Potassium

Question 1

What haematological disorder can result in spuriously low potassium results if the blood is unspun for a while?

Answer 1

leukaemia. WBCs take up the extra potassium

Question 2

What are the two forms of hypokalaemia periodic paralysis?

Answer 2

FHPP (Familial hypokalaemia period paralysis) and THPP (as above, but with thyrotoxicosis)

Question 3

Outline FHPP symptoms. Why do they arise?

Answer 3

Flaccid paralysis, arrhythmia. Tend to be provoked by anything that cause K+ to go into cells e.g. vigorous
exercise, sugar infusions.

Question 4

What mutation is most commmonly implicated in FHPP? What is the mutation inheritance pattern?

Answer 4

CACNA1S. Autosomal dominants. These relate to calcium-channels in skeletal muscle.

Question 5

How is it managed?

Answer 5

Oral potassium supplements, spironolactone, acetozolamide (not SCN4A mutations) .

Question 6

In what race is FHHPT most common? Does it resolve and how?

Answer 6

Chinese/Japanese. Even more marked male bias than FHHP. It will remit when the patient become euthyroid again.

Question 7

How much loss of potassium can there be in diarrhoea?

Answer 7

Up to 100mmol/day.

Question 8

How are resonium salts and geophagia linked?

Answer 8

Both bind K+ in gut, leading to lowering levels of K+.

Question 9

Why should haematinics be avoided in those with anaemia and low potassium?

Answer 9

The surge in reitculocyctes can drop potassium levels dangerously

Question 10

Renal loss of potassium has four subtypes. What are these?

Answer 10

Renal hypokalaemia acidosis, renal hypokalamic alkalosis (normotensive), renal hypokalaemic alkalosis (hypertensive), renal hypokalaemia with no specific acid-base disorder

Question 11

What two RTA can cause renal acidosis with hypokalaemia?

Answer 11

Type 1 (Distal) and 2 (proximal).

Question 12

renal acidosis with hypokalaemia can also be caused by what drug?

Answer 12

carbonic anhydrase inhibitors

Question 13

Uterosigmoid conduits, colonic conduits and colonic conduit diversion all cause hypokalaemia and acidosis. How?

Answer 13

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.

Question 14

Outline the expected metabolic status (pH, BP, K+ level) of someone with Bartter syndrome

Answer 14

Renal hypokalaemia alkalosis (normotensive)

Question 15

Outline the expected metabolic status (pH, BP, K+ level) of someone with Gitelmann syndrome

Answer 15

Renal hypokalaemia alkalosis (normotensive)

Question 16

Outline the expected metabolic status (pH, Cl-, K+ level) of someone abusing laxatives

Answer 16

metabolic alkalosis with hypokalaemia and hypochloraemia

Question 17

Outline the expected metabolic status (pH, Cl-, K+ level) of someone abusing diuretics

Answer 17

metabolic alkalosis with hypokalaemia and hypochloraemia

Question 18

What is the mechanism of congenital chloride losing diarrhoea? In what gastrin-producing syndrome does this also occur and how?

Answer 18

ileal defective chloride absorption. Gastrin results in diarrhoea with loss of chloride, potassium and bicarbonate.

Question 19

Which of the following does Bartter syndrome present with:

a) hypokalaemia acidosis hypereninaemia hyperaldosterone
b) hyperkalaemic alkalosis hyporeninaemic hypoaldoesterone
c) hypokalaemia alkalosis hyperinaemic hyperaldosteronism

Answer 19

c). There is renal wasting of potassium and chloride and patients are resistant to AII. As a result they are often slightly hypotensive.

Question 20

What gene is affected in Bartters?

Answer 20

The NKCC2 i.e. the sodium-potassium and two chloride transporter gene.

Question 21

What are the major additional electrolyte abnormalities with gitelmann’s syndrome, in addition to low potassium and alkalosis?

Answer 21

calcium and magnesium loss.

Question 22

The expected metabolic effects in terms of mineralocorticoid excess result in what in terms of sodium, fluid, and acid/base balance, potassium

Answer 22

potassium loss, sodium retention and acid loss in the distal tubules with fluid gain.

Question 23

Three familial forms of hyperaldosteronism exist. Which is glucocorticoid suppressible?

Answer 23

Type 1

Question 24

Liddle syndrome involves mutation in what channel and involves what change in blood pressure and potassium

Answer 24

EaNC result in sodium and fluid rentention and fluid loss. Present with malignant hypertension early in life. K is lost, along with acid.

Question 25

Name an example condition of pseudohyperaldosteronism

Answer 25

Liddle syndrome

Question 26

Excessive ingestion of liquorice results in hypertension. How?

Answer 26

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.

Question 27

Several drugs can induce kaliuresis. Give two examples.

Answer 27

Platinums and aminoglycosides

Question 28

How does magnesium deficiency result in low potassium

Answer 28

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.

Question 29

A 24hr potassium should be greater than what?

Answer 29

Certainly greater than 15. Anything less suggests extra renal loss.

Question 30

What tis the TTKG and how is it calculated?

Answer 30

Transtubular potassium gradient. Divide the urine/serum potassium by the urine/serum osmolality ratio. K+ conservation is expected to be <2.

Question 31

Urine chloride of less than what suggests retention of chloride at the renal level?

Answer 31

<20

Question 32

What is the maximum rate of ward level potassium infusion? Critical care?

Answer 32

20mmol per hour but up to 40mmol with appropriate monitoring

Question 33

What is familial pseudohyperkalamia?

Answer 33

These families have particularly leaky red blood cells that leak potassium excessively in vivo.

Question 34

There is a reverse of the FHPP. What is this? What gene is mutated and what drug is used to managed it?

Answer 34

Hyperkalaemic period paralysis. Again it is Scn4a. Salbutamol is used.

Question 35

Resection of urinary tract into what part of the GI tract can result in K+ retention?

Answer 35

Jejunum

Question 36

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

Answer 36

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

Question 37

PHA type 1 is marked by BP status of what. What age does it present?

Answer 37

Usually hypotensive. Infancy

Question 38

What is the cause of PHAs?

Answer 38

Either loss of function mineralcorticoid receptors or EaNC (kidney) or in type II (Gordons), wnk1 genes

Question 39

Generally with PHA, what is the K+ acid-base findings?

Answer 39

Usually they are hyperkalaemic with a metabolic acidosis.