Hyperprolactinemia — MCQs
Ramkali bai, a 35-year-old female presented with a one-year history of menstrual irregularity and galactorrhoea. She also had off and on headache, her examination revealed bitemporal superior quadrantanopia. Her fundus examination showed primary optic atrophy. Which of the following is a most likely diagnosis in this case -
A 30-year-old male presents with erectile dysfunction, low testosterone, and elevated prolactin levels. What is the most likely diagnosis?
Which of the following medications is not associated with causing hyperprolactinemia?
Maximum increase in prolactin level is caused by:-
A lady presents with amenorrhea and galactorrhea. What is the most likely cause?
Secretion of prolactin is inhibited by?
All are causes of anovulatory amenorrhea except which of the following?
Testicular feminization syndrome is characterized by all of the following except?
A female presents with normal breast development but scanty pubic hair. What is the most likely diagnosis?
Which of the following tests can differentiate Mullerian agenesis (MRKH syndrome) from complete androgen insensitivity syndrome (testicular feminization syndrome)?
Hyperprolactinemia Indian Medical PG Practice Questions and MCQs
Question 1: Ramkali bai, a 35-year-old female presented with a one-year history of menstrual irregularity and galactorrhoea. She also had off and on headache, her examination revealed bitemporal superior quadrantanopia. Her fundus examination showed primary optic atrophy. Which of the following is a most likely diagnosis in this case -
- A. Pituitary macroadenoma (Correct Answer)
- B. Craniopharyngioma
- C. Ophthalmic ICA Aneurysm
- D. Chiasmal Glioma
Explanation: ***Pituitary macroadenoma*** - **Menstrual irregularity**, **galactorrhoea**, and **headaches** are classic symptoms of a pituitary macroadenoma, especially if it secretes **prolactin** [1]. - **Bitemporal superior quadrantanopia** and **primary optic atrophy** are consistent with compression of the inferior chiasm by a large pituitary tumor [1]. *Craniopharyngioma* - While craniopharyngiomas can cause visual field defects and endocrine dysfunction, galactorrhoea is less common, and they typically affect children and young adults or older adults, not commonly presenting in a 35-year-old with this specific constellation. - The visual field defect from craniopharyngioma would more typically be a bitemporal hemianopia due to compression of the mid-chiasm, not primarily a superior quadrantanopia. *Ophthalmic ICA Aneurysm* - An ophthalmic ICA aneurysm can compress the optic nerve, leading to visual loss, but it typically causes unilateral visual field defects and is not usually associated with galactorrhoea or menstrual irregularity. - Endocrine symptoms like galactorrhoea are not characteristic of an unruptured internal carotid artery aneurysm. *Chiasmal Glioma* - Chiasmal gliomas are more common in children and can cause visual field defects and endocrine abnormalities, but galactorrhoea is not a typical presentation. - The progression of symptoms and specific visual field defect (bitemporal superior quadrantanopia) are less classic for a chiasmal glioma compared to a pituitary macroadenoma.
Question 2: A 30-year-old male presents with erectile dysfunction, low testosterone, and elevated prolactin levels. What is the most likely diagnosis?
- A. Craniopharyngioma
- B. Testicular failure
- C. Pituitary adenoma (Correct Answer)
- D. Cushing's syndrome
Explanation: Pituitary adenoma - Elevated prolactin levels in a male, coupled with symptoms of hypogonadism (erectile dysfunction, low testosterone), are highly suggestive of a prolactinoma, which is a type of pituitary adenoma [1]. - The prolactinoma suppresses gonadotropin-releasing hormone (GnRH), leading to secondary hypogonadism [1]. Craniopharyngioma - While it is a suprasellar tumor that can affect pituitary function, it typically causes symptoms related to compression of the optic chiasm (visual field defects) [3] and panhypopituitarism, which are not mentioned here. - Hyperprolactinemia is usually due to stalk compression rather than direct prolactin secretion, and other hormone deficiencies are typically more prominent [1]. Cushing's syndrome - Characterized by elevated cortisol levels, leading to symptoms like central obesity, moon facies, and skin changes, which are not described in this patient [4]. - Although it can sometimes be caused by a pituitary tumor (Cushing's disease), the primary hormonal imbalance is cortisol excess, not isolated hyperprolactinemia. Testicular failure - While it causes low testosterone and erectile dysfunction, it would lead to elevated LH and FSH (hypergonadotropic hypogonadism) due to the lack of negative feedback on the pituitary [2]. - Elevated prolactin is not a direct consequence of primary testicular failure.
Question 3: Which of the following medications is not associated with causing hyperprolactinemia?
- A. Haloperidol
- B. Trifluoperazine
- C. Metoclopramide
- D. Lasix (Correct Answer)
Explanation: ***Lasix*** - **Furosemide (Lasix)** is a loop diuretic primarily used to treat **edema** and **hypertension**. It acts on the kidneys to increase urine output and is not known to directly affect prolactin secretion pathways. - Its mechanism of action involves inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, a process unrelated to dopamine or prolactin regulation. *Metoclopramide* - **Metoclopramide** is a **dopamine D2 receptor antagonist** that can readily cross the blood-brain barrier, leading to increased prolactin secretion by blocking the inhibitory effect of dopamine on prolactin release from the pituitary gland. - It is often used as an **antiemetic** and **prokinetic agent**, and hyperprolactinemia is a common side effect. *Haloperidol* - **Haloperidol** is a potent **first-generation antipsychotic** that significantly blocks **dopamine D2 receptors** in the central nervous system. - This blockade directly inhibits the dopamine-mediated suppression of prolactin, leading to a dose-dependent increase in serum prolactin levels. *Trifluoperazine* - **Trifluoperazine** is another **first-generation antipsychotic** that also acts as a potent **dopamine D2 receptor antagonist**. - Its strong dopamine D2 receptor blockade frequently results in **hyperprolactinemia**, a common side effect of typical antipsychotics.
Question 4: Maximum increase in prolactin level is caused by:-
- A. Olanzapine (Primarily blocks 5HT2 receptors)
- B. Aripiprazole (D2 partial agonist)
- C. Risperidone (Potent D2 receptor antagonist) (Correct Answer)
- D. Clozapine (Primarily blocks 5HT2 receptors)
Explanation: ***Risperidone (Potent D2 receptor antagonist)*** - Risperidone is a **potent D2 receptor antagonist**, meaning it blocks dopamine's action at these receptors. Since dopamine inhibits prolactin release, blocking D2 receptors leads to a significant increase in **prolactin levels**. - Its high affinity for D2 receptors in the **tuberoinfundibular pathway** is a primary reason for its pronounced effect on prolactin. *Olanzapine (Primarily blocks 5HT2 receptors)* - While olanzapine can cause some prolactin elevation, its primary mechanism involves **5HT2 receptor blockade**, with less potent D2 antagonism compared to risperidone. - The degree of **hyperprolactinemia** associated with olanzapine is generally milder than that seen with risperidone. *Aripiprazole (D2 partial agonist)* - Aripiprazole is a **D2 partial agonist**, meaning it acts as an antagonist when dopamine levels are high and an agonist when dopamine levels are low, effectively stabilizing dopamine activity. - Due to its partial agonism, aripiprazole typically has a **low risk of hyperprolactinemia** and can even normalize elevated prolactin levels caused by other antipsychotics. *Clozapine (Primarily blocks 5HT2 receptors)* - Clozapine primarily blocks **5HT2 receptors** and has relatively weak D2 receptor antagonism, especially transient D2 blockade. - It generally causes **minimal to no prolactin elevation** and is considered a prolactin-sparing antipsychotic.
Question 5: A lady presents with amenorrhea and galactorrhea. What is the most likely cause?
- A. None of the options
- B. Pituitary adenoma (Correct Answer)
- C. Adrenal hyperplasia
- D. 7α-hydroxylase deficiency
Explanation: ### Pituitary adenoma - A **prolactin-secreting pituitary adenoma** (prolactinoma) is the most common cause of sustained **hyperprolactinemia**, leading to both **amenorrhea** and **galactorrhea** [1]. - **Elevated prolactin levels** inhibit gonadotropin-releasing hormone (GnRH) pulsatility, leading to reduced LH and FSH, causing anovulation and amenorrhea, alongside direct stimulation of breast tissue for galactorrhea [1], [2]. ### *None of the options* - This option is incorrect as **pituitary adenoma** is a highly plausible cause for the presented symptoms. - The combination of **amenorrhea** and **galactorrhea** is a classic presentation of hyperprolactinemia, often due to a pituitary adenoma [1]. ### *Adrenal hyperplasia* - **Adrenal hyperplasia** typically involves overproduction of androgens or cortisol, leading to symptoms like **hirsutism**, **virilization**, or **Cushing's syndrome**, rather than galactorrhea [3]. - While it can cause menstrual irregularities, it does not directly cause **galactorrhea**, which is primarily linked to prolactin excess [1], [3]. ### *7α-hydroxylase deficiency* - **7α-hydroxylase deficiency** is a rare genetic disorder affecting **bile acid synthesis**, not directly related to reproductive hormones or prolactin regulation. - Its clinical manifestations are primarily related to **liver disease** due to abnormal bile acid metabolism and would not present with amenorrhea and galactorrhea.
Question 6: Secretion of prolactin is inhibited by?
- A. Dopamine (Correct Answer)
- B. Serotonin
- C. Noradrenaline
- D. Adrenaline
Explanation: ***Dopamine*** - **Dopamine**, produced by the **hypothalamus**, is the primary physiological inhibitor of **prolactin secretion** from the anterior pituitary gland. - It acts on **D2 receptors** on lactotrophs, leading to a decrease in prolactin synthesis and release. *Serotonin* - **Serotonin** generally has a stimulatory effect on **prolactin secretion**, rather than an inhibitory one. - Elevated serotonin levels can lead to **hyperprolactinemia**. *Noradrenaline* - While **noradrenaline** can have complex effects on pituitary hormones, it is not considered the primary direct inhibitor of **prolactin secretion**. - Its influence is often indirect or less potent than that of **dopamine**. *Adrenaline* - **Adrenaline** (epinephrine) is a neurotransmitter and hormone primarily involved in the **"fight or flight" response** and does not directly inhibit **prolactin secretion**. - Its effects on pituitary hormone release are typically less direct compared to **dopamine's** specific action on lactotrophs.
Question 7: All are causes of anovulatory amenorrhea except which of the following?
- A. Hyperprolactinemia
- B. Drugs
- C. PCOD
- D. Gonadal dysgenesis (Correct Answer)
Explanation: ***Gonadal dysgenesis*** - This condition is a cause of **primary ovarian insufficiency**, leading to amenorrhea but not primarily due to anovulation in a previously cycling individual. - In gonadal dysgenesis, the **ovaries are malformed or absent**, resulting in a lack of follicles and thus no ovulation or estrogen production from the start. *PCOD* - **Polycystic Ovarian Disease** (PCOD/PCOS) is a common cause of anovulatory amenorrhea, characterized by **oligo- or anovulation**, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound. - The hormonal imbalance (e.g., elevated **androgens**, high **LH/FSH ratio**) disrupts normal follicular development and ovulation. *Hyperprolactinemia* - **Elevated prolactin levels** inhibit the pulsatile secretion of **GnRH (Gonadotropin-Releasing Hormone)** from the hypothalamus, which in turn reduces FSH and LH release from the pituitary. - This suppression of gonadotropins leads to impaired follicular development and **anovulation**, resulting in amenorrhea. *Drugs* - Various medications can cause anovulatory amenorrhea by interfering with the **hypothalamic-pituitary-ovarian axis**. - Examples include antipsychotics (which can increase **prolactin levels**), certain antidepressants, opioids, and chemotherapy agents that can damage ovarian function.
Question 8: Testicular feminization syndrome is characterized by all of the following except?
- A. Absent uterus
- B. Primary amenorrhea
- C. Normal breast development
- D. Presence of Barr body (Correct Answer)
Explanation: **Explanation:** **Testicular Feminization Syndrome (now known as Complete Androgen Insensitivity Syndrome - CAIS)** is a condition where a genetic male (46, XY) has a total resistance to androgens due to a defect in the androgen receptor. **Why Option D is the Correct Answer:** The **Barr body** represents an inactivated X chromosome, typically found in individuals with more than one X chromosome (e.g., 46, XX females or 47, XXY males). Since CAIS patients have a **46, XY genotype**, they possess only one X chromosome, which remains active. Therefore, they are **Barr body negative**. **Analysis of Other Options:** * **A. Absent uterus:** In these patients, the testes are present (usually intra-abdominal) and secrete **Anti-Müllerian Hormone (AMH)**. AMH causes the regression of Müllerian structures, leading to the absence of the uterus, fallopian tubes, and upper third of the vagina. * **B. Primary amenorrhea:** Due to the absence of a uterus and ovaries, these patients typically present during puberty with a failure to start menstruation. * **C. Normal breast development:** Peripheral conversion of testosterone to estrogen (aromatization) occurs. Since there is no androgen action to oppose this estrogen, patients develop normal, often feminine, breast contours (though the nipples/areolae may be pale). **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** 46, XY (Genetically male, Phenotypically female). * **Gonads:** Testes (Risk of gonadoblastoma; gonadectomy is recommended after puberty/attainment of height). * **Hair:** Characteristically **absent or scanty** axillary and pubic hair (due to androgen resistance). * **Vagina:** Blind-ending pouch (short vagina). * **Differential Diagnosis:** **Müllerian Agenesis (MRKH Syndrome)**. Distinguishing factor: MRKH has a 46, XX karyotype, normal pubic hair, and normal ovaries.
Question 9: A female presents with normal breast development but scanty pubic hair. What is the most likely diagnosis?
- A. Turner's syndrome
- B. Testicular feminizing syndrome (Correct Answer)
- C. Mullerian agenesis
- D. Gonadal dysgenesis
Explanation: **Explanation:** The clinical presentation of **normal breast development** paired with **scanty or absent pubic/axillary hair** is a classic hallmark of **Androgen Insensitivity Syndrome (AIS)**, historically known as **Testicular Feminizing Syndrome**. **1. Why the Correct Answer is Right:** In AIS, the individual has a **46, XY** karyotype and functioning testes that produce testosterone. However, due to a defect in androgen receptors, the body cannot respond to testosterone. * **Breast Development:** Occurs because the high levels of testosterone are peripherally converted to estrogen (aromatization). * **Scanty Pubic Hair:** Pubic and axillary hair growth is dependent on androgens. Since the receptors are non-functional, hair growth is minimal or absent. * **Anatomy:** MIF (Müllerian Inhibiting Factor) is produced, so there is no uterus or fallopian tubes (blind-ending vagina). **2. Why Incorrect Options are Wrong:** * **Turner’s Syndrome (45, XO):** Characterized by "streak gonads" and low estrogen. Patients typically present with **primary amenorrhea and absent breast development** (sexual infantilism). * **Müllerian Agenesis (MRKH Syndrome):** These patients are **46, XX** with normal ovaries. They have **normal breast development AND normal pubic hair** (since androgen receptors are functional), but lack a uterus and upper vagina. * **Gonadal Dysgenesis:** Similar to Turner’s, the lack of functional gonads leads to estrogen deficiency, resulting in a lack of secondary sexual characteristics (no breast development). **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** AIS is 46, XY; MRKH is 46, XX. * **Gonads:** In AIS, testes are often found in the inguinal canal or abdomen (risk of gonadoblastoma; requires removal after puberty). * **Differential Diagnosis:** The presence or absence of pubic hair is the most important clinical differentiator between AIS (absent) and MRKH (present).
Question 10: Which of the following tests can differentiate Mullerian agenesis (MRKH syndrome) from complete androgen insensitivity syndrome (testicular feminization syndrome)?
- A. 3D Ultrasound
- B. MRI
- C. Karyotyping (Correct Answer)
- D. Serum testosterone levels
Explanation: **Explanation:** Both **Mullerian Agenesis (MRKH Syndrome)** and **Complete Androgen Insensitivity Syndrome (CAIS)** present with primary amenorrhea, a blind vaginal pouch, and well-developed breasts. However, their underlying genetic and hormonal profiles are fundamentally different. **Why Karyotyping is the Correct Answer:** Karyotyping is the definitive diagnostic tool to differentiate these two conditions. * **MRKH Syndrome:** Patients are genetically female (**46, XX**). They have normal ovaries and female-range testosterone levels. * **CAIS:** Patients are genetically male (**46, XY**). They have undescended testes and male-range testosterone levels, but appear phenotypically female because their tissues are unresponsive to androgens. **Analysis of Incorrect Options:** * **A & B (3D Ultrasound/MRI):** While both imaging modalities are excellent for identifying the absence of a uterus and cervix, they cannot reliably distinguish between a 46,XX individual (MRKH) and a 46,XY individual (CAIS) based solely on pelvic anatomy, as both lack Mullerian structures. * **D (Serum Testosterone):** While testosterone levels are significantly higher in CAIS (male range) than in MRKH (female range), **Karyotyping** remains the gold standard for definitive diagnosis and is the preferred initial step in the workup of primary amenorrhea with absent internal organs. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pubic/Axillary Hair:** This is the most important clinical differentiator. It is **normal** in MRKH but **absent or scanty** in CAIS (due to androgen resistance). 2. **Gonads:** In MRKH, ovaries are present (normal ovulation/hormones). In CAIS, testes are present (usually intra-abdominal or inguinal). 3. **Management:** In CAIS, the gonads must be removed (gonadectomy) after puberty to prevent malignancy (gonadoblastoma/dysgerminoma). In MRKH, the focus is on vaginal creation (dilatation or vaginoplasty).
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