Phys 3 + 4 Flashcards

1
Q

How is K+ reabsorbed?

A

paracellularly

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2
Q

What does an increased flow rate mean for K+?

A

enhances secretion because the concentration build up doesn’t occur until later on because the concentration is diluted…there’s more Na+ in the later parts of the nephron, which leads to its reabsorption and K+s secretion

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3
Q

What does a decreased flow rate mean for K+?

A

the concentration builds up earlier, and without the gradient secretion slows

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4
Q

What is an important role of flow rate when Na+ levels increase?

A

aldosterone is down regulated, so increased flow rate (caused by increased GFR and decreased PCT Na+ reabsorption) helps to maintain levels of K+ excretion

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5
Q

What does chronic acidosis do?

A

stimulate K+ secretion

*acute decreases excretion

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6
Q

What’s the biologically active form of vitamin D called?

A

calcitriol

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7
Q

What is the role of calcitriol?

A

resorbs bone by stimulating osteoclasts–>increased Ca+ and phosphate plasma concentrations

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8
Q

What does calcitriol do to bone? intestine? kidney?

A
  1. promotes osteod mineralization; osteoclast mediated resorption
  2. increases Ca2+ and phosphorous absorption
  3. increased phosphorous and Ca2+ reabsorption

*works with PTH

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9
Q

What receptor does calcitriol use?

A

VDR (found throughout body)

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10
Q

What is the role of calcitonin?

A
  • lowers serum Ca2+ and phosphate by inhibiting bone resorption (decreases activity/number of osteoclasts)
  • promotes renal excretion of Ca2+ and phosphate

*works against PTH

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11
Q

What does calcitonin do to bone? kidneys?

A
  1. inhibits osteoclast bone respiration
  2. promotes phosphate and Ca2+ excretion

*used to treat osteoporosis, Paget’s disease, HyperCa2+

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12
Q

What does PTH do to bone? intestine? kidneys?

A
  1. increase osteoclast resorption
  2. Increase Ca2+/Pi absorption indirectly via calcitriol production
  3. increase reabsorption of Ca2+ (mainly in DCT); decreased–>reabsorption of Pi in PCT, Na+/H+ anti porter, and bicarbonate reabsorption
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13
Q

What can be caused by excessive PTH?

A

hypercalcemia, hypophosphatemia, hypercholermic metabolic acidosis

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14
Q

When is CaSR activated?

A

high levels of Ca2+

*inhibits Ca2+ reabsorption on apical membrane

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15
Q

How is Ca2+ reabsorbed in the PCT?

A

mainly paracellular (some trans cellular–>Ca2+ ATPase and Na-Ca2+ anti porter)

*major site

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16
Q

What does volume contraction do to Ca2+ reabsorption?

A

increases it

17
Q

Why is active transport needed for Ca2+ in the DCT?

A

because there is a negative transepithelial voltage

*TRPV5 is used to reabsorb Ca2+

18
Q

What four things can activate TRPV5? what can inhibit it?

A
  1. PTH, Vit D, Calcitriol, Thiazide diuretics; Alkalosis

2. Acidosis

19
Q

How does Pi cross the membrane in the PCT?

A

via it’s own, unidentified transporter and via the Na+/Pi symporter

20
Q

How is Vit. D activated in the Kidney?

A

1 alpha-hydroxylase/CYP1alpha/renal 1 alpha hydroxylase activates it in the PCT

21
Q

How do the following regulate Pi levels: FGF-23, PTH, Calcitriol, Insulin, Dietary, renal function?

A
  1. increase excretion
  2. increase excretion
  3. increase absorption
  4. lowers serum levels via cell uptake
  5. variable
  6. decrease reabsorption (bc no Vit. D)
22
Q

What is the most important hormone that regulates Pi excretion?

A

PTH

*inhibits Na+/Pi transporters and Na/H antiporter in apical membrane of PT cells

23
Q

How does chronic acidosis affect Pi excretion? alkalosis?

A
  1. increase

2. decrease

24
Q

Where does Mg fine tuning take place?

A

DCT

*crosses apical border via TRPM6

25
Q

What effect do the following have on Mg2+ reabsorption?

  1. Dietary depletion
  2. PTH
  3. Metabolic acidosis
  4. Metabolic alkalosis
  5. ECF volume expansion
  6. ECF volume contraction
A
  1. increase –> increase paracellular permeability
  2. increase
  3. decrease–> decrease paracellular permeability
  4. increase–> increase paracellular permeability
  5. decrease
  6. increase