Anatomy
1 questionsBlood tissue barrier in testis is formed by?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 401: Blood tissue barrier in testis is formed by?
- A. Basal lamina & interstitial cells
- B. Basal lamina & spermatogonia
- C. Basal lamina & leydig cells
- D. Adjacent Sertoli cells with basal lamina (Correct Answer)
Explanation: ***Adjacent Sertoli cells with basal lamina*** - The **blood-testis barrier** is primarily formed by **tight junctions** between adjacent **Sertoli cells**, which divide the seminiferous epithelium into basal and adluminal compartments [1]. - The **basal lamina** of the seminiferous tubule also contributes to this barrier, regulating the passage of substances from the interstitial fluid to the basal compartment [1]. *Basal lamina & interstitial cells* - While the **basal lamina** is part of the barrier, **interstitial cells (Leydig cells)** are located outside the seminiferous tubules and are primarily involved in **testosterone production**, not barrier formation [1]. - **Interstitial cells** are part of the connective tissue between the tubules and do not form tight junctions that would restrict molecular movement into the seminiferous epithelium. *Basal lamina & spermatogonia* - **Spermatogonia** are germ cells located in the **basal compartment** of the seminiferous tubule, *beneath* the Sertoli cell tight junctions [1]. - They are able to cross the barrier as they differentiate and move into the adluminal compartment, but they do not form the barrier itself. *Basal lamina & leydig cells* - As mentioned previously, **Leydig cells** (interstitial cells) are responsible for **androgen synthesis** and are located outside the seminiferous tubule [2]. - They do not form components of the physical blood-testis barrier.
Biochemistry
3 questionsWhich of the following is not an androgen?
What is the unit for a prolactin level of 20 in blood?
Which enzyme polymerises Okazaki fragments?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 401: Which of the following is not an androgen?
- A. 17α-hydroxyprogesterone (Correct Answer)
- B. Testosterone
- C. Dihydrotestosterone
- D. Androstenedione
Explanation: ***17α-hydroxyprogesterone*** - This is a **progesterone derivative** and an intermediate in the synthesis of androgens and corticosteroids, but it does **not possess significant androgenic activity** itself. - Its primary role is as a precursor, rather than a direct androgen. *Testosterone* - **Testosterone** is the **primary male sex hormone** and a potent androgen, responsible for the development of male secondary sexual characteristics. - It plays crucial roles in muscle mass, bone density, libido, and erythropoiesis. *Dihydrotestosterone* - **Dihydrotestosterone (DHT)** is a potent androgen, formed from testosterone by the enzyme 5α-reductase. - DHT is responsible for the development of external male genitalia during fetal development and contributes to prostate growth and male pattern baldness in adults. *Androstenedione* - **Androstenedione** is a **weak androgen** and an important **precursor hormone** in the biosynthesis of testosterone and estrogens. - It is produced in the adrenal glands and gonads, serving as an intermediate step in steroidogenesis.
Question 402: What is the unit for a prolactin level of 20 in blood?
- A. ng/ml (Correct Answer)
- B. mg/ml
- C. mg/l
- D. ng/l
Explanation: ***ng/ml*** - Prolactin levels in blood are typically measured in **nanograms per milliliter (ng/mL)**, reflecting the very small concentrations of hormones. - A value of 20 ng/mL falls within the typical reference range for prolactin. *mg/mL* - **Milligrams per milliliter (mg/mL)** is a unit used for much higher concentrations, more common for drugs or larger molecules, not hormones like prolactin. - If prolactin were measured in mg/mL, a value of 20 mg/mL would be an astronomically high and physiologically impossible level. *mg/L* - **Milligrams per liter (mg/L)** is also a unit for higher concentrations than those typically seen for hormones in blood. - 20 mg/L is equivalent to 20 µg/mL or 20,000 ng/mL, which would indicate severe hyperprolactinemia. *ng/L* - **Nanograms per liter (ng/L)** is a unit for extremely low concentrations. - A reading of 20 ng/L would be too low for normal physiological prolactin levels, as 1 ng/mL equals 1000 ng/L.
Question 403: Which enzyme polymerises Okazaki fragments?
- A. DNA polymerase I
- B. DNA polymerase II
- C. DNA polymerase III (Correct Answer)
- D. RNA polymerase
Explanation: ***DNA polymerase III*** - **DNA polymerase III** is the primary replicative enzyme in **prokaryotes (bacteria)** responsible for synthesizing new DNA strands, including the **polymerization of Okazaki fragments** on the lagging strand. - It possesses high processivity (can add ~500 nucleotides without dissociating), essential for rapid and efficient DNA synthesis during replication, adding nucleotides in a **5' to 3' direction**. - In **eukaryotes**, DNA polymerase δ (delta) performs the analogous function of polymerizing Okazaki fragments. *DNA polymerase I* - **DNA polymerase I** in prokaryotes primarily functions in **removing RNA primers** left by primase and **filling the resulting gaps** with DNA nucleotides. - It has 5' to 3' exonuclease activity for primer removal and polymerase activity for gap filling, but is **not the main enzyme for elongating Okazaki fragments**. - Its role is in **DNA repair and finishing replication**, not the extensive synthesis of Okazaki fragments. *DNA polymerase II* - **DNA polymerase II** in prokaryotes is primarily involved in **DNA repair mechanisms**, particularly in **restarting stalled replication forks** and responding to DNA damage. - It is not the main enzyme responsible for the polymerization of **Okazaki fragments** during normal DNA replication. *RNA polymerase* - **RNA polymerase** (specifically **primase**, a specialized RNA polymerase) synthesizes short **RNA primers** (8-12 nucleotides) during DNA replication, which provide the 3'-OH group necessary to initiate DNA synthesis. - It does not synthesize DNA or polymerize **Okazaki fragments**; its function is to create RNA primers, not extend DNA strands.
Internal Medicine
1 questionsChronic atrophy of adrenal gland will result in which hormone deficiency ?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 401: Chronic atrophy of adrenal gland will result in which hormone deficiency ?
- A. Aldosterone
- B. Dehydroepiandrosterone (DHEA)
- C. Epinephrine
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.
Pathology
3 questionsWhich is not a feature of paroxysmal nocturnal hemoglobinuria?
Localized Langerhans cell histiocytosis affecting head and neck is?
In which condition are Pseudo-Pelger-Huët cells typically seen?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 401: Which is not a feature of paroxysmal nocturnal hemoglobinuria?
- A. Thrombocytopenia
- B. Hemolysis
- C. Increased LAP score (Correct Answer)
- D. Thrombosis
Explanation: ***Increased LAP score*** - In paroxysmal nocturnal hemoglobinuria, the **LAP score** is typically **low** due to ineffective hematopoiesis and not elevated. - The presence of a low LAP score is inconsistent with the features of this condition, making it the correct choice. *Thrombosis* - Paroxysmal nocturnal hemoglobinuria is **associated with a high risk of thrombosis**, particularly in the **venous system** [2]. - This is due to **increased platelet activation** and excessive thrombin generation resulting from hemolysis. *Hemolysis* - **Hemolysis** is a hallmark feature of paroxysmal nocturnal hemoglobinuria, where there is **destruction of red blood cells** [2,3]. - Patients often present with signs of hemolytic anemia including **elevated bilirubin** and **low haptoglobin** levels. *Thrombocytopenia* - **Thrombocytopenia** is a common finding in paroxysmal nocturnal hemoglobinuria due to **expanded consumption** of platelets during episodes of hemolysis. - This can lead to an **increased risk of bleeding** in affected patients. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651.
Question 402: Localized Langerhans cell histiocytosis affecting head and neck is?
- A. Eosinophilic granuloma (Correct Answer)
- B. Letterer-siwe disease
- C. Pulmonary Langerhans cell histiocytosis
- D. Hand-Schuller-Christian disease
Explanation: ***Eosinophilic granuloma*** - This is a localized form of **Langerhans cell histiocytosis** that typically presents in the head and neck region, often affecting areas like the skull and mandible [1]. - Characterized by **bone lesions** and may present with **pain or swelling** in the affected area, making it a prominent form in children and young adults. *Pulmonary langerhans cell histiocytosis* - Primarily affects the **lungs** and is associated with **cough, dyspnea**, and pulmonary nodules, not the head and neck region. - Occurs predominantly in **smokers** and involves interstitial lung disease patterns on imaging studies. *Hand-schuller-christian disease* - This condition is a systemic form of Langerhans cell histiocytosis that affects multiple systems rather than being localized, commonly presenting with **diabetes insipidus** and bone lesions. - It is often associated with **exophthalmos** and may involve lymphadenopathy, affecting older children and adults, not localized head and neck involvement. *Letterer-siwe disease* - This represents the acute, disseminated form of Langerhans cell histiocytosis, affecting infants, and is marked by systemic symptoms like **fever**, **rash**, and **hepatosplenomegaly** [1]. - Typically presents with serious manifestations and not specifically localized in the **head and neck area** as seen in eosinophilic granuloma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 630.
Question 403: In which condition are Pseudo-Pelger-Huët cells typically seen?
- A. Hairy cell leukemia
- B. Multiple myeloma
- C. Hodgkin's lymphoma
- D. Myelodysplastic syndrome (Correct Answer)
Explanation: ***Mylodysplastic syndrome*** - Pseudo-Pelger-Huet cells are characteristic and often observed in myelodysplastic syndromes, indicating an ineffective hematopoiesis [1]. - These cells appear as **hyposegmented neutrophils** and are associated with dysplastic changes in the bone marrow [1]. *Hairy cell leukemia* - Typically presents with **hairy cells** in peripheral blood and often involves splenomegaly; pseudo-Pelger-Huet cells are not usual in this condition. - Associated with **PANCYTOPENIA** and reticulin fibrosis, differing from myelodysplastic syndrome. *Hodgkin's lymphoma* - Characterized by the presence of **Reed-Sternberg cells** and typically involves lymphadenopathy. - Peripheral blood findings generally do not include pseudo-Pelger-Huet cells; the focus is on lymphatic tissue. *Multiple myeloma* - Commonly presents with **plasma cells** and related symptoms like bone pain and renal failure, not associated with pseudo-Pelger-Huet cells. - It primarily causes an increase in monoclonal proteins rather than dysplastic changes seen in myelodysplastic syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.
Physiology
2 questionsWhich of the following hormones is not stored in cells?
LH surge is associated with?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 401: Which of the following hormones is not stored in cells?
- A. Thyroxin
- B. Renin
- C. Insulin
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - Cortisol is a **steroid hormone** that is synthesized from **cholesterol** on demand and is **not stored** in secretory vesicles or elsewhere within cells. - Being **lipophilic**, it diffuses freely across cell membranes immediately after synthesis. - Its release is regulated by the **hypothalamic-pituitary-adrenal (HPA) axis**, with synthesis and immediate secretion occurring upon stimulation. *Insulin* - Insulin is a **peptide hormone** synthesized as **proinsulin** and then cleaved into active insulin. - It is **stored in secretory granules** within pancreatic beta cells, allowing for rapid release in response to elevated blood glucose. *Thyroxine* - Thyroxine (T4) is a **thyroid hormone** that is synthesized from tyrosine and iodine. - It is **stored extracellularly** within the thyroid gland's follicles as part of a large protein called **thyroglobulin**. - Unlike cortisol (which is never stored), thyroxine has a **substantial storage pool** that can last weeks, though the storage is extracellular rather than intracellular. *Renin* - Renin is an **enzyme** produced by the **juxtaglomerular cells** of the kidney. - It is **stored in secretory granules** within these cells and released in response to decreased renal perfusion pressure or sympathetic stimulation.
Question 402: LH surge is associated with?
- A. Increased estrogen & decreased progesterone (Correct Answer)
- B. Increased estrogen & increased progesterone
- C. Decreased estrogen & increased progesterone
- D. Decreased estrogen & decreased progesterone
Explanation: ***Increased estrogen & decreased progesterone*** - The **LH surge** is triggered by a significant rise in **estrogen** levels from the dominant follicle, indicating ovarian readiness. - At the time of the LH surge, **progesterone** levels remain low; they only begin to rise significantly after ovulation, when the corpus luteum forms. *Increased estrogen & increased progesterone* - While **estrogen** levels are high, **progesterone** only significantly increases *after* ovulation, as the corpus luteum develops. - High estrogen *and* high progesterone together are typically seen in the **luteal phase**, not at the peak of the LH surge. *Decreased estrogen & increased progesterone* - A decrease in **estrogen** would suppress LH, not trigger a surge. - Increased **progesterone** would also inhibit LH release via negative feedback in the follicular phase if it were to occur pre-ovulation. *Decreased estrogen & decreased progesterone* - Both **decreased estrogen** and **decreased progesterone** would lead to low FSH/LH levels and would not promote an LH surge or ovulation. - This hormonal profile is more characteristic of the very early follicular phase or menopause.