Vasopressin

Front 1

How does ADH work? (ie. binds to what receptor to activate what, resulting in what)

Back 1

Binds to V2 receptors to activate cAMP which thus induces synthesis and insertion of aquaporins to the luminal surface of collecting tubules in nephrons. Thus, reabsorption of water occurs. How much water is absorbed depends on the medullary concentrating gradient.

Front 2

How do you calculate plasma osmolarity?

Back 2

Plasma osmolality = 2 [Na+] + [glucose]/18 + BUN/2.8

remember, normal is ~ 290 mOsm

Front 3

What are stimuli for ADH secretion?

Back 3

Increased plasma osmolality, decreased blood pressure, pain/nausea/emesis, anesthesia, nicotine, drugs

Front 4

What is the differential diagnosis in patients with polyuria?

Back 4

Diabetes mellitus - osmotic diuresis
Primary polydipsia
Diabetes insipidus - central
Diabetes insipidus - nephrogenic

Front 5

The autosomal dominant form of familial central DI is a
A. defect in vasopressin gene such that no vasopressin is produced
B. a defect in decreased bioactivity and normal vasopressin levels are present

Back 5

A. defect in vasopressin gene such that no vasopressin is produced

Front 6

True or False:
Lithium or demeclycycline can be a cause of nephrogenic DI

Back 6

True

Front 7

Most (90%) of inherited nephrogenic DI is due to
A. autosomal recessive mutations
B. autosomal dominant mutations
C. X-linked mutations

Back 7

C. X-linked mutations (specifically, in the V2 receptor)

Front 8

When doing the water deprivation test to test for diabetes insipidus, when will administration of ADH at completion of the fluid deprivation test result in an increase in urine osmolality?
A. Normal response to fluid deprivation
B. Nephrogenic DI response to fluid deprivation
C. Central DI response to fluid deprivation

Back 8

The responsiveness to ADH indicates normal kidney function, so given the choices, it'd be
C. Central DI response to fluid deprivation

Front 9

What is the treatment for central diabetes insipidus?

A. Desmopressin (DDAVP)
B. sodium restriction
C. Thiazide diuretics

Back 9

A. Desmopressin (DDAVP)

Front 10

What is the treatment for nephrogenic diabetes insipidus?

A. Desmopressin (DDAVP)
B. sodium restriction
C. Thiazide diuretics
D. fluid restriction
E. demeclocycline

Back 10

B. sodium restriction
C. Thiazide diuretics

strategy is to limit water delivery to collecting duct by limiting salt intake or causing sodium diuresis. Loss of sodium will lead to volume contraction resulting in increased sodium and water retention in proximal tubule leaving less to go to collecting ducts.

Front 11

SIADH is a diagnosis of exclusion. Other causes for increased ADH must be excluded. What are those common causes? (5)

Back 11

hypovolemia, hypotension, pain, adrenal insufficiency, hypothyroidism

ALL the following must be present:
- hyponatremia with decreased plasma osmolality
- inappropriately concentrated urine in face of hyponatremia
- excessive renal sodium excretion
- absence of hypotension, hypovolemia, or edema since these would be expected to be associated with increased vasopressin levels
- normal renal, adrenal and thyroid function

Front 12

SIADH is a diagnosis of exclusion. What six things are NEEDED to make the diagnosis?

Back 12

1. Normal renal function - normal creatinine
2. Normal thyroid function - normal TSH
3. Normal adrenal function
4. Hyponatremia
5. Inappropriately concentrated urine osmolality (usually > than serum osmolality)
6. Normal blood pressure and volume status

Front 13

High urine concentration despite hyponatremia is consistent with
A. DM
B. Central DI
C. Nephrogenic DI
D. SIADH

Back 13

D. SIADH

Front 14

Treatment of SIADH includes

A. Desmopressin (DDAVP)
B. sodium restriction
C. Thiazide diuretics
D. fluid restriction
E. demeclocycline

Back 14

D. fluid restriction (to correct hyponatremia)
E. demeclocycline (causes nephrogenic DI)