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Pathophysiology - Endocrine and Reproductive > Pharmacology of Female and Male Gonadal Medications > Flashcards

Pharmacology of Female and Male Gonadal Medications Flashcards

1
Q

Give three ways to increase bioavailability of a hormone agent?

A
  1. Alter structure (usually 17C position) to avoid first pass metabolism
  2. Use an alternate route of administration to avoid first pass metabolism
  3. Micronize the hormone molecules -> suspend in oil so they are protected from first pass metabolism
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2
Q

What portion of the estrogen is required for receptor binding? Other than saving from first pass metabolism, what other function does 17C modification have?

A

Phenolic A ring -> phenyl + alcohol

Also inhibits oral estrogens from binding sex hormone binding globulin, so they are more orally bioavailable

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3
Q

Who are the only women who can use estrogen alone? If you are starting estrogen therapy, what is the latest it can be started for postmenopausal symptoms?

A

Women without a uterus -> otherwise you need to give progesterone as well to prevent endometrial hyperplasia

Must start estrogen therapy within 10 years of menopause

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4
Q

What are the contraindications to estrogen therapy?

A
  1. Estrogen dependent neoplasma
  2. Undiagnosed genital bleeding
  3. Hepatic disease (decrease the metabolism)
  4. Pregnancy
  5. History of thromboembolic disorder (increased cardiovascular risk)
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5
Q

What is progesterone vs progestins?

A

Progesterone - natural
Progestins - synthetic

Umbrella term: Progestogens

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6
Q

What are the two primary indications for postmenopausal hormone replacement therapy (HRT)?

A
  1. High risk of osteoporosis - especially thin, white smokers with a family history (start before bone loss)
  2. Atrophic vaginitis
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7
Q

Is estrogen first line in osteoporosis? Does it restore bone loss?

A

No, not first line. Calcium / vitamin D / bisphosphonates are.

Does not restore bone loss -> must be started early (i.e. within 10 years of menopause). Can only prevent further progession.

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8
Q

How does estrogen affect your warfarin levels?

A

It decreases your warfarin levels (probably by CYP induction to some extent, idk)

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9
Q

What is the mechanism of oral contraceptives in the treatment of hirsutism and acne in androgen excess?

A
  1. Estrogens feedback negatively on LH, reducing ovarian androgen production
  2. Estrogens increase hepatic SHBG production, which reduces free androgen levels
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10
Q

What is the mechanism of action of spironolactone? What is it used for?

A

Competitive antagonist for androgen receptor (as well as aldosterone receptor), and inhibits androgen biosynthesis (like ketoconazole, 17,20 desmolase / 17a hydroxylase))
-> used for treatment of female hirsutism, i.e. as in PCOS

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11
Q

What vitamin / mineral combination has been used effectively in the treatment of hirsutism in PCOS?

A

Magnesium-zinc-calcium-vitamin D

Zinc inhibits 5a reductase

Others interfere with steroidogenesis or some shit

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12
Q

What drug is an antiandrogen by blocking 5alpha-reductase?

A

Finasteride

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13
Q

What are the three main synthetic progestins?

A
  1. Medroxyprogesterone
  2. Norethindrone
  3. Norgesterel
    - >look for a “-gest” and its probaly gucci
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14
Q

How should chronic anovulation with continuous estrogen stimulation of uterus be handled in PCOS?

A

Give oral contraceptives, especially containing synthetic progestins
-> Daily dose and then withdrawal to induce withdrawal bleeding

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15
Q

What are the benefits of metformin therapy in PCOS?

A
  1. Improve hepatic insulin senstivitiy
  2. Reduce androgen production in ovarian theca cells
  3. Induction of ovulation (like clomiphene)
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16
Q

What is clomiphene used for and why?

A

Treatment of infertility

  • > tends to block estrogen receptor in hypothalamus, which makes hypothalamus see low estrogen -> increasing GnRH release
  • > leads to increased FSH levels, and subsequent follicle stimulation
17
Q

Who is clomiphene only effective in and when should it be administered?

A

Only effective in infertile women with adequate estrogen levels (just not getting enough LH surge)

Should be administred for 5 days in early follicular phase -> before follicle dominance occurs to increase chance of multiple follicle recruitment (however, associated witih risk of multiple gestation)

18
Q

What other class of medications can induce ovulation by reducing circulating estrogen levels?

A

Aromatase inhibitors - i.e. Anastrozole, Letrozole, exemestane

  • > similar mechanism to clomiphene, increase FSH levels by causing hypoestrogen environment.
  • > Use at same time in follicular phase
19
Q

How can FSH / LH be directly used to induce ovulation? Describe the regimen.

A

FSH - give once daily during follicular phase

LH - normal surge will be inhibited due to negative feedback from FSH inducing estrogen. Thus, give hCG (mimics LH) roughly 36 hours before you want to ovulation.

20
Q

What is ovarian hyperstimulation syndrome?

A

An adverse effect occuring in women given ovulation induction / superovulation drugs. Results in increased vasoactive substances like VEGF being secreted during follicle luteinization.

VEGF causes ascites, hypovolemia, and hemoconcentration

21
Q

What are the three primary androgen drugs? Adverse effect of concern and how can it be avoided

A
  1. Testosterone salts - long IM release
  2. Methyltestosterone
  3. Fluoxymesterone

Adverse effect: hepatotoxicity if given orally -> recommend using patch, gel, on buccal mucosa, or subcutaneous pellet

22
Q

What is the clinical use of testosterone agonists?

A
  1. Treat hypogonadism + promote puberty (secondary sexual characteristics)
  2. Stimulate anabolism to promote recovery after a burn or injury
  3. Male hypogonadism in adulthood
23
Q

What are some symptoms and signs of male hypogonadism?

A

Decreased libido, erectile dysfunction, infertility, depression

Decreased body hair, decreased musscle mass, gynecomastia, osteoporosis, anemia

24
Q

What is one clear indication to discontinue testosterone therapy? What is one clear contraindication to starting?

A

If hematocrit is >54%.
-> Testosterone acts like erythropoietin to some extent.

Do not start if PSA > 4 ng/mL (causes prostate hyperplasia)

25
Q

What are likely side effects of testosterone therapy in children?

A
  1. Initial growth spurt followed by premature closure of the epiphyseal plates
  2. Gynecomastia -> children have more extraglandular aromatase activity
26
Q

What happens to females and males of all ages with testosterone therapy?

A

Females - virilization, male pattern baldness, hirsutism

Males - Decreased testicular size (decreased FSH / LH leads to gonadal atrophy)

27
Q

What is Danazol and what is it used for?

A

An ethinyl derivative of testosterone -> Weak androgen agonist and inhibitor of midcycle surge of FSH / LH.

Used in treatment of ENDOMETRIOSIS

28
Q

What are possible side effects of danazol?

A
  1. Pseudotumor cerebri

2. Excessive virilization / hepatotoxicity -> same effects as rest of testosterone treatments

29
Q

How does longterm use of anabolic steroids affect your cardiovascular risk?

A

Increases risk of MI and stroke

Lowers HDL, increases LDL and triglycerides

30
Q

Give a GnRH agonist and antagonist. Why might one be preferred over the other for treatment of prostate cancer?

A

GnRH agonist - Leuprolide
GnRH antagonist - Cetrorelix

Cetrorelix might be preferred because there is no initial LH spike which GnRH agonists give.

31
Q

Give two non-steroidal androgen receptor antagonists used in the treatment of prostate cancer. Which one has the better side effect profile? What are they given in combination with?

A

Flutamide
Bicalutamide (less hepatotoxic than flutamide)

Give in combination with GnRH agonist (i.e. leuprolide)

32
Q

What is the mechanism of action of abiraterone and what is it used for? What should it be given in combination with?

A

Inhibits testosterone synthesis by inhibiting CYP17A1 (17alpha hydroxylase), an enzyme needed to make androgens from progestins

Used for treatment of castration-resistant prostate cancer

Give in combination with prednisone

33
Q

What is the mechanism of action of finasteride and what are the indications?

A

5alpha reductase inhibitors (ur gonna have an ass to ride)

  1. Benign prostatic hyperplasia
  2. Androgenic alopecia
  3. Adjunctive therapy for prostate cancer
34
Q

What is the most common treatment for uterine fibroids?

A

GnRH agonist - Leuprolide. Since they are estrogen sensitive.

35
Q

What drug can be used in combination with replacement doses of hydrocortisone as an anti-androgen?

A

Ketoconazole

  • > very strong 17,20 desmolase blockade
  • > replacement of glucocorticoids is necessary

Pathophysiology - Endocrine and Reproductive (27 decks)

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