Answer is (e)- The implied drug class is antihistamines. Of the drugs given only 2, (c), and (e) are antihistamines. There are two classes of antihistamines, H1 and H2. H2, represented by cimetidine, are used to treat ulcers not skin conditions. H1
antihistamines are used to treat allergic reactions, and chlorpheniramine is an H1 drug. Thus the answer is (e).

(d) same question repeated three different ways

(c) meclizine is used for vertigo, the others for allergies

(a) Remember that Parkinsonism is a due to a deficiency of DA in the brain, and is currently treated with levodopa and carbidopa. However, prior to these, anticholinergic drugs were the first drugs found to be somewhat effective for treatment of this disease, in that cholinergic and dopaminergic tracts interact in the brain, and thus reducing cholinergic activity via anticholinergic drugs improves or enhances dopaminergic function, suggesting one is inhibitory to the other. Drugs with anticholinergic activity are often still the first drug tried. Antihistamine drugs such as diphenhydramine often have strong anticholinergic activity, which accounts for their effectiveness in drying nasal secretions associated with a cold. Therefore, the answer is (a). (e) is there to confuse you, but don’t be. Diphenhydramine does not stimulate dopaminergic nerves in the basal ganglia. Adrenergic blockers ((c)) do see some use in the treatment of Parkinson’s, but diphenhydramine has no adrenergic blocking activity. Diphenhydramine does have the actions given in (b) and (d), but these are not responsible for its efficacy in Parkinson’s.

(b) Answer is (b) – memorization – H1 antihistamines are competitive histamine receptor blockers. Many students answer (e), but this is the mechanism of action of cromolyn. (c) also draws some answers, but is wrong-epinephrine is the physiological antagonist of histamine.

Answer is (b)- This is a memorization question. Carbamazepine, as well as phenytoin, are the main drugs used to treat trigeminal neuralgia. Clonazepam is a benzodiazepine, succinylcholine is a depolarizing neuromuscular blocking agent, while acetazolamine is an anticonvulsant like carbamazepine.

The answer is (b), Cardiac arrthymias are the main bad side effect of epinephrine as a vasoconstrictor. Epi stimulates both alpha and beta receptors. Beta receptors are found in the heart and stimulation of beta receptors increases heart rate, force of contraction, cardiac output and oxygen utilization. (a) is wrong, epi elevates blood glucose. (c) is wrong- beta stimulation in smooth muscle and bronchi causes bronchodilation, and is thus a drug of choice for acute asthmatic attacks. (d) is obviously wrong- a decrease in blood pressure would not result from adrenergic stimulation, increased blood pressure is the rule.

The two major side effects are suspected carcinogenicity and the tendency to produce thromboembolisms. Liver function can be altered but this is reversible. Research has failed to prove the link between estrogen and breast cancer, and reproductive function eventually returns upon cessation of therapy.

The answer is (d). Miosis ((a)) is a cholinergic effect typically observed with opiates. Cocaine doesn’t cause this kind of effect for example. (b), tolerance, is common to many drugs such as opiates, barbiturates and sedatives, but has not been clearly demonstrated for all abused drugs. (c), physical dependence, is usually thought to be true only for morphine, alcohol, caffeine, and perhaps cocaine.

Answer is (e)- Alcohol inhibits the CNS, thus eliminating (a), (b), and (c), leaving the choice between 4 and 5. Alcohol has been postulated to inhibit GABA effects, the major inhibitory transmitter in the CNS, especially in the cortex. Thus (e) is the answer.

Answer is (c)- memorization- alpha agonists decrease insulin release, beta agonists increase it. Thus because both of these are adrenergic stimulation, (a) can’t be the answer. (b)- muscarinic agonists increase insulin release, but this is not the mechanism of sulfonylureas. They cause insulin release by (c), and are the primary oral antidiabetic agents used therapeutically.

Answer is (e)- Dicoumarol is an oral anticoagulant. Thus the risk in an extraction is that the patient may bleed excessively, or that a serious interaction with a drug that you might require in your management of the patient, such as barbiturates or salicylates may occur. You may need to adjust the anticoagulant activity to within a safe range for surgical procedures. Since dicoumarol prevents blood clotting by preventing the conversion of Vitamin K to prothrombin, (e) is the only appropriate test.

Answer is (c)- 2 gm at 0 hr, at 4 hrs 1/2 from first injection is gone, leaving 1 gm in the body and you inject 2 more for a total after the second injection of 3. At the third dose, 1/2 of 3 is gone, leaving 1.5 gms, you inject 2 more for a total of 3.5 immediately after the third dose.

(a) should be immediately obvious- go no further, do not pass go, do not collect $200. (b) is wrong-Protamine is an antagonist of heparin, not dicoumarol. (c): phenylbutazone enhances the toxicity of warfarin by displacing it from plasma protein binding sites. (d): hyperbaric oxygen would be a useful treatment for carbon monoxide poisoning, not CO2

Answer is (d)- remember, diabetes medications can be organized into 3 groups based on their onset and duration of action: 1)fast-acting: insulin injection, 2) intermediate acting: Isophane insulin suspension, and 3) long acting: protamine zinc insulin suspension

answer is (a)- most people answer 3, confusing protein binding sites from active receptor sites where drugs exert their effects. Protein binding sites are just uptake sites that take up a drug and keep it from getting to its real receptor site of action. Some drugs are extensively protein bound, for example coumarin is 97% protein bound and only 3% is left to reach effective sites. Administration with another drug that is also extensively plasma protein bound will displace the drug that is already on these sites via competition, and thus effectively increase the level of drug that can now get to an active receptor site.

Answer is (e)- Addison’s disease results from failure of the adrenal cortices to produce adrenocortical hormones such as aldosterone. Aldosterone is a mineralocorticoid that controls sodium retention and potassium excretion. Lack of aldosterone results in electrolyte imbalances, with the major problem being hyponatremia (sodium loss). Similar symptoms may also be seen when a patient is withdrawn from chronic adrenal steroid therapy. Due to depressed adrenal function, patients can’t respond to stressful situations (such as dental procedures) adequately, and an adrenal crisis may occur. The recommended treatment is (e), 100 mg of hydrocortisone hemisuccinate. Of the other corticosteroids given, he dose given for prednisolone ((b)) is too low, while triamcinolone lacks any effects on sodium retention. NE and Epi would not be used in this situation- they might be used in a case of adrenal medulla insufficiency.

Answer is (b)- usually biotransformation results in a more water soluble, more readily excreted form of the parent drug. In most cases this inactivates the drug, but there are some exceptions which involve the formation of metabolites with activity (diazepam) or when an inactive prodrug is given (levodopa) which becomes active after the first step in the biotransformation pathway (DOPA) sometimes are asked in questions of this form.

Answer is (c)- Remember that local anesthetics are either esters or amides. All of the other alternatives diverge widely in their structures.

Answer is (c)- Remember, cimetidine or “Tagamet” is an H2 antihistamine are used therapeutically to inhibit gastric secretion ((c)) in cases of peptic ulcer. This is its only clinical use. You might see it in a question regarding drug metabolism- it is also a
potent inhibitor of the mixed function oxidase drug metabolizing enzyme system in the liver. The other alternatives are to confuse you because you probably at least remember that it is an antihistamine, but you don’t know the difference between H1 and H2 antihistamines.

Answer is (d) – I would guess (d) because its the only one I’ve ever heard of, and since this wasn’t covered in class you might be one to guess it also. Wow, we got it right! Actually, if you look the others up, (a) & (b) are alkylating agents, (c) is an alkaloid derived from plants. (d) is a folate antagonist, which acts as an antimetabolite. Just for your future edification, most cancer chemotherapy drugs cause cell death by affecting the ability of cells to divide. The drugs thus inhibit one or more phases of the cell cycle or prevent a cell in Go (the nondividing phase) from entering into the cycle of cell division. Antimetabolites may act in 2 ways (1) by incorporation into a metabolic pathway and formation of a false metabolite which is nonfunctional or (2) by inhibition of the catalytic function of an enzyme or enzyme system. Methotrexate is an example of a cell cycle specific antimetabolite that inhibits DNA synthesis during the S phase. Vincristine acts during the mitotic phase

Answer is (b)- maintaining the concentration of Ca++ in extracellular fluid by regulating the deposition and mobilization of calcium from bone, absorption from the GI tract, excretion etc. is the main function of parathyroid hormone. Thyrocalcitonin is another
name for calcitonin. They hope to confuse you because there is a correlation between calcitonin and calcium, except that calcium concentrations regulate the synthesis and release of calcitonin. Glucagon is a pancreatic hormone that stimulates glucose production, thyrotropin is there to confuse you with parathyroid hormone, and aldosterone regulates Na+ levels not Ca++.

Answer is (d)- scopolamine is a muscarinic receptor blocker similar to atropine, thus (a) is wrong. Levodopa has nothing to do with this question. To counteract a competitive muscarinic receptor block, you need to increase the levels of agonist, in this case acetylcholine. However, you can’t give ACh because it is broken down almost instantaneously by acetylcholinesterase. The answer is to give a drug which knocks out the acetylcholinesterase, allowing endogenously released ACh to accumulate to overcome the action of scopolamine. The drug which will do this is physostigmine.

Answer is (a)- your choices are between tolerance and desensitization, (a) and (d). The latter refers to some alteration of receptors that leads to diminished response to the drug, and is really a mechanism whereby tolerance may occur. Thus the Gods of the Board questions have decreed that the answer shall be (a).

Answer is (c)- “a” can’t be right because exercise increases blood flow through muscles and thus improves absorption. Thus # 1 is wrong. “b” is obviously right for the same reason. “c” would also result in reduced blood flow so slower absorption would also be a problem. “d” is often used for prolonged and steady drug release so it also is true. The answer must thus be (c).

Answer is (e)- “Salicylism” is a mild toxic reaction to aspirin (acetylsalicylic acid), usually occurring after prolonged treatment with large doses. Nausea, tinnitus, vomiting and GI bleeding are all symptoms of salicylism. Other notable side effects of aspirin
which result from ingestion of a single large dose are disturbances of acid-base imbalance (acidosis or alkalosis), fever, hypoglycemia. Remember, aspirin, is contraindicated in children suffering from influenza or chicken pox: aspirin has been implicated in the development of Renee’s syndrome.

Answer is (b)- This is a pure memorization question. All of these drugs are benzodiazepines, which typically have a long duration of action because they are converted to pharmacologically active metabolites with long half-lives. Oxazepam, midazolam, and lorazepam are exceptions that are not converted to active metabolites. The answer is thus (b).

Answer is (a)- If you learned anything from pharmacology, you should instantly be able to identify (a) as the correct answer. The constant quest of pharmacology as a science is to design or identify drugs that have as narrow or specific range of action as possible, but not to many single action drugs have been identified. Alternatives (c) and (b) should remind you of phrases such as dose-response curves and therapeutic index (the ratio of a toxic or lethal dose to a therapeutic dose, LD50/ED50). A toxic effect can be broadly defined as any undesired effect of the drug, thus # 4 can’t be the exception. To rule out # 5, think of nerve gas.

Answer is (d)- Nalbuphine is a mixed agonist-antagonist that is analgesically equipotent with morphine (thus # 1 is ruled out). However, analgesia is produced by its agonistic effects at kappa opioid receptors. It has pronounced antagonistic effects at the mu receptor, and can be used clinically to reverse respiratory depression (by blocking mu receptors) without a loss of analgesic effects (by stimulating kappa receptors). Thus, # 2
is ruled out. # 4 is not likely. The mixed agonist-antagonists were designed to combine analgesia with enough antagonistic properties to prevent their abuse. Thus, # 3 is the right answer. Typically, these drugs can mimic the effect of morphine in a drug free patient, but antagonize opiate action in a dependent patient, thus precipitating withdrawal. Of this class of drugs, butorphanol is the exception- it will not precipitate withdrawal because it is only a weak mu antagonist.

Answer is (b)- Nonsynthetic reactions (phase I reactions) include the various transformations of molecular structure: oxidation, reduction, and hydrolysis; they represent the first stage of biotransformation. Synthetic (phase II) reactions consist of the conjugation of drugs or their metabolites with functional groups. Of the alternatives, (c) and (d) are conjugation reactions, and thus are wrong because they are synthetic reactions. Alternative (a) is tricky. It is made to sound like N-dealkylation, which is a nonsynthetic or phase I oxidative reaction. There is no reaction called N-alkylation. Thus (b), an oxidative phase I reaction is left as the right answer