Disorders of potassium balance Zhao Chenghai Pathophysiology

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Disorders of potassium
balance
Zhao Chenghai
Pathophysiology
Outline
• Potassium balance
• Disorders of potassium balance
– Hypokalemia
– Hyperkalemia
Potassium balance
Potassium balance
• Distribution of potassium
• Gains and losses of potassium
• Mechanisms of regulation
• Functions of potassium
Distribution of potassium
• The intracellular concentration of
potassium ranges from 140 to 150
mmol/L.
• The extracellular concentration of
potassium (3.5-5.0mmol/L) is
considerable less.
Gains and losses
• Food is the main source of potassium
intake.
• The kidneys are the main source of
potassium elimination.
Mechanisms of regulation
•
Renal regulation
•
Transcellular shift between the
intracellular and extracellular
compartments
Renal regulation
• Secretion of potassium by distal and
collecting tubules.
• Aldosterone --- a sodium-potassium
exchange system.
Sodium is transported back into blood.
Potassium is secreted into tubular filtrate.
Mineralocorticoid hormone
Plasma potassium levels control aldosterone
secretion by adrenal gland.
Transcellular shifts
• Sodium-potassium ATPase
– Both insulin and epinephrine increase the activity of
sodium-potassium pump.
(An increase in potassium level stimulates insulin
release. --- a feedback mechanism)
• Potassium channels
– ECF osmolality↑→H2O leaves cell→ ICF K+↑→ K+
moves out of cell through K+ channels →ECF K+
– Exercise
• Potassium-hydrogen exchange to maintain
electrical neutrality
– In acidosis
– In alkalosis
Functions of potassium
• Maintain the osmotic integrity of cells
– Osmotic pressure in ICF
• Maintain acid-base balance
– Through potassium-hydrogen exchange
• Contribute to the reactions that take place in
cells
– Transform carbohydrates into energy
– Convert amino acid to protein
– Change glucose into glycogen
• Play a critical role in the excitability of
skeletal, cardiac, and smooth muscle.
Resting membrane potential (RMP)
RMP≈-59.5lg[K+]i/[K+]e
Excitability of muscle cells can be affected
by the distance between RMP and
threshold potential.
Hypokalemia
Hypokalemia refers to a decrease
in plasma potassium level below
3.5 mmol/L.
Causes of hypokalemia
•
Inadequate intake
–
–
•
Excessive renal, gastrointestinal and skin
losses
–
–
–
•
inability to obtain or ingest food
Diet deficient in potassium
Diuretic therapy (thiazide and loop diuretics)
Increased aldosterone level (primary aldosteronism,
stress-cortisol)
burn, sweating increase, vomiting and diarrhea
Transcellular shift
–
–
–
Administration of insulin (to treat diabetic
ketoacidosis)
β-adrenergic agonist----albuterol (bronchodilator)
Alkalosis
Manifestations of hypokalemia
• Neuromuscular manifestations
– Muscle flabbiness, weakness and fatigue
– Muscle cramps and tenderness
– Paresthesia and paralysis
• Impaired kidney’s ability to concentrate the
urine
– polyuria, urine with low osmolality, polydipsia (ECF
osmolality↑)
• Gastrointestinal manifestations
– Anorexia, nausea, vomitting,
– Constipation, abdominal distension, paralytic ileus
• Cardiovascular manifestations
– Arrhythmias, increased sensitivity to digitalis toxicity
• Metabolic alkalosis
ECG changes in hypokalemia
•
•
•
•
Depression of the ST segment
Flattening of the T wave
Appearance of a prominent U wave
Prolongation of PR interval
Treatment of hypokalemia
• Increasing the intake of foods high in
potassium content
• Oral potassium supplements
• Giving potassium intravenously when
rapid replacement is needed.
– Only if the renal function is adequate
Hyperkalemia
• Hyperkalemia refers to an increase in
plasma levels of potassium in excess
of 5.0mmol/L.
Causes of hyperkalemia
• Decreased renal elimination
– Decreased renal function-renal failure
– Treatment with potassium-sparing diuretics
– Decreased aldosterone level
• Adrenal insufficiency (addison’s disease)
• Treatment with ACEI
• Angiotensin II receptor blocker
• Excessively rapid administration
• Movement of potassium from the intracellular
to extracellular compartment
– Tissue injury such as burns and crushing injuries
– Extreme exercise or seizures
– Acidosis
Manifestations of hyperkalemia
• Gastrointestinal manifestations
– Anorexia, nausea, vomitting, intestinal
cramps, diarrhea
• Cardiovascular manifestations
– Ventricular fibrillation and cardiac arrest
• Neuromuscular manifestations
– Paresthesias
– Weakness
– Muscle cramps
ECG changes in hyperkalemia
•
•
•
•
Appearance a peaked T wave
Widening of the QRS complex
Prolongation of the PR interval
Disappearance of the P wave
Treatment of hyperkalemia
• Decreasing intake or absorption of
potasssium.
• Using calcium to antagonize the
potassium.
• Using insulin and glucose
• Increasing potassium excretion
– hemodialysis
– peritoneal dialysis
Case1
• A 40-year-old man with advanced acquired
immunodeficiency syndrome (AIDS) presents
with an acute chest infection. Investigation
confirm a diagnosis of P.carinii pneumonia.
Although he is treated appropriately, his serum
sodium level is 118mmol/L. Tests of adrenal
function are normal.
• What type of disorders happened to this man?
• What is the likely cause of this electrolyte
disturbance?
Case 2
• A 70-year-old woman who is taking
furosemide (a loop diuretic) for congestive
heart failure complains of weakness, fatigue,
and cramping of the muscles in her legs. Her
serum potassium is 2.0mmol/L, and her
serum sodium is 140mmol/L. She also
complains that she notices a “strange heart
beat” at times.
• What is the likely cause of this woman’s
symptoms?
• What would be the treatment for this woman?
Case 3
• A 76-year-old woman was brought to the
hospital because she was lethargic and
refused to drink fluid. Her blood pressure is
100/60 mmHg. Serum sodium level is
170mmol/L, potassium level is 4.3mmol/L.
• What kind of electrolyte disturbance
happened to this woman?
• What is the cause of this kind of disorder?
• What is the most severe outcome of this
disorder?
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