01b: Post Pit Flashcards

1
Q

T/F: Both ADH and oxytocin are synthesized as large pro-hormones.

A

True

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2
Q

Pro-hormone is enzymatically cleaved into ADH and (X). In the case of oxytocin, it’s cleaved into the active hormone and (Y).

A

X = Y = neurophysin

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3
Q

AVP/ADH binds to renal (X) receptors and stimulates:

A

X = V2

cAMP/PKA (synthesis and insertion of AQP2)

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4
Q

Supra-physiologic AVP can bind to (X) receptors and have which extra-renal effect?

A

X = V1 receptors (on vascular smooth muscle)

Increase BP

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5
Q

List the four main mechanisms of AVP/ADH regulation

A
  1. Osmoreceptors (ant hypothalamus)
  2. Baroreceptors (atria)
  3. Nausea
  4. Thirst
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6
Q

Baroreceptors located in (X) will (increase/decrease) AVP secretion when (Y) is decreased by 5-10%.

A

X = atria
increase
Y = blood V

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7
Q

Nausea (increases/decreases) AVP secretion.

A

Increases (potently and rapidly)

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8
Q

Max AVP release level is with plasma osm of:

A

295 mOsm/kg

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9
Q

List the three main mechanisms behind DI.

A
  1. Central DI (less AVP produced/released)
  2. Gestational DI (increased metabolism of AVP)
  3. Nephrogenic DI (resistance to AVP in kidney)
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10
Q

T/F: In order for central DI to occur, the pituitary typically suffers a huge insult and loses 90% secretory capacity .

A

False - pituitary lesion alone insufficient; lesion must be in hypothalamus or stalk (with over 90% secretory capacity lost)

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11
Q

Central DI: (abrupt/insidious) onset of (X) symptoms, with (Y) as the most objective symptom.

A

Abrupt
X = polydipsia, polyuria, thirst
Y = nocturia

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12
Q

If patient has (adequate/restricted) water access, DI can cause which complications/presentation?

A

Restricted

Hypernatremia/hyperosm (mental status deterioration), hyperthermia, coma, brain shrinkage (vessel rupture)

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13
Q

List the 3 most important causes of Central DI

A
  1. Neurosurg/trauma
  2. Tumors
  3. Infiltrative disease
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14
Q

List 3 tumors that commonly cause central DI.

A
  1. Craniopharyngioma
  2. Germinoma
  3. Hypothalamic glioma
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15
Q

After nsurg, pt that develops central DI will go through which phases of response?

A
  1. Acute (low AVP)
  2. Interphase (high AVP spill)
  3. Permanent (low AVP)
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16
Q

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?

A

Drop (interphase period of triphasic response);

Not necessarily

17
Q

List some causes for nephrogenic DI

A

Hypokalemia, hypercalcemia, Li use

18
Q

The classic etiology for primary polydipsia is (X).

A

X = schizophrenia (over-concerned with belief that water is healthy)

19
Q

Beginning an evaluation of DI involves first eliminating (X) diagnosis. Which labs do you order to accomplish this?

A

X = osmotic diuresis

  1. Urine Osm
  2. Serum Osm
  3. Serum chemistry (electrolytes, glucose, Cr, Ca)
20
Q

The exact etiology of a patient’s DI can be separated from others by (X) test.

A

X = water deprivation

21
Q

T/F: Administration of DDAVP in water deprivation test will not affect the trajectory of increasing urine Osm in a normal individual.

A

True

22
Q

List the etiologies of DI that will have unaffected Urine Osm with DDAVP administration.

A
  1. Nephrogenic

2. Primary polydipsia

23
Q

List the etiologies of DI that will show little to no (increase/decrease) in urine Osm with water deprivation alone.

A

Increase;

  1. Nephrogenic
  2. Complete central DI
24
Q

Hypertonic saline infusion can be used to diagnose (X) etiology of DI. You measure (Y). How would you expect (Y) levels to change?

A
X = Central DI
Y = AVP

No change in AVP
(unlike rise in AVP if etiology was primary polydipsia, or nephrogenic DI)