Contraception

How does oestrogen affect the menstrual cycle at the hypothalamus and pituitary?

Oestrogen exerts negative feedback on GnRH, LH and FSH during most of the cycle, preventing excessive follicular recruitment. Around mid-cycle, sustained high oestrogen triggers a positive feedback loop, producing the LH surge that causes ovulation. In contraception, oestrogen maintains a constant high level, eliminating the LH surge and preventing ovulation.

How does oestrogen affect the endometrium?

Oestrogen stimulates proliferation of the endometrial lining during the follicular phase, increasing growth of glands and stroma. In combined hormonal contraception, continuous low-dose oestrogen stabilises the endometrium to prevent breakthrough bleeding, but does not allow the natural proliferative-to-secretory transition.

How does oestrogen affect the cervical environment?

Oestrogen produces thin, watery, stretchable cervical mucus (Spinnbarkeit). This facilitates sperm penetration during the fertile window. In contraception containing oestrogen, the progestogen component usually dominates mucus characteristics, so mucus tends to remain thick despite the presence of synthetic oestrogen.

How does progesterone affect the hypothalamus and pituitary?

Progesterone suppresses GnRH pulsatility, which reduces LH and prevents the LH surge required for ovulation. This suppression is the primary mechanism of progestogen-only contraceptives, though suppression may not be complete in all users.

How does progesterone affect the endometrium?

Progesterone converts a proliferative endometrium into a secretory one. In contraception, continuous progestogen causes endometrial glandular atrophy and thinning, making implantation unlikely. This is why progestogen-only methods often cause lighter periods or amenorrhoea.

How does progesterone affect cervical mucus?

Progesterone produces thick, viscous mucus that forms a barrier to sperm entry. This is one of the most reliable contraceptive actions of progestogen-only pills, implants and IUS systems.

How does progesterone affect the fallopian tubes?

Progesterone slows tubal ciliary beating and muscular contractions. This alteration reduces gamete and embryo transport. In contraceptive doses, this contributes to reduced fertilisation probability.

Combined Oral Contraception

COC gives continuous synthetic oestrogen + progestogen, creating a pseudo-pregnancy hormonal state. This suppresses the hypothalamic–pituitary–ovarian (HPO) axis, so ovulation does not occur. Ovulation suppression is the primary mechanism.

Step-by-step

1. Hormones taken daily

   • Tablet contains ethinylestradiol (oestrogen) + a progestogen (e.g. levonorgestrel, desogestrel).

   • Blood levels are steady and higher than normal cycle levels.

2. Negative feedback on the HPO axis

• High oestrogen + progestogen inhibit GnRH from the hypothalamus.

• This reduces FSH and LH release from the pituitary.

3. Ovulation is prevented

• ↓ FSH → follicles do not mature properly.

• ↓ LH → no LH surge, so no ovulation.

4. Cervical mucus thickens (progestogen effect)

• Mucus becomes thick and hostile to sperm, reducing sperm entry into the uterus.

5. Endometrium becomes thin and inactive

• The uterine lining is less receptive, making implantation unlikely.

• Progesterone is only “pro-implantation” when:

  • It rises after ovulation

  • On a lining already thickened by oestrogen

• In COC, progesterone is early, constant, and synthetic, so it has the opposite effect.

Why is ovulation not always absolutely suppressed in some CHC users?

Pharmacokinetic variation affects hormone levels; metabolism differs between individuals; missed pills or absorption issues can temporarily reduce suppression. Some degree of follicular development may still occur but usually without ovulation.

What are major benefits of combined hormonal contraception?

It is reliable, rapidly reversible, unrelated to intercourse, and under the woman’s control. It reduces ovarian and endometrial cancer risk by half, helps endometriosis, reduces dysmenorrhoea, menorrhagia and PMS, and allows cycle control including continuous use to stop periods.

What are risks of combined hormonal contraception?

Most COC risks come from oestrogen effects on clotting and liver metabolism and progestogen effects on vascular tone and metabolism. All listed risks are rare, but certain risk factors increase likelihood.

1. Cardiovascular risks

Arterial (mainly progestogen-related, risk-modified)

• Includes stroke and myocardial infarction

• Risk increases with:

  • Smoking (especially >35 years)

  • Hypertension

• Mechanism:

  • Progestogens can affect lipids and vascular tone

  • Smoking + oestrogen/progestogen → endothelial damage + thrombosis risk

Venous (mainly oestrogen-related)

• Includes VTE:

  • DVT

  • Pulmonary embolism

• Mechanism:

  • Oestrogen increases clotting factors (II, VII, IX, X) and reduces anticoagulants

• Higher risk in:

• Inherited clotting disorders

• Obesity

• Immobility

• Migraine with aura (important contraindication)

2. Neoplastic risks

• Breast cancer:

  • Slight increase while using COC

  • Risk returns to baseline after stopping

• Cervical cancer:

  • Slight increase with long-term use

• Liver tumours:

  • Rare (hepatic adenomas), oestrogen-related

• Protective effects (important exam point):

  • ↓ Ovarian cancer

  • ↓ Endometrial cancer

3. Gastrointestinal / metabolic

• Insulin resistance / carbohydrate metabolism

  • Oestrogen can reduce insulin sensitivity

• Weight gain

  • Evidence weak; often due to fluid retention rather than fat gain

4. Hepatic risks

• Liver metabolises steroid hormones → increased hepatic workload

• Can worsen:

  • Congenital non-haemolytic jaundice

  • Cholestasis

• ↑ Risk of gallstones

  • Oestrogen increases cholesterol in bile

5. Dermatological

• Chloasma (melasma)
  

  • Oestrogen increases melanocyte activity

• Acne

  • Depends on progestogen type (some androgenic, some anti-androgenic)

• Erythema multiforme

  • Rare immune-mediated reaction

6. Psychological

• Mood swings

• Depression

• Changes in libido

• Mechanism:

  • Steroid hormones interact with neurotransmitters (serotonin, GABA)

How do liver enzyme-inducing drugs affect CHC?

Drugs such as carbamazepine, phenytoin, rifampicin, topiramate and certain antiretrovirals increase hepatic metabolism of contraceptive hormones, lowering serum levels and reducing efficacy. Additional barrier methods are required.

What are the pill rules for CHC?

Start on day 1 of menstruation. Take 21 days of pills followed by a 7-day pill-free interval, restarting on day 8. Late or missed pills in the first week require condoms. Missing pills in the last 7 days means skipping the pill-free interval. Annual BP and BMI checks are required

How does the vaginal ring work?

The ring delivers the same hormones as CHC but via the vaginal route. It stays in for 21 days, is removed for 7 days, and then replaced. It avoids daily pill taking but still relies on correct insertion and timely replacement.

Progestogen-only contraception?

Progestogen creates a hostile reproductive environment—mainly by thickening cervical mucus. Ovulation suppression happens variably, depending on dose and delivery method.

What progestogen does in the body

1. Thickens cervical mucus (main mechanism for all methods)

• Mucus becomes thick, viscous, and impermeable

• Sperm cannot penetrate the cervix

• This effect happens even at low hormone levels

2. Thins the endometrium

• Progestogen suppresses endometrial proliferation

• Lining becomes thin, inactive, and unreceptive

• Implantation is unlikely

3. Suppresses ovulation (method-dependent)

• High, continuous progestogen → suppresses LH surge

• Reliability varies:

• Desogestrel POP, implants, injections → ovulation usually suppressed

• Traditional POPs → ovulation often still occurs

4. Reduces tubal motility

• Slows ciliary action and smooth muscle contraction

• Reduces sperm–egg transport efficiency

2. Progestogen-only methods

A. Long-acting reversible contraception (most reliable)

• Implants (e.g. etonogestrel)

• Hormone-releasing IUS (levonorgestrel)

• Injectables (e.g. medroxyprogesterone acetate)

Mechanism:

• Cervical mucus thickening

• Endometrial thinning

• Consistent ovulation suppression

B. User-dependent methods (POPs)

• Daily tablets

• Mechanism depends on type:

• Desogestrel POP → usually suppresses ovulation

• Older POPs → mainly rely on cervical mucus

• Timing is critical (missed pills reduce efficacy)

3. Why there is no oestrogen

• Avoids oestrogen-related risks:

• VTE

• Hypertension

• Migraine with aura

So it’s safe to use in:

• Breastfeeding

• Smokers >35

• Many cardiovascular risk groups

Copper IUDs

Copper IUCDs create a toxic, inflammatory intrauterine environment that is hostile to sperm and implantation. They work without hormones.

Step-by-step

Copper ion release

• The device continuously releases Cu²⁺ ions into the uterine cavity.

1. Direct spermicidal effect (primary mechanism)

   • Copper ions:

     • Are toxic to sperm

     • Reduce sperm motility and viability

     • Increase reactive oxygen species

• Fertilisation is usually prevented before sperm reach the egg.

2. Sterile inflammatory reaction

• Copper acts as a foreign body → local inflammatory response

• ↑ Leukocytes, macrophages, and prostaglandins

• This environment is hostile to:

  • Sperm

  • Eggs

  • Early embryos

Endometrial effects

• Prostaglandins + inflammation → endometrium unsuitable for implantation

• Also causes:

  • ↑ uterine contractility

  • ↓ implantation probability

3. Mechanical contribution

• Physical presence of the device adds a minor mechanical barrier, but this is not the main effect

Important clarifications (exam-relevant)

• Copper IUCDs do not disrupt an established pregnancy

• Main action is pre-fertilisation

• Can be used as emergency contraception (up to 5 days post-intercourse)

• No systemic hormonal effects

What are benefits of IUCDs?

They are extremely reliable, immediately effective, non-user dependent, long-acting, coitus-independent, rapidly reversible and free from major systemic risks

What are disadvantages of IUCDs?

They require trained insertion, may cause pain during fitting, may increase menstrual pain or bleeding (copper types), do not protect against STIs, and threads may be felt by partners.

What are risks of IUCDs?

Rare expulsion, rare uterine perforation, miscarriage risk if pregnancy occurs with IUCD in situ, and a small risk of ectopic pregnancy if pregnancy occurs.

What are absolute contraindications for IUCDs?

Current pelvic inflammatory disease, pregnancy, unexplained vaginal bleeding, and uterine cavity abnormalities.

Condoms

They create a physical barrier preventing semen from entering the vagina. They also provide protection against STIs by preventing direct mucosal contact and limiting fluid exchange.

What are advantages and disadvantages of male condoms?

Advantages include user control, STI protection and availability. Disadvantages include need for correct timing, potential latex allergy, potential erection-related issues, and higher failure rates with imperfect use.

What are advantages and disadvantages of female condoms?

Advantages include user control, STI protection, and usability independent of male erection. Disadvantages include cost, obtrusiveness, noise during intercourse and uncertain real-world failure rates.

Diaphragms and Caps work?

They are barrier methods that physically block the cervix, stopping sperm from entering the uterus. They rely on correct placement + spermicide.

Step-by-step

1. Insertion before sex

   • The diaphragm or cap is inserted into the vagina before intercourse.

   • It is positioned to cover the cervix completely.

2. Barrier effect

• The device forms a physical barrier over the cervical os.

• Sperm cannot pass from the vagina into the uterus.

3. Spermicide use (essential)

• Spermicide is applied to:

  • Kill sperm

  • Immobilise sperm that reach the device

• Barrier alone is not sufficient.

4. After intercourse

• Device must be left in situ for at least 6 hours.

• This ensures any remaining sperm are inactivated.

• Removing it earlier increases pregnancy risk.

2 types:

Diaphragm caps

• Made of latex

• Fit across the vagina, covering the cervix

• Come in different sizes (needs fitting)

Cervical (suction) caps

• Made of plastic

• Smaller, fits directly onto the cervix by suction

• Different sizes available

Key limitations (exam-relevant)

• User-dependent → higher failure rate

• Must be fitted correctly

• No STI protection

• Less effective in parous women (especially cervical caps)

What are advantages and disadvantages of diaphragms and caps?

Advantages include user control, advance insertion and perceived naturalness. Disadvantages include training requirements, higher failure rates, messy spermicide use and increased UTI or Candida risk.

How does fertility awareness–based contraception work?

It predicts the fertile window using cycle length, cervical mucus, basal body temperature and ovulation signs. Couples avoid unprotected sex during the fertile period or target intercourse during that window when trying to conceive.

Why is fertility awareness method effectiveness highly user dependent?

It requires accurate daily observation, partner cooperation, teaching from a trained practitioner, and consistent abstinence or alternative contraception during the fertile window. Any deviation reduces reliability.

Emergency Contraception

Emergency contraception works by preventing or delaying ovulation or by preventing fertilisation/implantation, depending on the method and timing. It does not terminate an established pregnancy.

1. Postcoital (emergency) pills

A. Levonorgestrel (LNG)

• Time window: up to 72 hours after unprotected sexual intercourse (UPSI)

• Main mechanism:

  • Delays or inhibits ovulation if taken before the LH surge

• Effectiveness:

  • Prevents ~7 out of 8 expected pregnancies

• Key limitation:

  • Ineffective if ovulation has already occurred

B. Ulipristal acetate (ellaOne)

• Time window: up to 120 hours (5 days) after UPSI

• Main mechanism:

  • Potent ovulation delay, even close to the LH surge

• Effectiveness:

  • More effective than levonorgestrel near ovulation

Pills mainly act in the first half of the cycle → “beware” if ovulation has already occurred.

2. Copper IUCD (most effective method)

• Time window:

  • Up to 5 days after ovulation, or

  • Up to 5 days after UPSI at any time in the cycle

• Mechanism depends on cycle phase:

  • Before ovulation: copper is toxic to sperm → prevents fertilisation

  • After ovulation: induces inflammatory endometrial response → prevents implantation

• Failure rate: extremely low (most effective emergency method)

• Provides ongoing contraception once inserted

Exam-critical distinctions

• Emergency contraception ≠ abortion

• Pills → mainly ovulation delay

• Copper IUCD → works before and after ovulation

What is the difference between perfect use and typical use when measuring contraceptive efficacy?

Perfect use refers to method use exactly as prescribed without errors. Typical use includes real-world behaviours such as missed pills or incorrect barrier use. Typical use failure rates are often significantly higher, especially for user-dependent methods.

Why are long-acting reversible contraceptives (LARCs) considered most effective in real-world settings?

They eliminate daily or situational user involvement, removing adherence errors. Implants, IUS and IUCDs show minimal difference between perfect use and typical use, making them the most reliable options.