Anti-Diuretic Hormone Flashcards by Kate Carmie

Anti diuretic means

to prevent urination

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What is the target organs of antidiuretic hormone?

Kidney

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Secreted by the posterior pituitary gland

Anti-diuretic hormone

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Promotes water re-absorption by kidneys

Anti-diuretic hormone

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“Too low”

Diabetes Insipidus

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“Too high”

SIADH

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Described as the passage of very large amounts of dilute urine

Diabetes insipidus

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2 forms of diabetes insipidus

Central (Neurogenic)
Nephrogenic

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Causes of Central (Neurogenic)

-Idiopathic
- Tumor-associated
- Post-Operative
- Head Trauma
- Hereditary (10%)

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Causes of Nephrogenic

-Lithium Toxicity
- Hypercalcemia
- Hypokalemia
-Hyperglycemia

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Its pathophysiology with ADH synthesis, transport, or release

Central (Neurogenic)

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Its pathophysiology is inadequate renal response to ADH despite presence of adequate ADH

Nephrogenic

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Clinical Manifestations of Diabetes Insipidus

-Polyuria
- Polydipsia
- Dilute urine
- Hypovolemia

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What is the normal specific gravity?

1.010-1.025

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Diagnostic Test of Diabetes Insipidus

Fluid Deprivation Test

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Assess ability of kidneys to concentrate urine under the influence of ADH

Fluid Deprivation Test

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Stages of Fluid Deprivation Test

-Fluids are deprived for 8 hours
-Plasma osmolality are checked q4h and urine volume and osmolality q2h
- Desmopressin acetate is given at the end of the 8 hours

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Medical Management of Central Diabetes Insipidus

Desmopressin (DDAVP)
- A synthetic vasopressin
-Given intranasally (nasal spray) q12 to 24 hours
- Caution: CAD

Chlorpropamide (Diabetes)
-Has an antidiuretic effect in vasopressin- sensitive DI

Nursing Management of Central Diabetes Insipidus

-During acute episodes
-Hypotonic IV fluids or D5 water, as ordered (to replace urine output)
-Encourage increased oral fluids as tolerated
-Monitor VS, urine output and specific gravity
-Monitor level of consciousness and for signs of dehydration

Management of Nephrogenic Diabetes Insipidus

-Thiazide diuretics
-Reduces blood flow to the ADH- sensitive distal nephrons
-Indomethacin
-Helps increase renal responsiveness to ADH

Collaborative & Nursing Management of Nephrogenic Diabetes Insipidus

-Low-sodium diet (no more than 3g/day) (helps decrease urine output)
- Encourage increased oral fluids as tolerated
- Monitor VS, urine output and specific gravity
- Monitor level of consciousness and for signs of dehydration

involves the continued secretion or action of arginine vasopressin (AVP) despite normal or increased plasma volume.

SIADH (Syndrome of Inappropriate Anti-Diuretic Hormone)

Causes of SIADH

-Malignancies
-Drugs
-CNS Disorders

Drugs that triggers the SIADH

-Vinca Alkaloids
-Opioids
-General Anesthetics
-Oxytocin
-Carbamazepine
-Antidepressants

CNS Disorders that triggers the SIADH

-Head Injury -Infection (CNS) - Stroke

SIADH tends to be self limiting if causes are:

Head trauma or Drugs

SIADH may become chronic if associated with:

Tumors or metabolic diseases

What is the first symptom of hyponatremia?

Headache

Excessive ADH can increased the reabsorption of water from the collecting ducts back into the circulation. What are the results or the manifestation of it?

-Decreased urine volume - Increased urine specific gravity

Excessive ADH can also increased blood volume. What are the factors or the clinical manifestations of it?

-Hypertension -Weight gain

3 classification of hyponatremia

-Mild hyponatremia - Moderate hyponatremia - Severe Hyponatremia

Serum sodium level of mild hyponatremia

130-134 mmol/L

Serum sodium level of moderate hyponatremia

125-129 mmol/L

Serum sodium level of severe hyponatremia

<120

Mostly asymptomatic but can report/present with headache, nausea, vomiting, fatigue, confusion, anorexia, muscle cramps

Mild Hyponatremia

Gait disturbances, headache, vomiting, fatigue, confusion, muscle cramps, depressed deep tendon reflexes

Moderate hyponatremia

Classification in hyponatremia where delirium, restlessness, agitation, or lethargy, seizures, brainstem herniation, respiratory arrest, coma, death

Severe hyponatremia

Emergency Management of SIADH with Severe Hyponatremia

-3% Hypertonic Saline -Furosemide (Lasix)- increases excretion of free water thereby limiting treatment-induced volume expansion

High yield concept of Emergency Management of SIADH with Severe Hyponatremia

-Sodium correction must be made gradually - Too rapid elevation of sodium levels causes CENTRAL PONTINE MYELINOLYSIS (CPM)

Medical Management of SIADH with Mild/Moderate Hyponatremia in Fluid Restriction

FLUID RESTRICTION (First Line of Treatment)

Medical Management of SIADH with Mild/Moderate Hyponatremia in VAPTANS

-Classified as aquaretics (blocks ADH action and increase water excretion) CONIVAPTAN -Given as IV -Used in combination with fluid restriction -Should not be used for more than 4 days TOLVAPTAN - Given as PO - Dose needs to be titrated after loading dose up to a max of 60 mg -Fluid restriction is avoided as it may cause too rapid sodium correction

Medical Management of SIADH with Mild/Moderate Hyponatremia in Loop Diuretics

-Drug of Choice: Furosemide (Lasix) -Reduces sodium reabsorption in the Loop of Henle - Lost sodium is replaced by either 3% saline or PNSS

Medical Management of Asymptomatic Chronic SIADH

VAPTANS (Alternative) -Chronic loop diuretic therapy with increased salt intake (UREA)-Safe to consume -Increases urine volume - Dissolve powder in water and take during or after meals -Antacids may be used if with GI upset (Mannitol)- Diuretic -Increases osmolarity of glomerular filtrate thereby preventing reabsorption of water