FMGE 2017 — Biochemistry
4 Previous Year Questions with Answers & Explanations
Vitamin K leads to?
Colipase is found in?
Which of the following has a polygenic pattern of inheritance?
Wernicke's encephalopathy is due to deficiency of:
FMGE 2017 - Biochemistry FMGE Practice Questions and MCQs
Question 1: Vitamin K leads to?
- A. β-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X
- B. α-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X
- C. γ-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X
- D. γ-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X (Correct Answer)
Explanation: ***γ-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X*** - Vitamin K acts as a **cofactor** for the enzyme **γ-glutamyl carboxylase**, which is essential for the post-translational modification of specific clotting factors. - This modification involves adding a **carboxyl group** to the **gamma-carbon** of certain **glutamic acid residues** within coagulation factors II (prothrombin), VII, IX, and X, converting them to **γ-carboxyglutamic acid (Gla) residues**. - These Gla residues enable the clotting factors to bind **calcium ions**, which is critical for their activation and proper function in the coagulation cascade. *β-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X* - This option incorrectly states **beta-carboxylation**, whereas the correct process is **gamma-carboxylation**. - The specific carbon atom modified (gamma position) is crucial for the proper function of the clotting factors. *γ-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X* - This option incorrectly identifies the amino acid residue involved as **aspartic acid**. - Vitamin K-dependent carboxylation specifically modifies **glutamic acid residues**, not aspartic acid. *α-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X* - This option incorrectly specifies both the carbon position involved (**alpha-carboxylation**) and the amino acid residue (**aspartic acid**). - The correct process is **gamma-carboxylation** of **glutamic acid residues**.
Question 2: Colipase is found in?
- A. Pancreatic juice (Correct Answer)
- B. Saliva
- C. Bile
- D. Succus entericus
Explanation: ***Pancreatic juice*** - **Colipase** is a co-enzyme secreted by the **pancreas** that is essential for the activity of pancreatic lipase. - It helps **pancreatic lipase** anchor to the surface of fat globules, preventing its inactivation by bile salts and facilitating fat digestion. *Saliva* - Saliva primarily contains **alpha-amylase** (ptyalin) for carbohydrate digestion and **lingual lipase** for initial fat digestion. - It does not contain colipase. *Bile* - **Bile** is produced by the liver and stored in the gallbladder, primarily aiding in fat emulsification. - It contains **bile salts**, cholesterol, bilirubin, and phospholipids but not digestive enzymes like colipase. *Succus entericus* - **Succus entericus**, or intestinal juice, is secreted by the small intestine and contains enzymes like **sucrase**, **maltase**, **lactase**, and peptidases. - It does not contain colipase, which is specifically a pancreatic enzyme.
Question 3: Which of the following has a polygenic pattern of inheritance?
- A. Diabetes mellitus (Correct Answer)
- B. Familial hypercholesterolemia
- C. Resistant rickets
- D. G6PD
Explanation: **Diabetes mellitus** - **Type 2 Diabetes Mellitus**, the most common form, is a classic example of a **polygenic disease**, meaning it results from the interaction of multiple genes and environmental factors. - Many genes contribute to aspects like **insulin resistance** and **beta-cell dysfunction**, leading to the disease. *Familial hypercholesterolemia* - This condition is inherited in an **autosomal dominant** pattern, primarily due to mutations in a single gene, most commonly the **LDL receptor gene**. - While other genes can influence cholesterol levels, the severe form of familial hypercholesterolemia is typically **monogenic**. *Resistant rickets* - **X-linked hypophosphatemia**, also known as vitamin D-resistant rickets, is inherited in an **X-linked dominant** pattern. - It is caused by mutations in the **PHEX gene**, which affects phosphate reabsorption in the kidneys. *G6PD* - **Glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency)** is an **X-linked recessive** disorder. - It is caused by mutations in a single gene on the X chromosome, making it a **monogenic** condition.
Question 4: Wernicke's encephalopathy is due to deficiency of:
- A. B6
- B. Thiamine (Correct Answer)
- C. B12
- D. Niacin
Explanation: ***Thiamine*** - **Wernicke's encephalopathy** is a serious neurological disorder directly caused by a severe deficiency of **thiamine (vitamin B1)**. - Thiamine is crucial for **glucose metabolism** in the brain; its deficiency impairs energy production, leading to neuronal damage and the characteristic symptoms of confusion, ataxia, and ophthalmoplegia. *B6* - Deficiency of **vitamin B6 (pyridoxine)** can cause peripheral neuropathy, seizures, and microcytic anemia. - It is not the primary cause of the acute neurological syndrome seen in Wernicke's encephalopathy. *B12* - Deficiency of **vitamin B12 (cobalamin)** is associated with megaloblastic anemia and subacute combined degeneration of the spinal cord. - While it can cause neurological symptoms, they differ from the specific triad of Wernicke's encephalopathy. *Niacin* - Deficiency of **niacin (vitamin B3)** causes **pellagra**, characterized by dermatitis, diarrhea, and dementia. - Although it involves neurological symptoms (dementia), the presentation is distinct from Wernicke's encephalopathy.