Renal 6 Flashcards

1
Q

Define secretion in terms of net movement of a solute.

A

Movement of a solute from the blood into the lumen of the nephron

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2
Q

Explain why all organic acids competitively inhibit secretion of other organic acids and why all organic bases competitively inhibit secretion of all other organic bases.

A
  • Because when you have a carrier-mediated transport that several different substances can use – secretion of one substance might be decreased in the presence of one of its competetitors. Rate of elimination decreases when 2 different drugs use the same carrier.
  • Organic anions actively pumped into basolateral cell, and passively moved from cap  interstitium and cell  tubule
  • Organic cations: electric force favors movement into cell
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3
Q

Explain the effect of low urine pH on the net secretion, excretion and plasma concentration of organic acids (e.g. aspirin).

A

Low pH and organic acids (aspirin): In general, membranes are more permeable to compounds in the associated form than the dissociated form. So higher concentration of H+ allows for more associated form of organic acid. This would allow for a larger back leak after secretion and a lower excretion of the organic acid. And vice versa with high pH.

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4
Q

Explain why alkalinizing the urine (by ingesting bicarbonate) would be helpful in treating an aspirin overdose.

A
  • Alkalinizing the urine would drive the oragnic acid to be in the dissociated form which will result in a higher excretion.
  • Weak bases, however, need more acidification to stay dissociated
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5
Q

Explain why an excretion rate that exceeds the filtration rate for a compound means that the compound was secreted.

A

If rate of excretion exceeds rate of filtration the compound had to be secreted. If the clearance rate for a compound is greater than the clearance rate for creatinine, the compound is said to be secreted.

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6
Q

Explain why the clearance of PAH is a measure of the effective renal plasma flow (ERPF).

A

Because all of PAH is removed either thru filtration or secretion, we know that clearance of PAH correlates with100% of the volume that is arriving at the afferent arteriole. “Effective” because only the blood flow that is measured by PAH secretion is that for which goes to the nephron and not the blood that only goes to renal fat.

  • the clearance of PAH is a measure of the volume of plasma that entered the kidney per unit time*
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7
Q

Calculate the ERPF when given the plasma and urinary concentrations of PAH and the rate of urine production.

A

ERPF = {(urine concentration of plasma) x (volume of urine collected/min)} /
(Plasma concentration of PAH)

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8
Q

Calculate the filtration fraction when given GFR and ERPF.

A

Filtration Fraction = GFR/ERPF

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9
Q

Explain why the nephron segments upstream of the distal tubule do not contribute to the regulation of potassium balance. (Hint: Does the percent of filtered potassium reabsorbed before the distal tubule depend on the concentration of potassium in the plasma?)

A

Because under hypokalemia, normal K+, and hyperkalemia  90% of filtered K+ is reabsorbed by the end no matter what case. If the body is trying to conserve K+, most of the rest is reabsorbed in the distal tubule or the collecting duct.

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10
Q
  1. Describe the effect of hyperkalemia on aldosterone secretion. 11. Describe the effect of increased plasma potassium on the Na+/K+ATPase pump on the basolateral membrane of the principal cells in the late distal tubule (second half of distal tubule) and collecting duct/tubule. What is the probable effect of aldosterone on this pump? What other effects does aldosterone have on the collecting ducts? 12. Describe the effect of increased aldosterone and increased potassium on the reabsorption or secretion of potassium in the late distal tubule (second half of distal tubule) and the collecting duct.
A
  • High K+ directly stimulates aldosterone secretion (not dependent on renin pathway)  stimulates Na/K ATPase pump on basolateral surface. This will pump K+ into the cell and then K+ can passively leave thru channels on the apical side.
  • High K+ also stimulates the Na/K ATPase pump on the basolateral side
  • Aldosterone also increases the number of active epithelial sodium channels (ENaCs). This increases the reabsorption of Na+ and secretion of K+. (ENaC is inhibitied by ANP)
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11
Q

Explain why diuretics which inhibit sodium and water reabsorption can cause the depletion of body potassium.

A
  • Loop diuretics inhibit the Na/K/Cl pumps in the thick ascending loop of Henle. This causes a higher flow of fluid thru late distal tubule and collecting duct which causes potassium secretion to increase.
  • Thiazide diuretics inhibit NaCl reabsorption in early distal tubule. Which also increases flow  affects prinicpal cells in late distal tubule  increased K+ secretion
  • Aldosterone blockers  will decrease Na and water reabsorption but do not increase K+ excretion.
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12
Q

State the effect of alkalosis on potassium. Does alkalosis cause hypokalemia or hyperkalemia?

A

Acute/Chronic metabolic alkalosis causes hypokalemia because metabolic alkalosis stimulates Na/K ATPase on basolateral membrane of principal cells. K+ increases in principial cells then flows out of the cell passively.

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13
Q

Explain why acute acidosis results in potassium retention and hyperkalemia.

A

Acute acidosis decreases the Na/K ATPase activity of principal cells  decreases permeability of apical membrane to K+  decreased K+ excretion  Hyperkalemia

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14
Q

State the effect of chronic acidosis on body potassium.

A

Chronic acidosis inhibits Na, Cl, and water reabsorption in proximal tubule  increased fluid flow in distal tubule  increased potassium secretion/excretion  hypokalemia

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