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Immunity > Hypersensitivity - Schein 4/11/16 > Flashcards

Hypersensitivity - Schein 4/11/16 Flashcards

1
Q

hypersensitivity

4 types

A

exaggerated response of the immune system to some antigen in a damaging way

  • aka allergic reaction

4 types:

type I : IgE mediated hypersensitivity - ab (Th2)

type II : antibody-mediated cytotoxic hypersensitivity - ab (Th2)

type III : immune complex-mediated hypersensitivity - ab (Th2)

type IV : Delayed Type hypersensitivity - T cells (Th1)

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2
Q

type I hypersensitivity

A

immediate (minutes) = allergy (atopy)

  • initial exposure: sensitization → Th2 activation → IgE made
    • IgE binds Fc receptor on mast cells and basophils, hangs out waiting for secondary exposure
  • secondary exposure: multivalent antigen causes cross-linking of surface IgEs → release of inflammatory mediators by mast cells, eosinophils, basophils
    • mast cell pdts attract eosinophils (primary defense against parasites/worms/etc)

ex. hay fever, asthma, allergy to penicillin, expulsion of worms/insect infections

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3
Q

allergy mediators

A

primary (stored)

  • histamine, serotonin (vascular permeability, smooth muscle contraction)
  • eosinophil chemotaxis mediators
  • neutrophil chemotaxis mediators
  • protease (mucus secretion, connective tissue degradation)

secondary (synthesized)

  • leukotrienes (vascular permeability, sm muscle contraction)
  • prostaglandins (vasodilation, sm muscle contraction, platelet activation)
  • bradykinin (vascular permeability, sm muscle contraction, pain)
  • cytokines (recruit immune cells, inflammation)
    *
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4
Q

manifestations of allergy

A

symptoms: sneezing, coughing, wheezing, diarrhea

local anaphylaxis: allergic rhinitis, asthma, urticaria (hives), atopic dermatitis (eczema), angioedema (swelling of soft tissues)

late phase rxn: cytokines recruit eosinoiphils, neutrophils, lymphocytes → promotes infl

systemic anaphylaxis:

  • disseminated mast cell activation → increased vasc permeability, constriction of sm muscle
    • leads to extravasation of fluid ( → hypotension), constriction of airways, epiglottis swelling
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5
Q

skin test for allergy

A

small amt of allergen introduced via intradermal injection or superficial scratching

local mast cells degranulate → increased permeability and fluid leakage, vasodilation and increased blood flow

  • wheal: swelling, local region of intense edema. appears white bc capillaries are occluded
  • flare: larger surrounding areas of redness due to vasodil
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6
Q

RAST test for allergy

A

radioallergosorbant test

detects level of IgE

  • allergens are coupled to beads
  • patient serum is added → IgE binds beads
  • radiolabeled anti-IgE is added, measured → IgE quantified
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7
Q

allergy shots

A

desensitization

introduce small amounts of antigen in increasing amounts over a period of time

goal: try to get isotype switching from IgE → IgA, IgG

  • trying to get Tregs going to suppress Th2 cells that are forming IgE
  • if it works; IgA and IgG will bind to and neutralize antigen when it’s encountered, prevent it from binding IgE → prevent it from setting off allergic rxn
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8
Q

hygiene hypothesis

A

modern day practice of hitting everything with antiseptics and avoiding all types of microbial contact → insufficient contact leading to insufficient stimulation of Th1 reactions

  • results in imbalance of Th1/Th2 → more Th2 → processing of innocuous environmental agents as threats → allergic responses

theory: exposure to diverse environmental antigens may actually prevent sensitization to any particular one

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9
Q

type II hypersensitivity

A

antibody-mediated cytotoxicity

hours (vs Type I minutes)

IgM or IgG dependent → bind to antigens on cell surfaces

opsonization →

  • phagocytosis by macrophages and neutrophils
  • neutrophil recog and secretion of lytic enzymes (antibody-dependent cell-mediated cytotoxicity = ADCC)
  • complement activation (MAC attack)
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10
Q

ADCC

A

antibody-dependent cell-mediated cytotoxicity

target cell is coated with antibodies → target cell is lysed by cytosolic effector cells

  • NK cells
  • macrophages
  • neutrophils

no complement required!!!

but dependent on prior antibody response

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11
Q

type II hypersensitivites (rxns)

A
  • transfusion reactions
  • hemolytic disease of newborn (HDN)
  • autoimmune diseases
  • drug-induced hemolytic anemia
    • antibiotics (cephalosporin, penicillin, streptomycin
    • cell membrane is carrier for hapten-carrier complexes

*hapten: small molecule that can bind an antibody but is not immunogenic in and of itself

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12
Q

type III hypersentitivity

A

4-12 hours

immune complex disease : caused by circulating antigen-antibody complexes that can lodge in small vessels and filtering organs

  • complexes = antigen + high-affinity IgG (lower affinity IgM)

mechanisms

1. large complexes are insoluble

  • fix complement → phagocytosed

2. small complexes can get into tissues where they can cause probs

  • not cleared as readily, can accumulate in blood, get deposited in vessels

3. complement C3a and C5a (anaphylatoxins)

  • induce mast cell degranulation (IgG, not IgE)
  • mediate inflammation response
    • release cytokines, attracts neutrophils to come through and phagocytose and release lytic enzymes (tissue injury)
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13
Q

Arthus reaction

A

type III rxn

  • acute response initiated by local deposition of Ag/Ab complexes
  • 4-12 hours to develop
    • immune complexes must form in situ → activate mast cells and neutrophils, activate complement
  • develops more slowly than type I hypersensitivity, more quickly than type IV hypersensitivity

looks like wheal and flare! BUT takes hours to form

  • pay attn to time course!
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14
Q

localized vs. systemic type III rxns

A

localized

  • local vasculitis: deposition of immune complexes in dermal blood vessels
  • insect bites
  • drugs/vaccines
  • intrapulmonary (inhaled bacterial spores, fungi (Farmer’s Lung), fecal proteins)

systemic

  • serum sickness
  • autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus)
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15
Q

example of arthus rxn

drunk pt who gets a laceration, needs a tetanus booster (no need for antiserum, bc already got vaccine 5 yrs ago)

pt struggles, shot thats supposed to be intramuscular is given intradermal

12 hours later → painful lesion.

what happened?

A

point of intramuscular protocol: let booster diffuse into lymphoid system so that antigen therein can trigger antibody-generation

intradermally injected shot cant diffuse out quickly → end up reacting with the antibody already present → localized type III hypersensitivity rxn

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16
Q

type IV hypersensitivity

A

delayed type hypersensitivity (DTH)

48-72 hours (symptoms start 24h after second exposure, peak in this window)

antibody independent : mediated by antigen-specific Th1 cells

  • recruit monocytes/macrophages, granuloma formation
  • activate CTLs → cell killing

process

  • Th1 cells are sensitized : APCs presented to Th1 by APC-MHC/antigen presentation → activated Th1 cells undergo clonal expansion
  • subsequent exposures?
    • memory T cells recognize antigens, go to work → secrete cytokines, recruit macrophages (main players, over 80% of infiltrate) and other nonspecific infl cells (neutrophils - secondary players)

ex. TB skin test

17
Q

type IV reactions

A
  • TB skin test
  • allergy to metal salts or other small reactive chemicals (haptens)
    • bind to proteins → create new epitopes
    • contact dermatitis to coins, jewelry
  • organ rejection
  • skin contact to poison ivy
18
Q

example of type IV rxn:

bone marrow transplant recipient gets transplant, presents soon after with skin rash, diarrhea, jaundice,

progressive worsening and indication of pneumonia and kidney failure

what happened?

A

gravt vs host disease!

graft contained some immunocompetent T cells that are active → recognize host MHC as foreign → attack whole host body as foreign :(

issue: donor cells have never seen foreign MHC before - read it as MHC+peptide, which is a target for attack

19
Q

hypersensitivity types

A

ABCD

I: anaphylactic: IgE mediated hypersensitivity

  • Allergic Anaphylaxis and Atopy

II: cytotoxic: antibody-mediated cytotoxic hypersensitivity

  • antiBody

III: ImmuneComplex: immune complex mediated hypersensitivity

  • immune Complex

IV: DTH: delayed type hypersensitivity

  • Delayed

or, ACID (anaphylaxis/atopy, cytotoxic, immunecomplex, delayed)

20
Q

atopic

A

predisposed to v severe allergic rxns

Immunity (18 decks)

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