Hypernatremia Flashcards

1
Q

How does ADH respond to volume hypertonicity?

A

ADH release is more sensitive to small changes in plasma tonicity than small decreases in EABV

however, it is exponentially stronger when changes in EABV are greater

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2
Q

symptoms of hypertonic hypernatremia

A

recognized as a SNa above 145 mEq/L, symptoms become obvious around 160 mEq/L

seizures

coma

somnolence

lethargy

thirstiness

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3
Q

What effect does hypertonicity have on cells?

A

produces cellular dehydration, unlike isotonic volume depletion

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4
Q

In the absence of ADH, how does volume depletion or decreased renal solute load affect H2O diuresis?

A

impairs H2O diuresis

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5
Q

What are the ways to develop hypertonic hypernatremia?

A

hypertonicity is almost always associated with some reduction in TBW

hypertonic salt infusion

persistent H2O losses not replaced by intake

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6
Q

What are the categories of hypertonic hypernatremia?

A

hypertonic Na gain

polyuric (increased CefH2O)

non-polyuric (decreased CefH2O)

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7
Q

What are the classifications of polyuric hypernatremia?

A

solute diuresis

pure H2O diuresis

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8
Q

What are the categories of pure H2O diuresis?

A

central diabetes insipidus

nephrogenic diabetes insipidus

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9
Q

What are the common causes of acute hypertonic Na gain?

A

drinking sea water

hypertonic feeding

hypertonic enemas

receiving 3% NaCl

receiving NaH2CO3

primary aldosteronism

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10
Q

What is the mechanism of acute hypertonic Na gain?

A

acute exposure to hypertonic Na solutions will result in a shift in TBW from ICF to ECF

results in brain shrinkage, cerebral blood vessel tears

limbic demyelination

elevation of EABV, and acute pulmonary edema

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11
Q

What are the common causes of non-polyuric hypertonic hypernatremia?

A

hypodipsia

fever

sweating

vomiting

diarrhea

cathartics

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12
Q

insensible daily losses

A

~500 mL/day/m2 or 800mL/day for a 70 kg person of which 60% is through the skin and 40% through respiration

fever and sweating produce greater hypotonic losses of about 1-1.5 L/day including ~20 mEq/L of Na and ~10 mEq/L of K

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13
Q

What are the mechanisms of non-polyuric hypertonic hypernatremia?

A

hypodipsia - lack of thirst or access to water

gastrointestinal losses - hypotonic losses

failure to replase H2O - leaves patient dehydrated, some oliguria due to high ADH

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14
Q

What urine output suggests polyuria? How is urine volume calculated?

A

greater than 3L/day

Urinve V = [solute excretion (mOsms)/day] / [average urine mOsms/L/day]

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15
Q

What is the conversion between calories/protein and renal solute load?

A

100 Calories = ~20 mOsm/day of renal solute

10 grams of protein/day = ~50 mOsm of urea/day

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16
Q

pure water diuresis

A

produces a urine osmolarity of ~200 mOsm/L

often in the range of 150-200 mOsm/L because as urine flow rate increases, there is less tubular time to remove solutes like NaCl

17
Q

solute diuresis

A

produces a urine osmolarity of ~300-350 mOsm/L because as urine flow rate increases there is less tubular time to remove H2O

urine losses are relatively H2O rich leaving the residual TBW hypertonic

18
Q

mechanisms of solute diuresis

A

excess H2O in the urine due to solute such as glucose

additional H2O reduces Na concentration and transport out of tubule

increased tubular flow rate increases and washes out intersitial gradient

relative electronegativity from Na uptake facilitates K+ loss

hypotonic loss of renal H2O raises the tonicity of the residual TBW, and thirst ensues

if access to H2O is restricted, hypernatremia worsens

19
Q

What are the common causes of central diabetes insipidus?

A

alcohol

pituitary tumors

post-surgery

trauma

cysts

granulomatosis

pregnancy

meningoencephalitis

genetic mutations - ADH

20
Q

What is the mechanism of central diabetes insipidus?

A

fewer ADH-producing neurons recues the the amount of ADH produces in response to increases in plasma osmolality

urine osmolality cannot be increased as a result

21
Q

causes of nephrogenic diabetes insipidus

A

hypercalcemia

hypokalemia

renal disease - MCD, SCD

drugs - lithium, V2RA, methoxyflurane, amphotericine B

genetic mutations - X-linked V2R and AD AQP2

22
Q

H2O deprivation test int he setting of polyuria

A

if SNa is > 145 mEq/L and the Uosm is less than the Posm, primary polydipsia can be excluded

start the test in the morning after 2-3 hours of fasting

measure UV, Uosm, and weight every hours, and SNa and Posm every 2 hours

continue test until either 1) the Uosm >600 mOsm/L, 2) the Uosm is stable on 2-3 hourly measurements despite a rising Posm, or 3) the Posm >295 or the SNa > 145 mEq/L

23
Q

In the H2o deprivation test, how does central diabetes insipidous respond to desmopressin?

A

Uosm rises > 100%

24
Q

In the H2o deprivation test, how does partial central diabetes insipidous respond to desmopressin?

A

Uosm rises 15-50% (>300 mOsm)

25
Q

In the H2o deprivation test, how does nephrogenic diabetes insipidus respond to desmopressin?

A

no increse in Uosm

26
Q

In the H2o deprivation test, how does partial nephrogenic diabetes insipidus respond to desmopressin?

A

small rise in Uosm (<300 mOsm)

27
Q

Treatment for acute Na intoxication with neurologic symptoms

A

administration of H2O as D5W

if the exposure is within 24 hours then the goal is to correct SNa to 145 mEq/L to minimize risk of cerebral shrinkage and limbic demyelination

if the exposure is longer than 40 hours, the SNa should not fall faster than 10 mEq/L/day to avoid cerebral edema

if there is pulmonary edema, diuretics should be used

28
Q

estimation of target water deficit

A

current TBW x [SNa/(140-1)]

TBW in men is 0.6 lean body weight, 0.5 in women, and 0.45 in elderly

29
Q

What is the equation to correct SNa for a higher serum glucose?

A

Correction = SNa + {[(Glucose - 100)/100] x 2 mEq/L}

30
Q

How do you treat hypernatremia that results from sweating, gastrointestinal losses, or solute diuresis?

A

0.45% saline with potassium

31
Q

equation describing rate of fall in SNa from a 1L infusion

A

[(infused Na + infused K) - SNa]/(TBW + 1)

32
Q

treatment of central diabetes insipidus

A

treat acutely with2 mcg desmopressin intravenously every 12 hours, and when the polyuria resolves and the patient is able, the patient can be switched to intranasal desmopressin

33
Q

treatment of nephrogenic diabetse insipidus

A

can be partially treated with a combination of low Na/low protein diet, thiazide diuretics, and NSAIDs