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Showing posts from September, 2022

GOUT

 Introduction: Gout is caused by the deposition of monosodium urate monohydrate (MSUM) crystals at synovial joints. It has a prevalence of 1–2%, and is more common in men, in certain ethnic groups and with increasing age. Uric acid mainly comes from the metabolism of purines within the body but some is ingested with food. Gout is becoming more common with increased longevity and prevalence of metabolic syndrome, of which hyperuricaemia is a component.   Clinical features Acute gout: This presents with rapid onset of severe pain in a single distal joint, commonly the first metatarsophalangeal joint. Other common sites include the ankle, midfoot, knee,  hand, wrist and elbow. Examination reveals marked synovitis with swelling, red shiny skin and extreme tenderness. Periarticular swelling and fever may also be present. Symptoms are usually selflimiting over 5–14 days. The differential diagnosis includes septic  arthritis, cellulitis and reactive arthritis.   Recurrent and chro

FIBROMYALGIA

  Introduction: This is a common cause of generalised regional pain and disability, and is frequently associated with medically unexplained symptoms in other systems. The prevalence in the UK is ~2–3%. It increases in prevalence with age, to reach a peak of 7% in women aged over 70. There is a female predominance of ~10 : 1. Risk factors include stressful life events, such as marital disharmony, alcoholism in the family, injury or assault, low income and self-reported childhood abuse. No structural, inflammatory or metabolic abnormality has been identified, although abnormalities of non-rapid eye movement (REM) sleep and of central pain processing have been postulated as potential aetiological factors.   Clinical features and investigations The main presenting feature is multiple regional pain, affecting the neck, back, both arms and both legs; it is unresponsive to analgesics and NSAIDs.  Patients commonly report fatigability, particularly in the morning, and reported disabi

SEPTIC ARTHRITIS

Introduction:  Septic arthritis is a medical emergency. It usually arises from haematogenous spread of bacterial infection from another site, commonly the skin or upper respiratory tract. Infection from direct puncture wounds or that secondary to joint aspiration is uncommon. Risk factors for septic arthritis include increasing age, pre-existing joint disease (especially RA), diabetes mellitus, immunosuppression and IV drug misuse.   Clinical features The usual presentation is with acute or subacute monoarthritis. The joint is usually swollen, hot and red, with pain at rest and on movement. The knee and hip are the most common sites. The usual culprit organism is Staphylococcus aureus . Disseminated gonococcal infection is another cause in young, sexually active adults. This presents with migratory arthralgia and low-grade fever, followed by the development of oligo- or monoarthritis. Painful pustular skin lesions may also be present. Lyme disease and brucellosis are less commo

SERONEGATIVE ARTHRITIS

  Introduction: This term is applied to a group of inflammatory joint diseases distinct from RA that share a number of clinical features: ● Ankylosing spondylitis. ● Reactive arthritis, including Reiter’sdisease. ● Psoriatic arthropathy. ● Arthritis associated with inflammatory bowel disease (Crohn’s disease, ulcerative colitis).   An association with HLA-B27 occurs in all seronegative spondarthritides but is particularly strong for ankylosing spondylitis and Reiter’s disease ( > 90%). The suggested pathogenesis is an aberrant response to infection in genetically predisposed individuals. In some situations a triggering organism can be identified, as in Reiter’s disease following bacterial dysentery or chlamydial urethritis, but in others the environmental trigger remains obscure.     Ankylosing spondylitis Ankylosing spondylitis is a chronic inflammatory arthritis predominantly affecting the sacroiliac joints and spine. The onset is typicallybetween the ages of

CONNECTIVE TISSUE DISORDER

Introduction:  These diseases share overlapping clinical features, characterised by dysregulation of immune responses, autoantibody production often directed at components of the cell nucleus, and widespread tissue damage.   Systemic lupus erythematosus Systemic lupus erythematosus (SLE) is a rare multisystem connective tissue disease, mainly occurring in women (90%), with a peak onset in the second and third decades. Prevalence is 0.2% in Afro- Caribbeans and 0.03% in Caucasians. Several autoantibodies are associated with SLE. Many of the target autoantigens are intracellular and intranuclear components. It is likely that the wide spectrum of autoantibody production results from polyclonal B- and T-cell activation. Although the triggers that lead to autoantibody production in SLE are unknown, one mechanism may be exposure of intracellular antigens on the cell surface during apoptosis.   Clinical features Fever, weight loss and mild lymphadenopathy occur during flaresof