Avascular necrosis (AVN) of the femoral head is a pathological process that results from disruption of the blood supply to the bone and occurs most commonly in the femoral epiphysis. Patients usually present with pain and limited joint motion. The mechanism involves impaired circulation to a specific area that ultimately becomes necrotic. AVN is most frequently associated with high doses of oral and intravenous corticosteroids and prolonged duration of therapy. Cancer patients receiving chemotherapy are usually also treated with corticosteroids.

Reactive arthritis, (formerly known as Reiter’s syndrome), is an autoimmune condition that occurs after a bacterial infection of the gastrointestinal or urinary tract. It is categorized as a seronegative spondylarthritis because of its association with HLA-B27. Reactive arthritis primarily affects young men and usually presents with musculoskeletal or extra‑articular symptoms. The characteristic triad consists of arthritis, conjunctivitis, and urethritis. The diagnosis is based on clinical features such as patient history and physical examination; there are no specific tests for reactive arthritis. Treatment is primarily symptomatic and consists of the administration of NSAIDs, as most patients recover spontaneously. extraarticular dermatologic manifestations include skin lesions of the glans resembling psoriasis (balanitis circinata); hyperkeratinisation of the palms and soles (keratoderma blenorrhagicum), oral ulcers. There usually is no rash and the diagnosis is unrelated to the presence of rheumatoid factor. This is a clinical diagnosis.

Women with Sjögren syndrome are likely to experience more complications during pregnancy than women without an autoimmune disease as the anti-Ro and anti-La antibodies cross the placenta and lead to various life threatening complications. Studies show a high incidence of poor fetal outcomes for these patients. Congenital heart block, neonatal lupus, congestive cardiac failure, hydrops fetalis can all be caused as a result of Sjogren syndrome.

TNF-alpha inhibitors are known to ameliorate the symptoms and disease activity of Arthritis mutilans (a rare and severe form of psoriatic arthritis), by disabling the cytokines that are involved in inflammation and joint destruction. From the mentioned choices, this would be the most effective option. Methotrexate is the most commonly used DMARD, followed by sulfasalazine used in mild to moderate forms of psoriatic arthritis but has not shown much efficacy in arthritis mutilans. Phototherapy, narrowband UVB light therapy can be very effective in clearing skin lesions.

Anti–Mi-2 antibodies are highly specific for dermatomyositis, but sensitivity is low; only 25% of patients with dermatomyositis demonstrate these antibodies. A positive antinuclear antibody (ANA) finding is common in patients with dermatomyositis, but is not necessary for diagnosis. Anti-Jo-1 antibodies are mostly associated with polymyositis. Anti Scl-70 antibodies and anti centromere antibodies are most commonly found in systemic scleroderma.

Angioedema secondary to C1 inhibitor deficiency has been rarely reported to be associated with systemic lupus erythematosus. A genetic defect of C1 inhibitor produces hereditary angioedema, which is usually presented with cutaneous painless oedema, but oedema of the genital area, gastrointestinal and laryngeal tracts have also been reported. In lupus patients, angioedema may be the result of an acquired type of C1 inhibitor deficiency, most probably due to antibody formation directed against the C1 inhibitor molecule.

Inclusion body myositis (IBM) is a progressive muscle disorder characterized by muscle inflammation, weakness, and atrophy (wasting). It is a type of inflammatory myopathy. IBM develops in adulthood, usually after age 50. The symptoms and rate of progression vary from person to person. The most common symptoms include progressive weakness of the legs, arms, fingers, and wrists. Some people also have weakness of the facial muscles (especially muscles controlling eye closure), or difficulty swallowing (dysphagia). Muscle cramping and pain are uncommon, but have been reported in some people. The underlying cause of IBM is poorly understood and likely involves the interaction of genetic, immune-related, and environmental factors. Some people may have a genetic predisposition to developing IBM, but the condition itself typically is not inherited. Elevated creatine kinase (CK) levels in the blood (at most ,10 times normal) are typical in IBM. Muscle biopsy may display several common findings including; inflammatory cells invading muscle cells, vacuolar degeneration, inclusions or plaques of abnormal proteins.

The typical “rheumatoid effusion” is a sterile exudative fluid with low pH (<7.3), low glucose (<60 mg. dL−1) and elevated lactate dehydrogenase (may be >700 IU). It should initially be treated with NSAIDs. Decortication should be reserved in patients with thickened pleura who have symptomatic dyspnoea.

Polymyositis is an inflammatory disorder causing symmetrical, proximal muscle weakness. It is thought to be a T-cell mediated cytotoxic process directed against muscle fibres. It may be idiopathic or associated with connective tissue disorders. It may also be associated with malignancy for example small cell lung carcinoma.
Dermatomyositis is a variant of the disease where skin manifestations are prominent, for example a purple (heliotrope) rash on the cheeks and eyelids.
It typically affects middle-aged, female: male 3:1. Features include proximal muscle weakness +/- tenderness, Raynaud’s phenomenon, respiratory muscle weakness, interstitial lung disease: e.g. fibrosing alveolitis or organising pneumonia, dysphagia, dysphonia. Investigations: elevated creatine kinase, other muscle enzymes (lactate dehydrogenase (LD), aldolase, AST and ALT) are also elevated in 85-95% of patients, EMG, muscle biopsy. Anti-Jo-1 antibodies are seen in pattern of disease associated with lung involvement, Raynaud’s and fever. Interstitial lung disease plays a major role in morbidity and mortality in patients with polymyositis and is considered a major risk factor for premature death in patients with myositis.

Anti-Sm antibodies are essential for diagnosis of SLE, especially in anti-dsDNA-negative patients. ANA are also found in 95% of the patients with SLE but they may also occur with other conditions like Juvenile inflammatory arthritis, chronic activity hepatitis, and Sjogren’s syndrome. Anti-Ro, although also found with SLE are more characteristic of Sjogren Syndrome. RF is usually associated with rheumatoid arthritis and cANCA with Wegener’s granulomatosis, Churg Strauss, and microscopic polyangiitis.