Differentiating between types of arthritis: A case study

In this case study, a patient presents with bony swelling at the DIP and PIP joints of the hands. It is important to differentiate between various types of arthritis to make an accurate diagnosis and provide appropriate treatment.

Osteoarthritis (OA) is characterized by loss of articular cartilage and overgrowth of underlying bone, commonly affecting the hips, knees, and small hand joints. Pain and swelling are common presenting features, along with crepitus on examination. Heberden’s and Bouchard’s nodes may also be present.

Osteoporosis, on the other hand, is a condition of reduced bone density and increased fragility, often diagnosed following a low-impact fracture or screening of high-risk patients. Pain and bony swelling are not typical features of osteoporosis.

Psoriatic arthritis is an inflammatory seronegative spondyloarthropathy associated with psoriasis, commonly affecting the hands but not causing the changes described in this case. Dactylitis is a usual examination finding with psoriatic arthritis.

Reactive arthritis is characterized by a triad of urethritis, conjunctivitis, and arthritis following an infection. It typically presents as an acute, asymmetrical lower-limb arthritis, occurring a few days to weeks after the initial infection.

Rheumatoid arthritis (RA) presents most often in women between the ages of 35 and 55 with symmetrical polyarticular arthritis, most often in the small joints of the hands or feet. Swelling is present at the metacarpophalangeal and PIP joints of the hands, along with other signs such as swan neck and Boutonnière deformities of the fingers, ulnar deviation of fingers, and Z deformity of the thumb.

In conclusion, careful examination and consideration of various types of arthritis are necessary for an accurate diagnosis and appropriate treatment plan.

According to the 2008 NICE guidelines, the initial treatment for osteoarthritis should involve the administration of paracetamol and topical NSAIDs, particularly for knee and hand joints.

The Role of Glucosamine in Osteoarthritis Management

Osteoarthritis (OA) is a common condition that affects the joints, causing pain and stiffness. The National Institute for Health and Care Excellence (NICE) published guidelines in 2014 on the management of OA, which includes non-pharmacological and pharmacological treatments. Glucosamine, a normal constituent of glycosaminoglycans in cartilage and synovial fluid, has been studied for its potential benefits in OA management.

Several double-blind randomized controlled trials (RCTs) have reported significant short-term symptomatic benefits of glucosamine in knee OA, including reduced joint space narrowing and improved pain scores. However, more recent studies have produced mixed results. The 2008 NICE guidelines do not recommend the use of glucosamine, and a 2008 Drug and Therapeutics Bulletin review advised against prescribing it on the NHS due to limited evidence of cost-effectiveness.

Despite the conflicting evidence, some patients may still choose to use glucosamine as a complementary therapy for OA management. It is important for healthcare professionals to discuss the potential benefits and risks of glucosamine with their patients and to consider individual patient preferences and circumstances.

Rheumatoid arthritis cases are often accompanied by Sjogren’s syndrome, which primarily affects women aged 40 to 60. This condition is characterized by arthralgia and sicca symptoms such as dry mouth and dry eyes. Other connective tissue disorders, as well as SLE, are also linked to Sjogren’s syndrome.

Understanding Sjogren’s Syndrome

Sjogren’s syndrome is a medical condition that affects the exocrine glands, leading to dry mucosal surfaces. It is an autoimmune disorder that can either be primary or secondary to other connective tissue disorders, such as rheumatoid arthritis. The onset of the condition usually occurs around ten years after the initial onset of the primary disease. Sjogren’s syndrome is more common in females, with a ratio of 9:1. Patients with this condition have a higher risk of developing lymphoid malignancy, which is 40-60 times more likely.

The symptoms of Sjogren’s syndrome include dry eyes, dry mouth, vaginal dryness, arthralgia, Raynaud’s, myalgia, sensory polyneuropathy, recurrent episodes of parotitis, and subclinical renal tubular acidosis. To diagnose the condition, doctors may perform a Schirmer’s test to measure tear formation, check for hypergammaglobulinaemia, and low C4. Nearly 50% of patients with Sjogren’s syndrome test positive for rheumatoid factor, while 70% test positive for ANA. Additionally, 70% of patients with primary Sjogren’s syndrome have anti-Ro (SSA) antibodies, and 30% have anti-La (SSB) antibodies.

The management of Sjogren’s syndrome involves the use of artificial saliva and tears to alleviate dryness. Pilocarpine may also be used to stimulate saliva production. Understanding the symptoms and management of Sjogren’s syndrome is crucial for patients and healthcare providers to ensure proper treatment and care.

Phenytoin treatment may lead to the development of Dupuytren’s contracture as a potential adverse effect.

Understanding Dupuytren’s Contracture

Dupuytren’s contracture is a condition that affects about 5% of the population. It is more common in older men and those with a family history of the condition. The causes of Dupuytren’s contracture include manual labor, phenytoin treatment, alcoholic liver disease, diabetes mellitus, and trauma to the hand.

The condition typically affects the ring finger and little finger, causing them to become bent and difficult to straighten. In severe cases, the hand may not be able to be placed flat on a table.

Surgical treatment may be necessary when the metacarpophalangeal joints cannot be straightened.

A possible cause of burning pain in the thigh is compression of the lateral cutaneous nerve, which can lead to a condition called meralgia paraesthetica. Meralgia paraesthetica, a condition characterized by burning pain in the thigh, may result from compression of the lateral cutaneous nerve of the thigh.

Understanding Meralgia Paraesthetica

Meralgia paraesthetica is a condition characterized by paraesthesia or anaesthesia in the distribution of the lateral femoral cutaneous nerve (LFCN). It is caused by entrapment of the LFCN, which can be due to various factors such as trauma, iatrogenic causes, or neuroma. Although not rare, it is often underdiagnosed.

The LFCN is a sensory nerve that originates from the L2/3 segments and runs beneath the iliac fascia before exiting through the lateral aspect of the inguinal ligament. Compression of the nerve can occur anywhere along its course, but it is most commonly affected as it curves around the anterior superior iliac spine. Meralgia paraesthetica is more common in men than women and is often seen in those aged between 30 and 40.

Patients with meralgia paraesthetica typically experience burning, tingling, coldness, or shooting pain, as well as numbness and deep muscle ache in the upper lateral aspect of the thigh. Symptoms are usually aggravated by standing and relieved by sitting. The condition can be mild and resolve spontaneously or severely restrict the patient for many years.

Diagnosis of meralgia paraesthetica can be made based on the pelvic compression test, which is highly sensitive. Injection of the nerve with local anaesthetic can also confirm the diagnosis and provide relief. Ultrasound is effective both for diagnosis and guiding injection therapy. Nerve conduction studies may also be useful. Overall, understanding meralgia paraesthetica is important for prompt diagnosis and management of this condition.

It is safe to continue using azathioprine during pregnancy, even if on an established dose. Discontinuing or reducing the medication could lead to disease progression and serious health risks for the patient. Therefore, the dose of azathioprine should not be lowered. Switching to corticosteroids would not be appropriate as the patient is already on a safe medication. Infliximab should only be used if necessary during pregnancy, so continuing with azathioprine is a better option. Methotrexate should never be used during pregnancy as it is known to be teratogenic.

Azathioprine is a medication that is broken down into mercaptopurine, which is an active compound that inhibits the production of purine. To determine if someone is at risk for azathioprine toxicity, a test for thiopurine methyltransferase (TPMT) may be necessary. Adverse effects of this medication include bone marrow depression, which can be detected through a full blood count if there are signs of infection or bleeding, as well as nausea, vomiting, pancreatitis, and an increased risk of non-melanoma skin cancer. It is important to note that there is a significant interaction between azathioprine and allopurinol, so lower doses of azathioprine should be used in conjunction with allopurinol. Despite these potential side effects, azathioprine is generally considered safe to use during pregnancy.

Clinical Features and Differential Diagnoses of Kawasaki Disease

Kawasaki disease is a rare but serious condition that primarily affects children under the age of five. To diagnose Kawasaki disease, a patient must have a fever for at least five days and four out of five classical features: bilateral, non-exudative conjunctival injection, changes in lips and oral cavity, oedema and erythema in the hands and feet, polymorphous rash, and cervical lymphadenopathy. However, tonsillar exudate, leukopenia, neck stiffness, and small submental lymph nodes are not classical features of Kawasaki disease and should prompt consideration of other differential diagnoses. Patients with confirmed Kawasaki disease should undergo echocardiographic examination to detect potential coronary artery aneurysms. Early diagnosis and treatment are crucial to prevent serious complications.

Common Causes of Ocular Symptoms: A Brief Overview

Giant Cell Arteritis: A large-vessel vasculitis that affects the temporal and ophthalmic arteries, causing headache, scalp tenderness, jaw pain, and visual disturbance. It is more common in females over the age of 70. In clinical practice, temporal artery biopsies performed for evaluation of patients with suspected GCA are positive in 25 to 35 percent of cases. So in this case this is the most likely diagnosis even in the absence of a positive biopsy.

Polyarteritis Nodosa (PAN): A necrotising vasculitis that can affect all age groups, but is more commonly associated with Hepatitis B. Symptoms include myalgia, arthralgia, fever, and weight loss. Ocular involvement is rare.

Diabetic Retinopathy: The most common cause of blindness in adults aged 30-65 in developed countries. Symptoms include microaneurysms, retinal haemorrhages, exudates, cotton wool spots, neovascularisation, and venous changes.

Sjögren Syndrome: An autoimmune disorder characterised by lymphocytic infiltration of salivary and lacrimal glands, resulting in dry eyes and dry mouth.

Central Retinal Vein Occlusion: Can occur in chronic simple glaucoma, arteriosclerosis, hypertension, and polycythaemia. Symptoms include a stormy sunset appearance of the fundus with red haemorrhagic areas and engorged veins.

The patient’s symptoms are suggestive of polymyalgia rheumatica (PMR), which is a common inflammatory condition in older adults. The sudden onset of pain and stiffness in the shoulders and hips, along with systemic symptoms such as fatigue and anorexia, are typical of PMR. Osteoarthritis, fibromyalgia, hypothyroidism, and adhesive capsulitis are less likely diagnoses, as they do not typically present with acute onset of symptoms or systemic involvement. However, it is important to rule out hypothyroidism by checking thyroid function. Frozen shoulder may cause shoulder pain and stiffness, but it is usually associated with restricted range of motion and does not typically cause systemic symptoms.

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 arteritis, 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 15mg/od. Patients typically respond dramatically to steroids, and failure to do so should prompt consideration of an alternative diagnosis.

Autoimmune Connective Tissue Diseases: Characteristics and Differences

Systemic lupus erythematosus (SLE), Sjögren syndrome, Behçet’s disease, granulomatosis with polyangiitis, and systemic sclerosis are all autoimmune connective tissue diseases with distinct characteristics. SLE is most prevalent in African-American women and presents with arthralgia, rashes, and fever. Sjögren syndrome is characterised by dry eyes and mouth, while Behçet’s disease is primarily characterised by recurrent mouth ulcers, genital ulceration, eye lesions, and cutaneous manifestations. Granulomatosis with polyangiitis predominantly affects the small vessels and presents with lesions involving the upper respiratory tract, lungs, and kidneys. Systemic sclerosis is a multisystem disease characterised by Raynaud’s phenomenon and either limited or diffuse cutaneous scleroderma. Understanding the differences between these diseases is crucial for accurate diagnosis and treatment.

The presence of antihistone antibodies is linked to drug-induced lupus, which is the likely cause of the patient’s symptoms. One of the drugs she was taking, isoniazid, is known to cause this condition. Rheumatoid factor is typically found in patients with rheumatoid arthritis, while anti Jo-1 antibody is associated with polymyositis and anti-Scl70 antibody is linked to diffuse systemic sclerosis.

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.

The correct diagnosis is lateral epicondylitis, which is caused by repetitive arm movements. The pain is typically more severe when the wrist is extended against resistance and the elbow is straightened. This description does not match the symptoms of anterior interosseous syndrome, carpal tunnel syndrome, or medial epicondylitis.

Understanding Lateral Epicondylitis

Lateral epicondylitis, commonly known as tennis elbow, is a condition that often occurs after engaging in activities that the body is not accustomed to, such as painting or playing tennis. It is most prevalent in individuals aged 45-55 years and typically affects the dominant arm. The primary symptom of this condition is pain and tenderness localized to the lateral epicondyle. The pain is often exacerbated by wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended. Episodes of lateral epicondylitis can last between 6 months and 2 years, with patients experiencing acute pain for 6-12 weeks.

To manage lateral epicondylitis, it is essential to avoid muscle overload and engage in simple analgesia. Steroid injections and physiotherapy are also viable options for managing the condition. By understanding the symptoms and management options for lateral epicondylitis, individuals can take the necessary steps to alleviate pain and discomfort associated with this condition.

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.

The presentation and examination strongly suggest a scaphoid fracture, making conservative treatment with splinting, pain relief, and physiotherapy unsuitable due to the risk of avascular necrosis caused by the scaphoid bone’s blood supply. While an outpatient x-ray is an option, some scaphoid fractures may not be visible on x-rays and may require a CT scan or MRI. As a result, the patient should be referred to an orthopaedic clinic, either directly or through the local emergency department.

Anatomy of the Scaphoid Bone

The scaphoid bone is a small bone located in the wrist. It has several important features that allow it to articulate with other bones in the wrist and hand. The bone has a concave surface that articulates with the head of the capitate and a crescentic surface that corresponds with the lunate. Proximally, it has a wide convex surface that articulates with the radius. Distally, it has a tubercle that can be felt and an articular surface that faces laterally and is associated with the trapezium and trapezoid bones.

The narrow strip between the radial and trapezial surfaces and the tubercle gives rise to the radial collateral carpal ligament. The tubercle also receives part of the flexor retinaculum, which is the only part of the scaphoid bone that allows for the entry of blood vessels. However, this area is commonly fractured and can lead to avascular necrosis. It is important to understand the anatomy of the scaphoid bone in order to properly diagnose and treat injuries to the wrist and hand.

Non-typhi salmonella (NTS) is known to cause blood and bone infections, particularly in children with sickle cell disease and malaria. The exact reason for this susceptibility is not fully understood, but it may be due to the bacteria’s affinity for iron, which is made available through haemolysis. Other bacteria such as E.coli and P. aeruginosa are not commonly associated with sickle cell disease, and Staphylococcus aureus is a gram-positive coccus. Aplastic anaemia and parvovirus can be ruled out as causes, as the child’s haemoglobin level is normal and parvovirus does not cause 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.

Reactive arthritis is a type of joint inflammation that occurs after an infection, often caused by dysentery or a sexually transmitted infection. It is more common in men who have the HLA-B27 gene. Reactive arthritis is part of a group of diseases called spondyloarthropathies, which also includes ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis, and undifferentiated arthritis. Unlike rheumatoid arthritis, reactive arthritis is not associated with rheumatoid factor. Symptoms of reactive arthritis include sudden, asymmetrical lower limb joint pain, which can occur a few days to weeks after the initial infection. Enthesitis, or inflammation where tendons and ligaments attach to bones, is also common and can cause plantar fasciitis or Achilles tendonitis. In some cases, reactive arthritis can also cause back pain and inflammation of the sacroiliac joint, as well as a sterile conjunctivitis. Treatment involves addressing the initial infection and may include medications such as sulfasalazine or methotrexate for relapsing cases. It is important to trace and treat sexual partners if necessary. Gout, rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis are other types of joint inflammation that have different symptoms and causes.

Ankylosing spondylitis is a type of spondyloarthropathy that is associated with HLA-B27. It is more commonly seen in young males, with a sex ratio of 3:1, and typically presents with lower back pain and stiffness that develops gradually. The stiffness is usually worse in the morning and improves with exercise, while pain at night may improve upon getting up. Clinical examination may reveal reduced lateral and forward flexion, as well as reduced chest expansion. Other features associated with ankylosing spondylitis include apical fibrosis, anterior uveitis, aortic regurgitation, Achilles tendonitis, AV node block, amyloidosis, cauda equina syndrome, and peripheral arthritis (more common in females).

Treatment and Management of Paracetamol Overdose

Paracetamol overdose is a serious medical emergency that requires prompt treatment and management. Here are some important steps to take:

Give intravenous acetylcysteine immediately for patients who have taken a staggered overdose, which is defined as ingesting a potentially toxic dose of paracetamol over a period of over one hour. Patients who have taken a dose of paracetamol > 150 mg/kg are at risk of serious toxicity.

Observe the patient for 24 hours after treatment.

Measure serum paracetamol level and give acetylcysteine if the level is above the treatment line. Patients who have ingested > 75 mg/kg of paracetamol over a period of less than one hour should have their serum paracetamol levels measured four hours after ingestion. If this level is above the treatment line, they should be treated with intravenous acetylcysteine. If blood tests reveal an alanine aminotransferase above the upper limit of normal, patients should be started on acetylcysteine regardless of serum paracetamol levels.

Start haemodialysis if patients have an exceedingly high serum paracetamol concentration (> 700 mg/l) associated with an elevated blood lactate and coma.

Take bloods including a coagulation screen and start acetylcysteine if clotting is deranged. In patients where a serum paracetamol level is indicated (patients who have ingested > 75 mg/kg of paracetamol over a period of less than one hour), deranged liver function tests are an indication to start acetylcysteine regardless of serum paracetamol levels.

In summary, prompt treatment with intravenous acetylcysteine is crucial for patients who have taken a staggered overdose of paracetamol. Monitoring of serum paracetamol levels, liver function tests, and clotting factors can help guide further management. Haemodialysis may be necessary in severe cases.

Women with low calorie intake or menstrual irregularities who increase their exercise are at risk of stress fractures due to the female athlete triad, which includes excessive exercise, reduced bone mineral density, and eating disorders or inadequate calorie intake. It is important to discuss eating habits and menstrual cycles when treating women with a history of stress fractures.

Stress fractures are small hairline fractures that can occur due to repetitive activity and loading of normal bone. Although they can be painful, they are typically not displaced and do not cause surrounding soft tissue injury. In some cases, stress fractures may present late, and callus formation may be visible on radiographs. Treatment for stress fractures may vary depending on the severity of the injury. In cases where the injury is associated with severe pain and presents at an earlier stage, immobilization may be necessary. However, injuries that present later may not require formal immobilization and can be treated with tailored immobilization specific to the site of injury.

Temporal arteritis should be considered in an older patient experiencing a sudden onset of unilateral headache accompanied by jaw claudication and elevated ESR. Trigeminal neuralgia typically does not cause jaw stiffness, while acute angle-closure glaucoma presents with a red eye and does not involve jaw claudication. Although TMJ dysfunction can cause pain during chewing and extend to the scalp and headache, there is no additional information to suggest this as the cause. Therefore, temporal arteritis is the more probable diagnosis.

Understanding Temporal Arteritis

Temporal arteritis is a type of large vessel vasculitis that often overlaps with polymyalgia rheumatica (PMR). It is characterized by changes in the affected artery that skip certain sections while damaging others. This condition typically affects individuals who are over 60 years old and has a rapid onset, usually occurring in less than a month. The most common symptoms include headache and jaw claudication, while vision testing is a crucial investigation for all patients.

Temporal arteritis can lead to various ocular complications, with anterior ischemic optic neuropathy being the most common. This results from the occlusion of the posterior ciliary artery, leading to ischemia of the optic nerve head. Patients may experience temporary visual loss or even permanent visual loss, which is the most feared complication of this condition. Other symptoms may include diplopia, tender and palpable temporal artery, and features of PMR such as aching, morning stiffness in proximal limb muscles, lethargy, depression, low-grade fever, anorexia, and night sweats.

To diagnose temporal arteritis, doctors may look for raised inflammatory markers such as an ESR of over 50 mm/hr or elevated CRP levels. A temporal artery biopsy may also be performed to check for skip lesions. Urgent high-dose glucocorticoids should be given as soon as the diagnosis is suspected, and an ophthalmologist should review patients with visual symptoms on the same day. Treatment may also involve bone protection with bisphosphonates and low-dose aspirin, although the evidence supporting the latter is weak.

In summary, temporal arteritis is a serious condition that requires prompt diagnosis and treatment to prevent irreversible visual damage. Patients who experience symptoms such as headache, jaw claudication, and visual disturbances should seek medical attention immediately.