Biochemistry
1 questionsWhat type of bond is involved in the side chain linkage of proteoglycans?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 371: What type of bond is involved in the side chain linkage of proteoglycans?
- A. Covalent (Correct Answer)
- B. Hydrogen bond
- C. Electrostatic bond
- D. Van-der Waal's force
Explanation: ***Covalent*** - Proteoglycans are formed by **glycosaminoglycan (GAG)** chains that are covalently linked to a protein core. - Specifically, an **O-glycosidic bond** forms between a xylose residue on the GAG chain and a serine residue on the core protein. *Hydrogen bond* - **Hydrogen bonds** are weaker intermolecular forces that stabilize protein secondary structures and interactions between water molecules. - They are not strong enough to form the primary structural linkage between the GAG chains and the core protein in proteoglycans. *Electrostatic bond* - **Electrostatic bonds**, or ionic bonds, involve attraction between oppositely charged ions. While proteoglycans have many charged groups, these bonds are not the primary linkage connecting the GAG chains to the protein core. - They contribute to the overall structure and interactions of proteoglycans with other molecules but do not form the main side chain linkage. *Van-der Waal's force* - **Van der Waals forces** are weak, short-range intermolecular forces that arise from temporary fluctuations in electron distribution. - These forces play a role in tertiary and quaternary protein structure and molecular packing, but they are far too weak to establish the covalent attachments of GAG chains to the proteoglycan core protein.
Internal Medicine
1 questionsWhich of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 371: Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
- A. HTN
- B. Increased urea
- C. Increased creatinine
- D. Normal C3 level (Correct Answer)
Explanation: ***Normal C3 level*** - In Post-streptococcal glomerulonephritis (PSGN), **C3 levels are typically decreased** due to complement consumption during the inflammatory process. [1] - A **normal C3 level** would not be consistent with PSGN, as it suggests no significant complement activation. *Increased urea* - Increased urea can occur due to **impaired renal function**, which is common in PSGN due to glomerular inflammation. [1] - It's a typical finding reflecting the kidneys' inability to excrete waste products properly. *HTN* - Hypertension is frequently associated with PSGN due to **volume overload** and activation of the renin-angiotensin system. [1] [2] - It is a common clinical feature that results from increased fluid retention. *Increased creatinine* - Increased creatinine levels indicate **renal impairment**, which is characteristic of PSGN as kidney function is affected during this condition. [1] - This finding highlights the reduction in glomerular filtration rate (GFR), typical in glomerulonephritis. [2]
Pathology
5 questionsWhich molecule is primarily responsible for nuclear fragmentation during apoptosis?
Which chromosomal translocation is associated with follicular thyroid carcinoma?
All of the following are features of granulomatous thyroiditis except?
What does Prussian blue staining specifically detect in histology?
Hyaline degeneration is found in -
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 371: Which molecule is primarily responsible for nuclear fragmentation during apoptosis?
- A. Caspases (Correct Answer)
- B. Apaf - 1
- C. Oxygen free radicals
- D. Endonuclease G
Explanation: ***Caspases*** - **Caspases** are a family of proteases that play a central role in the execution phase of apoptosis, including the **cleavage of nuclear proteins** and DNA fragmentation [1]. - Specifically, **executioner caspases** (e.g., caspase-3, -6, -7) activate **CAD (caspase-activated DNase)** by cleaving its inhibitor ICAD, leading to **nuclear fragmentation** and DNA laddering [1]. - This is the **primary mechanism** of nuclear breakdown in apoptosis. *Apaf-1* - **Apaf-1 (apoptotic protease activating factor 1)** is an adaptor protein that, upon activation by cytochrome c, forms the **apoptosome** [1]. - While essential for **caspase activation** (specifically caspase-9), Apaf-1 does not directly cleave nuclear components or cause fragmentation itself [1]. *Oxygen free radicals* - **Oxygen free radicals** (reactive oxygen species) can induce cellular damage and stress, and in high concentrations, can trigger apoptosis [2]. - However, they are generally upstream initiators of apoptosis pathways and do not directly mediate nuclear fragmentation; this process is carried out by **caspases**. *Endonuclease G* - **Endonuclease G** is a mitochondrial nuclease released during apoptosis that can contribute to DNA degradation. - However, it plays a **secondary role** and acts in a caspase-independent manner, whereas **caspases** remain the primary executors of nuclear fragmentation in apoptosis. **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, pp. 64-67. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 100-101.
Question 372: Which chromosomal translocation is associated with follicular thyroid carcinoma?
- A. PAX8 - PPARγ (Correct Answer)
- B. ALK - NPM1
- C. ETV6 - NTRK3
- D. RET - PTC1
Explanation: ***PAX8 - PPARγ*** - The **PAX8-PPARγ fusion oncogene** is a well-established molecular marker directly associated with **follicular thyroid carcinoma (FTC)**. - This translocation leads to the expression of a fusion protein that contributes to **thyroid cell proliferation** and **tumorigenesis**. *ALK - NPM1* - The **ALK-NPM1 fusion** is primarily observed in some types of **anaplastic large cell lymphoma**, not thyroid cancers. - This translocation typically results in an **activated anaplastic lymphoma kinase (ALK)**, driving lymphoproliferation. *ETV6 - NTRK3* - The **ETV6-NTRK3 rearrangement** is characteristic of **secretory carcinoma** (formerly mammary analogue secretory carcinoma), often affecting salivary glands, and is not a common finding in thyroid malignancies. - This fusion leads to the activation of the **NTRK3 receptor tyrosine kinase**, involved in cell growth and survival. *RET - PTC1* - The **RET-PTC1 rearrangement (RET/papillary thyroid carcinoma 1)** is specifically associated with **papillary thyroid carcinoma (PTC)**, which is histologically distinct from follicular thyroid carcinoma. - This fusion activates the **RET proto-oncogene**, promoting cell proliferation and survival in papillary thyroid cancer.
Question 373: All of the following are features of granulomatous thyroiditis except?
- A. Hyperthyroidism
- B. Giant cells on histology
- C. Painless (Correct Answer)
- D. Hypothyroidism
Explanation: ***Painless*** - Granulomatous thyroiditis is characterized by **painful** thyroid gland inflammation, which is a distinguishing feature. - Thus, describing it as **painless** contradicts the typical clinical presentation. *Hyperthyroidism* - Granulomatous thyroiditis may lead to **hyperthyroidism** initially due to the release of thyroid hormones from damaged follicles [1]. - However, this condition can also lead to transient thyroid function changes or even permanent hypothyroidism later on [1]. *Hypothyroidism* - While **hypothyroidism** can occur post-thyroiditis, it is not a feature of granulomatous thyroiditis at the outset like the **painless** descriptor. - This condition often starts with hyperthyroid symptoms and may evolve later, differing from primary hypothyroid disorders. *Giant cells on histology* - Histological examination typically reveals **multinucleated giant cells**, a hallmark of granulomatous inflammation, as seen in this thyroid condition. - This significant finding helps in differentiating it from other thyroid disorders. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1091-1092.
Question 374: What does Prussian blue staining specifically detect in histology?
- A. Ferric iron (Correct Answer)
- B. Ferrous iron
- C. Glycogen
- D. Lipids
Explanation: ***Ferric iron*** - The **Prussian blue reaction**, also known as Perls' stain, specifically identifies **ferric iron (Fe3+)** in tissue sections. - This stain is crucial for diagnosing conditions involving **iron overload**, such as hemochromatosis or hemosiderosis, by highlighting iron deposits as blue. *Ferrous iron* - The Prussian blue stain does **not react with ferrous iron (Fe2+)**; it specifically targets the ferric (oxidized) state of iron. - While ferrous iron is present in the body, it is not detected by this particular staining method for routine histological assessment of iron stores. *Glycogen* - **Glycogen** is a polysaccharide storage molecule and is typically stained using the **Periodic Acid-Schiff (PAS) stain**, which produces a magenta color. - Prussian blue staining is entirely unrelated to the detection of glycogen and would not highlight these molecules in tissue. *Lipids* - **Lipids** are fats and are typically stained with lipid-soluble dyes like **Oil Red O** or **Sudan Black**, especially in frozen sections to preserve their structure. - Prussian blue stain has no affinity for lipids and therefore cannot be used to detect them in histological samples.
Question 375: Hyaline degeneration is found in -
- A. Alzheimer's disease
- B. Alcoholic liver disease (Correct Answer)
- C. Acute myocardial infarction
- D. Acute appendicitis
Explanation: ***Alcoholic liver disease*** - **Mallory bodies**, a form of hyaline degeneration, are characteristic histologic findings in hepatocytes in alcoholic liver disease. - They represent aggregates of **intermediate filaments** and other proteins, indicating severe hepatocellular damage. *Acute myocardial infarction* - Characterized by **coagulative necrosis** of cardiac myocytes due to ischemia, not hyaline degeneration. - Inflammation and subsequent repair with **fibrosis** are key features. *Alzheimer's disease* - Defined by the presence of **senile plaques** (amyloid-beta deposits) and **neurofibrillary tangles** (hyperphosphorylated tau protein). - These are specific protein aggregates, distinct from hyaline degeneration of cellular components. *Acute appendicitis* - Involves acute inflammation of the appendix, leading to **neutrophilic infiltration** and often **fibrinopurulent exudate**. - There is no characteristic hyaline degeneration associated with this inflammatory process.
Pharmacology
3 questionsAlkaline diuresis in drug poisoning is not done in?
Regarding the concepts of efficacy and potency of a drug, which of the following statements is FALSE?
High volume of distribution is primarily determined by:
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 371: Alkaline diuresis in drug poisoning is not done in?
- A. Aspirin
- B. Morphine (Correct Answer)
- C. Phenobarbitone
- D. Methotrexate
Explanation: ***Morphine*** - **Morphine** is an **alkaline drug**, so its elimination is actually enhanced by **acidification of the urine**, not alkalinization. - Alkaline diuresis would decrease the ionization of morphine in the renal tubules, leading to **increased reabsorption** and reduced excretion. *Aspirin* - **Aspirin (acetylsalicylic acid)** is an **acidic drug**, and **alkaline diuresis** is effective in increasing its excretion by trapping the ionized form in the renal tubules. - This process prevents reabsorption and promotes clearance, which is a standard treatment for aspirin overdose. *Methotrexate* - **Methotrexate** is a **weak organic acid**, and **alkaline diuresis** is crucial in reducing its toxicity, especially in high-dose therapy. - By increasing urine pH, the renal elimination of methotrexate is significantly enhanced, preventing kidney damage and systemic accumulation. *Phenobarbitone* - **Phenobarbitone** is a **weak acid**, and **alkaline diuresis** is a well-established method to increase its renal excretion in cases of overdose. - Alkalinization of the urine promotes the ionization of phenobarbitone, reducing its reabsorption by the renal tubules and accelerating its elimination.
Question 372: Regarding the concepts of efficacy and potency of a drug, which of the following statements is FALSE?
- A. ED50 of the drug corresponds to efficacy (Correct Answer)
- B. Drugs that produce a similar pharmacological effect can have different levels of efficacy
- C. In a clinical setup, efficacy is more important than potency
- D. In the log dose response curve, the height of the curve corresponds with efficacy
Explanation: ***ED50 of the drug corresponds to efficacy*** - **ED50** (median effective dose) is the dose at which 50% of individuals exhibit the specified effect; it quantifies **potency**, not efficacy. - **Efficacy** refers to the maximum effect a drug can produce, while potency refers to the amount of drug needed to produce an effect. *In a clinical setup, efficacy is more important than potency* - **Efficacy** determines the maximal therapeutic benefit a drug can achieve for a patient, making it crucial for clinical outcomes. - While **potency** influences the dose required, a highly potent drug that is not very efficacious may not be clinically useful. *Drugs that produce a similar pharmacological effect can have different levels of efficacy* - Two drugs might act on the same receptor but elicit different maximal responses, indicating varying **efficacy**. - For example, a **partial agonist** and **full agonist** interacting with the same receptor will have different efficacies. *In the log dose response curve, the height of the curve corresponds with efficacy* - The **maximal response** or plateau of the dose-response curve represents the **efficacy** of a drug. - A higher plateau on the curve indicates a drug with greater intrinsic activity achieving a larger effect.
Question 373: High volume of distribution is primarily determined by:
- A. High lipid solubility (Correct Answer)
- B. High plasma protein binding
- C. Elimination rate
- D. Half-life of the drug
Explanation: ***High lipid solubility***- Highly **lipid-soluble** drugs readily cross biological membranes and distribute extensively into tissues, including adipose tissue, CNS, and intracellular compartments, leading to a **high volume of distribution (Vd)** [1, 2].- This property allows the drug to move out of the bloodstream and into various body compartments, increasing the apparent volume in which the drug is dissolved [1].*High plasma protein binding*- **High plasma protein binding** generally **restricts** drug distribution to tissues because only the **unbound (free) fraction** can diffuse across capillary membranes into interstitial fluid and cells [1].- This typically leads to a **lower Vd**, as the drug is largely retained within the plasma compartment.*Elimination rate*- The **elimination rate** determines how quickly the drug is removed from the body, affecting the **duration of action** rather than the extent of distribution.- It influences drug concentration changes over time but does not directly determine the physical space (volume) into which the drug distributes.*Half-life of the drug*- The **half-life (t½)** is the time required for drug concentration to reduce by half, and it is **determined by** both Vd and clearance (t½ = 0.693 × Vd/CL).- Half-life is a **consequence** of Vd and clearance, not a primary determinant of how widely a drug distributes [3].