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FPP Weeks 1 & 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Hypersensitivity

A

Excessive or abnormal secondary immune response to a sensitizing agent

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2
Q

Allergen

A

IgE mediated disease, require sensitization
Affects only those that are sensitized to the allergen
Not dose-dependent

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3
Q

Irritants

A

Not mediated through IgE

Dose dependent response, affects all

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4
Q

Type I Hypersensitivity

A

Mast cell and/or basophil dependent (IgE-dependent)
Initial response is immediate (within 15 mins)
Degranulates releasing preformed mediators

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5
Q

Histamine

A

Short half-life
Only produced by mast cells and basophils
At least 3 receptors (H1-3R)

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6
Q

Role of H1/H2R

A

Toxic to parasites
Increases vascular permeability
Causes smooth muscle contraction

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7
Q

Heparin

A

Released by mast cells

Similar effects as histamine

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8
Q

Mast Cell Enzymes

A

Tryptase: Two forms (Alpha - Constitutively, Beta - Activated mast cell)
Identifiable in serum for up to 4 hours after release
Only mast cells make this protein
Single best marker of mast cell activation
Leads to remodeling of connective tissue matrix
Chymase, Cathespin G, Carboxypeptidase: Remodeling of connective tissue matrives

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9
Q

Mast Cell Cytokines

A 
IL-4/13: Associated with Th2 cells and lead to Ig class switching in B cells to the production of IgE
IL-3/5, GM-CSF: Promote the survival and activation
TNF: Activates endothelium and leads to adhesion molecule expression, some exists as preformed mediator
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10
Q

Mast Cell Chemokines

A

MIP-1a (CCL3): Chemotactic for monocytes/macrophages/neutrophils/T cells/eosinophils
RANTES (CCL5) and Eotaxin (CCL11): Chemotactic for T cells and eosinophils

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11
Q

Mast Cell Lipid Mediators

A

Leukotrienes C4, D4, E4: Eosinophil migration, smooth muscle contraction, vascular permeability, mucus hypersecretion
Platelet activating factor (PAF): Attracts eosinophils and other leukocytes; activates eosinophils, neutrophils, and platelets; increases production of lipid mediators

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12
Q

What reduces the threshold for histamine release?

A 
Cytokines/chemokines
Antigen exposure
Histamine-releasing factor
Autoantibody
Psychological factors
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13
Q

What increases the threshold for histamine release?

A

Corticosteroids
Antihistamines
Cromolyn (in vitro)

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14
Q

What results in elevated eosinophil count?

A 
Neoplasia
Asthma
Allergy
Connective tissue disease
Parasitic disease
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15
Q

What is CCR3 for?

A

Eosinophil receptor for Eotaxin (only known receptor) and RANTES (CCL5)

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16
Q

What do corticosteroids result in?

A

Induce rapid apoptosis of eosinophils
Inhibit the production of IL-5
Inhibition of AP-1 and NFkB via GRa

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17
Q

What produces IL-5?

A

Th2 lymphocytes and other cells

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18
Q

IL-5 effects in vitro on eosinophils

A

Prolongs survival, enhances leukotriene production, cytotoxicity for parasites
Augments B2 integrin-mediated adhesion and transendothelial migration

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19
Q

IL-5 effects in vivo

A

Infusion causes eosinophilia
Levels increased in some diseases with eosinophilia
Levels increased in fluids obtained from sites of experimental allergic late phase reactions

20
Q

Function of lysophospholipase

A

Degrades lysophospholipids

21
Q

Function of MBP

A

Mast cell activation, helminthotoxic

22
Q

Function of ECP

A

Same as MBP plus neurotoxic

23
Q

Function of EDN

A

Neurotoxin

24
Q

Function of PAF

A

Bronchoconstriction and activates platelets

25
Q

Function of LTC4

A

Bronchoconstriction, mucus hypersecretion, edema

26
Q

Examples of Type I hypersensitivity

A

Allergic Rhinitis
Asthma
Anaphylaxis
Urticaria

27
Q

What causes allergic rhinitis?

A

Due to cross-linking of IgE in nasal mucosa and ocular conjunctiva with specific antigen exposure
Systemic symptoms are rare

28
Q

Mechanism of Asthma

A

Symptoms are due in part to IgE mediated disease in lower airways
Wheezing, shortness of breath due to increased airway constriction (prevents exhalation)
Increased mucus secretion and production (mucus plugging)

29
Q

Definition of Type II hypersensitivity

A

Antibody (IgG or IgM) binding to cell or matrix bound antigen

30
Q

Mechanism of Type II hypersensitivity

A

Phagocytic or NK cells bind ot the antibody via their Fc receptor
Target tissue is then destroyed
Complement may be involved (increases binding via C’ receptors on phagocytic cells)

31
Q

Mechanism of drug based Type II hypersensitivity

A

IgG is formed against drug-cell antigen
Erythrocytes and platelets are targeted resulting in spleen damage
Only targets cell-bound drug

32
Q

Examples of drug based Type II hypersensitivity

A

Penicillin, Quinidine, Methyldopa

33
Q

Definition of Type III hypersensitivity

A

Antibody (IgG) against a soluble antigen

34
Q

Mechanism of Type III hypersensitivity

A

Antigen-antibody complex activates complement
Activate FcyR expressing cells and complement
Large complexes cleared by phagocytes
Small complexes precipitate on blood vessel walls where leukocytes bind and activate against them

35
Q

Where is there high risk for Type III hypersensitivity?

A

Highly vascularized beds with narrow vessels, where the complexes are most likely to precipitate on the endothelial walls
Specifically: Kidneys, vessels, joints, and skins

36
Q

What cells are recruited with Type III hypersensitivity and what do they do?

A

Phagocytes (neutrophil predominant) release their lysosomal enzymes and cause tissue destruction

37
Q

Arthus reaction

A

Type III reaction when skin being sensitized when exposed to specific antigen
Involves activation of mast cell and other leukocytes via FcyRIII and not complement

38
Q

Serum sickness

A

Type III systemic reaction from injection of large quantities of foreign protein

39
Q

Timeframe of serum sickness

A

Reaction happens 7-10 days post exposure (time length for IgM to IgG) which is the peak of Ag-Ab complexes
Ag drops below Ab post this point
Next exposure will have a much shorter time course

40
Q

Symptoms of serum sickness

A

Flu-like, urticarial rash, arthritis, glomerulonephritis

41
Q

Farmer’s lung

A

Alveolitis due to a type III reaction against hay dust or mold spores
Inflammation in and destruction of the alveolar wall

42
Q

Examples of systemic antigen excess situations (Type III)

A

Autoimmune diseases
Infections: Viral hepatitis or subacute bacterial endocarditis
Recurrent antigen production

43
Q

Definition of Type IV hypersensitivity

A

Cell-mediated reaction (No antibodies)

44
Q

Mechanism of Type IV hypersensitivity

A

Antigen enters the skin (typically target) and then binds to self proteins
Bound antigen must be taken up and processed by APCs to T-cells
24-72 hour latency to reaction
Involves CD4+ Th1 cells or CD8+ T cells

45
Q

Mediators important in Type iV and role

A

IFN-y: Induces expression of adhesion molecules, activates macrophages
TNFa and Lymphotoxin (LT): Local tissue destruction, induces expression of adhesion molecules
IL-3 and GM-CSF: Stimulate monocyte production
Chemokines: Recruit macrophages to site

46
Q

Tuberculin response

A

Type IV hypersensitivity reaction where TB derived peptides are injected in skin
Th1 mediated response develops in 48-72 hours for previously exposed individuals

47
Q

What are contact hypersensitivity reactions and what is an example?

A

Chemical exposure to skin where compounds bind with self proteins and generate a response with extensive macrophage mediated inflammation
Example: Poison ivy or Rhus Dermatitis (due to pentadecacatechol)

FPP Weeks 1 & 2 (18 decks)

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