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DIABETES INSIPIDUS
DIABETES INSIPIDUS
 DI is an uncommon condition that occurs when the
kidneys are unable to conserve water as they perform
their fuction of filtering blood. The amount of water
conserved is controlled by antidiuretic
hormone(ADH), also called vasopression. ADH is a
hormone produced in a region of the brain called the
hypothalmus, it is then stored and released from the
pituitary gland, a small gland at the base of the
brain.the function of ADH is to regulate the level of
water in body drops, pituitary gland releases ADH to
conserve water and stop the production of urine.
Definition
 Diabetes insipidus results from lack of
antidiuretic hormones (ADH)or
arginine vasopressin(AVP) results in
polydypsia and polyuria.
Incidence
 Cases have been described in patients
from 8-18 years of age
TYPES
 Central Diabetes insipidus: The cause of
central diabetes insipidus usually damage to the
pituitary gland or hypothalmus, most commonly
due to cranial surgery, hypothalmic or pituitary
tumors, aneurysm, thrombosis, infection,
inflammation, head injury, skull fracture and
immunological disorder. In some cases the cause is
unknown. this damage disrupts the normal
production, storage and release of ADH.
 Nephrogenic diabetes insipidus:
Nephrogenic diabetes insipidus is caused by an
inadequate renal response to ADH. Nephrotic
diabetes insipidus occurs when there’s a defect in
the renal tubules- the structures in kidneys that
cause water to excreted or reabsoebed. This defect
makes kidneys unable to properly respond to
ADH. this defect may be due to an
inherited(genetic) disorder or a chronic kidney
disorder.
 Psychological Diabetes Insipidus:
Psychogenic diabetes insipidus is caused by an
extreme large fluid intake,which may be idiopathic
or related to psychosis. In this form of diabetes
insipidus excessive fluid intake leads to
suppression od ADH. drinking too much liquid
can be the result of abnormal thrist caused by
damage to the thrist-regulating mechanism,
situated in the hypothalamus.
 Gestational Diabetes Insipidus: Gestational
diabetes insipidus occurs only during pregnany and
when an enzyme made by the placenta-the system
of blood vessels and other tissue that allows the
exchange of nutrients and waste products between a
mother and her baby- destroys ADH in the mother.
CLINICAL FEATURES
 Polyuria and polydypsia
 Nocturnal enuresis
 Hypernatremic dehydration
 Anorexia, constipation & failure to thrive
 Hyperthermia & lack of sweating
 Weight loss
DIAGNOSTIC WORKUP
1. Careful history & examination
DOCUMENT PRESENCE OF POLYURIA (USUALLY 4-15
L/24h).
(Normal urine output is age-dependent:
Newborn and infant up to 1 year: 2 ml/kg/hour.
Older child: 0.5-1 ml/kg/hour
Adult: 40-80 ml/kg/hour
2. Urinalysis & microscopy together with plasma electrolytes
help exclude most of the causes of polyuria
DIAGNOSTIC WORKUP
3. Test for osmolality :
IN A NORMAL WELL HYDRATED SUBJECT PLASMA
OSMOLALITY IS <290 mOsml/l AND URINE OSMOLALITY IS 300-
450 mOsmol/l.
(osmolality is used to measure the number of
dissolved particles per unit of water ).
 IN PATIENTS WITH DI & FREE EXCESS TO WATER PLASMA
OSMOLALITY IS >290 mOsmol/l & URINE OSOLALITY IS 50-150
mOsmol/l
4. WATER DEPRIVATION TEST
 This test helps determine the cause of diabetes
insipidus. Patient will be asked to stop drinking
fluids two to three hours before the test so that
doctor can measure changes in body weight, urine
output and urine composition when fluids are
withheld. Doctor may also measure blood levels
of ADH durng this test. the water deprivation test
is performed under close supervision in children
and pregnant women to make sure no more than 5
percent of body weight is lost during the test.
5.Antidiuretic hormone test
 After the water deprivation test endocrinologist will
give a small dose of ADH, usually as an injection. this
will show how body reacts to the hormones and can
help identify which type of DI patient have.
6. MRI
 An MRI of the head is a noninvasive procedure that
uses a powerful magnet and radio waves to construct
detailed pictures of brain tissues. Doctor may want
to perform an MRI to look for abnormalities in or
near the pituitary gland.
TREATMENT
Central Diabetes Insipidus: Administration of
Desmopressin (ddavp), it has longer duration of action
(8-10 h), Route of Administration : IV, IM, SC,
intranasal,
 Nephrogenic Diabetes Insipidus: this
conditions is the result of kidneys not properly
responding to ADH, so desmopression is nota
treatment option. Instead, doctor may prescribe a
low salt diet to help reduce the amount of urine
kidneys make.patient will also need to drink enough
water to avoid dehydration.
drugs used to treat nephrogenic diabetes insipidus
include;
. anti inflammatory medications – indomethacin
. diuretics – hydrochlorothiazide and amiloride
COMPLICATIONS
 Hypernatremic dehydration & its neurological sequelea
 Growth retardation
 Hydronephrosis (due to excessive urine output)

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Diabets insipidus

  • 2. DIABETES INSIPIDUS  DI is an uncommon condition that occurs when the kidneys are unable to conserve water as they perform their fuction of filtering blood. The amount of water conserved is controlled by antidiuretic hormone(ADH), also called vasopression. ADH is a hormone produced in a region of the brain called the hypothalmus, it is then stored and released from the pituitary gland, a small gland at the base of the brain.the function of ADH is to regulate the level of water in body drops, pituitary gland releases ADH to conserve water and stop the production of urine.
  • 3. Definition  Diabetes insipidus results from lack of antidiuretic hormones (ADH)or arginine vasopressin(AVP) results in polydypsia and polyuria.
  • 4. Incidence  Cases have been described in patients from 8-18 years of age
  • 5. TYPES  Central Diabetes insipidus: The cause of central diabetes insipidus usually damage to the pituitary gland or hypothalmus, most commonly due to cranial surgery, hypothalmic or pituitary tumors, aneurysm, thrombosis, infection, inflammation, head injury, skull fracture and immunological disorder. In some cases the cause is unknown. this damage disrupts the normal production, storage and release of ADH.
  • 6.  Nephrogenic diabetes insipidus: Nephrogenic diabetes insipidus is caused by an inadequate renal response to ADH. Nephrotic diabetes insipidus occurs when there’s a defect in the renal tubules- the structures in kidneys that cause water to excreted or reabsoebed. This defect makes kidneys unable to properly respond to ADH. this defect may be due to an inherited(genetic) disorder or a chronic kidney disorder.
  • 7.  Psychological Diabetes Insipidus: Psychogenic diabetes insipidus is caused by an extreme large fluid intake,which may be idiopathic or related to psychosis. In this form of diabetes insipidus excessive fluid intake leads to suppression od ADH. drinking too much liquid can be the result of abnormal thrist caused by damage to the thrist-regulating mechanism, situated in the hypothalamus.
  • 8.  Gestational Diabetes Insipidus: Gestational diabetes insipidus occurs only during pregnany and when an enzyme made by the placenta-the system of blood vessels and other tissue that allows the exchange of nutrients and waste products between a mother and her baby- destroys ADH in the mother.
  • 9.
  • 10. CLINICAL FEATURES  Polyuria and polydypsia  Nocturnal enuresis  Hypernatremic dehydration  Anorexia, constipation & failure to thrive  Hyperthermia & lack of sweating  Weight loss
  • 11. DIAGNOSTIC WORKUP 1. Careful history & examination DOCUMENT PRESENCE OF POLYURIA (USUALLY 4-15 L/24h). (Normal urine output is age-dependent: Newborn and infant up to 1 year: 2 ml/kg/hour. Older child: 0.5-1 ml/kg/hour Adult: 40-80 ml/kg/hour 2. Urinalysis & microscopy together with plasma electrolytes help exclude most of the causes of polyuria
  • 12. DIAGNOSTIC WORKUP 3. Test for osmolality : IN A NORMAL WELL HYDRATED SUBJECT PLASMA OSMOLALITY IS <290 mOsml/l AND URINE OSMOLALITY IS 300- 450 mOsmol/l. (osmolality is used to measure the number of dissolved particles per unit of water ).  IN PATIENTS WITH DI & FREE EXCESS TO WATER PLASMA OSMOLALITY IS >290 mOsmol/l & URINE OSOLALITY IS 50-150 mOsmol/l
  • 13. 4. WATER DEPRIVATION TEST  This test helps determine the cause of diabetes insipidus. Patient will be asked to stop drinking fluids two to three hours before the test so that doctor can measure changes in body weight, urine output and urine composition when fluids are withheld. Doctor may also measure blood levels of ADH durng this test. the water deprivation test is performed under close supervision in children and pregnant women to make sure no more than 5 percent of body weight is lost during the test.
  • 14. 5.Antidiuretic hormone test  After the water deprivation test endocrinologist will give a small dose of ADH, usually as an injection. this will show how body reacts to the hormones and can help identify which type of DI patient have.
  • 15. 6. MRI  An MRI of the head is a noninvasive procedure that uses a powerful magnet and radio waves to construct detailed pictures of brain tissues. Doctor may want to perform an MRI to look for abnormalities in or near the pituitary gland.
  • 16. TREATMENT Central Diabetes Insipidus: Administration of Desmopressin (ddavp), it has longer duration of action (8-10 h), Route of Administration : IV, IM, SC, intranasal,
  • 17.  Nephrogenic Diabetes Insipidus: this conditions is the result of kidneys not properly responding to ADH, so desmopression is nota treatment option. Instead, doctor may prescribe a low salt diet to help reduce the amount of urine kidneys make.patient will also need to drink enough water to avoid dehydration. drugs used to treat nephrogenic diabetes insipidus include; . anti inflammatory medications – indomethacin . diuretics – hydrochlorothiazide and amiloride
  • 18.
  • 19. COMPLICATIONS  Hypernatremic dehydration & its neurological sequelea  Growth retardation  Hydronephrosis (due to excessive urine output)