2disorders of potassium balance 2
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Disorders of potassium balance
Zhao Chenghai
Pathophysiology
Outline
• Potassium balance
• Disorders of potassium balance– Hypokalemia– Hyperkalemia
Potassium balance
• Distribution of potassium
• Gains and losses of potassium
• Mechanisms of regulation
• Functions of potassium
Potassium balance
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+ mov
es 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
– inability to obtain or ingest food– Diet deficient in potassium
• Excessive renal, gastrointestinal and skin losses
– 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 ketoacido
sis)– 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 o
smolality↑)
• 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 cra
mps, 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 immu
nodeficiency 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 distur
bance?
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?