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Chapter: Medicine Study Notes : Endocrine and Electrolytes

Potassium - Electrolytes

Normal value of K: 3.5 – 5 mmol/L



·        Normal value of K: 3.5 – 5 mmol/L

·        Standard western diet contains ~ 70 mmol/day

·        Shifts from ICF to ECF in response to:

o  Insulin deficiency 

o  b-blockers

o  Acidosis

o  Cell necrosis


·        Excreted in the distal tubule (K and H swapped for Na) under the influence of aldosterone. High HCO3 excretion also ®­ K loss (eg alkalosis)

·        Investigations:

o  H+ 

o  HCO3-: usually ­ when K ¯ and visa-versa except when there is acidosis (eg renal tubular necrosis, diarrhoea) 

o  Creatinine 

o  Urinary K: > 20 mmol/L Þ renal K loss 

o  Na: ¯ in hyperkalaemia, consider renal tubule disorder, ¯mineralocorticoid

o  Glucose 

o  ECG (if widened QRS complexes give Ca).


·        Key differentials: Diabetic ketoacidosis, renal failure




·        Low: 

o  Redistribution: alkalosis, b-agonists

o  Loss: GI, renal, thiazide or loop diuretics

o  ¯Intake (starvation, surgery)

·        High:

o  Redistribution: acidosis

o  Massive cell lysis

o  ¯Excretion: DRUGS (eg ACE inhibitors), renal failure, hypoaldosteronism




·        Causes:


o  Usually ¯ renal excretion

o  Shift from ICF (eg acidosis, massive cell lysis)

o  Low aldosterone: ACE inhibitors (instead use spironolactone), ¯renin (renal disease, NSAIDs, diabetes), poor adrenal function (eg Addison‟s)

o  Renal unresponsive to aldosterone: interstitial nephritis, K sparing diuretics

o  Renal failure: hyperkalaemia once GFR < 25 ml/min


·        Signs: myocardial depression, peaked T wave, flat P wave, wide QRS, VF, diarrhoea, abdominal pain, muscle excitability

·        Treatment:

o  If severe (> 6.5 mmol/L) consider:

§  Glucose 50 g + soluble insulin 10 U over 15 mins

§  IV calcium gluconate – stabilises myocytes but doesn‟t change K

§  b2 agonist (salbutamol)

§  Dialysis if extreme


o  If moderate (5.5 – 6.5 mmol/L): Calcium resonium 15 g po (calcium binding resins), ­renal loss through diuretics, mineralocorticoids




·        Causes:

o  GI losses (ECF volume contraction):


§  Vomiting, NG suction ® alkalosis ® ­HCO3 in urine and ­aldosterone ® renal loss of K

§  Diarrhoea: ® K loss and metabolic acidosis

o  Urinary losses:

§  Diuretics: thiazides or loop

§  Alkalosis (also shift to ICF if significant alkalosis)

§  ECF normal or high: high aldosterone or hypermineralocorticoid (eg Cushing‟s)


o   K shift into cells: metabolic alkalosis, insulin, b-adrenergics

o   ¯Intake (starvation, surgery)

·        Symptoms:

o   Muscle weakness, cramps

o   GI: constipation, ileus

o   Polyuria, nocturia

o   Urine – if ­ volume then diuretics or osmotic diuresis, if not consider aldosterone action


·        Signs: arrhythmias, PR prolonged, inverted T waves, U waves, VF, GI ileus, muscle weakness, hypotonicity, digoxin toxicity, alkalosis


·        Treatment: May have large total body deficit (eg DKA).  Replacement KCl up to 40 mmol/hour


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