Posterior Pitutary
Quiz # 3 Material
Antidiuretic Hormone Vassopressin
ADH is critical to maintaining the volume and osmolality of the extracellular fluid, by controlling the final
volume and osmolality of the urine
 Uterotonic activity
 Vasoconstrictive activity
 Antidiuretlc activity
Changes in the plasma volume or osmolality from the ideal constant of 285 mOsm, controls the release of ADH.
Stimulation of osmoreceptors (Osmo-sodium receptors) in the hypothalamous and pressure (baroreceptors) in
the venous and arterial beds and heart result in the release of ADH
OSMORECEPTORS
The osmoreceptors respond to changes in extracellular sodium concentrations.
When the osmolarity becomes low, osmosis of water into the osmoreceptors causes them to swell, thus
decreasing the rate of impulse discharge.
Conversely, increased osmolarity in the extracellular fluid pulls water out of the osmoreceptors, causing them to
shrink and therby increasing the rate of impluse discharge.
The release of ADH, following osmoreceptor impulse stimulation increases the permeability of the collecting
ducts of the kidney and thus an increased conservation of water.
This results in a loss of sodium(excretion) causing a dilution of the extracellular sodium and a drop in the
osmolarity.
Conversely, when the extracellular fluid becomes too dilute (hypo-osmotic), less ADH is formed and excess
water is lossed, with sodium being conserved and the osmolarity increases.
The Ultimate Effects of ADH
1. To conserve water
2. To control sodium concentrations
3. To eliminate water
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Diabetes Insipidus
Diabetes Insipidus is a polyuric syndrome that results from a lack of ADH (pituitary) OR from a lack of ADH
effect (nephrogenic), sufficient to effect appropriate concentration of urine for the conservation of water.
 Pituitary Diabetes Insipidus
 Trauma to the pituitary
 A pituitary tumor (primary or metastatic)
 Infiltrations/inflammations of the pituitary
Idiopathic
in 30 to 40% of case there is no identifiable causes.
Most commonly Pituitary diabetes inspidus is the result of atrophy or destruction of the hypothalamic center
responsible for the production of ADH
A second mechanism responsible is a selective failure of the osmoreceptors to stimulate ADH release. This
form is often classed as “essential hypernatremia”, as high sodium concentrations do not stimulate ADH
release.
 Nephrogenic Diabetes Insipidus
Nephrogenic Diabetes Insipidus should be used to describe the state in which renal tubular unresponsiveness to
ADH is responsible for the polyuria and hyposthenuria.
May be either familial of acquired:
Familial occurs prirmarily inmalesand exogenous ADH produces no effect. The defect is believed to be in
the ADH receptor- adenylate cyclase system .
Acquired is most often secondary to drug therapy:
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antibiotics
methoxyflurane
Li (15 to 3O%)
systemic disease ( sarcoidosis, etc.)
Clinical Manifestations Of Diabetes Insipidus
 Polyuria is the foremost feature ( 3 to 15 L of urine per day)
 Thirst may be near continuous, often with a preference for cold water
 Nocturia is almost always present
The onset of pituitary diabetes insipidus is most often abrupt, with a peak urine flow reached in 1- 2 days.
Thus polyuria developing over weeks to months suggests a disorder other than diabetes insipidus.
Aside from the inconvenience of poluria and polydipisia, patients with diabetes insipidus usually suffer no ill
efects UNLESS they are deprived of water
When water is withheld, circulatory collapse or hypertonic encephalopathy can occur within hours.
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Hypertonic Encephalopathy
May be caused by NaCl or glucose concentrations which produce a serum osmolality > 350 mOsm/L.
These solutes cross cell membranes poorly and as a result, water is pulled out of the CNS cell in the presence of
high extracellular solute concentrations, producing cell shrinkage and CNS dysfunction. This can range from
lethargy to coma.
In children with hypernatremia (>160 mEqIL for 24hrs), the mortality rate is greater than 40%, with about 66%
of the survivors having some degree of permanent neurological damage.
Laboratory Findings of Diabetes Insipidus
Urine specific gravity of 1.005 or less
Urine osmolarity of less than 200 mOsm/L
Serum osmolarity usually normal (285 to 290 mOsmIL)
Serum sodium may be Increased (> 148 to 152 mEq/ml)
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The Polyuric Syndromes Diagnosis
Pituitary diabetes insipidus
 Absence or diminished production of ADH
 History of head trauma, tumor
 Sudden onset of polyuria
 Nocturia
 Random plasma osmolarity >290 mOsmIL
Nephrogenic diabetes insipidus
 Renal unresponsiveness to ADH
 Present since birth
 Slower onset of poluria
 Family history of diabetes insipidus
 History of exposure to ADH antagonists
Diabetes mellitus
Poluria,Polydipisia,Polyphagia Hyperglycemia,
Glycosuria
Primary Polydipisia
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The ingestion of unusually large volumes of water
Polyuria is an appropriate physiological response
Nocturia usually absent
Random plasma osmolarity usually normal
Diagnosis of Pituitary Insipidus
The basis of all tests for pituitary diabetes insipidus is the ability of the kidney to excrete a hypertonic urine
after an osmotic stimulus.
Water deprivation studies depend on endogenous ADH release in response to dehydration. However, these
tests have the potential for serious harm to the patient and are most often done in a hospital .
Diagnosis of Pituitary Diabetes Insipidus Exogenous ADH
Normal subjects:
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Urine osmolarity 2-4x > serum osmolarity
9% increase in urine osmolarity) post-ADH
Complete pituitary diabetes insipidus:
Urine osmolarity < serum osmolarity
50% increase in urine osmolarity) post-ADH
Partial Pituitary diabetes insipidus:
Urine osmolarity = or > serum osmolarity about a 10 to 15% increase in urine osmlarity) post-ADH
Direct ADH assay of the serum is probably the best in terms of simplicity and reproducibility
(NEJM 305:1539-1546, 1981)