Biochemistry
2 questionsLocation of gene on chromosome is identified by
Tyrosine kinase receptor is associated with proto-oncogene -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 351: Location of gene on chromosome is identified by
- A. Karyotyping
- B. Genetic mapping (Correct Answer)
- C. Microarray
- D. Genomic imprinting
Explanation: ***Genetic mapping*** - **Genetic mapping** (also called chromosome mapping) uses various techniques to determine the **physical location (locus)** of genes on a chromosome. - Techniques include **linkage analysis**, **FISH (Fluorescence In Situ Hybridization)**, chromosomal banding, and analysis of **inheritance patterns** of traits and genetic markers. - This identifies both the **relative positions** between genes and their **absolute chromosomal addresses**. *Karyotyping* - **Karyotyping** is a technique that visualizes the entire set of chromosomes in an organism. - While it can identify **large chromosomal abnormalities** like aneuploidy or major deletions/insertions, it does not pinpoint the exact location of a specific gene. *Microarray* - **Microarray** technology is used to study the expression levels of thousands of genes simultaneously or to detect specific genetic variations. - It does not directly map the physical location of a gene on a chromosome. *Genomic imprinting* - **Genomic imprinting** is an epigenetic phenomenon where certain genes are expressed in a **parent-of-origin-specific manner**. - It describes a mechanism of gene regulation rather than a method for identifying the location of a gene on a chromosome.
Question 352: Tyrosine kinase receptor is associated with proto-oncogene -
- A. RAS (RAt Sarcoma)
- B. RET (REarranged during Transfection) (Correct Answer)
- C. RB (Retinoblastoma gene)
- D. MYC (Myelocytomatosis oncogene)
Explanation: ***RET*** - RET is a **tyrosine kinase receptor** that plays a crucial role in cell signaling and development [1][2]. - It is associated with several **neoplasms**, including medullary thyroid carcinoma and multiple endocrine neoplasia type 2 [1]. *RB* - RB (Retinoblastoma protein) is a **tumor suppressor gene**, not a proto-oncogene or receptor. - Its role is largely in regulating the **cell cycle**, particularly in preventing excessive cell growth. *RAS* - RAS is a family of **GTPase proteins** involved in transmitting signals within cells, but it is not a receptor itself [1]. - It is classified as an **oncogene**, but does not function as a tyrosine kinase receptor [2]. *MYC* - MYC is a **transcription factor** involved in cell cycle progression and growth, not a tyrosine kinase receptor [2]. - It is considered an **oncogene** that promotes cellular proliferation, but it doesn't have tyrosine kinase activity [3][4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1097-1098. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 291-292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 28-29. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 293-294.
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 351: 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
6 questionsWhat is the initial event in serum sickness?
Which genetic condition is considered the most lethal due to monosomy?
Subepithelial deposits in the kidney are primarily associated with which condition?
Irregular scarred kidney with pelvic dilatation is seen with?
Reversible change from one cell type to another is known as -
Which of the following is an oncogene?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 351: 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 352: Which genetic condition is considered the most lethal due to monosomy?
- A. Autosomal monosomy (Correct Answer)
- B. Chromosomal monosomy
- C. Autosomal trisomy
- D. Chromosomal trisomy
Explanation: ***Autosomal monosomy*** - **Autosomal monosomy** is the most lethal form of monosomy because it involves the loss of an entire autosome, leading to a severe imbalance in gene dosage. [1] - The human body cannot typically survive with the loss of a whole autosome, resulting in early embryonic or fetal demise. [1] *Chromosomal monosomy* - This is a broader term that includes both **autosomal monosomy** and **sex chromosome monosomy**. - While many forms of chromosomal monosomy are lethal, **sex chromosome monosomy (e.g., Turner syndrome)** is survivable, making the general term "chromosomal monosomy" less specific for the *most lethal* condition. [1] *Autosomal trisomy* - **Autosomal trisomy** involves an extra copy of an autosome (e.g., Trisomy 21 for Down syndrome), which, while causing significant health issues, is generally less lethal than the complete loss of an autosome. [1] - Many individuals with autosomal trisomies can survive to birth and beyond, unlike most cases of autosomal monosomy. [1] *Chromosomal trisomy* - This refers to having an extra copy of any chromosome, including **autosomes** and **sex chromosomes**. - While conditions like **Trisomy 13 (Patau syndrome)** and **Trisomy 18 (Edwards syndrome)** are highly lethal, the presence of *extra* genetic material is typically less universally lethal than the *absence* of an entire autosome. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.
Question 353: Subepithelial deposits in the kidney are primarily associated with which condition?
- A. None of these conditions are associated with subepithelial deposits.
- B. Membranoproliferative Glomerulonephritis (MPGN) Type I
- C. Goodpasture's Syndrome (GPS)
- D. Post-Streptococcal Glomerulonephritis (PSGN) (Correct Answer)
Explanation: ***PSGN*** - Post-streptococcal glomerulonephritis (PSGN) is characterized by **subepithelial immune complex deposits** [1], typically after a streptococcal infection [1]. - It is associated with **hematuria**, **edema**, and elevated **anti-streptolysin O (ASO)** titers. *GPS* - Minimal change disease (often referred to as idiopathic nephrotic syndrome) does not primarily feature **subepithelial deposits** but rather **effacement of podocyte foot processes**. - Clinical presentation includes **nephrotic syndrome** symptoms, not glomerulonephritis like PSGN. *MPGN-1* - Membranoproliferative glomerulonephritis type 1 includes **subendothelial deposits** rather than subepithelial deposits associated with PSGN. - Symptoms often include **nephritic syndrome** and is commonly linked with conditions like **HCV infection**. *All* - While several conditions can show **deposits in kidney**, not all are characterized by **subepithelial deposits**, hence this option is inaccurate. - Each type of glomerular disease has specific types of deposits (immune complex vs. complement) associated with their pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-916.
Question 354: Irregular scarred kidney with pelvic dilatation is seen with?
- A. Chronic pyelonephritis (Correct Answer)
- B. Polycystic kidney
- C. Renal artery stenosis
- D. Tuberculosis of kidney
Explanation: ***Chronic pyelonephritis*** - Characterized by irregular scarring of the kidney and often leads to **pelvic dilatation** due to recurrent infections and obstruction [1]. - The damage from inflammation results in **cortical scarring** and can affect kidney function significantly over time [1]. *Renal artery stenosis* - Typically presents with **hypertension** and may lead to ischemic atrophy, but does not cause significant **pelvic dilatation**. - The kidney appears small and often asymmetric, but not typically irregular and scarred. *Tuberculosis of kidney* - Can cause damage to the kidney, but usually leads to **caseating granulomas** and can cause abscesses, not specifically irregular scarring with pelvic dilation. - Often presents with systemic symptoms such as fever and night sweats, along with hematuria. *Polycystic kidney* - Characterized by multiple cysts in both kidneys leading to enlarged kidneys, but does not typically present as **irregularly scarred kidneys**. - Usually associated with **hemodynamic issues** and hypertension but not pelvic dilatation in the sense of scarring or fibrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-939.
Question 355: Reversible change from one cell type to another is known as -
- A. Hypertrophy
- B. Dysplasia
- C. Hyperplasia
- D. Metaplasia (Correct Answer)
Explanation: ***Metaplesia*** - Refers to the **reversible change** from one cell type to another in response to chronic irritation or damage [1][2]. - It often occurs as an adaptive response in **epithelial tissues**, such as in the respiratory tract in smokers [1][2]. *Hypertrophy* - Represents an **increase in cell size** rather than a change in cell type [2]. - It is often a response to increased functional demand, as seen in **cardiac muscle** in athletes. *Hyperplesia* - Refers to an **increase in cell number** within a tissue or organ, not a change in cell type [2]. - Common in conditions such as **benign prostatic hyperplasia** but does not involve differentiation into other cell types. *Dysplasia* - Indicates an **abnormal growth or development** of cells, leading to disordered morphology rather than a transformation into another cell type. - It is often a precursor to cancer but does not signify the reversible nature of metaplasia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 49. [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. 85-92.
Question 356: Which of the following is an oncogene?
- A. WT-1
- B. Rb
- C. p53
- D. RAS (Correct Answer)
Explanation: ***RAS*** - RAS is an **oncogene**, not a tumor suppressor gene; it promotes cell proliferation and survival [1]. - Mutations in RAS lead to uncontrolled cell division, contributing to various cancers. *p53* - p53 is a crucial **tumor suppressor gene** responsible for regulating the cell cycle and preventing tumor formation [1,2]. - It functions by inducing apoptosis in cells with damaged DNA, preventing their proliferation [2]. *WT-1* - WT-1 is a **tumor suppressor gene** associated with Wilms' tumor and regulates kidney and gonadal development. - It plays a role in cell growth and differentiation, preventing tumorigenesis when functioning correctly. *Rb* - The Rb gene encodes the **retinoblastoma protein**, a key tumor suppressor that regulates the cell cycle by inhibiting cell division [1,2]. - Loss of Rb function is primarily associated with retinoblastoma and other cancers, indicating its critical role in tumor suppression [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-301. [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. 227-228.
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 351: 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.