Potassium Flashcards
What are examples of physiological processes which require strict potassium regulation?
Resting cellular-membrane potential
Propagation of action potentials
Hormone section and action
Vascular tone
GI motility
Systemic BP control
Acid-base homeostasis
Glucose and insulin metabolism
Renal concentrating ability
Fluid + electrolyte balance
Where is K+ primarily lost in healthy individuals?
Kidney= 90% GIT/skin= 10%
Where is the major of K+ located in the body?
What are reference ranges for K+ in serum?
ICF= 130-150mmol/L
Serum= 3.5-5.3 mmol/L (20-25mmol)
Why is rapid clearance ingested potassium required?
Meal contain more potassium than total plasma content meaning needs to be cleared by renal and extra-renal mechanisms to prevent variation in plasma potassium
What is the response in the serum and urine to potassium loading?
Serum:
K+ stimulates ATPase which stimulates increase release of hormones insulin, Catecholamine and aldosterone
Urine:
Renal cells stimulated to uptake and secrete K+
What does K+ redistribution in the ECF and ICF depend on?
Hormones
Acid base status
Plasma osmolality
Potassium sequestration into liver and muscle
What is the main regulator of K+ in the body? How is this achieved?
Kidney
600mmol/day K+ filtered = primarily at proximal tubule, then ALOH then distal tubule where aldosterone can further regulate
Which hormones are involved in K+ redistribution and how is this done?
Insulin + catecholamines increased K+ uptake by cells by activating Na+/K+ ATPase pump to lowers serum K+
Insulin= liver, SKM and adipose tissue
Cate= SKM
Aldosterone increased renal secretion= lowers serum K+ due to net loss of K+ and net gain of Na+
How is the RAAS system associated with hypokalaemia and hyperkalaemia?
Hypo:
Overactive RAAS i.e. Conn’s(hyperaldosteronism)/Cushing’s(hypercortisolism)/Renal artery stenosis (increased renin)
Hyper:
Under active RAAS i.e. adrenal insufficiency/ACEi/ Spironolactone
What is the difference between the action of insulin and catecholamines on increasing K+ uptake into cells via Na+/K+ ATPase?
Insulin causes indirect activation of pump by acting on Na+/H+ antiporter to increase Intracellular sodium to drive pump
Catecholamines (beta-adrenergic agent) acts directly on pump
What is the affect of metabolic acidosis on plasma potassium? Why does this occur?
Increase plasma K+
Inhibition of renal tubular K+ secretion due to H+ blocking K+ excretion
I.e. more H+ exchanged for Na+ rather than K+ due to body favouring excretion of H+ to maintain acid-base neutrality
Shift of K+ from ICF to ECF due to excess H+ in ECF entering cells in place of K+ leading to increase conc of K+ in ECF
I.e. body favours maintains acid-base neutrality over K+ homoestasis
Therefore= hyperkalaemia
When does a metabolic acidosis not result in hyperkalaemia? What is the mechanism behind this?
When acidosis is due to bicarbonate loss rather than H+ excess.
Bicarbinate loss leads to retention of Cl- to maintain electrochemical neutrality but Cl- ions cannot pass into cells
Therefore potassium is lost from cells to compensate and maintain neutrality
==HYPOKALAEMIA
What is the affect of metabolic alkalosis on potassium? Why is this?
Serum
Alkaline ph causes H+ to move out of cells to buffer the blood
K+ and Na+ enter the cell to maintain electrochemical neutrality leading to HYPOKALAEMIA
Urine
Plasma Na+ levels falling due to compensatory measures for alkalosis stimulates aldosterone release
Leads to increase renal excretion of K+ == HYPOKALAEMIA
How is hyperosmolarity associated with altered K+ levels?
Insulin deficiency causes water and K+ to move from ICF to ECF
== HYPERKALAEMIA
Osmotic diuresis leads to increased fluid delivary to lumen of kidneys and increases the excretion of K+
==HYPOKALAEMIA
How is hyperkalaemia defined?
What occurs when K+ conc >6.5mmol/L?
What potassium level is considered a medical emergency and why?
K+ conc >5.0 mmol/L
Altered electrical excitability
> 7.5mmol/L
Associated with arrythmias + MI
How can you identify hyperkalaemia on an ECG?
Tall peaked T wave
Loss of P wave
Wide QRS complex
Wide PR interval
What are the main causes of hyperkalaemia?
Increased intake i.e. oral or IV therapy
Reduced excretion i.e. renal failure or mineralocorticoid deficiency and tubular defects
Altered distribution of K+ i.e. acidosis, insulin deficiency, crush injuries or haemolysis
Haematological disorders
ACEi/ARBs
K+ sparing diuretics I.e. amiloride
Aldosterone anatagonists i.e. spironolactone
Potassium supplement
MOST COMMONLY= CKD + redistribution secondary to acidosis
When is urgent treatment indicated for hyperkalaemia? What are the main forms of treatment?
When K+ > 6.5mmol/L
Cardio protection TX i.e. prevent arrythmias
Calcium gluconate to increase threshold potentials
ECG monitoring
Redistribution TX
Glucose + insulin
B-agonist i.e. nebulised salbutamol
Bicarbonate i.e. when associated with acidosis
Removal
Loop diuretic i.e. furosemide
Ion-exchange resins
Dialysis/haemofiltration
When does chronic hyperkalaemia occur and how can it be managed?
Late complication of CKD
Treat underlying cause
Low K+ diet
Correct metabolic acidosis
What is artefactual high K+ and what are the most common causes?
K+ is falsely elevated without any pathological basis
Overnight storage prior to sample prep causing K+ to leak out of cells
Taken from vein above an IV infusion of K+/dextrose
Blood taken into EDTA anticoagulents
Haematological malignancies with v high WBC or platelets
What are the causes of hypokalaemia?
Loss
- GI= fistula, diarrhoea, villous adenoma, purgative abuse
- Renal= loop diuretics, renal tubular acidosis, mineralocorticoid excess
Inadequate intake (in combo with losses)
Redistribution
- insulin
- alkalosis
- salbutamol (beta-agonist acting on pump)
- hypokalaemia periodic paralysis
- familial periodic paralysis
What are the two causes of hypokalaemic acidosis?
Villous adenoma
Renal tubular necrosis
What are the consequences of hypokalaemia?
Skeletal muscle weakness and paralysis
Paralytic ileus
Impaired concentrating ability of kidney
Renal tubular defects
Cardiac conduction defects
Arrhythmias
Digoxin toxicity
Why does digoxin toxicity occur with hypokalaemia? How does it present
Low potassium means that digoxin can more readily bind to Na+/K+ ATPase due to it normally having to compete with K+ for the same binding site
Nausea, vomiting and irregular heartbeat
