Potassium and Electrolytes Flashcards

1
Q

What is the normal range of potassium?

A

3.5-5.0

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2
Q

What are the two hormones involved in potassium regulation?

A

Angiotensin II

Aldosterone

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3
Q

Explain the RAS system

A

Angiotensinogen is converted by RENIN to angiotensin I

Angiotensin I is coverted by ACE to angiotensin II

Angiotensin II stimulates the adrenal to produce aldosterone

Aldosterone stimulates sodium and water retention and potassium excretion in the kidney

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4
Q

Where is angiotensinogen produced?

A

liver

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5
Q

where is renin produced?

A

juxtoglomerular apparatus

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6
Q

Where is Angiotensin II produced

A

lung

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7
Q

Where is ALDOSTERONE produced?

A

liver

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8
Q

Which two molecules stimulate aldosterone release?

A

Angiotensin II

K+

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9
Q

How does aldosterone work?

A

It binds to MC receptors
This stimulates transcription of ENaC (sodium) channels
More Na+ from the lumen is reabsorbed
The lumen becomes negative
Subsequently, K+ moves down electrochemical gradient into the lumen

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10
Q

What are the main causes of hyperkalamia?

A
REDUCED EXCRETION OF POTASSIUM
Reduced GFR from renal impairment 
Reduced renin activity (NSAIDs, T4RTN)
Drugs: ACE inhibitors, ARB, Aldosterone antagonists (spironolactone)
Addisons (so less. aldosterone)

EXTRACELLULAR SHIFT
Potassium release from cells (rhabdomyolysis, acidosis)

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11
Q

How does acidosis cause hyperkalaemia?

A

High H+ in plasma means cells try to take in Moree H+ ions to normalise pH

To maintain electroneutrality, K+ comes out of cels

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12
Q

What are examples of diseases causing reduced renin activity?

A

Type 4 tubular necrosis

NSAIDs

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13
Q

What is the main ECG change with hyperkalaemia?

A

Peaked T waves

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14
Q

What is the management of hyperkalaemia?

A

10mL 10% calcium glutinate — for K+ > 6.5 or any ECG changes

50mL 50% dextrose + 10 units of insulin

Nebulised salbutamol

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15
Q

What are causes of hypokalaemia?

A
GI loss (loss of K+ through GI tract) 
Renal loss (hyperaldosteronism: Conn's, Cushing's, osmotic duiuresis: Loop and thiazide diuretics) 
Redistribution into cells (insulin, beta agonists, alkalosis) 
Rare causes: renal tubular acidosis1&2, hypomagnaesaemia
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16
Q

What are clinical ft of hypokalaemia?

A

Muscle weakness
Cardiac arrhythmia
Polyuria, polydipsia

17
Q

How do you manage hypokalaemia?

A

If K: 3.0-3.5 give oral KCl (SANDO-K)

If K: <3: IV KCl (max 10mmol/L otherwise irritating to peripheral veins)

18
Q

what drug and syndrome block the triple transporter in the loop of henle, preventing Na, K, Cl reabsorption

A

Loop diuretics

Bartter syndrome

19
Q

Give an example of a loop diuretic

A

Furosemide

20
Q

What drug and syndrome block the Na/Cl channel in the loop of henle, causing more Na to reach the distal nephron > change in electrochemical gradient > more K+ loss ?

A

Gitelman syndrome

THiazide diuretic

21
Q

What stimuli cause aldosterone release

A

low sodium

high k+

22
Q

what investigations should you get for hyperkalaemia and why

A
  1. Repeat sample (check for spurious sample)
  2. CK for rhabdomyolysis
  3. Creatinine, Urea
  4. Cortisol, short synachten test (addisons)
23
Q

give an example of a loop diuretic

A

Furosemide

24
Q

Explain renal tubular acidosis 1&2(&3)

A

Defect in hydrogen ion secretion into renal tubules > cannot secrete H+ into tubule

So secretes K+ instead to balance change with Na+ > hypokalaemia with acidosis

T1,2,3 differ in terms of where in the tubule the defect is (1: distal, 2: proximal, 3: both)

25
Q

Explain renal tubular acidosis T4

A

defect is in adrenal

ACIDOSIS with HYPERKALAEMIA

26
Q

what blocks the triple transporter in the loop of henle, preventing reabsorption of Na, K+, Cl and thereby causing hypokalaemia

A

Bartter syndrome

Loop diuretics e.g. furosemide

27
Q

what blocks the NaCl channel in the kidney preventing Na+ reabsorption and thereby causing hyponatraemia

A

Thiazide diuretic

28
Q

How do you work out the anion gap

A

Na + K - Cl - HCO3

29
Q

What is a normal anion gap

A

18-20

30
Q

what does a high anion gap suggest

A

that there is some other form of toxins in the patient’s blood (ketones, lactic acid)

31
Q

what is a form of poisoning responsible for a high anion gap

A

ethylene glycol poisoning