Physio 12 Flashcards
hyperkalemia
plasma K concentration above 5 mM. decreases outwardly directed K gradient, depolarizing the resting membrane potential. muscle hyperexcitability leading to ventricular arrhythmias and fibrillations. leads to metabolic acidosis
hypokalemia
plasma K concentration below 3.5 mM. increases outwardly directed K gradient, hyperpolarizing the membrane potential. Leads to hypoexcitability of the muscles, cardiac pace maker disturbances, and arrhythmias. can lead to metabolic alkalosis
external K+ balance
gastro-intestinal K+ uptake into the body balanced by renal and fecal removal of K from the body. amount of K excreted every day must equal the amount consumed
internal K+ balance
distribution of K+ between intracellular and extracellular fluids, due mostly to the Na/K ATPase pump. Most K+ is in muscle.
what promotes uptake of K+ into the cells?
insulin, epinephrine, and aldosterone. these hormones induce synth of Na/K ATPase
what happens during acidemia?
inhibition of Na/K ATPase and Na/K/2Cl cotransporter, causing loss of K+ from cells resulting in hyperkalemia
what happens during alkalemia?
stimulation of the Na/K ATPase causing uptake of K+ into cells, resulting in hypokalemia
renal handling of K+ equation
K excreted = (K filtered - K reabsorbed) + K secreted
where is K+ reabsorbed
proximal tubule
where is K+ secreted
distal nephron. some reabsorption happens here as well
how does K+ reabsorption in the proximal tubule happen?
paracellular. occurs by solvent drag and by passive electrodiffusion
how does K+ reabsorption happen in the thick ascending limb of the loop of Henle?
transcellular and paracellular. Transcellular uses Na-K-2Cl cotransporter and Na/K ATPase.
Paracellular is done using gradients
how is K+ reabsorbed in the distal nephron?
transcellular. Done by alpha intercalated cells. Uses K/H ATPase, transports K in and H out. Deficit of intracellular H increases HCO3 inside cell, which is put into the interstitial space using a Cl/HCO3 exchanger. can lead to metabolic alkalosis if K+ reabsorption is maximal
how is secretion of K+ performed?
transcellular. done by Principle cells in the distal nephron. Na/K ATPase on basolateral membrane gets K into cell, then it diffuses out passively into lumen
tubular flow dependence of distal tubule K+ secretion
faster flow = more secretion. the high flow sweeps away the K+ quickly, keeping the concentration gradient high.
slower flow = less secretion. slower flow means the concentration gradient is lower, allowing for slower secretion
regulation of K+ excretion at high dietary K+
increased secretion of K+ in the cortical distal nephron. DEcreased reabsorption of K+ in the cortical distal nephron
aldosterone effects
increases K+ secretion. induces increased capacity for Na+ reabsorption and K+ secretion in the distal nephron. Induces synth of Na/K ATPase, Na and K channels, and mitochondrial enzymes. increased Na conductance depolarizes membrane increasing driving force for K to go out of the cell
regulation of K+ excretion at low dietary K+
decreased secretion of K+ in the cortical distal nephron. increased reabsorption of K+ in the cortical distal nephron
how does alkalosis affect distal nephron K+ secretion?
increases it. decreased plasma [H+] increases intracellular K+. increased intracellular K+ increases driving force and rate of K+ transport out of the cell, leading to hypokalemia (hypokalemic metabolic alkalosis)
how does acidosis affect distal nephron K+ secretion
increased plasma [H+] induces decreased intracellular K+. thi decreases the driving force so less K+ goes out of the cell, leading to hyperkalemia (hyperkalemic metabolic acidosis)
why is potassium so important?
K+ concentration gradient across the cell membrane is largely responsible for the potential or voltage difference across the cell membrane.
