Immunopathology PATHOLOGY MCQS


  1. For each of the components of complement listed on the left select the most
    appropriate association from the features on the right.
    a. C3b.
    b. C5a.
    c. C5b-9 complex.
    A. Chemotactic for neutrophil polymorphs.
    B. Deficiency has no pathological effect.
    C. Inhibits mast cell degranulation.
    D. Macrophage surface receptor.
    E. Target cell plasma membrane injury.
    The answer is D, A, E. C3b – macrophage surface receptor. Macrophages (and
    polymorphs) have surface receptors for C3b which results in enhanced adherence of these
    cells to target cells with C3b on their surface.
    C5a – chemotactic for neutrophil polymorphs. C5a promotes the emigration and
    accumulation of neutrophil polymorphs and macrophages.
    C5b-9 complex – target cell plasma membrane injury. The final product of the
    complement cascade is a complex of C5b6789 which is inserted into the target cell plasma
    membrane resulting in cell lysis.
    Deficiency of the early stages of the complement cascade has no pathological effect.
    C3a and C5a both stimulate mast cell and basophil degranulation.
  2. If the following features of the atopic reaction were placed in their correct order
    which would come fourth?
    A. Antigen absorbed for the second time.
    B. Degranulation of mast cells.
    C. Inhalation of pollen.
    D. Mast cell binding by Fc component of IgE.
    E. Production of IgE.
    The answer is A. Atopy (anaphylactic, immediate or type 1 hypersensitivity) occurs
    when IgE binds to mast cells and causes degranulation; antigen is absorbed (C) and the
    immune response produces specific IgE (E) which binds by its Fc component to mast cells
    (D); subsequent exposure to the antigen (A) results in antigen trapping by the IgE Fab
    components on the mast cells with subsequent degranulation (B).
  3. For each of the hypersensitivity reactions on the left select the most appropriate
    association from the conditions on the right.
    a. Arthus reaction.
    b. Cytotoxic antibody reaction.
    c. Delayed hypersensitivity reaction.
    A. Asthma.
    B. Auto-immune haemolytic anaemia.
    C. Extrinsic allergic alveolitis.
    D. Infantile eczema.
    E. Tuberculoid leprosy.
    The answer is C, B, E. Artus reaction – extrinsic allergic alveolitis. Immune complex,
    Arthus type (type 3) reaction is the basis of extrinsic allergic alveolitis (farmer’s lung) which
    is a reaction to bacterial spores growing on mouldy hay.
    Cytotoxic antibody reaction – auto-immune haemolytic anaemia. Cytotoxic antibody
    (type 2) reactions are mediated by antibody which combines with cell surface antigenic
    determinants usually causing lysis. Auto-immune haemolytic anaemia, idiopathic
    thrombocytopenic purpura are examples.
    Delayed hypersensitivity reaction – tuberculoid leprosy. Delayed hypersensitivity (type
    4) reactions are mediated by primed T-lymphocytes; Tuberculoid leprosy, tuberculosis and
    contact dermatitis are examples.
    Asthma and infantile eczema are examples of atopy (type 1).
  4. Which ONE of the following is not an organ specific auto-immune disease?
    A. Auto-immune adrenalitis.
    B. Chronic auto-immune gastritis.
    C. Chronic auto-immune thyroiditis.
    D. Insulin dependent diabetes.
    E. Rheumatoid arthritis.
    The answer is E. Rheumatoid arthritis is one of the group of connective tissue diseases
    with evidence for an auto-immune pathogenesis. Rheumatoid factor consists of IgM antibodies
    to altered IgG which is autoantigenic. In insulin dependent diabetes the trigger for the autoimmune reaction may be a viral infection.
  5. For each of the types of immunological deficiency states listed on the left select
    the most appropriate association from those on the right.
    a. Di George syndrome.
    b. Infantile sex-linked agammaglobulinaemia.
    c. Severe combined immunodeficiency.
    A. Defective B-cell function.
    B. Defective B- and T-cell function.
    C. Defective T-cell function.
    D. Defective platelets.
    E. Defective vessels.
    The answer is C, A, B. Di George syndrome – defective TT-cell function. There is
    almost complete failure of development of the thymus and parathyroids from the third and
    fourth branchial arches.
    Infantile sex-linked agammaglobulinaemia – defective B-cell function. This selective
    B-cell defect (Bruton type) results in failure to produce IgG, IgM and IgA.
    Severe combined immunodeficiency – defective B- and T-cell function. This combined
    type (Swiss type) of agammaglobulinaema has failure of development of both thymus
    dependent and thymus independent systems.
    Platelets are abnormal (D) in the rare Wiskott-Aldrich syndrome in which T-cell
    function, IgM and IgA are also abnormal.
    Abnormal vessels (E) are a feature of ataxia telangiectasia in which there is abnormal
    cell mediated immunity and low levels of IgA and IgE.

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