Anatomy
2 questionsThe roof of the olfactory region is formed by?
Which of the following is NOT a content of the occipital triangle?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 381: The roof of the olfactory region is formed by?
- A. Nasal bone
- B. Sphenoid
- C. Temporal bone
- D. Cribriform plate of ethmoid (Correct Answer)
Explanation: ***Cribriform plate of ethmoid*** - The **cribriform plate** of the ethmoid bone forms the superior boundary, or roof, of the nasal cavity specifically in the olfactory region [1]. - It is perforated by numerous **olfactory foramina** through which the olfactory nerves pass from the nasal cavity to the olfactory bulb of the brain [2]. *Nasal bone* - The **nasal bones** form part of the bridge of the nose and contribute to the anterior part of the bony framework of the external nose. - They do not form the roof of the olfactory region within the nasal cavity. *Sphenoid* - The **sphenoid bone** is a complex bone at the base of the skull, contributing to the posterior wall of the nasal cavity and parts of the cranial floor. - It does not directly form the roof of the olfactory region. *Temporal bone* - The **temporal bones** are located on the sides and base of the skull, housing structures related to hearing and balance. - They are not involved in forming the roof of the nasal cavity or the olfactory region.
Question 382: Which of the following is NOT a content of the occipital triangle?
- A. Lesser occipital nerve
- B. Occipital artery
- C. Suprascapular nerve (Correct Answer)
- D. Great auricular nerve
Explanation: Suprascapular nerve - The **suprascapular nerve** originates from the brachial plexus and supplies the supraspinatus and infraspinatus muscles; it travels through the suprascapular notch and is not found within the occipital triangle. - Its primary course and innervation are associated with the shoulder, entirely separate from the neck region defining the occipital triangle. *Great auricular nerve* - The **great auricular nerve** emerges from the cervical plexus and supplies sensory innervation to the skin over the parotid gland, mastoid process, and auricle, courses superficially across the sternocleidomastoid in the region of the occipital triangle. - It is a recognized content of the posterior triangle of the neck, which encompasses the occipital triangle. *Lesser occipital nerve* - The **lesser occipital nerve** arises from the cervical plexus at C2 and C3, providing sensory innervation to the skin of the neck and scalp posterior to the auricle. - It ascends along the posterior border of the sternocleidomastoid muscle, placing it within the boundaries of the occipital triangle. *Occipital artery* - The **occipital artery** is a branch of the external carotid artery that supplies blood to the posterior scalp. - It traverses the apex of the posterior triangle (including the occipital triangle) as it ascends to the back of the head.
Biochemistry
3 questionsWhich defect in the urea cycle is an X-linked disease?
Which of the following organs does not primarily utilize the salvage pathway of purine nucleotide synthesis?
Rate limiting step in pyrimidine synthesis?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 381: Which defect in the urea cycle is an X-linked disease?
- A. Ornithine transcarbamylase (Correct Answer)
- B. Arginase
- C. Argininosuccinate synthase
- D. Carbamoyl phosphate synthetase I
Explanation: ***Ornithine transcarbamylase*** - **Ornithine transcarbamylase (OTC) deficiency** is the only **X-linked recessive** disorder among the urea cycle defects. - Males are usually more severely affected, while females can be symptomatic carriers. *Carbamoyl phosphate synthetase I* - **Carbamoyl phosphate synthetase I (CPS1) deficiency** is an **autosomal recessive** disorder. - It is one of the more severe urea cycle defects, leading to profound hyperammonemia. *Arginase* - **Arginase deficiency** (hyperargininemia) is an **autosomal recessive** disorder. - It typically presents with a distinct neurological phenotype, including spasticity and developmental delay. *Argininosuccinate synthase* - **Argininosuccinate synthase deficiency**, also known as **Citrullinemia type I**, is an **autosomal recessive** disorder. - It leads to the accumulation of **citrulline** and **ammonia** in the blood.
Question 382: Which of the following organs does not primarily utilize the salvage pathway of purine nucleotide synthesis?
- A. RBC
- B. Leukocytes
- C. Liver (Correct Answer)
- D. Brain
Explanation: ***Liver*** - The **liver** is capable of both *de novo* synthesis and the salvage pathway of purine nucleotides, but it primarily utilizes the **de novo pathway** due to its high metabolic capacity and central role in biosynthesis for the entire body. - While salvage pathways exist, the liver's robust *de novo* synthesis allows it to readily produce purines from simple precursors, making it less reliant on salvaging pre-formed bases. *Brain* - The **brain** relies heavily on the **salvage pathway** for purine nucleotide synthesis because it has a limited capacity for *de novo* purine synthesis. - This dependency makes the brain particularly vulnerable to deficiencies in salvage enzymes, such as in **Lesch-Nyhan syndrome** where HGPRT deficiency leads to severe neurological dysfunction. *RBC* - **Red blood cells (RBCs)** are anucleated and lack the machinery for *de novo* purine synthesis, making them entirely dependent on the **salvage pathway** to maintain their purine nucleotide pool. - They salvage pre-formed purine bases and nucleosides from the plasma to synthesize necessary adenine and guanine nucleotides. *Leukocytes* - **Leukocytes**, particularly lymphocytes, have a high turn-over rate and metabolic activity, and they primarily rely on the **salvage pathway** for purine nucleotide synthesis. - The **immune system's rapid proliferation** and response demand efficient nucleotide synthesis, and the salvage pathway offers a quick and energy-efficient way to achieve this.
Question 383: Rate limiting step in pyrimidine synthesis?
- A. Aspartate transcarbamoylase (ATCase)
- B. Dihydroorotate dehydrogenase
- C. Dihydro-orotase
- D. Carbamoyl phosphate synthase-II (Correct Answer)
Explanation: ***Carbamoyl phosphate synthetase II (CPS-II)*** - **CPS-II** is the **committed and rate-limiting enzyme** in **de novo pyrimidine synthesis** in **mammals (including humans)** - It catalyzes the formation of **carbamoyl phosphate** from glutamine, CO₂, and 2 ATP in the **cytoplasm** - This is the **first committed step** and the main **regulatory checkpoint**, inhibited by UTP (feedback inhibition) and activated by PRPP and ATP - CPS-II is part of the **CAD complex** (carbamoyl phosphate synthetase, aspartate transcarbamoylase, dihydroorotase) in mammals *Aspartate transcarbamoylase (ATCase)* - ATCase catalyzes the **second step**: condensation of carbamoyl phosphate with aspartate to form carbamoyl aspartate - While ATCase is the **rate-limiting step in bacteria** (E. coli), in **mammals** it is part of the CAD complex and **not the primary regulatory step** - This option is incorrect for human/mammalian biochemistry tested in NEET PG *Dihydro-orotase* - The **third enzyme** in the pathway, converting carbamoyl aspartate to dihydroorotate - Part of the CAD complex in mammals but **not the rate-limiting step** *Dihydroorotate dehydrogenase* - Catalyzes the **fourth step**: oxidation of dihydroorotate to orotate - Located on the **outer surface of the inner mitochondrial membrane** (only mitochondrial enzyme in the pathway) - Important enzyme but **not rate-limiting**
Internal Medicine
2 questionsResponse to iron therapy in iron deficiency anemia is denoted by?
Which of the following statements about Alport's syndrome is incorrect?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 381: Response to iron therapy in iron deficiency anemia is denoted by?
- A. Increase in hemoglobin
- B. Reticulocytosis (Correct Answer)
- C. Restoration of enzymes
- D. Increase in iron binding capacity
Explanation: Reticulocytosis - Reticulocytosis is one of the earliest signs of a positive response to iron therapy in iron deficiency anemia, occurring within 5-10 days. - It signifies that the bone marrow is effectively producing new red blood cells after iron supplementation. Restoration of enzymes - While iron is a crucial component of many enzymes (e.g., catalase, cytochrome oxidase), its restoration takes time and is not the primary immediate indicator of therapeutic response. - Clinical improvement and other hematological parameters precede the full restoration of enzyme function. Increase in hemoglobin - An increase in hemoglobin is a definitive sign of successful treatment, but it occurs later than reticulocytosis, typically visible after several weeks to months of therapy. - Hemoglobin levels rise as the new, iron-sufficient red blood cells fully mature and replace the older, iron-deficient ones. Increase in iron binding capacity - In iron deficiency anemia, total iron-binding capacity (TIBC) is typically increased due to more transferrin being available to bind iron [1]. - Successful iron therapy would lead to a decrease in TIBC as transferrin sites become saturated with iron, not an increase.
Question 382: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.
Pathology
1 questionsWhich of the following statements about sickle cell anemia is false?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 381: Which of the following statements about sickle cell anemia is false?
- A. Sickle cells are present in sickle cell anemia.
- B. Target cells are commonly seen in sickle cell anemia.
- C. Ringed sideroblasts are associated with sickle cell anemia. (Correct Answer)
- D. Howell Jolly bodies can be found in sickle cell anemia.
Explanation: ***Ringed sideroblast*** - **Ringed sideroblasts** are not typically associated with sickle cell anemia; they are indicative of disorders like **sideroblastic anemia**. - In sickle cell anemia, the primary findings include **hemolysis** and ineffective erythropoiesis, not ringed sideroblasts [3]. *Howell jolly bodies* - These bodies are remnants of nuclear material and can be found in individuals with **spleen dysfunction**, which can occur in sickle cell anemia [1]. - They are actually a common finding due to **hyposplenism** or **asplenia** in patients with sickle cell disease [2]. *Sickle cells* - The presence of **sickle-shaped red blood cells** is a hallmark of sickle cell anemia, caused by the mutation in the **beta-globin chain** [3]. - These sickle cells are responsible for the characteristic complications of the disease, such as **vaso-occlusive crises** [1][3]. *Target cells* - Target cells, or **codocytes**, are often seen in disorders like **thalassemia** and liver disease, and can also be present in sickle cell anemia. - They are formed due to an increase in the **surface area to volume ratio** of red blood cells, often secondary to **membrane abnormalities** seen in sickle cell changes [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-646. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 570-571. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.
Pharmacology
1 questionsMicrovesicular fatty liver is caused by ?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 381: Microvesicular fatty liver is caused by ?
- A. Valproate (Correct Answer)
- B. Chronic diabetes mellitus (DM)
- C. Prolonged starvation
- D. Chronic inflammatory bowel disease (IBD)
Explanation: ***Valproate*** - **Valproate** is a known cause of **microvesicular steatosis**, particularly in children, due to its interference with mitochondrial fatty acid oxidation. - This can lead to severe liver injury, including **acute liver failure**, as it impairs the liver's ability to metabolize fats. *Chronic diabetes mellitus (DM)* - Chronic DM is commonly associated with **macrovesicular steatosis** (NAFLD), not microvesicular, due to insulin resistance and increased hepatic lipid synthesis. - Unlike microvesicular steatosis, macrovesicular type usually does not immediately impair mitochondrial function. *Prolonged starvation* - Prolonged starvation can lead to **fatty liver**, usually **macrovesicular steatosis**, as the body mobilizes fatty acids from adipose tissue. - While it stresses the liver, it rarely causes the specific **microvesicular** pattern of fat accumulation. *Chronic inflammatory bowel disease (IBD)* - IBD can cause various liver complications, but **microvesicular fatty liver** is not a characteristic feature. - Liver issues in IBD are more often related to **sclerosing cholangitis** or secondary to nutritional deficiencies and medications.
Psychiatry
1 questionsWhich of the following develop first during dependence of a substance ?
NEET-PG 2013 - Psychiatry NEET-PG Practice Questions and MCQs
Question 381: Which of the following develop first during dependence of a substance ?
- A. Tolerance
- B. Physical dependence
- C. Psychological dependence (Correct Answer)
- D. Withdrawal symptoms
Explanation: ***Psychological dependence*** - **Psychological dependence** often develops first, characterized by an emotional need for the substance to experience pleasure or avoid discomfort. - This involves a strong **craving** and compulsive drug-seeking behavior despite negative consequences, driven by the substance's effect on brain reward pathways. *Tolerance* - **Tolerance** means that increasing doses of the substance are required to achieve the same effect previously achieved with lower doses. - While it often develops early in substance use, the initial "need" to use the substance is often psychological before physiological adaptations occur. *Physical dependence* - **Physical dependence** describes the body's physiological adaptation to the substance, leading to withdrawal symptoms if use is stopped or reduced. - It typically develops after consistent, prolonged use and is usually preceded by psychological dependence and often tolerance. *Withdrawal symptoms* - **Withdrawal symptoms** are the physiological and psychological signs that occur when a dependent person stops or drastically reduces their substance intake. - These are a direct manifestation of physical dependence and thus develop once physical dependence has been established.