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Adv Pharm 1 > Endo (pt 3/7) FSH/LH, Oxytocin, ADH > Flashcards

Endo (pt 3/7) FSH/LH, Oxytocin, ADH Flashcards

1
Q

Describe the cascade that leads to the release of FSH and LH?

A

1) Hypothalamus secretes GnRH
2) GnRH travels via the pituitary venous portal plexus
3) GnRH arrives at Anterior Pituitary
4) GnRH binds to the GPCR of gonadotroph cells
5) FSH and LH are released

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2
Q

What are the two ways GnRH can be administered?

A

-Pulsatile
-Nonpulsatile

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3
Q

________ GnRH secretion is required to stimulate the gonadotroph cell to produce and release LH & FSH.

A

Pulsatile

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4
Q

Continuous, ________ administration of GnRH or GnRH analogs INHIBITS the release of FSH and LH by the pituitary in both males and females (Hypogonadism)

A

Non-pulsatile

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5
Q

Why does non-pulsatile administration of GnRH inhibit the release of FSH & LH?

A

It signals negative feedback

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6
Q

T/F: Pulsatile administration of GnRH is super common and easy.

A

False: It is uncommon because it is expensive and inconvenient.

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7
Q

What are the GnRH agonists?

A

Gonadorelin (Acetate salt of synthetic human GnRH)

Synthetic analogs of GnRH (more potent and longer lasting):
-end in -relin

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8
Q

Explain the Biphasic response produced by continuous administration of Non-pulsatile Gonadorelin (or the longer acting analogs)

A

1) Flare: first 7-10 days. Inc concentration of gonadal hormones
2) Inhibition: as a result of the continued presence of GnRH, down-regulation and changes in the signaling pathways occurs (negative feedback)

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9
Q

What are the clinical indications for Pulsatile administration of GnRH (stimulation of gonadotrophic production)?

A

-Female infertility (questionable compared to hCG)
-Male infertility
-Diagnosis of LH responsiveness (delayed puberty)

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10
Q

What are the clinical indications for the administration of Non-Pulsatile, Continuous GNRH (suppression of gonadotrophic release/production)?

A

-Controlled ovarian hyperstimulation
-Endometriosis (can only use for about 6 months before bone issues)
-Uterine Leiomyomata (fibroids)
-Prostate Ca (Antiandrogen therapy is #1 medical therapy though)
-Central precocious puberty (<7 in g and <9 in b)
-Breast & Ovarian Ca

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11
Q

What are the advantages to using a GnRH Receptor ANTAGONIST over the GnRH AGONISTS?

A

1) Immediate antagonist effect, shorter use time
2) Does not have flare - straight to antagonistic effects (but wears off faster, so less suppressive response)
3) Less suppressive effect on the ovarian response to gonadotropin (decrease in the total duration and dose of gonadotropin)
4) Reduces concentrations of gonadotropins and androgens more rapidly than the agonists (no testosterone surge)

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12
Q

What are the GnRH Receptor Antagonists (Synthetic Decapeptides)?

A

-Ganirelix & Cetrorelix (approved for controlled ovarian hyperstimulation procedures)
-Degarelix & Abarelix (approved for advanced prostate Ca)

All produce a dose-dependent inhibition of the secretion of FSH & LH.

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13
Q

The GnRH Receptor Antagonists all produce what?

A

A dose-dependent inhibition of the secretion of FSH & LH.

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14
Q

-198-amino-acid peptide hormone
-Produced in the anterior pituitary
-Principal hormone responsible for lactation

A

Prolactin

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15
Q

Hyperprolactinemia can result from ?

A

Prolactin-secreting adenomas.
-Male – loss of libido & infertility
-Female – amenorrhea & galactorrhea

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16
Q

What drugs are known to increase Prolactin secretion?

A

-Antipsychotics
-Dopamine ANTAGONISTS

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17
Q

What drugs are known to inhibit prolactin release (act in the pituitary)?

A

Dopamine AGONISTS

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18
Q

Which Dopamine Agonists are ergot derivatives?

A

-Bromocriptine
-Cabergoline

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19
Q

What is ergot?

A

A fungus that causes pulmonary vasoconstriction

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20
Q

What dopamine agonist is not an ergot derivative?

A

Quinagolide

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21
Q

Which Dopamine Agonists have a high affinity for the D2 receptor?

A

Bromocriptine, Cabergoline, and Quinagolide

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22
Q

What is the function of the Dopamine agonists?

A

-Directly suppress PL release from the cells of the Anterior Pituitary
-At high doses, can suppress GH release

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23
Q

What are the typical side effects of Dopamine Agonists?

A

-Nausea
-HA
-Orthostatic HoTN
-Lightheadedness
-Fatigue
-Psychiatric Manifestations
-Stroke and/or coronary thrombosis (rare)

24
Q

High doses of ergot derivatives (Bromo and Caber) can cause what?

A

Cold-induced peripheral digital vasospasm (difficult to monitor pulse ox)

25
Q

Why is the Posterior pituitary lighter in color on both gross and microscopic exam?

A

It contains myelinated axon terminals of specialized neurons arising within hypothalamus.

26
Q

Where are the two hormones of the Posterior Pituitary produced?

A

The 2 hormones (vasopressin and oxytocin) are produced in the supraoptic and paraventricular nuclei and transported down the axons of the hypothalamo-hypophyseal tract to posterior pituitary where they are stored.

27
Q

How do the two hormones of the Posterior Pituitary get released?

A

Released into the capillary plexus of infundibulum, and then into the posterior hypophyseal portal veins for distribution to target cells.

28
Q

What are the target cells for ADH?

A

-Kidney (Collecting Ducts)
-Arterioles

29
Q

What are the target cells for oxytocin?

A

-Uterus
-Mammary glands

For labor and milk letdown

30
Q

A peptide hormone that stimulates contractions and lactation.
-Can be given IV to initiate & augment labor

A

Oxytocin

31
Q

What is the dose of Oxytocin to initiate and augment labor?

A

0.5 - 2 mU/min (increased every 30-60 min to desired contraction pattern)
-Max dose 20 mU/min (rates >10 mU/min are rare)

32
Q

What is the dose of oxytocin given IM/IV to control PP bleeding?

A

10-40 U added to 1L of fluid OR 10 U IM

33
Q

Why do you not want to rapidly IV push Oxytocin?

A

Risk of severe hypotension

34
Q

How is Oxytocin metabolized?

A

Renal and hepatic
T1/2 = 5 min
GPCR activity

35
Q

What are C/I to oxytocin therapy?

A

-Fetal distress
-Prematurity
-Abnormal fetal presentation
-Cephalopelvic disproportion
-Predisposition to uterine rupture

36
Q

What is an Oxytocin antagonist approved outside of the US for tx of preterm labor (tocolysis)?

A

Atosiban

37
Q

Vasopressin activates __ subtypes of GPCRs.

A

2: V1 and V2

38
Q

Vasopressin receptor found on vascular smooth muscle cells.
-Mediates vasoconstriction via Gq
-PLC

A

V1

39
Q

Vasopressin receptor found on renal tubule cells
-Reduces diuresis through increasing water reabsorption in the collecting tubules via Gs.
-Adenylyl Cyclase and cAMP

A

V2

40
Q

Extrarenal _______-like receptors regulate the release of coagulation factor VIII and Von Willebrand Factor

A

V2

41
Q

A long-acting, synthetic analog of vasopressin.
-Given IV, SQ, oral, or intranasal
-T1/2 = 1.5-2.5 hrs

A

Desmopressin Acetate (DDAVP)

42
Q

What is Vasopressin used in the tx of?

A

-DI
-Esophageal varices bleeding
-Colonic Diverticular bleeding

43
Q

What is Desmopressin used in the treatment of?

A

-DI
-Coagulopathy in Hemophila A and Von Willebrand Dz

44
Q

What are the two causes of DI?

A

1) Neurogenic: secondary to tumors of the pituitary and hypothalamus or from head injury (urine > 250 /hr)
2) Nephrogenic: impaired receptor sensitivity in collecting ducts of the kidney.

45
Q

What are the symptoms of Vasopressin/Desmopressin toxicity?

A

-HA, nausea, abd cramps, agitation (all masked under GA)
-Overdose = hyponatremia & seizures

46
Q

What is a C/I for vasopression?

A

Can cause vasoconstriction - caution in CAD patients.

47
Q

Occurs with tumors such as bronchogenic tumors of the lungs or tumors in the basal region of the brain.
-These tumors secrete ADH or a similar hormone.

A

Syndrome of Inappropriate ADH (SIADH)

48
Q

With the oversecretion of ADH, the body’s ECF increases ______, while the principle effect is to greatly _______ the Na concentration of the ECF.

A

only slightly; decrease

49
Q

Describe the sequence of events with SIADH?

A

1) a decrease in urine output and slight increase in blood volume
2) increase in arterial pressure and with a dilution of body fluids causes an increase in urine output
3) kidneys excreting a large amount of sodium but not water, reducing the sodium concentration in the extracellular fluid from a normal of 142 mEq/L to 110-120 mEq/L.

This can lead to sudden death from coma and convulsions.

50
Q

What is the tx for SIADH?

A

Treat underlying cause (excision of the tumor)

Acute: Hypertonic Saline (1-2 mL/kg over 3-4 hours) with furosemide
Chronic: Fluid restriction (1200-1800 mL/day)

Possible use of Vaptans.

51
Q

What are the Vaptans?

A

Vasopressin receptor antagonists. Not fully studied in SIADH.
-Tolvaptan
-Conivaptan.

52
Q

Has a high affinity for both the V1 and V2 receptors
-FDA approved for IV administration in hyponatremia.

A

Conivaptan

53
Q

Has a 30 fold higher affinity for V2 > V1 receptor.
-FDA approved for IV administration in hyponatremia.

A

Tolvaptan

54
Q

-High UOP
-Low ADH
-Hypernatremia
-Dehydrated
-Loss of fluid
-Excessive thirst

A

Diabetes Insipidus

55
Q

-Low UOP
-High ADH
-Hyponatremia
-Over hydrated
-Retain fluid
-Excessive thirst

A

SIADH

Adv Pharm 1 (28 decks)

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