Session 6 - Notes (SS only, add group work post-resp) Flashcards Preview

Semester 3 - Urinary > Session 6 - Notes (SS only, add group work post-resp) > Flashcards

Flashcards in Session 6 - Notes (SS only, add group work post-resp) Deck (7)
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1

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

2

Would use of ACE inhibitors cause hypokalaemia?

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

3

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

4

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

5

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.

6

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.

7

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.