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KG - Pharmacology 2 > KG - Pharm 2 Exam 3, Sex Hormones > Flashcards

KG - Pharm 2 Exam 3, Sex Hormones Flashcards

1
Q

Which groups of sex hormones are needed for secondary sex characteristics & functions?
(how do you know HOW to treat with these drugs?)

A

steroids

  • multiple levels for tx
  • determined by WHAT is needed
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2
Q

how does GnRH work?

A
  • release is pulsatile for stimulating FSH & LH release

- tonic GnRH admin leads to suppressed gonadotropin release

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3
Q

which drugs are GnRH LONG ACTING AGONISTS?

A

Leuprolide

Goserelin

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4
Q

Action of Leuprolide & Goserelin?

A
  • CONTINUOUS ADMIN SUPPRESSES RELEASE OF LH & FSH (after initial surge)
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5
Q

When are leuprolide/Goserelin used?

A
  • IVF
  • steroid dependent CAs
  • endometriosis
  • precocious puberty (will stop pre-pubertal development)
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6
Q

which drugs are GnRH ANTAGONISTS?

A

Cetrorelix

Ganirelix

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7
Q

Action of Cetrorelix & Ganirelix?

A
  • suppress LH and FSH
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8
Q

When are Cetrorelix & Ganirelix used?

A
  • IVF
  • steroid dependent CAs
  • endometriosis
  • precocious puberty (will stop pre-pubertal development)
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9
Q

How are GnRH agonists different from antagonists?

A
  • 4-5 tx w/ ANTAGONISTS, 3 wks tx w/ AGONIST to suppress gonadotropins
  • no initial surge of gonadotropins w/ ANTAGONIST
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10
Q

Which class of drugs demonstrates challenges during the start of tx when the pt has metastatic prostate cancer? (And what do you add to the tx plan?)

A

GnRD AGONISTS

- ADD ANTIANDROGEN

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11
Q

Side effects long acting GnRH agonists/antagonists?

A
  • menopausal symptoms

- testicular atrophy

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12
Q

Which hormone drives folliculogenesis during the menstrual cycle?

A

FSH

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13
Q

Which hormone, in high levels, causes a POSITIVE FEEDBACK on LH release?

A

estrogen

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14
Q

stages of menstruation?

A
  1. follicular/proliferative phase
  2. ovulation
  3. luteal/secretory phase
  4. menstruation
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15
Q

describe follicular/proliferative stage of the menstrual cycle

A

FSH DRIVES FOLLICULOGENESIS

  • get increased estrogen
  • get endometrial development and thickening
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16
Q

describe ovulation stage of the menstrual cycle

A

high, sustained levels of estrogen cause POSITIVE FEEDBACK on LH release

  • LH surge
  • ovulation
  • luteinization
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17
Q

describe luteal/secretory phase of the menstrual cycle

A

LH maintains corpus luteum

- progesterone and estrogen = MAINTENANCE OF ENDOMETRIUM

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18
Q

which hormones MAINTAIN the ENDOMETRIUM?

A

progesterone, estrogen

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19
Q

describe menstruation stage of the menstrual cycle?

A

loss of LH –> loss of CL –> loss of P&E

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20
Q

effects of FSH in women?

A

develop ovarian follicles & supports estrogen synthesis

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21
Q

effects of FSH in men?

A

stimulates spermatogenesis

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22
Q

which drug contains both FSH & LH?

A

human menopausal gonadotropins (hMG)

aka menotropins

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23
Q

for what are hMGs used for?

A

for FSH PROPERTIES ONLY

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24
Q

for what is Urofollitropin (uFSH) used?

A

PURIFIED FSH

with only FSH

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25
Q

what does LH do?

A
  • stimulates ovulation
  • stimulates luteinization of follicles
  • steroid production
    (women = progesterone synthesis, men = testosterone synthesis)
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26
Q

for what is hCG used?

A

LH AGONIST, USED INSTEAD OF LH

- BINDS TO LH RECEPTOR

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27
Q

pharmacokinetics of hCG?

A

longer half life than LH

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28
Q

why use gonadotropins?

A
  • reverse infertility
    (men = INDUCE SPERMATOGENESIS, LH increases testosterone –> FSH induces spermatogenesis)
    (women = IVF, FSH stimulates ovaries & estrogen production, single dose of LH given to induce ovulation)
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29
Q

how are FSH and LH usually used?

A

IN SEQUENCE

  • FSH for 9-12 days until estradiol levels normal
  • then SINGLE DOSE hCG (LH) to induce ovulation
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30
Q

side effects gonadotropins?

A
  • uncomplicated ovarian enlargement
  • OVARIAN HYPERSTIMULATION SYNDROME (life threatening)
  • MULTIPLE BIRTHS - 20%
  • GYNECOMASTIA
  • HA, depression, edema, precocious puberty
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31
Q

contraindications gonadotropins?

A

sex steroid dependent cancers

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32
Q

which are the major endogenous estrogens?

A

ESTRADIOL
ESTRIOL
ESTRONE

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33
Q

mechanism - estrogens?

A

NUCLEAR RECEPTORS

- interact w/ DNA

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34
Q

metabolism - estrogens?

A
  • conjugated by liver (excreted in bile)

- ENTEROHEPATIC CIRCULATION (reverses conjugation, increases bioavailability)

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35
Q

estrogen function - ovary?

A

prepare for ovulation

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36
Q

estrogen function - uterus?

A

ENDOMETRIAL GROWTH

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37
Q

estrogen function - vaginal epithelium?

A

proliferation, maintenance

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38
Q

estrogen function - endocervical glands

A

mucous

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39
Q

estrogen function - breasts

A

growth - pregnancy & puberty

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40
Q

estrogen function - puberty

A
  • growth & maturation

- CLOSES EPIPHYSES

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41
Q

estrogen function - bone

A

MAINTENANCE

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42
Q

estrogen function - blood clotting

A
  • SYNTHESIS OF CLOTTING PROTEINS

- INCREASED PLATELET ADHESIVENESS

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43
Q

estrogen function - metabolic

A

Liver

  • clotting factors
  • HORMONE BINDING PROTEINS: SHBG, CBG, TBG

INCREASED HDL, DECREASED LDL

Na+, H2O retention

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44
Q

why are there synthetic oral forms of estrogens?

A

naturally occurring not orally active

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45
Q

what forms are EXOGENOUS ESTROGENS?

A

synthetic –> oral contraceptives
conjugated –> HRT
estradiol –> creams/patches

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46
Q

uses - exogenous estrogens?

A
  • ORAL CONTRACEPTIVES
  • postmenopausal HRT
  • STIMULATING PUBERTAL DEVELOPMENT in hypogonadic girls
  • decrease uterine bleeding
  • suppressing ovulation in dysmenorrhea
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47
Q

adverse effects - estrogens

A
  • endometrial hyperplasia
  • nausea
  • breast tenderness
  • MIGRAINES
  • gallbladder dz
  • HTN
  • THROMBOEMBOLISM, thrombophlebitis, incr platelet aggregation, ACCELERATED BLOOD CLOTTING
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48
Q

contraindications - estrogens

A
  • ESTROGEN DEPENDENT NEOPLASMS (ie: breast CA)
  • undiagnosed genital bleeding
  • uncontrolled HTN
  • liver dz
  • THROMBOEMBOLIC DISORDERS
  • smoking & > 35 yo
  • pregnancy
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49
Q

tamoxifen - MOA

A

selective estrogen receptor modulator (SERM)

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50
Q

when is Tamoxifen an agonist?

A

BONE - limits bone loss

UTERUS - may increase risk uterine CA

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51
Q

when is Tamoxifen an antagonist?

A

BREAST - used as PALLIATIVE & PROPHYLACTIC TX IN BREAST

CANCER - reduces risk of further breast cancer

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52
Q

why would you use Raloxifene instead of Tamoxifene?

A

prevention better for osteoporosis

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53
Q

why would you use Toremifene instead of Tamoxifene?

A

similar to Tamoxifene but it will probably increase HDL

54
Q

clomiphene - MOA

A

Selective estrogen receptor modulator (SERM)

- ANTAGONIZES NEGATIVE FEEDBACK OF ESTROGEN IN HYPOTHALAMUS

55
Q

clomiphene - “adverse” effect?

A

multiple pregnancies (5-10%)

56
Q

fulvestrant - MOA?

A

full estrogen receptor antagonist

57
Q

list of aromatase inhibitors?

A

anastrozole
letrozole
exemastane

58
Q

aromatase inhibitors - MOA

A

do not inhibit adrenal steroid synthesis

59
Q

which aromatase inhibitor is irreversible?

A

Exemastane

60
Q

aromatase inhibitors - indications?

A
  • DOC - BREAST CANCER TREATMENT IN POSTMENOPAUSAL WOMEN

- ADVANCED BREAST CANCER AFTER TAMOXIFEN FAILURE IN POSTMENOPAUSAL WOMEN

61
Q

aromatase inhibitors - adverse effects?

A
  • diarrhea
  • abd pain
  • n/v
  • hot flashes
  • joint pain
62
Q

aromatase inhibitors - contraindications?

A
  • premenopausal women

- PREGNANCY = CAT X

63
Q

how is progesterone made?

A
  • produced by CORPUS LUTEUM

- produced by fetal/placental unit in pregnant women

64
Q

progesterone - MOA

A

NUCLEAR RECEPTOR

- interact w/ DNA

65
Q

progesterone - physiological effects, uterus?

A

converts endometrium to SECRETORY STATE

  • MAINTAINS PREGNANCY
  • suppresses contractility during pregnancy
66
Q

progesterone - physiological effects, endocervical glands?

A

regulates cervical mucous

67
Q

progesterone - physiological effects, breasts?

A

lobuloalveolar development at the end of the mammary ducts during pregnancy and puberty

68
Q

progesterone - physiological effects - thermogenic action?

A

increases body temperature

69
Q

why are there synthetic forms of progesterone?

A

progesterone is not orally active, so different formulations

70
Q

classes of progesterones?

A 
19-nortestosterones (progestin + androgenic activity)
progesterone derivatives (varying levels androgen activity)
71
Q

progestins - uses?

A
  • CONTRACEPTION
  • prevent ENDOMETRIAL HYPERPLASIA in HRT
  • tx of other problems when estrogens are contraindicated
72
Q

progestins - side effects?

A
  • possibly increased BP
  • high doses may reduce plasma HDL levels
  • depression, drowsiness
73
Q

list antiprogestins?

A

Mifepristone

Danazol

74
Q

Mifepristone - MOA?

A
  • PROGESTERONE/GLUCORTICOID receptor antagonist
75
Q

mifepristone - uses?

A
  • TERMINATE PREGNANCY (w/ prostaglandins)

- prevent implantation

76
Q

mifepristone - side effects?

A
  • vomiting
  • diarrhea
  • abd or pelvic pain
  • vaginal bleeding
77
Q

danazol - MOA?

A

weak progestin/androgen that suppresses ovarian function

78
Q

danazol - uses?

A

used to TREAT ENDOMETRIOSIS

79
Q

danazol - side effects?

A
  • weight gain
  • edema
  • acne/oily skin
  • hirsutism
  • deepening voice
  • headache
  • flush
  • libido changes
  • cramps
80
Q

what is the most common contraception option?

A

combination pill - estrogen + progestin

99.9% effective

81
Q

which combo contraception pill MUST YOU KNOW?

A

Drospirenone/ethinyl estradiol

82
Q

oral contraceptives - MOA?

A
  • INHIBIT OVULATION - no LH surge
  • change cervical mucous (block sperm)
  • change endometrium (DECREASE IMPLANTATION)
  • progestin withdrawal initiates bleeding at end of cycle
83
Q

what estrogens are usu in combo oral contraceptives?

A

ethinyl estradiol or mestranol

84
Q

what progestins are usu in combo oral contraceptives?

A

levonorgestrel or norethindrone

85
Q

what is most important when combining estrogens and progestins in a combo pill?

A

E:P ratio - MINIMAL AMTS desired

86
Q

how do combo contraceptives work?

A

21 days

  • estrogen stays the same = incr progestin content at each stage
  • 1 stage = mono phasic
  • 2 stages = biphasic
  • 3 stages = triphasic
87
Q

combo oral contraceptives mimic normal hormonal cycle… why?

A

MINIMIZE SIDE EFFECTS

88
Q

how are new oral contraceptives different from other combo oral contraceptives?

A

new pills provide longer cycle times or no cycle at all

  • Seasonale = 84 on, 7 off
  • Seasonique = 84 on, 7 estrogen only
  • Lybrel = always on pill
89
Q

new combo oral contraceptives - adverse effects

A
  • increased breakthrough bleeding (esp during first year)

- hard to tell if you’re pregnant

90
Q

Ethinyl estradiol/Drospirenone combo oral contraceptive - MOA

A

mineralcorticoid antagonist

91
Q

Ethinyl estradiol/Drospirenone combo oral contraceptive - advantages?

A
  • LESS WATER RETENTION - FDA APPROVED FOR PMDD

- very little androgenic properties

92
Q

newest combo pill (Natazia) - MOA

A
  • takes advantage of estradiol valerate to produce E2 in vivo
  • BIOIDENTICAL HORMONES
  • uses dienogest as progestin, weird 4 cycle regimen
93
Q

NuvaRing - how does it work?

A

vaginal ring containing 3 week supply of etongesterel & ethinyl estradiol

94
Q

progestin only - mini pills?

A
  • 87-98% EFFECTIVE FOR BIRTH CONTROL

- used for ADOLESCENTS & BREAST FEEDING

95
Q

progestin only - depo-provera?

A

3 month depot injection of medroxyprogesterone

96
Q

progestin only - implanon?

A
  • single silastic tube implanted in arm

- > 99% effective - 3 yrs

97
Q

progestin only - Mirena?

A
  • IUC w/ levonorgesterel

- 99.9% effective - up to 5 years

98
Q

emergency contraception - Plan-B?

A
  • lenonorgesterel only pill

- taken w/in 72 hrs after intercourse (better sooner, available w/out prescription to age 18+)

99
Q

emergency contraception - preven?

A

similar to plan B, but w/ ethyinyl estradiol

100
Q

emergency contraception - mifepristone (RU-486)?

A

can also be used to prevent implantation if w/in 72 hrs after intercourse

101
Q

combo oral contraceptives - adverse effects (common)?

A

common

  • WEIGHT GAIN
  • NAUSEA
  • EDEMA
  • DEPRESSION

breakthrough bleeding (progestin alone or too little estrogen)

TRY DIFFERENT COMBOS!

102
Q

combo oral contraceptives - adverse effects (CV + less common)?

A

CV PROBLEMS

  • CLOTTING (women 35+, SMOKING)
  • MILD HTN
  • MIGRAINE
  • MI/STROKE

cholestatic juice/gallbladder dz

TERATOGENESIS

FERTILITY - can be suppressed 3+ months

103
Q

combo oral contraceptives - benefits?

A
  • EFFECTIVE CONTRACEPTION
  • reduced risk for OVARIAN & ENDOMETRIAL CANCER (50% reduction even after 2 yrs, protection lasts 15 years after stopping), ovarian cysts, benign breast dz, ectopic pregnancy, iron def, RA, PMS, etc)
  • CONSENSUS = SAVES 1000s OF LIVES, DZ EPISODES & HOSPITALIZATION EVERY YEAR
104
Q

combo oral contraceptives - absolute contraindications?

A
  • thrombophlebitis
  • THROMBOEMBOLIC PHENOMENA
  • CV disorders
  • ESTROGEN-DEPENDENT NEOPLASMS
  • pregnancy
105
Q

combo oral contraceptives - relative contraindications?

A
  • LIVER DISEASE
  • teens prior to epiphyseal closure
  • asthma, eczema
  • migraine, HTN
  • DM
  • optic neuritis, retrobulbar neuritis
  • seizure disorders
  • smoking & > 35 yo
106
Q

combo oral contraceptives - drug interactions?

A
  • P450 inducers reduce effectiveness (phenytoin, rifampin, carbamazepine)
  • ANTIBIOTICS REDUCE EFFECTIVENESS (stop enterohepatic circulation)
  • decrease effectiveness of anticoags, anticonvulsants, tricyclic antidepressants, guanethidine, oral hypoglycemics
107
Q

what happens in menopause (general)?

A

reduced ovarian response to gonadotropins

  • decreased ovarian steroids
  • increased gonadotropins
108
Q

menopause - VASOMOTOR problems?

A
  • HA
  • palpitations
  • night sweats
  • insomnia
  • HOT FLASHES
109
Q

menopause - GENITOURINARY problems?

A
  • vaginal dryness
  • atrophy
  • pain
  • loss of trophic effects of estrogen
110
Q

menopause - OSTEOPOROSIS problems?

A
  • decrease in bone mass = serious problem
    (50% spinal compression fractures by 75)
    (20% hip fractures by 90)
111
Q

menopause - HEART DZ problems?

A
  • increased cholesterol & LDL

- decreased HDL

112
Q

Who should consider HRT?

A
  • younger pts tend not to have as many side effects(w/in ten yrs)
  • HYSTERECTOMIES - ESTROGEN ONLY
  • girls w/out ovarian development
113
Q

How is Raloxifene different?

A
  • does not affect CHD
  • DOES prevent osteoporosis & breast cancer
  • NO effect on hot flashes
114
Q

what might reduce adverse effects of HRT?

A

different routes of administration

  • creams for urogenital tract
  • transdermal good for osteoporosis w/ less CHD effects
115
Q

HRT - adverse effects?

A
  • endometrial cancer (progestins reduce)
  • BREAST CANCER - SMALL RISK (1.25 fold)
  • -> 8 cases per 10,000 women/yr
  • gallbladder dz
  • CARDIOVASCULAR
116
Q

HRT - advantages?

A
  • menopausal symptoms
  • osteoporosis
  • heart dz
117
Q

HRT - concerns?

A
  • breast cancer

- strokes

118
Q

when do the concerns outweigh the risks of HRT?

A

> 10 yrs after menopause

119
Q

androgens - physiological effects

A

VIRILIZING

  • spermatogenesis
  • sexual devleopment

ANABOLIC

  • incr bone density
  • incr amino acid incorporation into muscle
  • incr RBC mass
  • antagonize catabolic effects of glucocorticoids

PUBERTY
- development of secondary sexual characteristics, males

120
Q

androgens - uses (male)

A

TESTICULAR DEFICIENCY

121
Q

androgens - uses (women)

A

FEMALE HYPOPITUITARISM

- estrogens and androgens

122
Q

androgens - uses (both sexes)

A
  • hypoproteinemia of NEPHROSIS

- NEGATIVE NITROGEN BALANCE PATIENTS (ie: burn patients)

123
Q

androgens - side effects (men)

A
  • DECREASED SPERMATOGENESIS

- may exacerbate prostate cancer

124
Q

androgens - side effects (women)

A
  • MASCULINIZATION

- PSEUDOHERMAPHRODITISM of fetus in pregnant women

125
Q

androgens - side effects (both sexes)

A
  • baldness
  • fluid retention, edema
  • OILY SKIN (ACNE)
  • DECREASED HDL, increased LDL
  • PSYCHOLOGICAL CHANGES
126
Q

list androgen receptor antagonists

A
  • flutamide

- spironolactone

127
Q

flutamide - info

A
  • USED IN PROSTATE CANCER w/ LONG ACTING GnRH AGONIST

- hepatotoxic (reversible)

128
Q

spironolactone - info

A
  • mineralcorticoid antagonist
  • high doses anti androgen
  • uses = HIRSUTISM & PMS in women, PRECOCIOUS PUBERTY
129
Q

list 5 alpha reductase inhibitors

A

finasteride

dutasteride

130
Q

5 alpha reductase inhibitors - MOA

A
  • INHIBITS 5 alpha reductase (no DHT)

- suppresses male sex accessory organs w/out affecting libido

131
Q

5 alpha reductase inhibitors - uses

A
  • BENIGN PROSTATIC HYPERPLASIA

- MALE PATTERN BALDNESS

132
Q

5 alpha reductase inhibitors - warnings

A
  • teratogenic (even handling crushed pills!

KG - Pharmacology 2 (10 decks)

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