Exam (elaborations)
Exam (elaborations) clinical medicine
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This document consist of questions and their answers for Clinical medicine units.
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CLINICAL IMMUNOLOGY1. Please could you explain how lymphocytes (especially B) can maintain receptors on their
surfaces? Is this genetically related? If so, when the lymphocytes are first exposed to the
antigens, how could the antigen receptor be synthesized? Is there a mutation within the nuclei
of these lymphocytes when they learn to make the receptors? If there is, can you explain how
this occurs? Ans: B cells differentiate from lymphoid cells in the bone marrow in a way that
allows them to express an antigen receptor on the surface permanently. The expression of the
receptor is a definition of B cells and is a result of the differentiation pathway. The antigen
receptor varies from one immature B cell to another. There are billions of different receptors,
but any B cell will express only one type of receptor. The antigen does not ‘design’ the receptor;
rather, a clonal B cell that recognizes the antigen (very few B cells will recognize a given antigen)
will proliferate in response to the antigen and signals from T cells. As the B cells proliferate and
differentiate further, the DNA region that codes for the antigen receptor undergoes mutation,
and cells with mutations that recognize the antigen better are selected for further development,
while those that do not recognize the antigen die
2. I understand how nuclear factor-κB (NFκB) works in the inflammatory response but what is the
mechanism by which it causes cancer? Ans: NFκB is a transcription factor that alters cell
behaviour. It inhibits apoptosis and increases cell proliferation by increasing the production of
tumour necrosis factor (TNF-α).
3. What are the diseases associated with hypocomplementaemia and which complement
deficiency in particular? Ans: The following are the major patterns of deficiency:
● C3, C1q and factors H and I: susceptibility to capsulated bacteria, also systemic
lupus erythematosus (SLE)-like syndrome
● C5-9: susceptibility to disseminated neisserial infections
● C1 esterase deficiency: hereditary angio-oedema. (See K&C 7e, p. 71 for a discussion
of complement deficiency.)
4. What is meant by ‘B lymphocytes are sensitive to clonal deletion’? Ans: Clonal deletion occurs
during the development of immune tolerance. Clonal deletion occurs when lymphocytes of a
particular specificity are lost when in contact with ‘self’ or an extrinsic antigen.
5. What are the immunological implications of ‘bare lymphocyte syndrome’/MHC deficiency? Ans:
In the bare lymphocyte syndrome, a rare recessive condition, major histocompatibility
complexes are not expressed. The clinical manifestation is of severe combined immune
deficiency (SCID). Patients present in infancy with viral, bacterial, fungal and protozoal infections
that are difficult to control because of poor immunity.
6. Please explain oligoclonal and monoclonal Ans: ‘Oligoclonal’ antibodies are produced by more
than one clone (family) of cells, but not by as many as are involved in the production of
polyclonal antibodies. ‘Monoclonal’ indicates that the antibodies are produced by a single clone
of cells
7. I was wondering if there is any study regarding cell culture techniques of CD4 helper cells (stem
cell culturing) and, if so, is it of any benefit to HIV-infected patients? Ans: Cell culture techniques
of CD4 helper cells are available but we are unaware of their use in HIV-infected patients.
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