Immunology and Serology

  1. When do autoimmune diseases occur?
    Individual produces antibodie or T cell response to his/her own antigens
  2. What theory states that Burnet postulated that when an error in self-recognition occurs during fetal life and lymphs against an autoantigen are not destoryed, then autoantibodies are produced?
    Forbidden clone theory
  3. What theory states that clones developed during fetal life are not stimulated by low doses of antigens and the ability to produce antibodies against higher doses of antigens is still present?
    Clonal anergy
  4. What theory states that some antigens are hidden from the immune system during fetal development, and when tissue is damaged, the hidden cells are exposed?
    Sequestered antigen theory
  5. What theory states that supporessor T cells control antibody production by B cells and if suppressor T cells exhibit decreased activity, then antibodies against autoantigens are produced?
    Immunologic deficiency theory
  6. What theory states that an individual can make antibodies or reactive T cells to an infectious agent that cross reacts with self antigens?
    Molecular mimicry
  7. What theory states that a number of bacteria and viruses are known to nonspecifically stimulate B cells, and if these B cells have activity against self antigens, an autoimmune disease can result?
    Polyclonal B cell activation
  8. What clinical conditions are antinuclear antibodies (ANAs) associated with?
    • Systemic lupus erythematosis (SLE)
    • Mixed connective tissue disease (MCTD)
    • Rheumatoid arthritis (RA)
  9. What is an anti-antibody, typically IgM, that bind to the Fc portion of abnormal IgG?
    • Rheumatoid Factor (RF)
    • Chronic hepatitis
    • SLE
    • Syphilis
  10. What clinical conditions are associated with cryoglobulins?
    • Autoimmune diseases like:
    • Vasculitis
    • Glomerulonephritis
    • SLE
    • RA
    • Sjogren syndrome
  11. What clinical condition is a chronic, noninfectious inflammatory disease involving many organs and tissue injury is caused by autoantibodies and immune complexes deposited into the tissues?
    Systemic lupus erythematosus (SLE)
  12. What clinical condition is a chronic, noninfectious, systemic inflammatory disease that primarily afects the joints and is due to production of IgG or IgM antibodies against IgG in the synovium?
    Rheumatoid arthritis
  13. What clinical condition is consisten with the findings:
    ESR increased
    CRP increased
    RF positive
    Cryoglobulins positive
    ANA positive or negative
    Synovial fluid is cloudy with WBC between 5000-20000, increased protein
    Poor mucin clot development
    Complement decreased
    RF positive
    Rheumatoid arthritis
  14. What clinical condition is an inflammation of the salivary and lacrimal glands causing dryness of the mouth and eyes?
    Sjogren syndrome
  15. What clinical condition is consistent with the findings:
    Polycolonal hypergammaglobulinemia
    Autoantibodies agains the salivary glands
    RF positive
    ANA speckled or diffuse pattern
    Sjogren syndrome
  16. What clinical condition has:
    an increased rate of RBC destruction
    DAT positive
    Cold agglutinins (sometimes)
    Autoantibody against RBC antigens
    Autoimmune hemolytic anemia
  17. What disease occurs when
    Humoral and cellular immunity are activated
    Destruction of normal thyroid tissue leads to hypothyroidism
    Loss of thyroid function
    Low levels of thyroid hormones in the blood
    Detection of antithyroid antibodies
    Hashimoto disease
  18. What disease is characterized by:
    Hypoplasia and diffuse goiter caused by an autoantibody reacting with thyroid receptor on cells that overstimulates the thyroid gland
    Autoantibody mimics the activity of thyroid stimulating hormone (TSH)
    TT3 increased
    FT3 increased
    TT4 increased
    FT4 increased
    TSH decreased
    Infiltrative dermopathy
    Graves disease
  19. What disease is a:
    Neuromuscular disease in which the nerve muscles do not function normally
    Most patients exhibit antibodies to acetylcholine receptors
    Myasthenia gravis
  20. What disease is:
    Considered a chronic progressive inflammatory disease with demyelination of the nerves
    Active lesions (plaques) contain CTLs, T helper cells, and macrophages
    IgG increased in CSF
    Oligoclonal bands in CSF
    Multiple sclerosis (MS)
  21. What differentiates true increase of IgG due to a production rather than increases in permeability of the blood-brain barrier?
    IgG index
  22. What is the IgG index calculation?
    Image Upload 1
  23. What is the reference range for IgG index?
  24. What disease has:
    Islet cell destruction in the pancreas
    Autoantibodies and CTLs reactive against pancreatic beta cells produce marked atrophy and fibrosis of the islet cells - causing insulin deficiency
    Type 1 diabetes
  25. What types of responses are humoral mediated and immediate?
    Types I-III
  26. What type of responses are cell mediated at delayed?
    Type IV
  27. What type of hypersensitivity reaction is:
    Classified as an immediate hypersensitivity reaction b/c it occurs within minutes after reexposure
    After 1st exposure, basophils and mast cells are sensitized with IgE
    After 2nd exposure, IgE binds to a specific allergen and chemical mediators are released
    Type I hypersensitivity (anaphylactic)
  28. What do allergens contacting the bronchus cause?
  29. What is the systemic form of type I hypersensitivity?
  30. What mediator of Type I hypersensitivity:
    Causes contraction of bronchioles and smooth muscle of blood vessels
    Increases capillary permeability
    Increases mucus secretion in the airway
  31. What mediator of Type I hypersensitivity:
    Causes vasodialation 
    Increased vascular permeability
  32. What mediator of Type I hypersensitivity:
    Causes erythema and wheat formation
    Has 30-100 times the ability of histamine to cause bronchospasms
    Stimulate mucus secretion in the airways
  33. What type of hypersensitivity reaction is
    Due to IgG or IgM antibodies directed against cell surface antigens
    PMNs bind to antibody sensitized cells and destroy the cells by phagocytosis or antibody dependent cellular cytotoxicity reaction
    Type II hypersensitivity
  34. What occurs when antibody-antigen complex on cell surface activates the complement pathway to cause cell lysis?
    Complement mediated cell lysis
  35. Name an example of Type II hypersensitivity reactions
    Incompatible blood transfusions
  36. What type of hypersensitivity reaction is:
    When immune complexes are deposited on tissues, causing inflammation
    Can activate complement, which can lyse nearby (innocent bystander) cells
    Can stimulate degranulation of granulocytes, which triggers inflammation and tissue damage
    Type III hypersensitivity (immunecomplex)
  37. What 2 sites are where immune complexes are often deposited?
    • Heart valves
    • Renal glomeruli
  38. What happens when immune complexes are deposted into the renal glomeruli?
    • Causes inflammation of the kidney - glomerulonephritis
    • Possibly renal failure
  39. What hypersensitivity reaction is:
    Caused by soluble factors or lymphokines released by T cells
    Antibody and complement are NOT involved in this reaction
    Recruitment and activation of the cells takes 24-72 hours, and therefore referred to as delayed hypersensitivity
    Type IV hypersensitivity (cell mediated)
  40. How does Type IV hypersensitivity (cell mediated) reaction work?
    • Lymphokines are produced by T cells
    • These chemicals attract macrophages that become activated, cause them to degranulate
    • As more macrophages arrive at the site, ulceration and necrosis occurs
  41. Name examples of Type IV hypersensitivity (cell mediated)
    • Tuberculin-type hypersensitivity - swelling at the site of subcutaneous injection
    • Contact sensitivity (dermatitis) - allergens from poison ivy or poison oak
  42. What clinical condition is:
    Marked deficiency of all classes of immunoglobulins is detected after about 6 months of age
    Recurrent, life-threatening infections occur with encapsulated bacteria (Strep pneumo and H. influenzae)
    B cells are markedly decreased or absent
    Bruton X-linked agammaglobulinemia
  43. What clinical condition is:
    X linked genetic disease
    Serum IgM increased
    IgG and IgA are markedly decreased or absent
    Defect in CD40 ligand on T helper cells prevents class switching from IgM to IgG, IgA, or IgE
    Patients prone to respiratory tract infections
    Autoantibodies to platelets, RBCs, and neutrophils
    Hyper-IgM syndrome
  44. What clinical condition has:
    Patients present with small amounts or absence of serum and secretory IgA
    Usually caused by a genetic defect or by drugs (phenytoin and penicillin)
    Anaphylaxis may result if IgA is administered to someone with this deficiency (blood transfusion)
    Selective IgA defiency
  45. What clinical condition is:
    Autosomal recessive disorder that presents with ataxia, telanectasia, recurrent sinopulmonary infections, high incidence of malignancy, and variable immune defects
    IgA deficiency
    Sometimes IgE deficiency
    NOT primarily an immunodeficiency but a defect in a kinase gene that regulates the cell cycle
    B and T helper cells are affected
  46. What clinical condition has:
    Symptoms that include hypocalcemic tetany, due to underdevelopment of the thymus, and heart disease
    Immune defect is variable, from slight decrease in T cells to no T cells in bloodstream
    Patients very susceptible to opportunistic infections and have poor prognosis
    Congenital thymic hypoplasia (DiGeorge syndrome)
  47. What clinical condition has:
    Accumulation of nucleotide metabolites in all cells, which is particularly toxic to T and B cells
    T cells decreased
    Children often have an underdeveloped thymus, lack of tonsils or lymph nodes, hypogammaglobulinemia, and lymphopenia
    Defects in adenosine deaminase (ADA) or purine nucleotide phosphorylase (PNP)
  48. What clinical condition is:
    With an MHC class II deficiency, T helper cells fails to develop - patient present with hypogammaglobuminemia and no CMI response
    MHC class I defiency is less severe - loss of CTLs and response to intracellular pathogens
    Bare lymphocyte syndrome
  49. What clinical condition has:
    A mutation in the gene that codes for the Wiskott-Adrich syndrome protein (WASP) - a protein involved with cytoskeletal reorganization necessary for delivering cytokines
    Defect prevents T helper cells from delivering lymphokines to B cells, macrophages, and other target cells
    Patients demonstrate eczema, throbocytopenic purpura, and increase risk of infection
    Platelets are small and defective
    Wiskott-Aldrich syndrome
Card Set
Immunology and Serology
Autoimmune Disease, Hypersensitivity, Immune Deficiency