Lecture 30-Diabetes Insipidus Case Flashcards

1
Q

What are polyuria causing disorders?

A
  • primary polydipsia
  • osmoreceptor dysfunction
  • osmotic diuresis: diabetes mellitus
  • Diabetes insipidus: central, nephrogenic, gestational
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2
Q

When is AVP released?

A

in response to anything indicating low blood volume or high osmolarity:

  • angiotensin
  • hypovolemia
  • hyperosmolality
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3
Q

AVP release is inhibited when?

A

In response to baroreceptor activation (high blood pressure) and ANPs

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4
Q

What are the causes of neurogenic (central) DI?

A
  • 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
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5
Q

What are the causes of nephrogenic DI?

A

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
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6
Q

What are the 2 types of primary polydipsia?

A
  • dipsogenic

- psychogenic

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7
Q

Explain dipsogenic DI.

A

resetting thirst threshold usually a result of granulomatus disease, iopathic reasons, age, mass lesions

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8
Q

Explain psychogenic DI.

A

drinking for reasons other than thirst. Commonly seen in schizophrenic patients–called PIP: psychosis-intermittent hyponatremic polydipsia syndrome.

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9
Q

What is characteristic of DI? Which criteria must be met for a DI diagnosis?

A
  • 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
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10
Q

What are the cutoffs for diagnosis of DI with the outpatient method?

A
  • > 800 mOsm/kg rules it out, >600 mOsm/kg usually rules it out
  • serum [Na] will also be tested
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11
Q

What is the methodology of testing for DI with inpatient testing?

A
  • 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
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12
Q

Why does dDAVP not help someone with primary polydipsia?

A
  • 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.
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13
Q

When can plasma AVP differentiate CDI from other polyurias?

A
  • when Posm is >295 mOsm/kg
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14
Q

What are chloropropamide, indomethicin, and carbomazepine?

A

All anti-diuresis enhancing agents

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15
Q

What is used to treat DI

A
  • water
  • antidiuretics (AVP, dDAVP)
  • anti-diuresis enhancing agents (chloropropamide, carbomazepine, indomethacin)
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