Potassium

Question 1

Where does the majority of K reside?

Answer 1

In the intracellular fluid

Question 2

How is the K conc retained?

Answer 2

Regulated using the sodium-potassium exchange pump. Where 3 sodium ions from the ICF are exchanged for 2 potassium ions using ATP hydrolysis to exchange the two. Working against the conc gradient.

Question 3

Match term with appropriate serum conc of calcium

1. Hyperkalaemia
2. Hypokalaemia
3. Physiological range

A. >2.5 mmol/L
B. 3.5-5.3mmol/L
C. >6.5mmol/L

Answer 3

1. C
2. A
3. B

Question 4

When does potassium shift into the ICF?

Answer 4

Via the actions of insulin, beta agonists and during alkalosis (H+ enters the ICF and K+ enters ECF to maintain electron neutrality- DCT)

Question 5

When does potassium shift into the ECF?

Answer 5

Whereas potassium will shift out of the ICF during cell lysis, exercise, hypertonicity, alpha-agonists and during acidosis.

Question 6

What cells control the renal absorption of K?

Answer 6

principal cells

Question 7

What hormone can regulate potassium reabsorption? and whats the purpose?

Answer 7

Aldosterone acts to increase tubular reabsororption of K to increase BP

Question 8

Whats the role of the RAAS axis?

Answer 8

Important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure

Question 9

Briefly describe RAAS actions

Answer 9

Liver releases angiotensinogen in response to blood pressure dropping. A decrease in renal perfusion causes kidney to release renin. Renin cleaves angiotensiogen to angiotenisn I.. Angiotensin I is then further cleaved by ACE to make angiotensin II. The angiotensin II has a range of effector functions, such as increasing sympathetic function, increase tubular reabsorption, arteriolar vasoconstriction (increase BP), or increase H2O reabsorption in the collecting duct.

Question 10

What lab investigations are available to investigate the K homeostasis?

Answer 10

Investigation can be done by measuring sodium, urea & creatinine, magnesium, calcium and phosphate, glucose, bicarbonate, blood gases and urine potassium.

Question 11

What systems are affected by decreased potassium?

Answer 11

Changes to cardiovascular, neuromuscular, neuropsychiatric, renal and Gi systems.

Question 12

How does hypokalamaemia manifest in the ECG?

1. Decreased QST segment
2. Depressed ST
3. Inverted T waves
4. Depressed U waves
5. Prominent U waves

Answer 12

2,3,5

Question 13

Hypokalamaemia symptoms specific to renal

Answer 13

polyuria and sodium retention

Question 14

What is the goal of managing hypokalaemia?

Answer 14

Ensuring the minimal 40mmol/day is accounted for

Question 15

True or false. If the K is >2.5mmol/L then use IV K+ in normal saline, whilst <2.5mmol/L should use oral IV.

Answer 15

False. >2.5mmol/L use oral and if its <2.5mmol/L then use IV K+ in normal saline.

Question 16

What are some important treatment cautions? (hypokalaemia)

Answer 16

The replacement should occur slowly under 48/72 hr replacement, with regular K+ checks. Higher rates may be given in an ITU setting with cardiac monitoring

Question 17

What are some broad causes of hypokalaemia?

Answer 17

In vivo or In vitro redistribution or true deficit.

Question 18

What is the first step in investigating true deficit and what does it inidcate? hypokalaemia

Answer 18

Urine K+ measured
<10mmol/L means the cause is extra renal. Acid base balance needs to be assessed. There are some causes in normal acid:base and in metabolic acidosis.
If urine K>10mmol/L then its renal losses, e.g. metabolic acidois or alkalosis or variable acid base

Question 19

In hypokalameamia caused by renal loss due to metabolic alkalosis, what is the next step in investigation?

Answer 19

Urine chloride

Question 20

What are two syndrome associated with hypokalaemia?

Answer 20

Bartters and Gitelmans

Question 21

What causes Bartters and what does it result in?

Answer 21

Due to mutations in genes encoding proteins that transport ions across renal cells in the thick ascending limb of the nephron. This causes hyper-reninaemic hyper-aldosteronism. Presents with increased blood pH and normal to low BP. Polyuria and polydipsia is also common.

Question 22

What causes Gitelmans and what does it result in?

Answer 22

caused by inactivating mutations in the SLC12A3 gene resulting in a loss of function of the encoded thiazide-sensitive sodium chloride co-transporter (NCCT). This cell membrane protein participates in the control of ion homeostasis at the distal convoluted tubule portion of the nephron (reabsorbs one sodium for one chloride). Will present with high blood pH, low Cl,K,Mg, and decreased sodium excretion

Question 23

What are these conditions?

1. Familial hypokalaemic periodic paralysis
2. hypokalaemic periodic paralysis with thyrotoxicosis

Answer 23

These are autosomal dominant conditions affecting the muscles due to the redistribution of K+ from the ECF into the ICF
FHH is a mutation in skeletal muscle voltage-gated calcium channel. Both conditions manifest with flaccid paralysis of limbs and trunk. As well as cardiac arrythmias.

Question 24

What are some signs and symptoms of hyperkalaemia?

Answer 24

changes to cardiovascular, renal and neuromuscular systems

Question 25

Describe the ECG changes associated with hyperkalaemia

Answer 25

Tall T waves, prolonged PR intervals, flat P waves and the widening of QRS complex.

Question 26

Name 3 causes of hyperkalaemia

Answer 26

Redistribution, increased intake, decreased output and syndromes of hypoaldosteronims

Question 27

In investigating the cause of hyperkalaemia what is the first step?

Answer 27

To rule out pseudohyperkalamia, which can occur due to EDTA contamination (contaminate serum tube causing high K and undetectable Ca), IV contamination or in vitro redistribution

Question 28

What redistributions cause hyperkalaemia?

Answer 28

Due to acidosis, insulin deficiency with high glucose, drugs (beta blockers), acute tissue damage (hypoxia, tumour lysis) or hyperkalaemic periodic paralysis.

Question 29

How does hypoaldosteronims cause hyperkalaemia?

Answer 29

In simple aldosterone acts to excrete K+ into the DCT lumen. With decreased aldosterone we can retian more K+.

Question 30

What drugs can induce hyperkalaemia?

Answer 30

Drugs that reduce aldosterone secreiton (NSAID, ACEi), block aldosterone binding to receptor (spirolactone), inhibit activity of epithelial sodium (potassium sparing diuretics), alter transmembrane K+ movement (beta blockers)

Question 31

What lab investigations are done for hyperkalaemic cases?

Answer 31

1. The spurious (pseduohyperkalaemic) cases need to be excluded by looking at time/date (delayed separation)/storage/WCC/platelets/Ca/ and EDTA contamination. 2. The renal function can be assessed by calculating the eGFR. 3. Assessment of acid-base status as well as glucose 4. Consider the patients drug intake and cortisol levels 5. Renin & aldosterone levels need to be checked a. With caution. High potassium will stimulate aldosterone but suppresses the renin (blocking the axis by negative feedback), note as eGFR falls the aldosterone increases and renin decreases.

Question 32

What is hyperkalaemic periodic paralysis?

Answer 32

This is an autosomal dominant disorder with a K+ of 8mmol/L. Caused by mutation occurs in skeletal muscle voltage-gated sodium channel X-subunit. It can be investigated using an ECG showing tall T waves, but cardiac arrhythmias are rare. This condition can be managed by salbutamol inhalers (a beta-adrenergic agonists) to induce rebalance.

Question 33

What is the first step to managing hyperkalaemia?

Answer 33

To protect the heart by stabilising the myocardium using clacium gluconate or chloride, and ECG.

Question 34

What rate should calcium gluconate or chloride be administered? 1. 10ml of 10% over 10min intervals till ECG improves 2. 10ml of 25% over 30min intervals till ECG improves

Answer 34

1.10ml of 10% over 10min intervals till ECG improves

Question 35

How is the redistribution in hyperkalaemia assessed/treated?

Answer 35

using salbutamol (10-20mg) or using insulin + glucose (10 units of insulin in 25g glucose). In insulin + glucose, if K+ remains high a continuous infusion of insulin and glucose may be required.

Question 36

How can clinicians increase K+ excretion

Answer 36

sing haemodialysis or using calcium resonium (mild/moderate). The calcium resonium should be given four times a day (15g), but in enema 30g in 100ml may be given to asymptomatic hyperkalaemia. May take a couple of days to take effect. HD is required in persistent hyperkalaemia (>7mmol/L), severe or worsening metabolic acidosis (pH<7.2).

Question 37

Reducing intake load can be achieved by....

Answer 37

discontinue prescriptions and stopping K+ supplements, ACEi, or K-sparing diuretics