Anatomy
1 questionsWhich of the following is not a neural plate inducer?
NEET-PG 2012 - Anatomy NEET-PG Practice Questions and MCQs
Question 641: Which of the following is not a neural plate inducer?
- A. FGF upregulation
- B. Prechordal mesoderm
- C. High BMP (Correct Answer)
- D. Notochord appearance
Explanation: High BMP - **Bone Morphogenetic Proteins (BMPs)** are primarily involved in promoting epidermal differentiation in the ectoderm, and actively **inhibiting neural differentiation**. - Therefore, high levels of BMP would **prevent neural plate formation**, rather than induce it. *FGF upregulation* - **Fibroblast Growth Factors (FGFs)** are crucial in the early development of the nervous system. - They play a key role in **inducing neural plate formation** and maintaining its identity. *Prechordal mesoderm* - The **prechordal mesoderm**, located anterior to the notochord, is an important signalling center during early embryonic development. - It contributes to the **induction of the forebrain** and plays a role in patterning the anterior neural plate. *Notochord appearance* - The **notochord**, a transient rod-like structure, is a primary inducer of the neural plate. - It secretes factors like **Sonic Hedgehog (Shh)** which induce the overlying ectoderm to differentiate into neuroectoderm, forming the neural plate.
Internal Medicine
2 questionsAn 86-year-old lady presented with severe constipation. She was a known hypertensive on medications for 10 years. In clinic, her BP was 157/98 mm Hg with a heart rate of 58/min. On taking her BP in the supine position, it was found to be 90/60 mm Hg. She had a recent history of depression. She is taking atenolol, thiazide, imipramine, haloperidol, and docusate. What is the next best step in the management?
Serological testing of patient shows HBsAg, IgM anti-HBc and HBeAg positive. The patient has -
NEET-PG 2012 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 641: An 86-year-old lady presented with severe constipation. She was a known hypertensive on medications for 10 years. In clinic, her BP was 157/98 mm Hg with a heart rate of 58/min. On taking her BP in the supine position, it was found to be 90/60 mm Hg. She had a recent history of depression. She is taking atenolol, thiazide, imipramine, haloperidol, and docusate. What is the next best step in the management?
- A. Change atenolol and thiazide to calcium channel blocker and ACE inhibitor and add bisacodyl for constipation
- B. Change imipramine and haloperidol to fluoxetine and risperidone and add bisacodyl for constipation (Correct Answer)
- C. Only add bisacodyl for constipation and continue rest of the medications
- D. Discontinue all her medications and start her on steroids
Explanation: ***Change imipramine and haloperidol to fluoxetine and risperidone and add bisacodyl for constipation*** - The patient's presentation with **severe constipation** and **orthostatic hypotension** (supine BP 90/60 mmHg from 157/98 mmHg) strongly suggests drug-induced side effects. Older people are especially sensitive to drugs that can cause postural hypotension, and for any presenting problem in old age, the possibility that medication is a contributory factor should be considered [1]. Both **imipramine** (a tricyclic antidepressant) and **haloperidol** (an antipsychotic) have significant **anticholinergic effects**, which can cause severe constipation and worsen orthostatic hypotension. - Switching to **fluoxetine** (an SSRI with fewer anticholinergic effects) and **risperidone** (an atypical antipsychotic with less anticholinergic burden than haloperidol) would mitigate these side effects. Postural hypotension in older adults is defined as a drop in blood pressure of >20 mmHg systolic or >10 mmHg diastolic upon standing [2]. Adding **bisacodyl**, a stimulant laxative, directly addresses her severe constipation. *Change atenolol and thiazide to calcium channel blocker and ACE inhibitor and add bisacodyl for constipation* - While atenolol and thiazide can contribute to orthostatic hypotension, the primary drivers of her severe constipation and marked anticholinergic side effects are likely **imipramine** and **haloperidol**. - Changing the antihypertensive medications alone would not adequately address the severe constipation or the underlying pharmacological cause of her symptoms. *Only add bisacodyl for constipation and continue rest of the medications* - Simply adding a **laxative** without addressing the underlying drug-induced issues would not resolve the root cause of her severe constipation and orthostatic hypotension. Failure to recognise ADRs may lead to the use of further drugs to treat the problem, making matters worse [1]. - Continuing **imipramine** and **haloperidol** would perpetuate the significant anticholinergic side effects, leading to ongoing symptoms and potential complications. *Discontinue all her medications and start her on steroids* - **Discontinuing all medications** without a clear rationale is generally unsafe, especially in an elderly patient with multiple comorbidities like hypertension and depression. - **Steroids** are not indicated for constipation or orthostatic hypotension in this context and could introduce a new set of serious side effects.
Question 642: Serological testing of patient shows HBsAg, IgM anti-HBc and HBeAg positive. The patient has -
- A. Acute hepatitis B with high infectivity (Correct Answer)
- B. Chronic hepatitis with high infectivity
- C. Acute on chronic hepatitis
- D. Chronic hepatitis B with low infectivity (not acute)
Explanation: ***Acute hepatitis B with high infectivity*** - The presence of **HBsAg** (hepatitis B surface antigen) indicates active infection, while **IgM anti-HBc** (IgM antibody to hepatitis B core antigen) is a marker of recent or acute infection [1]. - **HBeAg** (hepatitis B e-antigen) positivity signifies active viral replication and a high likelihood of infectivity [1]. *Chronic hepatitis B with low infectivity (not acute)* - **Chronic hepatitis B** is characterized by the presence of **HBsAg for more than six months**, but **IgM anti-HBc** would typically be negative; instead, **IgG anti-HBc** would be positive [1]. - **Low infectivity** would be indicated by the absence of **HBeAg**, replaced by **anti-HBe** (antibody to HBeAg) [1]. *Chronic hepatitis with high infectivity* - This diagnosis would show positive **HBsAg and HBeAg**, but the absence of **IgM anti-HBc** (presence of **IgG anti-HBc** instead) would distinguish it from acute infection [1]. - The presence of **IgM anti-HBc** is a crucial marker for an acute phase of hepatitis B rather than chronic. *Acute on chronic hepatitis* - This scenario would involve a patient with pre-existing **chronic hepatitis B** (positive HBsAg, IgG anti-HBc) experiencing a new acute flare-up, which could involve a resurgence of **HBeAg** or a new acute viral insult. - While **HBsAg** and **HBeAg** would be positive, the key differentiator would be the presence of both **IgM anti-HBc** (indicating the acute component) and **IgG anti-HBc** (indicating the chronic component), which is not fully described here to confirm acute on chronic.
Microbiology
2 questionsWhich of the following substances is toxic to parasites?
Unsegmented eggs are in which parasite?
NEET-PG 2012 - Microbiology NEET-PG Practice Questions and MCQs
Question 641: Which of the following substances is toxic to parasites?
- A. Peroxidase (Correct Answer)
- B. Interferon-alpha
- C. IL-2 (Interleukin-2)
- D. IL-6 (Interleukin-6)
Explanation: ***Peroxidase*** - **Peroxidase** enzymes, especially those produced by **eosinophils**, generate toxic oxygen metabolites and hypohalous acids that are highly effective at damaging and killing parasites. - This enzyme plays a crucial role in the host's defense against larger parasites, such as **helminths (worms)**. *Interferon-alpha* - **Interferon-alpha** is an important cytokine primarily known for its **antiviral effects** and its role in activating natural killer (NK) cells. - While it modulates immune responses, it does not directly act as a toxic substance to parasites. *IL-2 (Interleukin-2)* - **IL-2** is a growth factor that primarily promotes the **proliferation and differentiation of T cells**, enhancing adaptive immune responses. - It does not directly kill parasites but rather supports the immune cells involved in parasite clearance. *IL-6 (Interleukin-6)* - **IL-6** is a pleiotropic cytokine involved in **inflammation, acute phase responses**, and the differentiation of B cells and T cells. - While it contributes to overall immune regulation, it lacks direct parasiticidal activity.
Question 642: Unsegmented eggs are in which parasite?
- A. Ancylostoma
- B. Necator americanus
- C. Dracunculus
- D. Trichuris trichiura (Correct Answer)
Explanation: ***Trichuris trichiura*** - *Trichuris trichiura* (whipworm) eggs are typically **unembryonated** or **unsegmented** when passed in feces. - Upon defecation, the eggs require a period of **development in soil** to become infective. *Ancylostoma* - **Hookworm (Ancylostoma)** eggs are typically **segmented** (possessing a 2-8 cell stage) when passed in feces. - They develop into **rhabditiform larvae** in the soil. *Necator americanus* - **Hookworm (Necator americanus)** eggs are also typically **segmented** (possessing a 2-8 cell stage) when passed in feces. - Like *Ancylostoma*, they require further development in soil to become infective. *Dracunculus* - *Dracunculus medinensis* (Guinea worm) does not lay eggs; instead, it releases **larvae** from the skin blister of the host into water. - The larvae are then ingested by **cyclops** (copepods) to continue their life cycle.
Ophthalmology
1 questionsToxoplasma in children causes:
NEET-PG 2012 - Ophthalmology NEET-PG Practice Questions and MCQs
Question 641: Toxoplasma in children causes:
- A. Chorioretinitis (Correct Answer)
- B. Keratitis
- C. Papillitis
- D. Conjunctivitis
Explanation: ***Chorioretinitis*** - **Toxoplasmosis** is a significant cause of **chorioretinitis** in children, particularly congenital infections. - Ocular toxoplasmosis often presents with **retinal lesions** that can lead to vision loss. *Conjunctivitis* - **Conjunctivitis** is an inflammation of the conjunctiva, typically caused by bacterial or viral infections. - While it can occur in children, it is not a primary or characteristic manifestation of **Toxoplasma infection**. *Keratitis* - **Keratitis** is an inflammation of the cornea, often caused by bacterial, viral, or fungal infections, or sometimes trauma. - Although eyes are affected by **Toxoplasma**, **keratitis** is not the typical ophthalmic presentation; **chorioretinitis** is. *Papillitis* - **Papillitis** refers to inflammation of the optic disc (optic nerve head). - While **Toxoplasma** can rarely affect the optic nerve, **papillitis** is not the most common or specific ocular manifestation compared to **chorioretinitis**.
Pharmacology
4 questionsWhich of the following has the least glucocorticoid activity?
Which of the following is the MOST CRITICAL indication for Acyclovir use during pregnancy?
What is the mode of action of azathioprine?
Resistance to Methotrexate develops due to?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 641: Which of the following has the least glucocorticoid activity?
- A. Fludrocortisone
- B. Cortisone (Correct Answer)
- C. Dexamethasone
- D. Betamethasone
Explanation: ***Cortisone*** - **Cortisone has the LEAST glucocorticoid activity** among the options listed. - It is a **prodrug** that must be converted to **hydrocortisone (cortisol)** by 11β-hydroxysteroid dehydrogenase in the liver to become active. - Its glucocorticoid potency is approximately **0.8** relative to hydrocortisone (when hydrocortisone = 1). - Due to variable hepatic conversion, it has **lower and less predictable glucocorticoid effects** compared to other agents. *Fludrocortisone* - Primarily used for its **potent mineralocorticoid activity** (125× that of hydrocortisone). - However, it retains **significant glucocorticoid activity** approximately **10-15 times** that of hydrocortisone. - Despite being marketed as a mineralocorticoid, its glucocorticoid potency is **considerably higher than cortisone**. *Dexamethasone* - **Highly potent synthetic glucocorticoid** with negligible mineralocorticoid activity. - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Long duration of action (36-72 hours) and excellent CNS penetration. *Betamethasone* - **Highly potent synthetic glucocorticoid**, structurally similar to dexamethasone (differs only in stereochemistry at C-16). - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Minimal mineralocorticoid activity, with similar clinical applications to dexamethasone.
Question 642: Which of the following is the MOST CRITICAL indication for Acyclovir use during pregnancy?
- A. Treatment of disseminated herpes (Correct Answer)
- B. Treatment of chickenpox in the first trimester
- C. Prophylaxis for recurrent herpes during pregnancy
- D. Prevention of cytomegalovirus infection in pregnancy
Explanation: ***Treatment of disseminated herpes*** - **Disseminated herpes** in pregnancy is a severe, life-threatening condition for both the mother and the fetus, making acyclovir use critically indicated. - This systemic infection can lead to **visceral organ involvement**, **encephalitis**, and significantly increased maternal and fetal morbidity and mortality. - Immediate treatment with intravenous acyclovir is essential to prevent **multi-organ failure** and death. *Treatment of chickenpox in the first trimester* - While chickenpox in the first trimester can be serious, leading to **congenital varicella syndrome**, acyclovir's role here is primarily to mitigate maternal illness, not as critical as disseminated herpes. - The risk of congenital varicella syndrome for the fetus is relatively low (around 0.4%) after maternal infection in the first trimester. *Prophylaxis for recurrent herpes during pregnancy* - **Prophylactic acyclovir** in the third trimester is commonly used to prevent recurrent genital herpes and reduce the risk of **neonatal herpes**, but it is not as acutely critical as treating disseminated disease. - This intervention aims to prevent transmission during delivery rather than managing an immediate, life-threatening maternal or fetal condition. *Prevention of cytomegalovirus infection in pregnancy* - Acyclovir has **minimal activity against CMV** and is not indicated for CMV prevention or treatment. - **Ganciclovir** or **valganciclovir** are the antivirals used for CMV, not acyclovir.
Question 643: 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 644: 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.