FMGE 2025 - Internal Medicine Practice Questions

Q: A 62-year-old male presents with left leg swelling and pain for 5 days and has a positive D-dimer test. Duplex ultrasonography confirms an extensive DVT involving the left popliteal and femoral veins. Which of the following is the most appropriate initial management strategy?

LMWH followed by oral anticoagulant. LMWH followed by oral anticoagulant - Low Molecular Weight Heparin (LMWH) is the preferred initial treatment for stable patients with extensive DVT due to its predictable response [1], [2], subcutaneous administration, and lower risk of heparin-induced thrombocytopenia (HIT) compared to UFH. - Following the initial parenteral therapy (LMWH or UFH), long-term treatment with an oral anticoagulant (such as a DOAC or warfarin) is necessary for at least 3 to 6 months to prevent thrombus extension and recurrent Pulmonary Embolism (PE) [1]. Unfractionated heparin followed by warfarin - Unfractionated Heparin (UFH) often requires hospitalization for IV administration and intense monitoring of aPTT levels [2], making LMWH the outpatient standard for stable patients. - UFH is typically reserved for patients with severe renal impairment (Creatinine Clearance < 30 mL/min) or those who are hemodynamically unstable and may require urgent reversal. Catheter-directed thrombolysis - This invasive therapy is reserved for patients with DVT accompanied by limb ischemia (phlegmasia cerulea dolens) [1] or for selected young patients with extensive proximal DVT and a low risk of bleeding. - It is associated with a significantly higher risk of major bleeding and is not the standard initial strategy for an uncomplicated extensive DVT [1]. IVC filter placement - An IVC filter is indicated only for patients with acute DVT who have an absolute contraindication to anticoagulation (e.g., active hemorrhage) or who experience recurrent PE despite adequate anticoagulation [1]. - Filter placement does not treat the existing deep vein clot and increases the long-term risk of recurrent DVT.

Q: A 58-year-old woman comes to the clinic for a routine follow-up. She has a history of mild hypertension, which is well-controlled with medication. She reports no symptoms such as palpitations, dizziness, or chest pain. Her ECG shows a prolonged PR interval of 0.24 seconds with regular 1:1 AV conduction and narrow QRS complexes. What is the most likely diagnosis based on these ECG findings?

First-Degree AV Block. ***First-Degree AV Block*** - This ECG demonstrates a fixed and prolonged **PR interval** that is greater than 0.20 seconds (more than 5 small squares), which is the defining characteristic of a first-degree AV block. - There is a consistent **1:1 conduction** between the atria and ventricles, meaning every P wave is followed by a QRS complex, distinguishing it from higher-degree blocks. *Second-Degree AV Block* - This condition is characterized by intermittently **non-conducted P waves**, resulting in 'dropped' QRS complexes, which are not present in this ECG. - It has two types: **Mobitz I (Wenckebach)** with progressive PR prolongation before a dropped beat, and **Mobitz II** with a constant PR interval before an unpredictable dropped beat. *Third-Degree AV Block* - Also known as complete heart block, this involves complete **AV dissociation**, where there is no relationship between P waves and QRS complexes. - On an ECG, P waves and QRS complexes would occur at their own independent, regular rates, which is contrary to the 1:1 conduction seen here. *Bundle Branch Block* - The primary feature of a bundle branch block is a **wide QRS complex** (≥0.12 seconds) due to delayed ventricular depolarization. - The QRS complex in this ECG is **narrow** (<0.12 seconds), which rules out a bundle branch block.

Q: A 35-year-old woman presents with fluctuating muscle weakness, especially affecting her speech and swallowing. Repetitive nerve stimulation shows a decremental response. Her blood tests are negative for acetylcholine receptor (AChR) antibodies. Which of the following antibodies is most likely responsible for her symptoms?

Anti-MuSK antibodies. Detailed clinical evaluation of myasthenia gravis reveals that anti-MuSK antibodies target Muscle-Specific Kinase (MuSK), essential for clustering AChR at the NMJ [1]. Their presence confirms the diagnosis of Myasthenia Gravis (MG) in patients who are seronegative for AChR antibodies, often presenting with prominent bulbar and facial weakness [1]. Anti-dsDNA antibodies are specific for Systemic Lupus Erythematosus (SLE), an autoimmune disease that primarily causes arthritis, renal disease, and malar rash [2]. Although SLE can cause myositis or neuropathy, it does not typically present with the isolated, fluctuating postsynaptic weakness characteristic of Myasthenia Gravis and the decremental response. Anti-thyroid peroxidase (TPO) antibodies are primary markers for Hashimoto's thyroiditis, leading to hypothyroidism; screening for associated autoimmune thyroid disease is recommended in MG patients [1]. Anti-Ro antibodies, characteristic of Sjögren's Syndrome and SLE [2], primarily involve sicca symptoms and occasionally present with myositis, but not the hallmark features of ocular or bulbar MG.

Q: Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Hypokalemia. ***Hypokalemia*** - Severe vomiting leads to significant loss of gastric acid and subsequent volume depletion, often resulting in **metabolic alkalosis** and substantial **potassium** loss (due to renal compensation and direct GI loss) [1]. - **Hypokalemia** directly affects cardiac muscle repolarization, predisposing the patient to various arrhythmias, including **ventricular tachycardia** (e.g., *Torsades de pointes*) [2], [3]. *Hyponatremia* - While severe vomiting can cause hyponatremia (due to volume loss and inappropriate ADH release), symptomatic effects are primarily **neurological** (e.g., seizures, confusion), not typically cardiac arrhythmias [2]. - The effect on the heart tends to be mild unless the drop is very rapid and severe; it primarily influences **myocardial contractility** through fluid shifts [2]. *Hyperkalemia* - Hyperkalemia causes severe and characteristic ECG changes (tall, peaked T waves, broadened QRS, possible asystole), but it is **not associated** with severe vomiting, which typically causes **hypokalemia** [2]. - Hyperkalemia is more commonly seen in conditions like **renal failure** or acidosis [4]. *Hypocalcemia* - Hypocalcemia primarily affects the heart by causing **prolongation of the QT interval**, which can increase the risk of *Torsades de pointes*, similar to hypokalemia. - However, calcium losses from simple gastric vomiting are generally **not as dramatic** or primary as the potassium losses, making hypokalemia the most direct and common cause of arrhythmia in this specific clinical scenario [1].

Q: A patient is positive for HBsAg and anti-HBc IgM. What is the most likely diagnosis?

Acute hepatitis. ***Acute hepatitis***- The simultaneous presence of **HBsAg** (Hepatitis B surface antigen) indicates active infection [1], paired with **anti-HBc IgM** (Immunoglobulin M against the core antigen) [2].- **Anti-HBc IgM** is the serological hallmark of a recent or **acute** Hepatitis B infection, typically detectable for up to 6 months after symptom onset [1].*Chronic hepatitis*- Chronic infection is defined by the persistence of **HBsAg** for **more than six months** [1].- The predominant core antibody present in chronic infection is **anti-HBc IgG**, whereas Anti-HBc IgM becomes undetectable [1].*Recovery phase*- The recovery phase is marked by the presence of **anti-HBs** (Hepatitis B surface antibody), indicating clearance of the virus and protective immunity [1].- During recovery, **HBsAg** is negative, and **anti-HBc IgM** is absent, leaving only **anti-HBc IgG** and anti-HBs [1].*Vaccination*- Successful vaccination only produces immunity against the surface antigen, resulting solely in the presence of **anti-HBs** [1].- Both **HBsAg** and **anti-HBc** (IgM or IgG) are universally negative following vaccination [1].

Q: A farmer presents with fever and subconjunctival hemorrhage. The microscopic agglutination test is found to be positive. What is the diagnosis?

Leptospira. ***Leptospira***- The clinical presentation of fever in a patient with an occupation involving exposure to animal habitats (farmer), coupled with the classic finding of **subconjunctival hemorrhage** (conjunctival suffusion), highly suggests **Leptospirosis** (Weil's disease) [1]. - The **Microscopic Agglutination Test (MAT)** is the gold standard serological test for the diagnosis of **Leptospirosis**, supporting this etiology [1]. *Brucella* - *Brucella* causes **Brucellosis** (Undulant Fever), characterized primarily by cyclical undulating fevers, night sweats, and localized infection (e.g., osteomyelitis or epididymitis), not typically subconjunctival hemorrhage. - Diagnosis usually involves blood culture or the Standard Tube Agglutination Test (SAT), not MAT. *E coli* - *E. coli* is a common cause of GI infections, UTIs, and sepsis; systemic *E. coli* disease does not typically manifest with the specific finding of subconjunctival hemorrhage. - MAT is not used for the diagnosis of *E. coli* infections, which are confirmed primarily through culture. *Staph aureus* - *S. aureus* can cause a wide range of infections (skin infections, endocarditis, sepsis) but is not associated with the specific syndrome presenting here (farmer, subconjunctival hemorrhage). - Diagnosis relies on culture, not serological tests like MAT, which is specific for spirochetes.

Q: A patient presents with fever, neck rigidity, headache, vomiting, and petechial rashes on the lower limbs. What is the most likely causative organism?

Neisseria meningitidis. ***Neisseria meningitidis***- This gram-negative diplococcus is the most likely causative agent as it classically causes **meningococcal meningitis** combined with **meningococcemia**, which highly correlates with the presence of **petechial or purpuric rashes** on the skin.- The rash results from **endotoxin** (lipooligosaccharide) damage to the blood vessel walls, leading to **vasculitis** and hemorrhage, often progressing to severe complications like the **Waterhouse-Friderichsen syndrome**.*Clostridium perfringens*- This organism is primarily known for causing **gas gangrene** (myonecrosis) and tissue necrosis, often following severe trauma or surgery.- It is not a common cause of primary community-acquired bacterial meningitis, and its clinical presentation focuses on localized **soft tissue infection** rather than systemic meningoencephalitis.*Cryptococcus neoformans*- This is a **fungal pathogen** that causes meningitis, usually in patients with **severe immunosuppression** (e.g., uncontrolled HIV infection).- Although it causes fever and signs of meningeal irritation, the presentation is typically subacute or chronic, and a hemorrhagic rash is not a standard clinical feature.*Clostridium difficile*- This bacterium is the causative agent of **antibiotic-associated diarrhea** and **pseudomembranous colitis**.- Its effects are localized almost exclusively to the colon, and it does not cause acute bacterial meningitis with systemic rash.

Q: A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Dysdiadochokinesis. ***Dysdiadochokinesis***- This term refers to the impairment in the ability to perform **rapid alternating movements**, directly matching the complaint of "difficulty switching between movements" [2].- It is a classic sign of **cerebellar dysfunction**, which also accounts for the associated **uncontrollable movements** (often reflecting associated **ataxia** or **dysmetria**) [3].*Intentional Tremor*- This tremor is absent at rest, but its amplitude increases significantly as the patient attempts to reach a **visual target** (e.g., during the finger-to-nose test).- While it is a sign of **cerebellar disease**, the primary complaint in the stem is difficulty *switching* movements, which is characteristic of **dysdiadochokinesis**.*Metamorphosis*- This neurological term typically refers to **perceptual distortion** (specifically, *metamorphopsia* is the distortion of visual size or shape), which is unrelated to motor control or coordination.- It is not the term used to describe the inability to perform **rapid alternating movements** or uncontrolled movements due to cerebellar pathology.*Resting Tremor*- A resting tremor is maximal when the limb is completely relaxed and **supported against gravity**, classically seen in **Parkinson's disease** [1].- This tremor usually **improves significantly** or disappears entirely when the patient performs voluntary action, distinguishing it from intentional tremors and general lack of coordination.

Q: A hypertensive patient’s lab results reveal hypernatremia, hypokalemia, and metabolic alkalosis. What is the most probable diagnosis?

Conn's Syndrome. ***Conn's Syndrome***- This condition, known as primary **hyperaldosteronism**, is defined by autonomous overproduction of aldosterone, leading to volume expansion and **hypertension** [1].- Aldosterone acts on the principal cells of the collecting duct to increase Na+ reabsorption (causing hypernatremia) while simultaneously promoting K+ and H+ excretion (causing **hypokalemia** and **metabolic alkalosis**) [2].*Addison’s Disease*- Addison’s disease is primary adrenal insufficiency, characterized by deficiency of mineralocorticoids and glucocorticoids [3].- This lack of aldosterone leads to impaired Na+ reabsorption and deficient K+ excretion, resulting in **hyponatremia** and **hyperkalemia** (the opposite of the clinical picture).*Diabetes Insipidus*- Diabetes Insipidus (DI) is a disorder of insufficient ADH action, resulting in polyuria and profound free water loss leading to **hypernatremia**.- DI does not arise from mineralocorticoid dysfunction, thus it would not typically cause **hypokalemia** or metabolic alkalosis.*Cushing's Disease*- Cushing's disease involves excess **cortisol** (a glucocorticoid), which can cause hypertension and occasionally hypokalemia.- However, the combination of **hypernatremia**, significant **hypokalemia**, and severe **metabolic alkalosis** strongly points toward primary **mineralocorticoid excess** rather than glucocorticoid excess [1].

Q: What is the primary mechanism behind tissue damage in long-standing diabetes?

Hyperglycemia. ***Hyperglycemia*** - Chronic exposure to high glucose levels is the fundamental upstream trigger initiating all harmful biochemical pathways that lead to **microvascular** and **macrovascular** complications [4]. - It directly leads to the formation of **Advanced Glycation End products (AGEs)**, activation of the **protein kinase C** pathway, and increased **oxidative stress**, all contributing to irreversible tissue damage. *Insulin resistance* - This is a key defect in **Type 2 Diabetes** [4] that *causes* hyperglycemia, but the resulting high glucose level is the direct downstream mechanism causing structural organ damage. - Its primary immediate effect is impaired glucose uptake and utilization in peripheral tissues [1], rather than the intrinsic structural damage seen in **vascular endothelium** or nerves. *Sorbitol accumulation* - This is a specific downstream consequence of chronic **hyperglycemia** activating the **polyol pathway**; therefore, it is a mechanism of damage, not the primary inciting cause. - Accumulation of **sorbitol** and resultant depletion of **NADPH** primarily contributes to osmotic stress and oxidative damage in specific cells like pericytes and Schwann cells (neuropathy). *Decreased insulin secretion* - This is the core pathophysiological defect in **Type 1 Diabetes** and a feature of advanced Type 2 Diabetes (**beta-cell failure**) that *results* in hyperglycemia [3]. - The lack of insulin elevates blood glucose, making **hyperglycemia** the direct variable driving the damaging biochemical process in target tissues over time [2].

Question 1

A 62-year-old male presents with left leg swelling and pain for 5 days and has a positive D-dimer test. Duplex ultrasonography confirms an extensive DVT involving the left popliteal and femoral veins. Which of the following is the most appropriate initial management strategy?

Accepted Answer

LMWH followed by oral anticoagulant

Answer

Unfractionated heparin followed by warfarin

Answer

Catheter-directed thrombolysis

Answer

IVC filter placement

Question 2

A 58-year-old woman comes to the clinic for a routine follow-up. She has a history of mild hypertension, which is well-controlled with medication. She reports no symptoms such as palpitations, dizziness, or chest pain. Her ECG shows a prolonged PR interval of 0.24 seconds with regular 1:1 AV conduction and narrow QRS complexes. What is the most likely diagnosis based on these ECG findings?

Accepted Answer

First-Degree AV Block

Answer

Third-Degree AV Block

Answer

Second-Degree AV Block

Answer

Bundle Branch Block

Question 3

A 35-year-old woman presents with fluctuating muscle weakness, especially affecting her speech and swallowing. Repetitive nerve stimulation shows a decremental response. Her blood tests are negative for acetylcholine receptor (AChR) antibodies. Which of the following antibodies is most likely responsible for her symptoms?

Accepted Answer

Anti-MuSK antibodies

Answer

Anti-TPO antibodies

Answer

Anti-dsDNA antibodies

Answer

Anti-Ro antibodies

Question 4

Which electrolyte abnormality will lead to cardiac arrhythmia in patients with severe vomiting?

Accepted Answer

Hypokalemia

Answer

Hyponatremia

Answer

Hyperkalemia

Answer

Hypocalcemia

Question 5

A patient is positive for HBsAg and anti-HBc IgM. What is the most likely diagnosis?

Accepted Answer

Acute hepatitis

Answer

Recovery phase

Answer

Vaccination

Answer

Chronic hepatitis

Question 6

A farmer presents with fever and subconjunctival hemorrhage. The microscopic agglutination test is found to be positive. What is the diagnosis?

Accepted Answer

Leptospira

Answer

Brucella

Answer

E coli

Answer

Staph aureus

Question 7

A patient presents with fever, neck rigidity, headache, vomiting, and petechial rashes on the lower limbs. What is the most likely causative organism?

Accepted Answer

Neisseria meningitidis

Answer

Cryptococcus neoformans

Answer

Clostridium difficile

Answer

Clostridium perfringens

Question 8

A patient reports difficulty switching between movements and experiences uncontrollable hand movements. What is the most likely diagnosis?

Accepted Answer

Dysdiadochokinesis

Answer

Metamorphosis

Answer

Resting Tremor

Answer

Intentional Tremor

Question 9

A hypertensive patient’s lab results reveal hypernatremia, hypokalemia, and metabolic alkalosis. What is the most probable diagnosis?

Accepted Answer

Conn's Syndrome

Answer

Addison’s Disease

Answer

Cushing's Disease

Answer

Diabetes Insipidus

Question 10

What is the primary mechanism behind tissue damage in long-standing diabetes?

Accepted Answer

Hyperglycemia

Answer

Insulin resistance

Answer

Sorbitol accumulation

Answer

Decreased insulin secretion

FMGE 2025 — Internal Medicine