Transcript Slide 1

Fluid, Electrolyte, and
Acid-Base Disorders
Darren Dreyfus, D.O.
Associates In Nephrology, P.C.
St. Vincent’s Health System
Question 1
Question 1
A 71-year-old man is evaluated because of
intermittent cough and increasing dyspnea on
exertion. He has smoked one pack of cigarettes
per day for 49 years. He has no other symptoms.
On physical examination, distant breath sounds are
audible in both lungs and there are scattered
rhonchi. Chest radiograph shows a perihilar mass.
Abnormal laboratory results include hemoglobin of
10.5 g/dL and a serum sodium of 127 meq/L.
Endobronchial biopsy reveals small-cell lung
cancer.
Question 1
Which of the following is most appropriate
treatment for this patient’s hyponatremia?
(A) Chemotherapy
(B) Hypertonic saline
(C) Fluid restriction
(D) Fluid restriction and demeclocycline
Answer
Question 1 - Answer
Answer: A
This patient with mild hyponatremia is newly
diagnosed with small-cell lung cancer. He has no
symptoms that are clearly attributed to the
hyponatremia and there initiating non-specific
therapy such as fluid restriction with or without
demeclocycline therapy, or aggressively treating
the hyponatremia with hypertonic saline is not
warranted. The most important therapeutic
intervention is to treat the underlying cancer with
chemotherapy.
Question 2
Question 2
A 78-year-old woman with metastatic breast cancer involving
the bones and soft tissues is evaluated in the emergency
department because of lethargy and weakness, nausea,
thirst, and dizziness. She has a history of congestive heart
failure that has been controlled with medications. On
physical examination she has orthostatic hypotension
associated with dizziness and dry mucous membranes. Her
lungs are clear and she has no dependent edema.
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Blood urea nitrogen – 42 mg/dL
Total serum calcium – 11.4 mg /dL
Serum creatinine – 1.6 mg/dL
Serum albumin – 3.0 g/dL
Question 2
Administration of which of the following is the
most appropriate treatment?
(A) A biophosphonate, intravenously
(B) Corticosteroids, intravenously
(C) Half-normal saline
(D) Normal saline
(E) Furosemide
Answer
Question 2 - Answer
Answer: D
The patient has hypercalcemia, the most common
metabolic complication of malignancy. She is
volume depleted as evidenced by her orthostatic
hypotension, dizziness and dry mucous
membranes. Despite her history of congestive
heart failure, the most appropriate initial therapy is
to replace vascular volume as vigorously as
possible with normal saline.
Question 2 - Answer
Furosemide must not be given until the patient has
first been adequately rehydrated. Administration of
a bisphosphonate is not an appropriate initial
therapeutic intervention in this patient because its
delayed onset of effect and her more urgent need
for volume repletion. Although corticosteroids can
be considered as an adjunctive therapy in a
patient with a potentially hormone-responsive
tumor such as breast cancer, the top priority is
volume repletion.
Question 3
Question 3
A 56-year-old man with a 25-pack-year smoking
history, distant cerebrovascular accident, and a 10year history of hypertension treated with
hydrochlorothiazide is evaluated because of
generalized fatigue. Blood pressure is 110/70 mm
Hg.
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Serum sodium – 128 meq/L
Serum potassium – 3.3 meq/L
Serum chloride – 79 meq/L
Serum biocarbonate – 38 meq/L
Arterial blood gases on room air:
► pH
– 7.50; PCO2 50 mm Hg, PO2 74 mm Hg
Question 3
Which of the following best explains the
patient’s acid-base disturbance?
(A) Metabolic alkalosis
(B) Respiratory acidosis
(C) Respiratory alkalosis
(D) Metabolic acidosis
Answer
Question 3 - Answer
Answer: A
The low blood pressure and hypochloremia suggest
volume-sensitive metabolic alkalosis due to
diuretic therapy. Metabolic alkalosis is indicated by
the high serum bicarbonate level and pH greater
than 7.4 Respiratory compensation for the
metabolic alkalosis is appropriate. The PCO2 is 50
mm Hg, showing the expected 10-mm Hg increase
that compensates for the 14-meq/L increase in
serum bicarbonate level.
Question 3 - Answer
Metabolic acidosis is not a possible diagnosis
since the bicarbonate level and pH are
elevated. The normal arterial-to-alveolar
oxygen gradient makes underlying chronic
obstructive pulmonary disease unlikely, and
blood gas values do not indicate concurrent
respiratory acidosis.
Question 4
Question 4
A 65-year-old man with chronic alcoholism is
evaluated because of a seizure 1 hour ago.
In the emergency department, he is
lethargic but conversant and oriented. He
reports a several-day history of diarrhea and
has muscle cramps. He has no history of
trauma or previous seizures. He is taking no
medication but has smoked 1 pack of
cigarettes daily for the past 30 years.
Question 4
On physical examination, blood pressure is
11/075 mm Hg, pulse rate is 100/min, and
respiration rate is 18/min. The neck is
supple. Carpopedal spasm and Chvostek’s
signs are present. The remainder of the
physical examination is normal.
Question 4
Serum
Serum
Serum
Serum
Serum
Serum
Serum
Serum
creatinine – 1.4 mg/dL
sodium – 136 meq/L
potassium 2.7 meq/L
chloride – 98 meq/L
bicarbonate – 23 meq/L
calcium – 7.6 mg/dL
magnesium – 0.5 mg /dL
phosphorus – 3.0 mg/dL
Question 4
Which of the following will best correct the
underlying deficiency responsible for this
patient’s electrolyte disorders?
(A) Calcium
(B) Magnesium sulfate
(C) Magnesium sulfate and potassium chloride
(D) Potassium chloride
Answer
Question 4 - Answer
Answer: C
Hypomagnesemia is frequently seen in
alcoholics and in persons with severe
diarrhea. If the serum magnesium level is
less than 1.0 mg/dL and carpopedal spasm,
Chvostek’s or Trousseau’s sign, or seizures
are present, intravenous treatment with
magnesium is indicated.
Question 4 - Answer
The hypokalemia is due to diarrhea and
volume depletion (volume depletion triggers
aldosterone release causing sodium
conservation at the expense of potassium
loss) and to the renal potassium wasting
induced by hypomagnesemia.
Attempts at correction of the hypokalemia will
be ineffective unless hypomagnesemia and
volume are also corrected.
Question 4 - Answer
The hypocalcemia is due to reduced secretion
and peripheral effects of parathyroid
hormone, which are caused by the
hypomagnesemia.
When the hypomagnesemia is corrected, the
parathyroid hormone levels will return to
normal and the serum calcium level will
normalize.
Question 5
Question 5
A 35-year-old man is evaluated because of
recurrent nepholithiasis and is found to have
a normal serum calcium concentration and
hypercalciuria.
Question 5
Which of the following diets should this man avoid in
order to reduce the risk of recurrent calcium
stones?
(A)
(B)
(C)
(D)
(E)
Low-sodium diet
Low-calcium diet
Low-oxalate diet
Low-protein diet
Low-purine diet
Answer
Question 5 - Answer
Answer: B
Risk factors for calcium nephrolithiasis include low
daily fluid intake, high dietary sodium and oxalate,
hyperoxaluria, hypercalciuria, hypocitrauria, and
hyperuricosuria.
Several studies in men and women have shown that
a high dietary calcium intake is associated with
reduced risk for calcium stone disease.
In a recent study, men with hypercalciuric
nephrolithiasis placed on a low-calcium versus a
high-calcium diet had greater risk of subsequent
stone formation.
Question 5 - Answer
Although not proven, it is believed that the risk for stone
formation is lower with high dietary calcium because higher
amounts of dietary calcium bind with dietary oxalate and
lessen oxalate absorption and urinary excretion. For this
same reason, oral magnesium therapy has also been used.
A low sodium diet can reduce renal calcium excretion and
may reduce calcium stone formation. A diet high in animal
protein increases urinary excretion of calcium and uric acid
while it decreases excretion of citrate, and is associated
with increased risk of calcium stone formation.
A diet low in animal protein may minimize this risk.
Question 5 - Answer
A low-purine diet reduces uric acid excretion
and, since uric acid crystals may act as a
nidus for formation of calcium stones, may
lessen calcium stone formation as well.
A low oxalate diet may decrease absorption of
oxalate and decrease urinary excretion of
oxalate.
Question 6
Question 6
A 26-year-old woman with type 1 diabetes mellitus is
evaluated in the emergency department because
of a serum glucose concentration of 450 mg/DL
and abdominal pain for the past 24 hours. Her
temperature is 38 oC (101 oF).
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Serum sodium – 133 meq/L
Serum potassium – 3.9 meq/L
Serum chloride – 97 meq/L
Serum bicarbonate – 10 meq/L
Arterial blood gases – pH 7.2; PCO2, 23 mm Hg
Whole blood lactacte - 0.6 mmol/L
Question 6
Which of the following best explains the patient’s
acid-base status?
Diabetic
(B) Diabetic
acidosis
(C) Diabetic
(D) Diabetic
(A)
ketoacidosis
ketoacidosis and proximal renal tubular
ketoacidosis and respiratory acidosis
ketoacidosis and metabolic alkalosis
Answer
Question 6 - Answer
Answer: A
The patient has an anion gap metabolic acidosis with
appropriate respiratory compensation consistent with a
diabetic ketoacidosis. Metabolic acidosis is indicated by a
low serum bicarbonate level and an arterial blood pH less
than 7.4. The respiratory compensation is appropriate;
thus, there is not a concomitant respiratory disorder
accompanying this metabolic acidosis.
The patient has an anion gap of 26. The change in the anion
gap is 14. The change in the bicarbonate level is 14,
calculated as the normal bicarbonate concentration minus
the measured bicarbonate concentration.
Question 6 - Answer
Thus, the ration between the change in the anion
gap and the change in the serum bicarbonate is 1,
suggesting that a concurrent non-anion gap
metabolic acidosis or a concurrent metabolic
alkalosis is not present.
Proximal renal tubular acidosis causes a non-anion
gap metabolic acidosis, and if it were present with
ketoacidosis, we would expect both a non-anion
gap and an anion gap metabolic acidosis. That is,
the ration between the change in the anion gap to
the change in the serum bicarbonate level would
be less than 1.
Question 7
Question 7
A 23-year-old woman with type 1 diabetes
mellitus is evaluated in the emergency
department because of a 2-day history of
dysuria and urinary frequency. Three years
ago she had “cystitis” twice in 6 months; in
both occasions, she was treated with
antibiotics. She uses insulin to control her
diabetes and takes 1 or 2 ibuprofen tablets
daily for headaches.
Question 7
On physical examination, the blood pressure
is 115/80 mm Hg, pulse rate is 80/min, and
temp is 37.4 oC (99.3 oF). Optic fundoscopy
reveals microaneurysms and the
neurological examination demonstrates
diminished sensitivity to pinprick and light
touch in the lower extremities. The
remainder of the examination is
unremarkable.
Question 7
Serum creatinine – 1.8 mg/dL (1.6 a month
ago)
Serum sodium – 138 meq/L
Serum chloride – 106 meq/L
Serum potassium – 6.2 meq/L
Serum bicarbonate – 21 meq/L
Urinalysis – Specific gravity 1.020; 3+
proteinuria; 25 leukocytes/hpf
Question 7
On renal ultrasonography, the right kidney is 11.0
cm and the left kidney is 10.9 cm. No
hydronephrosis or stones are present.
Which of the following is the most likely cause of her
hyperkalemia?
(A) Acute renal failure
(B) Diabetic ketoacidosis
(C) High sodium diet
(D) Hyporeninemic hypoaldosteronism
Answer
Question 7 - Answer
Answer: D
The most likely cause of hyperkalemia is hyporeninemic
hypoaldosteronism, a condition that occurs in 20% to 30%
of diabetic persons.
Hyperkalemia occurs most often in diabetic patients who have
mild to moderate renal failure (as in this case)
superimposed on the hyporenin hypoaldosterone state.
The later condition seems to be due to unresponsiveness of
the adrenal zona glomerulosa to stimulation by angiotensin
II, renin, and hyperkalemia itself.
Many diabetic patients with hyperkalemia have low renin
levels, caused by impaired conversion of prorenin to renin.
Question 7 - Answer
Since prostaglandins stimulate renin, use of
ibuprofen may contribute to the hypoaldosterone
state, but by itself rarely causes hyperkalemia.
Diabetic ketoacidosis is not present.
A change in serum creatinine concentration from 1.6
to 1.8 would not cause hyperkalemia in a patient
who had normal renin-aldosterone function.
A high-sodium diet does not cause hyperkalemia.
Question 8
Question 8
A 63-year-old man is evaluated because of upper
and lower extremity cramps and diffuse muscle
weakness of 2 weeks’ duration. He has been
taking aspirin for 6 weeks because of low back
pain. The physical examination is normal.
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Serum sodium – 135 meq/L
Serum potassium – 2.6 meq/L
Serum chloride – 117 meq/L
Serum bicarbonate – 15 meq/L
Arterial blood gases – pH, 7.30; PCO2, 31 mm Hg
Urine pH – 5.0
Question 8
Which of the following best explains his acidbase status?
(A)
(B)
(C)
(D)
Ethylene glycol toxicity
Lactic acidosis
Proximal renal tubular acidosis
Salicylate toxicity
Answer
Question 8 - Answer
Answer: C
The electrolyte and arterial blood gas patterns are consistent
with a non-anion gap metabolic acidosis.
Metabolic acidosis is indicated by a low serum bicarbonate
level and an arterial blood pH less than 7.4.
The anion gap, calculated as 135 – (117 + 15)=3, indicates a
non-anion gap acidosis.
A low anion gap (defined as less than 7) can be caused by an
increase in unmeasured cation such as calcium,
magnesium, lithium, or a positively charged paraprotein
produced by a myeloma.
A low anion gap can also be cause by a decrease in
unmeasured anions such as albumin.
Question 8 - Answer
The urine pH of 5.0 is consistent with a proximal
renal tubular acidosis in which distal tubular
function is normal. In these patients, when the
serum bicarbonate falls below the threshold for
complete proximal reabsorption, the distal tubule
is able to lower the pH normally. The low urine pH
rules out distal renal tubular acidosis. Proximal
renal tubular acidosis often causes hypokalemia
and a non-anion gap metabolic acidosis.
Question 8 - Answer
One cause of renal tubular acidosis is the
presence of a monoclonal light chain.
Proximal renal tubular acidosis due to a
monoclonal light chain may occur before
multiple myeloma is diagnoses.
Evaluation for multiple myeloma is warranted.
Salicylate toxicity, lactic acidosis, and ethylene
glycol toxicity all cause an anion gap
metabolic acidosis.
Question 9
Question 9
A 67-year-old woman is evaluated because of a 6month history of gradual-onset dementia. She has
smoked 1 to 2 packs per day of cigarettes for 40
years and she drinks 1 ounce of alcohol weekly.
On examination, she is disoriented to time and
place. Her blood pressure is 142/88 mm Hg,
without orthostatic change, pulse rate is 68/min,
respiration rate is 12/mi, and temperature 37 oC
(98.6 oF). There is no neck vein distention, the
lungs are clear, the cardiac and neurological
examinations are normal, and there is no
peripheral edema.
Question 9
Plasma glucose – 84 mg/dL
Blood urea nitrogen – 6 mg/dL
Serum creatine – 0.5 mg/dL
Serum sodium – 124 meq/L
Serum potassium – 4.2 meq/L
Serum chloride – 89 meq/L
Serum bicarbonate – 24 meq/L
Question 9
Serumn cholesterol – 182 mg/dL
Serum triglyceride – 60 mg/dL
Serum total protein – 7.5 g/dL
Serum osmolality – 255 mosmol/kg
Urine osmolality – 400 mosmo/kg
Question 9
Which of the following is the most likely cause
of her hyponatremia?
(A)
(B)
(C)
(D)
Cirrhosis
Pseudohyponatremia
Psychogenic polydipsia
Syndrome of inappropriate antidiuretic
hormone secretion
Answer
Question 9 - Answer
Answer: D
This patient has the syndrome of inappropriate
antidiuretic hormone secretion. The physical
examination; normal serum potassium level; and
low concentrations of blood urea nitrogen, serum
creatinine, and serum uric acid are consistent with
euvolemic hyponatremia and not with cirrhosis
which is associated with a decreased circulating
vascular volume.
The normal levels of cholesterol, triglycerides, and
total proteins rule out pseudohyponatremia.
Question 9 - Answer
In a patient with psychogenic polydipsia,
ingestion of large amounts of water would
result in hyponatremia. However, the
appropriate compensatory response would
be suppression of antidiuretic hormone,
which results in a dilute urine (excretion of
free water); this phenomenon is not present
in this patient, as evidences by the
inappropriately high urine osmolality.
Question 10
Question 10
A 39-year-old man is evaluated in the
emergency department because of a severe
left flank pain and hematuria after playing
softball. The pain is sharp and radiates to
the groin. He vomited eight times before
presentation. He has nonobstructing,
calcium-containing kidney stone in the
uretopelvic junction on the left side.
Question 10
On initial evaluation, his blood pressure was
130/90 mm Hg and pulse rate was 110/min.
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Serum sodum – 141 meq/L
Serum potassium- 4.0 meq/L
Serum chloride – 100 meq/L
Serum bicarbonate – 34 meq/L
Arterial blood gases – pH, 7.61; PCO2, 36 mg
Hg
Question 10
Which of the following best describes this
patient’s acid-base disorder?
(A)
(B)
(C)
(D)
(E)
Metabolic acidosis and respiratory alkalosis
Metabolic alkalosis
Metabolic alkalosis and respiratory acidosis
Metabolic and respiratory alkalosis
Respiratory alkalosis
Answer
Question 10 - Answer
Answer: D
Arterial blood gas values demonstrate a mixed
metabolic and respiratory alkalosis. Metabolic
alkalosis is indicated by the high serum
bicarbonate level and a pH greater than 7.4
Respiratory compensation for the metabolic alkalosis
is not appropriate; the PCO2 would be expected to
increase in compensation for the elevated serum
bicarbonate level, but instead, the PCO2 has
decreased to 36 mm Hg, indicated the presence of
a respiratory alkalosis.
Question 10 - Answer
The anion gap is 7, calculated as (141 – [100
+ 34]); thus, there is no hidden anion-gap
metabolic acidosis. The respiratory alkalosis
is most likely due to pain induced
hyperventilation from the kidney stone, and
metabolic alkalosis is probably a result of
vomiting.
Question 11
Question 11
The preceding patient is given intravenous
infusion of 0.9% normal saline at 200 mL/h.
Two days later, his flank pain worsens
dramatically, but nausea and vomiting have
resolved. Blood pressure and pulse rate are
unchanged.
Question 11
BUN – 8 mg/dL
Serum creatinine – 0.9 mg/dL
Serum sodum – 138 meq/L
Serum sodium – 138 meq/L
Serum potassium – 4.0 meq/L
Serum chloride – 105 meq/L
Serum bicarbonate – 22 meq/L
Arterial blood gases – ph, 7.48; PCO2, 30 mm Hg
Question 11
Which of the following best describes his acid-base
status?
Metabolic acidosis with respiratory alkalosis
(B) Metabolic alkalosis and respiratory alkalosis
(C) Respiratory acidosis and metabolic alkalosis
(D) Respiratory alkalosis
(A)
Answer
Question 11 - Answer
Answer: D
The patient has persistent respiratory alkalosis, as
indicate by the low PCO2, and a pH greater than
7.4. The condition is most likely due to
hyperventilation in response to pain from the
kidney stone.
For each 10 mm Hg drop in the PCO2, the serum
bicarbonate will decrease by 2. to 4.5 meq/L.
Since the serum bicarbonate level decreased by 2
meq/L, this confirms the diagnosis of a simple,
compensated respiratory alkalosis.
Question 12
Question 12
A 46-year-old man is evaluated because of a 20-year
history of difficult to control hypertension and
hypokalemia treated with amlodipine. He also has
irritable bowel syndrome and produces two semiformed stools daily. On examination, the blood
pressure is 150/88 mg Hg, and pulse rate is
74/min. The lungs are clear, and the heart rhythm
is regular, with no gallop or murmur. Abdominal
examination is normal. Pulses in the lower
extremities are normal, and no edema is present.
Question 12
Serum sodium – 142 meq/L
Serum potassium – 2.7 meq/L
Serum chloride – 105 meq/L
Serum bicarbonate – 30 meq/L
Urinalysis – pH 5.0; specific gravity 1.020; dipstick
negative for protein and blood
24-hour urine results:
 Sodum – 100 meq
 Potassium – 82 meq
 Calcium – 200 mg
Question 12
Which of the following is the most likely cause
of his hypokalemia?
(A)
(B)
(C)
(D)
Diarrhea
Distal renal tubular acidosis
Gitelman’s syndrome
Primary hyperaldosteronism
Answer
Question 12 - Answer
Answer: D
Primary hyperaldosteronism is associated with
hypertension, hypkalemia, and renal potassium
wasting. It is usually associated with a 24-hour
urinary potassium excretion greater then 30 meq
in the setting of a serum potassium concentration
less than 3.0 meq/L.
All of these features are present in this patient.
Distal renal tubular acidosis is incorrect because
the patient is not acidotic and has an acid urine
pH.
Question 12 - Answer
Gitelman’s syndrome is associated with hypokalemia,
renal potassium wasting, and hypocalciuria (which
is not present in this patient). And normotension.
Diarrhea would cause metabolic acidosis and may
cause hypokalemia but would not be associated
with renal potassium unless the patient is
hypovolemic resulting in stimulation of the reninangiotensin-aldosterone system.
Question 13
Question 13
A 60-year-old woman with a history of
essential hypertension is admitted to the
hospital after 7 years of vomiting. On
physical examination, she appears ill. The
systolic blood pressure is 110 mg Hg seated
and 70 mg Hg standing. The pulse rate
while seated is 120/min. The abdominal
examination reveals rebound tenderness
and no bowel sounds.
Question 13
Serum sodium – 140 meq/L
Serum potassium – 3.2 meq/L
Serum chloride – 80 meq/L
Serum bicarbonate – 11 meq/L
Arterial blood gases – pH, 7.29; PCO2, 24 mm
Hg
Question 13
Which of the following best describes her acid-base
status?
Anion gap metabolic acidosis
(B) Anion gap metabolic acidosis and metabolic
alkalosis
(C) Non-anion gap metabolic acidosis and metabolic
alkalosis
(D) Non-anion gap metabolic acidosis
(A)
Answer
Question 13 - Answer
Answer: B
The patient has an anion gap metabolic acidosis and
a con-current metabolic alkalosis. Metabolic
acidosis is indicated by the low serum bicarbonate
level and a pH less than 7.4. The distinctly
abnormal anion gap of 49, calculated as 140 – (80
+ 11), suggests the presence of an anion gap
metabolic acidosis, perhaps due to ischemic bowel
and resultant lactic acidosis.
Question 13 - Answer
The change in the anion gap is 37, calculated as the
anion gap (49) minus the expected normal anion
gap (12). The change in serum bicarbonate level is
13, calculated as the normal serum bicarbonate
level (24 meq/L) minus the actual serum
bicarbonate level (11 meq/L).
The ratio between the change in the anion gap and
the change in the serum bicarbonate level, or the
delta-delta, is greater than 2, thus suggesting a
concurrent metabolic alkalosis.
Question 13 - Answer
Vomiting causes hydrogen ion loss and is the
most likely cause of the metabolic alkalosis.
Respiratory compensation for the metabolic
acidosis is appropriate.
Question 14
Question 14
An 18-year-old male high school student is
evaluated in the emergency department
because of confusion, nausea, headache,
and decreased vision after a camping trip.
The patient’s friends state that he became ill
14 hours ago.
Question 14
BUN – 14 mg/dL
Serum creatinine – 1.0 mg/dL
Serum sodium – 140 meq/L
Serum chloride – 100 meq/L
Serum potassium – 4 meq/L
Serum bicarbonate – 12 meq/L
Serum glucose – 108 mg/dL
Measured serum osmolality – 326
Serum ketones – Negative
Serum lactate – 0.7 meq/L
Arterial blood gases – pH, 7.29; PCO2, 26 mm Hg
Question 14
Ingestion of which of the following best
explains the acid-base abnormalities?
(A)
(B)
(C)
(D)
Ethanol
Isopropyl alcohol
Methanol
Salicylate
Answer
Question 14 - Answer
Answer: C
The patient has an anion gap metabolic
acidosis. The differential diagnosis of an
anion gap metabolic acidosis can be
narrowed by calculating the osmolar gap.
Methanol causes both an anion gap metabolic
acidosis an an elevated osmolar gap.
Question 14 - Answer
Ethanol ingestion increases the osmolar gap but
does not cause this degree of metabolic acidosis
unless it is accompanied by concomitant lactic
acidosis or alcoholic ketoacidosis.
Ingestion of isopropyl alcohol also increases the
osmolar gap but does not produce anion gap
metabolic acidosis.
Use of salicylate causes anion gap metabolic acidosis
but does not increase the osmolar gap.
Finally, the clinical clue of decreased vision strongly
supports methanol and not ethanol as the poison;
methanol is toxic to the optic nerve.
Question 15
Question 15
A 28-year-old woman is evaluated because of
recurrent calcium-containing kidney stones.
She currently has no symptoms of renal
colic. For several years, she has had dry
eyes, dry mouth, and Raynaud’s
phenomenon. Crohn’s disease was
diagnosed 10 years ago; she is currently
asymptomatic and passes one formed stool
daily.
Question 15
She takes no medications. On examination,
the blood pressure is 115/74 mm Hg, pulse
rate is 72/min, and temperature is 37 oC
(98.6 oF). The physical examination is
unremarkable. Plain abdominal radiography
shows multiple calcifications within the renal
parenchyma bilaterally.
Question 15
Serum sodium – 138 meq/L
Serum potassium – 2.8 meq/L
Serum chloride – 109 meq/L
Serum bicarbonate – 19 meq/L
Serum calcium – 9.1 mg/dL
Serum phosphorus – 3.2 mg/dL
Urinalysis – pH 6.0; specific gravity 1.020; trace
hematuria, no proteinuria
Arterial blood pH – 7.29
Question 15
Which of the following is the most likely
etiology of her renal stone disease?
(A)
(B)
(C)
(D)
Distal renal tubular acidosis
Enteric hyperoxaluria
Idiopathic hypercalciuria
Primary hyperparathyroidism
Answer
Question 15 - Answer
Answer: A
This patient has renal tubular acidosis, as evidenced by
hypokalemia and inappropriately alkaline urine in the
presence of a metabolic acidosis.
Type I or distal renal tubular acidosis is associated with
increased urinary calcium excretion and an increased
incidence of nephrolithiasis and nephrocalcinosis.
Distal renal tubular acidosis can result from the
tubulointerstitial renal disease that occurs with Sjogren’s
syndrome, which is suggested in this case by the patient’s
Raynaud’s phenomenon and symptoms of dry eyes and
mouth.
Question 15 - Answer
The normal calcium and phosphate values
make hyperparathyroidism unlikely.
Enteric hyperoxaluria may be seen in
inflammatory bowel diseases, but usually
only in the setting of significant
gastrointestinal malabsorption and diarrhea.
Idiopathic hypercalciuria does not cause
metabolic acidosis or hypokalemia.
Question 16
Question 16
A 39-year-old man is admitted for elective right inguinal
hernia repair. He has bipolar disorder, for which he takes
lithium carbonate. In preparation for surgery, he has
received nothing by mouth for the previous 12 hours.
On examination, the patient is alert and in no distress, but is
thirsty. Blood pressure is 110/70 mm Hg seated and
standing, pulse rate 90/min, respiratory rate 12/min,
temperature 36.9 oC (98.4 oF). No neck vein distension is
present. Except for a right inguinal hernia, the remainder
of the examination is normal.
Question 16
BUN – 18 mg/dL
Serum creatinine – 1.1 mg/dL
Serum sodium – 150 meq/L
Serum potassium – 4.5 meq/L
Serum chloride – 112 meq/L
Serum bicarbonate – 26 meq/L
Urinalysis – Specific gravity 1.006
Question 16
Which of the following is the most likely cause
of the elevated serum sodium level?
(A)
(B)
(C)
(D)
Fluid restriction
High dietary sodium intake
Renal concentrating defect
Syndrome of inappropriate antidiuretic
hormone secretion
Answer
Question 16 - Answer
The patient probably has hypernatremia due to a renal
concentrating defect caused by lithium therapy. The urine
specific gravity is low despite an increased serum sodium
level, indicating a renal concentrating defect.
In healthy persons, 12 or more hours of fluid restriction
would result in renal water conservation and high specific
gravity of the urine and would not result in hypernatremia.
High dietary sodium intake does not cause hypernatemia, and
the syndrome of inappropriate antidiuretic hormone
secretion results in hyponatremia.
Question 17
Question 17
A 19-year-old man with epilepsy previously
well controlled with phenytoin therapy is
brought to the hospital by emergency
medical personnel because of a generalized
seizure. The patient had stopped taking
phenytoin about 3 weeks earlier. A second
seizure occurred shortly after arrival at the
emergency department and was
successfully treated with lorazepam.
Question 17
On examination, he is confused but his
physical examination is otherwise normal.






Serum sodium – 140 meq/L
Serum potassium – 4.0 meq/L
Serum chloride – 104 meq/L
Serum bicarbonate – 10 meq/L
Serum creatine kinase – 45 U/L
Arterial blood gasses – pH, 7.05; PCO2, 38 mm
Hg
Question 17
For the acid-base disorder, which of the following is
the most appropriate course of action?
(A)
(B)
(C)
(D)
(E)
Acetazolamide
Intravenous bicarbonate
Mechanical ventilation
0.45% normal saline
Observe
Answer
Question 17 - Answer
Answer: E
The patient has an anion gap metabolic acidosis with
concurrent respiratory acidosis. Lactic acidosis associated
with the seizure is the most likely explanation for the
metabolic acidosis. Since this state quickly reverses with
cessation of the seizure, observation alone is warranted.
Mechanical ventilation to correct the concurrent respiratory
acidosis is not needed if the patient is awake and breathing
normally.
Acetazolamide may cause a proximal renal tubular acidosis
with bicarbonate wasting and thus worsen the acidosis.
Question 17 - Answer
Intravenous fluids are not contraindicated, but
neither are they are necessary to correct the
acid-base disturbance.
Although the patient has an arterial blood pH
less than 7.2, the transient nature of the
acidosis along with the ability to regenerate
bicarbonate from lactate makes bicarbonate
therapy unnecessary.
Question 18
Question 18
A 64-year-old man with previously diagnosed
alcoholic cirrhosis is admitted to the hospital
with a 5-day history of lethargy and
confusion. Blood pressure is 110/70 mm Hg,
pulse rate is 87/min, and temperature is 36
oC (96.8 oF). The neck veins are not
distended. The lungs are clear, with
decreased breath sounds at both bases.
There is no S3. Ascites and 1+ ankle edema
are present.
Question 18
BUN – 15 mg/dL
Serum creatinine – 1.0 mg/dL
Serum sodium – 114 meq/L
Serum potassium – 4.1 meq/L
Serum chloride – 80 meq/L
Serum bicarbonate – 28 meq/L
Serum total protein – 6.9 g/dL
Cholesterol – 186 mg/dL
Serum osmolality – 241 mosmol/kg
Urine osmolaity – 400 mosmol/kg
Spot urine sodium – 10 meq/L
Question 18
What is the cause of this patient’s hyponatremia?
(A)
(B)
(C)
(D)
(E)
Nonosmotic stimulation of antidiuretic hormone
Hepatorenal syndrome
Low-sodium diet
Reset osmostat
Pseudohyponatremia
Answer
Question 18 - Answer
Answer: A
This patient with hyponatremia and excess
extracellular fluid volume has nonosmotic
stimulation of antidiuretic hormone due to
decreased arterial blood volume (decreased
effective circulating volume) from splanchnic
vasodilation.
Hyponatremia may be seen in the hepatorenal
syndrome, but his renal function is normal and it is
not the cause of the hyponatremia.
Question 18 - Answer
A low-sodium diet is almost never associated
with hyponatremia ; this patient’s urine is
inappropriately concentrated for the level of
serum hypotonicity. Pseudo-hyponatremia
occurs in patients with a normal osmolality
and very high serum levels of either
proteins or lipids.
Question 19
Question 19
A 48-year-old woman is found to have a serum
calcium concentration of 10.9 mg/dL on routine
screening.
Previously, a bone densitometry showed T scores at
the lumbar spine and left proximal femur of –2.14
and –2.64, respectively. There is no history or
evidence of renal stones, bone fracture, cognitive
impairment, or fatigue. The intact serum
parathyroid hormone level is 115 pg/mL (normal
range, 10 to 65 pg/mL).
Question 19
What is the most appropriate next step in the
treatment of this patient?
(A)
(B)
(C)
(D)
Biphosphonate therapy
Estrogen replacement therapy
Low-calcium diet
Parathyroid surgery
Answer
Question 19 - Answer
Answer: D
This patient has mild hypercalcemia and
osteoporosis of the hip. The most common cause
of this presentation is primary
hyperparathyroidism, which is confirmed in this
patient on the basis of an elevated serum
parathyroid hormone concentration.
According to the National Institutes of Health’s
recommendations for treatment of otherwise
asymptomatic patients with primary
hyperparathyroidism, this patient’s bone loss is
itself an indication for surgery.
Question 19 - Answer
She should be referred to an experienced
parathyroid surgeon for resection of what is likely
to be a single parathyroid adenoma.
The calcium metabolism should normalize
postoperatively, and bone density is like to
improve.
Estrogen replacement therapy or a biphosphonate
will reduce bone turnover and may stabilize bone
density, but patient with a recognized secondary
cause of bone loss, correction of the underlying
abnormality is more logical.
Question 19 - Answer
However, if surgery were considered too risky, or if
declined by the patient, medical antiresorptive
therapy may have a short-term salutary effect on
the skeleton in older women with
hyperparathyroidism.
Recent studies, however, have also demonstrated a
significant increase in the risk of breast cancer and
cardiovascular disease in women treated with
post-menopausal estrogen/progestin regimens.
Question 19 - Answer
A low-calcium diet will probably do little to
correct hypercalcemia, may increase the
parathyroid hormone concentration further,
and may increase the risk of further bone
loss.
Question 20
Question 20
A 44-year-old man comes to the emergency
department with polyuria and polydipsia. He
has a 2-year history of a brain tumor
involving the pons and middle cerebral
peduncles. A bone scan has shown multiple
areas of abnormal uptake and has been
receiving high-dose dexamethasone. Over
the past 2 weeks, he has noted increased
urination with nearly constant thirst.
Question 20
Physical examination reveals orthostatic
hypotension, cerebellar ataxia, and diffuse
muscle weakness. Admission laboratory
results included a serum sodium of 155
meq/L, plasma glucose of 150 mg/dL, and
urine osmolality of 117 mosm/kg. He has
significant increase in urine osmolality
(greater) than 50%) within 1 to 2 hours
after injection of arginine vasopression.
Question 20
What is the most likely cause of the
hypernatremia?
(A) Central diabetes insipidus
(B) Diabetes mellitus
(C) Diabetes insipidus, type undetermined
(D) Nephrogenic diabetes insipidus
(E) Primary polydipsia
Answer
Question 20 - Answer
Answer: A
This patient is clearly hyperosmolar, as estimated by
multiplying the serum sodium level by 2. The appropriate
renal response to hyperosmolality is to maximally
concentrate the urine. This response is not seen in this
patient. Thus, he has either diabetes insipidus or a solute
diuresis. A solute diuresis is most often caused by
hyperglycemia. This patient does have a plasma glucose
level of 180 mg/dL; however this degree of elevation is
unlikely to cause significant solute diuresis because the
renal threshold for glucose reabsorption is most persons is
200 to 225 mg/dL.
Question 20 - Answer
Furthermore, solute diuresis is usually characterized
by isotonicity of the urine, whereas this patient
has a markedly hypotonic urine. Consequently,
diabetes mellitus is unlikely.
Hyperosmolar patients without glucosuria who have
submaximally concentrated urine have diabetes
insipidus by definition.
Given his known brain tumor, central diabetes
insipidus is clinically more like than nephrogenic
diabetes insipidus.
Question 21
Question 21
A 22-year-old woman is evaluated in the
emergency department because of severe
dizziness, weakness, nausea, and vomiting
of 1 week’s duration. She has noted fatigue
and moderate weight loss over the
preceding 2 months. She has a history of
hypothyroidism and takes levothyroxine,
100 ug/d.
Question 21
On physical examination, the patient is 168
cm (66 in.) tall and weighs 53 kg (116 lb.)
Blood pressure is 90/60 mm Hg supine and
80/50 mm Hg standing, and pulse rate is
84/min supine and 96/min standing. The
skin is well tanned, and there is markedly
increased pigmentation of the gums and
palmar creases.
Question 21
Hematocrit – 40%
Serum creatinine – 1.2 mg/dL
Blood urea nitrogen – 39 mg/dL
Serum sodium – 124 meq/L
Serum potassium – 6.8 meq/L
Plasma glucose – 61 mg/dL
Question 21
What is the most likely underlying cause of
the hyponatremia?
(A) Acute adrenal hemorrhage
(B) Autoimmune adrenalitis (Addison’s
disease)
(C) Fulminant meningococcemia
(D) Pituitary apoplexy
(E) Tuberculosis
Answer
Question 21 - Answer
Answer: B
This patient presents with an acute adrenal crisis with volume
depletion, hyponatremia, and hyperkalemia, all of which
strongly suggest primary adrenal insufficiency.
Central adrenal insufficiency due to pituitary apoplexy can
present with an acute crisis, but headaches and visual field
abnormalities are usually prominent features and
hyperkalemia does not generally occur.
Primary adrenal insufficiency can result from all of the other
causes shown as options, but autoimmune adrenalitis
(Addison’s disease) is the most common of these in the
United States.
Question 21 - Answer
The presence of hypothyroidism in this patient
makes autoimmune adrenalitis even more likely,
since these two disorders occur together in
patients with autoimmune polyglandular
syndromes.
Fulminent meningococcemia is an unlikely cause of
adrenal insufficiency considering the protracted
time course of the patient’s illness, dark skin, and
the absence of a sepsis syndrome.
Question 22
Question 22
An 82-year-old man who is in the intensive care unit
with multiple system failure is evaluated for
hypocalcemia. He wad admitted 2 months ago
with multilobar pneumococcal pneumonia dn
respiratory failure. His course has been
complicated by difficulty in weaning from the
ventilator, myocardial infarction, prolonged ileus,
line sepsis, and sacral decubiti. The serum calcium
level has gradually decreased from 9.2 mg/dL on
admission to 7.6 mg/dL today.
Question 22
What is the first piece of information that is
needed to evaluate the hypocalcemia?
(A) Serum albumin concentration
(B) Urine calcium concentration
(C) Serum parathyroid hormone concentration
(D) Serum phosphate concentration
Answer
Question 22 - Answer
Answer: A
The measured serum calcium concentration
combines bound and free fractions. Because
calcium is bound to plasma proteins, chiefly
albumin, hypoalbuminemia invariably leads to a
decreased total serum calcium level, yet free or
ionized calcium levels will remain normal.
Therefore, before a diagnostic search is begun for
the cause of the hypocalcemia, it is necessary to
determine whether the ionized calcium level is
actually low.
Question 22 - Answer
In this patient with severe illness and multiple complications
affecting his nutritional status, substantial
hypoalbuminemia would be expected.
The serum phosphate level is elevated in patients with
hypoparathyroidism but is likely to be low-normal in this
patient (unless renal failure coexists).
For unclear reasons, parathyroid hormone levels tend to be
lower than expected in critically ill patients.
Large volume blood transfusions may decrease the serum
calcium level by complexing with citrate, the anticoagulant
in banked blood. This matter may be more pertinent if the
ionized calcium level is low.
End of Lecture
Thank you for your attendance.