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Flashcards in Biochemistry Potassium Deck (54):
1

Intracellular Potassium

98% - 2940 mmol

2

Extracellular

2% 60 mmol

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Plasma (extracellular)

0.5%-15 mmol (sampling this proportion)

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Transport out/into cells via

Na/K ATPase

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Potassium (plasma) maintains the

resting membrane potential

6

Determine via

Potassium inside cells vs. extracellular

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Resting potential of

-70mV

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Disturbing potassium problem

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

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The Na+ and K+ gradients are maintained by

by the sodium-potassium pump

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Intake

100 mmol per day

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Output

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

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Patient on IV fluids

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

13

Potassium – Renal Potassium Handling: Filtered

800 mmnol/day

14

Potassium – Renal Potassium Handling: Reabsorption

100% in proximal nephron

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Potassium – Renal Potassium Handling: Secretion via

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

16

Potassium – Renal Potassium Handling: Urine potassium excretion depends on

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

17

Potassium – Renal Potassium Handling: Output

• Input – other losses

18

Potassium – Renal Potassium Handling: Availability of sodium for exchange

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

19

Metabolic acidosis:

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

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Potassium depleted –

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.

21

Catecholamine effect on potassium/hydrogen

Salbutamol to treat hyperkalaemia as it stimulates Potassium excretion.

22

Insulin →

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

23

Re-feeding syndrome –

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.

24

Causes of Hypokalaemia

Renal Loss
Extra-renal loss

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Renal loss hypokalameia

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

26

Extra-renal loss hypokalaemia

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

27

Alkalosis

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

Hypokalaemia – may causes alkalosis

28

Diuretics

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

29

Mineralcorticoid excess

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.

30

Cushing’s

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

31

Ectopic ACTH

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

32

Renal tubular disease

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.

33

Hypomagnesium

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)

34

Anorexia Nervosa

Potassium intake low
Vomiting

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Acidosis with low potassium →

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

36

Clinical Features of Hypokalaemia →

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

37

Cardiac dysrhythmias in hypokalaemia

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

38

Causes of Hyperkalaemia →

Renal Cause
Extra-renal cause

39

Renal Cause






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

Mineralocorticoid deficiency
• Addison’s disease
• Hyporeninaemia hypoaldosteronism

40

Extra-renal cause hyperkalaemia

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

41

Renal Failure

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

42

Chronic renal failure

Potassium usually normal until late

43

Spironolacetone

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

44

ACE inhibitors and angtiotensin II blockers

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.

45

Pseudo Hypokalaemia

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

46

Leukocytosis

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

47

Malignancy

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

48

Hypoxia

Can operate sodium/potassium pump

49

Insulin deficiency

Results in deficient uptake of NA (DKA)

50

Clinical Features of Hyperkalaemia →

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

51

Treatment hyperkalaemia

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

52

Hypokalaemia treatment

Oral
Intravenous

53

Oral treatment

Sando-K
Bananas
Tomato juice

54

Intravenous

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

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