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Immunopathology Flashcards

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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
HLA-BW47
21-hydroxylase deficiency (also lack HLA-B8)
26
HLA-DR2
Multiple sclerosis
27
HLA-DR3
1. Graves disease | 2. SLE
28
HLA-DR4
Rheumatoid arthritis
29
HLA-DR3/DR4
Type 1 diabetes mellitus
30
HLA-DR5
Hashimoto thyroiditis
31
HLA-DQ2
Celiac disease
32
HLA-DQB1
Guilin-Barre syndrome
33
Immune defect in Bruton agammaglobulinemia
1. XR disorder 2. Failure of pre-B cells to become mature B cells 3. Due to mutated tyrosine kinase
34
Clinical features of Bruton agammaglobulinemia
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
35
Treatment for Bruton agammaglobulinemia
Intravenous gamma-globulin
36
Immune defect in IgA deficiency
Failure of IgA B cells to mature into plasma cells
37
Clinical features of IgA deficiency
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
Immune defect in common variable immunodeficiency (CVID)
Defect in B-cell maturation to plasma cells; this is an adult immunodeficiency disorder
39
Clinical features of CVID
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
Immune defect in DiGeorge syndrome (thymic hypoplasia)
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
Anti-acetylcholine receptor antibodies
Myasthenia gravis
42
Clinical features of DiGeorge syndrome
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
Most common congenital heart defects in DiGeorge syndrome
Tetralogy of Fallot, truncus arteriosus, defects in aortic arch
44
Inheritance pattern observed in hyper-IgM syndrome
X-linked recessive (70% of cases)
45
Genetic defect in hyper-IgM syndrome
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
Clinical features of hyper-IgM syndrome
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
Genetic lesions in severe combined immunodeficiency (SCID)
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
Clinical findings in severe combined immunodeficiency
1. Defective cell-mediated immunity due to lack of T cells 2. Decreased immunoglobulin levels 3. Thymic shadow absent on radiograph
49
Treatment for severe combined immunodeficiency (SCID)
Bone marrow transplant; pts with SCID do not reject allografts
50
Genetic basis for Wiskott-Aldrich syndrome
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
Clinical features of Wiskott-Aldrich syndrome
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
Treatment for Wiskott-Aldrich syndrome
Bone marrow transplantation is essential for survival
53
Genetic basis for ataxia-telangiectasia syndrome
Autosomal recessive inheritance pattern; mutation in a gene that encodes for DNA repair enzyme
54
Clinical features of ataxia-telangiectasia syndrome
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
Examples of type II HSRs
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
Examples of type III HSRs
1. Arthus reaction (e.g., swelling and inflammation following tetanus vaccine) 2. SLE 3. Polyarteritis nodosa 4. Poststreptococcal glomerulonephritis 5. Serum sickness
57
Examples of type IV HSRs
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
IgA-deficient individuals must receive blood products devoid of...
IgA
59
Anticardiolipin, lupus anticoagulant
1. SLE | 2. Antiphospholipid syndrome
60
Anti-desmosome (anti-desmoglein)
Pemphigus vulgaris
61
Anti-dsDNA, anti-Smith
SLE
62
Anti-glutamic acid decarboxylase (GAD-65)
Type 1 diabetes mellitus
63
Antihemidesmosome
Bullous pemphigoid
64
Anti-Jo-1, anti-SRP, anti-Mi-2
1. Polymyositis | 2. Dermatomyositis
65
Antimicrosomal, antithyroglobulin
Hashimoto thyroiditis
66
Antimitochondrial
Primary biliary cirrhosis
67
Anti-smooth muscle
Autoimmune hepatitis
68
Anti-U1 RNP
MCTD
69
IgA anti-endomysial, IgA anti-tissue transglutaminase
Celiac disease
70
MPO-ANCA/p-ANCA
Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
71
PR3-ANCA/c-ANCA
Granulomatosis with polyangiitis (Wegener)
72
Rheumatoid factor (IgM antibody that targets IgG Fc region), anti-CCP (more specific)
Rheumatoid arthritis
73
Post-splenectomy you see what in the peripheral blood?
1. Howell-Jolly bodies (nuclear remnants) 2. Target cells 3. Thrombocytosis (loss of sequestration and removal) 4. Lymphocytosis (loss of sequestration)
74
Describe the mechanism by which splenectomy leads to increased susceptibility to encapsulated organisms.
Splenectomy --> decreased IgM --> decreased complement activation --> decreased C3b opsonization --> increased susceptibility to encapsulated organisms
75
List the encapsulated bacteria.
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
HLA-A3
Hemochromatosis
77
HLA-B27
Psoriatic arthritis, ankylosing spondylitis, arthritis of inflammatory bowel disease, reactive arthritis (formerly Reiter syndrome) Remember: PAIR (Also known as seronegative arthropathies)
78
HLA-DQ2/DQ8
Celiac disease
79
HLA-DR2
1. Multiple sclerosis 2. Hay fever 3. SLE 4. Goodpasture disease
80
HLA-DR3
1. Diabetes mellitus type 1 2. SLE 3. Graves disease 4. Hashimoto thyroiditis
81
HLA-DR4
1. Rheumatoid arthritis | 2. Diabetes mellitus type 1
82
HLA-DR5
1. Pernicious anemia --> vitamin B12 deficiency | 2. Hashimoto thyroiditis
83
Post-splenectomy you see what in the peripheral blood?
1. Howell-Jolly bodies (nuclear remnants) 2. Target cells 3. Thrombocytosis (loss of sequestration and removal) 4. Lymphocytosis (loss of sequestration)
84
Describe the mechanism by which splenectomy leads to increased susceptibility to encapsulated organisms.
Splenectomy --> decreased IgM --> decreased complement activation --> decreased C3b opsonization --> increased susceptibility to encapsulated organisms
85
List the encapsulated bacteria.
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
HLA-A3
Hemochromatosis
87
HLA-B27
Psoriatic arthritis, ankylosing spondylitis, arthritis of inflammatory bowel disease, reactive arthritis (formerly Reiter syndrome) Remember: PAIR (Also known as seronegative arthropathies)
88
HLA-DQ2/DQ8
Celiac disease
89
HLA-DR2
1. Multiple sclerosis 2. Hay fever 3. SLE 4. Goodpasture disease
90
HLA-DR3
1. Diabetes mellitus type 1 2. SLE 3. Graves disease 4. Hashimoto thyroiditis
91
HLA-DR4
1. Rheumatoid arthritis | 2. Diabetes mellitus type 1
92
HLA-DR5
1. Pernicious anemia --> vitamin B12 deficiency | 2. Hashimoto thyroiditis

Pathology (8 decks)

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