Stiff And Painful Hands Case Study in Pathology

In this post, we are going to discuse the disease of STIFF AND PAINFUL HANDS.


A 28-year-old paralegal presents to her GP after having been bothered by stiff joints in both hands for the past few weeks. The stiffness is most prominent on waking and lasts for about an hour before improving during the day. She denies other musculoskeletal problems or involvement of other joints. Her only medical history is mild asthma. Her family history is positive for type 1 diabetes in her brother.


Physical examination reveals a slim, good-looking woman. Her metacarpophalangeal joints are slightly swollen bilaterally and mildly tender, and there is some tenderness in some of the interphalangeal joints in both hands. The metacarpal compression test is positive bilaterally.


1. Based on the history and examination findings, suggest a differential diagnosis.
Which diagnosis is most likely and why?
2. What further investigations are required, and which tests are most predictive for the
likely diagnosis?
3. Summarize the pathophysiology of the underlying diagnosis. What extra-articular
complications may arise with this condition?



The clinical picture in this case is highly suggestive of an inflammatory arthropathy with findings of joint swelling, morning stiffness, and evidence of synovitis. Therefore, key differential diagnoses include: • Rheumatoid arthritis (RA)

• Seronegative spondyloarthropathies (eg, psoriatic arthritis, arthritis associated with inflammatory bowel disease)

• Postviral or postinfectious arthropathy

• Connective tissue diseases (such as lupus and scleroderma)

• Crystal arthropathy (gout and pseudogout)

• Degenerative joint disease (osteoarthritis) The most likely diagnosis is rheumatoid arthritis, which is the most common inflammatory arthropathy and typically affects adults between 30 and 50 years of age. This is due to a history of bilateral joint problems, mainly in the small joints of the hand, as well as morning stiffness lasting more than an hour, which is highly suggestive of an inflammatory process rather than a degenerative one (in the latter, symptoms tend to get worse throughout the day and the stiffness usually lasts less than an hour). Similarly, the absence of a medical history or other symptoms makes seronegative arthritis, postviral arthritis, and connective tissue disease unlikely.

A diagnosis of rheumatoid arthritis, according to the American College of Rheumatology, requires the presence of four of the following (the first four for at least 6 weeks):

• Morning stiffness lasting >1 hour

• Symmetrical arthritis

• Arthritis of three or more joints areas

• Hand joint involvement

• Rheumatoid nodules

• Rheumatoid factor seropositivity

• Typical radiographic features (eg, erosions, juxtaarticular osteopenia). This patient meets three criteria from history and examination alone, and referral would be warranted to a rheumatology specialist. Additional investigations would include basic blood tests (complete blood count, possible anemia of chronic disease, kidney and liver function, which can guide the choice of medications) and tests for inflammatory activity.

The latter include CRP and ESR along with more specific tests for RA, namely rheumatoid factor (RF) and anti-CCP antibodies. Anti-CCP has similar sensitivity (65-85%) but much higher specificity (>95% vs. 80%) for RA in patients with suspected rheumatic disease than RF, and anti-CCP positivity is also reported. associated with a more severe clinical course. X-rays of the hand would also be helpful in looking for evidence of joint damage. The pathophysiology of RA is not completely understood and the cause remains unknown.

It is an autoimmune disease caused by exposure of a genetically susceptible individual to an as yet unidentified antigen. The interaction of genetic (eg, human leukocyte antigen [HLA]-DR4 allele) and environmental (eg, smoking, infection) factors lead to altered post-transcriptional regulation of proteins and citrullination of self proteins. Loss of tolerance to these new epitopes leads to the formation of autoantibodies (eg, anti-CCP) and stimulation of CD4 and B T-cell responses, which act against unknown target antigens in the joints and mediate injury. joint through the production of inflammatory cytokines such as TNF-α and IL-1.

These stimulate the proliferation of synovial cells and the production of matrix metalloproteinases, which aid in the destruction of articular cartilage, and the inflammation-rich hyperplastic synovium adheres and grows on the articular surfaces forming pannus. RA is also associated with an increased risk of cardiovascular disease, as a result of endothelial activation by inflammatory cytokines. This widespread inflammatory response may also explain the other systemic symptoms of RA, involving the lungs (fibrosis), bones (osteoporosis), and brain (reduced cognition), as well as an increased risk of lymphoma.



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