The quizzes about Gastrointestinal and Urinary Tract Pharmacology, Nutrition (Vitamins)

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Gastrointestinal and Urinary Tract Pharmacology, Nutrition (Vitamins)

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Question 1

A 65-year-old man will be undergoing elective total knee replacement He i s urged to start taking a specified stool softener several days before surgery, and i t will continue to be administered as needed for several days after the surgery. That i s because of one of the drugs he will receive in the operative and post-op periods (l i sted below) routinely causes severe constipation. Which drug i s that?

A	Ketorolac to supplement postoperative analgesia from morphine
B	Midazolam for sedation, anxiety relief, and induction of short-term amnesia
C	Morphine and/or a s imilar high-efficacy opioid for pain
D	Neostigmine as part of a protocol to reverse skeletal muscle paralysis
E	Ondansetron for management of postoperative nausea and vomiting

Question 1 Explanation:

Morphine (which is often used for short-term postop pain control) and fentanyl (which is often used for intraoperative pain prevention) cause numerous side effects. One of the gravest concerns for most patients is ventilatory depression, but that can be managed easily with such interventions as ventilatory support. Even in the absence of any lingering post-op ventilatory problems, constipation from a strong opioid poses a very common and potentially serious post-op management issue. That is why stool softeners or laxatives take on an important role for such patients. Neither ketorolac (a) nor midazolam (b) cause significant reductions of gut motility. Neostigmine (d), the most common acetylcholinesterase inhibitor used to reverse drug-induced skeletal muscle paralysis, would not likely to require a stool softener or laxative. Indeed, via neostigmine’s ability to increase gut motility (stimulates longitudinal gut muscle activity, relaxes sphincters) it is probably the least likely drug to necessitate use of a stool softener. Ondansetron (e), quite effective in managing perioperative nausea and vomiting, has a constipation-inducing risk far lower than that associated with strong opioids.

Question 2

A patient with multiple medical problems i s taking several drugs, including theophylline, warfarin, quinidine, and Despite the l ikelihood of interactions, dosages of each were adjusted carefully so their plasma concentrations and effects are acceptable. However, the patient suffers some GI distress and starts taking a drug provided by one of his “well-intentioned” friends. He presents with excessive or toxic effects from all his other medications, and blood tests reveal that plasma concentrations of all the prescribed drugs are high. Which drug did the patient most l ikely self-prescribe and take?

A	Antacid (typical magnesium-aluminum combination)
B	Cimetidine
C	Famotidine
D	Nizatidine
E	Ranitidine

Question 2 Explanation:

Cimetidine differs significantly from the other H2 blockers, famoti-dine (c), nizatidine (d), and ranitidine (e), in that it is a very effective inhibitor of the hepatic mixed function oxidase (P450) drug-metabolizing enzyme systems. (Cimetidine inhibits CYP1A2, 2C9, 2D6, and 3A4.) The other H2 blockers have no significant P450 effects, nor do they cause side effects as frequent or as problematic as those caused by cimetidine, especially at high doses. The outcome of P450 inhibition, of course, is reduced hepatic clearance of the interactants, leading to excessive plasma concentrations and effects if their dosages are not reduced properly. The examples cited in the question—phenytoin, warfarin, quinidine, and theophylline—are among the important interactants with cimetidine. They have rather low margins of safety (or therapeutic index: LD50/ED50), so even a slight increases in plasma levels (reductions of metabolic clearance) may be enough to cause toxicity. Given the fact that the alternative H2 blockers don’t inhibit the P450 system, there’s no rational reason for prescribing cimetidine to patients on multiple drug therapy (and in this case, the patient should have been warned about self-medicating with it). Antacids (a; particularly those that include an aluminum salt, which applies to the vast majority of OTC antacid combination products) tend to adsorb other drugs in the gut at or around the same time, and inhibit their absorption (rate, extent, or both). If this patient had taken an antacid with his other meds, on a regular basis, you would see reduced blood levels and effects—not increases as described in the question. Note: Not long after the newer H2 blockers came on the market, and we knew that they caused fewer side effects than cimetidine and certainly did not inhibit various CYP enzymes to cause drug-drug interactions, I asked a gastroenterologist why one would ever prescribe cimetidine. Her answer? She couldn’t think of a valid reason except cost. And now, as costs have come down, even that’s not a consideration. Finally, it is important to remember: cimetidine is still available OTC, and patients who should not be taking it (mainly because of interactions with other drugs they may be taking) can still use this drug without your OK or even your knowledge.

Question 3

A 53-year-old woman has been taking warfarin for prophylaxis of venous thromboembolism for the last 6 During that time the degree of anticoagulation, based on frequent measurements of her INR (International Normalized Ratio, an adjusted prothrombin time), has been in the desired therapeutic range, 2.5, and she suffered no adverse effects. Two weeks ago, she developed what she believed to be heartburn, and without consulting her MD began taking an over-the-counter medicine on a daily basis to control i t. She presents in cl inic today, reporting frequent epistaxis, and says her gums bleed when she brushes her teeth. Her INR i s now 9, well above the normal therapeutic range and indicative of excess warfarin effects. Which of the following medicines most l ikely interacted with the warfarin to cause these s igns and symptoms?

A	Bismuth salts (eg, Pepto-Bismol®)
B	Calcium carbonate
C	Cimetidine
D	Esomeprazole
E	Nizatidine

Question 3 Explanation:

Compared with all other drugs or drug groups listed, cimetidine stands out in terms of its ability to inhibit strongly the liver’s P450 system, which is important for the metabolic inactivation of warfarin (and many other drugs). PPIs such as esomeprazole (d) don’t share this property, nor do H2 blockers other than cimetidine (eg, nizatidine). [Ranitidine, not listed as an answer choice, is an H2 blocker that does have some P-450-inhibitory activity, but it is very weak—particularly in comparison with cimetidine—and the consequences of any potential drug interaction by this mechanism probably is not clinically important.] There is an interaction between warfarin (and many other orally administered drugs) with bismuth salts (a) and, especially, antacids (b, e) or antacid combinations, particularly Mg-Al combinations (e). They all tend to reduce the rate and extent of absorption of many oral drugs taken at or nearly at the same time. In such cases, the bioavailability of warfarin would be decreased, resulting in an INR that is lower—not higher—than would occur otherwise.

Question 4

Esomeprazole i s one of the medications prescribed for a patient you are seeing today in the general medicine cl Which one of the following statements best describes the actions or effects of esomeprazole and other drugs in i ts class?

A	Cause strong systemic atropine-like (antimuscarinic) effects that l imit their use in patients for whom atropine i tself i s contraindicated
B	Inhibit gastric acid secretion by s imultaneously and competitively blocking the actions of the agonists histamine, acetylcholine, and gastrin, on their parietal cell membrane receptors
C	Neutralize gastric acid faster than any other classes of drugs indicated for peptic ulcer disease or gastroesophageal reflux disease (GERD)
D	Profoundly inhibit an ATPase located on parietal cell membranes, thereby inhibiting acid secretion
E	Tend to cause bradycardia by antagonizing the positive chronotropic effects of histamine on cardiac H1 receptors

Question 4 Explanation:

You should look at the “stem” of the drug’s generic name. It ends in “- prazole,” and so you should realize that the drug is classified as a proton pump inhibitor (PPI). Esomeprazole, indeed all other “-prazoles,” have no antimuscarinic activity (a). Their antisecretory actions occur “downstream” of agonists such as ACh, histamine, and gastrin, and do not involve blockade/antagonism of those ligands on their receptors (b). PPIs have no acid-neutralizing activity (c; antacids work by that mechanism, and antacids provide the fastest relief of acid-related pain); they simply, yet effectively and rather profoundly, inhibit gastric acid secretion. Histamine does exert positive chronotropic effects on the heart, but that is not antagonized by any PPI, nor do the PPIs tend to cause bradycardia (e).

Question 5

A 60-year-old man has episodes of severe gastric and esophageal pain that i s ultimately l inked to gastric acid. Which one of the following drugs or drug classes, whether available over-the-counter or prescribed, i s most l ikely to relieve the acid-related symptoms the fastest when taken at usually effective/recommended doses?

A	Antacids (eg, magnesium-aluminum combinations)
B	Cimetidine (but not other drugs in i ts class)
C	H2 blockers, any of them
D	Misoprostol
E	Proton pump inhibitors

Question 5 Explanation:

Antacids, at usual recommended doses, relieve acid-related pain faster than any other drugs. Their acid-neutralizing effects occur instantaneously upon contact with gastric (hydrochloric) acid, and pain relief occurs within minutes of taking a dose. All the other drugs inhibit gastric acid secretion, some more effectively or completely than others, some quicker than others, but none alleviates acid-related pain or discomfort as quickly as antacids do. This includes cimetidine (b) or any other H2 blocker (c), misoprostol (d) and any of the PPIs (e). Several things worth noting here. Misoprostol has two main uses. One is as an adjunct to drug-induced termination of pregnancy, due to its strong uterine smooth muscle stimulating effects. In the context of this question in the GI section, misoprostol is sometimes used as an adjunct to reduce the incidence or severity of NSAID-induced gastric ulcer formation. For that purpose, misoprostol exerts what has been called a mucotropic or gastric cytoprotective effect: it enhances the formation of mucus in the gastric mucosa, thereby strengthening the “barrier” between the NSAID and its target of damage. Remember: No acid, no pain. This is a true statement. It basically means that the way to reduce gastric acid-related pain is either to neutralize sufficient amounts of acid (with an antacid) and/or inhibit sufficient amounts of gastric acid secretion, which can be accomplished with either H2 blocker or, more effectively, a PPI. Note that the rapidity of symptom relief does NOT parallel rate of ulcer healing. Remember, too, a somewhat related statement that is FALSE: No acid means no ulcer. What that means, clinically, is that we can neutralize acid, or inhibit gastric acid secretion rather quickly, but unless proper therapy is continued long enough, there still will be ulcers despite the lack of the major symptom, pain.

Question 6

Five days after starting self-medication for diarrhea and other GI complaints that arose after a trip to Central America, a very worried patient calls to report that his tongue has turned His stools have darkened too, but his description doesn’t at all fi t with what would be expected i f the patient had a bleed anywhere in the GI tract (eg, no “coffee grounds stools” suggestive of a gastric bleed.). Which drug most l ikely caused these s igns?

A	Bismuth salts
B	Calcium carbonate
C	Cimetidine
D	Esomeprazole
E	Magnesium-aluminum antacid combination
F	Nizatidine

Question 6 Explanation:

Among all the medications listed, black tongue and black stool are uniquely characteristic of the use of bismuth salts, including bismuth subsalicylate (most widely known, perhaps, as Pepto Bismol®). These effects are not worrisome (unless the patient isn’t forewarned about this likely occurrence, in which case they can cause much alarm), and otherwise indicate no toxicity or other potential adverse effects. None of the other drugs listed share this property.

Question 7

A patient who has been a high-dose alcohol abuser for many years presents with hepatic portal-systemic encephalopathy. What drug, given in relatively high doses, would be most suitable for the relief of some of the s igns and symptoms of this condition, and the l ikely underlying biochemical anomalies?

A	Diphenoxylate
B	Esomeprazole
C	Lactulose
D	Loperamide
E	Ondansetron

Question 7 Explanation:

Lactu-lose is a synthetic, nonabsorbable disaccharide (galactose-fructose). In moderate doses it acts as an osmotic laxative. In higher doses it binds intestinal ammonia and other toxins that accumulate in the intestine in severe liver dysfunction. These toxins, and perhaps more so the ammonia, contribute to the signs and symptoms of encephalopathy. None of the other drugs listed provide this benefit. Diphenoxylate (a) and loperamide (c) are opioid-like antidiarrheal drugs. Esomeprazole (b) is a proton pump inhibitor used to suppress gastric acid secretion. And ondansetron (e), a 5-HT3 antagonist, is mainly used to manage nausea and vomiting in response to chemotherapy

Question 8

Fat-soluble vi tamins, compared with their water-soluble counterparts, generally have a greater potential toxicity to the user when taken in excess. What property of those vi tamins—A, D, E, and K—is basically the main reason for this finding?

A	Administered in larger doses
B	Avidly stored by the body
C	Capable of dissolving membrane phospholipids
D	Involved in more essential metabolic pathways
E	Metabolized much more s lowly

Question 8 Explanation:

Fat-soluble vitamins, especially A and D (the others being vitamins E and K), can be stored in massive amounts and, hence, have a potential for serious toxicities. (On the bright side, this abundant storage means that relatively brief periods of inadequate intake are not likely to cause clinical signs and symptoms of deficiency.) Water-soluble vitamins are easily excreted by the kidneys and accumulation to toxic levels is much less common. However, inadequate dietary intake will lead to manifestations of deficiency relatively faster. On average, most people consume excessive amounts (a) of fat-soluble vitamins no more often than they do water-soluble ones. Even very large doses of fat-soluble vitamins that might be consumed will not alter membrane structure or function (c), although such effects can be demonstrated in certain in vitro settings that bear little relevance to intact humans. Differences involving greater or more roles in overall cell metabolism (d), or rates of the metabolism of the vitamins themselves (e), are not reasonable explanations for the relatively greater toxic potential of vitamins A, D, E, and K.

Question 9

A patient i s transported from a distant hospital to your surgical service by air He had abdominal surgery and in the postop care unit he received a drug that was clearly not indicated. The drug caused intense contraction of the detrusor and trigone muscles of his bladder. The fi rst dose failed to cause emptying of the bladder, so a second dose was given. However, and unknown to his prior care team, he had a mass that rather s ignificantly obstructed his urethra, and prior anatomical weakening in a portion of his bladder. Upon administration of the drug he fi rst suffered retrograde urine flow (from his bladder, back to the kidneys via the ureters), causing renal damage. Soon thereafter his bladder ruptured into his peritoneum. Which drug or drug class most l ikely caused these adverse effects?

A	Albuterol
B	Atropine or a s imilar antimuscarinic
C	Bethanechol
D	Furosemide
E	Propranolol or a s imilar β-blocker

Question 9 Explanation:

Bethanechol is a muscarinic agonist that is used to manage functional urinary retention—that is, urinary retention or a significant inability to void caused by some functional defect in the bladder musculature. It is contraindicated for patients with bladder walls that are damaged or unable to respond safely to drugs that stimulate the bladder musculature, and patients with mechanical obstruction of the urethra (from, say, prostatism or a prostatic cancer). This was what caused the bethanecholinduced problems for this patient. Albuterol (a), predominantly a β2 agonist used for its bronchodilator effects, has no significant effects on the healthy or damaged bladder: β- receptors just aren’t there. Atropine (b) or other antimuscarinics will weaken contraction of the trigone and detrusor, and stimulate contraction of the bladder sphincter, causing just the opposite of what I described. Furosemide (d) and other loop diuretics (torsemide, bumetanide, and ethacrynic acid) obviously increase the need to urinate and the volume of urine that is excreted. However, the bladder activation that ensues is mediated by reflexes triggered by a full bladder. There is no direct stimulation or inhibition of bladder musculature. Finally, just as β-agonists have no appreciable effect on bladder musculature, neither do drugs that block β-adrenergic receptors (e).

Question 10

A patient presents with malaise, and skin and mucous membranes appear Among the key findings from blood work are hypochromic, microcytic red cells and reduced red cell count/hematocrit; reduced reticulocyte count; and reduced total hemoglobin content. Which drug would be indicated, based on the presentation?

A	Cyanocobalamin (B12)
B	Folic acid
C	Iron
D	Vitamin C
E	Vitamin D

Question 10 Explanation:

The description contains many of the characteristics of “iron-deficiency anemia.” Oral iron salts (eg, ferrous sulfate, gluconate, or fumarate) are usually the first choice for management (after ruling out such causes as blood loss). Changes of gut motility (sometimes diarrhea, sometimes constipation), nausea, and heartburn are common complaints with oral iron salts, but using the oral drugs is often preferable to, just as effective as, and safer than using parenteral iron products such as iron-dextran (risk of anaphylaxis) or other iron complexes, which typically involve erythropoietin administration adjunctively. Megaloblastic anemia (in contrast with the microcytic anemia I described here) would be treated differently. If it is caused by vitamin B12 deficiency (vitamin malabsorption due to deficiency of intrinsic factor; answer a), we would treat with cyanocobalamin. The other cause, folate deficiency (inadequate dietary intake) is managed with oral folic acid (b). Deficiencies of vitamin C or D (answers d and e, respectively) don’t typically cause anemias.

Question 11

A patient will start taking one of the drugs l i sted As we hand them the prescription we advise them not to take supplemental vi tamin B₆ (pyridoxine), whether alone or as part of a multivitamin supplement, because the vi tamin i s l ikely to counteract a desired effect of the prescribed drug. To which drug does this advice apply?

A	Captopril for heart failure or hypertension
B	Haloperidol for Tourette syndrome
C	Levodopa/carbidopa for Parkinson disease
D	Niacin for hypertriglyceridemia
E	Phenytoin for epilepsy

Question 11 Explanation:

Recall that DOPA decarboxylase, an enzyme whose activity is dependent on pyridoxine, is responsible for metabolizing orally administered levodopa to dopamine in the gut; and that only unmetabolized levodopa crosses the blood-brain barrier to be efficacious in relieving parkinsonian signs and symptoms. Recall, too, that levodopa is often administered with carbidopa, a drug that inhibits the peripheral decarboxylase, sparing levodopa for entry into the brain and whose actions are antagonized by pyridoxine. Administering supplemental B6 will reduce the bioavailability of levodopa, thereby counteracting its antiparkinson effectiveness. None of the other drugs listed, whether used for the stated purpose or others, has its effects antagonized by pyridoxine.

Question 12

A patient with tuberculosis i s being treated with i She develops paresthesias, muscle aches, and unsteadiness. Which vi tamin needs to be given in supplemental doses in order to reverse these symptoms—or used from the outset to prevent them in high-risk patients?

A	Vitamin A
B	Vitamin B1 (thiamine)
C	Vitamin B6 (pyridoxine)
D	Vitamin C
E	Vitamin K

Question 12 Explanation:

Pyridoxine deficiencies arise often during isoniazid therapy because the antimycobacterial drug interferes with metabolic activation of the vitamin. The treatment or prophylaxis for at-risk patients is to administer relatively large doses of B6 (pyridoxine).

Question 13

A patient has severe gastroesophageal reflux disease (GERD). In addition to providing some immediate symptom relief, for which you will prescribe usually effective doses of an OTC combination antacid product, you want to suppress gastric acid completely as Which drug i s best suited for achieving that goal?

A	Atropine
B	Calcium carbonate
C	Cimetidine
D	Esomeprazole
E	Misoprostol

Question 13 Explanation:

Esomeprazole and related drugs (lansoprazole, omeprazole, rabeprazole, pantoprazole) inhibit the parietal cell H+-K+ATPase—the “proton pump”—that is the “final common pathway” for acid secretion triggered by all the major stimuli of gastric acid secretion. As a result, they are the most efficacious, causing near complete anti-acid secretory activity. Recall the main agonists that provoke acid secretion. One is gastrin, for which there are no clinically useful antagonists at this time. Histamine, arising from enterochromaffin-like (ECL) cells, activates H2 receptors, which then triggers acid secretion. Histamine’s effects can be blocked by cimetidine (c) or other H2 blockers (famotidine, nizatidine, and ranitidine; any of these alternatives are preferred to cimetidine, because they lack cimetidine’s P450 inhibitory effects). Acetylcholine increases gastric acid secretion by activating muscarinic receptors on both ECL cells and parietal cells. Its effects can be blocked by atropine (a), propantheline, pirenzepine (widely taught but never approved for use in the United States), and several other drugs with antimuscarinic activity. However, blocking only the histaminergic influences or only the cholinergic influences—or even blocking both types of receptors—only partially inhibits acid secretion. One additional disadvantage of muscarinic blockade is the prevalence of often disturbing and usually unwanted atropine-like side effects elsewhere, for example, on the eyes, heart, urinary tract, and exocrine gland secretions. Calcium carbonate (b), as well as aluminum and magnesium salts and sodium bicarbonate, are antacids. They have no inhibitory effects on acid secretion. Instead, they neutralize a component of acid that has already been secreted (and aluminum salts also adsorb pepsins). Calcium and aluminum salts tend to cause constipation, and magnesium salts, diarrhea/laxation. Sodium bicarbonate tends to cause no changes of gut motility, but the significant absorption of the sodium poses problems for many patients (eg, those with hypertension, heart failure, edema), and bicarbonate absorption causes metabolic alkalosis. Misoprostol (e) is unique in several ways. One way is that this prostaglandin analog mimics the effects of endogenous prostaglandins (mainly PGE2) on parietal cell prostaglandin receptors. Unlike the agonists noted above, one result of that is inhibition of acid secretion. Overall, the antiacid secretory effects are relatively weak. Ultimately, however, regardless of whether gastrin, ACh, or histamine is present, parietal cell acid secretion ultimately “funnels through” theproton pump. Block the receptors for any of the mediators noted above and you will suppress acid secretion caused only by that mediator—but that is only a fraction of total acid secretion. Block the proton pump and acid secretion will be inhibited nearly fully, no matter which one or more agonists are present.

Question 14

An opioid abuser, seeking something to self-administer for subjective responses, gets a large amount of diphenoxylate and consumes i t all at He i s not l ikely to do this again because he has consumed a combination product that contains not only the diphenoxylate but also another drug that causes a host of unpleasant systemic responses. What i s the other drug found in combination with the diphenoxylate?

A	Apomorphine
B	Atropine
C	Ipecac
D	Magnesium sulfate
E	Naltrexone

Question 14 Explanation:

Diphenoxylate is an opioid that has predominant antidiarrheal activity, and that is its sole approved use. It inhibits peristalsis and, hence, increases the passage time of the intestinal bolus. Typical antidiarrheal doses do not cause ventilatory depression, analgesia, or the euphoria for which opioids are mainly abused. However, should one attempt to take high doses to become euphoric, unpleasant effects will appear. That is because the product contains a small amount of atropine —usually not enough to cause side effects when the proper dose of the product is consumed, but clearly able to cause all the typical and unpleasant anti-muscarinic side effects of which you should be aware (see the chapter, “Autonomic Nervous System”) when excessive doses are taken. This pharmaceutical manufacturing “trick” discourages diphenoxylate abuse. Apomorphine (a) and ipecac (c) are dopaminergic emetics (for parenteral and oral administration, respectively) that are used in some poisonings where inducing emesis is desired and safe. Magnesium sulfate (“Epson salt”—clearly a foul-tasting substance; answer d) is occasionally and usually inappropriately used as a laxative or cathartic. Naltrexone (e) is an opioid antagonist (μ and κ receptors, naloxone-like, but given orally.)

Question 15

During a regular check-up, your patient states “You know, doc, sometimes after eating I get heartburn … you know, acid-indigestion.” Since the symptoms seem to be mild and infrequent, you suggest an empiric trial of an OTC antacid for prompt symptom relief, plus an oral anti-acid secretory drug for long-term You recommend several antacid brands for the patient to try. All the products you l i st are combination products that contain a magnesium salt and an aluminum salt. What i s main rationale or reason why the vast majority of these products contain these two particular drugs or salts?

A	Al salts counteract the gastric mucosal-irritating effects of Mg salts
B	Al salts require activation by an Mg-dependent enzyme in order to inhibit the parietal cell proton pumps
C	Mg salts cause a diuresis that helps reduce systemic accumulation of the Al salt by increasing renal Al excretion
D	Mg salts potentiate the ability of Al salts to inhibit gastric acid secretion
E	Mg salts tend to cause a laxative effect (increased gut motility) that counteracts the tendency of an Al salt to cause constipation

Question 15 Explanation:

Magnesium salts (eg, oxide/hydroxide, as found in ordinary milk of magnesia) used alone tend to cause a laxative effect. (Indeed, at dosages higher than those used for acid neutralization, magnesium salts are used for their laxative or cathartic effects.) Aluminum (and calcium) antacids, given alone, tend to cause constipation. Combining a magnesium salt with an aluminum salt (and/or calcium antacid) is an often successful approach to minimizing antacid-induced changes of net gut motility. Magnesium salts do not potentiate the antisecretory actions of Al or any other antacid. Indeed, none of the antacids inhibit gastric acid secretion (ie, they don’t have an antisecretory effect to begin with). They merely neutralize acid that has already been secreted (Mg, Ca, sodium bicarbonate) or adsorb acid and pepsins (most of the aluminum compounds). Although high concentrations of Mg salts may cause gastric irritation, the amounts and concentrations found in antacid products are not sufficient to do that. Remember that in order to minimize the risks of hypermagnesemia, even when otherwise reasonable doses are taken and especially when doses are higher than that, renal function must be “adequate.” As a result, many elderly patients and patients of any age who have renal dysfunction from other causes, are at increased risk for hypermagnesemia. Al salts don’t protect against any such potential effect. Magnesium salts do contribute to a diuresis, but it is not a significant effect. Al salts are “non-systemic” antacids: they are not absorbed to any appreciable degree, and therefore they don’t depend on renal processes for their elimination. The Al salts are effective in the form in which they are administered, and don’t require any enzymatic (or other type of) “activation” to exert their effects (which involves adsorption of acid, pepsins, etc).

Question 16

A patient with multiple GI complaints i s receiving ursodeoxycholic acid (ursodiol) as part of his drug What i s the most l ikely purpose for which this drug i s being given?

A	Dissolving cholesterol stones in the bile ducts
B	Enhancing intestinal digestion and absorption of dietary fats
C	Helping to reverse malabsorption of fat-soluble vi tamins from the diet
D	Stimulating gastric acid secretion in achlorhydria.
E	Suppressing steatorrhea and i ts consequences

Question 16 Explanation:

Ursodeoxycholic acid (ursodiol), one of several naturally occurring bile acids, is effective in some patients with cholesterol gallstones. Its main initial action is reduced hepatic cholesterol synthesis. That, in turn, lowers the cholesterol content in the bile, which favors the dissolution of cholesterol stones that have formed already and reduces the incidence of new stone formation. Ursodeoxycholic acid tends to inhibit (not enhance, answer b) intestinal fat digestion and absorption, and may contribute to (not reverse, answer c) impaired absorption of vitamins A, D, E, and K. The drug does not stimulate gastric acid secretion (d) and is not indicated for managing achlorhydria. Steatorrhea may develop in response to ursodeoxycholic acid; the incidence of fatty stools is not reduced (e) by the drug.

Question 17

Early-on in your general medicine clerkship you encounter a patient who i s taking a proton pump inhibitor, bismuth, metronidazole, and What i s the most l ikely condition for which this drug combination i s being used?

A	Antibiotic-associated pseudomembranous colitis
B	Irri table bowel syndrome (IBS)
C	Refractory or recurrent, and severe, gastric or duodenal ulcers secondary to H. pylori
D	“Traveler’s diarrhea,” severe, Escherichia coli-induced, from drinking contaminated water
E	Ulcers that occur in response to long-term, high-dose NSAID therapy for arthritis

Question 17 Explanation:

Several professional organizations, including the American College of Gastroenterology, have guidelines for managing severe, refractory, or recurrent duodenal and/or gastric ulcers, in which H. pylori clearly plays an important pathophysiologic role. Although several regimens have been suggested, all of them include an anti-acid secretory drug (usually a proton pump inhibitor, sometimes an H2 blocker), two or three antimicrobials (eg, amoxicillin, clarithromycin, or tetracycline, usually with metronidazole), and bismuth. In many cases, this so-called eradicative therapy can cause a clinical cure and prevent recurrences after about 8 weeks of treatment. (The treatment is expensive, but pales in comparison with the financial and personal costs of treating recurrent episodes or potentially serious complications such as GI bleeding or hemorrhage, either pharmacologically or surgically.) Antibiotic-associated pseudomembranous colitis (a) is typically managed with vancomycin or metronidazole, along with discontinuation of the causative agent (usually clindamycin). Dietary modifications (especially increased dietary fiber intake) and various drugs that alter gut motility (laxatives in constipation-predominant IBS; opioid, opioid-like, or serotonin antagonist antidiarrheals when diarrhea predominates) are often chosen to help manage irritable bowel syndrome (b). Doxycycline and/or bismuth salts are often used to prevent or treat E. coli-mediated diarrhea (d). If the goal is to prevent NSAID-induced gastric ulcers (e), a proton pump inhibitor (eg, esomeprazole), or misoprostol are reasonable choices.

Question 18

Several brand-name and store-brand “pink medications,” administered orally and available without prescription, are widely used to help alleviate occasional and short-lived nausea and vomiting, nonspecific GI distress, and diarrhea. They are also recommended for prophylaxis of “traveler’s diarrhea,” which typically i s caused by ingestion of foods or beverages contaminated with coli. These products contain bismuth subsalicylate, and because of the presence of an aspirin-like compound (a salicylate) they should not be taken by or administered to certain patients. Which patient-related factor or comorbidity contraindicates use of this drug or product?

A	Essential hypertension
B	Flu, chickenpox, or other vi ral i l lness in a child or adolescent
C	Hot flashes and other s igns/symptoms of menopause
D	Prostatic hypertrophy or glaucoma in elderly men
E	Rheumatoid or osteoarthritis
F	Severe seasonal allergy s igns and symptoms

Question 18 Explanation:

Bismuth salts such as the subsalicylate (best known, perhaps, as the brandname product Pepto Bismol®) exert antibiotic activity against H. pylori and probably E. coli also. They are commonly prescribed for the eradicative therapy of H. pylori-induced refractory gastric ulcers, along with an antibiotic and metronidazole. The salicylate in this formulation contraindicates its use in children with influenza or any other viral illness, owing to the risk of Reye syndrome. It is somewhat controversial what the term “children” means in this Reye-related context. The risk clearly applies to children in their adolescent (and earlier) years of age, but it may also extend to people younger than about 21 years of age. This is important to know, since children experiencing such viral illnesses as influenza, chick-enpox, or even a common cold may report that their “tummy hurts” and they may experience diarrhea for a variety of reasons. The “pink meds” described in the question are quite well known to many parents. Since they are available OTC (that automatically conveys the notion that they are “safe”) and effective, it’s not unlikely that the unknowing caregiver might give the child precisely the wrong drug. Warnings against the use of these bismuth-containing medications are printed on the labels of these products, but as you probably know by now many people don’t (or can’t) read product labels. The salicylate component also poses risks in other situations for which a salicylate should be avoided. Aspirin-sensitive asthma is a prime example. Bismuth salts (or the salicylate moiety specifically) lack significant effects on blood pressure or the effects of antihypertensive drugs (a). There are no well-documented beneficial or adverse effects on signs and symptoms typically associated with menopause (c). Likewise, there are no known desired or unwanted effects on prostate, urinary tract, or ocular function or disease (d), whether in older men or not; no effects on arthritic disease (the salicylate in bismuth subsalicylate is apparently sufficient to warrant the Reye syndrome warning, but not sufficient to favorably influence inflammatory diseases such as arthritis); nor affect signs and symptoms of seasonal (or other) allergic responses (f). The drug has no H2-blocking or muscarinic receptor-blocking activity. In the absence of any contraindications, bismuth subsalicylate may be useful for managing some cases of diarrhea, such as “traveler’s diarrhea” that often is caused by E. coli.

Question 19

A patient has undiagnosed multiple gastric ulcers. Shortly after consuming a large meal and large amounts of alcohol, he experiences s ignificant GI He takes an over-the-counter heartburn remedy. Within a minute or two he develops what he will later describe as a “bad bloated feeling.” Several of the ulcers have begun to bleed and he experiences searing pain. The patient becomes profoundly hypotensive from upper GI blood loss and i s transported to the hospital. Endoscopy confirms multiple bleeds; the endoscopist remarks that i t appears as i f the lesions had been l i terally stretched apart, causing additional ti ssue damage that led to the hemorrhage. Which drug or product did the patient most l ikely take?

A	An aluminum salt
B	An aluminum-magnesium combination antacid product
C	Magnesium hydroxide
D	Ranitidine
E	Sodium bicarbonate

Question 19 Explanation:

You’ve all done the experiment: mix vinegar and baking soda (sodium bicarbonate) and one product is CO2. This gas is formed when sodium bicarbonate—still used as a lay remedy for “heartburn” (esophageal reflux) and other acidrelated GI disturbances—reacts with HCl. Normally intragastric pressure is kept in check when the gastroesophageal sphincter opens. However, when pressure can’t be relieved quickly enough, or adequately, the stomach distends like a balloon. In the presence of ulcers, the lesions are stretched mechanically, favoring further damage that can lead to acute bleeding. Even in the absence of ulcers, any weakness of the gastric wall can lead to rupture. (Reports about this scenario, published in the lay press a while ago and laced with more than a little hyperbole, stated that “[the man’s] stomach exploded after a big night on the town”, followed by ingesting baking soda for relief.) None of the other antacids listed, whether alone or in combination, lead to production of CO2 or any other gas that might lead to the outcome described here. Aluminum salts (a) seldom are used alone for neutralizing gastric acid, but are used occasionally to reduce circulating phosphate levels in such patients as those with renal failure. Used alone, aluminum salts tend to cause constipation. Aluminum-magnesium combination products (b) are the most commonly prescribed or self-prescribed antacids. The rationale for this combination, aside from overall efficacy, is that the laxative effects of the magnesium salts (c) are counteracted by the constipating effects of the aluminum salts. (Calcium salts, particularly calcium carbonate, also have antacid effects and, when used alone, tend to cause constipation.) Ranitidine (d; and famotidine, nizatidine and the lesser-used cimetidine) are H2 blockers.

Question 20

You have a patient who has been consuming extraordinarily large amounts of alcohol for several years, and i s generally malnourished. He abruptly stops his alcohol intake and goes into acute alcohol withdrawal. Pertinent s igns and symptoms include nystagmus and bizarre ocular movements, and confusion (Wernicke encephalopathy). Although this patient’s alcohol consumption pattern has been accompanied by poor nutrient intake overall, you need to manage the Which drug i s most appropriate for this use?

A	α-tocopherol (vi tamin E)
B	Cyanocobalamin (vi tamin B12)
C	Folic acid
D	Phytonadione (vi tamin K)
E	Thiamine (vi tamin B1)

Question 20 Explanation:

Thiamine, administered parenterally before or at the same time as administering glucose, and often in high dosages, is used for Wernicke encephalopathy. It dramatically ameliorates the signs and symptoms. Thiamine must be given if glucose is to be given. Thiamine serves as a cofactor for many enzymatic reactions, including those involved in carbohydrate metabolism. If glucose is administered in a thiamine-deficient state, what little vitamin is left in the circulation will be depleted, aberrant glucose metabolism will continue, and the pathology (particularly neurologic) likely will be worsened. Thiamine deficiency is also responsible for Korsakoff psychosis (or Korsakoff amnestic syndrome), another accompaniment of severe, long-term alcohol consumption (especially without adequately nutritional diets). Unfortunately, the signs and symptoms of Korsakoff (short-term memory problems, a tendency to fabricate, polyneuropathies) are not reversible. Vitamin E (a) is not indicated for Wernicke encephalopathy. Supplements of that fat-soluble vitamin are often used (misused?) by the lay public for the vitamin’s “antioxidant” and “anti-aging” effects. Cyanocobalamin (B12; b) is often used for macrocytic anemias that involve deficiencies of intrinsic factor (see Question 348). Folic acid (c) supplements have a variety of uses, including reducing the risk of teratogenic or similar effects in pregnant women, especially if they are taking certain antiepileptic drugs. The most common use of phytonadione (vitamin K; d) is to help reverse excessive anticoagulant effects of warfarin.

Question 21

A patient has steatorrhea secondary to cystic Which drug usually i s considered the most reasonable and usually effective drug for managing the fatty stools?

A	Atorvastatin (or any other HMG Co-A-reductase inhibitor)
B	Cimetidine (or an alternative, eg, famotidine)
C	Bile salts
D	Metoclopramide
E	Pancrelipase

Question 21 Explanation:

Pancrelipase is an alcoholic extract of hog pancreas that contains lipase, trypsin, and amylase. (The related drug, pancreatin, is similar.) The goal in using it here is not so much to control the symptom, diarrhea, but do so by attacking the cause, which is endogenous pancreatic enzyme deficiency (lipases, amylase, chymotrypsin, and trypsin) that leads to impaired fat digestion and absorption. None of the other drugs mentioned (a statin, a; an H2 blocker, b; bile salts, c; metoclopramide, d) have actions that would be as effective (if effective at all) or specific as pancrelipase. Antidiarrheals, for example, would only treat the symptoms, not the underlying cause. Note: You may find pancrelipase administered with antacids, or an acid secretion inhibitor (H2 blocker or proton pump inhibitor). The purpose of combined therapy is not related to preventing adverse effects of acid on the gastric mucosa, but rather to raise gastric pH and prevent the pancrelipase from being hydrolyzed and inactivated by acid.

Question 22

You are meeting with a woman in whom pregnancy has just been confirmed, and as part of your holistic patient education you give her explicit advice to avoid taking supplements of a particular vi tamin, especially in high doses, because i t i s highly You also note the need to avoid any drugs that are derivatives of this nutrient during pregnancy, for the same reason. To which one of the following vi tamins does this precaution apply?

A	A
B	B12
C	C
D	E
E	Folic acid

Question 22 Explanation:

Pregnant women should not take more than 25% more than the normal (recommended) daily dietary allowance for vitamin A, because it is teratogenic, especially in the first trimester of pregnancy. Note that the vitamin A-like drug isotretinoin, which is mainly indicated for treating refractory or severe acne vulgaris, is contraindicated too. Of course, there are pregnancy-related recommendations for the other nutrients listed in the answer: vitamins B12 (b); C (c); E (d); and, especially, folic acid (e). However, and although excessive intake of these nutrients is not recommended, and doing so may pose risks to the mother or the fetus, the consequences are not “highly teratogenic.”

Question 23

A patient being cared for by the gastroenterology service i s being treated with What i s the most l ikely purpose for which i t i s being given?

A	Antibiotic-associated pseudomembranous colitis
B	E. coli-induced diarrhea
C	Gastric H. pylori infections
D	Inflammatory bowel disease
E	NSAID-induced gastric ulcer prophylaxis

Question 23 Explanation:

Sulfasalazine, which is a combination of sulfapryidine and 5-aminosalicylic acid (5-ASA) linked covalently (azo bond), is quite effective for managing inflammatory bowel disease (eg, ulcerative colitis and Crohn disease). Some of the sulfasalazine is absorbed, and a portion of that is excreted unchanged back into the colon. Colonic bacteria split the azo linkage, releasing the two drugs. The 5-ASA is responsible for local anti-inflammatory activity (suppression of inflammatory mediators, but how, is not well understood) and symptom relief. The other metabolite, sulfapyridine, is primarily responsible for side effects associated with this “two drugs in one” combination: nausea, vomiting, and headaches (dose-dependent); sulfonamide allergic reactions in “sulfa-sensitive” patients; and rare but potentially fatal blood reactions including immune-mediated hemolysis and aplastic anemia. A related drug, mesalamine, contains only the active 5-ASA. Lacking any sulfapyridine, the side effects, and adverse responses are very low compared with sulfasalazine. An even neater strategy is used by olsalazine: the drug is comprised of two azo-linked 5-ASA molecules; the bond is cleaved by gut bacteria, releasing two 5-ASA molecules for every molecule of olsalazine administered.

Question 24

A patient with renal failure i s undergoing periodic hemodialysis while awaiting a Between dialysis sessions we want to reduce the body’s phosphate load by reducing dietary phosphate absorption and removing some phosphate already in the blood. Which drug would be most suitable for this purpose?

A	Aluminum hydroxide
B	Bismuth subsalicylate
C	Magnesium hydroxide/oxide
D	Sodium bicarbonate
E	Sucralfate

Question 24 Explanation:

Aluminum hydroxide (and all other clinically useful aluminum salts other than the phosphate) has a high affinity for phosphate. In the gut, the aluminum salts bind phosphate and prevent its absorption quite well. They also induce a blood-to-gut gradient that favors elimination of circulating phosphate. (Used inappropriately, it may cause hypophosphatemia: sustained, high-dose use of aluminum-containing antacids is one of the most common causes of hypophosphatemia.) None of the other drugs listed are effective in or used for reducing phosphate absorption or lowering plasma levels. The main limitation to using an aluminum salt by itself is its tendency to cause constipation. This is usually dealt with, when aluminum salts are used as typical “antacids,” by coadministering a magnesium salt, which alone tends to cause laxation. (Giving a magnesium salt alone or in combination with another antacid would be inadvisable for patients with renal failure, such as this dialysis patient, who are often unable to excrete the cation at rates sufficient to avoid hypermagnesemia.)

Question 25

A woman has severe i rri table bowel syndrome (IBS) characterized by frequent, profuse, and symptomatic She has not responded to fi rst-l ine therapies and i s started on alosetron. What i s the most worrisome adverse effect associated with this drug?

A	Cardiac arrhythmias (serious, eg, ventricular fibrillation)
B	Constipation, bowel impaction, i schemic colitis
C	Parkinsonian extrapyramidal reactions
D	Pulmonary fibrosis
E	Renal failure

Question 25 Explanation:

Constipation is the most common and most worrisome adverse response to alosetron, which is often used for irritable bowel syndrome. This drug’s mechanism of desired action involves selective blockade of serotonin receptors (5-HT3) in the gut; the main outcomes include slowing of colonic transport time, increased sodium and water reabsorption from the colon, and reduced secretion of water and electrolytes into the colon.Although constipation (b) might be viewed as a trivial, minor, or merely annoying complaint with most drugs, with alosetron it is the most worrisome one. Constipation may (and has) progressed to fecal impaction, bowel perforation or obstruction, and ischemic colitis. Fatalities have occurred. The risks are such that the drug was pulled from the market in early 2000 and reapproved two years later with a limited indication (prolonged, severe diarrhea associated with IBS in women); abundant warnings in the package insert; and a comprehensive risk-management/avoidance program that includes a requirement for (among other things) a special “sign-off” by both the prescriber and the patient that they understand and acknowledge and can identify the risks and agree to treatment anyway. Serious cardiac arrhythmias (a), extrapyramidal reactions (c), pulmonary fibrosis (d), or renal failure (e) are not the most likely or most worrisome adverse effects associated with alosetron.

Question 26

A patient undergoing cancer chemotherapy gets ondansetron for prophylaxis of drug-induced nausea and Which best describes this drug’s main mechanism of action in this setting?

A	Activates μ-type opioid receptors in the chemoreceptor trigger zone (CTZ)
B	Blocks central serotonin (5-HT3) receptors
C	Blocks dopamine receptors
D	Blocks histamine H1 receptors in the brainstem and inner ear
E	Suppresses gastric motility and acid secretion via muscarinic blockade

Question 26 Explanation:

The antiemetic effects of ondansetron—a drug that is widely and effectively used to manage nausea and emesis associated with chemotherapy or many of several drugs typically administered during surgery—is mainly due to blockade of 5-HT3 receptors in the brain’s chemoreceptor trigger zone (CTZ) and, probably, in the solitary tract nucleus and in the stomach and small intestine. Activation of μ-opioid receptors in the CTZ (a) is what causes the nausea and emesis that is so common with such drugs as morphine and other opioid analgesics. Blockade of central dopamine receptors (c), particularly D2 receptors in the CTZ, is the main mechanism by which phenothiazines (eg, chlorpromazine, prochlorperazine) cause their antinausea/antiemetic effects. They are useful and effective for some patients with chemotherapyinduced nausea and vomiting, but better suited for prophylaxis of these symptoms due to other causes or for prophylaxis of motion sickness. Central antimuscarinic and antihistaminic actions may contribute to the overall effects. Blockade of H 1-histamine receptors (d) in the brain (brainstem) and vestibular apparatus of the inner ear accounts for the main mechanism of action of such drugs as cyclizine, diphenhydramine (and its derivative, dimenhydrinate), and hydroxyzine. Antimuscarinic effects of these antihistamines may contribute to the overall effect. They are best suited for motion sickness prophylaxis, less effective as “general antiemetics,” and not very or specifically effective for chemotherapy-induced symptoms. Antimuscarinic agents (e; scopolamine can be considered the prototype in terms of motion sickness or emesis control) do not exert their effects via actions on the GI musculature, although suppression of AChmediated GI motility and tone certainly occurs. Their effects are primarily central; their clinical utility is mainly limited to prophylaxis or treatment (lower efficacy) of motion sickness.

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1.A 65-year-old man will be undergoing elective total knee replacement He i s urged to start taking a specified stool softener several days before surgery, and i t will continue to be administered as needed for several days after the surgery. That i s because of one of the drugs he will receive in the operative and post-op periods (l i sted below) routinely causes severe constipation. Which drug i s that?

Ketorolac to supplement postoperative analgesia from morphine
Midazolam for sedation, anxiety relief, and induction of short-term amnesia
Morphine and/or a s imilar high-efficacy opioid for pain
Neostigmine as part of a protocol to reverse skeletal muscle paralysis
Ondansetron for management of postoperative nausea and vomiting

2. A patient with multiple medical problems i s taking several drugs, including theophylline, warfarin, quinidine, and Despite the l ikelihood of interactions, dosages of each were adjusted carefully so their plasma concentrations and effects are acceptable. However, the patient suffers some GI distress and starts taking a drug provided by one of his “well-intentioned” friends. He presents with excessive or toxic effects from all his other medications, and blood tests reveal that plasma concentrations of all the prescribed drugs are high. Which drug did the patient most l ikely self-prescribe and take?

Antacid (typical magnesium-aluminum combination)
Cimetidine
Famotidine
Nizatidine
Ranitidine

3. A 53-year-old woman has been taking warfarin for prophylaxis of venous thromboembolism for the last 6 During that time the degree of anticoagulation, based on frequent measurements of her INR (International Normalized Ratio, an adjusted prothrombin time), has been in the desired therapeutic range, 2.5, and she suffered no adverse effects. Two weeks ago, she developed what she believed to be heartburn, and without consulting her MD began taking an over-the-counter medicine on a daily basis to control i t. She presents in cl inic today, reporting frequent epistaxis, and says her gums bleed when she brushes her teeth. Her INR i s now 9, well above the normal therapeutic range and indicative of excess warfarin effects. Which of the following medicines most l ikely interacted with the warfarin to cause these s igns and symptoms?

Bismuth salts (eg, Pepto-Bismol®)
Calcium carbonate
Cimetidine
Esomeprazole
Magnesium-aluminum antacid combination
Nizatidine

4. Esomeprazole i s one of the medications prescribed for a patient you are seeing today in the general medicine cl Which one of the following statements best describes the actions or effects of esomeprazole and other drugs in i ts class?

Cause strong systemic atropine-like (antimuscarinic) effects that l imit their use in patients for whom atropine i tself i s contraindicated
Inhibit gastric acid secretion by s imultaneously and competitively blocking the actions of the agonists histamine, acetylcholine, and gastrin, on their parietal cell membrane receptors
Neutralize gastric acid faster than any other classes of drugs indicated for peptic ulcer disease or gastroesophageal reflux disease (GERD)
Profoundly inhibit an ATPase located on parietal cell membranes, thereby inhibiting acid secretion
Tend to cause bradycardia by antagonizing the positive chronotropic effects of histamine on cardiac H₁ receptors

5. A 60-year-old man has episodes of severe gastric and esophageal pain that i s ultimately l inked to gastric acid. Which one of the following drugs or drug classes, whether available over-the-counter or prescribed, i s most l ikely to relieve the acid-related symptoms the fastest when taken at usually effective/recommended doses?

Antacids (eg, magnesium-aluminum combinations)
Cimetidine (but not other drugs in i ts class)
H₂ blockers, any of them
Misoprostol
Proton pump inhibitors

6. Five days after starting self-medication for diarrhea and other GI complaints that arose after a trip to Central America, a very worried patient calls to report that his tongue has turned His stools have darkened too, but his description doesn’t at all fi t with what would be expected i f the patient had a bleed anywhere in the GI tract (eg, no “coffee grounds stools” suggestive of a gastric bleed.). Which drug most l ikely caused these s igns?

Bismuth salts
Calcium carbonate
Cimetidine
Esomeprazole
Magnesium-aluminum antacid combination
Nizatidine

7. A patient who has been a high-dose alcohol abuser for many years presents with hepatic portal-systemic encephalopathy. What drug, given in relatively high doses, would be most suitable for the relief of some of the s igns and symptoms of this condition, and the l ikely underlying biochemical anomalies?

Diphenoxylate
Esomeprazole
Lactulose
Loperamide
Ondansetron

8. Fat-soluble vi tamins, compared with their water-soluble counterparts, generally have a greater potential toxicity to the user when taken in excess. What property of those vi tamins—A, D, E, and K—is basically the main reason for this finding?

Administered in larger doses
Avidly stored by the body
Capable of dissolving membrane phospholipids
Involved in more essential metabolic pathways
Metabolized much more s lowly

9. A patient i s transported from a distant hospital to your surgical service by air He had abdominal surgery and in the postop care unit he received a drug that was clearly not indicated. The drug caused intense contraction of the detrusor and trigone muscles of his bladder. The fi rst dose failed to cause emptying of the bladder, so a second dose was given. However, and unknown to his prior care team, he had a mass that rather s ignificantly obstructed his urethra, and prior anatomical weakening in a portion of his bladder. Upon administration of the drug he fi rst suffered retrograde urine flow (from his bladder, back to the kidneys via the ureters), causing renal damage. Soon thereafter his bladder ruptured into his peritoneum. Which drug or drug class most l ikely caused these adverse effects?

Albuterol
Atropine or a s imilar antimuscarinic
Bethanechol
Furosemide
Propranolol or a s imilar β-blocker

10. A patient presents with malaise, and skin and mucous membranes appear Among the key findings from blood work are hypochromic, microcytic red cells and reduced red cell count/hematocrit; reduced reticulocyte count; and reduced total hemoglobin content. Which drug would be indicated, based on the presentation?

Cyanocobalamin (B12)
Folic acid
Iron
Vitamin C
Vitamin D

11. A patient will start taking one of the drugs l i sted As we hand them the prescription we advise them not to take supplemental vi tamin B₆ (pyridoxine), whether alone or as part of a multivitamin supplement, because the vi tamin i s l ikely to counteract a desired effect of the prescribed drug. To which drug does this advice apply?

Captopril for heart failure or hypertension
Haloperidol for Tourette syndrome
Levodopa/carbidopa for Parkinson disease
Niacin for hypertriglyceridemia
Phenytoin for epilepsy

12. A patient with tuberculosis i s being treated with i She develops paresthesias, muscle aches, and unsteadiness. Which vi tamin needs to be given in supplemental doses in order to reverse these symptoms—or used from the outset to prevent them in high-risk patients?

Vitamin A
Vitamin B₁ (thiamine)
Vitamin B₆ (pyridoxine)
Vitamin C
Vitamin K

13. A patient has severe gastroesophageal reflux disease (GERD). In addition to providing some immediate symptom relief, for which you will prescribe usually effective doses of an OTC combination antacid product, you want to suppress gastric acid completely as Which drug i s best suited for achieving that goal?

Atropine
Calcium carbonate
Cimetidine
Esomeprazole
Misoprostol

14. An opioid abuser, seeking something to self-administer for subjective responses, gets a large amount of diphenoxylate and consumes i t all at He i s not l ikely to do this again because he has consumed a combination product that contains not only the diphenoxylate but also another drug that causes a host of unpleasant systemic responses. What i s the other drug found in combination with the diphenoxylate?

Apomorphine
Atropine
Ipecac
Magnesium sulfate
Naltrexone

15. During a regular check-up, your patient states “You know, doc, sometimes after eating I get heartburn … you know, acid-indigestion.” Since the symptoms seem to be mild and infrequent, you suggest an empiric trial of an OTC antacid for prompt symptom relief, plus an oral anti-acid secretory drug for long-term You recommend several antacid brands for the patient to try. All the products you l i st are combination products that contain a magnesium salt and an aluminum salt. What i s main rationale or reason why the vast majority of these products contain these two particular drugs or salts?

Al salts counteract the gastric mucosal-irritating effects of Mg salts
Al salts require activation by an Mg-dependent enzyme in order to inhibit the parietal cell proton pumps
Mg salts cause a diuresis that helps reduce systemic accumulation of the Al salt by increasing renal Al excretion
Mg salts potentiate the ability of Al salts to inhibit gastric acid secretion
Mg salts tend to cause a laxative effect (increased gut motility) that counteracts the tendency of an Al salt to cause constipation

16. A patient with multiple GI complaints i s receiving ursodeoxycholic acid (ursodiol) as part of his drug What i s the most l ikely purpose for which this drug i s being given?

Dissolving cholesterol stones in the bile ducts
Enhancing intestinal digestion and absorption of dietary fats
Helping to reverse malabsorption of fat-soluble vi tamins from the diet
Stimulating gastric acid secretion in achlorhydria.
Suppressing steatorrhea and i ts consequences

17. Early-on in your general medicine clerkship you encounter a patient who i s taking a proton pump inhibitor, bismuth, metronidazole, and What i s the most l ikely condition for which this drug combination i s being used?

Antibiotic-associated pseudomembranous colitis
Irri table bowel syndrome (IBS)
Refractory or recurrent, and severe, gastric or duodenal ulcers secondary to H. pylori
“Traveler’s diarrhea,” severe, Escherichia coli-induced, from drinking contaminated water
Ulcers that occur in response to long-term, high-dose NSAID therapy for arthritis

18.Several brand-name and store-brand “pink medications,” administered orally and available without prescription, are widely used to help alleviate occasional and short-lived nausea and vomiting, nonspecific GI distress, and diarrhea. They are also recommended for prophylaxis of “traveler’s diarrhea,” which typically i s caused by ingestion of foods or beverages contaminated with coli. These products contain bismuth subsalicylate, and because of the presence of an aspirin-like compound (a salicylate) they should not be taken by or administered to certain patients. Which patient-related factor or comorbidity contraindicates use of this drug or product?

Essential hypertension
Flu, chickenpox, or other vi ral i l lness in a child or adolescent
Hot flashes and other s igns/symptoms of menopause
Prostatic hypertrophy or glaucoma in elderly men Rheumatoid or osteoarthritis
Severe seasonal allergy s igns and symptoms

19. A patient has undiagnosed multiple gastric ulcers. Shortly after consuming a large meal and large amounts of alcohol, he experiences s ignificant GI He takes an over-the-counter heartburn remedy. Within a minute or two he develops what he will later describe as a “bad bloated feeling.” Several of the ulcers have begun to bleed and he experiences searing pain.

The patient becomes profoundly hypotensive from upper GI blood loss and i s transported to the hospital. Endoscopy confirms multiple bleeds; the endoscopist remarks that i t appears as i f the lesions had been l i terally stretched apart, causing additional ti ssue damage that led to the hemorrhage. Which drug or product did the patient most l ikely take?

An aluminum salt
An aluminum-magnesium combination antacid product
Magnesium hydroxide
Ranitidine
Sodium bicarbonate

20. You have a patient who has been consuming extraordinarily large amounts of alcohol for several years, and i s generally malnourished. He abruptly stops his alcohol intake and goes into acute alcohol withdrawal. Pertinent s igns and symptoms include nystagmus and bizarre ocular movements, and confusion (Wernicke encephalopathy). Although this patient’s alcohol consumption pattern has been accompanied by poor nutrient intake overall, you need to manage the Which drug i s most appropriate for this use?

α-tocopherol (vi tamin E)
Cyanocobalamin (vi tamin B12)
Folic acid
Phytonadione (vi tamin K)
Thiamine (vi tamin B₁)

21. A patient has steatorrhea secondary to cystic Which drug usually i s considered the most reasonable and usually effective drug for managing the fatty stools?

Atorvastatin (or any other HMG Co-A-reductase inhibitor)
Cimetidine (or an alternative, eg, famotidine)
Bile salts
Metoclopramide
Pancrelipase

22. You are meeting with a woman in whom pregnancy has just been confirmed, and as part of your holistic patient education you give her explicit advice to avoid taking supplements of a particular vi tamin, especially in high doses, because i t i s highly You also note the need to avoid any drugs that are derivatives of this nutrient during pregnancy, for the same reason. To which one of the following vi tamins does this precaution apply?

A
B12
C
E
Folic acid

23. A patient being cared for by the gastroenterology service i s being treated with What i s the most l ikely purpose for which i t i s being given?

Antibiotic-associated pseudomembranous colitis
coli-induced diarrhea
Gastric H. pylori infections
Inflammatory bowel disease
NSAID-induced gastric ulcer prophylaxis

24. A patient with renal failure i s undergoing periodic hemodialysis while awaiting a Between dialysis sessions we want to reduce the body’s phosphate load by reducing dietary phosphate absorption and removing some phosphate already in the blood. Which drug would be most suitable for this purpose?

Aluminum hydroxide
Bismuth subsalicylate
Magnesium hydroxide/oxide
Sodium bicarbonate
Sucralfate

25. A woman has severe i rri table bowel syndrome (IBS) characterized by frequent, profuse, and symptomatic She has not responded to fi rst-l ine therapies and i s started on alosetron. What i s the most worrisome adverse effect associated with this drug?

Cardiac arrhythmias (serious, eg, ventricular fibrillation)
Constipation, bowel impaction, i schemic colitis
Parkinsonian extrapyramidal reactions
Pulmonary fibrosis
Renal failure

26. A patient undergoing cancer chemotherapy gets ondansetron for prophylaxis of drug-induced nausea and Which best describes this drug’s main mechanism of action in this setting?

Activates μ-type opioid receptors in the chemoreceptor trigger zone (CTZ)
Blocks central serotonin (5-HT₃) receptors
Blocks dopamine receptors
Blocks histamine H₁ receptors in the brainstem and inner ear
Suppresses gastric motility and acid secretion via muscarinic blockade

The quizzes about Gastrointestinal and Urinary Tract Pharmacology, Nutrition (Vitamins)

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Gastrointestinal and Urinary Tract Pharmacology, Nutrition (Vitamins)

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