Sodium and Potassium balance

Question 1

Normal sodium range

Answer 1

135-145

Question 2

Action of ADH

Answer 2

Act on V2 receoptors in collecting ducts

Increase AQA 2- causing more water to be reabsorbed

Question 3

What stimulates ADH release

Answer 3

High osmolarity - hypothalamic osmoreceptors

Low blood pressure- baroreceptors

Question 4

Cause of hypovolaemia hyponatraemia

Answer 4

Diuretics
D and V

Urine- low Na

Question 5

Cause of euvolaemia hyponatraemia

Answer 5

Hypothyroidism- reduced contractility
Adrenal insufficiency- less aldosterone- less Na reabsorption
SIADH

Question 6

Cause of hypervolaemic hyponatraemia

Answer 6

Cardiac failure
Liver cirrhosis- excess NO- low BP- ADH release
Renal failure

Question 7

Investigations if a patient demonstrated euvolaemia and low Na

Answer 7

TFT
Short synthACTHen
Plasma and urine osmolarity- SIADH- low plasma and high urine

Question 8

Signs of fluid overload

Answer 8

Raised JVP
Oedema
Bi-basal crackles

Question 9

Signs of fluid depletion

Answer 9

Tachy
Dry mucous membranes
Reduced urine output
Reduced skin turgor

Question 10

What is the most reliable test for knowing if patient is hypovolemic

Answer 10

Urine Sodium

Question 11

Diagnosis of SIADH

Answer 11

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

Question 12

Management of hypovolemic patient with hyponatraemia

Answer 12

Volume replacement with 0.9% saline

Question 13

Management of euvolaemic patient with hyponatraemia

Answer 13

Fluid restrict (<750ml/day + ABx infusions) + treat underlying cause

Question 14

Management of hypervolemic patient with hyponatraemia

Answer 14

Fluid restrict (<750ml/day + ABx infusions) + treat underlying cause

Question 15

Symptoms of severe hyponatraemia

Answer 15

o Reduced GCS
o Seizures

<120

Question 16

Management of severe hyponatraemia

Answer 16

o Seek expert help – treat with hypertonic 3% saline

Question 17

What happens if you correct sodium too quickly

Answer 17

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

Question 18

Drugs to treat SIADH

Answer 18

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

Question 19

Main causes of Hypernatraemia

Answer 19

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)

Question 20

Investigations for patient with suspected diabetes insipidus:

Answer 20

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)

Question 21

Management of hypernatraemia

Answer 21

Fluid replacement- dextrose

If the patient is also hypovolemic, then 0.9% saline and 5% dextrose water

Question 22

Normal potassium range

Answer 22

3.5-5.3 mmol/L

Question 23

Normal urea range

Answer 23

2.5-6.7 mmol/L

Question 24

Normal creatinine range

Answer 24

70-130 umol/L

Question 25

Describe the RAAS

Answer 25

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

Question 26

Cause of hyperkalaemia

Answer 26

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

Question 27

ECG changes with hyperkalaemia

Answer 27

Peak T waves
Broad QRS
Flat P waves
Prolonged PR

Question 28

High K management

Answer 28

10ml of 10% Calcium Gluconate
10 U insulin
50ml 50% dextrose

Question 29

Cause of hypokalaemia

Answer 29

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)

Question 30

Hypokalaemia management

Answer 30

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)

Question 31

What can you suspect if persistent HTN despite maximal control

Answer 31

Measure aldosterone: renin ratio for Conn’s