1 - University of California, San Diego
1) Which of the following conditions can be treated with Dopamine receptor antagonists? (5 ea)
a) Epilepsy
b) Parkinson’s Disease
c) Schizophrenia (Phenothiazines; Butyrophenones)
d) Angina pectoris
e) Nausea/Vomiting (Metoclopramide)
f) Diarrhea
2) Describe two clinical uses (+ mechanism) for the synthetic prostaglandin Misoprostol (10)
Inhibition of acid production by parietal cells => treatment of GERD, stomach ulcers etc.
Increase in uterine muscle tone => used to induce labor, or in combination with mifeprostone, to terminate pregnancy.
3) Which anti-diabetic drug group acts via the nuclear receptor PPARγ? Can these drugs be used for type I diabetes (explain!)? (10)
Glitazones: Upregulate signaling molecules downstream of the insulin receptor.
Useless for type I diabetes due to a complete lack of insulin production!
4) What is the “Minimal Alveolar Concentration (MAC)”? How does the MAC relate to the lipophilicity of the drug? (10)
The MAC is the concentration of the anesthetic at 1 atm that prevents a reaction to a painful stimulus in 50% of subjects. MAC decreases with increased lipophilicity.
5) Aspirin is contraindicated in which of the following conditions (5 ea)
a) Angina pectoris
b) Bronchial asthma
c) Hypertension
d) Arthritis
e) Gastritic ulcers
f) Bradycardia
6) The effects of which inhibitory neurotransmitter are intensified by alcohol? Which two drug classes have a strong synergistic sedating effect with alcohol based on this mechanism? Explain! (15)
GABA: Barbiturates mimic GABA action, benodiazepines increase affinity of GABA for the receptor. Alcohol also acts via GABA receptors => synergism.
7) During an outpatient procedure the physician accidentally injects lidocaine directly into the bloodstream. Within a few seconds the patient goes into cardiac arrest. WHY? (15)
Lidocaine (which in low doses is also used as an anti-arrhythmic drug) disrupts the cardiac impulse conduction (particularly from the AV node) => Cardiac arrest!
8) Which drug (group) reduces preload and afterload to alleviate symptoms of Angina pectoris? Briefly describe the basis for the efficacy (10)
Nitrates (nitroglycerol, ISMN, ISDN etc.) produce venous and arterial vasodilation via relaxation of vascular smooth muscle cells.
9) What are the specific indications for the opioid receptor antagonists Naloxone and Naltrexone? (10)
Naloxone: short-acting, for emergencies (Opiate overdose)
Naltrexone: long-acting: treatment of opiate addiction, alcoholism
10) Both Ranitidine and Lansoprazole are used to reduce stomach acid production. (15)
a) How do these drugs work (explain the mechanism)?
b) Which drug is likely to be more effective (explain your conclusion!)?
Ranitidine is a histamine H2 receptor antagonist which inhibits histamine-induced gastric secretion from parietal cells. Lansoprazole is a proton pump (K+/H+ ATPase) inhibitor which blocks secretion of acid from parietal cells.
Lansoprazole is more effective since it blocks stomach acid secretion directly. Ranitidine only blocks histamine-induced upregulation of stomach acid production, but does not, for instance, block muscarinic Ach-receptor mediated increases in stomach acid production.
11) Provide two distinct examples for the clinical use of estrogen receptor antagonists!
Name one drug in each group and describe the basis for their efficacy (20)
Tamoxifen: Estrogen-dependent cancers – blocks estrogen receptors on mammary tissue
Clomiphen: Infertility – blocks estrogen receptors in the pituitary gland => loss of feedback inhibition => ovulation
12) Provide an example of a drug (group) where addition of halogen atoms leads to increased potency and/or efficacy of the drug! (5)
Glucocorticoids (Betamethasone, Dexamethasone, …)
Quinolones (=> Fluoroquinolones: Ciprofloxazine, Levofloxazine…)
13) Provide an example of a (natural or synthetic) opiate derivative that is NOT used for analgetic purposes (name the drug and it’s use)! (10)
Dextrometorphane: Antitussive
Loperamide: Antidiarrheal
Etorphine: Animal “tranquilizer”
14) Finasteride is used to treat prostate enlargement/cancer as well as male baldness? Describe the mechanism of the drug action, and the basis for its efficacy against these disorders (10)
Finasteride inhibits 5-alpha reductase, the enzyme that converts testosterone into the more potent dihydrotestosterone (DHT). DHT promotes the growth of prostate cells, and is a major contributing factor in male baldness.
15) a) What does the “Amine Hypothesis of Depression” state? (5)
“Depression is caused by reduced levels of monoamines (serotonin, dopamine) in the brains”
b) Which three drug groups are predominantly used in the treatment of clinical depression (describe their mechanism of action)? (15)
MAO inhibitors: block degradation of serotonin and dopamine
TCAs: prevent reuptake of serotonin and dopamine
SSRIs: prevent reuptake of serotonin
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