Electrolyte Disorders - Hyponatremia Flashcards

1
Q

Def. hypoN and RFs

A

-Serum Na <135.

CHF
Cirrhosis
nephrotic syndrome
PNA legionella
post-op
ICU
older pt
meds
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2
Q

2 main systems that regulate sodium?

A
  • ADH system (amount of ADH is indirectly related to amount of urine produced!)
  • thirst mechanism.
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3
Q

What is normal Na

A

280-290 mOsm/L

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4
Q

What two stimuli trigger ADH to be released? the goal here would be to make urine that is NOT dilute

A
  1. Osmotic stimuli: osmoreceptors detect high osmolarity in serum –> concentrate urine to get rid of extra solutes
  2. Non-osmotic stimuli: baroreceptors detect low BP or blood volume –> concentrate urine to conserve fluid
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5
Q

What are other non-osmotic stimuli that trigger ADH release

A
Baroreceptors
Nausea
Hypoxia
Pain
Opiates &amp; Antidepressants
Pregnancy
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6
Q

Pathogen. of HypoN: what happens when you have decreased serum osmolarity i.e. too much free water retention?

A
  • Thirst suppression and suppression of ADH release

- ADH suppression= more urine= dilute urine

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7
Q

Pathogen. of HypoN: what happens when you have increased serum osmolarity i.e. too little free water?

A
  • Thirst stimulation and stimulation of ADH release

- ADH release=little urine=concentrated urine

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8
Q

Defective urine diluting ability (so all you’re doing is concentrating your urine!) + excess water intake = ?

A

Hyponatremia

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9
Q

Defective urine concentrating ability + inadequate water intake = ?

A

Hypernatremia

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10
Q

What results in hyponatremia?

A

Increases in TBW, not really from actual Na changes. Increased TBW due to excessive intake or decreased renal excretion …

(renal one is usually due to inability to suppress ADH…if you can’t suppress ADH you produce less urine thus increasing TBW and diluting out your Na)

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11
Q

Timing of acute v. chronic hyponatremia

A

Acute: <48h
Chronic: >48 h or unknown amount of time

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12
Q

Sx of hyponatremia

A

Usually present at <125mEq/L

HA, fatigue, dizziness, nausea, gait instability/falls, confusion, psychosis, seizures, coma due to cerebral edema

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13
Q

Whats the 2 step systematic approach to dx hypoN

A
  1. Measure serum osmolarity to determine if hypoN is hypotonic (true), isotonic or hypertonic (secondary)
  2. If it is hypotonic, assess fluid volume status because each volume status correlates w/ diff. etiologies.
    2a. Measure random urine Na level and urine osmolarity to weed out etiology. If considering SIADH, take serum uric acid. If low, could be SIADH.
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14
Q

What’s special about the labs in hyponatremia?

A

Must be drawn simultaneously ideally before any tx is given b/c that could alt. lab values

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15
Q

Hypovolemia PE

A
HypoTN
Orthostatics 
Tachy
Poor cap refill
Increased skin turgor
Dry mucosa/fissuring
Flat JV
Decreased urine output
>50% collapse of IVC during inspo on ECHO
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16
Q

Hypervolemia PE

A

HTN, Edema, JVD, Dilated IVC on ECHO

17
Q

Etiology:

  • Hypovolemic
  • Urine osm>300
  • Urine Na>20
A

RENAL FLUID LOSS

  • diuretic excess
  • adrenal insufficiency
  • osmotic diuresis
  • post obstructive diuresis post hydronephrosis
  • RTA
  • cerebral salt wasting
  • salt losing nephropathy
18
Q

Etiology:

  • Hypovolemic
  • Urine osm>300
  • Urine Na<20
A

EXTRARENAL FLUID LOSS

  • V/D
  • 3rd spacing (burns, pancreatitis)
  • Blood loss
  • Sweating
  • Lung losses
19
Q

Etiology:

  • Euvolemic
  • Urine osm<100
A

Psych issue causing primary polydipsia

20
Q

Etiology:

  • Euvolemic
  • Urine osm>300
  • Urine Na>20
A

-SIADH (tumor i.e. paraneoplastic syndrome pf #1 SCLC, CNS/pulm, SSRI, Nausea, Pain, hypoxia)

  • Hypothyroid
  • Adrenal insufficiency
  • Thiazides (one of the most common causes!!!)
21
Q

Etiology:

  • Hypervolemic
  • Urine osm>300
  • Urine Na<20
A

Nephrotic syndrome
CHF
Cirrhosis

all these lead to a defective circ. volume –> RAAS activation

22
Q

Etiology:

  • Hypervolemic
  • Urine osm>300
  • Urine Na>20
A

Acute or chronic kidney failure (will have low GFR)

23
Q

How is SIADH dx?

A

Exclude cortisol def., hypothryoid, other causes

24
Q

Most common causes of SIADH

A

SCLC!
Post-op!
Pulmonary disorders
Nervous system disorders

25
Q

What drugs are associated w/ SIADH

A
Antidepressants
Anticonvulsants
Antipsychotics
Cyclophosphamide for cancer
Opiates
MDMA
26
Q

Correction of acute hyponatremia

A

Can have rapid correction w/ little risk of ODS

27
Q

Correction of chronic hyponatremia

A

-Raise by 8-10 mEq/L/day w/ no more than 18mEq/L in first 48 hours

28
Q

If a pt is seizing (a complication of hypoN), what should you do?

A

Give HYPERTONIC SALINE (3%) to quickly raise Na by 3-4 mEq/L and stop sizure. Then slowly raise to normal.

29
Q

How to fix an overcorrection of Na?

A
  • D5W i.e. free water
  • DDAVP i.e. desmopressin
  • D5W and DDAVP
  • Discontinue therapies that are raising Na
30
Q

Tx for hypovolemic hypoN (both renal and extrarenal)

A
  • Isotonic saline if w/o sx

- Hypertonic saline if w/ sx

31
Q

Tx of euvolemic hypoN due to primary polydipsia

A
  • Water restriction

- Hypertonic saline if w/ sx

32
Q

Tx of euvolemic hypoN due to SIADH

A
  • Water restriction
  • Furosemide
  • Salt or urea tabs
  • Vaptans to inhibit ADH in kidney
  • Demeclocycline

-Other tx: thyroid replacement, prednisone, discontinue thiazine

33
Q

Tx of hypervolemic hypoN (both etiologies)

A

Water restriction and Furosemide

34
Q

Sx of ODS

A
  • Dysarthria and dysphagia
  • Paralysis
  • Behavior issues
  • Pseudobulbar palsy
  • Seizures
  • Lethargy
  • Confusion
  • Coma (*locked-in syndrome…terrifying)
  • Death
35
Q

Dx of ODS

A

MRI Head. Initial normal MRI does not R/O ODS b/c it can take 4 weeks for MRI abnormalities to be seen.

36
Q

Steps of developing ODS

A
  1. Normal brain w/ normal osmolality
  2. Sudden onset of hypotonic state
  3. Water moves ECM to ICM b/c there are more solutes IN the cells
  4. Rapid adaptation: we try to fix the edema by having Na, K, and Cl leave our cells so water will follow
  5. Slow adaptation: organic osmolytes leave
  6. BRANCH POINT:
    - proper therapy: slow increase of osmolytes and Na, K, Cl, etc.
    - overcorrection: cells shrink, axonal shear damage, BBB disruption all lead to demyelination