NEET-PG 2025 Practice Questions

Q: A patient with a known history of bronchial asthma is currently on salbutamol and ipratropium via MDI. He now presents with nocturnal worsening of symptoms and night time awakening. What is the next best step in management?

Start L.A.B.A + inhaled corticosteroids. ***Start L.A.B.A + inhaled corticosteroids*** - Nocturnal symptoms and night-time awakening indicate persistent or **partially controlled asthma**, necessitating a step-up in therapy (Step 3 or higher treatment based on GINA guidelines) [1]. - The preferred step-up involves adding a daily **low-dose inhaled corticosteroid (ICS)**, often combined with a **Long-Acting Beta Agonist (LABA)**, to address underlying inflammation and provide long-acting bronchodilation [1]. *Increase the dose of salbutamol* - **Salbutamol is a Short-Acting Beta Agonist (SABA)**, used for quick relief (rescue medication), not for controlling chronic inflammation or preventing nocturnal symptoms. - Increasing SABA use without adding anti-inflammatory medication (ICS) is an inappropriate strategy for managing **persistent asthma** and signals poor control. *Add theophylline* - Theophylline is a non-selective phosphodiesterase inhibitor, which is a **less preferred add-on therapy** (Step 4/5) due to its narrow therapeutic index and significant risk of **adverse effects** (e.g., arrhythmias, seizures). - This option is generally reserved for patients who remain symptomatic despite adequate ICS/LABA combination therapy. *Add Montelukast* - Montelukast (a **leukotriene receptor antagonist**) is an optional, less potent add-on therapy typically considered if symptoms persist despite ICS use or if the patient has significant **allergic rhinitis**. - It is **less effective** than adding an ICS-LABA combination when stepping up treatment for poorly controlled persistent asthma.

Q: The patient presents with fatigue and pruritus. LFT shows gross SALP elevation and elevated conjugated bilirubin. AMA is seen with liver biopsy shows florid bile ductular lesions. Diagnosis is

PBC. ***PBC*** - The presentation of **fatigue** and **pruritus**, severe **SALP elevation** (indicative of cholestasis), and a positive **Anti-Mitochondrial Antibody (AMA)** titer is the classic diagnostic hallmark of Primary Biliary Cholangitis [1], [3]. - The liver biopsy finding of **florid bile ductular lesions** (destruction of small to medium-sized intrahepatic bile ducts) is the pathognomonic histological feature of this disease [3]. *PSC* - While PSC (Primary Sclerosing Cholangitis) also causes cholestasis, it is typically **AMA-negative** and highly associated with Ulcerative Colitis [2], [3]. - Diagnosis of PSC requires imaging (MRCP/ERCP) showing characteristic **bile duct strictures** and **"beading"**, which are not implied by the provided histological description [2]. *UC* - Ulcerative Colitis is an **Inflammatory Bowel Disease (IBD)** affecting the colon, not a primary cholestatic liver disease itself. - Although UC is strongly linked to PSC, it does not explain the patient's **AMA positivity** or the specific destructive **florid bile duct lesions** seen on biopsy [3]. *CD* - Crohn's Disease is also an IBD, characterized by **transmural inflammation** and often affecting the terminal ileum and colon. - The primary features (pruritus, high SALP, AMA+) point directly to PBC, not the common clinical manifestations or liver associations typically seen with **Crohn's Disease**.

Q: A 30-year-old man develops an increase in shoe size with coarse facies and large hands. IGF1 is elevated. What is the investigation of choice?

Failure to suppress GH by OGTT. ***Failure to suppress GH by OGTT*** - This is the **gold standard dynamic test** for confirming acromegaly, as it proves autonomous and unregulated **Growth Hormone (GH)** secretion [1]. - In healthy individuals, glucose load suppresses GH levels (typically to <1 ng/mL), but this suppression fails in patients with GH-secreting tumors [1]. *IGF-1 levels* - While highly sensitive for screening and monitoring, elevated **Insulin-like Growth Factor 1 (IGF-1)** levels alone are not definitive for diagnosis [2]. - IGF-1 levels must be confirmed with a dynamic test because they can be influenced by other factors like malnutrition or chronic liver failure [2]. *Failure to suppress IGF-1 by OGTT* - The definitive OGTT suppression test measures the suppression of **GH**, not IGF-1; IGF-1 reflects integrated GH production [1]. - While IGF-1 levels are used for diagnosis and monitoring, measuring its failure to suppress during OGTT is not the primary definition of diagnostic test failure. *GH levels* - A single random measurement of **Growth Hormone (GH)** is unreliable for diagnosis because GH is secreted in a highly pulsatile manner [1]. - Dynamic testing, such as the **Oral Glucose Tolerance Test (OGTT)**, is mandatory to confirm the pathological non-suppressibility of GH [1].

Q: A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?

Decreased urinary citrate. ***Decreased urinary citrate*** - **Hydrochlorothiazide** (HCTZ) can cause hypokalemia associated with **metabolic alkalosis** - Metabolic alkalosis leads to **decreased urinary citrate** excretion (hypocitraturia) - **Citrate is a key inhibitor** of calcium oxalate and calcium phosphate stone formation by complexing with urinary calcium - Hypocitraturia theoretically increases stone formation risk by reducing this protective effect - **Clinical Note:** Despite this mechanism, thiazides are actually used to **prevent** recurrent calcium stones due to their dominant effect of reducing urinary calcium excretion *Increased urinary calcium* - This would promote stone formation, but thiazides actually **decrease** urinary calcium excretion (hypocalciuria) - The calcium-lowering effect is why thiazides are used therapeutically for **preventing** calcium nephrolithiasis - In this question, the mechanism relates to altered citrate, not calcium excretion *Decreased urinary calcium* - Thiazides do decrease urinary calcium, which is **protective** against stones, not causative - This is the primary beneficial effect that makes thiazides useful in preventing recurrent calcium nephrolithiasis - The stone formation in the question stem relates to the **citrate** mechanism, not calcium *Increased urinary citrate* - Increased citrate would be **protective** against stone formation by binding urinary calcium - Thiazides cause the opposite effect: **hypocitraturia** (decreased citrate) due to associated metabolic alkalosis - Higher urinary citrate is actually a therapeutic goal in stone prevention

Q: What is true about the investigation shown below?

Invasive procedure. ***Invasive procedure*** - The image depicts a form of **Urography** (likely Intravenous Urography or IVU), which requires the **intravenous injection** of a contrast medium, making it an invasive procedure. - If the image were a Retrograde Pyelogram (RGP), it would also be invasive, requiring instrumentation via **cystoscopy** up to the ureteric orifices. *Non invasive procedure to visualize ureteropelvic junction* - This statement is incorrect because the procedure requires the introduction of contrast material into the body, either intravenously or directly into the urinary system, which classifies it as **invasive**. - While it effectively visualizes the **ureteropelvic junction (UPJ)**, non-invasive imaging like **Ultrasound** or **Non-contrast CT** does not require contrast injection. *Gold standard for bladder cancer* - The gold standard investigation for diagnosing and staging bladder cancer is **Cystoscopy with Biopsy**, not urography. - Urography is primarily used to evaluate the **upper urinary tract** (kidneys and ureters) for filling defects, strictures, or stones. *Done percutaneously* - This procedure, typically an IVU, involves **intravenous access** for contrast injection, not a percutaneous stab into the kidney or other structures. - **Antegrade pyelography** is the investigation done percutaneously, usually through a **nephrostomy tube**, but this image represents broader visualization.

Question 1

A patient with a known history of bronchial asthma is currently on salbutamol and ipratropium via MDI. He now presents with nocturnal worsening of symptoms and night time awakening. What is the next best step in management?

Accepted Answer

Start L.A.B.A + inhaled corticosteroids

Answer

Add theophylline

Answer

Add Montelukast

Answer

Increase the dose of salbutamol

Question 2

The patient presents with fatigue and pruritus. LFT shows gross SALP elevation and elevated conjugated bilirubin. AMA is seen with liver biopsy shows florid bile ductular lesions. Diagnosis is

Accepted Answer

PBC

Answer

UC

Answer

CD

Answer

PSC

Question 3

A 30-year-old man develops an increase in shoe size with coarse facies and large hands. IGF1 is elevated. What is the investigation of choice?

Accepted Answer

Failure to suppress GH by OGTT

Answer

Failure to suppress IGF-1 by OGTT

Answer

GH levels

Answer

IGF-1 levels

Question 4

A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?

Accepted Answer

Decreased urinary citrate

Answer

Increased urinary citrate

Answer

Decrease urinary calcium

Answer

Increase urinary calcium

Question 5

What is true about the investigation shown below?

Accepted Answer

Invasive procedure

Answer

Gold standard for bladder cancer

Answer

Done percutaneously

Answer

Non invasive procedure to visualize ureteropelvic junction

NEET-PG 2025

Internal Medicine

Pharmacology

Radiology