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Autor:   •  December 19, 2016  •  Course Note  •  2,994 Words (12 Pages)  •  542 Views

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Examinations.

Answer two questions from four in two hours.

Un-annotated examination papers can be found under the Year Folder Biology/BMS essentials/ examination information

Here we give sample questions with answer guidance and in some cases a comment from the markers as to where some students ‘went wrong’. 

Note that these plans only refer to the question set.  Do not think that if you reproduce this plan as the basis for an answer to another question in the same area you will get good marks.  In final year one of the biggest failings is that students do not answer the question set.  Also if you just reproduce your lecture notes the best you can expect is usually a 2(ii) mark.

1.   Critically analyse the following statement: ‘In samples of serum and urine enzyme activities are more useful than products of metabolism for diagnosing hepatic and renal glomerular diseases’.

Answer guidance

Introduce by mentioning some examples of organ malfunction e.g. hepatocellular disease, Hep B infection; cholestatic disease, gall stones; renal glomerular disease, glomerular nephritis.

Hepatocellular disease: consider serum AST, ALT and bilirubin explaining why the latter is a metabolite and assessing the extent to which these markers in isolation and combination are indicative of hepatocellular disease.

Cholestatic disease: consider serum γGT, ALP and bilirubin assessing the extent to which these markers in isolation and combination are indicative of cholestatic disease. Good students will be able to comment on the presence/absence of bilirubin from urine in cholestatic disease vs. pre-hepatic jaundice and to distinguish between conjugated and unconjugated bilirubin.

Glomerular disease: consider serum creatinine and urea indicating why both are metabolites, how they are used, their strength and weaknesses, also stating that serum enzyme markers are not usually applicable in this context.

Finally good students might mention that urinary enzyme activities are rarely measured in routine analysis but that pancreatic amylase in acute pancreatitis would be an example.

Marker’s comment|: Here are some of the things that ‘went wrong’.  We mention this not to labour the point but to try to help subsequent students avoid such pitfalls.

  • Question spotting – some student produced ‘their essay’ on renal function others on hepatic disease.  To get good marks students needed to have revised both topics well.
  • Written definitions of GFR were still sometimes wrong and don’t forget the units in the formula.
  • Reference ranges.  By all means quote reference ranges but only if you can get the range correct and use the correct units.
  • Some confusions
  • Prognosis when diagnosis was meant (if you don’t know the meaning of these words there is a Glossary at the back of the Ahmed textbook)
  • Gilbert’s disease is not a form of pre-hepatic jaundice
  • Glucosuria is not an indicator of glomerular disease because glucose is normally filtered at the glomerulus
  • Confusion between serum enzymes and serum metabolites (the latter are produced by pathways of intermediary metabolism, the former are proteins)

2.  ‘The quality of any laboratory result is only as good as the presentation of the sample for analysis.’  Discuss the above statement with reference to the various blood sample tubes available, blood taking techniques and the organisation of a laboratory specimen reception.  As part of your answer, consider how you would organise a specimen reception for a large District General Hospital serving a widespread population compared to an inner city laboratory.

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