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CRRAB II- Week 1 > Popham- Natremic > Flashcards

Popham- Natremic Flashcards

1
Q

What is normal serum Na?

A

135-145

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2
Q

What is hyponatremia?

A

Less than 135

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3
Q

What is hypernatremia?

A

> 145

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4
Q

What is the main contributor to serum osmolality?

A

Na

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5
Q

If normal plasma/serum osmolality is 285-300 how can you estimate Na, BUN and glucose?

A

Na (2) + BUN/2.8 + Glucose/18

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6
Q

Are hyponatremia and hypernatremia usually water or salt problems?

A

almost always WATER problems

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7
Q

What causes the sxs of hypo/hyper natremia?

A

Alterations in plasma osmolality–>

changes in brain cells

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8
Q

What symptoms do you see with Hyponatremia?

A

Sxs d/t HYPOOSMOLALITY–> Brain cell swelling

<115: obtundation, seizures, coma

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9
Q

Are symptoms related to hyponatremia usually reversible?

A

YES!

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10
Q

When are hyponatremic sxs most severe?

A

If hyponatremia occurs QUICKLY and the brain doesn’t have time to adapt

(If hyponatremia develops gradually–> brain has time to adjust)

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11
Q

How do hyper and hyponatremia affect the brain?

A

Hypo> HYPOOSMOLALITY–> Brain cell swelling

Hyper> Extracellular hyperosmolality–> brain cell dehydration

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12
Q

What are the symptoms of hypernatremia?

A 
Lethargy
weakness
irritability
twitching
seizures
coma
death
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13
Q

What is commonly seen in the brain with hypernatremia?

A

Rupture of cerebral vessels due to decrease in brain volume

*Clinically significant water shift occurs with 30-35 mosm/kg osmolar gradient between plasma and brain or a Na elevation of 17 meq

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14
Q

What does ADH do?

A

Maintains appropriate plasma osmolality

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15
Q

Where is ADH produced and stored?

A

Produced in HYPOTHALAMUS in supraoptic and paraventricular nuclei, stored in secretory granules>
secretory granules move down supraopticohypophyseal tract to POSTERIOR LOBE of PITUITARY GLAND

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16
Q

What causes the release of ADH?

A
  1. Increase in plasma osmolarity
  2. baroreceptors–> hypovolemia or decreased ECV
  3. Pain
  4. Esophageal stimuli
  5. Various medications
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17
Q

What does ADH bind to and where? What does this do?

A

V2 receptor in COLLECTING TUBULE>
activates a protein kinase>
Aquaporin 2 to move from cytoplasm to luminal membrane and form water channels

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18
Q

What happens to water if ADH is present?

A

Water channels are present>
water is returned to blood>
lowers serum osmolality>
urine osmolality will be high

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19
Q

What happens to water in the collecting duct if ADH is absent?

A

Water channels are absent>
water is excreted in the urine>
raises serum osmolality>
urine osmolality will be low

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20
Q

What is the difference between high and low Posm?

A

Posm high> thirst, ADH released, CT permeable to water, High Uosm

Posm low> no thirst> no ADH release> Collecting tubules impermeable to water> low Uosm

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21
Q

What is indicated by high and low Uosm?

A

High Uosm: ADH present, kidney reabsorbing water

Low Uosm: ADH low/absent, kidney is excreting water

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22
Q

What is hte difference between high and low urine Na?

A

Tells you what the kidney thinks about volume status

High- kidney behaving as if body V is expanded, getting rid of excess Na

Low- kidney behaving as if body is V depleted, reclaiming Na

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23
Q

What is the range of urine osmolality in a normal functioning kidney?

A

50-1400

  • narrower in very old and very young
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24
Q

What happens if Uosm is < 100?

A

No ADH present and urine is maximally dilute

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25
Q

What happens if Uosm is >100?

A

the higher the Uosm the more ADH is present

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26
Q

What is the usual daily osmolar load from dietary protein/salt?

A

500-750 mosm

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27
Q

What is the minimum volume of water excreted daily?

A

Daily osmolar load/maximal urine osmolarity

500 mosm/day//1000 mosm = .5 L

750 msosm/day//1000 mosm=.75 L daily

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28
Q

What is the maximum volume of water excreted daily?

A

Daily osmolar load /minimal urine osmolarity

500 mosm/day//50 mosm/l = 10 liters/day
750 mosm/day//50 mosm/l = 15 liters/day

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29
Q

What happens to Na excretion in a steady state?

A

Dietary intake of Na = urinary excretion of Na

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30
Q

What happens to Na excretion if volume is depleted?

A

Kidney responds to hormones (Ang II, aldosterone) to RETAIN Na

31
Q

What percent of Na is reabsorbed by tubular cells? How?

A

65%

Luminal membrane: Na/K/2CLand NaCL

Basolateral membrane: NaKATP ase

32
Q

What influences Na reabsorption in tubular cells?

A

Hemodynamics and Ang II,
DA
NE

33
Q

What percent of Na is reabsorbed in the LOH? What is it dependent on?

A

23-35%

FLOW dependent

34
Q

What does the LOH do?

A

Generates DILUTE urine in ascending limb d/t water impermeability

35
Q

What percent of Na is reabsorbed in the distal tubule?

A

5%

FLOW Dependent

36
Q

What percent of Na is reabsorbed in the collecting tubule? What influences reabsorption?

A

4 %

Aldosterone, ANP

37
Q

What happens if htere is low urinary Na?

A

<10 meq/l

Kidney thinks ECV is depleted and holds onto Na

38
Q

What happens if there is HIGH urinary Na?

A

> 10 meq/l

Kidney thinks ECV is expanded OR

Kidney isn’t able to retain Na properly OR

Kidney is excreting Na as an obligate cation with something else

39
Q

How does hyponatremia relate to hypoosmolality?

A

Hyponatremia REFLECTS hypoosmolality

40
Q

What is Posm essentially equal to Na x2 if glucose is normal?

A

Posm = Na x 2 + glucose/18 + BUN/2.8

BUN- ineffective osmole, crosses membranes so doesnt’ contribute to osmotic gradient

If glucose is normal it doesn’t add much

41
Q

What causes hyponatremia with normal Posm?

A

Hyperlipidemia
Hyperproteinemia

Lipids/protein take up more plasma space, and reduces plasma water space, but Na+ still measured in total plasma space

42
Q

What causes hyponatremia with elevated Posm?

A

Hyperglycemia
Hypertonic mannitol

Water shifts out of cells to reestablish osmotic equilibrium, so Na+ is now more dilute in plasma water

43
Q

How does hyponatremia develop if mechanisms are in place to maintain plasma osmolarity w/in 1%?

A
  1. Osmotic stimuli to ADH would maintain plasma osmolarity within 1% by itself, without regard to ECV status
  2. Non-osmotic stimulus (from baroreceptors in kidney/carotid/heart) for ADH secretion maintain ECV at expense of plasma osmolarity

**Better to have brain perfusion than perfect plasma osmolarity

44
Q

How do you evaluate hyponatremia?

A
  1. Check Posm- confirm true hypoosmolar hypontaremia
  2. Check Uosm-is ADH acting?
    100: ADH present depsite hypoosmolar state
  3. Check UNa- kidneys perception of ECV
  4. Check patient/H&P: What is V status/clinical status
45
Q

What are physical exam signs for volume status?

A

neck veins, edema, rales, S3, orthostatic vital signs, skin turgor

46
Q

What labs are used to diagnose hyponatremia?

A 
electrolytes for metabolic alkalosis/acidosis
K
renal failure
Posm
Uosm
UNa
47
Q

What is happening in hyponatremia with Uosm<100? What are exceptions to this?

A

Excessive water intake (primary polydipsia- 10-15 L of water to overwhelm renal capacity to clear water)>
ADH not being produced d/t appropriate response to hypoosmolarity

*Beer potomania, Tea and Toast Syndrome

48
Q

How do you treat primary polydipsia?

A

Fluid restrictions>
body quickly gets rid of free water as NO ADH is present and no water channels in collecting tubules>
free water leaves kidney until plasma osmolarity is normalized

49
Q

What is Beer potamania or tea and toast syndrome?

A

Hyponatremia and LOW urine osmolaity WITHOUT excessive fluid intake

Big beer drinkers who don’t eat much else, or “little old ladies” eating only toast and drinking tea

Daily osmolar load for these folks can be as low as 100-250 mosm/day

This dictates that amount of free water they can clear daily is:
100 mosm/day/50 mosm/l = 2 liters/day
250 mosm/day/50 mosm/l = 5 liters/day

Can gradually develop hyponatremia even when fluid intake isn’t very high

50
Q

Where does most hyponatremia fall? What causes it?

A

Hyponatremia w/ Uosm>100

urine is more concentrated–> ADH is present

ADH release when plasma hypoosmotic is “inappropriate” from the standpoint of osmotic stimuli, but not if ECV depletion present

51
Q

What happens when Na via GI, skin (burn), DIURETICS, or through a cortisol deficiency?

A

UNa is <10 and volume is depleted

Kidney reabsorbs Na in effort to re-expand vascular space

52
Q

What happens to UNa and volume during CHF/Cirrhosis, nephrosis?

A

UNa is <10 and volume is expanded, but with ECV depletion

Kidney is receiving wrong signals

53
Q

What happens when UNa and volume when there is adrenal insufficiency, renal diseases, diuretics, or hypokelemia with metabolic acidosis?

A

UNa> 10 and volume depleted

Kidney is receiving wrong signals: salt wasting

54
Q

What happens to UNa and volume during SIADH, reset osmostate, or chronic kidney disease?

A

UNa> 10 and volume depleted

Brain/kidney are confused!

55
Q

What is SIADH? What causes it?

A

Syndrome of Inappropriate ADH secretion–> FIXED ADH excretion w/out regard to osmotic or volume stimuli

Ectopic production from tumors: oat cell carcinoma
Pulmonary process, especially TB, pneumonia, asthma
Drugs: chlorpropramide, tegretol, oxytocin, cytoxan
Esophageal process
Pain
Neuropsychiatric disorders

56
Q

How do you treat SIADH?

A
  1. Fluid restriction

2. Increase osmolar load: intake high Na or high protein diet–> body has more osms to work with to clear water

57
Q

How do you treat volume depleted hyponatremia?

A
  1. Vol depleted: NS to replenish vol & turn off ADH
58
Q

How do you treat volume neutral or expanded hyponatremia?

A
  1. Vol neut or expand: restrict H20 in, tx poor perfusion
59
Q

How do you treat severe hyponatremia?

A
  1. Severe hyponatremia – may need 3% saline to bring out of danger zone rapidly
    — Seizures or neurologic sx (tx underlying prob)
60
Q

How can be used for volume expanded hyponatremia?

A

ADH antagonist– use for vol expanded hyponat
— V1a and V1b: vasoconstriction & ACTH release
— V2: ADH
— Tolvaptan: oral, 30+ days → risk of liver fail
— Conivaptan: IV

61
Q

What’s important to consider when treating hyponatremia?

A
  1. Bring Na out of danger zone over several hours
  2. Then, 12 meq/l over 24 h (0.5 meq/l/h)
  3. Rapid correction → risk Central pontine syndrome!
  4. Less likely for hyponat that developed rapidly
  5. But for those that developed slowly (i.e. have less prominent sx), Slow and steady wins the race!!
62
Q

When is emergency use of 3% NaCl used?

A

To quickly bring serum Na+ out of danger range

3% NaCl = 513 meq Na+ per liter

Hyponatremic seizures: 100 cc 3% NaCl over 10 minutes, IV (about 51 meq Na+)

63
Q

What causes hypernatremia? Why are most of us protected from it?

A

excessive water losses and inadequate intake

Thirst stimulus is so profound, that most are protected from hypernatremia, even with water losses up to 10-15 liters daily

64
Q

In what pts do you usually see hypernatremia?

A

Young
elderly
patient with altered mental status

65
Q

What causes Hypernatremia?

A

• Na+ retention
— Hypertonic NaCl or NaHCO3 infusion
— Salt water drinkers
• H20 loss, w/ inadequate intake
— Insensible loss – sweat, fever, exercise, respir
— Renal loss – Diabetes insipidus, osmotic diuretics
— GI loss – malabs, infectious diarrhea
— H20 loss into cells – seizures, severe exercise
• Primary inadequate H20 intake
— Hypothalamic dysfunction

66
Q

How do you diagnose hypernatremia?

A

It’s based on CAUSE!

If Na>145, POsm will be >290, check UOsm

At POsm > 295, ADH release should be maximal, and UOsm should be 800-1400 (urine SG 1.025 – 1.030)

UOsm > 800: Primary Hypodipsia, increased insensible/GI losses, or Na+ overload

UOsm <300: severe CDI or NDI

UOsm 300-800: partial DI, volume depletion with DI, or osmotic diuresis

67
Q

What is the difference between Central DI and nephrogenic DI?

A

No ADH release from pituitary

Collecting ducts don’t respond to ADH

68
Q

How do you distinguish between CDI and NDI?

A

Ford CDI- exogenous ADH will increase Uosm

69
Q

What symptoms would suggest a diagnosis of DI?

A

Polyuria/polydipsia

70
Q

What drug can cause nephrogenic DI?

A

Lithium

71
Q

How do you treat DI?

A
  • Low Na diet & thiazide diuretic → mild vol depletion, decrease urine output by 50%
  • Moderate protein restriction → decrease osmolar load, decrease urine output
  • Cholorpropamide/clofibrate/carbamazepine → enhanced effects of ADH
  • NSAIDS → decreased renal PG effects that normally impair ADH
  • dDAVP (ADH) for CDI
72
Q

What happens in chronic hypernatremia? How should you correct it?

A

brain develops idiogenic osmoles to prevent cellular dehydration

SLOWLY to allow brain time to readjust

Safe rate: 0.5 meq/hour or 12 meq in 24 hours (same as for hyponatremia)

73
Q

How do you treat hypernatremia?

A
  • Calculate H20 deficiet
  • Replace H20 to lower plasma Na over 60 hours or rate of 125cc/h
  • Free H20 orally
  • D5W IV
  • Hypernat d/t vol deplete: ¼ NaCl
  • HypoTN w/ fluid loss: NS

CRRAB II- Week 1 (7 decks)

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