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Therapeutics > Exam 3 Pituitary Hormones > Flashcards

Exam 3 Pituitary Hormones Flashcards

1
Q

What are the anterior pituitary hormones?

A
  1. growth hormone
  2. somatostatin
  3. gonadotropins → FSH and LH
  4. gonadotropin releasing hormone (GnRH)
  5. prolactin
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2
Q

What are the posterior pituitary hormones?

A
  1. vasopressin
  2. vasopressin antagonists
  3. oxytocin
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3
Q

What are some things to know about the pituitary gland?

A
  1. the master gland
  2. also called the hypophysis
  3. size of a pea (0.5 g)
  4. has two lobes: frontal and posterior that secrete different hormones
  5. has nerve cells that connects posterior pituitary and hypothalamus
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4
Q

What are the two exceptions where vein connects two organs?

A
  1. portal vein that connects hypothalamus and pituitary gland
  2. hepatic portal vein that connects intestine to liver
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5
Q

What are the hormones associated in the hypothalamic-pituitary-endocrine gland axis?

A
  1. GnRH and SST (somatostatin) from the hypothalamus → anterior pituitary secretes GH → peripheral tissues
  2. TRH from hypothalamus → anterior pituitary secretes TSH → thyroid that secretes thyroxine and triiodothyroxine
  3. CRH from hypothalamus → anterior pituitary secretes ACTH → adrenal cortex secretes glucocorticoids
  4. GnRH from hypothalamus → anterior pituitary secretes FSH and LH → gonads secretes estrogen, progesterone, testosterone
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6
Q

What are things to know about growth hormone and prolactin?

A
  1. single chain protein hormones

2. activate receptors associated with JAK/STAT pathway

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7
Q

What are things to know about TSH, FSH, and LH?

A
  1. dimeric protein hormones sharing a common alpha chain → but have their own beta chain
  2. activate GPCRs
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8
Q

What are things to know about adrenocorticotropic hormone (ACTH)?

A
  1. single chain peptide

2. activates a GPCR

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9
Q

What are the functions of growth hormone?

A
  1. required during childhood and adolescence for attainment of normal adult size
  2. mediated primarily via increasing the production of insulin like growth factor I (IGF-I) in the liver, bone, cartilage, and muscle → for bone growth
  3. anabolic effects in the muscle → increases lean body mass
  4. catabolic effects in lipid cells → reduces central adiposity (get fat in the belly and harder to generate muscle)
  5. reduction in insulin sensitivity → compensated by the insulin activity of IGF-I
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10
Q

Does GH stimulate growth by itself?

A

NO! by itself, it does not stimulate growth but it stimulates IGF-I that promotes cellular growth of the bones!

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11
Q

What happens when someone has a deficiency of growth hormone?

A
  1. failure to reach the predicted adult height
  2. disproportionately increased body fat → central adiposity
  3. decreased muscle mass
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12
Q

What is the structure of growth hormone?

A
  1. 191 amino acid protein with two disulfide bonds
  2. similar to the structure of prolactin
  3. the recombinant form (rhGH, somatotropin) has the identical structure
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13
Q

What is the metabolism of growth hormone?

A
  1. half life of 20-25 minutes
  2. cleared by the liver
  3. rhGH is administered subcutaneously, active blood levels persist for about 36 hours
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14
Q

What are the clinical uses of growth hormone?

A
  1. growth hormone deficiency → congenital from genetic mutations, acquired from damage to pituitary or hypothalamus by a tumor, infection, surgery, or radiation therapy, short stature and adiposity in childhood, and hypoglycemia due to unopposed action of insulin
  2. treatment of pediatric patients with short stature without GH deficiency → for genetic disorders like Prader-Willi syndrome and Turner syndrome and for idiopathic short stature (controversial use since it costs $35K per inch)
  3. performance enhancer in athletics (banned by IOC)
  4. anti-aging? → skin can become smoother
  5. antiobesity (under investigation)
  6. use of recombinant bovine growth factor (rbGH) in dairy cattle → to make the cows make more milk but does not affect the quality of the milk
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15
Q

What is mecasermin?

A
  1. a recombinant human IGF-I (rhIGF-I)
  2. used in treatment of severe IGF-I deficiency → where people are not responsive to exogenous GH and/or have mutations in the GH receptor or development of neutralizing antibodies to GH
  3. prepared as a complex with recombinant human IGF-I binding protein-3 (rhIGFBP-3) → rhIGFBP-3 is needed to maintain an adequate half life of rhIGF-I
  4. hypoglycemia may occur due to the insulin activity of rhIGF-I since IGF has insulin like activity
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16
Q

What are the different growth hormone antagonists?

A
  1. GH secreting pituitary adenomas
  2. somatostatin analogs
  3. GH receptor antagonist
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17
Q

What are things to know about GH secreting pituitary adenomas (tumor that secretes hormones)?

A
  1. occur most commonly in adults → acromegaly (abnormal growth of cartilage, bone, and many other organs)
  2. occurrence before the epiphyseal closure leads to gigantism (rare)
  3. can be treated with GH antagonists (somatostatin analogs, GH receptor antagonist)
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18
Q

What are things to know about somatostatin analogs?

A
  1. octreotide
  2. lanreotide

they block the release of GH in the pituitary

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19
Q

What are things to know about GH receptor antagonists?

A
  1. Pegvisomat → PEG derivative of a mutant GH that binds to GH receptor but blocks signal transduction → doesn’t stimulate or activate the receptor
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20
Q

What are the effects of FSH?

A

in women: directs ovarian follicle development and stimulates the conversion of testosterone to estrogens

in men: regulates spermatogenesis and stimulates the conversion of testosterone to estrogens

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21
Q

What are the effects of LH?

A

in women: stimulates androgen production of in the follicular phase and controls estrogen and progesterone production in the luteal phase

in men: stimulates androgen production

22
Q

What are things to know about human chorionic gonadotropin (hCG)?

A
  1. produced in the placenta during pregnancy → what pregnancy tests detects
  2. nearly identical with LH (binds LH receptors)
  3. controls estrogen and progesterone production during pregnancy
23
Q

What are the structures of gonadotropins?

A
  1. FSH, LH, and hCG are all heterodimeric proteins that share the same alpha chain, have distinct beta chain that confers receptor specificity, and the beta chains of hCG and LH are nearly identical
  2. administered subcutaneous or intramuscular injection
  3. half life of 10-40 hours (dependent on the preparation and route of injection) → usually a daily injection
24
Q

What are the different preparations used clinically?

A
  1. menotropins
  2. urofollitropin (uFSH)
  3. follitropin alpha and follitropin beta
  4. lutropin alpha
  5. hCG
  6. choriogonadotropin alpha (rhCG)
25
Q

What are menotropins?

A
  1. human menopausal gonadotropins (hMG)
  2. first commercial gonadotropin product
  3. extracted from the urine of postmenopausal women
  4. mixture of FSH and LH
  5. lower potency than purified FSH or LH
26
Q

What is urofollitropin (uFSH)?

A
  1. FSH purified from the urine of postmenopausal women

2. LH activity is removed during purification

27
Q

What is follitropin alpha and beta?

A
  1. recombinant forms of FSH
  2. identical in amino acid sequence with FSH
  3. differ from each other and uFSH in carbohydrate chains
  4. considerably more expensive than uFSH
28
Q

What is lutropin alpha?

A
  1. recombinant form of LH
  2. approved for use in combination with follitropin alpha for stimulation of follicular development in infertile women with LH deficiency
  3. discontinued from the US market in 2012
29
Q

What is hCG?

A

extracted and purified from the urine of pregnant women

30
Q

What is choriogonadotropin alpha (rhCG)?

A

recombinant form of hCG → expensive and no difference in LH

31
Q

How are gonadotropins used for ovulation induction?

A
  1. in women with anovulation secondary to hypogonadotropic hypogonadism, PCOS, etc → but high cost, needs close monitoring during administration, and reserved for patients who fail to respond to other treatments (like clomiphene)
  2. controlled ovarian hyperstimulation in reproductive technology procedures
  3. protocols are based on the physiology of a normal menstrual cycle
32
Q

What is ovulation induction protocol?

A
  1. FSH preparations (hMG, uFSH) during the follicular phase → to prevent the premature endogenous surge in LH, the effects of endogenous GnRH need to be blocked by continuous administration of GnRH or GnRH receptor antagonist
  2. administration of hCG → ovulation → insemination or oocyte retrieval
  3. hormonal support during the luteal phase typically by exogenous progesterone
33
Q

How are gonadotropins used to treat male infertility?

A
  1. most of the symptoms of hypogonadism in men can be treated with exogenous androgens
  2. however treatment of infertility in hypogonadal men requires LH and FSH
  3. protocol: injection of hCG for 8-12 weeks (initial phase) then injection of hMG for months
  4. introduction of intracytoplasmic sperm injection (ICSI) reduces significantly the minimum requirement of spermatogenesis

need LH and FSH to make sperm → not just testosterone

34
Q

What are some adverse effects of gonadotropins?

A
  1. ovarian hyperstimulation syndrome → extra hormones and ovaries produce too many sex hormones and can make blood vessels leaky → occurs in 0.5-4% of patients where there is an overproduction of estrogen and progesterone that leads to vascular hyperpermeability and can lead to ovarian enlargement, ascites, hydrothorax, and hypovolemia
  2. multiple pregnancy → occurs in 15-20% when ovulation induction is used (occurs in 1% of population)
35
Q

What are things to know about gonadotropin releasing hormone?

A
  1. decapeptide hormone secreted by neurons in the hypothalamus
  2. binds to GPCRs on the plasma membranes of gonadotrope cells in the anterior pituitary
  3. example is gonadorelin → acetate salt of synthetic human GnRH with a half life of 4 mins (IV) or 3 hours (SQ)
36
Q

What are some synthetic analogs of GnRH?

A

goserelin, histrelin, leuprolide, nafarelin, triptorelin

37
Q

What are some things to know about synthetic analogs of GnRH?

A
  1. D-amino acid at position 6
  2. ethylamide substituted for glycine at position 10 (except nafarelin)
  3. more potent and longer lasting than GnRH and gonadorelin → daily shot
38
Q

What is the pulsatile secretion of GnRH?

A
  1. GnRH stimulates the production and release of LH and FSH only when its secretion is pulsatile
  2. in the pharmacological use of GnRH and its analog, the pulsatile secretion of GnRH is mimicked → IV administration every 1-4 hours
  3. nonpulsatile (at a constant level) administration of GnRH or GnRH analogs inhibits the release of FSH and LH in both women and men, resulting in hypogonadism → GPCR receptors are desensitized or even down regulated
39
Q

How is GnRH used for female infertility?

A
  1. injected IV in a pulsatile fashion using a portable battery powered programmable pump
  2. less likely than gonadotropins to cause multiple pregnancies and the ovarian hyperstimulation syndrome → advantage!
  3. not commonly used due to the inconvenience and cost
40
Q

How is GnRH used for male infertility?

A
  1. in men with hypothalamic hypogonadotropic hypogonadism
  2. pulsatile injection using a portable pump (for months)
  3. treatment with gonadotropins (hCG and hMG) is more favored
41
Q

What are the clinical uses of GnRH for suppression?

A
  1. continuous treatment with GnRH agonist → suppression of gonadotropin release
  2. controlled ovarian hyperstimulation → suppression of endogenous LH surge that could cause premature ovulation, involves daily SQ injection of leuprolide or daily nasal application of nafarelin
  3. endometriosis → supression of gonadotropin release leads to suppression of ovaries and reduced production of estrogen and progesterone
  4. prostate cancer → combination with an androgen receptor antagonist leads to reduction of testosterone levels and effects
  5. central precocious puberty → puberty that starts too early
42
Q

What are some points to know about GnRH agonists and antagonists?

A
  • relix → antagonist

- relin → agonist

43
Q

What are some things to know about GnRH receptor antagonists?

A
  1. synthetic decapeptides that function as competitive antagonists: ganirelix, cetrorelix, abarelix, degarelix
  2. controlled ovarian hyperstimulation (ganirelix, centrorelix) → produce an immediate antagonist effect so shorter duration of treatment and has lower risk of ovarian hyperstimulation syndrome
  3. advanced prostate cancer

antagonist effects are right away!!

44
Q

What is prolactin?

A
  1. 198 amino acid protein peptide hormone produced in the anterior pituitary
  2. structurally similar to growth hormone
  3. responsible for lactation
  4. dopamine inhibits the secretion of prolactin
45
Q

What is prolactin deficiency?

A
  1. rare form of pituitary abnormality

2. no preparation of prolactin is available

46
Q

What is hyperprolactinemia?

A
  1. caused by prolactin secreting adenomas
  2. inhibition of GnRH release
  3. amenorrhea and galactorrhea (may produce milk excessively) in women, loss of libido and infertility in men
  4. can be treated with dopamine agonists since dopamine inhibits prolactin secretion
47
Q

What are vasopressin and oxytocin?

A
  1. peptide posterior pituitary hormones
  2. synthesized in neuronal cell bodies in the hypothalamus
  3. transported via their axons to the posterior pituitary
48
Q

What are the structures of vasopressin and oxytocin?

A
  1. 9 amino acid peptide hormones with a ring formed by a disulfide bond → short peptide hormones
  2. the amino acid sequence of oxytocin is different from that of vasopressin at positions 3 and 8
  3. possess some cross activity
49
Q

What is desmopressin?

A
  1. long acting synthetic analog of vasopressin
  2. modification at position 1 and and D-amino acid at position 8
  3. has a longer half life
50
Q

What is vasopressin?

A
  1. antidiuretic hormone (ADH), arginine vasopressin (AVP)

2. released by the posterior pituitary in response to rising plasma tonicity (high Na+ levels) and falling blood volume

Therapeutics (15 decks)

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