The most common cause of a scaphoid fracture is falling onto an outstretched hand (FOOSH), which is the mechanism of injury reported by this patient. Although the initial x-ray of the wrist was normal, it is recommended that patients with suspected scaphoid fractures undergo a repeat x-ray (with dedicated scaphoid views) after 7-10 days, as these fractures may not appear on initial imaging.

Avascular necrosis is a potential complication of scaphoid fractures, which can cause gradually worsening pain in the affected wrist over time. If this occurs, referral to an orthopaedics team for further investigation (such as an MRI) and possible surgical intervention is necessary.

In this case, referral to a hand clinic for physiotherapy is not appropriate, as the patient requires further investigation and management. However, providing safety netting advice and a leaflet before discharge from the emergency department is good practice. It is important to refer the patient to the orthopaedics team before discharge.

The FRAX score is a tool used to assess a patient’s 10-year risk of developing an osteoporosis-related fracture, but it is not relevant to the diagnosis or management of avascular necrosis.

While MRI is the preferred imaging modality for avascular necrosis of the scaphoid, it is not appropriate to request an outpatient MRI with GP follow-up in one week. Instead, it is best to refer the patient directly to the orthopaedics team for specialist input and timely management, including arranging and following up on any necessary imaging and deciding on the need for surgical intervention.

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 development of avascular necrosis of the femoral head is strongly associated with long-term steroid use, as seen in this patient who is taking prednisolone for polymyalgia rheumatica.

Understanding Avascular Necrosis of the Hip

Avascular necrosis of the hip is a condition where bone tissue dies due to a loss of blood supply, leading to bone destruction and loss of joint function. This condition typically affects the epiphysis of long bones, such as the femur. There are several causes of avascular necrosis, including long-term steroid use, chemotherapy, alcohol excess, and trauma.

Initially, avascular necrosis may not present with any symptoms, but as the condition progresses, pain in the affected joint may occur. Plain x-ray findings may be normal in the early stages, but osteopenia and microfractures may be seen. As the condition worsens, collapse of the articular surface may result in the crescent sign.

MRI is the preferred investigation for avascular necrosis as it is more sensitive than radionuclide bone scanning. In severe cases, joint replacement may be necessary to manage the condition. Understanding the causes, features, and management of avascular necrosis of the hip is crucial for early detection and effective treatment.

Understanding Marfan’s Syndrome

Marfan’s syndrome is a genetic disorder that affects the connective tissue in the body. It is caused by a defect in the FBN1 gene on chromosome 15, which codes for the protein fibrillin-1. This disorder is inherited in an autosomal dominant pattern, meaning that a person only needs to inherit one copy of the defective gene from one parent to develop the condition. Marfan’s syndrome affects approximately 1 in 3,000 people.

The features of Marfan’s syndrome include a tall stature with an arm span to height ratio greater than 1.05, a high-arched palate, arachnodactyly (long, slender fingers), pectus excavatum (sunken chest), pes planus (flat feet), and scoliosis (curvature of the spine). In addition, individuals with Marfan syndrome may experience cardiovascular problems such as dilation of the aortic sinuses, mitral valve prolapse, and aortic aneurysm. They may also have lung issues such as repeated pneumothoraces. Eye problems are also common, including upwards lens dislocation, blue sclera, and myopia. Finally, dural ectasia, or ballooning of the dural sac at the lumbosacral level, may also occur.

In the past, the life expectancy of individuals with Marfan syndrome was around 40-50 years. However, with regular echocardiography monitoring and the use of beta-blockers and ACE inhibitors, this has improved significantly in recent years. Despite these improvements, aortic dissection and other cardiovascular problems remain the leading cause of death in individuals with Marfan syndrome.

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.

The appropriate management for osteomalacia, which is likely caused by chronic kidney disease, involves vitamin D supplementation with an initial loading dose regime. Blood tests for osteomalacia typically reveal low levels of calcium and phosphate, as well as high levels of alkaline phosphatase. Calcium supplementation may also be prescribed if the patient’s dietary intake is insufficient. Intravenous fluids and bisphosphonates are not recommended for the treatment of hypocalcaemia, while levothyroxine is used to manage hypothyroidism and oral bisphosphonates are used for osteoporosis.

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.

Osteomalacia is the likely diagnosis for an older woman experiencing bone pain, as indicated by low serum calcium, low serum phosphate, raised ALP, and raised PTH. This condition is caused by severe vitamin D deficiency, which impairs calcium and phosphate absorption from the gastrointestinal tract and kidneys. As a result, PTH secretion increases to compensate for low calcium, leading to increased bone resorption and elevated ALP levels. Osteitis fibrosis cystica, osteopetrosis, and osteoporosis are less likely diagnoses, as they present with different metabolic blood results.

Lab Values for Bone Disorders

When it comes to bone disorders, certain lab values can provide important information for diagnosis and treatment. In cases of osteoporosis, calcium, phosphate, alkaline phosphatase (ALP), and parathyroid hormone (PTH) levels are typically within normal ranges. However, in osteomalacia, there is a decrease in calcium and phosphate levels, an increase in ALP levels, and an increase in PTH levels.

Primary hyperparathyroidism, which can lead to osteitis fibrosa cystica, is characterized by increased calcium and PTH levels, but decreased phosphate levels. Chronic kidney disease can also lead to secondary hyperparathyroidism, with decreased calcium levels and increased phosphate and PTH levels.

Paget’s disease, which causes abnormal bone growth, typically shows normal calcium and phosphate levels, but an increase in ALP levels. Osteopetrosis, a rare genetic disorder that causes bones to become dense and brittle, typically shows normal lab values for calcium, phosphate, ALP, and PTH.

Overall, understanding these lab values can help healthcare professionals diagnose and treat various bone disorders.

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.

Scaphoid fractures may not be immediately visible on X-ray in most cases. However, failing to detect them can result in non-union and subsequent avascular necrosis of the proximal segment due to the retrograde blood supply of the scaphoid from the dorsal carpal branch of the radial artery. According to the NICE guidelines, if a scaphoid fracture is suspected but imaging is inconclusive, repeat imaging should be conducted after 7 days. Physiotherapy is not the appropriate immediate management as further movement may cause more damage. Instead, immobilisation with a splint is more suitable at this time.

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 patient is likely experiencing musculoskeletal lower back pain, which may have been worsened by physical labor. There is no indication of infection or cancer, and an MRI is not necessary at this point as it would not alter the treatment plan. It is recommended that patients with back pain remain physically active instead of being on strict bed rest. NSAIDs are the preferred initial treatment for back pain and are more effective than using only paracetamol. Opioids should not be the first choice for treatment.

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.

Bilateral carpal tunnel syndrome is frequently caused by rheumatoid arthritis, which is a common condition. This woman displays symptoms of bilateral carpal tunnel syndrome, which is an uncommon occurrence and typically results from conditions that enlarge the interstitial space with soft tissue growth or fluid. Although all of these conditions are linked to bilateral carpal tunnel syndrome, rheumatoid arthritis is the most probable cause in a 33-year-old. Acromegaly is more likely to cause carpal tunnel syndrome after the age of 50, and this association is well-known and frequently tested in exams.

Understanding Carpal Tunnel Syndrome

Carpal tunnel syndrome is a condition that occurs when the median nerve in the carpal tunnel is compressed. Patients with this condition typically experience pain or pins and needles in their thumb, index, and middle fingers. In some cases, the symptoms may even ascend proximally. Patients often shake their hand to obtain relief, especially at night.

During an examination, doctors may observe weakness of thumb abduction and wasting of the thenar eminence (not the hypothenar). Tapping on the affected area may cause paraesthesia, which is known as Tinel’s sign. Flexion of the wrist may also cause symptoms, which is known as Phalen’s sign.

Carpal tunnel syndrome can be caused by a variety of factors, including idiopathic reasons, pregnancy, oedema (such as heart failure), lunate fracture, and rheumatoid arthritis. Electrophysiology tests may show prolongation of the action potential in both motor and sensory nerves.

Treatment for carpal tunnel syndrome may include a 6-week trial of conservative treatments, such as corticosteroid injections and wrist splints at night. If symptoms persist or are severe, surgical decompression (flexor retinaculum division) may be necessary.

Psoriatic arthritis may be diagnosed even before psoriatic skin lesions appear, especially if there is a positive family history of psoriasis.

The correct answer is psoriatic arthritis, as the patient in the scenario presents with asymmetrical polyarthritis and >30 minutes of morning stiffness, which is a typical pattern of psoriatic arthritis. Additionally, the patient has a positive family history of psoriasis. In some cases, psoriatic arthritis can manifest before skin lesions, and a diagnosis can be made based on clinical patterns and family history.

Ankylosing spondylitis is an incorrect answer because it typically affects the spine and small joints of the digits, whereas the patient’s pattern of arthritis is more consistent with psoriatic arthritis.

Gout is also an incorrect answer because it usually affects only the small joints of the body, particularly the 1st metatarsophalangeal joint. Patients with gout are typically older and have a history of poor diet and lack of physical activity, which is not the case for this patient. The positive family history of psoriasis also makes psoriatic arthritis more likely.

Reactive arthritis is another incorrect answer because it usually presents with mono- or oligoarthritis, whereas the patient in the scenario has polyarthritis. Additionally, reactive arthritis is often preceded by a bacterial infection, such as gastroenteritis or a sexually transmitted infection, which is not the case for this patient. The recent viral illness and positive family history of psoriasis make psoriatic arthritis more likely.

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.

Early signs of rheumatoid arthritis can be observed through x-rays, specifically the presence of juxta-articular osteoporosis/osteopenia.

X-Ray Changes in Rheumatoid Arthritis

Rheumatoid arthritis is a chronic autoimmune disease that affects the joints, causing pain, stiffness, and swelling. X-ray imaging is often used to diagnose and monitor the progression of the disease. Early x-ray findings in rheumatoid arthritis include a loss of joint space, juxta-articular osteoporosis, and soft-tissue swelling. These changes indicate that the joint is being damaged and that the bones are losing density.

As the disease progresses, late x-ray findings may include periarticular erosions and subluxation. Periarticular erosions are areas of bone loss around the joint, while subluxation refers to the partial dislocation of the joint. These changes can lead to deformities and functional impairment.

It is important to note that x-ray findings may not always correlate with the severity of symptoms in rheumatoid arthritis. Some patients may have significant joint damage on x-ray but experience minimal pain, while others may have severe pain despite minimal x-ray changes. Therefore, x-ray imaging should be used in conjunction with other clinical assessments to determine the best course of treatment for each individual patient.

Avascular necrosis is strongly associated with prior chemotherapy treatment. Although initial x-rays may appear normal in patients with this condition, it is unlikely that they would not reveal any metastatic deposits that could cause pain.

Understanding Avascular Necrosis of the Hip

Avascular necrosis of the hip is a condition where bone tissue dies due to a loss of blood supply, leading to bone destruction and loss of joint function. This condition typically affects the epiphysis of long bones, such as the femur. There are several causes of avascular necrosis, including long-term steroid use, chemotherapy, alcohol excess, and trauma.

Initially, avascular necrosis may not present with any symptoms, but as the condition progresses, pain in the affected joint may occur. Plain x-ray findings may be normal in the early stages, but osteopenia and microfractures may be seen. As the condition worsens, collapse of the articular surface may result in the crescent sign.

MRI is the preferred investigation for avascular necrosis as it is more sensitive than radionuclide bone scanning. In severe cases, joint replacement may be necessary to manage the condition. Understanding the causes, features, and management of avascular necrosis of the hip is crucial for early detection and effective treatment.

In later stages of ankylosing spondylitis, apical fibrosis may be visible on a chest x-ray. Peripheral granulomas can develop due to inflammation, with potential causes including TB, infection, and sarcoidosis. Bilateral hilar lymphadenopathy is commonly associated with sarcoidosis and may also indicate lymphoma.

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.

AMA (Anti-mitochondrial antibodies)

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.

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.

Reactive arthritis is a condition that can develop after an infection, where the organism responsible cannot be detected in the joint. A patient who presents with arthritis, urethritis, and conjunctivitis, and has recently traveled, is highly suspicious of reactive arthritis. This condition is often associated with sexually transmitted diseases, with Chlamydia trachomatis being the most likely causative organism. However, the synovial fluid culture is negative as the organism cannot be recovered from the joint.

Gonococcal arthritis, on the other hand, is caused by disseminated gonococcal infection. It typically presents with arthritis-dermatitis syndrome and can progress to septic arthritis if left untreated. While it is a good differential diagnosis for young, sexually active males with mono- or oligoarthritis, it does not explain the other symptoms of dysuria and painful eye movements.

Gout is unlikely in a young male without predisposing factors and would not account for the patient’s urethritis and conjunctivitis. Rheumatoid arthritis, which typically presents as symmetrical arthritis affecting small joints such as PIP, MCP, or wrist joints, is also an unlikely diagnosis. Additionally, keratoconjunctivitis sicca is the most common ocular complication associated with rheumatoid arthritis, rather than conjunctivitis.

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, further 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 arthritis that occurs after an infection where the organism cannot be found in the joint. The post-STI form is more common in men, while the post-dysenteric form has an equal incidence in both sexes. The most common organisms associated with reactive arthritis are listed in the table below.

Management of reactive arthritis is mainly symptomatic, with analgesia, NSAIDs, and intra-articular steroids being used. Sulfasalazine and methotrexate may be used for persistent disease. Symptoms usually last for less than 12 months. It is worth noting that the term Reiter’s syndrome is no longer used due to the fact that Reiter was a member of the Nazi party.

The measurement of disease activity in rheumatoid arthritis is done using the DAS28 score. This score evaluates the level of disease activity by assessing 28 joints, hence the name DAS28, where DAS stands for disease activity score.

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.

The presence of systemic vasculitic symptoms, along with signs of hepatitis B and the absence of pulmonary symptoms, indicates that the patient may have polyarteritis nodosa. The patient’s symptoms appear to be viral, except for the presence of itchiness, scleral jaundice, haematuria, and purpura, which suggest vasculitis. The absence of respiratory symptoms helps to eliminate other possible diagnoses, such as polymyalgia rheumatica. The patient’s scleral jaundice and itchiness may indicate obstructive hepatic impairment. Polyarteritis nodosa is strongly associated with hepatitis B infection and does not typically present with respiratory symptoms, unlike other types of vasculitis.

Polyarteritis Nodosa: Symptoms, Features, and Diagnosis

Polyarteritis nodosa (PAN) is a type of vasculitis that affects medium-sized arteries, causing inflammation and aneurysm formation. It is more common in middle-aged men and is often associated with hepatitis B infection. Symptoms of PAN include fever, malaise, weight loss, hypertension, and joint pain. It can also cause nerve damage, testicular pain, and a skin condition called livedo reticularis. In some cases, patients may experience kidney damage and renal failure. Diagnosis of PAN may involve testing for perinuclear-antineutrophil cytoplasmic antibodies (ANCA) and hepatitis B serology. Angiograms may also be used to detect changes in the affected arteries.

The Beighton score is a valuable method for evaluating hypermobility, with a positive result indicating at least 5 out of 9 criteria met in adults or at least 6 out of 9 in children. In contrast, Schirmer’s test is commonly employed to diagnose Sjogren syndrome, while plain radiographs and MRI scans are not effective for assessing hypermobility.

Ehler-Danlos syndrome is a genetic disorder that affects the connective tissue, specifically type III collagen. This causes the tissue to be more elastic than usual, resulting in increased skin elasticity and joint hypermobility. Common symptoms include fragile and easily bruised skin, as well as recurrent joint dislocations. Additionally, individuals with Ehler-Danlos syndrome may be at risk for serious complications such as aortic regurgitation, mitral valve prolapse, aortic dissection, subarachnoid hemorrhage, and angioid retinal streaks.

When it comes to detecting lateral and medial meniscal tears, an MRI is the most sensitive option available. It surpasses the other choices in terms of sensitivity and should be requested for all patients who are suspected of having a meniscal injury. Ultrasound may be challenging to perform due to the patient’s probable swelling and pain. An X-ray may be necessary for patients with arthritis or a history of repeated meniscal tears.

Understanding Meniscal Tear and its Symptoms

Meniscal tear is a common knee injury that usually occurs due to twisting injuries. Its symptoms include pain that worsens when the knee is straightened, a feeling that the knee may give way, tenderness along the joint line, and knee locking in cases where the tear is displaced. To diagnose a meniscal tear, doctors may perform Thessaly’s test, which involves weight-bearing at 20 degrees of knee flexion while the patient is supported by the doctor. If the patient experiences pain on twisting the knee, the test is considered positive.

Patients diagnosed with antiphospholipid syndrome and a history of unprovoked thrombosis should receive lifelong warfarin as the preferred long-term anticoagulant. While unfractionated heparin or low molecular weight heparin may be used for acute episodes of thrombosis, they are not recommended for long-term anticoagulation in this condition. Failure to provide anticoagulation therapy to these patients is inappropriate due to their high risk of recurrent thrombosis. Additionally, the MHRA has advised against the use of direct-acting oral anticoagulants like rivaroxaban for long-term therapy in antiphospholipid syndrome patients due to an increased risk of thrombotic events compared to warfarin. Therefore, rivaroxaban is not a suitable management option.

Antiphospholipid syndrome is a condition that can be acquired and is characterized by a higher risk of both venous and arterial thrombosis, recurrent fetal loss, and thrombocytopenia. It can occur as a primary disorder or as a secondary condition to other diseases, with systemic lupus erythematosus being the most common. One important point to remember for exams is that antiphospholipid syndrome can cause a paradoxical increase in the APTT. This is due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade. Other features of this condition include livedo reticularis, pre-eclampsia, and pulmonary hypertension.

Antiphospholipid syndrome can also be associated with other autoimmune disorders, lymphoproliferative disorders, and, rarely, phenothiazines. Management of this condition is based on EULAR guidelines. Primary thromboprophylaxis involves low-dose aspirin, while secondary thromboprophylaxis depends on the type of thromboembolic event. Initial venous thromboembolic events require lifelong warfarin with a target INR of 2-3, while recurrent venous thromboembolic events require lifelong warfarin and low-dose aspirin. Arterial thrombosis should be treated with lifelong warfarin with a target INR of 2-3.

The diagnosis of chronic kidney disease is incorrect in this case. An eGFR below 90 can still be considered normal if it is above 60 and there are no abnormalities in the U&Es. The patient’s eGFR is 62 and their urea and creatinine levels are within normal range, indicating that they do not have CKD. In cases of CKD, secondary hyperparathyroidism may occur, which would result in different blood test results. Since the kidneys are responsible for activating vitamin D, which is essential for the absorption of calcium in the intestines, low serum calcium levels would be expected in CKD. Additionally, due to kidney dysfunction, there would be inadequate excretion of phosphate, leading to increased serum phosphate levels. This increase in phosphate levels would cause calcium to be deposited in the insoluble calcium phosphate salt, further lowering calcium levels. Therefore, the symptoms of hypercalcemia that the patient is experiencing would not be present in secondary hyperparathyroidism caused by CKD. In summary, hyperparathyroidism secondary to CKD would result in low calcium and high phosphate levels, rather than high calcium and low phosphate levels.

Lab Values for Bone Disorders

When it comes to bone disorders, certain lab values can provide important information for diagnosis and treatment. In cases of osteoporosis, calcium, phosphate, alkaline phosphatase (ALP), and parathyroid hormone (PTH) levels are typically within normal ranges. However, in osteomalacia, there is a decrease in calcium and phosphate levels, an increase in ALP levels, and an increase in PTH levels.

Primary hyperparathyroidism, which can lead to osteitis fibrosa cystica, is characterized by increased calcium and PTH levels, but decreased phosphate levels. Chronic kidney disease can also lead to secondary hyperparathyroidism, with decreased calcium levels and increased phosphate and PTH levels.

Paget’s disease, which causes abnormal bone growth, typically shows normal calcium and phosphate levels, but an increase in ALP levels. Osteopetrosis, a rare genetic disorder that causes bones to become dense and brittle, typically shows normal lab values for calcium, phosphate, ALP, and PTH.

Overall, understanding these lab values can help healthcare professionals diagnose and treat various bone disorders.

Compartment syndrome will be exacerbated by anticoagulation.

Compartment syndrome is a complication that can occur after fractures or vascular injuries. It is characterized by increased pressure within a closed anatomical space, which can lead to tissue death. Supracondylar fractures and tibial shaft injuries are the most common fractures associated with compartment syndrome. Symptoms include pain, numbness, paleness, and possible paralysis of the affected muscle group. Diagnosis is made by measuring intracompartmental pressure, with pressures over 20 mmHg being abnormal and over 40 mmHg being diagnostic. X-rays typically do not show any pathology. Treatment involves prompt and extensive fasciotomies, with careful attention to decompressing deep muscles in the lower limb. Patients may develop myoglobinuria and require aggressive IV fluids. In severe cases, debridement and amputation may be necessary, as muscle death can occur within 4-6 hours.

The diagnosis is osteomalacia, as indicated by the classic clinical features of widespread bone pain and proximal myopathy, along with laboratory results showing low serum calcium, low serum phosphate, raised ALP, and raised PTH. Osteopenia and osteoporosis are not the correct diagnoses, as they are quantitative disorders of bone mineralisation that require a DEXA scan for diagnosis. Primary hyperparathyroidism is also not the correct diagnosis, as it is characterised by hypercalcemia with a raised or inappropriately normal PTH.

Lab Values for Bone Disorders

When it comes to bone disorders, certain lab values can provide important information for diagnosis and treatment. In cases of osteoporosis, calcium, phosphate, alkaline phosphatase (ALP), and parathyroid hormone (PTH) levels are typically within normal ranges. However, in osteomalacia, there is a decrease in calcium and phosphate levels, an increase in ALP levels, and an increase in PTH levels.

Primary hyperparathyroidism, which can lead to osteitis fibrosa cystica, is characterized by increased calcium and PTH levels, but decreased phosphate levels. Chronic kidney disease can also lead to secondary hyperparathyroidism, with decreased calcium levels and increased phosphate and PTH levels.

Paget’s disease, which causes abnormal bone growth, typically shows normal calcium and phosphate levels, but an increase in ALP levels. Osteopetrosis, a rare genetic disorder that causes bones to become dense and brittle, typically shows normal lab values for calcium, phosphate, ALP, and PTH.

Overall, understanding these lab values can help healthcare professionals diagnose and treat various bone disorders.

The correct fundoscopic appearance for anterior ischemic optic neuropathy is a swollen pale optic disc with blurred margins. This condition is often seen in patients with temporal arthritis and can cause sudden unilateral vision loss. The patient in this case has classic symptoms of temporal arthritis, including new temporal headache, scalp tenderness, jaw claudication, and constitutional symptoms. Anterior ischemic optic neuropathy is caused by inflammation in the posterior ciliary artery, which leads to occlusion and subsequent ischemia to the head of the optic nerve.

A pale retina with a ‘cherry red’ spot is not the typical fundoscopic appearance for temporal arthritis. This is the typical finding in central retinal artery occlusion, which is not typically inflammatory and is more similar to a stroke. Cupping of the optic disc is also not seen in anterior ischemic optic neuropathy, as this is a typical finding in neuropathy due to glaucoma. Hazy fundus with an absent red reflex is also not related to temporal arthritis, as this is the typical finding in vitreous hemorrhage, which is often caused by bleeding from neovascularization in proliferative diabetic retinopathy, trauma, or retinal detachment.

Temporal arthritis, also known as giant cell arthritis, is a condition that affects medium and large-sized arteries and is of unknown cause. It typically occurs in individuals over the age of 50, with the highest incidence in those in their 70s. Early recognition and treatment are crucial to minimize the risk of complications, such as permanent loss of vision. Therefore, when temporal arthritis is suspected, urgent referral for assessment by a specialist and prompt treatment with high-dose prednisolone is necessary.

Temporal arthritis often overlaps with polymyalgia rheumatica, with around 50% of patients exhibiting features of both conditions. Symptoms of temporal arthritis include headache, jaw claudication, and tender, palpable temporal artery. Vision testing is a key investigation in all patients, as anterior ischemic optic neuropathy is the most common ocular complication. This results from occlusion of the posterior ciliary artery, leading to ischemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins. Other symptoms may include aching, morning stiffness in proximal limb muscles, lethargy, depression, low-grade fever, anorexia, and night sweats.

Investigations for temporal arthritis include raised inflammatory markers, such as an ESR greater than 50 mm/hr and elevated CRP. A temporal artery biopsy may also be performed, and skip lesions may be present. Treatment for temporal arthritis involves urgent high-dose glucocorticoids, which should be given as soon as the diagnosis is suspected and before the temporal artery biopsy. If there is no visual loss, high-dose prednisolone is used. If there is evolving visual loss, IV methylprednisolone is usually given prior to starting high-dose prednisolone. Urgent ophthalmology review is necessary, as visual damage is often irreversible. Other treatments may include bone protection with bisphosphonates and low-dose aspirin.

Understanding Greater Trochanteric Pain Syndrome

Greater trochanteric pain syndrome, also known as trochanteric bursitis, is a condition that results from the repetitive movement of the fibroelastic iliotibial band. This condition is most commonly observed in women aged between 50 and 70 years. The primary symptom of this condition is pain experienced over the lateral side of the hip and thigh. Additionally, tenderness is observed upon palpation of the greater trochanter.

Rheumatoid arthritis is a condition that can be diagnosed through initial investigations, including antibody tests and x-rays. One of the first tests recommended is the rheumatoid factor (RF) test, which detects a circulating antibody that reacts with the patient’s own IgG. This test can be done through the Rose-Waaler test or the latex agglutination test, with the former being more specific. A positive RF result is found in 70-80% of patients with rheumatoid arthritis, and high levels are associated with severe progressive disease. However, it is not a marker of disease activity. Other conditions that may have a positive RF result include Felty’s syndrome, Sjogren’s syndrome, infective endocarditis, SLE, systemic sclerosis, and the general population.

Another antibody test that can aid in the diagnosis of rheumatoid arthritis is the anti-cyclic citrullinated peptide antibody test. This test can detect the antibody up to 10 years before the development of rheumatoid arthritis and has a sensitivity similar to RF (around 70%) but a much higher specificity of 90-95%. NICE recommends that patients with suspected rheumatoid arthritis who are RF negative should be tested for anti-CCP antibodies.

In addition to antibody tests, x-rays of the hands and feet are also recommended for all patients with suspected rheumatoid arthritis. These x-rays can help detect joint damage and deformities, which are common in rheumatoid arthritis. Early detection and treatment of rheumatoid arthritis can help prevent further joint damage and improve overall quality of life for patients.

MRI is the preferred imaging technique for diagnosing osteomyelitis.

Understanding Osteomyelitis: Types, Causes, and Treatment

Osteomyelitis is a bone infection that can be classified into two types: haematogenous and non-haematogenous. Haematogenous osteomyelitis is caused by bacteria that enter the bloodstream and is usually monomicrobial. It is more common in children, with vertebral osteomyelitis being the most common form in adults. Risk factors include sickle cell anaemia, intravenous drug use, immunosuppression, and infective endocarditis. On the other hand, non-haematogenous osteomyelitis results from the spread of infection from adjacent soft tissues or direct injury to the bone. It is often polymicrobial and more common in adults, with risk factors such as diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.

Staphylococcus aureus is the most common cause of osteomyelitis, except in patients with sickle-cell anaemia where Salmonella species predominate. To diagnose osteomyelitis, MRI is the imaging modality of choice, with a sensitivity of 90-100%. Treatment for osteomyelitis involves a six-week course of flucloxacillin. Clindamycin is an alternative for patients who are allergic to penicillin.

In summary, osteomyelitis is a bone infection that can be caused by bacteria entering the bloodstream or spreading from adjacent soft tissues or direct injury to the bone. It is more common in children and adults with certain risk factors. Staphylococcus aureus is the most common cause, and MRI is the preferred imaging modality for diagnosis. Treatment involves a six-week course of flucloxacillin or clindamycin for penicillin-allergic patients.

Understanding Fat Embolism: Diagnosis, Clinical Features, and Treatment

Fat embolism is a medical condition that occurs when fat globules enter the bloodstream and obstruct blood vessels. This condition is commonly seen in patients with long bone fractures, particularly in the femur and tibia. The diagnosis of fat embolism is based on clinical features, including respiratory symptoms such as tachypnea, dyspnea, and hypoxia, as well as dermatological symptoms such as a red or brown petechial rash. CNS symptoms such as confusion and agitation may also be present. Imaging may not always show vascular occlusion, but a ground glass appearance may be seen at the periphery.

Prompt fixation of long bone fractures is crucial in the treatment of fat embolism. However, there is some debate regarding the benefit versus risk of medullary reaming in femoral shaft or tibial fractures in terms of increasing the risk of fat embolism. DVT prophylaxis and general supportive care are also important in the management of this condition. While fat embolism can be a serious and potentially life-threatening condition, prompt diagnosis and treatment can improve outcomes for patients.