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PHS 933 > Block 4 Lecture 1 -- Pituitary Hormones > Flashcards

Block 4 Lecture 1 -- Pituitary Hormones Flashcards

1
Q

What are the 3 structural groups of pituitary hormones?

A

1) somatropes
2) glycoprotein hormones
3) POMC-derived hormones

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2
Q

What are the somatotropes?

A

1) GH
2) PRL
3) PL

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3
Q

Describe somatotrope structure.

A

single polypeptide (22kDa, 190 AA)

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4
Q

What are the glycoprotein hormones?

A

1) LH
2) FSH
3) hCG
4) TSH (thyrotropin)

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5
Q

What are the POMC-derived hormones?

A

ACTH

alpha-MSH

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6
Q

Describe POMC-derived hormone structure?

A

short polypeptides

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7
Q

Describe glycoprotein hormone structure

A

heterodimeric protein
– common a
– unique b
sugar modified

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8
Q

What are the hypothalamic releasing hormones?

A

1) GHRH
2) GnRH
3) TRH
4) CRH
5) somatostatin

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9
Q

Describe the GHRH receptor.

A

Gs, increases cAMP and Ca++ release

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10
Q

What endogenous substances induce GH release?

A

1) ghrelin
2) DA
3) 5-HT
4) Arg
5) a-adrenergic agonists
6) GHRH

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11
Q

What activities induce GH secretion?

A

1) hypoglycemia
2) stress
3) exercise

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12
Q

How is GHRH release stimulated?

A

stress
sleep
exercise

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13
Q

What things inhibit GH release?

A

1) beta-agonists
2) FFAs
3) glucose
4) IGF-1
5) GH

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14
Q

Where is ghrelin produced?

A

endocrine cells of stomach

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15
Q

What is the function of ghrelin?

A

1) suppresses SST release

2) stimulates GHRH release from HT

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16
Q

What things increase GH-binding protein levels?

A

obesity
estrogens

(decreases free GH)

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17
Q

Describe the structure of SST.

A

SST-14 or SST-28
– proteolysis of precursor peptide

core is a 12-aa cyclic peptide formed by disulfide Cys-Cys

    • 4 aa sequence is essential to receptor binding
    • Phe-Trp-Lys-Thr
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18
Q

Describe SST receptors.

A

family of 5 Gi GPCRs

– SSTR2, 5 most important for GH regulation

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19
Q

Where is SST synthesized?

A

brain neurons and GI neuroendocrine cells

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20
Q

What are the functions of GH’s circulating binding protein?

A

binds 25-45%

    • delays GH clearance
    • dampens fluctuations from pulsatile secretion
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21
Q

Describe GH concentration across time

A
    • irregular pulsatile release
    • undetectable between pulses
    • greatest at night during sleep

– highest in children, esp. puberty

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22
Q

Describe the structure of GH.

A

2 forms, bioequivalent

– one is alternatively spliced

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23
Q

What is the most abundant AP hormone?

A

GH (40% of AP cells)

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24
Q

How is the ability of AP to suppress GH tested?

A

AP suppression test

– oral glucose

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25
Q

How is the ability of AP to secrete GH tested?

A

insulin tolerance test

    • generates hypoglycemia
    • GH released in 45-90 min
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26
Q

What are the effects of GH?

A

induces release of IGF-1 on target tissues

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27
Q

Where are the target sites of GH / where is IGF-1 produces?

A

liver, bone, adipose, muscle

    • liver is primary source of IGF-1
    • peripheral IGF-1 production is essential to growth
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28
Q

What are the effects of IGF-1?

A

causes anabolic and growth effects

– acts on secondary tissues thru IGF-1 receptor, which is on most cells

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29
Q

Where is the GH binding protein derived from?

A

GH receptor, by proteolysis

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30
Q

How is GH deficiency diagnosed in kids?

A

1) short stature/slow growth
2) delayed bone age
3) provocative test showing GH less than 10 ng/mL

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31
Q

How is GH deficiency diagnosed in adults?

A

1) IGF-1 levels below age/sex-adjusted values

2) failure of provocative test

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32
Q

GH deficiency is associated with:

A

1) CV morbidity and mortality
2) hyperlipidemia
3) decreased muscle mass and bone density

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33
Q

What are the somatropins?

A

GH preps identical to human GH

    • Serostim
    • Genotropin
    • Humatrope
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34
Q

What is Protropin?

A

modified GH

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35
Q

What is sermorelin acetate?

A

synthetic GHRH

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36
Q

What are “stacked” amino acids?

A

claims to stimulate GH

    • contain Arg and L-DOPA
    • no evidence of benefit in athletes as anabolic agent
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37
Q

What are GH replacement therapy ADRs in adults?

A 
dose-related
most common in older/obese patients
1) peripheral edema
2) carpal tunnel
3) arthralgia
4) myalgia
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38
Q

What are ADRs of GH replacement therapy in kids?

A 
rare
usually in first 8 wks
-- intracranial HTN
-- visual changes
-- HA
-- n/v
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39
Q

What are contraindications for GH therapy?

A

tumor and leukemia patients

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40
Q

What are symptoms of gigantism?

A

long bone growth due to unfused epiphyses

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41
Q

What are symptoms of acromegaly?

A 
--adults!
large hands and feet
arthropathy
carpal tunnel
visceromegaly
macroglossia
HTN
glucose intolerance
HA
sleep apnea
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42
Q

How is gigantism diagnosed?

A

OGTT in GH suppression

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43
Q

How is acromegaly diagnosed?

A

usually around 40-45 yo

    • acromegaly + GH or IGF-1 increase
    • failure of OGTT in GH suppression
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44
Q

Acromegaly is associated with…

A

1) shortened life expectancy

2) 2-fold increase in CVD

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45
Q

How is GH excess treated?

A
    • treatment of choice: transsphenoidal surgery
    • radiation
    • drugs, even after surgery
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46
Q

What are the somatostatin analogs?

A

octreotide (sandostatin)

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47
Q

What are the ADRs of octreotide?

A

GI in 50% of patients

    • diminish over time
    • nausea, diarrhea, pain
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48
Q

How is octreotide supplied?

A

1) SQ injection (duration = 12h)

2) IM monthly injection

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49
Q

What are the DA receptor agonists?

A

cabergoline (Dostinex)

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50
Q

What are the GH receptor antagonists?

A

pegvisomant (Somavert)

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51
Q

When is cabergoline used for GH excess?

A

acromegaly

    • best with tumors secreting PRL + GH
    • can be used with somatostatins
    • useful when patient refuses SST injection
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52
Q

What are the ADRs of cabergoline?

A

nausea, lightheadedness

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53
Q

What is the MoA of cabergoline in GH excess?

A

decreases GH secretion in some patients
– (increases secretion in normal patients)

much higher dose than hyper-PRL-emia

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54
Q

How is pegvisomant monitored?

A

1) dose titrated on serum IGF-1

2) liver enzymes: hepatotoxic

55
Q

How is pegvisomant supplied?

A

SQ injection

56
Q

Describe the structure of prolactin

A

related to GH

    • 23 kDa, 199 AA
    • 3 Cys-disulfides
    • some is glycosylated
57
Q

How is prolactin secretion induced?

A

1) sleep
2) stress
3) hypoglycemia
4) exercise
5) estrogen
6) breast suckling

58
Q

What are the effects of prolactin?

A

acts on PRL receptor to…

    • prepare for milk production and secretion
    • suppress GnRH (infertility)

PRL receptor are on many tissues; functions unknown

59
Q

How is prolactin secreted?

A

pulsatile
– cyclic in females; constant in males

in fetus, secreted by pituitary until bith

60
Q

How is prolactin secretion regulated?

A
    • mainly by DA (inhibitory)

- - TRH can induce secretion in severe hypothyroidism

61
Q

What are symptoms of hyperprolactinemia?

A 
women:
-- galactorrhea
-- amenorrhea
-- infertility
men:
-- impotence
-- loss of libido
-- infertility
62
Q

How is hyperprolactinemia treated?

A

surgery is preferred

D2 receptor agonists

63
Q

What are the D2 receptor agonists?

A

1) bromocriptine (Parlodel)
2) cabergoline (Dostinex)
3) quinagolide
4) pergolide (Permax)

64
Q

What are the effects of D2 receptor agonist therapy?

A

1) reduce symptoms
2) reduce tumor size
3) regain fertility, become pregnant

65
Q

What are the ADRs of bromocriptine?

A

tolerance developed over time

    • n/v (common)
    • HA; occasional CNS effects
    • postural hypotension
66
Q

How does cabergoline compare to bromocriptine?

A

1) 4x affinity
2) slightly more effective
3) less nausea

half-life is 65h (compared to 8h)

67
Q

When is quinagolide used?

A

only in Europe

68
Q

When is pergolide used?

A

(?)
it’s the cheapest
off-label (normally for PD)

69
Q

Describe PK of bromocriptine.

A

absorption good
rapid first-pass
t1/2 = 2-8 h

70
Q

What D2 agonist is preferred in patients trying to get pregnant?

A

bromocriptine

71
Q

Describe the structure of GnRH.

A

decapeptide from 92-aa precursor

72
Q

How is GnRH supplied clinically?

A

1) Gonadorelin

2) Factrel

73
Q

How are GnRH analogs supplied?

A

1) leuprolide
2) buserelin
3) nafarelin

74
Q

How are GnRH antagonists supplied?

A

1) cetrorelix
2) ganirelix
3) abarelix

75
Q

What GnRH depot (3-month) preparations are available?

A

1) goserelin (Zoladex)

2) triptorelin (Trelstar LA)

76
Q

How is GnRH used?

A

for differentiation of hypothalamic vs. pituitary defects

    • SQ or IV
    • monitor LH
77
Q

What are the indications for GnRH analogs?

A

1) pharmacological castration
2) precocious puberty
3) endometriosis and acute intermittent porphyria
4) infertility (not in the US)

78
Q

How do GnRH analogs compare to GnRH?

A
    • longer t1/2

- - higher affinity for receptor than GnRH

79
Q

What are GnRH antagonists used for?

A

symptomatic tx of hormonally-responsive tumors (prostate, breast)

80
Q

Describe the structure of oxytocin

A

cyclic nonapeptide related to vasopressin

81
Q

Where is oxytocin secreted?

A

1) posterior pituitary
2) ovarian luteal cells
3) endometrium
4) placenta

82
Q

What factors stimulate oxytocin release?

A
    • pain, dehydration, hemorrhage/hypovolemia
    • estrogen
    • cervicovaginal dilation (stage ii of labor)
83
Q

What factors inhibit oxytocin release?

A
    • EtOH

- - relaxin

84
Q

What are the effects of oxytocin?

A

1) breast, uterine muscle contraction
2) bind vasopressin receptors at pharmacological doses
3) increases force/frequency of uterine contractions during delivery

85
Q

For what is oxytocin used?

A

1) induction/augmentation of labor

2) to prevent hemorrhage post-delivery (uterine contraction)

86
Q

What should be monitored when oxytocin is given?

A

1) fetal HR
- - prevent hyperstimulation, uterine tetany
2) fluid intake
- - beware water intoxication (antidiuretic effect)

87
Q

What’s the t1/2 of oxytocin?

A

3 minutes

88
Q

What are the psychosocial roles of oxytocin?

A

1) contentment, anxiolytic, calmness, security
2) trust, generosity
3) mother-infant bonding

89
Q

What additional effects are given by IN oxytocin?

A

possibly inhibits amygdala
– reduced fear
– empathy and improved facial memory (esp happy) in healthy males
may reduce caloric intake in men

90
Q

Oxytocin levels are associated with:

A

1) mother-infant mutual gaze
2) human-dog mutual gaze/petting
3) orgasm
4) romantic attachment

91
Q

Describe the structure of vasopressin.

A

cyclic nonapeptide related to oxytocin

    • 2 aa difference
    • cleaved from pre-prohormone synthesized in HT
92
Q

What factors induce vasopressin secretion?

A

1) increased plasma osmolarity
2) severe hypovolemia/hypotension
3) AngII
4) TCAs, lithium, nicotine, morphine, ethanol, glucocorticoids

93
Q

What are the vasopressin receptors and where are they located?

A

GPCRs

1) V1a, V1b (Gq, Ca)
- - widespread in vasculature
2) V2 (Gs, phosphorylation)
- - distal tubule and collecting duct

94
Q

What are the effects of the V1a, V1b receptors?

A

vasoconstriction

95
Q

What are the effects of the V2 receptor?

A

1) insertion of preformed aquaporin-2s into apical (luminal) membrane
2) increased sodium recovery

96
Q

What is the MoA for DDAVP?

A

selective V2 receptor agonist
– 3000x higher affinity

eliminates pressor effect at therapeutic dose

97
Q

Describe the structure of DDAVP.

A

AVP, but..

    • D-Arg subbed for Arg at 8
    • deaminated N-terminus
98
Q

ADRs of DDAVP.

A

1) mild facial flushing
2) HA
3) allergic rxn
4) nasal congestion/rhinorrhea
caution: water intoxication

99
Q

How is DDAVP given?

A

IN or SQ 2-3 x/day
– nasal lasts 6-12h

po form, but $$ and hi-dose due to peptide degradation

100
Q

For what is DDAVP used?

A

1) central DI

2) some forms of von Willebrand’s disease

101
Q

What is von Willebrands disease?

A

clotting factor defect

DDAVP increases the vW-factor

102
Q

What are causes of central DI?

A

inadequate AVP secretion due to…

    • familial
    • injury
    • HT-pituitary tumor
103
Q

What are signs & symptoms of DI?

A

1) excessive urine production
2) polydipsia
3) dilute urine (less than 200 mOsm/L)

104
Q

What is the pathology of nephrogenic DI and what are its forms?

A

inadequate AVP response

    • congenital form
    • acquired form
105
Q

What causes acquired nephrogenic DI?

A

lithium is most common

    • interferes with V2-mediated activation of adenylate cyclase
    • reversible
106
Q

What causes congenital nephrogenic DI?

A

defective X-linked V2 receptors

or, defective aquaporin-2 channels

107
Q

How is nephrogenic DI treated?

A

not with DDAVP!!

  • -thiazides
  • -NSAIDs

–amiloride if lithium-induced

108
Q

How is central DI treated?

A

1st line) DDAVP
2nd line) chlorpropamide
– only when DDAVP not tolerated

adjuncts:

    • thiazides: added to chlorpropamide
    • NSAIDs (indomethacin)
109
Q

What is the MoA of chlorpropamide?

A

oral sulfonylurea

– potentiates AVP (AVP is required!)

110
Q

What is the MoA of thiazide diuretics?

A

promotes water recovery prior to collecting ducts

– enhanced by dietary sodium restriction

111
Q

What is the MoA of amiloride?

A

Na-channel blocker

    • blocks reuptake of lithium
    • reverses lithium-induced DI
112
Q

What are ADRs of amiloride?

A

GI upset, n/v

113
Q

What is the MoA of indomethacin when used for DI?

A

NSAID

    • decreases GFR
    • blocks PGs in juxtaglomerular apparatus
114
Q

Why is abarelix not used?

A

hypersensitivity reaction issue

– limited distribution

115
Q

What are treatment considerations for endometriosis and acute intermittent porphyria with GnRH analogs?

A

limit to 6 months!

116
Q

Why might GnRH analogs be useful in infertility?

A

available via a pump to stimulate ovulation

    • lower risk of multiple pregnancy
    • easy to measure
117
Q

Describe the secretion of GnRH across life?

A

pulsatile

    • begins as fetus; diminishes after 1 year
    • greater amplitude and frequency in puberty
118
Q

Describe GnRH receptor

A

Gq GPCR

  • -increases Ca
    • stimulates release of FSH and LH
119
Q

Describe feedback inhibition of GnRH secretion.

A
    • hypothalamic inhibition by gonadal steroids (E/P/T)
    • AP inhibitions of LH/FSH by gonadal steroids

– T may act, by conversion to E

120
Q

What are causes of hyperprolactinemia?

A

relatively common

    • usually PRL-secreting adenomas
    • HT/pituitary disease
    • hypothyroidism (hi TRH)
    • DAr antagonists
121
Q

What are the effects of octreotide use?

A

decreases pituitary tumor size

inhibits TSH secretion

122
Q

What are the effects of GH use in adults?

A

– increased bone and muscle mass

does NOT slow aging or improve strength in the elderly

123
Q

Why don’t GH therapy patients continue treatment after puberty?

A

provocative tests show that GH secretion is gained as adults

124
Q

How does sermorelin acetate compare to somatropins?

A
  • less expensive
  • less effective
  • not effective in AP disease (adults)
125
Q

How is sermorelin acetate monitored?

A

GH levels

126
Q

How is protropin treatment monitored?

A

IGF-1 (response, and compliance)

stop treatment when bone epiphyses close

127
Q

What is the presumption when GH deficiency is found in adults vs. children?

A

adults: AP disease
children: HT defect

128
Q

What impact did rGH have on GH therapy?

A

increased utilization

– eliminated risk of Creutzfeldt-Jakob disease from cadaver pituitaries

129
Q

GH deficiency causes:

A

proportionate dwarfism

130
Q

What is achondroplasia?

A

normal body size, but shortened limbs

131
Q

What are signs/symptoms of proportionate dwarfism?

A

1) normal body proportions and intelligence
2) growth less than 2 in/year
- - may appear after 2-3 yo
3) younger face
4) chubby build
5) delayed or absent puberty

132
Q

Pituitary hormones regulate…

A

1) growth/development
2) metabolism
3) reproduction
4) stress response

133
Q

Name the 7 dwarfs:

A

1) Doc
2) Grumpy
3) Happy
4) Sleepy
5) Bashful
6) Sneezy
7) Dopey

PHS 933 (14 decks)

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