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PHRM 100 – APPP > APPP 21: Hypersensitivity Reactions > Flashcards

APPP 21: Hypersensitivity Reactions Flashcards

1
Q

What are hypersensitivity reactions?

A

altered immunological response to an antigen that results in disease or damage to host

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2
Q

What are the 2 ways that hypersensitivity reactions can be classified by?

A
  • mechanisms that cause the disease (Gell and Coombs classification – type I-IV)
  • source of antigens
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3
Q

What are the 3 sources of antigens that can cause hypersensitivity reactions?

A
  • allergy: over-reactivity to otherwise unharmful environmental antigens or chemicals
  • autoimmunity: disturbance of immunological tolerance of self-antigens
  • alloimmunity: immunological reactions against tissues of another individual (blood transfusion, organ transplant, fetus during pregnancy)
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4
Q

Type I Hypersensitivity

A
  • IgE mediated
  • classic allergy
  • onset in minutes
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5
Q

Type II Hypersensitivity

A
  • IgG/IgM mediated
  • cytotoxic reactions
  • onset in hours to days
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6
Q

Type III Hypersensitivity

A
  • IgG/IgM
  • immune-complex diseases
  • onset in hours to weeks (1st encounter)
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7
Q

Type IV Hypersensitivity

A
  • T cell
  • delayed type hypersensitivity
  • onset in 2-3 days
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8
Q

Mechanism of Allergic Response

How does degranulation occur?

A
  1. allergen binds IgE/FceR1 on mast cell surface
  2. cross-links of two IgE to activate degranulation signal with tyrosine phosphorylation
  3. Ca2+ influx
  4. degranulation and release of inflammation mediators
  • granule contents include histamine, proteases, chemotactic factors (ECF, NCF)
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9
Q

What is an immediate phase event?

A
  • release of histamine and cytokines by mast cells
  • occurs within minutes following exposure to allergens
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10
Q

What is a late phase event?

A
  • induction and continuing synthesis of eicosanoids, cytokines, and chemokines
  • immune cell infiltrate (eosinophils and others)
  • smooth muscle contraction, edema
  • may last hours to days, and lead to chronic inflammatory reaction
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11
Q

Mechanism of Allergic Response

What is sensitization?

A
  • first antibodies made following antigen presentation are from IgM or IgG classes
  • repeated exposure is needed for switching (to IgE) in the presence of correct cytokines (IL-4)
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12
Q

Mechanism of Allergic Response

What is the effector stage?

A
  • high affinity IgE receptor (FceR1) found on mast cells, basophils, and activated eosinophils
  • subsequent to sensitization, increasing number of mast cells are primed with (already binding to) IgE on surface
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13
Q

How are we exposed to allergens?

A

commonly though mucosal exposure

  • airway
  • gastrointestinal
  • urogenital
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14
Q

Type I Hypersensitivity Reactions

What is localized anaphylaxis?

A

target organ responds to direct contact with allergens

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15
Q

Type I Hypersensitivity Reactions – Localized Anaphylaxis

Lung

  • disease
  • major symptoms
  • common allergens
  • route
A
  • asthma
  • wheezing, dyspnea
  • pollens, dust, danders
  • inhalation
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16
Q

Type I Hypersensitivity Reactions – Localized Anaphylaxis

Nose/Eyes

  • disease
  • major symptoms
  • common allergens
  • route
A
  • rhinitis (hay fever)
  • running nose, itchiness
  • pollens
  • mucous membrane
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17
Q

Type I Hypersensitivity Reactions – Localized Anaphylaxis

Skin

  • disease
  • major symptoms
  • common allergens
  • route
A
  • urticaria (hives)
  • itchiness and blisters
  • foods, medications
  • ingestion
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18
Q

Type I Hypersensitivity Reactions – Localized Anaphylaxis

GI Tract

  • disease
  • major symptoms
  • common allergens
  • route
A
  • allergic gastroenteropathy
  • vomiting, diarrhea
  • foods
  • ingestion
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19
Q

Type I Hypersensitivity Reactions

What is systemic anaphylaxis?

A

systemic vasodilation and smooth muscle contraction leading to severe bronchiole constriction, edema, and hypotension (shock)

  • tachycardia, arrhythmia, cyanosis, and cardiac arrest can occur
  • anaphylactic shock requires immediate medical interventions
  • biphasic presentations up to 30% of cases
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20
Q

Type I Hypersensitivity Reactions

What is atopy?

A

associated with genetic predisposition for localized anaphylaxis

  • atopic individuals have higher levels of IgE and eosinophils
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21
Q

Type I Hypersensitivity Reactions – Genetic Predisposition

What are the candidate polymorphic genes related to atopy? (5)

A
  • IL-4 receptor
  • IL-4 cytokine (promoter region)
  • FceRI: high affinity IgE receptor
  • class II MHC (present peptides promoting Th2 response)
  • inflammation genes
22
Q

Type I Hypersensitivity Reactions – Genetic Predisposition

What is the allergic triangle?

A

people who have one atopic condition are more likely to develop another atopic condition, and the trigger factors for each may be the same

23
Q

Type II: Cytotoxic Hypersensitivity

What is this hypersensitivity mediated by?

A

inappropriate binding of antibodies (IgG or IgM) to a tissue cell surface antigen, including:

  • extrinsic antigens presented on a cell surface following an infection
  • chemical that modified a cell surface component (ie. penicillin binding to RBC and quinine binding to platelet)
  • self antigen (auto-immune disease)
24
Q

Type II: Cytotoxic Hypersensitivity

Antibody binding directs cellular toxicity of target cells through ____________. (2)

A
  • classical complement pathway MAC
  • immune cell mediated ADCC
25
Q

Type II: Cytotoxic Hypersensitivity

What are some examples of type II hypersensitivity reactions? (3)

A
  • ABO hemolytic anemia (clinical mistakes in blood transfusions)
  • auto-immune hemolytic anemia (autoimmune disease)
  • Guillain Barre Syndrome (autoimmune reaction following viral infections)
26
Q

Type II: Cytotoxic Hypersensitivity

What are the special type II reactions?

A
  • known as type V in the UK
  • associated with cell surface receptors targeting antibodies
27
Q

Type II: Cytotoxic Hypersensitivity

What does mixing wrong blood types result in?

A

agglutination (clumping) and MAC

28
Q

Type III Hypersensitivity: Immune Complex Disease

What occurs in the 3 phases?

A

phase 1:

  • antigen presentation and antibody (IgG or IgM) production
  • formation of antigen-antibody complexes in circulation (soluble)

phase 2:

  • deposition of antigen-antibody complexes in tissues
  • frustrated phagocytes unable to clear these complexes

phase 3:

  • inflammation and tissue injury where antigen-antibody complexes are deposited (kidney, endothelial cells, joints)
29
Q

Type III Hypersensitivity: Immune Complex Disease

When are immune complexes (IC) formed?

A

when clusters of antibodies (mostly IgG, but also IgM) interlock after binding to soluble (not cell surface) foreign or tissue antigen (self antigen = autoimmune disease)

30
Q

Type III Hypersensitivity: Immune Complex Disease

Where are immune complexes (IC) found?

A
  • in circulation
  • in body fluids
  • deposited in tissue (ie. glomerular basement membrane)
31
Q

Type III Hypersensitivity: Immune Complex Disease

How are immune complexes normally removed and what happens if they aren’t?

A
  • normally rapidly removed through actions of phagocytic cells
  • when not effectively removed, they could become trapped in local tissues and cause degranulation of phagocytes
  • activation of complement system is also implicated in tissue injury caused by precipitated/trapped IC
32
Q

Type III Hypersensitivity: Immune Complex Disease

What are some common immune complex conditions? (3)

A
  • glomerulonephritis following streptococcal infection
  • rheumatoid arthritis (autoimmune)
  • systemic lupus erythematosus (autoimmune)
33
Q

Type III Hypersensitivity: Immune Complex Disease

What is systemic lupus erythematosus?

A
  • antibodies against dsDNA from apoptotic cells form immune complexes
  • these complexes are deposited in kidney’s glomerular structures and in blood vessels
  • immune complex deposition/formation eventually leads to immune-mediated tissue inflammation and damage
34
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What are the 2 phases?

A
  • sensitization phase: initial contact with antigen
  • effector phase: secondary contact with antigen
35
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What is DTH?

A

type of immune response classified by macrophage APC and T cell activation that results in tissue damage

  • can be the result of chronic infection or exposure to antigens
36
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What is contact dermatitis?

A

(example: response to poison ivy)

  • small molecules act as haptens and complex with skin proteins to be taken up by APCs and presented to Th1 cells to get sensitization
  • during secondary exposure, Th1 memory cells become activated by cytotoxic T cells to cause DTH
37
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What are some other haptens? (2)

A
  • heavy metals (nickel, cobalt, chromium, and zinc)
  • latex
38
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What are DTHs?

A
  • T-cell mediated inflammatory conditions
  • also implicated in some autoimmune diseases (type IV cell-mediated vs. type II and III antibody-mediated)
39
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

How do DTHs occur?

A
  • soluble protein antigens are presented by macrophages or dendritic cells to TH1 helper T-cells
  • in the classical TH1-macrophage feedback, TH1 cells secrete cytokines to recruit mononuclear cells and form granulomas
  • at the epidermis, Langerhans cells (dendritic cells specific to skin and mucosa) act as APC – small molecules bind to normal cellular proteins following skin contact, and present as modified epidermal antigens to elicit immune activation of cytotoxic T cells
40
Q

Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)

What are some examples of type IV hypersensitivity disorders? (2)

A
  • contact dermatitis (effector phase is cytotoxic T cell mediated)
  • tuberculin formation in tuberculosis (effector phase is TH1- macrophage)
41
Q

What are the causes of autoimmune disorders? (3)

A
  • breakdown in immune tolerance against self antigens
  • molecular mimicry of infectious microbe’s antigens resembling self-antigen
  • neo-antigen creation through hapten binding to cellular proteins, as well as somatic mutations that altered protein structures
42
Q

What are the risk factors in autoimmune disease? (4)

A
  • genetics: polymorphic forms of MHC II allotypes
  • sex: hormonal, X-inactivation, and micro-chimerism roles
  • infections in susceptible individuals (see mimicry above)
  • age: immunosenescence and loss of immune system self-regulatory capacity
43
Q

What hypersensitivity type is Guillain Barre disease?

A

II

44
Q

What hypersensitivity type is Graves Disease?

A

II

45
Q

What hypersensitivity type is Myasthenia Gravis?

A

II

46
Q

What hypersensitivity type is rheumatoid arthritis?

A

III

47
Q

What hypersensitivity type is systemic lupus erythematosus?

A

III

48
Q

What hypersensitivity type is celiac disease?

A

IV

49
Q

What hypersensitivity type is multiple sclerosis?

A

IV

50
Q

What hypersensitivity type is type I diabetes?

A

IV

PHRM 100 – APPP (23 decks)

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