cascade
  • Type III - immune complex type
    • IgG / IgM form antigen antibody complexes that deposit in post capillary venules → become bound by compliment → complement cascade
  • Type IV - cell-mediated
    • T-cells stimulate cell mediated rxns by many immune cells
    • delayed onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type I - IV hypersensitivity

  • define
  • describe mechanism
  • give examples
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the onset of type 1 hypersensitivity rxns

A

immediate onset: symptoms occur in seconds to minutes after allergen contact

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

discuss the general mechanism of type I hypersensitivity reactions

A
  • allergen cross-links IgE sensitized mast cells (mast cells that already have IgE bound to their Fc-receptors from previous exposure)
  • this triggers mast cell degranulation → histamine released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

discuss the affects of histamine throughout the body

A
  • GI tract: inc activity
    • fluid secretion
    • peristalsis → diarrhea, emesis
  • lungs:
    • bronchoconstriction
    • mucous secretion → coughing, sneezing
  • vasculature
    • vasodilation → inc blood flow
    • inc vascular permeability → leakage into tissues → edema
  • skin
    • uticaria (hives)
    • atopic dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • what causes anaphylaxis?
  • how is anaphylaxis treated?
A
  • systemic allergic rxns caused by wide-spread mast cell degranulation (type I)
  • tx = epinephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

discuss the symptoms of severe allergic reaction

A

same type I sx, just more severe

  • wide-spread vasodilation → catastrophic drop in BP
  • suffocation, d/t
    • air-way (bronchial) constriction
    • epiglottal swelling
  • GI - diarrhea / abdominal cramps / vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

discuss the common allergens, route of entry, and response for

  • systemic anaphylaxis
  • wheel and flare
  • allergic rhinitis
  • bronchial asthma
  • food allergy
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • other than common allergens, what triggers can cause allergy/anaphylactic reactions?
    • how do they do this?
A

all induce mast cell / basophil degranulation either by

  • binding cross linked IgE: lectins
  • directly increasing intracellular Ca+:
    • anaphylatoxins (C3a, C5a) - complement products that are degranulators
    • calcium ionophores
    • radiocontrast dyes
    • drugs
      • opiates: codeine, morphine
      • vancomycin
  • physical contact urticaria
    • cold induced
    • dermatographic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

other than allergens, what molecules can induce Type I hypersensitivity by binding IgEs on mast cells/basophils?

A

lectins

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

what substances increase intracellular Ca+? what does this lead to?

A
  • this leads to mast cell degranulation → type I hypersensitivity rxn
    • anaphylatoxins (C3a, C5a) - complement products that are degranulators
    • calcium ionophores
    • radiocontrast dyes
    • drugs
      • opiates: codeine, morphine
      • vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what “physical” means can induce a Type I hyper sensitivity rnx?

A
  • physical contact urticaria
    • cold induced
    • dermatographic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is atopy?

  • what causes atopy?
  • how does it present?
A
  • a genetic predisposition to make IgE
  • d/t defects in IgE response genes on chromosomes 5, 6, 11
    • Th2 gene cluster - chromosome 5
    • MHC-II - on chromosome 6
    • IgE Fc receptor - chromosome 11
  • classic presentation = triad
    • rhinitis
    • asthma
    • dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the stages of Type I Hypersensitivity reaction?

A
  1. sensitization
  2. activation
  3. effector phase
  4. late phase reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

outline the sensitization phase of Type I Hypersensitivity rxn

A
  • = initial exposure
    • antigen ingested by APC
    • antigen presented to TCR on T-helper cell (MHC-II-CD4+ binding)
    • this induces expansion of Th2 T-helper cell subset
    • Th2 produces IL-4 and IL-13
    • IL-4 and IL-13 induces B-cells → produce IgE (class switch)
    • IgE binds IgE Fc receptors on mast cells/basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

outline the activation stage of Type I hypersensitivity

A
  • = second exposure to antigen
    • allergen binds arms of IgEs that are bound (cross linked) to mast cells / basophils, inducing
    • methylation of membrane phospholipids, which
    • inc intracellular Ca+ → induces Ca+ influx, which
    • induces degranulation → release of mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

outline the effectors phase of Type I hypersensitivity rxn

A
  • response to release of mediators (formed and preformed) from mast cells/basophils
    • pre-formed mediators
      • histamine
      • serotonin
      • tryptase
      • heparin
      • ECF-A
      • inflammatory cytokines: IL-1, TNF-a, IL-8, IL-5, IL-4
    • newly synthesized mediators (produced from AA)
      • leukotrienes: LTC4, LTD4, LTE4
      • prostaglandins (PGF, PGE)
      • prostacyclin (PGI2)
      • thromboxane (TXA-2)
      • platelet activating factor (PAF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what pre-formed mediators are released from mast cells/basophils?

A

effector phase of Type I

  • histamine
  • serotonin
  • tryptase
  • heparin
  • ECF-A
  • inflammatory cytokines: IL-1, TNF-a, IL-8, IL-5, IL-4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what newly formed mediators are released from basophils/mast cells?

A

effector phase of Type I

  • products of AA pathway
    • leukotrienes: LTC4, LTD4, LTE4
    • prostaglandins (PGF, PGE)
    • prostacyclin (PGI2)
    • thromboxane (TXA-2)
    • platelet activating factor (PAF)
20
Q

what is histamine & its effects?

A

pre-formed mediator

  • binds to H1 receptors on smooth muscle
    • bronchoconstriction
    • vascular permeability / vasodilation
  • binds to H2 receptors on gut
    • mucous secretion
    • acid release
21
Q

how do anti-histamines work to nullify effects of histamine?

A
  • diphenhydramine (benadryl) blocks H1 stimulation (bronchoconstriction)
  • cimeditine (tagamet): blocks H2 stimulation (gut mucous/acid secretion)
22
Q

what is serotonin & its effect?

A

pre-formed mediator

  • functions like hsitamine
23
Q

what is tryptase & its effect?

A

pre-formed mediator

  • generates anaphylatoxins (C3a and C5a) → further mast cell degranulation
24
Q

what is ECF-A & its effects?

A

pre-formed mediator

  • attracts eosinophils
25
Q

what cytokines are released during the effector phase of Type I hypersensitivity & what do they do?

A

pre-formed mediators

  • IL-1, INFa: induce leukocyte migration
  • IL-8: attracts neutrophils
  • IL-4 (also made by Th2 cells)
    • sustains Th2
    • IgE production
  • IL-5: activate eosinophils
26
Q

what pre-formed mediators effect eisonophils in the effector phase of type I? what do they do?

A
  • ECF-A: attracts eosinophils
  • IL-5 (cytokine): activates eosinophils
27
Q

what are prostaglandins & their effect?

A

newly formed mediator (AA product)

  • bronchoconstriction
  • vasodilation
  • INHIBIT platelet aggregation
28
Q

what are thromboxanes (TXA) and their effect?

A

newly formed mediator (AA product)

  • induce platelet aggregation
29
Q

what are prostacyclins and their effects?

A

newly made mediator

  • vasodilation
  • INHIBIT platelet aggregation
30
Q

what are platelet activating factors (PAF) and their effects

A

newly made mediator

  • vasodilation
  • bronchoconstriction
  • INDUCE platelet aggregation
31
Q

which newly made mediators in the effector phase of type I rxn

  • induce platelet aggregation?
  • inhibit platelet aggregation?
A
  • induce platelet aggregation
    • TXA
    • PFA (platelet aggregation)
  • inhibit platelet aggregation
    • prostacyclins (PGI)
    • prostaglandins (PGF, PGE)
32
Q

prostaglandins, prostacyclins & PAF - compare/contrast effects

A
  • vasodilation - ALL
  • bronchoconstriction - ALL
  • platelet aggregation
    • PGIs, PGE/PGF = inhibit
    • PAF = induce
33
Q

what are leukotrienes and their effects?

A

newly made mediators (AA products made by SRS-A)

  • LTC-4, LTD-4, LTE-4
    • LTC-4: chemotactic for neutrophils
    • LTD-4, LTE-4: bronchoconstriction
34
Q

what type I mediators are chemotactic for neutrophils?

A
  • IL-8 (pre-made mediator)
  • LTB-4 (newly made mediator)
35
Q

what are the primary cause of anti-histamine resistant asthma?

A

leukotrienes

36
Q

outline the late phase of Type I rxn

A
  • formation of inflammatory infiltrate over next 24 hours
    • characterized by eosinophil degranulation
      • which is due to
        • ECF-A (attraction)
        • IL-5 (activation)
        • IgE binding Fc receptors (CD23) on surface (degranulation)
      • and leads to:
        • epithelial damage, due to
          • cytotoxins (major basic protein/cationic protein) → ROS → damage epithelium
        • shut-down of mast-cell products:
          • histaminase → inactivates histamine
          • anti-sulfatase → inhibits SRS-A release, inhibiting leukotriene production
37
Q

which component of the Type I hypersensitivty reactions inhibits histamine effects?

when/how does this occur?

A

anti-histaminase, made by eosinophils in the late phase (degrades histamine released from mast cells during activation phase)

38
Q

what is SRS-A? how is it produced/regulated?

A
  • made by mast-cells
  • allows production of leukotrienes (newly made mediators) during effector phase
    • LTB-4: neutrophil migration
    • LTC-5, LTD-4, LTE-4): smooth muscle constriction
  • inhibited by anti-sulfatase released by eiosinophils during the late phase
39
Q

anaphylaxis

  • m/c cause?
  • treatment?
A
  • m/c cause = penicillin
  • tx = epinephrine
40
Q
A

urticaria (hives) - erythematous, edematous (raised) wheels that

  • blanche with pressure
  • have a systemic distribution
  • are VERY PRURITIC

common manifestation of immediate (type I hypersensitivity)

41
Q
A

angioedema (swelling) that is

  • non-pitting
  • PAINFUL (instead of pruritic)
  • often in the face - eyes, nose, lips

common manifestation of immediately (type I) hypersensitivity

42
Q

what is the most common atopic disease? describe its presentation & cause

A

= allergic rhinitis (hay fever)

  • type I hypersensitivity
    • can be in context of HLA-DR2
  • presentation
    • congestion
    • sneezing / runny nose
    • itchy, watery eyes
43
Q

atopic dermatitis

  • hypersensitivity type
  • demographic
  • presentation
  • dx
A
  • both type II and type IV eczema presentations
    • demographics - usually young children
    • presentation
      • on FACE + FLEXOR SURFACES
      • scaly, itchy rashes
    • dx - papules containing eosinophils
44
Q

what are common causes of allergies d/t environmental antigens?

A
  • sulfur dioxide
  • nitrogen oxide
  • fly ash / diesel exhaust particles
45
Q

how does hyposensitization therapy work

A
  • sub-Q & sub-lingual administration:
    • both: shift away from Th2 → less IL-4/Il-13 → less IgE → BLOCKS MAST CELL DEGRNULATION
    • subcutaneous administration: shift to Th1 → more INF-y → more IgG1/IgG4
      • good for bee sting allergies
    • sublingual administration: shift to Treg → more IL-10 / TGF-B
      • foods, airborne allergens
46
Q

drug therapy for allergies

A
  • anti-histamines
    • blocks H1 receptors
    • good for urticaria, conjunctivits, rhinitis
    • NOT good for
      • asthma - give B-agonists, corticosteroids
      • anaphylaxis - give epinephrine

IMMUNO (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions