01b: Post Pit Flashcards
T/F: Both ADH and oxytocin are synthesized as large pro-hormones.
True
Pro-hormone is enzymatically cleaved into ADH and (X). In the case of oxytocin, it’s cleaved into the active hormone and (Y).
X = Y = neurophysin
AVP/ADH binds to renal (X) receptors and stimulates:
X = V2
cAMP/PKA (synthesis and insertion of AQP2)
Supra-physiologic AVP can bind to (X) receptors and have which extra-renal effect?
X = V1 receptors (on vascular smooth muscle)
Increase BP
List the four main mechanisms of AVP/ADH regulation
- Osmoreceptors (ant hypothalamus)
- Baroreceptors (atria)
- Nausea
- Thirst
Baroreceptors located in (X) will (increase/decrease) AVP secretion when (Y) is decreased by 5-10%.
X = atria
increase
Y = blood V
Nausea (increases/decreases) AVP secretion.
Increases (potently and rapidly)
Max AVP release level is with plasma osm of:
295 mOsm/kg
List the three main mechanisms behind DI.
- Central DI (less AVP produced/released)
- Gestational DI (increased metabolism of AVP)
- Nephrogenic DI (resistance to AVP in kidney)
T/F: In order for central DI to occur, the pituitary typically suffers a huge insult and loses 90% secretory capacity .
False - pituitary lesion alone insufficient; lesion must be in hypothalamus or stalk (with over 90% secretory capacity lost)
Central DI: (abrupt/insidious) onset of (X) symptoms, with (Y) as the most objective symptom.
Abrupt
X = polydipsia, polyuria, thirst
Y = nocturia
If patient has (adequate/restricted) water access, DI can cause which complications/presentation?
Restricted
Hypernatremia/hyperosm (mental status deterioration), hyperthermia, coma, brain shrinkage (vessel rupture)
List the 3 most important causes of Central DI
- Neurosurg/trauma
- Tumors
- Infiltrative disease
List 3 tumors that commonly cause central DI.
- Craniopharyngioma
- Germinoma
- Hypothalamic glioma
After nsurg, pt that develops central DI will go through which phases of response?
- Acute (low AVP)
- Interphase (high AVP spill)
- Permanent (low AVP)
After 6 days post-op, patient with surg-induced central DI has sudden (rise/drop) in urine output. Is he cured/recovered from the DI?
Drop (interphase period of triphasic response);
Not necessarily
List some causes for nephrogenic DI
Hypokalemia, hypercalcemia, Li use
The classic etiology for primary polydipsia is (X).
X = schizophrenia (over-concerned with belief that water is healthy)
Beginning an evaluation of DI involves first eliminating (X) diagnosis. Which labs do you order to accomplish this?
X = osmotic diuresis
- Urine Osm
- Serum Osm
- Serum chemistry (electrolytes, glucose, Cr, Ca)
The exact etiology of a patient’s DI can be separated from others by (X) test.
X = water deprivation
T/F: Administration of DDAVP in water deprivation test will not affect the trajectory of increasing urine Osm in a normal individual.
True
List the etiologies of DI that will have unaffected Urine Osm with DDAVP administration.
- Nephrogenic
2. Primary polydipsia
List the etiologies of DI that will show little to no (increase/decrease) in urine Osm with water deprivation alone.
Increase;
- Nephrogenic
- Complete central DI
Hypertonic saline infusion can be used to diagnose (X) etiology of DI. You measure (Y). How would you expect (Y) levels to change?
X = Central DI Y = AVP
No change in AVP
(unlike rise in AVP if etiology was primary polydipsia, or nephrogenic DI)