Digestion and Absorption — MCQs
In a patient with lipoprotein lipase deficiency, which of the following is increased following a fatty meal?
Trypsinogen is converted to trypsin by?
Which of the following reagents would be most useful in determining the N-terminal amino acid of a polypeptide?
Which transporter is responsible for the absorption of glucose in the intestine when a person is given Oral Rehydration Solution (ORS)?
A young boy presents with failure to thrive. Biochemical analysis of a duodenal aspirate after a meal reveals a deficiency of enteropeptidase (enterokinase). Which one of the following digestive enzymes would be affected by this deficiency?
A 69-year-old man is given a multivitamin containing vitamin B12. He feels well, reports no symptoms, and his physical examination is normal. His complete blood count is completely normal. Which of the following statements about vitamin B12 absorption is correct?
A baby boy is brought to the hospital because of convulsions. In the course of workup, his body temperature and plasma glucose are normal, but his CSF glucose is 12 mg/dL. A possible explanation is:
What is the primary glycerol-containing absorption product of dietary triglycerides in the gut?
Gastric acid secretion is stimulated during several phases associated with the ingestion and digestion of a meal. Which phase is primarily responsible for the majority of acid secretion?
Through which of the following means of transport is folic acid absorbed in the proximal jejunum?
Digestion and Absorption Indian Medical PG Practice Questions and MCQs
Question 1: In a patient with lipoprotein lipase deficiency, which of the following is increased following a fatty meal?
- A. Chylomicron (Correct Answer)
- B. LDL
- C. HDL
- D. Apo-A
Explanation: ***Chylomicron*** - Lipoprotein lipase (LPL) is essential for the breakdown of **chylomicrons** in the bloodstream. A deficiency in LPL means chylomicrons cannot be cleared effectively. - After a **fatty meal**, the body absorbs dietary fats as chylomicrons. Without functional LPL, these chylomicrons accumulate in the plasma, leading to **marked elevation** of chylomicron levels. - This results in **lipemic (milky) serum**, a characteristic finding in Type I hyperlipoproteinemia. *LDL* - **LDL (Low-Density Lipoprotein)** levels are primarily affected by the metabolism of VLDL (Very Low-Density Lipoprotein), which is a separate pathway from chylomicron metabolism. - LPL deficiency specifically impacts chylomicron clearance, not directly causing an increase in LDL. In fact, LDL may be normal or even low in severe hypertriglyceridemia. *HDL* - **HDL (High-Density Lipoprotein)** is involved in reverse cholesterol transport and is typically **decreased** (not increased) in LPL deficiency. - During normal lipolysis by LPL, surface components from chylomicrons are transferred to HDL. In LPL deficiency, this process is impaired, leading to **reduced HDL levels**. *Apo-A* - **Apolipoprotein A-I (Apo-AI)** is the primary apolipoprotein found on HDL particles and is crucial for HDL formation and function. - Since HDL levels are decreased in LPL deficiency, Apo-AI levels would also be decreased (not increased) following a fatty meal.
Question 2: Trypsinogen is converted to trypsin by?
- A. Combination of 2 molecules of trypsinogen
- B. Phosphorylation
- C. Addition of alkyl group
- D. Removal of specific amino acids from trypsinogen (Correct Answer)
Explanation: ***Removal of specific amino acids from trypsinogen*** - Trypsinogen is an **inactive zymogen** that is activated by the enzymatic cleavage of a **short N-terminal peptide**. - This cleavage event, primarily catalyzed by **enteropeptidase** (or trypsin itself), transforms trypsinogen into active **trypsin**, a process known as **proteolytic activation**. *Combination of 2 molecules of trypsinogen* - The activation of trypsinogen to trypsin is a **unimolecular conformational change** followed by proteolytic cleavage, not a combination reaction between two zymogen molecules. - While trypsin can activate other trypsinogen molecules, the initial activation does not involve the physical combination of two zymogen molecules. *Phosphorylation* - **Phosphorylation** is a common regulatory mechanism in proteins but is not the primary method for activating inactive trypsinogen. - Trypsinogen activation relies on a **proteolytic cleavage event**, rather than the addition of a phosphate group. *Addition of alkyl group* - The addition of an **alkyl group** is not a known mechanism for the physiological activation of trypsinogen. - Enzymatic activation typically involves **hydrolysis of peptide bonds** or other specific post-translational modifications.
Question 3: Which of the following reagents would be most useful in determining the N-terminal amino acid of a polypeptide?
- A. Trypsin
- B. Carboxypeptidase
- C. Phenylisothiocyanate (Correct Answer)
- D. Cyanogen bromide
Explanation: ***Phenylisothiocyanate*** - **Phenylisothiocyanate** (PITC), also known as Edman's reagent, is used in the **Edman degradation** method to identify the N-terminal amino acid. - It sequentially cleaves the **N-terminal amino acid** without hydrolyzing the rest of the peptide chain, allowing for identification by chromatography. *Trypsin* - **Trypsin** is a protease that cleaves peptide bonds at the carboxyl side of **lysine** and **arginine** residues. - It is used for peptide fragmentation, not for determining the N-terminal amino acid. *Carboxypeptidase* - **Carboxypeptidases** are exopeptidases that cleave amino acids from the **C-terminal end** of a polypeptide chain. - They are used to identify the C-terminal amino acid, not the N-terminal. *Cyanogen bromide* - **Cyanogen bromide (CNBr)** is a chemical reagent that specifically cleaves peptide bonds on the C-terminal side of **methionine** residues. - It is used for specific peptide fragmentation and not for N-terminal sequencing.
Question 4: Which transporter is responsible for the absorption of glucose in the intestine when a person is given Oral Rehydration Solution (ORS)?
- A. GLP-1
- B. SGLT-2
- C. SGLT-1 (Correct Answer)
- D. GLUT-1
Explanation: ***SGLT-1 (Sodium-Glucose cotransporter 1)*** - **SGLT-1** is the primary transporter responsible for the **active absorption of glucose** and galactose from the intestinal lumen into enterocytes, utilizing the electrochemical gradient of sodium. - The mechanism of **ORS** relies on the co-transport of sodium and glucose via SGLT-1, which also facilitates the osmotic movement of water, making it effective for rehydration. *GLP-1 (Glucagon-like peptide-1)* - **GLP-1** is an **incretin hormone** that stimulates insulin secretion and inhibits glucagon release from the pancreas, playing a role in glucose homeostasis. - It is not a transporter for glucose absorption from the intestine but rather a **signaling molecule** involved in metabolic regulation. *SGLT-2 (Sodium-Glucose cotransporter 2)* - **SGLT-2** is predominantly found in the **renal tubules**, where it is responsible for the majority of glucose reabsorption from the filtrate back into the bloodstream. - While it is a glucose transporter, its primary role is in the **kidney**, not in intestinal glucose absorption. *GLUT-1 (Glucose Transporter 1)* - **GLUT-1** is found in all cell types and is primarily responsible for **basal glucose uptake** by cells, particularly high in red blood cells and at the blood-brain barrier. - It is a **facilitated diffusion transporter** and is not the primary mechanism for glucose absorption from the intestinal lumen.
Question 5: A young boy presents with failure to thrive. Biochemical analysis of a duodenal aspirate after a meal reveals a deficiency of enteropeptidase (enterokinase). Which one of the following digestive enzymes would be affected by this deficiency?
- A. Amylase
- B. Pepsin
- C. Trypsin (Correct Answer)
- D. Lactase
Explanation: ***Trypsin*** - Enteropeptidase (enterokinase) is crucial for activating **trypsinogen** into its active form, **trypsin**. Without active trypsin, the entire cascade of pancreatic protease activation is disrupted. - Trypsin then activates other pancreatic proteases like chymotrypsin, elastase, and carboxypeptidases, all of which are essential for **protein digestion** in the small intestine. *Amylase* - **Amylase** is a carbohydrate-digesting enzyme, primarily involved in breaking down starch. Its activity is independent of enteropeptidase. - **Pancreatic amylase** is secreted in its active form and does not require proteolytic cleavage by trypsin for activation. *Pepsin* - **Pepsin** is an enzyme found in the stomach that initiates protein digestion. It is activated by **hydrochloric acid** from its inactive precursor, pepsinogen. - Its activity is entirely independent of enteropeptidase, which functions in the duodenum. *Lactase* - **Lactase** is a brush border enzyme located in the small intestine that digests the disaccharide **lactose** into glucose and galactose. - Its production and activity are genetically regulated and not dependent on the protein-digesting enzymes or enteropeptidase.
Question 6: A 69-year-old man is given a multivitamin containing vitamin B12. He feels well, reports no symptoms, and his physical examination is normal. His complete blood count is completely normal. Which of the following statements about vitamin B12 absorption is correct?
- A. absorbed primarily in the distal ileum
- B. not significantly affected by folic acid deficiency
- C. best absorbed in the presence of intrinsic factor (Correct Answer)
- D. absorbed equally well with or without intrinsic factor
Explanation: ***best absorbed in the presence of intrinsic factor*** - **Intrinsic factor** is a glycoprotein secreted by gastric parietal cells that binds to vitamin B12, forming a complex essential for its absorption in the **terminal ileum**. - This is the **most complete answer** as it identifies the critical requirement for efficient B12 absorption. - In conditions like **pernicious anemia**, where intrinsic factor is deficient, vitamin B12 absorption is severely impaired, leading to **megaloblastic anemia** and neurological symptoms. - Only about **1-2% of oral B12** can be absorbed by passive diffusion without intrinsic factor, which is insufficient for physiological needs. *absorbed primarily in the distal ileum* - While this statement is **technically correct** (B12 is indeed absorbed in the terminal/distal ileum), it is **incomplete** as it does not mention the essential role of intrinsic factor. - The **best answer** identifies not just the location but the critical mechanism (intrinsic factor requirement). - Without specifying intrinsic factor, this option misses the most clinically important aspect of B12 absorption. *not significantly affected by folic acid deficiency* - This is **incorrect** as **vitamin B12** and **folic acid** metabolism are intricately linked in one-carbon metabolism. - Both are crucial for DNA synthesis, particularly in rapidly dividing cells like bone marrow. - Vitamin B12 (as methylcobalamin) is required to convert 5-methyl-tetrahydrofolate to tetrahydrofolate, allowing folate to participate in DNA synthesis. - Deficiency in either can lead to **megaloblastic anemia** with similar hematologic findings. *absorbed equally well with or without intrinsic factor* - This statement is **incorrect** as **intrinsic factor is essential** for efficient vitamin B12 absorption. - The B12-intrinsic factor complex binds to specific receptors (cubilin) in the terminal ileum for absorption. - Without intrinsic factor, only minimal passive diffusion occurs (~1-2%), which is inadequate to meet daily requirements of approximately 2-3 mcg.
Question 7: A baby boy is brought to the hospital because of convulsions. In the course of workup, his body temperature and plasma glucose are normal, but his CSF glucose is 12 mg/dL. A possible explanation is:
- A. GLUT-1 45K deficiency in microglia
- B. GLUT 5 deficiency in cerebral capillaries
- C. SGLT 1 deficiency in astrocytes
- D. GLUT-1 55K deficiency in capillaries (Correct Answer)
- E. GLUT-3 deficiency in neurons
Explanation: ***GLUT-1 55K deficiency in capillaries*** - A CSF glucose of 12 mg/dL with normal plasma glucose strongly suggests a problem with **glucose transport across the blood-brain barrier (BBB)**. - The **GLUT-1 isoform (55K)** is the primary glucose transporter responsible for moving glucose from the blood into the brain across the **endothelial cells of the capillaries**, and its deficiency leads to profoundly low CSF glucose, causing seizures. *GLUT-1 45K deficiency in microglia* - The **GLUT-1 45K isoform** is found primarily on **astrocytes** and **neurons** in the brain, and while critical for neuronal glucose uptake, its deficiency alone would not cause such a profound drop in CSF glucose unless the 55K isoform in capillaries was also affected. - **Microglia** primarily express GLUT-5 and GLUT-3, but their function is not the primary determinant of CSF glucose levels. *GLUT 5 deficiency in cerebral capillaries* - **GLUT-5** is primarily a **fructose transporter** and is not the main glucose transporter in the brain or at the blood-brain barrier. - Its deficiency would not significantly impact **glucose transport** into the CSF. *GLUT-3 deficiency in neurons* - **GLUT-3** is the primary neuronal glucose transporter and is critical for neuronal metabolism. - However, GLUT-3 deficiency would affect **intracellular neuronal glucose uptake** rather than glucose transport across the BBB, so CSF glucose levels would remain normal while neurons might be energy-deprived. - The key finding of **low CSF glucose** indicates a problem at the **capillary level** (BBB), not at the neuronal uptake level. *SGLT 1 deficiency in astrocytes* - **SGLT1 (Sodium-Glucose Linked Transporter 1)** is an active glucose transporter primarily found in the **intestine** and **kidney**, and in some cells of the brain but not as the primary glucose transporter for the BBB. - Astrocytes primarily use **GLUT-1 (45K isoform)** for glucose uptake, not SGLT1, or for transport across capillaries.
Question 8: What is the primary glycerol-containing absorption product of dietary triglycerides in the gut?
- A. Fatty acids
- B. Mono acyl glycerol (Correct Answer)
- C. Diacyl glycerol
- D. Triglycerides
Explanation: ***Monoacylglycerol (2-MAG)*** - **Pancreatic lipase** hydrolyzes dietary triglycerides at positions 1 and 3, producing **2-monoacylglycerol** and **free fatty acids** as the two major products. - As the **primary glycerol-containing product**, 2-monoacylglycerol constitutes approximately **25% of digested lipid mass** and is essential for efficient **triglyceride resynthesis** in enterocytes. - Both 2-MAG and fatty acids are packaged into **mixed micelles** and co-absorbed, but 2-MAG is the predominant form containing the **intact glycerol backbone**. *Fatty acids* - **Free fatty acids** are co-absorbed with 2-monoacylglycerol in approximately a **2:1 molar ratio** (2 fatty acids per 1 monoacylglycerol). - While quantitatively significant, fatty acids do **not contain the glycerol backbone** structure. - Both products are required for efficient absorption and subsequent **triglyceride resynthesis** within enterocytes. *Diacylglycerol* - **Diacylglycerol** is a minor intermediate product during triglyceride hydrolysis. - It is rapidly hydrolyzed further by **pancreatic lipase** to yield **monoacylglycerol** and free fatty acids. - Not a significant absorption product in the intestinal lumen. *Triglycerides* - **Intact triglycerides** are too large and hydrophobic to be absorbed directly across the intestinal brush border. - They must first undergo **enzymatic hydrolysis** by pancreatic lipase into smaller absorbable units (2-MAG and fatty acids).
Question 9: Gastric acid secretion is stimulated during several phases associated with the ingestion and digestion of a meal. Which phase is primarily responsible for the majority of acid secretion?
- A. Cephalic
- B. Gastric (Correct Answer)
- C. Intestinal
- D. Interdigestive
Explanation: ***Gastric*** - The **gastric phase** is initiated by the presence of food in the stomach, leading to stomach distension and the presence of digested proteins and amino acids. - This phase accounts for approximately **60-70%** of total acid secretion, driven by local reflexes, vagovagal reflexes, and the release of gastrin. *Cephalic* - The **cephalic phase** is triggered by the **sight, smell, thought, or taste of food**, and accounts for about 20-30% of acid secretion. - It is mediated primarily by the **vagus nerve**, leading to the release of acetylcholine and gastrin. *Interdigestive* - The **interdigestive phase** refers to the period between meals when the stomach is empty. - During this phase, **basal acid secretion** is low and follows a circadian rhythm, primarily regulated by vagal tone and circulating gastrin. *Intestinal* - The **intestinal phase** begins once the chyme enters the small intestine and primarily functions to **inhibit** further gastric acid secretion. - While some stimulation can occur, inhibitory mechanisms, such as those from secretin, cholecystokinin (CCK), and gastric inhibitory peptide (GIP), dominate to regulate gastric emptying and acid production.
Question 10: Through which of the following means of transport is folic acid absorbed in the proximal jejunum?
- A. Facilitated diffusion
- B. Both active and passive transport (Correct Answer)
- C. Active transport
- D. Passive transport
Explanation: ***Both active and passive transport*** - **Folic acid** absorption in the **proximal jejunum** occurs through **both active and passive mechanisms**. - At **low physiological concentrations**, an **active carrier-mediated transport** system is primarily responsible, while at **higher concentrations** (e.g., from supplements), **passive diffusion** also plays a significant role. *Facilitated diffusion* - While a type of passive transport, **facilitated diffusion** alone does not fully encompass the entirety of folic acid absorption, especially at low concentrations. - It relies on a **concentration gradient** and **carrier proteins** but does not require metabolic energy. *Active transport* - **Active transport** is crucial for absorbing folic acid when its concentration is low in the gut lumen. - This process requires **energy** and specific **carrier proteins**, like the **reduced folate carrier (RFC)**, to transport folate against a concentration gradient. *Passive transport* - **Passive transport**, specifically **simple diffusion**, contributes to folic acid absorption but primarily at **high lumen concentrations**, such as after taking large doses of supplements. - It occurs down a **concentration gradient** and does not require energy or specific carriers.
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