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Sodium disorders Flashcards

1
Q

Normal serum Na+?

A

135-145 Meq/L

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2
Q

Normal plasma/serum osmolality?

A

285-300 Meq/L

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3
Q

Eqn to estimate plama/serum osmolality?

A

Na x 2 + BUN/2.8 + Gluc/18

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4
Q

Main contributor to serum osmolality?

A

Na

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5
Q

Symptoms of hypo/hypernatremia are due to effects on which orhan?

A

Brain

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6
Q

Sodium abnormalities are usually caused by ____________ NOT ___________.

A

Water problems

NOT

Salt problems

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7
Q

Extracellular hyp-O-osmolality have what effent on neurons?

A

swelling

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8
Q

Sx if Na+

A

nausea

malaise

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9
Q

Sx if Na+ = 115-120:

A

headache

lethargy

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10
Q

Sx if Na+

A

obtundation

seizures

coma

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11
Q

More severe sx in fast or slow hyp-O-natremia?

A

Fast

brain has less time to adapt

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12
Q

Effect of hyp-ER-natremia on neurons?

A

cells shrink

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13
Q

Sx of hyp-ER-natremia?

A

lethargy

weakness

irritability

twitching

seizures

coma

death

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14
Q

Decreased brain volume due to hyp-ER-natremia can have what effect on vasculature?

A

rupture cerebral vessels

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15
Q

Clinically significant water shift occurs with 30-35 mosm/kg osmolar gradient between plasma and brain; what is the corresponding rise in serum Na+?

A

17 meq/L

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16
Q

Hormone responsible for maintenance of plasma osmolality:

A

ADH

arginine vasopressin

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17
Q

Where is ADH produced?

A

supraoptic and paraventricular nuclei of hypothalamus

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18
Q

Where is ADH stored and released?

A

secretory granules

posterior pituitary

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19
Q

Osmotic stumuli of ADH release:

A

INCREASED plasma osmolality

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20
Q

Non-osmotic stimuli of ADH release:

A

hypovolemia –> baroreceptors

pain

esophageal stimuli

medications

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21
Q

What receptor binds ADH to release aquaporin 2 to luminal membrane?

Where does this occur?

A

V2 (activates protein kinase)

collecting tubule

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22
Q

With high presence of ADH:

Urine osmolality = ?

Plasma osmolality = ?

A

urine- increased

serum- decreased

**water flows out of tubule back into blood

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23
Q

In low/absent ADH state:

Urine osmolality= ?

Blood osmolality= ?

A

urine- increased

blood- decreased

**water excreted in urine

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24
Q

Physiologic responses to HIGH plasma osmolality:

A

thirst

ADH release

water reabsorption

concentration of urine –> high urine osmolality

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25
Physiologic response to LOW plasma osmolality:
No thirst No ADH release Loss of free water -- collecting tubules impermeable Low urine osmolality -- dilute urine
26
Plasma osmolality maintained within __%.
1%
27
Indicator of the presence of ADH?
Urine osmolality
28
What generally tells you what the kidney THINKS about the body's volume status?
urine sodium
29
Range of urine osmolality in a normal kidney?
50-1400 mosm/L
30
Normal daily osmolar load from dietary protein/salt?
500-750 mosm excreted in urine
31
If you have 500 mosm/day to get rid of and your maximum urine osmolarity is 1000 mosm/L, how much urine will be excreted?
0.5 L
32
If you have 500 mosm/day to get rid of and your minimum urine osmolarity is 50 mosm/L, how much urine will you excrete?
10 L
33
Hormones responsible for retention of sodium in volume depleted state?
Ang II Aldosterone
34
What is the kidney doing of urine sodium is
senses low effective circulating volume, so it's holding on to sodium
35
What's going on in the kidney if urine sodium is > 10 meq/L?
-sensing expanded ECV OR -not able to properly retain Na+ OR -excreting Na as an obligate cation with something else
36
What is pseudohyp-O-natremia? What causes this?
low Na with normal or elevated Plasma osmolality. Caused by: Hyperlipidemia (normal Posm) Hyperproteinemia (normal Posm) Hyperglycemia (elevated Posm) Hypertonic mannitol (elevated Posm)
37
How does hyponatremia develop if mechanisms are in place to maintain plasma osmolality within 1%?
Non-osmotic stimuli override osmotic stimuli (or lack of) to secrete ADH at the expense of plasma osmolarity **perfusion to brain is more important than perfect osmolality in plasma
38
Four steps in clinical eval of hyponatremia:
1. Check Posm: confirm true hypoosmolar hyponatremia 2. Check Uosm: is ADH acting? - 100 -- yes, despite hypoosmolar state, either appropriate for volume status or inappropriate 3. Check UNa+: what is the kidney's perception of ECV? 4. Check the patient: volume status/clinical picture?
39
Hyponatremia with Uosm
excess water intake (primary polydipsia) **need to drink 10-15 L/day to overwhelm kidney's ability to clear free water
40
Two exceptional causes of hyponatremia with Uosm
beer potomania tea and toast syndrome **not ingesting enough(or any) protein/solutes for an extended period (low daily osmolar load)
41
Treatment for primary polydypsia?
water restriction
42
UNa+
Reabsorbing Na+ in an effort to reexpand vascular space
43
UNa+
Recieving the wrong signal. Edematous states: think CHF/cirrhosis/nephrosis
44
UNa+ > 10, patient is volume depleted and hyponatremic. What is the kidney doing?
Salt wasting. Receiving the wrong signals. This is rare.
45
UNa+ > 10, patient is volume expanded and hyponatremic. What is the kidney doing?
Volume is appropriate or expanded Brain or kidney is confused
46
Causes of volume depleted hyponatremia with UNa+ of
GI-- N/V, diarrhea Skin-- burns Diuretics-- late Pure cortisol deficiency (Addison's???)
47
Causes of hyponatremia with UNa+
Edematous states/poor perfusion--reduced ECV - CHF - Cirrhosis/liver failure (low albumin?) - nephrotic syndrome (proteinuria?)
48
Causes of salt wasting (hyponatremia with volume depletion and UNa+ > 10):
adrenal insufficiency salt wasting renal disease Early diuretics Hypokalemia with metabolic alkalosis after vomiting (lose sodium and bicarb) hypothyroid
49
Causes of hyponatremia with UNa+ > 10 and appropriate or expanded volume:
SIADH-- Syndrome of Inappropriate ADH secretion - oat cell carcinoma (paraneoplastic) - pulmonary process (TB, PNA, asthma) - Drugs (chlorpropamide, oxytocin, tegretol, cytoxan) - esophageal process - pain - neuropsychiatric Reset osmostat CKD
50
Fixed ADH secretion without regard to osmotic or volume status:
SIADH
51
Tx for SIADH:
fluid restriction increase osmolar load (high protein/Na diet)
52
Treatment for volume depleted hyponatremia?
NS **replenish volume, turn off ADH
53
Tx for volume neutral or expanded hyponatremia:
restrict free water intake treat state of poor perfusion
54
Tx for severe hyponatremia not related to pure volume depletion OR with neurologic sx:
hypertonic saline
55
Pharm tx for volume expanded hyponatremia:
ADH antagonists Tolvaptan, Conivaptan
56
Rapid correction of hyponatremia risks?
Central Pontine Myelinolysis (BAD)
57
Brain's own mechanism of compensation for slowly developing hyponatremia:
idiogenic osmoles **more risk in rapid correction
58
V1a and V1b receptors response to ADH?
vasoconstriction and ACTH release
59
Hypothalamus/pituitary not releasing ADH?
Central diabetes insipidus
60
Collecting tublues don't respond to ADH:
nephrogenic diabetes insipidus
61
How could you differentiate central vs nephrogenic DI?
give exogenous ADH if UOsm increases --> central etiology
62
Dx of diabetes insipidus usually made by patient complaint of?
polyuria (usually not hypernatremia)
63
Drug to know that causes nephrogenic DI?
lithium
64
Safe rate for correcting hypernatremia?
slowly 0.5 meq/hour --> 12 meq/24 hr
65
What to give to replace free water deficit?
Free water ORALLY (NOT IV) D5W IV **can give 1/4 NaCl if volume depleted

CRRAB II (28 decks)

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