Contraception

1. Contraception Professor Hassan Nasrat Professor of Obstetrics and Gynecology Faculty of Medicine King Abdulaziz University Jeddah (Rabi II 1425/ May 2004)

2. Why Contraception Appropriate Family planning is for both health and social benefits for the family and the society

3. Impact Of Lack Of Contraception On Maternal Mortality: - Maternal Mortality Estimate 600.000 Women/Year. - 200,000 Due To Failure Or Lack Of Contraceptive Services. Impact Of Lack Of Contraception On Maternal Health: Unwanted Births Associated With Nonpsychotic Major Depression, Feelings Of Powerlessness, Increased Time Pressures, And Reduction In Overall Physical Health. Impact Of Lack Of Contraception On Infants Mortality: Infant Mortality In Developing Countries Could Be Decreased By One Third By Increasing The Spacing Between Births To 2 To 4 Years. Impact Of Lack Of Contraception On Infants And Children Health: Unwanted Children Had More Health Problems, E.G. LBW, Higher Mortality…etc. That Children From Large Families Generally Receive Less Education. Impact Of Lack Of Contraception On Societies: Population Explosion Is A Worldwide Problem Considering Limitation of Global Resources.

4. Factors Detriment The Effectiveness Of Contraception Method • Patient Motivation: Studies Setting Vs. Normal Life Setting. • More Failure in Couples Seeking To Delay A Wanted Birth Compared With Those Seeking To Prevent Any More Births. • The Woman's Age. • Socioeconomic Status And Level Of Education • Marital Status: • Failure Rates Reported In Prospective Studies Are Also Consistently Lower Than Those Of Retrospective Interview Studies Because Of Recall Bias. • Failure Rates Are Greater During The First Year Of Use Than In Subsequent Years, Yet Most Studies Report Only First-year-use Failure Rates.

6. Methods of Contraception • Reversible contraceptive • Intrauterine devices, contraceptive implants, and injectable contraceptives are associated with a low pregnancy rate regardless of the population studied, and the rate is minimally influenced by compliance. • Oral contraceptives • Other methods: diaphragm/cervical caps, condoms, spermicides, withdrawal, and periodic abstinence. • Irreversible Methods: • Tubal sterilization: • Vasectomy:

7. Hormonal Contraception: • Hormonal Contraceptives May Be Taken: • Orally • Transdermally • Parenteral • Implant • Released From An Intrauterine Contraceptive Device • Postcoital Hormonal Contraception (Emergency Contraception)

8. Mechanism Of Action Of Hormonal Contraceptives • Suppression Of Ovulation Through Estrogen-induced Inhibition Of The Midcycle Surge Of Gonadotropin. • Suppression Of Gonadotropin Secretion During The Follicular Phase Of The Cycle, Thereby Preventing Follicular Maturation. • Suppression Of Ovarian Steroid Production, Due To Suppression Of Gonadotropin Secretion. • Decrease In Responsiveness Of The Pituitary To Gonadotropin-releasing Hormone May Play A Role. Progestin-related Mechanisms: - Effects On The Endometrium, Rendering It Less Suitable For Implantation. - Alterations In Cervical Mucus, Which Becomes Less Permeable To Sperm - Impairment Of Normal Tubal Motility And Peristalsis.

9. Contraindications For OCs: • The Absolute Contraindications Are: • Previous Thromboembolic Event Or Stroke. • History Of An Estrogen-dependent Tumor • Active Liver Disease. • Pregnancy. • Undiagnosed Abnormal Uterine Bleeding. • Hypertriglyceridemia. • Women Over Age 35 Years Who Smoke Heavily (Greater Than 15 Cigarettes Per Day). • Relative Contraindications: • Poorly Controlled Hypertension • Migraine Headaches (With Focal Neurologic Symptoms) • Anticonvulsant Drug Therapy. • Diabetes Mellitus • Obesity

10. Non Contraceptive Benefits Of OCs Pills: • Treatment Of Some Menstrual Disorders, Cases of Hypothalamic Amenorrhea, And As Hormone Replacement In Women With Primary Hypogonadism. • Premenstrual Dysphoric Disorder (PMDD). • Endometriosis. • Elevation Of Hemoglobin Level. • Reduce Frequency Of Benign Breast Disease. • Reduce Ovarian Cysts (True in Higher Dose Estrogen Pills Only). • Lesser Risk of Ovarian and Endometrial Cancer. • Improve Bone Quality • Treatment Of Acne (Low Androgenic Progestin)

11. Drug Interactions: The Metabolism Of OCs Is Accelerated By Any Drug That Increases Liver Microsomal Enzyme Activity Such As Phenobarbital, Phenytoin, Griseofulvin, And Rifampin. On Some Occasions Individual Women Have Had Been Reported To Have Significant Decreases In The Plasma Concentrations Of Ethinyl Estradiol When Taking Certain Other Antibiotics, Such As Tetracycline, Penicillin Derivatives, And Cephalosporins.

12. Phases In Development Of Hormonal OCs: • Low Dose OCs: Contain < 50 µG Ethinyl Estradiol • First Generation OCs: Contain 50 µG Or More Of Ethinyl Estradiol. • Second Generation OCs: Contain Levonorgestrel, Norgestimate, And Other Members Of The Norethindrone Family And 30 Or 35 µG Ethinyl Estradiol. • Third Generation OCs: Contain Desogestrel, Or Gestodene With 20 Or 30 µG Ethinyl Estradiol. The Progestogens Has: - Low Affinity For Androgen Receptors - Little Effect On Serum (SHBG) Concentrations - Less Of An Effect On Carbohydrate And Lipid Metabolism. - More Effective In Reducing Acne And Hirsutism

13. Progesterone Only Contraceptive Pills

14. Types Of Combination Pills: • Monophasic Pills: Contain The Same Dose Of Estrogen And Progestin In Each Of The 21 Hormonally Active Pills. • Multiphasic Preparations:Biphasic & Triphasic • Multiphasic Regimens Slightly Decrease Total Steroid Content Over The Month. But No Proven Clinical Advantage Over Monophasic Preparations.

15. Adverse Effects Of OCs: • Direct (Minor) Side Effects: • Early (Transient) Effects: Bloating, Nausea, Breast Tenderness, And Mood Changes. • Breakthrough Bleeding: Due To Endometrium Adjusting To A New Thin State (More Common With Lower Dose Of Estrogen) • Amenorrhea: ( Occur in 5-10%) Due To Atrophic Endometrium.

16. Major (Indirect) Side Effects: Risk Of Cardiovascular Disease: An Increase In CV Morbidity And Mortality Occurred With The Early High-dose Pills. (The RCGP Study, The Oxford Family Planning Association Study, The Walnut Creek Contraceptive Drug Study, And The Group Health Cooperative Of Puget Sound Study, Stadel 1981) The Reduction In Estrogen Content (30 To 35 µG Of EE) Has Increased Safety Substantially. There Is No Evidence That Low-dose OCs Increase The Risk Of CVD In Women Under Age 30 Years Or In Nonsmoking Women Without Other Risk Factors (Chasan-taber Et Al 1998

17. Coronary Heart Disease: • Most Large Epidemiological Studies Have Confirmed An Increased Risk Of CHD Among OCs Users Who Are Old (>35 Years Of Age) AndHeavy Smokers (> 15 Cigarettes/Day) Or Already Hypertensive. • Any Increased Risk Of Myocardial Infarction Is Related To A Thrombotic Mechanism Rather Than The Development Of Atherosclerotic Plaques. Croft, P And Hannaford, Pc. 1989) , WHO Collaborative Study Of CVD And Steroid Hormone Contraception. Lancet 1997; 349:1202).

18. A Meta-analysis Of The Available Data Found That: “A Nonsmoking, Normotensive Woman's Annual Stroke Risk Would Be Expected To Increase From 4.4 To 8.5 Per 100,000 With Use Of Low Estrogen Oral Contraceptives. Treatment Of 24,000 Women Would Lead To One Additional Ischemic Stroke Each Year (i.e. The Absolute Increase In Risk Is Extremely Low) Risk Appears To Be The Same For Second And Third Generation Progestins. The Risk Of Hemorrhagic Stroke Is Not Increased. (Gillum, et al. Ischemic stroke risk with oral contraceptives: A meta-analysis. JAMA 2000; 284:72).

19. Effect On BP • Early Epidemiologic Studies Using High-dose Estrogen Found A Mean Elevation In BP Of 3-6/2-5 mmhg, With Approximately 5 Percent Of Women Developing Overt Hypertension. • It Is More Likely To Occur In Patients Who Developed Hypertension During A Prior Pregnancy Or Who Have A Family History Of Hypertension. • Cessation Of Therapy Typically Leads To A Return To Baseline Bp Within Two To 12 Months, But Proteinuria May Persist.

20. However, Current Preparations Contain As Little As 20 Percent Of The Estrogen And Progestin In Previous Preparations. A Report From The Nurses' Health Study Prospectively Evaluated Almost 70,000 Female Nurses, Aged 25 To 42 Years (Chasan-taber, L, Et Al 1996). After Adjustment For Age, Weight, Smoking, Family History And Other Risk Factors, The Relative Risk Of Hypertension in OCs Users Compared To Women Who Never Used OCs Was: - 1.8 For Current Users Vs. 1.2 For Previous Users. - Only 41.5 Cases Per 10,000 Person-years Could Be Attributed To OCs. This Risk Rapidly Declined With Cessation Of Therapy.

21. Venous Thromboembolic Disease An (VTE) Is Seen With Both High And Low Dose Estrogen OCs Preparations • The Mechanism Of Venous Thromboembolism Increased Risk With OCs Pills May Be Due To • Acquired Resistance To Activated Protein C. • A Greater Increase In Factors II And VII. • A Greater Decrease In Factor V. (Vandenbroucke, Et Al. Medical Progress: Oral Contraceptives And The Risk Of Venous Thrombosis. N Engl J Med 2001; 344:1527).

22. For 2nd Generation: (Low-dose EE & No Gestodene Or Desogestrel) Versus No Use — Odds Ratio 3.2. • For 3ed Generation (Low-dose EE With Desogestrel Or Gestodene) Versus No Use —Odds Ratio 4.8. • For 3ed Generation Vs. 2nd Generation Products — Odds Ratio 1.5. • The Probability Of Death From Thromboembolism Was Higher With 3ed Than With 2nd Generation OCs Or No OCs • (2.0 Vs. 1.4 Vs. 0.5 Per 100,000 Women Per Year, Respectively). Spitzer Et Al 1996, Who Collaborative Study On CVD And Steroid Hormone Contraception 1995

24. The Increase In Risk With The Third Generation Progestins Is Real, Clinically Important And May Apply Particularly To Women With Existing Cardiovascular Risk Factors Or An Inherited Or Acquired Thrombophilia.

25. Cerebral Vein Thrombosis At Higher Risk Of Cerebral Vein Thrombosis Is Present in: Carriers Of Hereditary Thrombophilias (Factor V Leiden, The Prothrombin Gene Mutation, And Deficiencies Of Protein S, Protein, C, And Antithrombin). Subjects With Hyperhomocysteinemia.

26. Glucose Metabolism: High-dose OCs Can Cause Abnormal GTT But Only Few Women Developed Diabetes. Women Taking Low-dose OCs Have Normal GTT, But May Develop Mild Insulin Resistance.

27. Lipid Metabolism: The Effect Depends Upon The Estrogen Dose And The Androgenicity Of The Progestin. The Estrogen: - Increases Serum Triglycerides And HDL Concentrations - Lowers Serum LDL Cholesterol Concentrations. The Progestin: - Increases Serum LDL C - Lowers Serum HDLc Concentrations, (Particularly The Androgenic Progestins Norgestrel And Levonorgestrel).

28. Contraceptives With Low-dose Norethindrone Lower Serum LDL Cholesterol And Raise Serum HDL Cholesterol Concentrations Because Of The Dominant Effects Of Estrogen And The Relatively Low Androgenicity Of Norethindrone. The Newer Progestins, Such As Desogestrel, Tend To Raise Serum HDL Cholesterol And Lower LD Cholesterol Concentrations. In A Meta-analysis Of 18 Studies, Administration Of A Desogestrel-containing OC Increased The Former By 5.8 Mg/Dl (0.2 Mmol/L) And Reduced The Latter By 4.5 Mg/Dl (0.1 Mmol/L).

29. Risk Of Cancer: Breast Cancer: In The Nurses' Health Study: Long-term OC Use Did Not Result In An Increase In Risk Of Breast Cancer Risk In Women Over Age 40 Years (Hankinson, SE, Et Al 1997). A Population-based, Case-control Study(Marchbanks, PA, Et Al 2002) Design: Women Ages 35 To 64 4574 Women With BC And 4682 Controls Over 75 % Using Or Had Used OCs. Result: The RR Of BC For Current Or Previous Oral Contraceptive Use Were 1.0 (95 Percent CI 0.8 To 1.2) And 0.9 (95 Percent CI 0.8 To 1.0), Respectively. Conclusion: BC Risk Was Not Associated With Estrogen Dose, Duration Of Use, Initiation At A Young Age (< Age 20), Or Race.

30. Cervical cancer OCs users has increased risk for developing cervical cancer. A systematic review of 28 studies (Smith, JS, et al 2003) including over 12,000 women with cervical cancer increased Risk with increasing duration of oral OC use. Even after adjusting for the number of sexual partners, previous cervical smears, smoking, histology (adenocarcinoma or squamous cell), HPV status, and use of barrier methods. It is not known if the increased risk of cervical cancer persists after discontinuation of OC's.

31. Most Studies Indicate HPV-negative OC Users Do Not Have An Increased Risk Of Cervical Cancer (De Villiers, EM. 2003). The Mechanism For An Increased Cervical Cancer Risk In HPV-positive OC Users: May Be Related To A Metabolite Of Estradiol, 16 Alpha-hydroxyestrone, Which Can Act As A Cofactor With Oncogenic HPV To Promote Cell Proliferation

33. Ovarian Cancer There Is A Decrease In The Risk Of Non-hereditary Forms Of Ovarian Cancer, Presumably Due To Inhibition Of Ovarian Stimulation. Data On OCs and Use and Risk Of Hereditary Forms, Such As Those Associated With Mutations In The BRCA1 Or BRCA2 Gene, Are Conflicting.

34. Endometrial Cancer OCs Decreases The Risk Of Endometrial Cancer. In One Study, Women Using Combination Oral Contraceptive Pills For At Least 12 Months Had A Relative Risk Of Endometrial Cancer Of 0.6 (95 Percent CI, 0.3 To 0.9) Compared With Nonusers. The Protective Effect Of Oral Contraceptives Persisted For At Least 15 Years After Cessation Of Use. This Benefit Is Likely Related To The Progestin Effect Which Suppresses Endometrial Proliferation.

35. Melanoma The Impact Of Oral Contraceptives On The Risk Of Melanoma Has Been Unclear. A Prospective Cohort Study Of Premenopausal Caucasian Women, Current Oral Contraceptive Use Was Associated With A Two-fold Increase In Risk, Particularly In Current Users With Ten Or More Years Of Use ( Feskanich D 1999). A Systematic Meta-analysis That Included 18 Case-control Studies Showed No Evidence For An Increased Risk Of Melanoma With The Use Of OCs ( Pfahlberg A Et Al 1997).

37. Low Estrogen Oral Contraceptives: Age-Specific Estimation of Cardiovascular Risk No. of excess cases of MI & Stroke attributed to OCs / 100,000 women-yr of use No. of pregnancy related deaths/100,000 live births

38. Emergency Contraception

39. Indications: Contraceptive Failure: E.G. A Condom Ruptures; A Diaphragm Or Cervical Cap Dislodges; An Intrauterine Device (IUD) Is Expelled; Or Birth Control Pills Are Lost, Forgotten, Or Poorly Absorbed In The Presence Of Gastrointestinal Hypermotility. Other Indications Rape Or Incestual Coitus.

40. Injectable contraceptives

41. Injectable Contraceptives: • Depo-medroxyprogesterone(dmpa) • Medroxyprogesterone Acetate/Estradiol Cypionate. • Advantages: • Highly Effective • Reversible, • Avoid The Need For Compliance. Daily • Reduce The Volume Of Menstrual Bleeding • DMPA Reduce The Risk Of Endometrial Cancer.

42. Depot Medroxyprogesterone Acetate (150 Mg Deep IM, Effective As Contraception For 3-4 Months. Theoretical And Actual Effectiveness Is 99.7 Percent. Mechanism Of Action: Inhibiting Ovulation. Changes In The Endometrium And Cervical Mucus, Resulting In Decreased Sperm Transport And Implantation. Advantages: - If Estrogen-containing OCs Is Either Contraindicated Or Causes Additional Health Concerns E.G. Migraine, Sickle Cell Anemia, Fibroids. - Older Women Who Smoke

43. Adverse Effects and Disadvantages: • Delay in the Return Of Fertility 6 To 9 may be Up To 18 Months. • Amenorrhea And Irregular Bleeding: • Other Adverse Effects (Related To Its Androgenicity): E.G. Acne. Headache., And Depression. • Weight Gain: Not Certain

45. Contraceptive Implants Transdermal Contraceptive Patch Contraceptive Vaginal ring Diaphragm and cervical cap Sponge

46. Two-rod Subdermal Levonorgestrel Implant • Significantly Easier To Insert( Than The 6 Rod Norplant) And Remove. • Protection From Pregnancy Occurs Within 24 Hours Of Insertion When Inserted In The First Week Of The Menstrual Cycle. • The Major Side Effect Is Irregular Bleeding. • Fertility Returns Rapidly After Removal Of The Rods. • The Cumulative Pregnancy Rate In Clinical Trials Was 0.3 At Three Years And 1.1 Percent At Five Years, Which Is A Lower Failure Rate Than That Of OCs And Most IUDs And Comparable To That Of Surgical Sterilization. • Efficacy May Be Reduced Slightly As Body Weight Increases.

47. Number 10 trocar illustrating first (1) and second (2) markings to guide placement of implants. After infiltration with local anesthetic, advance the trocar and obturator under the skin to the second mark nearer the hub.

48. Once the trocar is inserted to the second mark, remove the obturator and place an implant in the trocar Advance the obturator to the implant (to a point of gentle resistance Withdraw the trocar to the mark nearer the tip, leaving the implant behind

49. Redirect and advance the trocar and obturator while pushing the previously placed implant away from the trocar.

50. Vaginal ring (NuvaRing). The circular ring is flexible and easily inserted into the vagina. Unlike the diaphragm, the vaginal ring does not have to be in a specific position, because absorption of the hormones can occur anywhere in the vagina.