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pharma > B.15 > Flashcards

B.15 Flashcards

1
Q

Estrogens and antiestrogens

A
  1. Estrogen analogs: Ethinylestrogen, Estradiol
  2. SERM: Tamoxifene, Raloxifene, Clomifene
  3. Affecting GnRH: Goserelin, Degarelix
  4. Aromatase inhibitor: Anastrozole
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2
Q

SERM

A

Selective Estrogen Receptor Modulator

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3
Q

Palliative treatment

A

Medical care given to relieve the symptoms and improve the quality of life of patients with advanced or terminal cancer. This treatment doesn’t cure the cancer, but rather provide confort and support to the patient.

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4
Q

Ethinylestradiol

A

MOA: synthetic Estrogen analog (binds estrogen receptor and activates it)→ ↓LH→↓endometrial vascularizaiton. ↓GnRH→prevent ovulation.
It also ↑SHBG;
IND: Combined with other drugs for contraceptive, premenstrual dysphoric disorder, moderate acne, prevention of postmenopausal osteoporosis;
Kinetics: can be adm. s.c, as contraceptive patch, locally as vaginal ring (3week use-1 week pause), ↑PPB, metabolized in the liver, excreted in bile/urine/feces; has a long T1/2;
SEs: headache, dizziness, weight gain, impaired glucose tolerance, abnormal bleeding

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5
Q

Estradiol

A

MOA: Estrogen analog (binds estrogen receptor and activates it)→acts on vasomotor systems (such as hot flashes) and urogenital symptoms (such as vaginal dryness), inhibits bone resorption, have beneficial effect on plasma lipid profile;
IND: treatment of moderate-severe vasomotor symptoms and vulvar and vaginal atrophy due to menopause, hypoestrogenism due to hypogonadism /casteration /primary ovarian failue, prevention of postmenopausal osteoporsis, treatment of breast cc (only for Palliative treatment), treatment of androgen dependent prostate cc, in combination with other drugs as oral contraceptive pills

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6
Q

Clomifene

A

MOA: SERM, mechanism not completely understood (somehow it stimulates the release of GnRH, FSH and LH→ development and maturation of follicle→ovulation→development & function of the corpus luteum→pregnancy);
IND: Ovulation-inducing agent (e.g. in patients with anovulation→PCOS);
Kinetics: p.o adm., good absorption, hepatic metabolism, excreted mainly via feces, long T1/2

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7
Q

Tamoxifene

A

MOA: SERM (→competitively inhibits estrogen binding to its receptor→ inhibiting growth and promotes apoptosis in estrogen-R positive tumors), it also ↑SHBG (→↓the amount of freely available estradiol);
IND: Used in palliative treatment of estrogen-R positive breast cc in postmenopausal women;
Kinetics: has narrow therapeutic index (can lead to breathing diffculty or convulsions),

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8
Q

Raloxifene

A

MOA: SERM (exhibits estrogenic effects on bone&lipid metabolism, and antiestrogenic effects on uterine endometrium and breast tissues)→inhibits bone resorption, ↑bone mineral density;
IND: Prevention&treatment of post-menopausal osteoporosis, prevention &treatment of corticosteroid-induced bone loss, reduction in the risk of invasive breast cc in postmenopausal women with osteoporosis/women with high risk for invasive breast cc;
Kinetics: good p.o abs., ↑PPB, metabolized in liver and intestines, mostly fecal elimination

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9
Q

Anastrozole

A

MOA: non-steroidal Aromatase inhibitor;
IND: breast cc resistant to Tamoxifen

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10
Q

Goserelin

A

MOA: GnRH analogs (binds GnRH-R on the pituitary gonadotrophs and stimulate release of FSH and LH); IND: Hormone-dependent tumors (prostate, breast), Endometriosis, preterm puberty, Assisted fertillization (→stopping the pituitary function during preparation), Diagnostics (LH. FSH producing capacity), Hormone replacement (pulsatile→ hypothalamic hypogonadism, Kallmann sy.);
SEs: at the beginning of administration it can transiently worsen certain symptoms (→pain from bone metastases), secondary amenorrhea, reduced libido, erectile dysfunction, hypogonadism, hot flashes, osteoporosis

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11
Q

Degarelix

A

MOA: GnRH antagonist;
IND: Advanced hormone-dependent prostate cc;
SEs: erectile dysfunction, glucose tolerance↓, osteoporosis, QT↑, increased cardiovascular risk

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12
Q

Female sexual hormones

A

Hypothalamus secretes GnRH→ it stimulates the anterior pituitary (hypophysis) to release LH + FSH → they stimulate the ovary to secrete Estradiol + Progesterone→ they then go back and stimulate/inhibit the hypophysis in a negative feedback loop

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13
Q

The function of the ovary

A

Gametogenic and endocrine
- Quescient before puberty
- At puberty- begins 30-40 years period of cyclic function (menstrual cycle)
- Menopause::explain the stages during female life

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14
Q

Mechanism of action of estrogens

A

Binds Intracellular receptor →gene activation

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15
Q

Pharmacological effects of estrogen

A
  • Estrogens promote proliferation (endometrium, breast)
  • Cooperation with progestins
  • Female sexual maturation and growth, secondary sex characteristics, female libido
  • Metabolic and cardiovascular effects:
    • Normal structure and function of the skin and blood vessels::vascular system
    • Decrease the rate of bone resorption (inhibition of osteoclasts)
    • higher levels of CBG, TBG, SHBG, transferrin, fibrinogen
    • mild, advantageous changes in lipoproteins, TAGs, and cholesterol levels
  • Blood coagulation is enhanced (increased synthesis of coagulation factors)
  • Activation of the stress and the sympathetic system
  • Na+- retention and edema
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16
Q

Clinical use of estrogens

A
  1. Hormone replacement
    * Primary hypogonadism
    • Replacement therapy, started at 11-13 years of age
      * Postmenopausal hormonal therapy
    • either estrogen monotherapy
    • or in combination with progestins (if the patient has intact uterus)
  2. Estrogens + Progestins: ovarian suppression
    * Hormonal contraception
    * Other reasons:
    • Severe menstrual problems: intractable dysmenorrhea, polymenorrhea, dysfunctional bleeding, premenstrual syndrome
    • Treatment of hirsutism and amenorrhea due to excessive secretion of androgens by the ovary
17
Q

SEs of estrogens

A
  • Increased risk of endometrial cc (progestins are protective)
  • Increased risk of breast cc (Progestins are NOT protective)
  • Increased blood coagulation (increased risk of stroke and venous thrombosis)
  • Postmenopausal uterine bleeding
  • Nausea, breast tenderness, hyperpigmentation
  • Increase in frequency of migraines headaches, cholestasis, gallbladder disease, hepatic adenomas
  • Diethylstillbestrol: increased risk of vaginal adenocarcinoma in women whose mother was treated during pregnancy→should be avoided during pregnancy)
18
Q

Contra-IND of the estrogens

A
  • Patients with estrogen-dependent neoplasms (endometrial, breast cc)
  • Endometriosis
  • Patients with undiagnosed genital bleeding
  • severe liver disease
  • History of thrombotic disorder
  • Heavy smokers
19
Q

Pharmacokinetics of estrogens

A
  1. Natural estrogens:
    high first pass metabolism
    Estradiol binds to SHBG (and albumin) in the circulation
    Excretion in part with bile - enterohepatic cycling::metabolism, distribution, excretion
  2. Synthetic estrogens:
    good oral BA
20
Q

High first pass metabolism

A

-High ratio of hepatic to peripheral effects
- Increases the incidence of some SEs
* Undesired: coagulation, biliary
* Advantageous: lipid profile
- To avoid: transdermally, as an injection, or locally (vaginal use)
-Conjugated estrogens (e.g. estrogen valerate)
- I.m depot

21
Q

Natural estrogens

A
  • Estradiol (the major secretory product of the ovary)
  • Estrone and Estriol (formed in the liver from estradiol or in the peripheral tissues from androgens)
  • Equine estrogens
  • Phytoestrogens
22
Q

Synthetic estrogens

A
  • Steroidal structures: Ethinylestradiol, mestranol, quinestrol
  • Non-steroidal compounds: Dinestrol, Diethylstilbestrol, Chlorotrianisene, Methallenestril, Benzestrol, Hexestrol, Methestrol

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