Anatomy
1 questionsSertoli cells are derived from -
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 391: Sertoli cells are derived from -
- A. Genital swelling
- B. Coelomic epithelium (Correct Answer)
- C. Primordial germ cells
- D. Germinal epithelium
Explanation: Sertoli cells are derived from the **coelomic epithelium** (surface epithelium) of the urogenital ridge during gonadal development. - The coelomic epithelium proliferates to form the **primitive sex cords** (medullary cords in males), and cells within these cords differentiate into Sertoli cells. - These cells are essential for **spermatogenesis**, providing structural support and nutrition to developing germ cells, and producing **anti-Müllerian hormone (AMH)** which causes regression of Müllerian ducts in male development [1]. *Germinal epithelium* - This is an **outdated term** previously used for the surface epithelium of the gonad, based on the misconception that it gave rise to germ cells. - Modern embryology uses the term **coelomic epithelium** or surface epithelium instead. - While historically used, this terminology is no longer preferred in current medical literature. *Genital swelling* - **Genital swellings** (labioscrotal swellings) are external mesodermal structures that develop into the **scrotum** in males or **labia majora** in females. - These are external genitalia components and are not the source of internal testicular cells like Sertoli cells. *Primordial germ cells* - **Primordial germ cells (PGCs)** originate from the epiblast, migrate via the hindgut to the developing gonads, and differentiate into **spermatogonia** (males) or **oogonia** (females) [1]. - They form the **germ cell lineage** (gametes), not somatic support cells like Sertoli cells, which are of coelomic epithelial origin.
Biochemistry
3 questionsWhich of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
Enzyme deficient in Hers disease -
Fumarate is formed from which amino acid?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 391: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
- A. Glucokinase is induced by insulin. (Correct Answer)
- B. Hexokinase is specific for glucose.
- C. Glucokinase is inhibited by glucose-6-phosphate.
- D. Hexokinase has a high Km for glucose.
Explanation: ***Glucokinase is induced by insulin.*** - **Insulin** promotes glucose uptake and utilization in the liver and pancreatic beta cells, where glucokinase is primarily expressed. - Induction of **glucokinase** by insulin ensures that glucose is efficiently phosphorylated and trapped within hepatocytes when blood glucose levels are high. - This is a key mechanism for postprandial glucose homeostasis. *Incorrect: Hexokinase is specific for glucose.* - **Hexokinase** is NOT specific for glucose; it can phosphorylate various hexoses including **fructose**, **mannose**, and **galactose**. - Its broad substrate specificity distinguishes it from glucokinase, which has greater specificity for glucose. *Incorrect: Glucokinase is inhibited by glucose-6-phosphate.* - Unlike **hexokinase**, which is subject to product inhibition by glucose-6-phosphate, **glucokinase is NOT inhibited** by its product. - This lack of feedback inhibition allows glucokinase to continue phosphorylating glucose even when glucose-6-phosphate levels are elevated, which is appropriate for its role as a glucose sensor in liver and pancreatic beta cells. *Incorrect: Hexokinase has a high Km for glucose.* - **Hexokinase** has a **low Km** (~0.1 mM) for glucose, meaning it has high affinity and is saturated at normal blood glucose levels. - In contrast, **glucokinase** has a high Km (~10 mM), allowing it to respond proportionally to changes in blood glucose concentration.
Question 392: Enzyme deficient in Hers disease -
- A. Muscle phosphorylase
- B. Liver phosphorylase (Correct Answer)
- C. Acid maltase
- D. Debranching enzyme
Explanation: ***Liver phosphorylase*** - Hers disease, also known as Glycogen Storage Disease Type VI, is specifically caused by a deficiency of **liver phosphorylase**. - This enzyme is crucial for the breakdown of **glycogen in the liver**, leading to an inability to release glucose into the bloodstream during fasting. *Muscle phosphorylase* - Deficiency of **muscle phosphorylase** (myophosphorylase) causes **McArdle disease** (Glycogen Storage Disease Type V), which primarily affects muscle energy. - Patients typically present with exercise intolerance, muscle pain, and cramps, not the hepatic symptoms seen in Hers disease. *Acid maltase* - Deficiency of **acid maltase** (also known as alpha-glucosidase) is responsible for **Pompe disease** (Glycogen Storage Disease Type II), a lysosomal storage disorder. - This enzyme deficiency leads to glycogen accumulation in lysosomes in various tissues, including muscle, liver, and heart, causing muscle weakness and cardiomyopathy. *Debranching enzyme* - A deficiency in the **debranching enzyme** (amylo-1,6-glucosidase) causes **Cori disease** or **Forbes disease** (Glycogen Storage Disease Type III). - This results in the accumulation of abnormally structured glycogen with short outer branches in the liver, muscle, and heart.
Question 393: Fumarate is formed from which amino acid?
- A. Methionine
- B. Valine
- C. Histidine
- D. Tyrosine (Correct Answer)
Explanation: ***Tyrosine*** - **Tyrosine** is a **glucogenic and ketogenic amino acid** that is catabolized to acetoacetate and fumarate. - **Fumarate** then enters the **citric acid cycle (Krebs cycle)**, whereas acetoacetate is a ketone body. *Methionine* - **Methionine** is an **essential amino acid** and a precursor for **S-adenosylmethionine (SAM)**, a methyl donor in many reactions. - Its catabolism produces **succinyl CoA**, not fumarate, through a series of steps via propionyl CoA. *Valine* - **Valine** is a **branched-chain amino acid (BCAA)** that is exclusively **glucogenic**. - Its catabolism ultimately leads to the formation of **succinyl CoA**, which can enter the citric acid cycle. *Histidine* - **Histidine** is an **essential amino acid** that is catabolized to **formiminoglutamate (FIGLU)**. - FIGLU is then converted to **glutamate**, which can eventually be deaminated to α-ketoglutarate, a citric acid cycle intermediate, but not directly fumarate.
Internal Medicine
1 questionsWhat is the mode of inheritance for the most common form of hypophosphatemic rickets?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 391: What is the mode of inheritance for the most common form of hypophosphatemic rickets?
- A. Autosomal Recessive (AR)
- B. Autosomal Dominant (AD)
- C. X-Linked Recessive (XR)
- D. X-Linked Dominant (XD) (Correct Answer)
Explanation: ***X-Linked Dominant (XD)*** - The most common form of hypophosphatemic rickets is **X-linked hypophosphatemic rickets (XLH)**, which is inherited in an X-linked dominant pattern. - This condition is caused by mutations in the **PHEX gene** on the X chromosome, leading to impaired phosphate reabsorption in the kidneys. *Autosomal Recessive (AR)* - While some rare forms of hypophosphatemic rickets exist with **autosomal recessive** inheritance, they are not the most common. - These forms typically involve mutations in genes affecting phosphate transport or vitamin D metabolism, distinct from the primary defect in XLH. *Autosomal Dominant (AD)* - There are also rare **autosomal dominant** forms of hypophosphatemic rickets, such as hereditary hypophosphatemic rickets with hypercalciuria (HHRH) or autosomal dominant hypophosphatemic rickets (ADHR). - However, these are less common than the X-linked dominant form (XLH). *X-Linked Recessive (XR)* - **X-linked recessive** inheritance typically affects males more severely and exclusively, with carrier females usually unaffected or mildly affected. - In X-linked dominant conditions like XLH, both males and females are affected, though females may exhibit variable expressivity.
Pathology
2 questionsWhat is the initial event in serum sickness?
Which of the following is a chromosomal instability syndrome?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 391: What is the initial event in serum sickness?
- A. It is associated with hypocomplementemia.
- B. It is a type III hypersensitivity reaction.
- C. It occurs due to exposure to heterologous antigens. (Correct Answer)
- D. It can lead to leukocytoclastic vasculitis.
Explanation: ***Can lead to leukocytoclastic vasculitis*** - Serum sickness is characterized by the formation of **immune complexes**, which can trigger **leukocytoclastic vasculitis** affecting the blood vessels [1][2]. - Symptoms can include **rash, fever, and arthralgia**, typically occurring 1-3 weeks after exposure to the offending antigen [2]. *Can occur due to homologous antigen* - Serum sickness is usually a reaction to **heterologous** antigens, such as those from animal serum, not **homologous** ones. - Homologous antigens do not typically elicit the immune response seen in serum sickness; hence, this statement is incorrect. *Type 2 hypersensitivity* - Serum sickness is classified as a **Type III hypersensitivity** reaction due to the immune complex formation, not Type II [1]. - Type II is characterized by antibody-mediated destruction of **target cells**, which does not apply here. *Hypercomplementemia* - Serum sickness is associated with **hypocomplementemia** due to complement consumption from immune complex formation, not hypercomplementemia. - This can lead to **decreased complement levels** during the response, making this statement incorrect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173.
Question 392: Which of the following is a chromosomal instability syndrome?
- A. Bloom syndrome (Correct Answer)
- B. Fanconi anemia
- C. Ataxia-telangiectasia
- D. None of the options
Explanation: ***Bloom syndrome*** - Bloom syndrome is the **classic chromosomal instability syndrome** characterized by **spontaneous chromosomal breaks, gaps, and markedly increased sister chromatid exchanges (SCEs)**. - It is an **autosomal recessive disorder** caused by mutations in the BLM gene (RecQ helicase family), leading to impaired DNA repair and replication [1]. - Patients exhibit **growth deficiency, photosensitive facial erythema, immunodeficiency**, and a dramatically **increased risk of cancers** at an early age. - The **hallmark laboratory finding** is a 10-fold increase in sister chromatid exchanges, making it the **prototypical chromosomal instability disorder**. *Fanconi anemia* - Fanconi anemia is **also a chromosomal instability syndrome**, characterized by **chromosomal breakage** when lymphocytes are exposed to DNA crosslinking agents (DEB/MMC test) [1]. - However, it presents primarily with **progressive bone marrow failure, congenital anomalies** (thumb/radial ray, café-au-lait spots, short stature), and increased cancer risk (particularly AML and squamous cell carcinomas). - While chromosomal instability is present, the **clinical presentation is dominated by bone marrow failure**, distinguishing it from Bloom syndrome. *Ataxia-telangiectasia* - Ataxia-telangiectasia is **also a chromosomal instability syndrome** with chromosomal breaks and translocations (especially involving chromosomes 7 and 14) [1]. - Caused by **ATM gene mutations**, leading to defective DNA double-strand break repair and cell cycle checkpoint control. - However, it is **clinically characterized primarily by progressive cerebellar ataxia, oculocutaneous telangiectasias, immunodeficiency**, and elevated AFP levels. - The **neurological manifestations predominate** the clinical picture, distinguishing it from Bloom syndrome. *None of the options* - This option is incorrect because Bloom syndrome is the **classic and prototypical chromosomal instability syndrome**, characterized predominantly by chromosomal instability features rather than other system involvement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323.
Physiology
1 questionsThe major role of 2,3-bisphosphoglycerate in RBCs is -
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 391: The major role of 2,3-bisphosphoglycerate in RBCs is -
- A. Acid-base balance
- B. Reversal of glycolysis
- C. Release of oxygen (Correct Answer)
- D. Binding of oxygen
Explanation: ***Release of oxygen*** - **2,3-bisphosphoglycerate (2,3-BPG)** binds allosterically to **deoxyhemoglobin**, stabilizing its T (tense) state. - This binding reduces hemoglobin's affinity for oxygen, promoting the **release of oxygen** to tissues. *Acid-base balance* - While red blood cells play a role in **acid-base balance** through the bicarbonate buffer system, 2,3-BPG's primary role is not buffering. - The **chloride shift** and **carbonic anhydrase** are more directly involved in RBC acid-base regulation. *Reversal of glycolysis* - 2,3-BPG is an intermediate of the **Rapoport-Luebering shunt**, a side pathway of glycolysis. - It does not reverse glycolysis but rather is produced during glycolysis to serve a specific function in oxygen transport. *Binding of oxygen* - 2,3-BPG **decreases** hemoglobin's affinity for oxygen, thus promoting its *release* from hemoglobin, not its binding. - Oxygen binding to hemoglobin occurs primarily at the **heme iron** without 2,3-BPG.
Psychiatry
1 questionsAll of the following are true about Down syndrome except for one.
NEET-PG 2015 - Psychiatry NEET-PG Practice Questions and MCQs
Question 391: All of the following are true about Down syndrome except for one.
- A. Incidence of Robertsonian translocation is 1:1000 (Correct Answer)
- B. Most common cause is trisomy 21
- C. Mosaicism 21 has no association with maternal age
- D. Extra chromosome is of maternal origin
- E. Incidence increases with advanced maternal age
Explanation: **Incidence of Robertsonian translocation is 1:1000** - This statement is **not accurate** for Down syndrome. Robertsonian translocation accounts for only about **3-4% of Down syndrome cases**, not a general population incidence of 1:1000. - The vast majority of Down syndrome cases (~95%) are due to trisomy 21 from nondisjunction, not translocation. - This is the **correct answer** as it is the FALSE statement. *Extra chromosome is of maternal origin* - In approximately **90-95% of Down syndrome cases**, the extra copy of chromosome 21 originates from the mother due to **nondisjunction** during meiosis. - This maternal origin is strongly correlated with **advanced maternal age**. *Most common cause is trisomy 21* - **Trisomy 21** (due to meiotic nondisjunction) accounts for about **95% of all Down syndrome cases**, making it the most common genetic mechanism. - This results in three separate copies of chromosome 21 in all body cells. *Mosaicism 21 has no association with maternal age* - **Mosaic Down syndrome** occurs when nondisjunction happens *after fertilization* in early embryonic development, leading to a mixture of cells with normal and trisomic cells. - Because it is a **post-zygotic event**, its incidence is independent of **maternal age**, unlike full trisomy 21. *Incidence increases with advanced maternal age* - **TRUE statement** - The risk of Down syndrome (particularly trisomy 21) increases significantly with **maternal age**. - Risk is approximately 1:1500 at age 20, 1:1000 at age 30, 1:400 at age 35, and 1:100 at age 40. - This is due to increased risk of meiotic nondisjunction in older oocytes.
Surgery
1 questionsWhich solid organ is considered to have the lowest risk of rejection during transplantation?
NEET-PG 2015 - Surgery NEET-PG Practice Questions and MCQs
Question 391: Which solid organ is considered to have the lowest risk of rejection during transplantation?
- A. Pancreas
- B. Kidney
- C. Heart
- D. Liver (Correct Answer)
Explanation: ***Liver*** - The liver has a unique immunologic environment, often referred to as **immunologic privilege**, which contributes to its lower rates of rejection compared to other transplanted solid organs. - It produces various **immunosuppressive factors** and has a high capacity for regeneration and repair, adapting more readily to the recipient's immune system. - The liver's **dual blood supply** (hepatic artery and portal vein) and tolerogenic properties make it the most immunologically privileged solid organ. *Pancreas* - **Pancreas transplantation** carries a high risk of rejection, with rejection rates significantly higher than liver transplantation. - Pancreatic tissue is highly **immunogenic** due to its endocrine and exocrine functions, requiring aggressive immunosuppression. - Often transplanted with kidney in diabetic patients, and rejection episodes are common. *Kidney* - Kidney transplantation is common, but it carries a significant risk of both **acute and chronic rejection**, requiring lifelong immunosuppression. - The kidney expresses various **MHC antigens** that are readily recognized by the recipient's immune system, making it more immunogenic than the liver. *Heart* - **Heart transplantation** is associated with a high risk of rejection due to the rich vascularity and immunogenicity of cardiac tissue. - It often requires aggressive immunosuppressive regimens to prevent both **acute cellular rejection** and **antibody-mediated rejection**.