Question

Amanda Richards is a 20-year-old junior in college. She is majoring in biology and hopes someday to be a pediatrician. Beginning about a month ago, Amanda noticed that she was waking up once, sometimes twice a night, by the need to go to the bathroom. More recently, she has noticed that she needs to go to the bathroom during her school day much more frequently than before, sometimes as often as once every hour. At first Amanda thought that her increased frequency of urination was due to the coffee she drank, but when she reduced her coffee consumption to one cup in the morning, she still needed to go to the bathroom just as often. In addition, Amanda was buying bottled water by the case, and she found herself never without a beverage in her hand or nearby. She also noticed that her urine seemed pale and colorless. When Amanda told her mother of her problem, her mother became very concerned and arranged for Amanda to see the family physician. Her physician found no abnormalities on physical examination. However, a blood chemistry profile revealed Amanda’s plasma sodium level to be 149 mEq/L, plasma osmolarity was 308 mOsm/L, and her fasting plasma glucose was 85 mg/dl. An analysis of Amanda’s urine showed a urine osmolarity of 200 mOsm/L. The urine sample was negative for the presence of glucose. An extensive history revealed that no other member of the family had ever displayed Amanda’s symptoms. Amanda had no history of traumatic head injury and an MRI of her brain was normal. Next, a two-hour water deprivation test was performed on Amanda. After two hours of not being able to drink water, the osmolarity of her plasma and urine were measured a second time. This time her urine osmolarity was unchanged; however, the osmolarity of her plasma increased to 315 from 308 mOsm/L. She was then injected with a drug called DDAVP, a synthetic analogue of vasopressin. One hour after the injection, the osmolarity of her plasma decreased to 290 mOsm/L and the osmolarity of her urine increased to 425 mOsm/L. Based upon the results above, Amanda’s medical history, and the results of the MRI, a diagnosis of idiopathic pituitary diabetes insipidus (a form of central diabetes insipidus) was made.

Why was a form of central or pituitary diabetes insipidus diagnosed in Amanda’s case? (Assume she is not pregnant). Make sure to explain why the other types were ruled out.

Answer 1

ADH or Vasopressin homone is made by   hapothalamus. Next they will carried by nerve cells and remain stored in pituitary gland. From pituitary gland ADH is released into blood. ADH is mainly control the fluid volume in our body and also how much of fluid should be go out by urination. However, in central diabetes insipidus , body is unable to make the rewuired amount of ADH hormone and as a result kidneys perform a huge amount of water loss by urine.

Central Diabetes insipidus is tested mainly by performing urine tests, blood tests and also a water deprivation test. All these were done in Amanda Richards. She was also given DDAVP, a synthetic analogue of vasopressin. But after the applciation of DDAVP, although the osmolarity of her plasma decreased to 290 mOsm/L, but the urine increased to 425 mOsm/L. On the basis of the test result she was diagnosed to have idiopathic pituitary diabetes insipidus, as in idiopathic pituitary diabetes insipidus kidneys will not respond although vasopressin is still present or applied. This is occured due to presence of abnormal supply of blood in the pituitary gland.