Dental
1 questionsBrutonian lines on gums are seen in poisoning with which of the following substances?
NEET-PG 2012 - Dental NEET-PG Practice Questions and MCQs
Question 581: Brutonian lines on gums are seen in poisoning with which of the following substances?
- A. Lead (Correct Answer)
- B. Mercury
- C. Zinc
- D. Arsenic
Explanation: ***Lead*** - **Brutonian lines**, also known as **Burton's lines**, are a classic sign of chronic lead poisoning, appearing as a blue or blue-black line along the gum margin. - This discoloration is caused by the reaction of circulating lead with sulfur ions released by oral bacteria, forming lead sulfide deposits in the gingival tissue. *Mercury* - Mercury poisoning can cause **gingivitis**, **stomatitis**, and excessive salivation, but typically not the distinct Burton's lines. - A characteristic feature of chronic mercury poisoning is often **erected tremor** and **erethism** (changes in mood and irritability). *Arsenic* - Chronic arsenic poisoning can lead to **hyperkeratosis** and **hyperpigmentation** of the skin (rain drop pigmentation), as well as **peripheral neuropathy**. - It does not typically cause the specific gingival discoloration seen in lead poisoning. *Zinc* - Zinc intoxication is relatively rare and often results from excessive ingestion of zinc-containing supplements or industrial exposure. - Symptoms usually include **nausea, vomiting, diarrhea**, and sometimes **copper deficiency**, but not gum line discoloration.
Microbiology
1 questionsWhich part of bacteria is most antigenic?
NEET-PG 2012 - Microbiology NEET-PG Practice Questions and MCQs
Question 581: Which part of bacteria is most antigenic?
- A. Lipopolysaccharide (Correct Answer)
- B. Lipids
- C. Nucleic acid
- D. Protein coat
Explanation: ***Lipopolysaccharide (LPS)*** - The **O antigen** (polysaccharide component of LPS) in Gram-negative bacteria is one of the **most antigenic** bacterial components - Highly **immunogenic**, inducing strong antibody responses (both IgM and IgG) - Used as the basis for **serological typing** of Gram-negative bacteria (e.g., E. coli O157:H7) - The polysaccharide chains are structurally diverse with multiple epitopes, creating strain-specific immunity - While lipid A component has endotoxin activity, the polysaccharide portion is the primary antigenic determinant *Protein coat* - Bacterial **surface proteins** (flagella, pili, outer membrane proteins) are indeed antigenic - However, **polysaccharides** (including capsular polysaccharides and LPS) are classically considered more potent antigens - The term "protein coat" is also somewhat non-specific in bacteriology *Nucleic acid* - **Nucleic acids** (DNA, RNA) are generally **poor antigens** on their own - Not readily accessible to antibodies as they are intracellular - Can act as pathogen-associated molecular patterns (PAMPs) for innate immunity via TLRs, but are not major antibody targets *Lipids* - **Lipids** alone are generally **non-immunogenic** due to lack of structural complexity - Too small and lack sufficient epitopes to stimulate B cell responses effectively - May act as **haptens** requiring conjugation to carrier proteins
Pharmacology
8 questionsWhat is the mode of action of azathioprine?
Resistance to Methotrexate develops due to?
Sulphonamide injection causes decrease in folic acid by?
Which of the following drugs does not inhibit bacterial protein synthesis?
What is the mechanism of action of quinolones?
Romiplostim mimics which of the following receptors?
Which of the following is the most common side effect of Cimetidine?
Which diuretic exhibits paradoxical antidiuretic activity in diabetes insipidus?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 581: What is the mode of action of azathioprine?
- A. ↑ IL-2
- B. Decreased lymphophagocytic activity
- C. Wide-spread antitumor activity
- D. T-cell blockade (Correct Answer)
Explanation: ***T-cell blockade*** - Azathioprine is a **prodrug** that is metabolized into **6-mercaptopurine (6-MP)**, which then interferes with **purine synthesis** [1, 2]. - This interference inhibits the proliferation of **lymphocytes**, particularly **T-cells**, thereby blocking their immune response. *↑ IL-2* - An increase in **IL-2 (interleukin-2)** production would lead to enhanced T-cell proliferation and activity, which is the opposite effect of azathioprine. - **IL-2** is crucial for T-cell growth, differentiation, and survival, so drugs that increase it would boost, not suppress, the immune system. *Decreased lymphophagocytic activity* - This statement is not the primary mode of action of azathioprine. The drug's main effect is on the **synthesis of DNA and RNA** in rapidly dividing cells, including lymphocytes. - While immune suppression can indirectly affect various immune cell functions, the direct mechanism is not primarily a decrease in phagocytosis by lymphocytes. *Wide-spread antitumor activity* - Although 6-mercaptopurine, the active metabolite of azathioprine, is used in combination chemotherapy for some **hematological malignancies**, azathioprine itself is primarily known as an **immunosuppressant** in conditions like **autoimmune diseases** and **transplant rejection**. - Its antitumor activity is not typically described as "wide-spread," and its predominant use in pharmacology is for immune modulation.
Question 582: Resistance to Methotrexate develops due to?
- A. Rapid proliferation of cancer cells
- B. Thymidylate kinase deficiency
- C. Thymidylate synthetase deficiency
- D. Increased production of dihydrofolate reductase (DHFR) (Correct Answer)
Explanation: ***Increased production of dihydrofolate reductase (DHFR)*** - Methotrexate acts by inhibiting **dihydrofolate reductase (DHFR)**, an enzyme essential for **folate metabolism** and DNA synthesis. - An **increased production of DHFR** (through gene amplification or overexpression) by cancer cells allows them to bypass the drug's inhibitory effects, leading to resistance. - This is the **most common mechanism** of methotrexate resistance. *Rapid proliferation of cancer cells* - While **rapid cell proliferation** is a characteristic of cancer, it doesn't directly explain resistance to methotrexate. - Methotrexate targets fast-dividing cells (S-phase specific), so rapid proliferation often makes them **more susceptible**, not resistant, as long as the drug's mechanism is effective. *Thymidylate kinase deficiency* - **Thymidylate kinase** is involved in the phosphorylation of **thymidine** to produce **dTMP** (deoxythymidine monophosphate). - A deficiency in this enzyme would likely hinder DNA synthesis, potentially increasing sensitivity to DNA-targeting agents, rather than causing resistance to methotrexate. *Thymidylate synthetase deficiency* - **Thymidylate synthetase** converts dUMP to dTMP using **5,10-methylene-THF** as a cofactor. - Methotrexate **indirectly inhibits** thymidylate synthetase by depleting tetrahydrofolate cofactor pools through DHFR inhibition. - A **deficiency** of this enzyme would not cause resistance; rather, **increased thymidylate synthetase** expression can be an alternative resistance mechanism, though less common than DHFR overexpression.
Question 583: Sulphonamide injection causes decrease in folic acid by?
- A. Inhibition through competition with substrate (Correct Answer)
- B. Inhibition without competition
- C. Inhibition through a different site
- D. Inhibition that does not involve the active site
Explanation: ***Inhibition through competition with substrate***Sulphonamides are **structural analogs of p-aminobenzoic acid (PABA)**, a substrate crucial for dihydropteroate synthase [1, 2]. They competitively inhibit this enzyme, which synthesizes **dihydrofolic acid**, a precursor to **tetrahydrofolic acid (THF)**, thereby reducing folic acid production in bacteria [1, 2].*Inhibition without competition*This typically refers to **non-competitive inhibition**, where the inhibitor binds to an allosteric site and changes the enzyme's conformation, regardless of substrate concentration. Sulphonamides, however, specifically compete with PABA at the active site of **dihydropteroate synthase**.*Inhibition through a different site*This describes **allosteric inhibition** or non-competitive inhibition, where the inhibitor binds to a site other than the active site. Sulphonamides do not work through an allosteric mechanism; they directly interfere with the binding of PABA at the enzyme's active site.*Inhibition that does not involve the active site*This is another way to describe **non-competitive** or **allosteric inhibition**, where the inhibitor binds elsewhere on the enzyme, altering its function without directly blocking the active site. Sulphonamides' mechanism is distinct, as they closely resemble the natural substrate and directly compete for the active site of **dihydropteroate synthase**.
Question 584: Which of the following drugs does not inhibit bacterial protein synthesis?
- A. Aminoglycosides
- B. Chloramphenicol
- C. Clindamycin
- D. Sulfonamides (Correct Answer)
Explanation: ***Sulfonamides*** - Sulfonamides do **NOT** inhibit bacterial protein synthesis; instead, they inhibit **folic acid synthesis**. - They act as **competitive inhibitors** of dihydropteroate synthase, an enzyme involved in the synthesis of dihydrofolic acid. - Folic acid is essential for nucleotide synthesis and DNA replication, making sulfonamides bacteriostatic agents that work through a completely different mechanism than protein synthesis inhibitors. *Aminoglycosides* - Aminoglycosides bind to the **30S ribosomal subunit**, causing misreading of mRNA and premature termination of protein synthesis. - This leads to the production of **abnormal and non-functional proteins**, ultimately killing the bacterial cell. *Chloramphenicol* - Chloramphenicol binds to the **50S ribosomal subunit**, thereby inhibiting the peptidyl transferase enzyme. - This prevents the formation of **peptide bonds** between amino acids, effectively blocking protein elongation. *Clindamycin* - Clindamycin also binds to the **50S ribosomal subunit**, specifically at the P-site. - It interferes with the **translocation step** of protein synthesis, preventing ribosomal movement along the mRNA.
Question 585: What is the mechanism of action of quinolones?
- A. Inhibit tetrahydrofolate reductase
- B. Inhibit DNA gyrase (Correct Answer)
- C. Bind to 30S ribosomal subunit
- D. Bind to bacterial cell membrane
Explanation: ***Inhibit DNA gyrase*** - Quinolones, particularly **fluoroquinolones**, exert their bactericidal effect by targeting **bacterial DNA gyrase (topoisomerase II)** and **topoisomerase IV**. - This inhibition prevents the uncoiling and replication of bacterial DNA, leading to cell death. *Bind to 30S ribosomal subunit* - This mechanism is characteristic of **aminoglycosides** and **tetracyclines**, which disrupt bacterial protein synthesis. - Quinolones do not interfere with ribosomal function but rather with **DNA replication**. *Bind to bacterial cell membrane* - This is the mechanism of action for **polymyxins** and **daptomycin**, which disrupt the integrity of the bacterial cell membrane. - Quinolones specifically target **intracellular enzymes** involved in DNA handling. *Inhibit tetrahydrofolate reductase* - This enzyme name in the option is technically imprecise; **trimethoprim** actually inhibits **dihydrofolate reductase**, which is part of the **sulfonamide-trimethoprim (Bactrim)** combination. - This pathway is involved in **folic acid synthesis**, crucial for bacterial DNA and RNA production, a mechanism distinct from quinolones.
Question 586: Romiplostim mimics which of the following receptors?
- A. IL 6
- B. IL 8
- C. PGE 1
- D. Thrombopoietin (Correct Answer)
Explanation: ***Thrombopoietin*** - **Romiplostim** is a **thrombopoietin receptor agonist**, meaning it binds to and activates the **thrombopoietin receptor** [1]. - This activation mimics the effect of endogenous thrombopoietin, stimulating the production of **platelets** in the bone marrow [2].*IL 6* - **Interleukin-6 (IL-6)** is a cytokine involved in inflammation, immune response, and hematopoiesis, but it is not the primary target of romiplostim. - While IL-6 can influence platelet production indirectly, romiplostim directly targets the thrombopoietin pathway.*IL 8* - **Interleukin-8 (IL-8)** is a chemokine primarily involved in neutrophil chemotaxis and inflammation. - It plays no direct role in the mechanism of action of romiplostim.*PGE 1* - **Prostaglandin E1 (PGE1)** is a lipid compound with various effects, including vasodilation and inhibition of platelet aggregation. - Romiplostim's mechanism of action is distinct from that of prostaglandins, as it specifically targets platelet production rather than platelet function or vascular tone.
Question 587: Which of the following is the most common side effect of Cimetidine?
- A. Diarrhea
- B. Impotence
- C. CNS effects (confusion, dizziness) (Correct Answer)
- D. Gynaecomastia
Explanation: ***CNS effects (confusion, dizziness)*** - **Cimetidine** is a **H2-receptor antagonist** that can cross the **blood-brain barrier**, leading to **central nervous system (CNS) side effects**. - These effects, including **confusion, dizziness**, and **headache**, are more common in elderly patients or those with renal impairment due to reduced drug clearance. *Impotence* - While **cimetidine** can cause **endocrine effects** due to its anti-androgenic activity, **impotence** is a less common side effect compared to CNS disturbances. - It results from the drug's interference with **testosterone metabolism** and binding to **androgen receptors**. *Gynaecomastia* - **Gynaecomastia** is a known **endocrine side effect** of **cimetidine** due to its **anti-androgenic activity** and promotion of **prolactin release**. - However, CNS side effects are generally encountered more frequently in clinical practice. *Diarrhea* - **Gastrointestinal side effects** like **diarrhea** are possible with various medications, but they are not the most common or characteristic side effect of **cimetidine**. - Nausea and constipation are also reported, but generally less frequently than CNS effects.
Question 588: Which diuretic exhibits paradoxical antidiuretic activity in diabetes insipidus?
- A. Thiazide diuretics (Correct Answer)
- B. Aldosterone antagonists (Spironolactone)
- C. Loop diuretics (Furosemide)
- D. Potassium-sparing diuretics (Triamterene)
Explanation: ***Thiazide diuretics*** - Thiazides cause a modest **volume depletion**, leading to increased proximal tubular reabsorption of water and solutes [1]. - They also lower the **glomerular filtration rate**, further reducing the amount of fluid delivered to the collecting ducts, thus paradoxically reducing urine output in diabetes insipidus [2]. - This effect is particularly useful in **nephrogenic diabetes insipidus**, where the kidneys cannot respond to ADH [2]. *Potassium-sparing diuretics (Triamterene)* - Triamterene is a **potassium-sparing diuretic** that blocks epithelial sodium channels in the late distal tubule and collecting duct. - It increases sodium and water excretion, which would worsen, not improve, the polyuria of diabetes insipidus. *Aldosterone antagonists (Spironolactone)* - Spironolactone is a **mineralocorticoid receptor antagonist** that increases sodium and water excretion while conserving potassium in the collecting duct. - Its primary action is to counteract aldosterone, and it does not exhibit the paradoxical antidiuretic effect seen with thiazides in diabetes insipidus. *Loop diuretics (Furosemide)* - Loop diuretics like furosemide act on the **thick ascending limb of the loop of Henle** to inhibit sodium, potassium, and chloride reabsorption. - They cause significant diuresis and would **exacerbate the polyuria** in patients with diabetes insipidus, rather than improving it.