2002 Flashcards

1
Q

Renal plasma flow is an important determinant of glomerular filtration rate. Which one of the four Starling forces is influenced by RPF?

a. Glomerular capillary hydrostatic pressure
b. Glomerular capillary oncotic pressure
c. Bowman’s space oncotic pressure
d. Bowman’s space hydrostatic pressure

A

Glomerular capillary oncotic pressure

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2
Q

Which of the following hormones has the largest effect on urea clearance?

a. Parathyroid hormone
b. Vasopressin
c. Aldosterone
d. Cortisol

A

Vasopressin

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3
Q

During the course of a long hike on a particularly hot day, a normal subject loses a substantial amount of NaCl and water in her perspiration. She drinks enough water to restore her total body water content to normal, but does not have access to NaCl to replace the salt lost. After the loss of the NaCl, her intracellular fluid volume is:

a. Increased
b. Decreased
c. Normal
d. Insufficient information to determine

A

Increased

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4
Q

A medical student volunteers to take part in a drug study evaluating the potency of a new diuretic. Over several days, he loses substantial amounts of NaCl and KCl in his urine. He is given enough water to restore his total body water content to normal. However, he has become substantially Na and K depleted. In the face of the total body Na and K deficits, the volume of his intracellular fluid compartment is:

a. Increased
b. Decreased
c. Normal
d. Insufficient information to determine

A

D

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5
Q

(continued) . A second medical student enrolls in the study. He too loses substantial amounts of NaCl and KCl in his urine. However, he is given enough Na and water to restore his total body Na and water contents to normal. However, he receives no K replacement, and has a substantial total body K deficit. His intracellular fluid volume is:
a. Increased
b. Decreased
c. Normal
d. Insufficient information to determine

A

Decreased

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6
Q

All of the following statements about the plasma creatinine concentration are true EXCEPT:

a. It is used clinically to estimate glomerular filtration rate
b. It overestimates glomerular filtration rate in patients with renal failure
c. It is a function of muscle mass
d. It is a more accurate measure of glomerular filtration rate than the creatinine clearance

A

D

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7
Q

You are asked to see a patient because of hyponatremia. She has a normal blood pressure and heart rate, her cardiac exam is normal, and she has no peripheral edema. Her plasma and urine osmolalities are 270 and 75 mOsm/kg, respectively. The most likely cause of the hyponatremia is:

a. Syndrome of inappropriate antidiuretic hormone (SIADH)
b. Compulsive water drinking
c. Extracellular fluid volume depletion
d. Congestive heart failure

A

B

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8
Q

You are asked to evaluate a 79-year-old man because of change in personality, weight loss, and lethargy. He presented as an unkempt elderly man who was alert but oriented only to his name and the year. His blood pressure was 150/70 with a pulse rate of 72; there were no orthostatic changes and he was afebrile. His physical examination was reasonably normal although he would not cooperate for a careful neurological examination. His skin turgor was decreased, his oral mucous membranes were dry, and oral hygiene was very poor. Routine laboratory studies return with the following values: BUN = 30, serum Cr = 1.0 mg/dl; serum Na = 159, K= 4.5, Cl = 124, HCO3 = 24 mEq/L; urine osmolality = 875 mOsm/kg. What would be the best test to further evaluate the cause of his hypernatremia?

a. Plasma aldosterone level
b. Plasma vasopressin level
c. Ultrasound of the kidneys
d. Magnetic resonance scan of the head

A

D

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9
Q

QUESTION 18 (continued). You make a diagnosis and appropriate medical therapy is decided on. He has modest improvement with this treatment but returns to your office six months later with similar complaints by his family. However, he now also has frequent episodes of urinary incontinence. The physical examination is unchanged with the exception of the addition of a uriniferous odor. Laboratory studies show the following: BUN = 32, serum Cr = 1.1 mg/dl; serum Na = 159, K =4.6, Cl =125, HCO3 =25 mEq/L; urine osmolality = 80 mOsm/kg. Ideal therapy for his present condition would be:

a. Placement of a feeding tube to administer water through the gastro-intestinal tract
b. Placement of an indwelling intravenous catheter to administer 5% dextrose-in-water
c. Intranasal deamino-D-arginine vasopressin (dDAVP)
d. Furosemide to remove excess salt from the patient

A

C

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10
Q

You are consulted to see a 62 year-old man with a history of heavy smoking and lung cancer. His physical examination is completely normal with a blood pressure of 135/80, a pulse rate of 80, good skin turgor, moist mucous membranes and no peripheral edema. He is awake, alert and completely oriented. His laboratory studies return with: serum Na = 122 mEq/L; BUN = 10 and serum Cr = 0.9 mg/dl. Further laboratory studies show plasma and urine osmolalities of 246 and 480 mOsm/kg, respectively. The preferred therapy for his hyponatremia would be:

a. 0.9 % (isotonic) saline infused intravenously at 100 ml per hour for a total of 600 ml
b. 3% saline infused intravenously at 150 ml per hour for a total of 600 ml
c. Oral water restriction to a total of 600 ml per day
d. Furosemide 40mg intravenously followed by 0.9% saline infused intravenously at 100 ml per hour for a total of 600 ml

A

C

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11
Q

A 78 year old man comes to your office with exacerbation of congestive heart failure. He has a history of at least two myocardial infarctions in the distant past, and you have been treating him with digoxin, an angiotensin-converting enzyme (ACE) inhibitor and furosemide, with reasonably good control of his symptoms until quite recently. Over the past few weeks, his shortness of breath has increased, and he is unable to lie flat in bed at night because of shortness of breath. In addition, he has noticed progressive weight gain (despite adherence to the low Na diet you had prescribed) and worsening leg edema. Past medical history is otherwise unremarkable. He denies any recent episodes of chest pain, but has been bothered by headaches and has started taking an over the counter non-steroidal anti-inflammatory agent (naproxen) for this. Physical exam reveals a BP of 125/85 supine and erect, pulse 85 and regular. He is afebrile. He has jugular venous distension, a soft S3 gallop at the apex, and crackles posteriorly in both lung fields. Abdominal exam is unremarkable. He has 3+ pedal edema bilaterally. The EKG is unchanged and the chest X-ray shows cardiomegaly, pulmonary congestion and small bilateral pleural effusions. Routine laboratory evaluation reveals: BUN = 35, serum Cr = 1.8, serum glucose = 180 mg/dl; serum Na = 124, K =3.6, Cl = 84, HCO3 = 28 mEq/L. A spot urine osmolality = 625 mOsm/kg, and Na and K concentrations = 8 and 32 mEq/L, respectively. Which of the following statements best describes his volume status:

a. Extracellular fluid volume, plasma volume and effective arterial blood volume are all increased
b. Extracellular fluid volume and plasma volume are increased but effective arterial blood volume is decreased
c. Extracellular fluid volume is increased but plasma volume and effective arterial blood volume are normal
d. Extracellular fluid volume is increased but plasma volume and effective arterial blood volume are decreased

A

B

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12
Q

QUESTION 22 (continued). Which of the following statements best describes the cause of the hyponatremia:

a. Congestive heart failure decreases delivery of fluid to the renal diluting sites and increases circulating vasopressin levels
b. Furosemide directly inhibits the medullary diluting site in the thick ascending limb of Henle’s loop
c. Naproxen enhances vasopressin-stimulated water reabsorption in the collecting duct
d. Congestive heart failure activates the renin-angiotensin-aldosterone system, and angiotensin-II directly stimulates thirst and water intake

A

a or c

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13
Q

QUESTION 22 (continued). Which of the following statements best describes the most appropriate initial therapy:

a. Increase the dose of the angiotensin-converting enzyme inhibitor
b. Discontinue the naproxen, and use an analgesic such as acetaminophen (which does not inhibit prostaglandin synthesis) to control his headaches
c. Increase the dose of furosemide
d. Increase the delivery of fluid to the renal diluting sites by increasing dietary Na intake

A

b

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14
Q
  1. A 92 year old woman is admitted from a nursing home with “failure to thrive”. The only history that is available is that she has resided in the nursing home for “many years”, and although bed-ridden was “talking” until 3 or 4 days ago when she “suddenly took ill”. A medication list did not accompany the patient to the hospital. When you call the nursing home to get more information, the administrator tells you that the medical record is “unavailable” and that one of the nurses taking care of the patient was suspended yesterday because of “belligerent behavior” towards patients and other staff. The BP is 115/75, pulse 100 and regular, temperature 101.5O orally. Chest exam reveals tubular breath sounds at the right base. She is obtunded by reacts to painful stimuli. There are no focal neurologic signs, and there is no edema. The EKG is unremarkable and the chest X-ray shows right lower lobe consolidation compatible with pneumonia. Laboratory studies show: BUN = 20, serum Cr =0.7, glucose = 78 mg/dl; serum Na = 159; K= 4.8, Cl = 125, HCO3 = 24 mEq/L. Urine osmolality = 590 mOsm/kg. The most likely cause of the hypernatremia is:
    a. Intravenous administration of 3% (hypertonic) saline
    b. Administration of potent diuretics such as furosemide
    c. Discontinuation of steroid replacement therapy for primary adrenal insufficiency (Addison’s disease)
    d. Increased cutaneous insensible losses and poor water intake
A

d

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15
Q
  1. All of the following statements with regard to diuretic action are true EXCEPT:
    a. The magnitude of the response depends on the Na transport capacity of the site inhibited
    b. The magnitude of the response depends on the filtered load of the diuretic
    c. The magnitude of the response depends on the diuretic concentration in the tubular fluid
    d. The magnitude of the response depends on renal blood flow
A

B

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16
Q
  1. All of the following factors increase urinary ammonium excretion EXCEPT:
    a. Systemic acidemia
    b. Low urinary pH
    c. Aldosterone
    d. Hyperkalemia
A

D

17
Q
  1. Which of the following statements best describes the cellular effects of aldosterone in the cortical collecting tubule:
    a. Increases apical plasma membrane Na conductance
    b. Increases transepithelial potential difference
    c. Increases pertitubular cell membrane Na,K-ATPase activity
    d. All of the above
A

D

18
Q
  1. The most important cause of metabolic acidosis in renal failure is:
    a. Decreased proximal tubular HCO3 reabsorption
    b. Decreased distal tubular H-ATPase activity
    c. Decreased ammonia production
    d. Sulfate and phosphate retention
A

C

19
Q
  1. A 36 year old woman presents to her physician with a complaint of tiredness. She denies taking any medications. She is normotensive and does not exhibit any specific findings on physical examination. Laboratory tests are as follows: BUN = 12, serum Cr = 0.7 mg/dl; serum Na = 137, K = 2.7, Cl =116, HCO3 = 13 mEq/L; urine pH = 6.4; urine osmolality = 350 mOsm/kg; urine Na = 78, K = 31 mEq/L. The most likely cause for the metabolic acidosis is:
    a. Hyporeninemic hypoaldosteronism (Type IV RTA)
    b. Hypokalemic distal renal tubular acidosis (Type I RTA)
    c. Proximal renal tubular acidosis (Type II RTA)
    d. Bartter’s Syndrome
A

B

20
Q
  1. A patient in a clinical research study has the following laboratory studies: BUN = 15, serum Cr = 1.2 mg/dl; serum Na = 142, K =4.5, Cl = 107, HCO3 = 15 mEq/L. Minute ventilation and urinary net acid excretion are measured, and found to be unchanged from baseline (when there was no acid-base disturbance and the serum electrolytes were normal). The best explanation for the low HCO3 concentration is:
    a. Acute respiratory alkalosis
    b. Acute metabolic acidosis
    c. Chronic metabolic acidosis
    d. Chronic respiratory alkalosis
A

B

21
Q
  1. A 20 year old man was in good health until 12 hours prior to admission. The patient had been at a party and had consumed only one glass of wine, but a short time later appeared to be inebriated. Six hours later the patient was brought to the emergency room in a stuporous condition. On physical exam the blood pressure was 110/75 supine, pulse 85 and regular, respirations 24, temperature 95OF. Cardiac exam was unremarkable. Crackles were heard in both lung fields. Abdominal exam was normal. There was no edema. Fundoscopic exam was normal. There were no localizing neurologic signs. Reflexes were absent in all four extremities. The following initial laboratory data were obtained: BUN = 60, serum Cr = 3.5, glucose = 110 mg/dl; serum Na = 140, K= 4.4, Cl =105, HCO3 = 5 mEq/L; arterial pH = 7.14, pCO2 = 15 mm Hg, pO2 = 75 mm Hg. Plasma osmolality was 330 mOsm/kg. A toxicology screen showed only trace amounts of ethanol. The urine was not examined. What is the acid-base disturbance?
    a. Simple metabolic acidosis
    b. Mixed metabolic acidosis and respiratory acidosis
    c. Mixed metabolic acidosis and respiratory alkalosis
    d. Mixed metabolic acidosis and metabolic alkalosis
A

A

22
Q
  1. QUESTION 35 (continued). Given the clinical and laboratory data, the most likely cause of the metabolic acidosis is:
    a. Alcoholic ketoacidosis
    b. Salicylate intoxication
    c. Ethylene glycol intoxication
    d. Uremic acidosis
A

C

23
Q
  1. QUESTION 35 (continued). The NaHCO3 is infused intravenously over 2 hours, at which time a repeat arterial blood gas is obtained: pH = 7.19, pCO2 = 16 mm Hg, HCO3 = 6 mEq/L. Surprise! Surprise! Appropriately humbled the team is now willing to listen to you. You explain that the trivial effect of the infusion on the serum HCO3 concentration is because:
    a. NaHCO3 is a weak buffer in an open buffering system
    b. Intracellular buffering is not included in the standard calculation
    c. Insufficient time has elapsed for buffering to occur
    d. Ongoing acid production was not taken into account
A

D

24
Q
  1. A 69 year old woman with severe congestive heart failure is admitted to the hospital with one of many recent exacerbations of heart failure. She has been treated chronically with furosemide (a loop diuretic), lisinopril (an angiotensin II converting enzyme inhibitor), and digoxin. Upon admission, she is treated with increased doses of furosemide intravenously, with improvement in her shortness of breath. She is also given heparin subcutaneously, as prophylaxis for prevention of deep vein thrombosis. In response to recent evidence that spironolactone improves outcomes in patients with congestive heart failure, this is also started. You are called to see her on her 4th hospital day because of a low heart rate and lower than usual blood pressure. An electrocardiogram (ECG) shows a rate of 38, peaked T waves, and a wide QRS complex. You check the results of laboratory tests done that morning and find that the serum K concentration, which was 4.8 mEq/L on admission and 5.3 mEq/L yesterday, is now 6.8 mEq/L. Her serum creatinine is 2.2 mg/dl and the serum HCO3 is 19 mEq/L. You also note that the serum digoxin level is in the therapeutic range. You decide to first treat the patient’s potentially life-threatening problem before trying to decide why she became hyperkalemic. Therefore you:
    a. Give an extra dose of furosemide intravenously to acutely increase urinary K excretion
    b. Administer sodium polystyrene sulfonate (Kayexalate) to increase fecal K excretion
    c. Administer calcium gluconate and insulin intravenously to antagonize the effects of hyperkalemia on the heart and redistribute K into cells
    d. Page the nephrology fellow to emergently start hemodialysis to remove K from the body
A

C

25
Q
  1. QUESTION 39 (continued). After initiating appropriate treatment, you are gratified to see that the ECG changes have reverted to normal and that the serum K concentration has fallen to 5.1 mEq/L. You now begin to think about the cause of the hyperkalemia. Which of the following statements best describes the cause of the acute hyperkalemia in this patient:
    a. By inhibiting the Na,K-ATPase, digoxin reduced cellular K uptake
    b. By inhibiting aldosterone synthesis, heparin reduced cellular K uptake
    c. By blocking aldosterone-stimulated distal tubular K secretion, sprironolactone reduced urinary K excretion
    d. By blocking angiotensin II synthesis, lisinopril reduced urinary K excretion
A

C

26
Q
  1. You have graduated from Penn Medical School (yes, this will happen before you know it) and been accepted into your first choice Internal Medicine residency at the Hospital of Ultimate Prestige (HUP). A week into your internship, at 2 a.m., the Penn medical student working with you wants to know why the 18 year old patient you just admitted with diabetic ketoacidosis (DKA) is hyperkalemic. In particular, she wonders whether hypertonicity might be the cause of the hyperkalemia A quick perusal of the pertinent lab data reveals: serum glucose = 871, BUN = 25, serum Cr = 1.1 mg/dl; serum Na = 130, K = 5.9, Cl = 96, HCO3 = 12 mEq/L; arterial pH = 7.28, pCO2 = 26 mm Hg. You tell her that:
    a. Hypertonicity has no effect on internal K balance
    b. Insulin deficiency impairs net cellular K uptake
    c. Ketoacidosis increases the exchange of intracellular K for extracellular H
    d. Stress-related catecholamine release impairs cellular K uptake
A

B

27
Q
  1. QUESTION 41 (continued). Thirsting for knowledge the student next asks why you have included intravenous KCl as part of your therapeutic regimen, especially since the patient was hyperkalemic to start with. Wondering whether students learn anything at all in medical school, you reply:
    a. Total body K is very likely decreased, so K repletion is necessary to forestall the development of hypokalemia during therapy
    b. Total body K is very likely high, but intravenous K never hurt anyone
    c. Total body K is unpredictable, but K repletion is necessary to forestall the development of metabolic alkalosis during therapy
    d. Total body K is very likely normal, but K administration may help to restore pancreatic insulin synthesis
A

A

28
Q
  1. A thirty year old nurse takes you aside after rounds one day, and asks whether you would mind helping her with a personal problem. She tells you that she has been well all her life but in recent years has been concerned about her weight. Recently she went to see a well known internist to seek advice about dieting. She relates that she had nothing unusual to tell him about her medical history and that she takes no medications other than birth control pills. Her physical exam was unremarkable except for moderate obesity. In particular her blood pressure was normal. Routine laboratory studies were obtained, and she has just received the results, which include the following: serum glucose = 95, BUN = 20, serum Cr = 1.2 mg/dl; Na = 140, K = 2.9, Cl = 100, HCO3 =30 mEq/L. She is alarmed by the results, and since her follow-up appointment is not for another month, would like your opinion as to why her serum K concentration is so low. You tell her to send a spot urine to the lab and that you will meet with her later that day when the results are available. With this information in hand (urine Na = 35, K= 30, Cl = 55 mEq/L), you tell her that the most likely cause of the hypokalemia is:
    a. Surreptitious vomiting
    b. Primary hyperaldosteronism
    c. Laxative abuse
    d. Diuretic abuse
A

D

29
Q
  1. A 24 year old Type I diabetic presents to the emergency room with a one week history of fever, chills, cough and polyuria. He had been taking his insulin as prescribed until 3 days prior to admission when because of nausea and vomiting he was unable to eat or keep anything but a little water down, at which point he discontinued the insulin. The remainder of his past medical history and review of systems is unremarkable. BP is 105/70 supine and 80/60 erect. Pulse is 100 and regular supine, increasing to 115 in the erect position. Tubular breath sounds and crackles are present at the right base. Apart from the tacchycardia, cardiac exam is normal. Abdominal exam is likewise unremarkable except for mild mid-epigastric tenderness There is no edema. The neurological exam is normal. An ECG shows sinus tacchycardia, but is otherwise unremarkable. Chest X-ray reveals a right lower lobe pneumonia. Laboratory data: serum glucose = 695, BUN 38, serum Cr =1.9 mg/dl; Na = 146, K = 6.1, Cl =98 , HCO3 = 20 mEq/L. Arterial pH = 7.42, pCO2 = 30 mm Hg. Urine ketones are positive. What is the acid-base disturbance?
    a. Simple metabolic acidosis
    b. Metabolic acidosis and metabolic alkalosis
    c. Metabolic acidosis, metabolic alkalosis and respiratory alkalosis
    d. Metabolic acidosis, metabolic alkalosis and respiratory acidosis
A

C

30
Q
  1. The Chief Medical Resident presents you with the following set of electrolytes and arterial blood gases on rounds: serum Na = 141, K = 4.8, Cl = 107, HCO3 = 14 mEq/L; arterial pH = 7.40, pCO2 = 20 mm Hg, HCO3 = 12 mEq/L. He provides no history or other clinical information about the patient but requests an immediate acid-base diagnosis. Reflecting (to yourself) that he could not possibly be a graduate of Penn Med, you respond:
    a. Simple metabolic acidosis
    b. Chronic respiratory alkalosis
    c. Mixed metabolic acidosis and respiratory alkalosis
    d. Impossible to determine; the blood gases are internally inconsistent
A

C

31
Q
  1. You are asked to see a patient who has hypomagnesemia due to urinary magnesium losses as a result of Cisplatin administration. Despite aggressive oral and intravenous Mg supplementation, the patient has refractory hypocalcemia and hypokalemia. Which one of the following medications is most likely to help correct the hypomagnesemia?
    a. Furosemide
    b. Acetazolamide
    c. Hydrochlorthiazide
    d. Amiloride
A

D

32
Q
  1. A ten year old boy is admitted to the hospital with tetany and seizures. He is normotensive. CT scan and cerebrospinal fluid are normal. Serum glucose = 75, Ca = 5.8, PO4 = 7.7, Cr = 0.7, Mg = 1.6 mg/dl. Intact PTH = 108 ng/ml. Which one of the following is likely to be present?
    a. Thymic aplasia
    b. Intestinal malabsorption
    c. Short 4th metacarpals
    d. Low circulating 1,25 dihydroxyvitamin D (calcitriol)
A

C or D

33
Q
  1. A 35 year old man comes to your office for evaluation of fatigue and stress that he relates to his work. There is no history of weight loss, cough or shortness of breath, kidney stones, bone pain or fracture, peptic ulcer disease or hypertension. Physical exam is normal. Serum Ca = 12.7, PO4 = 3.1 mg/dl. Intact PTH = 58 pg/ml and 1,25 dihydroxyvitamin D (calcitriol) = 40 ng/ml. Twenty-four hour urine Ca = 90 mg. Your next step is:
    a. Family screening
    b. Parathyroid exploration
    c. PTH related peptide assay
    d. Bone scan
A

A

34
Q
  1. All of the following contribute to the hypophosphatemia commonly seen a day or two following the hospitalization of chronic alcoholics EXCEPT:
    a. Magnesium deficiency
    b. Poor dietary phosphate intake
    c. Intravenous glucose administration
    d. Hyperventilation
A

A