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MCQs in Fluid and Electrolyte Balance With Answers
MCQs in Fluid and Electrolyte Balance With Answers
MCQs in Fluid and Electrolyte Balance With Answers
Primary disturbance
Altered physiology
Clinical effect
Sodium
ECF volume
Circulatory changes
Water
ECF osmolality
Cerebral changes
Potassium
Action potential
Neuromuscular weakness,
cardiac effects
Hydrogen ion
Magnesium
Phosphate
Cellular energetic
1)
Page 2 of 50
2)
Page 3 of 50
If 1 L of solute-free water is lost from the body, how much fluid is lost by the ICF compartment?
a. 333 mL
b. 667 mL
T [ Water is distributed between the ICF and
the ECF in a 2:1 ratio. Therefore, a given amount of solute-free water loss will result in a
twofold greater reduction in the ICF compartment than the ECF compartment. If 1 L of
water is lost, the ICF volume will decrease by 667 mL, whereas the ECF volume will fall
by only 333 mL. If the 1L of fluid lost is isoosmotic, ECF compartment will decrease by 1
L because Na+ is largely restricted to the ECF.]
c. 1 L
d. None
5)
Page 4 of 50
until the osmolality in these two compartments is the same. Therefore, ECF osmolality is
equal to ICF osmolality.]
d. Any of the above depending on fluid intake
6)
ECF osmole(s)
a. Na+
b. Clc. HCO3d. All of the above
T [ Sodium is the predominant cation in ECF
and associates with the anions chloride and bicarbonate. These three electrolytes
account for more than 90% of the active osmoles in ECF. The predominant cation in ICF
is potassium. K+ is electrochemically balanced primarily by organic phosphates. In
addition, DNA, RNA, and phosphate esters (ATP, creatine phosphate, and phospholipids)
are anionic and provide a negative charge to balance the positive charge of potassium in
intracellular water (ICF). K+ and phosphate esters are the predominant ICF osmoles.
Solutes that are restricted to the ECF or the ICF determine the effective osmolality (or
tonicity) of that compartment. Na+ is largely restricted to the extracellular compartment.
Therefore, total body Na+ content is a reflection of ECF volume. Hyponatremia or
hypernatremia is due to disorders of water homeostasis.]
7)
ICF osmole(s)
a. ATP
b. Creatine phosphate
c. K+
d. Phospholipids
e. All of the above
T [ K+ is predominantly limited to the ICF.
The major intracellular anions are phosphates and negatively charged proteins. These
are necessary for normal cell function. Therefore, the number of intracellular particles is
relatively constant. Therefore, any change in ICF osmolality is usually due to a change in
ICF water content.]
b.
c.
d.
e.
9) What maintains the difference in cation concentration between the ICF and ECF?
Page 5 of 50
a. Sodium-potassium pump
10)What maintains the difference in cation concentration between the ICF and ECF?
a. Na+, K+-adenosine triphosphate
b. Cell membrane sodium conductance pathways
c. Cell membrane potassium conductance pathways
d. Free movement of water
e. All of the above
T [ Sodium is the major cation in the ECF.
Chloride and bicarbonate are the major accompanying anions in the ECF. Potassium is
the major cation in the ICF. Negative charges on organic molecules maintain
electroneutrality with potassium in the ICF. The difference in cationic solute composition
between these two compartments is maintained by the activity of Na+, K+-adenosine
triphosphate (ATPase) operating in concert with cell membrane sodium and potassium
conductance pathways. The free movement of water ensures that the sodium
concentration in ECF is nearly equivalent to the potassium concentration in ICF.]
Page 6 of 50
11)What regulates Na+ balance
a. Sodium intake and thirst
12)
13)
True statement(s)
a. Osmolality refers to the concentration of all solutes
b. Tonicity refers to the concentration of solutes that are effective in eliciting a water shift
between body fluid compartments
c. Urea is not an effective solute
[ Osmolality refers to the concentration of all
solutes. Tonicity refers to the concentration of solutes that are effective in eliciting a
water shift between body fluid compartments. Addition or removal of solutes causes shift
of water to restore the equality of solute concentrations. Therefore, they are considered
effective solutes. Solutes such as urea do not elicit such a sustained shift in water.
Therefore, urea is not considered effective solute, although they contribute to the
laboratory measurement of fluid osmolality.]
d. Addition of water without solutes results in reduction in both osmolality and tonicity
[ The addition of water without solutes
results in reduction in both osmolality and tonicity of all body fluid compartments. The
removal of water without solutes results in increase in both osmolality and tonicity of all
body fluid compartments.]
e. All of the above
T [ All are false statements.]
14)
Ineffective osmole
a. Sodium
[ The ECF volume is a reflection of total
body Na+ content. Na+ excess or deficit are manifest as edematous or hypovolemic
states, respectively.]
Page 7 of 50
b. Potassium
c. Urea
T [ Urea and glucose do not contribute to
water shift across cell membranes. Therefore, they are known as ineffective osmoles.]
d. Osmolytes
[ Osmolytes are organic solutes (e.g.,
inositol, betaine, and glutamine).]
15)
Which of the following is the least important source of obligate water loss?
a. Urine
[ Metabolism of a normal diet generates
about 600 mosmol/d. Therefore, 600 mosmols must be excreted per day through urine,
primarily as urea and electrolytes. The maximal urine osmolality that can be achieved is
1200 mosmol/kg. Thus, a minimum urine output of 500 mL daily is required for excreting
the daily solute load. Oliguria is urine output < 500 mL/day. Water intake must equal
water excretion to maintain a steady state. Daily water intake exceeds physiologic
requirements in normal physiological conditions.]
b. Stool
T [ Gastrointestinal excretion is only a minor
component of total water output. It becomes an important route of water loss in patients
with vomiting, diarrhea, or high enterostomyoutput states.]
c. Evaporation from the skin
[ Evaporative or insensitive water losses are
important in the regulation of body temperature.]
d. Evaporation from the respiratory tract
16)
17)
Page 8 of 50
Water
T [ Body water is the primary determinant of
extracellular fluid osmolality and disturbances in water balance primarily affect body fluid
tonicity. Disorders of body water balance can cause hypotonicity or hyperotonicity. When
there is an excess of body water relative to body solute, hypotonicity results. When there
is a deficiency of body water relative to body solute, hyperotonicity develops. The main
constituent of plasma osmolality is sodium. Therefore, hypotonic disease states are
characterized by hyponatremia and hypertonic disease states are characterized by
hypernatremia. Disturbances in sodium balance primarily affect ECF volume]
b. Glucose
c. Urea
d. Hemoglobin
a.
18)
19)
20)
Page 9 of 50
c. 300
d. 325
21)
Hypovolaemia
Thirst
Dizziness on standing
Weakness
Tachycardia
Hypotension
Dry tongue
Reduced skin turgor
Reduced urine output
Confusion
Symptoms
Signs
Hypervolaemia
Edema
Breathlessness
Peripheral edema
Raised JVP
Lung crepitations
Pleural effusion
Ascites
Weight gain
HYPOVOLEMIA
CAUSES OF SODIUM AND WATER DEPLETION
Mechanism
Examples
Inadequate intake
Internal sequestration
Page 10 of 50
In internal sequestration total body sodium and water may be normal or increased.
1) What is/are the cause(s) of hypovolemia with normal renal function?
a. High-protein hyperalimentation
[ Hypovolemia is volume depletion leading to
b.
c.
d.
e.
ECF volume contraction due to loss of both salt and water exceeding intake.
Increased renal filtration of non-reabsorbed solutes (e.g., glucose, urea) impairs
tubular reabsorption of Na+ and water, leading to an osmotic (solute) diuresis. This
occurs in poorly controlled diabetes mellitus and in patients receiving high-protein
hyperalimentation.]
Mannitol IV
[ The renal tubule is impermeable to
mannitol. Therefore, mannitol produces an osmotic diuresis because mannitol can be
excreted along with water only.]
Hypoaldosteronism
[ Mineralocorticoid deficiency
(hypoaldosteronism) causes salt wasting.]
Central diabetes insipidus
[ Central diabetes is due to impaired
secretion of AVP. Nephrogenic diabetes insipidus is due to renal unresponsiveness to
AVP.]
All of the above
T [ Excessive renal losses of Na+ and water
may also occur during the diuretic phase of acute tubular necrosis and following the
relief of bilateral urinary tract obstruction.]
History can determine the cause of hypovolemia (bleeding, vomiting, diarrhea, polyuria,
medications, diaphoresis).
a. 2 L
b. 5 L
c. 9 L
T [ About 9 L of fluid enters the GIT daily, 2 L
by ingestion and 7 L by secretion. Almost 98% of this volume is reabsorbed so that
fecal fluid loss is only 100 to 200 mL/d. Impaired gastrointestinal reabsorption or
increased secretion leads to volume depletion.]
d. 14 L
e. 20 L
3) Diarrhea causes
a. Metabolic alkalosis
4) Sweat
a. Usually hypertonic but may be isotonic
Page 11 of 50
b. Usually isotonic but may be hypertonic
c. Hypotonic
a. ECF
b. ICF
c. Both
d. Neither
T [ Examples of third-space are peritoneal
space, retroperitoneal space, lumen of GIT, and subcutaneous tissue. Third space
compartment is extracellular but is not in equilibrium with either the ECF or the ICF.
In pathologic conditions, ECF can be sequestered into third-space compartments
within the body without a history of fluid loss. In such cases, the clinical
manifestations are those of real hypovolemia because the sequestered compartment
is not in hemodynamic equilibrium with the ECF. The fluid is lost from the ECF and
can result in hypovolemia. Examples include sequestration of fluid in the bowel lumen
in gastrointestinal obstruction, in the subcutaneous tissues in severe burns or trauma,
in the retroperitoneal space in acute pancreatitis, and in the peritoneal cavity in
peritonitis or malignant ascites. These extrarenal causes of absolute hypovolemia
stimulate renal sodium and fluid retention.]
b.
c.
d.
e.
decreased.]
b. Vasodilatation of afferent arterioles
Page 12 of 50
d. Increased atrial natriuretic peptide
Page 13 of 50
b. Raised plasma urea
d.
e.
10)In hypovolemia
a. Low urine sodium
11)A patient has quickly lost 1 L of whole blood following an accident. What features can you
expect in such a patient? [ Answer all choices given below are true]
a. Tachycardia
b. Postural hypotension
c. Peripheral vasoconstriction with cool extremities
d. Oliguria - When fluid loss is extrarenal, there is water and sodium retention by the
kidneys. This normal renal response results in oliguria with an elevated urine specific
gravity (>1.020) and osmolality (>400 mOsm/kg), a sodium concentration less than
20 mEq/L and a fractional excretion of sodium < 1%.
Page 14 of 50
e. Collapsed neck veins - Jugular venous pressure may fall (CVP < 5 cm H2O)
f. Normal hemoglobin Hemoglobin may remain constant initially. Normal hemoglobin
levels do not rule out bleeding as a cause of hypovolemia. Later, hemoglobin falls
due to movement of ECF from the interstitial to the intravascular compartment
g. Normal blood urea - Blood urea may also remain constant initially. Later, blood urea
may increase reduced renal blood flow and the effects of destruction of erythrocytes
in the gastrointestinal tract
h. Normal serum sodium and potassium - Sodium and potassium concentration and
acid-base parameters are not likely to change initially
13)
Fluid
Glucose
Calories
Na+
Cl-
Other
5% dextrose
50 g
200
Normal saline
154
154
Page 15 of 50
What percentage of a unit of packed red blood cells given remains in the vascular
compartment?
a. 100
[ A unit of infused packed red blood cells
remains entirely in the vascular compartment. However, erythrocytes are actually
considered part of the intracellular compartment. Packed red cells are used in the
treatment of hemorrhage to restore oxygen carriage and delivery and not as ECF
volume replacement.]
b. 66
c. 33
d. 15
HYPERNATREMIA
1)
Page 16 of 50
Renal causes
Diuretics
Osmotic diuresis (glucose, urea, mannitol)
Postobstructive diuresis
Polyuric phase of acute tubular necrosis
Intrinsic renal disease
Gastrointestinal causes
Vomiting
Diarrhea
Nasogastric drainage
Cutaneous causes
Burns
Excessive sweating
Hypertonic sodium gain
Hypertonic sodium bicarbonate or sodium chloride infusion
Hypertonic feeding preparation
Ingestion of sodium chloride (e.g., sea water)
Hypertonic saline enemas
Intrauterine injection of hypertonic saline
Hypertonic dialysis
Primary hyperaldosteronism
Cushings syndrome
2)
Page 17 of 50
Hypernatremia is rare in conscious patients who have free access to water because of
the extreme sensitivity of the thirst mechanism.]
3)
If 1 L of water is lost from the body, how much fluid is lost by the ICF compartment?
a. 333 mL
b. 667 mL
T [ Water is distributed between the ICF and
the ECF in a 2:1 ratio. Therefore, a given amount of solute-free water loss will result in a
twofold greater reduction in the ICF compartment than the ECF compartment. If 1 L of
water is lost, the ICF volume will decrease by 667 mL, whereas the ECF volume will fall
by only 333 mL. If the 1L of fluid lost is isoosmotic, ECF compartment will decrease by 1
L because Na+ is largely restricted to the ECF.]
c. 1 L
d. None
4)
5)
6)
Fecal osmolality
a. Equal to the sum of stool concentrations of Na+ and K+
Page 18 of 50
7)
8)
9)
10)
Page 19 of 50
Hypernatremia can develop in patients with diabetes insipidus who have sustained a
large water loss. Diabetes insipidus causes nonosmotic urinary water loss and
hypernatremia. Total solute excretion must equal solute production. Persons eating a
normal diet generate about 700 mosmol/d of solutes. Therefore, daily solute excretion in
excess of 750 mosmol is an osmotic diuresis. This can be confirmed by measuring the
urine glucose and urea.]
b. Diabetes mellitus
T [ Osmotic diuresis is water loss in excess
of Na+ and K+. The most common cause of an osmotic diuresis is hyperglycemia and
glucosuria in poorly controlled diabetes mellitus.]
c. IV mannitol
d. High-protein diet
[ Intravenous administration of mannitol and
high-protein diet (increased production of urea) can also result in an osmotic diuresis.]
11)
Page 20 of 50
12)
13)
Page 21 of 50
15)
Treatment of hypernatremia
a. Loop diuretic
b. Desmopressin
c. Correct the water deficit
[ The most common cause of hypernatremia
is loss of water. Treatment of patients with hypernatremia secondary to dehydration is IV
or oral administration of water. The amount of water required to correct the deficit can be
calculated from the equation given below. Hypernatremic patients typically have reduced
blood volumes. Treat these patients first with the IV infusion of isotonic saline solutions
until the contracted ECF has been restored. Then give sufficient electrolyte-free water to
enable their renal function to produce concentrated urine and correct the hypernatremia.
In patients with prolonged hyperosmolality, aggressive treatment with hypotonic fluids
may cause cerebral edema, which can lead to coma, convulsions, and death. Lower Na+
only at a rate < 8 mEq/day. See figure below.]
d. Dialysis
e. Tetracycline
Total body water is approximately 50 of lean body weight in men and and 40% of lean body
weight in women
Page 22 of 50
Within minutes after the development of hypertonicity, loss of water from brain cells causes
shrinkage of the brain and an increase in osmolality. Partial restitution of brain volume occurs
within a few hours as electrolytes enter the brain cells (rapid adaptation). The normalization of
brain volume is completed within several days as a result of the intracellular accumulation of
organic osmolytes (slow adaptation). Slow correction of the hypertonic state reestablishes
normal brain osmolality without inducing cerebral edema, as the dissipation of accumulated
electrolytes and organic osmolytes keeps pace with water repletion. In contrast, rapid correction
may result in cerebral edema as water uptake by brain cells outpaces the dissipation of
accumulated electrolytes and organic osmolytes. Such overly aggressive therapy carries
the risk of serious neurologic impairment due to cerebral edema.
16)
How much is the free water deficit in a 50-kg woman with a plasma Na+ concentration of 160
mEq/L?
a. 1.9 L
b. 2.9 L
T [ (20 140) X (0.4 50). Rapid correction
of hypernatremia can be dangerous. A sudden decrease in osmolality may cause a rapid
shift of water into brain cells. Therefore, correct the water deficit slowly over at least 48.
The safest route of administration of water is by mouth. 5% dextrose in water or halfisotonic saline can be given intravenously safely.]
c. 3.9 L
d. 4.9 L
17)
What is the preferred route for administering fluids in a patient with hypernatremia?
Page 23 of 50
Page 24 of 50
19)
A 76-year-old man presents with confusion, dry mucous membranes, decreased skin turgor,
fever, tachypnea, and a blood pressure of 142/82 mm Hg without orthostatic changes. The
serum sodium concentration is 168 mEq per liter, and the body weight is 68 kg. Hypernatremia
caused by pure water depletion due to insensible losses is diagnosed, and an infusion of 5
percent dextrose is planned. How much is the estimated volume of total body water in liters?
a. 41
[ The estimated total body water (in liters) is
calculated as a fraction of body weight. The fraction is 0.6 in children; 0.6 and 0.5 in
nonelderly men and women, respectively; and 0.5 and 0.45 in elderly men and women,
respectively. Normally, extracellular and intracellular fluids account for 40 and 60 percent
of total body water, respectively. The estimated volume of total body water in a child
weighing 68 kg would be 68 X 0.6 = 40.8L]
b. 34
T [ 0.5 X 68]
c. 31
[ The estimated volume of total body water in
an elderly men and woman weighing 68 kg would be 68 X 0.45 = 30.6 L.]
d. 25
Page 25 of 50
20)
If 1 liter of 5 percent dextrose is given to the patient described above, what will be the fall in
serum sodium concentration?
a. 2.4 mEq per liter
b. 4.8 mEq per liter
T [ Change in serum Na+ = (infusate Na+ +
serum Na ) (total body water + 1). According to this formula, the retention of 1 liter of 5
percent dextrose will reduce the serum sodium concentration by 4.8 mEq per liter [ (0
168) (34+1) = - 4.8.]
c. 9.6 mEq per liter
d. 19.2 mEq per liter
21)
22)
A 62-year-old man with advanced alcoholic cirrhosis is on lactulose for hepatic encephalopathy.
Examination shows confusion, ascites, and asterixis. The blood pressure is 105/58 mm Hg in
the supine position, and the pulse is 110 beats per minute. The serum sodium concentration is
160 mEq per liter, the potassium concentration is 2.6 mEq per liter, and the body weight is 64
kg. What is the treatment?
a. Increase the dose of lactulose and give IV normal saline
b. Withdraw lactulose and give IV 0.2 percent sodium chloride
T [ The hypernatremia is due to hypotonic
sodium and potassium losses induced by lactulose therapy. Treatment is withdrawal of
lactulose and IV 0.2 percent sodium chloride containing 20 mEq of potassium chloride
per liter. With the presence of ascites, the estimated volume of total body water is about
38 liters (0.6 X 64).
c. Furosemide IV
d. Liver transplantation
e. Potassium chloride IV
23)
A 60-year-old man has received 10 ampoules of sodium bicarbonate over six hours during
resuscitation after recurrent cardiac arrest. He is stuporous and is undergoing mechanical
ventilation. His blood pressure is 138/86 mm Hg, and peripheral edema is present. The serum
Page 26 of 50
sodium concentration is 156 mEq per liter, the body weight is 85 kg, and the urinary output is 30
ml per hour. What is the treatment?
a. Furosemide
[ The hypernatremia is caused by hypertonic
sodium gain. For its correction, the excess sodium and water be excreted. Furosemide
alone is not enough, because furosemide- induced diuresis is equivalent to one-half
isotonic saline solution. Thus, the hypernatremia will be aggravated.]
b. Furosemide and electrolyte-free water
T [ The correct treatment is administration of
both furosemide and electrolyte-free water. The estimated volume of total body water is
51 liters (0.6 X85). If 1 liter of 5 percent dextrose is given, it will decrease the serum
sodium concentration by 3.0 mEq per liter (0 156) (51+1) = - 3.0. Since the patients
extracellular-fluid volume is expanded, fluids can be administered only with great
caution. Adjust fluid administration based on close monitoring of the patients clinical
status and serum sodium concentration.]
c. Hemodialysis
[ Hypernatremia with concurrent renal failure
and volume overload is a special problem. Diuretics cannot be relied on to reduce the
expanded extracellular-fluid volume. Therefore, hemodialysis, hemofiltration, or
peritoneal dialysis may be necessary.]
d. Peritoneal dialysis
e. Dopamine
24)
Not suited for correcting hypernatremia in a 50-year-old man with a serum sodium
concentration of 162 mEq per liter and a body weight of 70 kg is
a. Isotonic saline
T [ Isotonic saline is unsuitable for correcting
hypernatremia. Estimated volume of total body water is 42 liters (0.6 X 70). The retention
of 1 liter of 0.9 percent sodium chloride will decrease the serum sodium concentration by
only 0.2 mEq per liter ( 154 162) (42 + 1) = - 0.2). Although the sodium concentration
of the infusate is lower than the patients serum sodium concentration, it is not sufficiently
low to alter the hypernatremia substantially. The only indication for administering isotonic
saline to a patient with hypernatremia is a depletion of extracellular-fluid volume that is
sufficient to cause substantial hemodynamic compromise. Even in this case, after a
limited amount of isotonic saline has been administered to stabilize the patients
circulatory status, give a hypotonic fluid (i.e., 0.2 percent or 0.45 percent sodium
chloride). If a hypotonic fluid is not substituted for isotonic saline, the extracellular-fluid
volume may become seriously overloaded.]
b. 0.2 percent sodium chloride
c. 0.45 percent sodium chloride
d. All of the above
HYPONATREMIA
1)
Page 27 of 50
c. Hypernatremia
d. Diabetes insipidus
2)
Volume depletion
Cirrhosis
Heart failure
Nephrotic syndrome
SIADH
Hypothyroidism
Hypoadrenalism (Glucocorticoid deficiency)
Drugs
Pregnancy
Severe hypoalbuminemia
Low Circulating ADH
Page 28 of 50
a. Diuretics
b. Dilutional hyponatremia
T [ Dilutional hyponatremia is the most
common form of hyponatremia. It is most commonly caused by water retention due to
impaired renal excretion of water. With the exception of renal failure, these conditions are
characterized by high plasma concentrations of arginine vasopressin. In a minority of
cases, dilutional hyponatremia is caused by excessive water intake (e.g., primary
polydipsia). If water intake exceeds the capacity of the kidneys to excrete water, dilution
of body solutes results, causing hypo-osmolality and hypotonicity. Hypotonicity can lead
to cerebral edema.]
c. Hyperglycemia
[ Hypertonic hyponatremia is due to shift of
water from cells to the extracellular fluid. It is caused by solutes confined in the
extracellular compartment (e.g., hyperglycemia or mannitol). The serum tonicity is
increased causing dehydration of cells.]
d. Pregnancy
a. Decreased
b. Normal
c. Increased
d. Any of the above
T [ Hypotonic (dilutional) hyponatremia
means an excess of water in relation to existing sodium stores, which can be decreased,
essentially normal, or increased.]
5)
Page 29 of 50
6)
7)
8)
Page 30 of 50
Furosemide
[ Furosemide, bumetanide, and torsemide
are "loop" diuretics. They reversibly inhibit the reabsorption of Na+, K+, and Cl- in the
thick ascending limb of Henle's loop. Hypokalemia, hyperuricemia, and hyperglycemia
are observed occasionally. The reabsorption of free H2O is decreased. Loop diuretics
decrease the tonicity of the medullary interstitium and impair maximal urinary
concentrating capacity. This limits the ability of AVP to promote water retention.]
c. Bumetanide
d. Ethracrynic acid
e. Spiranolactone
b.
9)
What is/are the cause(s) of hyponatremia with increased ECF volume (hypervolemia)?
a. Congestive heart failure
[ Hypotonic hyponatremia is subdivided
according to the clinical ECF volume status. Hyponatremia with ECF volume expansion
is seen in edematous states, such as congestive heart failure, hepatic cirrhosis, and the
nephrotic syndrome. All these conditions have decreased effective circulating arterial
volume, leading to increased thirst and increased AVP levels.]
b. Cirrhosis
c. Nephrotic syndrome
d. Renal failure with oliguria
[ Oliguric renal failure may cause
hyponatremia if water intake is more than what the kidneys can excrete.]
e. All of the above
T [ The severity of hyponatremia often
correlates with the severity of the underlying condition and is an important prognostic
factor. See figure below.]
Page 31 of 50
10)Secondary hyperaldosteronism
a. Cardiac failure
b. Cirrhosis
c. Nephrotic syndrome
d. All of the above
T [ These conditions are associated with
sodium and fluid overload. The reduced effective blood volume stimulates reninangiotensin-aldosterone axis resulting in sodium and fluid overload. See figure above.]
11)
Page 32 of 50
Nephrotic syndrome
[ Patients with advanced renal disease
typically develop hyponatremia due to abnormal water retention.]
d. All of the above
T [ In hypervolemic hyponatremia, there is
an excess in total body water and total body sodium, resulting in edema or ascites. In
many cases, the increase in total body water is out of proportion to that of total body
sodium, causing hyponatremia. This pathophysiology occurs in congestive heart failure,
cirrhosis, and nephrotic syndrome.]
c.
12)
CAUSES OF HYPONATRAEMIA
14)
Volume status
Examples
Hypovolaemic
(sodium deficit with a
relatively
smaller water deficit)
Euvolaemic
(water retention alone)
Hypervolaemic
(sodium retention with
relatively
greater water retention)
Page 33 of 50
Adults
Thiazides
Postoperative state
SIADH
Polydipsia in psychiatric patients
Transurethral prostatectomy
Infants and children
Gastrointestinal fluid loss
Ingestion of dilute formula
Accidental ingestion of excessive water
Multiple tap-water enemas
17)
SIADH DIAGNOSIS
Page 34 of 50
18)
Cause(s) of SIADH
a. Hypopituitarism
[ Hypopituitarism can also lead to
hyponatremia. Hyponatremia is not due to mineralocorticoid deficiency. The main
regulator of aldosterone secretion is the RAAS and not ACTH secretion by the pituitary.]
b. Thyroid disease
[Patients with primary hypothyroidism have
impaired free water excretion. Decreased free water excretion in myxedema is due to an
alteration in renal perfusion and GFR (not due to inappropriate plasma AVP elevation).
The renal changes are secondary to systemic effects of thyroid hormone deficiency on
cardiac output and peripheral vascular resistance. This can be reversed by thyroid
hormone replacement.]
c. Adrenal disease
d. All of the above
e. None of the above
T [ SIADH is a diagnosis of exclusion and
can only be made in the setting of normal renal, thyroid, and adrenal function.]
19)
20)
What is/are the cause(s) of hyponatraemia with hypovolaemia due to increased renal loss of
sodium and water?
a. Diuretic therapy
[ Diuretic induced hyponatremia is more
common with thiazide diuretics than after loop diuretics. Though less potent than loop
diuretics, thiazide diuretics do not disrupt the medullary countercurrent concentrating
mechanism.]
b. Mineralocorticoid deficiency
c. Cerebral salt wasting
[ Head injury and intracranial hemorrhage
can induce negative sodium balance through urinary losses. The hypovolemia induces
release of AVP. This condition is frequently difficult to distinguish from hyponatremia
caused by the SIADH.]
d. Salt-losing nephropathy
e. All of the above
T
21)
Page 35 of 50
Edema is typical
[ Patients with hypervolemic hyponatremia
have excess total body sodium manifested by edema. Physical examination in a patient
with hypovolemic hyponatremia typically shows features of hypovolaemia (tachycardia,
orthostatic hypotension, dry mucous membranes, flat neck veins, absence of edema)]
c. Spot urine sodium concentration is always less than 20 mEq/L if renal function is normal
[ When volume losses are nonrenal (due to
hemorrhage, diarrhea, dermal losses, or third spacing of fluids as in pancreatitis or
peritonitis), the spot urine sodium concentration is typically less than 20 mEq/L. When
volume losses are due in part to renal sodium wasting, the spot urine sodium
concentration is greater than 20 mEq/L. Such renal sodium wasting may be seen in the
presence of active diuretics, mineralocorticoid deficiency, osmotic diuresis, salt-losing
nephropathy, bicarbonaturia (most commonly from vomiting), and ketonuria.]
d. All of the above
e. None of the above
T [ All are false statements.]
b.
22)
23)
Cause(s) of hyponatremia
a. Adrenal insufficiency
[ Cortisol deficiency that leads to
hypersecretion of AVP. AVP is cosecreted with corticotropin-releasing factor. Volume
depletion also causes hypersecretion of AVP. Decreased mineralocorticoids of adrenal
insufficiency may contribute to the hyponatremia.]
b. Hypothyroidism
[ Decreased cardiac output and GFR seen in
hypothyroidism lead to increased AVP secretion.]
c. SIADH
d. Primary polydipsia
[ The normal kidneys can excrete about 12 L
of water daily. In psychogenic or primary polydipsia, compulsive water consumption may
be much more than this. These patients often have psychiatric illnesses.
e. All of the above
T [ Metabolism of a normal diet generates
about 600 mosmol/d. The minimum urine osmolality is 50 mosmol/kg. Therefore, the
maximum daily urine output will be about 12 L (600 50 = 12).]
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Urine Na (mEq/L)
Low
Low
High
Diagnoses
Primary polydipsia
Malnutrition
Beer excess
Salt depletion
Hypovolaemia
Diuretic action (acute phase)
SIADH
Cerebral salt-wasting
Adrenal insufficiency
24)
What is the diagnosis in a patient with high urine sodium and low specific gravity?
a. SIADH
b. Adrenal insufficiency
c. Diuretic
T
d. Cardiac failure
e. Hypovolaemia
25)
What is potomania?
a. Fear of small pots
b. Fear of being photographed
c. Fear of cameras
d. Hyponatremia seen in beer drinkers
T [ Beer-drinkers potomania is caused by
a high in fluid (beer) intake that is low in solute. Consumption of large volumes of beer
may exceed the renal excretory capacity and result in hyponatremia. This phenomenon
is referred to as beer potomania.]
e. Seen in HIV infection
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26)
Page 38 of 50
Within minutes after the development of hypotonicity, water gain causes swelling of the brain
and a decrease in osmolality of the brain. Partial restoration of brain volume occurs within a few
hours as a result of cellular loss of electrolytes (rapid adaptation). The normalization of brain
volume is completed within several days through loss of organic osmolytes from brain cells
(slow adaptation). Low osmolality in the brain persists despite the normalization of brain
volume. Proper correction of hypotonicity reestablishes normal osmolality without risking
damage to the brain. Aggressive correction of hyponatremia can lead to irreversible brain
damage.
27)
Page 39 of 50
a. Cardiovascular
b. Respiratory
c. Neurologic
T [ The severity of symptoms depends
mainly on the rapidity of the decrease in serum Na+. Most patients are not symptomatic
until the serum Na+ decreases to less than 125 mEq/L. Symptoms are predominantly
neurologic (nausea, vomiting, headache, fatigue, irritability, and disorientation). See table
below. Severe hyponatremia can progress to seizures, brainstem herniation, and death.]
d. Renal
SYMPTOMS OF HYPONATREMIA
28)
29)
Page 40 of 50
adapts to this change. Solutes leave brain tissues within hours, thereby inducing water
loss and ameliorating brain swelling. This process of adaptation by the brain accounts for
the relatively asymptomatic nature of even severe hyponatremia if it develops slowly.]
c. Thirst
d. Osmotic demyelination
[ Osmotic demyelination can develop one to
several days after aggressive treatment and rapid correction of hyponatremia. Shrinkage
of the brain triggers demyelination of pontine and extrapontine neurons that can cause
neurologic dysfunction, including quadriplegia, pseudobulbar palsy, seizures, coma, and
even death.]
Page 41 of 50
Plasma osmolality
Urine osmolality
Urine Na+ concentration
Urine K+ concentration
Most patients with hyponatremia have a decreased plasma osmolality. The kidneys respond
to hypoosmolality by excreting maximum volume of dilute urine, i.e., urine osmolality will be
< 100 mosmol/kg and specific gravity will be < 1.003. This occurs in patients with primary
polydipsia.
If primary polydipsia is not present, decreased plasma osmolality suggests impaired free
water excretion due to the action of AVP on the kidney. The secretion of AVP may be a
Page 42 of 50
b.
c.
d.
e.
osmolality are the only tests required to diagnose the cause of hyponatraemia. Initial
laboratory evaluation also includes glucose, BUN, creatinine, and uric acid.]
Urine electrolytes
Urine osmolality
Plasma renin activity
[ Measurement of plasma renin activity is
useful when there is doubt about clinical signs of ECF volume.]
Plasma ADH
T [ Plasma ADH is not very helpful in
distinguishing between the causes of hyponatraemic states. ADH is activated both in
hypovolaemic and hypervolaemic states. Most chronic hypervolaemic states (cardiac
failure, cirrhosis and nephrotic syndrome) have impaired circulation that activates ADH
release through non-osmotic mechanisms. Indeed, these disorders may have higher
circulating ADH levels than patients with SIADH. ADH is suppressed in primary
polydipsia and iatrogenic water intoxication.]
Page 43 of 50
33)
34)
35)
36)
37)
50-year-old male admitted with seizures has a serum sodium level of 115 mEq/L. What is the
treatment?
a. Oral sodium
Page 44 of 50
b. Normal saline IV
c. Hypertonic saline IV
T [ Severe symptomatic hyponatremia
should be treated with hypertonic saline. Patients who have symptomatic hyponatremia
with concentrated urine (osmolality > 200 mOsm per kilogram of water) and clinical
euvolemia or hypervolemia require infusion of hypertonic saline. Hypertonic saline is
usually combined with furosemide to limit treatment induced expansion of the
extracellular-fluid volume. The plasma Na+ concentration should not be raised by more
than 12 mEq/L during the first 24 h.]
d. IV frusemide
In addition to its complete distribution in the extracellular compartment, this infusate induces osmotic
removal of water from the intracellular compartment.
Children = 0.6
Nonelderly men = 0.6
Nonelderly women = 0.5
Elderly men = 0.5
Elderly women = 0.45
Extracellular fluids = 40% of total body water
Intracellular fluids = 60% of total body water
Page 45 of 50
38)
How much sodium is needed to correct Na+ concentration from 115 mEq/L to 125 mEq/L in a
60-kg man?
a. 90 mEq/L
b. 180 mEq/L
c. 360 mEq/L
T [ The quantity of Na+ required to increase
the plasma Na+ concentration by a given amount is estimated by multiplying the deficit in
plasma Na+ concentration by the total body water. Normally, total body water is 60% of
lean body weight in men (50% of lean body weight in women). In this question sodium
needed is 125 115 X 60 X 0.60 = 360 mEq/L.]
d. 720 mEq/L
e. 1440 mEq/L
39)
40)
41)
Page 46 of 50
Within minutes after the development of hypotonicity, water gain causes swelling of the brain and a
decrease in osmolality of the brain. Partial restoration of brain volume occurs within a few hours as
a result of cellular loss of electrolytes (rapid adaptation). The normalization of brain volume is
completed within several days through loss of organic osmolytes from brain cells (slow adaptation).
Low osmolality in the brain persists despite the normalization of brain volume. Proper correction of
hypotonicity reestablishes normal osmolality without risking damage to the brain. Aggressive
correction of hyponatremia can lead to irreversible brain damage.
42)
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A previously healthy 30-year-old man has three generalized seizures two days after an
appendectomy. He was given diazepam and phenytoin intravenously and undergoes laryngeal
intubation with mechanical ventilation. Three liters of 5 percent dextrose in water had been
infused during the first day after surgery. He has subsequently drunk substantial amount of
water. Clinically, he is euvolemic, and he weighs 46 kg. He is stuporous and responds to pain
but not to commands. The serum sodium concentration is 112mEq per liter, the serum
potassium concentration is 4.1 mEq per liter, serum osmolality is 228 mOsm per kilogram of
water, and urine osmolality is 510 mOsm per kilogram of water. What is the treatment?
a. Water restriction
b. Infusion of 3 percent sodium chloride
c. Intravenous furosemide
d. All of the above
T [ This patient has hypotonic hyponatremia
due to water retention caused by the impaired excretion of water that is associated with
the postoperative state. The estimated volume of total body water is 23 liters (0.5 X 46).
The retention of 1 liter of 3 percent sodium chloride will increase the serum sodium
concentration by 16.7 mmol per liter (513 112) (23+1) =16.7.]
e. None of the above
44)
A 58-year-old man with small-cell lung carcinoma presents with severe confusion and lethargy.
Clinically, he is euvolemic, and he weighs 60 kg. The serum sodium concentration is 108 mEq
per liter, the serum potassium concentration is 3.9 mEq per liter, serum osmolality is 220 mOsm
per kilogram of water, the serum urea nitrogen concentration is 5 mg per deciliter, the serum
creatinine concentration is 0.5 mg per deciliter per liter, and urine osmolality is 600 mOsm per
kilogram of water. What is the treatment?
a. Water restriction
b. Infusion of 3 percent sodium chloride
c. IV furosemide
d. All of the above
T [ The diagnosis is tumor-induced
syndrome of inappropriate secretion of antidiuretic hormone on the basis of the presence
of hypotonic hyponatremia and concentrated urine in a euvolemic patient, the absence of
a history of diuretic use, and the absence of clinical evidence of hypothyroidism or
hypoadrenalism. The estimated volume of total body water is 36 liters. The retention of 1
liter of 3 percent sodium chloride is estimated to increase the serum sodium
concentration by 10.9 mEq per liter {(513 108) (36+1) = 10.9}. The initial goal is to
increase the serum sodium concentration by 5 mEq per liter over the next 12 hours.
Therefore, 0.46 liter of 3 percent sodium chloride (5 10.9), or 38 ml per hour, is
required.]
e. None of the above
Page 48 of 50
45)
46)
47)
A 72-year-old woman presents with a 2-day history of presyncope when rising from a chair. She
has been taking hydrochlorothiazide, 25 mg/d, for 5 years for systolic hypertension. Last week
she had a bout of viral gastroenteritis with marked diarrhea. She has been replacing the lost
fluids by drinking 3 L of water per day. When she rises from a seated position, her blood
pressure drops 20 mm Hg. Serum levels are as follows: sodium 128 mEq/L, potassium 3.1
Page 49 of 50
mEq/L, creatinine 1.5 mg% and urea nitrogen 60mg%. Which is/are true statements regarding
this patient?
a. ECF volume is contracted
[ The patient has postural hypotension which
indicates ECF volume contraction. The most likely cause is gastrointestinal losses of salt
and water, with only water replacement. It is also likely that the thiazide diuretic is
contributing to the hyponatremia. Thiazides impair the kidneys ability to reabsorb sodium
and to excrete free water.
b. Release of AVP is stimulated
[ ECF volume contraction from any cause
(diarrhea, vomiting, excessive sweating, diuretic use), stimulates the release of AVP. AVP
increases renal water reabsorption and ECF volume.]
c. Low urine sodium concentration
[ Volume contraction decreases renal
perfusion which stimulates renin release, and this causes the kidneys to avidly retain
sodium. The retention of water and sodium is appropriate in this setting and is supported
by a low urine sodium concentration (< 20 mmol/L) and a low urine volume. Often the
person who has a contracted ECF volume will drink water or another low-solute fluid
(e.g., tea), which contributes further to the hyponatremia. These patients have serum
sodium and body water levels that are lower than normal but have more loss of sodium
relative to loss of water.]
d. She needs potassium replacement
[ The ECF volume contraction, diarrheal
losses and diuretic use have resulted in hypokalemia in this patient. As ECF volume
contraction develops, the kidneys actively excrete potassium in exchange for sodium in
an attempt to preserve ECF volume. Volume restoration with normal saline and
potassium replacement is required until the postural drop in blood pressure is less than
10 mm Hg. She should then be treated conservatively with oral sodium and potassium
replacement.]
e. All of the above
T [ The management of this patient should
include temporary discontinuation of the thiazide diuretic.]
Water restriction will ameliorate all forms of hyponatremia, but it is not the optimal therapy in all
cases. Hyponatremias associated with the depletion of extracellular-fluid volume require
correction of the sodium deficit.
Isotonic saline is unsuitable for correcting the hyponatremia of the syndrome of inappropriate
secretion of antidiuretic hormone; if administered, the resulting rise in serum sodium is both
small and transient, with the infused salt being excreted in concentrated urine and thereby
causing a net retention of water and worsening of the hyponatremia.
Great vigilance is required in order to recognize and diagnose hypothyroidism and adrenal
insufficiency, since these disorders tend to masquerade as cases of the syndrome of
inappropriate secretion of antidiuretic hormone. The presence of hyperkalemia should always
alert the physician to the possibility of adrenal insufficiency.
Whereas patients with persistent asymptomatic hyponatremia require slow-paced management,
those with symptomatic hyponatremia must receive rapid but controlled correction.
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