Session 5

Question 1

What is the effect on low extracellular potassium on the membrane potential

Answer 1

More negative

Question 2

How is extracellular potassium regulated short and long term?

Answer 2

Short term - internal balance between ICF and ECF

Long term - external balance (renal excretion - regulated K+ SECRETION in late DT and early CD)

Question 3

What happens to potassium after a meal?

Answer 3

4/5ths moves into cells within minutes. After slight delay kidneys excrete the excess potassium.

Question 4

What factors increase potassium uptake into cells? (Na/K ATPase)

Answer 4

Hormones (insulin, aldosterone, catecholamines)
Increased concentration of potassium in ECF
Alkolosis

Question 5

What factors increase potassium shift out of cells? (K+ channel)

Answer 5

Exercise
Cell lysis
Increase in ECF osmolality
Low concentration of potassium in ECF
Acidosis

Question 6

What prevents hyperkalaemia during exercise?

Answer 6

There is potassium uptake by non contracting tissues and exercise produces catecholamines, which stimulate Na/K ATPase

Question 7

How do acid-base disturbances affect the ECF concentration of potassium?

Answer 7

They act as if there is a reciprocal shift between K+ and H+

E.g. Acidosis -> hyperkalaemia and hypokalaemia -> alkalosis

Question 8

What are the tubular factors that affect K+ secretion in principle cells of DT & CCD?

Answer 8

ECF [K+] - stimulates Na/K ATPase, increases permeability of apical K channels and stimulates aldosterone
Aldosterone - increases transcription of channels involved in K+ secretion
Acid base status - acidosis inhibits K+ secretion

Question 9

What are the luminal factors that affect K+ secretion in principle cells of DT & CCD?

Answer 9

Increased DT flow rate washes away luminal K+, increasing loss

Increased Na delivery to DT increases Na reabsorption, increasing K+ loss

Question 10

How is potassium absorbed by intercalated cells in the DT/CD?

Answer 10

Via H+/K+ ATPase (secreted acid)

Question 11

What are the causes of hyperkalaemia? [k+]>5mmol/L

Answer 11

Increased uptake (rare - only real Lin if inappropriate IV K+ dose given)
Decreased renal excretion- acute/chronic kidney injury, drugs blocking K+ secretion (ACEi, K+ sparing diuretics), low aldosterone state(addisons)
Internal shifts - diabetic ketoacidosis (no insulin & acidosis & plasma hyperosmolarity), cell lysis, metabolic acidosis, exercise

Question 12

What are the clinical features of hyperkalaemia?

Answer 12

Arrhythmias/heart block - heart less excitable because more fast Na channels remain inactive
Paralytic ileum - GI muscular dysfunction
Acidosis

Question 13

Describe the ECG changes seen in hyperkalaemia

Answer 13

Normal -> High T wave -> High T wave, prolonged PR, depressed ST -> Atrial standstill, IV block -> ventricular fibrillation

Question 14

What is the emergency treatment for hyperkalaemia?

Answer 14

Reduce the K+ effect on the heart - IV calcium gluconate
Shift k+ into cells by giving glucose plus insulin or nebulised B agonists (salbutamol)
Remove excess K+ - dialysis

Question 15

What is the longer term treatment for hyperkalaemia?

Answer 15

Treat cause - stop medication, treat DKA etc
Reduce intake
Remove excess K+ - dialysis, oral binding resins

Question 16

What are the causes of hypokalaemia? [k+]<3.5mmol/L

Answer 16

External balance - excessive loss by vomiting, diarrhoea, high aldosterone
Internal balance - shift into cells e.g. Metabolic alkalosis

Question 17

What are the clinical features of hypokalaemia?

Answer 17

Cardiac arrhythmias - hyperpolarised RMP means more fast Na channels so heart more excitable
Paralytic ileum -> GI muscular dysfunction
Skeltetal muscle weakness
Kindness unresponsive to ADH

Question 18

Describe the ECG changes seen in hypokalaemia

Answer 18

Normal -> low T wave -> low T wave, high U wave -> low T wave, high U wave, depressed ST segment

Question 19

What is the treatment for hypokalaemia?

Answer 19

Treat cause
IV/oral K+ replacement
K+ soaring diuretics that block aldosterone if that is the cause

Question 20

Describe the effects of alkalaemia

Answer 20

Lowers free calcium by causing them to come out of solution. This increases neuronal excitability and can lead to paraesthesia and tetany. 80% mortality at pH >7.65

Question 21

Describe the effects of acidaemia

Answer 21

Increases plasma K+ and denatures proteins<7.0

Question 22

Describe the process leading up to respiratory acidaemia

Answer 22

Hypoventilation -> hypercapnia -> acidaemia

Opposite for respiratory alkaemia

Question 23

Where is pCO2 detected and controlled?

Answer 23

Central chemoreceptors which change ventilation rate accordingly. Peripheral chemoreceptors are quicker but produce a smaller overall effect.

Question 24

Where is [HCO3-] detected and controlled?

Answer 24

Peripheral chemoreceptors

Question 25

What can cause metabolic alkalosis and what is the main problem?

Answer 25

Repeated vomiting - can only be partially compensated by decreasing ventilation due to hypoxia

Question 26

What is the role of the kidneys in maintaining pH?

Answer 26

They compensate for respiratory changes on pCO2 and also correct metabolic pH disturbances by varying excretion of HCO3-, or by making more.

Question 27

How do the kidneys increase plasma pH?

Answer 27

They recover all filtered HCO3-, make new HCO3- and secrete acid.

Question 28

Describe how the kidneys make new HCO3-

Answer 28

``` From CO2 (from metabolism) plus H2O in DCT. HCO3 enters the blood stream and H+ leaves in the urine via H+ ATPase. From glutamine in the PCT, producing NH4+, which enters urine. ```

Question 29

Describe how the kidneys recover HCO3- in the PCT

Answer 29

H+ enters lumen via NHE and reacts with HCO3-. CO2 enters cell and reacts with water. HCO3- leaves across basolateral membrane via Na-3HCO3- cotransporter. Carbonic anhydrase is present inside the cell and on apical membrane

Question 30

What factors does a decreased pH enhance in the kidney?

Answer 30

Activity of NHE in PCT (increasing HCO3 recovery) Ammonium production in PCT (increasing synthesis of HCO3) Activity of H+ ATPase in DCT (increasing synthesis of HCO3) Capacity to export HCO3 into ECF

Question 31

What is the anion gap and when does it increase?

Answer 31

The difference between [Na+] + [K+] and [Cl-] + [HCO3-]. | The gap increases if HCO3- is replaced by an anion other than Cl- (e.g. Lactate/ketone) in metabolic acidosis.

Question 32

Give an example of when metabolic acidosis does not produce an anion gap

Answer 32

Renal problems can cause decreased [HCO3-] and replace it with Cl-, hence no anion gap.