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Immunology > Oral Allergies and Immunologic Diseases > Flashcards

Oral Allergies and Immunologic Diseases Flashcards

1
Q

Type I HS

Ab

Ag

Response time

Appearance

Cells involved

A
  • Allergic or immediate HS rxn
  • Allergen specific IgE triggers release of histamine
  • Ab: IgE
  • Ag: exogenous
  • Wheal and flare
  • Basophils, mast cells, eosinophils activated
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2
Q

Type II HS

A

Results from IgG/ IgM Ab binding to self Ag developing cytotoxic reactions

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3
Q

Type III HS

A

Resuslts from non-clearance and deposition of immune complex and inflammation

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4
Q

Type IV HS

A

CD4 T cell mediated cutaneous contact reactions to nickel, latex or skin responses to leprosy and TB

Appears as erythema and induration

Macrophages and T cells are activated

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5
Q

Mechanism of Type I

A
  • First exposure to allergen
    • B cell activation and allergen-specific IgE production
    • IgE binds to IgE specific Fc receptors on mast cells/basophils
  • Second exposure
    • IgE on mast cells and basophils bind to allergen
    • Mast cells and basophils are activated to release
      • Histamine, leukotrienes, prostaglandins cytokines
    • Causes Smooth muscle contraction, increased vascular permeability, vasodilation, increased mucus secretion, inflammation
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6
Q

Mast cell Commpounds

A
  • Preformed mediators : immediate
    • Histamine
      • bronchoconstriction and vasodilation
    • Newly synthesized mediators: late phase
      • Leukotrienes, Prostaglandin D2: Bronchoconstriction and vasodilation
      • Cytokines- inflammation
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7
Q

Reaction to Type I HS

A

Local allergic

Systemic (Anaphylaxis)

Chronic inflammation

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8
Q

Diagnosis of Type I

A
  • History and signs
  • family history, genetics (atopic)
  • Detection of IgE Ab in patient
  • Evidence of the IgE
    • In vivo: Prick test and intradermal test
    • In vitro: RAST or ELISA
    • determines amt of IgE
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9
Q

Drugs and small molecules in Allergic Rxns

A
  • Drugs bind to proteins in the body
    • Penicillin core causes Type I
  • Drug-protein conjugate develops Th2 type of immune response and production of of IgE
  • Repeat exposure to drug triggers allergic reaction via mast cells
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10
Q

How can patients with penicillin alllergies be treated?

A

With cephalosporin

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11
Q

Drug- related Type I Allergies

A

Beta lactam antibiotics

Sulfonamides

Chemotherapy agents

HIV drug abacavir

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12
Q

Cross reactivity

A
  • Latex causes cross reactivity to fruits and vegtables
  • Called Oral Allergy SYndrome
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13
Q

Type IV DTH is encountered in

A
  • Allergic contact dermatitis from sensitization to chemicals including dental chemicals
  • Allergic reaction to many bacteria viruses and fungi
  • Tuberculin type HS
  • Granulomatous formation- TB leprosy
  • Rejection of transplants
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14
Q

Mechanism of Type IV

A
  • Sensitization
    • DC take up small molecule modified with protein Ag
    • Present molecule-protein conjugate to CD4 T cells
    • T cell activation and memory T cells
  • Elicitation
    • subsequent exposure
    • rapid secretion of proinflammatory cytokines: TNF and IL-1
    • Recruitment of effector cells, monocytes, MO and site inflammation
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15
Q

Granuloma Formation

Examples

A
  • DTH triggered via CD4 T cells response to pathogen
  • Failure to kill and clear
    • persistent antigenic stimuli prdoces chronic DTH- Chronic Granuloma
    • Body tries to wall it off
  • Leprosy, TB, measels mumps and herpes
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16
Q

Contact Dermatitis

A
  • Small molecules like nickel
  • Often lipophilic and cojugate with self proteins
  • Langerhans DC take up conjugate and present to Th cells
  • Th cells activate–> Allergic Contact Dermatitis
  • Observed in periodontal disease with nickel
  • TLR4 binds nickel –> inflammation
17
Q

Antihistamines

A
  • H1 receptor antagonists block binding of histamine to cells
18
Q

Adrenergic agents

A

Beta receptor agonists, bronchiole smooth muscle relaxant, elevation of cAMP (einephrine)

19
Q

Corticosteroids

A

Potent anti-inflammatory, prednisone, hydrocortisone

20
Q

3 Allergic Oral Mucosal Reactions

A

RAS RAU/ Canker sores

Orofacial Granulomatosis

Wegeners Granulomatosis

21
Q

RAS RAU Canker Sores

Prevelance

A
  • Most common
  • Triggered by a variety of causative agents with no single agent
  • Numerous pathophysiology hypothesis
  • Diff people have diff agents
    *
22
Q

Ras RAU Canker Sores Mech

A
  • Mucosal Mucosal destruction thru T cell mediated reaction
  • Decreased ratio of CD4 and CD8 T cells
  • Increased TNF–> Inflammation
  • Process may involve ADCC (Ab Dependent Cellular Cytotoxicity)
  • Genetic predisposition: HLA types, associated with RAU
  • Stress, vacation, travel
  • AIDS patients bc low CD4
23
Q

Orofacial Granulomatosis

Cause and presentation

A
  • Analogous to RAU
  • Cause is unknown and abnormal immune response
  • Gingiva swells, reythemia, pain, erosions, oral lesions
  • Non tender persistent swelling of lips
24
Q

Management of Orofacial Granulomatosis

A
  • Goal to discover initiating cause
  • Local measures to resolve
25
Q

Wegeners Granulomatosis

Cause, sysmptoms

A
  • Uncommon, unknown cause
  • Necrotizing granulomatus lesions and glomerulonephritis
  • Systemic vasculitis
  • localized may become systemic
  • Oral lesions, renal involvement, respiratory tract
26
Q

Wegeners Granulomatosis

Oral manifestation and drugs

A
  • Oral manifestation is gingival alteration:Strawberry gingivitis
  • Mixed inflammation
  • Drugs: cyclophosphamide and prednisone
27
Q

Allergic Mucosal Reactions to Synthetic drugs

A
  • Many drugs can cause it
  • Multiple mucosal alterations
28
Q

Allergic Mucosal Reactions to Synthetic drugs

Diagnosis

A
  • Chronic drug reactions
    • Definitive diagnosis can be made
      • Mucosal alterations resolve once you stop taking the drug
    • Presumptive diagnosis
  • In suspected lupus-like drug reactions
    • Evaluation for generic antinuclear Ab (ANA) and Abs against dsDNA and histones
29
Q

Allergic Mucosal Reactions to Synthetic drugs

Tratment and prognosis

A
  • Discontinue drug
  • Replace with diff drug
  • Localized acute rxns resolved with topical coticosteroids
  • Systemic manifestations (Anaphylatic stomatitis)
    • Requires systemic adrenaline, corticosteroids, antihistamines
  • Chronic oral lesions usually clear after stop taking drug
    • may need topical corticosteroids
    • Palliative care if cant stop taking drugs
30
Q

Hypersensitivities of Mixed Mechanisms

A

Many Diseases overlap different HS

Late phases of Type I in asthma and atopic dermatitis are mediated by cells causing inflammation, typical of DTH

Usually treated with NSAIDs or steroids to control inflammation

Patient counseling:Allergen avoidance

Immunology (11 decks)

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