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47 Cards in this Set

  • Front
  • Back
what is the normal range of k
3.5 -5
what is hyperkalemia
above 5
what is hypokalemia
below 3.5
what is the effect of k on membrane potential
it determines the resting membrane potential
how does hypokalemia effect the resting membrane potential
it makes it more difficult to depolarize
what does hyperkalemia do to the resting membrane potential
it makes it easier to reach threshold and therefore is hyperexcitable
more k's make you hyper
what effects on the ecg does hyperkalemia have
ventricular fibrillation
prolonged PR interval
depressed st segment
high t waves
what effects on the ecg does hypokalemia have
low t waves
high u waves
low st segment
how is k filtered in the bowman's capsule
it is freely filtered
what happens to the k in the nephron
it is 67% reabsorbed in proximal tubule
20% is reabsorbed in thick ascending limb of henle
and the physiological control occurs in the collecting duct
what type of cells in the collecting duct work on the concentration of k
principal cells - either reabsorb or secrete the k
what are the 5 factors that affect k secretion
extracellular k concentration
na concentration in tubular lumen
luminal flow rate
extracellular ph
what happens to the urinary k when there is an increase in plasma k conc
increases - you pee it out!
what situations alter the k handling
diuretics and a low sodium diet
how does diuretics alter the k handling
increase na volume delivery to late distal tubule and collecting duct and that increases K secretion
how does a low sodium diet effect k
hyperkalemia - less na delivery to the late distal tubule and collecting duct there is less k secretion and excretion
what should a low sodium diet person also be doing
eating less k
how does the tubular flow rate affect k secretion
more k secretion with higher tubular flow rates in the late distal and collecting duct
how is the plasma k effected by plasma pH
more alkaline pH more you secrete k
more acidic less secretion of k so acidemia favors hyperkalemia
higher extracellular protons causes the h/k exchange which does what
lowers the intracellular k concentration in the principal cells and therefore decreases k secretion
what stimulates the secretion of k in the distal tubule and the collecting duct
what is the mechanism of aldosterone's stimulation of k secretion
na/k atpase increase
and k channels
as k increases in the serum plasma what happens to aldosterone
it is stimulated
what are 2 disorders of aldosterone secretion
conn's disease and addison's
what is conn's
primary hyperaldosteronism
aldo secreting tumor
k secretion in collecting duct is in inappropriately stimulated
what do you see with conn's disease in regards to k
think the "con-man" stole all the k away
also the person is alkylotic
what is addison's
destruction of the adrenals
aldo not secreted
decreased k secretion
what is the concentration of k in addison's
what diuretics act at the proximal tubule
osmotic and carbonic anhydrase inhibitors
how does osmotic diuretics work
they inhibit reabsorption of water and secondarily of na
how does the carbonic anhydrase inhibitor work
it inhibits the hco3 reabsorption and therefore is also good for the alkalotic pt
how does furosimide work
lasix inhibits the na, k, 2cl cotransporter in the loop
it lessens the water reabsorption and should be used under careful medical supervision;
remember if not used properly can cause a fury in the loop
works on the distal convoluted tubule
inhibits na cl cotransport
potassium sparing diuretics
blocks na channels in collecting duct
aldosterone antagonist so is potassium sparing
low extracellular ca will do what
hypocalcemic tetany - this was definitely an old test question
where is 45% of the free ca
bound to albumin
what effect does pH have on the free Ca concentration
h competes with Ca for binding sites on plasma proteins
acidemia increases free ca
alkamemia decreases free ca
what occurs with severe alkalemia
pt develops hypocalcemic tetany
what is the mechanism of proximal tubular ca reabsorption
3 na in exchange for one ca
and ca pump using atp
where does paracellular ca reabsorption occur
in the thick ascending loop of henle via channels in tight junctions driven by 6 mV transepithelial potential
what hormones stimulate the ca reabsorption
decreased plasma ca does what to the parathyroid gland
causes the pth secretion
what does pth do
increases ec ca
where does 80% of the phosphate reabsorbed in the nephron
proximal tubule
what inhibits reabsorption of the phosphate in the proximal tubule
parathyroid hormone
where does the bulk of the mg handled in the nephron
thick ascending limb of the loop of henle via the paracellular route due to 6 mV transepithelial potential