ChemPath 4: Potassium and Electrolytes

Question 1

What is the Normal Value of sodium?

Answer 1

135-145 mmol/L

Question 2

What is the Normal Value of potassium?

Answer 2

3.5-5.3 mmol/L

Question 3

What is the Normal Value of urea?

Answer 3

2.5-6.7 mmol/L

Question 4

What is the Normal Value of creatinine?

Answer 4

• 70-100 micromol/L

Question 5

What is the Normal Value of Hb?

Answer 5

• Men: 130-180 g/L; Women: 115-160 g/L

Question 6

What is the Normal Value of WBCs?

Answer 6

• 4-11 x10⁹ cells/L

Question 7

What is the normal value of platelets?

Answer 7

• 150-400 x10⁹ cells/L

Question 8

What is the most abundant intracellular cation?

Answer 8

Potassium

Question 9

What is the most abundant extracellular cation?

Answer 9

Sodium

Question 10

What is the Potassium plasma/serum concentration?

Answer 10

3.5-5.3 mmol/L

Question 11

How is potassium regulated?

Answer 11

• Loss through the GI tract
• Renal regulation and secretion:
  
  • Angiotensin II
  • Aldosterone
• Movement from intracellular to extracellular

Question 12

Which cells does aldosterone act on?

Answer 12

principal cells of the cortical collecting tube

Question 13

Describe the renin-angiotensin-aldosterone system

Answer 13

• Angiotensinogen → Ang-1 [LIVER via renin from JGA]; renin release via…
  
  • Low BP (inrenalartery)
  • Low Na+ in macula dense by JGA
  • SNS beta-1 receptor activation
• Ang-1 → Ang-2 [LUNGS via ACE]
• Ang-2 acts on the adrenals to release aldosterone
• Aldosterone excretes K+ and increases Na+ retention
• Trigger for aldosterone release:
  
  • Angiotensin II
  • Potassium (high)

Question 14

What does aldosterone bind to?

Answer 14

• Aldosterone binds to MR steroid receptor…

Question 15

What happens once aldosterone binds to the MR steroid receptor?

Answer 15

(1) ENaC creation (Na resorption)

• Na+resorption from urine occurs through ENaC (Epithelial Sodium Channels) to create a -ve electrical potential in the renal lumen
• This drives K+ secretion into renal lumen through ROMK (Renal Outer Medullary Potassium) channel

(2) ROMK creation (K excretion)

(3) ­ Sgk1 (Serum Glucocorticoid Kinase 1)

• increased Sgk1
• → reduced Nedd4 (less phosphorylation or Nedd4)
• → reduced degradation of ENaC (sodium channels)
• → same happens as (1)

Question 16

What is the overall action of aldosterone?

Answer 16

Aldosterone increases the number of open Na+ channels in renal luminal membrane

→ Na+ resorption from renal lumen (urine)

→ this makes the lumen electronegative and creates an electrical gradient

→ K+ is secreted into the renal lumen (urine)

Question 17

What are the 2 stimuli for aldosterone secretion?

Answer 17

• Angiotensin II
• Potassium (high)

Question 18

What are the causes of hyperkalaemia?

Answer 18

1. reduced GFR
2. reduced Renin
   
   1. T4 RTA (diabetic nephropathy)
   2. NSAIDs
3. ACE inhibitors
4. ARBs (Angiotensin 2 Receptor Blockers)
5. Addison’s disease
6. Aldosterone antagonists (i.e. spironolactone)

Question 19

When is potassium released from cells?

Answer 19

• Rhabdomyolysis
  
  • (muscle death release K+)
• Acidosis
  
  • H+ taken into cells (to stabilise the disturbance) → H+/K+ transporter is disrupted → K+ is excreted in response (to maintain membrane electronegativity)

Question 20

What are the MAIN causes of hyperkalaemia?

Answer 20

• Renal impairment – reduced renal excretion
• Drugs – ACEi, ARBs, spironolactone
• Low aldosterone
  
  • Addison’s disease
  • T4 renal tubular acidosis (low renin, low aldosterone)
• Release from cells – rhabdomyolysis, acidosis

Question 21

What are the ECG changes associated with hyperkalaemia?

Answer 21

• Peaked T wave (early) - ‘tall, tented T waves’
• Broad QRS
• Flat P-wave
• Prolonged PR (and bradycardia)
• Sine wave (latest)

Question 22

What is the management of hyperkalaemia?

Answer 22

• 10mL 10% Calcium Gluconate (stabilise)
• 50mL 50% Dextrose (*drive K+ into cells)
• 10U Insulin*
• Nebulised salbutamol*
• Tx underlying cause

Question 23

What are the causes of hypokalaemia?

Answer 23

Question 24

How does increased Na+ delivery to DCT *cause Osmotic diuresis?

Answer 24

• Triple- or co-transporter is blocked →. less Na+ is resorbed in the ascending LoH → more goes to the DCT
  
  • Triple= (furosemide)
  • Co-transporter= (bendroflumethiazide)
• More Na+ reaches and is absorbed in the DCT → a more electronegative nephron
• This results in loss of K+ down the electrochemical gradient through ROMK channels

Question 25

What are the clinical features of hypokalaemia?

Answer 25

* Muscle weakness * Cardiacarrhythmias (ECG = ST depression, flat T-waves, U waves) * Polyuria and polydipsia (nephrogenic DI from low K+ or a high Ca2+)

Question 26

What is the main differential you must rule out in a patient with reduced K+ and hypertension?

Answer 26

Conn's syndrome

Question 27

What is the screening test for a patient with reduced K+ and hypertension?

Answer 27

Aldosterone: Renin ratio

Question 28

What happens to the Aldosterone: Renin ratio in Conn's?

Answer 28

* **HIGH aldosterone: renin ratio** * because aldosterone suppresses renin

Question 29

What is the management of Hypokalaemia?

Answer 29

Question 30

Hyperkalaemia is a side-effect of which of the following drugs? * Furosemide * Bendroflumethiazide * Salbutamol * Ramipril

Answer 30

Question 31

Hypokalaemia is a side-effect of which of the following drugs? * Spironolactone * Indomethacin * Perindopril * Furosemide

Answer 31

Question 32

What are the types of renal tubular acidosis (RTA)?

Answer 32

* **RTA T1** – ‘classic’ distal RTA * **RTA T2** – ‘proximal’ distal RTA * **RTA T4** – hypoaldosteronism

Question 33

What are the electrolyte disturbances seen in RTA T1?

Answer 33

Question 34

What are the electrolyte disturbances seen in RTA T2?

Answer 34

Question 35

What are the electrolyte disturbances seen in RTA T4?

Answer 35

Question 36

Summarise the 3 types of renal tubular acidosis (RTA)

Answer 36

Question 37

What would clinical assessment of this patient find?

Answer 37

Clinical assessment = **Hypovolaemic** (D&V and a diuretic)

Question 38

By which processes did this patient become hypovolaemic?

Answer 38

* Dehydration → lose Na+ AND H2O * Body resorbs H2O (no Na+) with ADH release * ADH binds to V2 → AQA2 insertion

Question 39

What are the 3 different findings that can be found on clinical assessment of a hyponatraemic patient, and what are their causes?

Answer 39

Question 40

How does hypovolaemic hyponatraemia occur?

Answer 40

Question 41

What is the management of this patient?

Answer 41

Question 42

What is this patient's underlying condition?

Answer 42

Congestive heart failure

Question 43

How might Congestive heart failure cause hyponatraemia?

Answer 43

CCF → low BP → detected by baroreceptors → ADH release

Question 44

What else can congestive heart failure cause, apart from hyponatraemia ?

Answer 44

hypervolaemia

Question 45

What is the Tx for this patient?

Answer 45

o Fluid restrict to 1L or 1.5L o Tx underlying cause

Question 46

What electrolyte imbalances does this patient have?

Answer 46

Hyponatraemia and hypervolaemia

Question 47

How might liver failure cause signs such as spenomegaly and spider naevi?

Answer 47

Liver failure (cirrhosis → NO release, BP down, ADH) **→ portal HTN** → clinical features of splenomegaly and spider naevi

Question 48

What will be/has been found on clinical assessment of this patient?

Answer 48

hypervolaemia → cirrhosis

Question 49

What is the Mx of this patient?

Answer 49

* Fluid restriction * Tx underlying cause

Question 50

1. What is the electrolyte disturbance in this patient? 2. What will be found on clinical assessment of this patient?

Answer 50

1. Hyponatraemia, low creatine 2. Euvolaemia

Question 51

What are the main differentials for this patient?

Answer 51

?**hypothyroidism** → do TFTs

Question 52

What is the Mx of this patient?

Answer 52

**thyroxine replacement** (Na isn’t that low and so no need to replace – correcting T4 should be enough)

Question 53

1. What is the electrolyte abnormality in this patient? 2. What will be found on clinical assessment of this patient?

Answer 53

1. Hyponatraemia, hyperkalaemia, high urea and creatine 2. Euvolaemia

Question 54

What is the main differential for this patient? How is this investigated?

Answer 54

?**adrenal insufficiency** → short SynACTHen test (test cortisol normally and then administer synthetic ACTH and measure cortisol 30 minutes later. If minimal response, likely Addison’s)

Question 55

What is the Mx of this patient?

Answer 55

hydrocortisone (steroid) and fludrocortisone (mineralocorticoid)

Question 56

1. What is the electrolyte abnormality in this patient? 2. What is found on clinical assessment of this patient?

Answer 56

1. hyponatraemia, high urea 2. euvolaemia

Question 57

What is the main differential for this patient? How is this investigated?

Answer 57

?**SIADH** (small cell lung cancer) → plasma and urine osmolarity

Question 58

How is SIADH diagnosed?

Answer 58

o No hypovolaemia, no hypothyroidism, no adrenal insufficiency o Reduced plasma osmolarity AND increased urine osmolarity (\>100)

Question 59

What are the causes of SIADH?

Answer 59

Question 60

What electrolyte abnormality is seen here?

Answer 60

Hypernatraemia

Question 61

What are the Causes of hypernatraemia?

Answer 61

Question 62

What are the Suspected diabetes insipidus investigations**?**

Answer 62

Question 63

What electrolyte abnormality is seen here?

Answer 63

hyperkalaemia

Question 64

What are the Conditions predisposing to hyperkalaemia?

Answer 64

Question 65

What electrolyte abnormality is seen here?

Answer 65

Hypokalaemia

Question 66

What are the Ix for this patient?

Answer 66

Persistent HTN despite maximal HTN control → **aldosterone: renin ratio (? Conn’s**) *Aldosterone drives sodium resorption (Na+/K+ exchanger in CD) → hypernatraemia (and subsequent HTN)*