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Serology > Autoimmune Diseases > Flashcards

Autoimmune Diseases Flashcards

1
Q

Hashiomoto’s Thyroiditis

A
  • Chronic lymphocytic thyroiditis T cell response targets thyroid antigens
  • (Anti-thyroglobulin – directed against thyroglobulin precursor in follicles
  • Anti-thyroid peroxidase (anti-TPO) – directed against thyroid peroxidase in microsomes)
  • Decreased production of thyroid hormones and uptake of thyroid hormone
  • Result – hypothyroidism
  • Autoantibodies also contribute to organ damage
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2
Q

Hashimoto’s Thyroiditis - Clinical Features

A
  • Onset of disease – 30-60 years of age
  • 5 times more common in♀than♂
  • Linked to disease predisposition: HLA-DR3, HLA-DR4, and HLA-DR5
  • Linked to protection from disease: HLA-DQB1
  • Patients have low T4 and high TSH
  • Prolonged hypothyroidism leads to myxedema Diagnosis- Autoantibodies can be detected by several methods: EIA, chemiluminescence, IFA (indirect immunofluorescence), hemagglutination
  • Treatment – thyroid hormone replacement
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3
Q

Grave’s Disease

A
  • Antibodies mimic TSH by binding to and activating TSH receptors
  • Thyroglobulin breakdown accompanied by production of T4 and T3
  • Result – hyperthyroidism
  • Onset of disease – 20-50 years of age 10 times more common in♀than♂
  • Lower incidence in African Americans vs. Caucasians In Caucasians, high risk may be linked to: DRB1*0304, DRB1*0301, or DQA1*0501
  • Linked to protection from disease: DRB1*07
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4
Q

Laboratory Testing for Grave’s Disease

A

Diagnosis often made on clinical symptoms alone Elevated T3 and T4; low TSH >50% of patients have anti-TPO abs; some patients have low anti-thyroglobulin

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5
Q

Type 1 Diabetes Mellitus

A
  • Also called insulin-dependent or juvenile diabetes 10% of diagnosed cases of diabetes in U.S.; chronic disease in children
  • Abrupt onset in children <20 years old
  • Now recognized as an autoimmune disease
  • Patients have antibody to the insulin-producing cells (beta cells) in the pancreas
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6
Q

Type 1 Diabetes Pathophysiology

A
  • A virus (Coxsackie B, rubella, rotavirus, or enterovirus) may initiate response: Antibodies cross-react with epitopes on pancreatic cells
  • Macrophages and Th1 lymphocytes activated and release cytokines
  • Atrophy and fibrosis of pancreas results
  • Stimulate formation of autoantibodies to native insulin or islet cell antigen, resulting reaction of these autoantibodies with tissue antigen causes termination of insulin production and hyperglycemia.
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7
Q

Type 1 Diabetes Disease

A

Hyperglycemia, ketoacidosis, and eventual absolute insulin deficiency.

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8
Q

Laboratory Tests for Type 1 Diabetes

A
  • Elevated serum and urine glucose
  • Increased ketone excretion
  • Decreased insulin levels in plasma
  • Antibodies to native insulin may be detected in plasma
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9
Q

Multiple Sclerosis Causative Factors

A
  • Progressive, relapsing inflammatory condition of CNS, leading to interruption of nerve impulses
  • Environmental and genetic factors trigger autoimmune response
  • Viruses such as EBV and HHV-6 suggested as causative agents
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10
Q

Multiple Sclerosis Disease

A
  • Characteristic plaques appear within white matter of central nervous system damage myelin sheath; produced by: Interaction of myelin-reactive T cells and macrophages with myelin epitopes and Inflammatory reactions
  • Peak incidence – 20-50 years of age
  • Twice as many women as men affected
  • Linked to disease predisposition: People of Northern European heritage HLA DRB1, DRB5, and DQB1
  • Acute attacks alternate with remission
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11
Q

Multiple Sclerosis Treatment

A

Steroids may decrease immune reactions

Routine injections with beta interferons and synthetic myelin protein have shown success in some patients

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12
Q

Laboratory Testing for Multiple Sclerosis

A

History, neurological exam, MRI most commonly used CSF protein – normal or slightly elevated

High IgG in CSF compared to serum IgG

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13
Q

Autoimmune Hepatitis

A

Has developed in some patients following acute hepatitis A infection If untreated, can cause fulminant hepatitis or cirrhosis

Hepatocytes destroyed by: Cell-mediated toxicity involving IL-2 and TNF Antibody-dependent cytoxocity (ADCC) involving IL-4 and IL-10

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14
Q

Laboratory Testing for Autoimmune Hepatitis

A
  • High alanine aminotransferase (ALT)
  • High bilirubin
  • Type I patients: High ANA antibodies; no characteristic pattern
  • High anti-SMA Type II patients: High anti-LKM Significant titers of these antibodies: >1:80 (adults); 1:20 (children)
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15
Q

Primary Biliary Cirrhosis

A

Anti-mitochondrial antibodies (MA) to mitochondrial antigens (usually enzymes) destroy intrahepatic bile ducts

Onset of disease – 50s and 60s 90% of patients are women

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16
Q

Laboratory Testing for Primary Biliary Cirrhosis

A

Elevation of 1 or more liver enzymes: Alkaline phosphatase, gamma glutamyl transpeptidase, alanine aminotransferase, aspartamine aminotransferase Increased: bilirubin, cholesterol, ceruloplasmin, IgM, urine excretion of copper, 50% have increased ANA antibodies 90% of patients have high anti-MA Detected by indirect FA

17
Q

Primary Sclerosing Colangitis

A
  • Rare hepatic autoimmune disease
  • Inflammation of intra- and extrahepatic bile ducts, leading to cirrhosis
  • Often seen in patients with inflammatory bile diseases
18
Q

Pernicious Anemia (Autoimmune)

A
  • Autoantibody against intrinsic factor (IF) binds and inhibits absorption of vitamin B12
  • Autoantibody to gastric parietal cells seen in 80% of patients
  • Onset of disease – ~60 years of age
  • Disease affects slightly more♀than♂
  • Treatment: monthly B12 injections
19
Q

Laboratory Tests for Pernicious Anemia

A
  • Peripheral blood smear: Macrocytic, normochromic RBCs, Hypersegmented neutrophils, Frequent pancytopenia
  • High MCV, High MCH; MCHC normal
  • Low serum vitamin B12; normal folate
  • Schilling’s test positive
  • Fluorescent methods for anti-parietal antibodies
20
Q

Systemic Autoimmune Diseases

A
  • Autoantibodies that react with antigens in multiple cells/organs of the body
  • Damage to collagen in vascular or connective tissue Immune complexes, autoantibodies, and acute inflammatory response cause most damage
  • Laboratory Testing: CBC, metabolic panel, urinalysis, C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR), test for rheumatoid factor, test for presence of antinuclear antibodies (ANA), complement levels
21
Q

Rheumatoid Arthritis

A
  • Chronic disease with inflammation and destruction of joints
  • Probable cause – infection with virus (EBV) or bacterium
  • Response to this foreign antigen attracts cells to the synovium; cytokines cause inflammatory response Immune complexes (IgM anti-IgG bound to IgG) in joint binds complement and attracts PMNs and macrophages
  • Cytokines released from macrophages and lymphocytes, lysozymes, and other proteases from neutrophils damage the cartilage in the joint
  • Treatment – non-steroidal anti-inflammatory drugs (NSAIDs) initially; as disease progresses, methotrexate, steroids, and biologic disease modifiers may be used
22
Q

Laboratory Testing for Rheumatoid Arthritis

A

Nonspecific findings: Normochromic, normocytic anemia, low serum iron, high total protein, high ESR, positive CRP

Laboratory marker for RA – presence of rheumatoid factor; not specific for RA, but ~80% of people with RA have high RF Positive – >60 U/ml by nephelometry; titer of >1:80 by agglutination

23
Q

Systemic Lupus Erythematosus

A
  • Circulating immune complexes deposited in various tissues cause inflammation and destruction
  • Joints, skin, kidney, brain, and lungs most commonly affected
  • Treatment: NSAIDs, steroids, antimalarial drugs for joint pain, methotrexate
24
Q

Sjogren’s Syndrome

A
  • Pathological changes in salivary and lachrimal glands
  • Can be a primary disease or secondary to another autoimmune condition or triggered by a viral infection Usually mild, but may become systemic
  • Patients may have high risk of malignant B cell lymphoma Immune reaction leads to chronic inflammation of salivary gland
  • Treatment – drugs to stimulate flow of saliva, artificial tears
25
Q

Laboratory Testing for Sjogren’s Syndrome

A

Diagnosis usually based on symptoms

Biopsy of salivary gland – classic inflammation with T and B cells

ANA with speckled pattern - 70% of patients are positive, typically of anti-SS-A/Ro or anti-SS-B/La

26
Q

Primary Immunodeficiencies

A
  • Severe combined immunodeficiency (SCID) is the most severe
  • Pure T cell disorders also usually severe since cytokines are important to the immune response
  • Pure B cell disorders are characterized by frequent serious bacterial infections
27
Q

SCID

A
  • Both T and B cell deficiency
  • Usually recognized in neonatal period Patient experiences failure to thrive, diarrhea, and persistent infections, Skin lesions common
  • Diagnosis – clinical symptoms, small thymus, hypogammaglobulinemia, profound lymphopenia
28
Q

SCID Treatment

A

Bone marrow or hematopoietic stem cell transplant 95% cure rate if performed in first 3 months of life

29
Q

Secondary Immunodeficiencies

A

Due to an exogenous agent or condition HIV, severe nutritional defects, burns, chemotherapy Immunodeficiency not always permanent

30
Q

Rheumatoid factor

A
  • A diverse group of immunoglobulins occurring in patients with rheumatoid arthritis, specifically these antibodies (mostly IgM) react with the Fc regions of IgG molecules
  • Positive reactions depend on the antigenic multivalency of IgG achieved by aggregation
  • They are not disease specific and can occur in situations of chronic inflammatory disease such as bacterial endocarditis, tuberculosis, and leprosy
31
Q

C3 and C4

A
  • Depressed levels indicate SLE and liver disease
  • Depressed C3 and normal C4 indicate acute poststreptococcal glomerulonephritis and PNH, The reverse is true for membranoproliferative glomerulonephritis and some coagulopathies
  • C4 is reduced in patients with rheumatoid arthritis
32
Q

CSF IgG in MS

A

There is a 30 to 40% false positive rate when applied to patients with meningitis (aseptic and carcinomatous), cerebral lymphoma, encephalitis, syphilis, Guillain Barre syndrome, post viral myelitis, cerebral arthritis, cerebral lupus erythematosus

33
Q

Primary Sclerosing Colangitis Laboratory testing

A
  • Not specific
  • Increased IgM
  • Increased p-ANCA antibodies (not specific for PSC)

Serology (8 decks)

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