CSIM 2.25 - ELECTROLYTE ABNORMALITIES SODIUM PROBLEMS Hyponatraemia1. Determine by plasma Na+ concentration: 135-144mmol/L2. Clinical features SymptomsSigns

none.headachenauseavomitingmuscle crampslethargydisorientationseizurecomacerebral oedemadeath

3. Aetiology a. Pseudohyponatraemia; Hyperglycemia, Hyperlipidaemia, Non-physiological osmolyteb. Sodium depletion; renal loss, diuretics, salt wasting nephropathy, hypoadrenalism, salt wasting, gut lossc. Excess water intake; dipsogenic DI, sodium-free, hypoosmolar, irrigant solutions, IV fluid therapyd. reduced renal free water clearance; cardiac failure, Nephrotic syndrome, hypothyroidism, hypoadrenalism, SIAD, NSIAD, hypovolaemia e. reduced renal free water clearance; hypovalaemia 4. CNS consequence of rapid Na+ correctiona. Clinical featuresi. 1-4d post change plasma Na+ ii. neurology quadriplegia opthalmoplegia pseudo-bulbar palsy comab. Pathologyi. de-myelination pontine extra-pontineii. necrosisHypernatremia 1. Too little water or too much salt. 2. Dehydration: the elderly, terminal illness, water loss > water intake. 3. Excess Na+ in IV therapy.

Potassium Problems Distal tubule is main control pointHypokalaemia 1. Presentation CardiovascularEndocrine & metabolic

abnormal electrocardiogram predisposition to digoxin toxicity atrial ventricular arrhythmias decreased insulin secretion carbohydrate intolerance growth retardation

NeuromuscularRenal & electrolyte

constipation/ileus bladder dysfunction weakness, cramps tetany paralysis myalgias rhabdomyolysis decreased GFR decreased renal blood flow renal concentrating defect chloride wasting metabolic alkalosis hypercalciuria phosphaturia dilation & vacuolization of proximal tubules medullary cyst formation interstitial nephritis

2. Causes Example of case Conns Syndrome3

1. GI Deficient intake GI losses; vomiting, diarrhoea, fistula, uretero-sigmoidostomy Renal Tubular disorders Renal tubular acidosis Laekaemia Liddles syndrome Varrters syndrome Gitelmans syndrome antibiotics Metabolic alkalosis Diuretics Mineralocorticoid/GC effects Cell shifts w/o depletion

Hyperkalaemia Presentation CardiovascularNeuromuscular

abnormal electrocardiogram atrial/ventricular arrhythmias pacemaker dysfunction parasthesias weakness paralysis

Endocrine & metabolicRenal & electrolyte

increased insulin secretion decreased renal NH4 production

Example of case Conns Syndrome Personal details; 34 History: tetany, paraesthesia & periodic weakness polyuria/dipsia Examination: mild hypertension Investigations: a. hypokalemic alkalosis, hypernatraemia, b. suppressed renin c. reduced free water excretiond. increased urine aldosterone Intervention Progress symptoms biochemistry; 10 days hypertension; 18 daysExample of case Barrters SYndrome 1. Increased Na+ delivery to distal control point2. Featuresa. metabolic alkalosisb. hypokalaemiac. hypercalciuriad. elevated renine. elevated aldosteronef. normal BP3. Mechanisma. loss of functionb. NKCC2c. Clc Cl- channel4. Diagnosisa. high urine K+b. high urine Cl-c. high renind. hypercalciuria