Rheumatoid Arthritis MCQs

Explanation: Hashimoto's thyroiditis is an autoimmune thyroid disease characterized by marked lymphocytic infiltration of the thyroid, follicular atrophy, and fibrosis . The disease is primarily mediated by T-cell-induced thyroid cell destruction , but autoantibodies serve as important clinical markers . The most relevant antibodies in Hashimoto's thyroiditis are: Anti-thyroid peroxidase (Anti-TPO) antibodies → most commonly present, clinically useful for diagnosis. Anti-thyroglobulin (Tg) antibodies → also present in many cases. (vs Option C) TSH-receptor blocking antibodies → seen in some patients, especially in thyroid atrophy, but less common. (vs Option B) Among these, anti-TPO antibodies are the most strongly associated and are the standard diagnostic marker. Anti-CCP (Option A): Seen in rheumatoid arthritis , not thyroid disease.

The symptoms of fevers, weight loss and lower back pain are classical for retroperitoneal fibrosis. There is an association with inflammatory conditions such as SLE, rheumatoid arthritis, ankylosing spondylitis, Hashimoto's thyroiditis and glomerulonephrosis. CT or MRI shows fibrotic para-aortic masses causing ureteral obstruction. Reference: Harrison's Principles of Internal Medicine, 21 st ed, Ch: 319 Pg: 2375

Among the newer agents, JAK inhibitors are the drugs that are given orally among the options. Conventional DMARDS are also oral agents. Biologicals are all parenteral agents. Reference: Harrison's Principles of Internal Medicine, 21st ed, Ch: 358, Pg: 2761-2764

The question deals with treatment endpoints in SLE. Complete permanent remission(no disease activity without any treatment) is seen in Aim of treatment in SLE is disease remission on treatment or low level disease activity. Disease activity is measured using SLEDAI 2k score and a score of > 4 indicates an active disease. Anti ds DNA titres and C3 complement levels are used as markers of disease flare. From among the given options, SLEDAI2K score of > 3 does not indicate active disease. Hence it is wrong. So statements 1,2 and 3 are correct. Reference: Harrison's principles of Internal Medicine 21st edition Ch : 356 Pg: 2740, 2746

TS DMARDS or targeted synthetic DMARDS are inhibitors of JAK and are therapeutically used in RA. The JAK family links the extracellular domains of the cytokines involved in RA to the intra cellular signals. They include Tofacitinib : JAK 1 and JAK 3 inhibitor Baricitinib: JAK 1 and JAK 2 inhibitors Upadacitinib: JAK 1 inhibitor They can be used as monotherapy or in combination with methotrexate. They cause neutropenia, increase in cholesterol levels and rise in serum creatinine and transaminases. Reference: Harrison's Principles of Internal Medicine, 21st ed, Ch: 358, Pg: 2761-2764

The conventional DMARDs that are useful in Psoriatic Arthritis are: Methotrexate, Sulfasalazine, Leflunomide. Biologicals that are used include: anti TNFα agents, anti IL17/23 agents and anti JAK agents like Tofacitinib. Phosphodiesterase inhibitor Apremilast is also used. Reference: Harrison's Principles of Internal Medicine 21 st ed, Ch: 362, Pg: 2800

The knees are most frequently involved in reactive arthritis, next most commonly affected are the ankles and small joints of the feet Reference : Harrison's Principles of Internal Medicine, 21 st ed, Ch: 362, Pg: 2797

The disease activity in SLE can be assessed by measuring the Serum ds DNA activity and a decrease in Serum complement levels(C3 or C4). ESR and CRP can be raised in disease flare or during infections and hence cant be used to differentiate them. Reference : Harrisons Principles of Internal Medicine, 21 st ed Ch: 356, Pg:2745