Types of Arthritis and Infections that can Cause Tenosynovitis

Tenosynovitis is a condition where the tendon sheath becomes inflamed, causing pain and swelling. It can be caused by various types of arthritis and infections. Here are some of the most common causes:

Systemic Sclerosis: This autoimmune disease causes fibrosis of connective tissue, resulting in hard and thickened skin, swollen digits, and Raynaud’s phenomenon. Tenosynovitis in systemic sclerosis is non-tender and without swelling of the tendons.

Rheumatoid Arthritis: Tenosynovitis due to rheumatoid arthritis causes pain and swelling of tendons. It usually involves the interphalangeal, metacarpophalangeal, and wrist joints, and can cause deformities such as swan neck and Boutonnière’s deformity.

Gout: Gout can cause tenosynovitis, which is very painful and presents with redness and swollen tendons. It typically affects the metatarsophalangeal joints.

Disseminated Gonococcal Infection: This infection can cause acute migratory tenosynovitis, especially in younger adults. Women may be asymptomatic, while men may present with urethral discharge or dysuria.

Reactive Arthritis: This type of arthritis causes pain and swelling of tendons, commonly affecting the knees or sacrum. It is an acutely inflammatory process and would therefore be swollen and tender.

In conclusion, tenosynovitis can be caused by various types of arthritis and infections, and it is important to identify the underlying cause in order to provide appropriate treatment.

Understanding the Diagnosis of Polymyalgia Rheumatica

Polymyalgia rheumatica (PMR) is a condition that causes pain and stiffness in proximal muscle groups, often accompanied by systemic symptoms. While other potential diagnoses such as infections or neoplasia should be considered, PMR is typically characterised by raised levels of inflammatory markers, particularly erythrocyte sedimentation rate (ESR). Treatment with corticosteroids usually results in rapid improvement, and lack of response to steroids may indicate a need to re-evaluate the diagnosis. Autoantibody screening and nerve conduction velocity tests are not helpful in diagnosing PMR, while muscle biopsy may be performed to exclude polymyositis. A temporal artery biopsy may be considered if the patient has symptoms of giant cell arthritis.

Differentiating Knee Conditions: A Case-Based Approach

A patient presents with a red, tender, and inflamed knee. The differential diagnosis includes prepatellar bursitis, osteoarthritis, localised cellulitis, rheumatoid arthritis, and gout.

prepatellar bursitis, also known as housemaid’s knee, carpet layer’s knee, or nun’s knee, is often caused by repetitive knee trauma. Treatment involves non-steroidal anti-inflammatory agents and local corticosteroid injection. Septic bursitis requires appropriate antibiotic cover and drainage.

Osteoarthritis is a diagnosis of exclusion and does not typically cause a red, tender, inflamed knee. Knee aspirate in this case would not show white cells.

Localised cellulitis may result in erythema but is unlikely to cause knee swelling. Knee aspirate in this case would not show white cells.

Rheumatoid arthritis is unlikely to present in men of this age and typically affects small joints of the fingers, thumbs, wrists, feet, and ankles.

Gout can be diagnosed through the presence of negatively birefringent crystals seen on joint microscopy.

In conclusion, a thorough evaluation of the patient’s symptoms and appropriate diagnostic tests are necessary to differentiate between these knee conditions.

Differentiating between Rheumatic Diseases: A Case Study

Polymyalgia rheumatica (PMR) is a common inflammatory rheumatic disease in the elderly population, presenting as pain and stiffness in the neck, shoulders, upper arms, and hips. In contrast, polymyositis is an autoimmune connective tissue disease that results in proximal muscle weakness. Multiple myeloma is a malignancy of plasma cells, causing bone pain, renal failure, and anaemia. Rheumatoid arthritis is a chronic inflammatory, symmetrical polyarthropathy that tends to cause joint stiffness and pain within the small joints, as well as causing fatigue. Osteoarthritis is a degenerative arthritis that commonly affects the knee, hip, spine, and hands.

In this case study, the patient presented with shoulder stiffness, fatigue, low-grade fever, and anaemia. A diagnosis of PMR was made clinically and with the aid of a raised ESR. Treatment is with oral prednisolone, which should be reduced gradually once symptoms are controlled to avoid the risks of chronic steroid use.

It is important to differentiate between these rheumatic diseases as they have different underlying causes, presentations, and treatments. A thorough history, physical examination, and appropriate investigations are necessary for accurate diagnosis and management.

Systemic lupus erythematosus (SLE) is an autoimmune disease that primarily affects young women. It is caused by the deposition of immune complexes and can have a wide range of clinical effects, including a butterfly-shaped rash on the cheeks and nose, joint pain, and involvement of multiple organ systems such as the kidneys, lungs, and heart. SLE is associated with the presence of ANA and dsDNA antibodies, as well as low levels of C3 and C4 in the blood.

Mixed connective tissue disease (MCTD) is a syndrome that shares features with several other rheumatological conditions, including SLE, scleroderma, myositis, and rheumatoid arthritis. Common symptoms include fatigue, joint pain, pulmonary involvement, and Raynaud’s phenomenon. MCTD is strongly associated with anti-RNP antibodies.

Rheumatoid arthritis is an inflammatory arthritis that typically affects middle-aged women and causes symmetrical joint pain and stiffness, particularly in the hands and feet. If left untreated, it can lead to deformities that affect function. Rheumatoid arthritis is associated with the presence of autoantibodies such as rheumatoid factor and anti-CCP.

Polymyositis is an autoimmune myositis that causes weakness and loss of muscle mass, particularly in the proximal muscles. Other symptoms may include malaise and difficulty swallowing. Polymyositis is associated with anti-Jo1 autoantibodies.

Systemic sclerosis, also known as diffuse scleroderma, is an autoimmune disease that primarily affects women aged 30-50. It causes collagen accumulation, leading to thickening of the skin and vasculitis affecting small arteries. Systemic sclerosis can affect multiple organ systems, including the skin, lungs, kidneys, and gastrointestinal tract. It is associated with anti-Scl70 antibodies.

Differentiating Autoantibodies in Connective Tissue Diseases

Connective tissue diseases are a group of autoimmune disorders that affect various parts of the body. Differentiating between these diseases can be challenging, but autoantibodies can provide valuable clues. Here are some common autoantibodies and the connective tissue diseases they are associated with:

1. Anti-centromere antibody: This antibody is most likely to be present in limited systemic sclerosis (CREST).

2. Anti-Scl-70: This antibody is found in diffuse systemic sclerosis.

3. Anti-RNP antibody: This antibody is found in mixed connective tissue disease.

4. Anti-Ro antibody: This antibody is classically positive in Sjögren’s syndrome or systemic lupus erythematosus.

5. Anti-Jo-1 antibody: This antibody is commonly raised in polymyositis.

By identifying the specific autoantibodies present in a patient, healthcare providers can better diagnose and manage connective tissue diseases.

Treatment Options for Paget’s Disease: Oral Bisphosphonates and More

Paget’s disease is a condition characterized by abnormal bone remodeling, which can lead to a range of symptoms including bone pain, fractures, and osteoarthritis. Diagnosis is typically made through radiograph findings and laboratory tests. Treatment options vary depending on the severity of symptoms, with physiotherapy and NSAIDs being effective for mild cases. However, for more severe cases, oral bisphosphonates and calcitonin may be necessary to inhibit osteoclastic activity. Chelation therapy, antidepressant medication, and chemotherapy for osteosarcoma are not indicated for Paget’s disease. Operative therapy may be necessary for patients with degenerative joint disease and pathological fractures, but should be preceded by treatment with oral bisphosphonates or calcitonin to reduce bleeding.

Mythbusting Gout: Clarifying Common Misconceptions

Gout is a painful and often misunderstood condition. Here are some common misconceptions about gout, and the truth behind them:

1. Gout may be seen in patients with chronic haemolytic anaemia.
2. Gout may occur in those with elevated urate levels (although levels may be normal during an acute attack) such as those with haemolytic anaemia.
3. Gout only affects the first metacarpophalangeal (MCP) joint.
4. Gout most commonly affects the first metatarsophalangeal joint. However, it is not the only joint affected.
5. Allopurinol is effective in the treatment of acute gout.
6. Acute gout is treated with non-steroidal anti-inflammatory drugs (NSAIDs), colchicine or prednisolone, but not allopurinol. Allopurinol is effective in the prevention of gout because it reduces serum urate levels by blocking urate production (xanthine oxidase inhibition).
7. A diagnosis of gout is made if there are positively birefringent crystals in the joint aspirate.
8. Gout is an inflammatory arthritis that occurs as a result of deposition of negatively birefringent urate crystals in the joint.
9. All cases of acute gout have an elevated serum urate.
10. Although a raised serum urate can be used to support the diagnosis, many will not be raised. Similarly, if a patient has a raised serum urate, they do not automatically have the clinical picture of gout.

In conclusion, it is important to dispel these common myths about gout in order to properly diagnose and treat this painful condition.

Differential Diagnosis for a Young Man with Purpura and Haematuria

The patient in question presents with a purpuric rash on the back, buttocks, and extensor surfaces of the lower limbs, as well as haematuria. The following is a differential diagnosis of possible conditions that could be causing these symptoms.

Henoch–Schönlein purpura (HSP)
The clinical presentation is entirely typical of HSP, a vasculitic process that results in a purpuric rash and haematuria. It should be noted that platelet numbers are usually normal or raised in HSP, so thrombocytopaenia is not expected.

Haemophilia A
This condition is not likely as it results in joint and muscle bleeding, which is not present in this case. Additionally, haemophilia would not cause haematuria.

Idiopathic thrombocytopaenic purpura (ITP)
While purpura is a symptom of ITP, a reduced platelet count is typically present. Without a discussion of platelet levels, it is difficult to justify a diagnosis of ITP. Additionally, ITP would not result in haematuria.

Leukaemia
If acute leukaemia were causing the symptoms, thrombocytopaenia might be expected. However, the clinical presentation is more compatible with HSP, and thrombocytopaenia alone would not result in haematuria.

Thalassaemia trait
There is no indication in the history to suggest this condition, and it would not result in purpura. Thalassaemia trait is typically asymptomatic.

In conclusion, the patient’s symptoms are most consistent with HSP, a vasculitic process that results in a purpuric rash and haematuria.

Sites of Crystal Deposition in Pseudogout

Pseudogout is a condition characterized by the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in various tissues of the body. The most common site of deposition is the synovial fluid, which can lead to joint inflammation and pain. However, CPPD crystals can also be deposited in other tissues such as cartilage, ligaments, tendons, and bursae.

Cartilage is another common site for CPPD crystal deposition, and pseudogout is also known as chondrocalcinosis. Deposition in the ligaments and tendons is possible but less common than in the synovium. Bursae deposition is also possible but less common than synovium deposition.

In summary, while CPPD crystals can be deposited in various tissues in pseudogout, the synovium is the most common site of deposition, followed by cartilage, ligaments, tendons, and bursae.