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Solutions to Midterm 6 - Pharmacology | BIMM 118, Exams of Pharmacology

Material Type: Exam; Class: Pharmacology; Subject: Biology/Molec Biol, Microbiol; University: University of California - San Diego; Term: Unknown 2006;

Typology: Exams

2009/2010

Uploaded on 03/28/2010

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BIMM118 – Midterm ’06
1) A competitive antagonist
a) binds to the same site on the receptor as the natural ligand
b) binds the receptor irreversibly
c) elicits a response from the receptor
d) shifts the dose-response curve to the right
e) shifts the dose-response curve to the right AND down
(5 pts each)
2) Which pharmacokinetic process is known as “First Pass Elimination”?
Drugs taken up in the intestine first reach the liver via the hepatic vein, and are therefore
subject to hepatic metabolism prior to entering the general circulation.
(10 pts)
3) Which of the following modifications would be expected to increase lipid
solubility of a drug:
a) glucoronidation
b) hydroxylation
c) sulfation
d) halogenation
e) alkylation
f) dealkylation
(5 pts each)
4) Provide an example of a food-drug interaction! Explain the underlying mechanism!
*) Grapefruit juice contains a CYP3A4 inhibitor, thereby preventing oxidative metabolism of
drugs such as acetaminophen, codeine, warfarin, erythromycin etc.
*) MAO inhibitors (anti-depressant) also prevent the metabolism of tyramine, an amino acid
found in red wine and ripe cheeses. If not degraded by MAO, tyramine competes with
(nor)epinephrine for re-uptake and storage in presynaptic vesicles, thereby promoting
sympathetic output.
(10 pts)
5) When a loading dose is administered, the initial drug concentration is dependent on
which of the following:
a) elimination rate constant
b) drug half-life
c) volume of distribution
d) clearance
e) metabolism
f) amount of drug administered
(5 pts each)
6) Which of the following drugs would be useful in treating malathione poisoning:
a) Dobutamine
b) Epinephrine
c) Atropine
d) Propranolol
e) Pancuronium
(5 pts each)
7) Explain the underlying mechanism for the stimulating effects of cocaine!
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BIMM118 – Midterm ’

  1. A competitive antagonist a) binds to the same site on the receptor as the natural ligand b) binds the receptor irreversibly c) elicits a response from the receptor d) shifts the dose-response curve to the right e) shifts the dose-response curve to the right AND down (5 pts each)
  2. Which pharmacokinetic process is known as “First Pass Elimination”? Drugs taken up in the intestine first reach the liver via the hepatic vein, and are therefore subject to hepatic metabolism prior to entering the general circulation. (10 pts)
  3. Which of the following modifications would be expected to increase lipid solubility of a drug: a) glucoronidation b) hydroxylation c) sulfation d) halogenation e) alkylation f) dealkylation (5 pts each)
  4. Provide an example of a food-drug interaction! Explain the underlying mechanism! *) Grapefruit juice contains a CYP3A4 inhibitor, thereby preventing oxidative metabolism of drugs such as acetaminophen, codeine, warfarin, erythromycin etc. *) MAO inhibitors (anti-depressant) also prevent the metabolism of tyramine, an amino acid found in red wine and ripe cheeses. If not degraded by MAO, tyramine competes with (nor)epinephrine for re-uptake and storage in presynaptic vesicles, thereby promoting sympathetic output. (10 pts)
  5. When a loading dose is administered, the initial drug concentration is dependent on which of the following: a) elimination rate constant b) drug half-life c) volume of distribution d) clearance e) metabolism f) amount of drug administered (5 pts each)
  6. Which of the following drugs would be useful in treating malathione poisoning: a) Dobutamine b) Epinephrine c) Atropine d) Propranolol e) Pancuronium (5 pts each)
  7. Explain the underlying mechanism for the stimulating effects of cocaine!

Cocaine inhibits norepinephrine reuptake into storage vesicle (=> NE increase), thereby acting as an indirect sympathomimetic. (10 pts)

  1. A patient is treated with a MAO inhibitor for his clinical depression. Since he is overweight, he wants to support his dieting efforts with a weight loss product containing ephedrine. What, if anything, might result from the co-administration of these drugs? Justify your conclusion! Ephedrine displaces NE from the presynaptic storage vesicles, increasing NE concentration in the synapse. MAO inhibitors also cause an increase in NE in the synapse, thus producing a synergistic effect with ephedrine => hypertension, agitation, tachycardia etc. (15 pts)
  2. Which of the following drugs can be used to treat hypertension: a) Propranolol b) Pancuronium c) Atropin d) Digoxin e) Nifedipine (5 pts each)
  3. Which drug, captopril or prazosin, is likely to be more effective in reducing high blood pressure? Justify your conclusion! Prazosin is an  1 -selective antagonist, causing dilation of blood vessels. Captopril is an ACE-inhibitor, preventing the production of angiotensin II. AT-II constricts blood vessels and increases blood volume by promoting retention of sodium and water. Consequently, the decrease in AT-II after captopril will yield a dilation of the blood vessels AND a reduction in blood volume, providing a “dual- action” and therefore stronger anti-hypertonic response. (15 pts)
  4. Dihydropyridines are considered “vasoselective” Ca2+^ channel blockers. a) Where do they find clinical application? Hypertension b) What is the underlying basis for the vasoselectivity? Specific inhibition of L-type Ca2+^ channel on vascular smooth muscle cells, little to no inhibition of cardiac T-type channels c) What is a common side-effect caused by the physiological response to these drugs (explain the reason)?
  5. Orthostatic hypotension and peripheral edema through vasodilation; 2) Reflex tachycardia due to feedback-mediated increased sympathetic output d) Which drug(group) could be used to prevent this side effect? Diuretics against edema; beta-blockers against reflex tachycardia (20 pts)