Scribd
Upload
21 views16 pages

Diabetes Insipidus & Syndrome of Inappropiate Antidiuretic Hormone

This document discusses Diabetes Insipidus (DI) and Syndrome of Inappropriate Antidiuretic Hormone (SIADH). It defines antidiuretic hormone (ADH) and its role in fluid balance. It describes central and nephrogenic DI, and covers causes, symptoms, pathophysiology, and diagnostic/treatment approaches for DI. SIADH is defined as impaired water excretion due to inability to suppress ADH secretion, which can lead to hyponatremia if water intake exceeds urine output. Signs, differential diagnosis, and treatment of SIADH are also reviewed.

Uploaded by

Stephanie Rivera
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
21 views16 pages

Diabetes Insipidus & Syndrome of Inappropiate Antidiuretic Hormone

This document discusses Diabetes Insipidus (DI) and Syndrome of Inappropriate Antidiuretic Hormone (SIADH). It defines antidiuretic hormone (ADH) and its role in fluid balance. It describes central and nephrogenic DI, and covers causes, symptoms, pathophysiology, and diagnostic/treatment approaches for DI. SIADH is defined as impaired water excretion due to inability to suppress ADH secretion, which can lead to hyponatremia if water intake exceeds urine output. Signs, differential diagnosis, and treatment of SIADH are also reviewed.

Uploaded by

Stephanie Rivera
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 16

DIABETES INSIPIDUS &

SYNDROME OF
INAPPROPIATE
ANTIDIURETIC HORMONE
Javier Sevilla-Rodriguez, MD
Ponce Health Science University
What is ADH?
• ADH- Antidiuretic Hormone: helps to
control blood pressure by acting on the
kidneys and the blood vessels. Its most
important role is to conserve the fluid
volume of your body by reducing the
amount of water passed out in the urine.

• In normal individuals, plasma ADH levels


are very low when the plasma osmolality
is below 280 mosmol /kg, thereby
permitting the excretion of ingested water,
and ADH levels increase progressively as
the plasma osmolality rises above 280
mosmol/kg. 
• Central DI — Central diabetes insipidus (also
called neurohypophyseal or neurogenic DI) is due
to deficient secretion of ADH. 

Diabetes • Nephrogenic DI — Nephrogenic diabetes


Insipidus insipidus is characterized by normal ADH
secretion but varying degrees of renal resistance
to its water-retaining effect. This problem, in its
mild form, is relatively common since most
patients who are older adults or who have
underlying kidney disease have a reduction in
maximum renal concentrating ability.
Most Common Cause of Central Diabetes
Insipidus
• The most common causes of central diabetes insipidus, accounting for most
cases are:
•  Idiopathic diabetes insipidus
•  Primary or secondary tumors
•  Infiltrative diseases
•  Neurosurgery
•  Trauma
Recognize the symptoms and signs of
Diabetes Insipidus
• Central diabetes insipidus  is characterized by decreased release of antidiuretic
hormone (ADH), resulting in a variable degree of polyuria

• Patients with untreated central diabetes insipidus typically present with polyuria,
nocturia, and, due to the initial elevation in serum sodium and osmolality,
polydipsia

• They may also have neurologic symptoms related to the underlying neurologic
disease
• Idiopathic CDI — Approximately 30 to 50% of
cases of CDI are idiopathic, being associated
with destruction of the hormone-secreting cells
in the hypothalamic nuclei. It has been
suggested that an autoimmune process is
Pathophysiology involved in many, if not most, patients.
of Central
• Neurosurgery or trauma — CDI can be induced
Diabetes by neurosurgery (usually transsphenoidal) or
Insipidus trauma to the hypothalamus and posterior
pituitary. The incidence of CDI in these patients
varies with the extent of injury, ranging from 10
to 20 percent after transsphenoidal removal of
an adenoma limited to the sella to as high as 60
to 80 percent after removal of very large
tumors.
Pathophysiology of Nephrogenic
Diabetes Insipidus
• Lithium toxicity — These adverse effects are mediated by
lithium entry into the principal cells in the collecting tubule via
the epithelial sodium channel (ENaC). At cytotoxic
concentrations, lithium inhibits signaling pathways that
involve glycogen synthase kinase type 3 beta (GSK3beta),
resulting in dysfunction of the aquaporin-2 water channel.
• Hypercalcemia — Calcium-sensing receptors are also
expressed on the luminal membrane of the cells of the inner
medullary collecting duct (IMCD). By reducing calcium and
sodium reabsorption in the loop of Henle, hypercalcemia is
associated with an increase in calcium delivery to the luminal
IMCD calcium-sensing receptors; their activation reduces the
antidiuretic hormone-induced increase in water permeability
• Hypokalemia — Persistent severe hypokalemia (plasma
potassium concentration usually < 3 mEq/L) can impair
urinary concentrating ability. As with hypercalcemia, both
decreased collecting tubule responsiveness to ADH (which
may be mediated by decreased expression of aquaporin-2)
and diminished sodium chloride reabsorption in the thick
ascending limb have been demonstrated in experimental
animals.
DIAGNOSTIC AND
THERAPEUTIC
APPROACH DIABE
TES INSIPIDUS 

1. 2 to 3–hr water deprivation followed by


ADH administration
2. Failure of urine osmolality to rise after
water deprivation suggests DI
3. A rise in urine osmolality following ADH
administration suggests central DI.
4. Failure of urine osmolality to rise after
ADH administration suggests
nephrogenic DI
DIAGNOSTIC AND THERAPEUTIC
APPROACH DIABETES INSIPIDUS
• An inappropriately low urine osmolality in the setting of an elevated serum
osmolality and hypernatremia in a patient with polyuria (>50 mL/kg/24 hours in
the absence of glucosuria) is diagnostic of diabetes insipidus. 

• Diabetes insipidus is treated with desmopressin administered intranasally, orally,


or subcutaneously; caution should be taken to avoid overreplacement as this can
result in hyponatremia, water intoxication, and volume overload. 
SIADH
• The syndrome of inappropriate secretion of antidiuretic hormone is a disorder of
impaired water excretion caused by the inability to suppress the secretion of
antidiuretic hormone (ADH)
• If water intake exceeds the reduced urine output, the ensuing water retention
leads to the development of hyponatremia 
SIGNS AND SYMPTOMS OF SIADH
• Should be suspected in any patient with hyponatremia, hypoosmolality, and a
urine osmolality above 100 mosmol/kg.
• In SIADH, the urine sodium concentration is usually above 40 mEq/L, the serum
potassium concentration is normal, there is no acid-base disturbance, and the
serum uric acid concentration is frequently low. 
Drugs associated with
SIADH secretion
DIFFERENTIA
L DX
SIADH Diagnosis and Treatment
• Euvolemic Hyponatremia:
• Decreased serum Osmolarity
• Increase Urine Osmolarity
• Increased Urine Sodium

• There are three components to the treatment of hyponatremia in SIADH:


• Fluid restriction
• Treatment of the underlying disease, if possible (ex. Cessation of offending drug)
• Initial therapy to raise the serum sodium (ex. IV hypertonic saline)

You might also like