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Combined oral contraceptives prevent pregnancy by inhibiting ovulation through suppression of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) but have no protective effect against STIs. They do not prevent pathogen transmission because they act systemically rather than as a physical barrier.

Intrauterine devices (IUDs) prevent pregnancy by causing a local inflammatory reaction toxic to sperm and ova or releasing hormones to thicken cervical mucus. They do not prevent STIs and can increase the risk of pelvic inflammatory disease if inserted in women with an active infection.

Contraceptive implants release progestin to inhibit ovulation and thicken cervical mucus. While highly effective for pregnancy prevention, they do not prevent exposure to pathogens during sexual activity and thus offer no protection from STIs.

Combined oral contraceptives contain both estrogen and progestin, increasing the risk of ischemic stroke in women with migraine with aura. Estrogen elevates hepatic production of clotting factors II, VII, IX, X, and fibrinogen, promoting a hypercoagulable state. This makes them contraindicated in such patients despite high contraceptive efficacy.

Transdermal contraceptive patches deliver systemic estrogen and progestin, carrying the same thromboembolic and cerebrovascular risks as COCs. They are contraindicated in women with migraine with aura due to estrogen’s vascular effects, even though they avoid daily pill intake.

Vaginal contraceptive rings release estrogen and progestin locally but still achieve systemic estrogen absorption comparable to COCs. This retains the same contraindications in women with migraine with aura due to increased stroke risk, making them inappropriate despite convenience and high efficacy.

Combined oral contraceptives contain estrogen, which reduces prolactin secretion and may decrease milk volume, especially within the first 6 weeks postpartum. Estrogen also increases the risk of thromboembolism during this period due to pregnancy-induced hypercoagulability, evidenced by elevated fibrinogen (normal 200–400 mg/dL) and clotting factors.

The transdermal contraceptive patch delivers systemic estrogen and progestin, posing the same risks to milk supply and thrombosis as COCs. Its estrogen exposure is continuous, potentially reducing daily milk output by disrupting prolactin-mediated milk synthesis.

The vaginal contraceptive ring releases estrogen and progestin, achieving systemic estrogen levels sufficient to impact prolactin. This estrogen exposure during exclusive breastfeeding may compromise milk production and should be avoided in the first 6 weeks postpartum.