5601 to 5650 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 5601 to 5650
Kerasin consists of
- a) Nervonic acid
- b) Lignoceric acid
- c) Cervonic acid
- d) Clupanodonic acid
Explanation:
Kerasin is a cerebroside (a type of glycosphingolipid) found in the myelin sheaths of nerves and brain tissue. It is composed of sphingosine, galactose, and the saturated fatty acid, lignoceric acid.
Why other options are incorrect:
Why other options are incorrect:
- • Nervonic acid: This is found in another cerebroside called nervon.
- • Cervonic acid: Also known as DHA, this is an omega-3 fatty acid, not a component of Kerasin.
- • Clupanodonic acid: This is a polyunsaturated fatty acid found in fish oils, unrelated to the structure of Kerasin.
Gangliosides are complex glycosphingolipids found in
- a) Liver
- b) Brain
- c) Kidney
- d) Muscle
Explanation:
Gangliosides are the most complex glycosphingolipids. They are primarily concentrated in the ganglion cells of the central nervous system, particularly in the brain, where they play vital roles in cell-cell recognition and signal transduction.
Why other options are incorrect:
Why other options are incorrect:
- • Liver: While the liver contains various lipids, it is not the primary site for the high concentration of complex gangliosides found in neural tissue.
- • Kidney: Glycosphingolipids are present, but gangliosides are not characteristically associated with kidney tissue as they are with brain tissue.
- • Muscle: Muscle tissue primarily contains other lipid types; gangliosides are not a defining feature of muscle cells.
Unsaturated fatty acid found in the cod liver oil and containing 5 double bonds is
- a) Clupanodonic acid
- b) Cervonic acid
- c) Elaidic acid
- d) Timnodonic acid
Explanation:
Clupanodonic acid (docosapentaenoic acid) is a long-chain polyunsaturated fatty acid found in fish oils (like cod liver oil) that contains 5 double bonds.
Why other options are incorrect:
Why other options are incorrect:
- • Cervonic acid: This is docosahexaenoic acid (DHA), which contains 6 double bonds.
- • Elaidic acid: This is a monounsaturated trans fatty acid (1 double bond).
- • Timnodonic acid: This is eicosapentaenoic acid (EPA), which contains 5 double bonds but is distinct from the C22 structure of Clupanodonic acid.
Phospholipid acting as surfactant is
- a) Cephalin
- b) Phosphatidyl inositol
- c) Lecithin
- d) Phosphatidyl serine
Explanation:
Lecithin (dipalmitoyl phosphatidylcholine) is the primary component of pulmonary surfactant. It acts by reducing the surface tension at the air-liquid interface in the alveoli, preventing lung collapse during expiration.
Why other options are incorrect:
Why other options are incorrect:
- • Cephalin: Primarily a structural component of biological membranes and involved in blood clotting, not a major pulmonary surfactant.
- • Phosphatidyl inositol: Primarily serves as a precursor for intracellular signaling molecules.
- • Phosphatidyl serine: Found mostly on the inner leaflet of the plasma membrane; when exposed on the outer leaflet, it acts as a signal for apoptosis (cell death).
An oil which contains cyclic fatty acids and once used in the treatment of leprosy is
- a) Elaidic oil
- b) Rapeseed oil
- c) Lanoline
- d) Chaulmoogric oil
Explanation:
Chaulmoogric oil contains unique cyclic fatty acids (such as chaulmoogric acid and hydnocarpic acid). It was historically the primary treatment for leprosy before the development of modern sulfonamide drugs.
Why other options are incorrect:
Why other options are incorrect:
- • Elaidic oil: This is a trans-fatty acid isomer, not a therapeutic oil for leprosy.
- • Rapeseed oil: Used primarily in the food industry; it does not contain therapeutic cyclic fatty acids.
- • Lanoline: A greasy substance obtained from sheep’s wool, used as a base in ointments and cosmetics, not a treatment for leprosy.
Unpleasant odours and taste in a fat (rancidity) can be delayed or prevented by the addition of
- a) Lead
- b) Copper
- c) Tocopherol
- d) Ergosterol
Explanation:
Tocopherols (Vitamin E) act as natural antioxidants. They function by terminating free radical chain reactions that cause lipid peroxidation, thereby preventing or delaying the development of rancidity in fats.
Why other options are incorrect:
Why other options are incorrect:
- • Lead & Copper: These are heavy metals that act as pro-oxidants, which actually accelerate the oxidation of fats and worsen rancidity.
- • Ergosterol: A sterol found in fungi and protozoa, which serves as a precursor to Vitamin D2 and has no antioxidant properties to prevent rancidity.
Gangliosides derived from glucosylceramide contain in addition one or more molecules of
- a) Sialic acid
- b) Glycerol
- c) Diacylglycerol
- d) Hyaluronic acid
Explanation:
Gangliosides are glycosphingolipids that consist of a ceramide backbone attached to a complex oligosaccharide chain. By definition, all gangliosides must contain one or more residues of N-acetylneuraminic acid (also known as sialic acid).
Why other options are incorrect:
Why other options are incorrect:
- • Glycerol: This is the backbone of triglycerides and phosphoglycerides, whereas sphingolipids (including gangliosides) use sphingosine.
- • Diacylglycerol: This is a lipid signaling molecule and intermediate in fat metabolism, not a component of complex glycosphingolipids.
- • Hyaluronic acid: This is a glycosaminoglycan found in the extracellular matrix, not a structural component of gangliosides.
’Drying oil’, oxidized spontaneously by atmospheric oxygen at ordinary temperature and forms a hard water proof material is
- a) Coconut oil
- b) Peanut oil
- c) Rape seed oil
- d) Linseed oil
Explanation:
Linseed oil is a classic example of a “drying oil.” It is rich in polyunsaturated fatty acids, particularly linolenic acid. When exposed to air, it undergoes polymerization through oxidation, forming a tough, solid, waterproof film, which is why it is widely used in paints and varnishes.
Why other options are incorrect:
Why other options are incorrect:
- • Coconut oil: A non-drying oil rich in saturated fatty acids; it remains liquid or solid but does not form a hard film upon exposure to air.
- • Peanut oil: A non-drying oil; it is stable and used primarily for cooking, not for coating surfaces.
- • Rape seed oil: A semi-drying oil, which does not oxidize and polymerize to the extent required to form a hard, durable waterproof material like linseed oil.
Deterioration of food (rancidity) is due to presence of
- a) Cholesterol
- b) Vitamin E
- c) Peroxidation of lipids
- d) Phenolic compounds
Explanation:
Rancidity occurs primarily due to the oxidative deterioration of fats and oils. This process, known as lipid peroxidation, involves the attack of oxygen on the double bonds of unsaturated fatty acids, resulting in the formation of aldehydes, ketones, and other breakdown products that produce foul odors and off-flavors.
Why other options are incorrect:
Why other options are incorrect:
- • Cholesterol: A structural lipid; it is not the primary cause of rancidity in food.
- • Vitamin E: This is an antioxidant that actually prevents or delays rancidity.
- • Phenolic compounds: These are also antioxidants often found in foods that protect against oxidation, rather than causing it.
The number of ml of N/10 KOH required to neutralize the fatty acids in the distillate from 5 gm of fat is called
- a) Reichert-Meissel number
- b) Polenske number
- c) Acetyl number
- d) Non volatile fatty acid number
Explanation:
The Reichert-Meissel (RM) number is a measure of the volatile, water-soluble fatty acids (primarily butyric and caproic acids) present in a fat. It is defined as the number of milliliters of 0.1 N KOH required to neutralize the soluble fatty acids distilled from 5 grams of fat.
Why other options are incorrect:
Why other options are incorrect:
- • Polenske number: Measures the volatile, water-insoluble fatty acids.
- • Acetyl number: Measures the number of hydroxyl groups in fats or oils.
- • Non-volatile fatty acid number: This is not a standard analytical constant used for fat identification.
Molecular formula of cholesterol is
- a) C27H45OH
- b) C29H47OH
- c) C29H47OH
- d) C23H41OH
Explanation:
Cholesterol is a sterol (a type of lipid) with the molecular formula C27H45OH. It consists of a tetracyclic cyclopenta[a]phenanthrene ring system, a hydroxyl group, and a hydrocarbon side chain.
Why other options are incorrect:
Why other options are incorrect:
- • C29H47OH: This is closer to the formula for stigmasterol or sitosterol, which have longer side chains than cholesterol.
- • C23H41OH: This formula does not correspond to any primary sterol found in human biology.
The cholesterol molecule is
- a) Benzene derivative
- b) Quinoline derivative
- c) Steroid
- d) Straight chain acid
Explanation:
Cholesterol is the most abundant steroid in the animal body. Its structure is based on the cyclopentanoperhydrophenanthrene (steroid nucleus) ring system, which consists of four fused hydrocarbon rings.
Why other options are incorrect:
Why other options are incorrect:
- • Benzene derivative: Cholesterol contains saturated rings, not the aromatic structure of benzene.
- • Quinoline derivative: Quinoline is a heterocyclic compound containing nitrogen, which is not present in cholesterol.
- • Straight chain acid: Cholesterol is a cyclic alcohol, not an acid, and does not have a straight-chain structure.
Salkowski test is performed to detect
- a) Glycerol
- b) Cholesterol
- c) Fatty acids
- d) Vitamin D
Explanation:
The Salkowski test is a classic qualitative test used for the detection of cholesterol. When concentrated sulfuric acid is added to a chloroform solution of cholesterol, the chloroform layer turns red or pink, and the sulfuric acid layer develops a green fluorescence.
Why other options are incorrect:
Why other options are incorrect:
- • Glycerol: Detected using the Acrolein test.
- • Fatty acids: Usually identified through their physical properties or titration (acid value) rather than colorimetric steroid tests.
- • Vitamin D: While it shares a sterol backbone, this specific test is the standard diagnostic indicator for cholesterol.
Palmitic, oleic or stearic acid ester of cholesterol used in manufacture of cosmetic creams is
- a) Elaidic oil
- b) Lanoline
- c) Spermaceti
- d) Chaulmoogric oil
Explanation:
Lanoline (wool wax) is a complex mixture of esters of high molecular weight alcohols (like cholesterol and lanosterol) with long-chain fatty acids (like palmitic, oleic, and stearic acid). Because of its excellent moisturizing properties and ability to form stable emulsions, it is widely used in the manufacture of cosmetic creams and ointments.
Why other options are incorrect:
Why other options are incorrect:
- • Elaidic oil: A trans-fatty acid, not used as a base in cosmetic creams.
- • Spermaceti: A wax obtained from sperm whales, primarily consisting of cetyl palmitate, not cholesterol esters.
- • Chaulmoogric oil: A therapeutic oil containing cyclic fatty acids, historically used for leprosy, not for cosmetics.
Dietary fats after absorption appear in the circulation as
- a) HDL
- b) VLDL
- c) LDL
- d) Chylomicron
Explanation:
After dietary fats are digested and absorbed by the intestinal epithelial cells, they are re-synthesized into triglycerides and packaged with proteins, cholesterol, and phospholipids into large lipoprotein particles called Chylomicrons. These are then released into the lymphatic system before entering the general blood circulation.
Why other options are incorrect:
Why other options are incorrect:
- • VLDL: These are synthesized in the liver to transport endogenously produced triglycerides.
- • LDL: These are formed in the circulation from the breakdown of VLDL; they primarily transport cholesterol to tissues.
- • HDL: These are synthesized in the liver and intestine, primarily involved in “reverse cholesterol transport” (removing cholesterol from tissues).
Free fatty acids are transported in the blood
- a) Combined with albumin
- b) Combined with fatty acid binding protein
- c) Combined with β -lipoprotein
- d) In unbound free salts
Explanation:
Free fatty acids (FFAs) are hydrophobic and cannot dissolve directly in the blood plasma. They are transported in the circulation bound non-covalently to serum albumin, which is the most abundant protein in the plasma.
Why other options are incorrect:
Why other options are incorrect:
- • Fatty acid binding protein (FABP): These proteins are found inside cells (cytosol) to transport fatty acids, not in the blood circulation.
- • β-lipoprotein: These primarily transport triglycerides, cholesterol, and phospholipids, not free fatty acids.
- • Unbound free salts: Fatty acids are insoluble in water and cannot exist freely in blood as unbound salts; they would form micelles or cause damage to cell membranes.
Long chain fatty acids are first activated to acetyl-CoA in
- a) Cytosol
- b) Microsomes
- c) Nucleus
- d) Mitochondria
Explanation:
Before undergoing β-oxidation in the mitochondria, long-chain fatty acids must be activated. This activation process involves their conversion into fatty acyl-CoA by the enzyme acyl-CoA synthetase (thiokinase), which takes place in the cytosol of the cell.
Why other options are incorrect:
Why other options are incorrect:
- • Mitochondria: While β-oxidation occurs inside the mitochondria, the initial activation to acyl-CoA occurs in the cytosol before the fatty acid is transported across the mitochondrial membrane.
- • Microsomes & Nucleus: These are not the primary sites for the activation and subsequent catabolism of long-chain fatty acids via β-oxidation.
The enzyme acyl-CoA synthase catalyses the conversion of a fatty acid of an active fatty acid in the presence of
- a) AMP
- b) ADP
- c) ATP
- d) GTP
Explanation:
The activation of a fatty acid into fatty acyl-CoA is catalyzed by the enzyme Acyl-CoA synthetase (thiokinase). This reaction requires ATP, which is converted to AMP and inorganic pyrophosphate (PPi) to provide the energy necessary to drive the reaction forward.
Why other options are incorrect:
Why other options are incorrect:
- • AMP & ADP: These are products or intermediates, but the initial energy source required to initiate this activation reaction is ATP.
- • GTP: While GTP is an energy carrier in other metabolic processes (like protein synthesis or the citric acid cycle), it is not the substrate used by acyl-CoA synthetase.
Carnitine is synthesized from
- a) Lysine and methionine
- b) Glycine and arginine
- c) Aspartate and glutamate
- d) Proline and hydroxyproline
Explanation:
Carnitine is synthesized in the liver and kidneys from the amino acids lysine and methionine. The epsilon-amino group of lysine provides the carbon backbone, while S-adenosylmethionine (SAM) serves as the methyl donor for the methylation steps in the pathway.
Why other options are incorrect:
Why other options are incorrect:
- • Glycine and arginine: These are the precursors for the synthesis of creatine.
- • Aspartate and glutamate: These are primarily involved in transamination and nitrogen metabolism, not carnitine synthesis.
- • Proline and hydroxyproline: These are primary constituents of collagen, not precursors for carnitine.
The enzymes of β-oxidation are found in
- a) Mitochondria
- b) Cytosol
- c) Golgi apparatus
- d) Nucleus
Explanation:
The process of β-oxidation of fatty acids takes place within the mitochondrial matrix. Therefore, the complete set of enzymes required for this pathway (such as acyl-CoA dehydrogenase, enoyl-CoA hydratase, etc.) are located in the mitochondria.
Why other options are incorrect:
Why other options are incorrect:
- • Cytosol: This is where fatty acid activation occurs, but not the site for β-oxidation.
- • Golgi apparatus & Nucleus: These organelles are involved in protein processing and genetic regulation respectively, and do not participate in fatty acid catabolism.
Long chain fatty acids penetrate the inner mitochondrial membrane
- a) Freely
- b) As acyl-CoA derivative
- c) As carnitine derivative
- d) Requiring Na dependent carrier
Explanation:
The inner mitochondrial membrane is impermeable to fatty acyl-CoA. Therefore, long-chain fatty acids must be converted to acyl-carnitine by the enzyme Carnitine Palmitoyltransferase I (CPT-I). They are then transported across the membrane as an acyl-carnitine derivative via the carnitine-acylcarnitine translocase.
Why other options are incorrect:
Why other options are incorrect:
- • Freely: Long-chain fatty acids are polar and cannot cross the lipid bilayer by simple diffusion.
- • As acyl-CoA derivative: Acyl-CoA cannot penetrate the inner mitochondrial membrane; that is specifically why the carnitine shuttle system is required.
- • Requiring Na dependent carrier: Transport is mediated by a specific translocase, not by a sodium-dependent carrier mechanism.
An important feature of Zellweger ’s syndrome is
- a) Hypoglycemia
- b) Accumulation of phytanic acid in tissues
- c) Skin eruptions
- d) Accumulation of C26-C38 polyenoic acid in brain tissues
Explanation:
Zellweger syndrome (cerebro-hepato-renal syndrome) is a peroxisomal biogenesis disorder. Due to the absence of functional peroxisomes, the body cannot oxidize Very Long Chain Fatty Acids (VLCFA). This leads to an accumulation of these acids (such as C26-C38 polyenoic acids) in the brain and other tissues, causing severe neurological damage.
Why other options are incorrect:
Why other options are incorrect:
- • Hypoglycemia: While some metabolic disorders cause this, it is not the defining diagnostic feature of Zellweger syndrome.
- • Accumulation of phytanic acid: This is the hallmark of Refsum disease, a different type of peroxisomal disorder.
- • Skin eruptions: These are not a clinical manifestation associated with the pathophysiology of Zellweger syndrome.
An important finding of Fabry’s disease is
- a) Skin rash
- b) Exophthalmos
- c) Hemolytic anemia
- d) Mental retardation
Explanation:
Fabry’s disease is an X-linked lysosomal storage disorder. A characteristic clinical finding is “angiokeratoma,” which presents as a reddish-purple skin rash (small papules) typically found in the “bathing trunk” area.
Why other options are incorrect:
Why other options are incorrect:
- • Exophthalmos: Typically associated with Graves’ disease (thyroid disorders), not lysosomal storage diseases.
- • Hemolytic anemia: Not a primary clinical feature of Fabry’s disease.
- • Mental retardation: While neurological symptoms occur (like neuropathic pain), intellectual disability is not a characteristic feature of Fabry’s disease, unlike other sphingolipidoses such as Tay-Sachs.
Gaucher’s disease is due to deficiency of the enzyme:
- a) Sphingomyelinase
- b) Glucocerebrosidase
- c) Galactocerbrosidase
- d) β-Galactosidase
Explanation:
Gaucher’s disease is the most common lysosomal storage disorder, caused by a deficiency of the enzyme glucocerebrosidase (also known as acid β-glucosidase), which leads to the accumulation of glucocerebroside in cells.
Why other options are incorrect:
Why other options are incorrect:
- • Sphingomyelinase: Deficiency causes Niemann-Pick disease.
- • Galactocerebrosidase: Deficiency causes Krabbe disease (globoid cell leukodystrophy).
- • β-Galactosidase: Deficiency is associated with GM1 gangliosidosis.
Characteristic finding in Gaucher’s disease is
- a) Night blindness
- b) Renal failure
- c) Hepatosplenomegaly
- d) Deafness
Explanation:
Gaucher’s disease is characterized by the accumulation of glucocerebroside in the lysosomes of macrophages (Gaucher cells). These cells infiltrate organs like the liver and spleen, leading to significant hepatosplenomegaly (enlarged liver and spleen).
Why other options are incorrect:
Why other options are incorrect:
- • Night blindness: Primarily caused by Vitamin A deficiency.
- • Renal failure: While Fabry’s disease is associated with renal failure, it is not a hallmark of Gaucher’s disease.
- • Deafness: Not a standard clinical feature associated with Gaucher’s disease.
An important finding in Niemann-Pick disease is
- a) Leukopenia
- b) Cardiac enlargement
- c) Corneal opacity
- d) Hepatosplenomegaly
Explanation:
Niemann-Pick disease is a lysosomal storage disorder caused by a deficiency of sphingomyelinase. The accumulation of sphingomyelin in macrophages leads to hepatosplenomegaly, which is a classic clinical finding, often accompanied by a “cherry-red spot” on the macula.
Why other options are incorrect:
Why other options are incorrect:
- • Leukopenia: While patients may develop cytopenias due to marrow infiltration, it is not the most defining clinical finding compared to organomegaly.
- • Cardiac enlargement: This is more commonly associated with disorders like Pompe disease (glycogen storage disease type II).
- • Corneal opacity: This is a characteristic feature of Fabry’s disease (cornea verticillata), not Niemann-Pick disease.
Fucosidosis is characterized by
- a) Muscle spasticity
- b) Liver enlargement
- c) Skin rash
- d) Kidney failure
Explanation:
Fucosidosis is a rare lysosomal storage disease caused by a deficiency of the enzyme alpha-L-fucosidase. It is characterized by progressive neurological deterioration, which includes muscle spasticity (hypertonia), seizures, and delayed psychomotor development.
Why other options are incorrect:
Why other options are incorrect:
- • Liver enlargement: While hepatomegaly can occur, it is a non-specific finding found in many storage diseases (like Gaucher’s) and is not the primary diagnostic differentiator for Fucosidosis.
- • Skin rash: Skin manifestations like angiokeratoma are the hallmark of Fabry’s disease, not Fucosidosis.
- • Kidney failure: This is a major clinical feature of Fabry’s disease, not typical for Fucosidosis.
Metachromatic leukodystrophy is due to deficiency of enzyme:
- a) α-Fucosidase
- b) Arylsulphatase A
- c) Ceramidase
- d) Hexosaminidase A
Explanation:
Metachromatic leukodystrophy is a lysosomal storage disease caused by a deficiency of Arylsulphatase A. This leads to the accumulation of sulfatides (sulfatide-galactosylceramide) in the central and peripheral nervous system, causing demyelination.
Why other options are incorrect:
Why other options are incorrect:
- • α-Fucosidase: Deficiency causes Fucosidosis.
- • Ceramidase: Deficiency leads to Farber disease (Farber’s lipogranulomatosis).
- • Hexosaminidase A: Deficiency results in Tay-Sachs disease.
A significant feature of Tangier disease is
- a) Impairment of chylomicron formation
- b) Hypotriacylglycerolmia
- c) Absence of Apo-C-II
- d) Absence of Apo-C-I
Explanation:
Tangier disease is a rare genetic disorder characterized by a severe deficiency or absence of HDL (High-Density Lipoprotein) in the blood. This condition is typically associated with hypotriacylglycerolmia (low levels of triglycerides in the blood) and very low levels of LDL cholesterol.
Why other options are incorrect:
Why other options are incorrect:
- • Impairment of chylomicron formation: This is a characteristic of Abetalipoproteinemia.
- • Absence of Apo-C-II: This results in Familial Lipoprotein Lipase Deficiency, which causes severe hypertriglyceridemia.
- • Absence of Apo-C-I: This is not the primary diagnostic or significant clinical feature defining Tangier disease.
A significant feature of Broad Beta disease is
- a) Hypocholesterolemia
- b) Hypotriacylglycerolemia
- c) Absence of Apo-D
- d) Abnormality of Apo-E
Explanation:
Broad Beta disease (also known as Type III Hyperlipoproteinemia or Dysbetalipoproteinemia) is characterized by an abnormality of Apo-E (specifically the E2/E2 homozygous genotype). This leads to the impaired clearance of chylomicron remnants and IDL (Intermediate-Density Lipoproteins) from the blood, resulting in elevated levels of both cholesterol and triglycerides.
Why other options are incorrect:
Why other options are incorrect:
- • Hypocholesterolemia: Broad Beta disease actually causes hypercholesterolemia.
- • Hypotriacylglycerolemia: This condition causes hypertriglyceridemia (elevated triglycerides).
- • Absence of Apo-D: Apo-D is not the protein involved in the pathogenesis of this disorder; the condition is strictly linked to Apo-E dysfunction.
Neonatal tyrosinemia improves on administration of
- a) Thiamin
- b) Riboflavin
- c) Pyridoxine
- d) Ascorbic acid
Explanation:
Neonatal tyrosinemia is a benign, transient condition often seen in premature infants due to the delayed maturation of the enzyme p-hydroxyphenylpyruvate dioxygenase. Administration of Ascorbic acid (Vitamin C) helps to activate or overcome the metabolic block, allowing for the proper oxidation of p-hydroxyphenylpyruvate.
Why other options are incorrect:
Why other options are incorrect:
- • Thiamin (B1): Used for conditions like Beriberi and Maple Syrup Urine Disease (in some cases).
- • Riboflavin (B2): A coenzyme for FAD/FMN, not involved in the remediation of tyrosinemia.
- • Pyridoxine (B6): Used for B6-responsive anemias and certain types of homocystinuria, but not for tyrosinemia.
Absence of phenylalanine hydroxylase causes
- a) Neonatal tyrosinemia
- b) Phenylketonuria
- c) Primary hyperoxaluria
- d) Albinism
Explanation:
Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by a deficiency or absence of the enzyme phenylalanine hydroxylase. This enzyme is responsible for converting the amino acid phenylalanine into tyrosine. Its absence leads to the accumulation of phenylalanine in the blood and tissues.
Why other options are incorrect:
Why other options are incorrect:
- • Neonatal tyrosinemia: Caused by a transient deficiency of p-hydroxyphenylpyruvate dioxygenase.
- • Primary hyperoxaluria: Related to defects in glyoxylate metabolism, not phenylalanine.
- • Albinism: Typically caused by a deficiency of tyrosinase, which converts tyrosine to melanin.
Plasma tyrosine level in Richner-Hanhart syndrome is
- a) 1–2 mg/dL
- b) 2–3 mg/dL
- c) 4–5 mg/dL
- d) 8–10 mg/dL
Explanation:
Richner-Hanhart syndrome (Tyrosinemia Type II) is caused by a deficiency of the enzyme tyrosine aminotransferase. This results in significant elevation of tyrosine levels in the blood, typically in the range of 8–10 mg/dL or even higher (normal levels are generally below 2 mg/dL).
Why other options are incorrect:
Why other options are incorrect:
- • 1–2 mg/dL: This is within the normal physiological range for plasma tyrosine.
- • 2–3 mg/dL: While slightly elevated, it does not represent the diagnostic range associated with the clinical presentation of Tyrosinemia Type II.
- • 4–5 mg/dL: This level is suggestive of mild elevation but does not reach the threshold typically diagnostic of the severe clinical manifestations (palmo-plantar keratosis and eye lesions) of Richner-Hanhart syndrome.
Amount of phenylacetic acid excreted in the urine in phenylketonuria is
- a) 100–200 mg/dL
- b) 200–280 mg/dL
- c) 290–550 mg/dL
- d) 600–750 mg/dL
Explanation:
In phenylketonuria (PKU), the metabolic block in phenylalanine metabolism leads to the accumulation of phenylalanine. This excess phenylalanine is diverted into alternative metabolic pathways, resulting in the excretion of large amounts of phenyl derivatives, specifically phenylpyruvate, phenyllactate, and phenylacetic acid, which is typically excreted in the range of 290–550 mg/dL in affected individuals.
Why other options are incorrect:
Why other options are incorrect:
- • 100–200 mg/dL: These levels are generally too low to be diagnostic of the metabolic accumulation seen in untreated PKU.
- • 200–280 mg/dL: While elevated compared to healthy individuals, they do not represent the standard clinical range for the characteristic phenylacetic acid excretion in this condition.
- • 600–750 mg/dL: These levels exceed the typically observed range for this specific metabolite in standard clinical cases.
Tyrosinosis is due to defect in the enzyme:
- a) Fumarylacetoacetate hydrolase
- b) p-Hydroxyphenylpyruvate hydroxylase
- c) Tyrosine transaminase
- d) Tyrosine hydroxylase
Explanation:
Tyrosinosis (also known as Tyrosinemia Type III) is a rare disorder of tyrosine catabolism caused by a deficiency in the enzyme p-hydroxyphenylpyruvate hydroxylase (also known as p-hydroxyphenylpyruvate dioxygenase). This defect leads to the accumulation of p-hydroxyphenylpyruvate and tyrosine.
Why other options are incorrect:
Why other options are incorrect:
- • Fumarylacetoacetate hydrolase: Deficiency of this enzyme causes Tyrosinemia Type I (Hepatorenal Tyrosinemia).
- • Tyrosine transaminase: Deficiency of this enzyme causes Tyrosinemia Type II (Richner-Hanhart syndrome).
- • Tyrosine hydroxylase: This enzyme is involved in the conversion of tyrosine to L-DOPA in the catecholamine synthesis pathway, not in tyrosine catabolism.
An important finding in Histidinemia is
- a) Impairment of conversion of α-Glutamate to α-ketoglutarate
- b) Speech defect
- c) Decreased urinary histidine level
- d) Patients can not be treated by diet
Explanation:
Histidinemia is caused by a deficiency of the enzyme histidase. A common clinical observation in symptomatic patients with histidinemia is a speech defect or language development delay, although many individuals remain asymptomatic.
Why other options are incorrect:
Why other options are incorrect:
- • Impairment of conversion of α-Glutamate to α-ketoglutarate: This is not related to histidine metabolism; it involves glutamate dehydrogenase.
- • Decreased urinary histidine level: Histidinemia actually results in increased (elevated) histidine levels in both blood and urine (histidinuria).
- • Patients can not be treated by diet: Histidinemia is often managed effectively by a low-histidine diet, particularly in individuals showing neurological or developmental symptoms.
An important finding in glycinuria is
- a) Excess excretion of oxalate in the urine
- b) Deficiency of enzyme glycinase
- c) Significantly increased serum glycine level
- d) Defect in renal tubular reabsorption of glycine
Explanation:
Primary glycinuria is a rare benign condition characterized by a specific defect in the renal tubular reabsorption of glycine. Because the kidneys fail to reabsorb glycine properly, it is excreted in large amounts in the urine, despite the serum glycine levels remaining normal.
Why other options are incorrect:
Why other options are incorrect:
- • Excess excretion of oxalate: This is a hallmark of Primary Hyperoxaluria, not simple glycinuria.
- • Deficiency of enzyme glycinase: Glycinuria is a transport defect, not an enzymatic defect.
- • Significantly increased serum glycine level: In pure glycinuria, blood levels of glycine are typically normal because the defect is localized to the kidneys.
Increased urinary indole acetic acid is diagnostic of
- a) Maple syrup urine disease
- b) Hartnup disease
- c) Homocystinuria
- d) Phenylketonuria
Explanation:
Hartnup disease is a disorder of neutral amino acid transport. In this condition, tryptophan is not absorbed properly in the intestine. Bacteria in the gut degrade the unabsorbed tryptophan into indole compounds (like indole acetic acid), which are then absorbed and excreted in the urine, making increased urinary indole acetic acid a diagnostic finding.
Why other options are incorrect:
Why other options are incorrect:
- • Maple syrup urine disease: Characterized by the excretion of branched-chain amino acids and their keto acids (leucine, isoleucine, valine).
- • Homocystinuria: Characterized by elevated levels of homocysteine and methionine in blood and urine.
- • Phenylketonuria: Characterized by the excretion of phenylpyruvate and phenylacetic acid, not indole compounds.
In glycinuria daily urinary excretion of glycine ranges from
- a) 100–200 mg
- b) 300–500 mg
- c) 600–1000 mg
- d) 1100–1400 mg
Explanation:
In primary glycinuria, there is a defect in the renal tubular reabsorption of glycine. This leads to significantly increased urinary glycine levels, which typically range from 600 to 1000 mg per day, compared to the much lower amounts excreted by healthy individuals.
Why other options are incorrect:
Why other options are incorrect:
- • 100–200 mg / 300–500 mg: These ranges are closer to, or only slightly above, the normal physiological excretion rates of glycine.
- • 1100–1400 mg: While glycinuria involves excessive excretion, these higher values are not the standard diagnostic range typically cited for this specific renal transport defect.
An inborn error, maple syrup urine disease is due to deficiency of the enzyme:
- a) Isovaleryl-CoA hydrogenase
- b) Phenylalanine hydroxylase
- c) Adenosyl transferase
- d) α-Ketoacid decarboxylase
Explanation:
Maple Syrup Urine Disease (MSUD) is caused by a deficiency of the branched-chain α-ketoacid dehydrogenase complex (often referred to as α-ketoacid decarboxylase). This enzyme is responsible for the oxidative decarboxylation of branched-chain amino acids (leucine, isoleucine, and valine).
Why other options are incorrect:
Why other options are incorrect:
- • Isovaleryl-CoA hydrogenase: Deficiency of this enzyme causes Isovaleric Acidemia.
- • Phenylalanine hydroxylase: Deficiency of this enzyme causes Phenylketonuria (PKU).
- • Adenosyl transferase: Deficiency is typically related to hypermethioninemia.
Maple syrup urine disease becomes evident in extra uterine life by the end of:
- a) First week
- b) Second week
- c) Third week
- d) Fourth week
Explanation:
Maple syrup urine disease (MSUD) typically presents within the first week of life (often within 48 to 72 hours) as the infant begins to ingest protein, leading to the accumulation of branched-chain amino acids.
Why other options are incorrect:
Why other options are incorrect:
- • Second, Third, and Fourth week: While symptoms can persist or worsen over time if untreated, the initial clinical manifestation typically occurs much earlier, specifically during the neonatal period (first week) once protein feeding is established.
Alkaptonuria occurs due to deficiency of the enzyme:
- a) Maleylacetoacetate isomerase
- b) Homogentisate oxidase
- c) p-Hydroxyphenylpyruvate hydroxylase
- d) Fumarylacetoacetate hydrolase
Explanation:
Alkaptonuria is caused by a deficiency of the enzyme Homogentisate oxidase, which leads to the accumulation of homogentisic acid in the body, resulting in dark-colored urine and ochronosis.
Why other options are incorrect:
Why other options are incorrect:
- • Maleylacetoacetate isomerase: Deficiency of this enzyme leads to Tyrosinemia type III.
- • p-Hydroxyphenylpyruvate hydroxylase: Deficiency of this enzyme results in Tyrosinemia type II (Richner-Hanhart syndrome).
- • Fumarylacetoacetate hydrolase: Deficiency of this enzyme leads to Tyrosinemia type I (hepatorenal tyrosinemia).
An important feature of maple syrup urine disease is:
- a) Patient can not be treated by dietary regulation
- b) Without treatment death, of patient may occur by the end of second year of life
- c) Blood levels of leucine, isoleucine and serine are increased
- d) Excessive brain damage
Explanation:
Maple syrup urine disease (MSUD) is a severe metabolic disorder. If left untreated, the accumulation of branched-chain amino acids leads to severe ketoacidosis and neurological deterioration, often resulting in death within the first two years of life.
Why other options are incorrect:
Why other options are incorrect:
- • Dietary regulation: MSUD is managed primarily through a strict, lifelong diet restricted in branched-chain amino acids.
- • Blood levels: It is specifically the levels of Leucine, Isoleucine, and Valine (not Serine) that are increased.
- • Brain damage: While neurological damage is a complication, “death by the second year” is the classic clinical description of the untreated prognosis.
Ochronosis is an important finding of:
- a) Tyrosinemia
- b) Tyrosinosis
- c) Alkaptonuria
- d) Richner Hanhart syndrome
Explanation:
Ochronosis refers to the deposition of dark pigments in connective tissues (like cartilage and skin) and is a hallmark clinical feature of Alkaptonuria, caused by the buildup of homogentisic acid.
Why other options are incorrect:
Why other options are incorrect:
- • Tyrosinemia: Refers to a group of disorders (Types I, II, and III) involving tyrosine metabolism, but not characterized by ochronosis.
- • Tyrosinosis: An older term often associated with Tyrosinemia Type I.
- • Richner-Hanhart syndrome: This is specifically Tyrosinemia Type II, characterized by corneal ulcers and palmoplantar keratoderma, not ochronosis.
Phrynoderma is a deficiency of:
- a) Essential fatty acids
- b) Proteins
- c) Amino acids
- d) None of these
Explanation:
Phrynoderma, also known as “toad skin,” is a follicular hyperkeratosis clinically associated with a deficiency of essential fatty acids (specifically linoleic and linolenic acid). It is often historically linked to Vitamin A deficiency as well, though the primary nutritional classification points to fats.
Why other options are incorrect:
Why other options are incorrect:
- • Proteins: Protein deficiency leads to conditions like Kwashiorkor or Marasmus, not follicular hyperkeratosis.
- • Amino acids: While part of protein metabolism, their individual deficiency does not manifest as phrynoderma.
The percentage of linoleic acid in safflower oil is:
- a) 73
- b) 57
- c) 40
- d) 15
Explanation:
Safflower oil is one of the richest dietary sources of polyunsaturated fatty acids. Specifically, high-linoleic varieties of safflower oil contain approximately 73% to 75% linoleic acid, which is an essential omega-6 fatty acid.
Why other options are incorrect:
Why other options are incorrect:
- • 57%: This is closer to the linoleic acid content found in sunflower oil.
- • 40%: This is significantly lower than the standard high-linoleic safflower oil concentration.
- • 15%: This level of linoleic acid is characteristic of oils much lower in polyunsaturated fats, such as olive oil or some varieties of canola oil.
The percentage of polyunsaturated fatty acids (PUFA) in soybean oil is:
- a) 62
- b) 10
- c) 3
- d) 2
Explanation:
Soybean oil is highly valued for its high polyunsaturated fatty acid (PUFA) content. It contains approximately 60% to 65% PUFA, primarily consisting of linoleic acid (omega-6) and alpha-linolenic acid (omega-3).
Why other options are incorrect:
Why other options are incorrect:
- • 10%, 3%, and 2%: These values are far too low and do not represent the fatty acid profile of soybean oil, which is categorized as a high-PUFA vegetable oil.
The percentage of polyunsaturated fatty acids (PUFA) in butter is:
- a) 60
- b) 37
- c) 25
- d) 3
Explanation:
Butter is primarily composed of saturated fats. The polyunsaturated fatty acid (PUFA) content in butter is very low, typically ranging between 2% to 4% of its total fat composition.
Why other options are incorrect:
Why other options are incorrect:
- • 60%, 37%, and 25%: These figures are significantly higher than the actual PUFA content found in butter, which is known for its high saturated fat and cholesterol content rather than polyunsaturated fats.
Dietary fibre denotes:
- a) Undigested proteins
- b) Plant cell components that cannot be digested by own enzymes
- c) All plant cell wall components
- d) All non digestible water insoluble polysaccharide
Explanation:
Dietary fibre is defined as the edible parts of plants or analogous carbohydrates that are resistant to digestion and absorption in the human small intestine, meaning they cannot be broken down by the human body’s own digestive enzymes.
Why other options are incorrect:
Why other options are incorrect:
- • Undigested proteins: These are not classified as dietary fibre.
- • All plant cell wall components: While many cell wall components (like cellulose) are fibre, this definition is too broad as it may include other substances.
- • All non-digestible water insoluble polysaccharide: This is incorrect because dietary fibre also includes soluble fibres (like pectins and gums), not just insoluble ones.
A high fibre diet is associated with reduced incidence of:
- a) Cardiovascular disease
- b) C.N.S. disease
- c) Liver disease
- d) Skin disease
Explanation:
A high fibre diet, particularly one rich in soluble fibre, helps lower LDL (bad) cholesterol levels and improves blood pressure control, which significantly reduces the risk of cardiovascular disease.
Why other options are incorrect:
Why other options are incorrect:
- • C.N.S. disease, Liver disease, and Skin disease: While a healthy diet overall supports general organ health, high fibre intake specifically has a well-documented and direct clinical association with the prevention of cardiovascular conditions and metabolic disorders like Type 2 diabetes and colorectal issues.
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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