SM 214: Hypernatremia Flashcards

1
Q

Equation for free water clearance

A

CefH2O = (Urine Volume)x(1 - (Uk + Una)/Sna)

Urine Volume = Solute Excretion Amount/Urine Conc.

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2
Q

What stimuli release ADH? Which one stimulates it more?

A

Stimulated by hypertonicity and low blood volume
ADH release more sensitive to hypertonicity than low blood volume
At less volume, ADH release more sensitive to hypertonicity

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3
Q

What is the definition of hypernatremia?

What are the symptoms of hypernatremia?

A

SNa > 145mEq/L

Sx: Thirst - Lethargy - Somnolence - Coma - Seizures

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4
Q

What is the brain’s response to hypernatremia?

A

Brain takes in solute to prevent cell shrinkage.

Upon volume restoration, risk of cerebral EDEMA (if SNa falls more than 8mEq/L/day)

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5
Q

What are the two mechanisms to hypertonic hypernatremia?

A
  1. High hypertonic salt intake

2. Persistent water loss not replaced by intake

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6
Q

Broad classes of DDx for Hypertonic Hypernatremia

A
  1. Hypertonic Na Gain
  2. Non-Polyuric Water Loss
  3. Polyuric Renal Water Loss
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7
Q

Mechanism and Cause of Hypertonic Na Gain (Hypertonic Hypernatremia)

A

high intake of hypertonic fluid = water shift from ICF to ECF = causes brain shrinkage, cerebral blood vessel tears, limbic demyelination, high EABV, acute pulm edema
Cause: Drink Sea Water/Salty feedings, receiving 3% NaCl, Primary Aldosteronism (lots of Na Reabsorption)

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8
Q

Mechanisms and Cause of Non-polyuric water loss causing hypertonic hypernatremia

A

Non-kidney hypotonic fluid loss
Primary hypodypsia: rare genetic variant and occurs in infirm elderly with less perceived thirst and no access to water
Mechanism: Water Loss > Water Gain - high insensible daily losses + fever/sweat
Cause: GI Loss (Vomit/non-secretory diarrhea)
May also have oliguria if volume deplete (due to ADH)

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9
Q

Mechanism of Polyuric Water Loss (Solute Diuresis) in Hypertonic Hypernatremia

A

Glycosuria: more water stays in tubule to hydrate non-reabsorbed glucose = decreases Na conc. = Less Na Reabsorption + more Na Excretion
Polyuria washes out interstitial gradient = ADH becomes less effective
Hypokalemia also accompanies this because ENaC activated to try to reclaim whatever Na it can
Hypotonic renal loss = low TBW = more thirst
Occurs with Glucose, mannitol, urea, diuretics, NaCl, NaH2CO3

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10
Q

Mechanisms of Polyuric Water Loss (Pure Water Loss) in Hypertonic Hypernatremia

A
  1. Central Diabetes Insipidus
    Brain can’t make/release ADH
    Cause: alcohol, pituitary tumors, post-brain surgery/brain trauma, genetic mutation in ADH
  2. Nephorgenic Diabetes Insipidus
    Kidneys can’t respond to ADH
    Cause: hypercalcemia (binds CaSR = less NKCC activity = less Na reabsorption = less interstitial gradient); hypokalemia (less urea reabsorption in PT = less interstitial gradient); renal disease, drugs, genetic mutations (x-linked V2R, AD AQP2)
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11
Q

What is a water deprivation test good for?

A

Test: restrict water intake, measure urine volume/OsM and plasma OsM for 2-3 hrs

If Urine OsM stable despite rising Plasma Osm - ADH is not working!

Test part 2: give 4mcg desmopressin IV and follow urine response (volume/OsM)

Central Diabetes Insipidus: Urine OsM doubles! (kidneys are functional)
Nephrogenic Diabetes Insipidus: Urine OsM does not change (kidneys not working)

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12
Q

How to treat acute Na intoxication

A

Administer Water as D5W (SNa should not fall more than 8mEq/L/day)

Estimate target H2O deficit: TBW x ([SNa]/140 - 1)

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13
Q

How do you correct Na in High Serum Glucose?

A

SNa,correct = SNa + [(Glucose - 100)/100 x 2]

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14
Q

How do you treat hypernatremia due to hypotonic loss?

A

Sweating, GI loss, Solute Diuresis
Replace Na, K, H2O with NS or half normal saline
Change in SNa from 1 L infusion = (infused Na + infused K - SNa)/(TBW+1)
Don’t forget to correct for insensible losses and renal losses (CefH2O) - with D5W

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15
Q

How do you treat Central and Nephrogenic DI

A

Central DI: desmopressin
Nephrogenic: Low Na/protein diet, thiazide diuretics (lose Na), NSAIDs (because lowers prostaglandin synthesis, which competes with ADH)

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