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DT4-Exam 1 > Pharm-Neuroendocrine-Melissa > Flashcards

Pharm-Neuroendocrine-Melissa Flashcards

1
Q

Release of the following hormones from the hypothalamus will induce/inhibit the release of which hormones from the anterior pituitary:
GHRH, CRH, TRH, GnRH, Dopamine

A 
GHRH--> GH
CRH--> ACTH
TRH--> TSH, PRL 
GnRH--> FSH +LH
DA--> INHIBITON of PRL release
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2
Q

What are the two hormones released by the posterior pituitary?

A
  • oxytocin

- ADH/ vasopressin

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3
Q

Describe the two negative feedback mechanisms imposed upon hypothalamic/ anterior pituitary system:

A

Target organ hormone–> Inhibit Pit + hypothalamus

Pit Hormone–> Inhibit hypothalamus

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4
Q

Which two hypothalamic hormones regulate the release of GH from the anterior pituitary?
What is the function of GH?

A

GHRH–> ^ Release GH
Somatostatin –> INHIBIT Release GH

GH induces synthesis of IGF-1 which regulates growth

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5
Q

How do we treat hypothalamic dwarfism; what is deficient in the disease?
What are 4 CI’s for this method of treatment?

A

Hypothalamic dwarfism = Deficient GHRH
Treat with GH replacement (+ sex hormones at puberty)

CI for GH therapy:

  • closing epiphyses
  • over 15 yoa
  • Inability to make IGF-1 (Laron dwarfism)
  • active malignancy
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6
Q

What are the GH preparations used to treat patients with hypothalamic dwarfism? (2)

A
  • Somatropin

- Sermorelin

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7
Q

Somatropin: what is the drug and what does it treat?

How is it administered?

A
  • Recombinant DNA match for human GH
  • Treats hypothalamic dwarfism etc.
  • Administer SQ 1x/ day
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8
Q

Sermorelin: what is the drug and what does it treat?

A
  • Synthetic GHRH
  • Formerly used to treat hypothalamic dwarfism etc.
  • Fell out of favor bc not as effective as direct GH therapy
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9
Q

List all the uses for GH therapy (6):

A
  • hypothalamic dwarfism
  • turner’s syndrome
  • prader willi (without obesity or sleep apnea = DEATH)
  • chronic renal insufficiency
  • idiopathic short stature
  • AIDS waisting (anabolic effects)
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10
Q

Two ADRS associated with GH therapy:

A
  • ^ ICP early in treatment
  • diabetogenic effects
  • Note: kids generally tolerate treatment well
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11
Q

Human recombinant IGF-1:
Therapeutic use (2)?
How is it administered?
ADRs (2)?

A

Treat growth problems assts with low IGF-1:

  • Laron dwarfism (GH-R mutations)
  • Pts with Abs against GH

Administer SQ 1-2x/day, preferably after meal to avoid hypoglycemia

ADRs:

  • Hypoglycemia
  • Lipohypertrophy
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12
Q

What is the problem with Laron Dwarfism?

A

Mutant GH-Rs–> Can not make IGF-1

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13
Q

Excess GH: effects in adults and kiddos

A

Kiddos: gigantism
Adults: Acromegaly

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14
Q

What are two somatostatin analogs used to treat ^GH in adults and kids? How do they work? ROA?

PAY ATTENTION TO SPECIAL NOTE REGARDING OCTREOTIDE ON OTHER SIDE OF THIS CARD. CAME FROM RX QUESTIONS!!!!

A

Octreotide + Lanreotide–>
Somatostatin analogs w longer t 1/2–>
INHIBIT GH secretion + DECREASE IGF-1

Administer SQ

–Special fact about octreotide: it inhibits gastric secretions and vasoconstricts: used to treat carcinoid syndrome!!

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15
Q

What are some of the ADRs associated with Octreotide and Lanreotide?

A
  • GI PROBLEMS: N/V/D/ Abdominal pain

- Gall stones (Decrease biliary cntrxn, GI time)

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16
Q

What is one possible alternative use for octreotide and lanreotide?

A

Treat thyrotrope adenomas because they decrease thyrotropin secretion

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17
Q

Pegvisomant:

MOA, Therapeutic use, ROA, ADRs (2)

A

MOA:
Competitive GH-R ANTAGONIST–> DECREASE IGF-1
Tx: ^^^ GH
ROA: SQ
ADR: Lipohypertrophy at injection site, Hepatotoxic
**Monitor liver function

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18
Q

What are 5 problems that can cause excessive prolactin release?

A
  • Hypothalamic lesion–> DECREASE DA
  • Antipsychotic DA-R antagonists
  • Prolactin secreting pituitary adenoma
  • Renal insufficiency (decrease breakdown prolactin)
  • Excess TRH (hypothyroidism)
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19
Q

Describe the hallmark sx of hyperprolactinemia (4):

A
  • amenorrhea
  • infertility ***
  • impotence
  • galactorrhea
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20
Q

Cabergoline + Bromocriptine:

MOA, Therapeutic use, differences between drugs–which is preferred?

A

MOA: D1 + D2 AGNONISTS
Tx: Hyperprolactinemia

Differences:

  • Cabergoline = preferred drug, selective D2 + longer t1/2
  • Bromocriptine also indicated for acromegaly
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21
Q

***ADRs asstd. with Cabergoline + Bromocriptine:

A
  • N/V/ Dizziness; LESS with cabergoline

- Valvular disease (cabergoline only)

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22
Q

Which drug do we use to diagnose hypothyroidism?

How do we know if the problem is primary, secondary, or tertiary?

A

PROTIRELIN: synthetic TRH–> ^ TSH release

  • ^TSH–> ^ T3/T4 = Hypothalamic defect (tertiary)
  • NO ^TSH–> NO ^ T3/T4 = Pituitary defect (secondary)
  • ^ TSH–> NO ^ T3/T4 = Thyroid defect (primary)
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23
Q

Cosyntropin:

MOA, Therapeutic use

A

MOA: synthetic ACTH analog (^ cortisol release)
Tx: Dx primary vs secondary adrenal insufficiency

24
Q

Describe the mechanism of GnRH naturally and how that is manipulated by long acting GnRH agents:

A

Normal:
PULSITILE GnRH–> FSH + LH release–> ^ E/ P/ T

Long Acting Agents:
CONSTANT GnRH–> DECREASE # GnRH-R’s–>
DECREASE FSH + LH release–> DECREASE E/ P/ T

25
Q

How does hCG work to ^ fertility?

A

mimics actions od LH–>

^ female ovulation (LH surge) + ^ male external sexual development (^ T)

26
Q

What are the indications for hCG therapeutic use? (2)

A
  • stimulating ovulation in women

- threat male infertility and cryptorchidism

27
Q

Menotropins (hMG)
What are the active components in these drugs?
What are the two therapeutic uses?

A
  • Contain equal LH and FSH
  • treats female infertility (^ follicular dvlpmt.)
  • ^ male spermatogenesis
28
Q

Urofollitropin:
What is the active component of this drug?
What are the two therapeutic uses?

A
  • Menotropin with most of LH removed; ^ FSH
  • treats female infertility (^ follicular dvlpmt.)
  • ^ male spermatogenesis
29
Q

What are the gonadotropin mimicking drugs (2)?

What is their MOA and what are they used to treat?

A

Follitropin beta + alpha (recombinant FSH)
- use like urofollitropin

Choriogonadotropin alpha (recombinant LH)
- use like hCG
30
Q

What are some ADRs associated with gonadotroipins? (3)

A
  • multiple births
  • ovarian hyperstimulation syndrome
  • gynecomastia (^E)
31
Q

What is ovarian hyper stimulation syndrome?

A

Leaky ovarian capillaries cause fluid to fill abdominal cavity
–> painful abdomen

32
Q

**Chlomiphene:
MOA
Therapeutic uses
ADRS

A

MOA:
Estrogen receptor ANTAGONIST–> INHIBIT E negative feedback to hypothalamus–> ^ LH + ^ FSH–> ^ fertility

Therapeutic uses:
- Infertility due to ovulatory disorder i.e. PCOS

ADRs:

  • multiple births
  • antiestrogenic effects (endometrium, ovarian cysts, developing follicle)
33
Q

Gonadorelin: MOA, therapeutic use?

A
  • Synthetic GnRH
  • Administered via pump–> ^ endogenous FSH +LH
  • Treats infertility in females
34
Q

Leuprolide, Goserelin, Nafarelin, Histrelin:

MOA, Dosing regimine?

A

Long acting Synthetic GnRH AGONIST

MOA:
DOWNREGULATES GnRH-R + INHIBIT GnRH Secretion

Dosing:
Admin continuously for 2-4 weeks

35
Q 
Leuprolide, Goserelin, Nafarelin, Histrelin: 
Therapeutic uses (4)?
A

Long acting Synthetic GnRH AGONIST

  • Endometriosis
  • Uterine fibroids
  • Prostate and breast cancers
  • Precocious puberty
36
Q

Leuprolide, Goserelin, Nafarelin, Histrelin: ADRs?

A

Long acting Synthetic GnRH AGONIST:

Problems with too low E and T… (like in menopause)

  1. Hot flashes, vaginal atrophy
  2. osteoporosis
  3. erectile dysfunction
37
Q

Flutamide + Bicalutamide:

MOA, Therapeutic use

A

MOA: Androgen receptor ANTAGONISTS

Therapeutic use:

  • **Combo treatment with long acting GnRH analogs
  • Treats metastatic prostate disease
38
Q

Why should Flutamide + Bicalutamide not be administered alone?

A

^ LH synthesis due to DECREASED testosterone mediated negative feedback–would ultimately lead to INCREASE in Testosterone production

39
Q

Flutamide + Bicalutamide: ADRs

A

BLACK BOX: Reversible Hepatotoxicity; check liver function prior to use

40
Q

Finasteride:

MOA, Therapeutic use?

A

MOA: 5-a reductase inhibitor; STOP T–> DHT

Therapeutic use:
BPH, prostate cancer, male pattern baldness

41
Q

Describe the difference between central and nephrogentic DI– How are the two diagnosed?

A

Central: inadequate ADH
- synthetic vasopressin = INCREASE urine osmolality

Nephrogentic: Kidneys fail to repsond to ADH
- synthetic vasopressin NO EFFECT ON urine osmolality

42
Q

What are two HIGH yield causes of nephrogenic DI?

A

LITHIUM + Dimiclocyclin!!

43
Q

What are the symptoms of DI (both types)?

A
  • polyuria and polydipsia

- dilute urine

44
Q

Desmopressin:

MOA (3), therapeutic use (3)?

A

MOA:

  • Exogenous vasopressin w REDUCED (V1) vasopressor activity and INCREASED (V2) antidiuretic effects
  • ^ factor VIII
  • ^ VWF

Therapeutic use:

  • CENTRAL DI
  • von Willibrand disease type1
  • primary nocturnal enuresis
45
Q

What are 3 of the ADRs associated with vasopressive therapy; with which drug are they worse?

A
  • Facial pallor
  • ^GI motility (N/Cramping)
  • OVERSTIMULATION of V2 receptors–> H2O toxicity

**Note that ADRs are worse with vasopressin than desmopressin

46
Q

***How do Lithium and Demeclocycline cause nephrogenic DI?

A

Lithium + Demeclocycline–> INHIBIT V2-Rs in collecting duct!

1/3 of all patients on lithium will get this!!!

47
Q

How do we treat/ prevent lithium induced nephrogenic DI?

What is the MOA here?

A

Administer AMILORIDE–>

BLOCKS Li+ uptake at the Na+ channel in the collecting duct–> reverse/ inhibit V2 effects

48
Q

Amiloride: therapeutic use?

A

Treat nephrogenic DI induced by Lithium

49
Q

What are three treatments used for nephrogenic DI?

A
  • ^ H2O intake
  • Administer THIAZIDE diuretics
  • Na+ restriction
50
Q

What is SIADH/ how does it present?

What 4 drug causes?

A

^^^ ADH–> hyoposmolality and hyponatremia
Patients present with lethargy, N/V, cramping, convulsion, death

4 drug causes:

  • SSRI
  • TCA
  • Sulfadrugs
  • vinka alkaloids
51
Q

Which tetracycline antibiotic is used to treat SIADH and how does it work?

A

Demeclocycline–> Inhibits vasopressin actions on collecting duct

52
Q

What are the two vaptan drugs?

How do they work and what do they treat?

A

Conivaptan (V1 + V2 ANTAGONIST)
Tolvaptan (V2 ANTAGONIST)

Therapeutic Use:
Euvolemic and hypervolemic hyponatremia asstd. with SIADH

53
Q

What are the three methods used to treat SIADH?

A
  • fluid restriction +/- hypertonic saline +/- loop diuretics
  • demeclocycline
  • vaptans
54
Q

What are the therapeutic uses for pharmacologic oxytocin (4)? Describe the ROA for each use.

A
  • abortion
  • induction of labor (IV)
  • postpartum hemorrhage (IM)
  • induction of lactation (intranasal)
55
Q

What are 2 ADRs associated with synthetic oxytocin use?

A
  • excessive uterine contraction–> harm mom and newborn

- water intoxication due to ^ resorption (has ADH effects)

DT4-Exam 1 (17 decks)

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