5. Regulation of K, Ca, PO4, and Mg Flashcards
What are the symptoms of hypokalemia?
A SIC WALT
Alkalosis, shallow respirations, irritability confusion/drowsiness, Weakness, arrhythmias (tachycardia or brady), lethargy, thready pulse
decrease in intestinal motility, nausea, vomit
What is addison’s disease?
hypoaldosteronism resulting in hyperkalemia
Hypoaldosteronism increases water and salt excretion and reduces potassium excretion
Destruction of adrenals: aldosterone isnt secreted
What is the normal range of plasma K?
2% in ECF
3.5-5.0 mEq/l
What is the acute effect of low EC K concentration on resting membrane potential of excitable tissues?
It lowers the resting membrane potential and makes it harder to excite the tissue
What are some factors that cause K to move from ICF to ECF?
Hyperosmolarity, Cell lysis, Heavy exercise, acidemia, hypokalemia, alpha-adrenergic agnoists
What factors affect the movement of K from the ECF to the ICF?
Hyperkalemia, alkalemia, beta-adrenergic agonists, insulin
If K moves from the ECF to the ICF, something has to be changed to maintain electroneutrality. What is exchanged and what can result if there is a high amount of exchange?
H+ ion is exchanged and can cause acidosis in the ECF
Patients with hyperkalemia are at risk of acidosis.
Why are diabetics at risk for hyperkalemia?
Because insulin moves K into the cells. Without insulin, the K stays in the ECF and causes hyperkalemia
Patients that have alkalosis are prone to what levels of K in the ECF? why?
Hypokalemia. The reduced extracellular H concentration favors movement out of the cell and to maintain electroneutrality, K and Na enter the cell
Vice versa can happen. Too much acid will result in hyperkalemia
K is handled differently in different segments of the nephron. Where is most of the K reabsorbed? How much is reabsorbed? What is the method of reabsorption?
In the proximal tubule
67% reabsorbed
Paracellular- solvent drag and diffusion (+lumen)
Where is 20% of K reabsorbed in the nephron?
Thick ascending limb of henle by the Na,K,2Cl cotransport
Where is physiological control of K exerted in the nephron?
collecting duct by principal cells that either reabsorb or secrete K depending on body’s K balance.
What are the FIVE factors which affect K secretion in collecting duct?
ECF K concentration
Na reabsorption: negative luminal voltage attracts K
Luminal fluid flow rate: dilution of secreted K results in conc. gradient
Extracellular pH: K/H exchange
Aldosterone: Collecting duct, maintain electroneutrality
Most classes of diuretics increase Na and volume delivery to late distal tubule and CD, which ________ K secretion
increases
Less Na delivery to late distal tubule and CD causes ______ K secretion
less, and may cause hyperkalemia
If there is an increase in extracellular H what cation exchanges happen in the collecting duct principal cells? What results?
H/K exchange on interstitial side of cell. It will cause H/K exchange which lowers intracellular K concentration and thus decreases K secretion and increases plasma K
What is the major regulator of plasma K?
aldosterone,
It goes into the nucleus to increase the amount of K channels and Ka/K ATPase
aldosterone does not monitor Na concentration
The presence of high aldosterone causes a negative feedback to what system?
RAAS, so in a patient with high aldosterone there can be low plasma renin
A person with hyperaldosteronism, what would you expect the Na concentration to be? why?
Normal because along with Na reabsorption, water is reabsorbed, maintaining concentration
In a patient with hypoaldosterionism, what would you expect the level of plasma Na to be?
Low because, Na will decrease because we are no longer holding onto it and losing it at a higher rate
What is Conn’s disease?
hyperaldosteronism resulting in hypokalemia
Aldossterone secreting tumor in adrenal cortex
K secretion by CD is inappropriately stimulated
What do osmotic diuretics do?
e.g. mannitol: inhibit reabsorption of water and secondarily, Na in the proximal tubule and thin descending limb of henle. Generate osmotic pressure gradient
What do carbonic anhydrase inhibitors do?
Acetazolamide: inhibit NaHCO3 reabsorption in the proximal tubule
reduce Na reabsorption by their effect on carbonic anhydrase and 1/3 of proximal tubule Na reabsorption occurs in exchange for H (Na/H antiporter)
Long term creates metabolic acidosis
*only used for altitude sickness
What are some examples of Loop diuretics?
Furosemide (lasix), bumetanide (bumex) and ethacrynic acid
