Sodium

Hyponatraemia

This is a low concentration of plasma Na+. As the concentration depends on both sodium levels and water volume, hyponatreamia can either be due to a lack of sodium ions or too much water.

Causes:

The main way to distinguish the causes is first assessing if the patient is dehydrated or full of water.

– If dehydrated, this suggests the primary problem is losing Na+ ions, and water indirectly follows as a result.

–> Kidney etiology – Addison’s disease or renal failure

–> Outside kidneys – Burns, diarrhea, small bowel obstruction

– If not dehydrated, this suggests that there is excessive relative water retention occurring, causing the plasma to become more diluted.

–> If patient has oedema (hypervolaemic), suggests kidney, liver, heart failure

–> If no oedema (euvolemic), either SIADH or water overload

Symptoms:

(Low osmolality will make the brain swell giving symptoms of raised ICP)

– Starts with anorexia, nausea and malaise

– Then get headache, confusion, low GCS and seizures

– Increased risk of falls in the elderly

Artefacts:

– Hyponatremia can occur if blood sample was taken from an arm with a drip

– If there are high levels of lipid/protein/glucose

– Iatrogenic hyponatremia ➔ if 5% glucose is infused IV without saline, glucose gets metabolized giving a hypotonic solution causing hyponatreamia. Can give cerebral oedema usually in young adults

Management

Correct underlying cause, never just treat Na+ concentration alone

– Fluid restriction and rehydration with saline 

Hypernatremia

This usually occurs due to water loss in excess of Na+ loss (high osmolality):

– DEHYDRATION –> vomit, burns

– DIABETES insipidus

– DOCTORS: incorrect IV fluid replacement (excessive saline)

Management:

If in coma –> glucose 5% IV slowly guided by fluid balance and sodium levels

– Again, be careful when correcting levels as quick correction can lead to cerebral oedema raising ICP 

Potassium

Hypokalaemia

This hyperpolarizes the cell and reduces the excitability of nerve and muscles, causing muscular weakness which leads to muscular paralysis and cardiac arrhythmias

Symptoms:

– Muscle weakness, with hypotonia and hyporeflexia (decreases excitability of nerve + muscle)

– Light-headedness – Arrhythmias + Palpitation – Constipation

Tests:

ECG shows small or inverted T waves, long PR interval + prominent U wave

– If person is on diuretics, raised HCO3- is best indicator that hypokalemia is long standing

Management:

– If mild, oral K+ supplement 

– If <2.5mM, IV KCl replacement with cardiac monitoring. (Max rate infusion = 10mM/hour)

Hyperkalaemia

This often due to renal failure where GFR drops below 20%

– Depolarises cells bringing them closer to threshold, increasing excitability of nerve and muscle and raising chances of cardiac arrhythmias.

Symptoms:

– Tachycardic irregular pulse,

– Palpitations, chest pain and light-headedness

Phosphate

Phosphate is key in making DNA, proteins and membranes – and is a key buffer for H+ ions in the body.

Hypophosphatemia

This is common and of little clinical significance unless very severe

Causes:

Vitamin D deficiency + primary hyperparathyroidism + inadequate intake + refeeding syndrome

Symptoms:

Muscle weakness/rhabdomyolysis, arrhythmias/cardiac arrest, white cell dysfunction

Treatment:

Oral phosphate supplementation

N.B. Never give IV phosphate to a patient who is hypercalcemic/hyperparathyroid (will give precipitates) 

Calcium

Management:

– If mild, give calcium 5mM/6h

– If severe, 10ml of 10% calcium gluconate

– If due to chronic kidney disease, treat with Vitamin D supplements, Alfacalcidol/Calcitriol

Hypercalcaemia

Most common reasons are malignancy (bone metastases, myeloma) and primary hyperparathyroidism.

– In the blood 40% of Ca2+ is bound to albumin, and the rest is free Ca2+

Symptoms:

– Bones –> Ectopic calcification (e.g. cornea) and bone pain

– Stones –> Renal stones and renal failure

– Groans –> Abdominal pain, vomiting, constipation

– Psychiatric Moans –> Confusion + irritability + Depression

– Other –> polyuria, polydipsia, weakness, fatigue (as it decreases excitability of nerve and muscle)

Investigations

– The main distinction to make is malignancy vs primary hyperparathyroidism

– Look at albumin first –> indicates whether it is due to dehydration (urea also raised) or just an artefact

– If albumin is normal, main determinant is PO43-

– If low, suggests hyperparathyroidism –> also gives high PTH

– If high, look at ALP –> raised ALP from bone turnover (bone metastases)

Hypomagnesaemia

Like hypocalcaemia this raises the excitability of nerve and muscle as there is less Ca2- reuptake into the SR

Causes:

– Drugs –> Loop and thiazide diuretics

– Poor supply –> Total parenteral nutrition

– Excessive loss –> diarrhea (natural or due to IBD)

– Secondary to low Ca2+, low K+ and low PO43-

Symptoms:

– Increased nerve and muscle excitability (tetany, seizures etc.), seizures, tetany, arrhythmias

– Secondary hypoparathyroidism –> as Mg is needed for PTH secretion

– Can exacerbate digoxin toxicity

Tests:

ECG resembles hypokalaemia (small or inverted T waves, long PR interval + prominent U wave)

Management:

– If <0.4mM –> IV replacement

– If >0.4mM, oral magnesium salts

Hypermagnesemia

Causes:

Renal Failure or iatrogenic (excessive antacids)

Symptoms:

(Weakness) neuromuscular depression, low BP, low pulse, CNS and respiratory depression

Management:

Rarely requires treatment unless very severe

Lipids

Raised cholesterol is a major risk factor for cardiovascular disease, which can be primary or secondary

(Primary) Familial hypercholesterolemia

This is a condition which is due to an autosomal dominant mutation in the LDL receptor

– Means that hepatocytes are unable to internalize LDLs, this raises the concentration in blood

– Should be suspected if cholesterol >7.5mM or cardiovascular events <60 years

Diagnosis:

– This involves measuring cholesterol/LDL level + 1 factor

– In adults, total cholesterol >7.5mM with LDL-C >4.9mM (Children > 6.7mM and LDL >4.0mM) +

– Tendon xanthoma in patients/relative or DNA evidence of FH

Management:

–Atorvastatin 80mg and referral to specialist clinic

N.B. For children if one parent affected, arrange test by age 10. If both parents affected, test by age 5.

(Secondary) Hypercholesterolemia

This can be due to nephrotic syndrome + cholestasis + hypothyroidism

– In these patients it is good to assess QRISK in these patients, this is a risk of CVD of 10% or more

Management:

– If QRISK > 10%, start atorvastatin 20mg 1st line

– If there is already established CVD, then atorvastatin 80mg is 1st line

If on statin, follow up patients every 3 months with full lipid profile ➔ can increase dose up to 80mg.

– Risk of congenital defects means that statins should be stopped in women 3 months before conception.