Diabetes Insipidus Clinical Correlation Flashcards

1
Q

Which three stimuli trigger the release of vasopressin?

A

1) Hyperosmolality
2) Hypovolemia
3) Release of angiotensin II (response to hypovolemia)

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2
Q

What mechanisms help regulate serum sodium concentration?

A

Hypothalamic circumventricular organ osmoreceptors and renal juxtaglomerular cells monitor plasma osmolality and produce hormones to regulate.

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3
Q

What are the forms of primary polydipsia?

A

1) Phychogenic - constant water drinking due to schizophrenia or other psychological reason
Dipsogenic: Reset of thirst threshold due to aging or disease (lesion, idiopathic)

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4
Q

What are 4 causes of central diabetes insipidus?

A

1) Hypothalamic lesion (40-50% of cases)
2) Pituitary lesion (only post-operative)
3) Idiopathic autoimmune
4) Genetic (delayed onset)

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5
Q

What is the downstream effect of increased vasopressin?

A

Upregulation of aquaporins in collecting duct cells to reabsorb water

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6
Q

What is the network of blood vessels called that is the destination of AVP?

A

Vasa Recta - deliver to collecting duct cells

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7
Q

What will be the effect of removing the entire pituitary gland on systemic AVP levels?

A

Levels will be unchanged because the cell bodies that produce AVP are in the hypothalamus; removal of pituitary will NOT cause central DI.

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8
Q

What are 2 idiopathic causes of central DI?

A

1) Autoimmune disorder called Lymphocytic Infundibularneurohypophysitis - causes thickening of the pituitary stalk
2) Langerhans cell histiocytosis

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9
Q

How can you differentiate between diabetes mellitus, central diabetes insipidus, and primary polydipsia?

A

1) DM would have high blood & urine glucose
2) Clinical water deprivation test, patients with central DI would still produce dilute urine
3) People with primary polydipsia, when deprived of water, will produce concentrated urine due to normal AVP levels.

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10
Q

What are two potential causes of nephrogenic DI?

A

1) Familial:
a) AVP V2 receptor mutation (X-linked recessive)
b) Aquaporin 2 mutation (autosomal dominant)
2) Acquired:
a) hypercalcemia, hypokalemia, drugs

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11
Q

What are the 4 criteria required to diagnose polyuria?

A

1) >50 ml/kg over 24 hr, ad lib water intake
2) Urine SG <300 (hypotonic)
4) Rule out glycosuria

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12
Q

What criterion defines diabetes insipidus diagnosis?

A

Output of hypotonic urine despite hyperosmolar serum.

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13
Q

What is the protocol for the outpatient water deprivation test? How is it interpreted?

A

Abstain from drinking fluids after dinner overnight; measure urine osmolality in the AM
->600-800 rules out DI

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14
Q

What is the protocol for inpatient water deprivation test? How is it interpreted?

A

1) Withhold fluids until BW decreases 3-5% OR urine osmolality is fully concentrated OR serum [Na+} > 145 mM
2) Administer AVP & monitor urine for 2 hr
3) If urine osmolality increases >50%, diagnosis is central DI, if <10%, diagnosis is nephrogenic DI

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15
Q

Why does primary polydipsia cause permanent impairment to the degree of urine concentration despite water deprivation?

A

1) Aquaporin is downregulated

2) Osmotic gradient in collecting ducts has been flushed out; less osmotic pressure driving reabsorption

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16
Q

What does a pituitary bright spot on MRI indicate?

A

<5% likelihood of central DI

17
Q

How is central DI treated?

A

1) Water
2) Antiduretic agents: AVP, ddAVP
3) Antidiuresis-enhancing agents:
- chlorpropamide
- carbamazepine
- indomethacin

18
Q

What are the consequences of osmoreceptor dysfuntion?

A

1) Inhibition of thirst

2) Prevents AVP release in response to high serum osmolality

19
Q

What is one measure that can differentiate central DI from other causes of polyuria?

A

Plasma AVP levels, only when plasma osmolality > 295

20
Q

What are 3 main differences between AVP and ddAVP?

A

1) Longer duration
2) ddAVP has no pressor effects at V1a receptors
3) Intranasal & oral bioavailability