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Renal Test 2 > Body Fluid Osmolality > Flashcards

Body Fluid Osmolality Flashcards

1
Q

Max osmolality at bottom of LoH

A

1200-1400 mOsm

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2
Q

osmolality at top of ascending LoH

A

100 mOsm (HYPOTONIC)

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3
Q

Osmolality difference maintained by TAL

A

200 mOsm difference btwn TAL and interstitium

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4
Q

causes of the medullary interstitial osmotic gradient

A
  1. water moves from the descend LoH–>interstitium via aquaporins
  2. LoH anatomy makes it more concentrated as it dips (bc of Na/K ATPase
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5
Q

purpose of the vasa recta

A

dictate the countercurrent multiplier by:

  • supplying blood to the medulla
  • SLOW blood flow
  • increased permeability to solutes and water
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6
Q

what is medullary washout

A

when the gradient dissipates bc the blood flows too fast

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7
Q

type of osmolality of blood entering the LoH

A

isotonic and 300mOsm

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8
Q

Osmolality of descending LoH & interstitium in step 1 or countercurrent multiplier

A

D loH = 300

interstitium =300

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9
Q

what moves out of the A LoH

A

salt (no water bc impermeable to water due to tight jcts)

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10
Q

How does salt move to the interstitium in the A LoH

A

via the NKCC

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11
Q

osmolality of D LoH, interstitium, and A LoH in step 2 of countercurrent multiplier

A

D LoH = 300
interstitium = 400
A LoH = 200

*medullary interstitial fluid is HYPERTONIC

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12
Q

osmolality of D LoH, interstitium, and A LoH in step 3 of countercurrent multiplier

A

D LoH = 300 entering, then 400
interstitium = 400
A LoH = 200

*D LoH is at EQUILIBRIUM with interstitium

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13
Q

What happens during step 4 of CCM?

osmolality of D LoH, interstitium, and A LoH in step 4 of countercurrent multiplier

A
  • more 300 TF pumped in from PCT to D LoH
  • bottom of LoH becomes more concentrated

D LoH = 300 - 300 - 400 - 400
interstitium = 300 (top) 400 - 400 - 400
A LoH = 200 top - 200 - 400 - 400

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14
Q

What happens during step 5 of CCM?

A

need to dilute the A LoH so solutes dumped from TF to interstitium (so diff is 200mOsm)

D LoH = 300 - 300 - 400 - 400
interstitium = 350 (top) - 500 - 500
A LoH = 150- 150 - 300 - 300

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15
Q

What are the final fluid and interstitium concentrations in the final stages of the CCM?

A

D LoH = 300 - 700 - 1000 - 1200
interstitium = 300 -700 - 1000 - 1200
A LoH = 100- 500 - 800 - 1000

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16
Q

what parts of the nephron are impermeable to urea

A
  1. TAL
  2. DCT
  3. Cortical CD
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17
Q

what creates increased [urea] in the TF

A
  1. formation of concentrated urine
  2. increased ADH
  3. DT water reabsorption
  4. cortical tube water reabsorption
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18
Q

UTA1

A

urea transporter

medullary CD –> TAL

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19
Q

UTA3

A

urea transporter

medullary CD –> D LoH

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20
Q

UTA3

A

urea transporter

medullary CD –> bottom of LoH

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21
Q

percentages of Urea present in PCT, D LoH, TAL, urine

A

PCT = 100%
D LoH= 50%
TAL = 100% (from urea recycling)
urine = 20%

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22
Q

where is ADH made

A

supraoptic and paraventricular nerves in the hypothalamus

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23
Q

where is ADH released

A

secretory vessels in the posterior pituitary (neurohypophysis)

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24
Q

what triggers ADH to be released

A

osmoreceptors detect high plasma osmolality

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25
Q

What happens as a result of the osmoreceptors detecting high plasma osmolality?

A
  1. ADH secretion (FAST response) –> Na & water reabsorption via
  2. trigger thirst
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26
Q

function of aldosterone

A

“salt-retaining” hormone

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27
Q

what triggers aldosterone to be released

A
  1. Angiotensin II

2. increased Plasma K+

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28
Q

where is aldosterone secreted from

A

adrenal cortex

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29
Q

Where does aldosterone act?

A

increases ENaC channels in principal cells to increase Na reabsorption

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30
Q

effects of aldosterone

A
  1. increase Na absorption (increase plasma Na)
  2. increase K secretion (decrease plasma K)
    - —-excess K+ in urine
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31
Q

how is Na reabsorbed in principal cells

A

active transport via Na/K ATPase on the basolateral membrane

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32
Q

how is K secreted in principal cells

A

Na/K ATPase AND it diffused down its electrochemical gradient

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33
Q

how is Cl- reabsorbed

A

paracellularly

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34
Q

how is water reabsorbed in principal cells

A

through aquaporins inserted on the apical/luminal membrane by ADH

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35
Q

What channel does aldosterone act on?

A

ENaCs

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36
Q

how does ADH affect hydration status

A

high ADH when hydrated

low ADH when dehydrated

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37
Q

where are aquaporins inserted in the nephron

A

the collecting duct

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38
Q

what does the presence of aquaporins in the CD do to urine

A

makes urine concentrated bc more water is reabsorbed (pulled into the blood stream instead of staying in the tubular fluid)

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39
Q

what part of the collecting duct is permeable to water at all times

A

the cortical collecting duct

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40
Q

hydrated osmolality status

A

275-295 mOsm

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41
Q

dehydrated osmolality status

A

300mOsm

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42
Q

when ADH is “turned off” what is the result

A
  • get dilute urine
  • excrete water
  • not holding on to salt
  • **plasma osmolality INCREASED to normal (bc excreting water in urine)
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43
Q

when ADH is “turned on” what is the result

A
  • add aquaporins to the CD
  • hold on to water
  • get concentrated urine
  • excrete solute
  • plasma osmolality is DECREASED to normal (bc adding water to blood)
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44
Q

what the main problem leading Central diabetes insipidus (DI)

A

can’t make ADH

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45
Q

another name for central diabetes insipidus (DI)

A

“Neurogenic” Diabetes Insipidus

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46
Q

causes of central DI

A

head injury
infection
congenital

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47
Q

what will you see in patients with central DI

A

large volume of dilute urine (>15L/day)

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48
Q

how do you Dx central DI

A

water deprivation test (water restriction)

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49
Q

how do you treat central DI

A

Main: desmopressin (ADH agonist)

water restriction -have to be careful bc it may cause dehydration

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50
Q

how does desmopressin work?

A

its an ADH analog (ADH agonist) that can bind to the V2 receptor and increase water permeability in late DCT and CT

51
Q

causes of nephrogenic DI

A

kidney can’t respond to ADH

52
Q

cause of nephrogenic DI

A
  • there’s no countercurrent (LoH impairments due to diuretics can affect concentrating ability)
  • DCT/CD don’t respond to ADH
  • medications such as:
    1. lithium (manic depression)
    2. tetracycline (antibiotic)
53
Q

what will you see inpatients with nephrogenic DI

A
  • increased volume of dilute urine
  • dehydration
  • hypernatremia (high plasma Na)
54
Q

how do you treat nephrogenic DI

A
  1. hydration
  2. low Na diet
  3. Thiazide (for Na excretion)
55
Q

what’s the main problem leading to SIADH (Syndrome of Inappropriate ADH)

A

excess ADH released

56
Q

what causes SIADH

A

lots of low Na (hypotonic) fluid is in the ECF

57
Q

what will be seen in patients with SIADH (physiological)

A

Main: Excess water retention

  • water will diffuse into the cells (ECF –> ICF)
  • cells will swell
  • *WATER INTOXICATION
  • Dilutional Hyponatremia (decreased plasma osmolality)
58
Q

Clinical Sx for SIADH patients

A
  1. thirst
  2. dyspnea
  3. vomiting
  4. confusion
  5. cramps
  6. lethargy
59
Q

how does SIADH affect GFR

A

increased GFR

why? hyponatremia and increasing the GFR will lead to bringing in more Na for reabsorption

60
Q

urinary output in DI

A

high

61
Q

urinary output in SIADH

A

low

62
Q

ADH levels in DI

A

low

63
Q

ADH levels in SIADH

A

high

64
Q

plasma Na in DI

A

hypernatremia

65
Q

plasma Na in SIADH

A

hyponatremia (dilutional hyponatremia)

66
Q

how is central DI distinguished from nephrogenic DI

A

administer desmopressin

*if the volume output does not decrease AND urine osmolarity does not increase in 2 hours after getting desmopressin, the Dx is NEPHROGENIC DI

67
Q

hydration status for DI

A

dehydrated

68
Q

hydration status for SIADH

A

over hydrated

69
Q

fluid status for DI

A

losing fluid (large urine output)

70
Q

fluid status for SIADH

A

retaining fluid (water intoxication)

71
Q

thirst status for DI

A

excessive thirst

72
Q

thirst status for SIADH

A

excessive thirst

73
Q

how does solute move out of the TF of the TAL into the interstitium

A

via NKCC

solute moves out
water is stuck inside TF

**this is key to diluting the urine

74
Q

what is hyponatremia

A

low plasma Na

excess water in the body

75
Q

what is hypernatremia

A

high plasma Na

free water deficit

76
Q

what causes hyponatremia

A

ADH in kidney (diminish free water excretion)

77
Q

what causes hypernatremia

A

impaired access and impaired thirst

78
Q

stimuli for hyponatremia

A 
Rx
pain
nausea
low arterial vol
strenuous exercise
79
Q

role of polydipsia in hyponatremia

A

NOT a cause!

80
Q

main reasons for hyponatremia

A
  1. true volume depletion
  2. effective circulating volume depletion
  3. SIADH (water intoxication)
  4. low solute intake
81
Q

main reasons for hypernatremia

A
  1. water depletion
  2. water + volume depletion
  3. osmotic diuresis
  4. DI
  5. salt intoxication
82
Q

urine osmolality in hyponatremia

A

> 300 mOsm/kg
(vol depletion, eff circ vol depletion, etc)

SIADH ?100-150 mOsm/kg (not maximally dilute)

83
Q

urine osmolality for water depletion in hypernatremia

A

> 600-800

84
Q

urine osmolality for water & volume depletion in hypernatremia

A

> 600-800

85
Q

how does osmotic diuresis affect urine osmolality in hypernatremia

A

> 300

caused by hyperglycemia, manitol

86
Q

how does DI affect urine osmolality

A

<300

<100 in complete neprogenic DI bc large volume of dilute urine

87
Q

how does salt intoxication affect urine osmolality and urine sodium

A

urine osmolality >600-800 mOsm/kg

urine Na >20 mmol/l (very high!)

88
Q

normal urine output in a healthy person

A

1-2L/day

89
Q

polyuria

A

too much urine

> 2.5L/day
40 ml/kg/day

90
Q

causes of polyuria

A 
DI
DM
Kidney Ds
Alcohol
Caffeine
Sickle Cell
Anemia
Diuretics
91
Q

oliguria

A

too little urine

300-500ml/day

92
Q

causes of oliguria

A 
dehydration
blood loss
kidney ds
cardiogenic shock
diarrhea
enlarged prostate
93
Q

anuria

A

no urine

<=50ml/day

94
Q

causes of anuria

A

kidney failure
obstruction (kidney stone/tumor)
enlarged prostate

95
Q

when would the DCT/CT be impermeable to water

A

when you drink too MUCH water

  • no ADH will be secreted
  • no medullary osmotic gradient made
96
Q

what 4 things happen when you drink too much water

A
  1. increase urine flow rate (V)
  2. decrease [urea] in inner medulla
  3. decrease urea diffusion
  4. increase dilute urine
97
Q

when would the DCT/CT be permeable to water

A

when you drink to LITTLE water

  • ADH will be secreted
  • aquaporins will be inserted to increase water reabsorption
98
Q

what 2 things happen when you drink too little water

A
  1. decrease urine output (volume)

2. increase urine concentration

99
Q

what happens as a result of the interstitium becoming super concentrated

A

TF will be hypoosmotic compared to the medullary interstitium

water from the TF (D LoH) will move OUT of the tube IN to the interstitium to try to reach osmotic equilibrium

when the water moves out of the TF, the tubular fluid then becomes more concentrated

100
Q

what 4 things cause polyuria

A
  1. increased fluid intake
  2. increase GFR
  3. increase solute output
  4. kidneys DO NOT reabsorb water in late DCT
101
Q

what impacts increased fluid intake in patients w/polyuria

A

psychogenic causes: stress and anxiety

102
Q

what impacts increased GFR in patients w/polyuria

A

hypOthyroidism
fever
hypErmatabolic states

103
Q

what impacts increased solute output in patients w/polyuria

A

DM
hypErthyroidism
hypErparathyroidism
diuretics (increase DCT solutes)

104
Q

what impacts the kidney’s inability to reabsorb water in the late DCT in patients w/polyuria

A

CDI (not making ADH)
NDI (not responding to ADH)
Drugs
Chronic renal failure (CRF)

105
Q

difference between water and solute diuresis

A

water diuresis: high water excretion and NO salts

solute diuresis: high water excretion WITH salt

106
Q

cause of water diuresis

A

high water intake

107
Q

cause of solute diuresis

A

high TF salt

108
Q

Diseases associated with water diuresis

A

polydipsia (HIGH water intake >6L/day or >100ml/kg/day)

DI

109
Q

Diseases associated with solute diuresis

A

IV NaCl
hyperglycemia
increased protein intake
AKI recover

110
Q

what is free water clearance

A

the rate that solute-free water leaves the kidneys

111
Q

what does a positive free water clearance indicate

A

excess water is EXCRETED in urine

112
Q

what does a negative free water clearance indicate

A

water is RETAINED/CONSERVED (solutes excreted)

113
Q

if you have a patient with the following things happening, what does it tell you about their free water clearance?

  • water retention
  • ADH secretion
  • Na retention
  • K+ secretion
  • low plasma K+
A

urine osmolality > plasma osmolality

NEGATIVE free water clearance

114
Q

equation for free water clearance

A

V - (Uosm x V)
——————
Posm

units: ml/min

115
Q

equation for obligatory urine volume

A

concentrating ability

116
Q

what is obligatory volume

A

the minimum volume of urine that you must excrete

117
Q

what urine volumes would cause you to suspect oliguria in infants

A

<1 ml/kg/hr

118
Q

what urine volumes would cause you to suspect oliguria in children

A

<0.5 ml/kg/hr

119
Q

what urine volumes would cause you to suspect oliguria in adults

A

<0.3-0.5 ml/kg/hr

120
Q

what does the ratio of urine osmolality tell you

A

your ability to concentrate or dilute urine

121
Q

what does a Uosm:Posm >1 mean

A

concentrated urine

122
Q

what does a Uosm:Posm =1 mean

A

urine is iso-osmotic with plasma

123
Q

what does a Uosm:Posm <1 mean

A

dilute urine

Renal Test 2 (9 decks)

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