Biochemistry Potassium Flashcards
Intracellular Potassium
98% - 2940 mmol
Extracellular
2% 60 mmol
Plasma (extracellular)
0.5%-15 mmol (sampling this proportion)
Transport out/into cells via
Na/K ATPase
Potassium (plasma) maintains the
resting membrane potential
Determine via
Potassium inside cells vs. extracellular
Resting potential of
-70mV
Disturbing potassium problem
Disturbs resting potential and therefore leading to the clinical symptoms of hypo or hyper
The Na+ and K+ gradients are maintained by
by the sodium-potassium pump
Intake
100 mmol per day
Output
30 mmol/day Skin – 10 mmnol Faeces – 10 mmol Urine >10 mmol Minimum loss – 7 mmoll/litre in urine
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.
Potassium – Renal Potassium Handling: Filtered
800 mmnol/day
Potassium – Renal Potassium Handling: Reabsorption
100% in proximal nephron
Potassium – Renal Potassium Handling: Secretion via
Controlled Na/K exchanger in distal convoluted tubule regulated by aldosterone – regulates potassium excretion to maintain potassium balance
Potassium – Renal Potassium Handling: Urine potassium excretion depends on
- Availability of sodium for exchange –
- Plasma aldosterone concentration
- Relative intracellular [K+] and [H+]
Potassium – Renal Potassium Handling: Output
• Input – other losses
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
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.
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.
Catecholamine effect on potassium/hydrogen
Salbutamol to treat hyperkalaemia as it stimulates Potassium excretion.
Insulin →
diabetic ketoacidosis: one effects after treatment (as normal high potassium with acidosis observed rapid reduction in plasma potassium.
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.
Causes of Hypokalaemia
Renal Loss
Extra-renal loss
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
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
Alkalosis
Reciprocal relation with potassium nd hydrogen
Alkalosis – favours potassium loss
Acidosis – inhibits potassium loss (getting rid of H+ ions)
Hypokalaemia – may causes alkalosis
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
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.
Cushing’s
Excess cortisol – glucocorticoids. Sufficiently high levels of cortisol leading to cross reactivity.
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
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.
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)
Anorexia Nervosa
Potassium intake low
Vomiting
Acidosis with low potassium →
Hypokalaemia with low bicarb – atypical (gastrointestinal loss) or renal tubular acidosis. • Diarrhoea • Villous adenoma (sigmoid) • Pancreatic fistula • Renal tubular acidosis
Clinical Features of Hypokalaemia →
- Muscle weakness/ hypotonia
- Paralytic ileus
- Exacerbation of hepatic encephalopathy
- Enhanced sensitivity to digoxin
- Polyuria (renal tubular vacuolation)
- Cardiac dysrhythmias
Cardiac dysrhythmias in hypokalaemia
a. Low T wave
b. ST segment depression (pathopneumonic)
c. Prominent U waves (pathopneumonic)
d. Wide OT interval
Causes of Hyperkalaemia →
Renal Cause
Extra-renal cause
Renal Cause
Renal Failure • Acute • End-stage chronic Drugs • Potassium-sparing diuretics → Amiloride → Spironolacetone • ACE inhibitors
Mineralocorticoid deficiency
• Addison’s disease
• Hyporeninaemia hypoaldosteronism
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
Renal Failure
If potassium is above 6/rising rapidly concenring feature for cardiac problems.
Chronic renal failure
Potassium usually normal until late
Spironolacetone
Blocks Potassium excretion in distal tubule via blocking Na-K channel.
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.
Pseudo Hypokalaemia
Artefact. Traumatise blood cells e.h. haemolyses blood samples.
Leukocytosis
High WCC/Platelets release potassium more than normal. Always check FBC with unexplained hyperpotassium.
Malignancy
Large amount of tissue being killed by chemo – tumourlysis (rapid release of potassium).
Hypoxia
Can operate sodium/potassium pump
Insulin deficiency
Results in deficient uptake of NA (DKA)
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
Treatment hyperkalaemia
Calcium Gluconate Salbutamol Insulin + 50% dextrose Na HCO3 (not used_ Calcium resonium Haemofiltration or Dialysis
Hypokalaemia treatment
Oral
Intravenous
Oral treatment
Sando-K
Bananas
Tomato juice
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
