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Pharmacology > Gonadal Hormones > Flashcards

Gonadal Hormones Flashcards

1
Q

When the primary follicle matures, it secretes

A

estrogen

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2
Q

Mature follicle releases ovum and then follicle transforms into

A

Corpus Luteum

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3
Q

Corpus Leuteum secretes

A

progesterone which is involved in maintenance of the endometrium

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4
Q

Ovarys release what hormones

A

estrogen and progesterone

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5
Q

Precursor for hormones

A

cholesterol

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6
Q

Enzyme transforms non aromatic onto aromatic

A

Aromatase

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7
Q

Main natural estrogen

A

estradiol

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8
Q

Genistein

A

Natural compound found in plants such as soy, used OTC , used to support women undergoing menopause. It can activate estrogen receptors similar to Estadiol.

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9
Q

Bisphenol A

A

Used in plastic bottles. Might have hormonal effects. Could be disruptive in developing fetuses.

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10
Q

Why use synthetic estrogens?

A

estrogen has low bioavailability when taken orally. Can increase the bioavailability when used as a cream, but it is still low.

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11
Q

Pharmokinetics of estrogens

A

Binds strongly to sex hormone binding globulin.
Biotransformation in the liver and excretion in bile (can compromise the liver).

Lipophilic , requires proteins for shuttling.

Cytoplasmic receptors, not transmembrane.

Binding estrogen forms complex with receptors, dimerizes then binds to DNA sequence. Different receptors than GCS, but same sequence of events.

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12
Q

Physiological effects of estrogens

A

Decrease rate of bone resorption

Reduce total plasma cholesterol

Endometrial effects

stimulate production of leptin

structure and function of skin and blood vessels.

Enhance blood coagulability

Maturation

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13
Q

Clinical uses of estrogens

A

hypogonadism

postmenopausal hormone therapy

hormonal contraceptive

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14
Q

Estrogen side effects

A

Uterine bleeding

Cancer (slightly enhanced risk of breast cancer, but rare)

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15
Q

Progestins produced by CL and synthesized in

A

ovary, testis, adrenal cortex, placenta during pregnancy

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16
Q

Progestins are metabolized in the

A

liver and secreted in the urine as a glucuronide conjugate

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17
Q

Progesterone favors

A

fat deposition, increased basal insulin levels and promotes glycogen storage

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18
Q

Progesterone competes with

A

aldosterone and decreases sodium reabsorption

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19
Q

Progesterone increases

A

body temp (indicator of ovulation)

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20
Q

Synthetic progestins do not

A

usually support implantation of fertilized egg

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21
Q

1:1 estrogen progesterone ratio

A

monophonic

22
Q

bi and tri phasic differs in

A

hormone levels

23
Q

continuous progestin therapy aka

A

mini pills

24
Q

Use mini pills when

A

patients don’t respond to estrogen

25
Q

Estrogens to known

A

Ethinyl Estradiol

Mestranol

Estradiol Valerate

26
Q

Progestins to know

A

norgestrel

desogestrel

norethindrone

27
Q

Main purpose of combined forms of estrogen and progesterone

A

prevent LH spike and inhibit ovulation

28
Q

Progestins mostly effect

A

endometrium and changes in the uterus

29
Q

Mini pills do not . . .

A

inhibit ovulation, but influence changes in the endometrium. Effects are purely on endometrium.

30
Q

Pharmacologic effects of hormonal contraceptives (1)

A

depression of ovarian function

hypertrophy of cervix

changes in cervical mucous

stimulation of breasts (risk of breast cancer)

31
Q

Pharm effects of hormonal contraceptives (2)

A

change in other hormones regulated to AP

increased pigmentation, changes in serum production

increased coagulation

beneficial changes in lipid profile

change in levels of globulins (more globulins that binds steroids = less bioavailability , only active in their free form)

32
Q

Adverse effects of estrogens (mild)

A

nausea, Mastalgia, edema, headache, lack of withdrawal bleeding

33
Q

Adverse effects of estrogens (moderate)

A

abnormal bleeding when its not time for the period

vaginal infections

weight gain

acne and hirsutism

amenorrhea

34
Q

Adverse estrogen effects severe

A

cancer, depression , vasular disorders

35
Q

SERMs

A

selective estrogen receptor modulators (not called antagonist because they inhibit some receptors in some tissues, but activate in other, depends on location.

36
Q

SERMs to know

A

tamoxifen

raloxifen

toremifene

clomifene

mifepristone

37
Q

How does tamoxifen, raloxifen, and toremifene work?

A

used in patients with breast cancer after mastectomy to prevent metastasis and used in cancer that responds to increase estrogens. Could cause hot flashes, no negative impacts on bone.

38
Q

How does clomifene work?

A

blocks only estrogen receptors in the brain. (hypothalamus and Ant pit) blocks the neg feedback , so CNS keeps pumping estrogens . Why use these? In fertility clinics , to stimulate fertilization.

39
Q

Mifepristone

A

Antagonist of GCS and MCS, but mainly blocks progesterone receptors. Will be used to induce abortions often used in combinations of drugs that will stimulate uterine contractions, certain prostaglandins may increase uterine contractions.

40
Q

Androgens are produced in

A

testes or adrenal glands

41
Q

Physiological form of Testosterone

A

Dihydrotestosterone

42
Q

Taking testosterone may increase estrogens

A

aromatase does this conversion

43
Q

Physiological effects of androgens

A

maturation

replacement therapy

low libido (also used in females)

growth stimulators (AIDS)

44
Q

Androgen side effects

A

prostatic hyperplasia

sleep apnea, agressiveness

Acne

masculinizing effects

45
Q

Drugs that inhibit androgens will be used in treating

A

prostate cancer or prostate hyperplasia

46
Q

Dihydrotestosterone may

A

stimulate balding , so drugs may block this to prevent balding

47
Q

Inhibits synthesize of steroids way up the pathway

A

Ketoconazole, spironolactone

48
Q

Inhibits 5 alpha reductase which converts testosterone to dihydrotestosterone

A

finasteride and Dutasteride

49
Q

Directly inhibits receptors of dihydrotestosterone

A

Flutamide, cyproterone, spironolactone

50
Q

Combination given for prostate hyperplasia

A

alpha 1 antagonist and 5 alpha reductase inhibitor

Pharmacology (20 decks)

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