By Dr. Marcus Judge

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Pharmacology

Contents

  1. Introduction
  2. Sex Steroid Hormones
  3. Hormonal Contraception
  4. Hormone Replacement Therapy
  5. Selective Modulators
  6. Hormonal Therapy in Cancer
  7. Drugs in Obstetric Practice
  8. Summary
  9. Drug Summary Table
  10. Quiz

Abstract

  • The sex steroid hormones (oestrogens, the main female sex hormones; progestogens, progesterone-like hormones; and androgens, male sex hormones such as testosterone) bind nuclear receptors and act through gene transcription. Drugs in this area are either analogues (drugs that copy the natural hormone), antagonists (drugs that block its action) or selective modulators, which act as an agonist in some tissues and an antagonist in others.
  • The combined oral contraceptive pill (COCP) contains a synthetic oestrogen and a progestogen and acts mainly by suppressing ovulation. The progestogen-only pill (POP) works mainly by suppressing ovulation (desogestrel and drospirenone pills). The older levonorgestrel and norethisterone POPs do not reliably suppress ovulation. They rely on thickening the mucus at the neck of the womb (cervical mucus), among other effects.
  • Hormone replacement therapy (HRT) relieves menopausal symptoms and lowers the risk of fragility fractures (fractures after a low-impact injury) while it is taken. It increases the risk of breast cancer (combined preparations) and of venous thromboembolism (VTE, blood clots in the veins) with oral preparations.
  • Selective receptor modulators include tamoxifen (SERM: antagonist in breast, agonist in endometrium and bone) and ulipristal acetate (SPRM: emergency contraception, fibroids).

Core

Introduction

Drugs acting on the reproductive hormone system are widely used in the UK, both for women's health (contraception, HRT, cancer treatment) and men's health (prostate disease, hormone-sensitive cancer). This article covers the principal classes at pre-clinical level. The underlying physiology is set out in the SimpleMed Reproductive System articles.

Sex Steroid Hormones

The three main classes (oestrogens, progestogens and androgens) are synthesised from cholesterol via the steroid biosynthetic pathway (the series of enzyme steps that builds steroid hormones) and act predominantly on nuclear receptors. The receptor-hormone complex moves into the nucleus (translocates) and modulates gene transcription, so the effects develop over hours to days rather than seconds.

Oestrogens

The oestrogens made by the body (endogenous oestrogens) are oestradiol (the most potent), oestrone and oestriol. Synthetic versions used in pharmacology include ethinylestradiol (in the COCP), oestradiol valerate, and conjugated equine oestrogens (in some HRT preparations).

Major actions: development of secondary sexual characteristics in puberty, regulation of the menstrual cycle, maintenance of bone density, and a number of metabolic and vascular effects. Drugs that make use of these actions include the combined oral contraceptive pill (COCP), hormone replacement therapy (HRT) and selective oestrogen receptor modulators (SERMs).

Progestogens

Progesterone made by the body (endogenous progesterone) is produced by the corpus luteum (the structure left in the ovary after ovulation) and the placenta. Synthetic progestogens used clinically include levonorgestrel (the progestogen-only pill or POP, emergency contraception, and the levonorgestrel intrauterine device or LNG-IUD, which used to be called an intrauterine system), desogestrel (POP), norethisterone, drospirenone and medroxyprogesterone (depot injection, a long-acting injection that releases the drug slowly; also HRT).

Major actions: preparation of the endometrium (the lining of the uterus) for implantation, maintenance of pregnancy, and breast development. Synthetic progestogens differ in their androgenic (male-hormone-like), mineralocorticoid (salt- and water-retaining) and glucocorticoid (cortisol-like) effects, which is why side-effect profiles vary across formulations.

Androgens

The principal androgen is testosterone, with the more potent metabolite dihydrotestosterone (DHT) formed from testosterone by the enzyme 5α-reductase. Therapeutic uses include replacement in hypogonadism (low sex hormone production by the testes or ovaries; testosterone preparations) and gender-affirming care.

Hormonal Contraception

The Combined Oral Contraceptive Pill

The combined oral contraceptive pill (COCP) contains an oestrogen (almost always ethinylestradiol) and a synthetic progestogen. Mechanisms:

  • Suppression of ovulation: negative feedback on the hypothalamus and pituitary suppresses gonadotrophin-releasing hormone (GnRH), follicle-stimulating hormone (FSH) and luteinising hormone (LH).
  • Thickening of cervical mucus (the mucus at the neck of the womb, or cervix).
  • Effects on the endometrium (the lining of the uterus) and on tubal motility (movement of the egg along the fallopian tube), which add to the contraceptive effect.

The contraceptive efficacy with perfect use is very high (around 0.3% failure per year), but typical-use failure is about 7 to 9% per year because of missed pills.

Non-contraceptive benefits: the COCP also reduces the risk of ovarian, endometrial and colorectal cancer, regulates the menstrual cycle, and improves acne and dysmenorrhoea (painful periods).

Side effects and risks:

  • Venous thromboembolism (VTE): the absolute risk is low in healthy young women. In one year, about 2 in 10,000 women who are not using a COCP develop a VTE. The figure is 5 to 7 in 10,000 for COCPs containing levonorgestrel, norethisterone or norgestimate, and 9 to 12 in 10,000 for COCPs containing drospirenone, desogestrel or gestodene. The UK Medical Eligibility Criteria (UKMEC) grade each method for each condition from 1 to 4. Category 4 means an unacceptable health risk. Category 3 means the method is not recommended because the risks outweigh the benefits. The COCP is category 4 after a previous VTE or after major surgery with prolonged immobilisation. It is category 3 with a body mass index (BMI) of 35 kg/m2 or more, a first-degree relative who had a VTE before the age of 45, or immobility unrelated to surgery.
  • Stroke and myocardial infarction (MI, heart attack): rare in healthy women. The COCP causes a very small increase in the risk of MI and about a two-fold increase in the risk of stroke. The risk is greatest in women who smoke and in women with diabetes, hypertension, a BMI of 35 kg/m2 or more, or migraine with aura (migraine preceded by visual or other sensory warning symptoms). The COCP is category 4 for migraine with aura, and for women aged 35 or over who smoke 15 or more cigarettes a day. It is category 3 for women aged 35 or over who smoke fewer than 15 cigarettes a day.
  • Breast cancer: small increased risk, falling after stopping.
  • Cervical cancer: small increase with prolonged use.
  • Hypertension, mood changes, breast tenderness, breakthrough bleeding (bleeding between periods).

Pharmacokinetic interaction (an interaction that changes how the body handles a drug): ethinylestradiol is metabolised by hepatic (liver) cytochrome P450 (CYP) enzymes. Enzyme-inducing drugs (drugs that make the liver break down other drugs faster) reduce contraceptive efficacy. Examples are rifampicin and rifabutin, several antiepileptics (carbamazepine, oxcarbazepine, phenytoin, phenobarbital, primidone and topiramate), some antiretrovirals (ritonavir, ritonavir-boosted protease inhibitors, efavirenz and nevirapine), and St John's wort. Standard non-enzyme-inducing antibiotics no longer require additional contraceptive precautions in current guidance from the Medicines and Healthcare products Regulatory Agency (MHRA) and the Faculty of Sexual and Reproductive Healthcare (FSRH), although they were historically thought to.

The Progestogen-Only Pill

The progestogen-only pill (POP) contains a single progestogen (commonly desogestrel or levonorgestrel). The desogestrel and drospirenone POPs work mainly by inhibiting ovulation, with an additional effect on cervical mucus. The older levonorgestrel and norethisterone POPs do not reliably inhibit ovulation. They rely on their effects on cervical mucus, the endometrium (which becomes thinner) and tubal motility, and they require strict timing.

The POP is one option when the COCP is not suitable. Examples are women aged 35 or over who smoke, women with a history of VTE, women less than 6 weeks after giving birth, and women with hypertension, migraine with aura or significant cardiovascular risk. Other progestogen-only methods and intrauterine methods can usually also be used in these groups, but the progestogen-only injection is category 3 (not recommended) after a VTE or when there are multiple cardiovascular risk factors.

Long-Acting Reversible Contraception

Long-acting reversible contraception (LARC) methods do not depend on remembering to take a pill every day. The implant and the intrauterine devices have typical-use failure rates of 0.1% to 0.8% per year, far lower than the COCP (about 7 to 9%). The injection has a typical-use failure rate of about 4% per year, which is lower than the COCP but higher than the implant and the intrauterine devices. NICE advises that everyone needing contraception is given information about, and offered a choice of, all methods, including LARC:

  • Progestogen-only injection (depot medroxyprogesterone acetate, "Depo"): every 12-13 weeks. Concerns about bone mineral density limit prolonged use in adolescents.
  • Progestogen-only implant (etonogestrel, Nexplanon): a rod placed under the skin (subcutaneous) that lasts 5 years according to current NHS and NICE Clinical Knowledge Summaries (CKS) advice (the British National Formulary, BNF, still gives the licensed duration as up to 3 years). Most effective reversible contraception (typical-use failure about 0.1% per year, similar to the LNG-IUD at 0.1% to 0.4%).
  • Levonorgestrel intrauterine device (LNG-IUD, for example Mirena), formerly called an intrauterine system (LNG-IUS): Mirena is effective for 8 years for contraception (or until age 55 if it is inserted at age 45 or over). It is also used for menorrhagia (heavy periods; effective for 5 years) and as the progestogen component of HRT, to protect the endometrium (Mirena is licensed for this for 4 years, but use for up to 5 years is supported).
  • Copper intrauterine device (Cu-IUD): non-hormonal; its main action is to prevent fertilisation, through the effect of copper on the egg and sperm; it can be used as emergency contraception.

Emergency Contraception

Three options are available in the UK:

  • Levonorgestrel 1.5 mg orally: effective up to 72 hours after unprotected sex; less effective with each passing hour. CKS advises ulipristal acetate, or a double dose (3 mg) of levonorgestrel, when the BMI is over 26 kg/m2 or the body weight is over 70 kg. A copper IUD, or a double dose (3 mg) of levonorgestrel, is also advised for people taking liver enzyme-inducing drugs (drugs that make the liver break down other drugs faster).
  • Ulipristal acetate 30 mg orally: a selective progesterone receptor modulator (SPRM), effective up to 120 hours (5 days) after unprotected sex.
  • Copper intrauterine device: the most effective option, can be inserted up to 5 days after unprotected sex (or up to 5 days after the earliest expected ovulation).

Hormone Replacement Therapy

Hormone replacement therapy (HRT) replaces oestrogen (and, in women with a uterus, a progestogen) lost at the menopause. NICE advises offering HRT for vasomotor symptoms (hot flushes and night sweats) and offering vaginal oestrogen for genitourinary symptoms (vaginal dryness and urinary symptoms). Fragility fracture risk is lower while taking HRT, but this benefit decreases once treatment stops.

Two principles to remember:

  • Women with a uterus need combined HRT (oestrogen + progestogen): unopposed oestrogen (oestrogen given without a progestogen) increases the risk of endometrial hyperplasia (overgrowth of the endometrium) and cancer.
  • Women without a uterus (post-hysterectomy) can have oestrogen-only HRT.

Routes: oral, transdermal (through the skin, as a patch or gel) and vaginal (local). Transdermal preparations avoid first-pass metabolism (breakdown in the liver before the drug reaches the rest of the body) and carry a lower VTE risk than oral preparations. NICE advises considering transdermal rather than oral HRT for people at increased risk of VTE, including those with a BMI over 30 kg/m2.

Risks:

  • Breast cancer: the risk increases with combined (oestrogen + progestogen) HRT, rises with the duration of use and persists for at least 10 years after stopping. There is very little or no increase with oestrogen-only HRT.
  • VTE: oral oestrogen increases risk; transdermal does not.
  • Stroke: small absolute increase with oral preparations.
  • Endometrial cancer: the risk increases if a woman with a uterus takes oestrogen without a progestogen.
  • Cardiovascular disease: HRT does not protect against heart disease (the early observational data were confounded, that is, distorted by other differences between the groups being compared), although starting HRT within 10 years of menopause is not associated with substantial cardiovascular harm.

Selective Modulators

Tamoxifen and Raloxifene (SERMs)

Selective oestrogen receptor modulators (SERMs) bind the oestrogen receptor but produce tissue-specific effects: agonist in some tissues, antagonist in others. The key examples:

Tamoxifen:

  • Active itself, but converted in the liver (mainly by the enzyme CYP2D6) to more potent metabolites, 4-hydroxytamoxifen and endoxifen. Tamoxifen and these metabolites compete with oestrogen at the oestrogen receptor (ER).
  • Antagonist in breast tissue: the basis of its use in oestrogen-receptor-positive breast cancer (cancer cells that carry oestrogen receptors, so oestrogen helps them grow), used as adjuvant therapy (treatment given after surgery to reduce the risk of the cancer returning). NICE includes tamoxifen among the options for pre-menopausal women. It also offers tamoxifen to post-menopausal women at low risk of recurrence or who cannot take an aromatase inhibitor, and to people with male reproductive organs. It is usually given for 5 years, and NICE says to consider extending it beyond 5 years.
  • Agonist in endometrium: increases the risk of endometrial hyperplasia and cancer.
  • Agonist in bone in post-menopausal women: helps to preserve bone mineral density. In pre-menopausal women it is possibly associated with bone density loss.
  • Increases VTE risk.

Raloxifene:

  • Antagonist in breast and endometrium.
  • Agonist in bone.
  • Used for the secondary prevention of osteoporotic fragility fractures (preventing further fractures after a first one) in post-menopausal women who cannot take or tolerate a bisphosphonate (a drug that slows bone loss).

Ulipristal and Mifepristone (SPRMs)

Selective progesterone receptor modulators (SPRMs) bind the progesterone receptor with similar tissue-specific behaviour:

  • Ulipristal acetate: emergency contraception (delays or inhibits ovulation if taken up to 120 hours after unprotected sex). Ulipristal 5 mg is also licensed for uterine fibroids (non-cancerous growths in the uterus), but because of rare, serious liver injury (hepatotoxicity) it is now limited to intermittent treatment of moderate to severe symptoms before the menopause, when surgery is not suitable or has failed.
  • Mifepristone (RU-486): progesterone receptor antagonist with significant antiglucocorticoid activity (it blocks the action of cortisol-like hormones). Used (with misoprostol) in medical termination of pregnancy. The BNF does not list Cushing's syndrome (a condition of excess cortisol) as a UK indication, although mifepristone is approved for it in some other countries, where its glucocorticoid receptor blockade is exploited.

Hormonal Therapy in Cancer

Aromatase Inhibitors

Anastrozole, letrozole and exemestane inhibit aromatase, the enzyme that converts androgens to oestrogens. They suppress oestrogen synthesis in peripheral tissues (the main source of oestrogen in post-menopausal women) and are the usual adjuvant therapy (treatment given after surgery to reduce the risk of recurrence) for oestrogen-receptor-positive breast cancer in post-menopausal women at medium or high risk of recurrence. NICE offers tamoxifen instead to those at low risk of recurrence, or if an aromatase inhibitor is not tolerated or is contraindicated.

Side effects relate to oestrogen deprivation: hot flushes, joint pains (common and limit adherence), accelerated bone loss (NICE advises a baseline DEXA scan, a bone density scan, and bisphosphonates, which are drugs that slow bone loss, for those at risk of fracture), and a small adverse effect on the lipid profile (blood fats such as cholesterol).

GnRH Analogues and Antagonists

GnRH analogues, also called GnRH agonists (goserelin, leuprorelin), initially stimulate the pituitary, then desensitise it, ultimately suppressing FSH and LH and producing a "medical castration" (drug-induced suppression of the sex hormones). The initial flare is a short-term rise in testosterone. It is clinically important: in prostate cancer it can cause a tumour flare, with increased bone pain, spinal cord compression or ureteric obstruction (a blocked tube from the kidney). To prevent this, an anti-androgen such as cyproterone acetate is started 5 to 7 days before the first dose of the analogue and continued for 3 to 4 weeks afterwards.

Indications:

  • Prostate cancer (androgen deprivation therapy).
  • Pre-menopausal hormone-sensitive breast cancer.
  • Endometriosis (womb-lining tissue growing outside the uterus) and uterine fibroids (non-cancerous growths in the uterus).
  • In vitro fertilisation (IVF) protocols.

GnRH antagonists (degarelix) act immediately without the flare. They have not replaced agonists in metastatic prostate cancer. NICE recommends degarelix only as an option for advanced hormone-dependent prostate cancer in people with spinal metastases (secondary tumours in the spine), and relugolix, an oral GnRH antagonist, as an option for advanced hormone-sensitive prostate cancer.

Anti-Androgens

  • Bicalutamide, flutamide, cyproterone acetate: competitive antagonists at the androgen receptor. They are used in prostate cancer. Cyproterone acetate 2 mg, combined with ethinylestradiol (co-cyprindiol), is also used for hirsutism (excess terminal hair growth in women, for example on the face and chest) and for moderate to severe acne. It also works as a contraceptive, but it should not be used solely for contraception: it is reserved for people who need treatment for androgen-dependent skin conditions. Cyproterone acetate carries a dose-related risk of meningioma (a tumour of the membranes around the brain), so it must not be used in anyone with a meningioma or a history of one. High doses are restricted, except in prostate cancer, to when alternative treatments are unavailable or inappropriate. Flutamide can cause liver damage (hepatitis and abnormal liver function, sometimes fatal).
  • Finasteride and dutasteride: 5α-reductase inhibitors; reduce DHT formation. Both are used in benign prostatic hyperplasia (BPH, non-cancerous enlargement of the prostate). Finasteride 1 mg is also used for male-pattern baldness (androgenetic alopecia); dutasteride is listed in the BNF for BPH only. Side effects include reduced libido and erectile dysfunction, which with finasteride may persist after treatment stops. The MHRA warns that finasteride is associated with depression and suicidal thoughts, and has added a precautionary warning about mood changes to dutasteride.
  • Spironolactone: antagonist at the mineralocorticoid receptor (the receptor through which aldosterone makes the kidney retain salt and water) that also has some anti-androgen activity at the androgen receptor, used for hirsutism in women. This use is not licensed.

Drugs in Obstetric Practice

A handful of obstetric drugs are routinely tested at pre-clinical level:

  • Oxytocin: given intravenously to induce or augment (speed up) labour, and as an intramuscular injection in active management of the third stage of labour (the time from the birth of the baby to the delivery of the placenta and membranes). The synthetic preparation is Syntocinon. Syntometrine is oxytocin combined with ergometrine. NICE says that Syntometrine may be more effective than oxytocin alone at reducing postpartum haemorrhage (PPH, heavy bleeding after birth) and advises it when there are risk factors for PPH. Syntometrine is more likely to cause nausea and vomiting, and it is contraindicated in women with severe hypertension, pre-eclampsia, eclampsia or severe cardiac, hepatic or renal disease.
  • Ergometrine: makes the smooth muscle of the uterus contract; used for PPH. It is contraindicated in eclampsia, severe hypertension, severe cardiac disease, vascular disease and sepsis, and in the first and second stages of labour.
  • Misoprostol: a prostaglandin E1 analogue (a synthetic version of a hormone-like chemical that softens the cervix and makes the uterus contract); uses include induction of labour (NICE offers low-dose 25 microgram oral tablets as one option), postpartum haemorrhage and miscarriage (the BNF notes that these two uses are not licensed), and (with mifepristone) medical termination of pregnancy. It induces uterine contractions and is teratogenic (can harm a developing baby) in the first trimester (roughly the first 12 weeks), so it is avoided when a pregnancy is to continue.
  • Tocolytics (drugs that suppress uterine contractions in preterm labour): nifedipine (a calcium channel blocker) is first-line in the UK, atosiban (an oxytocin receptor antagonist) is offered if nifedipine is contraindicated, and NICE advises against beta-agonists. Gestation is written as weeks+days, so 24+0 means 24 weeks and 0 days. NICE says to consider nifedipine from 24+0 weeks and to offer it from 26+0 to 33+6 weeks.
  • Magnesium sulfate: given intravenously. It is the anticonvulsant of choice for eclampsia (seizures in pregnancy), and diazepam and phenytoin should not be used instead. It is considered for severe pre-eclampsia (high blood pressure with organ involvement in pregnancy) when the woman is in critical care and birth is planned within 24 hours (NICE NG133). It is also offered for fetal neuroprotection (to protect the baby's brain) to women between 24+0 and 29+6 weeks who are in established preterm labour or having a planned preterm birth within 24 hours. NICE NG25 says to consider it between 30+0 and 33+6 weeks in the same situations, and to discuss it between 23+0 and 23+6 weeks.
  • Antihypertensives in pregnancy: labetalol is considered first, nifedipine if labetalol is not suitable, and methyldopa only if neither labetalol nor nifedipine is suitable. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) should be stopped if a woman becomes pregnant.
  • Anti-D immunoglobulin: given to RhD-negative women (women who lack the RhD antigen on their red blood cells) to prevent haemolytic disease of the fetus and newborn. NICE recommends routine antenatal anti-D prophylaxis for all RhD-negative pregnant women who are not known to be sensitised. It is also given after potential sensitising events (events in which fetal blood may enter the mother's circulation).

Summary

  • Sex steroid drugs act on nuclear receptors via transcription: effects are slow but durable.
  • The COCP contains ethinylestradiol and a progestogen; works mainly by suppressing ovulation; main risks are VTE, stroke and MI, with a small rise in breast cancer risk; efficacy reduced by enzyme-inducing drugs (rifampicin, antiepileptics, St John's wort).
  • The POP is one option when oestrogen is contraindicated; other progestogen-only methods and intrauterine methods can usually also be used.
  • Long-acting reversible contraceptives (implant, LNG-IUD, Cu-IUD, depot injection): the implant and the intrauterine devices have the lowest typical-use failure rates (0.1% to 0.8% per year), while the depot injection is less reliable in typical use (about 4%).
  • Emergency contraception: levonorgestrel up to 72 hours; ulipristal up to 120 hours; copper IUD most effective.
  • HRT relieves menopausal symptoms and lowers fragility fracture risk while it is taken; oral preparations increase VTE risk (transdermal preparations do not); combined HRT increases breast cancer risk; women with a uterus need a progestogen to prevent endometrial cancer.
  • Tamoxifen is a SERM: antagonist in breast (cancer treatment), agonist in endometrium (cancer risk) and, after the menopause, in bone (bone preservation).
  • Aromatase inhibitors (anastrozole, letrozole) are used in post-menopausal ER-positive breast cancer.
  • GnRH analogues produce medical castration: used in prostate cancer, endometriosis and fibroids.
  • Key obstetric drugs: oxytocin, ergometrine, misoprostol, nifedipine (tocolytic), magnesium sulfate (eclampsia), labetalol (hypertension in pregnancy), and anti-D immunoglobulin.

Drug Summary Table

Class Examples Use Key points / side effects
Combined oral contraceptive pill (COCP) Ethinylestradiol + progestogen Contraception, cycle regulation, acne VTE, ↑ BP, breast & cervical cancer; ↓ ovarian/endometrial cancer; reduced by enzyme inducers
POP Desogestrel, levonorgestrel Contraception when oestrogen contraindicated Irregular bleeding
LARC (progestogen) Implant (Nexplanon), depot injection (Depo-Provera), LNG-IUD (Mirena) Long-acting contraception, menorrhagia (heavy periods), HRT progestogen Implant and LNG-IUD: lowest typical-use failure rates; depot: about 4% typical-use failure, bone density concern
Emergency contraception Levonorgestrel (≤72 h), ulipristal (≤120 h), copper IUD (≤5 d) Post-coital prevention Copper IUD most effective
HRT Oestradiol ± progestogen Menopausal symptoms; lowers fragility fracture risk while taken Combined ↑ breast cancer; oral ↑ VTE; consider transdermal if VTE risk is increased
SERM Tamoxifen, raloxifene ER+ breast cancer (tamoxifen, pre-menopausal women); osteoporosis (raloxifene) Tamoxifen ↑ endometrial cancer & VTE
SPRM Ulipristal acetate; mifepristone Emergency contraception (ulipristal); medical termination of pregnancy (mifepristone) Mifepristone has antiglucocorticoid activity
Aromatase inhibitors Anastrozole, letrozole, exemestane Post-menopausal ER+ breast cancer Joint pain, bone loss (baseline bone density scan; bisphosphonates for those at risk)
GnRH analogues / antagonists Goserelin, leuprorelin (agonists); degarelix (antagonist) Prostate cancer, breast cancer (pre-menopausal), endometriosis, fibroids, IVF Initial flare with agonists; medical castration symptoms
Anti-androgens Bicalutamide, cyproterone (androgen receptor, AR, antagonists); finasteride, dutasteride (5α-reductase inhibitors) Prostate cancer (bicalutamide); BPH (finasteride, dutasteride), hair loss (finasteride) Reduced libido, erectile dysfunction (may persist); finasteride: depression, suicidal thoughts; cyproterone: meningioma
Obstetric drugs Oxytocin, ergometrine, misoprostol, nifedipine, magnesium sulfate, labetalol, anti-D immunoglobulin Labour induction/augmentation, postpartum haemorrhage (PPH), tocolysis, eclampsia, hypertension in pregnancy, RhD prophylaxis Misoprostol: avoid if the pregnancy is to continue (it induces contractions and is teratogenic in the first trimester); ergometrine: avoid in severe hypertension and pre-eclampsia; magnesium sulfate toxicity

Reviewed by: Dr. Marcus Judge

Quiz

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