Ovulation physiology US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Ovulation physiology. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Ovulation physiology US Medical PG Question 1: A 26-year-old woman comes to the emergency department because of a 3-day history of nausea and vomiting. Her last menstrual period was 9 weeks ago. A urine pregnancy test is positive. Ultrasonography shows an intrauterine pregnancy consistent in size with a 7-week gestation. The hormone that was measured in this patient's urine to detect the pregnancy is also directly responsible for which of the following processes?
- A. Development of breast tissue
- B. Preparation of the uterine endometrium for implantation
- C. Inhibition of preterm uterine contractions
- D. Maintenance of the corpus luteum (Correct Answer)
- E. Inhibition of ovulation
Ovulation physiology Explanation: ***Maintenance of the corpus luteum***
- The hormone measured in the urine pregnancy test is **human chorionic gonadotropin (hCG)**.
- **hCG** acts like **luteinizing hormone (LH)** to maintain the **corpus luteum** in early pregnancy, ensuring continued progesterone production until the placenta takes over.
*Development of breast tissue*
- **Estrogen** and **progesterone** are the primary hormones responsible for the development of breast tissue during pregnancy, preparing the breasts for lactation.
- While hCG indirectly supports these hormones, it does not directly cause breast tissue development.
*Preparation of the uterine endometrium for implantation*
- The **preparation of the uterine endometrium** for implantation is primarily driven by **progesterone**, produced by the corpus luteum initially and later by the placenta.
- hCG’s role is to maintain the corpus luteum, thus indirectly supporting progesterone production.
*Inhibition of preterm uterine contractions*
- **Progesterone** is the main hormone responsible for **inhibiting uterine contractions** during pregnancy to prevent preterm labor.
- While hCG supports progesterone production, it does not directly inhibit uterine contractions itself.
*Inhibition of ovulation*
- High levels of **estrogen** and **progesterone** during pregnancy suppress the hypothalamic-pituitary-gonadal axis, thereby **inhibiting ovulation**.
- While hCG maintains the corpus luteum which produces these hormones, hCG itself is not the direct inhibitor of ovulation.
Ovulation physiology US Medical PG Question 2: A 22-year-old woman comes to the physician to discuss the prescription of an oral contraceptive. She has no history of major medical illness and takes no medications. She does not smoke cigarettes. She is sexually active with her boyfriend and has been using condoms for contraception. Physical examination shows no abnormalities. She is prescribed combined levonorgestrel and ethinylestradiol tablets. Which of the following is the most important mechanism of action of this drug in the prevention of pregnancy?
- A. Inhibition of rise in luteinizing hormone (Correct Answer)
- B. Suppression of ovarian folliculogenesis
- C. Thickening of cervical mucus
- D. Prevention of endometrial proliferation
- E. Increase of sex-hormone binding globulin
Ovulation physiology Explanation: ***Inhibition of rise in luteinizing hormone***
- Combined oral contraceptives (COCs) primarily prevent pregnancy by **suppressing the hypothalamic-pituitary-ovarian axis**, which inhibits the mid-cycle **Luteinizing Hormone (LH) surge** necessary for ovulation.
- Without the LH surge, the mature follicle does not rupture, and the **ovum is not released**.
*Suppression of ovarian folliculogenesis*
- While COCs do **suppress follicular development**, this is a consequence of the feedback inhibition on FSH secretion, and not the primary contraceptive mechanism.
- The direct **prevention of ovulation** via LH surge inhibition is the most crucial step.
*Thickening of cervical mucus*
- Progestin components of COCs cause the **cervical mucus to become thick and impermeable** to sperm, acting as a secondary contraceptive mechanism.
- However, this is not the most important or primary mechanism, as ovulation can still be theoretically prevented even without this effect.
*Prevention of endometrial proliferation*
- The progestin in COCs causes the endometrium to become **thin and atrophic**, making it less receptive to implantation.
- This is an **ancillary contraceptive effect** but not the primary way pregnancy is prevented, as preventing ovulation is more fundamental.
*Increase of sex-hormone binding globulin*
- Estrogen in COCs can **increase levels of sex hormone-binding globulin (SHBG)**, affecting the bioavailability of endogenous androgens.
- This effect is largely responsible for reducing symptoms of androgen excess (e.g., acne) but plays **no direct role in contraception**.
Ovulation physiology US Medical PG Question 3: A 51-year-old woman presents to the primary care clinic complaining of trouble sleeping. She reports that she has episodes of "overheating" and "sweating" during the day and at night. The nightly episodes keep her from staying asleep. She also explains how embarrassing it is when she suddenly becomes hot and flushed during work meetings. The patient becomes visibly upset and states that she is worried about her marriage as well. She says she has been fighting with her husband about not going out because she is "too tired." They have not been able to have sex the past several months because "it hurts." Labs are drawn, as shown below:
Follicle stimulating hormone (FSH): 62 mIU/mL
Estradiol: 34 pg/mL
Progesterone: 0.1 ng/mL
Luteinizing hormone (LH): 46 mIU/mL
Free testosterone: 2.1 ng/dL
Which of the following contributes most to the production of estrogen in this patient?
- A. Adrenal glands
- B. Adipose tissue (Correct Answer)
- C. Bartholin glands
- D. Mammary glands
- E. Ovaries
Ovulation physiology Explanation: **Adipose tissue**
- In **postmenopausal women**, the ovaries no longer produce significant amounts of estrogen; instead, **adipose tissue** becomes the primary site for estrogen synthesis through the conversion of **androgens** (like androstenedione from the adrenal glands) into **estrone** via **aromatase**.
- The patient's presentation with **hot flashes**, **night sweats**, **sleep disturbance**, **vaginal dryness** (painful intercourse), and **elevated FSH/LH** with **low estradiol** is classic for **menopause**, highlighting the shift in estrogen production.
*Adrenal glands*
- The **adrenal glands** primarily produce **androgens** (e.g., androstenedione, DHEA) and a small amount of estrogens, but their main contribution to estrogen in menopause is indirect, by providing substrates for conversion in peripheral tissues.
- While they are a source of **androgens**, they do not directly contribute most significantly to **estrogen production** in a menopausal woman compared to the peripheral conversion in adipose tissue.
*Bartholin glands*
- **Bartholin glands** are located at the vaginal opening and produce **lubricating fluid**, but they play no role in **hormone production**, including estrogen.
- They are exocrine glands involved in lubrication during sexual arousal.
*Mammary glands*
- **Mammary glands** are primarily involved in **milk production** (lactation) and are target organs for sex hormones, but they do not produce significant amounts of **estrogen**.
- They respond to estrogen but do not synthesize it in substantial quantities.
*Ovaries*
- In premenopausal women, the **ovaries** are the primary source of **estrogen** (mainly estradiol), but in this 51-year-old woman with menopausal symptoms and high FSH/LH, ovarian function has significantly declined.
- The **elevated FSH and LH** levels, coupled with **low estradiol**, indicate **ovarian failure**, meaning the ovaries are no longer actively producing estrogen.
Ovulation physiology US Medical PG Question 4: Research is being conducted on embryoblasts. The exact date of fertilization is unknown. There is the presence of a cytotrophoblast and syncytiotrophoblast, marking the time when implantation into the uterus would normally occur. Within the embryoblast, columnar and cuboidal cells are separated by a membrane. Which of these cell layers begins to line the yolk sac cavity?
- A. Hypoblast (Correct Answer)
- B. Epiblast
- C. Syncytiotrophoblast
- D. Inner cell mass
- E. Endoderm
Ovulation physiology Explanation: ***Hypoblast***
- The **hypoblast** is a layer of cuboidal cells that forms from the inner cell mass around day 8 post-fertilization.
- It plays a crucial role in forming the **primary yolk sac** by migrating to line the exocoelomic cavity.
*Epiblast*
- The **epiblast** is composed of columnar cells located dorsal to the hypoblast and forms the floor of the **amniotic cavity**.
- It is the source of the **three primary germ layers** during gastrulation (ectoderm, mesoderm, and endoderm), not the yolk sac lining itself.
*Syncytiotrophoblast*
- The **syncytiotrophoblast** is the outer, invasive layer of the trophoblast that facilitates implantation and forms the fetal component of the placenta.
- It is not involved in lining the yolk sac cavity but rather in **invading the uterine endometrium** and producing hCG.
*Inner cell mass*
- The **inner cell mass (ICM)** is the cluster of cells within the blastocyst that gives rise to the embryoblast (which further differentiates into epiblast and hypoblast).
- The ICM itself does not line the yolk sac; rather, its derivative, the hypoblast, does.
*Endoderm*
- The **endoderm** is one of the three primary germ layers that forms during gastrulation from the epiblast derivative.
- It ultimately forms the linings of the **gastrointestinal and respiratory tracts**, not the primary yolk sac lining.
Ovulation physiology US Medical PG Question 5: A researcher is studying gamete production and oogenesis. For her experiment, she decides to cultivate primary oocytes in their arrested state and secondary oocytes just prior to fertilization. When she examines these gametes, she will find that the primary oocytes and secondary oocytes are arrested in which phases of meiosis, respectively?
- A. Anaphase I; anaphase II
- B. Interphase I; prophase II
- C. Metaphase I; metaphase II
- D. Metaphase I; prophase II
- E. Prophase I; metaphase II (Correct Answer)
Ovulation physiology Explanation: ***Prophase I; metaphase II***
- **Primary oocytes** are arrested in **prophase I** from embryonic development until puberty, when they resume meiosis in preparation for ovulation.
- **Secondary oocytes** are immediately arrested in **metaphase II** after completing meiosis I, and they will remain in this stage until fertilization occurs.
*Anaphase I; anaphase II*
- **Anaphase I** involves the separation of **homologous chromosomes**, and **anaphase II** involves the separation of **sister chromatids**. Neither primary nor secondary oocytes are arrested in these stages.
- Meiotic arrest occurs at earlier stages to prevent further division until specific triggers (ovulation or fertilization) are met.
*Interphase I; prophase II*
- **Interphase I** precedes meiosis I, during which DNA replication occurs, and it is not a stage of meiotic arrest for primary oocytes.
- **Prophase II** is a transient stage in meiosis II, and secondary oocytes are arrested later in **metaphase II**, not prophase II.
*Metaphase I; metaphase II*
- While **secondary oocytes** are indeed arrested in **metaphase II**, **primary oocytes** are arrested much earlier in **prophase I**, not metaphase I.
- The arrest in metaphase I is temporary for primary oocytes as they complete meiosis I to form secondary oocytes upon hormonal signaling.
*Metaphase I; prophase II*
- **Primary oocytes** are arrested in **prophase I**, not metaphase I. Meiosis I is completed before ovulation, leading to the formation of secondary oocytes.
- **Secondary oocytes** are arrested in **metaphase II**, not prophase II, awaiting fertilization to complete meiosis II.
Ovulation physiology US Medical PG Question 6: A 35-year-old man presents to his primary care physician for a routine visit. He is in good health but has a 15 pack-year smoking history. He has tried to quit multiple times and expresses frustration in his inability to do so. He states that he has a 6-year-old son that was recently diagnosed with asthma and that he is ready to quit smoking. What is the most effective method of smoking cessation?
- A. Nicotine replacement therapy alone
- B. Quitting cold turkey
- C. Bupropion in conjunction with nicotine replacement therapy and cognitive behavioral therapy (Correct Answer)
- D. Participating in a smoking-cessation support group
- E. Bupropion alone
Ovulation physiology Explanation: ***Bupropion in conjunction with nicotine replacement therapy and cognitive behavioral therapy***
- The combination of **pharmacological therapies** (Bupropion and NRT) with **behavioral support** (CBT) is consistently shown to be the most effective strategy for smoking cessation. This approach addresses both the physiological addiction and the psychological habits associated with smoking.
- **Bupropion** helps reduce cravings and withdrawal symptoms, while **nicotine replacement therapy (NRT)** manages nicotine withdrawal. **Cognitive behavioral therapy (CBT)** provides coping mechanisms and strategies to deal with triggers and prevent relapse.
*Nicotine replacement therapy alone*
- While **nicotine replacement therapy (NRT)** is an effective treatment, its efficacy significantly increases when combined with behavioral therapy or other pharmacotherapies.
- NRT alone primarily addresses the **physical dependence** on nicotine but may not fully address the psychological and behavioral aspects of addiction.
*Quitting 'cold-turkey'*
- **Quitting cold turkey** has a very low success rate, with only about 3-5% of individuals managing to quit long-term using this method.
- This method provides no support for severe **withdrawal symptoms** or cravings, making relapse highly likely, especially for heavy smokers.
*Participating in a smoking-cessation support group*
- **Support groups** provide valuable behavioral and social support, which is an important component of successful cessation.
- However, behavioral support alone is often less effective than when combined with **pharmacological interventions** that address the physiological addiction.
*Bupropion alone*
- **Bupropion** is an effective pharmacotherapy that helps reduce cravings and withdrawal symptoms and has been shown to improve cessation rates.
- While effective, its success rate is typically lower than when used in combination with **nicotine replacement therapy** and comprehensive behavioral support.
Ovulation physiology US Medical PG Question 7: A 12-year-old girl is brought to the emergency department 3 hours after the sudden onset of colicky abdominal pain and vomiting. She also has redness and swelling of the face and lips without pruritus. Her symptoms began following a tooth extraction earlier this morning. She had a similar episode of facial swelling after a bicycle accident 1 year ago which resolved within 48 hours without treatment. Vital signs are within normal limits. Examination shows a nontender facial edema, erythema of the oral mucosa, and an enlarged tongue. The abdomen is soft and there is tenderness to palpation over the lower quadrants. An abdominal ultrasound shows segmental thickening of the intestinal wall. Which of the following is the most likely cause of this patient's condition?
- A. T-cell mediated immune reaction
- B. Drug-induced bradykinin excess
- C. Leukotriene overproduction
- D. Immune-complex deposition
- E. Complement inhibitor deficiency (Correct Answer)
Ovulation physiology Explanation: ***Complement inhibitor deficiency***
- This patient's presentation with recurrent episodes of **angioedema** (face and lip swelling, enlarged tongue, intestinal wall thickening causing abdominal pain), particularly triggered by **trauma** (tooth extraction, bicycle accident), strongly suggests **hereditary angioedema (HAE)**. HAE is caused by a deficiency or dysfunction of **C1 esterase inhibitor**, a key complement inhibitor.
- A deficiency in C1 esterase inhibitor leads to uncontrolled activation of both the **complement cascade** and the **kallikrein-bradykinin pathway**, resulting in excessive **bradykinin production**, which causes increased vascular permeability and localized edema without urticaria or pruritus.
*T-cell mediated immune reaction*
- **T-cell mediated reactions** are typically associated with **delayed-type hypersensitivity reactions** (e.g., contact dermatitis, graft rejection) and **autoimmune disorders**, which do not fit the acute, recurrent, non-pruritic angioedema seen here.
- These reactions primarily involve cell-mediated cytotoxicity or cytokine release, rather than rapid fluid extravasation due to bradykinin excess.
*Drug-induced bradykinin excess*
- While drug-induced angioedema (e.g., from **ACE inhibitors**) can also cause bradykinin excess, this patient's history of episodes since childhood (after a bicycle accident) and the current exacerbation after a tooth extraction, makes a **hereditary predisposition** much more likely than an isolated drug reaction in a 12-year-old.
- The triggers (trauma, dental procedure) are classic for HAE, which involves an intrinsic defect in bradykinin regulation, not merely an external pharmaceutical cause.
*Leukotriene overproduction*
- **Leukotrienes** are potent mediators involved in **allergic reactions** and **asthma**, contributing to bronchoconstriction, vascular permeability, and inflammation.
- Conditions involving leukotriene overproduction, such as aspirin-exacerbated respiratory disease, typically present with bronchospasm, rhinitis, or urticaria, which are not the primary features here.
*Immune-complex deposition*
- **Immune-complex deposition** is characteristic of conditions like **serum sickness**, **lupus nephritis**, or **vasculitis**, leading to inflammation, fever, rash, and organ damage.
- These conditions do not typically present with isolated, recurrent, non-pruritic angioedema and do not involve the specific mechanism of bradykinin overproduction seen in this patient.
Ovulation physiology US Medical PG Question 8: Fertilization begins when sperm binds to the corona radiata of the egg. Once the sperm enters the cytoplasm, a cortical reaction occurs which prevents other sperm from entering the oocyte. The oocyte then undergoes an important reaction. What is the next reaction that is necessary for fertilization to continue?
- A. The second meiotic division (Correct Answer)
- B. Degeneration of the sperm tail
- C. Release of a polar body
- D. Formation of the spindle apparatus
- E. Acrosome reaction
Ovulation physiology Explanation: ***The second meiotic division***
- Upon **sperm penetration**, the secondary oocyte completes its **meiosis II**, forming a mature ovum and a second polar body.
- This completion of meiosis II is a critical step for the pronuclear fusion and subsequent **zygote formation**.
*Degeneration of the sperm tail*
- While the sperm tail does degenerate within the ooplasm, it occurs **after** the genetic material has been released and is not the immediate next critical reaction for continued fertilization.
- This is a process of degradation and assimilation, not an active cellular reaction of the oocyte vital for fertilization progression.
*Release of a polar body*
- The first polar body is released **before fertilization** (at the completion of meiosis I), and the second polar body is released **concomitantly with the completion of meiosis II**, which is the required reaction.
- Releasing a polar body is a consequence of meiotic division, not an independent reaction that drives fertilization forward.
*Formation of the spindle apparatus*
- The **spindle apparatus** is formed during both meiotic divisions to separate chromosomes, but its formation itself is not the immediate "next reaction" necessary for fertilization to continue after cortical reaction.
- The key event is the progression of meiosis, which the spindle facilitates, not the mere formation of the apparatus.
*Acrosome reaction*
- The **acrosome reaction** occurs **before** the sperm binds to the zona pellucida and penetrates the oocyte, enabling the release of enzymes to digest the egg's outer layers.
- This reaction has already taken place for the sperm to have entered the oocyte and initiated the cortical reaction.
Ovulation physiology US Medical PG Question 9: A 27-year-old woman with Kallmann syndrome (congenital GnRH deficiency) desires pregnancy. She has been on estrogen-progesterone replacement for bone health. Her physician plans to switch her to pulsatile GnRH therapy. After 6 weeks of treatment, labs show: LH 4 mIU/mL, FSH 5 mIU/mL, estradiol 120 pg/mL. Ultrasound shows a 16mm dominant follicle. Evaluate and synthesize the physiologic response to determine the appropriate next intervention for ovulation induction.
- A. Continue current GnRH dosing and monitor for spontaneous LH surge
- B. Add clomiphene citrate to augment endogenous gonadotropin release
- C. Increase GnRH pulse frequency to stimulate endogenous LH surge
- D. Administer exogenous hCG to trigger ovulation and time intercourse (Correct Answer)
- E. Switch to gonadotropin therapy with recombinant FSH and LH
Ovulation physiology Explanation: ***Administer exogenous hCG to trigger ovulation and time intercourse***
- In **Kallmann syndrome**, the absence of **GnRH neurons** means the patient cannot generate a spontaneous **LH surge** despite follicular maturation; **exogenous hCG** acts as an **LH analog** to trigger ovulation.
- The labs and ultrasound demonstrate successful **follicular development** with a **16mm follicle** and adequate **estradiol**, indicating the patient is ready for the final maturation trigger.
*Continue current GnRH dosing and monitor for spontaneous LH surge*
- A spontaneous surge will not occur because the patient lacks the endogenous **hypothalamic GnRH** release mechanism required to respond to **estrogen positive feedback**.
- Relying on the pump's fixed frequency will not mimic the necessary mid-cycle **GnRH surge** needed for natural ovulation.
*Add clomiphene citrate to augment endogenous gonadotropin release*
- **Clomiphene citrate** works by blocking **estrogen receptors** in the hypothalamus to increase GnRH; it is ineffective in Kallmann syndrome due to the lack of **functional GnRH neurons**.
- Therapeutic success in these patients requires bypassing the hypothalamus using either **pulsatile GnRH** or direct **gonadotropin therapy**.
*Increase GnRH pulse frequency to stimulate endogenous LH surge*
- Increasing pulse frequency does not replicate the complex **positive feedback** kinetics required to generate a massive **LH surge** in GnRH-deficient individuals.
- Fixed-frequency pulsatile pumps are designed for **folliculogenesis** but are generally insufficient to achieve the threshold required for **oocyte release** without additional triggers.
*Switch to gonadotropin therapy with recombinant FSH and LH*
- This switch is unnecessary because the patient is already showing an excellent physiologic response to **pulsatile GnRH therapy**, as evidenced by her **FSH**, **LH**, and **dominant follicle**.
- Pulsatile GnRH is often preferred when available because it maintains the **pituitary-ovarian axis** and carries a lower risk of **ovarian hyperstimulation syndrome (OHSS)** compared to exogenous gonadotropins.
Ovulation physiology US Medical PG Question 10: A 30-year-old woman at 28 weeks gestation with gestational diabetes managed with insulin presents with decreased fetal movement. Fetal monitoring shows category II tracing. Umbilical artery Doppler shows absent end-diastolic flow. Her glucose control has been suboptimal (HbA1c 7.8%). Maternal blood pressure is normal. Synthesize the pathophysiologic relationship between her metabolic condition and the Doppler findings to determine the primary mechanism.
- A. Maternal hyperglycemia causing fetal hyperinsulinemia and increased oxygen consumption
- B. Maternal ketoacidosis causing direct fetal myocardial depression
- C. Fetal polycythemia from chronic hypoxia increasing blood viscosity
- D. Uteroplacental insufficiency from diabetes-induced vasculopathy affecting spiral arteries (Correct Answer)
- E. Placental hypertrophy from fetal macrosomia compressing umbilical cord
Ovulation physiology Explanation: ***Uteroplacental insufficiency from diabetes-induced vasculopathy affecting spiral arteries***
- **Absent end-diastolic flow (AEDF)** in the umbilical artery signifies high **placental vascular resistance**, often due to maternal **decidual vasculopathy** and endothelial damage.
- Suboptimal glucose control in diabetes leads to **microvascular changes** in the **spiral arteries**, reducing oxygen and nutrient delivery, which results in placental insufficiency and compromised fetal wellbeing.
*Maternal hyperglycemia causing fetal hyperinsulinemia and increased oxygen consumption*
- While **maternal hyperglycemia** leads to **fetal hyperinsulinemia**, this metabolic state primarily drives **fetal macrosomia** and elective oxygen demand rather than structural vascular resistance in the umbilical artery.
- Increased oxygen consumption contributes to **fetal hypoxemia**, but it does not mechanistically explain the **AEDF** seen on Doppler studies.
*Fetal polycythemia from chronic hypoxia increasing blood viscosity*
- **Fetal polycythemia** is a compensatory response to **chronic hypoxia** triggered by erythropoietin release; it is a consequence rather than the primary driver of umbilical artery flow obstruction.
- Although increased **blood viscosity** can affect flow, the primary lesion in **AEDF** is high resistance within the **placental villous bed** due to vascular pathology.
*Maternal ketoacidosis causing direct fetal myocardial depression*
- **Maternal ketoacidosis** is an acute, life-threatening emergency that can cause **fetal distress**, but there is no clinical evidence (such as pH or anion gap) provided to support this diagnosis here.
- **AEDF** is typically a marker of chronic **placental resistance** over time, whereas myocardial depression would more likely reflect as **fetal bradycardia** or loss of variability.
*Placental hypertrophy from fetal macrosomia compressing umbilical cord*
- **Placental hypertrophy** is commonly associated with **gestational diabetes**, but the placenta does not compress the umbilical cord to the point of causing **AEDF**.
- **Umbilical cord compression** usually presents as **variable decelerations** on fetal heart monitoring, not a persistent high-resistance Doppler pattern in the umbilical artery.
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