Biochemistry
4 questionsTransport of lipids from the intestine to other tissues is by -
Which method is used to separate a mixture of lipids?
Bile acids are synthesized from ?
Most abundant source of fuel in starvation -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 411: Transport of lipids from the intestine to other tissues is by -
- A. Chylomicrons (Correct Answer)
- B. LDL
- C. HDL
- D. VLDL
Explanation: ***Chylomicrons*** - **Chylomicrons** are the **largest lipoprotein particles** that transport **dietary (exogenous) lipids** from the **intestine** to peripheral tissues - They are synthesized in **intestinal enterocytes** after fat absorption and enter the bloodstream via the **lymphatic system (thoracic duct)** - They carry **triglycerides (85-95%), cholesterol, phospholipids, and fat-soluble vitamins** (A, D, E, K) - **Apolipoprotein B-48** is the characteristic structural protein of chylomicrons - After delivering triglycerides to tissues (via lipoprotein lipase), chylomicron remnants are taken up by the **liver** *LDL (Low-Density Lipoprotein)* - LDL transports **cholesterol from the liver to peripheral tissues** (not from intestine) - It carries **endogenous cholesterol**, not dietary lipids from the intestine - Often called "**bad cholesterol**" due to its role in atherosclerosis - Contains **Apolipoprotein B-100** *HDL (High-Density Lipoprotein)* - HDL performs **reverse cholesterol transport** - moving excess cholesterol from peripheral tissues **back to the liver** - It does **not transport lipids from the intestine** to tissues - Called "**good cholesterol**" for its protective cardiovascular role - Contains **Apolipoprotein A-I and A-II** *VLDL (Very-Low-Density Lipoprotein)* - VLDL is synthesized in the **liver** (not intestine) and transports **endogenous triglycerides** to peripheral tissues - It carries lipids **from the liver**, not from the intestine - VLDL is converted to IDL and then LDL after losing triglycerides - Contains **Apolipoprotein B-100**
Question 412: Which method is used to separate a mixture of lipids?
- A. Electrophoresis
- B. Chromatography (Correct Answer)
- C. Isoelectric focusing
- D. PAGE
Explanation: ***Chromatography*** - **Chromatography** (e.g., thin-layer chromatography, gas chromatography, high-performance liquid chromatography) is widely used to separate lipids based on differences in their **polarity**, **molecular weight**, or **solubility** in various solvents. - This method allows for the isolation and identification of different lipid classes and individual lipid species from a complex mixture. *Electrophoresis* - **Electrophoresis** separates molecules based on their **charge** and **size** in an electric field, making it more commonly used for proteins and nucleic acids. - Lipids are generally **uncharged** or have very low charge, which makes them poorly suited for separation by standard electrophoretic methods without modification. *Isoelectric focusing* - **Isoelectric focusing** is a type of electrophoresis that separates molecules based on their **isoelectric point (pI)**, which is the pH at which a molecule has no net charge. - This technique is primarily used for **proteins** and **peptides**, as lipids typically lack ionizable groups necessary for establishing a distinct pI. *PAGE* - **PAGE** (Polyacrylamide Gel Electrophoresis) is a common method used to separate **proteins** and **nucleic acids** based on their size and charge. - Lipids are **hydrophobic** and do not readily migrate through an aqueous polyacrylamide gel matrix, making PAGE unsuitable for their direct separation.
Question 413: Bile acids are synthesized from ?
- A. Heme
- B. Ribulose
- C. Arachidonic acid
- D. Cholesterol (Correct Answer)
Explanation: ***Cholesterol*** - **Bile acids** are derivatives of **cholesterol**, synthesized in the liver through a multi-step enzymatic pathway. - The conversion of cholesterol to bile acids is a primary mechanism for the excretion and transport of cholesterol from the body. *Heme* - **Heme** is a component of hemoglobin and myoglobin, primarily involved in oxygen transport and storage. - Its degradation product is **bilirubin**, which forms part of bile but is distinct from bile acids. *Ribulose* - **Ribulose** is a 5-carbon sugar, playing a key role in the **pentose phosphate pathway** and the **Calvin cycle** in photosynthesis. - It is not a precursor for bile acid synthesis. *Arachidonic acid* - **Arachidonic acid** is a polyunsaturated fatty acid that serves as a precursor for **eicosanoids** (prostaglandins, thromboxanes, and leukotrienes). - These molecules are involved in inflammation and immune responses but are unrelated to bile acid synthesis.
Question 414: Most abundant source of fuel in starvation -
- A. Liver glycogen
- B. Muscle glycogen
- C. Adipose tissue (Correct Answer)
- D. Blood glucose
Explanation: ***Adipose tissue*** - **Adipose tissue** stores **triglycerides**, which are hydrolyzed into fatty acids and glycerol to serve as the body's primary energy source during prolonged starvation. - The energy reserve in adipose tissue is significantly larger than glycogen stores, providing **sustained fuel** for days or weeks. *Liver glycogen* - **Liver glycogen** is a readily available source of glucose but is rapidly depleted within **12-24 hours** during starvation. - Its primary role is to maintain **blood glucose levels** for glucose-dependent tissues like the brain. *Muscle glycogen* - **Muscle glycogen** is used primarily for **muscle contraction** and cannot be directly released into the bloodstream to maintain blood glucose levels. - While it's a significant energy reserve for working muscles, it does not contribute to systemic fuel needs during starvation. *Blood glucose* - **Blood glucose** is the immediate circulating fuel, but it is tightly regulated and its levels decrease during starvation as glycogen stores are depleted. - It is not an abundant stored source of fuel but rather a transport form of energy.
Internal Medicine
1 questionsWhich of the following statements about sickle cell disease is true?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 411: Which of the following statements about sickle cell disease is true?
- A. Sickling is completely reversible with oxygenation, making it clinically insignificant.
- B. Sickling leads to a significant increase in overall MCHC levels in the blood.
- C. Fetal hemoglobin inhibits sickling. (Correct Answer)
- D. Sickling occurs exclusively in the homozygous state and never in the heterozygous state.
Explanation: ***Sickling is reversible with oxygenation*** - When oxygen tension is restored, hemoglobin S can re-hydrate and revert to its normal shape, reducing sickling. - This reversible process is essential for managing episodes of vaso-occlusive crisis in sickle cell disease. *Fetal hemoglobin facilitates Sickling* - Fetal hemoglobin (HbF) actually inhibits sickling by stabilizing the erythrocyte shape and reducing the proportion of hemoglobin S [1]. - Individuals with higher levels of HbF experience fewer sickling-related complications [1]. *Sickling occurs both in heterozygous and homozygous state* - Sickling primarily occurs in the homozygous state (HbSS); heterozygotes (HbAS) usually do not experience significant sickling effects [1]. - Heterozygous individuals may have a selective advantage against malaria, but they are not prone to sickle cell crises. *Sickling Leads to decreased MCHC* - Sickling does not directly lead to decreased mean corpuscular hemoglobin concentration (MCHC); MCHC is typically normal in sickle cell patients. - In fact, sickle cell disease often results in hemolysis and can lead to increased MCHC in some cases.
Pathology
4 questionsConcentric hypertrophy of left ventricle is seen in -
Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
What is a distinguishing feature of reticulocytes?
Osmotic fragility test is commonly used for which of the following conditions?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 411: Concentric hypertrophy of left ventricle is seen in -
- A. Congenital aortic stenosis due to bicuspid aortic valve (Correct Answer)
- B. Mitral Stenosis
- C. Aortic Regurgitation
- D. Hypertrophic Obstructive Cardiomyopathy
Explanation: ***Congenital aortic stenosis due to bicuspid aortic valve*** - **Aortic stenosis** creates a **pressure overload** on the left ventricle, leading to a compensatory increase in myocardial wall thickness without significant chamber dilation, which is the classic example of **concentric hypertrophy** [1]. - A **bicuspid aortic valve** is a common congenital anomaly that causes aortic stenosis and thus concentric left ventricular hypertrophy [2]. - This represents **acquired concentric hypertrophy** due to hemodynamic stress. *Mitral Stenosis* - **Mitral stenosis** primarily causes a pressure overload on the **left atrium**, leading to left atrial enlargement [3]. - While it can indirectly affect the left ventricle, it typically does not cause **concentric left ventricular hypertrophy** itself. *Aortic Regurgitation* - **Aortic regurgitation** leads to a **volume overload** on the left ventricle as blood flows back into the ventricle during diastole. - This typically results in **eccentric hypertrophy**, where both the ventricular wall thickness and chamber size increase significantly (dilated ventricle with increased mass) [1]. *Hypertrophic Obstructive Cardiomyopathy* - **Hypertrophic obstructive cardiomyopathy (HOCM)** is a **primary genetic myocardial disease** characterized by **asymmetric septal hypertrophy** rather than uniform concentric hypertrophy. - While HOCM involves significant myocardial hypertrophy, it represents a distinct pathophysiologic entity with **asymmetric distribution** (predominantly septal), not the classic concentric pattern seen with pressure overload states. - The hypertrophy in HOCM is **intrinsic (genetic)** rather than **adaptive (hemodynamic)** like in aortic stenosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 562-563. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 533-534.
Question 412: Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
- A. lacks H- antigen
- B. lacks A-antigen
- C. All of the options
- D. lacks Fy(b) antigen (Correct Answer)
Explanation: ***lacks Fy(b) antigen*** - The **Duffy Fy(a-b-)** phenotype indicates absence of both Fy<sup>a</sup> and Fy<sup>b</sup> antigens on red blood cells. - Since the phenotype is **Fy(a-b-)**, it definitively lacks the **Fy<sup>b</sup> antigen** (indicated by the "b-" notation). - This phenotype is common in people of **African descent** and confers natural **resistance to Plasmodium vivax malaria**, as these antigens serve as receptors for the parasite to enter RBCs. *lacks H- antigen* - The **H antigen** belongs to the **H/h blood group system** and is a precursor to A and B antigens in the ABO system. - The absence of H antigen (Bombay phenotype - Oh) is completely **unrelated to the Duffy blood group system**. - Duffy antigens are on the **DARC (Duffy Antigen Receptor for Chemokines)** protein, distinct from the H antigen. *lacks A-antigen* - The **A antigen** is part of the **ABO blood group system** and defines blood types A and AB. - The Duffy blood group system is **genetically and structurally independent** from the ABO system. - Having Fy(a-b-) phenotype does not affect A antigen expression. *All of the options* - This is incorrect because the Duffy Fy(a-b-) phenotype **specifically refers only to the absence of Duffy antigens** (Fy<sup>a</sup> and Fy<sup>b</sup>). - It has **no relationship** with A, B, or H antigens, which belong to different blood group systems controlled by different genes on different chromosomes.
Question 413: What is a distinguishing feature of reticulocytes?
- A. Slightly larger in size than RBCs
- B. Presence of residual RNA and ribosomes (Correct Answer)
- C. Mature in bone marrow
- D. Constitute approximately 1% of the red cells
Explanation: ***Presence of residual RNA and ribosomes*** - This is the **defining and most distinguishing feature** of reticulocytes that differentiates them from mature red blood cells. - Reticulocytes contain residual **ribosomal RNA** and other organelles that are lost when they mature into erythrocytes. - This residual RNA forms a **reticular (network-like) pattern** when stained with supravital stains like **new methylene blue** or **brilliant cresyl blue**, which is the basis for their name and identification. - The presence of RNA allows for **reticulocyte counting**, an important marker of bone marrow erythropoietic activity. *Slightly larger in size than RBCs* - While reticulocytes may be slightly larger (polychromatophilic appearance), size variation is **not specific** and overlaps significantly with mature RBCs. - Size is not a reliable distinguishing feature and is not used for identification or counting. *Mature in bone marrow* - Reticulocytes are **released from the bone marrow** as immature red cells and complete their maturation in the **peripheral circulation** over 24-48 hours. - They do not fully mature in the bone marrow; their presence in peripheral blood is normal. *Constitute approximately 1% of the red cells* - Normal reticulocyte count is **0.5-2%** (or approximately 1%) of total red blood cells in healthy adults. - This is a **population characteristic** indicating normal erythropoietic activity, not a distinguishing cellular feature.
Question 414: Osmotic fragility test is commonly used for which of the following conditions?
- A. Megaloblastic anemia
- B. Aplastic anemia
- C. Hereditary spherocytosis (Correct Answer)
- D. Iron deficiency anemia
Explanation: ***Hereditary spherocytosis*** - The **osmotic fragility test** helps in diagnosing hereditary spherocytosis, where **spherical red blood cells** are more prone to hemolysis in hypotonic solutions [1][2]. - This condition is characterized by **spherocytes** (abnormally shaped RBCs) leading to increased osmotic fragility [1][3]. *Megaloblastic anemia* - Megaloblastic anemia is primarily associated with **deficiencies in B12 or folate**, affecting the size and maturation of red blood cells, not their osmotic fragility. - The diagnosis focuses on **serum vitamin levels** and **bone marrow examination** rather than osmotic fragility. *Iron deficiency anemia* - Iron deficiency anemia features **microcytic** and **hypochromic RBCs**, and its diagnosis relies on **iron studies**, not osmotic fragility tests. - The osmotic fragility test does not reveal significant changes in red blood cells for this condition. *Aplastic anemia* - Aplastic anemia involves **pancytopenia** due to bone marrow failure and does not typically show altered osmotic fragility. - The diagnosis is confirmed through **bone marrow biopsy**, not by assessing osmotic fragility. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.
Surgery
1 questionsAmount of blood loss in Stage I of hemorrhagic shock is -
NEET-PG 2015 - Surgery NEET-PG Practice Questions and MCQs
Question 411: Amount of blood loss in Stage I of hemorrhagic shock is -
- A. <10%
- B. <30%
- C. <15% (Correct Answer)
- D. <40%
Explanation: ***<15%*** - Stage I (Class I) hemorrhagic shock is characterized by **minimal blood loss of up to 15%** of total blood volume (up to 750 mL in a 70 kg adult). - This is the **universally accepted ATLS definition** for Class I hemorrhage. - At this level, compensatory mechanisms maintain normal vital signs with minimal clinical manifestations. - Patients typically show minimal or no symptoms, with possible mild tachycardia only. *<10%* - While this amount falls within Stage I, it represents only a **portion of the Stage I range** and is not the complete definition. - Stage I actually extends up to 15%, making this option incomplete. *<30%* - This range encompasses **both Stage I (up to 15%) and Stage II (15-30%)** hemorrhagic shock. - Stage II manifests with tachycardia (>100 bpm), tachypnea, and decreased pulse pressure, but blood pressure remains normal. - This is too broad to specifically define Stage I. *<40%* - This range covers **Stage I, II, and III** hemorrhagic shock. - Stage III (30-40% loss) presents with significant hypotension, marked tachycardia (>120 bpm), altered mental status, and decreased urine output. - This is far beyond the compensated Stage I definition.