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1) Hyperkalemia is plasma K+ concentration more than ----------- mEq/L
T [ Hyperkalemia is defined as a plasma (not
serum) K+ concentration > 5.0 mmol/L. Hyperkalemia may be due to release of K+ from cells or
decreased renal loss. Increased dietary K+ intake does not usually cause hyperkalemia since
renal K+ excretion increases in response to increases in dietary consumption.]

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2) What is/are the cause(s) of pseudohyperkalemia?
a. Prolonged use of a tourniquet
[ Pseudohyperkalemia is an increase in
potassium concentration only in vitro (or in the local blood vessel). It has no physiological
consequences. Pseudohyperkalemia is artificially elevated plasma K+ concentration due to
movement of K+ out of cells. Normally, intracellular concentration of K+ is high (140mEq/L) and
plasma concentration of K+ is low (5mEq/L). Small leaks of K+ out of blood cells can increase
serum K+ levels considerably. When blood is allowed to clot before centrifugation, enough K is
released from platelets to raise serum K by approximately 0.5 mEq/L. This is accounted for
within normal limits. However, excessive errors can occur in the presence of marked
thrombocytosis, marked leukocytosis, or hemolysis on obtaining blood samples. These
conditions are referred to as ‘‘pseudohyperkalemia.’’ This can occur immediately prior to or
following venepuncture. Prolonged use of a tourniquet with or without repeated fist clenching
is a contributing factor. Prolonged use of a tourniquet with fist exercises can increase the
serum potassium level by as much as l mEq/L.]
b. Hemolysis
[ In intravascular hemolysis, K+ is released from
the hemolysed RBCs. As 98% of body potassium is located within cells, cell death can result in
c. Leukocytosis
[ High leukocyte and platelet counts may also
artificially elevate potassium levels due to lysis of these cells after the blood is drawn. The
elevated serum K+ concentration is due to release of intracellular K+ following clot formation. If
plasma (not serum) K+ concentration is measured, it should be normal.]
d. Tumor lysis syndrome
[ Tumor lysis syndrome is caused by the
destruction of a large number of rapidly proliferating neoplastic cells. Potassium is the main
intracellular cation. Therefore, massive destruction of malignant cells may cause hyperkalemia.
Tumor lysis syndrome and rhabdomyolysis lead to K+ release from cells as a result of tissue
breakdown. Muscle breakdown from crush injury or rhabdomyolysis increase serum K+
e. All of the above
T [ Suspect pseudohyperkalemia in an otherwise
asymptomatic patient with no obvious underlying cause. In pseudohyperkalemia, no
electrocardiographic abnormalities are present.]

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3) Which of the following is not raised in tumor lysis syndrome?
a. Uric acid
[ Tumor lysis syndrome is caused by the
destruction of a large number of rapidly proliferating neoplastic cells. Effective treatment kills
malignant cells and leads to increased serum uric acid levels from the turnover of nucleic
acids. Uric acid can precipitate in the tubules, medulla, and collecting ducts of the kidney,
leading to renal failure. Uric acid crystals in the urine strongly suggest uric acid nephropathy.]
b. Phosphate
[ Hyperphosphatemia is caused by the release of
intracellular phosphate by tumor cell lysis. Hyperphosphatemia produces a reciprocal
depression in serum calcium.]
c. Potassium
[ Potassium is the main intracellular cation.
Therefore, massive destruction of malignant cells may cause hyperkalemia.]
d. Lactic acid
e. Calcium
T [ Tumor lysis syndrome is characterized by
various combinations of hyperuricemia, hyperkalemia, hyperphosphatemia, lactic acidosis, and
hypocalcemia. Acute renal failure is a common complication of the syndrome.]
4) Tumor lysis syndrome is most frequently associated with
a. Multiple myeloma
b. Burkitt's lymphoma
T [ Tumor lysis syndrome is most frequently
associated with the treatment of Burkitt's lymphoma, acute lymphoblastic leukemia, and other
high-grade lymphomas. The risk of tumor lysis syndrome in Burkitt's lymphoma is related to
the tumor burden and renal function. Hyperuricemia and high serum levels of lactate
dehydrogenase correlate with total tumor burden, also correlate with the risk of tumor lysis
c. Ovarian carcinoma

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d. Hypernephroma
5) Useful in the treatment of tumor lysis syndrome
a. Allopurinol
[ Prevention is the most important step in the
management. Allopurinol, urinary alkalinization, and aggressive hydration are the main
preventive measures.]
b. Rasburicase
[ Rasburicase is recombinant urate oxidase. Urate
oxidase catalyzes the conversion of poorly soluble uric acid to readily soluble allantoin. This
enzyme is not present in humans. Rasburicase decreases uric acid levels within hours.
Rasburicase is contraindicated in patients with glucose-6-phosphate dehydrogenase
c. Dialysis
[ Hemodialysis is often necessary and should be
considered early in the course.]
d. All of the above
T [ Prognosis is excellent.]
6) Cause of hyperkalemia
a. Metabolic acidosis
[ In metabolic acidosis, hydrogen ions enter the
cells and potassium ions come out of the cells.]
b. Insulin deficiency
[ Insulin stimulates entry of glucose and
potassium into cells. Thus, insulin lowers plasma potassium and is used in the treatment of
hyperkalemia. Insulin deficiency and hypertonicity due to hyperglycemia promote K+ shift from
the ICF to the ECF.]

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c. Exercise
[ Exercise-induced hyperkalemia is due to release
of K+ from muscles. The severity of exercise-induced hyperkalemia is related to the degree of
exertion. It is rapidly reversible and is often associated with rebound hypokalemia.
Hyperkalemic periodic paralysis is a rare autosomal dominant disorder characterized by
episodic weakness or paralysis. It is precipitated by stimuli that normally lead to mild
hyperkalemia (e.g., exercise).]
d. Beta blockers
[ Treatment with beta blockers rarely causes
e. All of the above
T [ Hyperkalemia may occur with severe digitalis
toxicity due to inhibition of the Na-K-ATPase pump.]
7) What is the most common cause of acute hyperkalemia?
a. Renal failure
T [ Acute renal failure is the most common cause
of rapid onset of hyperkalemia. Acute decreases in GFR lead to marked decreases in distal
delivery of salt and water, which secondarily decrease distal K secretion. Thus, when acute
renal failure is oliguric, hyperkalemia is frequent. When acute renal failure is nonoliguric, distal
sodium and water delivery is usually sufficient and hyperkalemia is unusual.]
b. Spiranolactone
[ Spironolactone, triamterene, beta-blockers,
cyclosporine and tacrolimus may cause hyperkalemia.]
c. Hemorrhagic infarction of both adrenal glands [ Damage to the adrenals can result in
d. Reperfusion of ischemic skeletal muscle
[ Reperfusion injury occurs at the completion of
arterial injury repair. Rhabdomyolysis leads to release of K+. Sodium bicarbonate can prevent
hyperkalemia and cardiac arrest. Give bolus IV infusion of sodium bicarbonate immediately
before reperfusion of the ischemic tissues by release of the arterial clamp. The bicarbonate
shifts potassium from the ECF across the cell membrane into ICF.]

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8) What is the most common cause of chronic hyperkalemia?
a. Hyperkalemic periodic paralysis
[ Hyperkalemic periodic paralysis is a rare
autosomal dominant disorder due to a mutation in the gene for the skeletal muscle Na+
channel. It is characterized by episodic weakness or paralysis. It is precipitated by stimuli that
normally lead to mild hyperkalemia (e.g., exercise).]
b. Succinylcholine
[ Succinylcholine can increase the plasma K+
concentration, especially in patients with massive trauma, burns, or neuromuscular disease.]
c. Decreased renal K+ excretion
T [ Chronic hyperkalemia is almost always due to
decreased renal K+ excretion due to hyporeninemic hypoaldosteronism.]
d. Angiotensin-converting enzyme inhibitors
[ Patients getting ACE inhibitors or angiotensin
receptor antagonists are at increased risk of hyperkalemia. Patients with diabetes mellitus,
renal insufficiency, decreased effective circulating arterial volume, and bilateral renal artery
stenosis are particularly at risk. Concurrent use of K+-sparing diuretics or NSAIDs also
increases the risk.]
[ NSAIDs inhibit renin secretion and the synthesis
of vasodilatory renal prostaglandins. Hyperkalemia may develop due to decrease in GFR and
K+ secretion.]
9) What is/are the cause(s) of hyporeninemic hypoaldosteronism?
a. Renal insufficiency
b. Diabetic nephropathy
[ Hyporeninemic hypoaldosteronism is the most
common cause of aldosterone deficiency states. It is the commonest cause of chronic
hyperkalemia among nondialysis patients. Hyporeninemic hypoaldosteronism is characterized
by euvolemia or ECF volume expansion and suppressed renin and aldosterone levels. As a
rule, the degree of hyperkalemia due to hypoaldosteronism is mild in the absence of increased
K+ intake or renal dysfunction. Diabetic nephropathy and interstitial renal disease are the most
common causes of hyporeninemic hypoaldosteronism.]

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c. Chronic tubulointerstitial disease
[ Diseases associated with inflammation in the
tubulointerstitium (e.g., SLE, renal transplant) can cause aldosterone resistance. When there is
aldosterone resistance, tubular secretion of potassium is impaired, even in the presence of
high aldosterone levels. Aldosterone resistance can also occur during therapy with potassium-
sparing diuretics.]
d. All of the above
T [ Drugs that inhibit the release of renin may
provoke hyperkalemia (ACE inhibitors, nonsteroidal anti-inflammatory agents, beta-blockers).
Therapy with angiotensin receptor antagonists, NSAIDs or beta-blocking drugs can cause
hyporeninaemic hypoaldosteronism.]
10) Which one of the following drugs decreases aldosterone synthesis?
a. Trimethoprim
[ Trimethoprim and pentamidine block distal
nephron Na+ reabsorption and thus impair K+ secretion.]
b. Heparin
T [ Heparin inhibits production of aldosterone by
the cells of the zona glomerulosa. Heparin can cause severe hyperkalemia in patients with
underlying renal disease, diabetes mellitus, or those receiving K+-sparing diuretics, ACE
inhibitors, or NSAIDs. Two other causes of decreased aldosterone synthesis are Addison's
disease (primary adrenal insufficiency) or congenital adrenal enzyme deficiency.]
c. Spironolactone
[ Spironolactone is a competitive aldosterone
d. Amiloride
[ Amiloride and triamterene block the apical Na+
channel of the principal cell. Amiloride and triamterene inhibit Na reabsorption, which
abolishes the lumen negative potential and therefore inhibits K secretion.]
e. 9a-fludrocortisone
[ 9a-fludrocortisone is a synthetic

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11) Renal cause(s) of hyperkalemia
a. Acute oliguric renal failure
[ Hyperkalemia is a common complication of
acute oliguric renal failure. Hyperkalemia is due to increased K+ release from cells (acidosis,
catabolism) and decreased excretion.]
b. Chronic renal failure
[ Increased distal flow rate and K+ secretion by
surviving nephrons may maintain normal plasma K+ concentration. However, these adaptive
mechanisms eventually fail to maintain K+ balance when the GFR falls below 10 to 15 mL/min
or oliguria ensues.]
c. Urinary tract obstruction
[ Urinary tract obstruction is an often overlooked
cause of hyperkalemia.]
d. Diabetic nephropathy
[ Other nephropathies associated with impaired
K+ excretion include drug-induced interstitial nephritis, lupus nephritis, sickle cell disease, and
diabetic nephropathy.]
e. All of the above
12) What is/are the clinical manifestion(s) of hyperkalemia?
a. Quadriparesis
[ The resting membrane potential is related to the
ratio of the ICF to ECF K+ concentration. Therefore, hyperkalemia partially depolarizes the cell
membrane. The most important manifestation of prolonged depolarization is muscle weakness.
The muscle weakness may progress to flaccid paralysis.]
b. Hypercapnia
[ Hypoventilation develops if the respiratory
muscles are involved.]
c. Metabolic acidosis
[ Hyperkalemia inhibits renal ammonia synthesis
and reabsorption of NH4+ in the thick ascending limb of the loop of Henle. Thus, H+ ion
excretion is impaired and results in metabolic acidosis. Metabolic acidosis further exacerbates
the hyperkalemia due to K+ movement out of cells.]

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d. Ventricular fibrillation
[ The most serious effect of hyperkalemia is
cardiac toxicity. It does not correlate well with the plasma K+ concentration. The earliest ECG
change is either increased T-wave amplitude or peaked T waves. Ventricular fibrillation or
asystole is usually a terminal event.]
e. All of the above
T [ Patients typically present with progressive
muscular weakness, but sometimes there are no symptoms until cardiac arrest occurs.
Potentially fatal hyperkalemia rarely occurs unless the plasma K+ concentration exceeds 7.5
mEq/L and is usually associated with profound weakness and absent P waves, QRS widening,
or ventricular arrhythmias on the electrocardiogram.]
13) What is the earliest electrocardiographic change of hyperkalemia?
a. Peaked T waves
T [ Cardiac toxicity does not correlate well with
the plasma K+ concentration. The earliest ECG change is either increased T-wave amplitude or
peaked T waves. See figure below.]
b. Prolonged PR interval
[ More severe degrees of hyperkalemia result in a
prolonged PR interval and QRS duration, atrioventricular conduction delay, and loss of P
c. Widening of the QRS complex
[ Progressive widening of the QRS complex and
merging with the T wave produces a sine wave pattern. Peaking of the T wave is an early ECG
sign, but widening of the QRS complex presages a dangerous cardiac arrhythmia. The terminal
event is usually ventricular fibrillation or asystole.]
d. Atrioventricular conduction delay
e. Loss of P waves

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14) What is the first step in the differential diagnosis of hyperkalemia?
a. Rule out pseudohyperkalemia
T [ The first step in the differential diagnosis of
hyperkalemia is to rule out pseudohyperkalemia. ECG abnormalities of hyperkalemia are
absent in pseudohyperkalemia. The absence of ECG changes does not eliminate true
hyperkalemia because ECG changes are rare in chronic hyperkalemia. Pseudohyperkalemia
should be suspected in conditions known to cause pseudohyperkalemia, such as
thrombocytosis or in vitro hemolysis (pink serum). In pseudohyperkalemia due to
thrombocytosis, both serum and plasma K+ should be obtained simultaneously.]
b. Measurement of a 24-hour urine K+
[ Once pseudohyperkalemia is ruled out, the next
step is to differentiate among the three major causes of hyperkalemia: increased K+ intake,
shift of K+ from the cell, and impaired renal excretion. A careful dietary history will be sufficient
to rule out hyperkalemia due to increased intake. Measurement of a 24-hour urine K+ will
distinguish increased intake from the other two causes. Although hyperkalemia due to a shift
of K+ from the cell would result in an increased urinary excretion of K+, renal excretion of K+ is
often not increased because impaired renal excretion of K+ often contributes to hyperkalemia.]
c. Blood urea and serum creatinine
[ Among the renal causes of hyperkalemia, acute
renal failure is the most common cause of acute hyperkalemia. This will be obvious from serum
creatinine and BUN.]

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d. Urinary excretion of Na+ and K+
[ Chronic hyperkalemia is almost always due to
impaired renal excretion. For differential diagnosis of chronic hyperkalemia of renal causes, the
first step is to measure plasma renin activity, plasma aldosterone, and urinary excretion of Na+
and K+. A very low urinary Na+ and a low K+ in the absence of polyuria suggest that the
aldosterone effect is normal. If urinary Na+ is adequate (> 20 mEq/L), plasma renin activity and
aldosterone should be measured.]
e. Plasma renin activity
[ Low PRA and low aldosterone suggest
hyporeninemic hypoaldosteronism. High PRA and low aldosterone suggest Addison's disease,
heparin therapy, and aldosterone biosynthetic defect. Treatment with potassium-sparing
diuretics (e.g., amiloride, triamterene, and spironolactone) increase both PRA and aldosterone.]

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15) Treatment of hyperkalemia
a. Calcium gluconate IV
[ Calcium gluconate decreases membrane
excitability. Calcium antagonizes the depolarization effect of elevated K+.]
b. Insulin
[ Insulin causes K+ to shift into cells from ECF
and will temporarily lower the plasma K+ concentration. Insulin is given with glucose to prevent
c. NaHCO3 IV
[ Alkalosis caused IV NaHCO3 therapy can also
shift K+ into cells.]
d. Beta 2 adrenergic agonists
[ Beta 2 adrenergic agonists promote cellular
uptake of K+ when administered parenterally or in nebulized form. The onset of action is 30 min
and the effect lasts 3 hours.]
e. All of the above
[ Potentially fatal hyperkalemia rarely occurs
unless the plasma K+ concentration exceeds 7.5 mEq/L and is usually associated with
profound weakness and absent P waves, QRS widening, or ventricular arrhythmias on the
16) What is the most rapid and effective way of lowering the plasma K+ concentration?
a. Loop diuretics
[ Loop and thiazide diuretics, often in
combination, enhance K+ excretion if renal function is adequate.]
b. Cation-exchange resin
[ Sodium polystyrene sulfonate is a cation-
exchange resin that binds potassium in the gut lumen (promotes the exchange of Na+ for K+ ).
Each gram binds 1 mEq of K+ and releases 2 to 3 mmol of Na+. It can be given by mouth or as a
retention enema. Chronic hyperkalemia associated with renal dysfunction can be managed by
oral or rectal administration of sodium polystyrene sulfonate.]

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c. Hemodialysis
T [ Hemodialysis is the most rapid and effective
way of lowering the plasma K+ concentration. It is indicated in patients with renal failure and
those with severe life-threatening hyperkalemia unresponsive to other treatments.
Hemodialysis is the most reliable method for controlling hyperkalemia in patients with acute
renal failure. Peritoneal dialysis is only 20% as effective as hemodialysis.]
d. Correction of metabolic acidosis
e. Mineralocorticoid
17) What is the first treatment in hyperkalemia with ECG changes?
a. Infusion of calcium gluconate
T [ If ECG changes are present, the first step
should be infusion of calcium gluconate to stabilise conductive tissue membranes. Calcium
has the opposite effect of potassium on conduction of an action potential.]
b. Insulin and glucose
[ Also use measures to shift potassium from the
ECF to the ICF. These act rapidly and may avert cardiac complications of hyperkalaemia.]
c. IV frusemide
[ This will remove K+ from the body if adequate
renal function is present.]
d. Ion-exchange resins
[ In renal failure, use ion-exchange resins acting
through the gastrointestinal tract and arrange for urgent dialysis.]
e. Urgent dialysis

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Stabilise cell membrane potential
IV calcium gluconate (if ECG changes suggestive
of hyperkalaemia and/or K > 7 mEq/L)
Shift K into cells
Inhaled beta 2 agonist
IV glucose and insulin
IV sodium bicarbonate (if acidosis present)
Remove K from body IV furosemide and normal saline (if adequate
residual renal function)
Ion-exchange resin


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