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Pham, Chapter 1 - Na/Water > Ch 1, part 1 - Hyponatremia > Flashcards

Ch 1, part 1 - Hyponatremia Flashcards

1
Q

Hyponatremia effects on:

1) Bones
2) Heart
3) Lifespan

A

1) Bones -> increase risk for osteoporosis, gait instability, fall, fracture.
2) Heart –> Myocardial fibrosis (rats)
3) Lifespan –> early senescence ( rats).

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2
Q

Copeptin - describe metabolism

A

Pre-pro-AVP –cleaved–> ADH + Copeptin + neurophysin II

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3
Q

Copeptin is surrogate for what? Why is this measured?

A

Surrogate for ADH levels.

Measured b/c more STABLE compound than ADH.

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4
Q

Copeptin increased/decreased in what conditions?

A

Increased in CHF, SIADH, sepsis

Reduced in cDI.

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5
Q

T/F: Copeptin shown to be increased earlier than troponin in acute MI and suggested to be used as marker of early MI.

A

True

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6
Q

Why do we not check copeptin in US?

A

not commercially available in US yet.

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7
Q

What would it mean if there is loss of “pituitary bright spot” on MRI?

A

ADH may be seen as Pituitary “bright spot” on MRI

If Pit bright spot is absent on MRI, that is suggestive of central DI.

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8
Q

range of clinical presentation of hyponatremia?

A 
Asymptomatic. 
Slowed mentation
Lethargy, HA, n/v, disorientation, 
Muscle cramps, 
Reduced reflexes. 
Seizures
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9
Q

What is Pseudohyponatremia? Why does it happen?

A

Happens with old technique (Flame photometric assay) where lipids/proteins get in the way in vitro.

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10
Q

How can we avoid pseudohyponatremia?

A

Newer methods avoid this via Ion-specific electrodes, supra-cenrifugation of serum removes paraproteins/lipids prior to measuring sNa.

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11
Q

Hyperosmolar Hypernatremia causes and mechanism

A

Mechanism: shift of water from intra –> extracellular space
Causes:
- hyperglycemia
- hypertonic mannitol
- sucrose, maltose (eg, mixed in IVIG solutions)

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12
Q

Renal salt wasting mechanism of hypoNa

A

volume depletion –> appropriate ADH release –> hyponatremia

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13
Q

Renal salt wasting causes/situations

A
    • Acute, recent diuretic use
    • HypoAldosterone
    • Cerebral salt wasting
    • hypovolemic pt but Una > 20-30 and Uosm > 300
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14
Q

Cytoxan is a/w SIADH (T/F)

A

True

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15
Q

symptomatic HIV is a/w SIADH (T/F)

A

True

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16
Q

Mechanism of Hypothyroidism and hypoNa

A

severe (eg, myxedema), TSH > 50 mIU/ml —> reduced CO, PVR, renal perfusion –> increased ADH secretion.

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17
Q

Kidney failure usually has what Uosm?

A

isosthenuric Uosm 300 mOsm/L.

can’t dilute or concentrate urine when kidneys don’t work

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18
Q

Situations where Uosm < 100

A

Polydipsia –> appropriate dilution of urine
Low solute intake –> need solute in nephron to get rid of water (see card 21).
Hypotonic fluids –> appropriate dilution

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19
Q

Hypocortisolism and hypoNa - mechanism?

A

Increased synthesis of Corticotropin-releasing hormone (co-expressed w/ ADH) –> thus, higher ADH.

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20
Q

Pregnancy and hypoNa – mechanism?

A

Reduced threshold for ADH secretion + increased thirst

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21
Q

Tea and toast/beer potomania: explain.

A

Kidneys can’t excrete just pure water, they need at least 50-100mOsm of solute to excrete every 1L of water.
Low solute states –> less Na delivery –> less water excretion.

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22
Q

Irrigation fluids: eg, Transurethral resection, Hysteroscopy, nephrolithotomy
Explain the hyponatremia. Which fluid should not cause hyponatremia?

A

HYPO-osmotic 1.5% glycine = 200mOsm/kg.
Note:When > 1.5-2L of it is used, ADH can be stimulated directly.

  • Hypo-osmotic 3% Sorbitol = 165mOsm/kg. Sorbitol becomes glc/fructose in liver, then CO2 + H2O.
  • Isotonic 5% mannitol does not cause hyponatremia (275 mOsm/L).
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23
Q

SIADH vs. NSIAD

Long answer

A

SIADH is inappropriate ADH release –> kidney –> water reabsorption

NSIAD = Nephrogenic syndrome of inappropriate anti-diuresis = Constitutively activated ADH receptor w/o presence of ADH. 
== X-linked gain of function mutation of AVP 2 receptor.
== Clinically, looks same as SIADH, but ADH levels low. 
== Confirmatory Diagnosis == Sequencing AVP2 receptor gene
== carriers of mutation have abnormal response to water-loading test.

(similar conceptually to cDI vs. nDI)

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24
Q

SIADH vs. NSIAD

Short answer

A

SIADH –> too much ADH

NSIAD –> low ADH, but abnormal V2 receptor (always active)

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25
Q

Diuretics that can lead to hyponatremia

A 
Most common -- thiazides, 
Less common: 
Indapamide (thiazide)
Amiloride (eNaC blocker, K sparing)
Lasix (if becomes hypovolemic)
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26
Q

2 ways drugs affect ADH

A

1) Increase hypothalamic ADH production

2) Potentiate ADH effect

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27
Q

Drugs that increase hypothalamic ADH

A

Anti-depressants

Anti-psychotics (thioridazine, trifluoperazine, haldol).

Anti-epileptics (Carbamezepine, Oxcarbazepine, Valproic acid),

ChemoTx (Vincristine, vinblastine, IV cytoxan, melphalan, ifosfamide, MTX, IFN alpha/gamma, levamisole, pentostatin, monoclonal antibodies),

Opiates.

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28
Q

ACEi – mechanism of hypoNa

A

Rare

AT 1 –> AT 2. ACEi blocks this in peripheral tissues, not in brain.
ACEi –> increased AT1 levels in periphery, AT1 then goes to brain –> makes more AT 2 in brain –> more thirst and ADH release –> hyponatremia.

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29
Q

Drugs that Potentiate ADH effect

A

Anti-epileptics (carbamezepine, lamotrigine)
IV Cytoxan
NSAIDs

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30
Q

How does IVIG cause hyponatremia

A

1) IVIG (w/ sucrose or maltose) –>
(i) PseudohypoNa if flame photometric assay used (lot of globulins);
(ii) hyper-osmolar (similar to hyperglycemia induced hyponatremia mechanism of water coming out to high sugar) - more likely to happen in renal insufficiency since there is reduced sugar excretion.

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31
Q

mechanism of Ecstasy and other amphetamines in hyponatremia

A

Increased hypothalamic ADH secretion + increased water intake due to hyperthermia.

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32
Q 
T/F
Less commonly associated w/ hyponatremia: 
Nicotine patch, 
Colchicine poisoning, Tacrolimus, 
PPIs, 
Hydroxyurea, 
Azithro, 
Glipizide, 
Heparin (unfractionated).
A

True

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33
Q

what is effect of hypoxemia in pt with hyponatremia

A

Hypoxemia can exacerbate hyponatremic encephalopathy

Oxygenation is therefore important.

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34
Q

As you correct the hypoNa, who is at risk of hypotonic polyuria the most?

A

Theme: loss or reduction of ADH = hypotonic polyuria

    • post - pituitary infarction (loss of ADH)
    • steroid replacement for cortisol deficiency (suppression of ADH release).
    • d/c of DDAVP in pts using it chronically (eg, central DI)
    • primary polydipsia
    • volume depleted pt who gets rapid volume expansion
    • recovery from acute resp failure
    • d/c of thiazides
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35
Q

T/F

K+ supplementation will increase Na+ and correct it same amount.

A

True

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36
Q

Pt needs 200meq Na to raise Na to goal, but also needs 75mEq K. What can you do?

A

Give 125meq Na + 75meq K = 200meq.
You don’t need to give 275, otherwise you’ll overshoot.
K+ = Na+ in terms of correction of hypoNa.

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37
Q

what are the concurrent factors that increase ODS risk?

A

ODS can happen independent of rate of Na correction

Concurrent HYPO: K, Mg, Phos, Thiamine, or any combo of these.
Classic: ALCOHOLIC

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38
Q

what % of increase in Na should reduce cerebral edema significantly?

A

~5%

eg, Na 115 (5% = 5.75), so ~6meq/L to Na 121 should do it.

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39
Q

Who is at high risk for ODS?

A
    • Na < 105
    • Alcoholic
    • Malnourished
    • Advanced Liver disease
    • Hypokalemia
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40
Q

How does ODS look in 1-2 days post over correction?

A

generalized encephalopathy

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41
Q

How does ODS look in 2-3 days post over correction?

A

behavioral changes, CN palsies, weakness, Quadriplegia (“locked in” syndrome), possible death

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42
Q

Is ODS reversible?

A

Partial to complete recovery of mild to moderate neurological complications possible.

DDAVP and hypotonic fluids to reverse overcorrection has been shown to be beneficial in rats and humans (case reports).

43
Q

What is recommended correction rate for acute hyponatremia (< 48 hr)?

A

6-8 mEq/L per 24 h

44
Q

What is recommended correction rate for chronic hyponatremia (> 48 hr)?

A

4-8meq/L per day

4-6meq/L per day for high risk ODS

45
Q

Don’t exceed ___ in 48 hours of hypoNa correction

A

not more than 18mEq/L in 48 hrs

46
Q

In whom to consider fluid restriction?

A

euvolemic/hypervolemic.

Anyone not hypovolemic basically.

47
Q

does “fluid” in fluid restriction only refer to “free water” intake?

A

no!

all fluids

48
Q

how much should pt fluid restrict by?

A

aim for 500ml BELOW pt’s average daily UOP.

49
Q

pt w/ euvolemic hyponatremia, making ~1200 mL UOP per day. How much should they fluid restrict themselves?

A

aim for 500ml BELOW pt’s average daily UOP.

~700mL/day

50
Q

who usually fails fluid restriction for hyponatremia tx?

A
  • -> High Uosm > 500
  • -> (Una + Uk) / SNa > 1 (high urine solutes)
  • -> Baseline urine volume < 1500ml/day
51
Q

when to use 0.9% saline in hyponatremia

A

hypovolemic (regardless of how high Uosm is).

52
Q

what to do if pt w/ severe symptomatic hyponatremia (eg, seizures, severely depressed mental status)?

A

3% NS 100ml every 10 min to break seizures or total 3 boluses (whichever is first).

53
Q

Other than in severe symptomatic hyponatremia, can we use hypertonic 3% saline in less symptomatic patients?

A

yes, could consider in SIADH pt w/ Na < 120 w/ very high Uosm&raquo_space; 300.

(We know 2% would be king here, but what do they know?? hehehehe)

54
Q

T/F
Any salt solution used should have higher osmolarity than the pt’s Uosm (in SIADH pts), otherwise may worsen hyponatremia.

A

True

If NS is used for SIADH w/ Uosm > 300, then desalination occurs and more water is retained than salt.

55
Q

how many mEq of Na are in:

1) 1gm NaCl tab
2) 0.9% NS
3) 3% NS

A

1) 1gm NaCl –> 18 meq Na
2) 0.9% NS –>154 mEq of Na
3) 3% NS –> 513 mEq of Na

56
Q

Give 3 ADH blockers

A

Demeclocycline
Tolvaptan
Conivaptan

57
Q

Mechanism and issues with Demeclocycline

A

Inhibits ADH binding to receptor.

Contraindicated in pregnancy, kids due to bone/teeth development/staining.

Nephrotoxic, photosensitive rash.

58
Q

this vaptan is given only PO

A

tOlvaptan (O for oral)

59
Q

this vaptan is given only IV

A

conIVaptan (IV in the name!)

60
Q

this vaptan blocks both V1a and V2 receptors

A

Conivaptan

61
Q

this vaptan blocks only V2 receptor

A

Tolvaptan

62
Q

why should conivaptan use be limited to 4 days

A

significant drug interactions w/ other agents metabolized by CYP3A4

63
Q

T/F

Vaptan use has been shown to improve long term survival in hyponatremia

A

False, it has not improved long term outcomes.

64
Q

(T/F)

If pt just came off 3% NS, it is highly recommended to start them on vaptan

A

False – can cause overcorrection

65
Q

in which situation is a vaptan ineffective

A

in renal failure (sCr > 3mg/dl)

66
Q

who is at risk of ODS on vaptan?

A

if they are also on diuretics and/or have little/no access to free water intake.

67
Q

T/F

you should d/c fluid restriction if you are starting a vaptan. why or why not?

A

True

to avoid dehydrating pt and causing overcorrection of hyponatremia.

68
Q

Has ODS been reported in overcorrection of hyponatremia with dialysis in ESRD patients?

A

Yes, therefore should follow same guidelines for non-uremic patients.

69
Q

What should the Hemodialysis Rx be for hyponatremia pt?

A

1) Low Na bath (aim for lowest possible based on pt’s Na, usually lowest is 130)
2) Lowest BFR possible.

70
Q

PROBLEM:
ESRD pt (female) with Na 120meq/L.
Weight 60kg
Goal Na is 126 mEq/L by end of iHD treatment.
If you will use Na bath 130mEq/L over 3 hours, what should be your BFR? Are there any other considerations re: the dialyzer?

A

every 1 L of blood w/ gain 10mEq Na
TBW = 30L
Total Na to add to pt = 6mEq/L x 30L = 180mEq Na
180mEq/10meq/L = 18 L that would need to pass through over 3 hours.
BFR = 18,000mL/180min = 100ml/min

Use pediatric mode on dialyzer.

71
Q

T/F

for acute water intoxication, re-lowering Na is necessary to avoid ODS

A

False, it is not necessary.

72
Q

What can you do to manage hyponatremia overcorrection?

A

1) d/c fluid restriction (ie, give PO water)
2) D5W IV to desired Na level.
3) DDAVP – 2-4mcg q8-12 hrs

73
Q

in addition to D5W, DDAVP, what else can you consider in severe overcorrection of hypoNa?

A

high dose steroids (eg, Dexamethasone 4mg q6h for 24-48 h)

74
Q

What are some long term strategies for a patient with primary polydipsia other than fluid restriction?

A

1) Behavioral therapy

2) Clozapine (anti-psychotic) has been reported to be useful in some cases.

75
Q

PROBLEM:
CHF pt w/ volume overload and hypoNa.
mild to moderate symptoms
Whats a good treatment strategy?

A

1) fluid restrict 1L/day
2) add loop diuretic for v/o
3) consider Tolvaptan

76
Q

PROBLEM:
CHF pt w/ severe sx hypoNa.
How to treat?

A

consider 3% NS + loop diuretics.

High risk for over-correction, need very close monitoring.

77
Q 
PROBLEM: 
NSIAD -- 
mild to moderate sx. Treatment?
severe sx?
what about Vaptans?
A

1) fluid restrict + increase solute intake (can consider Urea)
2) 3% NS
3) Vaptans not as effective b/c the receptor is constitutively active.

78
Q

What is osmolar clearance (Cosm)?

A

Cosm = (Uosm x V) / P

79
Q

What is the “typical” Cosm (osmolar clearance)?

A

< 3L per day

80
Q

What Cosm indicates a solute diuresis?

A

> 3L per day

81
Q

What is the Free water clearance equation?

A

FWC = Urine Volume x (1 - Uosm/Sosm)

82
Q

What does a positive free water clearance mean?

A

FWC = Urine Volume x (1 - Uosm/Sosm)

(+) means that pt is making urine that is hypotonic to plasma.

(-) is opposite (hypertonic urine).

83
Q

What is the electrolyte free water clearance equation?

A

EFWC = Vu x [1 - (Una+k/Sna + K)]

84
Q

Meaning of:

1) positive EFWC
2) negative EFWC

A

(+) –> pt’s urine has lower electrolyte (Na + K) than in plasma –> cause rise in sNa.

(-) –> pt’s urine has higher electrolyte (Na + K) than in plasma –> cause drop in sNa.

85
Q 
PROBLEM: 
pt w/ post-obstructive diuresis. 
sNa = 135
Posm = 297
UOP = 300ml/hr
Uosm = 450
Una = 73, Uk = 20
Is sNa expected to increase or decrease?
A

EFWC = 0.3L/h x (1 - 93/135) = 0.093L/h (positive)

positive means ‘hypotonic’ urine (less electrolytes than in plasma) –> rise in sNa.

86
Q

can a pt with Uosm > Sosm get hypernatremia?

A

Yes, as long as the EFWC is positive.

87
Q 
PROBLEM: 
CHF pt on Bumex gtt.
sNa 148
UOP 125cc/hr
Una = 75
Uk = 15
Which fluid would not worsen fluid overload and would keep sNa the same (assuming pt NPO and not on any other IVF).
A) 125ml/hr of NS 
B) 125ml/hr of 1/2NS
C) 50ml/hr of D5W
D) 75ml/hr of D5W
E) 125ml/hr of D5/1/4NS
A

EFWC of urine = 50ml/hr (positive)

Answer:
C –> EFWC of D5W = 50ml/hr x (1 - 0) –> 50cc/hr given to pt (same as fH2O loss) –> net even fluid balance and net even water balance.

88
Q 
PROBLEM: 
CHF pt on Bumex gtt.
sNa 148
UOP 125cc/hr
Una = 75
Uk = 15
Which fluid would not worsen fluid overload and would decrease the sNa. 
A) 125ml/hr of NS 
B) 125ml/hr of 1/2NS
C) 50ml/hr of D5W
D) 75ml/hr of D5W
E) 125ml/hr of D5/1/4NS
A

EFWC of urine = 50ml/hr (positive)

Answer:

D. EFWC of D5W here is 75cc/hr – net gain of 25cc/hr of fH20

89
Q

What is the average US diet urine solute load?

A

~800mOsm

90
Q

PROBLEM:

Can a pt with relatively low Uosm (150) to Posm (280) have a solute diuresis?

A

Yes.
Depends on urine volume.
If pt makes 10L urine/day at 150mosm/liter, then that is a Uosm 1500mosm per day.
Daily Uosm of American is ~800mosm/L so in this case there’s more Uosm being excreted per day than 800.

Using equation Cosm = Uosm x V/Posm = 150 x 10L/280 = 5.4L which is > 3L.
Average diet is < 3L/day.

91
Q

Can pt’s with hypernatremia get intra-cerebraland subarachnoid bleeding?

A

Yes, can occur due to rupture of cerebral veins with marked decrease in brain volume.

92
Q

What hypothalamic disorders lead to hypernatremia?

A

1) Primary hypodipsia
2) Reset osmostat in primary mineralocorticoid excess.
3) Adipsic DI

93
Q

How does hypernatremia occur in primary aldo excess? How is it a form of “reset osmostat”?

A

Chronic Na retention/volume expansion leads to mild chronic ADH suppression (in effect, is state of reset osmostat)

94
Q

How can one treat the hypernatremia in primary aldo excess?

A

Diuretics –> euvolemia –> less ADH suppression –> water reabsorption –> normonatremia

95
Q

What is the typical Na range in primary aldo excess?

A

~143-147 mEq/L

96
Q

How does hypernatremia occur in Adipsic DI? What is defective and what is intact?

A

There are combined defects in:

1) osmoreceptor function and
2) Thirst.

    • Osmolar dependent ADH secretion is defective.
    • But, volume regulated ADH secretion is intact!
97
Q

Adipsic vs. central DI

A

Typical central DI pt cannot stimulate ADH release with either hyperosmolar or hypovolemic states.

Adipsic DI responds to hypovolemic stimuli.

98
Q

Clinical presentation of adipsic DI?

A

1) typically asx since it is chronic.
2) Na ~155-190mEq/L
3) Pt may be hypovolemic + high renin/aldo –> hypokalemic met alk.

99
Q

Classic pt with adipsic DI

A

obese w/ sleep apnea, venous thrombi during hypernatremia, thermoregulatory dysfxn, seizures, and increased mortality.

100
Q

what are some causes of adipsic DI?

A

Congenital or acquired CNS lesions

Sarcoidosis

101
Q

Obese pt w/ sleep apnea, DVT. You’re called for hypernatremia 160mEq/L not correcting w/ hypotonic fluid.

What is the diagnosis?

A

Adipsic DI

pt can’t secrete ADH in response to hyperosmolality thus no ADH to reabsorb water that the pt is getting.
But pt can concentrate urine w/ fluid restriction.

102
Q

How can you treat adipsic DI?

A

DDAVP

…since they are able to concentrate urine but unable to secrete ADH to hyperosmolar stimulus.

103
Q

what is primary nephrogenic DI due to?

A

it is hereditary mutation of AQP2 channel

104
Q

What are some causes of 2* nDI?

A 
Electrolytes: Hypercalcemia, Hypokalemia
Pregnancy
Drugs: 
- Lithium
- Demeclocycline
- Vaptans
- Ampho B
- Foscarnet
- Aminoglycosides
- Cidofovir
- Methoxyflurane

Pham, Chapter 1 - Na/Water (2 decks)

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