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Pathology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

Anti-basement membrane antibodies

A

Goodpasture syndrome

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2
Q

Anticentromere antibodies

A
  1. CREST syndrome (limited scleroderma)

2. Diffuse systemic sclerosis

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3
Q

Antiendomysial IgA

A

Celiac disease

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4
Q

Antigliadin IgA

A

Celiac disease

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5
Q

Antihistone antibodies

A

Drug-induced lupus

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6
Q

Anti-insulin antibodies

A
  1. SLE

2. Type 1 diabetes

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7
Q

Anti-intrinsic factor antibodies

A

Pernicious anemia

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8
Q

Anti-parietal cell antibodies

A

Pernicious anemia

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9
Q

Anti-islet cell antibodies

A

Type 1 diabetes

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10
Q

Antimicrosomal antibodies

A

Hashimoto thyroiditis

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11
Q

Anti-Smith (Sm) antibodies

A

SLE

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12
Q

Anti-SS-A (Ro) antibodies

A
  1. Sjogren syndrome

2. SLE

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13
Q

Anti-SS-B (La) antibodies

A

Sjogren syndrome

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14
Q

Antithyroglobulin antibodies

A
  1. SLE

2. Hashimoto thyroiditis

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15
Q

Anti-tissue transglutaminase IgA

A

Celiac disease

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16
Q

Anti-DNA topoisomerase I (anti-Scl-70) antibodies

A

Diffuse systemic sclerosis

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17
Q

Antimitochondrial antibodies

A
  1. CREST syndrome

2. Primary biliary cirrhosis

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18
Q

Antimyeloperoxidase antibodies

A

Microscopic polyangiitis (p-ANCA)

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19
Q

Antinuclear antibodies

A
  1. SLE
  2. Systemic sclerosis
  3. Dermatomyositis
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20
Q

Antiproteinase 3 antibodies

A
  1. Polymyositis
  2. MCTD
  3. Primary biliary cirrhosis
  4. Wegener granulomatosis (c-ANCA)
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21
Q

Anti-ribonucleoprotein (RNP) antibodies

A
  1. MCTD

2. SLE

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22
Q

Anti-TSH receptor antibodies

A

Graves disease

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23
Q

HLA-A3

A

Hemochromatosis

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24
Q

HLA-B27

A
  1. Ankylosing spondylitis

2. Reactive arthritis

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25
Q

HLA-BW47

A

21-hydroxylase deficiency (also lack HLA-B8)

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26
Q

HLA-DR2

A

Multiple sclerosis

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27
Q

HLA-DR3

A
  1. Graves disease

2. SLE

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28
Q

HLA-DR4

A

Rheumatoid arthritis

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29
Q

HLA-DR3/DR4

A

Type 1 diabetes mellitus

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30
Q

HLA-DR5

A

Hashimoto thyroiditis

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31
Q

HLA-DQ2

A

Celiac disease

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32
Q

HLA-DQB1

A

Guilin-Barre syndrome

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33
Q

Immune defect in Bruton agammaglobulinemia

A
  1. XR disorder
  2. Failure of pre-B cells to become mature B cells
  3. Due to mutated tyrosine kinase
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34
Q

Clinical features of Bruton agammaglobulinemia

A
  1. Sinopulmonary infections, sepsis due to bacteria requiring opsonization and phagocytosis (S. pneumoniae, S. aureus, H. influenzae)
  2. Chronic meningitis due to enteroviruses (echovirus, poliovirus, coxsackievirus) that require neutralizing antibodies to keep them in check
  3. Giardia lamblia infection in small bowel (diarrhea, malabsorption) due to decrease in secretory IgA production
  4. Maternal antibodies are protective from birth to age 6 months
  5. Paradoxical increase in incidence of autoimmune disease (e.g., arthritis, dermatomyositis)
  6. All immunoglobulins are markedly decreased
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35
Q

Treatment for Bruton agammaglobulinemia

A

Intravenous gamma-globulin

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36
Q

Immune defect in IgA deficiency

A

Failure of IgA B cells to mature into plasma cells

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37
Q

Clinical features of IgA deficiency

A
  1. Most common primary immunodeficiency disease
  2. May be asymptomatic (80%) or sinopulmonary infections (most common infection); giardiasis
  3. Increased risk for autoimmune disease (rheumatoid arthritis, SLE, PA, ITP, celiac disease, ulcerative colitis) and atopic (IgE) disorders (asthma, rhinitis, food allergies, dermatitis, conjunctivitis)
  4. Anaphylaxis if exposed to blood products that contain IgA
  5. Decreased serum IgA and decreased secretory IgA
38
Q

Immune defect in common variable immunodeficiency (CVID)

A

Defect in B-cell maturation to plasma cells; this is an adult immunodeficiency disorder

39
Q

Clinical features of CVID

A
  1. Sinopulmonary infections (90-100%)
  2. GI infections (e.g., Giardia, Salmonella, Shigella, Campylobacter)
  3. Pneumonia
  4. Increased risk for autoimmune disease (ITP, AIHA) and malignancy (malignant lymphoma, gastric cancer)
  5. Viral infections: recurrent Herpes infection; enterovirus infections leading to meningitis
  6. Common pathogens: Actinomyces israelii, Streptococcus pneumoniae, Haemophilus influenzae, chronic infections – Staphylococcus aureus, Pseudomonas aeruginosa
  7. Decrease in serum immunoglobulins
40
Q

Immune defect in DiGeorge syndrome (thymic hypoplasia)

A
  1. Chromosome 22 deletion syndrome
  2. Failure of third and fourth pharyngeal pouches to develop
  3. Thymus (site for T cell synthesis) and parathyroid glands fail to develop
41
Q

Anti-acetylcholine receptor antibodies

A

Myasthenia gravis

42
Q

Clinical features of DiGeorge syndrome

A
  1. Bacterial sepsis
  2. Viral infections: CMV, EBV, varicella (chickenpox)
  3. Candida infections
  4. Pneumocystis jiroveci pneumonia
  5. Hypoparathyroidism (tetany): seizures in newborns
  6. Absent thymic shadow on radiograph
  7. Danger of GVH reaction
  8. Increased incidence of cleft lip and congenital heart defects (seen in ~80% of cases)
43
Q

Most common congenital heart defects in DiGeorge syndrome

A

Tetralogy of Fallot, truncus arteriosus, defects in aortic arch

44
Q

Inheritance pattern observed in hyper-IgM syndrome

A

X-linked recessive (70% of cases)

45
Q

Genetic defect in hyper-IgM syndrome

A

Mutation in gene encoding CD40 ligand in CD4+ T cells (CD40 ligand normally reacts with CD40 on surface of B cells to allow for Ig class switching; defect in ligand results in failure of B cells to switch from IgM to other classes of Igs)

46
Q

Clinical features of hyper-IgM syndrome

A
  1. Recurrent pyogenic infections (due to decreased IgG for proper opsonization)
  2. Pneumonia due to P. jiroveci (defect in CD4 T cells affects normal cell-mediated immunity)
47
Q

Genetic lesions in severe combined immunodeficiency (SCID)

A
  1. X-linked recessive inheritance pattern is most common (50-60% of cases); mutation in IL-2 receptor on T cells (lack gamma-chain, which is necessary for development of T cells)
  2. Various autosomal recessive forms have also been identified; adenosine deaminase deficiency (responsible for 15% of SCID cases) is one such form and is associated with an increase in deoxyadenosine, which is toxic to both B cells and T cells
48
Q

Clinical findings in severe combined immunodeficiency

A
  1. Defective cell-mediated immunity due to lack of T cells
  2. Decreased immunoglobulin levels
  3. Thymic shadow absent on radiograph
49
Q

Treatment for severe combined immunodeficiency (SCID)

A

Bone marrow transplant; pts with SCID do not reject allografts

50
Q

Genetic basis for Wiskott-Aldrich syndrome

A

X-linked recessive disorder involving mutation of a gene that encodes for a protein that is involved in the assembly of the actin filaments that make up the cytoskeleton of all hematopoietic cells; defect in actin causes problems in cell migration, signal transduction, and other cell functions

51
Q

Clinical features of Wiskott-Aldrich syndrome

A
  1. Symptom triad: atopic eczema, thrombocytopenia, sinopulmonary infections
  2. Increased risk for malignancy (lymphoma and leukemia)
  3. Infections due to viruses, encapsulated organisms (e.g., Streptococcus pneumoniae), and Pneumocystis jiroveci
  4. Defective cell-mediated immunity
  5. Decreased IgM
  6. Normal IgG
  7. Increased IgA and IgE
52
Q

Treatment for Wiskott-Aldrich syndrome

A

Bone marrow transplantation is essential for survival

53
Q

Genetic basis for ataxia-telangiectasia syndrome

A

Autosomal recessive inheritance pattern; mutation in a gene that encodes for DNA repair enzyme

54
Q

Clinical features of ataxia-telangiectasia syndrome

A
  1. Thymic hypoplasia
  2. Cerebellar ataxia
  3. Telangiectasia (dilated vessels) in the eyes and skin
  4. Increased risk for malignancy [lymphoma and/or leukemia; adenocarcinoma (e.g., stomach, breast)]
  5. Increased serum alpha-fetoprotein (AFP)
  6. Increased carcinoembryonic antigen (CEA)
  7. Defective cell-mediated immunity: decreased total lymphocyte count and defective T cell function
  8. Deficient antibody production to viral or bacterial antigens
  9. Decreased serum IgA levels
  10. Decreased serum IgE levels
  11. Normal to increased serum IgM levels
  12. Decreased serum IgG2/IgG4 levels
  13. Normal to decreased total IgG
55
Q

Examples of type II HSRs

A
  1. Acute hemolytic transfusion reactions
  2. Autoimmune hemolytic anemia
  3. Bullous pemphigoid
  4. Erythroblastosis fetalis
  5. Goodpasture syndrome
  6. Graves disease
  7. Guillain-Barre disease
  8. Idiopathic thrombocytopenic purpura
  9. Myasthenia gravis
  10. Pemphigus vulgaris
  11. Pernicious anemia
  12. Rheumatic fever
56
Q

Examples of type III HSRs

A
  1. Arthus reaction (e.g., swelling and inflammation following tetanus vaccine)
  2. SLE
  3. Polyarteritis nodosa
  4. Poststreptococcal glomerulonephritis
  5. Serum sickness
57
Q

Examples of type IV HSRs

A
  1. Contact dermatitis (e.g., poison ivy, nickel allergy)
  2. Graft-vs-host disease
  3. Multiple sclerosis
  4. PPD (test for M. tuberculosis exposure)
58
Q

IgA-deficient individuals must receive blood products devoid of…

A

IgA

59
Q

Anticardiolipin, lupus anticoagulant

A
  1. SLE

2. Antiphospholipid syndrome

60
Q

Anti-desmosome (anti-desmoglein)

A

Pemphigus vulgaris

61
Q

Anti-dsDNA, anti-Smith

A

SLE

62
Q

Anti-glutamic acid decarboxylase (GAD-65)

A

Type 1 diabetes mellitus

63
Q

Antihemidesmosome

A

Bullous pemphigoid

64
Q

Anti-Jo-1, anti-SRP, anti-Mi-2

A
  1. Polymyositis

2. Dermatomyositis

65
Q

Antimicrosomal, antithyroglobulin

A

Hashimoto thyroiditis

66
Q

Antimitochondrial

A

Primary biliary cirrhosis

67
Q

Anti-smooth muscle

A

Autoimmune hepatitis

68
Q

Anti-U1 RNP

A

MCTD

69
Q

IgA anti-endomysial, IgA anti-tissue transglutaminase

A

Celiac disease

70
Q

MPO-ANCA/p-ANCA

A

Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

71
Q

PR3-ANCA/c-ANCA

A

Granulomatosis with polyangiitis (Wegener)

72
Q

Rheumatoid factor (IgM antibody that targets IgG Fc region), anti-CCP (more specific)

A

Rheumatoid arthritis

73
Q

Post-splenectomy you see what in the peripheral blood?

A
  1. Howell-Jolly bodies (nuclear remnants)
  2. Target cells
  3. Thrombocytosis (loss of sequestration and removal)
  4. Lymphocytosis (loss of sequestration)
74
Q

Describe the mechanism by which splenectomy leads to increased susceptibility to encapsulated organisms.

A

Splenectomy –> decreased IgM –> decreased complement activation –> decreased C3b opsonization –> increased susceptibility to encapsulated organisms

75
Q

List the encapsulated bacteria.

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae type b
  3. Neisseria meningitidis
  4. Escherichia coli
  5. Salmonella spp.
  6. Klebsiella pneumoniae
  7. Group B streptococci

Remember: SHiNE SKiS

76
Q

HLA-A3

A

Hemochromatosis

77
Q

HLA-B27

A

Psoriatic arthritis, ankylosing spondylitis, arthritis of inflammatory bowel disease, reactive arthritis (formerly Reiter syndrome)

Remember: PAIR (Also known as seronegative arthropathies)

78
Q

HLA-DQ2/DQ8

A

Celiac disease

79
Q

HLA-DR2

A
  1. Multiple sclerosis
  2. Hay fever
  3. SLE
  4. Goodpasture disease
80
Q

HLA-DR3

A
  1. Diabetes mellitus type 1
  2. SLE
  3. Graves disease
  4. Hashimoto thyroiditis
81
Q

HLA-DR4

A
  1. Rheumatoid arthritis

2. Diabetes mellitus type 1

82
Q

HLA-DR5

A
  1. Pernicious anemia –> vitamin B12 deficiency

2. Hashimoto thyroiditis

83
Q

Post-splenectomy you see what in the peripheral blood?

A
  1. Howell-Jolly bodies (nuclear remnants)
  2. Target cells
  3. Thrombocytosis (loss of sequestration and removal)
  4. Lymphocytosis (loss of sequestration)
84
Q

Describe the mechanism by which splenectomy leads to increased susceptibility to encapsulated organisms.

A

Splenectomy –> decreased IgM –> decreased complement activation –> decreased C3b opsonization –> increased susceptibility to encapsulated organisms

85
Q

List the encapsulated bacteria.

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae type b
  3. Neisseria meningitidis
  4. Escherichia coli
  5. Salmonella spp.
  6. Klebsiella pneumoniae
  7. Group B streptococci

Remember: SHiNE SKiS

86
Q

HLA-A3

A

Hemochromatosis

87
Q

HLA-B27

A

Psoriatic arthritis, ankylosing spondylitis, arthritis of inflammatory bowel disease, reactive arthritis (formerly Reiter syndrome)

Remember: PAIR (Also known as seronegative arthropathies)

88
Q

HLA-DQ2/DQ8

A

Celiac disease

89
Q

HLA-DR2

A
  1. Multiple sclerosis
  2. Hay fever
  3. SLE
  4. Goodpasture disease
90
Q

HLA-DR3

A
  1. Diabetes mellitus type 1
  2. SLE
  3. Graves disease
  4. Hashimoto thyroiditis
91
Q

HLA-DR4

A
  1. Rheumatoid arthritis

2. Diabetes mellitus type 1

92
Q

HLA-DR5

A
  1. Pernicious anemia –> vitamin B12 deficiency

2. Hashimoto thyroiditis

Pathology (8 decks)

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