Regulation of K, Ca, PO4, Mg Flashcards
(35 cards)
Which ion has effects on membrane potential and muscle/nerve excitability when increased or decreased?
Potassium (K)
Hypokalemia on membrane potential
Hyperkalemia on membrane potential
Increased threshold needed to fire AP
Decreased threshold needed to fire AP
A patient is hyperkalemic. How might you tell from an EKG?
How to think about it?
High T wave
Low PR interval
Likes to re-polarize (high T)
Lower resting potential due to higher K (low PR)
A patient is hypokalemic. How might you tell from an EKG?
How to think about it?
Low T wave
High U wave
Likes to depolarize (smaller T wave)
U wave opposite of T wave (high U)
What situations will favor movement of K+ into ECF?
Why? (for each)
Hypokalemia - need to replenish plasma
Acidemia - buffering excess H+ moving INTO cells
Alpha-adrenergic agonists
What situations will favor movement of K+ into ICF?
Why? (for each)
Hyperkalemia - excess needs to go somewhere
Alkalemia - buffer H+ moving into plasma to replenish
Beta-adrenergic agonists
How is K+ reabsorbed in the:
PT
Loop
CD
PT - paracellular (+ lumen)
Loop - NaKCl2
CD - IC cells
Main physiologic control of K+ reabsorption/secretion is where?
How is K+ secreted?
CD
Principle cells and IC cells
A person is hypokalemic. What substance will be HIGH in the epithelial cells of the lumen?
Why?
Sodium (Na)
Less K+ to drive basolateral Na/K ATPase, so Na builds up in cell
Why does aldosterone cause up-regulations in K+ and H+ secretion?
Increases Na+ brought into cell (increases Na/K exchanger)
Increases negative lumen and need for electrochemical balancing
Reasoning for why high aldosterone causes alkalosis AND hypokalemia
Increased Na/H exchange = less H+ in body = H/K exchange = more K in cell = more Na/K exchange
OR just up-regulates both Na/H and Na/K exchangers
A patient is put on a diuretic for CHF. What is a potential side effect (potassium)?
What is the treatment? Why?
More Na+ delivery to CD –> more K+ secretion –> hypokalemia
Tx = Low-Na diet
Less excess delivery to CD = less K+ secretion
A patient is put on a low-sodium diet for health reasons. What is a potential side effect (potassium)?
Tx? Why?
Less Na+ delivered to CD –> Hyperkalemia
Tx = diuretic
More Na+ delivered to CD
Conn’s disease
Side effects?
Hyperaldosteronism
Hypokalemia (more Na/K exchange)
Alkalosis (more Na/H exchange)
Addison’s disease
Side effects?
Hypoaldosteronism
Hyperkalemia
Acidosis
Potential Tx for Conn’s disease?
Aldosterone antagonist
Potential Tx for Addison’s disease?
Upstream diuretic (increase Na+ delivery to CD)
A patient is on a loop diuretic. How will the RBF be affected?
Increased
More water excreted = volume depletion = compensation for low GFR by increasing RBF
Main C.A. inhibitor drug
Main osmotic diuretic
Acetazolamide
Mannitol
Main loop diuretics
Furosemide (Lasix)
Bumetanide (Bumex)
Main thiazide diuretic
Hydrochlorothiazide
Main aldosterone antagonist
Main K+ - sparing diuretics
Spironolactone
Amiloride, Triamterene
How do K+-sparing diuretics work?
Block Na+ channels in the CD
A patient comes in with rigid muscles. ABG values show high pH. What is the cause?
Low H+ = low free Ca++
Hypocalcemic tetany
