5851 to 5900 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 5851 to 5900
NADPH required for fatty acid synthesis can come from:
- a) Hexose monophosphate shunt
- b) Oxidative decarboxylation of malate
- c) Extramitochondrial oxidation of isocitrate
- d) All of these
Explanation:
NADPH required for fatty acid synthesis is supplied by several cytosolic pathways. These include the hexose monophosphate (HMP) shunt, the malic enzyme reaction converting malate to pyruvate, and the extramitochondrial oxidation of isocitrate by NADP+-dependent isocitrate dehydrogenase. Therefore, all of these can contribute NADPH.
Why other options are incorrect:
Why other options are incorrect:
- • Hexose monophosphate shunt: Correctly produces NADPH through the oxidative phase of the pathway.
- • Oxidative decarboxylation of malate: The malic enzyme converts malate to pyruvate and generates NADPH.
- • Extramitochondrial oxidation of isocitrate: Cytosolic NADP+-dependent isocitrate dehydrogenase produces NADPH.
Fatty liver may be prevented by all of the following except
- a) Choline
- b) Betaine
- c) Methionine
- d) Ethionine
Explanation:
Choline, betaine, and methionine are lipotropic agents that help prevent the accumulation of fat in the liver. Ethionine, however, is an antagonist of methionine and acts as a hepatotoxin that induces fatty liver.
Why other options are incorrect:
Why other options are incorrect:
- • Choline, Betaine, & Methionine: These are lipotropic factors that facilitate the synthesis of phosphatidylcholine, which is essential for the export of VLDL from the liver, thus preventing fat accumulation.
- • Ethionine: It is an ethyl analog of methionine. It interferes with cellular metabolism and protein synthesis, leading to the development of fatty liver rather than preventing it.
Human desaturase enzyme system cannot introduce a double bond in a fatty acid beyond:
- a) Carbon 9
- b) Carbon 6
- c) Carbon 5
- d) Carbon 3
Explanation:
The human desaturase enzyme system cannot introduce a double bond beyond carbon 9 from the carboxyl end of a fatty acid. Humans therefore cannot synthesize linoleic acid (ω-6) and α-linolenic acid (ω-3), making them essential fatty acids.
Why other options are incorrect:
Why other options are incorrect:
- • Carbon 6: Humans do possess desaturase enzymes capable of introducing double bonds at the Δ6 position.
- • Carbon 5: Humans possess Δ5-desaturase, which introduces a double bond at this position.
- • Carbon 3: A Δ3 desaturase limitation is not the key restriction in human fatty acid synthesis.
Which of the following lipid is absorbed actively from intestines?
- a) Glycerol
- b) Cholesterol
- c) Monoacylglycerol
- d) None of these
Explanation:
Lipids, including glycerol, cholesterol, and monoacylglycerols, are absorbed from the intestines via passive diffusion (often facilitated by bile salts forming micelles), not via active transport.
Why other options are incorrect:
Why other options are incorrect:
- • Glycerol: Being water-soluble, it is absorbed directly into the portal blood by simple diffusion.
- • Cholesterol & Monoacylglycerol: These are hydrophobic and are incorporated into mixed micelles with bile salts, which then diffuse across the brush border membrane of the enterocytes.
- • Active Transport: Active transport (requiring ATP) is typically used for sugars (like glucose) and amino acids, not for the absorption of dietary lipids.
C22 and C24, fatty acids required for the synthesis of sphingolipids in brain are formed by
- a) De novo synthesis
- b) Microsomal chain elongation
- c) Mitochondrial chain elongation
- d) All of these
Explanation:
The synthesis of long-chain fatty acids (like C22 and C24) required for the brain’s sphingolipids primarily occurs via the microsomal chain elongation system.
Why other options are incorrect:
Why other options are incorrect:
- • De novo synthesis: The standard cytosolic fatty acid synthase complex primarily produces Palmitate (C16).
- • Microsomal chain elongation: This is the major system responsible for elongating palmitate into the very-long-chain fatty acids (VLCFAs) found in sphingolipids (cerebrosides and sphingomyelin).
- • Mitochondrial chain elongation: While it exists, its physiological role is generally considered to be minor compared to the microsomal system in the context of producing VLCFAs for brain lipids.
Sphingomyelins are:
- a) Phospholipids
- b) Nitrolipids
- c) Alcohols
- d) None of these
Explanation:
Sphingomyelins are phospholipids containing sphingosine, a fatty acid, phosphoric acid, and a nitrogenous base such as choline. They are major components of cell membranes and myelin.
Why other options are incorrect:
Why other options are incorrect:
- • Nitrolipids: This is not the correct classification of sphingomyelin.
- • Alcohols: Sphingomyelin is a complex lipid, not simply an alcohol.
- • None of these: Incorrect because sphingomyelin is a phospholipid.
All of the following statements about hypoglycin are true except
- a) It is a plant toxin
- b) It causes hypoglycaemia
- c) It inhibits oxidation of short chain fatty acids
- d) It inhibits oxidation of long chain fatty acids
Explanation:
Hypoglycin (found in the unripe ackee fruit) is metabolized to methylene cyclopropyl acetic acid (MCPA). This metabolite inhibits Acyl-CoA dehydrogenases, specifically those involved in the oxidation of long-chain and branched-chain fatty acids.
Why ‘c’ is the incorrect statement:
Why ‘c’ is the incorrect statement:
- • Hypoglycin action: By inhibiting the beta-oxidation of fatty acids (especially long-chain), it reduces the production of ATP and NADH.
- • Impact: The lack of ATP inhibits gluconeogenesis, leading to severe hypoglycemia (the hallmark of Jamaican vomiting sickness).
- • Distinction: It specifically disrupts the metabolism of long-chain fatty acids; labeling it as an inhibitor of “short-chain” fatty acid oxidation is incorrect in this context.
Synthesis of prostaglandins is inhibited by:
- a) Glucocorticoids
- b) Aspirin
- c) Indomethacin
- d) All of these
Explanation:
Prostaglandin synthesis is inhibited by glucocorticoids, aspirin, and indomethacin. Glucocorticoids reduce the availability of arachidonic acid by inhibiting phospholipase A₂, while aspirin and indomethacin inhibit cyclooxygenase (COX) enzymes. Therefore, the correct answer is All of these.
Why other options are correct:
Why other options are correct:
- • Glucocorticoids: Inhibit phospholipase A₂ activity and reduce arachidonic acid availability.
- • Aspirin: Inhibits cyclooxygenase, thereby decreasing prostaglandin synthesis.
- • Indomethacin: Inhibits cyclooxygenase and reduces prostaglandin production.
Lipo-oxygenase is required for the synthesis of
- a) Prostaglandins
- b) Leukotrienes
- c) Thromboxanes
- d) All of these
Explanation:
The lipo-oxygenase enzyme pathway is responsible for the conversion of arachidonic acid into leukotrienes.
Why other options are incorrect:
Why other options are incorrect:
- • Prostaglandins: These are synthesized via the cyclooxygenase (COX) pathway, not lipo-oxygenase.
- • Thromboxanes: Similar to prostaglandins, these are synthesized from prostaglandin H2 via the cyclooxygenase pathway.
- • All of these: Since prostaglandins and thromboxanes are COX-dependent, this option is incorrect.
All of the following statements about multiple sclerosis are true except:
- a) There is loss of phospholipids from white matter
- b) There is loss of sphingolipids from white matter
- c) There is loss of esterified cholesterol from white matter
- d) White matter resembles gray matter in composition
Explanation:
In multiple sclerosis, demyelination causes loss of myelin lipids, particularly phospholipids and sphingolipids. The white matter consequently becomes more similar in composition to gray matter. Esterified cholesterol is not characteristically lost.
Why other options are incorrect:
Why other options are incorrect:
- • Phospholipids: These are lost from white matter due to destruction of myelin.
- • Sphingolipids: These are important components of myelin and are lost during demyelination.
- • White matter resembles gray matter: Demyelination reduces the lipid content of white matter, making its composition more similar to gray matter.
Release of free fatty acids from adipose tissue is increased by all of the following except:
- a) Glucagon
- b) Epinephrine
- c) Growth hormone
- d) Insulin
Explanation:
Insulin inhibits lipolysis in adipose tissue and promotes fat storage. Therefore, it decreases the release of free fatty acids into the blood. In contrast, glucagon, epinephrine, and growth hormone promote lipolysis and increase free fatty acid release.
Why other options are correct:
Why other options are correct:
- • Glucagon: Promotes mobilization of stored fat and increases fatty acid availability.
- • Epinephrine: Stimulates hormone-sensitive lipase and increases lipolysis.
- • Growth hormone: Has a lipolytic effect and promotes release of free fatty acids.
All the following statements about brown adipose tissue are true except:
- a) It is rich in cytochromes
- b) It oxidizes glucose and fatty acids
- c) Oxidation and phosphorylation are tightly coupled in it
- d) Dinitrophenol has no effect on it
Explanation:
Brown adipose tissue is specialized for heat production through non-shivering thermogenesis. It contains numerous mitochondria rich in cytochromes and uses both glucose and fatty acids as fuels. Oxidation is uncoupled from ATP synthesis through thermogenin (UCP1), so statement (c) is false.
Why other options are correct:
Why other options are correct:
- • Rich in cytochromes: Brown adipose tissue contains many mitochondria, giving it a high cytochrome content.
- • Oxidizes glucose and fatty acids: Both substrates can be oxidized to provide energy for thermogenesis.
- • Dinitrophenol: DNP is an uncoupling agent, but the characteristic physiological uncoupling of brown fat is mediated by UCP1 (thermogenin).
Lovastatin and mevastatin lower:
- a) Serum triglycerides
- b) Serum cholesterol
- c) Serum phospholipids
- d) All of these
Explanation:
Lovastatin and mevastatin belong to the class of drugs known as statins. They act by competitively inhibiting HMG-CoA reductase, the rate-limiting enzyme in the cholesterol biosynthesis pathway in the liver. By blocking this enzyme, they significantly reduce the endogenous production of cholesterol.
Why other options are incorrect:
Why other options are incorrect:
- • Serum triglycerides: While some statins may have a minor effect, it is not their primary mechanism or clinical purpose.
- • Serum phospholipids: These drugs do not specifically target phospholipid synthesis.
- • All of these: Since the primary and intended pharmacological effect is the reduction of cholesterol, “all of these” is incorrect.
Lovastatin is a:
- a) Competitive inhibitor of acetyl CoA carboxylase
- b) Competitive inhibitor of HMG CoA synthetase
- c) Non-competitive inhibitor of HMG CoA reductase
- d) Competitive inhibitor of HMG CoA reductase
Explanation:
Lovastatin is a member of the statin class of drugs. It functions as a competitive inhibitor of the enzyme HMG-CoA reductase, which catalyzes the conversion of HMG-CoA to mevalonate—the rate-limiting step in cholesterol biosynthesis.
Why other options are incorrect:
Why other options are incorrect:
- • Acetyl CoA carboxylase: This enzyme is involved in fatty acid synthesis, not cholesterol synthesis.
- • HMG CoA synthetase: This is a different enzyme in the cholesterol pathway, not the target of statins.
- • Non-competitive inhibitor: Statins are specifically competitive inhibitors because they structurally resemble the substrate (HMG-CoA) and compete for the enzyme’s active site.
Abetalipoproteinaemia occurs due to a block in the synthesis of:
- a) Apoprotein A
- b) Apoprotein B
- c) Apoprotein C
- d) Cholesterol
Explanation:
Abetalipoproteinemia is a rare autosomal recessive disorder caused by a mutation in the MTP (Microsomal Triglyceride Transfer Protein) gene. This protein is essential for the loading of lipids onto Apoprotein B. Consequently, the body cannot assemble or secrete chylomicrons (in the intestine) or VLDL (in the liver), leading to extremely low levels of plasma lipoproteins.
Why other options are incorrect:
Why other options are incorrect:
- • Apoprotein A: Associated with HDL; not the primary defect in this condition.
- • Apoprotein C: A cofactor for lipoprotein lipase; its absence causes hypertriglyceridemia, not abetalipoproteinemia.
- • Cholesterol: While plasma cholesterol is very low in this condition, it is a secondary effect of the inability to transport it, not a primary synthesis block.
All of the following statements about Tangier disease are true except:
- a) It is a disorder of HDL metabolism
- b) Its inheritance is autosomal recessive
- c) Apoproteins A-I and A-II are not synthesised
- d) Plasma HDL is increased
Explanation:
Tangier disease is an autosomal recessive disorder of HDL metabolism caused by defective ABCA1-mediated cholesterol efflux. It is characterized by extremely low plasma HDL levels, not increased HDL. Therefore, option (d) is the incorrect statement.
Why other options are correct:
Why other options are correct:
- • HDL metabolism: Tangier disease is primarily a disorder of cholesterol transport and HDL metabolism.
- • Autosomal recessive: The disease is inherited in an autosomal recessive pattern.
- • Apo A-I and Apo A-II: These apoproteins are markedly reduced because of impaired HDL formation and increased catabolism.
Genetic deficiency of lipoprotein lipase causes hyperlipoproteinaemia of following type:
- a) Type I
- b) Type IIa
- c) Type IIb
- d) Type V
Explanation:
Type I Hyperlipoproteinemia (also known as Familial Chylomicronemia Syndrome) is caused by a deficiency of Lipoprotein Lipase (LPL) or its obligatory cofactor, Apo C-II. This results in an inability to clear chylomicrons from the blood, leading to extremely high levels of serum triglycerides and chylomicrons.
Why other options are incorrect:
Why other options are incorrect:
- • Type IIa: Characterized by elevated LDL due to LDL receptor deficiency.
- • Type IIb: Characterized by elevated LDL and VLDL.
- • Type V: Characterized by an increase in both chylomicrons and VLDL; while related to LPL, Type I is the classic definition of primary LPL deficiency.
Chylomicrons are present in fasting blood samples in hyperlipoproteinaemia of following types:
- a) Types I and IIa
- b) Types IIa and IIb
- c) Types I and V
- d) Types IV and V
Explanation:
Normally, chylomicrons disappear from the blood within 6–8 hours after a meal. Their presence in a fasting blood sample indicates a failure in triglyceride clearance. This occurs specifically in Type I (deficiency of LPL or Apo C-II) and Type V (increased chylomicrons and VLDL) hyperlipoproteinemias.
Why other options are incorrect:
Why other options are incorrect:
- • Type IIa/IIb: These types are characterized by elevated LDL and/or VLDL; chylomicrons are typically absent in fasting states.
- • Type IV: This is characterized by elevated VLDL only, not chylomicrons.
Glutathione is a constituent of:
- a) Leukotriene A4
- b) Thromboxane A1
- c) Leukotriene C4
- d) None of these
Explanation:
Leukotriene C4 (LTC4) is formed by the conjugation of the unstable intermediate Leukotriene A4 (LTA4) with glutathione. This reaction is catalyzed by the enzyme glutathione-S-transferase. LTC4 is the parent compound of the cysteinyl leukotrienes, which are potent mediators of inflammation and bronchoconstriction.
Why other options are incorrect:
Why other options are incorrect:
- • Leukotriene A4: This is the precursor, not the product containing glutathione.
- • Thromboxane A1: Thromboxanes are derived from the cyclooxygenase pathway and do not contain glutathione.
Prostaglandins are inactivated by:
- a) 15-Hydroxyprostaglandin dehydrogenase
- b) Cyclo-oxygenase
- c) Lipo-oxygenase
- d) None of these
Explanation:
Prostaglandins have a very short biological half-life. They are rapidly inactivated primarily by the enzyme 15-hydroxyprostaglandin dehydrogenase, which oxidizes the hydroxyl group at the C-15 position into a keto group, rendering the molecule biologically inactive.
Why other options are incorrect:
Why other options are incorrect:
- • Cyclo-oxygenase (COX): This enzyme is involved in the synthesis of prostaglandins from arachidonic acid, not their inactivation.
- • Lipo-oxygenase: This enzyme is involved in the synthesis of leukotrienes, not the inactivation of prostaglandins.
Phenylbutazone and indomethacin inhibit:
- a) Phospholipase A1
- b) Phospholipase A2
- c) Cyclo-oxygenase
- d) Lipo-oxygenase
Explanation:
Phenylbutazone and indomethacin are Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). Their primary mechanism of action is the inhibition of the cyclo-oxygenase (COX) enzymes, which prevents the conversion of arachidonic acid into prostaglandins and thromboxanes, thereby reducing inflammation and pain.
Why other options are incorrect:
Why other options are incorrect:
- • Phospholipase A1 & A2: These enzymes are involved in releasing arachidonic acid from membrane phospholipids; they are typically inhibited by corticosteroids (via lipocortins), not NSAIDs.
- • Lipo-oxygenase: This enzyme leads to the production of leukotrienes; NSAIDs generally do not inhibit this pathway and can sometimes shunt arachidonic acid toward it.
For extramitochondrial fatty acid synthesis, acetyl CoA may be obtained from:
- a) Citrate
- b) Isocitrate
- c) Oxaloacetate
- d) Succinate
Explanation:
Since the mitochondrial membrane is impermeable to acetyl-CoA, it is transported to the cytosol as citrate. Once in the cytosol, the enzyme ATP-citrate lyase cleaves citrate back into acetyl-CoA and oxaloacetate, providing the necessary substrate for cytosolic (extramitochondrial) fatty acid synthesis.
Why other options are incorrect:
Why other options are incorrect:
- • Isocitrate: An intermediate of the TCA cycle, but it is not the transport vehicle for acetyl-CoA.
- • Oxaloacetate: Produced alongside acetyl-CoA in the cytosol after citrate cleavage, but it is not the source of acetyl-CoA.
- • Succinate: A later intermediate in the TCA cycle and is not involved in the shuttle mechanism for acetyl-CoA transport.
Fluidity of membranes is increased by the following constituent except:
- a) Polyunsaturated fatty acids
- b) Saturated fatty acids
- c) Integral proteins
- d) Cholesterol
Explanation:
Saturated fatty acids decrease membrane fluidity because their straight, long hydrocarbon chains allow them to pack tightly together, increasing intermolecular interactions (Van der Waals forces) and making the membrane more rigid.
Why other options are incorrect:
Why other options are incorrect:
- • Polyunsaturated fatty acids: The presence of “kinks” due to double bonds prevents tight packing, thereby increasing fluidity.
- • Cholesterol: Acts as a fluidity buffer; at physiological temperatures, it prevents the membrane from becoming too fluid by restricting phospholipid movement.
- • Integral proteins: Contribute to the fluid mosaic structure, and their movement/presence generally supports the fluid nature of the membrane.
Transition temperature of membranes may be affected by the following constituent of membranes:
- a) Peripheral proteins
- b) Integral proteins
- c) Cholesterol
- d) Oligosachharides
Explanation:
The transition temperature is the point at which a membrane shifts from a fluid (liquid) state to a rigid (gel/crystalline) state. Cholesterol plays a critical role in modulating this; by inserting itself between the phospholipid tails, it prevents them from packing too tightly at low temperatures, effectively broadening the transition range and preventing the membrane from freezing.
Why other options are incorrect:
Why other options are incorrect:
- • Peripheral/Integral proteins: While they are part of the membrane, they do not significantly alter the phase transition temperature of the lipid bilayer compared to cholesterol or the degree of fatty acid unsaturation.
- • Oligosaccharides: These are primarily involved in cell recognition and signaling and do not influence the phase transition properties of the lipid bilayer.
Acetyl CoA formed from pyruvate can be used for the synthesis of all the following except:
- a) Glucose
- b) Fatty acids
- c) Cholesterol
- d) Steroid hormones
Explanation:
Glucose cannot be synthesized from acetyl-CoA in humans. The conversion of pyruvate to acetyl-CoA by the pyruvate dehydrogenase complex is an irreversible step. Since the two carbons of acetyl-CoA are lost as CO2 during the TCA cycle, there is no net gain of carbon atoms that can be used for gluconeogenesis.
Why other options are correct :
Why other options are correct :
- • Fatty acids: Acetyl-CoA is the primary building block for de novo fatty acid synthesis.
- • Cholesterol: Acetyl-CoA is the source of all carbon atoms in the cholesterol biosynthesis pathway.
- • Steroid hormones: Since these are derived from cholesterol, they are ultimately synthesized from acetyl-CoA precursors.
Which of the following can be used as a source of energy in extrahepatic tissues?
- a) Acetoacetate
- b) Acetone
- c) Both (Acetoacetate) and (Acetone)
- d) None of these
Explanation:
Acetoacetate (along with 3-hydroxybutyrate) is a ketone body produced in the liver and transported to extrahepatic tissues (like muscle and brain). There, it is converted into Acetyl-CoA, which enters the TCA cycle to generate ATP.
Why other options are incorrect:
Why other options are incorrect:
- • Acetone: This is a non-metabolizable ketone body formed by the spontaneous decarboxylation of acetoacetate. It cannot be used for energy and is simply removed from the body as a waste product.
- • Both: Since acetone cannot be used for energy, this option is false.
Anti-inflammatory corticosteroids inhibit:
- a) Phospholipase A1
- b) Phospholipase A2
- c) Cyclo-oxygenase
- d) Lipo-oxygenase
Explanation:
Corticosteroids exert their potent anti-inflammatory effects by inducing the synthesis of a protein called lipocortin (annexin-1). This protein inhibits the enzyme phospholipase A2. By blocking this enzyme, corticosteroids prevent the liberation of arachidonic acid from membrane phospholipids, which is the precursor for both prostaglandins (via cyclo-oxygenase) and leukotrienes (via lipo-oxygenase).
Why other options are incorrect:
Why other options are incorrect:
- • Phospholipase A1: Not the primary target for anti-inflammatory steroids.
- • Cyclo-oxygenase: This is inhibited by NSAIDs (like aspirin or ibuprofen), not corticosteroids.
- • Lipo-oxygenase: Corticosteroids inhibit the pathway “upstream” by preventing the availability of arachidonic acid, whereas direct inhibitors of lipo-oxygenase (like zileuton) are a separate class of drugs.
Cyclo-oxygenase is involved in the synthesis of:
- a) Prostaglandins
- b) Thromboxanes
- c) Both (Prostaglandins) and (Thromboxanes)
- d) None of these
Explanation:
The cyclo-oxygenase (COX) pathway is the foundational step for synthesizing the prostanoid family. COX enzymes convert arachidonic acid into PGG2 and then PGH2. This intermediate (PGH2) is then processed by specific tissue-based synthases to produce various prostaglandins (like PGE2, PGF2α) or thromboxanes (like TXA2).
Why other options are incorrect:
Why other options are incorrect:
- • Prostaglandins only / Thromboxanes only: Selecting either one individually is incomplete, as the COX pathway is responsible for the initiation of both.
Leukotrienes cause:
- a) Increase in capillary permeability
- b) Aggregation of platelets
- c) Bronchodilatation
- d) None of these
Explanation:
Leukotrienes, especially the cysteinyl leukotrienes, are primary mediators in the inflammatory response. They significantly increase capillary permeability, leading to the leakage of fluid into tissues (edema).
Why other options are incorrect:
Why other options are incorrect:
- • Aggregation of platelets: This is primarily the role of Thromboxane A2.
- • Bronchodilatation: Leukotrienes actually cause powerful bronchoconstriction, which is why they play a critical role in the pathophysiology of asthma.
Prostaglandins decrease all of the following except:
- a) Gastric acid secretion
- b) Blood pressure
- c) Uterine contraction
- d) Platelet aggregation
Explanation:
The statement “Prostaglandins decrease uterine contraction” is **false**. Prostaglandins, particularly PGF2α and PGE2, are potent stimulators of smooth muscle in the uterus and are used to increase uterine contractions.
Why other options are correct :
Why other options are correct :
- • Gastric acid secretion: Prostaglandins (like PGE2 and PGI2) inhibit acid production in the stomach (cytoprotective effect).
- • Blood pressure: Many prostaglandins (like PGI2 and PGE2) are potent vasodilators, which help lower systemic blood pressure.
- • Platelet aggregation: Prostacyclin (PGI2) is a potent inhibitor of platelet aggregation.
Hypocholesterolaemia can occur in:
- a) Hyperthyroidism
- b) Nephrotic syndrome
- c) Obstructive jaundice
- d) Diabetes mellitus
Explanation:
Hypocholesterolaemia (low blood cholesterol) can occur in hyperthyroidism because increased thyroid hormone activity enhances cholesterol metabolism and clearance.
Why other options are incorrect:
Why other options are incorrect:
- • Nephrotic syndrome: Usually causes hyperlipidaemia, including increased cholesterol levels.
- • Obstructive jaundice: Typically causes increased serum cholesterol due to impaired bile excretion.
- • Diabetes mellitus: Commonly associated with dyslipidaemia and may cause elevated triglycerides and cholesterol.
De novo synthesis and oxidation of fatty acids differ in the following respect:
- a) Synthesis occurs in cytosol and oxidation in mitochondria
- b) Synthesis is decreased and oxidation increased by insulin
- c) NADH is required in synthesis and FAD in oxidation
- d) Malonyl CoA is formed during oxidation but not during synthesis
Explanation:
Fatty acid synthesis occurs in the cytosol using enzymes like fatty acid synthase, while fatty acid oxidation takes place in the mitochondria via the beta-oxidation pathway.
Why other options are incorrect:
Why other options are incorrect:
- • Insulin effect: Insulin increases synthesis and decreases oxidation.
- • Cofactors: Synthesis requires NADPH (not NADH), while oxidation produces NADH and FADH2.
- • Malonyl CoA: It is an intermediate in synthesis, and it acts as an inhibitor of fatty acid oxidation (by blocking CPT-1), not a product of oxidation.
Free fatty acids released from adipose tissue are transported in blood by:
- a) Albumin
- b) VLDL
- c) LDL
- d) HDL
Explanation:
Albumin is the primary transport protein for free fatty acids (also known as non-esterified fatty acids) in the bloodstream. While lipoproteins (VLDL, LDL, HDL) transport esterified lipids (triglycerides and cholesterol), free fatty acids are uniquely transported by binding to the hydrophobic pockets of albumin.
Why other options are incorrect:
Why other options are incorrect:
- • VLDL, LDL, and HDL: These are lipoproteins involved in transporting triglycerides and cholesterol within a phospholipid-protein shell, not the “free” fatty acids released during lipolysis.
The enzyme deficient in metachromatic leukodystrophy is:
- a) Arylsulphatase A
- b) Hexosaminidase A
- c) Ceramidase
- d) Sphingomyelinase
Explanation:
Metachromatic leukodystrophy is caused by a genetic deficiency of the enzyme Arylsulphatase A. This enzyme is responsible for the hydrolysis of cerebroside sulfate (sulfatides). Its deficiency leads to the accumulation of sulfatides in the nervous system, causing progressive demyelination.
Why other options are incorrect:
Why other options are incorrect:
- • Hexosaminidase A: Deficiency causes Tay-Sachs disease.
- • Ceramidase: Deficiency causes Farber disease.
- • Sphingomyelinase: Deficiency causes Niemann-Pick disease.
All of the following statements about generalized gangliosidosis are true except:
- a) It results from deficiency of GM1-β-Gangliosidase
- b) Breakdown of GM1 ganglioside is impaired
- c) GM2 ganglioside accumulates in liver and elsewhere
- d) It leads to mental retardation
Explanation:
Generalized gangliosidosis (GM1 gangliosidosis) is caused by deficiency of β-galactosidase, resulting in impaired breakdown and accumulation of GM1 ganglioside. GM1 accumulates in tissues, including the liver, spleen, and nervous system. GM2 accumulation is characteristic of GM2 gangliosidoses such as Tay-Sachs disease. Therefore, statement (c) is incorrect.
Why other options are correct:
Why other options are correct:
- • GM1-β-Gangliosidase deficiency: GM1 gangliosidosis results from deficiency of lysosomal β-galactosidase.
- • Impaired GM1 breakdown: Deficiency of the enzyme prevents normal degradation of GM1 ganglioside.
- • Mental retardation: Severe neurological involvement can cause developmental and intellectual impairment.
Hexosaminidase A is deficient in:
- a) Tay-Sachs disease
- b) Gaucher’s disease
- c) Niemann-Pick disease
- d) Fabry’s disease
Explanation:
Tay-Sachs disease is a lysosomal storage disorder caused by a deficiency of the enzyme Hexosaminidase A. This enzyme is required to break down GM2 gangliosides; without it, these lipids accumulate in neuronal cells, leading to progressive neurodegeneration.
Why other options are incorrect:
Why other options are incorrect:
- • Gaucher’s disease: Caused by a deficiency of glucocerebrosidase.
- • Niemann-Pick disease: Caused by a deficiency of sphingomyelinase.
- • Fabry’s disease: Caused by a deficiency of alpha-galactosidase A.
Mental retardation occurs in:
- a) Tay-Sachs disease
- b) Gaucher’s disease
- c) Niemann-Pick disease
- d) All of these
Explanation:
Tay-Sachs, Gaucher’s, and Niemann-Pick are all lysosomal storage disorders. These metabolic conditions involve the accumulation of harmful substances in cells, which frequently leads to progressive neurological damage and intellectual disability (mental retardation).
Why these are correct:
Why these are correct:
- • Tay-Sachs disease: A genetic disorder that destroys nerve cells in the brain and spinal cord.
- • Gaucher’s disease: While severity varies, certain types (especially neuronopathic forms) involve neurological impairment.
- • Niemann-Pick disease: A group of inherited metabolic disorders that lead to the buildup of lipids in organs, including the brain.
The enzyme deficient in Fabry’s disease is:
- a) α-Galactosidase
- b) β-Galactosidase
- c) α-Glucosidase
- d) β-Glucosidase
Explanation:
Fabry’s disease is an X-linked recessive lysosomal storage disorder caused by a deficiency of the enzyme α-galactosidase A, which leads to the accumulation of globotriaosylceramide (Gb3) in the body’s cells.
Why other options are incorrect:
Why other options are incorrect:
- • β-Galactosidase: Deficiency leads to GM1 gangliosidosis or Krabbe disease.
- • α-Glucosidase: Deficiency leads to Pompe disease (Glycogen storage disease type II).
- • β-Glucosidase: Deficiency leads to Gaucher’s disease.
Highest protein content amongst the following is present in:
- a) Wheat
- b) Rice
- c) Pulses
- d) Soyabean
Explanation:
Among the listed options, Soyabean has the highest protein content, typically containing about 36-40% protein by dry weight, which is significantly higher than cereals like wheat and rice, and even most other pulses.
Why other options are incorrect:
Why other options are incorrect:
- • Wheat & Rice: These are primarily carbohydrate-rich cereals with a much lower protein content (typically 7-12%).
- • Pulses: While they are a good source of plant-based protein (usually 20-25%), they still contain less protein per gram compared to soyabeans.
Daily protein requirement of an adult man is:
- a) 0.5 gm/kg of body weight
- b) 0.8 gm/kg of body weight
- c) 1.0 gm/kg of body weight
- d) 1.5 gm/kg of body weight
Explanation:
According to the World Health Organization (WHO) and the Recommended Dietary Allowance (RDA) guidelines, the safe level of protein intake for a healthy sedentary adult is 0.8 grams per kilogram of body weight per day.
Why other options are incorrect:
Why other options are incorrect:
- • 0.5 gm/kg: This is generally considered insufficient to maintain nitrogen balance in most healthy adults.
- • 1.0 – 1.5 gm/kg: While these levels may be recommended for athletes, growing children, or individuals recovering from surgery/trauma, they exceed the standard daily requirement for a healthy, sedentary adult male.
Daily protein requirement of an adult woman is:
- a) 0.5 gm/kg of body weight
- b) 0.8 gm/kg of body weight
- c) 1.0 gm/kg of body weight
- d) 1.5 gm/kg of body weight
Explanation:
The recommended daily protein requirement for a healthy adult woman is approximately 0.8 g/kg of body weight per day. Therefore, the correct answer is 0.8 gm/kg.
Why other options are incorrect:
Why other options are incorrect:
- • 0.5 gm/kg: Below the usual recommended daily requirement for healthy adults.
- • 1.0 gm/kg: Slightly above the standard adult recommendation.
- • 1.5 gm/kg: Higher than the standard requirement and generally used for specific increased needs.
Cysteine can partially meet the requirement of:
- a) Phenylalanine
- b) Threonine
- c) Methionine
- d) None of these
Explanation:
Cysteine can partially meet the requirement for methionine because cysteine can be synthesized from methionine through the transsulfuration pathway. Therefore, dietary cysteine can spare part of the body’s methionine requirement.
Why other options are incorrect:
Why other options are incorrect:
- • Phenylalanine: Its requirement can be partially met by tyrosine, not cysteine.
- • Threonine: Threonine is an essential amino acid and cannot be replaced by cysteine.
- • None of these: Incorrect because cysteine can partially spare the requirement for methionine.
Invisible fat is present in:
- a) Milk
- b) Coconut oil
- c) Groundnut oil
- d) Hydrogenated oils
Explanation:
“Invisible fats” refer to fats that are naturally integrated into the structure of food (such as in milk, meat, cereals, and nuts), rather than being added as free or visible fats like cooking oils, butter, or ghee.
Why other options are incorrect:
Why other options are incorrect:
- • Coconut oil, Groundnut oil, & Hydrogenated oils: These are classified as “visible fats.” They are extracted or processed specifically to be used as a concentrated source of fat for cooking or frying.
Visible fat is present in:
- a) Milk
- b) Pulses
- c) Coconut oil
- d) Egg yolk
Explanation:
Visible fat refers to fats that are readily identifiable as separate fats or oils in the diet. Coconut oil is a clear example of visible fat because it is consumed directly as an oil.
Why other options are incorrect:
Why other options are incorrect:
- • Milk: Contains fat, but the fat is naturally present within the food rather than being a separately visible fat.
- • Pulses: Contain small amounts of naturally occurring, invisible fat.
- • Egg yolk: Contains fat naturally within the yolk and is considered an invisible fat source.
Fat content of eggs is about:
- a) 7%
- b) 10%
- c) 13%
- d) 16%
Explanation:
The fat content of a whole egg is approximately 10–13%. Therefore, among the given options, 13% is the best answer. Most of the fat is present in the egg yolk.
Why other options are incorrect:
Why other options are incorrect:
- • 7%: Lower than the typical fat content of a whole egg.
- • 10%: Close to the actual value, but 13% is the expected answer in this question.
- • 16%: Higher than the usual fat content of a whole egg.
Fat content of pulses is about:
- a) 5%
- b) 10%
- c) 15%
- d) 20%
Explanation:
Pulses generally contain about 1–5% fat, depending on the type. Therefore, among the given options, approximately 5% is the closest answer.
Why other options are incorrect:
Why other options are incorrect:
- • 10%: Higher than the typical fat content of most pulses.
- • 15%: Considerably higher than the usual fat content of pulses.
- • 20%: Much higher than the typical fat content of pulses.
Predominant fatty acids in meat are:
- a) Saturated
- b) Monounsaturated
- c) Polyunsaturated
- d) Mono and poly-unsaturated
Explanation:
The predominant fatty acids in meat are generally saturated fatty acids, particularly palmitic and stearic acids. Meat also contains monounsaturated fatty acids, but saturated fatty acids are traditionally emphasized as the predominant type.
Why other options are incorrect:
Why other options are incorrect:
- • Monounsaturated: Present in meat but not considered the predominant group in this question.
- • Polyunsaturated: Present in smaller amounts compared with saturated fatty acids.
- • Mono and poly-unsaturated: Both are present, but they are not the predominant category in the given choices.
Oils having more than 50% polyunsaturated fatty acids (PUFA) include all of the following except:
- a) Groundnut oil
- b) Soyabean oil
- c) Sunflower oil
- d) Safflower oil
Explanation:
Groundnut (peanut) oil contains approximately 30–35% PUFA, which is less than 50%. Therefore, it is the exception. Soyabean, sunflower, and safflower oils contain more than 50% PUFA.
Why other options are incorrect:
Why other options are incorrect:
- • Soyabean oil: Contains more than 50% polyunsaturated fatty acids.
- • Sunflower oil: Traditionally contains a high proportion of PUFA, generally above 50%.
- • Safflower oil: Traditionally contains a very high proportion of PUFA, generally above 50%.
Cholesterol is present in all of the following except:
- a) Egg
- b) Fish
- c) Milk
- d) Pulses
Explanation:
Pulses are plant-based foods and do not contain cholesterol. Cholesterol is a sterol found primarily in animal tissues and animal-derived foods.
Why other options are incorrect:
Why other options are incorrect:
- • Egg: Egg yolk contains a significant amount of cholesterol.
- • Fish: Fish contains cholesterol because it is an animal-derived food.
- • Milk: Milk contains cholesterol, particularly in its fat component.
Which of the following has the highest cholesterol content?
- a) Meat
- b) Fish
- c) Butter
- d) Milk
Explanation:
Butter has a relatively high cholesterol content compared with meat, fish, and milk among the given options. It is a concentrated dairy fat and contains approximately 200–220 mg of cholesterol per 100 g.
Why other options are incorrect:
Why other options are incorrect:
- • Meat: Contains cholesterol, but generally less than butter among these options.
- • Fish: Contains cholesterol, but its amount varies by species and is generally lower than butter.
- • Milk: Contains cholesterol, but the concentration is considerably lower than that of butter.
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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