Rheumatology and Immunology Practice Questions

Q: All of the following are true regarding acute gouty arthritis, EXCEPT:

Allopurinol is effective to treat the acute attack. The correct answer is **A. Allopurinol is effective to treat the acute attack.** **1. Why Option A is correct (The False Statement):** Allopurinol is a **Xanthine Oxidase Inhibitor** used for chronic management (urate-lowering therapy) [1]. It should **never** be initiated during an acute attack. Rapidly lowering serum urate levels can cause the mobilization of urate from tissue stores, leading to the "shedding" of crystals into the joint space, which paradoxically worsens or prolongs the acute inflammation [1]. The primary goal in an acute attack is to reduce inflammation using NSAIDs, Colchicine, or Glucocorticoids. **2. Analysis of Incorrect Options:** * **Option B:** Monosodium urate (MSU) crystals are characteristically **needle-shaped** and show **strong negative birefringence** under polarized light (appearing yellow when parallel to the slow axis of the compensator) [2]. * **Option C:** Serum uric acid levels are unreliable during an acute flare. They may be **normal or low** because uric acid is an "acute-phase reactant" that can be excreted more rapidly by the kidneys during stress, or because the urate has precipitated out of the blood into the joints [3]. * **Option D:** **Tophi** are pathognomonic for chronic gout and consist of large aggregations of MSU crystals surrounded by a granulomatous inflammatory response [2]. **Clinical Pearls for NEET-PG:** * **First-line for acute gout:** NSAIDs (e.g., Indomethacin, Naproxen). * **Colchicine:** Most effective if started within 12–24 hours; its main side effect is diarrhea. * **Rule of Initiation:** If a patient is already on Allopurinol when an attack starts, **do not stop it**. If they are not on it, **do not start it** until the inflammation has completely subsided (usually 2 weeks later) [1]. * **Definitive Diagnosis:** Arthrocentesis showing needle-shaped, negatively birefringent crystals [2].

Q: A patient has been diagnosed with systemic sclerosis and has the presence of anti-RNA polymerase III antibodies. Which of the following is more commonly associated with this condition?

Acute onset of disease. Explanation: Systemic Sclerosis (SSc) is categorized into limited and diffuse types based on skin involvement and autoantibody profiles. **Anti-RNA polymerase III (anti-RNAP III)** antibodies are highly specific for the **Diffuse Cutaneous Systemic Sclerosis (dcSSc)** subtype. **1. Why "Acute onset of disease" is correct:** Anti-RNAP III antibodies are associated with a rapid and aggressive clinical course. Patients typically present with an **acute or subacute onset** of extensive skin thickening (scleroderma) that progresses rapidly over the trunk and proximal extremities [1]. **2. Analysis of Incorrect Options:** * **A. Reduced risk of scleroderma renal crisis:** This is incorrect. Anti-RNAP III is the strongest predictor for **Scleroderma Renal Crisis (SRC)**. Patients with these antibodies require frequent blood pressure monitoring. * **C. Reduced risk of malignancy:** This is incorrect. There is a well-documented temporal association between the onset of anti-RNAP III-positive SSc and **synchronous malignancy** (especially breast and GI cancers), suggesting a paraneoplastic trigger. * **D. Increased risk of pulmonary hypertension:** While it can occur, isolated Pulmonary Arterial Hypertension (PAH) is more classically associated with **Limited SSc** and **Anti-centromere antibodies**. Anti-RNAP III is more closely linked to skin and renal involvement. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Scl-70 (Anti-topoisomerase I):** Associated with Diffuse SSc and a high risk of **Interstitial Lung Disease (ILD)**. * **Anti-Centromere:** Associated with Limited SSc (CREST syndrome) and **Pulmonary Hypertension**. * **Anti-U1 RNP:** Associated with **Mixed Connective Tissue Disease (MCTD)**. * **Management Tip:** In patients with anti-RNAP III, avoid high-dose corticosteroids as they can precipitate a renal crisis.

Q: For a patient experiencing an acute attack of gout who cannot tolerate NSAIDs, which medication is the most appropriate choice?

Steroid. ### Explanation **Correct Option: B. Steroid** In the management of an **acute gouty attack**, the primary goal is to reduce inflammation and pain. The first-line agents are typically **NSAIDs** (e.g., Indomethacin, Naproxen) or **Colchicine**. However, if a patient has contraindications to NSAIDs (such as peptic ulcer disease, chronic kidney disease, or hypersensitivity), **Corticosteroids** (oral, intravenous, or intra-articular) are the most appropriate and effective alternative. They act by suppressing the recruitment of leukocytes and inhibiting the inflammatory response to urate crystals. **Why the other options are incorrect:** * **A & D (Allopurinol and Febuxostat):** These are **Xanthine Oxidase Inhibitors** used for *chronic* management (uricosuric therapy). They should **never be started during an acute attack**, as a rapid drop in serum uric acid levels can mobilize urate from tissues, potentially worsening or prolonging the acute inflammation. * **C (Probenecid):** This is a **Uricosuric agent** that increases uric acid excretion in the kidneys. Like Allopurinol, it is used for chronic prophylaxis and has no role in treating acute inflammation. **High-Yield NEET-PG Pearls:** * **Drug of Choice (DOC) for Acute Gout:** NSAIDs (specifically Indomethacin is traditionally preferred). * **DOC for Chronic Gout:** Allopurinol (a hypouricemic agent). * **Colchicine:** Used for acute attacks; its dose-limiting toxicity is **diarrhea**. It works by inhibiting microtubule polymerization (binding to tubulin). * **Rule of Thumb:** Never start or stop urate-lowering therapy (Allopurinol/Febuxostat) during an acute attack. If the patient is already on them, continue the same dose.

Q: A patient suffering from morning stiffness lasting more than 1 hour presents with the following abnormality in the X-ray. What is the most possible diagnosis?

Rheumatoid arthritis. ***Rheumatoid arthritis*** - **Morning stiffness lasting more than 1 hour** is a hallmark feature of RA, indicating significant **inflammatory synovitis**. - Classic X-ray findings include **periarticular osteoporosis**, **symmetric joint space narrowing**, and **marginal erosions** at **MCP/PIP joints**. *Psoriatic arthritis* - Typically presents with **asymmetric joint involvement** and characteristic **pencil-in-cup deformity** on X-ray. - Associated with **psoriatic skin lesions** and often affects **DIP joints**, unlike the pattern described. *Osteoarthritis* - Morning stiffness is typically **less than 30 minutes**, indicating mechanical rather than inflammatory pathology. - X-ray shows **osteophytes**, **joint space narrowing**, and commonly affects **DIP joints** with **Heberden's nodes**. *Relapsing polychondritis* - Primarily affects **cartilaginous structures** like ears, nose, and larynx rather than synovial joints. - Does not typically cause the **joint erosions** and **symmetric arthropathy** seen in inflammatory arthritis.

Q: Which of the following organs is least likely to be involved in Behcet's disease?

Liver. Behcet’s Disease is a chronic, multisystemic, relapsing inflammatory disorder classified as a **variable vessel vasculitis**. It is unique because it can involve blood vessels of all sizes (small, medium, and large) on both the arterial and venous sides [1]. **Why Liver is the correct answer:** While Behcet’s disease is multisystemic, it characteristically **spares the liver parenchyma**. While rare vascular complications like Budd-Chiari syndrome (hepatic vein thrombosis) can occur due to the disease's prothrombotic nature, the liver is not a primary target organ for the inflammatory process. In contrast, the skin, mucosa, eyes, joints, and CNS are classic sites of involvement. **Analysis of Incorrect Options:** * **CNS (Neuro-Behcet’s):** Involved in about 5–10% of cases. It typically presents as parenchymal disease (brainstem involvement) or non-parenchymal disease (dural sinus thrombosis). * **Joints:** Arthritis or arthralgia occurs in approximately 50% of patients. It is usually a non-erosive, asymmetrical oligoarthritis, most commonly affecting the knees and ankles. * **Eyes:** Ocular involvement is a hallmark of the disease (70% of cases). It typically presents as **bilateral panuveitis** or posterior uveitis, which can lead to blindness if untreated. **High-Yield Clinical Pearls for NEET-PG:** 1. **Classic Triad:** Recurrent oral ulcers (most common), genital ulcers (most specific), and uveitis. 2. **Pathergy Test:** A positive skin hyperreactivity test (formation of a sterile pustule 24–48 hours after a needle prick) is highly specific for Behcet’s. 3. **HLA Association:** Strongly associated with **HLA-B51**. 4. **Vascular:** It is a leading cause of pulmonary artery aneurysms (Hughes-Stovin Syndrome). 5. **Treatment:** Colchicine for mucocutaneous symptoms; Azathioprine or Anti-TNF agents for ocular and CNS involvement.

Q: A man developed frequent facial swelling with occasional laryngeal edema. What is the most probable diagnosis?

C1 esterase deficiency. The clinical presentation of recurrent facial swelling and life-threatening laryngeal edema without associated urticaria (hives) or pruritus is the classic hallmark of **Hereditary Angioedema (HAE)**, which is caused by **C1 esterase inhibitor deficiency**. [3] ### **Why C1 Esterase Deficiency is Correct** C1 esterase inhibitor (C1-INH) normally regulates the classical complement pathway and the kinin-generating cascade. A deficiency leads to the unregulated activation of kallikrein, resulting in excessive production of **bradykinin**. Bradykinin increases vascular permeability, leading to episodic, non-pitting edema of the face, extremities, and, most critically, the larynx. ### **Why Other Options are Incorrect** * **Allergy & Anaphylaxis:** These are Type I hypersensitivity reactions mediated by IgE and mast cell degranulation (histamine release). [1] They are almost always accompanied by **urticaria (wheals)**, intense itching, and hypotension. [3] The absence of "itchy rashes" in the history strongly points away from an allergic etiology. * **Not esterase deficiency:** This is a distractor that contradicts the clinical findings. ### **NEET-PG High-Yield Pearls** * **Inheritance:** Autosomal Dominant. * **Key Mediator:** Bradykinin (NOT histamine). * **Clinical Trigger:** Often precipitated by minor trauma, dental procedures, or stress. * **Diagnostic Screening:** Low **C4 levels** (best initial screening test, even between attacks). * **Management:** * *Acute attack:* Purified C1-INH concentrate or **Icatibant** (bradykinin B2 receptor antagonist). * *Prophylaxis:* **Danazol** (stanozolol) or Tranexamic acid. * **Note:** ACE inhibitors are contraindicated in these patients as they prevent bradykinin breakdown, worsening the edema. [2]

Q: Felty's syndrome is associated with which of the following?

Rheumatoid arthritis. **Explanation:** **Felty’s Syndrome** is a rare but serious extra-articular manifestation of long-standing, seropositive **Rheumatoid Arthritis (RA)** [1]. It is classically defined by a clinical triad: 1. **Rheumatoid Arthritis** (usually severe, erosive, and chronic). 2. **Splenomegaly.** 3. **Neutropenia** (Absolute Neutrophil Count <2000/mm³). **Why Rheumatoid Arthritis is correct:** Felty’s syndrome typically occurs in patients who have had RA for over 10 years [1]. These patients often have high titers of Rheumatoid Factor (RF) and anti-CCP antibodies, along with extra-articular features like rheumatoid nodules and vasculitis. The pathophysiology involves autoimmune-mediated destruction of neutrophils and splenic sequestration. **Why the other options are incorrect:** * **Osteoarthritis:** This is a degenerative joint disease, not an autoimmune systemic inflammatory disorder, and is not associated with splenomegaly or cytopenias. * **Ankylosing Spondylitis:** This is a seronegative spondyloarthropathy primarily affecting the axial skeleton (HLA-B27 associated); it does not manifest as Felty’s syndrome. * **Psoriatic Arthritis:** While an inflammatory arthritis, it belongs to the seronegative group and is characterized by skin lesions and dactylitis rather than the Felty’s triad [2]. **High-Yield Clinical Pearls for NEET-PG:** * **HLA Association:** Strongly associated with **HLA-DR4**. * **Risk of Infection:** The primary clinical concern is recurrent bacterial infections (skin and respiratory) due to profound neutropenia. * **Large Granular Lymphocyte (LGL) Leukemia:** There is a significant phenotypic overlap between Felty’s syndrome and T-cell LGL leukemia; both present with RA and neutropenia. * **Treatment:** Management focuses on controlling the underlying RA, typically using **Methotrexate**. Granulocyte colony-stimulating factor (G-CSF) may be used in severe cases.

Q: Which joint is typically spared in Rheumatoid arthritis?

Distal interphalangeal joints of the finger. Rheumatoid Arthritis (RA) is a chronic, systemic inflammatory disease characterized by symmetric polyarthritis [1]. The hallmark of RA is the involvement of small joints of the hands and feet, specifically targeting the synovium [1]. **1. Why the Distal Interphalangeal (DIP) joints are spared:** The DIP joints are typically spared in RA because they have minimal synovial tissue compared to other joints. Inflammation of the DIP joints is instead a classic feature of **Osteoarthritis (Heberden’s nodes)** and **Psoriatic Arthritis** [3]. If a patient presents with DIP involvement, clinicians should look for alternative diagnoses. **2. Analysis of Incorrect Options:** * **Metacarpophalangeal (MCP) joints:** These are the most commonly involved joints in the hand in RA, leading to characteristic deformities like ulnar deviation. * **Proximal Interphalangeal (PIP) joints:** These are frequently involved early in the disease, often resulting in "fusiform swelling" or "spindle-shaped" fingers [1]. * **Atlanto-axial joint (C1-C2):** While RA generally spares the lumbosacral spine, it characteristically involves the cervical spine. Synovitis of the transverse ligament can lead to **atlanto-axial subluxation**, a potentially life-threatening complication. **3. High-Yield Clinical Pearls for NEET-PG:** * **Joints Spared in RA:** DIP joints, Thoracolumbar spine, and Sacroiliac joints. * **Early Sign:** Symmetrical involvement of the MTP (Metatarsophalangeal) joints of the feet is often the earliest manifestation. * **Deformities:** Boutonnière deformity (PIP flexion, DIP hyperextension) and Swan-neck deformity (PIP hyperextension, DIP flexion). * **Serology:** Anti-CCP (Cyclic Citrullinated Peptide) is more specific than Rheumatoid Factor (RF) for diagnosis [2].

Question 1

All of the following are true regarding acute gouty arthritis, EXCEPT:

Accepted Answer

Allopurinol is effective to treat the acute attack

Answer

MSU crystals are needle shaped and negatively birefringent

Answer

Serum uric acid levels can be normal or low at the time of an acute attack

Answer

Tophi are made up of monosodium urate crystals (MSU)

Question 2

A patient has been diagnosed with systemic sclerosis and has the presence of anti-RNA polymerase III antibodies. Which of the following is more commonly associated with this condition?

Accepted Answer

Acute onset of disease

Answer

Reduced risk of scleroderma renal crisis

Answer

Reduced risk of malignancy

Answer

Increased risk of pulmonary hypertension

Question 3

A 37-year-old woman presents with complaints of severe heartburn with or without meals. She has a history of hypertension, which has been treated with captopril. She also has a history of Raynaud disease, multiple facial telangiectasias, and very taut skin on the dorsum of both hands. She has failed to obtain relief for her heartburn with large doses of antacids or omeprazole. Esophageal manometry is ordered. What are the most likely results of this test?

Accepted Answer

Decreased esophageal peristalsis and decreased LES pressure

Answer

Decreased esophageal peristalsis and increased LES pressure

Answer

Increased esophageal peristalsis and decreased LES pressure

Answer

Increased esophageal peristalsis and increased LES pressure

Question 4

For a patient experiencing an acute attack of gout who cannot tolerate NSAIDs, which medication is the most appropriate choice?

Accepted Answer

Steroid

Answer

Allopurinol

Answer

Probenecid

Answer

Febuxostat

Question 5

A patient suffering from morning stiffness lasting more than 1 hour presents with the following abnormality in the X-ray. What is the most possible diagnosis?

Accepted Answer

Rheumatoid arthritis

Answer

Psoriatic arthritis

Answer

Osteoarthritis

Answer

Relapsing polychondritis

Question 6

Which of the following organs is least likely to be involved in Behcet's disease?

Accepted Answer

Liver

Answer

CNS

Answer

Joints

Answer

Eyes

Question 7

Which of the following is FALSE regarding antiphospholipid antibody syndrome (APLA)?

Accepted Answer

>=2 unexplained consecutive spontaneous abortions in > 10 weeks of gestation

Answer

>=3 unexplained consecutive spontaneous abortions in < 10 weeks of gestation

Answer

>=1 unexplained death of a morphologically normal fetus >= 10 weeks of gestation

Answer

>=1 premature birth of a morphologically normal neonate < 34 weeks of gestation

Question 8

A man developed frequent facial swelling with occasional laryngeal edema. What is the most probable diagnosis?

Accepted Answer

C1 esterase deficiency

Answer

Allergy

Answer

Anaphylaxis

Answer

Not esterase deficiency

Question 9

Felty's syndrome is associated with which of the following?

Accepted Answer

Rheumatoid arthritis

Answer

Osteoarthritis

Answer

Ankylosing spondylitis

Answer

Psoriatic arthritis

Question 10

Which joint is typically spared in Rheumatoid arthritis?

Accepted Answer

Distal interphalangeal joints of the finger

Answer

Metacarpophalangeal joints of the hand

Answer

Proximal interphalangeal joints of the finger

Answer

Atlanto-axial joint

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

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