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
