Session 5 Flashcards
What is the effect on low extracellular potassium on the membrane potential
More negative
How is extracellular potassium regulated short and long term?
Short term - internal balance between ICF and ECF
Long term - external balance (renal excretion - regulated K+ SECRETION in late DT and early CD)
What happens to potassium after a meal?
4/5ths moves into cells within minutes. After slight delay kidneys excrete the excess potassium.
What factors increase potassium uptake into cells? (Na/K ATPase)
Hormones (insulin, aldosterone, catecholamines)
Increased concentration of potassium in ECF
Alkolosis
What factors increase potassium shift out of cells? (K+ channel)
Exercise Cell lysis Increase in ECF osmolality Low concentration of potassium in ECF Acidosis
What prevents hyperkalaemia during exercise?
There is potassium uptake by non contracting tissues and exercise produces catecholamines, which stimulate Na/K ATPase
How do acid-base disturbances affect the ECF concentration of potassium?
They act as if there is a reciprocal shift between K+ and H+
E.g. Acidosis -> hyperkalaemia and hypokalaemia -> alkalosis
What are the tubular factors that affect K+ secretion in principle cells of DT & CCD?
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
What are the luminal factors that affect K+ secretion in principle cells of DT & CCD?
Increased DT flow rate washes away luminal K+, increasing loss
Increased Na delivery to DT increases Na reabsorption, increasing K+ loss
How is potassium absorbed by intercalated cells in the DT/CD?
Via H+/K+ ATPase (secreted acid)
What are the causes of hyperkalaemia? [k+]>5mmol/L
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
What are the clinical features of hyperkalaemia?
Arrhythmias/heart block - heart less excitable because more fast Na channels remain inactive
Paralytic ileum - GI muscular dysfunction
Acidosis
Describe the ECG changes seen in hyperkalaemia
Normal -> High T wave -> High T wave, prolonged PR, depressed ST -> Atrial standstill, IV block -> ventricular fibrillation
What is the emergency treatment for hyperkalaemia?
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
What is the longer term treatment for hyperkalaemia?
Treat cause - stop medication, treat DKA etc
Reduce intake
Remove excess K+ - dialysis, oral binding resins
What are the causes of hypokalaemia? [k+]<3.5mmol/L
External balance - excessive loss by vomiting, diarrhoea, high aldosterone
Internal balance - shift into cells e.g. Metabolic alkalosis
What are the clinical features of hypokalaemia?
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
Describe the ECG changes seen in hypokalaemia
Normal -> low T wave -> low T wave, high U wave -> low T wave, high U wave, depressed ST segment
What is the treatment for hypokalaemia?
Treat cause
IV/oral K+ replacement
K+ soaring diuretics that block aldosterone if that is the cause
Describe the effects of alkalaemia
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
Describe the effects of acidaemia
Increases plasma K+ and denatures proteins<7.0
Describe the process leading up to respiratory acidaemia
Hypoventilation -> hypercapnia -> acidaemia
Opposite for respiratory alkaemia
Where is pCO2 detected and controlled?
Central chemoreceptors which change ventilation rate accordingly. Peripheral chemoreceptors are quicker but produce a smaller overall effect.
Where is [HCO3-] detected and controlled?
Peripheral chemoreceptors
What can cause metabolic alkalosis and what is the main problem?
Repeated vomiting - can only be partially compensated by decreasing ventilation due to hypoxia
What is the role of the kidneys in maintaining pH?
They compensate for respiratory changes on pCO2 and also correct metabolic pH disturbances by varying excretion of HCO3-, or by making more.
How do the kidneys increase plasma pH?
They recover all filtered HCO3-, make new HCO3- and secrete acid.
Describe how the kidneys make new HCO3-
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.
Describe how the kidneys recover HCO3- in the PCT
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
What factors does a decreased pH enhance in the kidney?
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
What is the anion gap and when does it increase?
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.
Give an example of when metabolic acidosis does not produce an anion gap
Renal problems can cause decreased [HCO3-] and replace it with Cl-, hence no anion gap.
