4651 to 4700 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.
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Questions 4651 to 4700
A carbohydrate, known commonly as invert sugar, is
- a) Fructose
- b) Sucrose
- c) Glucose
- d) Lactose
Explanation:
Sucrose is called invert sugar because its optical rotation “inverts” during hydrolysis. Sucrose is dextrorotatory (+66.5°), but once hydrolyzed, it forms a mixture of glucose and fructose that is levorotatory (-20°) due to the strong levorotatory nature of fructose.
Why other options are incorrect:
Why other options are incorrect:
- • Fructose: Known as fruit sugar or levulose; it is a component of invert sugar but not the original carbohydrate referred to by the term.
- • Glucose: Known as grape sugar or dextrose; like fructose, it is a product of the inversion process, not the source.
- • Lactose: Known as milk sugar; its hydrolysis yields glucose and galactose, and it does not undergo the specific “inversion” associated with sucrose.
A heteropolysaccharide among the following is
- a) Inulin
- b) Cellulose
- c) Heparin
- d) Dextrin
Explanation:
Heteropolysaccharides are composed of two or more different types of monosaccharide units. Heparin is a heteropolysaccharide (specifically a glycosaminoglycan) made up of repeating units of glucuronic acid (or iduronic acid) and glucosamine.
Why other options are incorrect:
Why other options are incorrect:
- • Inulin: This is a homopolysaccharide composed entirely of fructose units.
- • Cellulose: This is a homopolysaccharide composed entirely of glucose units linked by β-1,4-glycosidic bonds.
- • Dextrin: These are a group of low-molecular-weight homopolysaccharides produced by the hydrolysis of starch, consisting only of glucose units.
The predominant form of glucose in solution is
- a) Acyclic form
- b) Hydrated acyclic form
- c) Glucofuranose
- d) Glucopyranose
Explanation:
In aqueous solution, glucose exists in an equilibrium between its open-chain and cyclic forms. The Glucopyranose form (a six-membered ring) is the most stable and predominant, accounting for over 99% of glucose molecules in solution.
Why other options are incorrect:
Why other options are incorrect:
- • Acyclic form: The open-chain form is very unstable and represents less than 0.02% of the glucose in a solution.
- • Hydrated acyclic form: This is an intermediate state and exists only in negligible trace amounts.
- • Glucofuranose: This is a five-membered ring form of glucose; while it exists in solution, it is much less stable than the pyranose form and accounts for less than 1% of the total.
An L-isomer of monosaccharide formed in human body is
- a) L-fructose
- b) L-Erythrose
- c) L-Xylose
- d) L-Xylulose
Explanation:
While most monosaccharides in the human body are D-isomers, L-Xylulose is a notable exception. It is an intermediate formed during the uronic acid pathway (a pathway for glucose metabolism). In individuals with the rare condition essential pentosuria, L-xylulose accumulates due to a deficiency in the enzyme that reduces it to xylitol.
Why other options are incorrect:
Why other options are incorrect:
- • L-fructose: This is a synthetic sugar and is not naturally produced or metabolized by the human body.
- • L-Erythrose: This is not a standard metabolic intermediate in human biochemistry.
- • L-Xylose: This is not naturally synthesized in the human body; D-xylose is the common form found in dietary plant fibers.
Hyaluronic acid is found in
- a) Joints
- b) Brain
- c) Abdomen
- d) Mouth
Explanation:
Hyaluronic acid is a high-molecular-weight glycosaminoglycan (GAG) that is a major component of the synovial fluid in joints. It serves as a vital lubricant and shock absorber, ensuring smooth movement of the articular cartilage.
Why other options are incorrect:
Why other options are incorrect:
- • Brain: While the brain’s extracellular matrix contains some GAGs, hyaluronic acid’s primary functional and structural role is most significant in connective tissues and joints.
- • Abdomen: This is a general anatomical region; hyaluronic acid is not specifically localized to the abdominal cavity in the way it is in joint spaces.
- • Mouth: Although present in small amounts in the gingival tissues, the “textbook” and most critical location for its physiological function is the synovial joints.
The carbon atom which becomes asymmetric when the straight chain form of monosaccharide changes into ring form is known as
- a) Anomeric carbon atom
- b) Epimeric carbon atom
- c) Isomeric carbon atom
- d) None of these
Explanation:
When a monosaccharide cyclizes, the carbonyl carbon (C1 in aldoses like glucose, or C2 in ketoses like fructose) changes from being achiral to a new chiral/asymmetric center. This specific carbon is called the Anomeric carbon, and the resulting isomers are called alpha (α) and beta (β) anomers.
Why other options are incorrect:
Why other options are incorrect:
- • Epimeric carbon atom: Epimers are sugars that differ in configuration at only one specific chiral carbon atom (other than the anomeric one), such as Glucose and Galactose at C4.
- • Isomeric carbon atom: This is a general term for any carbon contributing to isomerism; it does not specifically describe the unique carbon created during ring formation.
- • None of these: This is incorrect because “Anomeric carbon” is the precise chemical term for this phenomenon.
The smallest monosaccharide having furanose ring structure is
- a) Erythrose
- b) Ribose
- c) Glucose
- d) Fructose
Explanation:
A furanose ring is a five-membered ring structure consisting of four carbon atoms and one oxygen atom. To form this ring, a monosaccharide must have at least four carbon atoms. Erythrose, being a tetrose (4-carbon sugar), is the smallest monosaccharide capable of forming this cyclic structure.
Why other options are incorrect:
Why other options are incorrect:
- • Ribose: This is a pentose (5 carbons). While it commonly forms a furanose ring (especially in RNA), it is larger than erythrose.
- • Glucose: This is a hexose (6 carbons). It predominantly forms a 6-membered pyranose ring and is much larger than erythrose.
- • Fructose: This is also a hexose (6 carbons). Although it often exists in furanose form, it is larger than the 4-carbon erythrose.
Which of the following is an epimeric pair?
- a) Glucose and fructose
- b) Glucose and galactose
- c) Galactose and mannose
- d) Lactose and maltose
Explanation:
Epimers are stereoisomers that differ in configuration at only one specific chiral carbon atom. Glucose and Galactose are C4-epimers because they are identical in every way except for the orientation of the hydroxyl (-OH) group at the 4th carbon atom.
Why other options are incorrect:
Why other options are incorrect:
- • Glucose and fructose: These are functional isomers (aldohexose vs. ketohexose), not epimers.
- • Galactose and mannose: These are diastereomers, but not epimers of each other. They differ at two positions (C2 and C4). However, both are individual epimers of glucose.
- • Lactose and maltose: These are disaccharides with different compositions and glycosidic linkages, not epimeric pairs of monosaccharides.
α-Glycosidic bond is present in
- a) Lactose
- b) Maltose
- c) Sucrose
- d) All of these
Explanation:
Maltose (malt sugar) is composed of two D-glucose units linked by an α(1→4) glycosidic bond. While Sucrose also contains an α-linkage (α1-β2), Maltose is the classic example used to demonstrate the α-linkage in contrast to the β-linkage found in Lactose.
Why other options are incorrect:
Why other options are incorrect:
- • Lactose: This disaccharide contains a β(1→4) glycosidic bond between galactose and glucose. Because it contains a β-linkage, “All of these” cannot be the correct answer.
- • Sucrose: While it does have an α-bond (from the glucose side), it is a unique α1-β2 linkage. In many introductory biochemistry contexts, Maltose is the primary answer for “α-glycosidic bond” questions.
- • All of these: This is incorrect because Lactose strictly contains a β-glycosidic bond.
Branching occurs in glycogen approximately after every
- a) Five glucose units
- b) Ten glucose units
- c) Fifteen glucose units
- d) Twenty glucose units
Explanation:
Glycogen is a highly branched polymer of glucose. While the main chain consists of α(1→4) glycosidic bonds, branches are formed by α(1→6) glycosidic bonds. These branches occur frequently, typically every 8 to 12 glucose units (averaging about 10), making the molecule very compact and allowing for rapid mobilization of glucose.
Why other options are incorrect:
Why other options are incorrect:
- • Five glucose units: This would be too dense for the molecular structure, leading to steric hindrance (crowding) between the chains.
- • Fifteen/Twenty glucose units: These intervals are more characteristic of amylopectin (a component of plant starch), which is much less branched than glycogen (branching every 24–30 units typically).
N–Acetylglucosamine is present in
- a) Hyaluronic acid
- b) Chondroitin sulphate
- c) Heparin
- d) All of these
Explanation:
Hyaluronic acid is a glycosaminoglycan (GAG) composed of repeating disaccharide units of D-glucuronic acid and N-acetyl-D-glucosamine. It is unique among GAGs because it is non-sulfated and not covalently attached to a protein core.
Why other options are incorrect:
Why other options are incorrect:
- • Chondroitin sulphate: This contains N-acetylgalactosamine rather than N-acetylglucosamine.
- • Heparin: This is composed of glucosamine and glucuronic/iduronic acid, but the glucosamine is primarily N-sulfated, not N-acetylated.
- • All of these: Since Chondroitin and Heparin have different amino sugar derivatives, this option is incorrect.
Iodine gives a red colour with
- a) Starch
- b) Dextrin
- c) Glycogen
- d) Inulin
Explanation:
Glycogen (often called animal starch) is a highly branched polysaccharide. When it reacts with iodine solution, it forms a complex that typically gives a reddish-brown or red color.
Why other options are incorrect:
Why other options are incorrect:
- • Starch: Gives a characteristic deep blue color with iodine due to the amylose component trapping iodine molecules in its helical structure.
- • Dextrin: This is a broad term; while Erythrodextrin gives a red color, Achrodextrin gives no color. Glycogen is the more definitive biological answer.
- • Inulin: This is a polymer of fructose and does not react with iodine to produce a color change; it remains the yellow/brown color of the iodine solution.
Amylose is a constituent of
- a) Starch
- b) Cellulose
- c) Glycogen
- d) None of these
Explanation:
The correct answer is Starch. Starch is a plant storage polysaccharide composed mainly of two glucose polymers: amylose and amylopectin. Amylose consists of glucose units linked primarily by α(1→4) glycosidic bonds.
Why other options are incorrect:
Why other options are incorrect:
- • Cellulose: Cellulose is composed of β-D-glucose units linked by β(1→4) bonds and does not contain amylose.
- • Glycogen: Glycogen is a highly branched glucose storage polymer and does not contain amylose.
- • None of these: Incorrect because amylose is a major constituent of starch.
Synovial fluid contains
- a) Heparin
- b) Hyaluronic acid
- c) Chondroitin sulphate
- d) Keratin sulphate
Explanation:
Hyaluronic acid is the major glycosaminoglycan found in synovial fluid. It is responsible for the high viscosity of the fluid, which allows it to act as a lubricant and shock absorber for the joints.
Why other options are incorrect:
Why other options are incorrect:
- • Heparin: This is an anticoagulant found in mast cells and the liver; it is not a structural component of synovial fluid.
- • Chondroitin sulphate: While found in the articular cartilage surrounding the joint, it is not the primary fluid component responsible for lubrication.
- • Keratin sulphate: Found mainly in the cornea of the eye and in bone/cartilage, but not the defining component of synovial fluid.
Gluconeogenesis is decreased by
- a) Glucagon
- b) Epinephrine
- c) Glucocorticoids
- d) Insulin
Explanation:
Insulin is the primary hormone that lowers blood glucose levels. It decreases gluconeogenesis by inhibiting key regulatory enzymes (such as PEPCK and Fructose-1,6-bisphosphatase) and by promoting the storage and utilization of glucose instead of its synthesis.
Why other options are incorrect:
Why other options are incorrect:
- • Glucagon: This hormone increases gluconeogenesis in the liver to raise blood sugar levels during fasting.
- • Epinephrine: Released during stress (fight or flight), it stimulates gluconeogenesis to ensure enough glucose is available for energy.
- • Glucocorticoids: These steroid hormones (like cortisol) stimulate the synthesis of glucose from non-carbohydrate sources to maintain blood sugar during prolonged stress.
Lactate formed in muscles can be utilised through
- a) Rapoport-Luebeling cycle
- b) Glucose-alanine cycle
- c) Cori’s cycle
- d) Citric acid cycle
Explanation:
The Cori cycle (also known as the Lactic Acid cycle) is the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted back to glucose through gluconeogenesis. This glucose then returns to the muscles to be used for energy.
Why other options are incorrect:
Why other options are incorrect:
- • Rapoport-Luebeling cycle: This occurs in mature erythrocytes (RBCs) for the synthesis of 2,3-bisphosphoglycerate (2,3-BPG), which regulates oxygen binding to hemoglobin.
- • Glucose-alanine cycle: This cycle involves the transport of nitrogen from muscles to the liver via the amino acid alanine, rather than the transport of lactate.
- • Citric acid cycle: While lactate can eventually be oxidized to CO2 and water after being converted back to pyruvate, the specific “cycle” describing the muscle-liver-muscle exchange of lactate is the Cori cycle.
Glucose-6-phosphatase is not present in
- a) Liver and kidneys
- b) Kidneys and muscles
- c) Kidneys and adipose tissue
- d) Muscles and adipose tissue
Explanation:
Glucose-6-phosphatase is the enzyme responsible for converting glucose-6-phosphate into free glucose, allowing it to be released into the blood. This enzyme is present in the liver, kidneys, and intestinal mucosa. However, it is absent in muscles and adipose tissue. Because muscles lack this enzyme, they cannot release glucose into the bloodstream from their glycogen stores; instead, the glucose-6-phosphate enters glycolysis for the muscle’s own energy use.
Why other options are incorrect:
Why other options are incorrect:
- • Liver and kidneys: These are the primary organs where this enzyme is highly active to maintain blood glucose levels.
- • Kidneys and muscles: While absent in muscles, it is present in the kidneys, making this pairing incorrect for a “not present in” question.
- • Kidneys and adipose tissue: Similarly, the enzyme is present in the kidneys, so this option does not satisfy the condition of being absent in both.
Pyruvate carboxylase is regulated by
- a) Induction
- b) Repression
- c) Allosteric regulation
- d) All of these
Explanation:
Pyruvate carboxylase, a key enzyme in gluconeogenesis, is regulated at multiple levels. It is allosterically activated by Acetyl-CoA. Additionally, its synthesis is subject to hormonal control: it undergoes induction (increased synthesis) by glucagon and glucocorticoids, and repression (decreased synthesis) by insulin.
Breakdown of Regulation:
Breakdown of Regulation:
- • Allosteric regulation: Acetyl-CoA acts as a mandatory activator; the enzyme is virtually inactive without it.
- • Induction: During fasting or stress, hormones like cortisol and glucagon increase the production of the enzyme to boost glucose synthesis.
- • Repression: High levels of insulin signal that blood glucose is already sufficient, leading to a decrease in the synthesis of this enzyme.
Fructose-2, 6-biphosphate is formed by the action of
- a) Phosphofructokinase-1
- b) Phosphofructokinase-2
- c) Fructose biphosphate isomerase
- d) Fructose-1, 6-biphosphatase
Explanation:
Fructose-2, 6-bisphosphate is a potent regulator of carbohydrate metabolism. It is synthesized from Fructose-6-phosphate by the enzyme Phosphofructokinase-2 (PFK-2). It is not an intermediate in glycolysis but acts as a powerful allosteric activator of PFK-1 and an inhibitor of Fructose-1, 6-bisphosphatase.
Why other options are incorrect:
Why other options are incorrect:
- • Phosphofructokinase-1: This enzyme catalyzes the conversion of Fructose-6-phosphate into Fructose-1, 6-bisphosphate, which is a key step in glycolysis.
- • Fructose biphosphate isomerase: Also known as Aldolase, it cleaves Fructose-1, 6-bisphosphate into DHAP and Glyceraldehyde-3-phosphate.
- • Fructose-1, 6-biphosphatase: This is a gluconeogenic enzyme that converts Fructose-1, 6-bisphosphate back into Fructose-6-phosphate.
The highest concentrations of fructose are found in
- a) Aqueous humor
- b) Vitreous humor
- c) Synovial fluid
- d) Seminal fluid
Explanation:
The seminal fluid (produced by the seminal vesicles) contains the highest concentration of fructose in the human body. Fructose serves as the primary energy source for the motility of spermatozoa. This is unique because most other tissues in the body rely primarily on glucose for energy.
Why other options are incorrect:
Why other options are incorrect:
- • Aqueous/Vitreous humor: These fluids in the eye primarily contain glucose and very low levels of other sugars to maintain the metabolism of the lens and cornea.
- • Synovial fluid: As established previously, this fluid is rich in hyaluronic acid for lubrication, but its carbohydrate content is mostly glucose derived from plasma.
Glucose uptake by liver cells is
- a) Energy-consuming
- b) A saturable process
- c) Insulin-dependent
- d) Insulin-independent
Explanation:
Glucose uptake in the liver is insulin-independent. Hepatocytes (liver cells) utilize the GLUT2 transporter, which is always present on the cell membrane and does not require insulin for its translocation or activity. This allows the liver to freely uptake glucose for storage (glycogenesis) when blood sugar levels are high.
Why other options are incorrect:
Why other options are incorrect:
- • Energy-consuming: Glucose uptake via GLUT transporters is a form of facilitated diffusion, which is a passive process and does not require ATP (energy).
- • A saturable process: While all protein-mediated transport is technically saturable, GLUT2 has a very high Km (low affinity), meaning it is functionally non-saturable under normal physiological glucose concentrations.
- • Insulin-dependent: This describes glucose uptake in muscle and adipose tissue, which utilize the GLUT4 transporter. GLUT4 requires insulin to move from intracellular vesicles to the cell surface.
Renal threshold for glucose is decreased in
- a) Diabetes mellitus
- b) Insulinoma
- c) Renal glycosuria
- d) Alimentary glycosuria
Explanation:
The Renal Threshold is the blood glucose concentration (normally about 180 mg/dL) at which the kidneys can no longer reabsorb all the glucose from the filtrate, causing it to appear in urine. In Renal Glycosuria, the threshold is pathologically lowered due to a defect in the renal tubules, meaning glucose appears in the urine even when blood glucose levels are perfectly normal.
Why other options are incorrect:
Why other options are incorrect:
- • Diabetes mellitus: Here, the renal threshold is usually normal (or even elevated in chronic cases), but blood glucose levels are so high that they exceed the threshold.
- • Insulinoma: This condition causes excessive insulin production, leading to severe hypoglycemia (low blood sugar), so the threshold is never reached.
- • Alimentary glycosuria: This is a temporary condition where blood glucose rises rapidly after a very high carbohydrate meal, exceeding the normal renal threshold; the threshold itself remains unchanged.
Active uptake of glucose is inhibited by
- a) Ouabain
- b) Phlorrizin
- c) Digoxin
- d) Alloxan
Explanation:
The active uptake of glucose occurs via SGLT (Sodium-Glucose Linked Transporters), which is a secondary active transport mechanism. Phlorrizin is a competitive inhibitor that specifically blocks these transporters in the small intestine (SGLT1) and the renal tubules (SGLT2), preventing glucose absorption and reabsorption.
Why other options are incorrect:
Why other options are incorrect:
- • Ouabain & Digoxin: These are cardiac glycosides that inhibit the Na+/K+ ATPase pump. While this indirectly affects glucose transport by dissipating the sodium gradient, they are not specific inhibitors of the glucose transporter itself.
- • Alloxan: This is a toxic glucose analog used in labs to induce experimental diabetes by selectively destroying the beta cells of the pancreas; it does not inhibit the transport proteins in the gut or kidney.
Glucose-6-phosphatase is absent or deficient in
- a) Von Gierke’s disease
- b) Pompe’s disease
- c) Cori’s disease
- d) McArdle’s disease
Explanation:
Von Gierke’s disease (Glycogen Storage Disease Type I) is caused by a deficiency of the enzyme Glucose-6-phosphatase. Because this enzyme is missing, the liver cannot convert Glucose-6-phosphate into free glucose, leading to severe fasting hypoglycemia and an abnormal accumulation of glycogen in the liver and kidneys.
Why other options are incorrect:
Why other options are incorrect:
- • Pompe’s disease (Type II): Caused by a deficiency of Acid α-glucosidase (acid maltase), which breaks down glycogen in lysosomes.
- • Cori’s disease (Type III): Caused by a deficiency of the Debranching enzyme, leading to the accumulation of limit dextrin-like glycogen.
- • McArdle’s disease (Type V): Caused by a deficiency of Muscle glycogen phosphorylase, affecting the ability of muscles to use glycogen for energy during exercise.
Debranching enzyme is absent in
- a) Cori’s disease
- b) Andersen’s disease
- c) Von Gierke’s disease
- d) Her’s disease
Explanation:
The correct answer is Cori’s disease. Cori’s disease (Glycogen Storage Disease Type III) is caused by a deficiency of the glycogen debranching enzyme. This results in accumulation of abnormal, partially degraded glycogen called limit dextrin.
Why other options are incorrect:
Why other options are incorrect:
- • Andersen’s disease: Caused by deficiency of glycogen branching enzyme.
- • Von Gierke’s disease: Caused by deficiency of glucose-6-phosphatase.
- • Her’s disease: Caused by deficiency of liver glycogen phosphorylase.
McArdle’s disease is due to the deficiency of
- a) Glucose-6-phosphatase
- b) Phosphofructokinase
- c) Liver phosphorylase
- d) Muscle phosphorylase
Explanation:
McArdle’s disease (Glycogen Storage Disease Type V) is caused by a deficiency of muscle glycogen phosphorylase (also known as myophosphorylase). This enzyme is essential for glycogenolysis in the muscles; without it, muscle cells cannot break down glycogen to provide energy for contraction, leading to exercise intolerance, fatigue, and painful cramps.
Why other options are incorrect:
Why other options are incorrect:
- • Glucose-6-phosphatase: Deficiency of this enzyme causes Von Gierke’s disease (Type I), primarily affecting the liver and blood sugar regulation.
- • Phosphofructokinase: Deficiency of the muscle isoform of this enzyme causes Tarui’s disease (Type VII), which has symptoms similar to McArdle’s but involves a different step in glycolysis.
- • Liver phosphorylase: Deficiency of this enzyme causes Hers’ disease (Type VI), which primarily results in liver enlargement (hepatomegaly) and mild hypoglycemia.
Tautomerisation is
- a) Shift of hydrogen
- b) Shift of carbon
- c) Shift of both
- d) None of these
Explanation:
Tautomerisation is a chemical process where a molecule undergoes a structural change involving the shift of a hydrogen atom (proton) accompanied by the relocation of a double bond. This results in two isomers (tautomers) existing in a state of dynamic equilibrium. A classic biological example is the keto-enol tautomerism.
Why other options are incorrect:
Why other options are incorrect:
- • Shift of carbon: Changes to the carbon skeleton result in structural isomers or rearrangements, but this is not called tautomerisation, which specifically involves the migration of a mobile hydrogen atom.
- • Shift of both: While a double bond moves, the primary defining movement is that of the hydrogen; the carbon atoms themselves do not change positions within the skeletal structure.
- • None of these: This is incorrect because “Shift of hydrogen” is the fundamental definition of the tautomerization mechanism.
In essential pentosuria, urine contains
- a) D-Ribose
- b) D-Xylulose
- c) L-Xylulose
- d) D-Xylose
Explanation:
Essential pentosuria is a rare, benign genetic disorder characterized by a deficiency of the enzyme L-xylulose reductase. In the normal uronic acid pathway, this enzyme converts L-xylulose to xylitol. When deficient, L-xylulose accumulates in the blood and is excreted in large amounts in the urine.
Why other options are incorrect:
Why other options are incorrect:
- • D-Ribose: This pentose sugar is a component of RNA and nucleotides; it is not the sugar involved in the metabolic block of pentosuria.
- • D-Xylulose: This is a different isomer. The specific enzyme deficiency in pentosuria affects the L-isomer, not the D-isomer.
- • D-Xylose: While it is a pentose, it is usually used in medical tests to evaluate intestinal absorption and is not the metabolite that accumulates in this specific condition.
Action of salivary amylase on starch leads to the formation of
- a) Maltose
- b) Maltotriose
- c) Both of the above
- d) Neither of these
Explanation:
Salivary amylase (also known as ptyalin) is an $\alpha$-amylase that cleaves the $\alpha(1\to4)$ glycosidic bonds in starch. Since it acts randomly on these internal bonds, it produces a mixture of smaller saccharides, primarily maltose (a disaccharide), maltotriose (a trisaccharide), and $\alpha$-limit dextrins.
Why ‘Both’ is the correct choice:
Why ‘Both’ is the correct choice:
- • Maltose formation: Amylase breaks down the long glucose chains of starch until mostly two-unit pieces (maltose) remain.
- • Maltotriose formation: Because the enzyme cleaves bonds at random, three-unit chains (maltotriose) are also frequent intermediate products before they are further broken down.
- • Limit Dextrins: Amylase cannot break the $\alpha(1\to6)$ branch points, leaving behind small branched fragments called limit dextrins.
Congenital galactosaemia can lead to
- a) Mental retardation
- b) Premature cataract
- c) Death
- d) All of the above
Explanation:
Congenital galactosaemia is a serious metabolic disorder (most commonly a deficiency of the enzyme GALT). If left untreated, the accumulation of galactose and its metabolites leads to systemic damage.
Why all options are correct:
Why all options are correct:
- • Mental retardation: High levels of galactose-1-phosphate in the brain tissue can cause permanent developmental delays and intellectual disabilities.
- • Premature cataract: Excess galactose is diverted to the polyol pathway, forming galactitol. Galactitol is osmotically active, causing water to enter the lens of the eye, leading to clouding (cataracts).
- • Death: In acute cases, infants may suffer from liver failure, jaundice, and a high risk of life-threatening E. coli sepsis if milk (lactose) is not immediately removed from their diet.
Uridine diphosphate glucose (UDPG) is
- a) Required for metabolism of galactose
- b) Required for synthesis of glucuronic acid
- c) A substrate for glycogen synthetase
- d) All of the above
Explanation:
Uridine diphosphate glucose (UDPG) is a high-energy “activated” form of glucose that serves as a versatile intermediate in several key metabolic processes.
Why all options are correct:
Why all options are correct:
- • Metabolism of galactose: In the Leloir pathway, the enzyme GALT uses UDPG to exchange its glucose for galactose, ultimately allowing galactose to enter mainstream glucose metabolism.
- • Synthesis of glucuronic acid: UDPG is oxidized by the enzyme UDP-glucose dehydrogenase to form UDP-glucuronic acid, which is used for detoxification (conjugation) and the synthesis of glycosaminoglycans.
- • Substrate for glycogen synthetase: During glycogenesis (glycogen synthesis), UDPG acts as the direct donor of glucose units to be added to the growing glycogen chain by the enzyme glycogen synthase.
The following is actively absorbed in the intestine:
- a) Fructose
- b) Mannose
- c) Galactose
- d) None of these
Explanation:
Galactose and Glucose are absorbed from the intestinal lumen by secondary active transport. This process is mediated by the SGLT1 (Sodium-Glucose Linked Transporter 1) protein, which uses the sodium gradient (maintained by the Na+/K+ ATPase pump) to move the sugar against its concentration gradient.
Why other options are incorrect:
Why other options are incorrect:
- • Fructose: This sugar is absorbed via facilitated diffusion using the GLUT5 transporter. Unlike galactose, it does not require energy or a sodium gradient.
- • Mannose: This is absorbed very slowly by the intestinal mucosa, primarily through facilitated diffusion rather than active transport.
- • None of these: This is incorrect because Galactose is a well-known example of an actively absorbed monosaccharide.
An amphibolic pathway among the following is
- a) HMP shunt
- b) Glycolysis
- c) Citric acid cycle
- d) Gluconeogenesis
Explanation:
An amphibolic pathway is one that functions in both catabolism (breakdown of molecules for energy) and anabolism (synthesis of complex molecules). The Citric acid cycle (Krebs cycle) is the classic example because it oxidizes Acetyl-CoA to produce energy (catabolic) while also providing essential intermediates like $\alpha$-ketoglutarate and oxaloacetate for the synthesis of amino acids and glucose (anabolic).
Why other options are incorrect:
Why other options are incorrect:
- • HMP shunt: This is primarily an anabolic (synthetic) pathway, focused on producing NADPH for fatty acid synthesis and ribose-5-phosphate for nucleotide synthesis.
- • Glycolysis: This is primarily a catabolic pathway, focused on the breakdown of glucose to pyruvate to generate ATP.
- • Gluconeogenesis: This is a strictly anabolic pathway, as it involves the synthesis of glucose from non-carbohydrate precursors.
Cori’s cycle transfers
- a) Glucose from muscles to liver
- b) Lactate from muscles to liver
- c) Lactate from liver to muscles
- d) Pyruvate from liver to muscles
Explanation:
The correct answer is Lactate from muscles to liver. During strenuous exercise, muscles convert pyruvate to lactate. Lactate travels through the blood to the liver, where it is converted back into glucose by gluconeogenesis. The glucose can then return to the muscles.
Why other options are incorrect:
Why other options are incorrect:
- • Glucose from muscles to liver: The main substance transported from muscles to liver in the Cori cycle is lactate.
- • Lactate from liver to muscles: Lactate moves primarily from exercising muscles to the liver.
- • Pyruvate from liver to muscles: Pyruvate is not the primary metabolite transported in the Cori cycle.
Excessive intake of ethanol increases the ratio:
- a) NADH : NAD+
- b) NAD+ : NADH
- c) FADH2 : FAD
- d) FAD : FADH2
Explanation:
The correct answer is NADH : NAD+. Ethanol is metabolized to acetaldehyde and then to acetate. Both reactions reduce NAD+ to NADH, causing an increase in the cellular NADH/NAD+ ratio.
Why other options are incorrect:
Why other options are incorrect:
- • NAD+ : NADH: This ratio decreases because NAD+ is consumed while NADH is produced.
- • FADH2 : FAD: Ethanol metabolism primarily affects the NAD+/NADH redox couple, not this ratio.
- • FAD : FADH2: This is not the major redox change caused by ethanol metabolism.
Ethanol decreases gluconeogenesis by
- a) Inhibiting glucose-6-phosphatase
- b) Inhibiting PEP carboxykinase
- c) Converting NAD+ into NADH and decreasing the availability of pyruvate
- d) Converting NAD+ into NADH and decreasing the availability of lactate
Explanation:
The metabolism of ethanol produces a large amount of NADH, shifting the NADH/NAD+ ratio. This high concentration of NADH drives the Lactate Dehydrogenase reaction to convert pyruvate into lactate. Because pyruvate is a primary substrate for gluconeogenesis, its depletion (by being diverted to lactate) effectively shuts down the production of new glucose, often leading to alcohol-induced hypoglycemia.
Why other options are incorrect:
Why other options are incorrect:
- • Inhibiting G6Pase/PEPCK: Ethanol does not directly inhibit these enzymes; the inhibition of the pathway is due to substrate (pyruvate) unavailability rather than enzyme blockage.
- • Decreasing availability of lactate: This is the opposite of what happens. Ethanol metabolism increases the production and availability of lactate (leading to lactic acidosis), while decreasing the availability of pyruvate.
Glycogenin is
- a) Uncoupler of oxidative phosphorylation
- b) Polymer of glycogen molecules
- c) Protein primer for glycogen synthesis
- d) Intermediate in glycogen breakdown
Explanation:
Glycogenin is a specialized protein that acts as a primer for the synthesis of glycogen. The enzyme glycogen synthase can only add glucose units to an existing chain of at least 8 glucose residues. Glycogenin autochemically attaches the first few glucose molecules to its own tyrosine residue, creating the starting point required for glycogen synthase to take over.
Why other options are incorrect:
Why other options are incorrect:
- • Uncoupler of oxidative phosphorylation: This refers to substances like DNP or thermogenin that decouple the electron transport chain from ATP synthesis.
- • Polymer of glycogen molecules: Glycogen itself is a polymer of glucose; glycogenin is the protein core at the center of that polymer.
- • Intermediate in glycogen breakdown: Breakdown intermediates include things like limit dextrins and glucose-1-phosphate; glycogenin is the starting point of synthesis, not a breakdown product.
During starvation, ketone bodies are used as a fuel by:
- a) Erythrocytes
- b) Brain
- c) Liver
- d) All of these
Explanation:
During prolonged starvation, the Brain undergoes a metabolic shift. Since glucose levels are low, it adapts to use ketone bodies (acetoacetate and β-hydroxybutyrate) as an alternative energy source to spare body protein.
Why other options are incorrect:
Why other options are incorrect:
- • Erythrocytes: Red blood cells lack mitochondria, which are necessary to oxidize ketone bodies; they rely solely on glucose (glycolysis).
- • Liver: Although the liver produces ketone bodies, it cannot use them for energy because it lacks the enzyme thiophorase (β-ketoacyl-CoA transferase).
- • All of these: Incorrect, as only specific extrahepatic tissues with mitochondria (like the brain, heart, and skeletal muscle) can utilize ketone bodies.
Animal fat is in general:
- a) Poor in saturated and rich in polyunsaturated fatty acids
- b) Rich in saturated and poor in polyunsaturated fatty acids
- c) Rich in saturated and polyunsaturated fatty acids
- d) Poor in saturated and polyunsaturated fatty acids
Explanation:
Animal fats (such as butter, lard, and tallow) are typically solid at room temperature because they are rich in saturated fatty acids. They contain relatively low amounts of polyunsaturated fatty acids compared to plant-based oils.
Why other options are incorrect:
Why other options are incorrect:
- • Option a: This description typically applies to vegetable oils (like sunflower or corn oil), which are liquid at room temperature.
- • Option c: While animal fats have some unsaturated fats, they are not “rich” in polyunsaturated fats; the high saturated content is their defining characteristic.
- • Option d: Animal fats are definitely not poor in saturated fats; they are one of the primary dietary sources of them.
In the diet of a diabetic patient, the recommended carbohydrate intake should preferably be in the form of:
- a) Monosaccharides
- b) Disaccharides
- c) Polysaccharides
- d) All of these
Explanation:
Polysaccharides (complex carbohydrates like starch and fiber) are recommended for diabetic patients because they are digested and absorbed more slowly than simple sugars. This results in a gradual rise in blood glucose levels rather than a rapid spike.
Why other options are incorrect:
Why other options are incorrect:
- • Monosaccharides: (e.g., Glucose, Fructose) These are absorbed almost immediately into the bloodstream, causing dangerous spikes in blood sugar levels.
- • Disaccharides: (e.g., Sucrose, Lactose) These are broken down very quickly into simple sugars, also leading to rapid increases in blood glucose.
- • All of these: Incorrect, as the management of diabetes specifically requires limiting simple sugars (mono and disaccharides) in favor of complex ones.
Obesity increases the risk of:
- a) Hypertension
- b) Diabetes mellitus
- c) Cardiovascular disease
- d) All of these
Explanation:
Obesity is a complex metabolic condition that serves as a major risk factor for all of the mentioned diseases. It causes systemic inflammation and metabolic changes that affect multiple organ systems.
How obesity contributes to these risks:
How obesity contributes to these risks:
- • Hypertension: Excess adipose tissue increases the demand for blood flow and can lead to structural changes in the kidneys and blood vessels, raising blood pressure.
- • Diabetes mellitus: Obesity is the primary cause of insulin resistance, where body cells stop responding correctly to insulin, leading to Type 2 diabetes.
- • Cardiovascular disease: High body fat is linked to increased LDL (bad cholesterol) and triglycerides, which lead to atherosclerosis and heart attacks.
Worldwide, the most common vitamin deficiency is that of:
- a) Ascorbic acid
- b) Folic acid
- c) Vitamin A
- d) Vitamin D
Explanation:
Vitamin A deficiency is recognized as a major global public health problem, particularly in developing countries. It is the leading cause of preventable blindness in children and increases the risk of disease and death from severe infections.
Why other options are incorrect:
Why other options are incorrect:
- • Ascorbic acid (Vitamin C): Scurvy is relatively rare today as most modern diets contain at least minimal amounts of citrus or vegetables.
- • Folic acid: While common among pregnant women and certain populations, its global prevalence as a clinical deficiency is generally ranked below Vitamin A.
- • Vitamin D: While extremely common in urban and northern populations (insufficiency), Vitamin A remains the most common “clinical” vitamin deficiency addressed by global health organizations like the WHO.
Consumption of iodised salt is recommended for prevention of:
- a) Hypertension
- b) Hyperthyroidism
- c) Endemic goitre
- d) None of these
Explanation:
Iodine is a crucial micronutrient required by the thyroid gland to produce thyroid hormones. A deficiency in iodine leads to the enlargement of the thyroid gland, a condition known as Endemic goitre. Adding iodine to common table salt is the most effective way to prevent this deficiency.
Why other options are incorrect:
Why other options are incorrect:
- • Hypertension: This is high blood pressure. In fact, excessive salt (sodium) intake is often linked to an increase in hypertension, not its prevention.
- • Hyperthyroidism: This refers to an overactive thyroid gland. Iodine deficiency typically leads to hypothyroidism (underactive thyroid) rather than hyperthyroidism.
- • None of these: This is incorrect because option (c) is the scientifically established reason for salt iodization.
Restriction of salt intake is generally recommended in:
- a) Diabetes mellitus
- b) Hypertension
- c) Cirrhosis of liver
- d) Peptic ulcer
Explanation:
Sodium (found in salt) causes the body to retain extra fluid, which increases blood volume and puts extra pressure on the arteries. Therefore, restricting salt intake is a primary lifestyle recommendation for managing and preventing Hypertension (high blood pressure).
Why other options are incorrect:
Why other options are incorrect:
- • Diabetes mellitus: The primary dietary restriction in diabetes is focused on sugar and carbohydrate intake to manage blood glucose levels.
- • Cirrhosis of liver: While salt restriction is sometimes used to manage fluid buildup (ascites) in advanced cirrhosis, it is most “generally” and universally associated with hypertension in clinical practice.
- • Peptic ulcer: Treatment focuses on neutralizing stomach acid or treating H. pylori bacteria; salt intake is not the primary factor in ulcer management.
Polyuria can occur in:
- a) Diabetes mellitus
- b) Diarrhoea
- c) Acute glomerulonephritis
- d) High fever
Explanation:
Polyuria is the production of abnormally large volumes of dilute urine. In Diabetes mellitus, high blood glucose levels exceed the kidney’s reabsorption capacity. The excess glucose is excreted in the urine, pulling water with it through osmotic diuresis, leading to frequent urination.
Why other options are incorrect:
Why other options are incorrect:
- • Diarrhoea: This leads to significant fluid loss through the gastrointestinal tract, causing dehydration and usually resulting in oliguria (decreased urine output).
- • Acute glomerulonephritis: This kidney inflammation typically reduces the glomerular filtration rate, often leading to oliguria or even anuria.
- • High fever: Fever causes fluid loss through sweating and increased respiration, which generally leads the kidneys to conserve water, resulting in dark, concentrated, and low-volume urine.
Normal specific gravity of urine is:
- a) 1.000–1.010
- b) 1.012–1.024
- c) 1.025–1.034
- d) 1.035–1.045
Explanation:
Specific gravity of urine is a measure of the concentration of solutes in the urine. It reflects the kidney’s ability to concentrate or dilute urine compared to plasma. The normal range for a healthy adult with a standard fluid intake is typically between 1.012 and 1.024 (though the full clinical range can span 1.005 to 1.030).
Why other options are incorrect:
Why other options are incorrect:
- • 1.000–1.010: These values represent very dilute urine. While 1.000 is the specific gravity of pure water, values in this range are seen after excessive water intake or in conditions like Diabetes Insipidus.
- • 1.025–1.034: This range represents highly concentrated urine, often seen in cases of dehydration or when there is an excess of substances like glucose or protein in the urine.
- • 1.035–1.045: These are abnormally high values. They typically indicate severe dehydration, the presence of contrast media after imaging tests, or very high levels of glucose (sucrosuria).
Specific gravity of urine is raised in all of the following except
- a) Diabetes mellitus
- b) Diabetes insipidus
- c) Dehydration
- d) Acute glomerulonephritis
Explanation:
The correct answer is Diabetes insipidus. In diabetes insipidus, there is impaired ADH action, causing excessive excretion of dilute urine and therefore a low specific gravity.
Why other options are incorrect:
Why other options are incorrect:
- • Diabetes mellitus: Glucose in the urine increases urine specific gravity.
- • Dehydration: Reduced water excretion produces concentrated urine with increased specific gravity.
- • Acute glomerulonephritis: Protein and blood cells in urine can increase its specific gravity.
Heavy proteinuria occurs in:
- a) Acute glomerulonephritis
- b) Acute pyelonephritis
- c) Nephrosclerosis
- d) Nephrotic syndrome
Explanation:
Nephrotic syndrome is clinically defined by “heavy” or massive proteinuria (typically greater than 3.5 grams per 24 hours). This occurs due to increased permeability of the glomerular filtration barrier, leading to hypoalbuminemia and edema.
Why other options are incorrect:
Why other options are incorrect:
- • Acute glomerulonephritis: While this condition involves proteinuria, it is usually mild to moderate. It is primarily characterized by hematuria (blood in urine) and hypertension (Nephritic syndrome).
- • Acute pyelonephritis: This is a bacterial infection of the kidney. The urine typically shows white blood cells (pyuria) and bacteria, but not massive amounts of protein.
- • Nephrosclerosis: This refers to the hardening of the kidney walls due to hypertension. It may cause mild to moderate proteinuria over time, but it does not reach the “heavy” levels seen in Nephrotic syndrome.
Mucopolysaccharides are:
- a) Homopolysaccharides
- b) Heteropolysaccharides
- c) Proteins
- d) Amino acids
Explanation:
Mucopolysaccharides (also known as glycosaminoglycans or GAGs) are Heteropolysaccharides because they are composed of repeating disaccharide units that contain two different types of sugars (typically an amino sugar and a uronic acid or galactose). Examples include hyaluronic acid and heparin.
Why other options are incorrect:
Why other options are incorrect:
- • Homopolysaccharides: These consist of only one type of monosaccharide unit throughout the chain (e.g., starch, glycogen, and cellulose).
- • Proteins: These are polymers of amino acids linked by peptide bonds, not carbohydrate chains.
- • Amino acids: These are the basic organic building blocks of proteins, not complex sugar molecules.
Bence-Jones protein precipitates at:
- a) 20°–40° C
- b) 40°–60° C
- c) 60°–80° C
- d) 80°–100° C
Explanation:
Bence-Jones proteins (monoclonal immunoglobulin light chains) have a unique thermal characteristic. They precipitate when heated to 40°–60° C, but unlike most proteins, they redissolve when the temperature reaches near boiling (100° C) and reappear when the urine cools back down to the 40°–60° C range.
Why other options are incorrect:
Why other options are incorrect:
- • 20°–40° C: This range is too low; the protein remains soluble at room and body temperatures.
- • 60°–80° C: While some precipitation might still be visible, the optimal and diagnostic range for initial precipitation is lower (40°–60° C).
- • 80°–100° C: Most standard proteins (like albumin) coagulate and stay precipitated at these high temperatures, whereas Bence-Jones proteins actually dissolve at this stage.
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.
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