FMGE 2017 - Internal Medicine Practice Questions

Q: Which of the following conditions should not be considered if JVP rises on deep inspiration?

Atrial fibrillation. The phenomenon of JVP rising on deep inspiration is known as **Kussmaul's sign**, which is indicative of impaired right ventricular filling and is not typically associated with **atrial fibrillation**. In **complete heart block**, there is dissociation between atrial and ventricular contractions. This can lead to **cannon 'a' waves** in the JVP, which are large prominent 'a' waves caused by right atrial contraction against a closed tricuspid valve [1]. **Constrictive pericarditis** is characterized by a rigid pericardium that restricts diastolic filling of the right ventricle. This condition is a classic cause of **Kussmaul's sign**, where the JVP rises paradoxically during inspiration due to increased venous return that cannot be accommodated by the constricted ventricle. **Restrictive cardiomyopathy** involves impaired diastolic filling of the ventricles due to myocardial stiffness. It can also cause a paradoxical rise in JVP during inspiration (**Kussmaul's sign**) because the stiffened right ventricle cannot adequately accommodate the inspiratory increase in venous return.

Q: Initial treatment for management of mild to moderate Crohn's disease is:

Budesonide. ***Budesonide*** - **Budesonide** is a **steroid** with high first-pass metabolism, meaning it works locally in the gastrointestinal tract with minimal systemic effects, making it suitable for mild to moderate Crohn's disease. - It is effective in inducing remission for mild to moderate ileocolonic Crohn's disease, with a better safety profile than systemic corticosteroids. *Mesalamine* - **Mesalamine (5-ASA)** is primarily used for **ulcerative colitis** and has limited efficacy in Crohn's disease, especially for moderate disease. - While it can be considered for very mild Crohn's disease, its role is often debated and not a first-line agent for moderate cases. *Infliximab* - **Infliximab** is a **biologic agent (anti-TNF-α)** used for moderate to severe Crohn's disease or for patients who have failed conventional therapy. - It works by blocking a key inflammatory cytokine and is not typically used as initial treatment for mild disease due to its potency and potential side effects. *Sulfasalazine* - **Sulfasalazine** is more effective in **colonic Crohn's disease** and **ulcerative colitis**, and its efficacy in small bowel Crohn's disease is limited [1]. - Many patients experience side effects such as **nausea**, **headaches**, and **allergic reactions**, limiting its use as a first-line agent.

Q: Which of the following leads to development of SIADH?

CNS disorders. ***CNS disorders*** - Neurological conditions such as **stroke**, hemorrhage, infection, and trauma can cause inappropriate **ADH release** due to damage or irritation of the hypothalamus or posterior pituitary [2]. - This leads to increased water reabsorption and subsequent **hyponatremia** characteristic of SIADH [1]. *Lung cancer* - Certain types of **lung cancer**, particularly **small cell lung carcinoma (SCLC)**, are known to produce ADH ectopically, leading to SIADH. - This represents a **paraneoplastic syndrome**, where the tumor cells independently synthesize and secrete ADH. *Pituitary adenoma* - While pituitary adenomas can cause various endocrine dysfunctions, they are generally **not a direct cause of SIADH**. - **SIADH** typically results from unregulated ADH secretion rather than a primary pituitary tumor's overproduction of ADH itself. *All of the options* - Although **lung cancer** and **CNS disorders** are well-established causes of SIADH, **pituitary adenomas** are not a common or direct cause. - Therefore, choosing "all of the options" would be incorrect due to the inclusion of pituitary adenoma as a direct cause.

Q: Which of the following is the best investigation for acute gout?

Uric acid in synovial fluid. ***Uric acid in synovial fluid*** - The definitive diagnosis of acute gout is established by identifying **negatively birefringent needle-shaped uric acid crystals** within the synovial fluid of the affected joint [1]. - This method directly confirms the presence of **monosodium urate crystals**, which are the hallmark of gout, offering diagnostic certainty [1]. *Uric acid in urine* - While urinary uric acid levels can help assess uric acid excretion, they are not diagnostic for acute gout and do not directly show the presence of **intra-articular crystals**. - This test is more relevant for investigating the **cause of hyperuricemia** (overproduction vs. underexcretion) rather than diagnosing an acute flare. *Anti CCP antibodies* - **Anti-cyclic citrullinated peptide (anti-CCP) antibodies** are markers for **rheumatoid arthritis** and are not relevant for the diagnosis of acute gout. - Their presence indicates an autoimmune inflammatory condition distinct from crystal-induced arthropathy. *Serum uric acid* - Serum uric acid levels are often elevated during an acute gout flare (**hyperuricemia**), but this is not diagnostic, as many individuals with hyperuricemia never develop gout [1]. - Approximately 30% of patients may have **normal serum uric acid levels** during an acute attack, making it an unreliable sole diagnostic criterion.

Question 1

Which of the following conditions should not be considered if JVP rises on deep inspiration?

Accepted Answer

Atrial fibrillation

Answer

Complete heart block

Answer

Constrictive pericarditis

Answer

Restrictive cardiomyopathy

Question 2

Initial treatment for management of mild to moderate Crohn's disease is:

Accepted Answer

Budesonide

Answer

Mesalamine

Answer

Infliximab

Answer

Sulfasalazine

Question 3

Which of the following leads to development of SIADH?

Accepted Answer

CNS disorders

Answer

Lung cancer

Answer

Pituitary adenoma

Answer

All of the options

Question 4

Which of the following is the best investigation for acute gout?

Accepted Answer

Uric acid in synovial fluid

Answer

Uric acid in urine

Answer

Anti CCP antibodies

Answer

Serum uric acid

FMGE 2017 — Internal Medicine