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Reproductive II - Exam 1 > Female Gonadal Hormones and Inhibitors (Linger DSA) - SRS > Flashcards

Female Gonadal Hormones and Inhibitors (Linger DSA) - SRS Flashcards

1
Q

What are the drug categories we need to know from this assignment? 9

A
  1. Menotropins (human menopausal gonadotropins, or hMG)
  2. Follicle stimulating hormone
  3. Leuteinizing hormone
  4. Human choriogonadotropin hormone
  5. Gonadotropin-releasing hormone analogs
  6. Gonadotropin-releasing hormone antagonists
  7. Estrogens
  8. Progestins
  9. Estrogen and progesterone inhibitors and antagonists
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2
Q

What are the three follicle stimulating hormones?

A
  1. Follitropin alfa (rFSH alfa)
  2. Follitropin beta (rFSH beta)
  3. Urofollitropin (uFSH)

Follitropins

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3
Q

What is the leutenizing hormone drug?

A

Lutropin alfa

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4
Q

What are the gonadotropin-releasing hormone analogs?

A
  1. Leuprolide (prototype)
  2. Goserelin
  3. Histrelin
  4. Nafarelin
  5. Triptorelin
  6. Gonadorelin (synthetic human GnRH)

mostly “relins”

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5
Q

What are the gonadotropin-releasing hormone antagonists?

A
  1. Cetrorelix
  2. Degarelix
  3. Ganirelix

“relix”

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6
Q

What are the four estrogens covered here?

A
  1. Conjugated estrogens (Premarin)
  2. Estradiol valerate
  3. Ethinyl estradiol
  4. Mestranol
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7
Q

What are the progestins?

A
  1. Desogestrel (inactive prodrug) and Etonogestrel (active metabolite)
  2. Drospinenone
  3. Medroxyprogesterone
  4. Norethindrone
  5. Norgestimate
  6. Norgestrel (L-norgestrel, levonorgestrel)
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8
Q

What are the estrogen and progesterone antagonists and inhibitors?

A
  1. Mifepristone
  2. Selective estrogen receptor modulators
    1. Raloxifene
    2. Tamoxifen
    3. Toremifene
  3. Selective estrogen receptor downregulators
    1. Clomiphene
    2. Fulvestrant
  4. Aromatase inhibitors
    1. Anastrazole
    2. Exemestane
    3. Letrozole
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9
Q

What are the SERMs this time around? 3

A
  1. Raloxifene
  2. Tamoxifen
  3. Toremifene
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10
Q

What are the SERDs (selective estrogen receptor downregulators)? 2

A
  1. Clomiphene
  2. Fulvestrant
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11
Q

What are the aromatase inhibitors we covered? 3

A
  1. Anastrazole
  2. Exemestane
  3. Letrozole
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12
Q

Menotropins (human menopausal gonadotropins, or hMG) are Purified FSH and LH extracted from the urine of postmenopausal women combined with an FSH like substance and an LH like substance. (Assuming I’m interpreting this from the DSA correctly, which may be a big if)/ What are the clinical uses for this?

3

A
  1. Used in conjunction with hCG to induce ovulation and pregnancy in infertile females experiencing anovulation not caused by primary ovarian failure
  2. Stimulation of multiple follicle development in ovulatory patients as part of an ART
  3. Unlabeled: Stimulation of spermatogenesis in hypogonadotropic hypogonadism
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13
Q

What is urofollitropin?

A

is purified human FSH extracted from the urine of postmenopausal women (no LH activity)

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14
Q

What are follitropin alfa and follitropin beta?

A

Recombinant FSH (rFSH), with AA sequences identical to human FSH

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15
Q

rFSH preparations have a shorter half-life but stimulate estrogen secretion equal to or greater than uFSH. Why might we prefer to use uFSH?

A

rFSH is very costly

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16
Q

rFSH and uFSH are used to stimulate ovulation in what 2 types of patients?

Which type is preferred for each?

A
  1. in patients who previously received pituitary suppression (uFSH)
  2. patients in whom the cause of infertility is functional and not caused by primary ovarian failure (rFSH alfa and beta)
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17
Q

What are two additional clinical uses of FSH drugs?

Which ones are useful for each?

A
  1. Spermatogenesis induction in men with hypogonadotropic hypogonadism in whom the cause of infertility is not due to primary testicular failure (rFSH alfa and beta)
  2. Development of multiple follicles with ART (uFSH, rFSH alfa and beta)
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18
Q

What is lutropin alfa?

What is its only use?

A

Recombinant form of human LH

  1. Only used in combination with rFSH alfa for stimulation of follicular development in infertile women with profound LH deficiency
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19
Q

What are the two types of hCG we use clinically?

A
  1. extracted and purified from the urine of pregnant females
  2. Choriogonadotropin alfa (rhCG) is a recombinant form of hCG
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20
Q

What is extracted hCG used standalone for?

What about in combination with rFSH?

A
  • Standalone: to induce ovulation and pregnancy in anovulatory, infertile females
  • With rFSH: treatment of hypogonadotropic hypogonadism, spermatogenesis induction with rFSH
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21
Q

In what female patients is rhCG used and for what purpose? 2

A
  1. induces ovulation in infertile females who have been pretreated with follicle stimulating hormones
  2. induces ovulation and pregnancy in infertile females when the cause of infertility is functional
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22
Q

What are the adverse effects of hCG?

A
  1. Multiple pregnancies (15 - 20% increase in ART patients)
  2. uncomplicated ovarian enlargement
  3. Ovarian hyperstimulation syndrome
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23
Q

hCG has the risk of inducing multiple pregnancies, apart from the unexpected burden of two children, why else might this be bad? 3

A

Increased risk of…

  1. Gestational Diabetes
  2. Preeclampsia
  3. preterm labor
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24
Q

As we established, hCG puts patients at risk for multiple pregnancies, overstimulation and enlargement of the ovary that spontaneously resolves, and ovarian hyperstimulation syndrome, which occurs in 0.5 - 4% of patients.

What is this last ADR characterized by? 5

A
  1. Ovarian enlargement
  2. ascites
  3. hydrothorax
  4. hypovolemia
  5. shock
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25
Q

What are the GONADOTROPIN-RELEASING HORMONE analogues?

A
  1. Leuprolide (prototype)
  2. goserelin
  3. histrelin
  4. nafarelin
  5. triptorelin
  6. gonadorelin
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26
Q

Using a GnRH analogue produces the following results…

During the first 7-10 days of administration, an agonist effect results in increased concentrations of gonadal hormones (referred to as a flare)

After the first 7-10 days, the continued presence of GnRH (or analog) results in an inhibitory action that manifests as a drop in the concentration of gonadotropins and gonadal steroids.

Explain this second part.

A

This is d/t receptor down-regulation and changes in the signaling pathways activated by GnRH.

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27
Q

What are two clinical uses of Leuprolide and friends? Which is more commonly employed?

A
  1. Clinical situations where stimulation of gonadotropin production is useful
  2. Clinical situations where suppression of gonadotropin production is useful (more commonly used here)
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28
Q

So what are two examples of clinical situations where Leuprolide is used to stimulate gonadotropin production?

A
  1. Female and male infertility (usually tx’d with more convenient and less costly gonadotropins)
  2. Diagnosis of LH responsiveness (determines whether delayed puberty in a hypogonadotropic adolescent is due to constitutional delay or to hypogonadotropic hypogonadism)
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29
Q

What are five clinical situations where Leuprolide and friends are used to suppress gonadotropin production?

A
  1. Controlled ovarian hyperstimulation (e.g., to prevent premature ovulation by endogenous LH in IVF patients)
  2. Endometriosis
  3. Uterine leiomyomata (benign, estrogen-sensitive uterine fibroids); treatment may reduce size
  4. Prostate cancer (often combined with androgen receptor antagonist; this strategy is as effective as surgical castration in reducing serum testosterone concentrations and effects)
  5. Central precocious puberty
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30
Q

What are some ADRs/toxicities of the Leuprolide type drugs in females? (lots, try to get the big ones)

A
  1. Continuous treatment of women with a GnRH analog causes the typical symptoms of menopause, which include hot flushes, sweats, and headaches
  2. Additional adverse effects include depression, diminished libido, generalized pain, vaginal dryness, and breast atrophy; decreased bone density and osteoporosis may occur with long-term use
  3. Ovarian cysts may develop during the first 2 months of treatment; discontinue therapy if cysts do not resolve after an additional 6 weeks
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31
Q

What are two contraindications to the use of Leuprolide and CO?

A

Breast feeding

pregnancy

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32
Q

What are some ADRs of Leuprolide in men? up to 8

A
  1. Continuous GnRH agonist administration in men cause hot flushes, sweats, edema, gynecomastia, decreased libido, decreased hematocrit, reduced bone density, and asthenia
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33
Q

What is the MOA of Ganirelix and cetrorelix?

A
  1. GnRH RECEPTOR ANTAGONISTS
    1. MOA: synthetic competitive antagonists of GnRH receptors - inhibit the secretion of FSH and LH in a dose-dependent manner
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34
Q

GnRH RECEPTOR ANTAGONISTS are used to suppress gonadotropin production, what are Ganirelix and cetrorelix used for?

A

Suppress LH surge during controlled ovarian hyperstimulation

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35
Q

What is Degarelix used for? Why?

A

Treatment of advanced prostate cancer by reducing gonadotropin and androgen concentrations at a much faster rate than GnRH agonists, and avoid the initial testosterone surge.

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36
Q

Short term use of GnRH receptor antagonists is generally well tolerated, but ADRs have occurred. What are they? 2

A
  1. Hypersensitivity reactions, including anaphylaxis, have been noted
  2. Adverse effects of long-term use for prostate cancer are similar to GnRH agonists
37
Q

What are the two types of estrogen drugs we use?

A

Natural Estrogens

Synthetic estrogens

38
Q

Where do we obtain natural estrogens from?

A
  1. sulfoconjugated equine estrogens derived from the pregnant mare (Premarin)
  2. esterified estrogens derived from plant sources (e.g., soybeans, chick peas, alfalfa sprouts, peanuts)
39
Q

Synthetic estrogens may be steroidal (share similar structure as estradiol) or nonsteroidal (do not possess the 4-ring cholesterol backbone but bind to the estrogen receptor). What are three examples of steroidal synthetic estrogens?

A
  1. Mestranol
  2. Estradiol valerate
  3. ethinyl estradiol
40
Q

What are two examples of nonsteroidal synthetic estrogens?

A
  1. chlorotrianisene
  2. methallenestril

(Get the impression these are low yield)

41
Q

Which, steroidal or nonsteroidal estrogens are most common in combination oral contraceptives?

A

Steroidal

42
Q

What are four major effects of Estrogen?

A
  1. Female maturation
  2. Endometrial effects
  3. Metabolic and cardiovascular effects
  4. Effects on blood coagulation - increase coagulability, but also increase plasminogen and decrease platelet adhesion
43
Q

What are four clinical uses of estrogens?

A
  1. Primary hypogonadism
  2. Postmenopausal hormone replacement therapy (HRT)
  3. Estrogens and progestins are used to suppress ovulation in patients with intractable dysmenorrhea or to suppress ovarian function for the treatment of hirsutism and amenorrhea due to excessive ovary androgen secretion
  4. Contraception
44
Q

What are the ADRs of estrogens?

A
  1. Breast cancer - ONLY IN PROLONGED THERAPY, and only a slight risk increase
  2. Endometrial carcinoma
  3. Uterine bleeding
  4. Nausea
  5. Breast tenderness
  6. hyperpigmentation
  7. migraines
  8. cholestasis
  9. gallbladder disease
  10. HTN
45
Q

By what factor does the addition of progesterone to estrogen therapy mitigate the risk of breast cancer?

A

To no degree, it may even, based on recent studies, significantly increase the risk of breast cancer.

46
Q

Studies show an increased risk of endometrial carcinoma in patients taking estrogens alone with the following increases.

  1. Up to 15 times greater in patients taking large estrogen doses for 5 or more years
  2. 2-4 times greater in patients receiving low estrogen doses for short periods of time

What can be done to diminish this risk?

A
  • Concomitant use of progestins and estrogens prevents the increased risk due to estrogen alone and may reduce the incidence to less than that in the general population
47
Q

Riddle me some contraindications to estrogen therapy. 6

A
  1. Patients with estrogen-dependent neoplasms (e.g., endometrial carcinoma, breast cancer) or at high risk for breast carcinoma
  2. Patients with undiagnosed genital bleeding
  3. liver disease
  4. a history of thromboembolic disorder
  5. heavy smokers
  6. Pregnancy/suspected pregnancy
48
Q

Which route of administration has a greater impact on the levels of sex-hormone binding globulin and angiotensinogen, oral or transdermal estrogens?

A

Oral, d/t first pass metabolism

49
Q

What is the most important progestin?

A

Natural progestin: progesterone

(Unclear based on the DSA if this is ever used as a drug, or if she is just talking about endogenously sourced)

50
Q

What are the synthetic progesterones? 3

A
  1. Levonorgestrel (L-norgestrel)
  2. norethindrone acetate
  3. medroxyprogesterone acetate
51
Q

What are the following drugs derived from?

And, what does this mean they have in common?

Norethindrone

Norethindrone acetate

Ethynodiol diacetate

L-Norgestrel

A

19-nortestosterone derivatives - which means they have androgenic effects (note, 2/5 of the listed derivatives of this do not have androgenic effects. However in lecture Linger generalized them all as having this characteristic)

52
Q

What are the isoforms of the progesterone receptor?

A

A

B

53
Q

Name 9 physiological effects of progesterone. Or as many as you can. Yeah lets go with that last one.

A
  1. Production during the luteal phase of the cycle decreases the frequency of GnRH pulses
  2. Decreases estrogen-driven endometrial proliferation
  3. Abrupt decline at the end of the cycle is the main determinant of the onset of menstruation
  4. Key in maintaining pregnancy and mammary gland development (with estrogen)
  5. Stimulates lipoprotein lipase and favors fat deposition
  6. Increases basal insulin levels and the insulin response to glucose
  7. Promotes glycogen storage and ketogenesis
  8. Can compete with aldosterone for the mineralocorticoid receptor, causing a decrease in sodium reabsorption (leads to increased secretion of aldosterone)
  9. Causes maturation and secretory changes in the endometrium that are seen following ovulation
54
Q

What are the two therapeutic applications of progesterone?

A
  1. Major use is for HRT (see estrogen above)
  2. hormone contraception (see below) - Progestins produce long-term ovarian suppression
55
Q

A 150 mg depot dose of medroxyprogesterone acetate, given IM every 90 days, produces prolonged anovulation and amenorrhea (considered high dose). What is this therapy protocol used to treat?

A
  1. Dysmennorhea
  2. endometriosis
  3. bleeding disorders
  4. hot flashes in post menopausal women who cannot take estrogen
  5. Contraception
56
Q

What are two diagnostic uses of progesterone?

A
  1. Progesterone can be used as a test of estrogen secretion (e.g., withdrawal bleeding may be induced in amenorrheic patients after administration of 5-7 days of progesterone only when the endometrium has been stimulated by estrogens)
  2. Estrogen-progestin combination can be given to test the responsiveness of the endometrium in patients with amenorrhea
57
Q

What are the ADRs associated with progestins?

A
  1. Breakthrough bleeding (most common when progestins alone are used for contraception)
  2. Progestins may increase blood pressure in some patients (typically a minor effect)
  3. The more androgenic progestins reduce plasma HDL levels in women
  4. HRT with an estrogen and progestin may increase the risks for cardiovascular problems and breast cancer compared to the risk in women taking estrogen alone
58
Q

What are the two types of oral contraception in use?

A

Combinations of estrogens and progestins

Continuous progestin therapy without estrogens.

59
Q

Combination hormonal contraception methods are divided into what three forms?

A
  1. Monophasic - constant dose of both components through the cycle
  2. biphasic - dosage of one or both components is changed once during the cycle
  3. triphasic - dosage of one or both components is changed twice during the cycle
60
Q

The Ortho Evra transdermal patch preparation consists of what two components?

A

ethinyl estradiol and norelgestromin

61
Q

What are the ADRs of transdermal patch preperations?

A

Similar to those of oral combo preperations but with more frequent..

  1. Breast discomfort
  2. Dysmenorrhea
  3. Nausea
  4. Vomiting
  5. skin irritation
62
Q

The NuvaRing contains ethinyl estradiol and etonogestrel and is inserted and left in place for 3 weeks followed by one ring-free week. What is an advantage of this type of contraception?

A

Rapid return to fertility after removal (back-up contraception should be used if removed for more than 3 hours)

63
Q

Injectable contraceptives containing medroxyprogesterone acetate are effective and eliminate the need for daily adherence. This Inhibits ovulation for at least 14 weeks and may be injected intramuscularly (Depo-Provera) or subcutaneously (Depo-SubQ Provera 104) every three months. Unpredictable irregular bleeding, particularly during the first year of use; amenorrhea is common.

How long before fertility can be expected to return?

What is another benefit?

What are two ADRs?

A

The return of fertility can be delayed 6-12 months after the last injection

Benefit: Long-term use reduces menstrual blood loss and may reduce risk of endometrial cancer

ADRs

  • reduction in bone density (reversible)
  • increased risk of atherosclerosis
64
Q

IUDs come in several different levonorgestrel-containing devices (Mirena, Skyla, Liletta, etc.) vary in size, hormone concentration, and duration of efficacy. The Mirena IUD is effective for up to 7, FDA approved for up to 5 years of consecutive use. These feature a rapid return to fertility after removal. What are some ADRs associate with this type of contraceptive device?

A
  1. Increased irregular bleeding for 3-6 months after placement; reduced total bleeding after that and 20% of users report amenorrhea after 1 year of use
  2. May increase risk of ovarian cysts
65
Q

A single-rod implant containing the progestin etonogestrel is the only implantable contraceptive preparation available in the United States. Where is it typically placed?

What is a common ADR?

A

Surgically inserted under the skin of the upper arm and is effective for three years; removal also requires surgery

Bleeding abnormalities are common

66
Q

Morning after contraception can prevent pregnancy following coitus by the administration of estrogens alone, progestins alone, estrogen and progestin combinations, or progesterone receptor modulators (e.g., ulipristal acetate), and are 99% effective if begun within 72 hours.

What are some ADRs associated with these drugs?

A
  1. Nausea
  2. Vomiting
  3. headache
  4. dizziness
  5. breast tenderness
  6. abdominal and leg cramps
67
Q

What is the MOA of mifepristone?

What is it commonly paired with?

A
  1. Mifepristone is a progesterone receptor antagonist that induces luteolysis;
  2. primarily used in combination with misoprostol (synthetic prostaglandin E1) for pregnancy termination
68
Q

Levonorgestrel (L-norgestrel, Plan B One-Step, Next Choice) is Available without a prescription for women ≥17 years old and with a prescription for younger women. The precise mechanism in emergency contraception is unknown (proposed mechanisms include inhibited or delayed ovulation, alterations in endometrial receptivity for implantation, interference with functions of the corpus luteum that maintains pregnancy, production of a cervical mucus that decreases sperm penetration, alterations in tubular transport of sperm, egg, or embryo, or disruption of the fertilization process).

What is a noteable limitation of this drug?

A
  1. Does not reverse a pregnancy that has already occurred (i.e., if the fertilized egg has already implanted in the uterus)
69
Q

Ulipristal acetate (Ella) is an emergency contraceptive. What are its MOAs? 2

A
  1. partial agonist at progesterone receptors; inhibits ovulation when taken up to five days after intercourse,
  2. may also block implantation of the fertilized egg
70
Q

What are the emergency contraceptive options? 3

A
  1. Ulipristal acetate
  2. Levonorgestrel
  3. Mifepristone
71
Q

How does the efficacy of Ulipristal acetate compare to levonorgestrel?

A
  1. As effective as levonorgestrel when used within 3 days and may be more effective 3-5 days after unprotected intercourse
72
Q

The incidence of serious known toxicities associated with the use of contraceptive drugs is low, far lower than the risks associated with pregnancy. Nonetheless, they do exist, and fall into mild, moderate and severe categories.

Mild includes stuff like headaches, N/V, bleeding

Moderate includes hirsutism, weight gain, acne, vaginal infections, and amenorrhea.

What are the severe adverse effects?

A

Vascular disorders: MI, DVT, cerebrovascular disease

Gastrointestinal disorders - cholestasis, hepatic adenomas

Depression

Cancer: she lists this here, but also states…

  1. Oral contraceptives reduce the risk of endometrial and ovarian cancer (not enough data on other forms of estrogen and progestin contraceptives)
  2. Lifetime risk of breast cancer in the population as a whole does not seem to be affected
  3. Relationship between oral contraceptives and risk of cervical cancer remains unclear

So I guess its actually not an ADR. This DSA is not Dr. Linger’s finest piece of work.

73
Q

Estrogen-containing contraceptives are not recommended for smokers ≥ 35 years old or patients with hypertension, coronary artery disease, cardiovascular and cerebrovascular disorders (or past history of these disorders), diabetes with end-organ damage, migraine headaches with focal neurological symptoms, vaginal bleeding of unknown cause, or patients with known or suspected tumors of the breast or other estrogen-dependent neoplasms, or adolescents in whom epiphysial closure has not yet been completed (progestin-only agents or non-hormonal methods are more appropriate).

Why are oral contraceptives CI in CHF?

A

D/t risk of edema

74
Q

What are some Non-contraceptive benefits of effects of combination oral contraceptives?

A
  1. reduced risk of epithelial ovarian and endometrial cancer,
  2. lower incidence of ectopic pregnancy and benign breast disease,
  3. reduction in dysfunctional uterine bleeding and dysmenorrhea,
  4. improvement in premenstrual symptoms, hirsutism, and acne
75
Q

Tamoxifen and toremifene can act as competitive partial agonists inhibitors of the estrogen receptor. How do they act in breast tissue and what does this make them useful for?

A
  1. Antagonist activity in breast tissue: Used to treat breast cancer (estrogen receptor positive or status unknown) and for chemoprevention of breast cancer in high-risk individuals
76
Q

MOA of Raloxifene?

A
  1. MOA: Agonist effects on lipids and bone; antagonist on endometrium and breast
77
Q

What are the Selective estrogen receptor downregulators (SERDs)?

A

Fulvestrant

Clomiphene

78
Q

What is the MOA of Fulvestrant?

A
  1. MOA: bind to ERs (estrogen receptors) and inhibit dimerization while increasing protein degradation. Thought to completely abolish the expression of estrogen-dependent genes.
79
Q

Fulvestrant Adverse effects include hot flashes, GI symptoms, headache, back pain, and pharyngitis.

What patients is this usually used on?

A

postmenopausal women with ER-positive breast cancer and pre- and postmenopausal women who have become resistant to tamoxifen

80
Q

What is the MOA of clomiphene? What is it used for?

A
  1. MOA: weak estrogen; acts as a competitive partial agonist inhibitor of endogenous estrogens
  2. Older drug; Used as an ovulation-inducing agent (see below)
81
Q

What are the ADRs associated with Clomiphene? 5

A
  1. Ovarian hyperstimulation
  2. increased multiple births
  3. ovarian cysts
  4. hot flashes
  5. blurred vision
82
Q

What is the MOA of mifepristone?

Use?

A
  1. MOA: a 19-norsteroid that acts as a progesterone receptor antagonist (also antagonizes the glucocorticoid receptor)

Used to terminate early pregnancies. Luteolytic properties account for its ability to be used as an emergency contraceptive agent

83
Q

What is the MOA of anastrazole, letrozole, exemestane?

A
  1. MOA: inhibit the function of aromatase (CYP19, responsible for the conversion of androstenedione and testosterone to the estrogens estrone and estradiol, respectively)
84
Q

What are the aromatase inhibitors used for?

A
  1. Treatment of breast cancer: AIs are only recommended for women who are postmenopausal, where their use can lead to profound estrogen deprivation; In general, AIs are contraindicated in premenopausal women because of concern they may result in reactivation of ovarian function
  2. AIs, especially letrozole, have been used off-label to induce ovulation
85
Q

What are some reasons why AI drugs might be preferable to SERMs and SERDs?

A
  1. Associated with a significantly lower incidence of vaginal bleeding, vaginal discharge, hot flashes, endometrial cancer, and deep vein thrombosis compared to SERMs and SERDs

“Fewer ADRS”

86
Q

What is the MOA of clomiphene?

A
  1. MOA: acts as a partial agonist at estrogen receptors and occupies estrogen receptor binding sites for a longer duration than estrogen. Occupation of hypothalamic ERs impairs normal estrogen feedback, which results in increased pulsatile GnRH release from the hypothalamus and subsequent pituitary FSH and LH release. Increased FSH and LH release induces growth and maturation of the ovarian follicle, followed by rupture
87
Q

Clinical use for clomiphene?

A
  1. : Stimulation of ovulation in women with oligomenorrhea or amenorrhea and ovulatory dysfunction
88
Q

ADRs of clomiphene?

A
  1. Hot flushes similar to those experienced during menopause, visual disturbances
  2. Stimulation of ovaries may lead to ovarian enlargement
  3. Increased incidence of multiple pregnancy (~10% compared to 1% in the general population)
89
Q

Nearly all the drugs discussed in this DSA have the same constitutional ADRs. Elaborate the intricacies of why this overlap exists.

Then, identify the disparate adverse effects/toxicities and discuss why these particular reactions are not shared between classes.

A

Just kidding.

Reproductive II - Exam 1 (12 decks)

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