Internal-Medicine

172 8: Kidneys
44. (B) Diuretics are a common cause of metabolic
alkalosis. The disorder can occur in volume
expanded patients in whom the alkalosis is
unresponsive to sodium chloride loading, as
in primary hyperaldosteronism or volume contraction
with secondary hyperaldosteronism,
as in this case. (Kasper, p. 268)
45. (A) INH can result in impaired oxygen utilization,
leading to lactic acidosis (type B), accumulation
of lactate, and increased anion gap.
(Kasper, p. 266)
46. (D) Chronic salicylate use can cause respiratory
alkalosis. Severe salicylate toxicity results in an
anion gap metabolic acidosis such as during an
overdose. During acute hyperventilation, plasma
bicarbonate concentrations fall by approximately
3 mEq/L when the arterial pressure of CO 2
falls
to about 25 mm Hg. Acute respiratory alkalosis
can be caused by anxiety, central nervous system
(CNS) disorders, drugs, or fever. Chronic respiratory
alkalosis occurs in pregnancy and liver
disease as well. (Kasper, p. 270)
47. (E) The diuretic phase of ATN is characterized by
large losses of sodium and water. (Kasper, p. 251)
48. (C) Primary polydipsia can cause greater
medullary washout than either nephrogenic or
central DI because primary polydipsia tends
to cause expansion of the ECF volume. This
tends to increase total delivery of sodium chloride
and water to the inner medulla. It also
increases renal blood flow, and increased flow
through the vasa recta reduces ability to trap
solutes in the medulla. (Kasper, p. 2098)
49. (A) Nephrogenic DI can be caused by
hypokalemia as well as hypercalcemia.
(Kasper, p. 2099)
50. (C) Both thioridazine and chlorpromazine have
been associated with primary polydipsia.
(Kasper, p. 251)
51. (A) There is little or no response to vasopressin
after fluid deprivation in complete nephrogenic
DI. Incomplete nephrogenic DI will show some
response. (Kasper, p. 2099)
52. (D) High protein tube feeds may cause a solute
diuresis because of excessive excretion of urea.
Other causes of solute diuresis include glucosuria,
mannitol, radiographic contrast media,
and chronic renal failure. (Kasper, p. 251)
53. (H) The combination of ECF volume contraction
with high urinary sodium (20 mmol/L) suggests
renal fluid loss. This is commonly caused by
diuretics or glucosuria. (Kasper, pp. 254–256)
54. (C) SIADH is associated with many CNS diseases
including meningitis, encephalitis, tumors,
trauma, stroke, and acute porphyria. It is
assumed that antidiuretic hormone (ADH) in
these patients is secreted in response to direct
stimulation of the hypothalamic osmoreceptors.
(Kasper, pp. 254–256)
55. (C) Amitriptyline is one of the psychoactive
drugs that cause SIADH. Others include phenothiazines,
serotonin reuptake inhibitors,
and monoamine oxidase inhibitors (MAOIs).
Antineoplastic drugs such as vincristine and
cyclophosphamide also cause SIADH, as does
the hypoglycemic agent chlorpropamide. (Kasper,
p. 2099)
56. (B) The combination of ECF volume contraction
and low urinary sodium (