GC160 The Woman Needs That Drug Oral Contraceptives Drugs Affecting Uterine Motility
Oral contraceptives are estrogen-progestin or progestin-only formulations that prevent ovulation, alter the endometrium, and thicken cervical mucus, while uterine motility drugs such as oxytocin, ergot alkaloids, prostaglandins, and tocolytics either stimulate or inhibit uterine contractions to manage labor, postpartum hemorrhage, or preterm labor.
Oral Contraceptives & Drugs Affecting Uterine Motility
Big Idea: This lecture bridges reproductive endocrinology and clinical pharmacology. It covers (1) how gonadotropins and gonadal hormones regulate the menstrual cycle, (2) how exogenous estrogen and progestin exploit these feedback loops for contraception, (3) the pharmacology and adverse-effect profiles of COCs vs POPs, (4) drug interactions that reduce OCP efficacy, (5) the physiology of labour onset, and (6) drugs that either promote (uterotonics) or suppress (tocolytics) uterine contractions.
Learning Objectives (from the slide deck) [1]:
| # | Objective |
|---|---|
| I | Describe functional relationships of gonadotropins (FSH, LH) and gonadal hormones (estrogen, progestin) in ovaries and uterus |
| II | Describe contraceptive actions of estrogen and progestin |
| III | Compare COCs and POPs — composition, dosing regimens, unwanted effects, drug-drug interactions |
| IV | Recognise resources available to guide patient counselling on contraception |
| V | Describe events underlying onset of labour and mediators (PG, OT) involved |
| VI | Describe uses of uterotonic drugs |
| VII | List examples of tocolytic drugs |
How it fits: This is a clinical pharmacology lecture that directly underpins O&G clinical practice — fertility regulation, induction of labour, management of postpartum haemorrhage, and emergency tocolysis for preterm labour. Expect MCQs on COC/POP differences, estrogen-related thromboembolic risk, progestin generations, mechanisms of uterotonics/tocolytics, and drug interactions.
1. Menstrual Cycle Hormonal Physiology (Review for Contraception)
High Yield: The lecture walks through a numbered 10-step feedback loop that you must understand to explain why contraceptives work. This is labelled "for your own review" but the contraceptive mechanism slides directly reference it. [1]
| Phase | Ovarian Event | Endometrial Event | Dominant Hormones |
|---|---|---|---|
| Menstrual | — | Shedding | Falling E & P |
| Follicular | Follicle development (FSH early, then LH & E late) | Proliferative (supported by E) | Rising FSH → rising E |
| Ovulatory | Ovulation | — | LH surge (triggered by very high E via +ve feedback) |
| Luteal | Corpus luteum | Secretory (supported by P) | High P & E from corpus luteum |
Critical feedback concepts from slides [1]:
- Rising E has little effect (via −ve feedback) on LH — this is why LH keeps rising in the follicular phase even as E rises.
- Continuous increase in E to reach above a threshold exerts +ve feedback to cause LH & FSH surge — the switch from negative to positive feedback is dose-dependent.
- Very high P level offsets E-mediated +ve feedback, causing FSH & LH to decrease — this is the basis of progestin-based contraception.
- FSH & LH begin to rise again as E & P levels fall — the trigger for a new cycle, and what happens during the hormone-free interval of COCs.
- Inhibin (from granulosa cells) also contributes to FSH suppression.
High Yield: Sustained E & P inhibits follicular development (via inhibiting FSH & LH), but no +ve feedback to increase FSH & LH → no LH surge → no ovulation → no corpus luteum. [1]
2.1 Four Mechanisms of Contraception (slide 9 summary) [1]
| Mechanism | Hormone Responsible | Why It Works |
|---|---|---|
| Suppression of ovulation | E + P together suppress FSH & LH; P prevents LH surge | No follicular maturation, no ovulation |
| Impaired endometrial development | Asynchronous P & E → thinner lining, altered secretions | Less favourable for implantation |
| Thickened cervical mucus | P | Impedes sperm penetration |
| Altered ovum transport | P & E alter tubal motility | Lower chance of fertilisation |
Why Sustained E Doesn't Cause an LH Surge in COC Users
In the normal cycle, the LH surge requires E to rise continuously past a threshold. In COC users, E is provided at a constant low dose — it never builds up enough for positive feedback. Additionally, the progestin component actively suppresses the LH surge by exerting negative feedback. The combination is therefore synergistic: estrogen suppresses FSH (preventing follicle development), while progestin suppresses LH (preventing ovulation even if some follicular development occurs).
3. Combined Oral Contraceptives (COCs)
Each COC pill contains an estrogen (E) + a progestin (P). [1]
Contraindicated in pregnancy, breast cancer & other conditions (that allow usage of POP instead) [1]
The "other conditions" relate to estrogen's vascular effects (detailed in POP section below).
3.3 Dosing Regimens
Each hormone-containing pill (containing same E & P dose) taken continuously for 21 or 24 days; one hormone-free pill for each of remaining 7 (of 21) days or 4 (of 24) days of cycle [1]
Purpose of hormone-free interval: to allow bleeding, as preferred by some patients, but no demonstrated medical benefit [1].
What happens during hormone-free days [1]:
- No exogenous estrogen → reduced negative feedback → FSH may stimulate some follicular development → endogenous estradiol secretion → endometrial growth → endometrial atrophy follows (similar to end of menstrual period) & bleeding.
| Feature | 21-day active + 7-day HFI | 24-day active + 4-day HFI |
|---|---|---|
| Example | Yasmin® (EE 0.03 mg + drospirenone 3 mg) | Yaz® (EE 0.02 mg + drospirenone 3 mg) |
| HFI length | 7 days | 4 days |
| Follicular development | More (longer HFI) | Less (shorter HFI) |
| Contraceptive efficacy | Slightly less | Better (less follicle rescue) |
| Unscheduled bleeding | Less | More (less endometrial development from lower E dose & shorter cycle) |
Shorter hormone-free period = better efficacy due to less-well developed follicle; shorter = increased chance of unscheduled bleeding due to less well-developed endometrium [1]
Other regimen options [1]:
- Extended-cycle (e.g. 84 active pills + 7 inert pills → bleeding every 3 months)
- Continuous (no scheduled bleeding at all)
Biphasic and triphasic COCs: lower total hormone dose taken in a cycle, aiming to mimic more closely changing ratios of E & P in a natural menstrual cycle [1]
- Comparable contraceptive efficacy as monophasic
- Generally reduced risk of unscheduled bleeding — better development & maintenance of endometrial tissue with phasically adjusting E:P ratio
- But more unscheduled bleeding in biphasic COCs than triphasic COCs — perhaps due to greater increase in P:E ratio → more atrophic endometrium, or inadequate progestin at later phase mimicking end of menstrual cycle
- May exacerbate estrogen-mediated mood symptoms (lower total E & P → less stable hormone levels)
High-dose (50 μg) no longer common for contraceptive use — more thromboembolic effects [1] Low-dose (20 to 35 μg) [1]
| EE Dose | Thromboembolic Risk | Unscheduled Bleeding |
|---|---|---|
| 50 μg (high) | Higher | Lower |
| 35 μg (low) | Lower | Lower |
| 20 μg (ultra-low) | Lowest (but depends on progestin) | Higher |
The 'Net Estrogenic Effect' Concept
The thromboembolic risk is not determined by EE dose alone. It depends on the net estrogenic effect, which is the EE effect minus the opposing androgenic/progestogenic activity of the progestin. If the progestin is anti-androgenic (like drospirenone), it enhances the estrogenic effect → more thromboembolism. If the progestin is androgenic (like levonorgestrel), it opposes the estrogenic effect → less thromboembolism. The slide explicitly states: "E" effect opposed by "P" & "A" [1].
This is a critical exam topic. The slide presents a conceptual framework of how different progestins modulate the "net estrogenic effect" [1].
| Generation | Example | Androgenicity | Anti-androgenicity | Net Estrogenic Effect | Thromboembolic Risk |
|---|---|---|---|---|---|
| 1G | Norethindrone (norethisterone) | Moderate | None | Baseline reference | Moderate |
| 2G | Levonorgestrel (L-norgestrel) | Higher | None | Lower than norethindrone | Lowest |
| 3G | Desogestrel | Lower (≈ "weak anti-androgenic") | Weak | Higher than norethindrone | Higher |
| 4G | Drospirenone | None | Strong | Highest | Highest |
More progestogenic & androgenic (1G: norethindrone, 2G: levonorgestrel) = less estrogenic = less thromboembolic [1] More anti-androgenic (4G: drospirenone) or less androgenic (3G: desogestrel) = more estrogenic = more thromboembolic [1]
Why does androgenicity matter for thrombosis? Estrogen promotes hepatic synthesis of clotting factors. Androgens oppose this effect. So:
- Androgenic progestins (levonorgestrel) → oppose estrogen's pro-coagulant hepatic effects → lower VTE risk.
- Anti-androgenic progestins (drospirenone) → do not oppose (and may enhance) estrogen's pro-coagulant effects → higher VTE risk.
Compared to norethindrone, drospirenone is strictly anti-androgenic (w/o any androgenicity), thus eliciting "estrogenic-like" thrombotic effects [1]
| Action | Mechanism |
|---|---|
| Suppress ovulation | Sustained E & P → −ve feedback → ↓ FSH & LH → no LH surge |
| Impair implantation | Asynchronous E & P → thin, atrophic endometrium with altered secretions |
| Impede sperm | P → thick cervical mucus |
| Alter transport | P & E → altered tubal motility → ↓ fertilisation chance |
4. Progestin-Only Pills (POPs)
Slightly lower efficacy than COC because ovulation is not always inhibited, owing to: progestin dose in POP much lower than in COC; less inhibition on FSH, so some follicular development & estradiol release can occur → possible ovulation from estradiol-triggered LH surge [1]
| Feature | COC | POP |
|---|---|---|
| Components | E + P | P only |
| Ovulation suppression | Reliable | Not always (some follicular development possible) |
| Dosing schedule | 21+7 or 24+4 | 28-day continuous (no pill-free period) — except drospirenone (24+4) |
| Contraindications | Pregnancy, breast cancer, estrogen-related vascular conditions | Pregnancy & breast cancer only |
| VTE risk | Increased | Not significantly increased |
Used by those contraindicated to COCs, usually due to estrogenic (or "estrogenic-like") effects on vascular conditions [1]
The slide details three mechanisms of estrogen-related vascular harm:
| Vascular Effect | Mechanism | Clinical Consequence |
|---|---|---|
| Endothelial dysfunction | Pro-thrombotic state enhanced by smoking | DVT/PE |
| Increased coagulation | Increased synthesis of clotting factors | Thrombotic disorders |
| Hypertension | More activated RAAS | Promotes thrombosis |
COC Contraindications — The Vascular Triad
Students often forget why COCs are contraindicated in smokers over 35, women with hypertension, and those with thrombotic history. It all comes back to estrogen's effects on endothelium, clotting factors, and RAAS. POPs avoid these issues because they lack estrogen. But remember: POPs are STILL contraindicated in breast cancer and pregnancy.
Most commonly taken every day (in 28-pill pack) without pill-free period — applies to progestins that are not "strongly" anti-androgenic or "weakly" androgenic, i.e. all progestins except drospirenone (which is taken for 24 days + 4 days of placebo) [1]
The slide (p. 20) categorizes adverse effects [1]:
| Category | Effect | Explanation |
|---|---|---|
| Estrogenic | Thromboembolic events (DVT/PE/stroke) | ↑ clotting factor synthesis, endothelial dysfunction, ↑ RAAS |
| Progestogenic/Androgenic | Weight gain, acne, hirsutism | More common with older 1G/2G progestins (norethindrone, levonorgestrel) |
| Breakthrough bleeding | Unscheduled bleeding | Most common with POP use; also common with low-dose COCs |
| Warning signs (ACHES) | Abdominal pain, Chest pain, Headache, Eye problems, Severe leg pain | May be indicative of stroke or other thrombotic conditions |
Breakthrough Bleeding Explained [1]
| Type | Cause | Mechanism |
|---|---|---|
| Progesterone breakthrough | High P:E ratio (POP, or late COC cycle) | Endometrium atrophic & ulcerated from lack of E → prone to frequent, irregular bleeding |
| Estrogen breakthrough | Excess E without adequate P | Endometrium proliferates in undifferentiated manner → portions slough irregularly → profuse bleeding |
"Progesterone breakthrough bleeding occurs when the progesterone-to-estrogen ratio is high... The endometrium becomes atrophic and ulcerated because of a lack of estrogen" [1]
ACHES Mnemonic for Danger Signs on OCP
ACHES = Abdominal pain, Chest pain, Headache (severe), Eye problems (visual disturbance), Severe leg pain — these are potential signs of thromboembolism or stroke and mandate immediate discontinuation and investigation. This is a common exam item.
P450 inducers, e.g. certain anti-epileptics, St. John's wort → increased OCP metabolism [1] Concurrent antibiotic use, especially beta-lactams, tetracyclines → reduced enterohepatic recycling [1]
Mechanism of Interaction
CYP450 inducers: EE (and some progestins) are metabolised by hepatic CYP3A4. Enzyme inducers accelerate metabolism → reduced plasma levels → reduced efficacy.
Antibiotics & enterohepatic recycling: EE is conjugated in the liver → excreted in bile → deconjugated by gut bacteria → reabsorbed. Antibiotics kill gut flora → less deconjugation → less reabsorption → lower EE levels [1].
| Interacting Drug | Mechanism | Clinical Consequence |
|---|---|---|
| Rifampicin (most potent) | CYP3A4 induction | Dramatically ↓ OCP efficacy; advise alternative contraception [3] |
| Carbamazepine, phenytoin, phenobarbital | CYP induction | ↓ OCP efficacy |
| St. John's wort | CYP3A4 induction | ↓ OCP efficacy (commonly tested!) |
| Beta-lactams, tetracyclines | ↓ enterohepatic recycling | ↓ EE levels |
The slide explicitly notes that the enterohepatic recycling diagram "also applies to progestin" [1]
Rifampicin and OCP
Rifampicin is such a potent CYP inducer that it reduces OCP levels by up to 50%. Recommend female patients of reproductive age to use other contraceptive methods other than pills when prescribing rifampicin [3]. This is a favourite cross-specialty exam question (TB management + contraception).
The lecture includes a case reference (slide 21, 34) for using COC/POP and NSAIDs in heavy menstrual bleeding (HMB):
Low-dose luteal-phase progestogens are no longer recommended for treatment of heavy but regular periods because they increase menstrual blood loss in this situation [1]
Progesterone withdrawal increases endometrial COX-2 enzyme → PGE2 and PGF2α synthesis. Women with HMB have increased prostaglandin synthesis and COX-2 enzymes. PGE2 may contribute to excessive bleeding by enhancing vasodilatation of spiral arteries [1]
Therefore: NSAIDs (which inhibit COX → ↓ PG synthesis) reduce menstrual blood loss and are used as medical management of HMB. COCs stabilize the endometrium and reduce menstrual flow. These are non-pregnant uses of the same pharmacological principles.
Family planning care should not have a singular focus of preventing unintended pregnancy... focus on people reaching their desired reproductive outcomes by supporting them to make informed decisions about their fertility and contraceptive use that are aligned with their preferences and reproductive goals [1]
Key counselling principles [1][4]:
- Informed choice — respect patient preferences
- Dual protection (condoms + hormonal methods)
- Compliance support
- Discussion of side effects, warning signs (ACHES)
- Drug interactions (especially anti-epileptics, antibiotics)
- Fertility return after discontinuation
9. Onset of Labour & Mediators
Labour = physiologic process to expel foetus from uterus as it contracts [1]
| State | Contractility |
|---|---|
| Non-pregnant | Spontaneous, weak, un-coordinated contractions |
| Early pregnancy | Contractions suppressed by both estrogen & progestin |
| Late pregnancy | Stronger, more coordinated contractions with increasing frequency |
| At parturition | Fully coordinated and forceful contractions |
Ripening state of cervix becomes critical in onset of labour [1]
9.2 Key Mediators
Increased PG synthesis & receptor expression under influence of estrogen
| PG | Receptor | Effect | Location |
|---|---|---|---|
| PGE1 & PGE2 | EP2 | Cervical ripening (softening) and dilation | More EP2 at cervix |
| PGE1 & PGE2 | EP3 (& EP1) | Uterine contraction | More EP3 at top of uterus |
| PGF2α | FP | Uterine contraction | Throughout myometrium |
Signalling: EP1, FP, OT receptor → PLC → IP3 → ↑ cytosolic Ca²⁺ (from SR release & extracellular Ca²⁺ entry via voltage-gated & store-operated Ca²⁺ channels) → contraction [1]
EP3 additional mechanism: EP3 receptor activation reduces cAMP production, thus suppressing uterine relaxation (i.e. promoting contraction) [1]
Increased OT receptor expression under influence of estrogen & PG → more prevalent in later stage of pregnancy Increased OT release from foetal stimulation (i.e. stretching) of cervix → uterine contraction OT also enhances PG release, thus promoting cervical ripening
This creates a positive feedback loop: cervical stretch → OT release → uterine contraction → more cervical stretch → more OT (Ferguson reflex).
10. Uterotonic Drugs
| Drug | PG Analogue | Primary Use | Key Points |
|---|---|---|---|
| Misoprostol | PGE1 | Terminate pregnancy (with anti-progestin, e.g. mifepristone, for abortion) | Risk of uterine hyperstimulation → not preferred for inducing labour; also used for PPH |
| Dinoprostone | PGE2 | Induce labour (cervical ripening) | Less likely to cause uterine hyperstimulation when used at lower doses for cervical ripening |
| Carboprost | PGF2α | Induction of labour, PPH | Acts via FP receptor → PLC → ↑ Ca²⁺ |
These PGs can also manage/prevent postpartum haemorrhage by constricting myometrial blood vessels [1]
Pulsatile administration resembles endogenous release pattern — more effective than continuous infusion [1] Requires favourable cervix for successful labour induction [1] May cause foetal distress & death due to placental blood flow interruption when given at high doses over prolonged period [1] Also used to prevent postpartum haemorrhage [1]
Signalling: OT receptor → PLC → IP3 → ↑ Ca²⁺ → contraction
Naturally derived compounds from fungi on plants (e.g. rye grass) [1] Effect depends on contracted state of uterus — cause more forceful contraction in relaxed than contracted uterus [1] Also used to prevent postpartum haemorrhage [1] May induce vomiting due to D2 receptor activation in chemoreceptor trigger zone (CTZ) [1]
Signalling: Activate α1-adrenergic & 5-HT receptors → PLC → IP3 → ↑ Ca²⁺ [1]
| Drug | Receptor | Mechanism | Side Effect |
|---|---|---|---|
| Misoprostol | EP1/EP3 | ↑ Ca²⁺, ↓ cAMP | Uterine hyperstimulation, diarrhoea |
| Oxytocin | OTR | ↑ Ca²⁺ | Water retention (ADH-like effect), foetal distress at high dose |
| Ergometrine | α1, 5-HT | ↑ Ca²⁺ | Vomiting (D2 in CTZ), hypertension |
"toco-" = childbirth; "-lytic" = to loosen, break [1]
| Drug | Mechanism | Key Points |
|---|---|---|
| NSAIDs (e.g. indometacin) | Inhibits PG synthesis → delays cervical ripening & reduces uterine contraction | Not for term pregnancy use — in utero closure of ductus arteriosus [1] |
| Progesterone | Reduces PG receptor expression & other cytokine production → delays cervical ripening [1] | Used in threatened preterm labour |
| Nifedipine | Blocks Ca²⁺ entry (L-type Ca²⁺ channel blocker) → reduces uterine contraction [1] | Also causes peripheral vasodilation |
| MgSO₄ | Blocks Ca²⁺ entry → reduces uterine contraction [1] | Also neuroprotective for preterm foetus |
| Atosiban | OTR partial agonist but antagonistic when OT levels are high → reduces contraction [1] | Selective, fewer systemic side effects |
| β₂ agonists (e.g. ritodrine) | Increases cAMP production & PKA activity → suppresses uterine contraction [1] | Cardiovascular side effects (tachycardia, hypotension) |
Why NSAIDs Cannot Be Used at Term
Indometacin inhibits PG synthesis. PGs (especially PGE2) keep the ductus arteriosus patent in utero. Inhibiting PG at term → premature closure of ductus arteriosus → right heart failure, pulmonary hypertension in the foetus. This is one of the most commonly tested points on tocolytics.
Atosiban — A Partial Agonist Paradox
Atosiban is a partial agonist at OTR. In early labour when OT levels are low, it may actually have mild agonistic activity. But at parturition when endogenous OT levels are high, it acts as an antagonist — competing with OT for the receptor but producing less downstream signalling. This is a classic pharmacological concept: partial agonists behave as antagonists in the presence of high levels of full agonist.
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| "COCs increase ovarian cancer risk" | Wrong — COCs DECREASE ovarian and endometrial cancer risk (protective effect of suppressing ovulation) |
| "All progestins have the same VTE risk" | Wrong — 3G (desogestrel) and 4G (drospirenone) have HIGHER VTE risk than 2G (levonorgestrel) because they are less androgenic/more anti-androgenic |
| "POPs reliably suppress ovulation" | Wrong — ovulation is not always inhibited with POPs due to lower progestin dose |
| "Misoprostol is first-line for labour induction" | Wrong — dinoprostone (PGE2) is preferred; misoprostol risks uterine hyperstimulation |
| "Oxytocin works regardless of cervical status" | Wrong — OT requires a favourable (ripened) cervix for successful induction |
| "NSAIDs are safe tocolytics at term" | Wrong — risk of premature closure of ductus arteriosus |
| "Ergometrine is safe in hypertensive patients" | Wrong — ergometrine causes vasoconstriction (via α1) → dangerous in hypertension |
| "Hormone-free interval in COCs has medical benefit" | The slide explicitly says "no demonstrated medical benefit" — it is for patient preference |
- Gallstones: OC pills are a risk factor for gallstones (estrogen increases cholesterol saturation in bile) [5][6]
- Pre-operative assessment: OCPs should be stopped pre-operatively to reduce VTE risk [7]
- Rifampicin interaction: A commonly examined drug interaction — recommend alternative contraception [3]
- Hyperprolactinaemia: Estrogen-containing medications can stimulate lactotrophs → hyperprolactinaemia [8]
Past Paper Questions
"Combined oral contraceptive (COC) pills contain two active components. Which of the following represents an example of oestrogen in a COC pill?" A. Estrone B. Ethinyl oestradiol C. Levonorgestrel D. Norethindrone
Answer: B. Ethinyl oestradiol
Rationale: The lecture explicitly states "most common E is ethinyl estradiol (EE)" [1]. Levonorgestrel (C) and norethindrone (D) are progestins. Estrone (A) is an endogenous estrogen but not used in COC formulations.
"A 51-year-old woman just had total abdominal hysterectomy and bilateral salpingo-oophorectomy for uterine fibroids 6 weeks ago... She complained of severe hot flushes... What management will you suggest to help her?" A. Oral oestrogen and progestogen B. Oral oestrogen only C. Oral progestogen only D. Vaginal oestrogen
Answer: B. Oral oestrogen only
Rationale: After total hysterectomy + BSO, there is no uterus → no need for progestogen (which is added to HRT only to protect the endometrium from unopposed estrogen). Vaginal oestrogen (D) would not adequately treat systemic vasomotor symptoms (hot flushes). This tests understanding of why progestogen is included in HRT — to oppose endometrial proliferation.
"A 26-year-old G0P0 woman attended the Family Planning Clinic for contraceptive advice... Which of the following is a recognised side effect of combined oral contraceptive pills?" A. Increased risk of endometrial cancer B. Increased risk of infertility in the future C. Increased risk of ovarian cancer D. Increased risk of venous thromboembolism
Answer: D. Increased risk of venous thromboembolism
Rationale: COCs are protective against endometrial and ovarian cancer (A, C are wrong). COCs do not cause permanent infertility (B is wrong). Estrogen increases synthesis of clotting factors that predisposes to thrombotic disorders [1].
"A 22-year-old female college student... on combined oral contraceptive pills for 2 years... noticed intermenstrual spotting in the past 3 months. Pregnancy test was negative. What investigation would you like to arrange?" A. Cervical smear B. Endocervical swab for Chlamydia trachomatis C. High vaginal swab for Trichomonas vaginalis D. Ultrasound scan of pelvis
Answer: B. Endocervical swab for Chlamydia trachomatis
Rationale: In a young sexually active woman on COC with new intermenstrual bleeding and negative pregnancy test, the most important cause to exclude is STI — particularly Chlamydia, which is often asymptomatic and a common cause of intermenstrual bleeding. Cervical smear (A) is for cancer screening, not the first-line investigation here. This connects the lecture concept of breakthrough bleeding to a clinical DDx.
"A 40-year-old woman attended the Family Planning Clinic for emergency contraception. The couple noted the male condom slipped during sexual intercourse the night before. She had completed her family with three children and had no further fertility wish. Which is the MOST APPROPRIATE treatment?" A. Copper intrauterine device B. Levonorgestrel 1.5 mg orally for a single dose C. Mifepristone 25 mg orally for a single dose D. Ulipristal acetate 30 mg orally for a single dose
Answer: A. Copper intrauterine device
Rationale: The copper IUD is the most effective emergency contraception (>99% effective) and can be left in place as ongoing contraception — ideal for a woman with no further fertility wish. Levonorgestrel (B) and ulipristal (D) are less effective, and mifepristone (C) at 25 mg is an anti-progestin used for medical abortion, not standard emergency contraception in this context.
"A 25-year-old woman... sometimes engaged in commercial sexual activities, and would like to consider a contraceptive method... which protects from pregnancy as well as sexually transmitted infections. Which of the following is the BEST contraceptive option?" A. Combined oral contraceptive pill B. Male condom C. Male condom added with spermicide D. Spermicidal vaginal suppository
Answer: B. Male condom
Rationale: COCs (A) do not protect against STIs. Spermicide alone (D) has high failure rates. Male condom + spermicide (C) — spermicide (especially nonoxynol-9) can cause mucosal irritation that may actually increase STI transmission risk. The male condom alone provides the best combination of pregnancy prevention and STI protection. This tests counselling principles from the lecture: dual protection is ideal, and informed choice aligned with patient needs.
"Ms. Chan, 46-year-old, attended the gynaecology clinic for heavy menstrual bleeding since 6 months ago... irregular period with cycle length ranging from 30 to 60 days..." (a) Physical examination focus areas? (b) Investigations? (c) Differential diagnoses? (d) Complications of hysterectomy?
Relevance: This connects to the lecture's discussion of COC/norethisterone for HMB management and the use of NSAIDs (via COX-2 inhibition) to reduce PG-mediated menstrual blood loss [1].
High Yield Summary
Oral Contraceptives:
- COCs contain EE + progestin; suppress ovulation (↓FSH/LH), thin endometrium, thicken cervical mucus.
- EE dose: lower = less VTE but more breakthrough bleeding.
- Progestin generation determines "net estrogenic effect": 2G levonorgestrel = lowest VTE risk; 4G drospirenone = highest VTE risk (anti-androgenic).
- POPs: lower efficacy (ovulation not always suppressed), no hormone-free interval (except drospirenone), used when COC contraindicated (vascular conditions, smoking).
- ACHES = danger signs of thromboembolism.
- Drug interactions: CYP450 inducers (rifampicin, St. John's wort, anti-epileptics) and antibiotics (↓ enterohepatic recycling) reduce OCP efficacy.
Uterotonics:
- Misoprostol (PGE1): abortion (with mifepristone), PPH; risk of hyperstimulation.
- Dinoprostone (PGE2): cervical ripening for labour induction.
- Oxytocin: pulsatile dosing, requires ripened cervix; PPH prevention.
- Ergometrine: α1/5-HT → contraction; D2 → vomiting; PPH prevention; avoid in hypertension.
Tocolytics:
- Indometacin: ↓PG synthesis; NOT at term (ductus arteriosus closure).
- Progesterone: ↓PG receptor expression.
- Nifedipine/MgSO₄: block Ca²⁺ entry.
- Atosiban: OTR partial agonist (antagonistic at high OT).
- Ritodrine (β₂ agonist): ↑cAMP → relaxation.
Active Recall - Lecture Notes
[1] GC 160. The woman needs that drug Oral contraceptives Drugs affecting uterine motility.pdf (all slides) [2] CFB (OG03) Fertility Regulation.pdf (mechanisms, methods, injectable contraceptives) [3] MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.178 — rifampicin drug interactions) [4] MBBS_SRH_2025.8.10.pdf (p.25, p.27 — teenage contraception, counselling principles) [5] Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf (OCP as gallstone risk factor) [6] MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.508 — gallstone risk factors including OCP) [7] GC 002 - Is he fit for surgery - Pre-operative assessment.pdf (p.32 — stopping OCPs pre-op) [8] Block A - I keep on bumping into people on my side_ pituitary tumours; hypopituitarism.pdf (p.9 — estrogen-containing medications and hyperprolactinaemia) [9] 2025 Fourth Summative MCQ.pdf (Q74, Q80) [10] 2021 Fourth Summative Assessment MCQ.pdf (Q10, Q11) [11] 2023 Fourth Summative MCQ.pdf (Q12) [12] 2022 Fourth Summative MCQ.pdf (Q14) [13] 2018 Fourth Summative SAQ.pdf (Q11)
GC159 Research Ethics (notes)
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GC161 Alcohol And The Brain From Psychiatric To Neuropsychiatric Perspectives
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