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DR. RAJENDRAN’S INSTITUTE OF MEDICAL EDUCATION Phone 0470 – 2604199, 09388852220.
FLUID AND ELECTROLYTE DISTURBANCES
MANIFESTATIONS OF DISORDERED WATER, ELECTROLYTE AND ACID-BASE STATUS
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
Acid-base Balance (pH)
Altered tissue function, respiratory compensation
Magnesium
Cell membrane Stability
Neuromuscular, vascular and cardiac effects
Phosphate
Cellular energetic
Widespread tissue effects
1)
What percentage of body weight in men is water? a. 15 b. 30 c. 60 T [ About 50% of body weight in women and 60% in men is water. Body fat content influences the proportion of body weight that is water. As body fat increases, water declines as a proportion of body weight. As muscle mass increases, water increases as a proportion of body weight. Intracellular fluid (ICF) is the largest compartment and is 60% of total body weight. Extracellular fluid (ECF) is 40% of TBW. The solutes in the ICF and ECF compartments are different. See figure below. In ICF the main cation is potassium and the anions are phosphates and bicarbonate. In ECF the main cation is sodium, and chloride and bicarbonate are the anions.] d. 90
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2)
What percentage of total body water is intracellular fluid? a. 30 b. 40 c. 60 T [ 55 to 75% of total body water is intracellular and 25 to 45% is extracellular. The total body water is approximately 40 liters. About 25 liters is inside cells (ICF compartment). Some 15 liters is in the extracellular fluid (ECF) compartment. The ECF is further subdivided into intravascular and extravascular spaces in a ratio of 1:3. Of the ECF, the plasma is only 3 liters. 12 liters is interstitial fluid outside the cells. See figure below.] d. 80
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3) Plasma volume is ------------- L a. 3 T [ 25% of the ECF is intravascular subcompartment. This corresponds to 3 - 3.5 L of plasma. The remaining 75% of ECF volume is in the interstitial spaces. This corresponds to 10 – 12 L.] b. 6 c. 9 d. 12 4)
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)
Extracellular osmolality in a healthy adult a. More than intracellular osmolality b. Less than intracellular osmolality c. Same as intracellular osmolality [ Osmolality is a measure of the total number of solutes per mass of water. Osmolality is the solute or particle concentration of a fluid. It is expressed as milliosmoles per kilogram of water (mosmol/kg H2O). The normal plasma osmolality is 275 to 290 mosmol/kg. The extracellular and intracellular solutes (or osmoles) are markedly different, but water crosses cell membranes to achieve osmotic equilibrium. Water moves across cell membranes and distributes between ICF and ECF
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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.]
8) The main extracellular cation a. Potassium
b. c. d.
e.
[ Potassium is the dominant cation in the ICF.] Calcium Magnesium Sodium T [ Sodium is the dominant extracellular cation. Chloride and bicarbonate are the dominant ECF anions. A typical diet contains more sodium than daily requirements. Therefore, dietary intake of Na+ results in ECF volume expansion. This in turn promotes increased renal Na+ excretion to maintain Na+ balance. The amount of sodium excreted is equal to the amount ingested per day.] Albumin [ An important difference between the plasma and interstitial compartments of the ECF is that only plasma contains significant concentrations of protein.]
9) What maintains the difference in cation concentration between the ICF and ECF?
Page 5 of 50 a. Sodium-potassium pump
T [ Themajor force maintaining the difference in cation concentration between the ICF and ECF is the sodium-potassium pump (Na,Kactivated ATPase) See figure below. Na+,K+-ATPase moves three sodium molecules out of the cell while concurrently two potassium ions in ECF enter the cell. With three cations transported out and two cations transported into the cell, the consequence of Na+,K+ATPase activity is a net negative intracellular charge.] b. RMP c. Osmotic pressure d. Intracellular proteins
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
[ Na+ balance is regulated by varying Na+ excretion.] b. GFR [ Na+ excretion is mainly regulated by tubular Na+ reabsorption (not by GFR).] c. Sodium reabsorption T [ About 65% of filtered Na+ is reabsorbed in the proximal convoluted tubule. Further reabsorption (30%) occurs in the thick ascending limb of the loop of Henle. About 5% of filtered Na+ is reabsorbed in the distal convoluted tubule. Final Na+ reabsorption occurs in the cortical and medullary collecting ducts. The amount of sodium excreted is equal to the amount ingested per day.] d. AVP [ Water metabolism is controlled primarily by arginine vasopressin. Sodium metabolism is predominately regulated by the reninangiotensin-aldosterone system.]
12)
Osmotic adaptation occurs in a. Placenta during delivery b. Glomeruli during water load c. Normal brain T [ Brain cells can vary the number of intracellular solutes to protect against large water shifts and resultant change in intraneuronal osmolality. This process is called osmotic adaptation and occurs in chronic hyponatremia and hypernatremia. Osmotic adaptation is mediated initially by shifts of K+ and Na+ and later by osmolytes.] d. Muscles during exercise
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.]
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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)
What is the primary stimulus for drinking water? a. Thirst T [ The primary stimulus for drinking water is thirst. The thirst center is situated in the organum vasculosum of the anterior hypothalamus. Thirst is caused by an increase in effective osmolality or a decrease in ECF volume or blood pressure. The osmotic threshold for thirst is about 295 mosmol/kg and varies among individuals. Reduction of ECF volume also stimulates thirst by means of angiotensin 2, even when body tonicity is not elevated.] b. Reduction of ECF volume [ Reduction of ECF volume is a very potent stimulus for release of AVP (carried by the ninth and tenth cranial nerves), even when body tonicity is not elevated. Reduction of ECF volume also stimulates thirst by means of angiotensin 2.] c. Hypothalamus [ Osmoreceptors are located in the supraoptic and paraventricular nuclei of the hypothalamus. They are stimulated by a rise in tonicity. The osmoreceptors stimulate the release of AVP from storage sites in the posterior pituitary gland. Even very small changes in tonicity (in the range of 2%) cause changes in release of AVP and the perception of thirst. An increase or decrease in tonicity is sensed by hypothalamic osmoreceptors, leading to enhancement or suppression of AVP secretion.] d. Glucose [ Urea and glucose are ineffective osmoles. They do not stimulate thirst.] e. Urea
17)
What is the primary determinant of extracellular fluid osmolality?
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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)
What determines plasma osmolality? a. Glucose b. Urea c. Sodium T [ Sodium is actively pumped out of cells by the Na+, K+-ATPase pump. As a result, 90% of all Na+ is extracellular. The major ECF solutes are Na+ salts. Therefore, plasma Na+ concentration determines osmolality. The normal plasma osmolality is 275 to 290 mosmol/kg. The plasma osmolality does not vary by more than 2%. The intake of solute-free water must be balanced by the loss of the same volume of electrolyte-free water. Impaired free water excretion will lead to hyponatremia.] d. Potassium e. Calcium
19)
What determines ECF volume? a. Sodium T [ Total body sodium is the principal determinant of ECF volume. Most of the body's sodium is located in the ECF. The regulation of sodium excretion by the kidney maintains normal ECF and hence plasma volume. The glomerular filtration rate is 125 ml/min (80 liters/day) in a typical adult. Over 99% of this filtered fluid is reabsorbed as a result of tubular reabsorption of sodium.] b. Renin c. Aldosterone d. Baroreceptors
20)
What is the osmotic threshold for AVP release? a. 275 b. 285 mosmol/kg T [ The major stimulus for AVP secretion is hypertonicity. The osmotic threshold for AVP release is 280 to 290 mosmol/kg. Arginine vasopressin (AVP) is a polypeptide synthesized in the supraoptic and para-ventricular nuclei of the hypothalamus and secreted by the posterior pituitary gland. An increase or decrease in tonicity is sensed by hypothalamic osmoreceptors, leading to enhancement or suppression of AVP secretion.]
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c. 300 d. 325 21)
What regulates water homeostasis a. Thirst [ Fluid homeostasis depends on proper water intake (regulated by thirst mechanism) and on urinary excretion of free water (regulated by AVP).] b. Arginine vasopressin c. Kidneys d. All of the above T [ The serum sodium concentration and thus serum osmolality are controlled by water homeostasis. Water homeostasis is mediated by thirst, arginine vasopressin, and the kidneys. Abnormal water balance manifests as an abnormality in the serum sodium concentration (hypernatremia or hyponatremia).] CLINICAL FEATURES OF HYPOVOLAEMIA AND HYPERVOLAEMIA
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
Environmental deprivation, inadequate therapeutic replacement
Gastrointestinal sodium Loss
Vomiting, diarrhea, nasogastric suction, external fistula
Skin sodium loss
Excessive sweating, burns
Renal sodium loss
Diuretic therapy, mineralocorticoid deficiency, tubulointerstitial disease
Internal sequestration
Bowel obstruction, peritonitis, pancreatitis, crush injury
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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).
2) How much fluid enters the gastrointestinal tract daily?
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
T [ Diarrhea often causes metabolic alkalosis because biliary, pancreatic, and intestinal secretions are alkaline (high HCO3concentration).] b. Metabolic acidosis [ Gastric secretions have high H+ concentration (low pH). Therefore, vomiting often causes metabolic acidosis.] c. Lactic acidosis d. Hyperkalemia
4) Sweat a. Usually hypertonic but may be isotonic
Page 11 of 50 b. Usually isotonic but may be hypertonic c. Hypotonic
T [ Sweat is hypotonic. Therefore, excessive sweating (e.g., febrile illnesses, prolonged heat exposure), more loss of water than Na+, but continued Na+ loss is manifest as hypovolaemia. The Na+ concentration of sweat is normally 20 to 50 mEq/L and decreases with profuse sweating due to the action of aldosterone.] d. Hypertonic 5) Third-space is in equilibrium with
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.]
6) ECF volume contraction results in a. Hypotension
b. c. d. e.
[ Clinically ECF volume contraction manifest as a decreased plasma volume and hypotension. Hypotension is due to decreased venous return (preload) and diminished cardiac output.] Stimulation of baroreceptors [ Hypotension stimulates baroreceptors in the carotid sinus and aortic arch.] Stimulation of sympathetic nervous system [ Hypotension activates the sympathetic nervous system and the renin-angiotensin system.] Stimulation of renin secretion All of the above T [ The net effect is to maintain mean arterial pressure and cerebral and coronary perfusion. In contrast to this cardiovascular response, the renal response attempts to restore the ECF volume.]
7) Renal response(s) to ECF volume contraction a. Increased GFR [ The GFR and filtered load of Na+ is
decreased.] b. Vasodilatation of afferent arterioles
[ Increased sympathetic tone decreases GFR by causing preferential afferent arteriolar vasoconstriction.] c. Increased reabsorption of sodium T [ There is increased tubular reabsorption of Na+. Increased sympathetic tone increases proximal tubular Na+ reabsorption.]
Page 12 of 50 d. Increased atrial natriuretic peptide
[ Sodium is also reabsorbed in the proximal convoluted tubule. Enhanced reabsorption of Na+ by the collecting duct is in response to increased secretion of angiotensin 2, aldosterone and AVP and suppressed ANP secretion.] e. All of the above
CLINICAL FEATURES OF ECF VOLUME CONTRACTION
Symptoms (nonspecific and secondary to electrolyte imbalances and tissue hypoperfusion) Fatigue and weakness Thirst Muscle cramps Postural dizziness Oliguria Confusion Cyanosis Signs of decreased interstitial fluid Diminished skin turgor Dry oral mucous membranes Signs of intravascular volume contraction Postural tachycardia Postural hypotension Decreased jugular venous pressure Signs of hypovolemic shock Tachycardia Hypotension Cold and clammy limbs Oliguria Altered mental status Cyanosis History is often helpful in determining the cause of hypovolemia (bleeding, vomiting, diarrhea, polyuria, medications, diaphoresis). Absence of symptoms does not exclude mild to moderate hypovolemia, especially if the volume loss has occurred gradually. Intravascular volume contraction of less than 5% does not usually cause symptoms or signs. Symptoms and signs begin to appear with intravascular volume contraction of 5 - 15%. Severe degrees of hypovolemia (intravascular volume contraction > 15%) cause hypotension, peripheral cyanosis, cold extremities, and reduced levels of consciousness. Thirst may be an early manifestation but more likely reflects a concomitant hypertonic state. Reduced skin turgor and dry mucous membranes are not reliable indicators of hypovolemia. 8) Laboratory finding(s) in loss of sodium and water a. Normal plasma sodium concentration
[ Plasma sodium concentration may be normal if losses of salt and water are parallel.]
Page 13 of 50 b. Raised plasma urea
[ The plasma urea concentration rises because urea excretion is reduced. Hypovolemia decreases GFR and urea excretion.] c. Normal plasma creatinine [ Plasma creatinine may be relatively normal early in hypovolaemic states.] d. Raised plasma uric acid e. All of the above [ The urine specific gravity and osmolality increases because urine concentrating mechanisms are activated to conserve water. Urine sodium concentration falls] 9) BUN:creatinine ratio of 20:1 a. Normal b. c.
d. e.
[ Normally, the BUN:creatinine ratio is about 10:1.] Glomerulonephritis Prerenal azotemia [ In hypovolemia, the blood urea nitrogen (BUN) and plasma creatinine concentrations tend to be elevated due to decreased GFR. In prerenal azotemia, hypovolemia leads to increased urea reabsorption and a proportionately greater elevation in BUN than plasma creatinine. Therefore, BUN:creatinine ratio is 20:1 or higher.] GI bleeding [ An increased BUN (relative to creatinine) may also be due to increased urea production that occurs with hyperalimentation (high-protein), glucocorticoid therapy, and gastrointestinal bleeding.] Both c and d are true T
10)In hypovolemia a. Low urine sodium
[ Hypovolemia causes enhanced renal Na+ and water reabsorption. Therefore, the urine Na+ concentration is usually <20 mEq/L.] b. High urine specific gravity [ The urine specific gravity in hypovolemic patients is usually > 1.015 due to increased AVP secretion.] c. High urine osmolality [ The urine osmolality in hypovolemic patients is usually > 450 mosmol/kg due to increased AVP secretion.] d. All of the above T [ All these are the appropriate renal response to hypovolemia. In hypovolemia due to diabetes insipidus, urine osmolality and specific gravity are very low and indicates dilute urine. If no ADH is circulating in plasma, the osmolality of urine produced by the kidney can be less than 100 mmol/kg H2O. If a maximum level of ADH is circulating in plasma, the osmolality of urine produced by the kidney can exceed 1200 mmol/kg H2O.]
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
12)How much sodium is present in 1 L of normal saline? a. 77 mEq/L [ Half-normal saline or 0.45% NaCl has77
mEq/L of Na+. Hypernatremia indicates a proportionally greater deficit of water than Na+. Therefore, its correction requires a hypotonic solution such as half-normal saline or 5% dextrose in water.] b. 154 mEq/L T [ Normal saline or 0.9% NaCl has 154 mEq/L of Na+. See table below. This is the solution of choice in normonatremic and mildly hyponatremic individuals. It should be administered initially in patients with hypotension or shock. Patients with significant hemorrhage, anemia, or intravascular volume depletion may require blood transfusion or colloid-containing solutions (albumin, dextran).] c. 513 mEq/L [ Severe hyponatremia may require hypertonic saline (3.0% NaCl or 513 mEq/L Na+). d. 616 mEq/L
COMPOSITION OF ISOTONIC IV FLUIDS (1 L)
13)
Fluid
Glucose
Calories
Na+
Cl-
Other
5% dextrose
50 g
200
0
0
0
Normal saline
0
0
154
154
0
What is the increase in plasma volume if 1 L of isotonic saline is given IV? a. 1000 mL b. 600 mL c. 300 mL T [ Retention of 1 L of infused isotonic saline increases plasma volume by about 300 mL. The remaining portion is distributed in the interstitial subcompartment of the ECF.] d. 150mL [ In contrast, a solution of 5% dextrose in water (D5W) is equivalent to administering solute-free water. It distributes uniformly throughout all body fluid compartments. A third of the retained volume of 5% dextrose remains in the ECF compartment and only 10 to 15% remains in the intravascular compartment). The retained solute-free volume reduces body tonicity and the plasma
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sodium concentration. 5% dextrose in water is useful when hypovolemia is accompanied by hypertonicity and hypernatremia.] e. 75 mL [ Infusing half isotonic saline (0.45% sodium chloride plus 5% glucose) is equivalent to infusing half that volume as solute-free water (distributed throughout body fluid compartments) and the other half as isotonic saline (confined to the ECF compartment).] 14)
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)
Hypernatremia is plasma Na+ concentration greater than -------- mEql/L a. 135 b. 145 T [ Hypernatremia is plasma Na+ concentration > 145 mEql/L. Patients have moderate hypernatremia if their serum Na+ is 146 to 159 mEq/L. Patients with Na+ greater than 160 mEq/L have severe, lifethreatening hypernatremia. Hypernatremia may be due to primary Na+ gain or water deficit. Water loss is the most common cause of acute hypernatremia. Hypernatremia can develop in patients who do not replace the water lost after excessive sweating in a hot environment, vomiting or diarrhea.] c. 155 d. 165 CAUSES OF HYPERNATREMIA
Net water loss Pure water Unreplaced insensible losses (dermal and respiratory) Hypodipsia Diabetes insipidus Hypotonic fluid
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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 Cushing’s syndrome
2)
Hypernatremia - True statement a. Hyperosmolar sate [ Na+ and its accompanying anions are the major effective ECF osmoles. Therefore, hypernatremia is a state of hyperosmolality and results in ICF volume contraction. Sodium is impermeable. It contributes to tonicity and induces the movement of water across cell membranes. Therefore, hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration, at least transiently.] b. Results in ICF volume contraction [ Hypernatremia causes hypertonicity of ECF. Therefore, water shifts out of cells, leading to a contracted ICF volume. Neurologic damage as a result of contraction of brain cell volume is the primary risk associated with hypernatremia.] c. Stimulates thirst [ Hypernatremia stimulates thirst and thus increases water intake. The severity of hyperosmolality is typically mild unless the thirst mechanism is abnormal or access to water is limited (infants, postoperative state, impaired mental status, and intubated patients in the intensive care unit.] d. Stimulates AVP secretion [ Another response to hypernatremia is excretion of a minimum volume of maximally concentrated urine. This is due to increased AVP secretion in response to hypertonia.] e. All of the above T [ The first question to be answered in any patient with hypernatremia is why there has been inadequate intake of water.
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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)
What is the most common cause of hypernatremia? a. Gain of sodium [ A primary Na+ gain is an uncommon cause of hypernatremia. For example, inadvertent administration of hypertonic NaCl or replacing sugar with salt in infant formula can produce this complication.] b. Hyperemesis gravidarum [ Pregnant women, in the second or third trimester, may develop nephrogenic diabetes insipidus due to excessive elaboration of vasopressinase by the placenta.] a. Loss of water T [ Most cases of hypernatremia are due to loss of free water. Hypernatremia with hypovolaemia results from fluid losses that is more than sodium loss. Renal water loss (e.g., diuretics) is the most common cause of hypernatremia. Diarrhea is the most common gastrointestinal cause of hypernatremia. Profuse sweating is also a major cause of fluid loss resulting in hypernatremia with hypovolaemia.] b. Renal failure c. Primary hypodipsia [ Primary hypodipsia results from damage to the hypothalamic osmoreceptors that control thirst. Thirst is impaired. Primary hypodipsia may be due to granulomatous disease, vascular occlusion, or tumors.]
5)
Which of the following is a cause of diarrhea with hyponatremia? a. Lactulose [ Osmotic diarrheas (induced by lactulose, sorbitol, or malabsorption of carbohydrate) and viral gastroenteritides cause more water loss than Na+ and K+ loss.] b. Sorbitol c. Malabsorption d. Viral gastroenteritides e. Cholera T [ Secretory diarrheas (e.g., cholera, carcinoid, VIPoma) have a fecal osmolality similar to that of plasma. Diarrhea due these present with ECF volume contraction and a normal plasma Na+ concentration or hyponatremia.]
6)
Fecal osmolality a. Equal to the sum of stool concentrations of Na+ and K+
Page 18 of 50
Half the sum of stool concentrations of Na+ and K+ Twice the sum of stool concentrations of Na+ and K+ T [ The stool osmolality is assumed to be 300 mosmol/kg H2O. When the calculated difference is > 50, an osmotic gap is present. This suggests that the diarrhea is due to a nonabsorbed dietary nutrient, e.g., a fatty acid and/or carbohydrate. When this difference is < 25, it is presumed that a dietary nutrient is not responsible for the diarrhea.] d. Thrice the sum of the stool concentrations of Na+ and K+ b. c.
7)
Insensible losses are increased with a. Fever b. Exercise c. Severe burns d. Mechanical ventilation e. All of the above T [ Insensible loss of water is due to evaporation from the skin and respiratory tract. Insensible losses are increased with fever, exercise, heat exposure, and severe burns and in mechanically ventilated patients. The Na+ concentration of sweat decreases with profuse perspiration, thereby increasing solute-free water loss.]
8)
What is the most common cause of hypernatremia? a. Renal water loss T [ Renal water loss is the most common cause of hypernatremia. The normal renal response to hypernatremia is for the nephron to generate hyperosmolar urine and retain water. However, renal correction of hypernatremia depends on the patient having access to water. Severe hypernatremia rarely occurs in conscious patients because intense thirst compels them to drink water. In contrast, severe hypernatremia can develop in sedated patients, disoriented patients, or patients in delirium tremens.] b. Insensible loss c. Rota virus d. Diabetes insipidus
9)
Cause(s) of hypervolemic hypernatremia a. Administration of hypertonic sodium bicarbonate [ Hypernatremia with hypervolemia can be caused by iatrogenic administration of hypertonic sodium chloride or hypertonic sodium bicarbonate.] b. Administration of hypertonic sodium chloride c. Mineralocorticoid excess [ Mineralocorticoid excess is suggested by the presence of hypertension and hypokalemic metabolic alkalosis. Urine sodium concentration will vary according to dietary intake.] d. All of the above T
10)
What is the most common cause of osmotic diuresis? a. Diabetes insipidus [ Failure to synthesize and release ADH or failure of the renal tubular cells to respond to ADH can result in hypernatremia.
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)
The main symptom of hypernatremia is due to a. Cerebral edema and coning [ Hyponaremia may cause cerebral edema.] b. Hypertension and cardiac failure [ Volume depletion is often present in patients with a history of excessive sweating, diarrhea, or an osmotic diuresis. History and physical examination will often provide clues as to the underlying cause of hypernatremia. Important points to note are the absence or presence of thirst, diaphoresis, diarrhea, polyuria and current drugs. Look for features of ECF volume contraction. Evaluate neurologic and mental status.] c. Altered mental status T [ Hypernatremia causes hypertonicity of ECF. Therefore, water shifts out of cells, leading to a contracted ICF volume. Brain cell volume is decreased. Hence, the major symptoms of hypernatremia are neurologic and include altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and occasionally coma or seizures.] d. Craving for ice-cold water [ Patients with polydipsia from central diabetes insipidus tend to prefer ice-cold water.]
Page 20 of 50
12)
What is the feature of hypernatremia due to primary Na+ excess? a. ECF volume expansion and urine Na+ concentration < 40 mEq/L b. ECF volume expansion and urine Na+ concentration >100 mmol/L T [ Measure urine volume and osmolality in the evaluation of hyperosmolality. ECF volume expansion and natriuresis (urine Na+ concentration >100 mEq/L) confirms a primary Na+ excess.] c. ECF volume contraction and urine Na+ concentration >100 mmol/L d. ECF volume contraction and urine Na+ concentration < 20 mEq/L
13)
What does a low volume of maximally concentrated urine indicate? a. Extrarenal water loss b. Remote renal water loss c. Administration of hypertonic Na+ salt solutions d. Any of the above T [ A urine specific gravity of 1.010 units or less is a dilute urine and suggests that ADH levels are low. A urine specific gravity greater than 1.030 units suggests that the urine being produced is close to maximum osmolality. The correct renal response to hypernatremia is the excretion of the minimum volume (500 mL/d) of maximally concentrated urine (urine osmolality > 800 mosmol/kg).
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These findings suggest extrarenal or remote renal water loss or administration of hypertonic Na+ salt solutions.] 14)
What is the solute excretion rate? a. Urine volume ÷ osmolality b. Urine volume X osmolality T [ The solute excretion rate is the product of the urine volume and osmolality.] c. Urine sodium + potassium + chloride d. { Urine sodium + potassium + chloride + glucose } ÷ urine osmolality e. { Urine sodium + potassium + chloride + glucose } ÷ urine volume
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
Water deficit = plasma sodium concentration – 140 140
X Total body water
Total body water is approximately 50 of lean body weight in men and and 40% of lean body
weight in women
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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?
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a. Intravenous through a peripheral vein b. Intravenous through a central vein c. Oral route T [ The preferred route for administering fluids is the oral route or a feeding tube. If neither is feasible, fluids should be given intravenously.] d. Per rectal 18)
Which fluid is least appropriate for managing hypernatremia? a. Pure water [ Only hypotonic fluids are appropriate, including pure water, 5 percent dextrose, 0.2 percent sodium chloride (one-quarter isotonic saline), and 0.45 percent sodium chloride (one-half isotonic saline). b. 5% dextrose c. 0.2 percent sodium chloride d. 0.45 percent sodium chloride e. Isotonic saline T [ Except in cases of frank circulatory compromise, 0.9 percent sodium chloride (isotonic saline) is unsuitable for managing hypernatremia.]
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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)
A 58-year-old woman with postoperative ileus is undergoing nasogastric suction. She is obtunded with diminished skin turgor and mild orthostatic hypotension. The serum sodium concentration is 158 mEq per liter, the potassium concentration is 4.0 mEq per liter, and the body weight is 63 kg. What is the treatment? a. 0.45% sodium chloride IV T [ Hypernatremia caused by hypotonic fluid loss is the correct diagnosis. The estimated volume of total body water is 31.5 liters (0.5 X 63). The infusion of 1 liter of 0.45 percent sodium chloride will reduce the serum sodium concentration by 2.5 mEq per liter (77 – 158) ÷ ( 31.5 + 1) = - 2.5. If the goal is to reduce the serum sodium concentration by 5 mEq per liter over the next 12 hours, 2 liters of the solution is required (5÷2.5). If 1 liter is added to compensate for ongoing losses of gastric and other fluids, a total of 3 liters will be administered for the next 12 hours, or 250 ml per hour.] b. 0.9% sodium chloride IV [ Although there is evidence of a depletion in the volume of extracellular fluid, the patient’s hemodynamic status is not sufficiently compromised to warrant the initial use of 0.9 percent sodium chloride.] c. Furosemide IV d. Furosemide oral e. Hemodialysis
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 patient’s extracellular-fluid volume is expanded, fluids can be administered only with great caution. Adjust fluid administration based on close monitoring of the patient’s 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 patient’s 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 patient’s 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)
How do disorders in sodium balance present? a. Altered ECF volume T [ Disorders in sodium balance present chiefly as altered ECF volume rather than altered sodium concentration.] b. Hyponatremia
Page 27 of 50
c. Hypernatremia d. Diabetes insipidus 2)
Hyponatremia is plasma Na less than ------------- mEq/L a. 125 b. 135 T [ The normal serum sodium ion concentration ranges between 135 and 145 mEq/L. Hyponatraemia is plasma Na < 135 mEq/L. Severe hyponatremia is defined as an Na+ less than 120 mEq/L. A falling Na+ indicates that the osmolality in ECF and ICF is also falling. Hypernatremia always indicates hypertonicity, but hyponatremia can be associated with low, normal, or high tonicity.] c. 145 d. 155
CAUSES AND CLASSIFICATION OF HYPONATREMIA
High Plasma Osmolality Hyperglycemia Hypertonic mannitol Normal Plasma Osmolality (Pseudohyponatremia) Hyperlipidemia Hyperparaproteinemia Low Plasma Osmolality High Circulating ADH
Volume depletion Cirrhosis Heart failure Nephrotic syndrome SIADH Hypothyroidism Hypoadrenalism (Glucocorticoid deficiency) Drugs Pregnancy Severe hypoalbuminemia Low Circulating ADH
Acute or chronic renal failure Low solute intake (beer potomania) Primary polydipsia Low solute intake (beer potomania) Primary polydipsia Posm in mOsm/kg H2O = (2 X serum Na in mEq/L) + (glucose in mg/dL/18) + (BUN in mg/dL/2.8)
Page 28 of 50
3) What is the most common cause of hyponatremia?
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
4) The total sodium stores of the body in dilutional hyponatremia is
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)
What is the most common cause of isotonic hyponatremia? a. Pseudohyponatremia T [ Isotonic hyponatremia is usually synonymous with so-called ‘‘pseudohyponatremia’’ and must be distinguished from true hypoosmolality. Normal serum is typically comprised of 93% water and 7% nonaqueous factors, including lipids and proteins. The nonaqueous components usually do not affect serum tonicity. In marked hyperproteinemia or hyperlipidemia, the nonaqueous proportion of serum is relatively increased with respect to the aqueous portion. The result is an artifactual decrease in the serum concentration of Na+ although the concentration of Na+ is unchanged. Isotonic hyponatremia does not cause movement of water between the ntracellular fluid (ICF) and extracellular fluid (ECF) compartments.] b. Hyperglycemia [ Hyperglycemia causes hypertonic hyponatremia.] c. High blood urea [ Unlike glucose, solutes that enter cells, such as urea or ethanol, do not cause intracellular-to-extracellular water shift and thus do not cause hyponatremia.] d. SIADH [ SIADH causes hypotonic hyponatremia.] e. All of the above
Page 29 of 50 6)
What is the most common cause of hypertonic hyponatremia? a. Hyperglycemia T [ High osmolality indicates the presence of excessive extracellular osmoles leading to the entry of intracellular water into the extracellular fluid and the dilution of the sodium in the extracellular fluid. High glucose level is the commonest cause of hypertonic hyponatremia. The increases in plasma glucose raise serum osmolality, which pulls water out of cells and dilutes the serum Na. Plasma Na+ concentration falls by 1.6 mEq/L for every 100 mg/dL rise in the plasma glucose concentration.] b. High blood urea [ Unlike glucose, solutes that enter cells, such as urea or ethanol, do not cause intracellular-to-extracellular water shift and thus do not cause hyponatremia.] c. Transurethral resection of the prostate [ Massive absorption of irrigant solutions that do not contain sodium (e.g., those used during transurethral prostatectomy) can cause severe hyponatremia. Isotonic or slightly hypotonic hyponatremia may complicate transurethral resection of the prostate or bladder. Large volumes of isoosmotic (mannitol) or hypoosmotic (sorbital or glycine) bladder irrigation solution can be absorbed and result in a dilutional hyponatremia.] d. IV mannitol [ Hypertonic hyponatremia may also be due to intravenous administration of mannitol.] e. Thiazide diuretics [ Thiazide diuretics lead to Na+ and K+ depletion and AVP-mediated water retention.]
7)
What is the most common cause of hypotonic hyponatremia? a. Hyperglycemia a. Primary polydipsia [ Hypotonic hyponatremia means that water intake exceeds the ability of the kidney to excrete water. A normal kidney can excrete 30 L of water per day. Therefore, hyponatremia with normal renal water excretion implies that the patient is drinking more than 30 L of water per day. This condition is referred to as primary polydipsia. These patients should have a urine osmolality less than 100 mOsm/L. Primary polydipsia is a common condition that leads to polyuria and polydipsia, but it is uncommon as the sole cause of hyponatremia.] b. Mannitol infusion c. Diuretics a. SIADH T [ Hypotonic hyponatremia is most commonly due to decreased renal water excretion (i.e., urine that is not adequately concentrated even when there is hypotonia). When there is hypotonic hyponatremia, the normal response of the kidneys is to excrete maximally diluted urine. A urine osmolality >100 mOsm/L is inappropriate in hypotonic hyponatremia. Inappropriately concentrated urine implies a defect in renal water excretion (failure to maximally suppress AVP levels.]
8)
Diuretic-induced hyponatremia is almost always due to a. Thiazides T [ Diuretic-induced hyponatremia is almost always due to thiazide diuretics. Thiazide diuretics lead to Na+ and K+ depletion and AVP-mediated water retention. Thiazide diuretics reduce the reabsorption of Na+ and Clin the first half of the distal convoluted tubule and a portion of the cortical ascending limb of the loop of Henle. However, thiazides can cause excretion of a hypertonic urine and contribute to dilutional hyponatremia.]
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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.]
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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)
Hypervolemic hyponatremia caused by a. Heart failure [ In CCF, even though there is total body ECF overload, the decreased cardiac output causes perceived intra-arteriolar volume depletion. There is a decrease in the effective arterial blood volume at the level of the carotid artery and the renal afferent arteriole baroreceptors. Decreased renal perfusion activates the RAAS, resulting in increased sodium and water reabsorption. Increased baroreceptor firing activates non-osmotic AVP secretion, resulting in increased free water reabsorption. These adaptive physiologic mechanisms further exacerbate hypervolemia and progressive hyponatremia. ACE inhibitors reduce mortality in this subgroup of patients with cardiac failure.] b. Cirrhosis [ Cirrhosis is the most common cause of ascites. 30% of patients with ascites develop hyponatremia. Gastrointestinal endotoxin is less efficiently cleared in cirrhosis due to portal-systemic shunting. This stimulates nitric oxide production and vasodilatation. Arterial dilatation in the splanchnic vasculature, leads to arterial underfilling and non-osmotic secretion of AVP. The increase in AVP secretion and water retention is proportional to the severity of cirrhosis. A serum Na+ less than 125 mEq/L often indicate end-stage disease.]
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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)
Hypervolemic hyponatremia - True statement a. Low intravascular volume [ These patients have low ECF volume secondary to heart failure, cirrhosis, or nephrotic syndrome. Low ECF volume stimulates nonosmotic release of vasopressin, renal water reabsorption, and subsequent hyponatremia.] b. Urinary sodium is very low [ Spot urinary sodium is very low (often <10 mEq/L) due to avid renal sodium retention.] c. Edema is typical [ Physical examination may show peripheral edema, ascites, pulmonary congestion, or jugular venous distention depending on the underlying cause.] d. Seen in renal failure [ Hypervolemic hyponatremia may be seen in acute or chronic renal failure where renal excretion of sodium and water is decreased. The hyponatremia is the result of water intake in excess of sodium intake (dilutional hyponatremia). It is a common finding in patients with end-stage renal disease. The UNa+ may be greater than 20 mEq/L.] e. All of the above T
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)
Renal Na losses (e.g., thiazides) Adrenocortical failure Gastrointestinal Na losses (e.g., Vomiting, Diarrhoea) Primary polydipsia Excessive electrolyte-free water infusion SIADH Hypothyroidism Congestive cardiac failure Cirrhosis Nephrotic syndrome Chronic renal failure (during free water intake)
MOST COMMON CAUSES OF SEVERE HYPONATREMIA
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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)
What is the most common cause of normovolemic hyponatremia? a. SIADH T [ Syndrome of inappropriate antidiuretic hormone secretion is the most common cause of normovolemic hyponatremia. It is due to the nonphysiologic release of AVP from the posterior pituitary or an ectopic source. AVP impairs renal excretion of free water while the regulation of Na+ balance is not affected. Small-cell lung cancer is the most common cause of SIADH. Other causes of SIADH include stroke, meningitis, pneumonia and TB. Patients with SIADH have a serum osmolality < 270 mmol/kg H2O along with inappropriately concentrated urine.] b. Hypothyroidism [ Other causes of euvolemic hyponatremia are hypothyroidism, glucocorticoid deficiency, acute emotional stress or psychosis, certain drugs (selective serotonin reuptake inhibitor, carbamazepine, nonsteroidal antiinflammatory drugs, vincristine, and oxytocin), and primary polydipsia.] c. Serotonin reuptake inhibitor [ Drugs associated with euvolemic hyponatremia act largely by stimulating release of ADH from the posterior pituitary gland.] d. Primary polydipsia [ Circulating ADH levels are high in all these disorders except for primary polydipsia.]
SIADH – DIAGNOSIS
Low plasma sodium concentration (< 130 mEq/L) Low plasma osmolality (< 270 mosmol/kg) Urine osmolality not minimally low (> 150 mmol/kg) Urine sodium concentration not minimally low (> 30 mEq/L) Low-normal plasma urea, creatinine, and uric acid No signs of hypovolemia (tachycardia, orthostatic hypotension, decreased skin turgor, dry mucous membranes) or hypervolemia (edema, ascites) No hypothyroidism, hypocortisolism or diuretic use
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)
What is/are the cause(s) of hyponatraemia with hypovolaemia? a. Diuretic therapy [ Thiazides are more commonly associated with severe hyponatremia than are loop diuretics such as furosemide. There is high urine sodium excretion (Na > 20 mEql/L).] b. Addison's disease c. Vomiting d. Burns e. All of the above T [ Clinical features of hypovolaemia (tachycardia, orthostatic hypotension, dry mucous membranes, flat neck veins, absence of edema) are common. Urinary sodium concentration is low and plasma renin activity is elevated.]
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)
Hypovolemic hyponatremia - True statement a. Low circulating ADH levels [ Patients with hypovolemic hyponatremia have a deficit in total body sodium causing low ECF volume and nonosmotic release of antidiuretic hormone (ADH). High circulating ADH levels stimulate renal water reabsorption and subsequent development of hyponatremia.]
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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)
What is the best index of effective arterial volume? a. Pulse and blood pressure T [ On physical examination, the best index of effective arterial volume is the pulse and blood pressure. The earliest clinical evidence of decreasing blood volume is tachycardia and postural fall in BP.] b. Low urinary sodium c. Low urinary chloride d. Low fractional excretions of sodium and chloride in the urine a. Blood urea [ BUN is very sensitive to effective arterial volume. In patients with normal serum creatinine, a high BUN suggests a low effective arterial volume and a low BUN suggests a high effective arterial volume. The plasma uric acid can also be used as a sensitive index of effective arterial volume.]
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).]
URINE Na+ AND OSMOLALITY IN HYPONATRAEMIA
Page 36 of 50 Urine Na (mEq/L)
Urine osmolality (mmol/kg)
Low (< 30)
Low (< 100)
Low
High (> 150)
High (> 40) High
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-drinker’s 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)
Hyponatremia - True statement a. Common abnormality [ Hyponatremia is a common electrolyte abnormality, often detected asymptomatically.] b. Often asymptomatic [ Patients with mild to moderate hyponatremia (Na+ >120 mEq/L) rarely have signs or symptoms of their hyponatremia. These patients are identified on laboratory testing.] c. Can cause severe cerebral dysfunction [ Cerebral symptoms are anorexia, nausea, vomiting, confusion, lethargy, seizures and coma. Brain cells adapt to hyponatremia by losing cellular potassium, organic solutes, and then other organic osmolytes. This adaptation requires 48 to 72 hours and is very effective in reducing brain swelling. Thus, when hyponatremia occurs slowly, patients have few or no symptoms. When hyponatremia develops in less than 48 hours, adaptation has not had time to occur. These patients are at high risk for developing cerebral edema and intracranial hypertension. Intracranial cell swelling in patients with acute severe hyponatremia causes headaches and confusion that may rapidly progress to coma or seizures.] d. Clinical features depends on the rate of development of hyponatremia [ Cerebral symptoms depends more on how fast hyponatremia develops than on the severity of hyponatremia. This is because when the plasma osmolality falls rapidly, water flows into cerebral cells which become swollen and ischaemic. When hyponatraemia develops gradually, cerebral neurons respond by reducing the intracellular osmolality. Cerebral neurons reduce intracellular osmolality by reducing its potassium concentration and synthesis of intracellular organic osmolytes.] e. All of the above T [ See figures below.]
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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)
Symptoms of hyponatremia are predominantly
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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)
What is the most important clinical manifestation of hyponatremia? a. Cerebral edema T [ Hyponatremia leads to increased ICF volume, specifically brain cell swelling. The symptoms of hyponatremia are primarily neurologic. Their severity dependents on the rapidity of onset and absolute decrease in plasma Na+ concentration. Patients may be asymptomatic at first. As the plasma Na+ concentration falls, headache, confusion, and obtundation develop. Seizures and coma do not usually occur unless the plasma Na+ concentration falls acutely below 120 mmol/L or decreases rapidly. Acute or severe hyponatremia (plasma Na+ concentration <115 mEql/L) present with altered mental status and/or seizures.] b. Cardiac failure c. Muscle weakness d. ECG changes e. Thirst
29)
What is the most important clinical manifestation of acute hyponatremia? a. Intracranial hypotension b. Intracranial hypertension T [ Hypotonic hyponatremia causes entry of water into the brain, resulting in cerebral edema. The surrounding cranium limits expansion of the brain. Therefore, intracranial hypertension may develop. Brain rapidly
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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.]
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DIAGNOSIS OF HYPONATREMIA – 4 TESTS 1. 2. 3. 4.
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
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physiologic response to hemodynamic stimuli or it may be inappropriate in the presence of hyponatremia and euvolemia. SIADH is characterized by hyponatremia with decreased plasma osmolality and concentrated urine (urine osmolality > 100 mosmol/kg and urine Na+ concentration usually greater than 40 mmol/L). Urine Na+ excretion rate is equal to intake. Patients are typically normovolemic. Na+ is the major ECF cation and is largely restricted to this compartment. Therefore, ECF volume contraction indicates a deficit in total body Na+ content. Volume depletion in patients with normal underlying renal function results in enhanced tubule Na+ reabsorption and a urine Na+ concentration < 20 mmol/L. Urine Na+ concentration > 20 mmol/L in hypovolemic hyponatremia suggests diuretic therapy, hypoaldosteronism, a salt-wasting nephropathy, or occasionally vomiting.
30)Which test is not useful for the diagnosis of hyponatraemia? a. Plasma electrolytes [ Plasma and urine electrolytes and
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.]
31)Plasma ADH level is low in a. SIADH b. Cardiac failure c. Cirrhosis d. Nephrotic syndrome e. Primary polydipsia 32)
T
What is the treatment of mild asymptomatic hyponatremia? a. Increase oral sodium intake b. Stop loop diuretic c. Loop diuretic d. Water restriction e. No treatment T [ Mild asymptomatic hyponatremia requires no treatment. The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction. In asymptomatic patients, the plasma Na+ concentration should not be raised by more than 0.5 to 1.0 mmol/L per h and 10 to 12 mmol/L over the first 24 h.]
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33)
What is the treatment of asymptomatic hyponatremia with ECF volume contraction? a. Increase oral sodium intake b. Stop loop diuretic c. Give thiazide d. Water restriction e. Isotonic saline T [ Give sodium as normal saline. The direct effect of the IV normal saline on the plasma Na+ concentration is trivial. When euvolemia is restored by normal saline, the stimulus for AVP release is removed allowing the excess free water to be excreted. Acute or severe hyponatremia (plasma Na+ concentration <110 to 115 mmol/L) usually present with altered mental status and/or seizures and requires more rapid correction.]
34)
What is the treatment of asymptomatic hyponatremia with edema? a. Restrict Na+ intake [ The hyponatremia associated with edematous states reflect the severity of the underlying disease. It is usually asymptomatic. These patients have increased total body water that exceeds the increase in total body Na+ content. Treatment is restriction of Na+ and water intake.] b. Restrict water intake [ Dietary water intake should be less than the urine output.] c. Correct hypokalemia [ Correction of the K+ deficit may raise the plasma Na+ concentration by shifting of Na+ out of cells as K+ moves in.] d. Loop diuretic [ Use loop diuretics to increase water loss. Replace a proportion of the urinary Na+ loss to ensure net free water excretion.] e. All of the above T
35)
Water restriction is useful in hyponatremia due to a. Cardiac failure b. Primary polydipsia c. SIADH d. Renal failure a. All of the above T [ 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.]
36)
What is the treatment of symptomatic hyponatremia with dilute urine? a. Water restriction T [ Patients with symptomatic hyponatremia and dilute urine (osmolality < 200 mOsm per kilogram of water) but with less serious symptoms usually require only water restriction and close observation.] b. Hypertonic saline [ Infusion of hypertonic saline is indicated only when severe symptoms (e.g., seizures or coma) are present.] c. Oral sodium d. Thiazide e. Furosemide
37)
50-year-old male admitted with seizures has a serum sodium level of 115 mEq/L. What is the treatment? a. Oral sodium
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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
FORMULAS FOR MANAGING HYPONATREMIA
† In addition to its complete distribution in the extracellular compartment, this infusate induces osmotic removal of water from the intracellular compartment.
ESTIMATED TOTAL BODY WATER (IN LITERS)
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
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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)
What is the treatment for severe hyponatraemia and convulsions? a. IV furosemide b. Dialysis c. Hypertonic sodium chloride T [ The symptoms and treatment for hyponatraemia depends on the rate of development and severity of hyponatraemia. If hyponatraemia has developed rapidly (over hours to days), cerebral edema may develop. In such circumstances, it is safe to correct the plasma sodium relatively rapidly. Infusion of hypertonic (3%) sodium chloride solutions may be indicated, especially when the patient is obtunded or convulsing.] d. Phenytoin 100mg every 8 hours e. Half-normal saline
40)
What is the treatment for severe asymptomatic chronic hyponatraemia? a. Hypertonic sodium chloride [ Rapid correction of hyponatraemia which has developed slowly (over weeks to months) can cause brain damage (central pontine myelinolysis). Cerebral cells adapt to slowly developing hyponatraemia and hypoosmolality by reducing the intracellular osmolality, thus maintaining normal cell volume. Rapid correction of hyponatraemia will cause an abrupt increase in extracellular osmolality. Rapid increase in extracellular osmolality can lead to water shifting out of the cerebral neurons, abruptly reducing their volume and risking detachment from their myelin sheaths ('myelinolysis'). Therefore, rate of correction of the plasma Na concentration in chronic asymptomatic hyponatraemia should not exceed 10 mEq/L/day.] b. Water and salt restriction T c. Demeclocycline [ Demeclocycline inhibits renal tubular responsiveness to ADH, leading to increased water excretion. Onset of action is 3 to 6 days.] d. V2-receptor antagonists [ V2-receptor antagonists (conivaptan) will likely become the first-line treatment for euvolemic and hypervolemic hypernatremia.] e. Furosemide [ Furosemide in combination with sodium chloride tablets will increase urine volume and allow more water intake.]
41)
What is the cause of osmotic demyelination syndrome? a. Inadequate steroid in multiple sclerosis
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Rapid correction of hyponatremia T [ The risk of correcting hyponatremia too rapidly is the development of the osmotic demyelination syndrome. See figure below. Patients with chronic hyponatremia are most susceptible. Hypertonic saline can cause sudden osmotic shrinkage of brain cells. It is characterized by flaccid paralysis, dysarthria, and dysphagia. Diagnosis is confirmed by neuroimaging studies. There is no specific treatment.] c. Fast diuresis in massive ascites d. More than 12 L of water intake in primary polydipsia [ Water restriction in primary polydipsia may also lead to too rapid correction of hyponatremia. IV saline in ECF volume-contracted patients may also lead to too rapid correction of hyponatremia. It is due to AVP suppression and brisk water diuresis. It can be prevented by administration of water or use of an AVP analogue to slow down the rate of free water excretion.] e. Toxic effect of AVP b.
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)
How does central pontine myelinolysis clinically present? a. Quadriplegia T [ Central pontine myelinolysis typically presents as quadriplegia and pseudobulbar palsy. Diagnosis is by MRI. Partial forms present as confusion, dysarthria, and/or disturbances of conjugate gaze without quadriplegia. Most cases are associated with rapid correction of hyponatremia or with
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hyperosmolar states. The pathology is demyelination without inflammation in the base of the pons.] b. Hyponatremia c. SIADH d. Intense thirst 43)
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)
A 68-year-old woman is brought to the hospital because of progressive drowsiness and syncope. She is being treated with a low-sodium diet and hydrochlorothiazide daily for essential hypertension; she has had diarrhea for the past three days. She is lethargic but has no focal neurologic deficits. She weighs 60 kg. Her blood pressure while in a supine position is 96/56 mm Hg, and the pulse is 110 beats per minute. The jugular veins are flat, and skin turgor is decreased. The serum sodium concentration is 106 mEq per liter, the serum potassium concentration is 2.2 mEq per liter, the serum urea nitrogen concentration is 46 mg per deciliter, the serum creatinine concentration is 1.4 mg per deciliter, serum osmolality is 232 mOsm per kilogram of water, and urine osmolality is 650 mOsm per kilogram of water. What is the treatment? a. 0.9% sodium chloride first followed by 0.45 % sodium chloride T [Diagnosis is hypotonic hyponatremia caused by thiazide therapy and gastrointestinal losses of sodium. There is associated depletion of potassium also. Treatment is to withhold hydrochlorothiazide and to infuse 0.9 percent sodium chloride solution containing 30 mEq of potassium chloride per liter. The estimated volume of total body water is 27 liters (0.45 X 60). The retention of 1 liter of this infusate will increase the serum sodium concentration by 2.8 mEq per liter {(154 + 30) – 106 ÷ (27 + 1) = 2.8}. As soon as the extracellular-fluid volume nears restoration, the nonosmotic stimulus to arginine vasopressin release will cease resulting in rapid excretion of dilute urine and correction of the hyponatremia at a rapid pace. Therefore, switch to 0.45 percent sodium chloride containing 30 mmol of potassium chloride per liter.] b. 0.45 % sodium chloride first followed by 0.9 % sodium chloride c. 5 % dextrose in water containing 30 mmol of potassium chloride d. 3 percent sodium chloride
46)
What is the long-term treatment of asymptomatic hyponatremia that accompanies cardiac failure? a. Water restriction T [Asymptomatic hyponatremia is common in edematous states and in syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia is due to a defect of water excretion. Water restriction (to <800 ml per day) is the mainstay of long-term management. Goal is to induce negative water balance.] b. Thiazide diuretic [ Loop, but not thiazide, diuretics reduce urine concentration and augment excretion of electrolyte-free water. Therefore, loop diuretics permit relaxation of fluid restriction.] c. Loop diuretics with high sodium intake [ In the syndrome of inappropriate secretion of antidiuretic hormone, but not in edematous disorders, loop diuretics should be combined with plentiful sodium intake (in the form of dietary sodium or salt tablets). This treatment increases water loss. If these measures fail, demeclocycline per day can help by inducing nephrogenic diabetes insipidus.] d. Demeclocycline
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
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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 kidney’s 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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