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ENT Board Study > Immunology/Allergy > Flashcards

Immunology/Allergy Flashcards

1
Q

What is an antigen?

A

Any molecule that can be specifically recognized by the specific immune system

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2
Q

What is an antibody?

A

Specific Ig produced by a specific B cell that recognizes and binds to specific antigens that are recognized as non-self

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3
Q

Where does the thymus develop from?

A

Third and fourth pharyngeal pouches

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4
Q

How is the thymus critical for the immune system?

A

Critical for major histocompatibility complex restriction (MHC) which is imposed on lymphoid precursors arising form the yolk sac, fetal liver, and bone marrow

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5
Q

Where do T-cells develop?

A

Thymus

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6
Q

What are the members of the secondary lymphoid system?

A

Waldeyer ring, lymph nodes, spleen, mucosa-associated lymphoid tissue

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7
Q

Where are B-cells primarily found in the lymph node?

A

Cortex and medulla

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8
Q

Where are T-cells primarily found in the lymph node?

A

Paracortex and medulla

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9
Q

What kind of Ig is produced by MALT?

A

Secretory IgA

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10
Q

CD2 and CD3 differentiate what types of cells?

A

All T-cells

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11
Q

Which types of T-cells have CD4?

A

Helper T-cells

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12
Q

What are helper T-cells responsible for?

A

Augmenting the interactions between T-T, T-B, and T-macrophage cells

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13
Q

Allergic inflammation is characterized by a TH1 or a TH2 response?

A

TH2

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14
Q

What do TH1 cells produce?

A

IL-2 and IFN-gamma

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15
Q

Do TH1 cells stimulate or inhibit B-cells?

A

Inhibit

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16
Q

What do TH2 cells produce?

A

IL-4, 5, 6, and 10

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17
Q

Do TH2 cells stimulate or inhibit B-cells?

A

Stimulate

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18
Q

CD8 T-cells function by doing what?

A

Specific killing of target cells, inhibit the response of B-cells and other T-cells

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19
Q

Which MHCs are associated with helper T-cells?

A

MHC II

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20
Q

What MHCs are associated with cytotoxic T-cells?

A

MHC I

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21
Q

In order for proper antigen recognition, what must an antigen be presented with?

A

MHC on the antigen-presenting cell

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22
Q

What induces proliferation of both T- and B-cells?

A

IL-1

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23
Q

What type of MHC is on the surface of B-cells?

A

MHC Class II

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24
Q

Which CD molecules are on B-cells?

A

CD 19, 20, 22

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25
Q

What is the purpose of NK cells?

A

Eliminate cells that become spontaneously malignant or are infected with virus

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26
Q

What type of receptors are on NK cells?

A

IgG receptors

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27
Q

Which CD molecules are on NK cells?

A

CD 16, 56

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28
Q

What is the principle function of the MHC?

A

Bind fragments of foreign protein to form complexes recognized by T-cells

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29
Q

How are endogenous antigens processed?

A

Pass through rough endoplasmic reticulum and are associated with MHC Class I molecules

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30
Q

How are exogenous antigens processed?

A

Hydrolyzed and associated with MHC Class II molecules

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31
Q

Where are MHC Class I molecules found?

A

On nearly all nucleated cells

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32
Q

Where are MHC Class II molecules found?

A

B-cells, macrophages of dendritic cells, endothelial cells

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33
Q

Which cells are responsible for producing IFN-alpha?

A

Leukocytes

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34
Q

How does IFN-alpha work?

A

Decreases viral replication and increases cell membrane proteins

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35
Q

Which cells produce IFN-beta?

A

Fibroblasts and epithelial cells

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36
Q

What are the functions of IFN-beta?

A

Decreases viral replication and increases cell membrane proteins

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37
Q

Which cells produce IFN-gamma?

A

Activated T-cells and NK cells

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38
Q

What are the functions of IFN-gamma?

A

Increases expression of cell membrane antigens, including Class I and II HLA and Fc receptors; potent activator of eosinophils

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39
Q

Clinically significant allergen-induced reactions are mediated by what?

A

IgE

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40
Q

What causes the immediate allergic reaction?

A

Release of mast cell mediators and proteases

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41
Q

When does the late phase of an allergic reaction begin?

A

Three to four hours after the immediate response

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42
Q

What is the significance of the IgE-mediated late phase response?

A

Thought to play a role in the triggering of allergic diseases such as asthma, atopic dermatitis, and allergic rhinitis

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43
Q

What cytokines are usually released after IgE cross-linking?

A

IL1, IL3, IL4, IL5, IL6, GM-CSF, and TNF-alpha

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44
Q

How does IL-4 affect T-cell proliferation?

A

Induces differentiation into a TH2 phenotype

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45
Q

How does IL-4 affect B-cells?

A

Enhances B-cell growth and antigen presentation of B-cells

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46
Q

What is the role of IL-13 in the allergic response?

A

Has IL-4 like activities on B-cells and monocyts and induces IgE isotype switching

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47
Q

What is the primary role of IL-5 in the allergic response?

A
  • Promotes differentiation of eosinophils
    • Chemotactic factor
    • Activates mature eosinophils
    • Reduces apoptosis
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48
Q

What cells act as antigen-presenting cells?

A
  • Macrophages
  • Endothelial cells
  • Dendritic cells found in the:
    • Skin & mucosa
    • Lymph node
    • Spleen
    • Thymus
  • Glia
  • Activated B-cells
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49
Q

What major cytokine is released by macrophages after antigen exposure?

A

IL-1, which stimulates precursor TH cell to develop into a mature TH

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50
Q

What is a Type I Gell & Coombs allergic reaction?

A

Occurs after cross-linking of IgE on mast cells leading to degranulation. Memory cells exposued to the allergen produce more IgE

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51
Q

What is a Type II Gell & Coombs allergic reaction?

A
  • First exposure-allergen induces a B-cell response with production of allergen
  • Second exposure-antibodies bind to cell surfaces expressing the allergen
    • Complement is activated and cell is lysed
    • The attached antibodies act as an opsonin and phagocytic cells are attracted
    • Damage is tissue-specific
  • Unclear if Type II reactions produce allergic symptoms
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52
Q

What is a Type III Gell & Coombs allergic reaction?

A
  • First exposure-allergen induces a B-cell response with production of antibodies
  • Second exposure-allergen circulating in the blood binds to the antibody to create an immune complex
    • When large quantities accumulate, they cannot be easily removed by the reticuloendothelial system
    • Complexes attached to small vessel endothelium and initiate a inflammatory response through complement activation
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53
Q

What is a Type IV Gell & Coombs allergic reaction?

A
  • First exposure-allergen sensitizes T cells
  • Second exposure-allergen is detected on a target cell surface
    • Previously sensitized T-cells lyse the target cell
    • Inflammatory response initiated
54
Q

What intracellular signalling pathway is used by mast cells for release of mediators?

A

cAMP/cGMP and calcium

55
Q

What is the major precursor to both prostaglandins and leukotrienes?

A

Arachadonic acid

56
Q

During metabolism of arachadonic acid, which pathway leads to production of leukotrienes?

A

Lipoxygenase

57
Q

During metabolism of arachadonic acid, which pathway leads to production of prostaglandins?

A

Cyclo-oxygenase

58
Q

What are the four major effects of histamine?

A
  1. Vasodilation
  2. Increased capillary permeability
  3. Bronchoconstriction
  4. Tissue edema
59
Q

Where are type 1 histamine receptors located?

A

Smooth muscle of vessels, bronchi, goblet cells, and GI mucosa

60
Q

Where are type 2 histamine receptors located?

A

Suppressor T-cells, basophils, mast cells, neutrophils, gastric cells

61
Q

What is the role of heparin in an allergic response?

A

Released by mast cells and causes histamine suppression, increased phagocytosis, and anticoagulation

62
Q

What is the role of leukotrienes in the allergic response?

A

Vasoactive, chemotaxis, bronchoconstriction

63
Q

What is the role of prostaglandins in the allergic response?

A

Bronchoconstriction, platelet aggregation, vasodilation

64
Q

What are Dennie’s lines?

A

Fine horizontal lines in the lower eyelids

65
Q

What are ocular clinical signs of allergies?

A
  • Allergic shiners
  • Dennie’s lines
  • Conjunctivitis
  • Lymphoid aggregates on the palpebral conjunctiva
66
Q

What are nasal clinical signs of allergies?

A
  • Itching
  • Allergic salute
  • Facial grimace
  • Nasal obstruction
  • Sneezing
67
Q

What are oral clinical signs of allergies?

A
  • Chronic mouth breathing secondary to nasal airway obstruction
  • Nocturnal tooth grinding
68
Q

What are pharyngeal clinical signs of allergies?

A
  • Dry, irritated, sore throat
  • Repeated throat clearing
  • Cobblestoning
69
Q

What are airway clinical signs of allergies?

A
  • Hoarseness
  • Asthma
  • Wet cough, especially with mold allergy
70
Q

What is house dust composed of?

A

Mites, cockroach, cotton particles, human scales

71
Q

What is the major allergenic component from dust mites?

A

Feces

72
Q

What is it that makes cats allergenic?

A

Fel D1 antigen produced in sebaceous glands and shed on skin scales

73
Q

What are the primary molds that cause allergic symptoms?

A

Aspergillus, Penicillium, Alternaria, Cephalosporium

74
Q

What is the first screening tool used for allergy testing?

A

Epicutaneous prick testing

75
Q

How is skin prick testing performed?

A

Antigen is inserted into the skin via a sterile #26 gauge needle

76
Q

What are the positive and negative controls used in skin prick testing?

A
  • Positive-histamine
  • Negative-glyercine
77
Q

What are the advantages to skin prick testing?

A
  • Rapid
  • Better correlation with intradermal tests
  • Relatively safe
78
Q

What are the disadvantages to skin prick testing?

A
  • Qualitative measure of allergy only (yes vs. no)
  • Will miss low degree of allergy (increased false negatives)
  • Grading of skin test is subjective
79
Q

What is the Patterson System for scoring skin prick testing?

A
  • Negative-no reaction or no different from control
  • One plus-erythema smaller than a nickel in diameter
  • Two plus-erythema larger than a nickel in diamter with no wheel
  • Three plus-wheal with surrounding erythema
  • Four plus-Wheal with pseudopods and surrounding erythema
80
Q

How many dilutions are made for intradermal dilution titration?

A

6 dilutions that are fivefold diluted compared to the previous

81
Q

Does dilution #1 have a higher or lower concentration of allergen than dilution #6 for IDT?

A

Higher

82
Q

What is standard concentration of the allergen concentrate?

A

1:20

83
Q

What is the concentration of dilution #1 for IDT?

A

1:100

84
Q

When doing IDT, which dilution is injected first?

A

6

85
Q

How much dilution is injected at a time during IDT?

A

0.01 ML, which produces a 4 mm wheal that enlarges (without reaction) to a 5 mm wheal

86
Q

What defines a postive, allergic response during SDET?

A

2 mm of wheal enlargement beyond the size of the original 5 mm wheal

87
Q

What is the endpoint in SDET?

A

The first dilution which yields a wheal at least 2 mm larger than the predecing negative wheal, and which is followed by a wheal at next stronger dilution that is at least 2 mm larger still

88
Q

What are the advantages of SDET?

A
  • Quantitative and qualitative measure
  • Highly reproducible
  • Very sensitive
  • Safe
89
Q

What are the disadvantages of SDET?

A
  • Time-consuming
  • Possible false positives in low degree of allergy
  • More office supplies needed
90
Q

How long should a patient be off of antihistamines before allergy testing?

A

36 hours

91
Q

How long should a patient be off tricyclic antidepressants before skin testing?

A

2-4 days

92
Q

What is the concern with patients being on Beta-blockers when doing allergy testing?

A

If the patient develops an anaphylactic response, you don’t want the beta-adrenergic receptors blocked and hamper the use of epinephrine

93
Q

What does RAST stand for?

A

RadioAllergoSorbent Test

94
Q

What is the purpose of RAST testing?

A

Measure the serum level of allergen-specific IgE

95
Q

How does RAST work?

A
  • A paper disc with antigen on the surface is placed in a test tube and patient serum is added
  • Allergen-specific IgE binds to the antigen on the disc
  • Radiolabeled anti-IgE antibody is added and binds to the patient IgE
  • Amount of bound radiolabel is then measured
96
Q

What are the advantages of RAST testing?

A
  • Eliminates variability of the skin response
  • Eliminates drug effects
  • More specific than skin testing
  • Can be used to determine starting doses for immunotherapy
  • Safe for patients on beta-blockers
97
Q

What are the disadvantages of RAST testing?

A
  • More expensive
  • Requires specialized lab equipment and technician training
  • May be less sensitive than skin testing
98
Q

What are indications for in vitro allergy testing?

A
  • Patients not responding to environmental control and medical management
  • Sytmptomatic patients with conditions in which in vivo skin testing is contraindicated
  • Patients doing poorly on immunotherapy
  • Diagnosis of IgE-mediated food sensitivity
99
Q

What are examples of first generation antihistamines?

A

Benadryl, Chlortrimeton, Phergan, Atarax, Vistaril

100
Q

What are examples of second-generation antihistamines?

A

Claritin, Zyrtec, Allegra

101
Q

Why are first generation antihistamines more sedating than second generation ones?

A

They are lipophilic and able to more easily cross the blood brain barrier

102
Q

What is the disadvantage of systemic decongestants?

A

Alpha-adrenergic effects which can lead to hypertension, decreased appetite, tachycardia & palpitations

103
Q

What is the complication associated with long-term nasal decongestant use?

A

Rhinitis medicamentosa

104
Q

Nasal steroid sprays are considered first-line therapy for what conditions?

A
  • Allergic rhinitis
  • Non-allergic rhinitis
  • Rhinitis medicamentosa
  • Nasal polyps
105
Q

Do systemic corticosteroids have increased efficacy compared to nasal corticosteroids for treatment of allergic rhinitis?

A

Efficacy is equivalent

106
Q

What is the reason for immunotherapy?

A

Leads to reduction in mediator release, antigen-induced eosinophil migration, and clinical symptoms from both immediate and late phase reactions

107
Q

What are the immunologic effects of immunotherapy?

A
  • Rise in serum IgG blocking antibody levels
  • Suppresion of annual season rise in IgE followed by a decline in the level of specific IgE over the course of immunotherapy
  • Increase in IgA and IgG levels in nasal secretions
108
Q

What are the starting doses for immunotherapy?

A
  • 0.05 mL of the endpoint dilution from SDET (dilution that produced the first positive reaction)
  • 0.05 mL of endpoint minus 1 or minus 2 for safety based on RAST
109
Q

How are immunotherapy doses escalated?

A
  • Generally, increasing by 0.05 mL each week is safe
  • Increasing by 0.10 mL each week may be used for weaker dilutions if well tolerated
  • Increasing by 0.20 mL each week may be used for weaker dilutions if shots are given outside of the blooming season
110
Q

How is the maintenance dose decided for immunotherapy?

A
  • Plateau of clinical improvement
  • Control of symptoms for at least one week
  • Local reaction of 2 to 3 cm that lasts for more than 48 hours
111
Q

When can dosing intervals be lengthened from weekly to every 2 or 3 weeks?

A

After the first full year of well-controlled symptoms

112
Q

When can immunotherapy be stopped?

A

After 3 to 5 years of maintenance

113
Q

What are contraindications to immunotherapy?

A
  • Nonimmune mechanism for symptoms
  • IgE-mediated mechanism
  • Mild symptoms easily controlled by conservative therapy
  • Easily avoidable allergen
  • Atopic dermatitis
  • GI food allergies
  • Noncompliant patients
  • Patients taking beta-blockers
  • Infants and children under 2
  • IgE-mediated drug and chemical sensitivity
114
Q

What are the complications of immunotherapy?

A
  • Local reactions-erythema larger than 3 cm with induration and lasting more than 24 hours
  • Worsening of allergic symptoms after a shot
  • Urticaria or angioedema
  • Anaphylactic shock
115
Q

What are the two major types of food allergy?

A

Cyclic & non-cyclic

116
Q

What are the vast majority of food allergies?

A
  • Cyclic
    • 60-95% of cases
    • Symptoms not apparent for 4-48 hours
    • Mostly IgG-mediated, immune complex
117
Q

What defines non-cyclic food allergies?

A
  • 5 to 40% of cases
  • Severity is fixed
  • Does not depend on dose or frequency of ingestion
  • Onset within minutes
  • IgE mediated
118
Q

How is cyclic food allergy diagnosed?

A
  • History-combined with 1 week food diary
  • Oral challenge
    • 4 days of not eating suspect food, evaluate for symptoms after a large amount is eaten
  • Prick testing
    • Many false positives and false negatives
    • Cyclic food allergy is not IgE mediated
  • Provocation (neutralization)
    • Allergen given sublingually, subcutaneously, or subdermally
    • Watch for onset of symptoms or pattern of skin test reactions
119
Q

How does one treat cyclic food allergy?

A
  • Elimination of food
  • Omission for 3 month interals with challenge test feedings for tolerance
  • Omission of the food until tolerance develops will then usually allow gradual reintroduction into the diet
120
Q

What organisms are usually associated with allergic fungal sinusitis?

A

Aspergillus, Bipoaris, Alternaria, Curvularia

121
Q

Name four radiographic features of allergic fungal sinusitis

A
  • Hypercalcified speckling of sinus opacity
  • Thickening of sinus walls
  • Bone erosion
  • Expansion of sinus volumes
122
Q

What are the histopathologic features of allergic fungal sinusitis?

A
  • Allergic mucin with eosinophils
  • Charcot-Leyden crystals
  • Fungal hyphae
123
Q

What is the major treatment of allergic fungal sinusitis?

A

Endoscopic drainage

124
Q

What are the major laryngeal manifestations of SLE?

A
  • Thickening of the vocal folds, hoarseness
  • Perichondritis/chondritis; loss of laryngeal cartilage support
  • Cricothyroid joint arthritis with airway obstruction
125
Q

What are the major nasal manifestations of SLE?

A
  • Butterfly rash over nose and cheeks
  • Nasal septal ulcers
  • Nasal septal perforation
126
Q

What are the major oral cavity manifestations of SLE?

A
  • Superficial ulcers with surrounding erythema
  • Petechiae and hemorrhagic bullae if thrombocytopenia develops
127
Q

What is the difference between primary and secondary Sjogren’s syndrome?

A

Secondary Sjogren’s is exocrine gland dysfunction in conjunction with other autoimmune conditions

128
Q

What are the primary manifestations of Sjogren’s syndrome?

A
  • Keratoconjunctivitis sicca
  • Xerostomia
  • Difficulty swallowing
  • Dental caries
  • Myositis
129
Q

What are the key laboratory markers for Sjogren’s syndrome?

A
  • ANA
  • anti-SSA
  • anti-SSB
  • RF
130
Q

What are the key histopathologic findings for Sjogren’s syndrome?

A

Aggregates of lymphoid proliferation around minor salivary gland remants from the lower lip

131
Q

What are the major ENT manifestations of Rheumatoid arthritis?

A
  • TMJ arthritis
  • Cricoarytenoid joint arthritis
  • Vocal fold thickening
  • Cervical spine subluxation
  • Synovitis of the ossicular chain which leads to erosion rather than fixation

ENT Board Study (3 decks)

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