Sodium and Potassium balance Flashcards
Normal sodium range
135-145
Action of ADH
Act on V2 receoptors in collecting ducts
Increase AQA 2- causing more water to be reabsorbed
What stimulates ADH release
High osmolarity - hypothalamic osmoreceptors
Low blood pressure- baroreceptors
Cause of hypovolaemia hyponatraemia
Diuretics
D and V
Urine- low Na
Cause of euvolaemia hyponatraemia
Hypothyroidism- reduced contractility
Adrenal insufficiency- less aldosterone- less Na reabsorption
SIADH
Cause of hypervolaemic hyponatraemia
Cardiac failure
Liver cirrhosis- excess NO- low BP- ADH release
Renal failure
Investigations if a patient demonstrated euvolaemia and low Na
TFT
Short synthACTHen
Plasma and urine osmolarity- SIADH- low plasma and high urine
Signs of fluid overload
Raised JVP
Oedema
Bi-basal crackles
Signs of fluid depletion
Tachy
Dry mucous membranes
Reduced urine output
Reduced skin turgor
What is the most reliable test for knowing if patient is hypovolemic
Urine Sodium
Diagnosis of SIADH
o No hypovolaemia (euvolaemia)
o No hypothyroidism
o No adrenal insufficiency
o Reduced plasma osmolality (resorbing lots of water) AND
o Increased urine osmolality (>100) (concentrating the urine) – need to know this ref range
Management of hypovolemic patient with hyponatraemia
Volume replacement with 0.9% saline
Management of euvolaemic patient with hyponatraemia
Fluid restrict (<750ml/day + ABx infusions) + treat underlying cause
Management of hypervolemic patient with hyponatraemia
Fluid restrict (<750ml/day + ABx infusions) + treat underlying cause
Symptoms of severe hyponatraemia
o Reduced GCS
o Seizures
<120
Management of severe hyponatraemia
o Seek expert help – treat with hypertonic 3% saline
What happens if you correct sodium too quickly
No greater correction than 8-10mmol/L in the first 24 hours)
o Risk of osmotic demyelination – Central Pontine Myelinolysis / Osmotic Demyelination Syndrome
o Signs/symptoms: Quadriplegia, dysarthria, dysphagia, seizures, coma, death
Drugs to treat SIADH
o Demeclocycline -induce nephrogenic diabetes insipidus - Reduces responsiveness of collecting tubule cells to ADH- Monitor U&Es as risk of nephrotoxicity
o Tolvaptan – V2 receptor antagonist
Main causes of Hypernatraemia
Increase in sodium
• Medical high intake (hypertonic saline, sodium bicarbonate)
• Dietary high intake (salty infant formula, high dietary salt)
• Conn’s syndrome (high aldosterone: renin ratio), BAH (high aldosterone: renin ratio)
• Renal artery stenosis (low GFR from RAS -low BP at JGA -high renin -high aldosterone)
• Cushing’s syndrome (overactivation of MR by cortisol aldosterone-like effect)
Loss of water: main determinant of hypernatraemia is WATER CONTROL (not salt)
• Renal losses:
o Osmotic diuresis
o Diabetes insipidus (less ADH action / release)
Investigations for patient with suspected diabetes insipidus:
o Serum glucose – exclude diabetes mellitus - osmotic diuresis
o Serum potassium – exclude hypokalaemia -nephrogenic DI
o Serum calcium – exclude hypercalcaemia - nephrogenic DI
o Plasma and urine osmolality – exclude hyperaldosteronism (high plasma osmolality, low urine osmolality)
o Water deprivation test (normal = concentrated urine, no ADH = carry on passing water – dilute urine)
Management of hypernatraemia
Fluid replacement- dextrose
If the patient is also hypovolemic, then 0.9% saline and 5% dextrose water
Normal potassium range
3.5-5.3 mmol/L
Normal urea range
2.5-6.7 mmol/L
Normal creatinine range
70-130 umol/L
Describe the RAAS
Renin is released from the JGA and acts on angiotensinogen (from liver) which is converted by ACE in the lung to ANGII
This causes release of aldosterone in the adrenals- this casques reabsorption of Na and K to move in the opposite direction
Cause of hyperkalaemia
o Renal impairment – reduced renal excretion
o Drugs – ACEi, ARBs, spironolactone
o Low aldosterone-Addison’s disease, T4 renal tubular acidosis (low renin, low aldosterone)
o Release from cells – rhabdomyolysis, acidosis
ECG changes with hyperkalaemia
Peak T waves
Broad QRS
Flat P waves
Prolonged PR
High K management
10ml of 10% Calcium Gluconate
10 U insulin
50ml 50% dextrose
Cause of hypokalaemia
GRRR
GI loss
Renal loss- hyperaldosteronism/Conns, thiazide and loop diuretics
Redistribution- Insulin, alkalosis- swap H from K
Rarer - low Mg (needed to correct K)
Hypokalaemia management
o [K+] = 3.0-3.5mmol/L
-Oral KCl 2 SandoK tablets, TDS, 48 hours
o [K+] = <3.0mmol/L
-IV KCl
-Maximum rate 10mmol/hour (rate >20mmol/hour irritate peripheral veins)
o Tx underlying cause (i.e. with spironolactone – a K+-sparing diuretic)
What can you suspect if persistent HTN despite maximal control
Measure aldosterone: renin ratio for Conn’s
