Joint Lesions Flashcards
Osteoarthritis
- Degenerative arthropathy with multifactorial etiology
- Most common cause of chronic joint pain in geriatric age group
- Associated with joint stiffness and decreased range of motion
- Classic radiologic features include loss of joint space, subchondral bone sclerosis, cysts and osteophyte formation
- Usually affects old age group
- More common in women than men
Rheumatoid arthritis
- Rheumatoid arthritis (RA) is a chronic autoimmune disorder often characterized by symmetrical and progressive destructive arthritis
- Rheumatoid arthritis often affects women and frequently presents with symmetric arthritis, often involving the small bones of the hands and feet
- Patients may have an increase in serum acute phase reactants and positive autoantibodies, including rheumatoid factor and anticitrullinated protein antibodies
- Microscopic findings typically show thickening of the synovial lining, abundant lymphocytes and plasma cells, angiogenesis and erosion of bone and cartilage
- Extra-articular manifestations are common and can include rheumatoid nodules, pleuritis, vasculitis and scleritis
- Twice as common in women than men; M:F between 1:2 and 1:4
- May begin at any age with peak frequency in the fourth and fifth decades
- Rheumatoid Factor –> antibody against the Fc portion og IgG
- RF and IgG form complex
Micro:
Rheumatoid arthritis (joint involvement)
* Synovial hypertrophy and hyperplasia
* Synoviocyte layer can have 5 or more cells in thickness
* Hypertrophic synoviocytes have microvilli protruding from the surface
* Synovium can be replaced by granulation tissue and fibrin with increased blood vessels
* Synovium with prominent lymphocytic and polyclonal plasma cell infiltrate
* Lymphocytes tend to aggregate, forming follicles and occasionally germinal centers
* Mixed inflammatory infiltrate includes T lymphocytes, B lymphocytes, macrophages, plasma cells and mast cells
* Neutrophils may be present, especially in an acute flare and early arthritis
* Tendons may have necrosis, myxoid degenerative change and vascular growth
Rheumatoid nodules
* Rheumatoid nodules have zones of central eosinophilic fibrinoid necrosis surrounded by palisading histiocytes and an outer layer of granulation tissue, chronic inflammation and fibrous tissue
* Rheumatoid nodules become more hyalinized and fibrotic as they mature, extent of necrosis varies with age of the lesion
* Fibrosis may be extensive
Gout and gouty arthritis
- Core mechanism for pathogenesis of gout is an augmented serum level of uric acid following a reduced renal excretion
- Alcohol and drugs
- HGPRT enzyme deficiency
- Leish-nehyn syndrome –> complete absence of hGPRT
Gout and pseudogout are both forms of arthritis that result from the deposition of crystals in the joints, but they differ in the type of crystals involved, the affected joints, and certain clinical characteristics.
- Cause and Crystals
Gout: Caused by the deposition of uric acid crystals in the joints. Uric acid is a waste product of purine metabolism, and when it builds up in the body (often due to high levels of uric acid in the blood, a condition called hyperuricemia), it forms needle-shaped crystals that can deposit in the joints, leading to inflammation and pain.
Pseudogout: Caused by the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the joints. These crystals are often referred to as “pseudo-gout” crystals because their effects mimic gout, but they are chemically different.
- Affected Joints
Gout: Primarily affects the big toe (a condition called podagra) but can also affect other joints, especially those in the lower extremities like the ankles and knees. Gout tends to affect one joint at a time (acute attacks), though multiple joints can eventually be involved in chronic cases.
Pseudogout: Most commonly affects the knee, but it can also affect the wrists, shoulders, hips, and other joints. It can cause more widespread joint involvement compared to gout, especially in older individuals.
- Onset and Symptoms
Gout: Gout attacks are often sudden and severe, occurring after a trigger like eating purine-rich foods (e.g., red meat, shellfish), drinking alcohol (especially beer), dehydration, or trauma. Symptoms include intense pain, redness, warmth, and swelling in the affected joint. The attack often comes on overnight and can be extremely painful.
Pseudogout: The onset is also often sudden but may not be as dramatic or painful as gout. The symptoms of pseudogout can be less intense initially, and the pain tends to be more chronic or recurrent rather than the sharp, sudden attacks seen in gout. Swelling, redness, and warmth are common, but the inflammation may be more prolonged.
- Age and Risk Factors
Gout: Gout is more common in middle-aged and older men, though it can occur in women, especially after menopause. Risk factors for gout include obesity, high blood pressure, kidney disease, alcohol consumption, and a diet rich in purines (e.g., red meat, seafood). Genetics also play a role in its development.
Pseudogout: Pseudogout is more common in older adults and is often associated with conditions such as osteoarthritis, hyperparathyroidism, hypothyroidism, and certain genetic factors. It’s less commonly seen in younger individuals compared to gout.
- Diagnosis
Gout: Diagnosis is typically confirmed through the identification of uric acid crystals in the joint fluid obtained during joint aspiration (arthrocentesis). Blood tests may show elevated uric acid levels, though some people with gout do not have high uric acid levels during an acute attack.
Pseudogout: Diagnosis is confirmed by identifying calcium pyrophosphate crystals in joint fluid. These crystals are rhomboid-shaped and positively birefringent under polarized light. X-rays may show joint damage or calcification of cartilage, a common feature of pseudogout.
- Treatment
Gout: Treatment focuses on reducing inflammation during an acute attack with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids. Long-term management includes medications to lower uric acid levels (e.g., allopurinol, febuxostat) and lifestyle changes such as dietary modifications and weight management.
Pseudogout: Treatment for pseudogout involves managing the acute flare with NSAIDs, colchicine, or corticosteroids. For chronic cases, joint injections or physical therapy may be recommended. Unlike gout, there is no treatment to lower the level of calcium pyrophosphate crystals in the body.
- Prognosis
Gout: With proper treatment, acute gout attacks can be managed effectively. Chronic gout can lead to joint damage and tophi (deposits of uric acid crystals under the skin) if left untreated.
Pseudogout: While pseudogout can also lead to joint damage over time, it is generally less aggressive than gout. However, repeated episodes of pseudogout can result in cartilage damage and contribute to the development of osteoarthritis in the affected joints
Reiter’s Syndrome
- Key Features of Reiter’s Syndrome (Reactive Arthritis):
Arthritis: Inflammation and pain, usually affecting large joints such as the knees, ankles, and feet. The arthritis is typically asymmetric, meaning it affects different joints on either side of the body.
Conjunctivitis: Inflammation of the eyes, leading to redness, pain, and sometimes light sensitivity. It’s an important diagnostic feature of the condition.
Urethritis: Inflammation of the urinary tract, often leading to painful urination, frequent urination, and discharge.
Additional Symptoms: Some patients may also experience skin rashes, mouth ulcers, sausage-like swelling of fingers or toes (dactylitis), and enthesitis (inflammation at the sites where tendons or ligaments attach to bones).
Causes of Reiter’s Syndrome:
Reiter’s syndrome is often triggered by an infection. Infections that can lead to the development of reactive arthritis include:
- Gastrointestinal infections caused by bacteria like Salmonella, Shigella, Campylobacter, or Yersinia.
- Genitourinary infections caused by Chlamydia trachomatis (a sexually transmitted infection).
- Respiratory infections, though less common, can also be a trigger, particularly infections involving Mycoplasma pneumoniae.
After the infection, the body’s immune system may mistakenly attack healthy tissues, leading to inflammation in the joints and other affected areas, even though the original infection has been cleared.
