Anatomy
1 questionsCephalic index is calculated as
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 1251: Cephalic index is calculated as
- A. Biparietal Diameter / Occipitofrontal Diameter (Correct Answer)
- B. Biparietal Diameter / Head Circumference
- C. Head Circumference / Femur Length
- D. Occipitofrontal Diameter / Biparietal Diameter
Explanation: ***Biparietal Diameter / Occipitofrontal Diameter*** - The **cephalic index** is a measure used in **craniometry** to describe the shape of the skull, calculated by dividing the maximum **biparietal diameter** (width) by the maximum **occipitofrontal diameter** (length) and multiplying by 100. [1] - This ratio helps classify head shapes into **brachycephalic** (short, wide), **mesocephalic** (medium), and **dolichocephalic** (long, narrow). *Biparietal Diameter / Head Circumference* - This ratio is not the standard definition for the **cephalic index**; head circumference is a measure of overall head size, not its proportional shape in terms of width to length. - While both parameters are used in fetal biometry, their ratio does not define the **cephalic index**. *Head Circumference / Femur Length* - This ratio is completely unrelated to the **cephalic index**. - **Head circumference** estimates head size, and **femur length** estimates fetal long bone growth, both used for gestational age assessment, but not for skull shape. *Occipitofrontal Diameter / Biparietal Diameter* - This formula represents the inverse of the **cephalic index**, which would yield a different and non-standard index for skull shape. - The traditional and medically recognized formula for the **cephalic index** places the **biparietal diameter** in the numerator.
Internal Medicine
1 questionsWhich of the following is NOT typically associated with Kallmann's syndrome?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 1251: Which of the following is NOT typically associated with Kallmann's syndrome?
- A. Hypogonadotropic hypogonadism
- B. Anosmia
- C. Amenorrhea
- D. Excess stimulation of the HPO axis (Correct Answer)
Explanation: ***Excess stimulation of the HPO axis*** - Kallmann's syndrome is characterized by **hypogonadotropic hypogonadism**, meaning there is a deficiency in the secretion of **gonadotropin-releasing hormone (GnRH)** [1] from the hypothalamus. - This deficiency leads to *reduced* stimulation of the **hypothalamic-pituitary-ovarian (HPO)** axis, not excess stimulation. *Amenorrhea* - **Amenorrhea** (absence of menstruation) is a common presentation in females with Kallmann's syndrome due to the **hypogonadotropic hypogonadism**. - The lack of GnRH results in insufficient **follicle-stimulating hormone (FSH)** and **luteinizing hormone (LH)**, preventing ovarian function and regular menstrual cycles. *Hypogonadotropic hypogonadism* - This is a **defining feature** of Kallmann's syndrome, where the **hypothalamus fails to produce enough GnRH**, leading to low levels of FSH and LH from the pituitary. - The low gonadotropin levels subsequently cause the gonads (testes or ovaries) to produce insufficient sex hormones, resulting in **delayed or absent puberty** [1]. *Anosmia* - **Anosmia** (the inability to smell) is a classic and diagnostic feature of Kallmann's syndrome, distinguishing it from other forms of hypogonadotropic hypogonadism. - It occurs because the **GnRH-producing neurons** originate in the olfactory placode and fail to migrate correctly into the hypothalamus during embryonic development, disrupting both smell and GnRH secretion.
Obstetrics and Gynecology
5 questionsWhat is the primary hormonal cause of hot flushes experienced during menopause?
What is the recommended dose of folic acid for a patient with a history of neural tube defect (NTD) in a previous pregnancy?
A G2P1L1 female presents at 28 weeks of gestation with a 1:4 anti-D titre. What is the most appropriate management option?
Number of stem villi at term in human placenta is?
The window of implantation occurs at which of the following time periods after fertilization?
NEET-PG 2015 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 1251: What is the primary hormonal cause of hot flushes experienced during menopause?
- A. Increased noradrenaline with normal estrogen levels
- B. Increased noradrenaline
- C. Decreased estrogen levels (Correct Answer)
- D. Both increased noradrenaline and decreased estrogen levels
Explanation: ***Decreased estrogen levels*** - **Decreased estrogen** is the primary hormonal change during menopause, leading to thermoregulatory dysfunction in the hypothalamus. - This hormonal imbalance causes the **vasomotor symptoms** like hot flushes and night sweats. *Increased noradrenaline* - While **noradrenaline** (norepinephrine) is involved in thermoregulation, its increase is a **secondary event** triggered by the initial estrogen deficiency, not the primary cause. - Increased noradrenaline can exacerbate the **vasodilation** and heat dissipation experienced during a hot flush. *Increased noradrenaline with normal estrogen levels* - This option is incorrect because hot flushes are characteristic of menopause, which is defined by **decreased estrogen levels**. - **Normal estrogen levels** would typically prevent the severe thermoregulatory instability that causes hot flushes. *Both increased noradrenaline and decreased estrogen levels* - Although both factors are involved, the question asks for the **primary hormonal cause**. **Decreased estrogen** initiates the cascade of events, including the subsequent alteration of neurotransmitter levels like noradrenaline. - Noradrenaline's role is more of a **mediator** in the physiological response to the primary estrogen deficiency.
Question 1252: What is the recommended dose of folic acid for a patient with a history of neural tube defect (NTD) in a previous pregnancy?
- A. 0.5 mg
- B. 1 mg
- C. 2 mg
- D. 4 mg (Correct Answer)
Explanation: ***4 mg*** - For women with a prior history of a **neural tube defect (NTD)-affected pregnancy**, a higher dose of **4 mg of folic acid daily** is recommended to significantly reduce the risk of recurrence. - This increased dosage is crucial for achieving adequate maternal folate levels to prevent NTDs, starting at least one month before conception and continuing through the first trimester. *0.5 mg* - This dose is lower than the standard recommendation for women without a history of NTDs and is insufficient for high-risk individuals. - Suboptimal folic acid levels can still lead to a higher risk of NTD recurrence in patients with a history of NTD-affected pregnancies. *1 mg* - While 1 mg is higher than the general recommendation, it is still insufficient for women with a **history of NTD in a previous pregnancy**. - Current guidelines suggest a significantly higher dose for secondary prevention due to altered folate metabolism or higher requirements in these individuals. *2 mg* - This dose is also lower than the **established recommendation for high-risk women** who have had a previous NTD-affected pregnancy. - It does not provide the optimal level of protection required to reduce the risk of recurrence effectively.
Question 1253: A G2P1L1 female presents at 28 weeks of gestation with a 1:4 anti-D titre. What is the most appropriate management option?
- A. MCA Doppler (Correct Answer)
- B. Caesarean section
- C. Induction of labour
- D. Amniocentesis
Explanation: ***MCA Doppler*** - The presence of anti-D antibodies in a pregnant woman indicates **Rh isoimmunization**, which can lead to **hemolytic disease of the fetus and newborn (HDFN)**. - Even though a titre of **1:4 is below the critical threshold** (usually 1:16 or 1:32), any detectable anti-D titre at 28 weeks warrants **fetal surveillance** to detect early signs of fetal anemia. - **Middle cerebral artery (MCA) Doppler** is the **non-invasive gold standard** for detecting fetal anemia by measuring peak systolic velocity (PSV), which increases in anemic fetuses due to hyperdynamic circulation. - Serial MCA Doppler monitoring allows timely intervention if fetal anemia develops, avoiding unnecessary invasive procedures. *Caesarean section* - This is a mode of delivery and would only be considered if there were severe **fetal compromise** or other obstetric indications after proper monitoring and management. - At 28 weeks gestation with a low anti-D titre, immediate delivery is **not indicated** and would result in significant prematurity risks. *Induction of labour* - Induction of labour is a delivery method that would only be planned at term or for specific indications like severe fetal compromise unresponsive to other interventions. - At **28 weeks gestation**, the focus should be on **monitoring and prolonging pregnancy** while ensuring fetal wellbeing, not on delivery. *Amniocentesis* - Historically used to assess **bilirubin levels (ΔOD450)** in amniotic fluid as an indirect measure of fetal hemolysis, but it is an **invasive procedure** with risks (miscarriage ~1%, infection, worsening sensitization). - **MCA Doppler has largely replaced amniocentesis** for initial and serial assessment of fetal anemia due to its non-invasive nature, high sensitivity, and ability to be repeated safely.
Question 1254: Number of stem villi at term in human placenta is?
- A. 60
- B. 240 (Correct Answer)
- C. 120
- D. 480
Explanation: ***240*** - At term, the **human placenta** contains numerous **stem villi** which branch extensively to form the villous tree. - The approximate number of **stem villi** at term is around **240**, contributing to the large surface area for maternal-fetal exchange. *60* - This number is significantly **lower** than the actual count of **stem villi** found in a mature, term placenta. - Such a low number would result in an **insufficient surface area** for effective nutrient and gas exchange. *120* - While higher than 60, this number is still **underestimated** for the quantity of **stem villi** present in a full-term human placenta. - A placenta with only 120 stem villi might not be able to adequately support a fetus at term. *480* - This number is an **overestimation** of the typical count of **stem villi** in a human placenta at term. - While villi are extensive, 480 stem villi represent a significantly higher number than usually observed.
Question 1255: The window of implantation occurs at which of the following time periods after fertilization?
- A. 6-10 days (Correct Answer)
- B. 12 days
- C. 12 weeks
- D. 6 weeks
Explanation: ***6-10 days*** - The uterus is most receptive to implantation during the **"window of implantation,"** which occurs roughly **6 to 10 days post-fertilization**, coinciding with the mid-luteal phase. - During this period, the **endometrial lining** undergoes specific changes, guided by hormonal signals from **progesterone**, making it optimal for the blastocyst to attach. *12 days* - While implantation can still occur, the **peak receptivity window** is generally considered to be narrower, between 6 and 10 days. - By day 12, changes in the **endometrial environment** may start to reduce the likelihood of successful implantation. *12 weeks* - **12 weeks** refer to the end of the first trimester of pregnancy and is far too late for the initial implantation event. - Implantation must have occurred much earlier for a viable pregnancy at this stage. *6 weeks* - **6 weeks** refers to an established pregnancy, at which point implantation would have occurred several weeks prior. - The process of implantation is completed within the first two weeks post-fertilization.
Pediatrics
1 questionsWhich of the following is true regarding precocious puberty:
NEET-PG 2015 - Pediatrics NEET-PG Practice Questions and MCQs
Question 1251: Which of the following is true regarding precocious puberty:
- A. Sexual maturity is attained early (Correct Answer)
- B. Mental function is increased
- C. Reproductive function is absent
- D. Body proportions remain unchanged
Explanation: ***Sexual maturity is attained early*** - **Precocious puberty** is defined by the development of secondary sexual characteristics significantly earlier than the average age. - This early onset of puberty means that affected individuals reach **sexual maturity** at a younger chronological age. *Mental function is increased* - Precocious puberty does not inherently lead to an increase in **mental function** or cognitive abilities. - While hormonal changes can influence mood and behavior, they do not enhance intelligence. *Reproductive function is absent* - Precocious puberty implies the premature activation of the **hypothalamic-pituitary-gonadal axis**, leading to the appearance of secondary sexual characteristics and, in many cases, the potential for **reproductive function**. - Girls, for example, can experience early menarche and boys can produce sperm, meaning fertility is not absent but rather accelerated. *Body proportions remain unchanged* - Precocious puberty often results in changes in **body proportions**, particularly due to the early closure of epiphyseal plates. - Although there is an initial growth spurt, the premature fusion of growth plates can lead to a shorter-than-average adult height.
Physiology
2 questionsThe role of human placental lactogen is :
Antimullerian hormone is secreted by ?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 1251: The role of human placental lactogen is :
- A. Stimulate milk production
- B. Promotes growth of breast for lactation.
- C. Supports fetal growth and development. (Correct Answer)
- D. Provide fetal nutrition by antagonizing the action of insulin in maternal circulation, breakdown of fats and proteins and transport of fatty acids and amino acids from maternal to fetal circulation.
Explanation: ***Supports fetal growth and development.*** - Human placental lactogen (hPL) acts as a **growth hormone** for the fetus, primarily by altering maternal metabolism to favor fetal nutrient supply. - It increases **maternal insulin resistance**, leading to higher maternal glucose and free fatty acids, which are then shunted to the fetus, supporting its growth and development. *Stimulate milk production* - **Prolactin**, secreted by the anterior pituitary, is the primary hormone responsible for stimulating milk production (lactogenesis). - While hPL has some structural similarity to growth hormone and prolactin, its primary role is not to directly stimulate milk production during pregnancy; rather, it prepares the breasts. *Promotes growth of breast for lactation.* - hPL, along with **estrogen** and **progesterone**, contributes to the **mammary gland development** during pregnancy, preparing the breasts for lactation. - However, its direct role is more about **mammary gland proliferation and differentiation** rather than initiation of milk production. *Provide fetal nutrition by antagonizing the action of insulin in maternal circulation, breakdown of fats and proteins and transport of fatty acids and amino acids from maternal to fetal circulation.* - This is a highly detailed and largely accurate description of *how* hPL supports fetal growth and development, making it a mechanism rather than the primary, concise role. - It describes the metabolic changes induced by hPL, which ultimately lead to the **support of fetal growth and development**.
Question 1252: Antimullerian hormone is secreted by ?
- A. Theca cells
- B. Leydig cells
- C. Both Sertoli cells and granulosa cells (Correct Answer)
- D. None of the above
Explanation: ***Both Sertoli cells and granulosa cells*** - **Antimullerian hormone (AMH)** is produced by **Sertoli cells in males** and **granulosa cells in females** - In **males**: Sertoli cells secrete AMH during fetal development to cause **regression of Müllerian ducts** (which would otherwise develop into uterus, fallopian tubes, and upper vagina) - In **females**: Granulosa cells of developing ovarian follicles secrete AMH, which serves as a **marker of ovarian reserve** and inhibits excessive follicle recruitment - This is the only option that correctly identifies both cell types that produce AMH *Theca cells* - Theca cells are found in ovarian follicles and produce **androgens** (androstenedione and testosterone), not AMH - These androgens are converted to estrogens by granulosa cells via aromatase enzyme - Theca cells do not produce antimullerian hormone *Leydig cells* - Leydig cells are located in the **testes** and produce **testosterone** - They do not produce antimullerian hormone - Only Sertoli cells (not Leydig cells) produce AMH in males *None of the above* - This is incorrect because AMH is indeed produced by specific cell types: **Sertoli cells in males** and **granulosa cells in females**