Potassium Balance Flashcards
Outline Potassium intake and output, and where they’re stored
What are the main roles of Potassium?
What are the measures in place for potassium homeostasis?
- Intake - leafy vegetables, fruit, potatoes
Output - urine, stools, sweat
Most is stored in cells (mainly muscle), with the rest in the ECF
- Determining ICF osmolality, RMP, vascular resistance.
- Internal measures: Acute regulation - distribution between ECF and ICF compartments
External measures: Chronic regulation - adjustment of kidney potassium excretion and reabsorption
How does Na+ and K+ in the ECF work to produce the RMP?
The Na/K ATPase pump maintains the High [K+] and Low [Na+] intracellularly.
What affects the ECF [K+]?
What does the ECF [K]+ say about the stage of action potentials in the heart?
What are the ECG changes?
- Insulin, Adrenaline, Aldosterone, PH
- Low [K+] = hyper polarisation, High [K+] = depolarisation.
Hypokalaemia: ↓amplitude T-wave, prolong Q-U interval, prolong P-wave
Hyperkalaemia: ↑QRS complex, ↑amplitude T-wave, eventual loss P-wave
What causes Hypokalaemia?
What is the affect of Hypokalaemia on the body?
- <3.5mmol - due to renal/extra-renal loss of K+, restricted intake, diuretics without K supplementation, prolonged vomiting, diarrhoea, Hyperaldosteronism (Conn’s)
- ↓Aldosterone, Adr, Insulin release
What causes Hyperkalaemia?
What is affect of Hyperkalaemia on the body?
What are some of the treatment options?
- > 5.5mmol - due to prolonged exercise (K moves from muscle to ECF), insufficient renal excretion, ↑release from damaged body cells (e.g. chemotherapy), Long-term use of K-sparing diuretics, Addison’s disease (adrenal insufficiency)
- Plasma [K+] > 7mmol is life-threatening → Asystolic cardiac arrest
- Insulin-Gluose infusion, given other hormones e.g. Aldosterone, Adrenaline.
How does the kidney try to handle Na+ and K+?
Preserve Na+
Excrete K+
How is K+ REABSORBED in the PCT?
LOOK AT DIAGRAMS!!
- K+ is actively transported into epithelial cells via the Na/K pump on the basolateral membrane - pump inhibited by Dopamine/Digitalis
- K+ then goes back into the ECF via the K+ channels on the basolateral membrane
- Passive, facilitated diffusion of Na+ (via symporter and antiporter) on the luminal membrane into cell
- Passive, paracellular uptake of Na+ and K+ from lumen to ECF
How is K+ REABSORBED in the Loop of Henle?
LOOK AT DIAGRAMS!!
- In ascending limb, a Symporter transports K+, Na+, and 2Cl- into cell from lumen - inhibited by Loop diuretics = Hypokalaemia
- Active transport of K+ into cell from ECF via Na/K pump on the basolateral membrane
- K+ goes into the ECF from cell via K+ channels on the basolateral membrane
How is K+ SECRETED in the DCT?
LOOK AT DIAGRAMS!!
What determines K+ secretion in the DCT? How is this achieved?
- Since most K+ is reabsorbed, it has to be further adjusted by secretion - occurs in principal cells of the late DCT and CD:
- ENaC (epithelial Na channel) transporter (ALDOSTERONE-SENSITIVE) brings Na+ into cell from lumen - inhibited by K-sparing diuretics
- The Na/K pump and K+ channels work to create an electrochemical gradient = net K+ movement into lumen
- ↑K+ intake and PH changes (acidosis/alkalosis) - is achieved by the Na/K pump, electrochemical gradient, and permeability of the luminal membrane channels.
The factors that affect K+ secretion in DCT are:
- Aldosterone
LOOK AT DIAGRAMS!!
Aldosterone acts to ↑K+ secretion by:
• ↑Na/K pump activity on basolateral membrane = ↑K+ moved into cell
• ↑ENaC activity = ↑Na+ reabsorption = ↑gradient across luminal membrane
• Redistributes ENaC from being inside cell to being on the membrane
• ↑Permeability of K+ across the luminal membrane
- Increase in Plasma [K+]
LOOK AT DIAGRAMS!!
It ↑K+ secretion in 3 ways to prevent hyperkalaemia:
- Slows down exit of K+ through basolateral membrane = ↑cell [K+] and ↑cell-lumen conc. gradient
- ↑Na/K pump activity on basolateral membrane = ↑K+ moved into cell
- Stimulates Aldosterone secretion = even more K+ secretion
- Acidosis and Alkalosis
LOOK AT DIAGRAMS!!
Acidosis (↓PH):
• INHIBITS Na/K pump = ↓[K+] in cell = ↓K+ secretion
Alkalosis (↑PH):
• ↑Na/K pump = ↑[K+] in cell = ↑K+ secretion
• ↑Luminal membrane permeability
- Increase in Tubular Flow Rate
LOOK AT DIAGRAMS!!
It ↑K+ secretion by:
• Moves away the K+ to make the filtrate [K+] low again; maintain concentration gradient for continuous secretion.
- Tubular flow can be increased by ↑GFR, Inhibition of reabsorption, K-wasting diuretics.
What cells are active in severe hypokalaemia and what does their activity result in?
α-intercalated cells of late DCT/CD = ↑K+ reabsorption = ↑plasma [K+]
Explain the role of the RAAS in Na/K balance
LOOK AT DIAGRAMS!!
- JGA and Macula Densa sense a ↓BP and a ↓Na+ = Renin secretion from JGA.
- Renin → Ang II, which causes vasoconstriction (↑BP) and stimulates Aldosterone secretion from adrenals.
- Aldosterone acts on Principal cells of late DCT/CD = ↑increase Na+ reabsorption and K+ secretion - the Na+ also brings water with it so the BP and Na levels are restored.
- Aldosterone also acts on the intercalated cells = ↑Na+ and K+ reabsorption, and H+ secretion.
* ALDOSTERONE HAS DIFFERING EFFECTS ON POTASSIUM DEPENDING ON WHICH CELL IT ACTS ON!
