Electrolyte disturbances

Causes:

• hypovolaemic: loss of water from urine (salt wasting, diuretics, renal failure, adrenocortical insufficiency) or outside of urine (vomiting, diarrhoea, sweating, burns)
• euvolaemic: SIADH, psychogenic polydipsia, malnutrition, glucocorticoid insufficiency, severe hypothyroidism
• hypervolaemic: primary polydipsia, cirrhosis, renal failure, nephrotic syndrome, HF

Sx: headache, anorexia, N+V, lethargy, muscle cramps/weakness, confusion/altered consciousness, seizures, drowsiness, ataxia, signs of dehydration (if hypovolaemic), oedema/ ascites/raised JVP (if hypervolaemic)

Ix: determine fluid status, U+Es, urinary sodium, TFTs, ACTH stimulation/serum cortisol, CT head, CXR if considering HF

Mgmt: correct underlying cause if possible, hypertonic saline if severe (not too rapid as risk of osmotic demyelination)

Causes: inadequate water intake, diabetes insipidus, water loss (burns/sweating, GI losses, diuretics, acute tubular necrosis), iatrogenic (hypertonic saline/dialysis, tube feeding, IV drugs containing sodium), excessive salt intake, hyperaldosteronism

Sx: thirst, polydipsia, polyuria, CNS dysfunction (confusion, seizures, lethargy, weakness), signs of dehydration

Ix: glucose, U+Es, lithium levels where appropriate (increased risk of lithium toxicity), urinary sodium, serum osmolality, neuroimaging where appropriate

Mgmt: treat underlying disorder if possible, correct dehydration, assess severity

Causes:

• increased loss: thiazide/loop diuretics, renal tubular acidosis, hypomagnesaemia, tubulo-interstitial disease, D+V, burns, erythroderma, sweating (XS, CF)
• transcellular shift: alkalosis, insulin, beta2 agonists, hypothermia
• decreased intake: malnitrition, inadequate IV replacement
• other: chronic alcoholism, chronic peritoneal dialysis, plasmapheresis

Sx: may be asymptomatic, muscle weakness/pain (leads to resp failure), constipation, ileus, paraesthesia, ARRHYTHMIAS

Ix: ECG (flattened T waves, ST depression, U waves), U+Es, other electrolytes, glucose

Mgmt: potassium replacement (KCl) with careful monitoring

Causes:

• renal: AKI, CKD, potassium sparing diuretics, mineralocorticoid deficiency, drugs that interfere with renin-angiotensin system (ACEIs, ARBs, NSAIDs, heparin)
• increased circulation of potassium: exogenous (supplements), endogenous (tumour lysis syndrome, rhabdomyolysis, trauma, burns)
• shift from intra to extracellular: acidosis, medications (digoxin, theophylline, beta-blockade)

Sx: nonspecific, weakness, fatigue, palpitations/chest pain, bradycardia, depressed/absent reflexes

Ix: U+Es, other electrolytes, FBC (suggestive of haemolysis), glucose, ABG (metabolic acidosis), ECG (tall tented T waves)

Mgmt: ABCDE, stop further potassium accumulation, 10ml 10% calcium gluconate, insulin-glucose infusion

AKA primary hyperaldosteronism

Sx: HTN, hypokalaemia, alkalosis (elevated bicarbonate), high aldosterone, suppressed renin, (hypernatraemia), may have polyuria + polydipsia, may have weakness, lethargy and headache due to electrolyte disturbance

Causes: adenoma, bilateral adrenal hyperplasia

Ix: BP (check control, often treatment resistant), U+Es, check renin (low in primary causes), check aldosterone, ECG, CT/MRI (CT is 1st line but MRI is more sensitive), adrenal vein sampling (gold standard)

Thiazide-like defect in DCT Na/Cl transporter

Autosomal recessive, most common renal tubular disorder in Caucasians

Characterised by: hypokalaemia, metabolic alkalosis, hypomagnesaemia, hypocalciuria, causes secondary hyperaldosteronism (with high renin), normal BP

Mostly onset of Sx in adulthood: transient muscle weakness and tetany, abdominal pain, chondrocalcinosis. 50% have prolonged QT interval

Group of autosomal recessive disorders affecting loop of Henle

Characterised by: metabolic acidosis, hypokalaemia, salt wasting, hypercalciuria

Usually present >5yrs old with vascular volume depletion, polyuria and polydipsia

Normocalcaemia and normomagnesaemia

Causes:

• drug induced: thiazide diuretics, SSRIs, carbamazepine, TCAs, cyclophosphamide, opiates, vincristine, NSAIDs, PPIs
• CNS: inflammatory, tumour, infection
• tumour-associated: SCLC
• chest disease: structural, infection

Dx: hyponatraemia, serum osmolality <275mOsmol/kg, urine osmolality >100mOsmol/kg, urine Na >30mmol/L, no recent diuretic use, absence of hypotension/hypovolaemia/non-osmotic AVP release/oedema/adrenal, thyroid and renal insufficiency

Most common metabolic disturbance/emergency in malignancy. 

Sx: thirst, polyuria, renal stones, muscle pain/weakness, bone pain, depression, confusion, anorexia, vomiting, constipation

Causes: primary hyperparathyroidism, humoral hypercalcaemia of malignancy (PTHrP-related), bone disease (diffuse, bony mets), myeloma, drugs, vitamin D intoxication, sarcoidosis, renal failure, hyperthyroidism, Addison's disease, phaeochromocytoma

Mgmt: baseline PTH (1st presentation), IV saline (dehydration), bisphosphonates

Common malignancies for bony mets: lung, breast, prostate. High risk of pathological fractures, often have bone pain

Common malignancies for HHM: lung, breast, oesophagus, gynaecological, skin, myeloma, renal, bladder

Causes: low vitamin D, hypoparathyroidism, drugs (phosphate, chemotherapy, bisphosphonates), contrast, renal failure, acute illness (pancreatitis, rhabdomyolysis)

Symptoms: paraesthesias, muscular twitching, leg cramps, stridor, tetany, seizures, Trousseau's sign (wrist flexion with BP cuff), Chvostek's sign (facial twitching), papilloedema, hyperreflexia, prolonged QT interval

Causes: benign solitary parathyroid adenoma (85%), 4-gland parathyroid hyperplasia (15%), carcinoma (<1%)

Prevalence 1:1000, F>M, peak age 50-70yrs

Biochemistry: hypercalcaemia, hypophosphataemia, raised/normal PTH, elevated ALP, elevated/normal urinary calcium, mild hyperchloraemic metabolic acidosis

Complications: renal stones, renal impairment, pathological fractures, osteoporosis, brown tumours of bone, ?HTN

Mgmt: exploratory neck surgery (if symptoms/complications), conservative mgmt (only if asymptomatic), calcimimetic drugs (calcium receptor agonists) e.g. cinacalcet

Causes: post-surgical (thyroidectomy), congenital absence of parathyroid glands, autoimmune (with candidiasis and Addison's), reset PTH setpoint, peripheral PTH resistance (pseudohypoparathyroidism), infiltration, defective PTH molecule

Biochemistry: hypocalcaemia, hyperphosphataemia, low/undetectable circulating PTH, ormal renal function, hypocalciuria