This document summarizes several conditions involving joints: rheumatoid arthritis, gout, and tenosynovial giant cell tumour. It describes the pathogenesis, clinical features, laboratory findings, treatment and histological features of each condition. Rheumatoid arthritis is a chronic inflammatory condition that predominantly affects the small joints of the hands and feet, causing pain and swelling. Gout is caused by urate crystal deposition in joints and organs and is characterized by acute inflammatory flares. Tenosynovial giant cell tumour is a benign neoplasm most commonly affecting the tendons of the fingers.
2. RHEUMATOID ARTHRITIS
• Chronic multisystem disease
• Most prominent manifestation- inflammatory arthritis of peripheral
joints usually with symmetrical distribution
• Systemic manifestations- hematologic, pulmonary, neurological,
cardiovascular abnormalities
3. • 3-5 times higher preponderance in females
• Peak incidence in 3rd – 4th decades of life
• Prodrome- fatigue, weakness, joint stiffness, vague arthalgias &
myalgias
• PAIN and SWELLING of joints of hands, wrists and feet in symmetrical
pattern
6. LABORATORY FINDINGS:
1. About 80% cases are positive for RA factor.
2. HLA-DR4 and HLA-DR1 association in familial cases.
3. Mild normocytic normochromic anemia, elevated ESR, mild
leucocytosis and hypergammaglobulinemia
4. Advanced cases show characteristic radiologic abnormalities such
as narrowing of joint space and ulnar deviation of the fingers and
radial deviation of the wrist
7. MORPHOLOGIC FEATURES
• RA involves first the small joints of hands and feet and then
symmetrically affects the joints of wrists, elbows, ankles and knees.
• The proximal interphalangeal and metacarpophalangeal joints are
affected most severely.
• Frequently cervical spine is involved but lumbar spine is spared.
8. HISTOLOGICALLY:
• Numerous folds of large villi of synovium
• Marked thickening of synovial membrane due to edema,
congestion and multilayering of synoviocytes
• Intense inflammatory cell infiltrate in the synovial membrane with
predominance of lymphocytes, plasma cells and some
macrophages, at places forming lymphoid follicles
• Foci of fibrinoid necrosis and fibrin deposition
Diffuse proliferative synovitis with formation of pannus.
9. • The pannus progressively destroys the underlying cartilage and
subchondral bone.
• This invasion of pannus results in demineralistaion and cystic
resorption of underlying bone.
• Later, fibrous adhesions or even bony ankylosis may unite the two
opposing joint surfaces.
10.
11.
12. EXTRA-ARTICULAR LESIONS:
• Non-specific inflammatory changes (acute vasculitis) are seen in the
blood vessels, lungs, pleura, pericardium, myocardium, lymph nodes,
peripheral nerves and eyes.
• RHEUMATOID NODULES- found in the subcutaneous tissue over
pressure points such as elbows, occiput and sacrum. The centre of
these nodules consists of an area of fibrinoid necrosis and cellular
debris, surrounded by several layers of palisading large epitheioid
cells, and peripherally there are numerous lymphocytes, plasma cells
and macrophages.
13.
14. VARIANT FORMS OF RA:
1. JUVENILE RA
2. FELTY’S SYNDROME
3. ANKYLOSING SPONDYLITIS OR RHEUMATOID SPONDYLITIS
15. TREATMENT
• NSAIDs: Nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve
pain and reduce inflammation. ...
• Steroids: Corticosteroid medications, such as prednisone, reduce
inflammation and pain and slow joint damage. ...
• Disease-modifying antirheumatic drugs (DMARDs)
• Biologic agents : adalimumab, infliximab
16. GOUT & GOUTY ARTHRITIS:
Gout is due to hyperuricemia and deposition of monosodium urate
crystals in joints and viscera and uric acid kidney stones
• Primary gout (90%): idiopathic (85%) with overproduction of uric acid
(may have normal excretion) or known enzyme defects (partial
hypoxanthine-guanine phosphoribosyl transferase deficiency
[HGPRT])
• Secondary gout (10%): increased nucleic acid turnover due to
leukemia/lymphoma, chronic renal disease, HGPRT deficiency
17. • Need serum urate > 7 mg/dl for deposition (saturation threshold for
urate at 98.6 F)
• Uric acid / urate is product of metabolic breakdown of purine
nucleotides.
• There is an cute inflammatory response and deposits of rhomboid
crystals on the articular cartilage, ligaments, tendons and joint
capsule, termed chondrocalcinosis.
18. CLINICAL FEATURES
• Males more commonly affected
• Risk factors for gout with hyperuricemia are age > 30 years, familial
history of gout, alcohol use, obesity, thiazide administration, lead
• The involvement may be monoarticular or polyarticular but large
joints such as knees, hips & shoulders are more often affected.
• Synovial fluid Aspirate: grossly white gray and granular; strongly
negative birefringent needle shaped crystals under polarized light;
foreign body giant cells
21. A gouty tophus, showing central aggregate of urate crystals surrounded by inflammatory
cells, fibroblasts and occasional giant cells.
22. TREATMENT:
Drugs to relieve gout pain include:
• nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin,
ibuprofen, and naproxen
• Corticosteroids
Drugs that prevent gout attacks include:
• xanthine oxidase inhibitors, such as allopurinol and febuxosta
23. TENSOSYNOVIAL GIANT CELL TUMOUR
• Giant cell tumour of tendon sheath
• Nodular tenosynovitis
• Second most common tumor of the hand (after ganglion cyst)
• Most commonly seen in the tendons of fingers
• Fourth or fifth decade of life most frequent
• F>M (2:1)
• Skin colored nodule without specific features; most are slow growing and
painless
24. Pathogenesis:
• Initially regarded as inflammatory in origin ( synovitis)
• Currently, cytogenetic studies have shown clonal proliferation of cells
indicating that the lesions are neoplastic
• Majority of cases contain a subset of cells with a translocation
involving CSF1 gene at 1p13
25. • Well circumscribed and
lobulated swelling in the digits,
usually in close association
with a tendon
• Other locations have been
reported, such as wrist, ankle,
knee, hip, elbow.
• Intra-articular localized
tenosynovial giant cell tumors
are most frequent in the knee
26. Histologically:
• Well encapsulated
• Composed of variable
proportions of mononuclear
cells, osteoclast-like giant cells,
foamy histiocytes and
hemosiderin laden histiocytes
and irregular bundles of
collagen