1. NAME: NORAZREENA BT ANDUL GHANI
ENDOCRINE SYSTEM
DIABETES INSIPIDUS
NAME: NORAZREENA BT ANDUL GHANI
MATRIX NO:

2. GLANDS

3. DIABETES INSIPIDUS
Diabetes insipidus is the condition characterized by polydipsia ( excessive thirst ) and polyuria ( excessive urine volume) due to decreased secretion or resistance to the antidiuretic hormone (ADH) .

4. WHO ARE MOST AFFECTED?
Diabetes insipidus is uncommon, with a prevalence of 1 case per 25,000 people.
No significant sex differences in central or nephrogenic diabetes insipidus exist.
Male and female prevalence are equal.
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5. PATHOPHYSIOLOGY
Hormones control the function of the kidneys in regulating the water content of the body.
The hypothalamus, a small but very important gland located in the middle of the brain, manufactures the antidiuretic hormone, ADH (also known as arginine vasopressin) for subsequent storage in the posterior pituitary gland that is attached to the hypothalmus by a thin stalk.
ADH is released when the blood volume decreased , when a large amount of salt shows up in blood, or when pain or stress are present.
ADH release by the pituitary gland stimulates reabsorption of water into the blood. If water intake is not enough to make up for the water lost in perspiration and in breathing, the pituitary gland releases more ADH, thus reducing the amount of water released in urine.
If the blood is too dilute, the pituitary gland reduces the secretion of ADH, causing a larger flow of water into urine.

6. PHATOGENESIS http://www.google.com.my
ADH is a hormone produced in a region of the brain called the hypothalamus. It is then stored and released from the pituitary gland, a small gland at the base of the brain
ADH- helps manage the amount of water in the body by acting on the kidneys.

7. MANIFESTATION Symptoms Polydipsia ( excessive thirst)
Polyuria ( excessive urination , 2.5 liters to 15 liter of urination per day )
Nocturia ( urinary frequency at night )
Dehydration – headache, dizziness, fainting, dry mouth

8. MANIFESTATION Signs Hypotension Dilute urine
Reduced capillary refill time
Cold extremities
Crying, growth retardation , irritability , weight loss in infants
Anorexia, Enuresis ( Bed wetting) , growth defects in children

9. DISEASE CLASSIFICATION
4 types of DI:
Neurogenic
Nephrogenic
Dipsogenic
Gestational

10. NEUROGENIC NDI more commonly known as central
Central DI is due to lack of ADH secretion
Causes increased urine production and dehydration
Idiopathic – 25% of cases.

11. CAUSES
Because vasopressin is produced by the hypothalamus & released by the posterior pituitary gland, pathology impacting either of these glands has the potential to cause diabetes insipidus.
The lack of vasopressin production usually results from some sort of damage
benign tumor (20 percent of cases),
trauma (17 percent of cases),
neurosurgery (9 percent of cases)
rare causes which include hemochromatosis, sarcoidosis, and histiocytosis.
Neurogenic diabetes insipidus can be a failure of production at the hypothalamus, or a failure of release at the pituitary.
Benign tumour: Pituitary adenoma’s (20%), Craniopharyngiomas
Trauma:Head injury
Haemochromotosis - deposition of iron in pituitary/hypothalamic tissue causing damage

12. NEPRHOGENIC
Nephrogenic diabetes insipidus is a form of diabetes insipidus due primarily to pathology of the kidney.
which is caused by insufficient levels of antidiuretic hormone (ADH)/Argenine Vasopressin (AVP).
Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH,
leading to a decrease in the ability of the kidney to concentrate the urine by removing free water.
The kidneys are responsible for reabsorbing fluid when ADH binds to their receptors.  Anything which interferes with this binding or damages the kidneys has the potential to cause diabetes insipidus.
 This is in contrast to central/neurogenic diabetes insipidus,

13. NEPRHOGENIC
Acquired 
Metabolic – hypercalcaemia, hyperglycaemia, hypokalaemia
Drugs – lithium, demeclocycline – both interfere with the binding of ADH¹
Chronic renal disease – polycystic kidney’s
Amyloidosis
Post obstructive uropathy¹
hypercalcaemia( high levels of calcium in the body)

14. DIPSOGENIC
Dipsogenic DI is due to a defect or damage to the thirst mechanism, which is located in the hypothalamus.
This defect results in an abnormal increase in thirst and fluid intake that suppresses vasopressin secretion and increases urine output.

15. GESTATIONAL
Gestational DI only occurs during pregnancy. During pregnancy, all women produce vasopressinase in the placenta, which breaks down ADH.
Gestational diabetes insipidus is therefore thought to be caused by overproduction of vasopressinase by the placenta causing a lack of functional vasopressin.
Most cases of gestational DI can be treated with desmopressin.

16. SIGNIFICANT LAB TEST clinical findings, laboratory test
radiological imaging
Routine urine test: urine specific gravity or less and osmolality of urine is less than 200 mOsm/kg .
fluid deprivation test
Radiological imaging includes MRI may show abnormality of pituitary or hypothalamus gland .

17. SIGNIFICANT LAB TEST
The fluid deprivation test is the most useful in diagnosing diabetes insipidus
Helps determine cause of DI – neurogenic, nephrogenic, primary polydipsia
Patient is allowed fluids overnight
Patient is then deprived of fluids for 8 hours (or until loss of 5% of body weight if earlier)
The patient is weighted hourly
Plasma osmolality is measured every 4 hours

18. SIGNIFICANT LAB TEST
Urine volume & Osmolality is measured every 2 hours
At the end of the deprivation period the patient is given 2mcg of IM Desmopressin
Urine volume & Serum osmolality are then measured over the next 4 hours

19. IMAGING CONSIDERATION
Brain MRI - scan head looking for tumours
Pituitary MRI: T1-weighted images of the healthy posterior pituitary yield a hyperintense signal. In patients with central diabetes insipidus, this signal is absent except in the rare familial form of central diabetes insipidus where the signal is still present.

20. RADIOLOGICAL APPEARANCES
Sagittal MRI of suprasellar cystic craniopharyngioma in a child presenting with hypothalamic diabetes insipidus. The child presented with a 2-month history of polyuria and polydipsia. Treatment was with cyst decompression and sub-total surgical excision.

21. RADIOLOGICAL APPEARANCES
Figure 11. Loss of the posterior pituitary 'bright spot' on T1 weighted MRI in hypothalamic diabetes insipidus. The normal posterior pituitary can be demonstrated as a 'bright spot' within the sella turcica on T1-weighted MRI (a). This increased signal intensity can be lost in HDI (b). An ectopic posterior pituitary 'bright-spot' can be seen some cases of childhood onset hypopituitarism, implying failure to complete normal developmental migration. Function can be normal despite the aberrant position

23. REFERENCES http://ckj.oxfordjournals.org -retrieved on 12 May 17, 2012