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Would an impaired ability of the kidney to reabsorb Na+ ions cause hypokalaemia? (Bartters syndrome)

Yes, mimics the effect of loop diuretics by downregulating NaKCC in TAL


Would use of ACE inhibitors cause hypokalaemia?

ACE inhibitors will result in depressed aldosterone secretion, hence K+ retention and hyperkalaemia.


Why should late distal diuretics not be administered in parallel with ACE inhibitors?

Late distal diuretics also dispose towards hyperkalaemia, and this is why these drugs must never be administered in parallel


Would Conn’s syndrome (primary hyperaldosteronism), most commonly arising from adrenal adenoma cause hyper/hypokalaemia?

Conn's syndrome may be associated with hypokalaemia due to enhanced K+ loss


Would chronic laxative abuse cause hypokalaemia?

Chronic laxative abuse, like diarrhoea, causes hypokalaemia. This is because the high intestinal fluid content will lead to the K+ within it being relatively dilute. One of the factors affecting the rate of washout of K+ from cells lining the intestinal tract will be the intra-/extra-cellular K+ concentration gradient. When this is increased, as in laxative abuse, more cellular K+ will lost from these cells.


Heavy exercise

Heavy exercise causes transient hyperkalaemia for 2 reasons. Firstly, K+ will be released into the plasma from mechanically ruptured red cells. Secondly, many cell types, including myocytes, contain ATP sensitive K+ channels; these are normally blocked by ATP. As ATP is depleted, these channels become unblocked and K+ leaks out. This has a beneficial effect, because K+ ions are vasodilators, and blood flow to exercising muscle is thus increased.


Liddle’s syndrome is a rare genetic defect resulting from hyperconductivity of the Na+ ion channels in the luminal membranes in the distal tubule. It is characterised by raised blood pressure low levels of circulating renin (hyporeninaemia) hypokalaemia and metabolic alkalosis. Most of you will never see a case of Liddle’s syndrome. Try to work out how this enhancement of Na+ ion reabsorption leads to the symptoms listed; this will be a good indication of how well you understand the important interrelationships between Na+, K+ and H+ ion transport in the distal nephron

Liddle’s syndrome results from genetically determined hyperactivity of the luminal Na+ ion channels in the distal part of the nephron. This leads to systemic Na + overload and an increase in Extra-cellular Fluid Volume (ECFV). Although transient increases in ECFV do not necessarily lead to elevation of blood pressure, chronic overload will result in hypertension, which down-regulates the RAAS, hence hyporeninaemia. The luminal membrane of distal cells will become excessively depolarized, enhancing K + leakage, hence hypokalaemia. The equilibrium of the intra-cellular free/buffered cation relationship will be shifted to the left, increasing the availability of H + ions for secretion, hence alkalosis.