E: Posterior Pituitary

Front 1

What are the two hormones produced by the posterior pituitary?
- where are they produced? where are they stored? how to they get to where they are stored?

Back 1

Vasopressin (ADH) and Oxytocin
- synthed in magnocellular neurons of the supra-optic and paraventricular nuclei of the hypothalamus
- prohormones transported intracellularly down axons
- stored in secretory granules at nerve terminals.

Front 2

What is the normal fx of oxytocin?

Back 2

- causes uterine smooth mus contraction when stim by uterine distention
- caues mammary smooth mus contraction --> milk ejection (not production) when stim by suckling

Front 3

What are the three normal fx of vasopressin, and what are the receptors associated with these functions?

Back 3

V1: vasoconstrictor actv
- low affinity
- platelet activation, endothelial release of fVIII-vWF

V2: AD actv
- kidneys
- HIGH affinty

V3: stim ACTH from pituitary

Front 4

What is Pitocin, and what is it used for?

Back 4

synthetic oxytocin, used to stimulate contractions and milk let down.

Front 5

Are they any known human diseases associated with excess or deficiency of oxytocin?

Back 5

No.

Front 6

Where are the direct osmoreceptors in the body?
- how sensitive are the direct osmo receptors? What does they do when osm is low?
- which are more sensitive, osmoreceptors or baroreceptors?

Back 6

hypothalamic osmoreceptors ant to the 3rd ventricle
- respond to as little as 1% change in osm: supp. AVP when osm is low so that more water is excreted.
- osmoreceptors.

Front 7

Hypotension effects which change in AVP via which mechanism(s)?

Are baroreceptors synergistic with osmoreceptors?

Back 7

hypotension *releases* AVP from inhibition by the carotid sinus and cardiac baroreceptors that normally inhibit AVP via CN IX and X.

Yes, e.g., decreased LAP increases osmotic AVP release due (i.e. blood loss increases amount of AVP release due to hypertonicity)

Front 8

Is thirst regulation less or more sensitive to water deprivation than AVP-inducing osmoreceptors?

What does nausea do to AVP regulation? Pain & emotional stress?

Back 8

less sensitive.

potent stim.

stim.

Front 9

When should you think diabetes insipidis?
- cause?

Back 9

plasma hyperosmolality w/ urinary hypoosmolality.
- hyperNa w/o appropiate urinary Na excretion.

Deficit of, or insensitivity to, AVP.

Front 10

Give me the Osm equation. What is ~ normal osmolality?

Back 10

Osm = 2Na + BUN/2.8 + G/18
~289

Front 11

Urinary output >3L/day is the definition of what?
- causes?
+ esp. comment on ion causes and drug causes

Back 11

polyuria.
- diuresis
- osmotic polyuria (like too much G in urine)
- Neuphrogenic DI (renal insensitivity to AVP)
+ hyperCa, hypoK, Lithium, cisplatin, furosimide,
+ renal dz (sickle cell, amyloid, sarcoid, RTacidosis, obstructive uropathy)
- gestational DI
- dipsogenic DI (primary polydipsia)
- central DI: AVP deficiency

Front 12

What chromosome is the AVP gene on?
- What is DIDMOAD? chromosome?

Back 12

- 20
- Wolfram's Syndrome; 4p or 4q.

Front 13

Name some dz that can cause destruction of hypothalamus and pituitary. (Do it by category)

Back 13

- inflamm: sarcoid, TB, amyloid, histiocytosis
- infectious: meningitis, encephalitis
- tumors: craniopharyngioma, lymphoma, meningioma, metastatic carcinoma, other brain tumors
Xrt
- Trauma: whiplash, surgery

Front 14

What test can you do for DI?
- what factor can make this test uninterprible?

What about if you want to assess *response* to AVP?
- what does this help differentiate b/t?

Back 14

water deprivation test : induce hyperosmolality --> would usually stim AVP (Thirst is so powerful pts will drink enough H20 to keep themselves in normal ranges unless you induce hyper-osmolality!)
- nausea (b/c it stim AVP nonosmotically)

- admin dDAVP when the sodium is high (>148); give H20 freely.... then monitory serum and urine NA.
+ central DI and nephrogenic DI.

Front 15

dDAVP is selective for which AVP receptor?
- side effects?
- indications?
- stronger or weaker than AVP?
- safe in pts w/ CAD?

Back 15

V2.
- rare: HA, nausea, nasal congestion, flushing.
- DI and conWillebrand's
- stronger on V2.
- yes, because no V1 effects.

Front 16

What are some strategies for adjunctive tx for mild DI? examples of these?

Back 16

enhance AVP release in partial CDI
- chlorpropamide, clofibrate, carbamazepine

non-hormonal effects, helpful for NDI
- HCT: Vol contraction (1) \GFR (2) reduces diluting capacity of distal nephron (3) impair Na reabs --> \ free water excretion.
+ result: \Vol, ^concentration (strange)
- Amiloride: blunts Li uptake in DT and CD
- Indomethacin: inhib prostaG (prostaglandins typically inhibit AVP action)

Front 17

If you see serum hypo-osmolality w/ inappropriately concentrated urine, what might you think?
- what do you have to rule out to get this dx? (work through why these might cause it too)

Back 17

SIADH
- Hypocortisolism, hypothyroidism, primary polydipsia

Front 18

Most of hypoNa is due to what?

What are the 5 criteria for this?

Back 18

SIADH

hypoNA w/ low plasma osmolal; urine osmolality > plasma osmolality; inappropiate renal Na excretion > 20mmol/L; absence of hypotension, hypovolemia, and edema-forming states; normal renal and adrenal fx

Front 19

What are the types of hyponatremia?

Back 19

hypertonic (usually followed by correcting diuresis)
- hyperG
- mannitol

non-hypotonic (pseudohyponatruemia)
- severe hyperlipidemia
- paraproteinemia (multiple myeloma)

Hypotonic Hyponatremia

Front 20

What other processes can be associated with SIADH? Drug classes?

Back 20

SCLC of lung, SSC of lung, COPD;

SSRIs, TCA, narcotics, NSAIDS, Chlorpropamide, clofibrate, carbamazepine, dDAVP OD.

Front 21

SIADH sx?

Back 21

can have none

- HA, N&Vm Confusion, personality changes, seizures, coma (from water intoxication)

Front 22

Tx of SIADH w/o CNS sx?
- chronic SIADH?
- w/ CNS sx?
+ have to watch for what?
- What are the aquaretics?

Back 22

if no CNS sx, just use fluid restriction.
- demeclocycline.
- IV NS or 3% saline and loop diuretics
+ watch rate of Na correction to avoid myelinolysis (pontine)
- V2 receptor antag: Anti-anti diuretic hormone... (conivaptan, tolvaptan.... they're new drugs)

Front 23

Can you correct hyponatremia more quickly if it's chronic or if it's acute?

Back 23

acute. Correct chronic too quickly can cause cellular dehydration and central pontine myelinolysis.

Front 24

Inpatient @ UNC hospitals shows evidence of ataxia, lethary, mutism and dysarthria. Pt has hx of correction of hyponatremia one week ago. What's happened?
- tx?
- predisposing factors?
- can it cause seizures, coma, and death too?

Back 24

Central pontine myelinolysis
- no known tx
- malnutrition, hypoK, liv dz
- yes

Front 25

What are the general methodologies of SIADH tx? (3)

Back 25

fluid restriction
increased salt
new V2 receptor antagonists