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SP1 Physiology/Microanatomy 2 > Lecture 37 4/12/24 > Flashcards

Lecture 37 4/12/24 Flashcards

1
Q

Why is precise control of ECF potassium necessary?

A

many cell functions are sensitive to changes in ECF potassium concentration

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2
Q

Where is potassium contained within the body?

A

-98% within the cells
-2% in the ECF

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3
Q

Why is it important that the ECF is rapidly rid of ingested potassium?

A

daily potassium intake is often high enough to cause severe, life-threatening hyperkalemia if the potassium is not removed and/or stored in the cells

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4
Q

What does potassium homeostasis depend on?

A

-excretion of potassium by the kidneys
-control of potassium distribution between the extracellular and intracellular compartments

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5
Q

How does insulin affect the distribution of potassium between the cells and the ECF?

A

insulin stimulates Na+/K+ ATPase activity, which transports potassium into the cells

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6
Q

How do catecholamines affect the distribution of potassium between the cells and the ECF?

A

catecholamines activate beta2-adrenergic receptors which stimulate Na+/K+ ATPases, causing transport of potassium into the cells

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7
Q

How does alkalosis affect the distribution of potassium between the cells and the ECF?

A

-causes activation of Na+/H+ exchanger, which leads to an increase in intracellular Na+
-blocks the H+/K+ exchanger to prevent K+ from leaving the cell
-increased intracellular Na+ activates the Na+/K+ ATPase to bring K+ into the cell

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8
Q

How does increased potassium intake affect the distribution of potassium between the cells and the ECF?

A

stimulates the secretion of aldosterone, which increases cell potassium uptake

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9
Q

How does metabolic acidosis affect the distribution of potassium between the cells and the ECF?

A

-blocks the Na+/H+ exchanger; decreased intracellular Na+ prevents Na+/K+ ATPase activity
-activates the H+/K+ exchanger
-both lead to increased ECF potassium conc.

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10
Q

Why is cell destruction associated with hyperkalemia?

A

cell destruction releases stored potassium into the ECF

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11
Q

Renal potassium excretion is determined by the sum of which three processes?

A

-rate of potassium filtration
-rate of potassium reabsorption by the tubules
-rate of potassium secretion by the tubules

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12
Q

Where does potassium reabsorption occur?

A

-65% in the proximal tubule
-25-30% in the LOH (active co-transport with Na and Cl)
-variable rates in collecting tubules and ducts

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13
Q

Which cells in the late distal and collecting tubules can reabsorb potassium when potassium intake is low?

A

type A intercalated cells

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14
Q

Which mechanisms are thought to be behind type A intercalated cell reabsorption of potassium?

A

-H+/K+ ATPase transport
-diffusion through potassium membrane channels

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15
Q

Which regions of the nephron excrete extra potassium when intake is high?

A

distal and collecting tubules

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16
Q

What are the steps involved in secretion of potassium from the blood into the tubular lumen?

A

-uptake from the interstitium into the cell via Na+/K+ pump
-passive diffusion of K+ from the cell interior into the tubular fluid

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17
Q

Which channels are present in the principal cell membranes that allow for rapid potassium diffusion?

A

-renal outer medullary potassium (ROMK) channels
-high-conductance, “big” potassium (BK) channels

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18
Q

Which steps are involved in type B intercalated cells excreting extra potassium during high intake?

A

-potassium pumped into cells via H+/K+ ATPase
-diffusion of potassium into the tubular lumen

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19
Q

Which factors stimulate potassium secretion?

A

-increased ECF K+ concentration
-increased aldosterone
-increased tubular flow rate

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20
Q

What does increased ECF K+ lead to increases in?

A

-principal cell activity/Na+/K+ ATPase activity
-BK and ROMK channels
-K+ gradient from the renal interstitium
-aldosterone

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21
Q

How does aldosterone lead to increased K+ excretion?

A

-aldosterone stimulates active reabsorption of Na+, which is mediated by Na+/K+ pumps
-aldosterone also increases the number of potassium channels in cells

22
Q

In addition to increased excretion, how else does aldosterone lower the ECF conc. of K+?

A

by increasing cellular uptake of potassium

23
Q

How does a high-volume flow rate increase potassium secretion?

A

-causes secreted potassium to be continuously flushed down the tubule, minimizing tubular K+ conc. and increasing net secretion
-increases number of BK channels in the luminal membrane

24
Q

Why is it important that high sodium intake increases distal flow rate?

A

-increased distal flow rate increases potassium secretion
-this counterbalances the decrease in potassium secretion that occurs due to aldosterone, which also accompanies high sodium intake
-counterbalance ensures that potassium excretion remains constant even though sodium intake changes

25
Q

What percent of the body’s calcium mass is contained within the ECF?

A

0.1%

26
Q

What happens when ECF calcium concentration drops?

A

-increased excitability of nerve and and muscle cells
-hypocalcemic tetany

27
Q

What happens when ECF calcium concentration rises?

A

-depression of neuromuscular excitability
-cardiac arrhythmias

28
Q

How does plasma hydrogen ion concentration influence calcium binding to plasma proteins?

A

-acidosis leads to less calcium being bound to plasma proteins
-alkalosis leads to more calcium being bound to plasma proteins

29
Q

Where is the majority of calcium excreted?

A

feces

30
Q

What happens when calcium conc. is low?

A

-stimulates release of PTH
-increased vit. D activation
-increased intestinal calcium reabsorption
-increased renal calcium reabsorption
-increased calcium release from bones

31
Q

Why is only 50% of plasma calcium filtered at the glomerulus?

A

-only 50% of plasma calcium is ionized
-the other 50% is either bound to plasma proteins or complexed with anions

32
Q

What percent of filtered calcium is excreted?

A

1%

33
Q

Where is calcium reabsorbed in the nephron?

A

-proximal tubule
-LOH
-distal and collecting tubules

34
Q

What is the breakdown of calcium reabsorption in the proximal tubule?

A

-80% paracellular
-20% transcellular

35
Q

What are the steps of transcellular calcium reabsorption in the proximal tubule?

A

-calcium exits the cell via Ca++-ATPase pump and Na+/Ca++ counter-transporter
-calcium diffuses from tubular lumen into the cell down an electrochemical gradient due to the higher conc. of calcium in the lumen

36
Q

What are the characteristics of calcium reabsorption in the LOH?

A

-only occurs in thick ascending limb
-50% paracellular
-50% transcellular, under PTH control
-calcitonin and calcitriol contribute slightly

37
Q

What are the characteristics of calcium reabsorption in the distal tubule?

A

-almost entirely active transport
-involves Ca++-ATPase and Na+/Ca++ counter-transporter
-stimulated by PTH
-calcitonin and calcitriol contribute slightly

38
Q

Which factors decrease calcium excretion?

A

-inc. PTH
-dec. ECF Ca++ conc.
-dec. blood pressure
-inc. plasma phosphate conc.
-metabolic alkalosis
-vitamin D

39
Q

Which factors increase calcium excretion?

A

-dec. PTH
-inc. ECF Ca++ conc.
-inc. blood pressure
-dec. plasma phosphate conc.
-metabolic acidosis

40
Q

Why is it important that calcium reabsorption is independent of PTH in the proximal tubule?

A

in cases of extracellular volume expansion or increased arterial pressure, calcium reabsorption is reduced along with sodium and water reabsorption

41
Q

What are the characteristics of renal phosphate excretion?

A

-controlled by an overflow mechanism
-when the level of phosphate in the glomerular filtrate is less than the normal transport maximum in the tubules, no phosphate is excreted
-when the level of phosphate in the glomerular filtrate exceeds the transport maximum, excess phosphate is excreted

42
Q

Where in the nephron is phosphate reabsorbed?

A

-75-85% in the proximal tubule
-10% in the distal tubule
-10% excreted

43
Q

What are the characteristics of phosphate reabsorption in the proximal tubule?

A

-primarily via transcellular pathway
-involves sodium/phosphate co-transporter
-may involve a counter-transport mechanism in which phosphate is exchanged for an anion

44
Q

How is PTH involved in phosphate conc. regulation?

A

-PTH promotes bone resorption, which releases large amounts of phosphate into the ECF
-PTH decreases the abundance of sodium/phosphate co-transporters, which reduces reabsorption
-net function of increased PTH is increased phosphate excretion

45
Q

Which factors decrease phosphate excretion?

A

-decreased dietary phosphate
-vitamin D
-metabolic alkalosis
-thyroid hormones

46
Q

Which factors increase phosphate excretion?

A

-increased dietary phosphate
-PTH
-metabolic acidosis
-hypertension

47
Q

What percent of the body’s magnesium is in the ECF?

A

1%

48
Q

How much of the magnesium in the plasma is bound to plasma proteins?

A

more than half

49
Q

What percent of magnesium in the glomerular filtrate is excreted by the kidneys?

A

10-15%

50
Q

Where is magnesium reabsorbed within the nephron?

A

-25% in proximal tubule
-65% in LOH
-small amount in distal and collecting tubules

SP1 Physiology/Microanatomy 2 (50 decks)

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