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Renal Exam #2 > Etc. Part 1 > Flashcards

Etc. Part 1 Flashcards

1
Q

What us the first step in the counter-current exchange mechanism?

A

NaCl secretion into the interstitium from the ascending limb.

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2
Q

What happens if the rate of blood flow thru the vasa recta is too high?

A

Medullary washout. Dissipates gradient established by counter-current echange.

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3
Q

Why is urea recycling ADH dependent?

What is the effect if ADH is present?

A

It is used as a means to reabsorb water.

If ADH is present, urea is reabsorbed.

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4
Q

What channel does aldosterone act on?

A

ENaC. On luminal side.

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5
Q

Where are AQPs inserted?

A

Apical membrane of PCs.

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6
Q

What does aldosterone do to urine?

A

Concentrate it

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7
Q

What portion of the CD is always permeable to water?

What portion is under hormonal control?

A

CCD

MCD

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8
Q

Normal Osm?

Dehydrated Osm?

A

275-295 mOsm

>300 mOsm

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9
Q

CNDI is caused by:

A

Head injuries, congenital abnormalities, infections.

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10
Q

How is CNDI treated?

Where does it bind?

A

Desmopressin

V2 receptors in DCT and CD.

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11
Q

What further actvates Nephrogenic DI?

A

Li, tetracyclines

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12
Q

What is the fluid shift occurring in SIADH?

A

From ECF to ICF causing water intoxication.

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13
Q

What does SIADH to do Na+ levels?

A

Decreases Na+ as it produces highly concentrated urine

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14
Q

What segment is dilution depending on? Why?

A

TAL of LoH.
It is the only portion where solutes are reabsorbed w/o water. Uses NaKCC2 channel.
It is impermeable to water.

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15
Q

How does Hyponatremia develop?

A

Increased ADH in kidneys and decreased water excretion.

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16
Q

What are the stimuli for hyponatremia?

A

Nonosmotic ones.

Nausea, pain, drugs, exercise, etc.

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17
Q

How does hypernatremia develop?

A

Decreased fluid intake. Usually in elderly and accompanies vol. depletion.

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18
Q

4 main causes of polyuria

A

Increased fluid intake
Increased GFR
Increased solute output
Kidney doesn’t absorb water in DCT well.

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19
Q

Equation for free water clearance

A

= V - (Uosm - V)/Posm

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20
Q

ECV

A

Volume of ECF in arterial system actively perfusing tissues.

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21
Q

How much of ECF is the ECV?

A

5% of ECF and 20 % of plasma

Not measurable

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22
Q

CHF

A

Decreased ECV due to decreased CO.
Pts retain Na and water causing edema.
Pts add to ECF vol but do not change their ECV.

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23
Q

Intrarenal receptors activate:

A

RAAS

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24
Q

When Na+ is low, what hormone is activated? Via what receptors?

A

Aldosterone

Baroreceptors

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25
Q

When water is low, what hormone is activated? Via what receptors?

A

ADH

Osmoreceptors

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26
Q

Effect of activating RAAS

A

Increased angiotensin and Na+ reabsorption along the nephron.
Increased aldosterone.
Activation of ADH

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27
Q

Effect of activating SNS

A

Decreased GFR
Activated RAAS
Increased NaCl reabsorption

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28
Q

Effect of activating ANP/BNP/Urodilatin

A 
Increased GFR
Inhibits RAAS
Inhibits aldosterone
Inhibits NaCl reabsorption
Decreased ADH
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29
Q

3 Methods of secreting renin

A

SNS
Perfusion pressure decreases
Tubuloglomerular feedback

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30
Q

Where does fluid shift during hyponatremia?

A

ECF to ICF. Cells swell.

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31
Q

Role of epinephrine in K+ balance

A

Causes extrarenal cells to increase uptake of K+.

Causes renal cells to secrete more K+.

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32
Q

Role of insulin in K+ balance

A

Activates Na/K ATPase.

Leads to a decrease in K+ levels.

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33
Q

What can insulin and Glc treat?

A

Hyperkalemia

34
Q

Role of aldosterone in K+ balance

A

Increased K+ secretion by kidney.

Increased K+ secretion into intestines and saliva.

35
Q

B-catecholamine function

A

Same as insulin.

+ Na/K ATPase

36
Q

a-catecholamine function

A
  • Na/K ATPase

Increase serum K+

37
Q

What is the role of Na+ in the Pt in affecting K+ secretion in the DT?

A

Indirect.

The more Na+ reabsorbed here, the less that is available in the DT for K+ secretion.

38
Q

How is K+ reabsorbed in the PT?

A

TEPD.
Na leaves.
Cl leaves.
K+ leaves.

39
Q

LoH recycling of K+ pathway

A

K+ screted into CCD
K+ reabsorbed by MCD and enters the interstitium
K+ secreted back into the late PT and DL of LoH.

40
Q

What is the point of K+ recycling?

A

To excrete more K+ during times of increased K+ intake.

Large K+ inhibits NaKCC2, increasing the amount of Na being delivered to the DT. This increases secretion of K+.

41
Q

Where is K+ secreted and/or reabsorbed?

A

Late DT and CCD due to body’s needs.

42
Q

What is the effect of flow rate on K+ secretion?

Why?

A

Increased tubular flow rate increases K+ secretion.

increases gradient for K+ and increases Na+ delivery to DT.

43
Q

What happens when there is too much K+?

A 
\+ Na/K ATPase
Decreases leak of K+ into interstitium
\+ synthesis of K+ channels on luminal membrane
\+ aldosterone
Increase flow rate
44
Q

Acute alkalosis and K+
Na/K ATPase
K+ diffusion into lumen
Leads to:

A

+ Na/K ATPase
+ K+ diffusion into lumen
Leads to: HYPOkalemia

45
Q

Acute acidosis and K+
Na/K ATPase
K+ diffusion into lumen
Leads to:

A
  • Na/K ATPase
  • K+ diffusion into lumen
    Leads to: HYPERkalemia
46
Q

What happens to K+ in chronic acidosis?

How?

A

+ K+ secretion.

The Na/K ATPase is inhibited at the PT and RAAS is activated.

47
Q

Ca levels during hypoalbuminemia

A

Increased

48
Q

Ca levels during hyperalbuminemia

A

Decreased

49
Q

Ca levels during acidosis

A

Increased plasma Ca as less is bound to albumin

50
Q

Ca levels during alkalosis

A

Decreased plasma Ca as more is bound to albumin

51
Q

Alkalosis can lead to:

A

Hypocalcemic tetany

52
Q

Calcitriol function:

How?

A

Increase Ca and P.
Bone: resorption
GI: Increased absorption of Ca/P
Kidney: Increased reabsorption of Ca/P

53
Q

Calcitonin function:

How?

A

Decrease Ca and P.
Bone: inhibitbone resorption.
Kidneys: Increase Ca and P excretion.

54
Q

PTH function:

How?

A

Increase Ca and decrease P.
Bone: increase bone resorption
GI: increase Ca absorption via calcitriol
Kidneys: increase Ca reabsorption in DT and decrease P reabsorption in PT.

55
Q

Where is the CaSR and what is its function?

A

Apical membrane of the TAL.

Inhibits NaKCC2, causing a dcrease in Na reabsorption and thus a decrease in Ca reabsorption.

56
Q

How does Ca reabsorption occur in the PT?

How much occurs here?

A

Mostly paracellularly, but some transcellularly.
Passive mainly.
65-70%

57
Q

What 2 transported exist in the PT and aid in Ca movement across the BL membrane?

A

Ca ATPase

Ca/Na antiporter

58
Q

How does volume expansion affect Ca levels?

A

Decreases Ca levels (increases secretion).

59
Q

How does volume contraction affect Ca levels?

A

Increases Ca levels (increases reabsorption).

60
Q

How is Ca reabsorbed in the TAL?

A

Via TEPD paracellularly

61
Q

What is the effect of loop diuretics on Ca excretion?

A

Increases Na excretion, thus increases Ca excretion by lowering TEPD.
Can treat hypercalcemia.

62
Q

How is Ca reabsorbed in the DT?

A

Via active transport due to -TEPD.

Uses TRPV5 on luminal side, then NCE.

63
Q

What is the effect of thiazide on Ca reabsorption?

A

Decreases Na reabsorption and increases Ca reabsorption.

64
Q

Acidemia and Ca balance

A

Increases Ca excretion by inactivating TRPV5

65
Q

Alkalemia and Ca balance

A

Decreases Ca excretion by activating TRPV5

66
Q

Activated TRPV5 does what to Ca balance?

A

Causes Ca reabsorption

67
Q

How is P reabsorbed in the early PT?

A

The Na-P symporter on luminal side.

P leaves luminal cell via unknown channel and Na leaves via Na/K ATPase

68
Q

FGF-23

A

Released by bone in response of calcitriol, PTH, hyperohosphaturia to increase P excretion.

69
Q

How is calcitriol activated (which enzyme)?

A

Renal 1a-hydroxylase

70
Q

What is the effect of CaSR on Renal 1a-hydroxylase?

A

Inhibits it.

CaSR signals high Ca, so no need to produce calcitriol

71
Q

1,25 (OH)2 D3 causes:

A

Increased P by intestinal reabsorption.

72
Q

Insulin effect on P balance

A

Decreases P by moving it into cells to be excreted (same as K+)

73
Q

What is the effect of PTH on Na-P and Na-H transporters in PT cells?

A

PTH inhibits them

74
Q

Chronic acidosis does what to P excretion?

A

Increases P excretion

75
Q

Chronic alkalosis does what to P exrcetion?

A

Decreases P excretion

76
Q

Where is most Mg reabsorbed?

A

TAL (70%)

77
Q

How is Mg reabsorbed at the PT?

A

Paracellularly/passively.

Follows Na and water.

78
Q

How is Mg reabsorbed at TAL?

A

Depends on NaKCC2 and TEPD.

79
Q

How is Mg reabsorbed at DT?

A

Crosses border via TRPM6 then the BL membrane via unknown channel.

80
Q

Mg levels during vol. expansion?

Contraction?

A

E: decrease reabsorption
C: increase reabsorption

81
Q

Mg levels during acidosis?

Alkalosis?

A

Acidosis: decrease reabsorption
Alkalosis: increase reabsorption

Renal Exam #2 (7 decks)

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