Unit 4: Renal Phys. -- ion and Urea Handling by the Nephron/ H2O Balance Flashcards

1
Q

What are the percentages for the Filtered load for the following ions?

  1. Na+
  2. K+
  3. PO4^3-
  4. Ca++
  5. Mg++
A
  1. 100%
  2. 100%
  3. 90%
  4. 60%
  5. 80%
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2
Q

What ion has the lowest filtered load?

A

Ca++

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3
Q

What ions has the highest filtered load?

A

Na+ and K+

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4
Q

What ion has the most variability of excretion?

A

K+

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5
Q

What ions are basically 100% reabsorbed?

A

Na+ and Ca++

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6
Q

What ion has some reabsorption taking place in the Proximal Straight Tubule?

A

Phosphate

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7
Q

What are all the locations that

Na+ is reabsorbed?

A

PCT– 67%
TAL – 25%
DCT – 5%
CD –3%

Excretion <1%

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8
Q

What are all the locations that K+ is reabsorbed or excreted?

A

PCT – 67%
TAL – 20%
DCT/CD – only if low in diet

CD– variable excretion

Excretion varies 1-100%

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9
Q

What are all the locations where phosphate is reabsorbed?

A

PCT – 70%
Proximal Straight Tubule– 15%**

Excretion ~15% (serves as buffer in urine for H+)

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10
Q

What are all the locations that Ca++ is reabsorbed?

A

PCT – 67%
TAL – 25%
DCT – 8%

Excretion <1%

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11
Q

What inhibits Na+ reabsorption in the DCT?

A

thiazide diuretics

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12
Q

What inhibits Phosphate reabsorption in the PCT?

A

PTH

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13
Q

What inhibits Ca++ reabsorption in the TAL?

A

Furosemide (loop diuretic)

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14
Q

What stimulates Ca++ reabsorption in the DCT?

A

PTH

Thiazide diuretics

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15
Q

What inhibits Mg++ reabsorption in the TAL?

A

Furosemide (loop diuretic)

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16
Q

What are all the locations that Mg++ is reabsorbed?

A

PCT– 30% (lowest of all)
TAL– 60%
DCT– 5%

Excretion ~5%

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17
Q

What two ions absorption are inhibited by Furosemide (loop diuretic in the TAL?

A

Ca++ and Mg++

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18
Q

How much Urea is in the tubules prior to the PCT? What about after the PCT? What happens in the Thin descending limb?
How much urea is in the DCT? What happens in the CD?

A
prior to PCT-- 100%
after PCT -- 50%
Thin descending limb--> secreted
in DCT--> 110%
CD--> UT1 takes 70% urea out

Excretion id ADH present = 40%

(if no ADH– then all is secrete)

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19
Q

What is important on the basolateral side in order to keep Na+ low in the cell so Na+ can come in passively on the luminal side?

A

Na+ K+ ATPase pump

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20
Q

Where does most reabsorption take place?

A

in the proximal convoluted tubule

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21
Q

What part of of the nephron is impermeable to H2O?

A

the Thick Ascending Limb

22
Q

Where is tubular fluid diluted in the nephron? Why?

A

in the Thick Ascending Limb b/c it is impermeable to water –> only solute can be pulled out of tubule and therefore dilutes urine

23
Q

What hormone increases K+ secretion by principal cells?

A

Aldosterone

24
Q

When there is an increase in plasma osmolarity due to water deprivation what gets stimulated and where?

A

stimulate osmole receptors in anterior hypothalamus

25
Q

During water deprivation, what will stimulation of osmole receptors in the anterior hypothalamus have of ADH?

A

increase ADH release–> therefore increase H2O permeability of principal cells (in DT and CD)–> will increase H2O reabsorption —> therefore increasing urine osmolarity and decreasing urine volume–> decreasing plasma osmolarity toward normal

26
Q

During water deprivation, stimulation of osmole receptors in the anterior hypothalamus will cause the stimulation of what two things?

A
  1. increase ADH release

2. increase thirst

27
Q

What will too much H2O intake cause? and what will our body’s response be?

A

decrease in plasma osmolarity–> inhibit osmole receptors in anterior hypothalmus

28
Q

What will the inhibition of osmole receptors in the anterior hypothalamus cause during H2O intake?

A
  1. decrease ADH release

2. decrease thirst

29
Q

What is the gradient of osmolarity in interstitial fluid from the cortex to the tip of the papilla?

A

Corticopapillary osmotic gradient

30
Q

What solutes contribute to the Corticopapillary osmotic gradient?

A
  • NaCl

- Urea

31
Q

What mechanisms will deposit NaCl and Urea into the ISF to create the Corticopapillary osmotic gradient?

A
  1. Countercurrent multiplication–> deposits NaCl in deeper regions
  2. Urea Recycling –> deposits urea; a fxn of inner medullay CD
32
Q

What is the two step process for Countercurrent Multiplication? What are the two steps repeated until?

A
  1. Single Effect
  2. Flow of Tubular Fluid

they are repeated until full corticopapillary gradient is established

33
Q

What does the size of the Corticopapillary gradient depend on? What is it in humans?

A

depends on length of loop on Henle

1200 mOsm/L at bend of juxtamedullary nephrons in humans

34
Q

What CREATES/establishes the corticopapillary gradient?

A

Countercurrent multiplication

two step process– Single Effect and Flow of Tubular Fluid

35
Q

What helps MAINTAIN the gradient b/w the ISF and tubules?

A

Countercurrent Exchange

36
Q

What does the Single Effect step of the Countercurrent Multiplication refer to the function of?

A

to the function of the Thick Ascending Limb

  • here Na+ is reabsorbed via Na+K+2Cl- cotransporter
  • its activity is increased by ADH
  • TAL is impermeable to water and this dilutes fluid in TAL

Recall: Descending limb is permeable to water

Result:

  • osmolatrity in ISF and descending limb increases
  • osmolarity in ascending limb decreases
37
Q

Describe the “Flow of Tubular Fluid” step for Countercurrent Multiplication.

A
  • there is continuous tubular flow entering the Proximal Tubule going to the Descending Limb that carries the osmolarity of 300 mOsm/L
  • this pushes down higher osmolarity tubular fluid toward bend in loop of Henle
38
Q

Give me the first four steps of Countercurrent Multiplication.

A
  1. Single effect–> NaCl reabsorbed out of ascending limb and into ISF; increasing ISF osmolarity and diluting ascending limb tubular fluid; descending limb tubular fluid equilibrates w/ ISF
  2. Flow of Fluid–> new fluid w/ 300 osmolarity enters DL from PT; fluid shifts; pushing high osmolarity of fluid down loop of Henle
  3. Single effect–> NaCl reabsorbed out of ascending limb and into ISF;increasing ISF and descending limb’s osmolarity; ascending limb further diluted
  4. Flow of Fluid–> new fluid w/ 300 osmolarity enters again and pushes fluid
39
Q

What is the main point to why Countercurrent Multiplication works? (I.e. Single effect, flow of fluid, single effect, flow of fluid)

A

the ascending limb is impermeable to H2O

= diluting segment

40
Q

How does Urea recycling contribute to the conc. gradient?

A
  • causes buildup of high conc. of urea in inner medulla
  • is secreted in Thin Descending Limb– 110% of filtered load
  • TAL, DCT, cortical CT, outer medullary CD = impermeable to Urea
  • —> therefore under ADH water is absorbed and urea left behind and that increase conc. of urea in tubule
  • UT1 in inner medullary CD is activated by ADH and will use facilitated diffusion to reabsorb 70% of Urea
  • therefore 40% filtered load is excreted (under ADH influence)
41
Q

How percentage of the filtered load of Urea is excreted under influence of ADH? How?

A

40%

due to secreting 110% in Thin Descending limb and reabsorbing 70% via facilitated diffusion viw UT1 in inner medullary CD

42
Q

What are the capillaries that serve the medulla and papilla called? What type of nephrons are they specifically assoc. with? What are they involved with?

A

Vasa Recta; assoc. w/ juxtamedullary nephrons

Countercurrent Exchange (NOT countercurrent mulitiplication)

43
Q

What is the Countercurrent Exchange?

A
  • involves Vasa Recta in juxtamedullary nephrons
  • passive
  • helps MAINTAIN the gradient (NOT create it)
44
Q

What are the three cations that ADH has on the renal tubule?

A
  1. increase H2O permeability of principal cells in late DT and CD
  2. increase activity of Na+ K+ 2Cl- cotransporter in TAL–> enhancing size of osmotic gradient
  3. increase urea permeability in inner medullary CD–> enhance Urea recycling and osmotic gradient (via UT1)
45
Q

How do we have production of Hyperosmotic Urine? What syndrome can cause this to occur?

A
  • PCT = no change is osmolarity (300)
  • TAL = impermeable to H2O and reabsorb NaCl and dilutes tubular fluid
  • Early DCT –> reabsorbs NaCl and is impermeable to H2O
  • Late DCT–> presence of ADH causes Principal Cells permeable to H2O; and since tubular fluid is dilute, the H2O gets reabsorbed
  • CD– H2O continues to be reabsorbed

~Syndrome of Inappropriate ADH (secrete too much ADH)

46
Q

How do we have production of Hyposmotic Urine? What condition may cause this?

A
  • Low ADH (central diabetes) or ineffective ADH (nephrogenic diabetes)
  • Reabsorption in PCT is independent of ADH
  • TAL–> absorb NaCl and not H2O
  • Early DCT –> reabsorb NaCl and not H2O
  • W/o ADH; Last DCT and CD remain impermeable to H2O and some NaCl is reabsorbed; further diluting urine
47
Q

What areas of the nephron depend on ADH in order to become permeable to water and therefore reabsorb water?

A

Distal convoluted tubule and collecting duct

48
Q

What is defined as distilled water that is free of solutes?

A

Free Water Clearance

49
Q

In the nephron where is free water generated?

A

in diluting segment where solute is reabsorbed and water is left behind–> in the Thick Ascending Limb

50
Q

Measurement of free water clearance is a way to assess what?

A

assessing the kidney’s ability to dilute or concentrate the urine

51
Q

When there is low ADH or it is ineffective, will the urine be hyposmotic or hyperosmotic? What will the free water clearance be, positive or negative?

A

all the free water generated in the TAL and early DCL is excreted b/c it cannot be reabsored by CD

Urine = hyposmotic

Free water clearance = positive (producing a dilute urine)

52
Q

When ADH is high, will the urine be hyposmotic or hyperosmotic? What will the free water clearance be, positive or negative?

A

all free water generated in TAL and early DCT will be reabsorbed by the last DCT and CD

Urine = hyperosmotic

Free water clearance = negative (therefore called “free water reabsorption”)