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DEN 7102 Micro & Immuno Concepts > Exam 3 - Hypersensitivity and Autoimmunity Part 1 > Flashcards

Exam 3 - Hypersensitivity and Autoimmunity Part 1 Flashcards

1
Q

Helminthic infection

A

Worm/parasite infection

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2
Q

True or false: eosinophils are PMN

A

True

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3
Q

Eosinophils stain with

A

Eosin

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4
Q

Helminthic infections stimulate ___ in the GI

A

Th2 response

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5
Q

In a helminthic infection, ____ can coat eggs and helminths to prevent _____

A

IgA and IgM; Prevent new adherence and further colonization

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6
Q

___ produces distinct response to adherent helminths that break the mucosal barrier

A

IgE

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7
Q

IgE is associated with

A

Atopic, allergic response

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8
Q

IgE ___ domain binds to ____ on basophils and mast cells

A

CH4 (extra CH domain); Fce receptors

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9
Q

FceRI receptor on eosinophils is ____

A

High affinity

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10
Q

FceRII receptor on eosinophils is ____

A

Low affinity

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11
Q

FceRI receptor on basophils and mast cells is ____

A

High affinity

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12
Q

Eosinophils, basophils, and mast cells are found in high concentrations in:

A
  • skin
  • respiratory tract
  • GI tract
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13
Q

FceRI degranulation releases _____ which are toxic to ____

A

major basic protein and eosinophil cationic protein; helminths

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14
Q

In addition to major basic protein and eosinophil cationic protein, eosinophils also contain:

A
  • histamine
  • lactoferrin
  • lysozyme
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15
Q

What is associated with atopic (allergic) response?

A
  • Type I hypersensitivity
  • Anaphylaxis
  • Elevated IgE levels
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16
Q

Type I hypersensitivity is ___ mediated

A

IgE

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17
Q

Routes of allergen encounter

A
  • inhalation
  • contact
  • ingestion
  • injection
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18
Q

Type I hypersensitivity may include:

A

Anaphylaxis

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19
Q

Common contact allergens

A
  • latex gloves
  • dental dam
  • condoms
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20
Q

Common ingested allergen

A

Antibiotics

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21
Q

Sensitization

A

process of coating mast cell with IgE, becoming sensitive to activation by subsequent encounter of that antigen

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22
Q

IgE is bound to mast cells for how long?

A

12-14 days

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23
Q

Antibodies that bind to cells like mast cells are known as

A

Cytotrophic antibodies

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24
Q

When the IgE + Mast Cell complex encounters the antigen again it causes:

A

Immediate degranulation (overwhelming and inappropriate response)

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25
Q

Immediate phase response during Type I hypersensitivity includes

A
  • rapid degranulation
  • histamine
  • heparin
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26
Q

Delayed phase response in Type I hypersensitivity includes

A
  • lipid mediators (arachidonic acid metabolites PGE2, PGD2, LB4)
  • cytokines
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27
Q

Immediate phase Type I hypersensitivity occurs ___ after exposure

A

5-30 min

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28
Q

What happens during immediate phase Type I hypersensitivity

A
  • mast cell (tissue) degranulation
  • may cause anaphylaxis if systemic degranulation (basophil)
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29
Q

Delayed phase Type I hypersensitivity occurs after ____

A
  • 8-12 hours (lipid mediators)
  • days to weeks (cytokines)
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30
Q

What happens during delayed phase Type I hypersensitivity

A
  • inflammatory cell infiltration
  • continual symptoms
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31
Q

Vasoactive amines

A
  • histamines
  • blood vessel dilation
  • vascular permeability
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32
Q

Histamines have what receptors

A

H1-H4

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33
Q

Chemotactic factors

A
  • Eosinophil chemotactic factor
  • neutrophil chemotactic factor
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34
Q

Heparin, Vasoactive amines, and chemotactic factors are examples of

A

Immediate (acute) mediators

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35
Q

H1R (histamine receptor) is located on:

A
  • smooth muscle
  • endothelium
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36
Q

Activation of H1R causes:

A
  • vasodilation and mucosal secretion
  • venule, capillary permeability
  • bronchial, gut constriction
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37
Q

H4R histamine receptor is located on

A

Basophils and mast cells

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38
Q

Activation of H4R causes:

A

mediation of chemotaxis and inflammation

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39
Q

Prostaglandin E2/PGD2

A

Increases vasodilation

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40
Q

Leukotriene B4

A

Chemoattraction of PMN

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41
Q

Lipoxin A4

A

Inhibits inflammation and chemotaxis

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42
Q

Type I hypersensitivity produces a ____ response to a _____ and an abnormally high response to an ____

A

abnormal; non-allergen; allergen

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43
Q

Type I hypersensitivity - mechanism

A
  • overproduction of IgE
  • priming of mast cells via FceRI
  • increases IgE half life
  • Degranulation releases histamine
  • causes inflammation
  • leads to production of arachidonic acid metabolites
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44
Q

Clinical manifestation of Type I Hypersensitivity

A
  • Urticaria
  • Edema
  • Erythema
  • Rhinorrhea
  • Bronchoconstriction
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45
Q

Urticaria

A

Hives (intraoral or dermal)

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46
Q

Edema

A

Swelling

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47
Q

Erythema

A

Redness

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48
Q

Rhinorrhea

A

Runny nose

49
Q

Bronchoconstriction

A

Shortness of breath

50
Q

Clinical diagnosis of allergies

A
  • Immunologic testing: skin test involves wheal and flare
  • Abnormal IgE serum levels
  • abnormal eosinophil count
  • Eosinophils in sputum
51
Q

Wheal

A

Granular response (histamine)

52
Q

Flare

A

Inflammatory response (PGE2, LB4)

53
Q

OTC antihistamines - name

A

Diphenhydramine

54
Q

Diphenhydramine is commonly used for ____ and competes with histamine for ____

A

hay fever and nasal allergies; H1 receptor

55
Q

Prescription anti-inflammatory medications

A
  • leukotriene receptor antagonists (Singulair)
  • Epinephrine or bronchodilators (Primatene mist)
  • Cromolyn sodium (blocks calcium influx, mast cells)
  • Asthma inhaler (inhibits degranulation)
56
Q

Hyposensitization

A

Repeated administration of sub-clinical allergen dose

57
Q

Type II hypersensitivity is ____ mediated

A

Antibody (IgG)

58
Q

Type II hypersensitivity is often called:

A

Cytotoxic hypersensitivity

59
Q

Rhesus disease is also called

A

Erythroblastosis fetalis; hydrops fetalis

60
Q

Most common cause of Rhesus disease is:

A

Rhesus incompatibility

61
Q

In Rhesus disease during pregnancy, mother is ____ and baby is ____

A

Rh -; Rh +

62
Q

Can Rhesus disease be prevented?

A

Yes - Rhogam

63
Q

Rhesus disease - subsequent children

A

IgG can be transferred to fetus

64
Q

Rhesus disease diagnosis via:

A

Coombs test

65
Q

Rheumatic fever involves:

A

Group A Strep

66
Q

Rheumatic fever is associated with antibody response to ____ which has structural similarity to some ____

A

protein M; cardiac antigens

molecular mimicry

67
Q

Some people with rheumatic fever develop immune response against

A

Cardiac antigens

68
Q

Diseases related to Type II hypersensitivity

A
  • Hemolytic disease of the newborn (Rhesus disease)
  • Rheumatic fever
  • Sympathetic Opthalmia
  • Drug-induced hemolytic anemia
69
Q

Sympathetic opthalmia is a form of

A

Uveitis

70
Q

What causes sympathetic opthalmia

A
  • Penetrating injury to the eye that releases sequestered antigens
  • ocular antigens stimulate conjunctival lymphatics
  • IgG and lymphocytes return via blood vessels
  • can damage eye, cause blindness
71
Q

Drug-induced hemolytic anemia includes what drugs

A
  • a-methyldopa
  • ibuprofen
  • pencillin
  • cephalosporins
  • quinine
72
Q

Drug-induced hemolytic anemia can modify or bind:

A
  • modify Rhesus antigens
  • bind erythrocytes
73
Q

What happens to RBC in drug-induced hemolytic anemia?

A

antibodies destroy RBC in presence of drug

74
Q

Treatment of drug-induced hemolytic anemia

A
  • removal of causative agent (drug)
  • treatment with prednisone (corticosteroid) if needed
75
Q

Gra’es disease, also known as ____, affects the ____

A

Toxic diffuse goiter; affects thyroid

76
Q

Grave’s disease - agonist

A

Thyroid stimulating immunoglobulin (TSI) to TSH receptor

77
Q

Most common cause of hyperthyroidism in the US

A

Grave’s disease (50-80% cases)

78
Q

Grave’s disease RR for female:male

A

7:1

79
Q

Most common symptoms of Grave’s disease

A
  • elevated levels of T3 and T4; low TSH
  • Exopthalmos (periorbital edma, bulding eyes)
80
Q

Hashimoto’s disease also known as

A

Hashimoto’s thyroiditis

81
Q

Most common cause of hypo-thyroidism in the US

A

Hashimoto’s disease

82
Q

Hashimoto’s disease - most common symptoms include:

A
  • weight gain
  • fatigue
  • depression
  • cold intolerance
  • constipation
83
Q

Goodpasture syndrome is known as ____ disease

A

Anti-globular basement membrane disease

84
Q

Goodpasture syndrome - most auto-antibodies are to:

A

alpba-3 subunit of Type IV collagen

85
Q

Goodpasture syndrome antibodies against:

A

Basement membrane in lung and kidneys

May lead to permanent lung, kidney damage, or death

86
Q

Pernicious anemia is a form of

A

Vitamin B12 deficiency

87
Q

In pernicious anemia, antibodies are formed against:

A

Gastric intrinsic factor (GIF) which is needed for B12 absorption

88
Q

Pernicious anemia can lead to

A

Macrolytic or megaloblastic anemia

89
Q

Common symptoms of pernicious anemia

A
  • pallor, low grade fever, weight loss, tingling, numbness
  • Glossitis (inflammation and depapillation of tongue)
90
Q

Pernicious anemia prevalence

A

400,000 in US; age-associated (>50)

91
Q

Myasthenia gravis is a

A

Long term neuromuscular disease

92
Q

Myasthenia gravis: autoimmune antibodies against

A

Nicotinic Ach receptors; prevents nerve impulses from triggering muscle contractions

93
Q

Myasthenia gravis symptoms

A
  • ptosis (drooping upper eyelid)
  • dysphagia (swallowing difficulties)
  • hanging jaw/facial weakness
94
Q

Myasthenia gravis is more common in:

A

women; ages 50-70

95
Q

Sjogren’s syndrome

A

Autoimmune disorder or moisture producing glands

96
Q

What is affected in Sjogren’s syndrome

A
  • Sjogren syndrome autoantibodies (SSA)
  • salivary and lachrymal (exocrine) glands
97
Q

Primary manifestation of Sjogren’s syndrome

A
  • xerostomia: dry mouth
  • keratoconjunctivitis sicca (KCS): dry eyes
98
Q

Tx for Sjogren’s syndrome

A
  • artificial tears/saliva
  • Pilocarpine may be used
99
Q

Sjogren’s syndrome characterized by:

A

CD4+ T cell and B cell infiltrate

100
Q

Lymphocytic infiltrate associated with:

A

Exocrine glands (salivary, lachrymal)

101
Q

Xerostomia increases:

A

Caries risk (500,000-2,000,000)

102
Q

Linear IgA disease

A

Linear IgA deposition in basement membrane zone (BMZ)

103
Q

True or false: Linear IgA is a type of Type II hypersensitivity

A

True even though it’s IgA and not IgG

104
Q

Linear IgA may present similar to

A

EBA

105
Q

There is a drug induced form of Linear IgA disease, called

A

vancomycin-induced Stevens-Johnson syndrome

106
Q

EBA antibodies against:

A

Auto-immunity IgG against type 7 collagen

107
Q

EBA disorder characterized by

A
  • blisters in skin or mucosa
  • can be spontaneous or trauma induced
  • occurs in areas of high contact (feet, hand, mouth)
108
Q

Pemphigus is:

A

Group of rare autoimmune blistering diseases

109
Q

Pemphigus antibodies against

A

Autoantibodies IgG against desmoglein - causes separation between cells

110
Q

Pemphigus vulgaris against:

A

Desmoglein 3

111
Q

Pemphigus foliaceus against:

A

Desmoglein-1

112
Q

Pemphigus vulgaris mostly affects desmosomes of

A

stratified squamous epithelium

113
Q

Pemphigus vulgaris - lesions may form on

A

Tongue and palate

114
Q

Pemphigoid

A

Antibodies are to BP-1 hemidesmosome in basement membrane

115
Q

____ can have cicatricial presentation (no skin involved)

A

Pemphigoid

116
Q

_____ rarely affects the mouth - mostly the skin

A

Bullous pemphigoid

117
Q

Bullous pemphigoid and Cicatricial pemphigoid can both be classified as

A

Type II hypersensitivity

118
Q

Cicatricial pemphigoid commonly presents in the ___ and can cause ____

A

mouth; desquamative gingivitis

119
Q

Bullous pemphigoid most commonly manifests in:

A

Skin lesions

DEN 7102 Micro & Immuno Concepts (26 decks)

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