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4 - Y5 a Path lectures 2021/22 > ChemPath 4: Potassium and Electrolytes > Flashcards

ChemPath 4: Potassium and Electrolytes Flashcards

1
Q

What is the Normal Value of sodium?

A

135-145 mmol/L

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2
Q

What is the Normal Value of potassium?

A

3.5-5.3 mmol/L

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3
Q

What is the Normal Value of urea?

A

2.5-6.7 mmol/L

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4
Q

What is the Normal Value of creatinine?

A
  • 70-100 micromol/L
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5
Q

What is the Normal Value of Hb?

A
  • Men: 130-180 g/L; Women: 115-160 g/L
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6
Q

What is the Normal Value of WBCs?

A
  • 4-11 x109 cells/L
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7
Q

What is the normal value of platelets?

A
  • 150-400 x109 cells/L
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8
Q

What is the most abundant intracellular cation?

A

Potassium

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9
Q

What is the most abundant extracellular cation?

A

Sodium

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10
Q

What is the Potassium plasma/serum concentration?

A

3.5-5.3 mmol/L

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11
Q

How is potassium regulated?

A
  • Loss through the GI tract
  • Renal regulation and secretion:
    • Angiotensin II
    • Aldosterone
  • Movement from intracellular to extracellular
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12
Q

Which cells does aldosterone act on?

A

principal cells of the cortical collecting tube

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13
Q

Describe the renin-angiotensin-aldosterone system

A
  • 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)
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14
Q

What does aldosterone bind to?

A

• Aldosterone binds to MR steroid receptor…

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15
Q

What happens once aldosterone binds to the MR steroid receptor?

A

(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)
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16
Q

What is the overall action of aldosterone?

A

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)

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17
Q

What are the 2 stimuli for aldosterone secretion?

A
  • Angiotensin II
  • Potassium (high)
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18
Q

What are the causes of hyperkalaemia?

A
  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)
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19
Q

When is potassium released from cells?

A
  • 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)
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20
Q

What are the MAIN causes of hyperkalaemia?

A
  • 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
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21
Q

What are the ECG changes associated with hyperkalaemia?

A
  • Peaked T wave (early) - ‘tall, tented T waves’
  • Broad QRS
  • Flat P-wave
  • Prolonged PR (and bradycardia)
  • Sine wave (latest)
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22
Q

What is the management of hyperkalaemia?

A
  • 10mL 10% Calcium Gluconate (stabilise)
  • 50mL 50% Dextrose (*drive K+ into cells)
  • 10U Insulin*
  • Nebulised salbutamol*
  • Tx underlying cause
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23
Q

What are the causes of hypokalaemia?

A
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24
Q

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

A
  • 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
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25
Q

What are the clinical features of hypokalaemia?

A
  • Muscle weakness
  • Cardiacarrhythmias (ECG = ST depression, flat T-waves, U waves)
  • Polyuria and polydipsia (nephrogenic DI from low K+ or a high Ca2+)
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26
Q

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

A

Conn’s syndrome

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27
Q

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

A

Aldosterone: Renin ratio

28
Q

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

A
  • HIGH aldosterone: renin ratio
  • because aldosterone suppresses renin
29
Q

What is the management of Hypokalaemia?

A
30
Q

Hyperkalaemia is a side-effect of which of the following drugs?

  • Furosemide
  • Bendroflumethiazide
  • Salbutamol
  • Ramipril
A
31
Q

Hypokalaemia is a side-effect of which of the following drugs?

  • Spironolactone
  • Indomethacin
  • Perindopril
  • Furosemide
A
32
Q

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

A
  • RTA T1 – ‘classic’ distal RTA
  • RTA T2 – ‘proximal’ distal RTA
  • RTA T4 – hypoaldosteronism
33
Q

What are the electrolyte disturbances seen in RTA T1?

A
34
Q

What are the electrolyte disturbances seen in RTA T2?

A
35
Q

What are the electrolyte disturbances seen in RTA T4?

A
36
Q

Summarise the 3 types of renal tubular acidosis (RTA)

A
37
Q

What would clinical assessment of this patient find?

A

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

38
Q

By which processes did this patient become hypovolaemic?

A
  • Dehydration → lose Na+ AND H2O
  • Body resorbs H2O (no Na+) with ADH release
  • ADH binds to V2 → AQA2 insertion
39
Q

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

A
40
Q

How does hypovolaemic hyponatraemia occur?

A
41
Q

What is the management of this patient?

A
42
Q

What is this patient’s underlying condition?

A

Congestive heart failure

43
Q

How might Congestive heart failure cause hyponatraemia?

A

CCF → low BP → detected by baroreceptors → ADH release

44
Q

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

A

hypervolaemia

45
Q

What is the Tx for this patient?

A

o Fluid restrict to 1L or 1.5L

o Tx underlying cause

46
Q

What electrolyte imbalances does this patient have?

A

Hyponatraemia and hypervolaemia

47
Q

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

A

Liver failure (cirrhosis → NO release, BP down, ADH)

→ portal HTN

→ clinical features of splenomegaly and spider naevi

48
Q

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

A

hypervolaemia → cirrhosis

49
Q

What is the Mx of this patient?

A
  • Fluid restriction
  • Tx underlying cause
50
Q
  1. What is the electrolyte disturbance in this patient?
  2. What will be found on clinical assessment of this patient?
A
  1. Hyponatraemia, low creatine
  2. Euvolaemia
51
Q

What are the main differentials for this patient?

A

?hypothyroidism → do TFTs

52
Q

What is the Mx of this patient?

A

thyroxine replacement

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

53
Q
  1. What is the electrolyte abnormality in this patient?
  2. What will be found on clinical assessment of this patient?
A
  1. Hyponatraemia, hyperkalaemia, high urea and creatine
  2. Euvolaemia
54
Q

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

A

?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)

55
Q

What is the Mx of this patient?

A

hydrocortisone (steroid) and fludrocortisone (mineralocorticoid)

56
Q
  1. What is the electrolyte abnormality in this patient?
  2. What is found on clinical assessment of this patient?
A
  1. hyponatraemia, high urea
  2. euvolaemia
57
Q

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

A

?SIADH (small cell lung cancer)

→ plasma and urine osmolarity

58
Q

How is SIADH diagnosed?

A

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

59
Q

What are the causes of SIADH?

A
60
Q

What electrolyte abnormality is seen here?

A

Hypernatraemia

61
Q

What are the Causes of hypernatraemia?

A
62
Q

What are the Suspected diabetes insipidus investigations?

A
63
Q

What electrolyte abnormality is seen here?

A

hyperkalaemia

64
Q

What are the Conditions predisposing to hyperkalaemia?

A
65
Q

What electrolyte abnormality is seen here?

A

Hypokalaemia

66
Q

What are the Ix for this patient?

A

Persistent HTN despite maximal HTN control → aldosterone: renin ratio (? Conn’s)

Aldosterone drives sodium resorption (Na+/K+ exchanger in CD) → hypernatraemia (and subsequent HTN)

4 - Y5 a Path lectures 2021/22 (37 decks)

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