Contraceptives

Chapter 54


Contraceptives


Pegah C. Dixon




DRUG OVERVIEW


































































































































































































































































































































































































































































































































































































































Class Subclass Generic Name Trade Name
Combination estrogen and progestin Oral monophasic ethinyl estradiol and norethindrone Ovcon 50
      Ovcon 35
      Balziva
      Cyclafem 1/35
      Nortrel 0.5/35
      Nortrel 1/35
      Norinyl 1+35
      Ortho-Novum 1/35
      Femcon FE
      Brevicon
      Modicon
      Generess FE
      Gildess FE 1.5/30
      Gildess FE 1/20
      Loestrin FE 1.5/30
      Loestrin 1/20
      Loestrin FE 1/20
      Loestrin 24 FE
      Junel 1.5/30
      Junel FE 1.5/30
      Junel 1/20
      Junel 1/20 FE
      Microgestin 1.5/30
      Microgestin FE 1.5/30
      Microgestin 1/20
      Microgestin FE 1/20
      Necon 0.5/35-21
      Necon 0.5/35-28
      Necon 1/35-28
      Zenchent
      Zenchent FE
      Zeosa and as chewable tablet
    ethinyl estradiol and levonorgestrel Portia 0.15/30
      Nordette 0.15/30
      Amethyst
      Levlen 21
      Levlen 28
      Alesse 28
      Aviane 21
      Lessina 28
      Levlite 28
      Levora 15/30
      Lybrel
      Lutera
      Orsythia
      Sronyx
    ethinyl estradiol and norgestrel Cryselle
      Lo/Ovral28
      Ogestrel 28
      Low-Ogestrel
    ethinyl estradiol and ethynodiol diacetate Kelnor 1/35
Zovia 1/35
    ethinyl estradiol and desogestrel Apri
      Desogen
      Ortho-Cept 28
      Emoquette
      Reclipsen
    ethinyl estradiol and drospirenone Beyaz
      Sayfral
      Yasmin 28
      Yaz
      Gianvi
      Loryna
      Ocella
      Syeda
      Zarah
    ethinyl estradiol and norgestimate Ortho-Cyclen
      MonoNessa
      Sprintec
    mestranol and norethindrone Norinyl 1+50
      Ortho-Novum 1/50
      Necon 1/50
  Oral biphasic ethinyl estradiol and norethindrone Necon 10/11
      Lo Loestrin FE
    ethinyl estradiol and desogestrel Azurette
      Kariva
      Mircette
  Oral triphasic ethinyl estradiol and norethindrone Aranelle
      Tri-Norinyl
      Ortho-Novum 7/7/7
      Estrostep Fe
      Cyclafem 7/7/7
      Leena
      Necon 7/7/7
      Nortrel 7/7/7
      Tilia FE
      Tri-Legest FE 28
    ethinyl estradiol and norgestimate Ortho Tri-Cyclen
      TriNessa
      Ortho Tri-Cyclen Lo
      Tri-Sprintec
    ethinyl estradiol and levonorgestrel Enpresse
      Trivora-28
    ethinyl estradiol and desogestrel Cyclessa
      Caziant
      Velivet
  Oral four-phasic estradiol valerate/dienogest Natazia
  Oral extended cycle levonorgestrel/ethinyl estradiol Amethia
      Camrese
      Introvale
      Jolessa
      Quasense
      LoSeasonique
      Seasonale
      Seasonique
  Contraceptive patch ethinyl estradiol and norelgestromin Ortho Evra
  Intravaginal ring ethinyl estradiol and etonogestrel ring NuvaRing
Progestin-only Emergency contraception levonorgestrel Plan B One-Step
  Progestin-only oral contraceptive (POP) norethindrone Next Choice
      Camila
      Errin
      Heather
      Jolivette
      Ortho Micronor
      Nor-QD
      Nora-BE
  Progestin-only injection medroxyprogesterone Depo-Provera IM and SQ
  Progestin subdermal implants etonogestrel Implanon
  Intrauterine device levonorgestrel Mirena image
Progestin receptor modulators Emergency contraception ulipristal Ella
Nonhormonal Intrauterine device   ParaGard


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image Top 100 drug.




INDICATIONS





Agents in this class can be divided into progestin-only agents and combination agents including both estrogen and progestin. Combined hormonal contraceptives are formulated for oral, transdermal, and intravaginal routes of administration. Progestin-only agents may be administered orally, intramuscularly, subcutaneously, in intrauterine systems, and via implants. Oral contraceptives (OCs) are commonly known as “birth control pills” or “the pill.”


This chapter is intended to provide the basic information necessary to understand contraception. Because these medications are used to prevent an unwanted pregnancy and not to treat a disease, the patient should always be invited to share in the decision making about contraceptive methods. This, like other components of medicine and surgery, makes selecting the best contraceptive method more of an art than a science. This is a rapidly changing field, with new information and new products. The provider will want to read further on this topic and check for the latest information before prescribing contraceptives.


The first OC pills, which were developed in the 1950s, contained only high doses of progestin. These early pills caused significant breakthrough bleeding (BTB). During manufacture, they became “contaminated” with estrogen. The women who took the contaminated pills had less BTB, so the estrogen was left in. The first combined birth control pill, which contained much higher doses of hormones than are found in the pills used today, was released in 1960.


In the 1970s, researchers first noted a dose-response relationship between high-estrogen pills and the risk of venous thromboembolism. This was caused by the action of oral estrogen on hepatic induction of fibrinogen, which increased the tendency to form blood clots. Early pills had roughly three times more estrogen and nine times more progestin than the pills that are available today. As doses of estrogen have been decreased to below 50 mcg of ethinyl estradiol (EE), thrombus risk has markedly diminished.


The original hormonal contraceptives were monophasic (same daily dose). Progestin-only pills and phasic preparations (estrogen and/or progestin doses that change during the 21-day cycle in an attempt to mimic the typical menstrual cycle) were introduced in the 1970s. Longer-acting progestin-only methods (e.g., medroxyprogesterone, a 3-month progestin-only injection; and Norplant, a 5-year implanted rod system) were approved for the U.S. market in the 1980s. Norplant was taken off the market because of adverse publicity over litigation regarding dose standardization and removal problems. Implanon, a single-rod implant, was introduced in 2006. A new radiopaque implant, Nexplanon, is now available.


In 2002, transdermal and vaginal hormone delivery systems were approved for use in preventing pregnancy. The trend for new contraceptives continues with the introduction of additional combination OCs with lower estrogen levels and different formulations of estrogen and progesterone. In 2003, extended-cycle contraceptives that contain levonorgestrel and an ethinyl estradiol tablet were introduced. Women who take this product experience fewer menstrual cycles per year, or menstruation may be suppressed entirely. Other new products include formulations with more active pills and shortened placebo intervals.



Therapeutic Overview


Anatomy and Physiology


The Menstrual Cycle


The menstrual cycle, which is a 28-day preparation cycle, is a classic negative feedback loop involving the hypothalamus, anterior pituitary gland, and ovaries. Menstruation begins on day 1 of the cycle, with shedding of the endometrium in response to declining estrogen and progesterone levels. Cycles consist of a follicular phase and a luteal phase that are nearly equal in length. Cycle lengths vary among individuals, and variability is increased in adolescents and in women who are close to perimenopause. Most variation occurs in the follicular phase. At the end of a menstrual cycle in which a pregnancy has not occurred, the hypothalamus responds to low circulating levels of estrogen and progesterone and secretes gonadotropin-releasing hormone (GnRH). GnRH stimulates the anterior pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH); these stimulate the ovaries to begin the ovulation cycle anew. The ovaries are the female gonads, which are responsible for secretion of the sex steroid hormones estrogen, progesterone, and testosterone. These gonads also store the ovarian follicles, which in turn are the home of oocytes. When a woman is born, her ovaries contain approximately 2 million follicles, and by puberty, 300,000 remain to carry her to menopause. Only about 500 follicles ovulate during the reproductive years.


FSH stimulates follicular growth and ovarian development. During each cycle, 18 to 20 follicles are stimulated; all except one dominant follicle eventually die off. The dominant follicle produces estrogen and promotes an environment favorable to healthy development of the follicle and its oocyte, in preparation for eventual ovulation. Enlargement of this dominant follicle causes estrogen levels to gradually increase. Near the middle of a cycle (around day 12 to 13 of a 28-day cycle), estrogen in the blood reaches a critical level that sends a hormonal message to the pituitary gland indicating that the follicle is mature and that ovulation is imminent. The pituitary gland responds by sending out the hormonal messenger, LH. The midcycle LH surge induces ovulation. The follicle, now a “bubble” on the side of the ovary, bursts and releases the egg into the ampulla of the fallopian tube. At the site of ovulation, the remains of the follicle form a cyst, called the corpus luteum. At this time, estrogen levels drop sharply and then stabilize as the corpus luteum assumes the role of hormone production, with production of progesterone predominating over that of estrogen.


Progesterone levels are very low during the first half of the cycle but climb sharply after ovulation, with the appearance of the corpus luteum. Progesterone dominates in the second half of the cycle, or the luteal phase. The corpus luteum cyst, maintained by LH, is a “hormone factory” that produces large amounts of progesterone. The corpus luteum typically remains functional for approximately 12 days. If no additional hormonal message (e.g., fertilization and implantation) is sent, the corpus luteum dies and regresses on day 26 of a 28-day cycle. With the demise of the corpus luteum, blood progesterone levels drop dramatically. By the last day of the cycle, baseline progesterone and estrogen levels signal the hypothalamus to start a new menstrual cycle.



Endometrial Changes


The thickness of the endometrial, or uterine, lining parallels the changing hormone levels, shedding from day 1 to about day 5 back to almost basement lining. Increasing estrogen levels in the first half of the cycle stimulate endometrial proliferation. Progesterone, which is produced in large amounts by the corpus luteum in the second half of the cycle, stabilizes the endometrium by increasing its blood supply and glycogen stores, producing a secretory endometrium that is receptive to implantation. Under the influence of progesterone, the endometrium ceases to grow in thickness but becomes significantly denser. The proliferative effects of estrogen must be present in the first half of the cycle for progesterone to produce a secretory endometrium. Without the stabilizing influence of progesterone, the endometrium would continue to thicken but, if unsupported by an adequate blood supply, would shed irregularly. This condition is seen in the woman with anovulatory cycles, who, lacking the secretion of progesterone by the corpus luteum has unpredictable, often heavy noncyclic bleeding as a result of lack of production of progesterone. Similarly, the secretion of large amounts of progesterone without adequate secretion of estrogen (i.e., unopposed progesterone) produces a thin endometrium that is not receptive to implantation.


If fertilization occurs and the egg implants, the embryo and the developing placenta produce human chorionic gonadotropin (hCG), which maintains the corpus luteum cyst for about 100 days until the placenta is advanced enough to produce its own progesterone. After the placenta matures, the corpus luteum declines.


In summary, the uterine lining proliferates in response to rising estrogen levels in the first half of the cycle. In the second half of the cycle, progesterone maintains a secretory endometrium. At the end of the menstrual cycle during which conception did not take place, progesterone and estrogen levels drop off, and the unsupported uterine lining sheds (Figure 54-1).


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FIGURE 54-1 Menstrual cycle events: hormone levels, ovarian and endometrial patterns, and cyclic temperature and cervical mucus changes. (From Hatcher RA et al: Contraceptive technology, ed 18 rev, New York, 2007, Ardent Media Trade, Inc.)


Hormone Physiology


Hormones are chemical messengers produced in the body that travel through the bloodstream from a gland to a distant site, where they exert their effects on specific organs or tissue.


The ovary produces three classes of sex steroid hormones: progestins, androgens, and estrogens. These steroid hormones can be synthesized in the ovaries in situ or derived from serum cholesterol that enters the ovaries. Several steps are included in the steroid biosynthesis pathway. Through a series of intermediary steps, cholesterol (a 27-carbon molecule) is broken down to progestins (21-carbon molecules), then to androgens (19-carbon molecules), and finally to estrogens (18-carbon molecules). During steroidogenesis, the number of carbon atoms can be reduced but never increased. Therefore, the metabolic breakdown of progestins can have progestational, androgenic, and estrogenic actions. The metabolic breakdown of androgens can have androgenic and estrogenic actions, but the metabolic breakdown of estrogens will have only estrogenic actions. In women, the principal circulating sex hormones—estrogen, estradiol, and the androgen testosterone—are also directly produced by the ovary. Most estradiol and testosterone (69%) are bound to sex hormone–binding globulin (SHBG), a protein carrier. Roughly 30% is loosely bound to albumin, leaving only 1% unbound and free. It is this free 1% that determines the biologic effects of estradiol and testosterone. Estrogen administration increases SHBG levels, thereby decreasing the quantities of free, or active, sex steroids. Progestins and androgens decrease SHBG, thereby increasing the quantities of free sex steroids. All combined oral contraceptive pills (COCPs) increase SHBG, although some do so more than others, depending on the progestin component and the ratio of estrogen to progestin. Because all COCPs increase SHBG, free testosterone is always decreased by some degree in women who are taking COCPs.



Progestins

Progesterone is secreted in significant amounts (20 to 30 mg/day) in the second half of the normal menstrual cycle by the corpus luteum. During the first half of the cycle, estrogen dominates and progesterone is secreted in minute amounts (2 to 3 mg/day) by the ovaries and the adrenals. During pregnancy, the placenta secretes very large amounts of progesterone.


The plasma half-life of progesterone is only 5 to 10 minutes, after which it is degraded to other steroids that have no progestational effect. Progesterone in its natural state cannot be used in oral form because of its rapid breakdown by the liver, so chemical modifications of synthetic progestins in hormonal contraceptives were made to deliberately slow down liver metabolism, making it possible to use the oral route (Table 54-1).



Effects of progesterone in the body are limited and are seen primarily in the reproductive tract and the breast; other effects are evident as changes in metabolism. Progesterone is the dominant hormone of pregnancy; it produces a secretory endometrium, decreases uterine contractions, and stimulates alveolar epithelial growth in the breast.


Norethindrone, the progestin originally used in OCs, was derived from ethisterone, an orally active form of testosterone. The removal of a 19-carbon molecule from ethisterone results in the formation of norethindrone and changes the major effect from that of an androgen to that of progesterone, but the androgenic component is never totally eliminated, and the potential for anabolic and androgenic effects remains. See Table 54-2 for biologic effects of progestins and estrogen. This is a dose–effect relationship: The lower the dose of progestins given, the lesser is the androgenic effect. At today’s very low doses of progestin in COCPs, clinical effects are usually negligible. As with estrogens, serious side effects, especially adverse serum lipid changes, have been associated with high doses of progestins; therefore, the lowest effective doses available should be used. Through the years, changes have been made in the chemical structure of progestins in the quest to produce new progestins that have more potent progestational activity with fewer androgenic side effects. Many different progestins are marketed in the United States for use in hormonal contraception.



TABLE 54-2


Biologic Effects of Estrogens and Progestins

























































































































































Organ and/or System Effects Estrogenic Effects Progestational Effects
Adrenal gland Increases cortisol-binding globulin (transcortin) Increases free cortisol
  Increases free cortisol  
Bone Promotes bone formation  
  Stimulates osteoblasts  
  Increases efficiency of calcium absorption  
  Promotes calcitonin synthesis  
Breast Stimulates ductal growth Stimulates glandular growth
  Promotes growth of estrogen receptor–positive cancers Inhibits proliferation decrease in fibrocystic disease
CNS Improves quality of sleep Sedation
  Antidepressant  
  Vasomotor stability  
Gallbladder Alteration in composition of gallbladder bile, increases cholesterol saturation  
  Increases gallstones in women already at risk during first 2 years of estrogen use  
Hematologic effects Increased fibrinogen; clotting factors VI, VII, IX, X, and prothrombin; ESR; transferrin Increased hematocrit; fibrinolytic activity
  Decreased antithrombin III  
Liver/serum lipids Influence synthesis of hepatic DNA and RNA, hepatic cell enzymes, serum liver enzymes, and plasma proteins Decrease HDL
  Increase HDL Increase ratio of total cholesterol to HDL
  Increase triglycerides Increase LDL
  Decrease ratio of total cholesterol to HDL  
Metabolic effects Fluid retention (breast discomfort, headaches) Glucose intolerance (increases peripheral resistance to insulin action)
  Maintenance of muscular strength Anabolic weight gain
  Nausea Increased appetite
  Increased prolactin Depression, fatigue
REPRODUCTIVE TRACT
Uterus Proliferative endometrium: endometrial growth due to gland maturation and enlargement; stromal development, capillary proliferation Secretory endometrium: restrained growth endometrium becomes thicker, more dense; progressive tortuosity of glands; glands become secretory
  Primes progesterone receptors  
Fallopian tubes Increase secretions, ciliary activity, and peristalsis to improve ovum transport Slow peristalsis and decrease secretions
Cervical mucus Increases amount, spinnbarkeit, permeability to sperm Thick, impermeable to sperm
    Increases candidiasis
    Cervicitis
MISCELLANEOUS
Skin Increases secretions, lubrication Oily skin, acne, sebaceous cysts, pilonidal cysts, hirsutism
  Increases elasticity  
  Chloasma (patchy increase in facial pigment)  
Thyroid Increases T3, thyroxine-binding globulin, total T4  
  Normal free T4  
Summary: Combined effects of estrogen and progesterone Increased angiotensin I and II, total iron binding capacity (TIBC) due to increased globulins, vitamin A nonharmful); decreased prothrombin time, B6 (pyridoxine), B12, folic acid, ascorbic acid  


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Estrogens

The human body produces three estrogens: estradiol, estrone, and estriol. The major estrogen is estradiol. It is 12 times more potent than estrone and 80 times more potent than estriol. The primary source of estrogen in women with normal menstrual cycles is estradiol, which is secreted by the ovary. The ovarian follicle secretes 100 to 300 mcg of estradiol daily, depending on the phase of the menstrual cycle. Estradiol levels of greater than 200 mcg are required for ovulation to occur. The ovary also secretes small amounts of estrone, but most comes from adrenal androgens that are converted to estrone in peripheral tissues, such as adipose, skin, and muscle. Estriol is a metabolite of estrone and estradiol.


Estrogens are conjugated in the liver to form glucuronides and sulfates. About one fifth of these conjugated products are excreted in the bile; the rest are excreted by the kidneys. Synthetic estrogens, such as ethinyl estradiol (EE), are degraded very slowly in the liver and other tissues, which causes their high intrinsic potency.


Estrogens are important in the development and maintenance of the female reproductive tract. Estrogen has effects throughout the body that are most notable in the breasts, bones, liver, and urogenital structures. See Table 54-2 for estrogen effects on the body.


Two estrogenic compounds are used in COCPs in the United States: EE and mestranol. Mestranol is considered pharmacologically weaker because it must first be converted to EE. Therefore, unconjugated EE is the active estrogen in the blood in both mestranol and EE. All of the low-dose pills are low-estrogen pills. They contain ≤35 mcg of estrogen pills (EE). Mestranol is available in only a few pills in a 50-mcg dose, which is roughly equivalent to 35 mcg EE. A relatively safe dose of EE is ≤35 mcg. Pills that include 50-mcg EE are reserved for women on medications that induce liver enzymes that degrade estrogen, requiring higher initial doses, and they are rarely used. It is more common practice to use other methods with women who require higher-dose pills. High-dose EE should be given under special circumstances and generally is not used in primary care. In this chapter, COCPs are assumed to contain ≤35 mcg of EE (Table 54-3).



TABLE 54-3


Medications with Dosages




























































































































































































































































































































































































































































































































































































































































Generic Name Trade Name Estrogen, mcg Progestin, mg
COMBINATION
Monophasic
ethinyl estradiol and norethindrone Ovcon 50 50 1
  Cyclafem 1/35 35 1
  Necon 1/35 35 1
  Nortrel 1/35 35 1
  Norinyl 1+35 35 1
  Ortho-Novum 1/35 3535 1
  Brevicon 35 0.5
  Modicon 35 0.5
  Necon 0.5/35 35 0.5
  Nortrel 0.5/35 3535 0.5
  BalzivaFemcon FE 35 0.4
  Ovcon 35 35 0.4
  Zenchent 35 0.4
  Zenchent Fe 30 0.4
  Zeosa 30 0.4
  Gildess FE 1.5/30 30 1.5
  Junel 1.5/30 30 1.5
  Junel FE 1.5/30 30 1.5
  Loestrin 1.5/30 35 1.5
  Loestrin FE 1.5/30 20 1.5
  Microgestin 1.5/30 20 0.8
  Microgestin Fe 1.5/30 20 1
  Generess FE 20 1
  Gildess FE 1/20 10 1
  Junel 1/20   1
  Junel 1/20 FE   1
  Loestrin 1/20    
  Loestrin FE 1/20    
  Microgestin 1/20    
  Microgestin Fe 1/20    
ethinyl estradiol and levonorgestrel Portia, Nordette, Levlen 21, Levlen 28, Levora 30 0.15
  Alesse 21 30 0.15
  Aviane 21 20 0.1
  Lessina 28 20 0.1
  Levlite 28 20 0.1
  Lutera 20 0.1
  Orsythia 20 0.1
  Sronyx 20 0.1
  Amethyst 20 0.1
  Lybrel 20 0.09
    20 0.09
ethinyl estradiol and norgestrel Ogestrel 28 50 0.5
  Cryselle 30 0.3
  Lo/Ovral 28 30 0.3
  Low-Ogestrel 28 30 0.3
ethinyl estradiol and ethynodiol diacetate Kelnor 1/35 35 1
  Zovia 35 1
      1
ethinyl estradiol and desogestrel Apri 30 0.15
  Desogen 30 0.15
  Emoquette 30 0.15
  Ortho-Cept 30 0.15
  Reclipsen 30 0.15
ethinyl estradiol and drospirenone Ocella 30 3
  Safyral 30 3; 451 mcg folate
  Syeda 30 3
  Yasmin 28 30 3
  Zarah 30 3
  Beyaz 20 3; 451 mcg folate
  Gianvi 20 3
  Loryna 20 3
  Yaz 20 3
ethinyl estradiol and norgestimate MonoNessa 35 0.25
  Ortho-Cyclen 35 0.25
  Sprintec 35 0.25
mestranol and norethindrone Necon 1/50 50 1
  Norinyl 1+50 50 1
  Ortho-Novum 1/50 50 1
Biphasic
ethinyl estradiol and norethindrone Necon 10/11 35 0.5 × 10 day then
  Lo Loestrin FE 10 1 × 11 day
      1 × 24 day then
      0 × 2 day
ethinyl estradiol and desogestrel Azurette, Kariva, Mircette 20 × 21 day then 0.15 × 21 day then
    10 × 5 day 0 × 5 day
Triphasic
ethinyl estradiol and norethindrone Aranelle, Leena, Tri-Norinyl 35 0.5 × 7 day then
  Cyclafem 7/7/7, Necon 7/7/7, Nortrel 7/7/7, Ortho-Novum 7/7/7, Estrostep Fe, Tilia FE, Tri-Legest FE 35 1 × 9 day then
    20 × 5 day then 0.5 × 5 day
    30 × 7 day then 0.5 × 7 day then
    35 × 9 day 0.75 × 7 day then
      1 × 7 day
      1
ethinyl estradiol and norgestimate OrthoTri-Cyclen, TriNessa, Tri-Sprintec 35 0.18 × 7 day then
  OrthoTri-Cyclen Lo 25 0.215 × 7 day then
      0.25 × 7 day
      0.18 × 7 day then
      0.215 × 7 day then
      0.25 × 7 day
ethinyl estradiol and levonorgestrel Enpresse, Trivora-28 30 × 6 day then 0.05 × 6 day then
    40 × 5 day then 0.075 × 5 day then
    30 × 10 day 0.125 × 10 day
ethinyl estradiol and desogestrel Caziant, Cyclessa, Velivet 25 0.1 × 7 day then
      0.125 × 7 day then
      0.15 × 7 day
Four-phasic
Estradiol valerate and dienogest Natazia 0 mg × 2 day then 3 × 2 day then
    2 mg × 5 day then 2 × 5 day then
    2 mg × 17 day then 3 × 17 day then
    2 mg × 2 day 0 × 2 day
Extended cycle
levonorgestrel/ethinyl estradiol Seasonale, Introvale, Jolessa, Quasense 30 mcg × 91 day 0.15 × 91 day
    30 × 84 day then 0.15 × 84 day then
  Seasonique, Camrese 10 × 7 day 0 × 7 day
  LoSeasonique 20 × 84 day then 0.1 × 84 day then
    10 × 7 day 0 × 7 day
EMERGENCY CONTRACEPTION
levonorgestrel Plan B One-Step 0 1.5 mg once. Take ASAP after unprotected intercourse; maximum efficacy w/in 72 hours, moderate efficacy w/in 120 hours.
  Next Choice 0 0.75 mg × 1 dose 12 hours apart ASAP after unprotected intercourse; maximum efficacy within 72 hours, moderate efficacy within 120 hours; Alt: 2 tabs po × 1
Progestin receptor modulators Ulipristal   30 mg once; ASAP within 120 hours of unprotected intercourse
PROGESTIN ONLY
norethindrone Camila 0 0.35
  Errin 0 0.35
  Heather 0 0.35
  Jolivette 0 0.35
  OrthoMicronor 0 0.35
  Nor-QD 0 0.35
  Nora-BE 0 0.35
TRANSDERMAL SYSTEM
ethinyl estradiol and norelgestromin Ortho-Evra 20/24 hr 0.15/24 hr q wk × 3, then no patch × 1 wk
    20 mcg/day  
VAGINAL
ethinyl estradiol and etonogestrel ring NuvaRing 15/24 hr 0.12/24 hr for 3 wk, then off 1 wk, self-inserted
  15 mcg/day    
INTRAUTERINE
Nonhormonal IUD ParaGard   q10yr
levonorgestrel IUD Mirena   52 mg q5yr
INJECTION
medroxyprogesterone Depo-Provera   150 mg q12wk (IM) or 104 mg SQ q12wk
PROGESTIN SUBDERMAL IMPLANT
etonogestrel Implanon, Nexplanon (radiopaque)   68-mg implant, one implant subdermally q3y
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Jul 22, 2016 | Posted by in PHARMACY | Comments Off on Contraceptives

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