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CMOD > Hypersensitivity/ Allergy > Flashcards

Hypersensitivity/ Allergy Flashcards

1
Q

State of heightened reactivity to antigen

A

Hypersensitivity

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2
Q

immune responses to innocuous antigens that lead to symptomatic reactions upon re-exposure

A

hypersensitivity reactions

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3
Q

damage to host tissue caused by hypersensitivity reactions to typically innocuous antigens

A

hypersensitivity disease

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4
Q

Involves IgE-dependent triggering of mast cells

A

Immediate Type/ Type I hypersensitivity

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5
Q

Commonly referred to as allergy

A

Immediate Type/ Type I

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6
Q

Involves IgG antibody that is reactive with cell-surface or matrix antigens

A

Type II: Altered Self

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7
Q

involves production of antigen:antibody complexes

A

type III: Immune complex

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8
Q

altered host hypersensitivity

A

Type II: altered self

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9
Q

immune complex hypersensitivity

A

type III: Immune complex

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10
Q

T cell mediated hypersensitivity

A

Type IV: Delayed type

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11
Q

delayed type hypersensitivity

A

Type IV: Delayed Type

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12
Q

Antigens that elicit a Type I hypersens. response are called

A

allergens–> slectively stimulate Th2 cells that can drive class switching from IgM to IgE (weakly opsonizing/low dose/extracellular)

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13
Q

Main cell type involved in type I hypersensitivity upon first encounter with the antigen

A

Th2 CD4+–> b/c it can promote class switiching to IgE which is taken up by the high affinity IgE receptor on mast cells etc…

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14
Q

Type I hypersensntitivity MOA

A

Antigen selectively stimulates a TH2 response that drives class switiching to IgE specific for the encountered antigen

  • ->then mast cells take up the IgE ab’s on their FCgammaR1 (high affinity IgE receptor)–>second exposure to Antigen–> massive degranulation of MAST CELLS
  • TH2 driven IgE responses
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15
Q

Common features of most allergens

A
  1. Small
  2. Highly Soluble
  3. Carried on Dessicated particles (stable)
  4. diffuse into the mucosa from the particles
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16
Q

High or Low dose exposure for allergens?

A

Low Dose ( will cause Th0 to become a TH2)

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17
Q

Th2 release which cytokines

A

3 4 5 10 13 TGF beta

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18
Q

Many common allergens have______

A

enzymatic activity

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19
Q

IgE is important in the immune response to _____

A

parasites
(They produce proteases that aid in the parasites own movement through the host’s tissue–>therefore, IgE response to protein allergens is largely physiologic–> but becomes pathologic in response to innoccuous environmental allergens

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20
Q

protein (enzymatic*) allergen +TH0–> TH2–>promotes class switching in Naive B lymphocytes to IgE specific to that protein

A

know that

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21
Q

One of the pre-requisites for Type I hypersensitivity is that the initial response must be….

A

IgE response

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22
Q

How does class switiching to IgE occur

A

TCR of an Effector CD4 TH2 t cell becomes ligated (by specific peptide antigen presented on MHC II molecules) on the B cell (an antigen presenting cell)–> TH2 secretes IL-4, 5, and 13–> mediates class switching to IgE

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23
Q

All the cells hat can INITIATE Type I Hypersensitivity reaction

A

Mast Cells (primary)
Eosinophils
Basophils
–>all of these have the high affinity IgE FC receptor

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24
Q

Cross-Linking of IgE receptors on a mast cell, basophil and eosinophil leads to what?

A

degranulation of granules that contain mainly histamine…Leukotriens, Prostaglandins, TNF, Cytokines, PAF and neutral proteases

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25
Q

What does atopic mean

A

predisposed to IgE allergens

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26
Q

Is there a genetic basis to atopy

A

yes 40% of Caucasian population

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27
Q

Chromosomes involved in genetic basis for atopy

A

11–> high affinity IgE receptor

5–>IL 3 4 5 9 13 and GM-CSF (isotype swithcing and mast cell survival)

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28
Q

First step of response to allergens in skin test

A

Wheal and Flare response

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29
Q

What happens in a Wheal and Flare Response

A

Mast cell degranulation–>releases histamine–> increased permeability–> edema (Wheal)
increased blood flow (flare)

30
Q

2nd step in response to allergen skin test

A

6-8 hours after injection (late phase reaction)second reaction at the site of injection
*wiki says primarily cytokine mediated

31
Q

The effects of IgE mediated allergic reactions vary with_____

A

site of mast cell activation

*only those cells at the site of action will cross-link and be degranulated

32
Q

Major sites of allergen-Mast cell response

A

mucosa of the respiratory tract, GI tract

33
Q

Insect bite allergens gain access to?

A

connective tissues and blood

34
Q

Body responses (coughing, diarrhea) to allergens are a response to

A

expel “parasites” from the body

35
Q

Systemic anaphylaxis

A

allergens in the blood
*widespread activation of mast cell degranulation causing both an increase in vascular permeability and widespread constriction of smoothe muscle

36
Q

Fluid leaving the blood in response to allergens in the blood–>

A

Low Blood pressure and anaphylactic shock

37
Q

Reactions that resemble anaphylactic responses but do not involved IgE and allergen

A

Anaphalactoid

38
Q

tx. for anaphylactic and anaphalactoid

A

epinephrine-> stiimulates reformation of tight junction between endothelial cells-> reduces blood vessel permeability->repletes blood volume–>diminishes swelling and rapidly restores blood pressure

39
Q

Rhinitis and Asthma are caused by_____

A

inhaled allergen

40
Q

mild allergic response characterized by violent bursts of sneezing and runny now in response to inhaled allergens

A

allergic rhinitis

  • allergens that diffuse across the mucous membranes of nasal passages and activate mucosal mast cells
  • release of mucous rich in eosinophils
41
Q

Allergic Rhinitis can extend to

A

ear and throat–> leading to accumulation of fluid in Eustachian Tubes (bacterial infections)

42
Q

Disease causing CHRONIC breathing difficulties

A

Allergic Asthma

although wiki says it is the RESULT of chronic inflammation

43
Q

Triggered when submucosal mast cells in LOWER respiratory tract are stimulated by allergen/IgE interaction

A

allergic asthma

44
Q

Pulmonary findings in allergic asthma

A
  1. increase in fluid and mucours into respiratory tract
  2. bronchial CONSTRICTION do to contraction of bronchial smooth muscles
  3. chronic asthma related inflammation can result in persistent infiltration of TH@’s, eosinophils, neutrophils)
45
Q

overall effect of asthma

A

trapping of air in lungs making breathing more difficult–> can be fatal

46
Q

Chronic asthma can be considered

A

Type IV hypersensitivity (antigen independent)–> excacerbated by immune response to bacterial or viral infections of respiratory tract (infections that elicit Th2 cells)

47
Q

hives=

A

urticaria ( caused by release of histamine by mast cells IN THE SKIN)
*essentially a wheal and flare reaction

48
Q

angioedmea

A

inflammation caused by mast cells IN THE SUBCUTANEOUS TISSUE)
*SWELLING IS MORE DIFFUSE THAN URTICARIA

49
Q

FOOD ALLERGEN MOA

A

allergen passes through wall of gut and binds to IgE receptors on mast cells–> accumulation of fluid in the gut

  • diarrhea, cramps, vomiting all caused by smooth muscle contraction
  • can have hives and angioedema too
50
Q

Therapy for PREVENTION of allergic reaction

A
  1. modify pt.’s behavior
  2. pharmacologic: give drugs that reduce the impact of contact with allergen
  3. prevent production of allergen specific IgE
    * desensitization: a series of shots of increasing allergen doses that gradually changed the Th2 IgE response to a Th1 response in which no IgE is produced
51
Q

Type of Hypersensitivity induced by antibodies specific for alterd components of Human Cells

A

Type II

52
Q

Most common examples of Type II

A

hemolytic anemia and thrombocytopenia following drugs administration

53
Q

common drugs that cause Type II

A

penicllin (most common)
quinidine
methyldopa

54
Q

Penicillin allergy MOA

A
  1. new epitopes are generated by the drug binding to RBC’s
  2. Penicillin Bound RBC’s are also coated with compliment (a inevitability given that there is an infection going on you are treating)
  3. Phagocytosis by macrophages
  4. Phagocytes present “new” epitopes to T cells–> Th2 phenotype effector is the product
  5. Th2 interacts with B cell–> IgG for altered host RBC is the outcome
  6. IgG binds to RBC’s and initiation MAC–> hemolysis (anemia)
55
Q

Immune complex hypersensitivity

A

Type III

56
Q

Small or Large Immune complexes are the trouble with Type III

A

Small–> inneficient compliment activation–>not taken up by macrophages properly and
*they remain in circulation and get deposited along blood vessels

57
Q

Type III once immune compexes get depositied onto vessel wall–>

A

tissue damage when sufficient number of immune complexes aggregate
*circulating leukocytes recognize immune compxe aggregates via Fc and compliment receptors and are activated to promote INFLAMMATION

58
Q

Type III EXPERIMENTAL TEST that takes place under the SKIN

A

Arthus reaction

59
Q

Serum sickness

A

immune responses to non-self material administered into the blood stream as a tx. for a variety of illnesses
*caused by systemic circulation of immune complexes–> eventually a systemic inflammatory response

60
Q

Serum sickness presents as

A

fever, chills, glomerulonephritis, rash, arthritis

61
Q

Farmer’s lung

A

Continual inhlation of dust and mold spores that occurs over a long period of time–> body makes and IgG mediated response (not IgE) and the resultant inflammation caused by immune complex build up in the lungs causes respiratory dysfunction

62
Q

Bird breeders lung

A

Type II hypersensitivity to avian antigens

63
Q

Hypersensitivity mediated by antigen specific t cells

A

Delayed Type Hypersensitivity

64
Q

time frame of DTH

A

1-3 days

65
Q

time frame for immediate type hypersensitivities

A

within minutes

66
Q

DTH require_____ quantities of antigen

A

100-1000 fold larger due to inefficient antigen processing and presentation

67
Q

common DTH antigens

A

poison ivy
nickel
insect venom
mycobacterial proteins

68
Q

positive TB test will show

A

inflammation around the site 24-72 hours after test

*Cytokines here are produced by Th1 cells that were activated by resident macrophages

69
Q

lipid-like molecule responsible for poison ivy

A

pentadecacatechol

70
Q

What happens on initial poison ivy interaction

A

poison covalently interacts with host tissues after penetrating skin and forms NEW antigens–> these are recognized as NON SELF
>local APC’s take up this antigen and present it to naive cells which
>formation of an effecto CD4 t cell army
VERY LITTLE INFLAMMATION RESPONSE
CTL’S CAN BE ACTIVATED DIRECTLY BY APC’S AS WELL

71
Q

SECOND POISON IVY RESPONSE

A

> ANTIGEN SPECIFIC CTL’S AND ANTIGEN SPECIFIC TH1 CELLS (DESTROY TISSUE WITH PENTADECACATECHOL)
AND
TH1’S THAT ACTIVATE MACROPHAGES AND PRODUCE INFLAMMATION

72
Q

EXAMPLE OF CONTRACTILE SENSITIVITY

A

poison ivy and nickel

*contact with the allergen is required to initiate the allergic response

CMOD (19 decks)

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