Biochemistry
4 questionsWhat is the pH of the zwitterion as shown in the titration curve of glycine?
The PRIMARY mechanism of toxicity of which substance is NOT through Cytochrome C oxidase inhibition?
A 90 kg obese man is taking a carbohydrate-rich diet. Which of the following enzymes/intermediates will be elevated in him? 1. Malonyl CoA 2. Acetyl CoA Carboxylase 3. PDH 4. Citrate Lyase
Match the following blotting techniques with the type of biomolecule they detect: Blotting Technique Detects A. Southern blot 1. RNA B. Northern blot 2. Lipids C. Western blot 3. DNA D. Eastern blot 4. Protein
INI-CET 2025 - Biochemistry INI-CET Practice Questions and MCQs
Question 171: What is the pH of the zwitterion as shown in the titration curve of glycine?
- A. 6 (Correct Answer)
- B. 2
- C. 9
- D. 4.4
Explanation: ***Correct Option: 6*** - The pH of the zwitterion corresponds to the **isoelectric point (pI)**, the pH at which the amino acid has a net charge of zero. According to the curve, this occurs at pH 5.97, which is approximately 6. - The pI is calculated as the average of the two pKa values: **pI = (pKa1 + pKa2) / 2 = (2.34 + 9.60) / 2 = 5.97**. *Incorrect Option: 4.4* - At a pH of 4.4, which is between pKa1 and pI, the glycine molecule would have a net **positive charge** as the concentration of the cationic form ([NH3+-CH2-COOH]) would still be significant. - This value does not represent any specific inflection or equivalence point on the titration curve for glycine. *Incorrect Option: 2* - A pH of approximately 2 is near the **pKa1 (2.34)** of the carboxyl group, which is the point where the concentration of the fully protonated form equals the concentration of the zwitterion. - At this pH, the molecule has a net **positive charge**, as the amino group is fully protonated and the carboxyl group is only half-deprotonated. *Incorrect Option: 9* - A pH of approximately 9 is near the **pKa2 (9.60)** of the amino group, representing the buffering region for this group. - At this pH, the molecule has a net **negative charge**, as there is a significant amount of the fully deprotonated form ([NH2-CH2-COO-]) present.
Question 172: The PRIMARY mechanism of toxicity of which substance is NOT through Cytochrome C oxidase inhibition?
- A. Nitric oxide (NO)
- B. Cyanide (CN)
- C. Oligomycin
- D. Carbon monoxide (CO) (Correct Answer)
Explanation: ***Carbon monoxide (CO)*** - **Primary mechanism of toxicity** is through binding to hemoglobin forming **carboxyhemoglobin**, preventing oxygen transport - While CO can bind to **cytochrome oxidase**, its **dominant clinical effect** occurs at the oxygen delivery level, not cellular respiration *Hydrogen sulfide (H₂S)* - **Direct inhibitor** of cytochrome C oxidase by binding to the **heme iron center** - Functions similarly to cyanide, causing **histotoxic hypoxia** by blocking cellular oxygen utilization *Nitric oxide (NO)* - **Potent reversible inhibitor** of cytochrome C oxidase competing with oxygen at the active site - Physiological regulator of **cellular respiration** and important in hypoxia signaling pathways *Cyanide (CN⁻)* - **Classic inhibitor** of cytochrome C oxidase, binding with high affinity to the **oxidized cytochrome a₃** - Causes rapid **metabolic failure** by completely blocking the electron transport chain at Complex IV
Question 173: A 90 kg obese man is taking a carbohydrate-rich diet. Which of the following enzymes/intermediates will be elevated in him? 1. Malonyl CoA 2. Acetyl CoA Carboxylase 3. PDH 4. Citrate Lyase
- A. $1,2,3,4$ (Correct Answer)
- B. $1,2,3$
- C. $1,3,4$
- D. $2,3,4$
Explanation: ***Correct Answer: 1,2,3,4 (All of them)*** In an obese person consuming a carbohydrate-rich diet, **high insulin levels** drive maximum flux through **lipogenesis (fatty acid synthesis)**. This results in elevation of ALL enzymes and intermediates in the pathway: - **PDH (Pyruvate Dehydrogenase)**: Activated by insulin to convert pyruvate → Acetyl CoA in mitochondria - **Citrate Lyase**: Elevated to cleave citrate → cytosolic Acetyl CoA (substrate for fatty acid synthesis) - **Acetyl CoA Carboxylase (ACC)**: The **rate-limiting enzyme** of fatty acid synthesis, activated by insulin (dephosphorylation) and citrate - **Malonyl CoA**: The **first committed intermediate** in fatty acid synthesis, product of ACC action on Acetyl CoA All four components work sequentially in the pathway from glucose → fatty acids, and all are upregulated in this metabolic state. *Incorrect Option: 1,2,3* This incorrectly excludes **Citrate Lyase**, which is essential for providing cytosolic Acetyl CoA from mitochondrial citrate. Without elevated Citrate Lyase activity, fatty acid synthesis cannot proceed efficiently despite high carbohydrate intake. *Incorrect Option: 2,3,4* This incorrectly excludes **Malonyl CoA**, the direct product of Acetyl CoA Carboxylase and the committed intermediate for fatty acid synthesis. When ACC is highly active (as it would be with high insulin), Malonyl CoA concentration must be elevated. *Incorrect Option: 1,3,4* This incorrectly excludes **Acetyl CoA Carboxylase (ACC)**, the **rate-limiting enzyme** of the entire fatty acid synthesis pathway. In a high carbohydrate/high insulin state, ACC is maximally activated by dephosphorylation and allosteric activation by citrate, making this a critical error.
Question 174: Match the following blotting techniques with the type of biomolecule they detect: Blotting Technique Detects A. Southern blot 1. RNA B. Northern blot 2. Lipids C. Western blot 3. DNA D. Eastern blot 4. Protein
- A. A-3, B-1, C-4, D-2 (Correct Answer)
- B. A-4, B-2, C-1, D-3
- C. A-2, B-4, C-3, D-1
- D. A-1, B-3, C-2, D-4
Explanation: ***A-3, B-1, C-4, D-2*** - **Southern blot** is named after Edwin Southern and is the foundational technique used to detect specific **DNA** sequences. - **Northern blot** detects specific **RNA** sequences, while **Western blot** targets specific **Proteins** using antibodies. ***A-1, B-3, C-2, D-4*** - This option incorrectly matches Southern blot (A) with RNA (1) and Northern blot (B) with DNA (3). - The standard nomenclature links Southern with **DNA** and Northern with **RNA** due to their evolutionary development from the original technique. ***A-4, B-2, C-1, D-3*** - This option incorrectly assigns Southern blot (A) to Protein (4) and Northern blot (B) to Lipids (2). - Western blot (C) detects **Protein**, not RNA (1), as suggested here. ***A-2, B-4, C-3, D-1*** - This option incorrectly matches Southern blot (A) with Lipids (2) and Western blot (C) with DNA (3). - **Eastern blot** (D) is a technique designed to detect **post-translational modifications** (like lipids and carbohydrates) on proteins, making the D-2 match plausible, but the other matches are incorrect (i.e., **Southern blot** detects DNA).
Community Medicine
1 questionsAlleles of a gene pool belong to a:
INI-CET 2025 - Community Medicine INI-CET Practice Questions and MCQs
Question 171: Alleles of a gene pool belong to a:
- A. Population (Correct Answer)
- B. Cell
- C. Individual
- D. Family
Explanation: ***Population (Correct)*** - A **gene pool** is the total collection of all alleles and genes within a **population** of a specific species capable of interbreeding - The concept is fundamental to **population genetics** and evolution, measuring overall genetic diversity available to the group - Includes genetic information from **all reproductive members** of the population in a geographical area *Individual (Incorrect)* - An individual possesses only a small subset of alleles from the gene pool (typically two alleles per gene locus) - Represents the **genotype** of a single organism, not the collective genetic diversity - The gene pool requires pooling genetic information from **multiple individuals** *Family (Incorrect)* - A family represents a limited subgroup within a population (related by kinship) - Does not encompass the entire **genetic variability** of the species' local reproductive unit - Too narrow a concept compared to the population-level gene pool *Cell (Incorrect)* - A cell contains the **genome** or **genotype** of an individual organism - The **gene pool** is a population-level concept extending beyond a single cell's genetic material - Represents the smallest unit of genetic information, not the collective diversity
Internal Medicine
2 questionsWhich gene would you test if the patient has a family history of breast and ovarian cancer?
Multiple lytic lesions on skull are seen in which thyroid carcinoma?
INI-CET 2025 - Internal Medicine INI-CET Practice Questions and MCQs
Question 171: Which gene would you test if the patient has a family history of breast and ovarian cancer?
- A. P53
- B. CDH1
- C. BRCA1/2 (Correct Answer)
- D. PTEN
Explanation: ***BRCA1/2*** - Mutations in **BRCA1** and **BRCA2** genes are responsible for the majority of hereditary breast and ovarian cancer syndromes (*Hereditary Breast and Ovarian Cancer syndrome*). [1] - Testing these genes is the standard procedure when a patient presents with a strong family history of both breast and ovarian cancers, as they are **tumor suppressor genes** involved in DNA repair. [1] ***P53*** - Mutations in the **TP53** gene are associated with **Li-Fraumeni syndrome**, which increases the risk for a wide spectrum of cancers, including breast cancer, sarcomas, brain tumors, and adrenocortical carcinoma. - While breast cancer is a component, Li-Fraumeni is less specifically linked to the combined presentation of breast and ovarian cancer compared to BRCA mutations. ***PTEN*** - Mutations in the **PTEN** gene cause **Cowden syndrome**, characterized by multiple hamartomas and an increased risk of breast, thyroid, and endometrial cancers. - Ovarian cancer is a less prominent feature of Cowden syndrome, making it a secondary consideration after BRCA testing. ***CDH1*** - Mutations in the **CDH1** gene (which encodes **E-cadherin**) are primarily associated with **Hereditary Diffuse Gastric Cancer (HDGC)**. - These mutations also confer an increased risk for **lobular breast cancer**, but they are not the primary drivers for a syndrome involving both significant breast and ovarian cancer risk.
Question 172: Multiple lytic lesions on skull are seen in which thyroid carcinoma?
- A. Follicular carcinoma (Correct Answer)
- B. Thyroid lymphoma
- C. Papillary carcinoma thyroid
- D. Hurthle cell carcinoma
Explanation: ***Follicular carcinoma*** - Follicular thyroid carcinoma (FTC) classically spreads hematogenously to distant sites, most commonly the **bone (skull, spine, pelvis)** and lungs. - Bone metastases, especially in the skull, are typically **lytic** and may present as solitary or multiple lesions with a characteristic **"cannonball" appearance** on imaging if involving the lungs. ***Papillary carcinoma thyroid*** - Papillary thyroid carcinoma (PTC) predominantly spreads locally via **lymphatics** to regional neck lymph nodes, rarely causing distant metastases early in the disease course. - Distant metastases, when they occur, are usually to the lungs (small micronodules) and are less common as lytic skull lesions compared to FTC. ***Hurthle cell carcinoma*** - Hurthle cell carcinoma (a variant of follicular carcinoma) also has a high propensity for **hematogenous spread** to bone and lung. - While it can cause lytic bone lesions, it is best classified under the broader category of follicular carcinoma for its metastatic pattern, but FTC is the most common association for lytic skull lesions among the choices. ***Thyroid lymphoma*** - Thyroid lymphoma is rare and usually presents as a **rapidly enlarging thyroid mass** in an older patient, often associated with a background of Hashimoto's thyroiditis. - It typically causes diffuse thyroid involvement and local invasion into the neck structures; distant metastases, especially lytic skull lesions, are highly **uncommon**.
Pathology
2 questionsCaspase-1 mediated cell death with inflammation is known as
Least common finding in diabetic kidney is
INI-CET 2025 - Pathology INI-CET Practice Questions and MCQs
Question 171: Caspase-1 mediated cell death with inflammation is known as
- A. Pyroptosis (Correct Answer)
- B. Necroptosis
- C. Necrosis
- D. Ferroptosis
Explanation: ***Pyroptosis*** - This form of programmed cell death is characterized by the formation of an **inflammasome** complex [2], activating **Caspase-1** [1]. - Caspase-1 activation leads to the cleavage of pro-IL-1$\beta$ and pro-IL-18 into their active forms, resulting in a highly **inflammatory** process and cell lysis [1]. *Necroptosis* - This programmed, but non-apoptotic, cell death is mediated by the **RIPK1/RIPK3/MLKL** signaling pathway, involving receptor-interacting protein kinases [1]. - It is morphologically similar to necrosis but can be pharmacologically inhibited; it is **Caspase-independent** [3]. *Ferroptosis* - Ferroptosis is a form of regulated necrosis driven by **iron-dependent lipid peroxidation**. - It is characterized by the accumulation of reactive oxygen species and is typically **Caspase-independent**. *Necrosis* - Necrosis is an uncontrolled, **non-programmed** form of cell death resulting from acute cellular injury or pathology (e.g., ischemia). - It involves cell swelling, rupture of the plasma membrane, and leakage of cellular contents, leading to massive local inflammation, but is **not directly mediated by Caspase-1**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 71. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 196. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71.
Question 172: Least common finding in diabetic kidney is
- A. Podocyte loss
- B. GBM thickening
- C. Armanni-Ebstein (Correct Answer)
- D. Mesangial widening
Explanation: ***Armanni-Ebstein*** - **Armanni-Ebstein lesion** (also known as Armanni-Ebstein change) refers to severe **glycogen accumulation** in the tubular epithelial cells, typically the proximal tubules. - This finding is relatively rare and seen mainly in cases of **poorly controlled acute diabetes mellitus** or acute hyperglycemia, making it the least common routine finding compared to the other structural changes. ***Podocyte loss*** - **Podocyte injury (podocytopathy)** and subsequent loss are a central and early feature in the pathogenesis of diabetic nephropathy, leading to **proteinuria**. - Progressive effacement, detachment, and eventual depletion of these highly specialized cells are constant findings in established **diabetic kidney disease (DKD)**. ***Mesangial widening*** - **Mesangial expansion/widening** is considered the earliest and most specific histological change in **diabetic nephropathy**. - This pathology progresses, leading eventually to **diffuse or nodular glomerulosclerosis** (**Kimmelstiel-Wilson lesions**), making it a universal finding in established DKD. ***GBM thickening*** - **Glomerular basement membrane (GBM) thickening** occurs very early in **diabetic nephropathy**, often preceding clinical proteinuria [1]. - It is a consistent and measurable structural abnormality caused by increased synthesis and altered composition of **extracellular matrix** components in the GBM [1], [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1119-1121. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 907-908.
Physiology
1 questionsWhich of the following tissues will not be able to take up glucose in insulin resistance/insulin absence/diabetes mellitus?
INI-CET 2025 - Physiology INI-CET Practice Questions and MCQs
Question 171: Which of the following tissues will not be able to take up glucose in insulin resistance/insulin absence/diabetes mellitus?
- A. Kidney
- B. Skeletal muscle (Correct Answer)
- C. Brain
- D. Red blood cells
Explanation: ***Skeletal muscle*** - Skeletal muscle is an **insulin-dependent** tissue, meaning glucose uptake is facilitated by the insulin-driven translocation of the **GLUT4** transporter to the cell membrane. - In conditions of insulin resistance or insulin deficiency (diabetes mellitus), the translocation of **GLUT4** is impaired, severely reducing the muscle's ability to take up circulating glucose. *Red blood cells* - Glucose uptake by red blood cells (RBCs) is primarily mediated by the **GLUT1** transporter. - **GLUT1** is constitutively active and highly **insulin-independent**, ensuring that RBCs maintain their glucose supply regardless of the patient's insulin status. *Brain* - The brain relies on transporters like **GLUT1** and **GLUT3** (often considered the primary neuronal glucose transporter) for continuous glucose supply. - Glucose uptake in the brain is **insulin-independent** to guarantee stable energy provision to the central nervous system, even in high-demand states. *Kidney* - The kidney utilizes primarily **GLUT1** and **GLUT2** transporters for glucose uptake into its cells and for reabsorption of filtered glucose in the renal tubules. - These transporters operate independently of insulin levels, classifying the kidney as an **insulin-independent** tissue for glucose metabolism.