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Immunology > Immunology Exam 4 (Hypersensitivies and Autoimmune disorders) > Flashcards

Immunology Exam 4 (Hypersensitivies and Autoimmune disorders) Flashcards

1
Q

Hypersensitivity Type I notable diseases

A

Anaphylaxis

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2
Q

Hypersensitivity Type II notable diseases

A

HDFN, transfusion reactions

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3
Q

Hypersensitivity Type III notable diseases

A

SLE, serum sickness, RA, cellular drug reactions

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4
Q

Hypersensitivity Type IV notable diseases

A

Contact dermatitis (poison ivy), PPD

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5
Q

What antibodies are involved in Type IV hypersensitivies?

A

None

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6
Q

What antibodies are involved in Type III hypersensitivies?

A

IgM and IgG

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7
Q

What antibodies are involved in Type II hypersensitivities?

A

IgM and IgG

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8
Q

What antibodies are involved in Type I hypersensitivities?

A

IgE

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9
Q

What cells are involved in Type IV hypersensitivities? What is the “reaction”?

A

Reaction = T cell dependent (Cell-mediated/delayed type)
Cells = Stimulated T helper cells, Macrophages, CD8 T cells
Complement is NOT involved

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10
Q

What cells are involved in Type III hypersensitivities? What is the “reaction”?

A

Reaction = Immune complex mediated
Cells = Macrophages, PMNs, Mast cells
Complement is involved

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11
Q

What cells are involved in Type II hypersensitivities? What is the “reaction”?
Is complement involved?

A

Reaction = Antibody-mediated cytotoxic
Cells = macrophages and neutrophils
Complement is involved

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12
Q

What cells are involved in Type I hypersensitivities? What is the “reaction”? Is complement involved?

A

Reaction = Anaphylaxis
Cells = Mast cells, basophils, APCs
Complement is NOT involved

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13
Q

What is the mechanism of injury for Type I hypersensitivities? Are cytokines involved?

A

Allergic/anapylactic reactions
Cytokines are involved (histamine)

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14
Q

What is the mechanism of injury for Type II hypersensitivities? Are cytokines involved?

A

Targeted cell lysis, cell mediated cytotoxicity
Cytokines are NOT involved

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15
Q

What is the mechanism of injury for Type III hypersensitivities? Are cytokines involved?

A

Immune complexes (Ab/Ag)
Cytokines are involved

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16
Q

What is the mechanism of injury for Type IV hypersensitivities? Are cytokines involved?

A

Immune complexes (Ab/Ag)
Cytokines are involved

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17
Q

Hypersensitivity

A

Exaggerated, but normal, immune response to an antigen that produces inflammation

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18
Q

Allergy

A

Atopy; any altered reaction to external substances mediated by IgE antibodies

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19
Q

Anaphylaxis

A

Type 1 hypersensitivity reaction resulting in systemic immune reactions affecting respiratory, cardiovascular, GI, and integumentary systems

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20
Q

What are the FOUR categories of hypersensitivities?

A

Type 1 - anaphylactic
Type 2 - cytotoxic antibody
Type 3 - immune complex formation
Type 4 - T cell dependent

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21
Q

What are the immediate reaction hypersensitivities? What are the delayed reaction hypersensitivities?

A

Immediate - Type 1,2,3
Delayed - Type 4

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22
Q

What cells are involved in Type IV hypersensitivies?

A

Stimulated T helper cells
Macrophages
CD8 T cells

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23
Q

What cells are involved in Type III hypersensitivies?

A

Macrophages
PMNs
Mast cells

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24
Q

What cells are involved in Type II hypersensitivies?

A

Macrophages
Neutrophils

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25
Q

What cells are involved in Type I hypersensitivies?

A

Mast cells
Basophils
APCs (B cells, macrophages)

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26
Q

Which hypersensitivities involve complement?

A

II and III

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27
Q

Auto-immune disorders are more common in ________ (males/females).

A

Females

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28
Q

Auto-immune disorders are more common in __________ (dizygotic/monozygotic twins).

A

Monozygotic twins

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29
Q

Autoimmune disorders are the result of loss of ______________.

A

Self tolerance

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30
Q

Where does Central Tolerance occur?

A

Primary lymphoid organs (bone marrow and thymus)

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31
Q

Where does Peripheral Tolerance occur?

A

Secondary lymphoid organs (spleen, lymph nodes)

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32
Q

Anergy

A

Absence of normal immune response to a particular antigen

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33
Q

Explain the genetic and environmental factors in the development of autoimmunity.

A

Certain environmental/endogenous triggers raise the risk of autoimmune disorders such as female hormones, tissue injury, microbial infections, or epigenetic factors. A genetically susceptible individual possesses a certain HLA or gene and can lose immunologic tolerance that leads to an autoimmune disease.

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34
Q

Influential factors for developing auto-immune disorders

A
  • Genetics (more common in females, certain HLA proteins correlate with AI disorders)
  • Age (peak age is 60-70, risk increases w/ age)
  • Exogenous factors (UV light exposure, drugs, viruses, chronic infectious diseases)
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35
Q

How can microbial infections be an endogenous factor to an autoimmune disorder?

A

Molecular mimicry
- Antigens of pathogens are structurally similar to host proteins and creates cross-reactivity of antibody response against the pathogen (Ex. S. pyogenes and Rheumatic Fever)

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36
Q

What is the bystander effect?

A

Presence of pathogens in tissue create inflammatory responses that recruit WBCs/APCs for T cell activation and accidental antigens are processed for allo-recognition
(Wrong place, wrong time)

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37
Q

Superantigens

A

Proteins produced by microbes that bind to MHC class II and TCRs regardless of MHC restriction/binding sites (Ex. Staphylococcal enterotoxins and toxic shock syndrome)

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38
Q

What are ANAs?

A

Anti-Nuclear Antibodies
Heterogenous group of circulating antibodies that can either be IgG, IgM, or IgA

True auto-antibodies that are classified by:
- Antibodies to DNA (native dsDNA or denatured ssDNA) histones, non-histones, or nucleolar antigens

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39
Q

How are ANAs detected?

A

Via IFA

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40
Q

ANA screening with IIF titers

A

1:80 and 1:160 dilutions performed because low titer positives may occur in healthy people, positive samples may be further diluted to determine titer

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41
Q

Homogenous ANA pattern

A
  • Interphase and metaphase positive
  • Uniform staining of entire nucleus
  • Associated with SLE, drug-induced lupus, AI hepatitis, and JIA
    Presents as solid, green circles!
42
Q

Speckled ANA pattern

A
  • Interphase positive, metaphase negative
  • Associated with anti-ENAs in SLE, Sjogrens, SSc, and SARDs
    Presents as speckled cells with metaphase cells having a greyed out area/line down the middle!
43
Q

Centromere ANA pattern

A
  • Interphase and metaphase positive
  • Associated with CREST syndrome
    Presents as speckled cells with metaphase cells having a bright green fluorescence down the middle!
44
Q

Nucleolar ANA pattern

A
  • Interphase positive, metaphase negative
  • ONLY nucleoli fluoresce
  • Associated with anti-RNA in patients w/ SSc or SARDs
    Presents as large fluorescing circles inside the cell representing the nucleoli
45
Q

What are the “other” ANA detection methods?

A

Oucherlongy double diffusion
Solid phase immunoassays (ELISA)
Immunoassays using Crithidia luciliae

46
Q

Peripheral/rim ANA pattern

A

Outer rim of nucleus will fluoresce green

47
Q

Anti-dsDNA is an autoantibody associated with which disease and immunofluorescent pattern?

A

SLE; homogenous

48
Q

Anti-ssDNA is an autoantibody associated with which disease and immunofluorescent pattern?

A

SLE, not detected on routine screen

49
Q

Anti-Sm is an autoantibody associated with which disease and immunofluorescent pattern?

A

Diagnostic for SLE, Coarse speckled pattern

50
Q

Anti-SS A (Ro) is an autoantibody associated with which disease and immunofluorescent pattern?

A

SLE, Sjogren’s syndrome
Fine Speckled

51
Q

Anti-SS B (La) is an autoantibody associated with which disease and immunofluorescent pattern?

A

SLE, Sjogren’s syndrome
Fine speckled

52
Q

Anti-Scl-70 is an autoantibody associated with which disease and immunofluorescent pattern?

A

Systemic sclerosis, scleroderma
Compound pattern with speckling

53
Q

Anti-centromere is an autoantibody associated with which disease and immunofluorescent pattern?

A

CREST syndrome
Discrete speckled

54
Q

Anti-RNP is an autoantibody associated with which disease and immunofluorescent pattern?

A

SLE
Speckled

55
Q

Examples of SARDs (Systemic autoimmune rheumatic diseases)

A

RA
SLE
Scleroderma
Osteoporosis
Gout
Systemic sclerosis
Sjogrens syndrome

56
Q

Scleroderma

A

SARD associated with anti-SSc, anti-Scl70
Centromere ANA pattern
Excessive fibrosis of skin, abnormal vasculature, & internal organ damage by 30 y/o
Raynaud’s phenomenon is common

57
Q

What does CREST syndrome stand for and what AI disorder is it aligned with?

A

C = calcinosis
R = Raynaud’s phenomenon
E = eosophageal dysmotility
S = sclerodactyly
T = telangiectasia
Associated w/ Scleroderma

58
Q

Sjogren’s Syndrome (what is it, signs and symptoms)

A

Chronic inflammation of exocrine glands (predominantly lacrimal and salivary glands)
S&S: dry eyes and mouth AKA “sicca syndrome”, hoarse voice, dry vagina, failure to produce acidic urine

59
Q

Lab diagnosis of Sjogren’s Syndrome and associated ANA patterns

A

Hypergammaglobulinemia
Anti-SSA and Anti-SSB, sometimes Anti-Sm
Fine speckled or homogenous pattern

60
Q

What is SLE?

A

Chronic inflammatory disorder involving joints, connective tissue, collagen during disease progression

61
Q

Variants of lupus?

A

Can be discoid, systemic, drug-induced, and neonatal

62
Q

Which AI disorder involved anti-phospholipid antibodies that bind T cells?

63
Q

Treatment for SLE

A

Hydroxychloroquine, systemic glucocorticoids, and steroids, newer therapies include monoclonal antibodies Belimumab and Ritiximab

64
Q

SLE is considered to be a hypersensitivity type _____ reaction.

65
Q

Clinical symptoms of SLE

A

Multi-joint involvement
Bilateral rash on nasal bridge
Renal involvement (Nephritis = major death cause)
Neurological symptoms
Anemia/leukopenia/thrombocytopenia

66
Q

What are some lab tests to assist in the diagnosis of SLE?

A

CBC (anemia, leukopenia)
Urinalysis (Renal disease)
CRP/ESR (elevated during flare ups)
Complement deficiencies
ANAs - anti-dsDNA, anti-Sm, anti-SSA/SSB

67
Q

Lupus anticoagulants are anti-phospholipids associated with _________ activation, meaning:

A

prothrombin activation; meaning patient is more likely to form a clot instead of bleed

68
Q

What is immunofluorescence using Crithidia luciliae?

A

IIF using a non-pathogenic trypanosome as the substrate to detect anti-dsDNA in Lupus patients
Positive result = stained kinetoplast

69
Q

Rheumatoid arthritis lab values

A

Increased uric acid levels
Increased CRP
Disruption of synovial fluid - exudative/transudative
Increased ESR
ANA reactivity

70
Q

Lab diagnosis for RA

A

Low serum iron
Low TIBC
Elevated ESR and CRP
Elevated complement
Elevated a2-macroglobulins and gamma globulins
Immune complexes
RF and anti-CCP

71
Q

What is a specific marker for RA?

72
Q

Treatment for RA

A

NSAIDs
Methotrexate - reduces pyrimidine and nucleotide synthesis and pro-inflammatory cytokines like TNF-alpha

73
Q

What is Wegener’s granulomatosis?

A

Rare AI disease involving inflammation of small to medium sized blood vessels and respiratory tract showing reoccurring rhinitis, sinusitis, and otitis media

74
Q

What disease is associated with ANCA (anti neutrophil cytoplasmic antibody) ?

A

Wegener’s granulomatosis

75
Q

Lab ID of Wegener’s granulomatosis

A

Normocytic, normochromic anemia
Leukocytosis, eosinophilia
Elevated ESR
Decreased albumin
Severe renal insufficiency (Decreased GFR)
Elevated CRP
Positive ANCA

76
Q

What is ANCA?

A

Anti neutrophil cytoplasmic antibodies
Produced against proteins in neutrophil granules
Two fluorescent patterns: Cytoplasmic (Anti-PR3) and perinuclear (Anti-MPO)

77
Q

C-ANCA is associated with anti- ______ ?

78
Q

P-ANCA is associated with anti- ______ ?

79
Q

Standout features of Warm AIHA

A

Most common
Antibodies react at 37C, IgG, complement involvement
Pan-agglutination in blood bank

80
Q

Standout features of Cold AIHA

A

Cold agglutinin disease due to cold ab
Complement involvement
IgM
Associated w/ mycoplasma pneumoniae or lymphoma
Raynaud’s phenomenon may occur

81
Q

Standout features of PCH

A

Associated with viral infections in children
Autoantibody to IgG that reacts at colder temps of the body that binds complement
Associated with anti-p specificity
Donath-landsteiner antibody

82
Q

Drug induced hemolytic anemia: Drug adsorption

A

Drug binds to a membranous protein forming a RBC/hapten complex that stimulates antiibody production
Extravascular

83
Q

Drug induced hemolytic anemia: Immune complexing

A

Drugs in the serum are viewed as foreign and antibodies bind to them forming immune complexes in serum
Intravascular hemolysis

84
Q

ITP

A

Autoimmune disorder characterized by petechiae, bruising, and menorrhagia
Marked thrombocytopenia
Commonly seen in children

85
Q

Addison’s disease: Target cells/tissues and associated autoantibodies

A

Adrenal glands
Antibody to adrenal cells

86
Q

Celiac disease: Target cells/tissues and associated autoantibodies

A

Small intestine and others
Anti-transglutaminase (tTG)
Anti-DGPs
Endomysial antibodies

87
Q

Goodpasture’s syndrome: Target cells/tissues and associated autoantibodies

A

Kidneys/lungs
Antibody to an antigen in the renal and pulmonary basement membranes

88
Q

Grave’s disease: Target cells/tissues and associated autoantibodies

A

Thyroid gland
TRAbs, anti-thyroglobulin, anti-TPO

89
Q

Hashimoto’s thyroiditis: target cells/tissues and associated autoantibodies

A

thyroid gland
Anti-thyroglobulin
anti-TPO

90
Q

Multiple sclerosis: target cells/tissues and associated autoantibodies

A

Myelin sheath of nerves
Antibodies to myelin basic protein

91
Q

Myasthenia gravis: target cells/tissues and associated autoantibodies

A

Nerve-muscle synapses
Antibodies to AChR, MuSK, LRP4

92
Q

Pernicious anemia: target cells/tissues and associated autoantibodies

A

Stomach
Intrinsic factor antibody

93
Q

Type 1 diabetes mellitus: target cells/tissues and associated autoantibodies

A

Pancreas
Anti-insulin
Islet cell antibodies
Anti-GAD

94
Q

Hashimoto’s vs Grave’s

A

Hashimotos: hypothyroidism, cold intolerance, brittle hair, goiter, Anti-Tg/Anti-TPO

Grave’s: hyperthyroidism, heat intolerance, TRAbs antibodies

95
Q

Celiac disease

A

Affects small intestine triggered by gluten ingestion

96
Q

Autoimmune hepatitis liver diseases

A

Anti-mitochondrial Abs (AMAs)
Elevated liver enzymes, jaundice, etc
Must be differentiated from hepatitis viruses

97
Q

Goodpasture’s syndrome

A

Autoantibodies against basement membranes that line renal glomeruli and lung alveoli
Antibodies to GBM
Renal failure, respiratory problems such as shortness of breath and hemoptysis

98
Q

Pernicious anemia

A

Megaloblastic anemia (MCV >100), def. in vitamin B12
Autoimmune response against parietal cells in stomach degrade intrinsic factor
Associated with D. latum infections

99
Q

Multiple sclerosis

A

Inflammation/destruction of CNS
Plaques form in white matter of brain and spinal cord (destruction of myelin sheath)
Pins and needles, weakness, vision loss

100
Q

Lab diagnosis of MS

A

Electrophoresis will show Tau protein (carbohydrate deficient transferrin protein)

101
Q

Myasthenia gravis

A

Affecets neuromuscular junctions resulting in weak/easily fatigued skeletal muscle (dropping of eyelids, double vision)
Autoantibodies against acetylcholine receptors used for muscle contraction

Immunology (6 decks)

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