Electrolytes Flashcards

1
Q

What is the normal reference range for sodium?

A

135-145mmols/L

Values less than 120 or more than 150 are potentially dangerous

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2
Q

What can contribute to sodium abnormalities?

A

Intake
Loss or retention (gut, sweat, renal)
Water intake/loss/retention

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3
Q

What are the clinical features of hypernatraemia?

A
H2O depletion (Vol decrease):
Unconscious/confused pts
Infants
Thirst centre damage
Dehydration

Conn’s/Cushings (Aldo increase)

DI (ADH Deacrease):
Cranial – no ADH
Nephrogenic – ADH ineffective

Addison’s (Adrenal insufficiency) (Aldo )

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4
Q

What are the clinical features of hyponatraemia?

A

H2O excess (vol increase):
infusion of hypotonic fluid
psychogenic DI

Na+ depletion (Na+ decrease from gut/skin/sweat)

Heart failure (Renal blood flow decrease)

SIADH (ADH increase)

Diuretics (Vol decrease)

Loss of Na+ and H2O (Vol decrease):
Osmotic diuresis (eg diabetes)
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5
Q

What are the common causes of hyponatraemia?

A
Iatrogenic eg fluid mismanagement
Drugs especially diuretics
Renal failure
Addison’s disease
Hypothyroidism
Liver failure 
Heart failure
SIADH
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6
Q

What is the reference range for potassium?

A

3.5-5mmol/L

Values less than 3 or more than 6 are potentially dangerous

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7
Q

What are the normal intracellular and extracellular concentrations of potassium?

A

Intra- 150mmol/L

Extra- 5mmol/L

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8
Q

Describe acidosis

A

ATPase slows
Less potassium into cells
Hyperkalaemia

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9
Q

Describe alkalosis

A

ATPase speeds up
More potassium into cells
Hypokalaemia

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10
Q

How is ATPase usually regulated in the red blood cells?

A

Catecholamines (e.g. Adrenaline)

Insulin

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11
Q

How is ATPase usually regulated in the kidney?

A

Mineralocorticoid activity:
Aldosterone
(Cortisol)

Diuretics:
Spironolactone
Amiloride

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12
Q

What are some of the common causes of potassium abnormalities?

A

Intake

Distribution

Loss/Retention:
Renal
Gut
Oral

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13
Q

What are the clinical features of hyperkalaemia?

A
Spurious (common):
Haemolysis – release from cells
Delay – release from cells
EDTA contamination – direct from K+ salt of EDTA
Drip arm – K+ drip
Mineralocorticoid deficiency – decreased Na+  K+/H+ exchange:
Addison’s disease
RTA IV (hyporeninaemic hypoaldosteronism)

Acidosis – Distribution:
Diabetic ketoacidosis
Lactic acidosis
Chronic respiratory acidosis

Hypoxia & related – ineffective pumps:
Hypoxia
Renal failure

Potassium sparing diuretics:
Spironolactone – aldosterone inhibitor
Amiloride - Na+  K+/H+ pump inhibitor

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14
Q

What are the clinical features of hypokalaemia?

A
Mineralocorticoid excess – increased Na+  K+/H+ exchange:
Conn’s syndrome
Cushing’s syndrome
Licorice
Secondary hyperaldosteronism

Increased cellular uptake:
Insulin excess
Alkalosis: plus increased renal loss
Increased catecholamines

Renal tubular acidosis (RTA):
Type I – H+ excretion impaired
Type II – HCO3- reabsorption impaired

Excess Na+ for exchange:
Prolonged saline infusion – more Na+ to reabsorb in exchange for K+
Loop/thiazide diuretics – inhibit Na reabsorption earlier in tubule

Extra-renal causes – may also cause secondary hyperadosteronism due to fluid loss:
Diarrhoea
Laxative abuse
GI infection
Prolonged vomiting
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15
Q

How do you avoid leaky red cells giving a spurious potassium result in the lab?

A

Check using heparinised sample & arrange for rapid analysis by the laboratory.

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16
Q

Why is magnesium important in electrolyte balance?

A

Mg is essential for K+ reabsorption in the kidney & for normal intracellular distribution of K+
Decreased Mg is often associated with hypocalcaemia as it is a co-factor for PTH release