BIMM118 – SP’06 Final
NOTE: WRONG answers on multiple choice questions will result in the
DEDUCTION of the points !!!!!
1) Provide two examples for the clinical use of MAO inhibitors! (10)
a) Depression (Tranylcypromine)
b) Parkinson’s Disease (Selegeline)
2) The dopamine precursor L-Dopa is used as a prodrug to treat Parkinson’s disease (10)?
a) What is the most prevalent peripheral side effect of this drug?
Renal hypertension, nausea due to elevated peripheral dopamine levels
b) How can the peripheral side effects of L-Dopa be prevented?
By combining L-Dopa with the de-carboxylase inhibitor Carbidopa, which does not
penetrate the BB barrier => only CNS dopamine levels increase
3) When a loading dose is administered, the initial drug concentration is dependent on which of
the following (5 ea)?
a) Elimination rate constant
b) Drug half-life
c) Volume of distribution
d) Clearance
e) Metabolism
f) Amount of drug administered
4) Provide an example of altered drug metabolism due to genetic variations among the
population! Briefly explain the underlying mechanism! (15)
a) Mutation in alcohol-dehydrogenase => patient can not metabolize alcohol
b) Mutation in aldehyde-dehydrogenase => patient can not metabolize acetaldehyde
(disulfiram effect)
c) Mutation in CYP2D6 => patient can not metabolize codeine into morphine => loss
of analgesic effecacy
d) Mutation in CYP2C19 => patient can not metabolize phenytoin => risk of OD
5) What are the two major drug classes used in the treatment of elevated blood cholesterol?
Briefly describe their molecular targets! (20)?
a) Statins: inhibit HMG-CoA-Reductase, the rate limiting enzyme in the cholesterol
synthesis pathway => increased uptake of LDL from plasma
b) Fibrates: PPAR agonists that trigger upregulation of fatty acid metabolizing enzymes
and stimulate lipoprotein-lipase activity.
6) Oral hypoglycemic drugs are only effective in Type II, but not in Type I diabetes. Explain why?
(10)
Oral hypoglycemic drugs stimulate insulin production of beta-cells, or increase sensitivity
of the target tissue to existing insulin, which will improve the symptoms of Type II
diabetes.
In Type I diabetes, the beta-cells are destroyed, therefore no insulin can be produced.
