Biochemistry
2 questionsWhich cofactor is primarily associated with the activity of glutamate dehydrogenase?
Where does omega oxidation of fatty acids occur?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 421: Which cofactor is primarily associated with the activity of glutamate dehydrogenase?
- A. NAD+ (Correct Answer)
- B. FAD
- C. FMN
- D. FADH2
Explanation: ***NAD+*** - Glutamate dehydrogenase catalyzes the oxidative deamination of **glutamate** to **α-ketoglutarate** and ammonia, and this reaction primarily uses **NAD+** as an electron acceptor. - In some organisms and contexts, it can also use **NADP+**, but **NAD+** is the more common and significant cofactor for its catabolic role. *FAD* - **FAD (flavin adenine dinucleotide)** is typically associated with **flavoproteins** and enzymes involved in oxidation-reduction reactions, such as those in the **electron transport chain** and the **Krebs cycle**. - Enzymes like **succinate dehydrogenase** use FAD, not glutamate dehydrogenase. *FMN* - **FMN (flavin mononucleotide)** is another flavin coenzyme, similar to FAD, and is found in various **flavoproteins** and enzymes of the **electron transport chain**, such as **NADH dehydrogenase (Complex I)**. - It does not serve as a primary cofactor for **glutamate dehydrogenase** activity. *FADH2* - **FADH2** is the reduced form of **FAD**, carrying high-energy electrons to the **electron transport chain** for ATP synthesis. - It's a product or reactant of various metabolic pathways, but not a direct cofactor for **glutamate dehydrogenase**.
Question 422: Where does omega oxidation of fatty acids occur?
- A. Endoplasmic Reticulum (Correct Answer)
- B. Cytosol
- C. Mitochondria
- D. None of the options
Explanation: ***Endoplasmic Reticulum*** - **Omega oxidation** of fatty acids occurs in the **endoplasmic reticulum (microsomes)** of liver and kidney cells. - This pathway involves **hydroxylation of the terminal omega carbon** by **cytochrome P450 enzymes** located in the smooth ER. - The omega carbon is then oxidized to a **carboxyl group**, forming a **dicarboxylic acid**. - This is a **minor pathway** that becomes important when **beta-oxidation is impaired** or for metabolism of **medium-chain fatty acids**. *Cytosol* - The cytosol is involved in **fatty acid synthesis**, not omega oxidation. - While some later steps of fatty acid metabolism occur in the cytosol, the initial hydroxylation step of omega oxidation requires ER-localized cytochrome P450 enzymes. *Mitochondria* - **Mitochondria** are the primary site for **beta-oxidation** of fatty acids, not omega oxidation. - Beta-oxidation sequentially removes **two-carbon units from the carboxyl end**, which is distinct from omega oxidation. - The dicarboxylic acids produced by omega oxidation may subsequently undergo beta-oxidation in mitochondria. *None of the options* - This option is incorrect because the endoplasmic reticulum is the correct cellular location for omega oxidation. - The ER contains the necessary cytochrome P450 enzymes for the hydroxylation reaction that initiates this pathway.
Internal Medicine
3 questionsWhich of the following conditions is the classic example of acute intravascular hemolysis triggered by oxidative stress?
What is the most common site of gastrointestinal stromal tumors (GISTs)?
PNH patients have deficient surface proteins that normally protect red blood cells from activated complements. Which two surface proteins are deficient in these patients?
NEET-PG 2012 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 421: Which of the following conditions is the classic example of acute intravascular hemolysis triggered by oxidative stress?
- A. Hereditary spherocytosis
- B. Sickle cell disease
- C. Acute G6PD deficiency (Correct Answer)
- D. None of the options
Explanation: ***b and c*** - Intravascular hemolysis is commonly associated with both **Acute G6PD deficiency** and **Hereditary spherocytosis**, leading to destruction of red blood cells in the bloodstream [1]. - These conditions are characterized by **high levels of hemoglobinuria** and **low haptoglobin**, indicative of intravascular hemolysis. *Sickle cell ds* - Sickle cell disease primarily causes **extravascular hemolysis** due to splenic sequestration rather than **intravascular** destruction [3]. - The clinical features include **vaso-occlusive crises** and splenic infarction rather than hemolysis within the blood vessels. *Acute G6PD* - While acute G6PD deficiency can lead to hemolysis, it is typically **triggered by oxidative stress** rather than occurring continuously [2]. - The hemolysis in G6PD deficiency occurs more in an **extravascular** manner unless acute stress occurs, which can result in **acute intravascular hemolysis, marked by anemia, hemoglobinemia, and hemoglobinuria** [4]. *Hereditary spherocytosis* - This condition primarily causes **extravascular hemolysis** through the spleen, where abnormal spherocytes are destroyed [1]. - Although it leads to anemia, the hallmark of hereditary spherocytosis is the **spleen's role** in hemocyte destruction rather than intravascular hemolysis.
Question 422: What is the most common site of gastrointestinal stromal tumors (GISTs)?
- A. Ileum
- B. Esophagus
- C. Colon
- D. Stomach (Correct Answer)
Explanation: Stomach - The stomach is the most common site for gastrointestinal stromal tumors (GISTs), accounting for approximately 60-70% of cases. - GISTs in the stomach often present with symptoms like abdominal pain or bleeding and are associated with mutations in the KIT gene. Ileum - Although GISTs can occur in the ileum, they are far less common than those found in the stomach, representing about 10-15% of cases [1]. - GISTs in the ileum tend to present differently, often with intestinal obstruction or pain [1]. Esophagus - Esophageal GISTs are rare and account for only about 5% of GIST cases, making them an uncommon location. - Symptoms are usually related to dysphagia or chest pain, not typical for GISTs arising from more common sites. Colon - Although GISTs can occur in the colon, their frequency is much lower compared to the stomach and represents a small percentage of cases. - Clinical features in colonic GISTs can mimic other colorectal tumors, often causing obstruction or bleeding rather than classic GIST symptoms.
Question 423: PNH patients have deficient surface proteins that normally protect red blood cells from activated complements. Which two surface proteins are deficient in these patients?
- A. CD 55 and CD 58
- B. CD 45 and CD 55 (Correct Answer)
- C. CD 55 and CD 59
- D. CD 51 and CD 55
Explanation: ***CD 55 and CD 59*** - **CD 55 (decay accelerating factor)** and **CD 59 (protectin)** are crucial for inhibiting the complement system, protecting red blood cells from lysis in PNH. - Deficiencies in these proteins lead to increased **susceptibility** of red cells to **complement-mediated hemolysis**. *CD58 and CD 59* - **CD 58** is involved in T-cell interaction but does not solely protect red cells from complement. - While **CD 59** is a correct answer, the absence of **CD 55** makes this option incorrect for PNH. *CD 45 and CD 59* - **CD 45** is primarily a **leukocyte common antigen**, not involved in protecting red cells from complement activation. - This orrectly mentions **CD 59**, but lacks **CD 55**, making it unsuitable as an answer. *CD 51 and CD 59* - **CD 51** is associated with integrin functions and does not play a role in protecting red blood cells from complements. - Although **CD 59** is relevant, the deficiency in **CD 55** highlights the incompleteness of this option.
Pathology
2 questionsHelmet cells are characteristic of anemia of?
Which condition is characterized by spongiform degeneration of the cerebral cortex?
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 421: Helmet cells are characteristic of anemia of?
- A. Hemolytic uremic syndrome (HUS) (Correct Answer)
- B. Disseminated intravascular coagulation (DIC)
- C. Thrombotic thrombocytopenic purpura (TTP)
- D. Autoimmune hemolytic anemia (AIHA)
Explanation: ***Hemolytic uremic syndrome*** - Helmet cells are **fragmented red blood cells** associated with **microangiopathic hemolytic anemia** [1], commonly seen in hemolytic uremic syndrome. - This condition frequently results in **thrombocytopenia** and acute renal failure. *Acanthocytosis* - Acanthocytosis is characterized by **spiky red blood cells** (acanthocytes) rather than helmet cells. - It is commonly associated with **liver disease** and **abetalipoproteinemia**, not hemolytic anemia. *Polysplenia* - Polysplenia is a condition involving multiple spleens but does not typically relate to the **formation of helmet cells**. - It may cause **asplenic complications**, but anemia characteristics do not include helmet cells. *Spherocytosis* - Spherocytosis involves the presence of **spherical red blood cells** rather than fragmented (helmet) cells. - It is associated with **hereditary conditions** like hereditary spherocytosis, which leads to increased hemolysis but not typically to helmet cells. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.
Question 422: Which condition is characterized by spongiform degeneration of the cerebral cortex?
- A. Creutzfeldt-Jakob disease (Correct Answer)
- B. Subacute sclerosing panencephalitis
- C. Fatal familial insomnia
- D. Cerebral toxoplasmosis
Explanation: ***Creutzfeldt-Jakob disease*** - This is a **prion disease** characterized by rapid cognitive decline, myoclonus, and distinctive EEG changes, with **spongiform degeneration of the cerebral cortex** as the hallmark neuropathological feature [1]. - The spongiform changes are due to intracellular vacuoles within neurons and astrocytes, giving the brain tissue a **spongy appearance** [2]. - CJD shows **widespread cortical involvement**, making it the classic answer for cortical spongiform degeneration [2]. *Subacute sclerosing panencephalitis* - This condition is a rare, **chronic, progressive encephalitis** caused by persistent measles virus infection. - It is characterized by widespread **demyelination, gliosis, and intranuclear inclusion bodies**, but not spongiform degeneration. *Fatal familial insomnia* - This is another **prion disease** that also exhibits spongiform degeneration, but the key difference is **anatomical distribution** [2]. - FFI primarily affects the **thalamus** (a subcortical structure) and causes severe insomnia, dysautonomia, and motor signs [2]. - While spongiform changes occur in FFI, they are most prominent in the **thalamus rather than the cerebral cortex**, making CJD the better answer for cortical spongiform degeneration [2]. *Cerebral toxoplasmosis* - This is an **opportunistic infection of the brain** caused by **_Toxoplasma gondii_**, primarily seen in immunocompromised individuals. - It typically results in the formation of **abscesses or ring-enhancing lesions**, rather than spongiform degeneration. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 712-713. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1284-1286.
Physiology
3 questionsGas exchange in tissues takes place at?
From the given pressure-volume curve, identify the end-diastolic volume (EDV) and end-systolic volume (ESV), then calculate the ejection fraction using the formula EF = (EDV - ESV)/EDV × 100%.

Which of the following factors increases stroke volume?
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 421: Gas exchange in tissues takes place at?
- A. Artery
- B. Capillary (Correct Answer)
- C. Vein
- D. Venules
Explanation: ***Capillary*** - **Capillaries** are the smallest and most numerous blood vessels, with very thin walls (only one cell thick), which facilitates the efficient exchange of gases, nutrients, and waste products between blood and tissues. - Their extensive network ensures close proximity to nearly every cell in the body, maximizing the surface area and minimizing the diffusion distance for **gas exchange**. *Artery* - Arteries carry **oxygenated blood** away from the heart to the tissues but have thick, muscular walls designed for high pressure and transport, not for direct exchange with tissues. - They branch into smaller arterioles, which then lead to capillaries, making them a conduit rather than an exchange site. *Vein* - Veins carry **deoxygenated blood** back to the heart from the tissues and have relatively thin walls compared to arteries but are still too thick for efficient gas exchange. - They primarily serve as blood return vessels and reservoirs. *Venules* - Venules are small blood vessels that merge from capillaries and eventually combine to form veins; they primarily function in collecting blood from capillary beds. - While slightly more permeable than larger veins, their main role is still collection and transport, not the extensive gas exchange facilitated by capillaries.
Question 422: From the given pressure-volume curve, identify the end-diastolic volume (EDV) and end-systolic volume (ESV), then calculate the ejection fraction using the formula EF = (EDV - ESV)/EDV × 100%.
- A. 40%
- B. 50%
- C. 55%
- D. 60% (Correct Answer)
Explanation: ***60%*** - From the pressure-volume loop, the **end-diastolic volume (EDV)** is the volume at point 'a', which is **130 mL**. - The **end-systolic volume (ESV)** is the volume at point 'd', which is **50 mL**. - Using the formula EF = (EDV - ESV) / EDV × 100% = (130 mL - 50 mL) / 130 mL × 100% = 80 mL / 130 mL × 100% = **61.5%**, which rounds to **60%** (the closest option). *40%* - To obtain an ejection fraction of 40%, the ESV would need to be higher, or the EDV lower, than what is indicated by the points 'a' and 'd' on the graph. - (130 - ESV) / 130 = 0.40 => 130 - ESV = 52 => ESV = 78 mL. This isn't consistent with the graph. *50%* - An ejection fraction of 50% would mean that the heart ejected half of its EDV. - (130 - ESV) / 130 = 0.50 => 130 - ESV = 65 => ESV = 65 mL. This value for ESV is not depicted at point 'd'. *55%* - For an ejection fraction of 55%, the calculation would yield a different ESV than what is presented in the curve. - (130 - ESV) / 130 = 0.55 => 130 - ESV = 71.5 => ESV = 58.5 mL. This is not the ESV at point 'd'.
Question 423: Which of the following factors increases stroke volume?
- A. Increased end-diastolic and end-systolic volumes
- B. Decreased end-diastolic and end-systolic volumes
- C. Increased end-diastolic volume and decreased end-systolic volume (Correct Answer)
- D. Decreased end-diastolic volume and increased end-systolic volume
Explanation: ***Increased end-diastolic volume and decreased end-systolic volume*** - **Stroke volume (SV)** is calculated as **End-Diastolic Volume (EDV)** minus **End-Systolic Volume (ESV)**. Therefore, increasing the volume before contraction while decreasing the volume after contraction will maximize the ejected blood. - A higher **EDV** signifies greater **preload** (more blood filling the ventricle), and a lower **ESV** indicates more complete ejection of blood, often due to increased **contractility** or decreased **afterload**. *Increased end-diastolic and end-systolic volumes* - While an **increased EDV** would tend to increase stroke volume, an **increased ESV** suggests that the heart is ejecting less blood per beat, which would decrease stroke volume. - The combined effect makes it less likely to unequivocally increase stroke volume, as the increase in ESV might offset or even surpass the effect of increased EDV. *Decreased end-diastolic and end-systolic volumes* - Both a **decreased EDV** (less filling) and a **decreased ESV** (more complete ejection) work against each other in terms of stroke volume calculation. - If **EDV** decreases, there's less blood to eject, and if the decrease in **EDV** is proportionally larger than the decrease in **ESV**, stroke volume will decrease. *Decreased end-diastolic volume and increased end-systolic volume* - A **decreased EDV** means less blood is available for ejection, reducing preload and the amount of blood the heart can pump. - An **increased ESV** means the heart is ejecting less blood with each beat, indicating reduced contractility or increased afterload, both of which would decrease stroke volume.