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Mandal > Oral Allergies and Immunologic Diseases > Flashcards

Oral Allergies and Immunologic Diseases Flashcards

1
Q

Definition of Hypersensitivity/ allergic reactions

A

immune response that cause tissue injury and disease

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2
Q

Hypersensitivity traits (3)

A
  1. Excessive or aberrant immune Responses
  2. Causes tissue damage
  3. manifested on second/subsequent contact w/ an antigen
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3
Q

Who came up w/ classfication of Hypersensitivity?

A

Coombs and Gell

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4
Q

Type I Hypersensitivity

A

allergic or immediate hypersensitivity reaction: allergen-specific IgE triggers histamine release (mast cells)

Binding to self protein

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5
Q

Type II Hypersensitivity

A

results from IgG/IgM Antibody binding to self Antigen developing cytotoxic reactions

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6
Q

Type III hypersensitivity

A

results from non-clearance & deposition of immune complex, and inflammation

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7
Q

Type IV hypersensitivity

A
  • CD4 T Cell-mediated cutaneous contact reactions to nickel, latex, or skin responses to leprosy or TB
  • Delyaed hypersensitivity 48-72hrs
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8
Q

Antibody

  1. Type I ( anaphylactic)
  2. Type-IV (delayed type)
A
  1. IgE
  2. None
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9
Q

Antigen

  1. Type I ( anaphylactic)
  2. Type-IV (delayed type)
A
  1. Exogenous
  2. Tissues & organs
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10
Q

Response Time

  1. Type I ( anaphylactic)
  2. Type-IV (delayed type)
A
  1. 15-30 minutes
  2. 24-72 hours
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11
Q

Appearance

  1. Type I ( anaphylactic)
  2. Type-IV (delayed type)
A
  1. wheal and flare
  2. erythema (redness) and induratoin (swelling)
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12
Q

Histology

  1. Type I ( anaphylactic)
  2. Type-IV (delayed type)
A
  1. Basophils, mast cells and eosinophil
  2. Macrophages and T cells
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13
Q

Examples

  1. Type I ( anaphylactic)-4
  2. Type-IV (delayed type)-2
A
  1. Allergic asthma, hay fever, uticaria, penicillin exposure
  2. Contact with Metal, latex, granuloma
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14
Q

Type I

First exposure to antigen

A
  • B cell activation →allergen-specific IgE production
  • IgE binds to IgE-specific Fc receptors on mast cells/basopils
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15
Q

Type I

Second Exposure to same allergen

A
  • IgE on the mast cells/basophils binds to the allergen
  • Activation of mast cells/basophils
  • triggers immediate and late phase allergic reactions
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16
Q

Type I

activation of mast cells/basophils release

A
  • Activation of mast cells/basophils
    • Release of histamine
    • leukotrienes
    • prostaglandin
    • cytokines
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17
Q

Type I

Triggers immediate & late phase allergic reaction via

A
  • Smooth muscle contractoin
  • increase vascular permeability
  • vasodilatation
  • increased mucus secretion and inflammation
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18
Q

TH2 secretes

A

IL-4

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19
Q

Type I allergy mechanisms

A
  • APC (TH2) secrete IL-4
  • IgE secreting B cell
  • IgM class switches to IgG
  • IgG becomes IgE
  • IgE releases Histamine
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20
Q

What are the two classes of active compounds that mast cell degranulation release ?

A
  • Pre-formed mediators: immediate
  • Newly synthesized mediators: late phase
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21
Q

pre-formed mediators that mast cell degranulation releases

A
  • immediate
  • Histamine
    • bronchoconstriction& vasodilation
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22
Q

newly synthesized mediators: late phase that mast cells degranulations release

A
  • Leukotrienes and Prostaglandin D2
    • bronchoconstriction & vasodilation
  • Cytokines
    • Inflammation
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23
Q

Type I Hypersensitivity Major Reactions

A
  • Local allergic reaction
  • Systemic Reaction
  • Chronic inflammation
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24
Q

Type I

Local allergic reaction

(4)

A
  1. Rhinitis
  2. Uticaria
  3. Dental Allergy
  4. Drug Allergy
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25
Q

Type I

Systemic Reaction

A
  • A rapid, vascular and smooth muscle reaction
  • Anaphylaxis (severe)
    • Vasodilation: fall in BP
    • Bronchoconstriction: shortness in breath
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26
Q

treatment of anaphylaxis

A
  • epinephrine
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27
Q

type I chronic inflammation examples

A
  • asthma
  • atopic dermatitis
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28
Q

Atopic Allergy

A
  • genetic predisposition to have high IgE level by inheritance of
    • HLA genes
    • Cytokine genes
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29
Q

Diagnosis of Allergy

A
  • History of signs and symptoms
  • Family history
  • Detection of allergen specific IgE Antibody
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30
Q

How to detect IgE (responsible for allergic symptoms) via testing

A
  • In Vivo Tests
    • In patient’s body
    • ​determines allergen-specific IgG in patient
    • prick test and intradermal test
  • In Vitro Tests
    • blood sample
    • RAST
    • ELISA
    • Determines IgE total/ for a specific allergen
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31
Q

Another name for Type IV ?

A

Delayed-type Hypersensitivity

(DTH)

32
Q

DTH is primarly a

A

CD4+ T helper cell-mediated inflammatory response

(not antibody dependent)

33
Q

DTH is encountered in

A

(type IV)

  • Allergic contact dermatitis (ACD)
  • Allergic reactions
  • Tuberculin-type hypersensitivity
  • Granulomatous formation
  • Rejection of transplanted tissue
34
Q

ACD

A
  • Allergic contact dermatitis
  • resulting from sensitization to chemicals including dental chemicals
  • type IV/DTH
35
Q

Dental Chemicals

A
  • Glutaraldehyde
  • Methacrylates
  • Epoxy Resins
  • Metals (nickel)
  • Antimicrobials
  • chemicals found in latex/synthetic gloves
36
Q

granulomatous formation examples

A
  • TB
  • Leprosy
37
Q

Sensitization portion of Hypersensitivity reactions

A
  • Present small molecule-protein conjuagtes to CD4 T cells
  • T cell activation and memory T cell formation
  • Dendritic cells
    • Take up small molecule modified with protein Antigen
38
Q

Elicitation of hypersensitivity reaction

A
  • Subsequent exposure to the same contact Ag leads
    • Rapid secretion of pro-inflammatory cytokines: TNF alpha, IL-1
    • Recruitment of effector T cells, monocytes and macrophages to the site of inflamation
39
Q

Type IV

Granuloma Formation triggered by

A

CD4 T cell response to pathoges

40
Q

In type IV what happens when the the Immue Response fails to kill and clear the pathogens

A
  • persistent antigenic stimulation produces chronic delyaed-type hypersensitivity reactions
  • Chronic granuloma
41
Q

chronic granuloma

A

an attempt by the body to wall off the pathogen

42
Q

Examples of granuloma formation

(type IV)

A

Leprosy

tuberculosis

Measles

Herpes

43
Q

granuloma forms by

A

macrophage engulfs the pathogens that are now repicating in the macrophage.

Macrophage just contains

pathogens will still release antigens

44
Q

contact dermatitis caused by

A
  • small molecules such as nickel usually too small to be antigenic
45
Q

haptens conjugate with

A

lipophilic an conjugate with self proteins

46
Q

contact dermatitis caused by small molecule sensitization reaction

A
  • small molecule conjugate with self proteins
  • Langerhans’ cells (skin) take up conjugates and present to Th-cells
  • Lead to Allergic Contact Dermatitis (ACD)
47
Q

what is common and obsereved to form of ACD in periodontal procendures

A

Nickel Allergy

(TLR4 binds to nickel and cause inflammation)

48
Q

ACD caused by

A

small molecules contact allergens

49
Q

Nickel sensitivity due to

A

Eczema

ACD

50
Q

Mixed Mechanisms hypersensitivity

A

late phase of the type I reactions in asthma and atopic dermatitis are mediated by cells causing inflammation, typical of Type IV reaction

51
Q

How are mixed mechainisms for asthma and atopic dermatitis treated?

A

NSAIDs

steroids controlling inflammation

patient counseling: allergen avoidance

52
Q

occupation based allergies

A
  • NRL protein induces ACD
  • no cure
  • Avoid
53
Q

Treatment for allergic reactions Type I/ Type IV

A
  1. Environmental Measures( avoid exposure)
  2. Pharmacologic Intervention
  3. Allergen Immunotherapy( desensitization to allergen)
54
Q

Type I and IV Pharmacologic Intervention

A
  • Antihistamines
  • Adrenergic agents
  • Corticosteroids
55
Q

Antihistamines function

A

H1 receptor antagonists block binding of histamine to cells

56
Q

Adrenergic agents function

A

Beta receptor agonists, bronchiole smooth muscle relaxant, elevation of cAMP

Epinephrine (adrenaline)

57
Q

Corticosteroids function

A

anti-inflammatory, prednisone, hydrocortisone

Fluticasone (Advair)

58
Q

Treatment for poisin ivy

A
  • Contact dermatitis type of DTH
  • corticosteroid- containing topical cream
  • oral corticosteroid prednisone
59
Q

Allergic Oral Mucosal Reactions

A
  1. Recurrent Aphthous Stomatitis (RAS) recurrent Aphthous Ulcerations (RAU)/ Canker Sores
  2. Oralfacial Granulomatosis
  3. Wegener’s Granulomatosis
60
Q

Which the the most common oral mucosal pathology?

What is it caused by?

A

Recurrent Aphthous Stomatitis (RAS) recurrent Aphthous Ulcerations (RAU)/ Canker Sores

variety of caustive agents ( not just one)

61
Q

RAS/RAU/Canker Sores

Pathophysiology

A
  • mucosal destruction thru a T cell- mediated reaction
  • Decrease ratio of CD4+ : CD8+ T lymphocytes
  • Increased TNF-alpha level
  • ADCC
62
Q

Aphthous Stomatitis increases because

(AS)

A
  • Genetic Predisposition (HLA-B12)
  • Stress and travel
  • AIDS
63
Q

Pathogenic involvement in RAS/RAU Canker sores

A
  • Streptococci
  • Herpes Simple Virus (HSV)
  • Varicella-Zostert virus (VZV)
  • Adenovirus
  • Cytomegalovirus (CMV)
64
Q

Three clinical variations of AS are

A
  • Minor Most Common
  • Major
  • Herpetiform
65
Q

Treatments of RAS/RAU Canker sores

A
  • Topical Corticosteroids
  • Betamethasone Syrup
  • 0.01% dexamethasone
66
Q

Major Aphthous Ulcerations

(MAU)

A
  • Large ulceration
  • treated by betamethasone syrup
67
Q

Orofacial Granulomatosis

cause

symptomns

Histopathology

A
  • similar to aphthous stomatitis
  • cause is idiopathic (unknown)
  • Gingiva swell,
  • erythema, pain, oral lesions (variable)
  • Hist: granulomatous inflammation
68
Q

Treatment of Orofacial Granulomatosis

A
  • Find cause
  • treat with variable drugs
    • Antibotics
    • Intralesional triamcinolone (Corticosteroids)
    • radiotherapy
69
Q

what disease causes the lip to swell?

A

Orofacial Granulomatosis

70
Q

Wegener’s Granulomatosis causes

A
  • Unknown cause
  • Necrotizing granulomatous lesions on respiratory tract
  • Necrotizing glomerulonephritisn
  • Systemic Vasculitis
  • Leads to renal involvement at an advanced stage of the disease
71
Q

Wegener’s Granulomatosis

Drug treatment

A

Cyclophosphamide

Prednisone

72
Q

What disease has Hemorrhagic gingiva (strawberry gingivitis)

Heavy inflammatory infiltrate of lymph, PMN etc?

A

Wegener’s granulomatosis

73
Q

Allergic Mucosal Reactions to Systemic Drug Administration

A
  • medications can cause potiental intraoral complicatons
  • 150 prescribed medicatoin associated with 46 oral side effects
74
Q

Oxaprozin

A
  • Drug causes irregular erosion of the ventral surface of the tongue
75
Q

Allopurinol

A
  • Lichenoid drug reaction
  • superficail erosion and lesions on tounge
76
Q

Oral Lichenoid Eruption due to

A

drug therapy for Insomnia and mood swings

77
Q

In suspected lupus-like drug reactions

A
  • Evaluation for ANA, dsDNA, and histones

Mandal (7 decks)

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