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BIMM118 __________________________ WI'08 Final NOTE: WRONG answers on multiple choice questions will result in the DEDUCTION of the points !!!!! 1) Which of the following drug groups is/are likely to exacerbate asthmatic conditions (5 ea)? a) NSAIDs b) D2-antagonists c) Statins d) Tetracyclines e) 2 antagonists 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 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. 4) High glucocorticoid concentrations (e.g. during therapy lead to Na + and water retention and consequently hypertension. Why? (10) GCs at high concentrations also stimulate the mineral-corticoid (=aldosterone) receptors => increased Na+ reabsorption and water retention 5) Which of the following drugs would be the obvious choice to prevent the glucocorticoid side effect described in #4? (5) a) Prazosin b) Propranolol c) Spironolactone d) Captopril e) Nifedipine 6) 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 7) Both Phenytoin and Lidocaine are Na+ channel blockers. How do they differ in their mode of action and in their clinical applications? (10) Phenytoin traps sodium channel in their refractory phase => prolonged recovery period => high frequency signals blocked: used as antiepileptic. Lidocaine inhibits sodium channels in their open configuration => all signals are blocked: used as local anesthetic, anti-arrhythmic. 8) Provide three examples for the clinical use of histamine receptor antagonists! (9) Anti-allergy medication (H1) Sleeping aid (H1) Antiemetic (H1) Reduction of stomach acid production (H2) 9) Cocaine produces symptoms similar to those observed in schizophrenic patients! Why? (10) Schizophrenia is characterized by elevated dopamine levels in the brain. Amphetamines cause increases in brain dopamine levels, thus producing schizophrenic symptoms. 10) 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. 11) Describe the 4 phases of general anesthesia and the drugs employed at each phase (include the rational behind the use of each drug)! (16) Pre-medication Anxiolytic (Benzodiazepines), reduce patient anxiety Analgesic (Opiods, Fentanyl) Autonomic Stabilization (Atropine) Induction Unconsciousness (Thiopental, Benzodiazepine) Muscle relaxation; intubation (Succinylcholine) Maintenance Unconsciousness (Halothane) Analgesic (Nitrous Oxide) Muscle relaxation (Pancuronium) Recovery Reversal Neuromuscular of Block (Neostigmine) 12) Would furosemide increase or decrease the effects of cardiac glycosides? Explain! (10) Increase: Diuretics cause a loss of potassium, resulting in lower potassium concentrations. Potassium competes with CG for binding the the Na +/K+ antiporter system => reduced K+ means less competition => increased effect of CG. 13) Local anesthetics display a significantly reduced effect in inflamed tissue due to the acidic pH in that environment. Explain the molecular mechanism! (10) Local anaesthetics are weak bases with pKa 8-9. The action of local anaesthetics is dependent on their ability to penetrate the nerve sheath in their non-ionized form. They are only partially ionized at physiologic pH, but decreased pH would result in significant ionization and reduced ability to cross membranes and therefore elicit a response. 14) Provide two examples of sex-steroid receptor antagonists and describe their clinical uses (10) Tamoxifen - EstrogenR antagonist: Breast cancer Clomiphen - EstrogenR antagonist: Infertility Mifepristone - ProgesteroneR antagonist: Pregnancy termination Flutamide - TestosteroneR antagonist: Prostate cancer 15) Describe two drugs (mechanism and use) whose efficacy is based on altering the conductance of K+ channels (10). Minoxidil - increases K+ current in vascular smooth muscle cells => membrane hyperpolarization => less Ca++ influx => vasodilation: reduction in blood pressure Bretylium, Amiodarone - block K+ current => prolonged repolarization phase => extended AP: treatment of cardiac arrhythmias Sulfonylureas: inhibit ATP-gated K+-channels => lower depolarization threshold => opening of voltage-gated Ca2+-channels => increased exocytosis of insulin 16) A patient arrives in the ER with signs of peripheral and pulmonary edema, and breathing difficulties. Closer examination reveals hypertrophy of the heart and decreased cardiac output. What treatment(s) would be indicated to improve the patients condition? (10) Patient is likely suffering from congestive heart failure and should be treated with a cardiac glycoside to achieve a positive inotropic affect. In addition, diuretics (furosemide) might be useful to reduce the edema. 17) Which two drugs are used in the treatment of chronic alcoholism? Briefly describe their mode of action (10)? Disulfiram: blocks acetaldehyde dehydrogenase => accumulation of acetaldehyde after alcohol consumption => nausea, vomiting Naltrexone: opiate receptor antagonist => inhibition of endorphine-mediated reward responses => desire to drink diminishes 18) Sulfonylureas and Glitazones are used as oral anti-hyperglycemic drugs. Explain their distinct molecular mechanisms of action. (10) Sulfonylureas: inhibit ATP-gated K+-channels => lower depolarization threshold => opening of voltage-gated Ca2+-channels => increased exocytosis of insulin. Glitazones: PPAR agonists => transcriptional upregulation of proteins involved in glucose transport and metabolism => increased insulin sensitivity 19) Describe the mechanism of action of Benzodiazepines and provide two examples of their clinical uses (10) Benzodiazepines increase the affinity of GABA for the inhibitory GABA receptor => CNS depression Clinical used as anxiolytics, anticonvulsants, sedatives/hypnotics, premedication before anesthesia, 20) How do NSAIDs and Glucocorticoids differ in their anti-inflammatory mechanisms. Which group is more potent? (10) NSAIDs inhibit COX => no PG production, but more LTs GCs produce inhibition of PLA2 => no AA => no PG or LT => GCs are more potent

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