Biochemistry Potassium

Question 1

Intracellular Potassium

Answer 1

98% - 2940 mmol

Question 2

Extracellular

Answer 2

2% 60 mmol

Question 3

Plasma (extracellular)

Answer 3

0.5%-15 mmol (sampling this proportion)

Question 4

Transport out/into cells via

Answer 4

Na/K ATPase

Question 5

Potassium (plasma) maintains the

Answer 5

resting membrane potential

Question 6

Determine via

Answer 6

Potassium inside cells vs. extracellular

Question 7

Resting potential of

Answer 7

-70mV

Question 8

Disturbing potassium problem

Answer 8

Disturbs resting potential and therefore leading to the clinical symptoms of hypo or hyper

Question 9

The Na+ and K+ gradients are maintained by

Answer 9

by the sodium-potassium pump

Question 10

Intake

Answer 10

100 mmol per day

Question 11

Output

Answer 11

30 mmol/day
	Skin – 10 mmnol
	Faeces – 10 mmol
	Urine >10 mmol
Minimum loss – 7 mmoll/litre in urine

Question 12

Patient on IV fluids

Answer 12

The patient would start to build up a hypo as no input but still output therefore supplementing input with potassium however must be observed.

Question 13

Potassium – Renal Potassium Handling: Filtered

Answer 13

800 mmnol/day

Question 14

Potassium – Renal Potassium Handling: Reabsorption

Answer 14

100% in proximal nephron

Question 15

Potassium – Renal Potassium Handling: Secretion via

Answer 15

Controlled Na/K exchanger in distal convoluted tubule regulated by aldosterone – regulates potassium excretion to maintain potassium balance

Question 16

Potassium – Renal Potassium Handling: Urine potassium excretion depends on

Answer 16

• Availability of sodium for exchange –
• Plasma aldosterone concentration
• Relative intracellular [K+] and [H+]

Question 17

Potassium – Renal Potassium Handling: Output

Answer 17

• Input – other losses

Question 18

Potassium – Renal Potassium Handling: Availability of sodium for exchange

Answer 18

Cant excrete potassium unless exchanged for sodium. Acute renal failure – less potassium being filtrerd but the main factor is reduced filtration of sodium (most reabsorb in proximal nephron. Little sodium gets to distal tubule therefore limited capacity for potassium xcretion = severe hyperalaemia in acute kidney injury

Question 19

Metabolic acidosis:

Answer 19

Kidney is required to excrete more H+ - less capacity for K= excretion as H+ being excreted in lieu of potassium. Hyperkalaemia in these patients.

Question 20

Potassium depleted –

Answer 20

Hypokalaemia alkalosis With an increased plasma bicarb concentration.
→ Reduction in intracellular potassium. Less potassium needing to be excreted. Potassium depletion there is enhanced H+ loss.
Also bicarb generation produced.

Question 21

Catecholamine effect on potassium/hydrogen

Answer 21

Salbutamol to treat hyperkalaemia as it stimulates Potassium excretion.

Question 22

Insulin →

Answer 22

diabetic ketoacidosis: one effects after treatment (as normal high potassium with acidosis observed rapid reduction in plasma potassium.

Question 23

Re-feeding syndrome –

Answer 23

redistribution of electrolytes post starving and start eating. When carbohydrate delivered exaggerated insulin and catecholamines (stress) response and get redistribution of potassium magnesium etc.
→ If a patient has not had a normal diet for +10 days feeding must be at a low dose. Monitor carefully.

Question 24

Causes of Hypokalaemia

Answer 24

Renal Loss

Extra-renal loss

Question 25

Renal loss hypokalameia

Answer 25

Alkalosis – favours potassium loss in kidney.
Drugs – diuretics (thiazides and loop)
Mineralcorticoid excess
•	1o hyperaldosteronism
•	2o hyperaldosteronism
•	Cushing’s syndrome
•	Ectopic ACTH
Renal disease
•	Renal tubular acidosis
•	Interstitial nephritis
•	Polyuric ATH
Miscellaneous
•	Hypomagnesaemia
•	Hypercalcaemia

Question 26

Extra-renal loss hypokalaemia

Answer 26

GI loss
•	Diarrhoea
•	Villous adenoma (sigmoid)
•	Pancreatic fistula
EC to IC shift
•	Insulin
•	Catecholamines
•	Refeeding syndrome
Inadequate intake
•	Alcoholism
•	Anorexia nervosa

Question 27

Alkalosis

Answer 27

Reciprocal relation with potassium nd hydrogen
Alkalosis – favours potassium loss
Acidosis – inhibits potassium loss (getting rid of H+ ions)

Hypokalaemia – may causes alkalosis

Question 28

Diuretics

Answer 28

Most common cause
Block sodium reabsorption and therefore increased water loss.
Work in first half of nephron – causes increased delivery of sodium to distal nephron. So more sodium being reabsorb and encourages/enhances potassium/hydroden loss
→Hypokalaemia alkalosis

Question 29

Mineralcorticoid excess

Answer 29

Driving Sodium reabsorption
Hall mark of primary aldosteronism – hypokalaemia
Clinical picture → Resistant hypertension with low potassium (unless diuretics causing it) - suspicious for conn’s syndrome.

Question 30

Cushing’s

Answer 30

Excess cortisol – glucocorticoids. Sufficiently high levels of cortisol leading to cross reactivity.

Question 31

Ectopic ACTH

Answer 31

Stimulates adrenal gland.
Biochemical pattern just like conn’s syndrome. But aldostere is normal.
Treat people with a longtime
Case:28:00 mins re-listen.
→ Hypokalaemia alkalosis often with a relatively high sodium

Question 32

Renal tubular disease

Answer 32

Renal tubular acidosis → acidosis of renal tubular origin. The defect in the ability of the kidney to excrete hydrogen ions. Therefore the kidney favours potassium loss in exchange of sodium.
Proximal tubule dysfunction – loss of potassium as failure to reabsorb.

Question 33

Hypomagnesium

Answer 33

Magnesium is a vital cofactor with ATP. So with magnesium depletion ATP cant work and cant fuel pump/receptor mechanisms. Therefore if leakage of Potassium out of cells and leaking out of kidney because pumps not working.
Causes of low magnesium
 Gut → diarrhoea
 Renal tubular toxicity (platinum chemo drugs)
 Sigmoid adenoma
Exocrine pancreatic fistula (electrolyte rich loss in intestine) – bicarb rich also. Acidosis with a low potassium Hypokalaemia with low bicarb (atypical but points towards these causes)

Question 34

Anorexia Nervosa

Answer 34

Potassium intake low

Vomiting

Question 35

Acidosis with low potassium →

Answer 35

Hypokalaemia with low bicarb – atypical (gastrointestinal loss) or renal tubular acidosis.
•	Diarrhoea
•	Villous adenoma (sigmoid)
•	Pancreatic fistula
•	Renal tubular acidosis

Question 36

Clinical Features of Hypokalaemia →

Answer 36

1. Muscle weakness/ hypotonia
2. Paralytic ileus
3. Exacerbation of hepatic encephalopathy
4. Enhanced sensitivity to digoxin
5. Polyuria (renal tubular vacuolation)
6. Cardiac dysrhythmias

Question 37

Cardiac dysrhythmias in hypokalaemia

Answer 37

a. Low T wave
b. ST segment depression (pathopneumonic)
c. Prominent U waves (pathopneumonic)
d. Wide OT interval

Question 38

Causes of Hyperkalaemia →

Answer 38

Renal Cause

Extra-renal cause

Question 39

Renal Cause

Answer 39

Renal Failure
•	Acute
•	End-stage chronic
Drugs
•	Potassium-sparing diuretics
→ Amiloride
→ Spironolacetone
•	ACE inhibitors

Mineralocorticoid deficiency
• Addison’s disease
• Hyporeninaemia hypoaldosteronism

Question 40

Extra-renal cause hyperkalaemia

Answer 40

Pseudohyperkalaemia
•	Haemolysis – blood sample
•	Leukocytosis – WCC/platelets release more potassium
•	Thrombocytosis
Increased potassium input
•	Exogenous
•	Endogenous
→ Tissue necrosis
             → Haemolysis
             →  Malignancy
              → Chemotherapy

IC to EC shift
 Acidosis
 Hypoxia
 Insulin deficiency

Question 41

Renal Failure

Answer 41

If potassium is above 6/rising rapidly concenring feature for cardiac problems.

Question 42

Chronic renal failure

Answer 42

Potassium usually normal until late

Question 43

Spironolacetone

Answer 43

Blocks Potassium excretion in distal tubule via blocking Na-K channel.

Question 44

ACE inhibitors and angtiotensin II blockers

Answer 44

If a patient has renal artery stenosis. Relying on high renin levels to drive function of kidney. If you suddenly inhibit that system. Causes an acute rise in potassium.

Question 45

Pseudo Hypokalaemia

Answer 45

Artefact. Traumatise blood cells e.h. haemolyses blood samples.

Question 46

Leukocytosis

Answer 46

High WCC/Platelets release potassium more than normal. Always check FBC with unexplained hyperpotassium.

Question 47

Malignancy

Answer 47

Large amount of tissue being killed by chemo – tumourlysis (rapid release of potassium).

Question 48

Hypoxia

Answer 48

Can operate sodium/potassium pump

Question 49

Insulin deficiency

Answer 49

Results in deficient uptake of NA (DKA)

Question 50

Clinical Features of Hyperkalaemia →

Answer 50

Tall peaked tented T waves [T wave larger than R wave in more than 1 lead]

Prolonged PR interval
Flattened or about P waves

Widened QRS [greater than 0.12 seconds]
Sine wave pattern (S and T waves merging)
Bradycardia
Ventricular tachycardia

Question 51

Treatment hyperkalaemia

Answer 51

Calcium Gluconate
Salbutamol
Insulin + 50% dextrose
Na HCO3 (not used_
Calcium resonium
Haemofiltration or Dialysis

Question 52

Hypokalaemia treatment

Answer 52

Oral

Intravenous

Question 53

Oral treatment

Answer 53

Sando-K
Bananas
Tomato juice

Question 54

Intravenous

Answer 54

a. Only if oral supplementation impossible
b. Concentration less than 40 mmol/L (peripherally)
c. Rate less than 20 mmol/h
d. Frequent monitoring of serum potassium concentration
e. Consider ECG monitoring