Obstetrics and Gynecology
1 questionsWhich drug is contraindicated before delivery of the baby (during first and second stages of labor)?
NEET-PG 2015 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 411: Which drug is contraindicated before delivery of the baby (during first and second stages of labor)?
- A. Mifepristone
- B. Oxytocin
- C. Misoprostol
- D. Ergometrine (Correct Answer)
Explanation: ***Ergometrine*** - **Ergometrine** is a potent uterotonic agent that causes **tetanic (sustained) uterine contractions**. - It is **absolutely contraindicated before delivery of the baby** (during first and second stages of labor) because: - Sustained contractions lead to **fetal hypoxia** and **fetal distress** by reducing placental blood flow - Risk of **uterine rupture** due to excessive uterine tone - **Obstructed labor** and **cervical lacerations** from forcing delivery against sustained contraction - Ergometrine is **only used after delivery of the baby** in the third stage for active management and prevention of postpartum hemorrhage. *Mifepristone* - **Mifepristone** is an antiprogesterone used for medical abortion in early pregnancy or cervical ripening before labor induction. - It is not relevant during active labor as it acts by blocking progesterone receptors, not by causing immediate uterine contractions. *Oxytocin* - **Oxytocin** is the drug of choice for induction and augmentation of labor. - It causes **rhythmic, intermittent contractions** that allow for adequate placental perfusion between contractions. - Safe to use during first and second stages when properly monitored. *Misoprostol* - **Misoprostol** is a prostaglandin E1 analog used for cervical ripening and labor induction. - Can be used before and during labor for induction, though requires careful monitoring. - Unlike ergometrine, it does not cause sustained tetanic contractions when used in appropriate doses.
Pathology
4 questionsWhich antigen is tested in routine Rh typing?
What is the most common type of graft rejection?
Which of the following is a type of small vessel vasculitis?
Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 411: Which antigen is tested in routine Rh typing?
- A. C antigen
- B. D antigen (Correct Answer)
- C. A antigen
- D. B antigen
Explanation: ***D antigen*** - Routine Rh typing specifically tests for the **D antigen**, which determines the Rh status of an individual as Rh-positive or Rh-negative [1]. - The presence of the **D antigen** is crucial for blood transfusions and pregnancy management [1]. *A antigen* - The **A antigen** is tested in the context of the ABO blood group system, not specifically for Rh typing. - It does not provide information regarding the Rh factor which is critical in blood compatibility. *C antigen* - Similar to the **A antigen**, the **C antigen** is part of the broader Rh system but is not routinely assessed in standard Rh typing. - Its testing is typically reserved for specific clinical scenarios involving Rh incompatibility. *B antigen* - The **B antigen** pertains to the ABO blood group and does not relate to the Rh factor or routine Rh typing. - Rh typing is solely focused on the **presence of the D antigen** to determine the Rh status. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.
Question 412: What is the most common type of graft rejection?
- A. Hyperacute
- B. Acute (Correct Answer)
- C. Chronic
- D. Acute on chronic
Explanation: ***Acute*** - **Acute rejection** is the most common type of graft rejection, occurring in **10-40% of transplant recipients**. [1] - It typically occurs **days to weeks to months** after transplantation (most commonly within the first 6 months). [1] - Mediated primarily by **T-lymphocytes** (cellular rejection) or **antibodies** (antibody-mediated rejection) reacting against donor antigens. [1] - Usually **responsive to immunosuppressive therapy** when detected early. *Hyperacute* - **Hyperacute rejection** is rare (occurs in <1% of cases) due to routine **pre-transplant cross-matching**. - Occurs within **minutes to hours** after transplantation due to **pre-existing circulating antibodies** against donor antigens. [1] - Results in immediate thrombosis and graft necrosis, requiring **immediate graft removal**. [1] *Chronic* - **Chronic rejection** (chronic allograft dysfunction) develops **months to years** after transplantation. - It is the **most common cause of late graft failure**, but not the most common type of rejection episode. - Characterized by **gradual, progressive loss of graft function** with vascular and fibrotic changes. - **Largely irreversible** and poorly responsive to treatment. *Acute on chronic* - This is **not a primary category** of graft rejection but represents an **acute rejection episode superimposed** on a graft already undergoing chronic changes. - Reflects exacerbation in a chronically rejecting graft. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-242.
Question 413: Which of the following is a type of small vessel vasculitis?
- A. Classical PAN
- B. Giant cell arteritis
- C. Granulomatosis with polyangiitis (GPA) (Correct Answer)
- D. None of the options
Explanation: ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.
Question 414: Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -
- A. PAF (Correct Answer)
- B. NF-kB
- C. TNF-α
- D. TGF-β
Explanation: ***PAF*** - **Platelet-activating factor (PAF)** is primarily involved in **anaphylaxis**, **asthma**, and **allergic responses**, mediating inflammation through platelet aggregation and smooth muscle contraction. - While it has pro-inflammatory effects, it is **not a primary mediator** of the specific inflammatory cascade seen in radiotherapy-induced radiation pneumonitis. *TNF-α* - **Tumor Necrosis Factor-alpha (TNF-α)** is a crucial **pro-inflammatory cytokine** that plays a significant role in the initial acute phase of radiation pneumonitis. - It induces **cytotoxicity**, **apoptosis**, and the production of other inflammatory mediators, contributing to lung tissue damage. *TGF-β* - **Transforming Growth Factor-beta (TGF-β)** is a key cytokine involved in the **fibrotic phase** of radiation pneumonitis. - It promotes **fibroblast proliferation**, collagen synthesis, and extracellular matrix deposition, leading to lung scarring. *NF-kB* - **Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB)** is a master **transcription factor** that regulates the expression of numerous genes involved in inflammation and immune responses. - Radiation exposure **activates NF-kB**, leading to the transcription of various pro-inflammatory cytokines, including TNF-α, which contribute to radiation pneumonitis.
Pharmacology
4 questionsWhich class of antihypertensive drugs is known to cause erectile dysfunction?
Propranolol is most commonly prescribed as first-line therapy for which condition?
Which of the following is NOT a side effect of atropine?
Maximum cycloplegic action of atropine is seen at ?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 411: Which class of antihypertensive drugs is known to cause erectile dysfunction?
- A. Calcium channel blocker
- B. ACE inhibitors
- C. AT1 receptor antagonists
- D. Beta-blockers (Correct Answer)
Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients
Question 412: Propranolol is most commonly prescribed as first-line therapy for which condition?
- A. Atrioventricular (AV) block
- B. Hypertension (high blood pressure)
- C. Cardiac arrest
- D. Thyrotoxicosis (excessive thyroid hormones) (Correct Answer)
Explanation: ***Thyrotoxicosis (excessive thyroid hormones)*** - **Propranolol** is commonly prescribed as **first-line symptomatic therapy** for **thyrotoxicosis** to manage symptoms such as **tachycardia, tremors, palpitations, and anxiety**. - It works by **blocking peripheral conversion of T4 to T3** and providing rapid **symptomatic relief** through beta-blockade. - While it does not treat the underlying thyroid disorder, it is the **immediate first-line agent** for symptom control while definitive treatment (antithyroid drugs, radioiodine, or surgery) is being arranged. - **Clinical pearl:** Propranolol is preferred over selective beta-blockers due to its additional effect on T4 to T3 conversion. *Hypertension (high blood pressure)* - **Propranolol** is **NOT a first-line agent** for hypertension in current guidelines (JNC 8, ESC/ESH). - First-line agents include **ACE inhibitors, ARBs, thiazide diuretics, and calcium channel blockers**. - Non-selective beta-blockers like propranolol are typically **third-line or later** due to unfavorable metabolic effects and side effect profile. - Selective beta-blockers (atenolol, metoprolol) may be used in specific hypertension scenarios, but propranolol is rarely first-line. *Atrioventricular (AV) block* - **Propranolol** is **absolutely contraindicated** in **AV block** as it further slows conduction through the AV node. - Beta-blockers can precipitate **complete heart block** in patients with pre-existing conduction abnormalities. *Cardiac arrest* - **Propranolol** is **contraindicated** in acute management of **cardiac arrest** as it reduces cardiac contractility and can worsen outcomes. - Cardiac arrest management involves **CPR, defibrillation, epinephrine, and amiodarone**.
Question 413: Which of the following is NOT a side effect of atropine?
- A. Diarrhoea (Correct Answer)
- B. Urinary retention
- C. Confusion of elderly
- D. Blurring of vision
Explanation: ***Diarrhoea*** - Atropine is a **muscarinic antagonist** that blocks the action of **acetylcholine** on muscarinic receptors in the gastrointestinal tract. - This leads to **decreased GI motility** and **decreased secretions**, typically causing **constipation**, NOT diarrhoea. - Diarrhoea would be associated with **cholinergic agonists** or anticholinesterases, which increase GI motility. *Blurring of vision* - Atropine causes **mydriasis** (pupil dilation) and **cycloplegia** (paralysis of the ciliary muscle). - **Cycloplegia** impairs accommodation for near vision, leading to **blurring of vision**. - This is a common anticholinergic side effect. *Urinary retention* - Atropine blocks **M3 receptors** on the **detrusor muscle**, causing bladder relaxation and reduced contractility. - This leads to **urinary retention**, especially in patients with pre-existing conditions like **prostatic hypertrophy**. *Confusion in elderly* - Atropine can cross the **blood-brain barrier** and cause **CNS effects** including confusion, agitation, and delirium. - Elderly patients are particularly susceptible to these **central anticholinergic effects**.
Question 414: Maximum cycloplegic action of atropine is seen at ?
- A. 1-3 hours (Correct Answer)
- B. 1-2 weeks
- C. 4-6 hours
- D. 30-60 minutes
Explanation: ***1-3 hours*** - Atropine, a **non-selective muscarinic antagonist**, reaches its **peak cycloplegic effect** approximately 1 to 3 hours after topical administration. - This peak activity is crucial for accurate retinoscopy and **refractive error measurement** in children, as it effectively paralyzes the ciliary muscle. *4-6 hours* - While atropine's cycloplegic effect is still present at 4-6 hours, it is generally **past its peak action** by this time. - Slower-acting cycloplegics might have their peak around this window, but not atropine. *1-2 weeks* - The **duration of action** for atropine's cycloplegic and mydriatic effects can last for 1-2 weeks, but this is the total duration, not when the maximum action is observed. - Patients are often instructed about the **prolonged effects** and potential for blurred vision and photophobia over this period. *30-60 minutes* - While some mydriatic effects might start within 30-60 minutes, the **full cycloplegic effect** of atropine, which requires maximum paralysis of the ciliary muscle, is not achieved in this short timeframe. - Shorter-acting cycloplegics like **cyclopentolate** or **tropicamide** would show peak action within this earlier interval.
Physiology
1 questionsRebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 411: Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?
- A. Parietal cell hyperplasia
- B. Increased histamine release
- C. Hypergastrinemia (Correct Answer)
- D. Hypersensitivity of Ach receptors
Explanation: ***Hypergastrinemia*** - Proton pump inhibitors (PPIs) create a state of **hypochlorhydria** (reduced stomach acid), which in turn stimulates the **G cells** in the stomach to produce more **gastrin**. - This elevated gastrin level leads to a compensatory increase in the number and activity of **parietal cells**, causing a rebound hypersecretion of acid when PPI therapy is discontinued. *Parietal cell hyperplasia* - While parietal cell hyperplasia can occur, it is a consequence of chronic **hypergastrinemia**, not the primary driver of rebound acid secretion. - The direct effect of increased gastrin stimulating existing parietal cells is more immediate and significant for the rebound phenomenon. *Increased histamine release* - Elevated histamine release from **enterochromaffin-like (ECL) cells** is a downstream effect of hypergastrinemia, as gastrin stimulates ECL cells. - While increased histamine contributes to acid secretion, the root cause for its increase in this context is the **hypergastrinemia** induced by PPIs. *Hypersensitivity of Ach receptors* - **Acetylcholine (Ach) receptors** on parietal cells are involved in direct neural stimulation of acid secretion. - There is no evidence that stopping PPIs causes an increased sensitivity of these receptors, or that this is the primary mechanism of rebound acid secretion.