5751 to 5800 MCQs for Lab Technician and Technologist Exam Preparation
5000 Plus MCQs for Lab Technician and Technologists are designed to test the knowledge and proficiency of laboratory professionals who work in the field of clinical laboratory science. These questions cover a wide range of topics related to laboratory science, including anatomy, physiology, microbiology, chemistry, and hematology.
If You like then share this to your friends and other social media.
If You have any question and suggestions then please Contact us Here
Questions 5751 to 5800
Acylsphingosine is also known as
- a) Sphingomyelin
- b) Ceramide
- c) Cerebroside
- d) Sulphatide
Explanation:
Acylsphingosine is the chemical name for a Ceramide. It consists of a sphingosine base linked to a fatty acid by an amide bond.
Why other options are incorrect:
Why other options are incorrect:
- • Sphingomyelin: A type of sphingolipid that contains a phosphocholine or phosphoethanolamine head group.
- • Cerebroside: A sphingolipid with a single sugar residue (glucose or galactose) attached.
- • Sulphatide: A galactosylceramide that contains a sulfate group attached to the sugar.
The highest phospholipids content is found in
- a) Chylomicrons
- b) VLDL
- c) LDL
- d) HDL
Explanation:
HDL (High-Density Lipoprotein) contains the highest percentage of phospholipids (approximately 25-30%) among the major lipoprotein classes, which helps in maintaining the stability of the lipoprotein particle.
Why other options are incorrect:
Why other options are incorrect:
- • Chylomicrons: Primarily composed of triglycerides (nearly 90%), used for the transport of dietary lipids.
- • VLDL: Also high in triglycerides, which are the main component used for delivery to tissues.
- • LDL: Primarily composed of cholesterol esters; it is the major carrier of cholesterol in the blood.
The major lipid in chylomicrons is
- a) Triglycerides
- b) Phospholipids
- c) Cholesterol
- d) Free fatty acids
Explanation:
Triglycerides are the major component of chylomicrons, accounting for approximately 85-90% of their total lipid content. Their primary function is to transport dietary triglycerides from the intestines to the rest of the body.
Why other options are incorrect:
Why other options are incorrect:
- • Phospholipids: While present on the surface layer of chylomicrons, they are a minor component compared to triglycerides.
- • Cholesterol: Present in smaller amounts; cholesterol esters are found in the core but do not constitute the majority.
- • Free fatty acids: These are usually transported in the blood bound to albumin, not as the primary cargo within chylomicrons.
Number of carbon atoms in cholesterol is
- a) 17
- b) 19
- c) 27
- d) 30
Explanation:
Cholesterol is a sterol with a steroid backbone consisting of four fused rings and a side chain; it contains a total of 27 carbon atoms.
Why other options are incorrect:
Why other options are incorrect:
- • 17: This corresponds to the number of carbons in the gonane (steroid nucleus) structure.
- • 19: This is the number of carbons found in androgens like testosterone.
- • 30: This corresponds to the number of carbons in squalene, the precursor to cholesterol synthesis.
The lipoprotein richest in cholesterol is
- a) Chylomicrons
- b) VLDL
- c) LDL
- d) HDL
Explanation:
LDL (Low-Density Lipoprotein) is known as the “bad cholesterol” because it contains the highest concentration of cholesterol (specifically cholesterol esters) among all the lipoprotein classes, transporting it to peripheral tissues.
Why other options are incorrect:
Why other options are incorrect:
- • Chylomicrons: Their primary cargo is dietary triglycerides (not cholesterol).
- • VLDL: Primarily transports endogenous triglycerides synthesized in the liver.
- • HDL: Contains a high proportion of protein and phospholipids, and its main role is “reverse cholesterol transport,” where it clears cholesterol from tissues back to the liver.
The major storage form of lipids is
- a) Esterified cholesterol
- b) Glycerophospholipids
- c) Triglycerides
- d) Sphingolipids
Explanation:
Triglycerides (triacylglycerols) are the primary storage form of energy in the body. They are stored in adipose tissue and provide a highly concentrated, anhydrous source of metabolic fuel.
Why other options are incorrect:
Why other options are incorrect:
- • Esterified cholesterol: Primarily involved in cellular functions and membrane structure, not energy storage.
- • Glycerophospholipids: These are structural components that form the lipid bilayer of cell membranes.
- • Sphingolipids: These serve as essential components of cell membranes, particularly in the nervous system, rather than energy stores.
Cerebonic acid is present in
- a) Triglycerides
- b) Cerebrosides
- c) Esterified cholesterol
- d) Sphingomyelin
Explanation:
Cerebrosides (specifically galactocerebrosides) contain a C24 hydroxy fatty acid known as Cerebonic acid (or cerebronic acid), which is a characteristic component of the myelin sheath in the nervous system.
Why other options are incorrect:
Why other options are incorrect:
- • Triglycerides: Composed of glycerol and three fatty acids, typically not including specialized hydroxylated fatty acids like cerebonic acid.
- • Esterified cholesterol: Composed of cholesterol and a single long-chain fatty acid, typically not cerebonic acid.
- • Sphingomyelin: Contains sphingosine and a fatty acid (usually long-chain), but does not typically contain cerebonic acid as a defining structural component.
The nitrogenous base in lecithin is
- a) Ethanolamine
- b) Choline
- c) Serine
- d) Betaine
Explanation:
Lecithin is the common name for Phosphatidylcholine. The nitrogenous base attached to the phosphate group in this phospholipid is Choline.
Why other options are incorrect:
Why other options are incorrect:
- • Ethanolamine: Found in Phosphatidylethanolamine (Cephalin), not Lecithin.
- • Serine: Found in Phosphatidylserine.
- • Betaine: A derivative of glycine and choline, but not the base component of the lecithin molecule.
All the following are omega-6-fatty acids except
- a) Linoleic acid
- b) α-Linolenic acid
- c) γ-Linolenic acid
- d) Arachidonic acid
Explanation:
α-Linolenic acid (ALA) is an omega-3 fatty acid, not an omega-6 fatty acid. Linoleic acid, γ-linolenic acid, and arachidonic acid are omega-6 fatty acids. Therefore, the correct answer is α-Linolenic acid.
Why other options are incorrect:
Why other options are incorrect:
- • Linoleic acid: An essential omega-6 fatty acid (18:2, n-6).
- • γ-Linolenic acid: An omega-6 fatty acid (18:3, n-6).
- • Arachidonic acid: An omega-6 fatty acid (20:4, n-6), synthesized from linoleic acid.
All the following have 18 carbon atoms except
- a) Linoleic acid
- b) Linolenic acid
- c) Arachidonic acid
- d) Stearic acid
Explanation:
Linoleic acid, linolenic acid, and stearic acid each contain 18 carbon atoms. Arachidonic acid contains 20 carbon atoms and has four double bonds (20:4). Therefore, arachidonic acid is the correct answer.
Why other options are incorrect:
Why other options are incorrect:
- • Linoleic acid: Contains 18 carbon atoms and two double bonds (18:2).
- • Linolenic acid: Contains 18 carbon atoms and three double bonds (18:3).
- • Stearic acid: Contains 18 carbon atoms and is saturated (18:0).
A 20-carbon fatty acid among the following is
- a) Linoleic acid
- b) α -Linolenic acid
- c) β -Linolenic acid
- d) Arachidonic acid
Explanation:
Arachidonic acid is a polyunsaturated omega-6 fatty acid that contains 20 carbon atoms and four double bonds (C20:4).
Why other options are incorrect:
Why other options are incorrect:
- • Linoleic acid: An 18-carbon fatty acid (C18:2).
- • α-Linolenic acid: An 18-carbon fatty acid (C18:3).
- • β-Linolenic acid: Also known as γ-linolenic acid, it is an 18-carbon fatty acid (C18:3).
Triglycerides are transported from liver to extrahepatic tissues by
- a) Chylomicrons
- b) VLDL
- c) HDL
- d) LDL
Explanation:
VLDL (Very Low-Density Lipoprotein) is synthesized by the liver to transport endogenous triglycerides to extrahepatic tissues (such as adipose and muscle tissue) for storage or energy production.
Why other options are incorrect:
Why other options are incorrect:
- • Chylomicrons: Transport dietary triglycerides from the intestine (exogenous pathway), not the liver.
- • HDL: Primarily involved in “reverse cholesterol transport,” moving cholesterol from tissues back to the liver.
- • LDL: Primarily transports cholesterol to peripheral tissues after VLDL has been processed.
Cholesterol is transported from liver to extrahepatic tissues by
- a) Chylomicrons
- b) VLDL
- c) HDL
- d) LDL
Explanation:
LDL (Low-Density Lipoprotein), often called “bad cholesterol,” is the primary lipoprotein responsible for carrying cholesterol from the liver to the peripheral tissues for use in cell membranes and steroid synthesis.
Why other options are incorrect:
Why other options are incorrect:
- • Chylomicrons: Transport dietary lipids from the intestine.
- • VLDL: Primarily transports endogenous triglycerides from the liver.
- • HDL: Performs “reverse cholesterol transport,” moving excess cholesterol from tissues back to the liver (the “good” cholesterol).
Elevated plasma level of the following protects against atherosclerosis:
- a) Chylomicrons
- b) VLDL
- c) HDL
- d) LDL
Explanation:
HDL (High-Density Lipoprotein) is known as “good cholesterol” because it participates in reverse cholesterol transport, removing excess cholesterol from peripheral tissues and arterial walls and transporting it back to the liver for excretion. This process helps prevent the formation of atherosclerotic plaques.
Why other options are incorrect:
Why other options are incorrect:
- • Chylomicrons & VLDL: High levels are associated with high triglycerides, which can increase cardiovascular risk.
- • LDL: Known as “bad cholesterol,” elevated levels promote the deposition of cholesterol in arterial walls, leading to atherosclerosis.
All the following amino acids are nonessential except
- a) Alanine
- b) Histidine
- c) Cysteine
- d) Proline
Explanation:
Histidine is an essential amino acid, meaning it must be obtained from the diet because the human body cannot synthesize sufficient amounts. Alanine, cysteine, and proline are generally classified as nonessential amino acids.
Why other options are incorrect:
Why other options are incorrect:
- • Alanine: A nonessential amino acid that can be synthesized in the body.
- • Cysteine: Generally considered conditionally essential but can be synthesized from methionine.
- • Proline: A nonessential amino acid synthesized from glutamate.
Sulphydryl group is present in
- a) Cysteine
- b) Methionine
- c) Both (A) and (B)
- d) None of these
Explanation:
The Sulphydryl (-SH) group (also known as a thiol group) is a characteristic functional group of Cysteine. It is this group that allows for the formation of disulfide bonds, which are crucial for protein structure.
Why other options are incorrect:
Why other options are incorrect:
- • Methionine: While it is a sulfur-containing amino acid, it contains a thioether group (-S-CH3), not a free sulphydryl (-SH) group.
- • Both (A) and (B): Incorrect because methionine lacks the -SH group.
Oligosaccharide-pyrophosphoryl dolichol is required for the synthesis of:
- a) N-linked glycoproteins
- b) O-linked glycoproteins
- c) GPI-linked glycoproteins
- d) All of these
Explanation:
The synthesis of N-linked glycoproteins involves the assembly of an oligosaccharide precursor on a lipid carrier called dolichol phosphate, forming oligosaccharide-pyrophosphoryl dolichol, which is then transferred to the asparagine residue of the protein.
Why other options are incorrect:
Why other options are incorrect:
- • O-linked glycoproteins: These are synthesized by the sequential addition of sugars directly to the hydroxyl groups of serine or threonine residues in the Golgi apparatus, not via a dolichol-pyrophosphate carrier.
- • GPI-linked glycoproteins: While they also utilize a phosphatidylinositol lipid anchor, they follow a different biosynthetic pathway than the dolichol-linked N-glycosylation.
- • All of these: Incorrect, because the dolichol-pyrophosphate intermediate is specific to the N-linked glycosylation pathway.
In N-linked glycoproteins, oligosaccharide is attached to protein through its:
- a) Asparagine residue
- b) Glutamine residue
- c) Arginine residue
- d) Lysine residue
Explanation:
In N-linked glycosylation, the oligosaccharide chain is attached to the amide nitrogen of an Asparagine (Asn) residue within a specific consensus sequence (usually Asn-X-Ser/Thr, where X is any amino acid except proline).
Why other options are incorrect:
Why other options are incorrect:
- • Glutamine: Although it contains an amide group, it is not the target for N-linked glycosylation.
- • Arginine: A basic amino acid involved in protein structure and ionic interactions, but not a site for N-linked oligosaccharide attachment.
- • Lysine: While lysine can undergo various post-translational modifications (like ubiquitination or acetylation), it does not participate in N-linked glycosylation.
De novo synthesis of fatty acids occurs in:
- a) Cytosol
- b) Mitochondria
- c) Microsomes
- d) All of these
Explanation:
The primary pathway for the de novo synthesis of fatty acids (specifically palmitate) from Acetyl-CoA occurs in the cytosol of the cell, catalyzed by the fatty acid synthase multienzyme complex.
Why other options are incorrect:
Why other options are incorrect:
- • Mitochondria: While the mitochondria contain enzymes for fatty acid oxidation (beta-oxidation) and elongation of existing fatty acids, they are not the primary site for de novo synthesis.
- • Microsomes: These are involved in the elongation and desaturation of fatty acids, but not the initial de novo synthesis process.
- • All of these: Incorrect, because the central pathway for synthesizing new fatty acids from basic building blocks is localized strictly to the cytosol.
Acyl Carrier Protein (ACP) contains the vitamin:
- a) Biotin
- b) Lipoic acid
- c) Pantothenic acid
- d) Folic acid
Explanation:
The prosthetic group of the Acyl Carrier Protein (ACP) is 4′-phosphopantetheine, which is derived from pantothenic acid (Vitamin B5). This group acts as a flexible arm to carry the growing fatty acid chain during synthesis.
Why other options are incorrect:
Why other options are incorrect:
- • Biotin: Used as a cofactor for carboxylase enzymes (e.g., Acetyl-CoA carboxylase), not as part of the ACP.
- • Lipoic acid: Functions as a coenzyme in the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes.
- • Folic acid: Primarily functions as a donor/acceptor of one-carbon units in various metabolic pathways, not involved in ACP structure.
Which of the following is required as a reductant in fatty acid synthesis?
- a) NADH
- b) NADPH
- c) FADH2
- d) FMNH2
Explanation:
NADPH (Nicotinamide adenine dinucleotide phosphate) is the essential reducing agent required for the biosynthetic reactions of fatty acid synthesis. It provides the electrons necessary to reduce the keto groups to hydroxyl groups and subsequently to methylene groups during the elongation of the fatty acid chain.
Why other options are incorrect:
Why other options are incorrect:
- • NADH: Primarily involved in catabolic reactions (like glycolysis and the citric acid cycle) and serves as an electron donor for the electron transport chain to generate ATP.
- • FADH2: Primarily acts as an electron carrier in catabolic processes, such as the oxidation of succinate or beta-oxidation of fatty acids.
- • FMNH2: Like FADH2, it is a flavin-based coenzyme generally involved in oxidation-reduction reactions within the electron transport chain or specific enzymatic oxidations, not fatty acid biosynthesis.
Hepatic lipogenesis is stimulated by:
- a) cAMP
- b) Glucagon
- c) Epinephrine
- d) Insulin
Explanation:
Insulin is the primary hormonal stimulator of lipogenesis. It promotes the process by increasing the activity of Acetyl-CoA carboxylase (the rate-limiting enzyme) through dephosphorylation and by increasing the expression of enzymes involved in fatty acid synthesis.
Why other options are incorrect:
Why other options are incorrect:
- • cAMP: Acts as a second messenger that generally triggers protein kinase A (PKA), which phosphorylates and inactivates key enzymes of lipogenesis.
- • Glucagon: Opposes insulin; it raises intracellular cAMP levels and triggers the phosphorylation and inhibition of Acetyl-CoA carboxylase, thereby shutting down lipogenesis.
- • Epinephrine: Like glucagon, it stimulates the breakdown of fats (lipolysis) and inhibits synthesis during times of stress or energy demand.
De novo synthesis of fatty acids requires all of the following except
- a) Biotin
- b) NADH
- c) Pantothenic acid
- d) ATP
Explanation:
De novo fatty acid synthesis requires biotin, pantothenic acid, ATP, and NADPH. NADH is not the reducing cofactor used by fatty acid synthase. Therefore, the correct answer is NADH.
Why other options are incorrect:
Why other options are incorrect:
- • Biotin: Required as a cofactor for acetyl-CoA carboxylase.
- • Pantothenic acid: A component of CoA and the acyl carrier protein (ACP).
- • ATP: Required for the carboxylation of acetyl-CoA to malonyl-CoA.
Acetyl CoA carboxylase regulates fatty acid synthesis by which of the following mechanisms?
- a) Allosteric regulation
- b) Covalent modification
- c) Induction and repression
- d) All of these
Explanation:
Acetyl-CoA carboxylase (ACC) is the major regulatory enzyme of fatty acid synthesis. Its activity is controlled by allosteric regulation, covalent modification, and long-term regulation through induction and repression of enzyme synthesis. Therefore, all of these mechanisms are involved.
Why other options are incorrect:
Why other options are incorrect:
- • Allosteric regulation: Citrate activates ACC, while long-chain fatty acyl-CoA inhibits it.
- • Covalent modification: Phosphorylation generally decreases ACC activity, whereas dephosphorylation activates it.
- • Induction and repression: Hormonal and nutritional signals regulate ACC expression over the longer term.
β-Oxidation of fatty acids requires all the following coenzymes except
- a) CoA
- b) FAD
- c) NAD
- d) NADP
Explanation:
β-Oxidation requires CoA, FAD, and NAD⁺. FAD is used in the first oxidation step, while NAD⁺ is used in the second oxidation step. NADP⁺ is not required for the β-oxidation pathway. Therefore, the correct answer is NADP.
Why other options are incorrect:
Why other options are incorrect:
- • CoA: Required for formation of fatty acyl-CoA and the thiolysis step.
- • FAD: Required for the first oxidation reaction in each cycle.
- • NAD: NAD⁺ is required for the second oxidation reaction in each cycle.
Which of the following can be oxidized by the β-oxidation pathway?
- a) Saturated fatty acids
- b) Monounsaturated fatty acids
- c) Polyunsaturated fatty acids
- d) All of these
Explanation:
Saturated, monounsaturated, and polyunsaturated fatty acids can all undergo β-oxidation. Unsaturated fatty acids require additional enzymes to handle the double bonds before entering the standard β-oxidation sequence.
Why other options are incorrect:
Why other options are incorrect:
- • Saturated fatty acids: Undergo the standard β-oxidation pathway.
- • Monounsaturated fatty acids: Can undergo β-oxidation after the double bond is handled by an auxiliary enzyme.
- • Polyunsaturated fatty acids: Can also undergo β-oxidation with additional enzymes such as 2,4-dienoyl-CoA reductase.
Propionyl CoA is formed on oxidation of:
- a) Monounsaturated fatty acids
- b) Polyunsaturated fatty acids
- c) Fatty acids with odd number of carbon atoms
- d) None of these
Explanation:
During the β-oxidation of fatty acids with an odd number of carbon atoms, the final round of cleavage produces one molecule of Acetyl-CoA and one molecule of Propionyl-CoA (a 3-carbon unit), whereas even-chain fatty acids produce only Acetyl-CoA.
Why other options are incorrect:
Why other options are incorrect:
- • Monounsaturated/Polyunsaturated: The primary products of β-oxidation for these are Acetyl-CoA units, as the double bonds are simply dealt with by auxiliary enzymes and do not inherently produce 3-carbon units.
- • None of these: Incorrect, because the oxidation of odd-chain fatty acids is specifically known for this unique product.
An enzyme required for the synthesis of ketone bodies as well as cholesterol is:
- a) Acetyl CoA carboxylase
- b) HMG CoA synthetase
- c) HMG CoA reductase
- d) HMG CoA lyase
Explanation:
HMG CoA synthetase is the shared enzyme. It catalyzes the condensation of Acetyl-CoA and Acetoacetyl-CoA to form HMG-CoA (3-hydroxy-3-methylglutaryl-CoA), which serves as a common intermediate for both ketogenesis (in the liver mitochondria) and cholesterol synthesis (in the cytosol).
Why other options are incorrect:
Why other options are incorrect:
- • Acetyl CoA carboxylase: Primarily involved in fatty acid synthesis, not ketogenesis or cholesterol synthesis.
- • HMG CoA reductase: Specifically involved in cholesterol synthesis as the rate-limiting step; it is not involved in ketogenesis.
- • HMG CoA lyase: Required only for ketogenesis (to break down HMG-CoA into acetoacetate); it is not involved in cholesterol synthesis.
Ketone bodies are synthesized in:
- a) Adipose tissue
- b) Liver
- c) Muscles
- d) Brain
Explanation:
The liver is the primary site for the synthesis of ketone bodies (ketogenesis). This occurs mainly in the mitochondrial matrix of hepatocytes when the rate of fatty acid oxidation is high and the resulting Acetyl-CoA exceeds the capacity of the citric acid cycle.
Why other options are incorrect:
Why other options are incorrect:
- • Adipose tissue: Primarily functions to store and release fatty acids, not to synthesize ketone bodies.
- • Muscles: These tissues utilize ketone bodies as an energy source, but they lack the necessary enzymes (specifically HMG-CoA lyase) to synthesize them.
- • Brain: Like muscles, the brain uses ketone bodies as an alternative fuel source during prolonged fasting or starvation, but it does not synthesize them.
All the following statements about ketone bodies are true except:
- a) Their synthesis increases in diabetes mellitus
- b) They are synthesized in mitochondria
- c) They can deplete the alkali reserve
- d) They can be oxidized in the liver
Explanation:
Ketone bodies are synthesized in the mitochondria of the liver, especially during prolonged fasting and uncontrolled diabetes mellitus. They are acidic and, when produced in excess, can consume bicarbonate and decrease the alkali reserve. However, the liver cannot oxidize ketone bodies because it lacks the enzyme thiophorase (succinyl-CoA:acetoacetate CoA transferase). Therefore, option D is the incorrect statement.
Why other options are incorrect:
Why other options are incorrect:
- • Their synthesis increases in diabetes mellitus: True. Insulin deficiency promotes fatty acid oxidation and ketogenesis.
- • They are synthesized in mitochondria: True. Hepatic ketone bodies are formed in the mitochondrial matrix.
- • They can deplete the alkali reserve: True. Excess ketone bodies contribute to metabolic acidosis by consuming bicarbonate.
All the following statements about carnitine are true except
- a) It can be synthesised in the human body
- b) It can be synthesized from methionine and lysine
- c) It is required for transport of short chain fatty acids into mitochondria
- d) Its deficiency can occur due to haemodialysis
Explanation:
Carnitine is required for the transport of long-chain fatty acyl groups into mitochondria for β-oxidation. Short-chain fatty acids can enter mitochondria without the carnitine shuttle. Therefore, option C is the incorrect statement.
Why other options are incorrect:
Why other options are incorrect:
- • It can be synthesised in the human body: True. Carnitine can be synthesized endogenously.
- • It can be synthesized from methionine and lysine: True. Lysine and methionine provide the carbon skeleton and methyl groups required for carnitine synthesis.
- • Its deficiency can occur due to haemodialysis: True. Carnitine can be removed during hemodialysis, potentially causing deficiency.
Which of the following can be synthesized in the human body if precursors are available?
- a) Oleic acid
- b) Palmitoleic acid
- c) Arachidonic acid
- d) All of these
Explanation:
Humans can synthesize oleic acid and palmitoleic acid by introducing double bonds into saturated fatty acids. Arachidonic acid can also be synthesized from linoleic acid through elongation and desaturation when the precursor is available. Therefore, all of these can be synthesized if the required precursors are available.
Why other options are incorrect:
Why other options are incorrect:
- • Oleic acid: Can be synthesized from stearic acid by Δ9 desaturation.
- • Palmitoleic acid: Can be synthesized from palmitic acid by Δ9 desaturation.
- • Arachidonic acid: Can be synthesized from linoleic acid by further desaturation and elongation.
All the following can be oxidized by β-oxidation except:
- a) Palmitic acid
- b) Phytanic acid
- c) Linoleic acid
- d) Fatty acids having an odd number of carbon atoms
Explanation:
Phytanic acid cannot be oxidized directly by standard β-oxidation because it has a methyl group at the β-carbon position, which blocks the process. It must first undergo α-oxidation to remove the terminal carbon.
Why other options are incorrect:
Why other options are incorrect:
- • Palmitic acid: A standard saturated fatty acid that undergoes normal β-oxidation.
- • Linoleic acid: An unsaturated fatty acid that can be oxidized via β-oxidation (with the help of isomerases/reductases).
- • Fatty acids with odd carbon atoms: These undergo β-oxidation normally, yielding acetyl-CoA units until a final 3-carbon propionyl-CoA remains.
Anti-inflammatory corticosteroids inhibit the synthesis of
- a) Leukotrienes
- b) Prostaglandins
- c) Thromboxanes
- d) All of these
Explanation:
Anti-inflammatory corticosteroids inhibit phospholipase A₂ activity by inducing lipocortin (annexin A1). This prevents the release of arachidonic acid from membrane phospholipids, thereby decreasing the synthesis of leukotrienes, prostaglandins, and thromboxanes.
Why other options are incorrect:
Why other options are incorrect:
- • Leukotrienes: Their synthesis decreases because less arachidonic acid is available as substrate.
- • Prostaglandins: Their synthesis decreases due to reduced arachidonic acid release and subsequent COX pathway activity.
- • Thromboxanes: Their synthesis also decreases because they are derived from arachidonic acid through the cyclooxygenase pathway.
Diets having a high ratio of polyunsaturated: saturated fatty acids can cause:
- a) Increase in serum triglycerides
- b) Decrease in serum cholesterol
- c) Decrease in serum HDL
- d) Skin lesions
Explanation:
Polyunsaturated fatty acids (PUFAs) are known to have a hypocholesterolemic effect. Diets with a high ratio of PUFAs to saturated fatty acids help in lowering serum total cholesterol and LDL cholesterol levels.
Why other options are incorrect:
Why other options are incorrect:
- • Increase in serum triglycerides: PUFAs typically do not increase triglycerides; in many cases, they help reduce them.
- • Decrease in serum HDL: While extreme intake might have minor effects, the primary clinically recognized effect of high PUFA intake is the lowering of LDL and total cholesterol, not a significant reduction in protective HDL.
- • Skin lesions: These are generally associated with a deficiency of essential fatty acids, not a high ratio of PUFAs.
Thromboxanes cause:
- a) Vasodilation
- b) Bronchoconstriction
- c) Platelet aggregation
- d) All of these
Explanation:
Thromboxane A2 (TXA2) is a potent mediator produced primarily by platelets. Its primary physiological function is to promote platelet aggregation and vasoconstriction during the process of hemostasis.
Why other options are incorrect:
Why other options are incorrect:
- • Vasodilation: Thromboxanes act as vasoconstrictors, not vasodilators (Prostacyclin/PGI2 is the primary vasodilator).
- • Bronchoconstriction: While some leukotrienes cause bronchoconstriction, Thromboxane A2 is primarily associated with cardiovascular effects rather than airway constriction.
- • Platelet aggregation: This is the key biological activity of Thromboxane A2, which helps in blood clot formation.
Prostaglandins lower cAMP in
- a) Adipose tissue
- b) Lungs
- c) Platelets
- d) Adenohypophysis
Explanation:
Prostaglandins, particularly PGE₁, can lower intracellular cAMP levels in adipose tissue by inhibiting adenylate cyclase. This reduces lipolysis and inhibits the release of free fatty acids from adipocytes.
Why other options are incorrect:
Why other options are incorrect:
- • Lungs: Prostaglandins have several effects in the lungs, but this is not the classic site associated with lowering cAMP in this context.
- • Platelets: Prostaglandins such as prostacyclin (PGI₂) increase cAMP in platelets and inhibit platelet aggregation.
- • Adenohypophysis: Prostaglandins can influence pituitary hormone secretion, but lowering cAMP is not the classic association in this question.
Slow reacting substance of anaphylaxis (SRS-A) is a mixture of:
- a) Prostaglandins
- b) Prostacyclins
- c) Thromboxanes
- d) Leukotrienes
Explanation:
The Slow Reacting Substance of Anaphylaxis (SRS-A) was historically identified as a mixture of cysteinyl leukotrienes, specifically LTC4, LTD4, and LTE4. These are potent mediators of inflammation released during allergic reactions.
Why other options are incorrect:
Why other options are incorrect:
- • Prostaglandins: These are eicosanoids produced via the cyclooxygenase pathway, not the lipoxygenase pathway responsible for SRS-A.
- • Prostacyclins: A type of prostaglandin (PGI2) involved in vasodilation and inhibiting platelet aggregation.
- • Thromboxanes: Also products of the cyclooxygenase pathway, primarily involved in vasoconstriction and platelet aggregation.
Dipalmitoyl lecithin acts as:
- a) Platelet activating factor
- b) Second messenger for hormones
- c) Lung surfactant
- d) Anti-ketogenic compound
Explanation:
Dipalmitoyl lecithin, also known as dipalmitoylphosphatidylcholine (DPPC), is the major phospholipid component of pulmonary surfactant. It serves to reduce surface tension at the air-liquid interface in the alveoli, preventing lung collapse (atelectasis) during expiration.
Why other options are incorrect:
Why other options are incorrect:
- • Platelet activating factor: This is a different class of phospholipid (an ether-linked phospholipid).
- • Second messenger: Second messengers are molecules like cAMP, cGMP, or IP3, not structural phospholipids.
- • Anti-ketogenic compound: This is not the biological role of dipalmitoyl lecithin; it is specifically a structural component of surfactant.
Reichert-Meissl number is defined using:
- a) 0.1 N KOH
- b) 0.5 KOH
- c) 0.1 N NaOH
- d) 0.5 NaOH
Explanation:
The Reichert-Meissl (R-M) number is the number of milliliters of 0.1 N KOH (or NaOH) required to neutralize the soluble volatile fatty acids distilled from 5 grams of a fat sample. 0.1 N alkali is the standard concentration used for this titration.
Why other options are incorrect:
Why other options are incorrect:
- • Concentration: Using 0.5 N or other concentrations would not correspond to the standard definition of the Reichert-Meissl value.
- • KOH vs NaOH: While 0.1 N NaOH is sometimes used in practice, 0.1 N KOH is the traditional and standard reagent specified in the analytical definition of the R-M number.
In glycerophospholipids, a polyunsaturated fatty acid is commonly attached to which of the following carbon atom of glycerol?
- a) Carbon 1
- b) Carbon 2
- c) Both (A) and (B)
- d) None of these
Explanation:
In glycerophospholipids, the polyunsaturated fatty acid (PUFA) is commonly esterified to the hydroxyl group at carbon 2 (sn-2) of glycerol. The saturated fatty acid is more commonly found at carbon 1 (sn-1).
Why other options are incorrect:
Why other options are incorrect:
- • Carbon 1: Usually carries a saturated fatty acid in glycerophospholipids.
- • Both (A) and (B): PUFA is preferentially located at the sn-2 position rather than both positions.
- • None of these: Incorrect because the PUFA is commonly attached to carbon 2.
Lysolecithin is formed from lecithin by removal of:
- a) Fatty acid from position 1
- b) Fatty acid from position 2
- c) Phosphorylcholine
- d) Choline
Explanation:
Lysolecithin (lysophosphatidylcholine) is produced by the action of the enzyme Phospholipase A2, which specifically hydrolyzes the ester bond of the fatty acid attached to the C-2 position of the glycerol backbone in lecithin (phosphatidylcholine).
Why other options are incorrect:
Why other options are incorrect:
- • Position 1: Removal of the fatty acid from position 1 is catalyzed by Phospholipase A1, which results in a different isomer.
- • Phosphorylcholine/Choline: Removing these groups would result in different molecules (like phosphatidic acid or diglycerides), not lysolecithin.
Sphingosine is synthesized from:
- a) Palmitoyl CoA and Choline
- b) Palmitoyl CoA and ethanolamine
- c) Palmitoyl CoA and serine
- d) Acetyl CoA and choline
Explanation:
The initial and rate-limiting step in sphingolipid biosynthesis is the condensation of Palmitoyl-CoA and the amino acid Serine. This reaction is catalyzed by the enzyme serine palmitoyltransferase (which requires pyridoxal phosphate as a cofactor) to produce 3-ketosphinganine, which is subsequently reduced to sphinganine and then desaturated to form sphingosine.
Why other options are incorrect:
Why other options are incorrect:
- • Choline/Ethanolamine: These are polar head groups added later in the synthesis of specific sphingolipids like sphingomyelin, but they are not the precursors for the sphingosine backbone.
- • Acetyl CoA: While involved in fatty acid synthesis, it is not the primary precursor used to build the sphingoid base.
For synthesis of sphingosine, all the following coenzymes are required except
- a) Pyridoxal phosphate
- b) NADPH
- c) FAD
- d) NAD
Explanation:
Sphingosine synthesis requires pyridoxal phosphate (PLP), NADPH, and FAD as important cofactors in the pathway. NAD is not required.
Why other options are incorrect:
Why other options are incorrect:
- • Pyridoxal phosphate: Required for the serine palmitoyltransferase reaction.
- • NADPH: Provides reducing equivalents during sphingolipid synthesis.
- • FAD: Required for the oxidation step in sphingosine synthesis.
- • NAD: Not required as a coenzyme in the synthesis of sphingosine.
Cerebrosides contain all the following except
- a) Galactose
- b) Sulphate
- c) Sphingosine
- d) Fatty acid
Explanation:
Cerebrosides are glycosphingolipids composed of sphingosine, a fatty acid, and a single sugar residue, usually galactose or glucose. They do not contain phosphate or sulphate groups.
Why other options are incorrect:
Why other options are incorrect:
- • Galactose: Commonly present in galactocerebrosides.
- • Sphingosine: Forms the sphingolipid backbone of cerebrosides.
- • Fatty acid: Attached to sphingosine to form the ceramide portion.
Niemann-Pick disease results from deficiency of:
- a) Ceramidase
- b) Sphingomyelinase
- c) Arylsulphatase A
- d) Hexosaminidase A
Explanation:
Niemann-Pick disease (specifically types A and B) is a lysosomal storage disorder caused by a deficiency of the enzyme sphingomyelinase. This deficiency leads to the abnormal accumulation of sphingomyelin within lysosomes in various organs, particularly the liver, spleen, and brain.
Why other options are incorrect:
Why other options are incorrect:
- • Ceramidase: Deficiency causes Farber disease.
- • Arylsulphatase A: Deficiency causes Metachromatic leukodystrophy.
- • Hexosaminidase A: Deficiency causes Tay-Sachs disease.
Chylomicron remnants are catabolised in:
- a) Intestine
- b) Adipose tissue
- c) Liver
- d) Liver and intestine
Explanation:
After chylomicrons have delivered their triacylglycerols to peripheral tissues (via lipoprotein lipase), they become “chylomicron remnants.” These remnants, which are rich in cholesterol esters, are recognized by specific receptors (ApoE receptors) and are taken up and catabolized primarily by the liver.
Why other options are incorrect:
Why other options are incorrect:
- • Intestine: The intestine is the site of chylomicron synthesis, not their catabolism.
- • Adipose tissue: This tissue is the site for the action of lipoprotein lipase, which removes triglycerides from chylomicrons, but it does not catabolize the remnants themselves.
- • Liver and intestine: While both are involved in lipid metabolism, the specific task of clearing remnants from the circulation is a function performed by the liver.
VLDL remnant may be converted into
- a) VLDL
- b) LDL
- c) HDL
- d) Chylomicrons
Explanation:
VLDL remnants (IDL) can be further metabolized by hepatic lipase to form LDL. LDL is therefore a major metabolic product of VLDL remnants.
Why other options are incorrect:
Why other options are incorrect:
- • VLDL: VLDL is the precursor of its remnant (IDL), not the usual product.
- • HDL: HDL has a separate pathway of synthesis and metabolism.
- • Chylomicrons: Chylomicrons transport dietary lipids and are formed in intestinal cells.
Receptors for chylomicron remnants are:
- a) Apo A specific
- b) Apo B-48 specific
- c) Apo C specific
- d) Apo E specific
Explanation:
Chylomicron remnants are cleared from the circulation by the liver through a receptor-mediated process. The hepatic remnant receptors (such as the LDL receptor and LDL receptor-related protein) specifically recognize and bind to Apo E present on the surface of the chylomicron remnants.
Why other options are incorrect:
Why other options are incorrect:
- • Apo A: Primarily associated with HDL.
- • Apo B-48: A structural protein unique to chylomicrons and their remnants, but it does not serve as the ligand for hepatic uptake.
- • Apo C: Involved in the activation or inhibition of lipoprotein lipase, not in the hepatic uptake of remnants.
Nascent HDL of intestinal origin lacks
- a) Apo A
- b) Apo C
- c) Apo E
- d) Apo C and Apo E
Explanation:
Nascent HDL synthesized by the intestine contains Apo A, particularly Apo A-I, but initially lacks Apo C and Apo E. These apolipoproteins are acquired later from circulating lipoproteins.
Why other options are incorrect:
Why other options are incorrect:
- • Apo A: Present in nascent HDL and is the major structural apolipoprotein of HDL.
- • Apo C: Nascent intestinal HDL initially lacks Apo C.
- • Apo E: Nascent intestinal HDL initially lacks Apo E.
Answer Key Summary
The questions are typically designed to assess the technical skills and knowledge required for the laboratory profession, including the ability to analyze laboratory test results, perform laboratory procedures, and maintain laboratory equipment.
To prepare for these MCQs, candidates should have a thorough understanding of the key concepts and principles of laboratory science. They should also be familiar with common laboratory equipment and procedures, as well as laboratory safety protocols.
Candidates may also benefit from studying specific laboratory science textbooks or taking online courses that cover the material tested in the MCQs. Additionally, practicing sample MCQs and reviewing the answers can help candidates identify areas where they may need to improve their knowledge or skills.
Overall, the MCQs for lab technologists are designed to be challenging and comprehensive, requiring candidates to demonstrate a high level of proficiency in the field of laboratory science.
📚 This article may have been prepared using trusted medical literature, clinical guidelines, textbooks, and peer-reviewed sources.
View Possible References Used →
Virulent factor in pneumococcus is?
Capsule
Emdotoxins
Cell wall
Mesosomes
The answer is capsule but you have given cell wall .