Potassium Flashcards
What haematological disorder can result in spuriously low potassium results if the blood is unspun for a while?
leukaemia. WBCs take up the extra potassium
What are the two forms of hypokalaemia periodic paralysis?
FHPP (Familial hypokalaemia period paralysis) and THPP (as above, but with thyrotoxicosis)
Outline FHPP symptoms. Why do they arise?
Flaccid paralysis, arrhythmia. Tend to be provoked by anything that cause K+ to go into cells e.g. vigorous
exercise, sugar infusions.
What mutation is most commmonly implicated in FHPP? What is the mutation inheritance pattern?
CACNA1S. Autosomal dominants. These relate to calcium-channels in skeletal muscle.
How is it managed?
Oral potassium supplements, spironolactone, acetozolamide (not SCN4A mutations) .
In what race is FHHPT most common? Does it resolve and how?
Chinese/Japanese. Even more marked male bias than FHHP. It will remit when the patient become euthyroid again.
How much loss of potassium can there be in diarrhoea?
Up to 100mmol/day.
How are resonium salts and geophagia linked?
Both bind K+ in gut, leading to lowering levels of K+.
Why should haematinics be avoided in those with anaemia and low potassium?
The surge in reitculocyctes can drop potassium levels dangerously
Renal loss of potassium has four subtypes. What are these?
Renal hypokalaemia acidosis, renal hypokalamic alkalosis (normotensive), renal hypokalaemic alkalosis (hypertensive), renal hypokalaemia with no specific acid-base disorder
What two RTA can cause renal acidosis with hypokalaemia?
Type 1 (Distal) and 2 (proximal).
renal acidosis with hypokalaemia can also be caused by what drug?
carbonic anhydrase inhibitors
Uterosigmoid conduits, colonic conduits and colonic conduit diversion all cause hypokalaemia and acidosis. How?
Electrolytes are exchanged at bowel surface but it is hard to predict how and it what quantities. Generally ileal segments have low complications. Sigmoid colon diversion result in lost bicarbonate and may result in lost potassium if the colon cannot reabsorb it all.
Outline the expected metabolic status (pH, BP, K+ level) of someone with Bartter syndrome
Renal hypokalaemia alkalosis (normotensive)
Outline the expected metabolic status (pH, BP, K+ level) of someone with Gitelmann syndrome
Renal hypokalaemia alkalosis (normotensive)
Outline the expected metabolic status (pH, Cl-, K+ level) of someone abusing laxatives
metabolic alkalosis with hypokalaemia and hypochloraemia
Outline the expected metabolic status (pH, Cl-, K+ level) of someone abusing diuretics
metabolic alkalosis with hypokalaemia and hypochloraemia
What is the mechanism of congenital chloride losing diarrhoea? In what gastrin-producing syndrome does this also occur and how?
ileal defective chloride absorption. Gastrin results in diarrhoea with loss of chloride, potassium and bicarbonate.
Which of the following does Bartter syndrome present with:
a) hypokalaemia acidosis hypereninaemia hyperaldosterone
b) hyperkalaemic alkalosis hyporeninaemic hypoaldoesterone
c) hypokalaemia alkalosis hyperinaemic hyperaldosteronism
c). There is renal wasting of potassium and chloride and patients are resistant to AII. As a result they are often slightly hypotensive.
What gene is affected in Bartters?
The NKCC2 i.e. the sodium-potassium and two chloride transporter gene.
What are the major additional electrolyte abnormalities with gitelmann’s syndrome, in addition to low potassium and alkalosis?
calcium and magnesium loss.
The expected metabolic effects in terms of mineralocorticoid excess result in what in terms of sodium, fluid, and acid/base balance, potassium
potassium loss, sodium retention and acid loss in the distal tubules with fluid gain.
Three familial forms of hyperaldosteronism exist. Which is glucocorticoid suppressible?
Type 1
Liddle syndrome involves mutation in what channel and involves what change in blood pressure and potassium
EaNC result in sodium and fluid rentention and fluid loss. Present with malignant hypertension early in life. K is lost, along with acid.
Name an example condition of pseudohyperaldosteronism
Liddle syndrome
Excessive ingestion of liquorice results in hypertension. How?
Licorice contains glycchirizic acid. Normally, cortisol is inactivated in the kidney by 11 beta hydroxy steroid dehydrogenase, allowing mineralcorticoids act alone. glycchirizic inactivates this enzyme allowing cortisol to act.
Several drugs can induce kaliuresis. Give two examples.
Platinums and aminoglycosides
How does magnesium deficiency result in low potassium
Thought to be due to Mg being required for Na/K pumps in the kidney working - low Mg means they retain more sodium at the expense of K. That and ROMK channels.
A 24hr potassium should be greater than what?
Certainly greater than 15. Anything less suggests extra renal loss.
What tis the TTKG and how is it calculated?
Transtubular potassium gradient. Divide the urine/serum potassium by the urine/serum osmolality ratio. K+ conservation is expected to be <2.
Urine chloride of less than what suggests retention of chloride at the renal level?
<20
What is the maximum rate of ward level potassium infusion? Critical care?
20mmol per hour but up to 40mmol with appropriate monitoring
What is familial pseudohyperkalamia?
These families have particularly leaky red blood cells that leak potassium excessively in vivo.
There is a reverse of the FHPP. What is this? What gene is mutated and what drug is used to managed it?
Hyperkalaemic period paralysis. Again it is Scn4a. Salbutamol is used.
Resection of urinary tract into what part of the GI tract can result in K+ retention?
Jejunum
What is the expected renin and aldosterone levels in the following:
a) Addisons
b) Hepatin
c) CAH
d) ACE inhibition
e) Pseudohypoaldoesteronism type 1
f) Pseudohypoaldoesteronism type 2
R A
a) H L
b) H L
c) N/H N/L
d) N/H N/L
e) H H
f) L L/N
PHA type 1 is marked by BP status of what. What age does it present?
Usually hypotensive. Infancy
What is the cause of PHAs?
Either loss of function mineralcorticoid receptors or EaNC (kidney) or in type II (Gordons), wnk1 genes
Generally with PHA, what is the K+ acid-base findings?
Usually they are hyperkalaemic with a metabolic acidosis.
