Free ASCP MLS Biochemistry Mock Test: Part 47 – Carbohydrate Metabolism & Glucose Regulation Practice Exam

Sodium fluoride inhibits enolase, an enzyme in the glycolytic pathway, preventing cells in the blood from consuming glucose.
This helps preserve the true glucose concentration in the sample until analysis.

Why the other options are incorrect:

• a) Serve as a coenzyme for the hexokinase reaction: Sodium fluoride is an enzyme inhibitor, not a coenzyme. The hexokinase method is a common laboratory assay for measuring glucose, and it uses ATP and NAD⁺ as cofactors, not fluoride.

• b) Precipitate proteins for a clearer sample: Fluoride does not precipitate proteins. Other additives or processes (like centrifugation) are used to obtain clear plasma or serum.

• d) Prevent reactivity of non-glucose reducing substances: This is not the function of fluoride. Modern enzymatic methods for glucose (like hexokinase) are highly specific for glucose and are not affected by other reducing substances.

In aerobic glycolysis, glucose is converted to pyruvate.
If oxygen is present, pyruvate is subsequently transported into mitochondria and converted to acetyl-CoA for entry into the citric acid cycle.
In anaerobic conditions, pyruvate is reduced to lactate.

Why the other options are incorrect:

• a) Lactate: This is the final product of anaerobic glycolysis (or lactic acid fermentation), not aerobic glycolysis.

• c) Acetyl-CoA: This is the product of the pyruvate dehydrogenase reaction, which occurs after glycolysis in the mitochondria.

• d) Carbon dioxide: This is a final product of the complete oxidation of glucose in the Krebs cycle and the electron transport chain, which occurs long after glycolysis is complete.

Strenuous aerobic exercise increases glycolytic activity, producing more pyruvate.
Some pyruvate is converted to lactate by lactate dehydrogenase.
Thus, both lactate and pyruvate levels are elevated post-exercise, reflecting increased anaerobic and aerobic metabolism.

Why the other options are incorrect:

• a) Normal lactic acid, low pyruvate: This is the opposite of what happens. Strenuous exercise dramatically increases the levels of both, not decreases them.

• b) Low lactic acid, elevated pyruvate: This is inconsistent. If pyruvate is elevated due to high glycolysis, the anaerobic conditions will force its conversion to lactate, raising lactate levels, not lowering them.

• c) Elevated lactic acid, low pyruvate: This is illogical. Lactic acid is produced from pyruvate. If pyruvate is low, there is no precursor to form elevated levels of lactate.

Glucose-6-phosphatase deficiency impairs gluconeogenesis and glycogenolysis, preventing the liver from releasing free glucose into the blood.
This causes Von Gierke’s disease (glycogen storage disease type I), characterized by hypoglycemia, hepatomegaly, and lactic acidosis.

Why the other options are incorrect:

• a) Diabetes insipidus: This is a disorder of water balance caused by a deficiency of antidiuretic hormone (ADH) or kidney resistance to it, unrelated to glucose metabolism.

• c) Addison’s disease: This is primary adrenal insufficiency, leading to cortisol and aldosterone deficiency, not an enzyme defect in glucose metabolism.

• d) Maple syrup urine disease: This is caused by a defect in the branched-chain alpha-keto acid dehydrogenase complex, leading to the accumulation of branched-chain amino acids and their keto acids, not glucose-6-phosphatase.

The Embden–Meyerhof pathway is the classic glycolytic pathway in which glucose is broken down into pyruvate, producing ATP and NADH.
It occurs in the cytoplasm and is a key step in cellular energy production.

Why the other options are incorrect:

• a) Gluconeogenesis: This is the synthesis of new glucose, essentially the reverse of glycolysis.

• c) Glycogenolysis: This is the breakdown of glycogen to glucose-1-phosphate.

• d) Pentose phosphate pathway (PPP): This is an alternative pathway for glucose oxidation that generates NADPH and pentose sugars, not ATP as its primary product.

Glycolysis occurs in the cytoplasm of the cell.
It does not require mitochondria or oxygen, making it an anaerobic pathway for the breakdown of glucose into pyruvate, producing ATP and NADH.

Why the other options are incorrect:

• a) Nucleus: The nucleus contains DNA and is the site of transcription, not energy metabolism.

• c) Mitochondria: The mitochondria are the site of the Krebs cycle and oxidative phosphorylation, which occur after glycolysis when oxygen is present. Pyruvate, the end product of glycolysis, is transported into the mitochondria for further processing.

• d) Endoplasmic reticulum (ER): The ER is involved in protein synthesis (rough ER) and lipid metabolism (smooth ER), not glycolysis.

Insulin and glucagon are primary regulators of blood glucose levels.
Thyroxine indirectly affects glucose metabolism by increasing basal metabolic rate and gluconeogenesis.
Oxytocin primarily regulates uterine contraction and milk ejection and has no direct role in glucose regulation.

Why the other options 

• a) Insulin: Lowers blood glucose by promoting cellular uptake and inhibiting glucose production.

• b) Glucagon: Raises blood glucose by stimulating glycogen breakdown and gluconeogenesis in the liver.

• c) Thyroxine (a thyroid hormone): While not a rapid-acting regulator like insulin or glucagon, it has a significant indirect role by influencing the basal metabolic rate. An increase in thyroxine generally raises blood glucose levels by increasing the rate of glycogenolysis and gluconeogenesis.

HbA1c reflects average blood glucose over the lifespan of red blood cells (~120 days).
In hemolytic anemia, RBCs are destroyed prematurely, shortening their lifespan.
This reduces the time for glycation, leading to falsely lower HbA1c values, even if glucose levels are normal or elevated.

Why the other options are incorrect:

• b) An increase in the glycated Hb value: This is not caused by hemolysis itself. Falsely high HbA1c can occur in situations where RBC lifespan is increased (e.g., after splenectomy) or due to certain hemoglobin variants.

• c) Little or no change in the glycated Hb value: Hemolysis has a direct and significant impact on HbA1c by shortening the exposure time of hemoglobin to glucose.

• d) An elevated HbA2 value: HbA2 is a minor hemoglobin component used in the diagnosis of beta-thalassemia trait. Its level is not directly affected by hemolytic anemia in a way that would explain a change in the HbA1c test result.

Glucose is rapidly consumed by red blood cells, leukocytes, and platelets through glycolysis if the blood specimen is not processed promptly.
After 8 hours at room temperature, glucose levels can fall significantly, whereas cholesterol, triglycerides, and creatinine remain relatively stable.

Why the other options are incorrect:

• a) Cholesterol: Cholesterol is a stable molecule and its concentration does not change significantly in a serum sample left at room temperature for 8 hours.

• b) Triglyceride: Triglycerides are generally stable for at least 24-48 hours at room temperature if the sample is properly sealed to prevent evaporation.

• c) Creatinine: Creatinine is very stable in serum and can withstand room temperature for at least 24 hours without significant change.

Arterial or capillary blood generally has a slightly higher glucose concentration than venous blood after a meal because tissues extract glucose as blood passes through the capillaries, causing venous glucose to be slightly lower.

Why the other options are incorrect:

• a) It is approximately 1-5 mg/dL lower: This is the opposite of the true physiological relationship.

• c) It is approximately 10-15 mg/dL lower: This magnitude of difference is not typical and would suggest a significant physiological or measurement error.

• d) It is identical: While the difference is small, it is physiologically significant and consistent. The concentrations are not identical, especially after a meal.

Glucose oxidase catalyzes the oxidation of glucose to gluconic acid and hydrogen peroxide.
In laboratory assays, the produced hydrogen peroxide reacts with a chromogen via peroxidase, allowing spectrophotometric measurement of glucose in blood or other body fluids.

Why the other options are incorrect:

• a) Glycogen: Glycogen is measured using enzymatic methods involving enzymes like amyloglucosidase, not glucose oxidase.

• c) Urea: Urea is commonly measured using the enzyme urease.

• d) Lactate: Lactate is measured using the enzyme lactate dehydrogenase (LDH).

The hydrogen (H₂) breath test is the preferred noninvasive method to diagnose lactase deficiency.
When lactose is not digested in the small intestine, it is fermented by colonic bacteria, producing hydrogen, which is absorbed into the blood and exhaled in the breath.

• a) Plasma Aldolase level: Aldolase is a glycolytic enzyme. Its level is measured to assess muscle damage (e.g., in muscular dystrophy) or sometimes liver damage, not for lactose intolerance.

• b) D-xylose test: This test assesses general small intestinal malabsorption by checking the integrity of the intestinal mucosa. It is not specific for lactase deficiency.

• d) Lactate Dehydrogenase (LD) level: LD is a cellular enzyme found in many tissues. Its level in blood is a non-specific marker of cell damage or turnover (e.g., hemolysis, myocardial infarction, cancer) and has no role in diagnosing lactase deficiency.

Why the other options are incorrect:

• a) 110 mg/dL (6.1 mmol/L): This value falls within the prediabetes range (FPG between 100 mg/dL and 125 mg/dL). It indicates impaired fasting glucose (IFG) and an increased risk for developing diabetes.

• b) 120 mg/dL (6.7 mmol/L): This value also falls within the prediabetes range.

• d) 140 mg/dL (7.8 mmol/L): While this value is clearly elevated and would be diagnostic, the official diagnostic cutoff is 126 mg/dL, not 140 mg/dL. The 140 mg/dL threshold was used in older guidelines but was lowered to the current standard to allow for earlier diagnosis and intervention.

Glycogenolysis is the enzymatic breakdown of glycogen into glucose-1-phosphate, which can then be converted to glucose-6-phosphate for energy production or released as free glucose by the liver.

Why the other options are incorrect:

• a) Glycogenesis: This is the process of synthesizing glycogen from glucose for storage. It is the opposite of glycogenolysis.

• c) Gluconeogenesis: This is the process of producing new glucose from non-carbohydrate precursors (like lactate, amino acids, glycerol), not from glycogen.

• d) Glycolysis: This is the pathway that breaks down glucose itself into pyruvate, not the breakdown of glycogen.

In a healthy individual, the 2-hour postprandial glucose should be less than 140 mg/dL (7.8 mmol/L).
A value of ~100 mg/dL after 2 hours reflects normal glucose metabolism and appropriate insulin response.

Why the other options are incorrect:

• a) 55 mg/dL (3.0 mmol/L): This value represents hypoglycemia. A sharp drop below the fasting level indicates an overactive insulin response, which is not normal.

• c) 180 mg/dL (9.9 mmol/L): This value is in the diabetic range according to ADA criteria (a 2-hour postprandial value ≥200 mg/dL is diagnostic, and 180 mg/dL is strongly indicative of impaired glucose tolerance or diabetes).

• d) 260 mg/dL (14.3 mmol/L): This value is clearly diagnostic of diabetes mellitus and represents a severe failure of the body to regulate blood glucose after a meal.

Glycolysis is the anaerobic breakdown of glucose (or other hexoses) into pyruvate, which can be further converted to lactate under low-oxygen conditions.
It produces ATP and NADH as energy sources for the cell.

Why the other options are incorrect:

• a) Glycogenesis: This is the process of synthesizing glycogen from glucose for storage. It is the opposite of glucose breakdown.

• b) Glycogenolysis: This is the process of breaking down glycogen into glucose-1-phosphate, which can then enter the glycolytic pathway. Glycolysis specifically refers to the breakdown of the glucose molecule itself.

• c) Gluconeogenesis: This is the process of synthesizing new glucose from non-carbohydrate precursors (like lactate, pyruvate, glycerol, and amino acids). It is essentially the reverse of glycolysis.

Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors (e.g., lactate, glycerol, amino acids).
The liver is the primary site, with the kidneys contributing to a lesser extent, especially during prolonged fasting.

Why the other options are incorrect:

• a) Brain: The brain is a major consumer of glucose but lacks the enzymatic machinery for gluconeogenesis.

• c) Skeletal muscle: Muscles lack the enzyme glucose-6-phosphatase, which is essential for releasing free glucose into the bloodstream. Therefore, they cannot contribute directly to blood glucose via gluconeogenesis.

• d) Pancreas: The pancreas is an endocrine organ that regulates glucose levels by secreting insulin and glucagon, but it does not perform significant gluconeogenesis.

Preterm and low birth weight infants normally have lower plasma glucose levels compared to adults due to immature gluconeogenesis and glycogen stores.
Hypoglycemia thresholds in these infants are lower than the adult cut-off of ≤70 mg/dL (3.9 mmol/L), and clinical context must be considered.

Why the other options are incorrect:

• a) The same as adults: This is incorrect and dangerous, as it would fail to identify neonates who are critically hypoglycemic by their own physiological standards.

• c) The same as a normal full-term infant: While closer, preterm infants often have even lower thresholds and less metabolic reserve than healthy full-term infants.

• d) Higher than a normal full-term infant: This is the opposite of the truth. Preterm infants are more susceptible to hypoglycemia and have lower defined thresholds, not higher ones.

The glucose tolerance test (GTT) assesses the body’s ability to regulate blood glucose after a standardized glucose load.
It primarily reflects insulin secretion and action, helping diagnose diabetes mellitus or impaired glucose tolerance.

Why the other options are incorrect:

• a) Liver enzyme activity: While the liver plays a key role in glucose storage and production, the GTT is not a specific test for liver enzymes. Abnormal GTT results can be influenced by liver disease, but that is not its primary purpose.

• c) Kidney function: The GTT is not used to assess kidney function. Tests like serum creatinine and BUN are used for that purpose. However, the kidneys do play a role in glucose reabsorption.

• d) Lipid metabolism: The GTT assesses carbohydrate metabolism, not lipid metabolism. A lipid panel is used to evaluate cholesterol and triglycerides.

The ADA recommends HbA1c for long-term monitoring of glycemic control in diabetic patients.
It reflects average blood glucose over the previous 2–3 months and is widely used to adjust therapy and assess treatment effectiveness.

Why the other options are incorrect:

• a) HbA1a & c) HbA1b: These are other minor fractions of glycated hemoglobin, but they are not used for routine clinical monitoring. HbA1c is the major and most clinically relevant fraction.

• b) HbA2: This is a normal, non-glycated hemoglobin variant that makes up a small percentage of total hemoglobin. Its measurement is used primarily in the diagnosis of beta-thalassemia trait, not for monitoring diabetes.

Vomiting during an OGTT compromises the ingestion and absorption of the glucose load, invalidating the test.
The recommended action is to draw a blood sample at the time of vomiting (to document any effect) and discontinue the test, then reschedule if necessary.

Why the other options are incorrect:

• a) Give the patient orange juice and continue the test: This would introduce an unstandardized and unknown amount of carbohydrate, completely invalidating the standardized protocol of the OGTT.

• b) Start the test over immediately with a 50 g carbohydrate dose: The test cannot be restarted immediately because the patient’s system already has an unknown amount of glucose from the first, partially absorbed dose. Furthermore, the standard dose must be used for a valid result.

• d) Place the patient in a recumbent position and continue the test: Changing position will not resolve the fundamental problem that the standardized glucose load was not fully absorbed, rendering the test results invalid.

Glucagon, secreted by pancreatic alpha cells, raises blood glucose by:

• Stimulating glycogenolysis in the liver

• Promoting gluconeogenesis
  Insulin lowers blood glucose, while estrogen and oxytocin have minimal direct effects on glucose regulation.

Why the other options are incorrect:

• a) Insulin: This hormone lowers blood glucose levels by promoting cellular uptake of glucose and inhibiting glucose production in the liver.

• b) Estrogen: While estrogen can have complex effects on metabolism, it is not a primary regulator of blood glucose levels.

• d) Oxytocin: This hormone is involved in childbirth and lactation, not glucose regulation.

NAD⁺ (Nicotinamide adenine dinucleotide) is essential in glycolysis to accept electrons during the oxidation of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate, producing NADH.

Why the other options are incorrect:

• a) Brain: The brain is a major consumer of glucose but lacks the enzymatic machinery for gluconeogenesis.

• c) Skeletal muscle: Muscles lack the enzyme glucose-6-phosphatase, which is essential for releasing free glucose into the bloodstream. Therefore, they cannot contribute directly to blood glucose via gluconeogenesis.

• d) Pancreas: The pancreas is an endocrine organ that regulates glucose levels by secreting insulin and glucagon, but it does not perform significant gluconeogenesis.

HbA1c reflects the average blood glucose over the previous 2–3 months, as glucose irreversibly binds to hemoglobin.
It is the preferred test for long-term monitoring of glycemic control in diabetes mellitus.

Why the other options are incorrect:

• a) Weekly fasting serum glucose: This provides only a single snapshot of glucose control at the time of the test and is heavily influenced by recent food intake, stress, and other short-term factors. It does not reflect overall control between tests.

• b) 2-hour postprandial serum glucose: This test measures the peak glucose level after a meal and is useful for adjusting mealtime insulin or medication. However, like the fasting glucose, it is a short-term measure and does not represent long-term control.

• c) Fructosamine: This test measures glycated serum proteins and reflects average glucose levels over the preceding 2 to 3 weeks. While it is useful in situations where HbA1c is unreliable (e.g., hemoglobinopathies, hemolytic anemia, pregnancy), it is not the best test for standard long-term (3-month) monitoring. HbA1c’s longer window is superior for routine management.

The first step of glycolysis is the phosphorylation of glucose to glucose-6-phosphate, catalyzed by hexokinase (or glucokinase in the liver).
This traps glucose inside the cell and prepares it for further metabolism in the glycolytic pathway.

Why the other options

• a) Insulin: Lowers blood glucose by promoting cellular uptake and inhibiting glucose production.

• b) Glucagon: Raises blood glucose by stimulating glycogen breakdown and gluconeogenesis in the liver.

• c) Thyroxine (a thyroid hormone): While not a rapid-acting regulator like insulin or glucagon, it has a significant indirect role by influencing the basal metabolic rate. An increase in thyroxine generally raises blood glucose levels by increasing the rate of glycogenolysis and gluconeogenesis.

Ion-exchange chromatography separates hemoglobin species based on charge differences.
Hemoglobin variants like HbS can co-elute with HbA1c, producing falsely elevated HbA1c values.
Other conditions (iron deficiency, pernicious anemia, thalassemias) may affect RBC lifespan, potentially lowering HbA1c, but do not directly cause this chromatographic artifact.

Why the other options .

• a) Iron Deficiency Anemia: This condition can cause a true increase in HbA1c due to prolonged red cell lifespan, not an analytical interference with the ion-exchange method itself.

• c) Pernicious Anemia: This is a type of megaloblastic anemia. It does not typically involve a structural hemoglobin variant that would interfere with the charge-based separation of HbA1c.

• d) Thalassemias: Thalassemias can cause falsely low or high HbA1c results depending on the method and the specific type

Diabetes mellitus is characterized by chronic hyperglycemia due to defective insulin secretion, action, or both, leading to impaired carbohydrate metabolism.
Secondary disturbances in lipid and protein metabolism also occur but are consequences of the primary carbohydrate disorder.

Why the other options are incorrect:

• a) Protein metabolism: While diabetes can lead to increased protein catabolism (breakdown) due to insulin deficiency, this is a secondary effect, not the primary disorder.

• b) Lipid metabolism: Diabetes causes abnormalities in lipid metabolism (e.g., increased lipolysis, ketoacidosis), but these are also secondary consequences of the underlying carbohydrate disorder and insulin dysregulation.

• d) Mineral metabolism: Diabetes can affect mineral balance (e.g., magnesium, potassium), but this is not the core defect.

Acetone is one of the ketone bodies, along with acetoacetate and beta-hydroxybutyrate. Ketone bodies are produced in the liver during the metabolism of fatty acids.

Why the other options are incorrect:

• a) Carbohydrates: A defect in carbohydrate metabolism (like the lack of insulin in diabetes) is the common underlying cause that triggers the accelerated fat breakdown. However, the acetone itself is a direct product of the resulting altered fat metabolism.

• c) Urea Nitrogen: Urea is the end product of protein and amino acid metabolism. A defect here would affect the urea cycle and cause hyperammonemia, not ketosis.

• d) Uric Acid: Uric acid is the end product of purine metabolism. Defects here are associated with conditions like gout, not the accumulation of acetone.

HbA1c measures the percentage of hemoglobin irreversibly glycated by glucose.
Since red blood cells have a lifespan of ~120 days, HbA1c reflects long-term (2–3 months) average blood glucose levels, making it a reliable tool for monitoring diabetic control.

Why the other options are incorrect:

• a) Short-term glucose fluctuations: This is measured by frequent blood glucose monitoring or continuous glucose monitors, not HbA1c.

• c) Renal glucose excretion: This is unrelated to HbA1c. Urine glucose tests measure renal excretion.

• d) Daily fasting glucose variation: A single fasting glucose test captures one point in time. HbA1c provides a long-term average that smooths out daily variations.

According to ADA criteria, a 2-hour postprandial (or oral glucose tolerance test) glucose ≥200 mg/dL (11.1 mmol/L) is diagnostic of diabetes mellitus.
Values below this indicate normal glucose tolerance or impaired glucose tolerance depending on the range.

Why the other options are incorrect:

• a) 150 mg/dL (8.3 mmol/L): This value is within the normal range for a postprandial glucose test and is not diagnostic of diabetes.

• b) 170 mg/dL (9.4 mmol/L): This value falls within the prediabetes range (140–199 mg/dL or 7.8–11.0 mmol/L for the 2-hour OGTT), indicating impaired glucose tolerance.

• c) 180 mg/dL (9.9 mmol/L): This value also falls within the prediabetes range and is not high enough to be diagnostic of diabetes.

Glucose, galactose, and fructose are simple sugars that cannot be hydrolyzed into smaller carbohydrate units.
They are classified as monosaccharides, the basic units of carbohydrates.

Why the other options are incorrect:

• a) Amino acids: These are the building blocks of proteins, containing both amino and carboxyl groups (e.g., glycine, alanine).

• c) Disaccharides: These are carbohydrates composed of two monosaccharide units (e.g., sucrose, lactose, maltose).

• d) Ketones: This is a class of organic compounds characterized by a carbonyl group. While fructose is a ketose (a type of monosaccharide with a ketone group), the category “ketones” is too broad and incorrect for grouping these sugars. Acetone is a common ketone.

Whole blood glucose is slightly lower than serum glucose because glucose is distributed in the plasma (the aqueous portion), and red blood cells occupy part of whole blood volume.
Since serum/plasma is mostly water, its glucose concentration appears higher than in whole blood.

Glycogen synthase is the key enzyme in glycogenesis, catalyzing the addition of glucose units from UDP-glucose to a growing glycogen chain.
This process stores excess glucose in the liver and muscle for later energy use.

Why the other options are incorrect:

• a) Glycogenolysis: This is the breakdown of glycogen, which is catalyzed by the enzyme glycogen phosphorylase, not glycogen synthase.

• c) Gluconeogenesis: This is the synthesis of new glucose from non-carbohydrate precursors. Glycogen synthase is not involved in this pathway.

• d) Glycolysis: This is the breakdown of glucose to pyruvate. Glycogen synthase is involved in storing glucose, not breaking it down for energy.

A fasting glucose of 95 mg/dL is within the normal range (70–99 mg/dL).
During fasting, blood glucose is maintained primarily by hepatic glycogenolysis and gluconeogenesis, not by skeletal muscle, since muscle lacks glucose-6-phosphatase.

Why the other options are incorrect:

• b) Normal; reflecting glycogen breakdown by skeletal muscle: This is incorrect. Skeletal muscle lacks the enzyme glucose-6-phosphatase, so it cannot release free glucose into the bloodstream. Muscle glycogen is used only by the muscle itself for energy.

• c) Abnormal; indicating diabetes mellitus: A fasting glucose of 95 mg/dL is normal. Diabetes is diagnosed with a fasting glucose ≥126 mg/dL.

• d) Abnormal; indicating hypoglycemia: Hypoglycemia is typically defined as a glucose level <55 mg/dL for clinical purposes. A value of 95 mg/dL is normal and not indicative of hypoglycemia.

Glycolysis is the anaerobic metabolic pathway in which glucose is converted to pyruvate, producing ATP and NADH.
It is the first step in cellular respiration and occurs in the cytoplasm of cells.

Why the other options are incorrect:

• a) Gluconeogenesis: This is the synthesis of new glucose from non-carbohydrate precursors (like lactate, pyruvate, glycerol). It is essentially the reverse of glycolysis.

• b) Glycogenesis: This is the process of synthesizing glycogen from glucose for storage.

• d) Glycogenolysis: This is the process of breaking down glycogen into glucose-1-phosphate, which can then enter the glycolytic pathway.

While the general threshold for hypoglycemia in a diabetic patient is often considered ≤70 mg/dL (3.9 mmol/L), which serves as a warning sign to take action, the definition is stricter for a non-diabetic individual, especially in the context of diagnostic testing like a fasting blood glucose test or during a prolonged fast.

Why the other options are incorrect:

• a) ≤70 mg/dL (≤3.9 mmol/L): This is the alert value for people with diabetes, indicating a need for intervention. In a non-diabetic person, a value this low may occur transiently but is not typically used to define pathological hypoglycemia.

• b) ≤60 mg/dL (≤3.3 mmol/L): While low, this value is not the standard diagnostic cutoff. The more stringent ≤55 mg/dL is used to increase the specificity for diagnosing pathological conditions.

• d) ≤45 mg/dL (≤2.5 mmol/L): This represents severe hypoglycemia, often associated with profound neuroglycopenia (impaired brain function). It is a consequence of hypoglycemia, not the standard definition for its onset in a non-diabetic person.

CSF contains glucose that can be rapidly consumed by cells or bacteria in the sample.
Immediate analysis (or proper preservation with fluoride) is required to prevent falsely low glucose results.

Why the other options are incorrect:

• a) To prevent contamination: While preventing contamination is always important, it is not the primary reason for immediate glucose testing. Contamination affects microbiology cultures more than chemistry tests.

• b) To avoid precipitation of proteins: Protein precipitation is not a significant concern for glucose analysis and does not necessitate immediate testing.

• d) To ensure accurate electrolyte measurement: While electrolytes should also be tested promptly, glucose is the most time-critical CSF analyte due to rapid glycolysis. Electrolytes are more stable.

• NADPH, used in biosynthetic reactions like fatty acid and steroid synthesis

• Ribose-5-phosphate, used for nucleotide and nucleic acid synthesis
  It is an alternative pathway for glucose metabolism that does not primarily produce ATP.

Why the other options are incorrect:

• b) ATP and pyruvate: These are the primary products of glycolysis, not the pentose phosphate pathway.

• c) Lactate and NAD⁺: These are associated with anaerobic glycolysis (lactic acid fermentation), not the PPP.

• d) GTP and glucose-1-phosphate: GTP is produced in the Krebs cycle, and glucose-1-phosphate is an intermediate in glycogen metabolism, not the PPP.

Insulin, secreted by the pancreatic β-cells, lowers blood glucose by:

• Promoting glucose uptake into cells

• Stimulating glycogen synthesis in the liver and muscle

• Inhibiting gluconeogenesis and glycogenolysis

Why the other options are incorrect:

• a) Glucagon: This hormone raises blood glucose levels by stimulating glycogenolysis and gluconeogenesis in the liver.

• b) Cortisol: This is a glucocorticoid hormone that elevates blood glucose by promoting gluconeogenesis and reducing glucose uptake by tissues.

• d) Epinephrine: This “fight-or-flight” hormone increases blood glucose by stimulating glycogen breakdown (glycogenolysis) in the liver and muscles.

The hexokinase method is the most specific enzymatic assay for glucose measurement.
It involves two reactions:

1. Glucose + ATP → Glucose-6-phosphate (via hexokinase)

2. Glucose-6-phosphate + NADP⁺ → 6-phosphogluconate + NADPH (via glucose-6-phosphate dehydrogenase)

Why the other options are incorrect:

• a) Glucose Oxidase: This method is very common, especially in dry reagent strips and portable meters, but it is less specific than hexokinase. It can be subject to interference from substances like uric acid, glutathione, and ascorbic acid. While an additional enzyme (peroxidase) is used to create the color change, the overall system is more prone to chemical interference.

• b) Glucose Dehydrogenase: This method is used in some point-of-care meters. However, different isoforms of this enzyme can react with other sugars besides glucose (e.g., GDH-PQQ reacts significantly with maltose and galactose), leading to falsely high results, especially in patients receiving certain parenteral therapies.

• c) Glucose-6-Phosphatase: This is not a method for measuring glucose. It is an enzyme involved in producing glucose in the liver during glycogenolysis. It acts in the opposite direction of the assay enzymes.

Normal fasting blood glucose in healthy adults ranges from 70 to 110 mg/dL (3.9–6.1 mmol/L).
Values below 70 mg/dL indicate hypoglycemia, while above 110 mg/dL may suggest impaired fasting glucose or diabetes.

Why the other options are incorrect:

• a) 40–70 mg/dL: This range is too low and falls into hypoglycemia. Values below 70 mg/dL are considered low, and below 55 mg/dL are diagnostic of clinical hypoglycemia.

• c) 120–160 mg/dL: This range is elevated. A fasting level of ≥126 mg/dL on two separate occasions is diagnostic of diabetes mellitus.

• d) 160–200 mg/dL: This range is significantly elevated and represents poorly controlled diabetes.

The most common form of galactosemia is due to deficiency of galactose-1-phosphate uridyl transferase (GALT).
This blocks the conversion of galactose-1-phosphate to UDP-galactose, leading to accumulation of galactose and its metabolites, which can cause liver damage, cataracts, and developmental issues.

Why the other options are incorrect:

• a) Glucose-6-Phosphatase: A deficiency in this enzyme causes von Gierke disease (Glycogen Storage Disease Type I), not galactosemia.

• b) Galactokinase: A deficiency in this enzyme causes a rarer form of galactosemia characterized primarily by early-onset cataracts, but it is not the most frequent cause. It lacks the severe systemic symptoms of classic transferase-deficient galactosemia.

• d) Uridine Diphosphate 4 Epimerase: A deficiency in this enzyme is very rare and can cause symptoms similar to classic galactosemia, but it is not the most frequent cause.

The liver plays a central role in glucose homeostasis:

• It stores glucose as glycogen after meals (glycogenesis)

• Releases glucose during fasting via glycogenolysis and gluconeogenesis
  The pancreas regulates glucose via hormones, but does not store it.

Why the other options are incorrect:

• a) Pancreas: The pancreas is an endocrine organ that regulates glucose levels by secreting the hormones insulin (which lowers glucose) and glucagon (which raises glucose). It does not store a significant amount of glucose itself.

• c) Kidney: The kidneys help regulate glucose by reabsorbing it from the filtrate and can also perform gluconeogenesis, but they are not the primary site for glycogen storage and release.

• d) Spleen: The spleen is involved in immune function and red blood cell filtration, not glucose metabolism or storage.

The brain relies almost exclusively on glucose under normal conditions because:

• It has limited glycogen stores

• Fatty acids cannot cross the blood-brain barrier efficiently
  During prolonged fasting, the brain can partially use ketone bodies, but glucose remains its primary energy source.

Why the other options are incorrect:

• a) Skeletal muscle: Can use glucose, fatty acids, and ketone bodies for energy. During rest, it primarily uses fatty acids.

• c) Liver: Is a central metabolic processing organ. It uses various fuels (fatty acids, amino acids, lactate) and its main role is to produce and store glucose for other organs, not just consume it.

• d) Kidney: Can use glucose, fatty acids, lactate, and glutamine for energy. It also performs gluconeogenesis during fasting.

In the liver, glucokinase catalyzes the phosphorylation of glucose to glucose-6-phosphate.
Unlike hexokinase, glucokinase has a higher Km and is not inhibited by glucose-6-phosphate, allowing the liver to store excess glucose as glycogen after meals.

Why the other options are incorrect:

• a) Hexokinase: This enzyme performs the same reaction in most other tissues (like muscle and brain). It has a low Km (high affinity) for glucose, ensuring glucose uptake even when blood levels are low, and it is inhibited by glucose-6-phosphate.

• c) Phosphatase: This is a general term for enzymes that remove phosphate groups (e.g., glucose-6-phosphatase), not add them.

• d) Aldolase: This enzyme catalyzes the cleavage of fructose-1,6-bisphosphate into two triose phosphates in glycolysis, not the phosphorylation of glucose.

Glucagon, secreted by pancreatic alpha cells, raises blood glucose by stimulating glycogenolysis and gluconeogenesis in the liver.
It is released when blood glucose falls, such as between meals.

Why the other options are incorrect:

• a) Insulin: Insulin is secreted in response to rising blood glucose levels (e.g., after a meal). Its action is opposite to glucagon—it promotes glucose uptake by cells and lowers blood sugar.

• b) Cortisol: Cortisol is a steroid hormone that helps raise blood glucose, but it does so as part of a slower, long-term stress response (diurnal rhythm) and is not the primary, rapid responder to a mid-morning dip in blood sugar.

• c) Epinephrine: Epinephrine (adrenaline) is released during acute stress or fight-or-flight situations and can rapidly increase blood glucose.

Glycogen is the primary storage form of glucose in humans, found mainly in the liver and skeletal muscle.
It serves as a readily mobilizable energy reserve to maintain blood glucose and supply energy during activity.

Why the other options are incorrect:

• a) Glucose: While glucose is the primary circulating sugar and main energy source, it is not a storage form. Blood glucose levels are tightly regulated, and excess glucose is converted into glycogen or fat for storage.

• b) Sucrose: This is common table sugar (a disaccharide of glucose and fructose). It is a dietary carbohydrate but is not synthesized or stored in the human body.

• d) Cellulose: This is a structural polysaccharide found in the cell walls of plants. Humans lack the enzyme (cellulase) to digest it, so it serves as dietary fiber, not an energy store.

Glucose is dissolved in the aqueous portion of blood.
Since erythrocytes have lower water content than plasma, the glucose concentration in whole blood depends on the proportion of red blood cells (hematocrit).
Higher hematocrit → less plasma water → slightly lower whole blood glucose compared to plasma/serum.

Why the other options are incorrect:

• a) Leukocyte Count: The number of white blood cells is too low to significantly affect the overall water content of blood.

• b) Hemoglobin Concentration: While hemoglobin concentration is correlated with hematocrit, it is the volume of the RBCs (the hematocrit), not the hemoglobin concentration itself, that directly determines the water content.

• d) Erythrocyte Indices: These values (MCV, MCH, MCHC) describe the size and hemoglobin content of individual RBCs, but the overall factor that determines the total water content in a blood sample is the total volume occupied by RBCs, which is the hematocrit.

Total glycosylated hemoglobin (including HbA1c) reflects the average blood glucose over the lifespan of red blood cells (~120 days).
It provides a long-term assessment of glycemic control, not just a single point-in-time glucose measurement.

Why the other options are incorrect:

• a) Blood glucose level at the time the sample is drawn: This is measured by a plasma or serum glucose test, not an HbA1c test. HbA1c does not change with short-term fluctuations.

• b) Average blood glucose levels for the past week: This is too short a timeframe. While the most recent 2-4 weeks contribute more heavily to the final value, the test reflects an average over the full 2-3 month period. The test fructosamine measures glycated proteins and reflects control over the past 2-3 weeks.

• d) HbA1c level at the time the sample is drawn: This statement is circular and inaccurate. The HbA1c level is the measurement itself, and it reflects a long-term average, not an instantaneous level.

Hexokinase catalyzes the phosphorylation of glucose to glucose-6-phosphate using ATP.
This is the first step of glycolysis, effectively trapping glucose inside the cell for metabolism.

Why the other options are incorrect:

• a) Glucose to fructose: This isomerization is catalyzed by phosphoglucose isomerase in glycolysis.

• c) Glucose-6-phosphate to pyruvate: This describes the entire process of glycolysis, which involves multiple enzymes, not just hexokinase.

• d) Glucose to glycogen: The synthesis of glycogen from glucose is called glycogenesis and involves enzymes like glycogen synthase, not hexokinase.

Ascorbic acid (Vitamin C) is a reducing agent that can interfere with the peroxidase reaction in the glucose oxidase–peroxidase method, leading to falsely low glucose measurements by inhibiting chromogen formation.

Why the other options are incorrect:

• a) Bilirubin: Bilirubin can also interfere, but it typically acts as an oxidizing agent in this assay, sometimes leading to falsely elevated results, not inhibition of chromogen production. Ascorbic acid is a more classic and potent reducing interferent.

• c) Uric Acid: Uric acid is a weak reducing agent, but its interference in modern methods is minimal and not as significant as ascorbic acid.

• d) Hemoglobin: Hemoglobin itself does not significantly inhibit the chromogen reaction. However, hemolysis can cause spectral interference or release intracellular substances like glutathione (a reducing agent) which may cause a slight negative interference.

Before a standard glucose tolerance test (OGTT), the patient should consume a high-carbohydrate diet (≥150 g/day) for 3 days.
This ensures adequate glycogen stores and normal insulin response, providing an accurate assessment of glucose metabolism.

Why the other options are incorrect:

• a) A low carbohydrate diet for 3 days: This is incorrect and would be detrimental. A low-carb diet can lead to “starvation diabetes” or physiological insulin resistance, causing an exaggerated blood glucose response and potentially a false-positive diagnosis of diabetes.

• b) Fasting for 48 hours prior to testing: This is excessive. The required fasting period is only 8-14 hours. Prolonged fasting can also lead to physiological insulin resistance and ketosis, invalidating the test.

• d) Bed rest for 3 days: Physical inactivity can impair glucose metabolism, but enforced bed rest is not a standard requirement for the test. Patients are, however, advised to avoid strenuous exercise prior to the test.

Monosaccharides (e.g., glucose, fructose, galactose) are the simplest carbohydrates and serve as the building blocks for disaccharides and polysaccharides.

Why the other options are incorrect:

• b) Disaccharide: This is a molecule made from two basic units (monosaccharides).

• c) Polysaccharide: This is a polymer made from many basic units (monosaccharides).

• d) Glycoprotein: This is a complex molecule that contains carbohydrates (monosaccharides) attached to a protein backbone.

In the hexokinase method, glucose is first converted to glucose-6-phosphate (G6P) by hexokinase.
Then G6P is oxidized by glucose-6-phosphate dehydrogenase, reducing NAD⁺ to NADH.
The formation of NADH is measured spectrophotometrically at 340 nm, which reflects the glucose concentration.

Why the other options are incorrect:

• a) The amount of hydrogen peroxide produced: This is the end product measured in the glucose oxidase method, not the hexokinase method.

• c) The condensation of glucose with an aromatic amine: This describes the chemistry of older, non-enzymatic methods like the o-toluidine method.

• d) The amount of glucose combined with bromcresol purple: Bromcresol purple is a pH indicator, not a reagent used in standard enzymatic glucose methods like the hexokinase assay.

Glucose-6-phosphate is converted back to glucose by glucose-6-phosphatase, an enzyme present in liver and kidney cells.
Muscle and adipose tissue lack this enzyme, so glucose-6-phosphate is used locally for energy rather than released into the blood.

Why the other options are incorrect:

• a) Muscle cells: Lack glucose-6-phosphatase. They retain glucose-6-phosphate for their own energy use (glycolysis) and cannot release free glucose into the blood.

• c) Red blood cells: Do not have mitochondria or complex metabolic pathways like gluconeogenesis and lack glucose-6-phosphatase.

• d) Adipose tissue: Uses glucose for lipid synthesis and energy, but it lacks glucose-6-phosphatase and cannot release free glucose into the bloodstream.

Glucose is transported from the blood into the cerebrospinal fluid (CSF) via facilitated diffusion across the blood-brain barrier and the choroid plexus. This process does not concentrate glucose; instead, it results in a CSF glucose level that is approximately 50-80% of the blood glucose level in a healthy individual.

Given a blood glucose of 80 mg/dL, the expected CSF glucose would be:

• 80 mg/dL × 0.6 (60%) ≈ 48 mg/dL

• 80 mg/dL × 0.7 (70%) ≈ 56 mg/dL

Therefore, a value around 50 mg/dL (2.3 mmol/L) falls perfectly within this expected range and is the most likely result.

Why the other options are incorrect:

• a) 25 mg/dL (1.4 mmol/L): This value is too low (only ~30% of blood glucose). It would be highly suggestive of a pathological condition, such as bacterial meningitis or hypoglycorrhachia, where glucose transport into the CSF is impaired or where cells (like bacteria or leukocytes) are consuming the glucose.

• c) 100 mg/dL (5.5 mmol/L): This value is higher than the blood glucose level, which is physiologically impossible under normal circumstances. Glucose is not actively transported into the CSF to create a concentration gradient.

• d) 150 mg/dL (8.3 mmol/L): This value is nearly double the blood glucose level, which is also impossible and would indicate a severe error in the laboratory measurement.

Phosphofructokinase-1 (PFK-1) catalyzes the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate.
It is the rate-limiting step of glycolysis, highly regulated by ATP, AMP, and citrate to control the pathway’s flux according to cellular energy needs.

Why the other options are incorrect:

• a) Hexokinase: This is the first enzyme of glycolysis and is regulated, but it is not considered the primary rate-limiting step. Its product, glucose-6-phosphate, can enter other pathways.

• c) Pyruvate kinase: This is the third regulated enzyme of glycolysis, but it is not the main rate-limiting step. It catalyzes the final ATP-generating step.

• d) Glucose-6-phosphate dehydrogenase: This is the rate-limiting enzyme of the pentose phosphate pathway, not glycolysis.

Under anaerobic conditions, cells lack sufficient oxygen for the mitochondria to oxidize pyruvate.
Pyruvate is reduced to lactate by lactate dehydrogenase, regenerating NAD⁺ to allow glycolysis to continue producing ATP.

Why the other options are incorrect:

• a) Acetyl-CoA: This conversion, catalyzed by the pyruvate dehydrogenase complex, requires oxygen and occurs in the mitochondria during aerobic conditions.

• c) Citrate: Citrate is formed in the Krebs cycle from the condensation of acetyl-CoA and oxaloacetate, an aerobic process.

• d) Oxaloacetate: Pyruvate can be carboxylated to form oxaloacetate (anaplerotic reaction), but this is not the primary or defining fate during anaerobic glycolysis. The dominant pathway is reduction to lactate.

Gluconeogenesis synthesizes glucose from non-carbohydrate precursors like lactate, glycerol, and amino acids, primarily to maintain blood glucose levels during fasting.
It is essentially the reverse of glycolysis, with some bypass reactions.

Why the other options are incorrect:

• a) Convert glucose to glycogen: This process is called glycogenesis (glycogen synthesis).

• c) Produce pyruvate from glucose: This describes glycolysis.

• d) Convert glycogen to glucose: This process is called glycogenolysis (glycogen breakdown).

Pregnant women with polyuria, polydipsia, or unexplained weight loss may have gestational diabetes.
A glucose tolerance test (OGTT) is the recommended diagnostic test to assess how the body handles a glucose load during pregnancy.

Why the other options are incorrect:

• a) Tolbutamide Test: This is an outdated test used to assess insulin secretion in the diagnosis of insulinomas (pancreatic beta-cell tumors), not for screening or diagnosing diabetes in pregnancy.

• b) Lactose Tolerance Test: This test is used to diagnose lactose intolerance (lactase deficiency), which causes bloating, diarrhea, and abdominal cramps after dairy consumption, not thirst and polyuria.

• c) Epinephrine Tolerance Test: This is not a standard test for diabetes. Epinephrine can be used to assess glycogen storage diseases or other metabolic disorders, but it is not relevant for diagnosing diabetes.