When someone falls on an outstretched hand, they may suffer from a scaphoid fracture, which is a common injury. However, the problem with this type of fracture is that it may not show up on an X-ray. This is because the scaphoid bone receives a retrograde blood supply from the dorsal carpal branch of the radial artery, which increases the risk of avascular necrosis if the fracture goes undetected. Symptoms of a scaphoid fracture include wrist pain, especially when the thumb is compressed longitudinally and the wrist is deviated ulnarly. Signs of this injury include tenderness over the anatomical snuffbox and wrist joint effusion. To diagnose a suspected scaphoid fracture, a scaphoid series of x-rays should be performed. If the fracture cannot be imaged, MRI scans can be used. If an undisplaced fracture is detected, a neutral forearm cast should be applied for 6-8 weeks. It is important to note that rest alone will not heal a scaphoid fracture, and without treatment, it can progress to avascular necrosis. Immediate screw fixation is not necessary for an undisplaced scaphoid fracture. If a fracture is suspected but cannot be imaged, a cast should still be applied, and the patient should be re-imaged using x-ray scans in two weeks. Screw fixation may be used to treat a displaced scaphoid fracture, as casting alone is less likely to promote healing.

Understanding Scaphoid Fractures

A scaphoid fracture is a type of wrist fracture that typically occurs when a person falls onto an outstretched hand or during contact sports. It is important to recognize this type of fracture due to the unusual blood supply of the scaphoid bone. Interruption of the blood supply can lead to avascular necrosis, which is a serious complication. Patients with scaphoid fractures typically present with pain along the radial aspect of the wrist and loss of grip or pinch strength. Clinical examination is highly sensitive and specific when certain signs are present, such as tenderness over the anatomical snuffbox and pain on telescoping of the thumb.

Plain film radiographs should be requested, including scaphoid views, but the sensitivity in the first week of injury is only 80%. A CT scan may be requested in the context of ongoing clinical suspicion or planning operative management, while MRI is considered the definite investigation to confirm or exclude a diagnosis. Initial management involves immobilization with a splint or backslab and referral to orthopaedics. Orthopaedic management depends on the patient and type of fracture, with undisplaced fractures of the scaphoid waist typically treated with a cast for 6-8 weeks. Displaced scaphoid waist fractures require surgical fixation, as do proximal scaphoid pole fractures. Complications of scaphoid fractures include non-union, which can lead to pain and early osteoarthritis, and avascular necrosis.

The most likely fracture resulting from a fall onto an outstretched hand (FOOSH) is Colles fracture. This type of fracture occurs in the distal radius and typically does not involve the joint. It is the most common type of distal radius fracture. Bennett fracture, Dupuytren fracture, and Galeazzi fracture are all incorrect answers as they describe different types of fractures in other parts of the body.

Understanding Colles’ Fracture

Colles’ fracture is a type of distal radius fracture that typically occurs when an individual falls onto an outstretched hand, also known as a FOOSH. This type of fracture is characterized by the dorsal displacement of fragments, resulting in a dinner fork type deformity. The classic features of a Colles’ fracture include a transverse fracture of the radius, located approximately one inch proximal to the radiocarpal joint, and dorsal displacement and angulation.

In simpler terms, Colles’ fracture is a type of wrist fracture that occurs when an individual falls and lands on their hand, causing the bones in the wrist to break and shift out of place. This results in a deformity that resembles a dinner fork. The fracture typically occurs in the distal radius, which is the bone located near the wrist joint.

Types of Bone Tumours

Bone tumours can be classified into two categories: benign and malignant. Benign tumours are non-cancerous and do not spread to other parts of the body. Osteoma is a common benign tumour that occurs on the skull and is associated with Gardner’s syndrome. Osteochondroma, on the other hand, is the most common benign bone tumour and is usually diagnosed in patients aged less than 20 years. It is characterized by a cartilage-capped bony projection on the external surface of a bone. Giant cell tumour is a tumour of multinucleated giant cells within a fibrous stroma and is most commonly seen in the epiphysis of long bones.

Malignant tumours, on the other hand, are cancerous and can spread to other parts of the body. Osteosarcoma is the most common primary malignant bone tumour and is mainly seen in children and adolescents. It occurs most frequently in the metaphyseal region of long bones prior to epiphyseal closure. Ewing’s sarcoma is a small round blue cell tumour that is also seen mainly in children and adolescents. It occurs most frequently in the pelvis and long bones and tends to cause severe pain. Chondrosarcoma is a malignant tumour of cartilage that most commonly affects the axial skeleton and is more common in middle-age. It is important to diagnose and treat bone tumours early to prevent complications and improve outcomes.

Reactive arthritis typically develops up to 4 weeks after an infection and can have a relapsing-remitting course over several months. The patient’s symptoms suggest reactive arthritis, which is a sterile arthritis triggered by distant gastrointestinal or urogenital infections. It usually presents with polyarticular arthralgia, urethritis, and uveitis, and is more common in people who are positive for the HLA-B27 gene. Behcet’s disease and systemic lupus erythematosus are unlikely diagnoses as they do not match the patient’s symptoms. Systemic juvenile idiopathic arthritis may have a more gradual onset with additional symptoms such as morning stiffness, spiking fevers, and a flat, pale pink rash.

Understanding Reactive Arthritis: Symptoms and Features

Reactive arthritis is a type of seronegative spondyloarthropathy that is associated with HLA-B27. It was previously known as Reiter’s syndrome, which was characterized by a triad of urethritis, conjunctivitis, and arthritis following a dysenteric illness during World War II. However, later studies revealed that patients could also develop symptoms after a sexually transmitted infection, now referred to as sexually acquired reactive arthritis (SARA).

Reactive arthritis is defined as an arthritis that develops after an infection, but the organism cannot be recovered from the joint. The symptoms typically develop within four weeks of the initial infection and last for around 4-6 months. Approximately 25% of patients experience recurrent episodes, while 10% develop chronic disease. The arthritis is usually an asymmetrical oligoarthritis of the lower limbs, and patients may also experience dactylitis.

Other symptoms of reactive arthritis include urethritis, conjunctivitis (seen in 10-30% of patients), and anterior uveitis. Skin symptoms may also occur, such as circinate balanitis (painless vesicles on the coronal margin of the prepuce) and keratoderma blennorrhagica (waxy yellow/brown papules on palms and soles). A helpful mnemonic to remember the symptoms of reactive arthritis is Can’t see, pee, or climb a tree.

In conclusion, understanding the symptoms and features of reactive arthritis is crucial for early diagnosis and treatment. While the condition can be recurrent or chronic, prompt management can help alleviate symptoms and improve quality of life for affected individuals.

Osteogenesis imperfecta is a collagen disorder that is identified by blue sclera, multiple fractures during childhood, dental caries, and deafness due to otosclerosis. It is often mistaken for child abuse or neglect, but the presence of blue sclera is a crucial indicator of osteogenesis imperfecta. In contrast, rickets is more likely to cause growth stunting and deformities rather than multiple fractures.

Osteogenesis imperfecta, also known as brittle bone disease, is a group of disorders that affect collagen metabolism, leading to bone fragility and fractures. The most common type of osteogenesis imperfecta is type 1, which is inherited in an autosomal dominant manner and is caused by a decrease in the synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides. This condition typically presents in childhood and is characterized by fractures that occur following minor trauma, as well as blue sclera, dental imperfections, and deafness due to otosclerosis.

When investigating osteogenesis imperfecta, it is important to note that adjusted calcium, phosphate, parathyroid hormone, and ALP results are usually normal. This condition can have a significant impact on a person’s quality of life, as it can lead to frequent fractures and other complications. However, with proper management and support, individuals with osteogenesis imperfecta can lead fulfilling lives.

Psoriatic arthropathy is a type of inflammatory arthritis that is associated with psoriasis. It is classified as one of the seronegative spondyloarthropathies and is known to have a poor correlation with cutaneous psoriasis. In fact, it often precedes the development of skin lesions. This condition affects both males and females equally, with around 10-20% of patients with skin lesions developing an arthropathy.

The presentation of psoriatic arthropathy can vary, with different patterns of joint involvement. The most common type is symmetric polyarthritis, which is very similar to rheumatoid arthritis and affects around 30-40% of cases. Asymmetrical oligoarthritis is another type, which typically affects the hands and feet and accounts for 20-30% of cases. Sacroiliitis, DIP joint disease, and arthritis mutilans (severe deformity of fingers/hand) are other patterns of joint involvement. Other signs of psoriatic arthropathy include psoriatic skin lesions, periarticular disease, enthesitis, tenosynovitis, dactylitis, and nail changes.

To diagnose psoriatic arthropathy, X-rays are often used. These can reveal erosive changes and new bone formation, as well as periostitis and a pencil-in-cup appearance. Management of this condition should be done by a rheumatologist, and treatment is similar to that of rheumatoid arthritis. However, there are some differences, such as the use of monoclonal antibodies like ustekinumab and secukinumab. Mild peripheral arthritis or mild axial disease may be treated with NSAIDs alone, rather than all patients being on disease-modifying therapy as with RA. Overall, psoriatic arthropathy has a better prognosis than RA.

ITP is a Type II hypersensitivity reaction where the body’s defective B cells produce IgM or IgG antibodies that attack platelets, causing thrombocytopenia. This is an antibody-mediated reaction where the antibodies directly attack host antigens.

Classification of Hypersensitivity Reactions

Hypersensitivity reactions are classified into four types according to the Gell and Coombs classification. Type I, also known as anaphylactic hypersensitivity, occurs when an antigen reacts with IgE bound to mast cells. This type of reaction is responsible for anaphylaxis and atopy, such as asthma, eczema, and hay fever. Type II, or cytotoxic hypersensitivity, happens when cell-bound IgG or IgM binds to an antigen on the cell surface. This type of reaction is associated with autoimmune hemolytic anemia, ITP, Goodpasture’s syndrome, and other conditions. Type III, or immune complex hypersensitivity, occurs when free antigen and antibody (IgG, IgA) combine to form immune complexes. This type of reaction is responsible for serum sickness, systemic lupus erythematosus, post-streptococcal glomerulonephritis, and extrinsic allergic alveolitis. Type IV, or delayed hypersensitivity, is T-cell mediated and is responsible for tuberculosis, graft versus host disease, allergic contact dermatitis, and other conditions.

In recent times, a fifth category has been added to the classification of hypersensitivity reactions. Type V hypersensitivity occurs when antibodies recognize and bind to cell surface receptors, either stimulating them or blocking ligand binding. This type of reaction is associated with Graves’ disease and myasthenia gravis. Understanding the different types of hypersensitivity reactions is important in diagnosing and treating various conditions. Proper identification of the type of reaction can help healthcare professionals provide appropriate treatment and management strategies.

If a patient presents with renal impairment, respiratory symptoms, joint pain, and systemic features, ANCA associated vasculitis should be considered. Granulomatosis with polyangiitis (Wegener’s granulomatosis) is a type of ANCA associated vasculitis that often presents with these symptoms, as well as ENT symptoms. A chest X-ray may show nodular, fibrotic, or infiltrative opacities. The best diagnostic test for granulomatosis with polyangiitis is cANCA. ANA is typically associated with autoimmune conditions like SLE, systemic sclerosis, Sjogren’s syndrome, and autoimmune hepatitis. pANCA is more specific for eosinophilic granulomatosis with polyangiitis (Churg-Strauss), which presents with asthma and eosinophilia and is often associated with conditions like ulcerative colitis, primary sclerosing cholangitis, and anti-GBM disease. If a patient presents with haemoptysis, weight loss, and cavitary lesions on chest X-ray, sputum acid-fast stain would be the appropriate diagnostic test for tuberculosis. However, if the patient also has haematuria, arthralgia, sinusitis, and epistaxis, granulomatosis with polyangiitis is more likely.

ANCA Associated Vasculitis: Common Findings and Management

Anti-neutrophil cytoplasmic antibodies (ANCA) are associated with small-vessel vasculitides such as granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, and microscopic polyangiitis. ANCA associated vasculitis is more common in older individuals and presents with renal impairment, respiratory symptoms, systemic symptoms, and sometimes a vasculitic rash or ear, nose, and throat symptoms. First-line investigations include urinalysis, blood tests for renal function and inflammation, ANCA testing, and chest x-ray. There are two main types of ANCA – cytoplasmic (cANCA) and perinuclear (pANCA) – with varying levels found in different conditions. ANCA associated vasculitis should be managed by specialist teams and the mainstay of treatment is immunosuppressive therapy.

ANCA associated vasculitis is a group of small-vessel vasculitides that are associated with ANCA. These conditions are more common in older individuals and present with renal impairment, respiratory symptoms, systemic symptoms, and sometimes a vasculitic rash or ear, nose, and throat symptoms. To diagnose ANCA associated vasculitis, first-line investigations include urinalysis, blood tests for renal function and inflammation, ANCA testing, and chest x-ray. There are two main types of ANCA – cytoplasmic (cANCA) and perinuclear (pANCA) – with varying levels found in different conditions. ANCA associated vasculitis should be managed by specialist teams and the mainstay of treatment is immunosuppressive therapy.

The correct diagnosis for a patient presenting with bone pain, muscle tenderness, and a waddling gait due to proximal myopathy is osteomalacia. This condition is caused by a demineralization of bone, often due to a deficiency in vitamin D. Laboratory tests may reveal hypocalcemia, low vitamin D levels, normal or elevated phosphate levels, and elevated alkaline phosphatase. Myositis, myotonic dystrophy, and osteoporosis are incorrect diagnoses as they do not present with the same symptoms or laboratory findings.

Understanding Osteomalacia

Osteomalacia is a condition that occurs when the bones become soft due to low levels of vitamin D, which leads to a decrease in bone mineral content. This condition is commonly seen in adults, while in growing children, it is referred to as rickets. The causes of osteomalacia include vitamin D deficiency, malabsorption, lack of sunlight, chronic kidney disease, drug-induced factors, inherited conditions, liver disease, and coeliac disease.

The symptoms of osteomalacia include bone pain, muscle tenderness, fractures, especially in the femoral neck, and proximal myopathy, which may lead to a waddling gait. To diagnose osteomalacia, blood tests are conducted to check for low vitamin D levels, low calcium and phosphate levels, and raised alkaline phosphatase levels. X-rays may also show translucent bands known as Looser’s zones or pseudofractures.

The treatment for osteomalacia involves vitamin D supplementation, with a loading dose often needed initially. Calcium supplementation may also be necessary if dietary calcium intake is inadequate. Understanding the causes, symptoms, and treatment options for osteomalacia is crucial in managing this condition effectively.

Syndesmophytes, which are ossifications of the outer fibers of the annulus fibrosus, are a common feature of ankylosing spondylitis. This patient is exhibiting symptoms of inflammatory joint pain, which is most likely caused by ankylosing spondylitis given his age, gender, and the nature of his pain. Plain x-rays can reveal the presence of ossifications within spinal ligaments or intervertebral discs’ annulus fibrosus. It is incorrect to assume that his symptoms would not improve with naproxen, as NSAIDs are commonly used to alleviate inflammatory joint pain. A bamboo spine on plain x-ray is a rare late sign that is not typically seen in clinical practice. While ankylosing spondylitis may be associated with apical lung fibrosis, this would present as a restrictive defect on spirometry, not an obstructive one.

Investigating and Managing Ankylosing Spondylitis

Ankylosing spondylitis is a type of spondyloarthropathy that is associated with HLA-B27. It is more commonly seen in males aged 20-30 years old. Inflammatory markers such as ESR and CRP are usually elevated, but normal levels do not necessarily rule out ankylosing spondylitis. HLA-B27 is not a reliable diagnostic tool as it can also be positive in normal individuals. The most effective way to diagnose ankylosing spondylitis is through a plain x-ray of the sacroiliac joints. However, if the x-ray is negative but suspicion for AS remains high, an MRI can be obtained to confirm the diagnosis.

Management of ankylosing spondylitis involves regular exercise, such as swimming, and the use of NSAIDs as the first-line treatment. Physiotherapy can also be helpful. Disease-modifying drugs used for rheumatoid arthritis, such as sulphasalazine, are only useful if there is peripheral joint involvement. Anti-TNF therapy, such as etanercept and adalimumab, should be given to patients with persistently high disease activity despite conventional treatments, according to the 2010 EULAR guidelines. Ongoing research is being conducted to determine whether anti-TNF therapies should be used earlier in the course of the disease. Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis, and ankylosis of the costovertebral joints.

The presence of anti-nuclear antibodies (ANA) is common in the adult population, but it is not a reliable diagnostic tool for autoimmune rheumatic disease without additional clinical features. To accurately diagnose systemic lupus erythematosus (SLE), the presence of anti-dsDNA antibodies, low complement levels, or anti-Smith (Sm) antibodies in patients with relevant clinical features is highly predictive. However, these markers cannot be used as rule-out tests, as there is still a chance of SLE even with a negative result. Anti-Ro/La antibodies are less specific to SLE, as they are also found in other autoimmune rheumatic disorders.

Systemic lupus erythematosus (SLE) can be investigated through various tests, including antibody tests. ANA testing is highly sensitive, making it useful for ruling out SLE, but it has low specificity. About 99% of SLE patients are ANA positive. Rheumatoid factor testing is positive in 20% of SLE patients. Anti-dsDNA testing is highly specific (>99%), but less sensitive (70%). Anti-Smith testing is also highly specific (>99%), but only 30% of SLE patients test positive. Other antibody tests include anti-U1 RNP, SS-A (anti-Ro), and SS-B (anti-La).

Monitoring of SLE can be done through various markers, including inflammatory markers such as ESR. During active disease, CRP levels may be normal, but a raised CRP may indicate an underlying infection. Complement levels (C3, C4) are low during active disease due to the formation of complexes that lead to the consumption of complement. Anti-dsDNA titres can also be used for disease monitoring, but it is important to note that they are not present in all SLE patients. Proper monitoring of SLE is crucial for effective management of the disease.

Understanding Drug-Induced Lupus

Drug-induced lupus is a condition that shares some similarities with systemic lupus erythematosus, but not all of its typical features are present. Unlike SLE, renal and nervous system involvement is rare in drug-induced lupus. The good news is that this condition usually resolves once the drug causing it is discontinued.

The most common symptoms of drug-induced lupus include joint pain, muscle pain, skin rashes (such as the malar rash), and pulmonary issues like pleurisy. In terms of laboratory findings, patients with drug-induced lupus typically test positive for ANA (antinuclear antibodies) but negative for dsDNA (double-stranded DNA) antibodies. Anti-histone antibodies are found in 80-90% of cases, while anti-Ro and anti-Smith antibodies are only present in around 5% of cases.

The most common drugs that can cause drug-induced lupus are procainamide and hydralazine. Other less common culprits include isoniazid, minocycline, and phenytoin.

Methylprednisolone, an intramuscular steroid, is commonly used to manage acute flares of rheumatoid arthritis. Glucocorticoids, such as methylprednisolone acetate and triamcinolone acetonide, are effective short-term treatment options that can be administered via intra-articular injection, intramuscular injection, or orally. Disease modifying anti-rheumatic drugs (DMARDs) like methotrexate may take several months to become effective, so they are not suitable for treating acute flare-ups. Non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen can be used for a short period to reduce pain and inflammation, but their potential side effects and risks must be considered. Paracetamol can help with pain relief, but it does not address the inflammation associated with rheumatoid arthritis and is therefore not the most effective treatment option.

Managing Rheumatoid Arthritis with Disease-Modifying Therapies

The management of rheumatoid arthritis (RA) has significantly improved with the introduction of disease-modifying therapies (DMARDs) in the past decade. Patients with joint inflammation should start a combination of DMARDs as soon as possible, along with analgesia, physiotherapy, and surgery. In 2018, NICE updated their guidelines for RA management, recommending DMARD monotherapy with a short course of bridging prednisolone as the initial step. Monitoring response to treatment is crucial, and NICE suggests using a combination of CRP and disease activity to assess it. Flares of RA are often managed with corticosteroids, while methotrexate is the most widely used DMARD. Other DMARDs include sulfasalazine, leflunomide, and hydroxychloroquine. TNF-inhibitors are indicated for patients with an inadequate response to at least two DMARDs, including methotrexate. Etanercept, infliximab, and adalimumab are some of the TNF-inhibitors available, each with their own risks and administration methods. Rituximab and Abatacept are other DMARDs that can be used, but the latter is not currently recommended by NICE.

When a man is suspected to have osteoporosis, it is important to check his testosterone levels through a blood test. This is because hypogonadism, which is a common cause of osteoporosis in men, can be classified as either hypergonadotropic or hypogonadotropic. Androgens play a twofold role in male bone metabolism by stimulating bone formation during puberty and preventing bone resorption during and after puberty. Other tests such as alpha fetoprotein, calcitonin, and serum protein electrophoresis are not useful in evaluating osteoporosis, but may be used to screen for other conditions such as Down syndrome, neural tube defects, thyroid cancer, and multiple myeloma.

Understanding the Causes of Osteoporosis

Osteoporosis is a condition that affects the bones, making them weak and brittle. It is more common in women and older adults, with the prevalence increasing significantly in women over the age of 80. However, there are many other risk factors and secondary causes of osteoporosis that should be considered. Some of the most important risk factors include a history of glucocorticoid use, rheumatoid arthritis, alcohol excess, parental hip fracture, low body mass index, and smoking. Other risk factors include a sedentary lifestyle, premature menopause, certain ethnicities, and endocrine disorders such as hyperthyroidism and diabetes mellitus.

There are also medications that may worsen osteoporosis, such as SSRIs, antiepileptics, and proton pump inhibitors. If a patient is diagnosed with osteoporosis or has a fragility fracture, further investigations may be necessary to identify the cause and assess the risk of subsequent fractures. Recommended investigations include blood tests, bone densitometry, and other procedures as indicated. It is important to identify the cause of osteoporosis and contributory factors in order to select the most appropriate form of treatment. As a minimum, all patients should have a full blood count, urea and electrolytes, liver function tests, bone profile, CRP, and thyroid function tests.

The patient’s symptoms suggest osteoarthritis, which commonly affects small joints in the hand and can cause swelling at the distal interphalangeal joints (Heberden’s nodes). Gout, pseudogout, and reactive arthritis are unlikely diagnoses based on the patient’s symptoms.

Understanding Osteoarthritis of the Hand

Osteoarthritis of the hand, also known as nodal arthritis, is a condition that occurs when the cartilage at synovial joints is lost, leading to the degeneration of underlying bone. It is more common in women, usually presenting after the age of 55, and may have a genetic component. Risk factors include previous joint trauma, obesity, hypermobility, and certain occupations. Interestingly, osteoporosis may actually reduce the risk of developing hand OA.

Symptoms of hand OA include episodic joint pain, stiffness that worsens after periods of inactivity, and the development of painless bony swellings known as Heberden’s and Bouchard’s nodes. These nodes are the result of osteophyte formation and are typically found at the distal and proximal interphalangeal joints, respectively. In severe cases, there may be reduced grip strength and deformity of the carpometacarpal joint of the thumb, resulting in fixed adduction.

Diagnosis is typically made through X-ray, which may show signs of osteophyte formation and joint space narrowing before symptoms develop. While hand OA may not significantly impact a patient’s daily function, it is important to manage symptoms through pain relief and joint protection strategies. Additionally, the presence of hand OA may increase the risk of future hip and knee OA, particularly for hip OA.

The most specific autoantibody associated with dermatomyositis is anti-Jo-1. This is consistent with the patient’s symptoms, which include proximal myopathy, Gottron’s papules, mechanic’s hands, and a heliotrope rash. Anti-Ro antibody, anti-Smith antibody, and antinuclear antibody are not specific to dermatomyositis and are associated with other rheumatological conditions.

Dermatomyositis is a condition that causes inflammation and muscle weakness, as well as distinct skin lesions. It can occur on its own or be associated with other connective tissue disorders or underlying cancers, particularly ovarian, breast, and lung cancer. Screening for cancer is often done after a diagnosis of dermatomyositis. Polymyositis is a variant of the disease that does not have prominent skin manifestations.

The skin features of dermatomyositis include a photosensitive macular rash on the back and shoulders, a heliotrope rash around the eyes, roughened red papules on the fingers’ extensor surfaces (known as Gottron’s papules), extremely dry and scaly hands with linear cracks on the fingers’ palmar and lateral aspects (known as mechanic’s hands), and nail fold capillary dilation. Other symptoms may include proximal muscle weakness with tenderness, Raynaud’s phenomenon, respiratory muscle weakness, interstitial lung disease (such as fibrosing alveolitis or organizing pneumonia), dysphagia, and dysphonia.

Investigations for dermatomyositis typically involve testing for ANA antibodies, which are positive in around 80% of patients. Approximately 30% of patients have antibodies to aminoacyl-tRNA synthetases, including antibodies against histidine-tRNA ligase (also called Jo-1), antibodies to signal recognition particle (SRP), and anti-Mi-2 antibodies.

If patients with polymyalgia rheumatica do not respond well to steroids, it is important to consider other possible diagnoses. While alendronic acid is useful for protecting bones during long-term steroid use, it will not alleviate symptoms. Amitriptyline is better suited for chronic or neuropathic pain rather than inflammatory conditions. Aspirin and naproxen may provide some relief due to their anti-inflammatory properties, but the response will not be as significant as with prednisolone.

Polymyalgia Rheumatica: A Condition of Muscle Stiffness in Older People

Polymyalgia rheumatica (PMR) is a common condition that affects older people. It is characterized by muscle stiffness and elevated inflammatory markers. Although it is closely related to temporal arthritis, the underlying cause is not fully understood, and it does not appear to be a vasculitic process. PMR typically affects patients over the age of 60 and has a rapid onset, usually within a month. Patients experience aching and morning stiffness in proximal limb muscles, along with mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, and night sweats.

To diagnose PMR, doctors look for raised inflammatory markers, such as an ESR of over 40 mm/hr. Creatine kinase and EMG are normal. Treatment for PMR involves prednisolone, usually at a dose of 15 mg/od. Patients typically respond dramatically to steroids, and failure to do so should prompt consideration of an alternative diagnosis.

According to the updated NICE guidelines in 2016, NSAIDs are now the first choice for managing lower back pain. The recommended NSAIDs are ibuprofen or naproxen, and it is advisable to consider co-administration of PPI. Paracetamol alone is not recommended for lower back pain, and for patients who cannot tolerate NSAIDs, co-codamol should be considered. If patients report spasms as a feature of their pain, a short course of benzodiazepines may be considered. NICE recommends referring patients to physiotherapy only if they are at higher risk of back pain disability or if their symptoms have not improved at follow-up. Additionally, there may be some delay in attending physiotherapy, and NSAIDs can be started immediately.

Management of Non-Specific Lower Back Pain

Lower back pain is a common condition that affects many people. In 2016, NICE updated their guidelines on the management of non-specific lower back pain. The guidelines recommend NSAIDs as the first-line treatment for back pain. Lumbar spine x-rays are not recommended, and MRI should only be offered to patients where malignancy, infection, fracture, cauda equina or ankylosing spondylitis is suspected.

Patients with non-specific back pain are advised to stay physically active and exercise. NSAIDs are recommended as the first-line analgesia, and proton pump inhibitors should be co-prescribed for patients over the age of 45 years who are given NSAIDs. For patients with sciatica, NICE guidelines on neuropathic pain should be followed.

Other possible treatments include exercise programmes and manual therapy, but only as part of a treatment package including exercise, with or without psychological therapy. Radiofrequency denervation and epidural injections of local anaesthetic and steroid may also be considered for acute and severe sciatica.

In summary, the management of non-specific lower back pain involves encouraging self-management, staying physically active, and using NSAIDs as the first-line analgesia. Other treatments may be considered as part of a treatment package, depending on the severity of the condition.

Hand osteoarthritis is characterized by involvement of the carpometacarpal and distal interphalangeal joints, as well as the presence of painless swellings known as Heberden’s nodes. Gout, pseudogout, and psoriatic arthritis are less likely diagnoses due to their acute presentation, involvement of different joints, and/or lack of a psoriasis history.

Understanding Osteoarthritis of the Hand

Osteoarthritis of the hand, also known as nodal arthritis, is a condition that occurs when the cartilage at synovial joints is lost, leading to the degeneration of underlying bone. It is more common in women, usually presenting after the age of 55, and may have a genetic component. Risk factors include previous joint trauma, obesity, hypermobility, and certain occupations. Interestingly, osteoporosis may actually reduce the risk of developing hand OA.

Symptoms of hand OA include episodic joint pain, stiffness that worsens after periods of inactivity, and the development of painless bony swellings known as Heberden’s and Bouchard’s nodes. These nodes are the result of osteophyte formation and are typically found at the distal and proximal interphalangeal joints, respectively. In severe cases, there may be reduced grip strength and deformity of the carpometacarpal joint of the thumb, resulting in fixed adduction.

Diagnosis is typically made through X-ray, which may show signs of osteophyte formation and joint space narrowing before symptoms develop. While hand OA may not significantly impact a patient’s daily function, it is important to manage symptoms through pain relief and joint protection strategies. Additionally, the presence of hand OA may increase the risk of future hip and knee OA, particularly for hip OA.

Colchicine is known to induce diarrhoea as a side effect.

One of the common side effects of colchicine, a medication utilized for treating acute gout attacks, is diarrhoea. Due to this, some physicians opt for naproxen or prednisolone instead of prescribing colchicine. The remaining drugs on the list are not typically associated with diarrhoea.

Gout is caused by chronic hyperuricaemia and is managed acutely with NSAIDs or colchicine. Urate-lowering therapy (ULT) is recommended for patients with >= 2 attacks in 12 months, tophi, renal disease, uric acid renal stones, or prophylaxis if on cytotoxics or diuretics. Allopurinol is first-line ULT, with an initial dose of 100 mg od and titrated to aim for a serum uric acid of < 300 µmol/l. Lifestyle modifications include reducing alcohol intake, losing weight if obese, and avoiding high-purine foods. Consideration should be given to stopping precipitating drugs and losartan may be suitable for patients with coexistent hypertension.