FMGE 2023 — Internal Medicine
43 Previous Year Questions with Answers & Explanations
A large 'V' wave on jugular venous pulse (JVP) examination is characteristic of:
Which of the following is least likely to cause mucormycosis?
A 35-year-old woman takes aspirin for a headache, later presented with wheezing and breathlessness. Along with these two symptoms, what other clinical findings are likely to be found in this condition?
A 20-year-old male presented with yellowish discoloration of his skin and sclera. He is otherwise normal. He gives a history of viral infection 10 days ago, which was resolved 2 days back. He also gives a history of similar episodes in the past following any illness. Lab values are given below. What is the most likely diagnosis? Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1mg/dL Conjugated bilirubin: 0.3mg/dL Serum AST and ALT: Normal
A 25-year-old male presents with mild jaundice noticed during a recent febrile illness. He gives a history of similar episodes in the past following any illness or periods of fasting. Physical examination reveals mild icterus with no hepatosplenomegaly. Lab values are given below: Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1 mg/dL Conjugated bilirubin: 0.3 mg/dL Serum AST and ALT: Normal What is the most likely diagnosis?
Which of the following is a sensitive and specific marker of intestinal inflammation?
A patient comes to you with increased cough, increased breathlessness, and decreased exercise capacity. Chest X-ray shows pulmonary fibrosis. Which drug can be administered in the given condition?
A 50-year-old female patient with a known case of ovarian cancer presents with difficulty in activities like climbing stairs, getting up from a chair, combing hair, etc. The following characteristic sign was found on examination. The most probable diagnosis is:
A young male patient presents with ptosis and muscle weakness, which reportedly worsens in the evening and improves in the morning. This is relieved by neostigmine. What is the likely diagnosis?
A diabetic patient developed DVT with a necrolytic migratory rash. What is the most likely diagnosis?
FMGE 2023 - Internal Medicine FMGE Practice Questions and MCQs
Question 1: A large 'V' wave on jugular venous pulse (JVP) examination is characteristic of:
- A. Tricuspid regurgitation (Correct Answer)
- B. Aortic regurgitation
- C. Tricuspid stenosis
- D. Atrial fibrillation
Explanation: ***Tricuspid regurgitation*** - A large **'V' wave** (ventricular systole) on JVP signifies increased pressure in the right atrium due to substantial **regurgitant flow** back from the right ventricle against a closed tricuspid valve.- This results in the rapid filling and distention of the right atrium during ventricular systole, often accompanied by the blunting or absence of the normal **'x' descent** (the 'x' descent is replaced by a systolic wave).*Aortic regurgitation* - Aortic regurgitation (AR) primarily affects the **left heart** and does not directly alter the established right heart pressure waveforms seen in the JVP [1].- Clinical signs of AR include a wide **pulse pressure**, **water-hammer pulse**, and diastolic murmur, but not specific waveform changes on JVP [3].*Tricuspid stenosis*- **Tricuspid stenosis** causes resistance to flow from the RA to the RV, leading to an exaggerated pressure rise during RA contraction, resulting in a prominent (tall) **'a' wave** [2].- The **'y' descent** is typically slow or attenuated because the rapid filling phase of the RV is impaired by the stenotic valve [2].*Atrial fibrillation* - In **atrial fibrillation (AFib)**, the uncoordinated atrial activity eliminates the mechanical contraction of the atria, causing the JVP tracing to lose the distinct **'a' wave**.- The ventricular rate is typically rapid and irregular, making JVP waveforms irregular, but it does not specifically cause a massive 'V' wave.
Question 2: Which of the following is least likely to cause mucormycosis?
- A. Neutropenia
- B. Broad spectrum antibiotics (Correct Answer)
- C. Uncontrolled diabetes without DKA
- D. Prolonged use of steroid
Explanation: ***Broad spectrum antibiotics*** - While broad-spectrum antibiotics predispose to many fungal infections (especially *Candida* infections) by disrupting the normal **microbiome**, they are not typically considered a direct, primary risk factor for **mucormycosis** [1]. - *Mucorales* are ubiquitous molds, and their pathogenicity is primarily related to defects in **phagocytic function** (like in neutropenia) [2] or **acidosis/iron overload** (like in DKA), not bacterial flora changes [2]. *Neutropenia* - Profound **neutropenia** (low neutrophil count) significantly impairs the host's ability to clear fungal spores, making it one of the most important risk factors for invasive mold infections, including **mucormycosis** [2]. - Neutrophils are crucial for the primary defense against **Mucorales** by killing the spores and hyphae. *Uncontrolled diabetes without DKA* - Even without **diabetic ketoacidosis (DKA)**, poorly controlled diabetes leads to impaired phagocyte function and immunosuppression, increasing the risk of invasive fungal infections like *Mucorales* and **Candida** [2], [3]. - The high glucose environment, especially in the **nasal mucosa**, can facilitate the growth and invasion of these fungi. *Prolonged use of steroid* - Glucocorticoids cause generalized **immunosuppression** by impairing the function of phagocytes and T-lymphocytes, thereby increasing susceptibility to opportunistic infections [3]. - High-dose or prolonged corticosteroid use is a well-established risk factor for severe and disseminated **mucormycosis** as it compromises the innate immune response.
Question 3: A 35-year-old woman takes aspirin for a headache, later presented with wheezing and breathlessness. Along with these two symptoms, what other clinical findings are likely to be found in this condition?
- A. IgE release
- B. Nasal polyp (Correct Answer)
- C. Extrinsic asthma
- D. Drug interaction
Explanation: ***Nasal polyp***- This clinical scenario is classic for **Aspirin-Exacerbated Respiratory Disease (AERD)**, also known as **Samter's Triad**, a condition characterized by three key components.- The three components of Samter's Triad are **asthma** (wheezing/breathlessness), chronic rhinosinusitis with **nasal polyps**, and sensitivity to aspirin/NSAIDs [1].*IgE release*- **Aspirin sensitivity** is a pseudoallergic reaction driven by abnormal metabolism of **arachidonic acid**, specifically involving the COX-1 pathway, and is thus typically **non-IgE mediated**.- This pathway disturbance leads to the overproduction of bronchoconstrictive **leukotrienes** (LTC4, LTD4, LTE4), which are the primary mediators of the reaction.*Extrinsic asthma*- **Extrinsic asthma** refers to allergic asthma, which relies on **IgE-mediated Type I hypersensitivity** reactions triggered by environmental allergens.- AERD is classified as a form of **intrinsic (non-allergic) asthma** because the trigger mechanism is pharmacological/metabolic rather than immunological (allergen-specific IgE) [1].*Drug interaction*- The adverse reaction seen here is an **idiosyncratic drug hypersensitivity reaction** stemming from the patient's underlying disease (AERD), not interaction with another drug.- A true **drug interaction** occurs when one drug alters the absorption, distribution, metabolism, or excretion of another drug, which is irrelevant to leukotriene overproduction.
Question 4: A 20-year-old male presented with yellowish discoloration of his skin and sclera. He is otherwise normal. He gives a history of viral infection 10 days ago, which was resolved 2 days back. He also gives a history of similar episodes in the past following any illness. Lab values are given below. What is the most likely diagnosis? Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1mg/dL Conjugated bilirubin: 0.3mg/dL Serum AST and ALT: Normal
- A. Criggler-Najar type 1 syndrome
- B. Gilbert syndrome (Correct Answer)
- C. Rotor syndrome
- D. Dubin-Johnson syndrome
Explanation: ***Gilbert syndrome*** - This condition is characterized by **unconjugated hyperbilirubinemia** (as seen by 2.1 mg/dL unconjugated vs. 0.3 mg/dL conjugated) that is mild, typically <3 mg/dL, and intermittent. [1] The history of similar episodes following **stress**, **vigorous exercise**, or **illness** (like the recent viral infection) is a classic trigger for this condition, which is caused by reduced activity of the **UGT1A1 enzyme**. [1] *Dubin-Johnson syndrome* - This syndrome results in **conjugated (direct) hyperbilirubinemia** due to defective excretion of conjugated bilirubin (MRP2 transporter defect). *Criggler-Najar type 1 syndrome* - This is a severe congenital deficiency of the **UGT1A1 enzyme**, leading to markedly and persistently elevated **unconjugated bilirubin** (often >20 mg/dL) and usually resulting in **kernicterus** and death in infancy. [1] The patient presents later in life (20 years old) with only mild, fluctuating unconjugated hyperbilirubinemia, ruling out Type 1 severity. *Rotor syndrome* - Similar to Dubin-Johnson, Rotor syndrome causes **conjugated (direct) hyperbilirubinemia** due to hepatocyte storage and transport defects, which contradicts the patient's lab findings of predominantly unconjugated bilirubin. Unlike Dubin-Johnson, Rotor syndrome does **not** cause black pigmentation of the liver.
Question 5: A 25-year-old male presents with mild jaundice noticed during a recent febrile illness. He gives a history of similar episodes in the past following any illness or periods of fasting. Physical examination reveals mild icterus with no hepatosplenomegaly. Lab values are given below: Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1 mg/dL Conjugated bilirubin: 0.3 mg/dL Serum AST and ALT: Normal What is the most likely diagnosis?
- A. Dubin-Johnson syndrome
- B. Gilbert syndrome (Correct Answer)
- C. Rotor syndrome
- D. Criggler-Najar type 1 syndrome
Explanation: ***Gilbert syndrome*** - It is characterized by isolated, mild, intermittent **unconjugated hyperbilirubinemia** (total bilirubin <4 mg/dL), often triggered by stress, fasting, illness, or dehydration, matching the patient's history of episodes following illness [1]. - The underlying cause is reduced activity (typically 30%) of the enzyme **uridine diphosphoglucuronate glucuronosyltransferase (UGT1A1)**, necessary for conjugating bilirubin, but liver function (AST/ALT) remains normal [1], [3]. *Dubin-Johnson syndrome* - This is characterized by **conjugated (direct) hyperbilirubinemia** due to defective excretion of bilirubin into the bile canaliculi, contrasting with the predominantly unconjugated pattern seen here [2]. - The liver tissue typically shows **black pigmentation** due to epinephrine metabolite accumulation, which is a key pathological feature. *Criggler-Najar type 1 syndrome* - This syndrome involves a severe or complete absence of the **UGT1A1 enzyme**, leading to very high levels of **unconjugated bilirubin** (often >20 mg/dL) that cause **kernicterus** and usually death in infancy, which is not consistent with a history of recurrent mild episodes in an adult [1]. - It requires lifelong treatment, typically with **phototherapy** and **liver transplantation**, due to the severe defect [1]. *Rotor syndrome* - Similar to Dubin-Johnson syndrome, Rotor syndrome also causes **conjugated (direct) hyperbilirubinemia** due to impaired hepatic storage and excretion of conjugated bilirubin, which contradicts the laboratory findings of mostly unconjugated bilirubin.
Question 6: Which of the following is a sensitive and specific marker of intestinal inflammation?
- A. Procalcitonin
- B. Fecal lactoferrin (Correct Answer)
- C. High-sensitivity C-reactive protein
- D. Tissue transglutaminase IgA
Explanation: ***Fecal lactoferrin***- This is an excellent proxy marker for active intestinal inflammation because **lactoferrin** is a highly concentrated protein released by **activated neutrophils** migrating into the gut lumen [1].- Elevated fecal levels often correlate well with endoscopic and histological evidence of mucosal inflammation [2], making it a sensitive and specific non-invasive test for conditions like **Inflammatory Bowel Disease (IBD)**.*Procalcitonin*- Primarily serves as a highly specific marker for diagnosing and monitoring **sepsis** and severe **systemic bacterial infection**.- It generally reflects systemic inflammatory responses and is not specific for inflammation localized to the **intestinal mucosa**.*Tissue transglutaminase IgA*- This is an autoantibody primarily used for screening and diagnosing **Celiac disease**, an autoimmune condition triggered by **gluten**.- It indicates underlying autoimmunity causing villous atrophy but is not used as a general marker of acute or chronic **intestinal inflammation** (like IBD).*High-sensitivity C-reactive protein*- It is a widely used, but **non-specific**, acute-phase reactant indicating **systemic inflammation** originating from any part of the body [1].- While elevated in IBD, its sensitivity and specificity for identifying isolated or localized intestinal inflammation are inferior to non-invasive **fecal markers** like lactoferrin or calprotectin.
Question 7: A patient comes to you with increased cough, increased breathlessness, and decreased exercise capacity. Chest X-ray shows pulmonary fibrosis. Which drug can be administered in the given condition?
- A. Pirfenidone (Correct Answer)
- B. Imatinib
- C. Bortezomib
- D. Roflumilast
Explanation: ***Pirfenidone***- This drug is an **antifibrotic agent** used specifically in the management of **Idiopathic Pulmonary Fibrosis (IPF)** to slow disease progression and decline in lung function [1].- It works by reducing the synthesis of **Transforming Growth Factor-beta (TGF-$\beta$)** and inhibiting collagen deposition, thus limiting fibrotic remodeling.*Bortezomib*- **Bortezomib** is a **proteasome inhibitor** primarily used in the treatment of hematological malignancies, such as **multiple myeloma** and mantle cell lymphoma.- It has no established role in the pathological treatment or management of the underlying lung fibrosis.*Roflumilast*- **Roflumilast** is a selective **phosphodiesterase-4 (PDE-4) inhibitor** used to reduce the risk of exacerbations in patients with severe **COPD** associated with chronic bronchitis [2].- It is an anti-inflammatory maintenance therapy for COPD, but it is not indicated as an antifibrotic treatment for pulmonary fibrosis [2].*Imatinib*- **Imatinib** is a selective **tyrosine kinase inhibitor** effective against the **BCR-ABL fusion protein**, making it the primary treatment for **Chronic Myeloid Leukemia (CML)**.- While tyrosine kinases are sometimes implicated in fibrosis pathways, Imatinib is not an approved or standard treatment for pulmonary fibrosis.
Question 8: A 50-year-old female patient with a known case of ovarian cancer presents with difficulty in activities like climbing stairs, getting up from a chair, combing hair, etc. The following characteristic sign was found on examination. The most probable diagnosis is:
- A. Systemic lupus erythematosus
- B. Dermatomyositis (Correct Answer)
- C. Systemic sclerosis
- D. Cushing syndrome
Explanation: ***Dermatomyositis*** - This diagnosis is strongly suggested by the combination of **symmetric proximal muscle weakness** (difficulty climbing stairs, combing hair) and the characteristic **Shawl sign**, an erythematous rash over the shoulders, neck, and upper back as shown in the image. - Dermatomyositis is a well-known **paraneoplastic syndrome**, frequently associated with underlying malignancies, particularly **ovarian cancer** in women, which aligns perfectly with the patient's history. *Systemic lupus erythematosus* - The classic cutaneous feature of SLE is a **malar rash** (butterfly rash) on the face; while other photosensitive rashes can occur, the Shawl sign is more specific to dermatomyositis. - Although SLE can present with myositis, the strong association with an underlying ovarian cancer makes dermatomyositis a more probable diagnosis. *Systemic sclerosis* - The primary feature of systemic sclerosis is **widespread fibrosis** and thickening of the skin (**scleroderma**), typically starting in the fingers (**sclerodactyly**), which is not described. - Muscle weakness in systemic sclerosis is usually due to disuse atrophy or fibrosis rather than a primary inflammatory myopathy, and it does not present with the rash seen. *Cushing syndrome* - While Cushing syndrome can cause **proximal muscle weakness** due to steroid myopathy, its characteristic skin findings include **violaceous striae**, easy bruising, and plethora, not a Shawl sign. - The inflammatory nature of the rash seen in the image is inconsistent with the endocrine and metabolic changes of Cushing syndrome.
Question 9: A young male patient presents with ptosis and muscle weakness, which reportedly worsens in the evening and improves in the morning. This is relieved by neostigmine. What is the likely diagnosis?
- A. Myasthenia gravis (Correct Answer)
- B. Huntington chorea
- C. Amyotrophic lateral sclerosis
- D. External ophthalmoplegia
Explanation: ***Myasthenia gravis***- The presentation of muscle weakness, specifically **ptosis**, that worsens with fatigue (evening) or activity and improves with rest (morning), is the classic hallmark of the autoimmune condition **Myasthenia Gravis (MG)**.- The dramatic improvement upon administration of **neostigmine** (an acetylcholinesterase inhibitor) is diagnostic, confirming impaired transmission at the **neuromuscular junction** due to autoantibodies against **acetylcholine receptors (AChR)** [1].*Huntington chorea*- This is a progressive, inherited neurodegenerative disorder primarily characterized by involuntary, jerky movements (**chorea**) and cognitive decline. - It is related to excessive CAG trinucleotide repeats on chromosome 4, leading to neuronal loss in the **caudate nucleus**, and does not respond to neostigmine.*Amyotrophic lateral sclerosis*- ALS is a motor neuron disease characterized by progressive and unrelenting weakness due to the loss of both **upper and lower motor neurons**.- The weakness in ALS is permanent, not fluctuating diurnally, and does not improve with acetylcholinesterase inhibitors like neostigmine.*External ophthalmoplegia*- This is a descriptive term referring to weakness or paralysis of the external eye muscles; while it is often seen in MG (where it is often called ocular MG), it is a symptom, not the overall diagnosis.- This term does not explain the generalized muscle weakness, the pattern of **fatigability**, or the characteristic response to **neostigmine**.
Question 10: A diabetic patient developed DVT with a necrolytic migratory rash. What is the most likely diagnosis?
- A. VIPoma
- B. Insulinoma
- C. Gastrinoma
- D. Glucagonoma (Correct Answer)
Explanation: ***Glucagonoma***- This paraneoplastic syndrome, caused by excessive glucagon secretion, is classically associated with the triad of **diabetes mellitus** (due to glucagon's counter-regulatory effect), **necrolytic migratory erythema (NME)**, and a high incidence of **venous thrombosis** (DVT/PE).- The classic rash, **NME**, is an erythematous, scaling rash that begins peripherally and migrates, often causing eroded, painful lesions [1].*Insulinoma*- The primary manifestation is **hypoglycemia** (Whipple's triad), leading to neuroglycopenic symptoms like confusion and seizures.- This tumor does not cause the characteristic **necrolytic migratory rash** or have a strong association with DVT.*Gastrinoma*- Gastrinomas cause **Zollinger-Ellison syndrome**, characterized by severe, refractory **peptic ulcer disease** (PUD) and chronic diarrhea.- The clinical presentation lacks the key features of hyperglycemia, DVT, and **necrolytic migratory erythema (NME)**.*VIPoma*- VIPomas cause the **WDHA syndrome** (**W**atery **D**iarrhea, **H**ypokalemia, **A**chlorhydria), leading to profound dehydration and electrolyte imbalances.- This tumor is not associated with the pathogenesis of **necrolytic migratory erythema** or the hypercoagulable state responsible for DVT.