Water Homeostasis Flashcards

1
Q

when renal free water balance is zero, serum sodium concentration is ?

A

NORMAL (136-145 mmol/L)

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2
Q

when renal free water balance is positive, serum sodium concentration is ?

A

LOW = HYPONATREMIA (<136 mmol/L)

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3
Q

when renal free water balance is negative, serum sodium concentration is ?

A

HIGH = HYPERNATREMIA

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4
Q

osmolarity - defined

A

number of solute particles per 1 L of solvent

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5
Q

osmolality - defined

A

number of solute particles in 1 kg of solvent

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6
Q

water balance - defined

A

*regulation of the osmolality of body fluids
*purpose of regulating water balance is to maintain constant osmolality in your cells and body fluids
*purpose is to prevent movement of water between fluid compartments
*regulated by regulating renal water excretion

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7
Q

renal water excretion is determined by

A
  1. amount of solute in urine
  2. osmolality of urine
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8
Q

urine water excretion = ? (equation)

A

urine solute excretion / osmolality of urine

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9
Q

regulation of the osmolality of body fluids - overview

A

osmoreceptors in the hypothalamus act as sensor → modulate antidiuretic hormone AND triggers thirst mechanisms

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10
Q

major factors that regulate H2O handling

A

PATHWAY:
1. osmoreceptors
2. ADH
3. aquaporin water channels

DRIVING FORCE = hyperosmolar medulla

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11
Q

pathway leading to increased water excretion

A

decreased serum osmolality detected by osmoreceptors → suppression of ADH → water excretion

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12
Q

pathway leading to water retention

A

increased serum osmolality detected by osmoreceptors → activation of ADH → insertion of aquaporin channels + hyperosmolar medulla → water reabsorption

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13
Q

ADH & aquaporin (AQP2) channels - overview

A

*ADH binds V2 receptors in the principal cells (in cortical collecting duct) → increased cAMP → insertion of AQP2 channels on apical membrane that are permeable only to water → increased water reabsorption

note - aquaretics (vaptans) block this V2 receptor (prevent ADH from binding V2 → excrete additional water)

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14
Q

medullary concentration gradient

A

*concentration difference of solutes (NaCl, urea) within the kidney’s medulla
*creating a progressively increasing osmotic pressure from the outer → inner layer of the medulla
*allows for the concentration of urine by facilitating water reabsorption from the collecting duct

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15
Q

mechanisms contributing to making the medullary interstitium hypertonic

A
  1. reabsorption of NaCl without water
    -occurs in thick ascending loop of Henle via active transport via NKCC
    -no H2O absorption
    -diluting segment
  2. urea entry into the inner medullary interstitium
    -via passive diffusion at the collecting duct
    -urea re-enters tubular fluid at the loop
  3. vasa recta
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16
Q

reabsorption of NaCl without water → hypertonic medullary interstitium

A

-occurs in thick ascending loop of Henle via active transport via NKCC
-no H2O absorption
-diluting segment

17
Q

urea entry into the inner medullary interstitium → hypertonic medullary interstitium

A

*when ADH is present, additional urea is reabsorbed into the medullary interstitium → increased medullary concentration gradient → promotes water reabsorption in the collecting duct
*via passive diffusion
*urea re-enters tubular fluid at the loop

18
Q

vasa recta contributes to → hypertonic medullary interstitium

A

*vasa recta helps to maintain the concentration gradient
*counter current mechanism utilizes energy to develop an osmotic concentration gradient along the medullary interstitium
*the layout of the vasa recta around its own Loops of Henle and the counter current flow that allows for the maintenance of the osmotic gradient

19
Q

diluting vs. concentrating urine

A

*if volume overloaded, kidneys dilute urine to excrete increased H2O in excess of solute to dump the excess volume
*if volume depleted, kidneys concentrate urine to excrete less H2O in relation to solute to conserve H2O
*this is achieved by not only the presence/absence of ADH but also through development/maintenance of the hypertonic medullary interstitium

20
Q

ADH secretion is regulated by

A
  1. plasma osmolality
  2. arterial volume

note - plasma osmolality is the primary trigger (arterial volume only contributes if there are large changes > 15%)

21
Q

plasma osmolality & regulation of ADH secretion

A

*increased plasma osmolality → sensed by osmoreceptors → release of ADH (from posterior pituitary) to maintain osmolality → increased free water reabsorption

*decreased plasma osmolality → suppressed ADH release → decreased free water reabsorption (increased water excretion)

22
Q

arterial volume & regulation of ADH secretion

A

*decreased arterial volume → decreased arterial stretch → increased ADH → increased water reabsorption → increased blood volume

*increased arterial volume → increased arterial stretch → decreased ADH → decreased water reabsorption (increased water secretion)

23
Q

what is the MAIN trigger for ADH secretion

A

increased plasma osmolality

24
Q

impaired free water excretion in diabetes insipidus

A

*a condition characterized by inability to concentrate urine & conserve water
*central: ADH not produced (hypothalamic or pituitary issue)
*nephrogenic: kidneys do not respond to ADH
*result: HYPERNATREMIA (increased serum sodium due to lack of water to dilute it)

25
Q

impaired water excretion in syndrome of inappropriate ADH secretion (SIADH)

A

*sustained increase in ADH secretion that is NOT due to changes in plasma osmolality or changes in arterial volume
*sustained increase in ADH → increased water reabsorption → HYPONATREMIA (due to increased water volume AND increased sodium excretion due to plasma volume expansion)

26
Q

effects of decreased Na+ and water intake on kidneys (SIMPLE)

A

*kidneys should REABSORB SODIUM AND WATER (i.e. decreased excretion of sodium and water)

27
Q

effects of increased Na+ and water intake on kidneys (SIMPLE)

A

*kidneys should EXCRETE MORE SODIUM AND WATER (i.e. decreased reabsorption of sodium and water)