Anatomy
1 questionsWhat is the preferred site for intramuscular injection in the gluteus muscle?
NEET-PG 2012 - Anatomy NEET-PG Practice Questions and MCQs
Question 351: What is the preferred site for intramuscular injection in the gluteus muscle?
- A. Inferolateral
- B. Superolateral (Correct Answer)
- C. Superomedial
- D. Inferomedial
Explanation: ***Superolateral*** - This quadrant is preferred because it avoids the **sciatic nerve** and major **blood vessels**, minimizing the risk of injury. - The muscle mass in this region, primarily the **gluteus medius**, is sufficient for medication absorption. *Inferomedial* - This area carries a high risk of damaging the **sciatic nerve**, which runs through the lower, medial part of the gluteus. - Injecting here can also hit major **blood vessels**, leading to bleeding or hematoma. *Superomedial* - While somewhat safer than the inferomedial quadrant, this area is still closer to the **sciatic nerve** exit point and major vessels compared to the superolateral region. - The muscle bulk is also less prominent here compared to the superolateral aspect. *Inferolateral* - This quadrant is still in the vicinity of the **sciatic nerve** and major blood vessels, making it riskier than the superolateral site. - There is less muscle mass here compared to the superior quadrants, which can lead to improper drug absorption.
Biochemistry
3 questionsAt which positions does pancreatic lipase hydrolyze the ester linkages of triacylglycerides?
Which of the following usually require a RNA intermediate for cloning/replication?
The primary defect which leads to sickle cell anemia is:
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 351: At which positions does pancreatic lipase hydrolyze the ester linkages of triacylglycerides?
- A. 1 and 2
- B. 2 and 3
- C. Only 3
- D. 1 and 3 (Correct Answer)
Explanation: **Correct: 1 and 3** - Pancreatic lipase specifically targets the **ester bonds at the sn-1 and sn-3 positions** (primary alcohol positions) on the glycerol backbone of triacylglycerides. - This positional specificity results in the formation of **2-monoacylglycerol (2-MAG)** and **two free fatty acids**. - This is the characteristic action of pancreatic triacylglycerol lipase during fat digestion in the intestinal lumen. *Incorrect: 1 and 2* - Hydrolysis at positions 1 and 2 would produce a 3-monoacylglycerol and free fatty acids, which is not the physiological product of pancreatic lipase. - The enzyme's positional specificity favors the outer sn-1 and sn-3 positions, not the middle sn-2 position. *Incorrect: 2 and 3* - Hydrolysis at positions 2 and 3 would yield a 1-monoacylglycerol and free fatty acids, which does not reflect pancreatic lipase activity. - The enzyme specifically spares the sn-2 position due to its structural specificity. *Incorrect: Only 3* - If only position 3 were hydrolyzed, the product would be a 1,2-diacylglycerol and one free fatty acid. - This represents incomplete hydrolysis; pancreatic lipase typically hydrolyzes **both outer positions (sn-1 and sn-3)** due to its regiospecificity.
Question 352: Which of the following usually require a RNA intermediate for cloning/replication?
- A. Cosmids
- B. Retroviruses (Correct Answer)
- C. Plasmids
- D. Transposons
Explanation: ***Retroviruses*** - **All retroviruses require an RNA intermediate** for their replication cycle, making this the correct answer. - Retroviruses have an **RNA genome** that must be **reverse transcribed into DNA** by reverse transcriptase enzyme before integration into the host genome. - The integrated DNA (provirus) is then transcribed back to RNA, which serves both as mRNA for viral proteins and as genomic RNA for new virions. - Examples include **HIV, HTLV**, and other retroviruses that definitively use this RNA → DNA → RNA replication strategy. *Transposons* - This option is **too broad** to be correct. Only **retrotransposons** (Class I transposons) use RNA intermediates via a "copy-and-paste" mechanism involving reverse transcription. - However, **DNA transposons** (Class II) move by a "cut-and-paste" DNA mechanism **without any RNA intermediate**. - Since the question asks what "usually requires" RNA intermediate, and many common transposons (like bacterial Tn5, Tn10) are DNA transposons, this answer is imprecise. *Cosmids* - Cosmids are **hybrid cloning vectors** containing cos sites from bacteriophage lambda combined with plasmid sequences. - They replicate as **DNA plasmids** in bacteria using DNA-dependent DNA polymerase. - No RNA intermediate is involved in their replication mechanism. *Plasmids* - Plasmids are **extrachromosomal circular DNA molecules** that replicate independently within bacterial or yeast cells. - Replication occurs via **DNA-to-DNA synthesis** using DNA polymerase. - No RNA intermediate is required for plasmid propagation.
Question 353: The primary defect which leads to sickle cell anemia is:
- A. An abnormality in porphyrin part of hemoglobin
- B. A nonsense mutation in the β-chain of HbA
- C. Substitution of valine by glutamate in the α-chain of HbA
- D. Replacement of glutamate by valine in β-chain of HbA (Correct Answer)
Explanation: ***Replacement of glutamate by valine in β-chain of HbA*** - The primary defect in sickle cell anemia is a **point mutation** that leads to the replacement of **glutamic acid** with **valine** in the **sixth position** of the β-globin chain [1]. - This mutation causes the hemoglobin (HbS) to polymerize under low oxygen conditions, resulting in the characteristic **sickle-shaped red blood cells** [1]. *A nonsence mutation in the I3-chain of HbA* - A nonsense mutation leads to a **premature stop codon**, which is not the mechanism behind sickle cell anemia. - This mutation does not involve the β-globin chain, which is critical in this specific disorder. *Substitution of valine by glutamate in the a-chain of HbA* - This statement is incorrect as sickle cell anemia specifically involves the **β-chain**, not the **α-chain**. - Substituting valine with glutamate does not cause sickling but rather the opposite of the actual defect observed in this condition. *An abnormality in porphyrin part of hemoglobin* - Sickle cell anemia does not arise from **porphyrin metabolism issues**, which are related to conditions like **porphyrias**. - The primary defect is a change in the amino acid sequence, not in the porphyrin structure of hemoglobin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.
Microbiology
1 questionsWhich of the following is the most potent stimulator of Naive T-cells?
NEET-PG 2012 - Microbiology NEET-PG Practice Questions and MCQs
Question 351: Which of the following is the most potent stimulator of Naive T-cells?
- A. Macrophages
- B. B-cell
- C. Mature dendritic cells (Correct Answer)
- D. Follicular dendritic cells
Explanation: ***Mature dendritic cells*** - **Mature dendritic cells** are the most potent professional antigen-presenting cells (APCs) for activating **naive T cells** due to their efficient antigen processing, presentation abilities, and high expression of costimulatory molecules (e.g., CD80, CD86) and MHC-peptide complexes. - Activated by pathogens or inflammatory signals, they migrate to secondary lymphoid organs where they initiate primary immune responses by presenting antigens to and activating naive T cells. *Follicular dendritic cells* - **Follicular dendritic cells** primarily present intact antigens to **B cells** in germinal centers of secondary lymphoid organs, playing a crucial role in B cell maturation, selection, and antibody production. - They lack MHC class II molecules and thus cannot directly present antigens to naive T cells. *Macrophages* - While **macrophages** are professional APCs, they are generally less efficient than mature dendritic cells at activating **naive T cells**, especially in the initiation of primary immune responses. - They are more involved in presenting antigens to already activated T cells and clearing pathogens, often acting as secondary APCs. *B-cell* - **B cells** can act as APCs, but they are generally less efficient than **dendritic cells** in activating **naive T cells**, especially for the primary immune response. - Their primary role in antigen presentation is to present processed antigens to **helper T cells** to receive costimulation for their own activation and differentiation into plasma cells, often after being activated themselves.
Pathology
4 questionsWhat type of anaemia is primarily associated with leukaemia?
What is the term for a localized malformation composed of an excessive but disorganized arrangement of cells and tissues indigenous to the site?
In which organ do atheromatous changes of blood vessels typically occur early in the disease process?
Which of the following best describes the shape of Birbeck granules?
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 351: What type of anaemia is primarily associated with leukaemia?
- A. Aplastic anaemia
- B. Iron deficiency anaemia
- C. Megaloblastic anaemia
- D. Myelophthisic anaemia (Correct Answer)
Explanation: ***Myelophthisic anaemia*** - This condition arises from the **displacement of normal hematopoietic tissue** in the bone marrow by abnormal cells, like those seen in leukaemia, leading to **extramedullary hematopoiesis**. - Marrow infiltration causes **pancytopenia** and often results in the presence of **immature granulocytes** and **nucleated red blood cells** in the peripheral blood (leukoerythroblastosis). *Iron deficiency anaemia* - This type of anaemia is caused by insufficient iron for **hemoglobin synthesis**, often due to chronic blood loss or inadequate dietary intake. - While leukaemia patients can develop iron deficiency due to bleeding, it is not the **primary type of anaemia** directly resulting from the marrow infiltration by leukaemic cells. *Megaloblastic anaemia* - Characterized by the production of abnormally large, immature red blood cells, primarily due to **vitamin B12** or **folate deficiency**. - There is no direct causal link between leukaemia and the development of megaloblastic anaemia as a **primary haemato-pathological mechanism**. *Aplastic anaemia* - Characterized by **pancytopenia** due to bone marrow failure with hypocellular marrow, not marrow infiltration. - While both leukaemia and aplastic anaemia can present with cytopenias, aplastic anaemia shows a **hypocellular marrow** whereas leukaemia shows a **hypercellular marrow** with infiltration by malignant cells.
Question 352: What is the term for a localized malformation composed of an excessive but disorganized arrangement of cells and tissues indigenous to the site?
- A. Hamartoma (Correct Answer)
- B. Malignant tumor
- C. Choristoma
- D. None of the options
Explanation: ***Hamartoma*** - A **hamartoma** is an overgrowth of cells and tissues that are normally found in the affected area, but in a disordered fashion, creating a tumor-like growth [1]. - It's a **benign (non-cancerous)** lesion, often congenital, that grows at the same rate as the surrounding tissues. *Malignant tumor* - A **malignant tumor** is characterized by uncontrolled cell growth that invades surrounding tissues and can metastasize to distant sites. - Unlike a hamartoma, a malignant tumor consists of **abnormal, dysplastic cells** that do not resemble the normal tissues of the organ. *Choristoma* - A choristoma is a **benign tumor-like growth** consisting of normal cells or tissues that are **heterotopic**, meaning they are located in an abnormal site. - An example is the presence of pancreatic tissue in the wall of the stomach, which is normal tissue in an abnormal location, unlike a hamartoma which has normal tissue in the correct location but in a disorganized manner. *None of the options* - This option is incorrect because **hamartoma** accurately describes the overgrowth of a skin structure at a localized region made of normal, but disorganized, tissue [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 651-652.
Question 353: In which organ do atheromatous changes of blood vessels typically occur early in the disease process?
- A. Kidney
- B. Heart (Correct Answer)
- C. Liver
- D. Spleen
Explanation: ***Heart*** - The **coronary arteries**, which supply the heart, are particularly susceptible to **atherosclerosis** due to high blood flow turbulence and shear stress [1]. - Early atheromatous changes often begin in these arteries, leading to conditions like **coronary artery disease (CAD)** [1]. *Kidney* - While the kidneys can be affected by **atherosclerosis** (renal artery stenosis), it typically occurs later in the disease process or in the presence of more widespread disease [1]. - The primary early site for systemic atherosclerosis is generally not the renal arteries. *Liver* - The liver is not a primary site for the development of **atherosclerosis** within its own blood vessels. - Liver disease can influence lipid metabolism, but directly developing atheroma within hepatic arteries is uncommon. *Spleen* - The spleen is rarely the primary or early site for **atheromatous changes**. - Its blood vessels are generally less prone to the turbulent flow and plaque formation seen in major arteries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 499-508.
Question 354: Which of the following best describes the shape of Birbeck granules?
- A. Resembling a tennis racket (Correct Answer)
- B. Resembling a hockey stick
- C. Resembling a bat
- D. Resembling a ball
Explanation: ***Tennis racket*** [1] - Birbeck granules are distinctive for their **tennis racket shape**, consisting of an elongated area and a bulbous end [1]. - They are typically found in **Langerhans cell histiocytosis** and are associated with **CD1a+** staining [1]. *Bat* - The term "bat" does not accurately describe the structure or morphology of Birbeck granules. - Unlike bats, Birbeck granules have a **specific elongated shape** with a bulbous tip rather than bat wings. *Hockey stick* - This shape implies a straight handle and a flat blade, which does not represent the **widely tapered ends** of Birbeck granules. - The **characteristic morphology** does not align with any hockey stick features. *Ball* - The term "ball" indicates a spherical shape, which is not fitting for Birbeck granules, as they are **elongated** and striated. - Birbeck granules are defined specifically by their **tapered structure**, contrasting markedly with a circular form. **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.
Physiology
1 questionsNonshivering thermogenesis in adults is due to:
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 351: Nonshivering thermogenesis in adults is due to:
- A. Muscle metabolism
- B. Thyroid hormone
- C. Noradrenaline
- D. Brown fat between the shoulders (Correct Answer)
Explanation: ***Brown fat between the shoulders*** - In adults, the primary **effector tissue** for **non-shivering thermogenesis** is **brown adipose tissue (BAT)**, with major depots located between the shoulders, around the neck, and along the spine. - **BAT** contains specialized mitochondria with **uncoupling protein 1 (UCP1)** that uncouples oxidative phosphorylation, generating heat instead of ATP. - This is the tissue where non-shivering thermogenesis actually occurs, making it the direct answer to what non-shivering thermogenesis is "due to." *Noradrenaline* - **Noradrenaline** is the key neurotransmitter that **activates brown fat** via **β3-adrenergic receptors** to initiate non-shivering thermogenesis. - While noradrenaline is the **trigger/stimulus**, the actual heat production occurs in brown adipose tissue. - Noradrenaline itself does not produce heat directly; it acts as the signal that activates the thermogenic machinery in BAT. *Thyroid hormone* - **Thyroid hormone** increases **basal metabolic rate** and can potentiate the thermogenic response by upregulating UCP1 expression in brown fat. - Its role is **permissive and long-term** rather than being the immediate effector of acute non-shivering thermogenesis. - It modulates overall cellular metabolism but is not the primary mechanism for rapid heat generation in cold exposure. *Muscle metabolism* - **Muscle contraction** during shivering generates heat through increased ATP hydrolysis, which is **shivering thermogenesis**. - **Non-shivering thermogenesis** specifically refers to heat production **without muscle contraction**, making muscle metabolism the mechanism for shivering, not non-shivering, thermogenesis.