- 1 1. What methods of contraception are currently available to women in the United States?
- 2 2. With typical use (as opposed to perfect use) of a given method of contraception, what percentage of women will have an unintended pregnancy within the first year of use?
- 3 3. What is the mechanism of action of oral contraceptives?
- 4 4. What is the association of OCPs with myocardial infarction?
- 5 5. What is the association of oral contraceptives with stroke?
- 6 6. What is the relationship between second- and third-generation OCPs and the risk of deep vein thrombosis?
- 7 7. What are some of the therapeutic uses of oral contraceptives?
- 8 8. What are the noncontraceptive benefits of OCPs?
- 9 9. What is the association of oral contraceptives with cancer?
- 10 10. List the contraindications for oral contraceptive use.
- 11 11. Describe some other methods of hormonal contraception, aside from oral contraceptives.
- 12 12. What potential problems and side effects are attributed to long-acting hormonal contraception?
- 13 13. What is the effect of hormonal contraception on pregnancy?
- 14 14. What methods of emergency contraception are currently available?
- 15 15. What is the mechanism of action of emergency contraceptives?
- 16 16. What is the mechanism of action of an IUD?
- 17 17. List the absolute contraindications for an IUD insertion.
- 18 18. What are the major risks associated with IUD use?
- 19 19. What is the appropriate time for IUD insertion?
- 20 20. Describe the mechanism of action of barrier methods of contraception.
- 21 21. What are some of the advantages and disadvantages of barrier methods of contraception?
- 22 22. What is the role of permanent sterilization as a contraceptive method?
1. What methods of contraception are currently available to women in the United States?
– Abstinence, withdrawal, and fertility awareness
– Permanent sterilization
- (a) Oral contraceptives (OCPs; combination and progestin-only)
- (b) Injectables:
- – Depot medroxyprogesterone acetate (Depo-Provera)
- – Lunelle (estradiol cypionate and medroxyprogesterone acetate)
- (c) Implant:
- – Norplant (6 rods of levonorgestrel)
- (d) Vaginal ring (NuvaRing: ethinyl estradiol and etonorgestrel)
- (e) Transdermal patch (Evra: ethinyl estradiol and norgestimate)
– Intrauterine device (IUD)
- (a) Levonorgestrel (Mirena)
- (b) Copper (Paragard)
- (a) Diaphragm
- (b) Cervical cap
- (c) Condoms (male and female)
– Emergency contraception (hormonal and copper IUD)
2. With typical use (as opposed to perfect use) of a given method of contraception, what percentage of women will have an unintended pregnancy within the first year of use?
* Limited data on “typical use” for these methods.
3. What is the mechanism of action of oral contraceptives?
Estrogenic effects: inhibition of ovulation in part by the suppression of follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
Progestational effects: inhibition of ovulation by suppressing LH; thickening of cervical mucus, thus hampering sperm transport; possible inhibition of sperm capacitation; production of a decidualized endometrium with exhausted and atrophic glands; altered motility of the uterus and fallopian tubes
4. What is the association of OCPs with myocardial infarction?
Recent evidence shows that the association between current combined oral contraceptive use (containing 35 mcg of ethinyl estradiol) and myocardial infarction (MI) is weak, with a relative risk ranging from 0.9 to 2.5. There is no evidence to support an increased or decreased risk of MI due to past OCP use compared to no use. Smoking has been identified as an independent risk factor for MI; the combination of smoking and OCP use can be synergistic for increasing the risk of an MI.
5. What is the association of oral contraceptives with stroke?
The link between high-dose oral contraceptive pills and ischemic stroke has historically been reported. Subsequent studies showed a decrease in the odds ratio and relative risk with a decrease in the estrogen dose. There is no significant increase in risk of ischemic stroke in women younger than 45 years old who use OCPs. In addition, there is no consistent, strong evidence linking OCP use to hemorrhagic stroke. Since smoking, hypertension, and migraine headaches all are independent risk factors for stroke, women with other independent risk factors (e.g., smoking, diabetes) may have a slightly increased risk of stroke while taking an oral contraceptive.
6. What is the relationship between second- and third-generation OCPs and the risk of deep vein thrombosis?
Deep vein thrombosis (DVT) and pulmonary embolism are the most common, serious side effects of estrogen-containing hormonal contraception. Risk increases approximately threefold with modern oral contraceptives (35 mcg of ethinyl estradiol)-less than the increase associated with pregnancy. There is no biological evidence that specific progestins have different effects on clotting factors.
In the mid-1990s, however, epidemiological studies reported that women using third-generation OCPs (containing the progestins gestodene and desogestrel) had a higher risk of venous thromboembolism compared to women using second-generation oral contraceptives (containing norethindrone and levonorgestrel). Studies performed since then have shown a weak association between OCP use and venous thromboembolism (strength of association ranging from 0.7 to 2.3). After reanalysis of the data, the U.S. Food and Drug Administration issued a statement that the risk of DVT with the third-generation progestins “is not great enough to justify switching to other products.”
Factor V Leiden mutation occurs in 3-5% of Caucasians and is responsible for the majority of cases of venous thrombosis in which there is an identifiable risk factor. This mutation may independently increase the risk of DVT.
7. What are some of the therapeutic uses of oral contraceptives?
Hyperandrogenism: Combination OCPs suppress ovarian, adrenal, and peripheral androgen metabolism. The estrogen component of oral contraceptives also increases sex hormone-binding globulin levels and inhibits 5-alpha-reductase in the skin, resulting in lower levels of dihydrotestosterone. OCPs, alone or with other agents, can successfully treat both acne and hirsuitism. No randomized controlled trial has found one formulation to be better than another in the treatment of acne. From a clinical standpoint, over 60% of women with hirsuitism respond to OCPs. Current low-dose progestin-only pills do not stimulate an androgenic response.
Menstrual disorders: Primary dysmenorrhea in most women can be successfully treated with oral contraceptives. Oral contraceptives should be used after an attempt of the first-line treatment of nonsteroidal anti-inflammatory medications is unsuccessful. OCPs can be used to treat heavy and inter-menstrual bleeding by restoring synchrony to the endometrium. For acute episodes of menorrhagia (seen commonly with anovulation) with associated anemia, high-doses (three or four pills a day) of combination formulations can effectively suppress bleeding. Once the bleeding has stopped, the high-dose regimen can be tapered and then stopped to allow withdrawal bleeding. For episodes of heavy bleeding without anemia, one or two pills of a high-dose formulation can be effective until bleeding abates, followed by a withdrawal bleed.
Endometriosis: Clinicians often use oral contraceptives to reduce pelvic pain associated with endometriosis and for long-term suppression after initial medical or surgical therapy. A recent Cochrane Collaboration review supported the use of OCPs as a “long-term alternative treatment for the painful symptoms of endometriosis.”
Hypoestrogenic states: OCPs have been used in women with hypothalamic amenorrhea as a method of hormone replacement therapy. The majority of these patients are adolescents with eating disorders or exercise-induced amenorrhea. Oral contraceptive use in the perimenopausal period has several distinct advantages: it prevents pregnancy, regulates uterine bleeding in a predictable fashion, and treats vasomotor and vaginal dryness symptoms at the same time. Estrogen replacement in the form of oral contraceptives can also benefit patients who are amenorrheic after radiation, chemotherapy, or bilateral oophorectomy.
Ovarian cysts: Even though oral contraceptives are sometimes prescribed to induce regression of ovarian cysts, little evidence exists to support this treatment.
Other menstrual-related disorders: OCPs may be useful in managing premenstrual-related mood disturbances (premenstrual dysphoric disorder). Some randomized controlled studies have shown benefits of oral contraceptives for this purpose, while others have not. Menstrual migraines occur immediately prior to the onset of menses and not at any other time during the cycle. These headaches may be triggered by changes in estrogen levels immediately prior to menstrual flow and can be treated with OCPs that deliver a continuous dose of estrogen, thereby minimizing hormone fluctuation.
8. What are the noncontraceptive benefits of OCPs?
- Reduction of ovarian and endometrial cancer risk
- Decreased risk of benign breast disease (fibroadenomas, fibrocystic change)
- Decreased risk of symptomatic pelvic inflammatory disease
- Decreased risk of ectopic pregnancy
- Increase in bone mineral density
- Possible reduction in colorectal cancer risk
- Possible improvement in symptoms of rheumatoid arthritis
- Decrease in menstrual flow
- Decreased incidence of anemia
- Decrease in primary dysmenorrhea
- Improvement in hirsutism and acne
9. What is the association of oral contraceptives with cancer?
Ovarian cancer: Users of oral contraceptives are less likely to develop ovarian cancer than never-users. The risk of developing epithelial ovarian cancer decreases by 40% with as little as 3-6 months of OCP use. Further declines in risk are seen with longer periods of use. The protective effect persists for at least 15 years after OCP discontinuation. OCPs may provide primary prevention for women at risk for hereditary ovarian cancer as well.
Endometrial cancer: Pill users have a 50% reduction in endometrial cancer risk compared to never-users. Risk is reduced by 20% with 1 year of use, 40% with 2 years of use, and 60% with 4 or more years of use. This reduction in risk persists for at least 15 years after discontinuation. Protection is seen with all monophasic preparations, including pills with less than 50 mcg of ethinyl estradiol, but there are no data thus far with multiphasic or progestin-only preparations.
Breast cancer: Evidence suggest that there is a slight increase in the relative risk of localized breast cancer associated with current (relative risk 1.24) or recent (relative risk 1.16 for use within 1-4 years) use of oral contraceptives compared to never use. However, breast cancers diagnosed in OCP users were significantly less advanced than those in never-users. Family history of breast cancer does not influence the association between current or recent oral contraceptive use and breast cancer risk. Also, duration of use, dosage, and formulation do not influence the risk of breast cancer. Young women have a very low baseline risk of breast cancer. This risk is slightly increased by the use of OCPs, but does not persist beyond 4 years after cessation of use.
Key points: contraception
- Combination oral contraceptives work by inhibiting ovulation through suppression of LH and FSH, thickening cervical mucus, and decreasing tubal motility.
- Venous thromboembolic events are the most common serious side effects of oral contraceptives.
- OCPs decrease the risk of ovarian and endometrial cancers but may increase the risk of breast cancer.
- Short-term, higher dose than OCP, combination estrogen and progesterone pills or progesterone-only pills (emergency contraception) can be taken within 72 hours of intercourse to prevent pregnancy after intercourse has occurred.
- A major additional advantage of barrier contraceptive methods, especially condoms, is prevention of STDs.
10. List the contraindications for oral contraceptive use.
Women with the following conditions should not use oral contraceptives:
- Known presence or history of deep venous thrombosis or pulmonary embolism
- History of cerebral vascular accident, coronary artery disease, or ischemic heart disease
- Diabetes with microvascular complications (neuropathy, retinopathy), or duration greater than 20 years
- History of estrogen-dependent cancer including known or history of breast cancer
- Current pregnancy
- Migraines with focal neurologic symptoms
- Age > 35 years in the setting of smoking more than 20 cigarettes a day
- Hypertension (blood pressure > 160/100 mmHg) or with vascular disease
- Active liver disease (benign hepatic adenoma, liver cancer, active viral hepatitis, or severe cirrhosis)
- Major surgery with prolonged immobilization or any surgery of the legs
- Presence or family history of hypercoagulable disorder
11. Describe some other methods of hormonal contraception, aside from oral contraceptives.
- Depo-Provera: intramuscular injection every 12 weeks of medroxyprogesterone acetate
- Lunelle: monthly injection of estradiol cypionate and medroxyprogesterone acetate
- Norplant: levonorgestrel; progestin-only implant lasting for 5 years
- NuvaRing: a vaginal ring combination of ethinyl estradiol and etonorgestrel placed every 3 weeks
- Evra: a transdermal combination patch of norgestimate and ethinyl estradiol placed every week
12. What potential problems and side effects are attributed to long-acting hormonal contraception?
Menstrual side effects are the most common side effects of hormonal contraception, particularly the progestin-only methods. Almost all women using Depo-Provera, Norplant, and progestin-only oral contraceptives experience irregular bleeding and spotting initially. With Depo-Provera, amenorrhea is common after 1 year of use (50%). Headaches are the most common nonmenstrual side effect. Both of these complaints often lead to method discontinuation. With the exception of Depo-Provera, return of fertility tends to be rapid for hormonal methods of contraception (approximately 1 month for most methods; 8.5 months for Depo-Provera).
The clinical significance of decreased bone mineral density (BMD) in Depo-Provera users is still under investigation. Studies have shown that small decreases in BMD do occur shortly after initiation of Depo-Provera use, but reverse after discontinuation-a trend that is similar to that seen during lactation.
13. What is the effect of hormonal contraception on pregnancy?
The use of any hormonal method of contraception early in pregnancy does not increase the risk of congenital anomalies or early pregnancy loss.
14. What methods of emergency contraception are currently available?
The emergency contraception formulations available in the United States include combined OCP tablets, progestin-only contraceptive tablets, and the copper-T IUD.
Combination methods: With the Yuzpe method, 200 mcg of ethinyl estradiol and 1 mg of levonorgestrel in two divided doses 12 hours apart is given. The risk of pregnancy is reduced by 74%. Preven is a prepackaged kit containing instructions for emergency contraceptive pill use, appropriately dosed estrogen and progestin pills, and a pregnancy test.
Progestin (levonorgestrel)-only methods: Plan B is a prepackaged form of progestin-only pills for emergency contraceptive use. It has similar or better effectiveness as the combination Yuzpe method and fewer side effects (nausea, vomiting).
All oral emergency contraception is best used within 72 hours of unprotected intercourse; use sooner, however, may be more effective.
Copper IUD: The IUD is a less frequently used method of emergency that can be inserted up to 7 days after ovulation to prevent pregnancy. The failure rate is very low, 0.1%. Also, this method has the additional advantage of providing long-term contraception.
15. What is the mechanism of action of emergency contraceptives?
Emergency contraception likely inhibits or delays ovulation and may also impair endometrial receptivity. Other possible mechanisms include interference with corpus luteum function, thickening of cervical mucus, and alterations in tubal transport of sperm, egg, or embryo. Emergency contraceptives do not interrupt an already established pregnancy.
16. What is the mechanism of action of an IUD?
An IUD causes a foreign-body reaction within the uterine cavity, thus altering sperm motility/integrity. It alters tubal fluids, thereby interfering with ova and sperm transport and interaction. Finally, an IUD alters the uterine lining so that it becomes unfavorable for implantation.
17. List the absolute contraindications for an IUD insertion.
- Confirmed or suspected pregnancy
- Known or suspected pelvic malignancy
- Undiagnosed vaginal bleeding
- Acute or chronic pelvic infection
- High-risk behavior for sexually transmitted diseases (i.e., multiple sexual partners, having partners at risk for sexually transmitted infections)
- Hyperbilirubinemia secondary to Wilson’s disease (for copper-containing devices only)
18. What are the major risks associated with IUD use?
- Displaced string
- Uterine perforation and difficult removal
- Pelvic infection: the IUD itself does not cause pelvic infection; in general, with IUDs there is an increased risk for pelvic inflammatory disease with exposure to sexually transmitted infections. The modern progestin-only IUDs may actually decrease the risk of pelvic infection by thickening cervical mucus.
19. What is the appropriate time for IUD insertion?
The levonorgestrel IUD should be inserted within 7 days of onset of menstruation or immediately after early pregnancy loss; it can then be replaced by a new system at any time of the menstrual cycle. The Copper IUD can be inserted at any point in the cycle as long as the patient is not pregnant. This IUD can be inserted immediately postpartum, postabortion, or as an “interval” insertion. An “interval” insertion is defined as insertion in women who are neither postpartum nor postabortion, or an insertion in women 6 weeks after delivery.
20. Describe the mechanism of action of barrier methods of contraception.
Both the male and female condoms provide a physical barrier that prevents sperm and egg interaction. Diaphragms, caps, and sponges use two different mechanisms, a physical barrier as well as a spermicidal chemical.
21. What are some of the advantages and disadvantages of barrier methods of contraception?
Vaginal barriers have many advantages, including protection against sexually transmitted infections, provision of immediate protection without much prior planning, easy access, and no systemic side effects. Disadvantages include the need for a high degree of motivation for use, discomfort with placement/use, possible latex allergy (condoms), and increased incidence of urinary tract infections (diaphragm).
22. What is the role of permanent sterilization as a contraceptive method?
Sterilization (female tubal sterilization and vasectomy) has become one of the most widely used methods of family planning worldwide. In fact, sterilization is the most common method of contraception used by couples over the age of 30 in the U.S. today. Both types are meant to be permanent and are comparable in effectiveness. Less than 1% of women will become pregnant after tubal sterilization in the first year. The risk of failure, however, persists for years after the procedure and varies by method of tubal occlusion and age of the patient.