The quizzes about Endocrine and Reproductive Pharmacology - Part 2

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Endocrine and Reproductive Pharmacology- Part 1

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Question 1

A 55-year-old male patient with a 20-year history of type 2 diabetes mellitus comes to your cl inic for his regular check-up. He looks good, feels However, over the last year his HbA₁c levels hovered around 9.5% (equivalent to an average plasma glucose of around 225 mg/dL). Current diabetes medications are metformin and glyburide. The patient says he i s doing “the best he can” with recommended diet and exercise plans. He has other personal and familial ri sk factors for coronary heart disease. He takes a statin and metformin to control his l ipids, but his LDL and triglyceride levels are far too high. He i s taking verapamil for Stage 1 hypertension, but his pressure i s sti l l higher than you’d l ike i t to be. Two years ago, he had severe angina from atherosclerotic coronary disease and underwent angioplasty and placement of a stent. He has had no i schemic episodes s ince. You’re thinking about adding niacin to get further control of triglyceride levels, adding another antihypertensive drug, and adjusting his diabetes treatment by adding another hypoglycemic drug (perhaps insulin). Which comorbidity or other factor would weigh against your selection of an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) as the add-on antihypertensive drug for this patient?

A	Bilateral renal artery stenosis and albuminuria
B	Bradycardia
C	Had two episodes of hyperosmolar hyperglycemic nonketotic syndrome in past 2 years
D	Has heart failure
E	Niacin will indeed be prescribed

Question 1 Explanation:

Persistently high plasma glucose and cholesterol levels obviously have many untoward consequences, one of which is renovascular disease that may lead to eventual renal failure and death. He already has microalbuminuria, so some renal damage is likely present. When the arterial supply to both kidneys is reduced because of stenosis (or other factors), that weighs against using an ACE inhibitor or an ARB. Angiotensin II has a critical role in maintaining glomerular filtration by increasing efferent arteriolar pressure. Blocking A-II synthesis, or its receptor-mediated vasoconstrictor effects, can significantly reduce renal perfusion and GFR and, eventually and sometimes precipitously, lead to renal failure. ACE inhibitors or ARBs do not cause bradycardia (b), whether directly or via baroreceptor-related reflex mechanisms. Prior episodes of hyperosmolar hyperglycemic nonketotic syndrome (HHNKA, c) reflect periods of severe, symptomatic hyper-glycemia (and poor glycemic control). In the absence of bilateral renal disease or other renal pathologies (or if the patient is not a woman who is pregnant or of child-bearing potential), an ACE inhibitor or ARB would be a logical choice for controlling hypertension; heart failure does not contraindicate (d) the use of these medications. Neither hypercholesterolemia or hypertriglyceridemia (or both), nor the use of niacin or other drugs for dyslipidemias (e), has any impact on the decision to use an ACE inhibitor or ARB in the absence of other contraindications.

Question 2

A patient has an inoperable pancreatic i s let cell carcinoma and i s chronically Which drug would be most l ikely chosen for relatively long-term oral therapy that attempts to raise blood glucose levels into a more acceptable range?

A	Atenolol (or metoprolol)
B	Diazoxide
C	Glucagon
D	Octreotide (somatostatin analog)
E	Oxytocin

Question 2 Explanation:

Oral diazoxide is indicated for the very situation described in the question. It is, chemically, a benzothiadiazide (like hydrochlorothiazide, many other diuretic/antihypertensives), but it is more efficacious in terms of reducing parenchymal cell (skeletal muscle, adipocytes) responsiveness, or sensitivity to insulin, thereby helping to raise blood glucose levels. (Recall that thiazides tend to cause hyperglycemia as a side effect. That is due to their insulin-desensitizing effects.) Neither diazoxide or a thiazide diuretic has any significant effects to inhibit insulin synthesis, release, or blood levels. Indeed, they tend to cause hyperinsulinism in response to hyperglycemia. Atenolol, metoprolol (a), and other drugs that block β-adrenergic receptors tend to suppress insulin release, cause hypoglycemia, delay recovery from hypoglycemic episodes by inhibiting hepatic glycogenolysis and suppressing insulin release, and block tachycardia (a tip-off to some diabetic patients that their blood glucose levels are getting quite low) that tends to occur in response to hypoglycemia. (The degree or extent to which β-adrenergic blockers exert their effects on glucose depends on the overall profile of the individual agents—nonselective [propranolol, others]; atenolol or metoprolol [largely β1 selective]; labetalol or carvedilol [nonselective β- plus α1 blockade]; pindolol [nonselective β-blockade with intrinsic sympathomimetic activity]). Glucagon (c) is used to manage hypoglycemia (as a supplement to intravenous glucose administration), but it is an injectable drug used only as an adjunct (to IV glucose) for short-term, severe, and symptomatic hypoglycemia. Octreotide (d), identified as a somatostatin analog, is used to inhibit growth hormone (GH) release and the effects of GH on insulin-like growth factor (IGF-1) in such cases as acromegaly and carcinoid syndrome, and is also used to control bleeding from esophageal varices. It is about 40% to 50% more potent than somatostatin in terms of suppressing GH release, but relatively weak in terms of suppressing insulin secretion. It would not be a reasonable choice here, given the alternatives. Oxytocin (e), a posterior pituitary hormone used mainly as a uterine stimulant (that’s where we got the terms oxytocic drug or oxytocic effect), has no clinically useful effects on glycemic control or the responses of target tissues to insulin or glucose deficiency or excess.

Question 3

A patient with type 2 diabetes mellitus i s notoriously noncompliant with medication and diet However, he thinks he’s smart enough to fool the physician into thinking otherwise: he takes his medication and eliminates nearly all carbohydrate intake for a few days before each cl inic vis i t, knowing he will get a finger stick for a spot check of plasma glucose levels. What would be the s implest, most cost- effective, and most informative way for the physician to assess for past drug and diet compliance and long-term glycemic control?

A	Glucose concentration in venous blood sample
B	Glucose tolerance test (oral)
C	HbA1c
D	Plasma levels of the antidiabetic drug
E	Urine ketone levels (in a sample donated at the time of cl inic vis i t)
F	Urine glucose levels

Question 3 Explanation:

Blood-borne glucose reacts nonenzymatically with hemoglobin to form glycated hemoglobin products (eg, HbA1c). The rate of HbA1c formation is related to ambient glucose levels, and the amount of HbA1c measured in any given blood sample reflects the average blood glucose levels over the last 2 to 3 months. Thus, although the patient’s plasma glucose levels may be acceptable after a couple of days’ fast, HbA1c measurements give the big picture about how good glycemic control was on a more long-term (and more important) timeline. Note that although measuring HbA1c gives important information about the long-term, it does not provide any information about day-to-day fluctuations in glucose levels or what’s happening “right now,” and such information is important to optimal control of diabetes and its symptoms. Nonetheless, regular, periodic checks of HbA1c should be part of the monitoring for every patient with diabetes (type 1 or 2), not so much as a way to assess for noncompliance as to make sure that the current treatment plan with which the patient is complying is working. It is a common and relatively inexpensive assay. Having the clinical lab measure glucose in a venous blood sample won’t give any additional or meaningful information: handheld glucometers, used properly, are remarkably accurate. Glucose tolerance tests, even those done with oral glucose, will provide little historic information, and they are expensive. Few clinical labs are set up to measure plasma concentrations of most oral antidiabetic drugs, and the cost for these nonstandard tests would be quite expensive. Measuring urine ketone levels are of no benefit for our purposes. All that they might prove is that our patient has fasted for several days. Urine glucose monitoring is not very enlightening either. Recall that glucose appears in the urine only when plasma concentrations exceed a renal threshold for reabsorption (around 180 mg/dL or so). A glucose-free urine sample, then, would only indicate that plasma glucose levels are below the threshold: they still could be unacceptably high, or normal, or low, and you would never know just by urine testing.

Question 4

A 70-year-old man complains of progressive difficulty starting his urine stream, and having to get up several times during each night to Rectal examination reveals a generally enlarged, smooth-surfaced prostate. Prostate-specific antigen (PSA) ti ters are s ignificantly elevated. You decide to start finasteride treatment. Eventually urine flow increases, nocturesis episodes decrease, and overall prostate s i ze decreases. Which phrase best summarizes the most l ikely mechanism by which finasteride caused symptom relief?

A	Blocks α-adrenergic receptors
B	Blocks testosterone receptors
C	Inhibits dihydrotestosterone synthesis
D	Inhibits testosterone synthesis
E	Lowers plasma testosterone levels by increasing i ts renal clearance

Question 4 Explanation:

Finasteride competitively inhibits steroid 5-reductase, the enzyme necessary for synthesis of the active form of testosterone (dihydrotestosterone) in the prostate. Testosterone synthesis (d) and circulating testosterone levels (e) do not fall in response to the drug. PSA titers will, however, fall. Recall that α 1-adrenergic blockers (eg, prazosin as the overall prototype and, particularly, tamsulosin in terms of use for BPH) provide symptomatic relief in some men with enlarged prostates by relaxing smooth muscle in the urethra, bladder neck, and prostate capsule; moreover, they do so without any effects on testosterone or its cellular actions. Finasteride, however, has no α-adrenergic receptor blocking activity (a).

Question 5

A 38-year-old woman presents in the endocrinology and metabolism cl inic One of the drugs she i s taking i s classified as a dipeptidyl peptidase-4 (DPP-4) inhibitor. Which statement best describes the main actions of this drug?

A	Activates hydroxylases required for cortisol and aldosterone synthesis
B	Cleaves active insulin from the proinsulin molecule
C	Enzymatically splits levothyroxine from thyroglobulin
D	Helps normalize physiologic release of estrogen and progesterone
E	Inhibits inactivation of incretins, raises glucagon-like peptide levels

Question 5 Explanation:

DPP-4 degrades incretins, which play a crucial role in regulating insulin and glucagons release, particularly in response to a meal. The DPP-4 inhibitors (ie, sitagliptin and other “gliptins”) thereby indirectly raise blood levels of endogenous glucagon-like peptide-1 (GLP-1). The two most important consequences of the now-raised GLP-1 levels are an increase of blood glucose-mediated insulin release, and a simultaneous reduction of glucagon release. The gliptins are oral agents used as adjuncts to the treatment of type 2 diabetes in certain patients who fail to get adequate glycemic control in response to exercise, proper diet, and more traditional oral antidiabetic agents (ie, metformin, a sulfonylurea, or even pioglitazone, alone or in combination). DPP-4 inhibitors have no actions on, or clinical utility related to, steroidogenesis (a), cleavage of insulin from preinsulin (b), thyroid hormone storage or release (c), or estrogen or progesterone metabolic pathways (d)

Question 6

A 54-year-old woman who has not seen a physician for several years presents with a previously undiagnosed thyroid cancer and One drug that i s administered as part of early management, and may be l i fesaving, i s propranolol. Which of the following best summarizes the objective for administering this drug?

A	Block parenchymal cell receptors for thyroid hormones
B	Block thyroid hormone release by a direct effect on the gland
C	Inhibit thyroid hormone synthesis
D	Lessen dangerous cardiovascular s igns and symptoms of thyroid hormone excess
E	Lower TSH levels

Question 6 Explanation:

In thyrotoxicosis/thyroid storm, essentially the only effect of administering a β-adrenergic blocker—and it is an important effect, to be sure—is to provide prompt relief of both relatively innocuous manifestations of thyroid hormone excess, such as tremor, and those that are much more dangerous, including significant and potentially lifethreatening increases in cardiac rate, contractility, and automaticity. Circulating thyroid hormone levels modulate the responsiveness of β- adrenergic receptors to their agonists (eg, epinephrine, norepinephrine). When thyroid hormone levels are excessive, so is adrenergic receptor responsiveness. Therefore, we can reduce the adrenergic consequences of the hormone excess using a β-blocker. There are no effects on thyroid hormone levels or thyroid gland function or control. None of the β-adrenergic blockers block the agonist effects of thyroid hormones on their receptors (a), nor do they inhibit thyroid hormone release (b) or synthesis (c). They do not alter TSH levels (e) directly or indirectly

Question 7

A woman deemed at high ri sk of postmenopausal osteoporosis i s started on What i s this representative bisphosphonate’s main mechanism of action?

A	Activates vi tamin D and so facilitates absorption of dietary calcium
B	Contains lots of calcium, which supplements dietary calcium intake
C	Directly forms hydroxyapatite crystals in bone
D	Provides supplemental phosphate, which indirectly elevates plasma Ca 2+
E	Reduces the number and activity of osteoclasts in bone

Question 7 Explanation:

Whether used for osteoporosis (prevention or management, men or women, idiopathic or drug-induced) or Paget disease of the bone, bisphosphonates exert their effects on osteoclasts and osteoblasts. The drug is incorporated into bone. When drug-containing bone is resorbed by the osteoclasts, osteoclast function (and, so, subsequent bone resorption) is inhibited. The bisphosphonates also recruit osteoblasts, which then produce a substance that further inhibits osteoclast activity. Bisphosphonates in general, or alendronate in particular, do not activate vitamin D (a); are not calcium-rich drugs (b) nor phosphate-rich drugs (d); and they do not form or stimulate formation of hydroxyapatite crystals in bone (c)

Question 8

Some patients who are taking high doses of a bisphosphonate for Paget disease of the bone develop an endocrine-metabolic What disorder would that be?

A	Cushing disease (cushingoid symptoms)
B	Diabetes insipidus
C	Diabetes mellitus
D	Hyperparathyroidism
E	Hyperthyroidism

Question 8 Explanation:

You should be able to deduce hyperparathyroidism as the answer by recalling that the bisphosphonates ultimately affect bone Ca2+ metabolism, and the parathyroid gland is the main regulator of plasma Ca2+ levels. When a bisphosphonate is given to a patient with Paget disease of the bone, after about a week the dramatic inhibition of bone resorption markedly lowers plasma Ca2+ levels (because an important portion of plasma Ca2+ arises from bone that is being resorbed). When plasma Ca2+ falls considerably, parathyroid hyperfunction can develop. The easiest way to prevent this is to administer dietary calcium supplements along with the bisphosphonate.

Question 9

Metyrapone i s useful in testing hyper- or hypo-function of certain endocrine conditions or biological processes those glands normally When we administer this drug for diagnostic purposes, which structure or function are we most l ikely assessing?

A	α cells of pancreatic i s lets
B	β cells of pancreatic i s lets
C	Leydig cells of the testes
D	Pituitary-adrenal axis
E	Thyroid gland’s response to TSH

Question 9 Explanation:

Metyrapone, because it decreases plasma levels of cortisol by inhibiting the 11β- hydroxylation of steroids in the adrenal, can be used to assess function of the pituitary-adrenal cortical axis. When metyrapone is given to normal persons, the adenohypophysis secretes more ACTH. This causes a normal adrenal cortex to synthesize increased amounts of 17-hydroxylated steroids, which can be measured in the urine. However, patients who have disease of the hypothalamic-pituitary axis do not produce ACTH in response to metyrapone. As a result, we find no increased levels of the steroids in the urine. Before administering metyrapone we need to test responsiveness of the adrenal cortex to respond to administration of ACTH.

Question 10

A 60-year-old man on long-term therapy with a drug develops hypertension, hyperglycemia, and decreased bone Blood tests indicate anemia. Some of his stool samples initially were positive for occult blood, and then the stool developed a “coffee-grounds” appearance. Which drug i s most l ikely responsible for the patient’s symptoms?

A	Beclomethasone
B	Hydrochlorothiazide
C	Metformin
D	Pamidronate
E	Prednisone

Question 10 Explanation:

These findings are characteristic of what one would expect with long-term (and/or high dose) systemic glucocorticoid therapy (ie, prednisone and many others, but not beclometha-sone, which is given by oral inhalation and is not absorbed appreciably). Psychoses, peptic ulceration with hemorrhage (coffee-grounds stool, indicative of gastric bleeding) or without (possibly causing guaiac-positive stools), increased susceptibility to infection, edema, osteoporosis, myopathy, and hypokalemic alkalosis can occur. Other adverse reactions include cataracts, hyperglycemia, slowed lineal growth in children, and iatrogenic Cushing syndrome. Hydrochlorothiazide (and other thiazide and thiazide-like diuretics, such as chlorthalidone or metolazone) can increase blood glucose levels. However, they typically lower blood pressure (as evidenced by their widespread use as antihypertensives) and tend to raise, not lower, plasma calcium levels (which would be inconsistent with the decreased bone density described in this man). None of the other drugs listed would cause a collection of findings consistent with what I described here.

Question 11

A woman with atrial fibrillation i s being treated long-term with amiodarone (and warfarin). This antiarrhythmic can cause biochemical changes and cl inical s igns and symptoms that resemble those associated with which endocrine disease/disorder?

A	Addisonian cris i s
B	Cushing syndrome
C	Diabetes insipidus
D	Diabetes mellitus
E	Hypothyroidism
F	Ovarian hyperstimulation syndrome

Question 11 Explanation:

Amiodarone, an iodine-rich drug, has several actions that can lead to clinical hypothyroidism—or, more often and mainly in persons with iodine-deficient diets, hyperthyroidism. How can these seemingly opposite outcomes occur? Before we get to that, let’s summarize the other adverse responses associated with amiodarone therapy: the potential for pulmonary fibrosis (may become serious); abnormal pigmentation of the skin (is photosensitive, too); corneal deposits (often described as “halo vision”); neuropathies; and hepatotoxicity. Now, the thyroid issue: amiodarone inhibits a deiodinase that removes iodine on both the 5 and 5′ positions and that converts thyroxine to triiodothyronine (T3), mainly in the liver. This process is the main contributor to the production of endogenous (circulating) T3 that is used by most target tissues in the body. Inhibit this enzyme and the peripheral tissues have less T3 to utilize, and signs and symptoms of hypothyroidism can ensue. The excess iodine derived from metabolism of amiodarone may also contribute to the hypothyroidism. The mechanism is analogous to the way in which administering large doses of iodide are clinically useful for suppressing thyroid function in hyperthyroid individuals: iodide limits its own transport into follicular cells, and, acutely at least, high circulating levels of iodide inhibit thyroid hormone synthesis. And how might amiodarone cause hyperthyroidism? The iodine cleaved from the drug during its metabolism can be incorporated, along with dietary iodine, into thyroid hormone synthetic pathways. Although amiodarone can cause clinically significant effects on thyroid status, it does not affect the metabolism or responses to other hormones, including cortisol (a, b), insulin (d, f), and ADH (c)

Question 12

A 22-year-old woman has been sexually assaulted and she wishes to have the pregnancy terminated by pharmacologic What i s generally the most appropriate drug, assuming no contraindications?

A	Ergonovine (or methylergonovine)
B	Mifepristone
C	Raloxifene
D	Ritodrine
E	Tamoxifen

Question 12 Explanation:

Mifepristone (perhaps better known as RU-486) is a synthetic drug used as an abortifacient. (In some other countries, but not in the United States, it is used as a postcoital contraceptive.) Although the drug blocks glucocorticoid receptors, that effect does not account for its use or effects in the context described here. Here the actions arise from blocking uterine progesterone receptors. They include detachment of the conceptus from the uterine wall, softening and dilation of the cervix, and increased myometrial contraction that expels the conceptus. (The latter arises from both a drug-induced increase of local prostaglandin synthesis and greater myometrial responsiveness to them.) If mifepristone fails to induce expulsion of the fetus, misoprostol is usually given to increase uterine contractions further. (Estrogens used alone or in combination with progestins have also proven effective in postcoital contraception.) Ergonovine and methylergonovine (a) are ergot compounds that cause uterine contraction, and are used postpartum to control bleeding, by increasing uterine tone, mainly in the face of postpartum uterine atony. They are abortifacient drugs, but not used for postcoital contraception. Ralxoifene (c) and tamoxifen (e) are estrogen receptor agonists or antagonists (which effect occurs depends on the tissue) that are used to treat certain estrogen-dependent breast cancers. Ritodrine (d) is a β2-adrenergic agonist that has been used to slow uterine contractions and reduce overall uterine tone in premature labor.

Question 13

A patient has hyperthyroidism from a thyroid cancer, and the medical team concludes that oral radioiodine (sodium iodide 131 [131I]) i s the preferred treatment. The dosage i s calculated correctly, and the drug i s What statement about this approach i s also correct?

A	A β-adrenergic blocker should not be used for symptom control i f or when 131I i s used
B	Hyperthyroidism symptoms resolve almost completely within 24 to 48 hours after dosing with 131I
C	Many patients treated with 131I develop metastatic nonthyroid cancers in response to the drug
D	Oral antithyroid drugs should be administered up to and including the day of 131I administration
E	There i s a high incidence of delayed hypothyroidism after using 131I for eradication of a thyroid tumor, and so thyroid hormone supplements may be needed later on

Question 13 Explanation:

Hypothyroidism is the most common adverse outcome of using 131I to treathyperthyroidism. No matter how accurately the dose is calculated, according to some studies about 8 of 10 treated patients develop symptomatic hypothyroidism (that needs to be treated) by 10 or more years after treatment. It results, of course, from excessive thyroid cell destruction. Substantive symptom relief from 131I takes from several weeks to a couple of months to develop (although blood chemistries change somewhat faster). Until a euthyroid state develops, drugs such as β-adrenergic blockers or oral antithyroid drugs may be needed for symptom control. Oral antithyroid drugs can be given before 131I treatment, but they should be stopped for a couple of days before radiotherapy so as not to prevent radioiodine uptake into the gland. Thyroid and other cancers, metastatic or not, are rare after 131I therapy

Question 14

A 20-year-old woman, otherwise healthy, presents with i rregular and occasionally missed menstrual periods, oily facial skin and acne, and s l ight She was a competitive runner during high school and now i s in training for a triathlon. She i s not taking any medications other than an estrogen-progesterone oral contraceptive. A pelvic ultrasound evaluation reveals numerous immature ovarian follicles (generally but incorrectly referred to as cysts). The diagnosis i s polycystic ovarian syndrome (PCOS). Which drug would be the most rational initial therapy to prescribe to help provide symptom relief without compromising the woman’s ability to conceive?

A	Estrogen (dose higher than in her oral contraceptive)
B	Ketoconazole
C	Metformin
D	Prednisone (or a s imilar oral glucocorticoid)
E	Testosterone

Question 14 Explanation:

Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder in young postpubertal women, and is characterized by not only the signs and symptoms noted in the question, but also others that are accompanied or caused by relative androgen excess (thus eliminating testosterone, e, as an answer). Just as metformin is often helpful in type 2 diabetes, through its insulin-sensitizing effects on parenchymal cells (adipocytes, skeletal muscle), so it is in PCOS; an added benefit, indirectly, is a reduction of circulating androgen levels. Higher dosages of estrogen (a) might help the signs and symptoms of PCOS, but obviously that approach would not preserve or improve fertility as long as the drug is being taken. Ketoconazole (b), a powerful inhibitor of steroidogenesis, is too nonselective in terms of its powerful inhibitory effects on steroido-genesis. Prednisone (d) or another glucocorticoid would be irrational, if for no other reason than the fact that these drugs will further raise blood glucose levels—a particularly unwanted effect considering the parenchymal cell insulin resistance that is a component of PCOS. Testosterone (e) is obviously inappropriate given the relative androgen excess already present in PCOS.

Question 15

A 50-year-old woman with a high ri sk of breast cancer i s started on tamoxifen for What i s the main mechanism of action of this drug?

A	Blocks estrogen receptors in breast ti ssue
B	Blocks estrogen receptors in the endometrium
C	Increases the ri sk of osteoporosis
D	Raises plasma LDL cholesterol and total cholesterol, lowers HDL
E	Reduces the ri sk of thromboembolic disorders

Question 15 Explanation:

Tamoxifen is often referred to as a selective estrogen receptor modifier (SERM). It blocks estrogen receptors in some tissues and stimulates them in some others. The drug can be used to prevent or treat estrogen-dependent breast cancers, and it works as an estrogen receptor antagonist there. A receptor-agonist action also accounts for one of the drug’s more distressing and common side effects, hot flashes. In contrast, the drug activates estrogen receptors in the uterus, increasing the risk of endometrial cancers. Other estrogen-activating (estrogen-like) consequences include a reduced risk of osteoporosis, desirable changes in plasma cholesterol profiles (reduced LDL and total cholesterols; increased HDL), and an increased risk of thromboembolic events. The related drug, raloxifene, is largely tamoxifen-like with one main exception: it does not activate uterine estrogen receptors, and so does not increase the risk of endometrial cancers.

Question 16

A 50-year-old woman i s recently diagnosed with type 2 diabetes Exercise and diet do not provide adequate glycemic control, so drug therapy needs to start. The physician contemplates prescribing metformin. Which statement about this drug i s correct?

A	Beneficial and unwanted actions are unaffected by l iver function status
B	Lactic acidosis occurs frequently, but i t i s seldom serious
C	Metformin-induced hypoglycemia seldom occurs
D	Useful for type 1 diabetes also
E	Weight gain i s a common and unwanted s ide effect

Question 16 Explanation:

Metformin, classified as a biguanide, “sensitizes” peripheral cells (skeletal muscle, adipocytes) to insulin, thereby facilitating glucose uptake and metabolic use, and suppresses release of glucose from the liver and into the blood. It is ineffective in the absence of insulin and so is approved only for type 2 diabetes (used alone or in conjunction with such other drugs as a sulfonylurea or insulin). Like other oral agents (and some parenteral drugs such as exenatide), metformin has no beneficial effect in patients with type 1 diabetes (d). Weight loss during metformin therapy is much more common than weight gain (e). This is probably due to an appetite-suppressing effect (leading to reduced caloric intake), rather than because of a specific drug-related effect on some metabolic reaction(s) or anorexia secondary to GI side effects. Why does metformin seldom—if not rarely—cause hypoglycemia? Rather than actively driving down blood glucose levels (as, say, insulin does), the drug acts as if it “puts a lid” on physiologic rises of blood glucose concentrations. (Thus, it has been described as being an antihyperglycemic drug, rather than a hypoglycemic agent.) Metformin is not metabolized by the liver, but liver dysfunction is one contraindication. That’s mainly because of the risks of the drug’s most important adverse effect, lactic acidosis, which is rare but often fatal (not common and seldom serious, answer b) when it does occur. Impaired liver function impairs lactate elimination and favors its accumulation to toxic levels (and so answer a is not correct). However the main primary cause of the lactic acidosis is renal insufficiency (plasma creatinine >1.5 mg/dL in men, 1.4 mg/dL in women), whether caused by renal disease or by renal hypoperfusion (ischemia, as might occur with heart failure and/or hypotension).

Question 17

Most therapeutic insulins nowadays are modifications of native human insulin, done by substituting some amino acids in the native protein using recombinant DNA For all these genetically modified insulins, what i s the one common result of such changes?

A	Changes the onsets, durations of action
B	Enables administration by either subcutaneous or intravenous routes
C	Prevents cellular K+ uptake as glucose enters cells
D	Reactivates endogenous (pancreatic) insulin synthesis
E	Selectively affects glucose metabolism, l i ttle/no effects on l ipids

Question 17 Explanation:

Insulin modifications, whether by rDNA technology to substitute amino acids, or by physical means (eg, in the case of NPH insulin), alter onsets and durations of action. (Recall that regular insulin, given by SC injection, has an onset of about 30 minutes, peaks in about 3 hours, and has a duration of about 7-8 hours. Lispro and aspart insulins work faster, peak earlier, and have the shortest durations [rapid/short]; NPH insulins [“intermediate-acting”] have onsets, times to peak, and durations longer than regular insulins; and insulin glargine has the slowest onsets [4-6 hours], with durations that are on par with NPH.) In general, the modified human insulins rarely cause allergic responses (not the case with the few other insulins). Beyond that, however, the modifications yield clinically useful pharmacokinetic—not biochemical—changes.

Question 18

You have prescribed an oral agent to help control a patient’s blood glucose He has type 2 diabetes. In explaining how the drug works, you describe i t as a “starch blocker” that inhibits the intestinal uptake of complex carbohydrates in the diet. You advise also that flatus or some cramping or “grumbling sounds” in the belly may develop. Which drug fi ts this description?

A	Acarbose
B	Any thiazolidinedione (“glitazone”)
C	Glipizide
D	Metformin
E	Tolbutamide

Question 18 Explanation:

Acarbose and the newer related drug, miglitol, act in intestinal brush border cells to inhibit monosaccharide formation from complex carbohydrates and oligosaccharides, and in so doing inhibit/slow the absorption of monosaccharides (eg, glucose) from the gut. The enzymatic targets are α-glucosidases in the brush border of intestinal cells. The main consequence in terms of glycemic control is a blunting of usual postprandial rises of blood glucose. The most common side effects of acarbose affect the GI tract, as described in the question. Used alone, hypoglycemia due to acarbose is rare; however, the drug is often used as an adjunct to a sulfonylurea, and their propensity for causing hypoglycemia is not at all reduced by acarbose. It is important to note that the usual patient-centered approach to managing an episode of hypoglycemia, as might occur when certain oral antidiabetic drugs are used (eg, sulfonylureas, glitazones), is to ingest table sugar (sucrose) or some beverage or food that contains it. If the hypoglycemic patient is taking acarbose, this approach will not correct blood glucose levels adequately or promptly

Question 19

A patient with type 1 diabetes i s being treated with insulin What cl inically important property sets this particular insulin apart, or otherwise differentiates i t, from nearly all the other insulin formulations that might be used instead?

A	Blood levels, hypoglycemic effects, following insulin glargine injection are more accurately described as a plateau rather as a definite “spike” or peak
B	Disulfiram-like reactions (acetaldehyde accumulation from inhibited EtOH metabolism) more common, severe, with insulin glargine
C	Has an extremely fast onset, useful for immediate postprandial control of plasma glucose elevations
D	Poses l i ttle or no ri sk of hypoglycemia i f the patient skips several meals in a row
E	Sensitizes parenchymal cells to insulin (eg, the administered insulin i tself), not s imply providing or replacing insulin, thereby enhancing glycemic control

Question 19 Explanation:

Insulin glargine is a genetically engineered insulin that is poorly (but adequately) soluble at physiologic pH values. The drug dissolves and enters the bloodstream slowly and in such a way that there is more of a stable plateau in terms of blood levels and hypoglycemic effects. It does not cause a well-defined peak in blood levels and effects (a). The plateau is rather “flat” over the typical 24-hour period following a subcutaneous injection. Thus, the drug is better able than most other insulins to maintain roundthe-clock glycemic control, but less able to suppress the postprandial elevation of glucose that is necessary for some patients. Insulin glargine’s onset and duration of action are comparable to such preparations as NPH insulin. It is what happens in between, temporally, that distinguishes this formulation from the rest. Insulin glargine—indeed all the insulin formulations—has no disulfiram-like effects (b). As with all the insulins, insulin glargine poses a risk of hypoglycemia (and so answer d is incorrect). Finally, the drug has no parenchymal cell insulin-sensitizing effects (e), and like all insulins it is given solely as hormone replacement therapy

Question 20

A patient presents in the emergency department (ED) with a massive overdose of a The most worrisome s igns and symptoms include excessive cardiac stimulation (severe tachycardia, palpitations, angina, etc). The ED physician orders IV administration a β-adrenergic blocker, saying (correctly) i t i s the only drug l ikely to normalize cardiac function quickly and save the patient’s l i fe. What was the most l ikely drug the patient overdosed on?

A	A second-generation sulfonylurea (eg, gl ipizide, glyburide)
B	Insulin
C	Levothyroxine
D	Prednisone (oral glucocorticoid)
E	Propylthiouracil

Question 20 Explanation:

Tachycardia, palpitations, tachyarrhythmias, and the possibility of acute myocardial ischemia are among the hallmarks of thyrotoxicosis or thyroid hormone overdoses. Thyroid hormone levels regulate the “responsiveness” of β- adrenergic receptors to epinephrine and norepinephrine (or exogenous β-agonists), and this probably contributes to the clinical picture. Although excesses of thyroid hormone are the cause of the problems, management is symptomatic and aimed at suppressing β-mediated responses. Hence the use of propranolol or some other suitable β-adrenergic blocker for immediate and quite possibly lifesaving symptom control. Sulfonylureas (a; first or second generation) would not cause the signs or symptoms noted above, and β-blocker therapy for overdoses of one of those drugs would do more harm than good. The same applies to insulin (b); β-blockers might control increases of cardiac rate, but they are more likely to further lower blood glucose levels and slow or otherwise attenuate rises of blood glucose levels when appropriate therapy to render the patient euglycemic is started. Overdoses of prednisone (d) or propylthiouracil (e) are not likely to present as described, and they are not properly managed with a β-blocker.

Question 21

This week finds you accompanying an attending in her outpatient endocrinology cl One patient, a 56-year-old woman, i s taking exena- tide, which i s classified as an incretin mimetic. What phrase best describes exenatide’s actions or main cl inical use?

A	Antagonizes testosterone effects, useful for treating hirsutism in men or women
B	Is a new adjunct to metformin and/or sulfonylurea therapy of hyperthyroidism
C	Often used as an add-on to a bisphosphonate for prophylaxis of postmeno-pausal osteoporosis
D	Preferred stimulant of cortisol production for treating Addison disease
E	Useful adjunct for some patients with poorly controlled type 2 diabetes mellitus

Question 21 Explanation:

Exenatide was the first in a new class of antidiabetic agents, the incretin mimetics. It is administered by subcutaneous injection and used adjunctively to improve glycemic control in type 2 diabetes patients already taking metformin, a sulfonylurea, or both. It is not indicated for type 1 diabetes. Exenatide is a synthetic analog of glucagon-like peptide-1 (GLP-1), a peptide hormone in the incretin family. Under physiologic conditions, GLP-1 and other incretins are released from cells of the GI tract after a meal. Exenatide binds to receptors for GLP-1. In doing so it slows gastric emptying, stimulates glucose-dependent insulin release, inhibits postprandial release of glucagon, and suppresses appetite. Dose-related hypoglycemia is common when exenatide is combined with a sulfonylurea (but not when used with only metformin, which seldom causes hypoglycemia). Nausea, vomiting, and diarrhea are the most common side effects. The drug is also apparently linked to the development of pancreatitis, and so monitoring for it is essential. Some patients taking exenatide develop antibodies directed against the drug. Antigen-antibody reactions to exenatide do not cause adverse effects (eg, allergic or anaphylactoid reactions), but can reduce the intensity of exenatide’s effects. At this time, the drug is classified in FDA Pregnancy Risk Category C. Given the years of experience with using insulin for diabetes during pregnancy, and the benefits and safety it provides, there’s little justification in using exenatide. Incretin and incretin mimetics have no effects on testosterone (whether antagonism or intensification; answer a). Metformin and sulfonylureas are, of course, antidiabetic drugs and are not indicated for thyroid disorders (b). Exenatide has no effects on calcium metabolism or osteoporosis management (c); and no direct effects on corticosteroid metabolism (d), whether in hyposecretory (Addisonian) or hypersecretory (cushingoid) states.

Question 22

A patient with hypothyroidism following thyroidectomy will require l i felong hormone replacement What drug or formulation generally would be most suitable?

A	Levothyroxine (T4)
B	Liothyronine
C	Liotrix
D	Protirelin
E	Thyroid, desiccated

Question 22 Explanation:

Levothyroxine is usually considered the first choice for long-term maintenance therapy of hypothyroidism, such as that which occurs after thyroidectomy or radiation therapy of the thyroid. Once absorbed, we get the slow-onset and rather steady, long-lasting effects of the T4. In addition, some of the administered T4 is deiodinated in the tissues to T3, “automatically” providing usually adequate levels and effects of this more rapidly and shorter-acting hormone without the need to administer T3 (liothyronine) separately. If the patient develops profound hypothyroidism (eg, myxedema), some clinicians may still prefer T3 for its prompt effects. However, in this instance too, T4 is generally regarded as the preferred way to replace both hormones and reestablish a euthyroid state (administered with corticosteroids for myxedema coma). Liothyronine (b) is synthetic T3; liotrix (c) is a mixture of synthetic T3 and T4; protirelin (d) is a synthetic tripeptide, chemically identical to thyrotropin-releasing hormone (TRH), that is used to diagnose some thyroid disorders; desiccated thyroid products (e) are outmoded for managing hypothyroidism, given the availability of synthetic hormone preparations.

Question 23

A patient develops marked skeletal muscle tetany soon after a recent The attending confirms the diagnosis, in part, by l ightly tapping the patient’s cheek in front of the ear. Stimulating the facial nerves in this manner leads to spasms of the local (oris) muscle (Chvostek s ign). Which drug i s most l ikely to be chosen to manage this adverse response to surgery?

A	Calcitonin
B	Calcium gluconate
C	Pl i camycin (mithramycin)
D	PTH (parathyroid hormone)
E	Vitamin D

Question 23 Explanation:

We’re dealing with hypocalcemia in this patient with tetany postthyroidectomy, because the parathyroid gland was damaged or removed during the surgery. Administration of intravenous calcium gluconate would immediately correct the tetany. Parathyroid hormone (d) could be considered appropriate for long-term management of hypocalcemia, but it has a slower onset of action that would not be of much help in a tetanic state. We would then probably use vitamin D (e) and dietary modifications for long-term control of plasma calcium levels. Calcitonin (a) is a hypocalcemic antagonist of parathyroid hormone. (Note that calcitonin or calcitriol will raise plasma calcium levels faster than vitamin D, but in this emergent situation they will not work fast enough, which is why we need direct administration of ionic calcium.) Plicamycin (c; mithramycin) is used to treat Paget disease and hypercalcemia. The dose employed is about one-tenth the amount used for plicamycin’s cytotoxic action when it is used as a chemotherapeutic drug.

Question 24

A 40-year-old man with a symmetrically enlarged thyroid gland associated with elevated levels of T₃ and T₄ i s treated with propylthiouracil (PTU). Which phrase best summarizes the principal mechanism of action of PTU?

A	Blocks iodide transport into the thyroid
B	Increases hepatic metabolic inactivation of ci rculating T4 and T3
C	Inhibits proteolysis of thyroglobulin
D	Inhibits thyroidal peroxidase
E	Releases T3 and T4 into the blood

Question 24 Explanation:

Propylthiouracil, a thioamide use to manage many patients with hyperthyroidism, has three main actions. It inhibits a peroxidase, and in doing so inhibits oxidation of inorganic iodide to iodine, and the iodination of tyrosine. It also blocks coupling of iodotyrosines and inhibits deiodination of T4 to T3 in the periphery. Propylthiouracil, and the thioamides in general, do not: block thyroid uptake of iodide (a); affect metabolic inactivation of T3 and T4 (b); inhibit thyroglobulin’s proteolysis (c); or directly release thyroid hormones into the circulation (e). Note: Most texts and other publications refer to this group of drugs as I have: thioamides. However, occasionally you will find an alternative term used: thionamide, thioamine, and even thionamine.

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1.The attending in the endocrine/metabolic diseases cl inic prescribes colesevelam as add-on therapy for a 58-year-old male with type 2 diabetes who i s not getting adequate glycemic control (based on high levels of HbA₁c measured twice in the last 12 months) from his current medications: metformin and The man has been a pack-a-day cigarette smoker for 40 years and says he “can’t seem to quit.” In addition to the diabetes and nicotine addiction he has several other comorbidities that are not optimally managed with his current medications for each, or recommended l i festyle modifications (he largely ignores them). The attending states that the cole-sevelam might just help one of those comorbidities in addition to possibly lowering HbA₁c levels after a few months on the drug. What is the “other condition” that i s most l ikely to be favorably and rather directly influenced by the colesevelam?

Chronic bronchitis (or emphysema)
Hyperlipidemias
Hyperuricemia, gout
Nicotine addiction
Prostatism (ie, benign prostatic hypertrophy)

2. Your patient, who is taking an oral contraceptive, has heard about and asks about the risk of thromboembolism as a result of taking these To reduce the ri sk of this potentially severe adverse hematologic response, but sti l l provide reasonably effective contraception, what would you prescribe?

A combination product with a higher estrogen dose
A combination product with a higher progestin dose
A combination product with a lower estrogen dose
A combination product with a lower progestin dose
A product that contains only estrogen

3. A 27-year-old woman i s diagnosed with hypercortism. To determine whether cortisol production i s independent of pituitary gland control, you decide to suppress ACTH production by giving a high-potency Which drug would be the best choice for this purpose?

Dexamethasone
Hydrocortisone
Methylprednisolone
Prednisone
Triamcinolone

4. A patient with Cushing syndrome i s being treated by X-irradiation of the It may take several months of this therapy for adequate symptomatic and metabolic improvement. Until that time, which drug would be administered to suppress glucocorticoid synthesis?

Cimetidine
Cortisol (massive doses)
Fludrocortisone
Ketoconazole
Spironolactone

5. A woman who has been taking an oral contraceptive (estrogen plus progestin) for several years i s diagnosed with epilepsy and started on What i s the most l ikely consequence of adding the phenytoin?

Agranulocytosis or aplastic anemia, requiring stopping both drugs immediately
Breakthrough seizures from increased phenytoin clearance
Phenytoin toxicity, s ignificant and of fast onset
Profoundly increased ri sk of craniofacial abnormalities in the fetus Reduced contraceptive efficacy
Thromboembolism from the estrogen component of the contraceptive

6. A woman wants a prescription for an oral contraceptive, and your choice i s between an estrogen-progestin combination and a “minipill” (progestin only). Compared with a hormone combination product, what i s the main difference that would occur when a progestin-only approach i s used?

Better contraceptive efficacy
Direct spermicidal effects
Higher ri sk of thromboembolism
More menstrual i rregularities (i rregular cycle length, amenorrhea, spotting, etc)
Poorer compliance due to taking the drug on an i rregular cycle, rather than daily

7. A woman i s taking a combination estrogen-progestin combination oral She experiences a multitude of s ide effects. Which s ide effect i s most l ikely due to what can be described as an “estrogen excess,” and not l ikely due to the progestin content of the medication?

Fatigue
Hypertension
Hypomenorrhea
Increased appetite
Weight gain

8. A comatose patient with an endocrine disorder undergoes a computed tomography (CT) diagnostic procedure that involves contrast media that has a tendency to induce lactic He i s also taking a drug that, in i ts own right, may cause lactic acidosis. Normally the drug would be stopped, at least temporarily, two days before the CT, but due to the patient’s acute and serious i l lness that could not be done. Lactic acidosis indeed develops and the patient nearly dies. Which drug was the most l ikely cause of this severe and potentially fatal metabolic derangement?

Insulin glargine, prescribed for type 1 diabetes mellitus
Levothyroxine, prescribed to maintain euthyroid status following thyroidectomy
Metformin, prescribed for type 2 diabetes mellitus
Propylthiouracil, prescribed for hyperthyroidism
Spironolactone, prescribed for an adrenal cortical tumor

9. A patient with type 2 diabetes mellitus begins gaining weight after several months of therapy with an oral antidiabetic A complete work-up indicates edema and other s igns and symptoms of heart failure. Which antidiabetic drug or group was the most l ikely cause?

Acarbose
Biguanides
Metformin
Pioglitazone
Sulfonylureas, both fi rst- and second-generation agents (eg, tolbutamide, chlorpropamide, glyburide, gl ipizide)

10. A woman goes into premature labor early enough that there are great concerns about inadequate fetal lung development and the ri sk of fetal respiratory distress Suitable uterine-relaxing drug therapy i s started to s low labor, but parturition seems imminent. What other adjunct should be administered prepartum, specifically for the purpose of reducing the ri sks and complications of the newborn’s immature respiratory system development?

Albuterol (β₂ agonist)
Betamethasone
Ergonovine (or methylergonovine)
Indomethacin
Magnesium sulfate

11. We prescribe etidronate for a postmenopausal woman who i s at great ri sk for developing for Which s ide effect or adverse response to this drug i s the patient most l ikely to experience?

Cholelithiasis
Esophagitis
Fluid/electrolyte loss from profuse diarrhea
Hepatic necrosis
Renal damage from calcium stone formation
Tetany

12. A 75-year-old man had surgery for prostate carcinoma, and local metastases were found intraoperatively. What i s the most appropriate follow-up drug aimed at treating the metastases?

Aminoglutethimide
Fludrocortisone
Leuprolide
Mifepristone
Spironolactone

13. A 53-year-old woman with type 2 diabetes mellitus i s started on Diet, exercise, and usually effective doses of metformin have not provided adequate glycemic control based on periodic measurements of HbA₁c. What i s the primary mechanism by which the glyburide i s l ikely to provide better glycemic control?

Decrease insulin resistance by lowering body weight
Enhance renal excretion of glucose
Increase insulin synthesis
Promote glucose uptake by muscle, l iver, and adipose ti ssue via an insulin-independent process
Release insulin from the pancreas

14. A 75-year-old woman with type 2 diabetes i s taking an oral anti-diabetic One day she goes without eating for 18 hours, but takes her drug nonetheless. She i s transported to the emergency after passing out. Her plasma glucose concentration i s 48 mg/dL (hypoglycemic) upon arrival at the ED, and she i s in very serious condition. Which drug, that most l ikely aggravated this fasting hypoglycemia, did she take?

Acarbose
Colesevelam
Glyburide
Metformin
Pioglitazone

15. A man with type 2 diabetes i s receiving a combination of oral drugs to maintain glycemic He becomes hypoglycemic one afternoon and ingests some orange juice and two chocolate bars—all containing abundant amounts of complex carbohydrates. Despite his ingestion of orange juice and several chocolate bars, his blood glucose levels remain low, his symptoms persist. Which antidiabetic that he was taking accounted for the failure of oral sugars to restore his plasma glucose?

Acarbose
Glyburide
Metformin
Repaglinide
Rosiglitazone

16. A 35-year-old woman has Graves disease, a small goiter, and symptoms that are deemed “mild-to-moderate.” Propylthiouracil i s What i s the most serious adverse response to this drug, for which close monitoring i s required?

Agranulocytosis
Cholestatic jaundice
Gout
Renal tubular necrosis Rhabdomyolysis
Thyroid cancer

17. A 60-year-old man with type 2 diabetes mellitus i s treated with pioglitazone (in addition to a proper diet and exercise). Which phrase summarizes best this drug’s main mechanism of action?

Blocks intestinal carbohydrate absorption
Causes glycosuria (increased renal glucose excretion)
Increases hepatic gluconeogenesis
Increases release of endogenous insulin
Increases target ti ssue sensitivity to insulin

18. A patient with a history of type 2 diabetes mellitus presents in the ED. His complaints include nonspecific gastrointestinal symptoms, including nausea and He states he i s bloated and has abdominal pain. His appetite has been suppressed for several days. He has malaise and difficulty breathing. His l iver i s enlarged and tender; l iver function tests indicate hepatic damage. Plasma bicarbonate i s low and lactate levels are high. Kidney function i s falling rapidly.

The diagnosis i s lactic acidosis, and the suspicion i s that i t was caused by an antidiabetic drug. Which of the following drugs i s this patient most l ikely to be taking?

Acarbose
Glipizide
Glyburide
Metformin
Pioglitazone

19. A patient i s transported to the ED shortly after taking a massive overdose of her levothyroxine in an apparent suicide Which of the following drugs should be administered for prompt control of the hormone-related effects that are most l ikely to lead to her death i f not correctly managed?

Iodine/iodide
Liothyronine
Propranolol
Propylthiouracil
Radioiodine (131I)

20. There are two main formulations of oral contraceptives: those that are estrogen-progestin combinations, and those that contain only progestin (“minipill”). What i s the main mechanism by which these drugs exert their desired contraceptive effects?

Acidify the cervical mucus, thereby making the mucus spermicidal
Displace/detach a fertilized egg from the endometrium
Inhibit nidation (implantation of a fertilized ovum)
Inhibit ovulation
Reduce uterine blood flow such that the fertilized ovum becomes hypoxic and dies

21. A 55-year-old postmenopausal woman develops weakness, polyuria, polydipsia, and s ignificant increases of plasma creatinine A computed tomogram (CT scan) indicates nephrocalcinosis. A drug i s considered to be the cause. Which drug was most l ikely responsible?

Estrogens
Etidronate
Glipizide
Prednisone
Vitamin D

22. A patient has severe Cushing Surgery cannot be scheduled for several months, so the physician plans to treat the patient in the interim with a drug that she describes as a “potent inhibitor of corticosteroid synthesis.” Which drug best fi ts that description?

Dexamethasone
Hydrocortisone
Ketoconazole
Prednisone
Spironolactone

23. You prescribe bromocriptine for a woman with primary Normal menstruation returns about a month after starting therapy. Which statement best describes the mechanism by which bromocriptine caused i ts desired effects?

Blocked estrogen receptors, enhanced gonadotropin release
Increased follicle-stimulating hormone (FSH) synthesis
Inhibited prolactin release
Stimulated ovarian estrogen and progestin synthesis
Stimulated gonadotropin-releasing hormone (GnRH) release

24. A patient has had his parathyroid glands excised during a total In addition to requiring supplemental thyroid hormone, interventions aimed at correcting hypoparathyroidism will be necessary. What i s the main physiologic action or role of parathyroid hormone—one that necessitates suitable therapy?

Decreases active absorption of Ca from the small intestine
Decreases excretion of phosphate
Decreases renal tubular reabsorption of calcium
Decreases resorption of phosphate from bone
Increases mobilization of calcium from bone

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