NEET-PG 2025 Practice Questions

Q: Hyperpigmentation in Addison's disease is due to increased secretion of:

B. ACTH. ***ACTH*** - In **primary adrenal insufficiency** (Addison's disease), low cortisol production results in loss of negative feedback to the pituitary gland, leading to massively increased secretion of **ACTH** (Adrenocorticotropic Hormone) [1]. - ACTH is synthesized from the precursor molecule **Pro-opiomelanocortin (POMC)**. Cleavage of POMC also generates Melanocyte-Stimulating Hormone (MSH) (or ACTH itself acts like MSH), which stimulates melanocytes, causing **hyperpigmentation** [1]. *Cortisol* - Cortisol levels are **low** in Addison's disease because of adrenal gland destruction, which is the underlying pathological issue [2]. - Cortisol is a glucocorticoid and its primary role is metabolic; it does not directly stimulate **melanogenesis**. *Aldosterone* - Aldosterone, a mineralocorticoid, is also deficient in primary Addison's disease, leading to **salt-wasting** and electrolyte disturbances (hyponatremia, hyperkalemia) [2]. - Aldosterone's synthesis pathway is distinct from that of the pituitary hormone ACTH and therefore does not influence **skin pigmentation**. *Renin* - Renin levels are often **elevated** in Addison's disease due to hypovolemia and hypotension resulting from aldosterone deficiency (activation of the **Renin-Angiotensin-Aldosterone System**) [3]. - Renin is an enzyme secreted by the kidney and has no direct mechanism or shared precursor pathway related to stimulating **melanocytes**.

Q: A 55-year-old man presents with altered sensorium and deep labored breathing. ABG is given below. What is the most likely acid-base disorder? pH: 7.20 pCO₂: 31 mmHg HCO₃⁻:16 mEq/L Na⁺: 130 mEq/L Cl⁻: 84 mEq/L PaO₂: 80 mmHg

Metabolic acidosis. ***Metabolic acidosis*** - The **low pH (7.20)** indicates **acidosis** [2]. The primary cause is low **bicarbonate (HCO₃⁻ 16 mEq/L)**, defining it as metabolic acidosis [1]. - This patient presents with **Kussmaul breathing** (deep, labored breathing) as a respiratory attempt to compensate (blowing off CO₂) for the underlying metabolic acidosis, suggested by the low **pCO₂ (31 mmHg)** [1]. *Metabolic alkalosis* - This would be characterized by a **high pH (>7.45)** and a **high HCO₃⁻** level, which is the opposite of the current findings [3]. - Commonly caused by conditions like **vomiting** or excessive intake of **alkali** substances [3]. *Respiratory acidosis* - This requires a **high pCO₂ (>45 mmHg)**, which is the cause of acidemia, typically due to **hypoventilation** or respiratory failure [2]. - The current pCO₂ (31 mmHg) is low, indicating **hyperventilation** (compensation). *Respiratory alkalosis* - This would show a **high pH (>7.45)** caused by a **low pCO₂ (<35 mmHg)** due to **hyperventilation** (e.g., anxiety, high altitude) [2]. - While pCO₂ is low, the pH is acidic (7.20), not alkaline, ruling out primary respiratory alkalosis [2].

Q: Old man underwent joint replacement surgery 3 days ago. Today he develops SOB with chest pain. O/E : pulse 100/min, BP 100/70 mm Hg, RR28/min and sp02: 85% room air. D-dimer is elevated. Which is the next best test

CTPA. ***CTPA*** - This is the **gold standard** for diagnosing acute pulmonary embolism (PE) by visualizing the filling defects in the pulmonary arteries [2]. - Given the high clinical suspicion (post-operative status, classical symptoms, elevated D-dimer) and hemodynamic instability, rapid confirmation with **CTPA** is essential for determining the need for treatments like thrombolysis [2], [3]. *V/Q scan* - **V/Q scans** are generally reserved for patients where CTPA is contraindicated, such as in severe renal failure or certain allergies, and are typically not performed in unstable patients [2]. - It frequently yields an intermediate probability result, which is less conclusive than a CTPA, especially when a definitive, rapid diagnosis is needed due to **hemodynamic compromise**. *ECG* - **ECG** is a vital part of the initial assessment to rule out conditions like acute myocardial infarction and to check for signs of right heart strain common in massive PE (e.g., S1Q3T3 pattern) [1]. - Although crucial for risk stratification, it is only a **supportive test** and is not the definitive diagnostic tool for confirming the presence of PE. *CXR* - The **CXR** is primarily useful for excluding other pulmonary pathologies that mimic PE, such as pneumonia or pneumothorax, and is often normal in the setting of acute PE [1]. - Findings associated with PE (like **Westermark's sign** or **Hampton hump**) are often subtle, non-specific, and lack the sensitivity required to confirm the diagnosis [1].

Q: A 56-year-old diabetic patient is currently on Metformin and Insulin Glargine. His HbA1c is 8.2 %, indicating suboptimal glycemic control. Echocardiography reveals a reduced ejection fraction (EF) of 35 %. Which of the following is the most appropriate agent to add to his current regimen?

Empagliflozin. ***Empagliflozin*** - Empagliflozin, an SGLT2 inhibitor, is the preferred agent due to its confirmed benefit in reducing **cardiovascular mortality** and **hospitalization for heart failure** (HFrEF, EF 35%). - Current guidelines recommend SGLT2 inhibitors as the **first-line add-on** for patients with Type 2 DM and established HFrEF, regardless of baseline glycemic control. *Pioglitazone* - Thiazolidinediones like Pioglitazone are **contraindicated** in patients with symptomatic or established heart failure (NYHA Class III or IV, which this patient likely approaches) due to the risk of **fluid retention** [1]. - This fluid retention can worsen the patient's existing **reduced ejection fraction** and precipitate acute decompensation [1]. *Glimepiride* - Sulfonylureas significantly increase the risk of **hypoglycemia**, which can be dangerous, especially in patients with co-existing severe cardiac disease. - Glimepiride offers no benefit in reducing **cardiovascular events** or **heart failure hospitalization** compared to the benefits provided by SGLT2 inhibitors. *Sitagliptin* - DPP-4 inhibitors are generally **weight and CV neutral** (aside from Saxagliptin, which is associated with increased HF risk in some studies). - They lack the robust evidence of **cardioprotective and renovasculoprotective effects** seen with SGLT2 inhibitors and are consequently suboptimal for a patient with established HFrEF.

Q: A 60-year-old man with chronic kidney disease presents with complaints of increasing fatigue, dyspnea on exertion, and signs of congestive heart failure. On evaluation, he is found to have anemia. What is the most appropriate next step in management?

Intravenous iron infusion. Intravenous iron infusion - Patients with chronic kidney disease (CKD) and anemia often have associated iron deficiency, which is necessary to correct before starting erythropoiesis-stimulating agents (ESAs). [1] - Intravenous iron is strongly preferred over oral iron in CKD, especially in dialysis patients, due to poor gastrointestinal absorption and high risk of non-compliance. Oral iron therapy - Oral iron is less effective and poorly tolerated in patients with CKD due to altered absorption and potential for gastrointestinal side effects. - It is not the initial treatment of choice when a rapid and efficient iron correction is needed to prepare for ESA therapy. Blood transfusion - This is reserved for patients with symptomatic severe anemia (e.g., severe dyspnea, hemodynamic instability) that is refractory to other treatments or requires immediate intervention. - Transfusion carries risks like volume overload (especially in heart failure) and sensitization, making it unsuitable as a routine initial step. Darbepoetin alfa - Darbepoetin alfa (an ESA) is used to correct the underlying erythropoietin deficiency in CKD-related anemia. [1] - ESAs are typically initiated only after iron stores have been adequately replenished (target ferritin >500 ng/mL or transferrin saturation >30%) to maximize response and minimize dosing.

Q: Patient with COPD presents with progressive dyspnea. ABG shows pH:7.32, pCO2 60 mm Hg and HCO3. which of the following is seen in

Chronic respiratory acidosis. ***Chronic respiratory acidosis*** - The high **pCO2 (60 mmHg)** indicates primary respiratory acidosis, while the relatively stable pH (**7.32** is mildly acidotic) implies significant renal compensation (elevated **HCO3-**) [1]. - This compensated state, where the pH is buffered despite chronic hypercapnia, is characteristic of a long-standing disease like **COPD** [1], [3]. *Acute respiratory acidosis* - If the acidosis were acute, there would be insufficient time for the kidneys to retain bicarbonate, resulting in a **more severe acidemia** (pH typically <7.25) for a pCO2 of 60 mmHg [2]. - An acute picture is less typical in a patient with stable COPD, which is inherently a **chronic condition** [1]. *Metabolic acidosis* - Metabolic acidosis is defined by a primary reduction in **HCO3-**, leading to a low pH [2]. - In this case, the acidemia is driven by the primary elevation of **pCO2** (hypercapnia), not a decrease in bicarbonate. *Metabolic alkalosis* - This condition is characterized by a primary increase in **HCO3-**, leading to an elevated pH (**alkalemia**). - Since the patient's pH is low (**acidemic**), and the primary driving force is CO2 retention, this diagnosis is incorrect.

Q: A young man presents with chronic lower back pain and morning stiffness and pain on bending that improves with activity. X ray of LS spine is normal. Ocular examination shows anterior uveitis. Which diagnostic modality will pick up the disease process at the earliest?

MRI of the sacroiliac joints. ***MRI of the sacroiliac joints*** - **MRI** is the most sensitive and specific tool for detecting early inflammatory changes in the **sacroiliic joints** (sacroiliitis), such as bone marrow edema (osteitis) [1]. - It is crucial when plain radiography is normal, as it detects inflammatory lesions years before structural bony changes become visible on X-ray or CT scan, facilitating early diagnosis of **Ankylosing Spondylitis**. *Anti CCP antibody* - The **Anti-Cyclic Citrullinated Peptide (Anti-CCP)** antibody is highly specific for **Rheumatoid Arthritis (RA)**, which presents differently, typically affecting small peripheral joints [2]. - The clinical presentation of chronic back pain, morning stiffness improving with activity, and anterior uveitis is classic for **Spondyloarthritis** (like Ankylosing Spondylitis), not RA [3]. *CT scan of the sacroiliac joints* - **CT scan** is excellent for visualizing bony erosions, sclerosis, and joint fusion, which are **late structural changes** in sacroiliitis. - However, it is less sensitive than MRI in detecting the **early, active inflammatory phase** (bone marrow edema) that occurs before joint damage is established. *Bone scan* - A **Bone scan** (Technetium-99m) is sensitive but **not site-specific**; it shows increased tracer uptake in inflamed areas but cannot distinguish between degenerative, traumatic, or inflammatory causes [2]. - Its use in diagnosing sacroiliitis is largely superseded by **MRI** due to the latter's superior spatial resolution and ability to depict active inflammation directly.

Q: A patient presents with morning stiffness and tests positive for anti-CCP antibodies. Which of the following histological features is most characteristic of the underlying disease?

Pannus formation and erosive joint damage. ***Pannus formation and erosive joint damage*** - **Anti-CCP antibodies** along with morning stiffness heavily suggest **Rheumatoid Arthritis (RA)**, whose defining feature is the proliferation of hyperplastic synovial tissue known as the **pannus** [1]. - The **pannus** invades and destroys the adjacent articular cartilage and subchondral bone, leading to characteristic joint **erosions** [1] and deformities [3]. *Non-caseating granulomas* - These histological findings are characteristic of systemic inflammatory conditions such as **Sarcoidosis** or certain types of inflammatory bowel disease like **Crohn's disease**. - Granulomas are distinct structures involving epithelioid macrophages and do not represent the primary destructive pathology in RA [1]. *Subepidermal blister with IgA deposits* - This pathology is specific to the skin disease **Dermatitis Herpetiformis**, often associated with Celiac disease. - It involves IgA deposition in the dermal papillae, which is completely irrelevant to the underlying joint pathology of RA. *Tophi with monosodium urate crystals* - These structures are the histological hallmarks of chronic **Gout**, resulting from the deposition of precipitated **monosodium urate** crystals usually surrounded by foreign-body giant cells [2]. - Gouty arthritis is clinically and immunologically distinct from RA, lacking anti-CCP antibody positivity. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1218-1220. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1214.

Q: Patient presents with dry cough, dyspnea and stridor. HPE of hilar LN shows stellate granulomas with giant cells and circular lamellated concretions on histopathology. Which of the following is the most likely diagnosis?

Sarcoidosis. ***Sarcoidosis*** - The histopathological finding of **stellate granulomas** (non-caseating) in the lymph node, combined with **circular lamellated concretions** (**Schaumann bodies**), is highly characteristic, if not pathognomonic, of **Sarcoidosis**. - The presentation of hilar lymphadenopathy (inferred from HPE of hilar LN) with dry cough and dyspnea is the most common manifestation of pulmonary sarcoidosis [1]. *Tuberculosis* - **Tuberculosis** typically results in granulomas that display **caseating necrosis** (cheese-like), a feature absent from the description of stellate granulomas. - Although TB causes hilar lymphadenopathy, it does not typically produce **Schaumann bodies** or exhibit the distinct, non-necrotizing stellate granuloma morphology. *GPA* - **Granulomatosis with Polyangiitis (GPA)** is characterized by **necrotizing vasculitis** and widespread **necrotizing granulomatous inflammation** involving the upper and lower respiratory tracts. - GPA granulomas are generally large and necrotizing, and they do not contain the specific organization or inclusion bodies like **Schaumann bodies** seen in sarcoidosis. *Hypersensitivity pneumonitis* - This condition involves scattered, often poorly formed, **non-necrotizing granulomas** typically located in the lung interstitium (centrilobular distribution). - Unlike sarcoidosis, generalized hilar lymph node involvement and the presence of classical **Schaumann bodies** or well-defined stellate granulomas are rare in Hypersensitivity Pneumonitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.

Q: A patient with recurrent episodes of PSVT (Paroxysmal Supraventricular Tachycardia) is being considered for long-term prophylactic therapy to prevent future episodes. Which of the following is the most appropriate preventive treatment?

Oral Verapamil. ***Oral Verapamil*** - This is a non-dihydropyridine **Calcium Channel Blocker** that effectively slows conduction and increases refractoriness in the **AV node**. - It is a standard oral medication used for the **long-term prevention (prophylaxis)** of recurrent PSVT, especially in cases of AVNRT or AVRT. *IV lignocaine* - Lignocaine (Lidocaine) is a **Class IB antiarrhythmic** primarily used to treat and prevent **ventricular arrhythmias** (premature ventricular contractions, VT). - It is generally ineffective for chronic prophylaxis of supraventricular tachycardias like PSVT. *IV Adenosine* - **Adenosine** is the preferred drug for the **acute termination** of PSVT due to its potent, transient block of the AV node (half-life of <10 seconds). - It has an extremely short half-life, making it unsuitable for a chronic, **oral preventive regimen**. *Oral Nifedipine* - Nifedipine is a **dihydropyridine Calcium Channel Blocker** primarily acting as a **peripheral vasodilator**. - It has minimal effects on the **AV nodal conduction** properties required for PSVT prophylaxis and is therefore not used for this purpose.

Question 1

Hyperpigmentation in Addison's disease is due to increased secretion of:

Accepted Answer

B. ACTH

Answer

C. Aldosterone

Answer

D. Renin

Answer

A. Cortisol

Question 2

A 55-year-old man presents with altered sensorium and deep labored breathing. ABG is given below. What is the most likely acid-base disorder?
pH: 7.20
pCO₂: 31 mmHg
HCO₃⁻:16 mEq/L
Na⁺: 130 mEq/L
Cl⁻: 84 mEq/L
PaO₂: 80 mmHg

Accepted Answer

Metabolic acidosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Answer

Metabolic alkalosis

Question 3

Old man underwent joint replacement surgery 3 days ago. Today he develops SOB with chest pain. O/E : pulse 100/min, BP 100/70 mm Hg, RR28/min and sp02: 85% room air. D-dimer is elevated. Which is the next best test

Accepted Answer

CTPA

Answer

CXR

Answer

ECG

Answer

V/Q scan

Question 4

A 56-year-old diabetic patient is currently on Metformin and Insulin Glargine. His HbA1c is 8.2 %, indicating suboptimal glycemic control. Echocardiography reveals a reduced ejection fraction (EF) of 35 %. Which of the following is the most appropriate agent to add to his current regimen?

Accepted Answer

Empagliflozin

Answer

Sitagliptin

Answer

Glimepiride

Answer

Pioglitazone

Question 5

A 60-year-old man with chronic kidney disease presents with complaints of increasing fatigue, dyspnea on exertion, and signs of congestive heart failure. On evaluation, he is found to have anemia. What is the most appropriate next step in management?

Accepted Answer

Intravenous iron infusion

Answer

Blood transfusion

Answer

Darbepoetin alfa

Answer

Oral iron therapy

Question 6

Patient with COPD presents with progressive dyspnea. ABG shows pH:7.32, pCO2 60 mm Hg and HCO3. which of the following is seen in

Accepted Answer

Chronic respiratory acidosis

Answer

Metabolic acidosis

Answer

Metabolic alkalosis

Answer

Acute respiratory acidosis

Question 7

A young man presents with chronic lower back pain and morning stiffness and pain on bending that improves with activity. X ray of LS spine is normal. Ocular examination shows anterior uveitis. Which diagnostic modality will pick up the disease process at the earliest?

Accepted Answer

MRI of the sacroiliac joints

Answer

CT scan of the sacroiliac joints

Answer

Bone scan

Answer

Anti CCP antibody

Question 8

A patient presents with morning stiffness and tests positive for anti-CCP antibodies. Which of the following histological features is most characteristic of the underlying disease?

Accepted Answer

Pannus formation and erosive joint damage

Answer

Subepidermal blister with IgA deposits

Answer

Tophi with monosodium urate crystals

Answer

Non-caseating granulomas

Question 9

Patient presents with dry cough, dyspnea and stridor. HPE of hilar LN shows stellate granulomas with giant cells and circular lamellated concretions on histopathology. Which of the following is the most likely diagnosis?

Accepted Answer

Sarcoidosis

Answer

GPA

Answer

Hypersensitivity pneumonitis

Answer

Tuberculosis

Question 10

A patient with recurrent episodes of PSVT (Paroxysmal Supraventricular Tachycardia) is being considered for long-term prophylactic therapy to prevent future episodes. Which of the following is the most appropriate preventive treatment?

Accepted Answer

Oral Verapamil

Answer

IV Adenosine

Answer

Oral Nifedipine

Answer

IV lignocaine

NEET-PG 2025

Internal Medicine

Pathology

Pharmacology