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Pharmacology > Estrogens-Progestins > Flashcards

Estrogens-Progestins Flashcards

1
Q

Describe the therapeutic and adverse effects of Tamoxifen

A

Therapeutic:

  1. Decrease breast CA growth
  2. decrease bone osteoclasts/bone reabsorption (TR)

*neutral= urogenital fxn

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2
Q

Describe the therapeutic and adverse effects of Raloxifene

A

Therapeutic:

  1. Decrease breast CA growth
  2. ++ decrease bone osteoclasts/bone reabsorption (R>T)
  3. decrease lipids
  4. decrease LH-FSH

Adverse Rxns:

    • endometrium CA growth
    • no vasomotor fxn
    • increase clotting factors (T>R)

*neutral= endometrium CA growth and urogenital fxn

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3
Q

What are the physiologic Effects of Estrogen ( and what ones have adverse or beneficial effects in pharmacotherapy)

A
  1. Breast growth — CA
  2. Endometrium growth– CA
  3. Increased clotting factors in liver
  4. LH-FSH release decrease
  5. Vasomotor fxn
  6. Decrease LDL, increase HDL
  7. Urogenital fxn
  8. Bone OC decrease
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4
Q

Examples of GnRH Agonists and GnRh antagonists

A

GnRH Agonists: Leuprolide [Lupron]

GnRH Antagonists: Degarelix [Firmagon]

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5
Q

What is the fxn of FSH

A
  1. Follicular development
  2. Gametogenesis
  3. Spermatogenesis
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6
Q

What is the fxn of LH

A
  1. Follicular development

2. Testosterone production in leydig cells (in concert w/ FSH)

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7
Q

What are clinical uses of FSH and LH

A
  1. Pit.-hypothalamic hypogonadism w/ infertility

(FSH + LH (hCG) sequentially in F or concomitantly in M

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8
Q

SE of FSH/LH

A
  1. Ovarian enlargement
  2. Multiple births
  3. Gynecomastia
  4. Spontaneous abortion
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9
Q

Describe the mechanism of estrogen-SERM action

A

*Majority of estrogen AGONIST (estradiol) actions are mediated by binding to ERa or ERBeta

  1. Diffuse through membrane
  2. enter nucleus and bind to an ER (alpha or beta)
  3. conformational change and Receptor dimerization
  4. Recruit co-activators
  5. initiate transcription/ mRNA synthesis

*ANTAGONISTS (tamoxifen and raloxifene) recruit co-repressors and reduce transcription

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10
Q

___ undergo extensive enterophepatic recirculation, thus when given orally there will be _______

A

Estrogen

  • Increased hepatic effects
  • 1st pass + enterohepatic recirculation!
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11
Q

What are examples of SERMs

A

Antagonists: Tamoxifen and raloxifene

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12
Q

What are non-hormonal treatments for menopause

A
  1. SSRI/SNRI
  2. Gabapentine
  3. Clonidine
  4. Vitamin E
  5. Phytoestrogen in soy
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13
Q

What are Clinical uses of Estrogen

A

MHT (symptomatic and prophylaxis)

Symptomatic:

  1. Hot flashes- need systemic
  2. Postcoital bleeding-topical
  3. Vaginal atrophy/itching
  4. Reduced endometrial risk w/ progrestin (Medroxyprogesterone)

Prophylaxis:
5. osteoporosis (Raloxifene)

***NOT approved for proph. CV dz)

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14
Q 
A 70-year-old woman is being treated with raloxifene for osteoporosis. Which of the following is a concern with this therapy? 
A.  Breast cancer 
B.  Endometrial cancer 
C.  Hot flashes 
D.  Venous thrombosis 
E.  Hypercholesterolemia
A

C.  Hot flashes

D.  Venous thrombosis

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15
Q

SE of estrogen

A
  1. Postmenopausal bleeding
  2. HTN
  3. Endometrial and breast CA
  4. N/V/D/A
  5. Gallstones
  6. Clots
  7. Breast tenderness
  8. Migraines
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16
Q

A 53 year-old woman has severe vasomotor symptoms (hot flushes) associated with menopause. She has no pertinent past medical or surgical history. Which of the following would be most appropriate for her symptoms?
A.  Conjugated estrogens vaginal cream
B.  Estradiol transdermal patch
C.  Oral estradiol and medroxyprogesterone
D.  Injectable medroxyprogesterone acetate
E.  Oral tamoxifen

A

C.  Oral estradiol and medroxyprogesterone

*Some clinicians prefer micronized progesterone** due to lower CHD risk

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17
Q

Contraindications to MHT

A
  1. Active thrombosis
  2. Active liver dz
  3. Hx of breast CA
  4. Hx of endometrial CA
  5. Vaginal bleeding
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18
Q

Precursor to estrogens, androgens and adrenocorticoids

A

Progestin

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19
Q

When does progesterone get released

A

large increase in secretion in the luteal phase

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20
Q

What are the physiological effects of progestin

A
  1. Fat deposition via LPL stimulation
  2. Liver glycogen storage
  3. Insulin levels and response increase
  4. Compensatory aldosterone secretion
  5. Ketogenesis
  6. Anti-estrogen action on endometrial proliferation
  7. Body temp increase (1F)
  8. Increase ventilatory response to COs
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21
Q

What are synthetic progestins

A
  1. Medroxyprogesterone– derivative
  2. Norethindrone (1st gen.)
  3. Desogestrel (3rd gen. )
  4. Drospirenone (4th gen.– spironolactone analog)
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22
Q

Describe the use and risks of Norethindrone

A
  1. 1st gen.
  2. Lower P activity than 2nd gen.
  3. OCP use*
    * increased risk of unscheduled spotting/bleeding
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23
Q

Describe the use and risks of Desogestrel

A
  1. 3rd gen.
  2. Lower androgenic activity
  3. OCP**
  4. Acne**

*increased risk of VTE

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24
Q

Describe the use and risks of Drospirenone

A
  1. 4th gen.
  2. spironolactone analog–> anti-MC and anti-androgenic activity
  3. OCP

*highest increase risk of VTE

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25
Q

Clinical uses of Progestin

A
  1. Contraception (oral and implant)
  2. OSA (medroxyprogesterone)
  3. MHT WITH estrogen
  4. Endometriosis bleeding
  5. Hirsutism
  6. AIDS w/ anorexia/wt. loss
  7. Dysmenorrhea (NSAIDs preferred)
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26
Q

Adverse reactions of Progestins

A 
Breast enlargement
Breast tenderness
HTN
HA
Depression
Edema
Wt. gain
Sleepy
Nausea
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27
Q

A young woman complains of abdominal pain at the time of menstruation. Careful evaluation indicates the presence of significant endometrial deposits on the pelvic peritoneum. Which of the following would be the most appropriate medical therapy for this patient?
A.  Bicalutamide orally
B.  Medroxyprogesterone acetate by intramuscular injection
C.  Norgestrel as an IUD
D.  Oxandrolone by intramuscular injection
E.  Raloxifene orally

A

B.  Medroxyprogesterone acetate by intramuscular injection

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28
Q

Describe the mortality related to OCs

A

reduced in women less than 35 who do not smoke

*increased 2-4 fold in those over 35 who smoke– largely due to cerebrovascular dz

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29
Q

Describe the MOA of HC

A

Inhibition of ovulation via:

  1. Suppression of FSH and follicular development (estrogen)
  2. prevention of ovulatory LH surge (progestin)
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30
Q

____ results in decreased likelihood of implantation

A

estrogen + progestin

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31
Q

__ component of HC contributes to prompt, brief, withdrawal bleeding

A

Progestin

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32
Q

Progestin alone decreases the frequency of ___, but has less reliable ___

A

hypothalamic GnRH pulses

LH suppression

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33
Q

Describe the Combined OC actions on the menstrual cycle

A
  1. Progestin inhibits GnRH pulse generator (lowers FSH/LH release)– but less reliable LH suppression
  2. Progestin has anti-proliferative effects on endometrium and cervix
  3. Estrogen blocks ovulation by preventing the LH surge

*stay in follicular stage NOT luteal phase

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34
Q

what estrogen is commonly used in Combined OC

A

ethinyl estradiol (there are HD and LD formulations)

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35
Q

What progestins are commonly used in combined OC

A
  1. Norethindrone (1st gen)
  2. Levonrgesterl (2nd gen.)
  3. Desogestrel (3rd gen.)
  4. Drospirenone (4th gen.)
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36
Q

Describe the risk of VTE with different progestins

A

Drospirenone (4th)> Desogestrel (3rd)> > Levonorgestrel (2nd)

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37
Q

Describe the different extended COC formulations and indications

A
  1. Seasonale (84/7)
  2. Amethyst (no pill-free interval)

May improve problems w/:

  1. menorrhagia
  2. anemia
  3. endometriosis
  4. dysmenorrhea
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38
Q

Mild-moderate Sx of COC due to Estrogen excess

A
  1. Nausea
  2. Edema
  3. Breast tenderness
  4. Cholasma (brown pigmentation on face)
  5. HTN
  6. Migraines
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39
Q

Mild-moderate Sx of COC due to Estrogen and progestin deficiency

A
  1. Early/mid-cycle breakthrough bleeding/spotting

2. Hypomenorrhea

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40
Q

Mild-moderate Sx of COC due to Progestin excess

A
  1. Weight gain
  2. Adverse lipid changes
  3. Fatigue
  4. Hair growth
  5. Depression
41
Q

Severe adverse reactions of COC

A
  1. Depression
  2. Thromboemoblic events (VTE, MI, cerebrovascular dz)
  3. Cervical CA w/ >5yr LT w/ persistent HPV (DECREASED RISK OF ENDOMETIRAL, OVARIAN, and COLORECTAL CA)
  4. Breast CA
  5. Cholestatic Jaundice (increased cholesterol content in bile)
42
Q 
A 26-year-old female is using injectable medroxyprogesterone acetate as a method of contraception. An adverse effect of concern with long-term use of this therapy is: 
A.  Hyperkalemia 
B.  Male pattern baldness 
C.  Osteoporosis 
D.  Weight loss 
E.  Weight gain
A

C.  Osteoporosis
E.  Weight gain

IM progesterin

43
Q

What are contraindications of COC

A
  1. Smokers >35
  2. Uncontrolled HTN
  3. Migraines w/ aura
  4. DM w/ end organ damage
  5. HX breast CA or VTE
  6. Hx of liver dz
  7. Incomplete epiphyseal closure in adolescents
44
Q 
Which of the following would be the most appropriate oral contraceptive for a patient with moderate acne? 
A.  Ethinyl estradiol - levonorgestrel 
B.  Ethinyl estradiol - norethindrone 
C.  Ethinyl estradiol - desogestrel 
D.  Medroxyprogesterone 
E.  Ulipristal
A

C.  Ethinyl estradiol - desogestrel –> Lower androgenic activity

*Ethinyl estradiol

45
Q

What drugs can interfere w/ COC

A

drugs that induce or enhance estrogen metabolism!

  1. Rifampin (NOT rifabutin)
  2. Carbamazepine
  3. Phenobarbital
  4. griseofulvin (anti-fungal)

*It is now thought that oral antibiotics DO NOT decrease the effectiveness of oral contraceptives via effect on intestinal flora

46
Q

When meds can be used for postcoital contraception

A
  1. Levonorgestrel (plan B)

2. Ulipristal (Ella)

47
Q

Describe the MOA of emergency postcoital contraception Plan B

A

alterned oviduct motility or endometrial changes

*give 1 or 2 doses 12 hrs apart w/in 72 hrs of unprotected sex–> best if w/in 24hrs

48
Q

Describe the MOA of emergency postcoital contraception Ulipristal (Ella)

A
  1. Selective progesterone receptor modulator that delays follicular rupture if taken before ovulation
  2. may also cause endometrial changes that affect implantation
49
Q

Adverse effects of IM contraception

A

**like progestin only

  1. Irregular/unpredictable bleeding
  2. wt gain
  3. osteoporosis
50
Q

Adverse effects w/ COC

A
  1. VTE
  2. MI and stroke in older 35 who smoke
  3. nausea
  4. HA
  5. Problems w/ BF
51
Q 
A 50-year-old woman with a positive mammogram undergoes lumpectomy and a small carcinoma is removed. Biochemical analysis of the cancer reveals the presence of estrogen and progesterone receptors. After this procedure she will probably receive which of the following drugs? 
A.  Bicalutamide 
B.  Clomiphene
C.  Leuprolide 
D.  Mifepristone 
E.  Tamoxifen 
F.   Testosterone enanthate
A

E.  Tamoxifen

52
Q

Describe the clinical use of Mifepristone

A

pharmacotherapeutic abortionof up to 9 weeks duration

-dose followed in 48hr by PGE Misoprostol (PO) for synergistic effect on endometrium

53
Q

Adverse Effects of Mifepristone

A 
Prolonged bleeding
Abdominal pain 90%
N/V/D
Continued pregnancy
Incomplete abortion
54
Q

What are the clinical uses of Tamoxifen

A
  1. TREAT* and prevent (T>R) breast CA
    * in ER+ breast CA can reduce recurrence, death, and metastatic dz
  2. protection against postmenopausal bone loss (less than w/ estrogen tho)
  3. Reduce hot flashes
55
Q

What are the clinical uses of Raloxifen

A
  1. Prevent breast CA (T>R)
  2. Postmenopausal bone loss** (less than w/ estrogen tho)
  3. Reduce hot flashes
56
Q

Uses of medroxyprogesterone

A
  1. OCP (w/ endometrial sx)
  2. OSA
  3. Endometrial risks/deposits
57
Q

What is the MOA of Mifepristone

A
  1. competitive antagonist of progesterone receptor that cause decidual breakdown and detachment of blastocyst
  2. blocks GC receptor

*luteolytic effect

58
Q

What is the clinical use of misoprostol

A
  1. Used 48hrs after Mifepristone induced medical abortion for synergistic effects on the endometrium
  2. Cervical effacement (in testing topically)
  3. Induction of labor via inducing uterine contraction
59
Q

Describe the MOA of misoprostol

A

PGE analog

  • cervical effacement
  • Oxytocic agent
60
Q

What are abortifacient agents

A
  1. Mifepristone (Mifeprex)
  2. misoprostol (Cytotec)
  3. Methotrexate
61
Q

What are cervical effacement and Oxytotic agents

A

PGEs (dinoprostone- PGE2, misoprostol-PGE1)

*CONTRACT`

62
Q

What are Tocolytic agents

A
  1. NSAIDs (indomethacin)
  2. CCBs (nifedipine)
  3. B2 agonists (terbutaline)
  4. Magnesium sulfate
  5. calcium channel?

*RELAX

63
Q

MOA and use of Letrozole

A

Aromatase inhibitor (prevents conversion of testosterone to estrogen)

*adjuvant therapy for tx in ER+ breast CA

64
Q

define labor

A

regular, rhythmic, forceful contractions of the uterine smooth muscle

65
Q

Cervical dilation is dependent upon ___

A

prostaglandins

66
Q

What drugs delay the onset of labor and prolong gestation?

A
  • *PGE synthesis inhibitors
    1. NSAIDs (ASA, ibuprofen, naproxen)
    2. Cox-2 selective inhibitors (celecoxib)
67
Q

Describe the stages of labor

A
  1. Cervical Effacement and dilation
  2. Descent of the presenting part and delivery of the fetus
  3. Separation and delivery of the placenta
68
Q

Cervical effacement is inhibited by ____ and stimulated by __ and __

A

progesterone

descent of the fetal head and PG synthesis

*Targets of Stage I of labor

69
Q

Uterine contractions are stimulated by ___ via ___

A

PGs and oxytocin

Ca++ movement thru L-Type Ca++ channels

*Target of Stage II of labor

70
Q

Uterine smooth muscle also expresses __ receptors that mediate ___

A

β2-adrenergic

relaxation

*Target of Stage II of labor

71
Q

___ promotes hemostasis via contraction of uterine smooth muscle in stage III of pregnancy

A

Oxytocin

72
Q

What do oxytocic and tocolytic agents do?

A

Oxytocic–> contract

Tocolytic—> relax

73
Q

What drugs are used to induce labor

A

*oxytocic–> contract

  1. PGE (dinoprostone gel, mosprostol)
  2. Oxytocin
74
Q

Describe the clinical uses of dinoprostone

A
  1. stimulates cervical effacement/ripening (when applied vaginally)
  2. induce pregnancy

**applied topically

75
Q

Adverse reactions of dinoprestone

A
  1. Intestinal cramping
  2. diarrhea
  3. nausea

*When administered systemically ONLY

76
Q

Adverse reactions of Misoprostol

A

**fewer systemic SE than dinoprestone

77
Q

Uses of Oxytocin (Pitocin)

A
  1. uterine contractions– MC used for labor induction after cervical ripening
  2. Postpartum hemorrhage
78
Q

SE of oxytocin

A
  1. Water intoxication w/ HD (similar to ADH)
  2. Coma
  3. Convulsion
  4. Death
  5. Uterine rupture
  6. Impaired fetal oxygenation
79
Q

Which one of the following is characteristic of oxytocin?
A.  Readily crosses the placenta where it can cause harmful side effects in the fetus
B.  Drug of choice for cervical ripening
C.  Drug of choice for induction of labor
D.  Plasma half-life of minutes
E.  Uterine sensitivity is greater to oxytocin than to PGs in early pregnancy
F.   The drug cannot be given orally

A

C.  Drug of choice for induction of labor
D.  Plasma half-life of minutes
F.   The drug cannot be given orally

80
Q

A 30-year-old woman presents to the ED with severe abdominal cramping and moderate to severe uterine bleeding following a spontaneous abortion. After oxytocin fails to control bleeding ergot alkaloids are administered. Which of the following is correct concerning the use of ergot alkaloids in this patient?
A.  Oral administration of a large dose of ergonovine is the fastest and most efficacious means for providing immediate relief
B.  Ergot alkaloids are used to treat oxytocin toxicity
C.  Ergot alkaloids in conjunction with magnesium sulfate may have effectively saved the pregnancy
D.  Large doses of ergot alkaloids act to reduce bleeding by causing sustained contraction of the uterus
E.  Prostaglandins are more effective than ergot alkaloids for management of severe uterine bleeding

A

D.  Large doses of ergot alkaloids act to reduce bleeding by causing sustained contraction of the uterus

81
Q

A pregnant woman presents at term for induction of labor. The best pharmacological approach would be:
A. Administration of PGE2 vaginal gel until the woman is in active labor
B. Administration of PGE2 vaginal gel with concurrent administration of IV oxytocin through an infusion pump
C. Administration of oxytocin IM
D. Administration of PGE2 vaginal gel until the cervix has ripen followed in 6 hrs by administration of IV oxytocin through an infusion pump if active labor has not occurred
E. IV administration of egonovine

A

D. Administration of PGE2 vaginal gel until the cervix has ripen followed in 6 hrs by administration of IV oxytocin through an infusion pump if active labor has not occurred

82
Q

What drugs are used to inhibit labor

A

*tocolytic agents–> relax uterus

  1. PGE inhibitors (NSAIDS/indomethasine)
  2. CCB (Nifedipine)
  3. B2 adrenergic agonist (Terbutaline)
  4. Magnesium sulfate
83
Q

What drugs is 1st line therapy at 32-34 weeks to prolong gestation?

A

CCB- Nifedipine (PO)

84
Q

What drugs is 1st line therapy at 24-32 weeks to prolong gestation?

A

Indomethacin (NSAID) )PO or IV)

85
Q

What are adverse effects of Indomethacin

A
  1. Closure of the ductus arteriosus in utero can lead to PHTN postnatally
    * safest to to use acetaminophen during pregancy
86
Q

Complication of nifedipine

A

fall in moms BP may have neg effect on blood flow btwn uterus and placenta

*fewer SE than B-agonists and magnesium

87
Q

Clinical uses of B2 andrenergic agonists

A
  1. suppress contractions
  2. tx premature labor
    * *less effective if the cervix has dilated and membranes have ruptured (no not affect local production of PGs)
88
Q

Adverse Reactions of Terbutaline

A
  1. Tachycardia/palps
  2. Jitteriness
  3. HypoK
  4. HyperGlycemia
  5. Hypotension
  6. Pulmonary edema
  7. BLACK BOX WARNING: cannot use for prevention or for tx beyond 48-72 hrs–> potenital for serous maternal heart problems or death
89
Q

Which one of the following is characteristic of the use of beta-2 agonists for promoting uterine relaxation?
A.  No risk of cardiovascular side effects
B.  Inhibition of COX-1 and COX-2
C.  Loss of effectiveness caused by tachyphylaxis
D.  More commonly used for primary dysmenorrhea
E.  A risk of maternal hyperglycemia
F.   A risk of fetal hypoglycemia

A

C.  Loss of effectiveness caused by tachyphylaxis
E.  A risk of maternal hyperglycemia
F.   A risk of fetal hypoglycemia

90
Q

MgSO4 generally sedating, depresses smooth muscle contractions by __-

A

antagonizing Ca2+ actions

91
Q

Clinical uses of MgO4

A
  1. Pre-eclampsia
  2. Eclampsia
  3. NO evidence to show preventing preterm birth–> but rather increase in total pediatric mortality
92
Q

Adverse reactions of MgSO4

A

rare but life-threatening

  1. pulmonary edema
  2. hypotension
  3. muscle paralysis
  4. respiratory arrest
93
Q

MIfepristone’s anti-progesterone actions also lead to ___ and a ___

A

increased uterine PGE level

prostaglandin-sensitized myometrium

94
Q

A drug or drug class that will cause uterine contractions and deliver the products of conception following interruption of an established pregnancy (< 7 weeks gestation) with mifepristone is (are):
A.  Oxytocin
B.  Beta-2 agonists (e.g., terbutaline)
C.  Calcium channel blockers (e.g., nifedipine)
D.  Prostaglandin analogs (e.g., misoprostol)
E.  Cyclooxygenase inhibitors (e.g., indomethacin)

A

D.  Prostaglandin analogs (e.g., misoprostol)

95
Q

Describe the MOA of methotrexate

A

folic acid antagonist that disrupts rapidly growing tissue, espically trophoblasts

96
Q

Clinical use of methotrexate

A

NOT FDA approved but sometimes used as medical abortifacient

*given as single IM followed in 7 days by vaginal misoprostoal can terminate pregnancy at 8 weeks or less

97
Q

Adverse effects of Methotrexate

A
  1. incomplete abortion

2. Systemic toxicity (dose-dependent)

98
Q

Uses of HD ethinyl estradiol vs low dose ethinyl estradiol

A

HD: pharmacologic suppression of Ovulation
LD: physiologic replacement to prevent hypoestrogenic menopausal sx

Pharmacology (31 decks)

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