A known type 1 diabetic presents with glucose 799 mg/dL, Na+ 128 mEq/L, Cl- 88 mEq/L, and signs of dehydration. Which of the following is NOT used in the initial management?
Hyperpigmentation in Addison's disease is due to increased secretion of:
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
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
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?
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?
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
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?
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?
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
NEET-PG 2025 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 21: A known type 1 diabetic presents with glucose 799 mg/dL, Na+ 128 mEq/L, Cl- 88 mEq/L, and signs of dehydration. Which of the following is NOT used in the initial management?
- A. 0.9 % Normal saline
- B. Potassium monitoring
- C. 3 % Saline (Correct Answer)
- D. IV infusion insulin
Explanation: Hypotonic conditions in Diabetic Ketoacidosis (DKA) are typically addressed with isotonic fluids. 3% saline is not used in initial management because it is reserved for severe cerebral edema or profound hypovolemia [3]. The immediate priority for fluid resuscitation in DKA is often 0.9% Normal Saline to correct volume depletion and hypotonicity [2], [4]. *0.9 % Normal saline* - This is essential for volume resuscitation to correct the severe dehydration (due to osmotic diuresis) and is the standard initial fluid administered in DKA [1], [2]. - It helps restore effective circulating volume and is initiated before insulin therapy to prevent vascular collapse [4]. *IV infusion insulin* - After initial fluid therapy is initiated, IV regular insulin infusion is crucial to transition the patient from a catabolic to an anabolic state, stopping ketone production and lowering blood glucose levels [2]. - Insulin therapy must be delayed until fluid resuscitation begins to prevent vascular collapse [4]. *Potassium monitoring* - Continuous and careful potassium monitoring is vital because acidosis and cellular shifts lead to rapid changes in serum potassium levels [2], [3]. - Potassium supplementation is often required if the serum potassium is < 5.5 mmol/L (or 5.2 mEq/L) to prevent life-threatening cardiac arrhythmias [2].
Question 22: Hyperpigmentation in Addison's disease is due to increased secretion of:
- A. C. Aldosterone
- B. D. Renin
- C. B. ACTH (Correct Answer)
- D. A. Cortisol
Explanation: ***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**.
Question 23: 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
- A. Respiratory acidosis
- B. Respiratory alkalosis
- C. Metabolic alkalosis
- D. Metabolic acidosis (Correct Answer)
Explanation: ***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].
Question 24: 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
- A. CXR
- B. CTPA (Correct Answer)
- C. ECG
- D. V/Q scan
Explanation: ***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].
Question 25: 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?
- A. Sitagliptin
- B. Empagliflozin (Correct Answer)
- C. Glimepiride
- D. Pioglitazone
Explanation: ***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.
Question 26: 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?
- A. Blood transfusion
- B. Darbepoetin alfa
- C. Intravenous iron infusion (Correct Answer)
- D. Oral iron therapy
Explanation: 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.
Question 27: 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
- A. Metabolic acidosis
- B. Metabolic alkalosis
- C. Chronic respiratory acidosis (Correct Answer)
- D. Acute respiratory acidosis
Explanation: ***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.
Question 28: 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?
- A. CT scan of the sacroiliac joints
- B. Bone scan
- C. MRI of the sacroiliac joints (Correct Answer)
- D. Anti CCP antibody
Explanation: ***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.
Question 29: 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?
- A. Add theophylline
- B. Add Montelukast
- C. Increase the dose of salbutamol
- D. Start L.A.B.A + inhaled corticosteroids (Correct Answer)
Explanation: ***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.
Question 30: 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
- A. UC
- B. CD
- C. PSC
- D. PBC (Correct Answer)
Explanation: ***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**.