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Renal Final > Mechanisms To Adjust Urine Concentration > Flashcards

Mechanisms To Adjust Urine Concentration Flashcards

1
Q

Describe water and sodium permeability in the thin descending segment of the LOH

A

Water permeable

NaCl remains in the tubule and concentrates during the descent

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2
Q

Describe water and sodium permeability in the thin and thick ascending LOH

A

Water impermeable

NaCl is reabsorbed in the tubule - dilutes during ascent

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3
Q

In the thick ascending LOH, Na/K ATPase maintains ____ intracellular Na and favors movement of Na from lumen into cell via _______ co-transporter and _____ countertransporter

Luminal electrochemical gradient favors movement of other positively charged ions out of the tubule

There is passive leakage of ____ and _____

A

Low; Na-K-2Cl; Na-H

K+ and Cl-

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4
Q

T/F: Loop diuretics will reduce magnitude of lumen-positive charge

A

True

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5
Q

Early DT reabsorbs what ions? Is it water permeable or impermeable?

A

reabsorbs Na, Cl, Ca

Water impermeable

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6
Q

Late DT cell types and their permeability/functions

A

Principal cells: Na+ reabsorption, K+ secretion, water reabsorption

Intercalated cells: acid-base balance

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7
Q

Do thiazide drugs act on early or late segment of DT?

A

Early, at the NCC channel

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8
Q

What diuretcs act at late DT?

A

K-sparing diuretics act on principal cells

Na channel blockers (amiloride, triamterene)

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9
Q

Which region/cells of the nephron respond in conditions of acidosis and what is the mechanism?

A

Late segment DT: alpha-intercalated cells

Convert carbonic acid to bicarb and H+

H+ ATPase and H/K ATPase transporters move H+ out of the cell into tubular lumen

H+ is excreted and HCO3 is reabsorbed

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10
Q

Which region/cells of the nephron respond in conditions of alkalosis and what is the mechanism?

A

Late segment DT: beta intercalated cells

Carbonic acid is converted to bicarb and H+

H+ ATPase and H/K ATPase transporters move H+ out of the cell into renal interstitium

H+ is reabsorbed and bicarb is secreted

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11
Q

What hormones regulate water permeability at the leate DT and CCD and what are their actions?

A

ADH -> upregulates aquaporin 2 in apical membrane

ANP and BNP inhibit ADH

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12
Q

T/F: Water transport along the nephron is active

A

False; passive!

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13
Q

Describe passive reabsorption of Cl

A

Chloride follows sodium

  1. Transport of Na+ leaves a negative charge behind that pushes Cl- from the area
  2. When water is reabsorbed, solutes are concentrated behind it, Cl- can build up. Cl- will passively diffuse away as a result
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14
Q

Describe active reabsorption of Cl-

A

Na-Cl co-transporter (distal tubule)

Na-K-2Cl co-transporter (TAL)

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15
Q

2 components of countercurrent multiplier mechanism

A
  1. The single effect

2. Fluid flow

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16
Q

What determines the size of the gradient generated by CC multiplier mechanism?

A

The length of the LOH

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17
Q

CC multiplier mechanism consists of single effect and fluid flow. Describe the single effect

A

NaCl leaves the ascending limb, interstitium becomes hyperosmotic

Water leaves descending limb in attempt to equalize the interstitium osmolality

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18
Q

CC multiplier mechanism consists of single effect and fluid flow. The single effect is when NaCl leaves the ascending limb, interstitium becomes hyperosmotic. Water then leaves descending limb in attempt to equalize the interstitium osmolality.

Describe the fluid flow aspect of CC multiplication

A

Fluid is always flowing through the tubule; new fluid enters descending limb from above, pushing tubular fluid downward and developing a gradient –> multiplies the effect of the single effect

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19
Q

During CC exchange: reabsorbed water is returned to the circulatory system via the _____ _____. Because the blood flow through these capillaries is very ______, any solutes that are reabsorbed into the bloodstream diffuse back into the interstitial fluid, which maintains the solute gradient in the medulla.

A

Vasa recta

Slow

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20
Q

Describe urea recycling

A

Urea in the interstitium drives up osmolality, which further enhances passive water reabsorption in the LOH. The recirculation of urea helps trap urea in renal medulla and contributes to hyperosmolarity of the renal medulla.

Renal transporters:
UT-AI and UT-A3 (medullary CD)
UT-A2 (thin limb)
Activated by ADH

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21
Q

What happens to urea cycling if you eat a high protein diet?

A

More urea in the body helping to concentrate medullary interstitium - so you will generate more concentrated urine

22
Q

Medullary osmolallity is due to the presence of what 2 compounds?

A

NaCl and urea

23
Q

________ = continuous reabsorption of solutes and failure to reabsorb water leading to high urine volume and low medullary solute concentrations

A

Diuresis

24
Q

______ ______ ______ is calculated based on the idea that the maximal concentrating ability of the kidney dictates how much urine volume must be excreted each day to rid the body of metabolic waste products and ions that are ingested

A

Obligatory urine volum

25
Q

What osmolarity is the max our kidneys can produce?

A

1200-1400 mOsm/L

26
Q

Antidiuresis requires what 2 things?

A

High ADH

High osmolality of renal medullary interstitial fluid

27
Q

Which has a higher concentration of urea, the CCD or the DT?

A

CCD, the DT is impermeable to urea

28
Q

Describe the water permeability of the collecting ducts when ADH levels are high

A

High ADH increaes the water permeability of the collecting ducts to very high levels

[High ADH also increases the permeability of the apical membrane of the thick ascending limb to NaCl, leading to an increase in the osmolality of the peritubular interstitium (d/t countercurrent multiplication). These effects combined result in water being rapidly reabsorbed from the cortical and outer medullary portions of the collecting duct system via aquaporin water channels, resulting in the production of a small volume of hypertonic urine, with osmolality approaching that of the inner medullary interstitium]

29
Q

During antidiuresis:

______ in ADH

_____ in urea concentration in CD

A

Increase

Increase

[urea will passively diffuse out of the tubule]

30
Q

What role does the vasa recta play in the hyperosmolarity of the medulla?

A

VR minimizes solute washout from the interstitium - thus it does not create the hyperosmolarity but plays a role in preventing it from being dissipated

31
Q

The total clearance of solutes from the blood can be expressed as ______ ________; this is the volume of plasma cleared of solutes each minute in the same way that clearance of a single substance is calculated

A

Osmolar clearance

32
Q

Osmolar clearance equation

A

Cosm = (Uosm x V)/Posm

33
Q

_______ ______ ______ = rate at which the body excretes solute-free water

A

Free water clearance

34
Q

Equation for free water clearance

A

C(H2O) = V - C(osm)

35
Q

What does it mean when C(H2O) is negative?

A

Excess solutes are removed; water is being conserved

36
Q

What does it mean when C(H2O) is positive?

A

Water is being excreted, forming dilute urine, water is in excess

37
Q

_______ _______ = Percentage of filtered substance that actually gets excreted

A

Fractional excretion

38
Q

Equation for fractional excretion

A

(Ux)(PCr)/(Px)(UCr)

39
Q

Interpret a fractional excretion of 1.0

A

100% of what gets filtered is excreted

40
Q

Interpret a fractional excretion of 0.9

A

90% of what is filtered gets excreted (reabsorption has occurred!)

41
Q

Interpret a fractional excretion of 1.1

A

110% of what gets filtered gets excreted (secretion occurred!)

42
Q

A FeNa of below 1% would indicate what type of AKI?

A

Pre-renal

The physiologic response to a decrease in renal perfusion is an increase in sodium reabsorption to control hyponatremia, often caused by volume depletion or decrease in ECV (e.g., low output heart failure)

43
Q

A FeNa of above 2% would indicate what type of AKI?

A

Intra-renal or post-renal

Either excess sodium is lost d/t tubular damage, or the damaged glomeruli result in hypovolemia resulting in the normal response of sodium wasting

44
Q

What 2 conditions relating to sodium and water balance does chronic SIADH lead to?

A

Hyponatremia

Euvolemia (TBW slightly increased)

45
Q

Possible underlying causes of euvolemic hyponatremia

A

SIADH
COPD
Malignancy

46
Q

Possible causes of hypervolemic hyponatremia

A

CHF
Renal impairment
Cirrhosis

47
Q

3 P’s of diabetes insipidus

A

Polyuria

Polydipsia

Polyphagia

48
Q

Central diabetes insipidus

A

Deficient secretion of ADH from hypothalamus or pituitary

49
Q

Nephrogenic diabetes insipidus

A

Renal insensitivity to ADH

50
Q

SIADH effect on:

Urinary output
ADH levels
Plasma sodium
Hydration status
Thirst
Body water content
A

Urinary output decrease

ADH level increase

Plasma sodium decrease

Hydration status increase

Thirst increase

Body water content normal or slightly increased

51
Q

Diabetes insipidus effect on:

Urinary output
ADH levels
Plasma sodium
Hydration status
Thirst
Body water content
A

Urinary output increase

ADH decrease (central) or same (nephrogenic)

Plasma sodium increase

Hydration status decrease

Thirst increase

Body water content decrease

Renal Final (10 decks)

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