Protein Digestion and Absorption — MCQs

10 questions

A 35-year-old Caucasian female presents with anemia, malaise, bloating, and diarrhea. Past genetic testing revealed that this patient carries the HLA-DQ2 allele. The physician suspects that the patient's presentation is dietary in cause. Which of the following findings would definitively confirm this diagnosis?

Which of the following is not elevated in a child presenting with jaundice, icterus, pruritus and clay-colored stools?

A patient is found to have sun-sensitive dermatitis, diarrhea, and dementia. He must be suffering from the deficiency of which of the following?

In Cystinuria, all of the following amino acids are excreted in urine, except:-

Because free ammonia in the blood is toxic to the body, it is transported in which of the following non-toxic forms?

Which of the following is an example of an exopeptidase?

Destruction of fat in acute pancreatitis is due to ?

Creatinine is formed from -

The limiting amino acid in maize is

Q10

Which amino acid in Jowar is responsible for its pellagragenic effect?

Protein Digestion and Absorption Indian Medical PG Practice Questions and MCQs

Question 1: A 35-year-old Caucasian female presents with anemia, malaise, bloating, and diarrhea. Past genetic testing revealed that this patient carries the HLA-DQ2 allele. The physician suspects that the patient's presentation is dietary in cause. Which of the following findings would definitively confirm this diagnosis?

A. CT scan showing inflammation of the small bowel wall
B. Biopsy of the duodenum showing atrophy and blunting of villi (Correct Answer)
C. Biopsy of the colon showing epithelial cell apoptosis
D. Esophageal endoscopy showing lower esophageal metaplasia
E. Liver biopsy showing apoptosis of hepatocytes

Explanation: ***Biopsy of the duodenum showing atrophy and blunting of villi*** - This finding is the **gold standard** for diagnosing **celiac disease**, which aligns with the patient's symptoms (anemia, malaise, bloating, diarrhea), genetic predisposition (HLA-DQ2 allele), and suspected dietary cause. - The characteristic **villous atrophy** and **crypt hyperplasia** seen in duodenal biopsies are hallmark pathological changes in celiac disease due to gluten exposure. *CT scan showing inflammation of the small bowel wall* - While a CT scan can show **inflammation**, it is not specific enough to definitively diagnose celiac disease, as many other conditions can cause small bowel inflammation. - It does not provide the **histopathological detail** necessary to confirm villous atrophy, which is key for celiac diagnosis. *Biopsy of the colon showing epithelial cell apoptosis* - **Epithelial cell apoptosis** in the colon is not a primary diagnostic feature of celiac disease, which primarily affects the **small intestine**. - This finding might be associated with other inflammatory bowel conditions or infections, not gluten-induced enteropathy. *Esophageal endoscopy showing lower esophageal metaplasia* - **Lower esophageal metaplasia**, or **Barrett's esophagus**, is a pre-cancerous condition of the esophagus, often caused by chronic acid reflux. - This finding is unrelated to celiac disease and does not explain the patient's gastrointestinal symptoms or genetic predisposition. *Liver biopsy showing apoptosis of hepatocytes* - **Apoptosis of hepatocytes** (liver cell death) would indicate liver damage or disease, such as hepatitis or drug-induced injury. - While celiac disease can sometimes have **hepatic manifestations**, liver apoptosis is not a primary or definitive diagnostic criterion for celiac disease itself.

Question 2: Which of the following is not elevated in a child presenting with jaundice, icterus, pruritus and clay-colored stools?

A. Serum amylase
B. Glutamate dehydrogenase
C. Lactate dehydrogenase
D. Creatine kinase (Correct Answer)

Explanation: ***Creatine kinase*** - **Creatine kinase (CK)** is a muscle enzyme found primarily in cardiac and skeletal muscle - CK elevation indicates **muscle injury** (rhabdomyolysis, myositis, myocardial infarction), NOT hepatobiliary disease - In **obstructive cholestasis** (jaundice, pruritus, clay stools), CK remains **normal** - **This is the correct answer** - CK is not elevated in cholestatic liver disease *Serum amylase* - May be **mildly elevated** if biliary obstruction causes **ampullary obstruction** or secondary pancreatic duct involvement - In pediatric biliary atresia or choledochal cyst, amylase is usually normal unless there is concurrent **pancreatitis** - Less specific than hepatobiliary markers but can be elevated in complicated cases *Glutamate dehydrogenase* - **GLDH** is a mitochondrial liver enzyme that reflects **hepatocellular necrosis** - In **prolonged cholestasis**, secondary hepatocellular damage occurs, leading to GLDH elevation - Elevated in biliary atresia with progressive liver damage *Lactate dehydrogenase* - **LDH** is a non-specific enzyme found in liver, RBCs, and many other tissues - Elevated in **hepatocellular injury**, hemolysis, and tissue damage - Can be elevated in cholestatic liver disease with hepatocyte damage or associated hemolysis

Question 3: A patient is found to have sun-sensitive dermatitis, diarrhea, and dementia. He must be suffering from the deficiency of which of the following?

A. Iron
B. Riboflavin
C. Niacin (Correct Answer)
D. Folic acid

Explanation: ***Niacin*** - The combination of **sun-sensitive dermatitis**, **diarrhea**, and **dementia** is the classic triad of symptoms for **pellagra**, a deficiency of **niacin (vitamin B3)**. - Niacin is crucial for **NAD+** and **NADP+** synthesis, which are essential coenzymes in over 400 enzymatic reactions, particularly in energy metabolism and DNA repair. *Riboflavin* - Deficiency of **riboflavin (vitamin B2)** typically presents with **cheilosis**, **angular stomatitis**, and **glossitis**, not the dermatological, gastrointestinal, and neurological issues described. - **Ariboflavinosis** can also cause oily, scaly rashes and light sensitivity, but not the pellagra triad. *Iron* - **Iron deficiency** leads to **anemia**, characterized by fatigue, pallor, and weakness. - While it can affect cognitive function (e.g., **"brain fog"** and **pica**), it does not cause the specific skin rash or chronic diarrhea associated with pellagra. *Folic acid* - **Folic acid deficiency** primarily causes **macrocytic anemia** and can lead to **neural tube defects** in developing fetuses. - Neurological symptoms like depression and cognitive impairment can occur, but it does not cause the characteristic **dermatitis** or **diarrhea** seen in pellagra.

Question 4: In Cystinuria, all of the following amino acids are excreted in urine, except:-

A. Cystine
B. Leucine (Correct Answer)
C. Ornithine
D. Arginine

Explanation: ***Leucine*** - Cystinuria is a disorder characterized by impaired transport of **dibasic amino acids** and **cystine**, not neutral amino acids like leucine. - Therefore, **leucine** would be properly reabsorbed and not significantly excreted in the urine. *Cystine* - **Cystine** is one of the four amino acids whose reabsorption is impaired in cystinuria, leading to its excessive excretion in urine and potential **kidney stone** formation. - The defect is in the **renal tubular transport system** for dibasic amino acids and cystine. *Ornithine* - **Ornithine** is a **dibasic amino acid** and its renal reabsorption is defective in cystinuria. - Like cystine, ornithine is excessively excreted in the urine due to the shared transport system. *Arginine* - **Arginine** is also a **dibasic amino acid** whose renal reabsorption is impaired in cystinuria. - Its presence in the urine is increased, along with cystine, ornithine, and lysine, forming the classic pattern of amino acid excretion in this condition.

Question 5: Because free ammonia in the blood is toxic to the body, it is transported in which of the following non-toxic forms?

A. Glutamine and urea
B. Alanine and glutamine (Correct Answer)
C. Phenylalanine and methionine
D. Histidine and urea

Explanation: ***Alanine and glutamine*** - **Glutamine** is the primary transporter of ammonia from most peripheral tissues to the liver and kidneys, where it can be safely released and processed. - **Alanine** transports ammonia from muscles to the liver via the glucose-alanine cycle, allowing for hepatic urea synthesis and glucose production. *Glutamine and urea* - While **glutamine** is a major ammonia transporter, **urea** is the *end product* of ammonia detoxification and is primarily synthesized in the liver for excretion. - Urea itself is not a transport form of ammonia *within* the blood before its synthesis; rather, it is the waste product. *Phenylalanine and methionine* - **Phenylalanine** and **methionine** are essential amino acids involved in protein synthesis and various metabolic pathways. - They do not serve as significant carriers for the transport of toxic free ammonia in the bloodstream. *Histidine and urea* - **Histidine** is an amino acid involved in protein synthesis and histamine production, but not primarily in ammonia transport. - As mentioned, **urea** is the final excretory form of detoxified ammonia, not a transport form within the blood.

Question 6: Which of the following is an example of an exopeptidase?

A. Trypsin
B. Chymotrypsin
C. Elastase
D. Carboxypeptidases (Correct Answer)

Explanation: ***Carboxypeptidases*** - **Carboxypeptidases** are enzymes that cleave the **C-terminal** (carboxyl end) amino acid from a polypeptide chain, making them a type of exopeptidase. - They are crucial in protein digestion, releasing individual amino acids from the end of protein chains. *Trypsin* - **Trypsin** is an **endopeptidase** that cleaves peptide bonds within protein chains, specifically at the carboxyl side of **lysine** or **arginine** residues. - It does not cleave amino acids from the ends of polypeptide chains. *Chymotrypsin* - **Chymotrypsin** is an **endopeptidase** that cleaves peptide bonds within a polypeptide chain, primarily at the carboxyl side of **tyrosine**, **tryptophan**, or **phenylalanine**. - Its action is internal to the protein sequence, not at the termini. *Elastase* - **Elastase** is also an **endopeptidase** that cleaves peptide bonds internally, specifically targeting small, uncharged amino acid residues like **alanine**, **glycine**, and **valine**. - Its primary role is to break down elastin, an elastic protein in connective tissues, but it does so by internal cleavage.

Question 7: Destruction of fat in acute pancreatitis is due to ?

A. Lipase (Correct Answer)
B. Trypsin
C. Secretin
D. Elastase

Explanation: ***Lipase*** - **Lipase** is the primary enzyme responsible for **fat necrosis** in acute pancreatitis. - It hydrolyzes triglycerides into **fatty acids and glycerol**. - The released fatty acids combine with calcium to form **soap (saponification)**, visible as chalky white areas of fat necrosis. - This is a characteristic pathological finding in acute pancreatitis. *Trypsin* - **Trypsin** is a proteolytic enzyme that breaks down **proteins**, not fats. - While trypsin activation is central to the pathogenesis of pancreatitis (it activates other pancreatic enzymes), **it does not directly destroy fat**. - Its primary role is in the autodigestion of pancreatic tissue and activation of the enzymatic cascade. *Secretin* - **Secretin** is a hormone that regulates pancreatic bicarbonate secretion and gastric acid secretion. - It plays **no role** in the enzymatic destruction of fat in acute pancreatitis. *Elastase* - **Elastase** is a protease that digests elastin in blood vessel walls and other proteins. - It contributes to vascular damage and hemorrhage in pancreatitis but **does not directly destroy fat**. - Fat necrosis is specifically caused by lipolytic enzymes, not proteases.

Question 8: Creatinine is formed from -

A. Creatine (Correct Answer)
B. Lysine
C. Leucine
D. Histidine

Explanation: ***Creatine*** - **Creatinine** is a waste product formed from the non-enzymatic, irreversible degradation of **creatine** and **creatine phosphate**, primarily in muscles. - **Creatine** itself is synthesized endogenously from three amino acids: **glycine, arginine, and methionine** (as S-adenosylmethionine) through a two-step enzymatic process in the kidney and liver. - The amount of creatinine produced daily is relatively constant and directly proportional to an individual's **muscle mass**, making it a useful marker for renal function. *Lysine* - **Lysine** is an **essential amino acid** and a precursor for various compounds like **carnitine** but is not involved in creatinine or creatine formation. - Deficiency can lead to impaired protein synthesis but does not impact creatinine levels. *Leucine* - **Leucine** is another **essential amino acid** and a **branched-chain amino acid (BCAA)** crucial for muscle protein synthesis and repair. - It does not serve as a direct precursor for creatinine or creatine. *Histidine* - **Histidine** is an **essential amino acid** and a precursor for **histamine** and other important compounds, but not creatinine or creatine. - It plays roles in immune response and gastric acid secretion.

Question 9: The limiting amino acid in maize is

A. Phenylalanine
B. Tryptophan
C. Lysine (Correct Answer)
D. Cysteine

Explanation: ***Lysine*** - **Lysine** is the **primary limiting amino acid** in maize (corn). - This means that maize contains a relatively low amount of lysine compared to the body's requirements, which limits the overall protein quality and biological value when maize is the sole protein source. - **Quality Protein Maize (QPM)**, developed through breeding programs, has significantly increased levels of **lysine** and **tryptophan** to improve nutritional quality. - Lysine deficiency in maize-based diets can lead to **pellagra** when combined with low niacin intake, as tryptophan (also deficient) is a precursor for niacin synthesis. *Tryptophan* - **Tryptophan** is the **second limiting amino acid** in maize, but not the primary one. - While maize is relatively low in tryptophan, the lysine deficiency is more pronounced and nutritionally significant. - Tryptophan is important as a precursor for **niacin (vitamin B3)**, **serotonin**, and **melatonin**. *Phenylalanine* - **Phenylalanine** is an **essential amino acid** but is generally present in sufficient quantities in maize and is **not considered a limiting factor**. - It serves as a precursor for **tyrosine**, **dopamine**, **epinephrine**, and **norepinephrine**. *Cysteine* - **Cysteine** is a **non-essential (conditionally essential) amino acid** in humans, as the body can synthesize it from methionine. - Therefore, it is **not considered a limiting amino acid** for dietary protein quality assessment.

Question 10: Which amino acid in Jowar is responsible for its pellagragenic effect?

A. Leucine (Correct Answer)
B. Lysine
C. Tryptophan
D. Methionine

Explanation: ***Leucine*** - A high intake of **leucine**, an essential amino acid, interferes with the metabolism of **tryptophan** and niacin, leading to **pellagra**. - Jowar (sorghum) contains high levels of leucine, which, when it forms a major part of the diet, can induce **niacin deficiency**. *Lysine* - Lysine is an essential amino acid and is generally considered to be in **limited supply** in many cereal grains, making it a desirable amino acid to increase in diets. - It does not directly contribute to the pellagragenic effect; rather, a deficiency in lysine can be a nutritional concern. *Tryptophan* - Tryptophan is a **precursor to niacin (Vitamin B3)** in the body; a deficiency in tryptophan can lead to pellagra. - The high leucine content in jowar interferes with the conversion of tryptophan to niacin, thus exacerbating niacin deficiency. *Methionine* - Methionine is an **essential sulfur-containing amino acid** important for various metabolic functions and protein synthesis. - It is not directly implicated in the pellagragenic effect associated with high jowar consumption.

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