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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
Type I Systemic Reaction
* A rapid, vascular and smooth muscle reaction * Anaphylaxis (severe) * Vasodilation: fall in BP * Bronchoconstriction: shortness in breath
26
treatment of anaphylaxis
* epinephrine
27
type I chronic inflammation examples
* asthma * atopic dermatitis
28
Atopic Allergy
* genetic predisposition to have **high IgE** level by inheritance of * HLA genes * Cytokine genes
29
Diagnosis of Allergy
* History of signs and symptoms * Family history * Detection of allergen specific IgE Antibody
30
How to detect IgE (responsible for allergic symptoms) via testing
* 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
31
Another name for Type IV ?
Delayed-type Hypersensitivity | (DTH)
32
DTH is primarly a
CD4+ T helper cell-mediated inflammatory response (not antibody dependent)
33
DTH is encountered in
(type IV) * Allergic contact dermatitis (ACD) * Allergic reactions * Tuberculin-type hypersensitivity * Granulomatous formation * Rejection of transplanted tissue
34
ACD
* Allergic contact dermatitis * resulting from sensitization to chemicals including dental chemicals * type IV/DTH
35
Dental Chemicals
* Glutaraldehyde * Methacrylates * Epoxy Resins * Metals (nickel) * Antimicrobials * chemicals found in latex/synthetic gloves
36
granulomatous formation examples
* TB * Leprosy
37
Sensitization portion of Hypersensitivity reactions
* 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
Elicitation of hypersensitivity reaction
* 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
Type IV Granuloma Formation triggered by
CD4 T cell response to pathoges
40
In type IV what happens when the the Immue Response fails to kill and clear the pathogens
* persistent antigenic stimulation produces chronic delyaed-type hypersensitivity reactions * Chronic granuloma
41
chronic granuloma
an attempt by the body to wall off the pathogen
42
Examples of granuloma formation | (type IV)
Leprosy tuberculosis Measles Herpes
43
granuloma forms by
macrophage engulfs the pathogens that are now repicating in the macrophage. Macrophage just contains pathogens will still release antigens
44
contact dermatitis caused by
* small molecules such as nickel usually too small to be antigenic
45
haptens conjugate with
lipophilic an conjugate with self proteins
46
contact dermatitis caused by small molecule sensitization reaction
* small molecule conjugate with self proteins * Langerhans' cells (skin) take up conjugates and present to Th-cells * Lead to Allergic Contact Dermatitis (ACD)
47
what is common and obsereved to form of ACD in periodontal procendures
Nickel Allergy (TLR4 binds to nickel and cause inflammation)
48
ACD caused by
small molecules contact allergens
49
Nickel sensitivity due to
Eczema ACD
50
Mixed Mechanisms hypersensitivity
late phase of the type I reactions in asthma and atopic dermatitis are mediated by cells causing inflammation, typical of Type IV reaction
51
How are mixed mechainisms for asthma and atopic dermatitis treated?
NSAIDs steroids controlling inflammation patient counseling: allergen avoidance
52
occupation based allergies
* NRL protein induces ACD * no cure * Avoid
53
Treatment for allergic reactions Type I/ Type IV
1. Environmental Measures( avoid exposure) 2. Pharmacologic Intervention 3. Allergen Immunotherapy( desensitization to allergen)
54
Type I and IV Pharmacologic Intervention
* Antihistamines * Adrenergic agents * Corticosteroids
55
Antihistamines function
H1 receptor antagonists block binding of histamine to cells
56
Adrenergic agents function
Beta receptor agonists, bronchiole smooth muscle relaxant, elevation of cAMP Epinephrine (adrenaline)
57
Corticosteroids function
anti-inflammatory, prednisone, hydrocortisone Fluticasone (Advair)
58
Treatment for poisin ivy
* Contact dermatitis type of DTH * corticosteroid- containing topical cream * oral corticosteroid prednisone
59
Allergic Oral Mucosal Reactions
1. Recurrent Aphthous Stomatitis (RAS) recurrent Aphthous Ulcerations (RAU)/ Canker Sores 2. Oralfacial Granulomatosis 3. Wegener's Granulomatosis
60
Which the the most common oral mucosal pathology? What is it caused by?
Recurrent Aphthous Stomatitis (RAS) recurrent Aphthous Ulcerations (RAU)/ Canker Sores variety of caustive agents ( not just one)
61
RAS/RAU/Canker Sores Pathophysiology
* mucosal destruction thru a T cell- mediated reaction * Decrease ratio of CD4+ : CD8+ T lymphocytes * Increased TNF-alpha level * ADCC
62
Aphthous Stomatitis increases because | (AS)
* Genetic Predisposition (HLA-B12) * Stress and travel * AIDS
63
Pathogenic involvement in RAS/RAU Canker sores
* Streptococci * Herpes Simple Virus (HSV) * Varicella-Zostert virus (VZV) * Adenovirus * Cytomegalovirus (CMV)
64
Three clinical variations of AS are
* Minor Most Common * Major * Herpetiform
65
Treatments of RAS/RAU Canker sores
* Topical Corticosteroids * Betamethasone Syrup * 0.01% dexamethasone
66
Major Aphthous Ulcerations | (MAU)
* Large ulceration * treated by betamethasone syrup
67
Orofacial Granulomatosis cause symptomns Histopathology
* similar to aphthous stomatitis * cause is idiopathic (unknown) * Gingiva swell, * erythema, pain, oral lesions (variable) * Hist: granulomatous inflammation
68
Treatment of Orofacial Granulomatosis
* Find cause * treat with variable drugs * Antibotics * Intralesional triamcinolone (Corticosteroids) * radiotherapy
69
what disease causes the lip to swell?
Orofacial Granulomatosis
70
Wegener's Granulomatosis causes
* Unknown cause * Necrotizing granulomatous lesions on respiratory tract * Necrotizing glomerulonephritisn * Systemic Vasculitis * Leads to renal involvement at an advanced stage of the disease
71
Wegener's Granulomatosis Drug treatment
Cyclophosphamide Prednisone
72
What disease has Hemorrhagic gingiva (strawberry gingivitis) Heavy inflammatory infiltrate of lymph, PMN etc?
Wegener's granulomatosis
73
Allergic Mucosal Reactions to Systemic Drug Administration
* medications can cause potiental intraoral complicatons * 150 prescribed medicatoin associated with 46 oral side effects
74
Oxaprozin
* Drug causes irregular erosion of the ventral surface of the tongue
75
Allopurinol
* Lichenoid drug reaction * superficail erosion and lesions on tounge
76
Oral Lichenoid Eruption due to
drug therapy for Insomnia and mood swings
77
In suspected lupus-like drug reactions
* Evaluation for ANA, dsDNA, and histones

Mandal (7 decks)

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