Polymyalgia rheumatica is identified by the sudden appearance of bilateral early morning stiffness in individuals over the age of 60. The most probable diagnosis is polymyalgia rheumatica, as there is a sudden onset of difficulty in moving arms in a patient over 50 years old without any weakness. This stiffness is a common symptom, but not always present. Other key features that aid in diagnosis include loss of appetite, low-grade fever, and morning symptoms. Dermatomyositis is a possible differential diagnosis, but it can be challenging to rule out. However, the absence of rash, detectable weakness, and muscle tenderness makes it unlikely. Rheumatoid arthritis is uncommon at this age without symmetrical polyarthritis, and the acute onset makes it even less likely. Osteoarthritis typically affects hips and knees more than other joints and has a gradual onset without fever.

Understanding Polymyalgia Rheumatica

Polymyalgia rheumatica (PMR) is a condition commonly seen in older individuals that 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 individuals over the age of 60 and has a rapid onset, with symptoms appearing in less than 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. Weakness is not considered a symptom of PMR.

To diagnose PMR, doctors look for elevated inflammatory markers, such as an ESR greater than 40 mm/hr. Creatine kinase and EMG are typically normal. Treatment for PMR involves the use of prednisolone, with a typical dose of 15 mg/od. Patients usually respond dramatically to steroids, and failure to do so should prompt consideration of an alternative diagnosis. Understanding the symptoms and treatment options for PMR can help individuals manage their condition and improve their quality of life.

Start alendronate without waiting for a DEXA scan in patients over 75 years who have had a fragility fracture.

Osteoporosis is a condition that weakens bones, making them more prone to fractures. When a patient experiences a fragility fracture, which is a fracture that occurs from a low-impact injury or fall, it is important to assess their risk for osteoporosis and subsequent fractures. The management of patients following a fragility fracture depends on their age.

For patients who are 75 years of age or older, they are presumed to have underlying osteoporosis and should be started on first-line therapy, such as an oral bisphosphonate, without the need for a DEXA scan. However, the 2014 NOGG guidelines suggest that treatment should be started in all women over the age of 50 years who’ve had a fragility fracture, although BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women.

For patients who are under the age of 75 years, a DEXA scan should be arranged to assess their bone mineral density. These results can then be entered into a FRAX assessment, along with the fact that they’ve had a fracture, to determine their ongoing fracture risk. Based on this assessment, appropriate treatment can be initiated to prevent future fractures.

Double-stranded DNA antibody (dsDNA) inhibitor

Drug-induced lupus is a condition that differs from systemic lupus erythematosus in that it does not typically involve renal or nervous system complications. This condition can be resolved by discontinuing the medication that caused it. Symptoms of drug-induced lupus include joint and muscle pain, skin rashes (such as a malar rash), and pleurisy. Patients with this condition will test positive for ANA, but negative for dsDNA. Anti-histone antibodies are found in 80-90% of cases, while anti-Ro and anti-Smith are only present in around 5%. The most common causes of drug-induced lupus are procainamide and hydralazine, while less common causes include isoniazid, minocycline, and phenytoin.

Management of Giant Cell Arteritis: Starting Prednisone and Urgent Treatment

Giant cell arteritis (GCA) is a serious condition that can lead to sudden unilateral visual loss if left untreated. The definitive diagnostic test is a temporal artery biopsy, but treatment with high-dose prednisolone should not be delayed while awaiting biopsy. The histological features on biopsy include intimal hypertrophy, inflammation of the intima and sub-intima, breaking up of the internal elastic lamina, and giant cell infiltration of the internal elastic lamina. Treatment with prednisolone is both diagnostic and dramatic, with a symptom response that confirms the diagnosis. Around three-quarters of patients require between 1 and 3 years of steroid therapy, while the remaining quarter may require continued steroids for some years. Urgent treatment is necessary to prevent potential visual impairment, and investigations such as immunoglobulin testing and CT scan of the head should not delay treatment. A temporal artery biopsy can be booked for surgical list in 5 days’ time to confirm the diagnosis.

The diagnosis is dermatomyositis. The patient exhibits a rash that is sensitive to sunlight, as well as a rash around the eyelids known as heliotrope rash, and Gottron’s papules. The rash distribution is consistent with dermatomyositis. Lupus typically presents with a butterfly-shaped rash that is erythematous and sensitive to sunlight, and there may be a history of joint and neurological symptoms. Lichen planus is a purple and itchy rash that appears in patches, with a distribution similar to psoriasis.

Understanding Dermatomyositis

Dermatomyositis is a condition that causes inflammation and weakness in the muscles, as well as distinct skin lesions. It can occur on its own or be associated with other connective tissue disorders or underlying malignancies. Patients with dermatomyositis may experience symmetrical, proximal muscle weakness, and photosensitive skin rashes. The skin lesions may include a macular rash over the back and shoulders, a heliotrope rash in the periorbital region, Gottron’s papules, and mechanic’s hands. Other symptoms may include Raynaud’s, respiratory muscle weakness, interstitial lung disease, dysphagia, and dysphonia.

To diagnose dermatomyositis, doctors may perform various tests, including screening for underlying malignancies. The majority of patients with dermatomyositis are ANA positive, and around 30% have antibodies to aminoacyl-tRNA synthetases, such as anti-synthetase antibodies, antibodies against histidine-tRNA ligase (Jo-1), antibodies to signal recognition particle (SRP), and anti-Mi-2 antibodies.

In summary, dermatomyositis is a condition that affects both the muscles and skin. It can be associated with other disorders or malignancies, and patients may experience a range of symptoms. Proper diagnosis and management are essential for improving outcomes and quality of life for those with dermatomyositis.

Arthropathy in Hereditary Haemochromatosis

Hereditary haemochromatosis is a condition that should be suspected in patients with liver cirrhosis, diabetes mellitus, hypogonadism and impotence, skin hyperpigmentation, fatigue and arthropathy. The arthropathy in hereditary haemochromatosis is due to calcium pyrophosphate crystal deposition and can include pseudo-gout, chondrocalcinosis and chronic arthropathy. Biochemical findings include high serum iron, ferritin and transferrin saturation, and liver biopsy shows staining for excess iron.

Cystinosis is a metabolic disease that causes end-stage renal function due to the accumulation of cysteine. Osteomalacia is often asymptomatic and bilateral knee joint pain is not a common presentation. Ochronosis describes the pigment deposition that occurs in the connective tissues of patients with alkaptonuria, which is not associated with the bronze appearance of the skin in this patient. Gout would present with hot, tender, swollen joints and subcortical bone cysts, but bilateral knee involvement would be unusual. Monosodium urate crystal deposition is not associated with hereditary haemochromatosis.

There are different types of calcium channels in the body, including L-type, P-type, N-type, R-type, and T-type. L-type calcium channels are found in various tissues, including skeletal muscle, smooth muscle, osteoblasts, and ventricular myocytes. Dihydropyridine calcium channel blockers like amlodipine target vascular smooth muscle, while non-dihydropyridine calcium channel blockers like diltiazem and verapamil are specific to the heart. P-type calcium channels are found in the cerebellum, but there are currently no specific drugs that target them. N-type calcium channels are found throughout the brain and peripheral nervous system and are a promising target for treating chronic neuropathic pain. R-type calcium channels are found in cerebellar granule cells, but their function is not well understood. T-type calcium channels are found in neurons and cardiac pacemaker cells and are a potential target for treating diabetic neuropathy and Parkinson’s disease.

The patient has lupus pernio, a specific skin manifestation of sarcoidosis. The differential diagnosis for bilateral hilar adenopathy includes sarcoidosis, lymphoma, tuberculosis, pneumoconiosis, berylliosis, and fungal diseases. Tuberculosis granulomata show caseating necrosis. The differential diagnosis for lupus pernio includes granulomatosis with polyangiitis, lymphoma cutis, and cutaneous lupus. Clinical presentation helps differentiate some lesions, but a biopsy may be required. The most common cutaneous manifestations of systemic lupus erythematosus are discoid lesions and the butterfly rash, often accompanied by arthralgias.

Diarrhoea can be caused by various factors, including medication such as colchicine and antibiotics that target anaerobes. It is uncommon to experience diarrhoea four days after completing a course of antibiotics. However, the most concerning possibility is the development of pseudomembranous colitis due to Clostridium difficile infection from the use of tazocin. Negative test results for antigens and toxins may be accurate, but delayed transportation of samples to the lab can result in a false negative outcome. There is no indication of cancer recurrence or norovirus outbreak in this case.

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 a delayed start recommended until inflammation has settled. Lifestyle modifications include reducing alcohol intake, losing weight if obese, and avoiding high-purine foods. Other options for refractory cases include febuxostat, uricase, and pegloticase.

Anti-Phospholipid Antibody Syndrome in Systemic Lupus Erythematosus Patients

Patients with systemic lupus erythematosus (SLE) are at risk of developing anti-phospholipid antibody syndrome (APAS). This syndrome is characterized by the presence of anticardiolipin antibodies or lupus anticoagulant on two occasions over a period of 12 weeks, along with a history of thrombus or recurrent pregnancy loss. If a patient has experienced one pregnancy loss greater than 10 weeks in gestation, and other causes of pregnancy loss have been excluded, they may also be diagnosed with APAS. Patients with APAS may have either primary or secondary APAS, depending on whether or not they have an associated autoimmune condition.

It is important to note that other causes of shortness of breath in SLE, such as shrinking lung syndrome and pneumonitis, do not present acutely. Therefore, pulmonary function tests or HRCT scans are unlikely to be of any benefit in diagnosing APAS. Early detection and management of APAS is crucial in preventing complications such as thrombosis and recurrent pregnancy loss.