5651 to 5700 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 5651 to 5700
Dietary fibres are rich in
- a) Cellulose
- b) Glycogen
- c) Starch
- d) Proteoglycans
Explanation:
Dietary fibres consist of plant-based carbohydrates that the human body cannot digest. The primary component of dietary fibre is cellulose, which forms the structural part of plant cell walls.
Why other options are incorrect:
Why other options are incorrect:
- • Glycogen: This is the form in which glucose is stored in animals and humans, not in plant fibres.
- • Starch: While found in plants, starch is a digestible carbohydrate used for energy, not classified as dietary fibre.
- • Proteoglycans: These are compounds consisting of a protein core with attached glycosaminoglycan chains, commonly found in animal connective tissues.
A bland diet is recommended in
- a) Peptic ulcer
- b) Atherosclerosis
- c) Diabetes
- d) Liver disease
Explanation:
A bland diet consists of foods that are soft, not very spicy, and low in fiber. It is commonly recommended for individuals suffering from peptic ulcers or gastrointestinal irritation to prevent further damage to the stomach lining and reduce acid secretion.
Why other options are incorrect:
Why other options are incorrect:
- • Atherosclerosis: Requires a low-fat, low-cholesterol, and heart-healthy diet rather than just a bland diet.
- • Diabetes: Requires a diet focused on glycemic control, high fiber, and complex carbohydrates.
- • Liver disease: Generally requires a balanced diet, often modified for sodium, protein, or fluid intake depending on the stage of the disease.
A dietary deficiency in both the quantity and the quality of protein results in
- a) Kwashiorkar
- b) Marasmus
- c) Xerophtalmia
- d) Liver diseases
Explanation:
Marasmus is a form of severe malnutrition caused by an overall deficiency in energy and protein intake (both quantity and quality). It is characterized by severe wasting of muscle and fat tissue.
Why other options are incorrect:
Why other options are incorrect:
- • Kwashiorkar: Primarily caused by a severe deficiency of protein alone, often with adequate caloric intake.
- • Xerophtalmia: A condition caused by a deficiency in Vitamin A, leading to dry eyes and potentially blindness.
- • Liver diseases: These can be caused by various factors, including infections, toxins, or metabolic issues, rather than being the direct clinical definition of protein-energy malnutrition.
The deficiency of both energy and protein causes
- a) Marasmus
- b) Kwashiorkar
- c) Diabetes
- d) Beri-beri
Explanation:
Marasmus is a condition of severe malnutrition resulting from a prolonged deficiency of both total caloric intake (energy) and protein. It leads to extreme muscle wasting and loss of subcutaneous fat.
Why other options are incorrect:
Why other options are incorrect:
- • Kwashiorkar: This is specifically a protein-deficiency disease, often occurring when caloric intake might be sufficient but protein intake is critically low.
- • Diabetes: This is a metabolic disorder characterized by high blood sugar levels resulting from insulin issues, not protein-energy malnutrition.
- • Beri-beri: This condition is caused specifically by a deficiency of Vitamin B1 (thiamine).
Kwashiorkar is characterized by
- a) Night blindness
- b) Edema
- c) Easy fracturability
- d) Xerophthalmia
Explanation:
Kwashiorkor is a form of severe protein-energy malnutrition. A hallmark clinical sign of this condition is edema (swelling, particularly in the legs and abdomen) caused by low levels of albumin in the blood, which prevents proper fluid balance in the tissues.
Why other options are incorrect:
Why other options are incorrect:
- • Night blindness: This is a symptom of Vitamin A deficiency.
- • Easy fracturability: This is typically associated with deficiencies in calcium, Vitamin D, or bone-related disorders like osteoporosis.
- • Xerophthalmia: Also a condition resulting from a severe deficiency of Vitamin A, leading to dry eyes.
A characteristic feature of Kwashiorkar is
- a) Fatty liver
- b) Emaciation
- c) Low insulin lever
- d) Occurrence in less than 1 year infant
Explanation:
In Kwashiorkor, the liver becomes enlarged and fatty (hepatomegaly). This occurs because the lack of protein prevents the synthesis of lipoproteins required to transport fat out of the liver, leading to fat accumulation within liver cells.
Why other options are incorrect:
Why other options are incorrect:
- • Emaciation: While muscle wasting is present, “emaciation” is more characteristic of Marasmus, as Kwashiorkor patients often have edema which masks weight loss.
- • Low insulin lever: Kwashiorkor is not primarily defined by low insulin levels; it is defined by a lack of dietary protein.
- • Occurrence in less than 1 year infant: Kwashiorkor typically occurs in children aged 1 to 3 years, often after weaning, whereas Marasmus is more common in infants under 1 year.
A characteristic feature of marasmus is
- a) Severe hypoalbuminemia
- b) Normal epinephrine level
- c) Mild muscle wasting
- d) Low insulin and high cortisol level
Explanation:
Marasmus is characterized by an adaptive response to prolonged starvation. This results in suppressed insulin levels (due to low glucose intake) and elevated cortisol levels, which promote the breakdown of muscle and fat stores to provide energy for the body.
Why other options are incorrect:
Why other options are incorrect:
- • Severe hypoalbuminemia: This is a characteristic feature of Kwashiorkor, causing edema, rather than Marasmus.
- • Normal epinephrine level: In starvation, hormone levels are significantly altered, not normal.
- • Mild muscle wasting: Marasmus is defined by “severe” muscle wasting and fat loss, not mild.
Obesity generally reflects excess intake of energy and is often associated with the development of
- a) Nervousness
- b) Non-insulin dependent diabetes mellitus
- c) Hepatitis
- d) Colon cancer
Explanation:
Obesity is a major risk factor for Type 2 diabetes (NIDDM). Excess adipose tissue, particularly visceral fat, leads to insulin resistance, making it difficult for the body to regulate blood sugar levels effectively.
Why other options are incorrect:
Why other options are incorrect:
- • Nervousness: This is a psychological or neurological symptom not directly caused by the metabolic state of obesity.
- • Hepatitis: This is an inflammation of the liver, typically caused by viral infections or toxins, whereas obesity is more commonly associated with non-alcoholic fatty liver disease (NAFLD).
- • Colon cancer: While there is some statistical correlation between obesity and various cancers, NIDDM is the most direct and well-established metabolic consequence of excess energy intake and obesity.
Atherosclerosis and coronary heart diseases are associated with the diet:
- a) High in total fat and saturated fat
- b) Low in protein
- c) High in protein
- d) High in carbohydrate
Explanation:
Diets high in total fat and saturated fat contribute to elevated levels of LDL cholesterol in the blood. This cholesterol can accumulate as plaque on the inner walls of arteries, leading to atherosclerosis (narrowing of the arteries) and increasing the risk of coronary heart disease.
Why other options are incorrect:
Why other options are incorrect:
- • Low in protein: While imbalanced, this does not directly cause plaque buildup in the coronary arteries.
- • High in protein: Excessive protein intake is not a primary driver of atherosclerosis; in fact, healthy protein sources are often part of a heart-healthy diet.
- • High in carbohydrate: While excessive intake of refined sugars can contribute to metabolic issues, high saturated fat is the most clinically recognized dietary cause of atherosclerosis.
Cerebrovascular disease and hypertension is associated with
- a) High calcium intake
- b) High salt intake
- c) Low calcium intake
- d) Low salt intake
Explanation:
Excessive sodium (salt) intake leads to water retention in the blood vessels, increasing blood volume and pressure (hypertension). Chronic hypertension is a primary risk factor for damage to the blood vessels in the brain, leading to cerebrovascular diseases like strokes.
Why other options are incorrect:
Why other options are incorrect:
- • High calcium intake: Generally considered beneficial for bone health and does not cause hypertension; some studies even suggest it may help regulate blood pressure.
- • Low calcium intake: While deficiencies can cause other health problems, high salt is the most significant dietary trigger for hypertension.
- • Low salt intake: This is actually the recommended medical intervention for managing and preventing hypertension and associated vascular diseases.
The normal range of total serum bilirubin is
- a) 0.2–1.2 mg/100 ml
- b) 1.5–1.8 mg/100 ml
- c) 2.0–4.0 mg/100 ml
- d) Above 7.0 mg/100 ml
Explanation:
The normal range for total serum bilirubin in an adult is typically between 0.1 to 1.2 mg/dL (or mg/100 ml). Bilirubin is a yellow pigment produced during the normal breakdown of red blood cells; levels outside this range can indicate liver dysfunction or blood disorders.
Why other options are incorrect:
Why other options are incorrect:
- • 1.5–1.8 mg/100 ml: These levels are considered borderline and may indicate mild jaundice or underlying liver issues.
- • 2.0–4.0 mg/100 ml: Levels in this range are significantly elevated and are clinically indicative of jaundice.
- • Above 7.0 mg/100 ml: This indicates severe hyperbilirubinemia, which requires urgent medical investigation for serious hepatic or biliary conditions.
The normal range of direct reacting (conjugated) serum bilirubin is
- a) 0–0.1 mg/100 ml
- b) 0.1–0.4 mg/100 ml
- c) 0.4–0.6 mg/100 ml
- d) 0.5–1 mg/100 ml
Explanation:
Direct or conjugated bilirubin is the form of bilirubin that has been processed by the liver. In healthy adults, the normal range for direct bilirubin is generally considered to be 0.1 to 0.4 mg/dL (or mg/100 ml), representing a small fraction of the total bilirubin.
Why other options are incorrect:
Why other options are incorrect:
- • 0–0.1 mg/100 ml: This is a very low range and does not represent the standard upper limit for normal conjugated bilirubin.
- • 0.4–0.6 mg/100 ml: Levels exceeding 0.4 mg/dL are often suggestive of biliary obstruction or hepatic dysfunction.
- • 0.5–1 mg/100 ml: These values are considered elevated and are clinically significant indicators of conjugated hyperbilirubinemia.
The normal range of indirect (unconjugated) bilirubin in serum is
- a) 0–0.1 mg/100 ml
- b) 0.1–0.2 mg/100 ml
- c) 0.2–0.7 mg/100 ml
- d) 0.8–1.0 mg/100 ml
Explanation:
Indirect or unconjugated bilirubin makes up the majority of the total bilirubin in healthy individuals. The standard clinical reference range for indirect bilirubin is approximately 0.2 to 0.7 mg/dL (or mg/100 ml). It is “indirect” because it is bound to albumin and requires a catalyst to react in laboratory tests.
Why other options are incorrect:
Why other options are incorrect:
- • 0–0.1 mg/100 ml: This is well below the physiological normal for unconjugated bilirubin levels in healthy adults.
- • 0.1–0.2 mg/100 ml: This range is too low; indirect bilirubin typically accounts for the largest portion of the total serum bilirubin.
- • 0.8–1.0 mg/100 ml: While these values are close, they are on the higher end of the reference range and may indicate early stages of increased red blood cell breakdown or mild Gilbert syndrome.
Jaundice is visible when serum bilirubin exceeds
- a) 0.5 mg/100 ml
- b) 0.8 mg/100 ml
- c) 1 mg/100 ml
- d) 2.4 mg/100 ml
Explanation:
Clinical jaundice—the yellowing of the skin and the whites of the eyes—typically becomes clinically apparent (overt) only when total serum bilirubin levels rise above 2.0 to 2.5 mg/100 ml. Levels between 1.0 and 2.0 mg/100 ml are referred to as latent or subclinical jaundice.
Why other options are incorrect:
Why other options are incorrect:
- • 0.5 mg/100 ml: This is well within the normal healthy range and will not cause jaundice.
- • 0.8 mg/100 ml: This is also within the normal range for total bilirubin.
- • 1 mg/100 ml: While this is at the upper limit of the normal range, it is not high enough to cause visible yellowing (jaundice) of the skin.
An increase in serum unconjugated bilirubin occurs in
- a) Hemolytic jaundice
- b) Obstructive jaundice
- c) Nephritis
- d) Glomerulonephritis
Explanation:
Hemolytic jaundice is caused by the excessive breakdown of red blood cells (hemolysis). This releases massive amounts of heme, which is converted into bilirubin faster than the liver can conjugate it, leading to a significant rise in serum unconjugated (indirect) bilirubin.
Why other options are incorrect:
Why other options are incorrect:
- • Obstructive jaundice: Characterized by an increase in conjugated (direct) bilirubin, as the bile duct is blocked and the liver cannot excrete bilirubin into the intestine.
- • Nephritis / Glomerulonephritis: These are inflammatory conditions of the kidneys, which are primarily involved in filtration and waste excretion, not in the metabolism or conjugation of bilirubin.
One of the causes of hemolytic jaundice is
- a) G-6-PD deficiency
- b) Increased conjugated bilirubin
- c) Glucokinase deficiency
- d) Phosphoglucomutase deficiency
Explanation:
G-6-PD (Glucose-6-phosphate dehydrogenase) deficiency is a genetic disorder that leaves red blood cells vulnerable to oxidative stress. When exposed to certain triggers, these cells rupture (hemolysis), releasing bilirubin into the blood faster than the liver can process it, causing hemolytic jaundice.
Why other options are incorrect:
Why other options are incorrect:
- • Increased conjugated bilirubin: This is a result of obstructive jaundice, not a cause of hemolytic jaundice.
- • Glucokinase deficiency: Affects glucose metabolism in the liver/pancreas (often linked to MODY diabetes), not red blood cell stability.
- • Phosphoglucomutase deficiency: Involved in glycogen metabolism and is not a recognized cause of hemolysis or jaundice.
Increased urobilinogen in urine and absence of bilirubin in the urine suggests
- a) Obstructive jaundice
- b) Hemolytic jaundice
- c) Viral hepatitis
- d) Toxic jaundice
Explanation:
In hemolytic jaundice, the massive breakdown of red blood cells produces large amounts of unconjugated bilirubin, which is processed by the liver into increased amounts of urobilinogen. Since unconjugated bilirubin is not water-soluble, it does not appear in the urine, but the excess urobilinogen excreted by the kidneys does.
Why other options are incorrect:
Why other options are incorrect:
- • Obstructive jaundice: Characterized by the presence of bilirubin in the urine (bilirubinuria) and decreased or absent urobilinogen.
- • Viral hepatitis & Toxic jaundice: These typically present with both bilirubin and urobilinogen in the urine due to hepatocellular damage affecting both conjugation and excretion pathways.
Increased urobilinogen in urine and absence of bilirubin in the urine suggests
- a) Obstructive jaundice
- b) Hemolytic jaundice
- c) Viral hepatitis
- d) Toxic jaundice
Explanation:
In hemolytic jaundice, the massive breakdown of red blood cells produces large amounts of unconjugated bilirubin, which is processed by the liver into increased amounts of urobilinogen. Since unconjugated bilirubin is not water-soluble, it does not appear in the urine, but the excess urobilinogen excreted by the kidneys does.
Why other options are incorrect:
Why other options are incorrect:
- • Obstructive jaundice: Characterized by the presence of bilirubin in the urine (bilirubinuria) and decreased or absent urobilinogen.
- • Viral hepatitis & Toxic jaundice: These typically present with both bilirubin and urobilinogen in the urine due to hepatocellular damage affecting both conjugation and excretion pathways.
Fecal stercobilinogen is increased in
- a) Hemolytic jaundice
- b) Hepatic jaundice
- c) Viral hepatitis
- d) Obstructive jaundice
Explanation:
In hemolytic jaundice, the accelerated breakdown of red blood cells leads to an overproduction of bilirubin. This excess bilirubin is excreted by the liver into the intestine, resulting in significantly increased production of fecal stercobilinogen (the byproduct of urobilinogen in the gut).
Why other options are incorrect:
Why other options are incorrect:
- • Obstructive jaundice: Characterized by “clay-colored” stools because bile—and therefore bilirubin—cannot reach the intestine to be converted into stercobilinogen.
- • Hepatic jaundice & Viral hepatitis: These conditions involve hepatocellular damage, which often impairs the liver’s ability to process and excrete bilirubin, typically leading to decreased or normal stercobilinogen levels rather than an increase.
Fecal urobilinogen is increased in
- a) Hemolytic jaundice
- b) Obstruction of biliary duct
- c) Extrahepatic gall stones
- d) Enlarged lymphnodes
Explanation:
In hemolytic jaundice, the rapid destruction of red blood cells leads to an excessive production of bilirubin. This surplus is conjugated by the liver and secreted into the gut, where it is converted into increased amounts of urobilinogen and stercobilinogen, resulting in dark-colored stools and elevated fecal urobilinogen.
Why other options are incorrect:
Why other options are incorrect:
- • Obstruction of biliary duct & Extrahepatic gall stones: Both cause obstructive jaundice, preventing bile from reaching the intestine, which leads to a dramatic decrease or absence of fecal urobilinogen.
- • Enlarged lymphnodes: While these can compress the bile duct (causing obstruction), the lymph nodes themselves are not a primary cause of increased bilirubin or urobilinogen production.
A mixture of conjugated and unconjugated bilirubin is found in the circulation in
- a) Hemolytic jaundice
- b) Hepatic jaundice
- c) Obstructive jaundice
- d) Post hepatic jaundice
Explanation:
Hepatic (hepatocellular) jaundice involves damage to liver cells. This damage impairs the liver’s ability to conjugate bilirubin (leading to increased unconjugated levels) and also causes the leakage of already conjugated bilirubin back into the bloodstream (leading to increased conjugated levels). Thus, a “mixed” hyperbilirubinemia is characteristic of liver diseases like hepatitis or cirrhosis.
Why other options are incorrect:
Why other options are incorrect:
- • Hemolytic jaundice: Primarily results in elevated unconjugated bilirubin because the liver is functioning normally and can conjugate what is sent to it.
- • Obstructive/Post hepatic jaundice: Primarily results in elevated conjugated bilirubin because the liver cells are working, but the bile duct is blocked, causing bile to back up into the blood.
Hepatocellular jaundice as compared to pure obstructive type of jaundice is characterized by
- a) Increased serum alkaline phosphate, LDH and ALT
- b) Decreased serum alkaline phosphatase, LDH and ALT
- c) Increased serum alkaline phosphatase and decreased levels of LDH and ALT
- d) Decreased serum alkaline phosphatase and increased serum LDH and ALT
Explanation:
In hepatocellular jaundice, there is significant damage to liver cells, leading to a marked rise in liver enzymes like ALT (Alanine Aminotransferase) and LDH. In contrast, obstructive jaundice is primarily characterized by a massive elevation in Alkaline Phosphatase due to bile duct obstruction. Therefore, compared to obstructive jaundice, hepatocellular jaundice shows significantly higher ALT/LDH and relatively lower (or only mildly elevated) Alkaline Phosphatase.
Why other options are incorrect:
Why other options are incorrect:
- • Increased serum alkaline phosphate, LDH and ALT: While LDH and ALT are high, Alkaline Phosphatase is typically much higher in obstructive jaundice, making this choice less accurate as a comparison.
- • Decreased serum alkaline phosphatase, LDH and ALT: Liver damage generally causes an increase, not a decrease, in these markers.
- • Increased serum alkaline phosphatase and decreased levels of LDH and ALT: This describes the profile of obstructive jaundice, not hepatocellular damage.
Icteric index of an normal adult varies between
- a) 1–2
- b) 2–4
- c) 4–6
- d) 10–15
Explanation:
The icteric index is a historical clinical test used to measure the intensity of the yellow color of serum compared to a standard potassium dichromate solution. In a normal healthy adult, this index typically ranges between 4 and 6 units.
Why other options are incorrect:
Why other options are incorrect:
- • 1–2 and 2–4: These values are considered below the normal threshold and do not accurately reflect the expected yellowness of normal serum.
- • 10–15: Values in this range indicate hyperbilirubinemia, which is associated with jaundice.
Clinical jaundice is present with an icteric index above
- a) 4
- b) 8
- c) 10
- d) 15
Explanation:
The icteric index measures the degree of yellow pigmentation in the serum. While values between 6 and 15 may indicate latent (subclinical) jaundice, the index is typically considered to be in the range of overt clinical jaundice when it exceeds 15 units.
Why other options are incorrect:
Why other options are incorrect:
- • 4: This is the lower limit of the normal range for a healthy adult.
- • 8 and 10: While these values are above the normal limit, they generally represent mild or latent hyperbilirubinemia rather than overt, visible clinical jaundice.
Normal quantity of urobilinogen excreted in the feces per day is about
- a) 10–25 mg
- b) 50–250 mg
- c) 300–500 mg
- d) 700–800 mg
Explanation:
In a healthy adult, the daily excretion of urobilinogen (which is converted into stercobilin, giving feces its characteristic brown color) ranges between 50 and 250 mg. This amount varies depending on the rate of red blood cell destruction and the subsequent metabolism of bilirubin by intestinal bacteria.
Why other options are incorrect:
Why other options are incorrect:
- • 10–25 mg: This range is significantly lower than the normal physiological output and may indicate reduced bile flow or intestinal transit issues.
- • 300–500 mg & 700–800 mg: These ranges are considered abnormally high, usually indicative of increased bilirubin production resulting from conditions like hemolytic anemia.
Fecal urobilinogen is decreased in
- a) Obstruction of biliary duct
- b) Hemolytic jaundice
- c) Excess fat intake
- d) Low fat intake
Explanation:
Urobilinogen is formed in the intestine by the bacterial reduction of bilirubin, which reaches the gut via bile. In cases of biliary duct obstruction (obstructive jaundice), bilirubin is prevented from entering the intestine. Consequently, no bilirubin is available to be converted into urobilinogen, leading to a marked decrease or complete absence of fecal urobilinogen.
Why other options are incorrect:
Why other options are incorrect:
- • Hemolytic jaundice: Causes an increase in fecal urobilinogen due to the overproduction of bilirubin.
- • Excess fat intake / Low fat intake: These dietary variations do not directly inhibit the bile pathway or the conversion of bilirubin to urobilinogen in the gut.
A complete absence of fecal urobilinogen is strongly suggestive of
- a) Obstruction of bile duct
- b) Hemolytic jaundice
- c) Intrahepatic cholestasis
- d) Malignant obstructive disease
Explanation:
The presence of urobilinogen in feces is dependent on bilirubin reaching the intestines. When there is a complete obstruction of the bile duct (e.g., by a large stone or complete blockage), bile cannot reach the gut. Since no bilirubin enters the intestine, no urobilinogen can be formed by bacterial action, resulting in acholic (clay-colored) stools that lack urobilinogen.
Why other options are incorrect:
Why other options are incorrect:
- • Hemolytic jaundice: Leads to a significant increase, not absence, of fecal urobilinogen.
- • Intrahepatic cholestasis: Often causes reduced bile flow, but rarely leads to the “complete” obstruction and total absence of fecal urobilinogen seen in mechanical bile duct blockage.
- • Malignant obstructive disease: While it causes obstruction, “Obstruction of bile duct” is the general physiological state that directly leads to the absence; it is the most fundamental answer for the cause of the metabolic finding.
Immediate direct Vanden Bergh reaction indicates
- a) Hemolytic jaundice
- b) Hepatic jaundice
- c) Obstructive jaundice
- d) Megaloblastic anemia
Explanation:
The Van den Bergh reaction tests for bilirubin. An “immediate direct” reaction occurs when conjugated bilirubin is present in high concentrations in the serum. This is a classic hallmark of obstructive jaundice (cholestasis), where the liver conjugates bilirubin normally, but the obstruction of the bile ducts causes it to reflux into the bloodstream.
Why other options are incorrect:
Why other options are incorrect:
- • Hemolytic jaundice: Gives an “indirect” (or delayed) reaction, as it involves primarily unconjugated bilirubin.
- • Hepatic jaundice: Typically shows a “biphasic” reaction, as it contains a mixture of both conjugated and unconjugated bilirubin.
- • Megaloblastic anemia: Primarily a hematological condition and not a direct cause of conjugated hyperbilirubinemia or a positive direct Van den Bergh reaction.
The presence of bilirubin in the urine without urobilinogen suggests
- a) Obstructive jaundice
- b) Hemolytic jaundice
- c) Pernicious anemia
- d) Damage to the hepatic parenchyma
Explanation:
In obstructive jaundice, conjugated bilirubin is unable to pass into the intestine. It backs up into the blood and is excreted in the urine (bilirubinuria). Because no bilirubin reaches the intestine to be converted into urobilinogen by bacteria, there is no urobilinogen to be reabsorbed and excreted in the urine.
Why other options are incorrect:
Why other options are incorrect:
- • Hemolytic jaundice: Characterized by increased urobilinogen in the urine, but the bilirubin present is mostly unconjugated, which is not water-soluble and does not appear in the urine.
- • Pernicious anemia: A type of hemolytic anemia that would increase urobilinogen production, not bilirubinuria.
- • Damage to the hepatic parenchyma: Typically results in both bilirubin and urobilinogen being present in the urine due to impaired processing and excretion.
Impaired galactose tolerance test suggests
- a) Defect in glucose utilisation
- b) Liver cell injury
- c) Renal defect
- d) Muscle injury
Explanation:
The galactose tolerance test is used to assess the functional capacity of the liver. The liver is the primary site for the metabolism of galactose into glucose. Therefore, impaired tolerance indicates significant liver cell injury or impaired hepatic function.
Why other options are incorrect:
Why other options are incorrect:
- • Defect in glucose utilisation: This is typically evaluated by glucose tolerance tests, not specifically galactose.
- • Renal defect: While the kidneys excrete excess galactose, the tolerance test itself is a measure of hepatic metabolic capacity.
- • Muscle injury: Muscle metabolism is not the primary factor measured by the galactose tolerance test.
Increased serum ornithine carabamoyl transferase activity is diagnostic of
- a) Myocardial infarction
- b) Hemolytic jaundice
- c) Bone disease
- d) Acute viral hepatitis
Explanation:
Ornithine carbamoyltransferase (OCT) is a urea cycle enzyme found almost exclusively in the liver. It is a highly specific marker for hepatocellular damage; therefore, significantly elevated serum levels are diagnostic of acute viral hepatitis or other forms of liver necrosis.
Why other options are incorrect:
Why other options are incorrect:
- • Myocardial infarction: Cardiac damage is typically diagnosed via Troponins or CK-MB, not urea cycle enzymes.
- • Hemolytic jaundice: This involves the breakdown of red blood cells (pre-hepatic), not liver cell enzyme leakage.
- • Bone disease: This is generally associated with elevated Alkaline Phosphatase (ALP) levels, not OCT.
The best known and most frequently used test of the detoxicating functions of liver is
- a) Hippuric acid test
- b) Galactose tolerance test
- c) Epinephrine tolerance test
- d) Rose Bengal dye test
Explanation:
The Hippuric acid test is the classic and most frequently used test to evaluate the detoxifying (conjugating) capacity of the liver. It involves the conjugation of benzoic acid with glycine by the liver to form hippuric acid, which is then excreted in the urine.
Why other options are incorrect:
Why other options are incorrect:
- • Galactose tolerance test: Primarily used to measure the carbohydrate metabolic capacity of the liver.
- • Epinephrine tolerance test: Used to assess the glycogenolytic function of the liver.
- • Rose Bengal dye test: Used to measure the excretory capacity of the liver, not its detoxifying conjugation function.
The ability of liver to remove a dye like BSP from the blood suggests a normal
- a) Excretory function
- b) Detoxification function
- c) Metabolic function
- d) Circulatory function
Explanation:
Bromsulphalein (BSP) is a dye that is removed from the bloodstream by the liver, conjugated, and then excreted into the bile. The rate at which the dye is cleared from the blood is an excellent indicator of the liver’s overall excretory capacity.
Why other options are incorrect:
Why other options are incorrect:
- • Detoxification function: This is specifically measured by tests like the Hippuric acid synthesis test.
- • Metabolic function: This relates to the processing of nutrients (e.g., carbohydrate/protein metabolism), not dye excretion.
- • Circulatory function: While blood flow affects clearance, the test specifically targets the functional ability of hepatocytes to excrete dyes.
Removal of BSP dye by the liver involves conjugation with
- a) Thiosulphate
- b) Glutamine
- c) Cystein component of glutathione
- d) UDP glucuronate
Explanation:
Bromsulphalein (BSP) is taken up by the liver and conjugated with glutathione, specifically via the cysteine residue present in the glutathione molecule, catalyzed by the enzyme glutathione-S-transferase before being excreted into the bile.
Why other options are incorrect:
Why other options are incorrect:
- • Thiosulphate: Not involved in the conjugation pathway of organic dyes like BSP.
- • Glutamine: Typically involved in ammonia detoxification, not dye excretion.
- • UDP glucuronate: Used for the glucuronidation of bilirubin and various drugs, but not for BSP conjugation.
Normal value of plasma total proteins varies between
- a) 3–4 gm/100ml
- b) 6–8 gm/100ml
- c) 10–12 gm/100ml
- d) 14–16 gm/100ml
Explanation:
The normal range for total plasma protein in a healthy adult is typically between 6.0 and 8.0 g/dL (or gm/100ml). This concentration is maintained primarily by the liver, which synthesizes the majority of plasma proteins, including albumin.
Why other options are incorrect:
Why other options are incorrect:
- • 3–4 gm/100ml: This range is significantly low (hypoproteinemia) and would likely lead to edema.
- • 10–12 gm/100ml: This is abnormally high (hyperproteinemia), which can occur in conditions like multiple myeloma or severe dehydration.
- • 14–16 gm/100ml: This level is pathologically high and rarely seen in clinical practice.
A decrease in albumin with increased production of other unidentified proteins which migrate in β, γ region suggests
- a) Cirrhosis of liver
- b) Nephrotic syndrome
- c) Infection
- d) Chronic lymphatic leukemia
Explanation:
In cirrhosis of the liver, there is impaired synthesis of albumin (hypoalbuminemia) alongside a polyclonal increase in gamma globulins (hypergammaglobulinemia) due to chronic inflammation and failure of the liver to clear antigens. The characteristic finding on serum protein electrophoresis is “beta-gamma bridging.”
Why other options are incorrect:
Why other options are incorrect:
- • Nephrotic syndrome: Primarily characterized by a massive loss of albumin in the urine, leading to low total protein, but not typically the beta-gamma bridging seen in liver disease.
- • Infection: Usually leads to an increase in acute-phase reactants (alpha and beta globulins), not the characteristic albumin-gamma pattern of cirrhosis.
- • Chronic lymphatic leukemia: Often presents with monoclonal spikes (M-proteins) rather than the diffuse increase in the gamma region seen in cirrhosis.
An increase in α2-Globulin with loss of albumin in urine suggests
- a) Primary immune deficiency
- b) Nephrotic syndrome
- c) Cirrhosis of liver
- d) Multiple myeloma
Explanation:
In nephrotic syndrome, the glomerular membrane becomes highly permeable, leading to a massive loss of low-molecular-weight proteins like albumin in the urine. To compensate for the resulting low oncotic pressure, the liver increases the synthesis of various proteins, including alpha-2 macroglobulin, leading to a characteristic rise in the α2-globulin fraction on electrophoresis.
Why other options are incorrect:
Why other options are incorrect:
- • Primary immune deficiency: Typically presents with low or absent gamma globulins (hypogammaglobulinemia).
- • Cirrhosis of liver: Characterized by the beta-gamma bridge and decreased albumin, not an increase in α2-globulin.
- • Multiple myeloma: Characterized by a monoclonal “M-spike” in the gamma or beta region, not specific α2-globulin elevation.
The normal levels of prothrombin time is about
- a) 2 sec
- b) 4 sec
- c) 14 sec
- d) 10–16 sec
Explanation:
The Prothrombin Time (PT) measures the integrity of the extrinsic and common coagulation pathways. For a healthy adult, the normal reference range is typically between 10 and 16 seconds, although this can vary slightly depending on the laboratory’s reagents and testing methods.
Why other options are incorrect:
Why other options are incorrect:
- • 2 sec & 4 sec: These times are physiologically impossible for clot formation in standard testing, as they are too rapid.
- • 14 sec: While 14 seconds falls within the normal range, it represents a single point rather than the full reference interval used in clinical diagnostics.
In obstructive jaundice prothrombin time
- a) Remains normal
- b) Decreases
- c) Responds to vit K and becomes normal
- d) Responds to vit K and increases
Explanation:
In obstructive jaundice, bile flow to the intestine is blocked. Since Vitamin K is a fat-soluble vitamin, its absorption requires bile salts. Lack of Vitamin K absorption leads to a deficiency of clotting factors (II, VII, IX, and X), resulting in prolonged prothrombin time. Administering Vitamin K corrects this deficiency, returning the prothrombin time to normal.
Why other options are incorrect:
Why other options are incorrect:
- • Remains normal: It becomes prolonged due to the malabsorption of Vitamin K.
- • Decreases: A “decreased” time would imply faster clotting, whereas the lack of clotting factors slows it down (increases the time).
- • Responds to vit K and increases: Vitamin K restores the factors and brings the prothrombin time down to the normal range, not increases it.
In parenchymatous liver disease the prothrombin time
- a) Remains normal
- b) Increases
- c) Decreases
- d) Responds to Vit K
Explanation:
In parenchymatous liver disease (such as cirrhosis or hepatitis), the liver cells are damaged and lose their synthetic capacity. Since the liver is responsible for synthesizing clotting factors, their production drops, leading to an increase (prolongation) in prothrombin time.
Why other options are incorrect:
Why other options are incorrect:
- • Remains normal: Liver damage causes a deficiency in coagulation factors, so PT cannot remain normal.
- • Decreases: A decrease (shorter time) would mean clotting is happening faster than normal, which is the opposite of this condition.
- • Responds to Vit K: Unlike obstructive jaundice, parenchymatous liver disease generally does not show a significant response to Vitamin K because the liver is unable to synthesize the clotting factors even if Vitamin K is present.
Urea clearance test is used to determine the
- a) Glomerular filtration rate
- b) Renal plasma flow
- c) Ability of kidney to concentrate the urine
- d) Measurement of tubular mass
Explanation:
The urea clearance test measures the volume of blood cleared of urea by the kidneys per unit of time. It is a clinical test used to assess the Glomerular Filtration Rate (GFR), as the filtration of urea at the glomerulus is a primary indicator of renal function.
Why other options are incorrect:
Why other options are incorrect:
- • Renal plasma flow: This is measured using Para-aminohippuric acid (PAH) clearance.
- • Ability of kidney to concentrate the urine: This is typically assessed using concentration/dilution tests or urine osmolarity measurements.
- • Measurement of tubular mass: This refers to tests like TmG (Tubular maximum for glucose), which measure the transport capacity of renal tubules.
The formula to calculate maximum urea clearance is U × V / B, where U denotes
- a) Concentration of urea in urine in gm/24hr
- b) Concentration of urea in urine in mg/100 ml
- c) Concentration of urea in blood in mg/100 ml
- d) Volume of urine in ml/mt
Explanation:
In the clearance formula (C = UV/B), the symbols represent:
U = concentration of the substance (urea) in the urine (mg/100 ml),
V = volume of urine excreted per minute (ml/min), and
B = concentration of the substance in the blood (mg/100 ml).
Why other options are incorrect:
Why other options are incorrect:
- • gm/24hr: Clearance formulas require units that match per minute flow rate.
- • Concentration of urea in blood (B): This is represented by ‘B’ in the formula, not ‘U’.
- • Volume of urine (V): This is represented by ‘V’ in the formula.
Average maximum urea clearance is
- a) 30 ml
- b) 50 ml
- c) 75 ml
- d) 90 ml
Explanation:
The maximum urea clearance (Cm) is the volume of blood cleared of urea per minute when the urine flow is 2 ml/min or greater. The average normal value for an adult is approximately 75 ml/min (typically ranging from 60 to 100 ml/min).
Why other options are incorrect:
Why other options are incorrect:
- • 30 ml & 50 ml: These values are too low and would suggest impaired renal function.
- • 90 ml: While within the upper end of the normal range, 75 ml/min is the classically accepted average value in clinical biochemistry textbooks.
Urea clearance is lowered in
- a) Acute nephritis
- b) Pneumonia
- c) Early stage of nephritic syndrome
- d) Benign hypertension
Explanation:
Urea clearance is a measure of Glomerular Filtration Rate (GFR). In acute nephritis (inflammation of the kidney/glomeruli), the filtration capacity of the nephrons is significantly impaired, leading to a decrease in the amount of urea cleared from the blood into the urine.
Why other options are incorrect:
Why other options are incorrect:
- • Pneumonia: This is a respiratory condition and does not directly affect the glomerular filtration rate.
- • Early stage of nephrotic syndrome: GFR is often preserved in the early stages, unlike in nephritic conditions.
- • Benign hypertension: While chronic hypertension can eventually damage the kidneys, it does not typically cause a rapid or significant decrease in urea clearance in its benign/early stage compared to acute nephritis.
Glomerular filtration rate can be measured by
- a) Endogenous creatinine clearance
- b) Para-aminohippurate test
- c) Addis test
- d) Mosenthal test
Explanation:
Endogenous creatinine clearance is the most frequently used clinical test to estimate the Glomerular Filtration Rate (GFR). Creatinine is produced by muscles at a relatively constant rate and is freely filtered by the glomeruli with minimal tubular secretion or reabsorption, making it a reliable marker for GFR.
Why other options are incorrect:
Why other options are incorrect:
- • Para-aminohippurate (PAH) test: Used to measure Effective Renal Plasma Flow (ERPF).
- • Addis test: A test used to count the number of red blood cells, white blood cells, and casts in a 24-hour urine sample.
- • Mosenthal test: Used to assess the concentrating and diluting ability of the renal tubules.
At normal levels of creatinine in the blood, this metabolite is
- a) Filtered at the glomerulus but not secreted nor reabsorbed by the tubule
- b) Secreted by the tubule
- c) Reabsorbed by the tubule
- d) Secreted and reabsorbed by tubule
Explanation:
Creatinine is an ideal substance for measuring GFR because it is filtered by the glomerulus and is essentially neither reabsorbed nor significantly secreted by the renal tubules at normal physiological concentrations. This allows the clearance rate to accurately reflect the rate of glomerular filtration.
Why other options are incorrect:
Why other options are incorrect:
- • Secreted by the tubule: While minor secretion can occur at very high plasma levels, it is negligible at normal levels.
- • Reabsorbed by the tubule: Unlike urea, creatinine is not reabsorbed by the renal tubules.
- • Secreted and reabsorbed: This description does not apply to creatinine’s handling under normal physiological conditions.
The normal values for creatinine clearance varies from
- a) 20–40 ml/min
- b) 40–60 ml/min
- c) 70–85 ml/min
- d) 95–105 ml/min
Explanation:
The normal range for creatinine clearance in a healthy adult (corrected for body surface area) is typically cited as 95–105 ml/min, with many clinical sources often rounding this range to 80–120 ml/min depending on age and gender. Among the provided options, 95–105 ml/min is the most accurate reflection of the standard reference range.
Why other options are incorrect:
Why other options are incorrect:
- • 20–40 ml/min: This would indicate moderate to severe renal impairment.
- • 40–60 ml/min: This would indicate moderate renal impairment.
- • 70–85 ml/min: While this is closer to the lower limit of normal, it represents a range below the standard healthy reference.
Measurement of insulin clearance test is a measure of
- a) Glomerular filtration rate
- b) Filtration factor
- c) Renal plasma flow
- d) Tubular secretory mass
Explanation:
Inulin (not to be confused with insulin, the hormone) clearance is the gold standard for measuring the Glomerular Filtration Rate (GFR). Because inulin is a polysaccharide that is freely filtered by the glomerulus and is neither secreted, reabsorbed, nor metabolized by the renal tubules, its clearance rate is exactly equal to the GFR.
Why other options are incorrect:
Why other options are incorrect:
- • Filtration factor: Calculated as GFR divided by Renal Plasma Flow (RPF).
- • Renal plasma flow: Measured using substances like Para-aminohippuric acid (PAH).
- • Tubular secretory mass: Measured by the transport maximum (Tm) of specific substances that undergo active secretion.
The polysaccharide inulin is
- a) Filtered at the glomerulus but neither secreted nor reabsorbed by the tubule
- b) Filtered at the glomerulus and secreted by the tubule
- c) Filtered at the glomerulus and reabsorbed by the tubule
- d) Filtered at the glomerulus, secreted and reabsorbed by the tubule
Explanation:
Inulin is an exogenous polysaccharide that is physiologically inert. Because it is small and not protein-bound, it is freely filtered at the glomerulus. Crucially, it passes through the renal tubules without being subject to active or passive secretion or reabsorption, making its rate of excretion exactly equal to its rate of filtration.
Why other options are incorrect:
Why other options are incorrect:
- • Secreting/Reabsorbing: If inulin were secreted or reabsorbed, its clearance would not be an accurate measure of GFR.
Normal inulin clearance is
- a) 40 ml/1.73 sqm
- b) 60 ml/1.73 sqm
- c) 80 ml/1.73 sqm
- d) 120 ml/1.73 sqm
Explanation:
The normal GFR, as measured by inulin clearance, is approximately 120–125 ml/min when corrected to the standard body surface area of 1.73 square meters (sqm). This value represents the standard healthy filtration rate for an adult human.
Why other options are incorrect:
Why other options are incorrect:
- • 40, 60, & 80 ml/1.73 sqm: These values are significantly below the normal range and indicate varying degrees of renal impairment or decreased glomerular function.
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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