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Renal System and Diuretic Pharmacology
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1.After a few weeks on a drug that was prescribed by another physician, a patient reports fine tremors of his fingers, headache and fatigue, and transient GI More worrisome to him i s that he i s constantly thirsty and urinates copiously and frequently throughout the day and night. A 24-hour urine collection produces nearly 5 L of hypotonic urine. Blood tests show that levels of the causative drug are within i ts therapeutic range. Nonetheless, the cl inical picture leads you to hypothesize that the offending drug i s causing renal responses quite s imilar to a syndrome characterized by reduced production or renal response to ADH. Which drug most l ikely caused or contributed to these s igns and symptoms?
- Li thium
2. A patient taking an oral diuretic for about 6 months presents with elevated fasting and postprandial blood glucose You check the patient’s HbA1c and find i t i s elevated compared with normal baseline values obtained 6 months ago. You suspect the glycemic problems are diuretic-induced. What was the most l ikely cause?
3. A patient with severe heart failure i s in the ICU. His urine output i s dangerously You begin an intravenous infusion of dopamine at a usual therapeutic dose and urine output ri ses quickly and dramatically. What i s the most l ikely mechanism by which the dopamine caused this effect?
- Blocked β-adrenergic receptors in the juxtaglomerular apparatus, thereby inhibiting renin release and susequent angiotensin-mediated aldosterone release from the adrenal cortex.
- Directly inhibited a renal Na+, K+, 2Cl- cotransporter in the Loop of Henle.
- Improved renal blood flow and glomerular fi l tration
- Lowered the medullary-to-cortical osmotic gradient, such that normal urine concentrating mechanisms were impaired
- Reduced the permeability of the ascending l imb, Loop of Henle, and of the collecting ducts, to water
4. Usual doses of a thiazide diuretic (eg, hydrochlorothiazide) produce a urine that i s relatively ri ch in sodium and potassium, but contains relatively l i ttle increase in urine volume (ie, comparatively l i ttle free water loss compared with the relative loss of ions). An action at what s i te in the nephron mainly accounts for the ability of the thiazides to cause these responses?
- Ascending l imb of the loop of Henle
- Cortical diluting segment of the proximal nephron
- Cortical-to-medullary “countercurrent multiplier”
- Descending l imb of the loop of Henle
- Principal cells of the nephron
5. A patient with essential hypertension i s being treated with hydro-chlorothiazide and a calcium channel blocker, and i s doing He also takes atorvastatin for hypercholesterolemia, and aspirin to reduce his ri sk of an acute coronary syndrome. He i s now diagnosed with a seizure disorder. We begin therapy with one of the suitable anticonvulsants that, fortunately, does not alter the metabolism of any of the medications prescribed for his cardiovascular problems. We’ve also read that systemic administration of acetazolamide may prove to be a useful adjunct to the anticonvulsant therapy: the metabolic acidosis i t causes may help suppress seizure development or spread. So, we start acetazolamide therapy too. What i s the most l ikely outcome of adding the acetazolamide?
- Excessive ri ses of plasma sodium concentration
- Hypertensive cris i s (antagonism of both antihypertensive drugs)
- Hypokalemia via synergistic actions with the thiazide
- Spontaneous bleeding (potentiation of aspirin’s actions)
- Sudden ci rculating volume expansion, onset of heart failure
6. A patient has very high plasma uric acid levels, has had two acute gout attacks in the last 8 months, and i s at imminent ri sk of developing acute uric acid We will treat the patient with proper anti-inflammatory drugs and other agents, but feel that reducing solubility of uric acid in the urine might help ward-off the development of renal problems. What drug i s best able to produce this desired renal effect vis-á-vis urate solubility without appreciably increasing systemic ri sks of the hyperuricemia?
- Antidiuretic hormone (ADH) (vasopressin [VP])
- Ethacrynic acid
7. A patient with heart failure has been managed with digoxin and furosemide and i s doing well by all measures, for 3 He develops acute rheumatoid arthritis and i s placed on rather large doses of a very efficacious nonsteroidal anti-inflammatory drug—one that inhibits both the COX- 1 and -2 cyclooxygenase pathways. What i s the most l ikely outcome of adding the NSAID?
- Hyperchloremic acidosis indicative of acute diuretic toxicity
- Dramatic increase of furosemide’s potassium-sparing effects
- Edema, weight gain, and other s igns/symptoms indicative of reduced diuresis
- Increased digoxin excretion
- Reduced digoxin effects because the NSAID competes with digoxin for myocyte receptor-binding s i tes
8. A patient was in a recumbent position for a 45-minute oral surgery procedure. When the surgery was completed the patient stood up quickly and promptly got l ight-headed and fainted. The cause was hypotension due to hypovolemia from excessive diuresis, attributed to a drug prescribed by her physician and taken for several What drug was the most l ikely cause?
9. One of your cl inic patients i s being treated with Which statement correctly describes a property of this drug?
- Contraindicated in heart failure, especially i f severe
- Inhibits Na+ reabsorption in the proximal renal tubule of the nephron
- Interferes with aldosterone synthesis
- Is a rational choice for a patient with an adrenal cortical tumor
- Is generally preferred to a thiazide in most patients with essential hypertension
10. Chlorthalidone and torsemide are members of different diuretic classes, in terms of mechanisms of action and chemical structure, but they share the ability to cause Which statement best describes the general and common mechanism by which these drugs cause their effects that lead to net renal potassium loss?
- Act as aldosterone receptor agonists, thereby favoring K+ loss
- Block proximal tubular ATP-dependent secretory pumps for K+
- Increase delivery of Na+ to principal cells in the distal nephron, where tubular Na+ i s transported into the cells via a sodium channel in exchange for K+, which gets eliminated in the urine
- Stimulate a proximal tubular Na, K-ATPase such that K+ i s actively pumped into the urine
- Lower distal tubular urine osmolality, thereby favoring passive diffusion of K+ into the urine
11. A 52-year-old man presents to your cl inic for his fi rst vis i t with you, after moving from a distant His only medications are a statin, aspirin, (81 mg/day) and metolazone. The pharmacist who fi l led his prescriptions explained to the gentleman why he was taking the aspirin and the statin, but merely referred to the metolazone as a “water pill.” Thus, you’re asked about i t. What i s the most l ikely reason why the metolazone was prescribed?
- Adjunctive management of an adrenal cortical tumor
- Adjunctive management of hepatic ci rrhosis from years of excessive alcohol consumption
- Hypertension accompanied by a history of gout and diabetes
- Treatment of essential hypertension
- Treatment of edema and ascites from heart failure
12. Urinary potassium concentrations are measured before and after several weeks of administering a loop diuretic (eg, furosemide, at typical daily dosages). We find that post-treatment urine K+ concentrations are substantially lower than those measured at What i s the most l ikely explanation for this observation?
- An expected response to the drug
- Loop diuretics cause potassium-wasting only in in vi tro experimental models
- Measurements of post-treatment urine K+ concentrations were erroneous
- The patient has hypoaldosteronism from bilateral adrenalectomy
- Potassium secretion by principal cells of the nephron are inhibited by loop diuretics
13. You have just completed your third-year medicine clerkship, having spent some time in general internal medicine, cardiology, nephrology, and endocrine-metabolism cl In each of those venues you have reviewed charts of patients taking eplerenone. What phrase best describes a characteristic or other property of this drug?
- Facilitates renal sodium water loss and potassium retention
- Inhibits steroidogenesis (steroid hormone production)
- Mimics antidiuretic hormone (vasopressin)
- Specifically inhibits aldosterone synthesis
- Used to counteract glycosuria in patients with type 1 or 2 diabetes mellitus
14. A 58-year-old man with a history of hypertension and hypercholesterolemia i s diagnosed with heart We start therapy with furosemide as one of several medications. Which of the following would you expect to occur along with the increased urine volume caused by this diuretic?
- Dilute (hypotonic) urine because normal urine concentrating mechanisms are impaired
- Hypercalcemia due to impaired renal Ca 2+ excretion
- Reduced net excretion of Cl –
- Metabolic acidosis due to increased renal bicarbonate excretion
- Reduced plasma uric acid (urate) concentrations because of increased urate excretion
15. A patient post-head trauma i s in the neurosurgery unit at your He has become hypervolemic and hyponatremic from two main causes: (1) trauma probably increased vasopressin release from his posterior pituitary gland; and (2) the staff was not sufficiently careful when administering IV fluids, which further increased blood volume and lowered blood sodium concentrations. This patient also has symptomatic heart failure that would be further compromised by additional ri ses of blood volume, even i f s l ight or short-lived. He had been on a number of drugs prior to admission. One was oral potassium-supplements to counteract diuretic-induced hypokalemia. Unfortunately, the supplement dose was excessive, and the patient was borderline-hyperkalemic too. What drug would be the most rational to administer, with the goal of normalizing or at least improving blood volume and electrolyte composition and without further compromising the patient’s hemodynamic status?
- Sodium chloride 0.9% (normal saline)
16. A 60-year-old man has multiple medical problems, including severe hepatic ci rrhosis from hepatitis at age 40, and over 30 years of excessive alcohol intake. Three days after a vis i t to a physician, who prescribed a drug for a condition unrelated to the l iver dysfunction, the man i s found He i s transported to the emergency department. What drug, prescribed 3 days before, most l ikely induced or contributed to the onset coma in this man?
17. Your patient, who l ives in Death Valley, California (240 feet below sea level) i s planning a vacation that includes a short hike to the top of Mount Everest (approx. 29,000 feet above sea level). You’re concerned about “altitude s i ” He has no other s ignificant medical conditions, and takes no other drugs that would interact with the drug you will prescribe for his trip. Which drug would you recommend that this adventurer start taking before his trek, and continue until he returns to an altitude much closer to sea level?
18. A patient presents with chronic open angle What “renal” drug, or a drug in the same chemical and pharmacologic class, might be prescribed as an adjunct to lower intraocular pressure and help manage this condition?
19. A patient has unacceptably low cardiac output and intense reflexmediated sympathetic activation of the peripheral vasculature that i s attempting, unsuccessfully, to keep vi tal organ perfusion pressure sufficiently The patient i s edematous because of the poor cardiac function and renal compensations for i t. Which one of the following drugs should be avoided in this patient because i t i s most l ikely to compromise function of the already-failing heart and the ci rculatory system overall?
- Ethacrynic acid
20. A patient i s recently diagnosed with adrenal cortical Among the pertinent Cushingoid s igns and symptoms are hypertension and weight gain from fluid retention; and hypernatremia and hypokalemia. Which drug would be the most rational to prescribe, alone or adjunctively, to specifically antagonize both the renal and the systemic effects of the hormone excess?
21. A patient has been referred to your academic medical center because of recent-onset ventricular ectopy, second-degree AV nodal block, chromatopsia, and other extracardiac s igns and symptoms of digoxin intoxication. His family doctor, who has been treating him for a host of common medical problems over the last 30 years, had prescribed furosemide and digoxin for this gentleman’s heart Blood tests show that digoxin levels are well within a normal range. We believe the problems are diuretic-induced. What did the diuretic most l ikely do to precipitate the digoxin toxicity?
- Caused hypercalcemia
- Caused hypokalemia
- Caused hyponatremia
- Displaced digoxin from ti ssue binding s i tes
- Inhibited digoxin’s metabolic elimination
22. A 48-year-old man with bilateral diabetic nephropathy develops acute heart failure and additional, and s ignificant, declines of renal function (eg, declines of GFR) as two of several consequences of You will administer appropriate antibiotics, vasodilators, and cardiac inotropes, but also need to administer a diuretic to promptly reduce ci rculating fluid volume and “unload” the failing heart. What drug would be most appropriate in terms of managing the hemodynamic problems for this patient?
- Metolazone (or chlorthalidone)
23. A patient with severe infectious disease i s being treated with an aminoglycoside Which diuretic should be avoided, i f possible, for this patient, because of the ri sk of a serious adverse effect shared by both drugs?
24. Amiloride i s a useful drug for managing hypokalemia caused by other drugs. Which phrase best describes the mechanism by which i t causes i ts potassium-sparing effects?
- Blocks the agonist effects of aldosterone with i ts renal tubular receptors
- Blocks distal tubular sodium channels and, ultimately, Na+-K+ exchange
- Hastens metabolic inactivation of aldosterone
- Stimulates a proximal tubular Na, K-ATPase
- Suppresses cortisol and aldosterone synthesis and release in the adrenal cortex
25. A patient who admits to drinking many l i ters of water each day has had recurrent episodes of symptomatic hyponatremia, and i s at great ri sk of recurrences. Because of another medical problem he now requires administration of a Which drug i s most l ikely to precipitate another recurrence of the hyponatremia, whether or not the patient’s daily water intake i s reduced to a more acceptable level?
- Ethacrynic acid
26. A hypertensive patient has been on long-term therapy with l i s inopril, a long-acting ACE inhibitor, for The drug i sn’t controlling pressure as well as wanted, so the physician decides to add amiloride. What i s a potential, i f not l ikely, outcome of adding this diuretic to the ACE inhibitor regimen?
- Blood pressure would ri se abruptly
- Blood pressure would fall again once amiloride was added (better BP control), but there’s a l ikelihood that the patient would become hyperkalemic
- Cardiac depression, because both drugs directly depress heart rate and left ventricular contractility
- Diabetes insipidus-like syndrome with production of large volumes of dilute urine, plus dilutional hyponatremia
- Hypokalemia because of the two drugs’ additive or synergestic effects on renal potassium handling
27.Consider again the patient described in the previous He now presents with diuretic-induced hyponatremia. The condition is symptomatic and severe enough that the excessively low Na+ concentration needs to be corrected promptly. In addition to cautious intravenous administration of Na Cl , adjunctive drug therapy i s indicated. Which drug or drug class would be the most rational to use adjunctively, in addition to IV Na Cl and stopping the causative diuretic at least temporarily, to help correct sodium concentration?
- Thiazide-like diuretic (eg, metolazone)
28. The table below shows the urinary electrolyte excretion patterns typical of various prototype These are qualitative changes, and do not reflect the magnitude of the changes. They show whether excretion of an electrolyte (net amount) is increased or decreased; they do not reflect changes in urine concentrations of these substances.
Which drug causes effects most s imilar, i f not identical, to unknown drug 2, above?
Your answer choices are: