Oestradiol MCQs With Answer offers B. Pharm students a focused, clinically relevant review of 17β-oestradiol pharmacology, mechanisms, formulations, metabolism, therapeutic uses, adverse effects, and drug interactions. This concise introduction emphasizes estrogen receptor biology (ERα/ERβ), hepatic first‑pass effects, routes of administration (oral, transdermal, parenteral), metabolic pathways (aromatase, 17β‑HSD, conjugation), and safety concerns such as thromboembolism and endometrial hyperplasia. Keywords included: Oestradiol MCQs With Answer, estradiol pharmacology, estrogen receptor, HRT, contraceptives, pharmacokinetics, drug interactions, and monitoring. The questions challenge understanding beyond basics to clinical application and formulation choices. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. Which enzyme directly converts testosterone to 17β‑oestradiol in peripheral tissues?
- Aromatase
- 17β‑Hydroxysteroid dehydrogenase
- 5α‑Reductase
- Sulfotransferase
Correct Answer: Aromatase
Q2. Which estrogen receptor subtype is most strongly associated with proliferative effects in the uterus?
- ERα
- ERβ
- GPR30 (GPER)
- Progesterone receptor
Correct Answer: ERα
Q3. What is the main reason oral 17β‑oestradiol increases hepatic protein synthesis more than transdermal delivery?
- Higher systemic bioavailability of oral estradiol
- First‑pass hepatic metabolism exposes the liver to higher concentrations
- Transdermal route increases enterohepatic recycling
- Oral estradiol binds less to SHBG
Correct Answer: First‑pass hepatic metabolism exposes the liver to higher concentrations
Q4. Which metabolic transformation converts estrone to the more potent 17β‑oestradiol?
- 17β‑Hydroxysteroid dehydrogenase (reduction)
- Aromatase hydroxylation
- Glucuronidation
- Sulfation
Correct Answer: 17β‑Hydroxysteroid dehydrogenase (reduction)
Q5. Which formulation of estradiol is preferred to minimize venous thromboembolism (VTE) risk in hormone replacement therapy?
- Oral micronized estradiol
- Transdermal estradiol patch
- Conjugated equine estrogens oral tablets
- Intramuscular oil injection
Correct Answer: Transdermal estradiol patch
Q6. Ethinylestradiol differs from natural estradiol primarily because:
- It is less potent at estrogen receptors
- It contains an ethinyl group that increases oral potency and hepatic effects
- It is converted to estrone by 17β‑HSD
- It has no effect on SHBG levels
Correct Answer: It contains an ethinyl group that increases oral potency and hepatic effects
Q7. Which laboratory method provides the most specific measurement of low serum estradiol concentrations?
- RIA (radioimmunoassay)
- ELISA
- LC‑MS/MS (liquid chromatography‑tandem mass spectrometry)
- Colorimetric assay
Correct Answer: LC‑MS/MS (liquid chromatography‑tandem mass spectrometry)
Q8. A patient on oral estradiol starts rifampicin for tuberculosis. What is the expected effect on estradiol levels?
- Marked increase due to CYP inhibition
- Marked decrease due to CYP induction and increased clearance
- No change because estradiol is not metabolized by CYP enzymes
- Immediate estrogen toxicity
Correct Answer: Marked decrease due to CYP induction and increased clearance
Q9. Which adverse effect is most specifically associated with unopposed estrogen therapy in women with an intact uterus?
- Osteoporosis
- Endometrial hyperplasia and carcinoma risk
- Reduced LDL cholesterol
- Decreased breast density
Correct Answer: Endometrial hyperplasia and carcinoma risk
Q10. Which transporter or binding protein carries the majority of circulating estradiol in plasma?
- Albumin only
- Sex hormone‑binding globulin (SHBG)
- Transferrin
- α1‑Acid glycoprotein
Correct Answer: Sex hormone‑binding globulin (SHBG)
Q11. Aromatase inhibitors reduce estradiol levels by blocking which step?
- Conversion of androstenedione/testosterone to estrogens
- Conversion of cholesterol to pregnenolone
- Conversion of estrone to estradiol
- Glucuronidation of estradiol
Correct Answer: Conversion of androstenedione/testosterone to estrogens
Q12. Which drug class acts as tissue‑selective estrogen receptor modulators and can antagonize estradiol in breast tissue?
- Aromatase inhibitors
- SERMs (e.g., tamoxifen)
- GnRH agonists
- Progestins
Correct Answer: SERMs (e.g., tamoxifen)
Q13. Which hepatic effect is observed with oral estrogens and may affect coagulation risk?
- Decrease in clotting factor synthesis
- Increase in synthesis of clotting factors and fibrinogen
- Complete inhibition of CYP450 enzymes
- Increase in bile acid excretion only
Correct Answer: Increase in synthesis of clotting factors and fibrinogen
Q14. Which metabolite pathway contributes to enterohepatic recirculation of estradiol?
- Glucuronidation and biliary excretion followed by gut bacterial deconjugation
- Oxidation by monoamine oxidase
- Sulfation and renal elimination without reabsorption
- Direct renal secretion of free estradiol
Correct Answer: Glucuronidation and biliary excretion followed by gut bacterial deconjugation
Q15. In male patients, high doses of exogenous estradiol were historically used to treat prostate cancer because:
- Estradiol directly kills prostate cancer cells via alkylation
- Estrogen suppresses gonadotropin release and reduces testosterone production
- Estrogen increases PSA levels to toxic ranges
- Estradiol is aromatized to testosterone
Correct Answer: Estrogen suppresses gonadotropin release and reduces testosterone production
Q16. Which clinical monitoring parameter is most appropriate when initiating systemic estrogen therapy in an older woman?
- Regular monitoring of serum creatinine only
- Assess VTE risk, blood pressure, and breast/cervical screening as indicated
- No monitoring is required once therapy starts
- Daily measurement of serum estradiol levels
Correct Answer: Assess VTE risk, blood pressure, and breast/cervical screening as indicated
Q17. Which statement about estradiol valerate is correct?
- It is an immediate‑release oral form identical to micronized estradiol
- It is an ester prodrug of estradiol that is hydrolyzed to active estradiol
- It cannot be used in combined oral contraceptives
- It is inactive until converted to ethinylestradiol
Correct Answer: It is an ester prodrug of estradiol that is hydrolyzed to active estradiol
Q18. Which adverse effect is commonly reported early after starting estrogen therapy?
- Hot flashes improvement only
- Nausea and breast tenderness
- Severe hypoglycemia
- Immediate hair loss
Correct Answer: Nausea and breast tenderness
Q19. Which drug interaction can reduce the contraceptive efficacy of combined oral contraceptives containing ethinylestradiol?
- Fluoxetine (CYP2D6 inhibitor)
- Rifampicin (CYP3A4 inducer)
- Warfarin
- Levothyroxine
Correct Answer: Rifampicin (CYP3A4 inducer)
Q20. Which physiological protein increases in plasma after estrogen therapy and affects free hormone fractions?
- Albumin decreases markedly
- Sex hormone‑binding globulin (SHBG) increases
- C‑reactive protein decreases
- Transcortin increases only
Correct Answer: Sex hormone‑binding globulin (SHBG) increases
Q21. Which contraceptive estrogen is most associated with predictable daily oral dosing and strong hepatic effects?
- 17β‑Oestradiol (micronized)
- Ethinylestradiol
- Estriol topical cream
- Estrone suppository
Correct Answer: Ethinylestradiol
Q22. Which of the following best describes non‑genomic estrogen receptor signaling?
- Estrogen binding that directly alters gene transcription via nuclear ER only
- Rapid signaling through membrane‑associated receptors activating kinases and second messengers
- Irreversible covalent modification of DNA by estradiol
- Estrogen acting solely through mitochondrial DNA receptors
Correct Answer: Rapid signaling through membrane‑associated receptors activating kinases and second messengers
Q23. In postmenopausal hormone therapy, adding a progestin to estrogen is recommended primarily to:
- Enhance bone loss prevention beyond estrogen alone
- Prevent endometrial hyperplasia in women with an intact uterus
- Increase estrogen hepatic metabolism
- Reduce breast cancer risk
Correct Answer: Prevent endometrial hyperplasia in women with an intact uterus
Q24. Which lipid effect is typically observed with estrogen therapy?
- Increase LDL and decrease HDL
- Decrease LDL and increase HDL
- No change in lipid profile
- Increase triglycerides only with transdermal route
Correct Answer: Decrease LDL and increase HDL
Q25. Which clinical condition is a contraindication to systemic estrogen therapy?
- Controlled hypothyroidism
- Active or recent venous thromboembolism
- Migraine without aura in young women
- Osteopenia alone
Correct Answer: Active or recent venous thromboembolism
Q26. Which enzymatic conjugation increases water solubility for renal elimination of estradiol metabolites?
- 17β‑Reduction
- Glucuronidation and sulfation
- Aromatization
- Desaturation
Correct Answer: Glucuronidation and sulfation
Q27. Which pharmacological strategy is used to reduce endometrial risk in women taking estrogen for contraception or HRT?
- Administer estrogen alone continuously
- Combine estrogen with a progestin cyclically or continuously
- Use higher doses of estrogen only at night
- Switch to topical estriol without progestin
Correct Answer: Combine estrogen with a progestin cyclically or continuously
Q28. Which clinical measurement is least useful to monitor directly when managing estradiol therapy?
- Serum estradiol concentration in routine maintenance
- Blood pressure and VTE risk factors
- Breast and pelvic examinations as appropriate
- Lipid profile and liver function tests when indicated
Correct Answer: Serum estradiol concentration in routine maintenance
Q29. Which statement about estriol compared with estradiol is correct?
- Estriol is the most potent estrogen for systemic effects
- Estriol has weaker systemic estrogenic potency and is prominent in pregnancy
- Estriol is synthetic and used widely in oral contraceptives
- Estriol cannot be measured in urine
Correct Answer: Estriol has weaker systemic estrogenic potency and is prominent in pregnancy
Q30. Which is a pharmacological rationale for preferring transdermal estradiol in older women?
- Transdermal route increases hepatic synthesis of clotting factors
- Transdermal route avoids first‑pass hepatic stimulation and may lower VTE risk
- Transdermal estradiol is ineffective for vasomotor symptoms
- Transdermal route always causes greater SHBG elevation than oral
Correct Answer: Transdermal route avoids first‑pass hepatic stimulation and may lower VTE risk

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