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SIADH

WHAT IS ADH? AND FROM WHERE


IT IS SECRETED? AND FUNCTIONS
OF ADH.
• Anti diuretic hormone. Secreted by posterior
pituitary or neurohypophysis to the distal
convoluted tubules and collecting tubules of
the nephron.
• Functions:-function of ADH on the kidneys
is to control the amount of water reabsorbed
by kidney nephrons and causes the retention
of water, but not solute. Hence, ADH activity
effectively dilutes the blood.
hypothalamus( osmoreceptors)

posterior pituitary
ADH
aquaporins (DCT and CT)

urine out put


• ADH is secreted to prevent water loss in the kidneys.
When water is ingested, it is taken up into the
circulation and results in a dilution of the plasma.
This dilution, otherwise described as a reduction in
plasma osmolality, is detected by osmoreceptors in
the hypothalamus of the brain and these then switch
off the release of ADH.
• The decreasing concentration of ADH effectively
inhibits the aquaporins in the collecting ducts and
distal convoluted tubules in the nephrons of the
kidney. Hence, less water is reabsorbed, thereby
increasing urine output, decreasing urine osmolality,
and increasing (normalization of) blood osmolality.
WHAT IS SIADH AND ITS CAUSES
AND CLINICAL FEATURE.

• This is a syndrome characterized by


excessive release of antidiuretic hormone
(ADH or vasopressin) from the posterior
pituitary gland.
• The result is hyponatremia, and
sometimes fluid overload
Some common causes of SIADH
include:
• meningitis (treated with fluid restriction and diuretics)
• Head injury
• Subarachnoid hemorrhage
• Cancers
• Lung cancer (especially small cell lung cancer, as well
as other small-cell malignancies of other organs)
• Infections
• Brain abscess
• Drugs
• Carbamazepine
• Selective serotonin reuptake inhibitors (SSRIs, a class
of antidepressants)
• Methylenedioxymethamphetamine (MDMA)
c/f
• In general, increased ADH causes water retention
and extracellular fluid volume expansion without
edema or hypertension, owing to natriuresis
(retention of water and passing of sodium in urine).
• The water retention and sodium loss both cause
hyponatremia, which is a key feature in SIADH.
Hyponatremia and concentrated urine (UOsm >300
mOsm) are seen, as well as no signs of edema or
dehydration.
• When hyponatremia is severe (sodium <120 mOsm),
or acute in onset, symptoms of cerebral edema
become prominent (irritability, confusion, seizures,
and coma).
WHAT IS THE DIANGNOSIS AND
MANAGEMENT OF SIADH
Dx ( c/f and lab findings)
• Hyponatremia <130 mEq/L, and POsm <270 mOsm/kg.
• Other findings include-

• Urine sodium concentration >20 mEqlL (inappropriate


natriuresis)
• Maintained hypervolemia
• Suppression of renin-angiotensin system
• No equal concentration of atrial natriuretic peptide
• Low blood urea nitrogen (BUN)
• Low creatinine
• Low uric acid
• Low albumin
management
• Treating underlying causes when possible.
• Fluid restriction to 800-1,000 ml/d should
be obtained to increase serum sodium.
• Intravenous saline - For very symptomatic
patients (severe confusion, convulsions, or
coma) hypertonic saline (5%) 200-300 ml
IV in 3-4 h should be given.
• Drugs
• Demeclocycline can be used in chronic situations
when fluid restrictions are difficult to maintain;
demeclocycline is the most potent inhibitor of AVP
action.
• Conivaptan - an approved antagonist of both V1A
and V2 vasopressin receptors. Its indications are
"treatment of euvolemic hyponatremia (e.g. the
syndrome of inappropriate secretion of antidiuretic
hormone, or in the setting of hypothyroidism,
adrenal insufficiency, pulmonary disorders, etc.) in
hospitalized patients."[1]