Lecture 30-Diabetes Insipidus Case Flashcards
What are polyuria causing disorders?
- primary polydipsia
- osmoreceptor dysfunction
- osmotic diuresis: diabetes mellitus
- Diabetes insipidus: central, nephrogenic, gestational
When is AVP released?
in response to anything indicating low blood volume or high osmolarity:
- angiotensin
- hypovolemia
- hyperosmolality
AVP release is inhibited when?
In response to baroreceptor activation (high blood pressure) and ANPs
What are the causes of neurogenic (central) DI?
- 40-50% are from HYPOTHALAMIC tumors,
- -> PITUITARY tumors are usually insufficient to cause DI until post-op
- 20-30% are idiopathic (autoimmune, histiocytosis, sarcoidosis)
- <5% are genetic and are usually late onset
What are the causes of nephrogenic DI?
familial mutations:
- either x-linked recessive V2 R mutation
- autosomal dominant AQP2 mutation
acquired:
- hypercalcemia (Ca > 13)
- hypokalemia (K < 2.5)
- drugs like lithium or demeclocycline
What are the 2 types of primary polydipsia?
- dipsogenic
- psychogenic
Explain dipsogenic DI.
resetting thirst threshold usually a result of granulomatus disease, iopathic reasons, age, mass lesions
Explain psychogenic DI.
drinking for reasons other than thirst. Commonly seen in schizophrenic patients–called PIP: psychosis-intermittent hyponatremic polydipsia syndrome.
What is characteristic of DI? Which criteria must be met for a DI diagnosis?
- characterized by hypotonic polyuria
- > 50 ml/kg in 24 hr period
- Uosm <300 mOsm/kg
- no solute diuresis (urine negative for glucose)
and must show hypotonic urine in the presence of hyperosmolar serum
What are the cutoffs for diagnosis of DI with the outpatient method?
- > 800 mOsm/kg rules it out, >600 mOsm/kg usually rules it out
- serum [Na] will also be tested
What is the methodology of testing for DI with inpatient testing?
- measure urine and plasma osm until:
- body water decreases by 3-5%
- Uosm plateaus for 2-3 measurements
- [Na] >145 and still outputting hypotonic urine
- administer dDAVP/AVP to distinguish btw central and nephrogenic DI
- Central: Uosm will increase by >50% of Uosm
- nephrogenic: Uosm will increase by <10% of Uosm
Why does dDAVP not help someone with primary polydipsia?
- they have completely downregulated all of their AQP2 because they’re drinking in excess of 50 ml/kg
- They have disrupted the gradient between the cells and the collecting duct lumen so there is less of a driving force to pull water in.
When can plasma AVP differentiate CDI from other polyurias?
- when Posm is >295 mOsm/kg
What are chloropropamide, indomethicin, and carbomazepine?
All anti-diuresis enhancing agents
What is used to treat DI
- water
- antidiuretics (AVP, dDAVP)
- anti-diuresis enhancing agents (chloropropamide, carbomazepine, indomethacin)