ADH Disorders (DI & SIADH) Flashcards

1
Q

What happens to cells when blood is hypernatremic?

A

Cells shrink

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2
Q

What happens to cells when blood is hyponatremic?

A

Cells swell

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3
Q

What is ADH’s response to increased plasma osmolality or to decreased circulating fluid volume?

A

Increased ADH secretion from posterior pituitary–> Decreased water excretion–> increased water retention–> increased circulation fluid volume–> decreased ADH

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4
Q

What is the body’s thirst response to increased plasma osmolality or to decreased circulating fluid volume?

A

Increased thirst –> increased fluid intake –> increased water retention–> increased circulating fluid volume –> decreased thirst

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5
Q

Another term for ADH

A

Vasopressin

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6
Q

What does SIADH stand for?

A

Syndrome of Inappropriate ADH

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7
Q

What happens in SIADH?

A

There is an overproduction of ADH which causes excess water reabsorption. This has a dilutional effect on serum sodium levels. Cells swell as fluid shifts into intracellular spaces.

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8
Q

What is the most common cause of SIADH?

A

Ectopic ADH production from lung cancer cells

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9
Q

What kind of disorder is occurring when lung cancer cells secrete ADH?

A

This is an example of a paraneoplastic disorder. The vasopressin is secreted by a tumor.

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10
Q

Why does diabetes insipidus occur?

A

There is an underproduction of ADH

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11
Q

What are the 2 causes of DI?

A
  1. Neurogenic causes
  2. Nephrogenic causes

There are also psychogenic causes

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12
Q

What is an example of a neurogenic cause of DI?

A

Head trauma, especially trauma to the pituitary

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13
Q

What is the most common cause of drug-induced nephrogenic DI?

A

Lithium

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14
Q

What is the pathology behind nephrogenic DI?

A

There may be adequate ADH levels in the blood, but the kidneys do not respond

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15
Q

What is the pathophysiology behind SIADH?

A

Increased ADH–> increased water reabsorption in the renal tubules –> increased intravascular fluid volume–> Dilutional hyponatremia & decreased serum osmolality

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16
Q

What serum level of sodium causes severe symptoms of SIADH?

A

<100-115 mEq/L

17
Q

What are the clinical manifestations of SIADH?

A

Depend on severity & rate of onset of hyponatremia, but S/S of hyponatremia:

  • Muscle cramping
  • Dyspnea
  • Fatigue
  • Neurologic symptoms: dulled sensorium, confusion, lethargy
  • GI symptoms: impaired taste, anorexia
18
Q

What are 2 priority nursing problems for SIADH patients?

A
  1. Fluid volume excess

2. Risk for injury (due to altered mental status r/t hyponatremia)

19
Q

What are nursing interventions for SIADH patients?

A

Assess for S/S fluid volume overload
Monitor I&Os; daily weights
Monitor LOC & changes in mental status
Restrict fluids as ordered
Administer IVF per order (closely monitor rate)
Administer meds as ordered (not 1st line treatment)
Support patient & family

20
Q

What is the immediate goal when caring for a patient with SIADH?

A

To restore normal fluid volume & osmolality

21
Q

Generally, how is drug therapy used in SIADH patients?

A

Only used in patients with chronic SIADH. Sometimes diuretics are used; sometimes demeclocycline (which blocks the effects of ADH) is used

22
Q

If an SIADH patient has severe symptoms and/or severe hyponatremia (<120 mEq/L), what IVF do they receive?

A

Hypertonic NS (3-5%) IV VERY SLOWLY over hours to days to prevent abrupt fluid shifts within the brain cells

23
Q

What is the pathophysiology of diabetes insipidus?

A

Decreased ADH –> decreased water reabsorption in renal tubules–> decreased intravascular fluid volume –> increased serum osmolality (hypernatremia) AND excessive urine output

24
Q

Describe the onset & nature of neurogenic (“central”) causes of DI.

A

Usually abrupt onset
Has the most severe signs & symptoms
If caused by head trauma
It is self-limiting meaning it will resolve on its own, but the symptoms need to be treated.

25
Q

Describe the onset & nature of nephrogenic causes of DI.

A

Less abrupt onset & less severe symptoms than central DI

26
Q

What are the characteristics of a DI patient’s urine?

A

They would produce 5-20 L/day (polyuria)
Very low specific gravity (<1.010); very diluted
Very low urine osmolality

27
Q

What are the characteristics of a DI patient’s blood?

A

High osmolality/very concentrated (300 mOsm or greater)

28
Q

Clinical manifestations of DI

A
  1. Polyuria (5-20 L/day)
  2. Polydipsia (extreme thirst as a mechanism to dilute their very concentrated blood)
  3. Fatigue (unable to sleep due to nocturia)
  4. Weakness
29
Q

2 priority nursing problems for DI

A
  1. Fluid volume deficit

2. Risk for injury (altered mental status r/t hypernatremia)

30
Q

What is the expected range for urine specific gravity?

A

1.010-1.030

31
Q

What is the expected range for serum osmolality?

A

270-290 mOsm

32
Q

What is the expected serum sodium level?

A

135-145 mEq/L

33
Q

Nursing care for deficient fluid volume in DI patients

A

Administer IVFs
Pharmacotherapy
I&Os; daily weights
Monitor labs (urine specific gravity, serum osmolality, serum sodium)
Notify HCP if increase in urine volume w/decreased specific gravity

34
Q

Drug therapy for neurogenic DI

A

Desmopressin (DDAVP), which is synthetic ADH

35
Q

What routes can desmopressin be administered?

A

Nasal spray, PO, IV, SQ