Potassium Balance Flashcards
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What are the most prevalent cations in body fluids?
→ Na+ and K+
Where is potassium found?
→ in leafy vegetables
→ Most fruit and juice
→ potatoes
What is the intra and extracellular concentration of potassium?
→ I : 150mmol/L
→E : 4.5 mmmol/L
What cell types have the most potassium?
→ Muscle cells
What is the internal potassium balance maintained by?
→ Insulin
→ Adrenaline
→ pH
→ Aldosterone
What is the external potassium balance maintained by?
Input
→Diet
Output
→ urine & stools
→ sweat
What is acute regulation of K+?
→The distribution of K+ through ICF and ECF compartments
What is chronic regulation of K+?
→ Kidney adjusting K+ excretion + reabsorption
What are the 2 functions of K+?
- Determines ICF osmolality
- Determines resting membrane potential
- Affects vascular resistance
What does the sodium/potassium pump do?
→ Na+ ions are pumped out of the cell
→ K+ pumped into the cell
→ energy driving the pump is released by ATP hydrolysis
What happens to K+ concentration after a meal?
→ Increase in plasma K+
→ shifted into ICF compartment
What hormones is the ICF K+ shift due to?
→ insulin
→ adrenaline
→ aldosterone
→ pH changes
What is hyperkalaemia defined as?
→ plasma K+ is above 5.5 mM
What is hypokalaemia defined as?
→ plasma K+ is below 3.5 mM
What is resting potential formed from?
→ ionic gradients
What is the normal distribution between IC and EC K+?
→ External - 3.5 mM
→ Internal - 140 mM
What happens to the equilibrium potential when you have hyperkalaemia?
→ Less negative
What happens to the equilibrium potential when you have hypokalaemia?
→ More negative
What happens during hyperpolarization (less K+) ?
→ more negative voltage across the membrane
→ Decreased excitability of neurons
→Longer to reach threshold
→ Longer to reach action potential
What happens during depolarization (more K+)?
→ Less negative voltage
→ Threshold is approached quicker
→ Increased excitability
What is hypokalaemia caused by?
→ Renal or extra renal loss of K+
What are causes of hypokalaemia?
→ Diuretics without KCl
→ Hyperaldosteronism ( Conn’s syndrome)
→ Prolonged vomiting (Increased aldosterone secretion)
→ Profuse diarrhoea
What does hypokalaemia result in?
→ Decrease adrenaline, aldosterone and insulin
What is hyperkalaemia caused by?
→ Prolonged exercise
→ Kidneys excrete K+ easily
What are disease states that cause hyperkalaemia?
→ Insufficient renal excretion
→ Increased release from damage body cells
→ Long term use of potassium sparing diuretics
→ Addisons disease
What happens if plasma K+ is above 6.5 mM?
→ Systolic cardiac arrest
What is used to drive K+ into the cells?
→ Insulin/glucose infusion
What hormones stimulate the Na+-K+ pump?
→ Aldosterone
→ Adrenaline
What is external balance of K+ regulated by?
→ the kidneys
What are human kidneys designed to do?
→ Conserve Na+ and excrete K+
What drugs raise serum K+ levels?
→ B blockers
→ ACE inhibitoris
What drug causes hypokalaemia?
→ loop diuretics
Why do the plasma and glomerular fluid have the same concentration?
→ Na+ and K+ are freely filtered at the glomeruli
How is K+ maintained at high levels within the kidney cells?
→ Sodium travels from the tubular lumen to the ECF bringing glucose and AA with it
→the Na+ and K+ pump maintains this on the basolateral side
→ Maintains K+ at high levels in the kidney cells
How do Na+ and K+ move in the loop of henle?
→Active reabsorption/pumping of Na+ & Cl- out of the fluid into the medulla
→done via a Na+/2Cl-/K+ symporter on the luminal membrane
→driven by the [Na+] gradient from lumen-cell.
→You also have entry of Na+ from Na+-H+ antiporter
→On the basolateral side you have a Na+/K+ ATPase pump and co-transport of Cl- & K+ out of the cell (especially in the thick ascending limb).
Where is 90% of the potassium reabsorbed?
→ PCT and loop of henle
What is excretion of K+ into urine controlled by?
→ secretion in principal cells of late DCT and CD
How do you get the K+ to go into the urine in the DCT?
→ eNAC channels are present on the luminal side
→ activated by aldosterone
→ as Na+ enters the cell it changes the electrical potential on the luminal side
→ allow K+ to be secreted out
→ there are K+/Cl- symporters that pump K+ out
What inhibits eNAC channels?
→ diuretics
What determines K+ secretion in the DCT?
→ Increased K+ intake
→ Changes in blood pH
What happens to K+ during alkalosis?
→ Increased excretion of K+
→ Decreased serum K+
What happens to K+ during acidosis?
→ Decreased excretion of K+
→ Increased serum K+
What causes the switch between secretion and absorption?
→ Activity of Na+ / K+ pump
→ Electrochemical gradient
→ Permeability of luminal membrane channel
What effect does aldosterone have on the Na+/ K+ pump?
→ Increase K+ influx
→ Increase intracellular potassium
→ increase cell-lumen concentration gradient
What is the major regulator of K+ balance?
→ aldosterone
What effect does aldosterone have on the eNAC channels?
→ More eNAC channels → Increased Na+ reabsorption → Decreased cell negativity → Increased lumen negativity → Increase voltage gradient
What does aldosterone do to the luminal membrane?
→ Makes it more permeable to K+
How does an increase in plasma K+ increase K+ secretion?
→ Slows exit from basolateral membrane
→ Increases concentration gradient towards urine
→ Increases activity of Na+/K+ ATPase
→ Stimulates aldosterone secretion
Flow chart for what happens during increased K+ intake
Increased K+ intake ↓ Increased plasma K+ ↓ Increased aldosterone secretion from adrenal cortex ↓ Increased plasma aldosterone ↓ Increased K+ secretion from cortical collecting ducts ↓ Increased K+ secretion
How is K+ secreted during alkalosis?
→ Increased activity of Na+/K+ pump and increased K+ in the cell
→ Favours the concentration gradient for K+ secretion
→ Increase in tubular fluid pH
→ increases permeability of luminal membrane
How is K+ secreted during acute acidosis?
→ increase in H+ of ECF reduces the activity of the Na+/K+ ATPase pump
→ Decreases intracellular K+
→ reduces passive diffusion of K+
What does an increase in tubule fluid flow rate result from?
→ increased GFR or inhibition of reabsorption upstream or diuretics
What does an increase in tubule fluid flow rate result in?
→ sweeping away of K+
→ makes tubular K+ low
→ more rapid rate of net secretion
What does anti diuretic hormone do?
→ Stimulates K+ secretion by increasing the conductance of the luminal membrane
Where does reabsorption of K+ occur in severe hypokalaemia?
→ alpha intercalated cells of late DCT
→ K+/H+ pump
Flow chart for when ECFV decreases
Adrenal cortex increases aldosterone secretion and proximal tubule increases Na+ reabsorption
↓
tubules decrease flow rate
↓
cortical collecting ducts increase K+ secretion (aldosterone) and decrease K+ secretion (flow rate)
↓
K+ unchanged
How does the RAAS system regulate sodium and BP?
→ JGA senses a fall in BP
→ Macula densa detects low Na+ in the DCT
→ Renin is released from JGA → Angiotensin II
→ Causes vasoconstriction and stimulates adrenal cortex
How does aldosterone restore BP?
→ Acts on DCT to increase Na+ reabsorption
→ Increases activity and inserts more Na+/K+ ATPase pumps
→ Na+ ions bring water with them via osmosis
How is renin release suppressed?
→ suppressed by -ve feedback with angiotensin II
How does aldosterone increase serum pH?
→ Acts on intercalated cells
→ Increase activity of Na+, H+ antiporter and influences acid- base status
→ Increases H+ secretion
What factors shift K+ into cells?
→ Insulin
→ Aldosterone
→ Beta adrenergic stimulation
→ Alkalosis
What factors shift K+ out of cells?
→ Insulin deficiency → Aldosterone deficiency → Beta adrenergic blockade → Acidosis → Cell lysis → Strenuous exercise → Increased ECF osmolarity
What does the adrenal cortex produce?
→ Gluco corticoid hormones
→ Mineralocorticoud hormones
→Sex hormones
What is primary adrenal insufficiency / Addisons?
→ Damage to cortex
→ Decreased hormone production
→ numerous symptoms
What is a result of a deficiency in aldosterone?
→ Secretion of large amounts of Na+
→ Low serum Na+ levels
→ Body retains K+
What is the treatment of addisons?
→ Treatment usually involves corticosteroid replacement for life
What is secondary adrenal insufficiency?
→ pituitary secretes less ACTH
→ Decrease cortisol
→ Adrenal glands shrink
What is hyperaldersteronism/Conns syndrome?
→ excess release of aldosterone
→ due to tumor
→ Aldosterone release without angiotensin II
What does an increase in plasma aldosterone mean?
→ Kidneys to stimulate Na+ reabsorption and K+ excretion
→ increase BP and Na delivery to macula densa
→ decrease release of renin
→ Increase fluid volume
→ Hypokalaemia, hypernatremia and alkalosis
What is the treatment for Conns syndrome?
→ surgical removal of tumor containing adrenal gland
→ Hypertension and hyperkalaemia
