FMGE 2025 - Internal Medicine Practice Questions

Q: CSF shows abundant PMNs with low sugar and elevated proteins. Diagnosis is?

Acute bacterial meningitis. ***Acute bacterial meningitis*** - The findings of abundant **Polymorphonuclear leukocytes (PMNs)**, **low CSF glucose** (due to bacterial consumption), and **elevated protein** are the classic triad for an acute bacterial infection of the meninges [1]. - A high PMN count indicates an acute inflammatory response, and the profound hypoglycemia and marked protein elevation distinguish it from most viral etiologies [1]. *Tubercular Meningitis* - While also associated with **low CSF glucose** and **elevated protein**, the predominant cell type is typically **lymphocytic** (mononuclear cells), not PMNs [3]. - The CSF often appears xanthochromic, and organisms like *M. tuberculosis* generally cause a subacute or chronic presentation rather than the acute presentation suggested by abundant PMN presence [3]. *Viral encephalitis* - CSF analysis usually reveals a **lymphocytic pleocytosis** (a higher proportion of lymphocytes), not a PMN predominance. - Glucose levels are typically **normal**, and protein elevation is usually mild to moderate, not markedly elevated. *Viral meningitis* - Similar to viral encephalitis, viral meningitis primarily causes a **lymphocytic pleocytosis** with a transient PMN phase early on, which quickly shifts to lymphocytes [2]. - The defining feature differentiating it from bacterial or tubercular meningitis is the **normal CSF glucose** level and milder protein elevation [2].

Q: Which of the following is a recommended treatment for esophageal varices?

Endoscopic ligation. ***Endoscopic ligation*** - This is a first-line endoscopic therapy for both actively bleeding esophageal varices and for the primary and secondary prevention of variceal hemorrhage [1]. - The procedure, also known as **variceal banding**, involves placing small rubber bands around the varices to ligate them, leading to thrombosis and eventual sloughing off [1]. *Transjugular intrahepatic portosystemic shunt (TIPS)* - TIPS is considered a second-line or salvage therapy for variceal bleeding that is refractory to endoscopic and pharmacological treatments [2]. - It is an invasive procedure that creates a shunt to reduce **portal pressure**, but it is reserved for uncontrolled bleeding due to risks such as **hepatic encephalopathy** [2]. *Intravenous labetalol* - While non-selective beta-blockers like **propranolol** or **nadolol** are used for the prophylaxis of variceal bleeding, they are not the treatment for an acute bleed. Vasoactive drugs like **terlipressin** or **octreotide** are used instead [1]. - Labetalol is a beta-blocker primarily used to manage **hypertension** and is not indicated for the acute management of variceal hemorrhage. *Oral amoxicillin* - Antibiotic prophylaxis (typically with intravenous third-generation cephalosporins like **ceftriaxone**) is recommended in patients with cirrhosis and variceal bleeding to prevent **spontaneous bacterial peritonitis (SBP)**. - Antibiotics do not treat the varices directly or stop the bleeding; they are given to reduce mortality associated with infections in this patient population.

Q: A follow-up patient of GERD on endoscopy was having a nodule in the 2nd part of the duodenum, which hormone are you suspecting to be raised?

Gastrin. ***Gastrin*** - The presence of a nodule in the second part of the duodenum, a common location within the **gastrinoma triangle** (Passaro's triangle), combined with GERD, strongly suggests a **gastrinoma**. - Gastrinomas cause **Zollinger-Ellison Syndrome (ZES)** by secreting excessive **gastrin**, which leads to gastric acid hypersecretion, resulting in refractory peptic ulcers and severe GERD [1]. *Inulin* - **Inulin** is a polysaccharide, not a hormone, and it is used clinically to measure the **glomerular filtration rate (GFR)**. - If this option meant **insulin**, an insulinoma would cause symptoms of **hypoglycemia**, such as sweating, tremors, and confusion, not GERD. *VIP* - A tumor secreting **Vasoactive Intestinal Peptide (VIPoma)** causes **WDHA syndrome**, characterized by **W**atery **D**iarrhea, **H**ypokalemia, and **A**chlorhydria. - This condition is associated with **low stomach acid** (achlorhydria), which is contrary to the hyperacidity that causes GERD. *Glucagon* - A **glucagonoma** is a tumor that secretes excess glucagon, leading to a syndrome characterized by **diabetes mellitus** and a classic skin rash known as **necrolytic migratory erythema**. - It is not associated with gastric acid hypersecretion or duodenal nodules presenting with GERD.

Q: A 16-year-old boy presents with multiple episodes of abdominal pain and a history of passing blood in his stools. On examination, he has darkly pigmented spots on his lips and oral mucosa. Endoscopy reveals multiple hamartomatous polyps in the small intestine. What is the most likely diagnosis?

Peutz-Jeghers Syndrome. ***Peutz-Jeghers Syndrome*** - This is an autosomal dominant disorder characterized by the classic triad of **hamartomatous polyps** in the GI tract (especially the small intestine), **mucocutaneous hyperpigmentation** (dark spots on lips, oral mucosa), and an increased risk of cancer [1]. - The patient's symptoms of abdominal pain and GI bleeding are common complications due to the polyps, which can lead to **intussusception** or ulceration. *Familial Adenomatous Polyposis* - This syndrome is defined by the presence of hundreds to thousands of **adenomatous polyps** in the colon, not hamartomatous polyps as seen in this patient [1]. - It is not associated with the characteristic **perioral mucocutaneous pigmentation** which is a hallmark feature of Peutz-Jeghers syndrome. *Juvenile Polyposis Syndrome* - This condition also involves **hamartomatous polyps**, but they are most commonly found in the colon and rectum, and the syndrome lacks the distinct mucocutaneous pigmentation [1]. - While patients can present with GI bleeding, the combination of small intestine polyps and pigmented lip spots points away from this diagnosis. *Cronkhite-Canada Syndrome* - This is a rare, non-hereditary syndrome typically affecting older adults, characterized by GI polyposis along with ectodermal changes like **alopecia** (hair loss) and **onychodystrophy** (nail changes). - Patients often present with severe diarrhea and **protein-losing enteropathy**, which are not features described in this case.

Q: A young patient experiences shortness of breath specifically during exercise in winter, which subsides after using salbutamol. What is the most likely explanation for this condition?

Exercise-induced bronchoconstriction triggered by cold air. ***Exercise-induced bronchoconstriction triggered by cold air*** - This patient presents with classic **Exercise-Induced Bronchoconstriction (EIB)**, previously known as exercise-induced asthma - **Key clinical features:** Dyspnea occurring during/after exercise, worsened by cold/dry air, rapid response to beta-2 agonists (salbutamol) [1] - **Pathophysiology:** Exercise increases ventilation → inhalation of cold, dry air → water loss from airway surface → increased osmolarity → mast cell degranulation and inflammatory mediator release → bronchoconstriction - Cold air is a potent trigger as it increases airway heat and water loss - Salbutamol (short-acting beta-2 agonist) provides rapid bronchodilation, confirming bronchospasm as the mechanism *Decreased cardiac output stimulates baroreceptors* - Baroreceptors respond to changes in blood pressure, not directly related to bronchospasm - Would not explain the rapid response to salbutamol - Cardiac dysfunction would present with different symptoms (fatigue, peripheral edema) [1] *Hyperventilation-induced respiratory alkalosis* - While exercise increases respiratory rate, respiratory alkalosis causes paresthesias, lightheadedness, not primarily dyspnea - Does not explain the seasonal (winter) pattern - Would not respond specifically to bronchodilators *Vagal stimulation due to cold air exposure* - Cold air can trigger vagal reflexes, but this would cause bradycardia and peripheral vasoconstriction - Vagal bronchomotor tone increases airway resistance but doesn't fully explain the exercise + cold air synergy - The dramatic response to salbutamol indicates beta-2 receptor-mediated bronchodilation is the primary mechanism

Q: A patient presents with fatigue, anemia, and hepatomegaly. Hemoglobin electrophoresis reveals the presence of HbS. What will be the appropriate treatment?

Hydroxyurea. Correct: Hydroxyurea - This is the primary disease-modifying therapy for Sickle Cell Disease (SCD), significantly reducing the frequency of vaso-occlusive crises and acute chest syndrome [1]. - It works by increasing the production of fetal hemoglobin (HbF), which interferes with HbS polymerization and subsequent sickling of red blood cells [1]. - Hydroxyurea is the first-line chronic management for symptomatic SCD patients [1]. *Incorrect: Blood transfusion* - Transfusions are reserved for acute, life-threatening complications of SCD, such as aplastic crisis, severe exacerbation of anemia, or prevention of stroke in high-risk patients [1]. - Chronic routine transfusions carry risks of iron overload (hemosiderosis) and alloimmunization, making them generally unsuitable for standard chronic management. *Incorrect: Iron supplementation* - Sickle cell anemia is a hemolytic anemia typically resulting in elevated iron stores due to chronic hemolysis, and if transfusions are given, iron overload (hemosiderosis) is a major concern. - Iron supplementation is contraindicated unless a specific, documented iron deficiency is present, as it can worsen iron deposition in vital organs. *Incorrect: Vitamin B12 supplementation* - Vitamin B12 is primarily used to treat megaloblastic anemia resulting from B12 deficiency (e.g., pernicious anemia). - SCD anemia is caused by chronic extravascular hemolysis, and while folic acid is often required due to high cell turnover, B12 is not the targeted treatment for HbS pathology.

Q: Which of the following genetic mutations is most commonly associated with familial cases of Amyotrophic Lateral Sclerosis (ALS)?

SOD1 gene mutation. ***SOD1 gene mutation***- Mutations in the **Superoxide Dismutase 1 (SOD1)** gene are historically significant and account for approximately 15–20% of all familial ALS cases.- The SOD1 protein is located in the cytoplasm and mitochondria, and mutations lead to toxic misfolding and aggregation, resulting in **motor neuron death**.*CFTR gene mutation*- The **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene mutation is critically linked to the development of **Cystic Fibrosis**, a severe disorder of exocrine glands.- This mutation primarily affects chloride ion transport across epithelia, leading to highly viscous secretions, particularly in the airways and pancreas, not motor neuron disease.*HTT gene mutation*- Mutations involving the **HTT (Huntingtin)** gene, specifically expanded **CAG trinucleotide repeats**, cause **Huntington's disease**.- Huntington’s disease is characterized by progressive degeneration of the **striatum** and cortex, leading to movement abnormalities (*chorea*), cognitive decline, and psychiatric symptoms, distinct from ALS.*FMR1 gene mutation*- The **FMR1 (Fragile X Messenger Ribonucleoprotein 1)** gene is responsible for **Fragile X syndrome**, the most common inherited cause of intellectual disability.- The mutation involves expansion of the **CGG trinucleotide repeat**, typically leading to transcriptional silencing and symptoms like macroorchidism and behavioral issues, not primary motor neuron degeneration.

Q: A patient with chronic kidney disease presents with severe anemia. Laboratory tests reveal normocytic, normochromic anemia. What is the most appropriate treatment to manage this patient's anemia?

Darbepoetin alfa. ***Darbepoetin alfa*** - Anemia in **Chronic Kidney Disease (CKD)** is predominantly caused by decreased production of **erythropoietin** by the failing kidneys, resulting in normocytic, normochromic anemia [1] - **Darbepoetin alfa** is a long-acting **Erythropoiesis-Stimulating Agent (ESA)** that replaces the deficient hormone, directly correcting the underlying cause of anemia in CKD - This is the **standard of care** for managing anemia in CKD patients with normocytic, normochromic presentation *Folic acid supplementation* - Indicated for **megaloblastic anemia** due to **folate deficiency**, which presents as macrocytic anemia (high MCV) [2] - Does not stimulate red blood cell production directly and is ineffective against the primary defect of **erythropoietin deficiency** in CKD - The patient's normocytic anemia excludes folate deficiency [2] *Vitamin B12 injection* - Standard treatment for Vitamin B12 deficiency (e.g., **pernicious anemia**), which causes macrocytic, megaloblastic anemia [2] - The patient presents with **normocytic** anemia, indicating the deficiency is not related to B12 or folate metabolism - No indication for B12 supplementation in this clinical scenario *Iron chelation therapy* - **Iron chelation** is used to treat severe **iron overload** (hemochromatosis) or toxicity, not to treat anemia - Patients with CKD-related anemia often require supplemental **iron** to enhance their response to ESAs like Darbepoetin alfa - Using chelation would be counterproductive and worsen the anemia

Question 1

CSF shows abundant PMNs with low sugar and elevated proteins. Diagnosis is?

Accepted Answer

Acute bacterial meningitis

Answer

Viral encephalitis

Answer

Tubercular Meningitis

Answer

Viral meningitis

Question 2

Which of the following is a recommended treatment for esophageal varices?

Accepted Answer

Endoscopic ligation

Answer

Transjugular intrahepatic portosystemic shunt (TIPS)

Answer

Intravenous labetalol

Answer

Oral amoxicillin

Question 3

A follow-up patient of GERD on endoscopy was having a nodule in the 2nd part of the duodenum, which hormone are you suspecting to be raised?

Accepted Answer

Gastrin

Answer

Inulin

Answer

Glucagon

Answer

VIP

Question 4

A 16-year-old boy presents with multiple episodes of abdominal pain and a history of passing blood in his stools. On examination, he has darkly pigmented spots on his lips and oral mucosa. Endoscopy reveals multiple hamartomatous polyps in the small intestine. What is the most likely diagnosis?

Accepted Answer

Peutz-Jeghers Syndrome

Answer

Cronkhite-Canada Syndrome

Answer

Juvenile Polyposis Syndrome

Answer

Familial Adenomatous Polyposis

Question 5

A young patient experiences shortness of breath specifically during exercise in winter, which subsides after using salbutamol. What is the most likely explanation for this condition?

Accepted Answer

Exercise-induced bronchoconstriction triggered by cold air

Answer

Decreased cardiac output stimulates baroreceptors

Answer

Vagal stimulation due to cold air exposure

Answer

Hyperventilation-induced respiratory alkalosis

Question 6

A patient presents with fatigue, anemia, and hepatomegaly. Hemoglobin electrophoresis reveals the presence of HbS. What will be the appropriate treatment?

Accepted Answer

Hydroxyurea

Answer

Blood transfusion

Answer

Iron supplementation

Answer

Vitamin B12 supplementation

Question 7

Which of the following genetic mutations is most commonly associated with familial cases of Amyotrophic Lateral Sclerosis (ALS)?

Accepted Answer

SOD1 gene mutation

Answer

HTT gene mutation

Answer

CFTR gene mutation

Answer

FMR1 gene mutation

Question 8

A 15-year-old boy presents with tremors, difficulty in speech, and behavioral changes. On examination, he has hepatomegaly and a golden-brown ring at the limbus of the cornea (Kayser-Fleischer ring). Wilson's disease is suspected. Which of the following is the best investigation to support the diagnosis?

Accepted Answer

Liver biopsy for copper estimation

Answer

Serum ceruloplasmin

Answer

Copper excretion in urine

Answer

Serum copper

Question 9

A 39-year-old male with symptoms of stress and work-life imbalance is diagnosed with Stage 2 hypertension (blood pressure 150/95 mmHg on three separate occasions) and impaired fasting glucose (120 mg/dL). What is the most appropriate pharmacological management?

Accepted Answer

Start telmisartan

Answer

Start thiazide diuretic

Answer

Advise rest only, no pharmacological treatment

Answer

Start glucocorticoids

Question 10

A patient with chronic kidney disease presents with severe anemia. Laboratory tests reveal normocytic, normochromic anemia. What is the most appropriate treatment to manage this patient's anemia?

Accepted Answer

Darbepoetin alfa

Answer

Vitamin B12 injection

Answer

Folic acid supplementation

Answer

Iron chelation therapy

FMGE 2025 — Internal Medicine