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.

The drug that can cause drug-induced pancreatitis is mesalazine. This patient is exhibiting the typical symptoms of acute pancreatitis, such as severe epigastric pain that is relieved by leaning forward, accompanied by vomiting and fever. Although there can be multiple causes of this condition, drug-induced pancreatitis is a common one. Mesalazine has been identified as a causative agent, but the exact mechanism is still unknown. It is believed that salicylic acid may increase the permeability of the pancreatic duct, leading to inflammation.

Phenytoin is a medication used to manage seizures, but it has not been shown to cause pancreatitis, although it can cause hepatitis and other side effects. Clozapine is an atypical antipsychotic used to treat complicated schizophrenia, but it has not been linked to pancreatitis, although it can cause agranulocytosis, neutropenia, constipation, myocarditis, and seizures. Ramipril is an angiotensin-converting enzyme inhibitor that has not been associated with pancreatitis, but it may cause cough, angioedema, and hyperkalemia.

Acute pancreatitis is a condition that is mainly caused by gallstones and alcohol in the UK. A popular mnemonic to remember the causes is GET SMASHED, which stands for gallstones, ethanol, trauma, steroids, mumps, autoimmune diseases, scorpion venom, hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia, ERCP, and certain drugs. CT scans of patients with acute pancreatitis show diffuse parenchymal enlargement with oedema and indistinct margins. It is important to note that pancreatitis is seven times more common in patients taking mesalazine than sulfasalazine.

It is improbable for pseudocysts to be detected within 4 weeks of an episode of acute pancreatitis. Nevertheless, they are more prevalent during this period and are linked to an elevated amylase level.

Acute pancreatitis can lead to various complications, both locally and systemically. Local complications include peripancreatic fluid collections, which occur in about 25% of cases and may develop into pseudocysts or abscesses. Pseudocysts are walled by fibrous or granulation tissue and typically occur 4 weeks or more after an attack of acute pancreatitis. Pancreatic necrosis, which involves both the pancreatic parenchyma and surrounding fat, can also occur and is directly linked to the extent of necrosis. Pancreatic abscesses may result from infected pseudocysts and can be treated with drainage methods. Haemorrhage may also occur, particularly in cases of infected necrosis.

Systemic complications of acute pancreatitis include acute respiratory distress syndrome, which has a high mortality rate of around 20%. Local complications such as peripancreatic fluid collections and pancreatic necrosis can also lead to systemic complications if left untreated. It is important to manage these complications appropriately, with conservative management being preferred for sterile necrosis and early necrosectomy being avoided unless necessary. Treatment options for local complications include endoscopic or surgical cystogastrostomy, aspiration, and drainage methods. Overall, prompt recognition and management of complications is crucial in improving outcomes for patients with acute pancreatitis.

The Yellow Card Scheme for Reporting Adverse Reactions to Medications

The Yellow Card scheme is a widely recognized method for reporting adverse reactions to medications. It is managed by the Medicines and Healthcare products Regulatory Agency (MHRA). The scheme is designed to encourage healthcare professionals and patients to report any suspected adverse drug reactions, including those related to new medicines, off-label use of medicines, and herbal remedies.

The MHRA recommends that all suspected adverse drug reactions for new medicines, identified by the black triangle symbol, should be reported. Additionally, all suspected adverse drug reactions occurring in children, even if a medicine has been used off-label, should be reported. Serious suspected adverse drug reactions for established vaccines and medicines, including unlicensed medicines, should also be reported.

Yellow Cards can be found at the back of the British National Formulary (BNF) or completed online through the Yellow Card website. It is important to note that any suspected reactions, not just confirmed ones, should be reported. Patients can also report adverse events through the scheme.

Once Yellow Cards are submitted, the MHRA collates and assesses the information. The agency may consult with the Commission on Human Medicines (CHM), an independent scientific advisory body on medicines safety, to further evaluate the reported adverse reactions. Reactions that are fatal, life-threatening, disabling or incapacitating, result in or prolong hospitalization, or are medically significant are considered serious.

Differentiating between possible causes of acute shortness of breath: A medical analysis

When a patient presents with acute shortness of breath, it is important to consider a range of possible causes. In this case, the patient’s symptoms suggest panic attacks rather than left ventricular failure, acute asthma attacks, COPD, or anaemia.

Panic attacks are characterized by sudden onset and spontaneous resolution, numbness of extremities, and normal examination and peak flow measurement. They can be triggered or occur unexpectedly, and may be due to a disorder such as panic disorder or post-traumatic stress disorder, or secondary to medical problems such as thyroid disease. Treatment includes psychological therapies, breathing exercises, stress avoidance, and pharmacological therapies such as selective serotonin reuptake inhibitors.

Left ventricular failure, on the other hand, would cause respiratory problems due to pulmonary congestion, leading to reduced pulmonary compliance and increased airway resistance. Examination of someone with left ventricular failure would reveal pulmonary crackles and possibly a small mitral regurgitation murmur. However, it is unlikely that a woman would experience acute episodes such as these due to heart failure.

Acute asthma attacks are typically triggered by inhaled allergens or other factors such as cold/dry air, stress, or upper respiratory tract infections. The absence of triggers in this case suggests that asthma is not the diagnosis.

COPD is a possible differential due to the patient’s smoking history, but it is unlikely to have worsened so acutely and resolved in a matter of minutes. The normal peak expiratory flow rate also suggests that COPD is not the cause.

Finally, anaemia would not account for acute episodes of shortness of breath, which are present normally on exertion in anaemic patients. Signs of anaemia such as pallor, tachycardia, cardiac dilation, or oedema are not mentioned in the patient’s history.

In conclusion, a careful analysis of the patient’s symptoms and medical history can help differentiate between possible causes of acute shortness of breath, leading to appropriate treatment and management.

Polymyalgia rheumatica is an inflammatory disease that causes pain and stiffness in the shoulder and pelvic girdle muscles, along with systemic symptoms such as fever and weight loss. It is often associated with giant cell arthritis. Diagnosis can be difficult, but response to a moderate dose of steroids is a useful indicator. Non-steroidal anti-inflammatories are not recommended. Other inflammatory conditions should be excluded, such as rheumatoid arthritis, systemic lupus erythematosus, polymyositis, and polyarteritis nodosa.

Medications Associated with Gynaecomastia

Gynaecomastia, the enlargement of male breast tissue, can be caused by various medications. Spironolactone, ciclosporin, cimetidine, and omeprazole are some of the drugs that have been associated with this condition. Ramipril has also been linked to gynaecomastia, but it is a rare occurrence.

Aside from these medications, other drugs that can cause gynaecomastia include digoxin, LHRH analogues, cimetidine, and finasteride. It is important to note that not all individuals who take these medications will develop gynaecomastia, and the risk may vary depending on the dosage and duration of treatment.

The most effective way to confirm a diagnosis of ankylosing spondylitis is through the detection of sacro-ilitis on a pelvic X-ray. This condition is commonly found in males between the ages of 20 and 30. While radiographs may not show any abnormalities in the early stages of the disease, later changes may include sacroiliitis, lumbar vertebrae squaring, and bamboo spine. ANA and rheumatoid factor tests are not useful in diagnosing ankylosing spondylitis, as they are positive in other autoimmune diseases. HLA-B27 testing is also not a reliable indicator, as it can be positive in individuals with or without the disease. Inflammatory markers such as ESR and CRP are often elevated in patients with ankylosing spondylitis, but normal levels do not necessarily rule out the condition.

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.

Location of Gastric Cancers: Changing Trends

Gastric cancers can arise from different parts of the stomach, including the cardia, body, fundus, antrum, and pylorus. In the past, the majority of gastric cancers used to originate from the antrum and pylorus. However, in recent years, there has been a shift in the location of gastric cancers, with the majority now arising from the cardia. This change in trend highlights the importance of ongoing research and surveillance in the field of gastric cancer.

Multiple Myeloma

Multiple myeloma is a type of cancer that affects plasma cells found in the bone marrow. These plasma cells are derived from B lymphocytes, but when they become malignant, they start to divide uncontrollably, forming tumors in the bone marrow. These tumors interfere with normal cell production and erode the surrounding bone, causing soft spots and holes. Since the malignant cells are clones derived from a single plasma cell, they all produce the same abnormal immunoglobulin that is secreted into the blood.

Patients with multiple myeloma may not show any symptoms for many years, but eventually, most patients develop some evidence of the disease. This can include weakened bones, which can cause bone pain and fractures, decreased numbers of red or white blood cells, which can lead to anemia, infections, bleeding, and bruising, and kidney failure, which can cause an increase in creatinine levels. Additionally, destruction of the bone can increase the level of calcium in the blood, leading to symptoms of hypercalcemia. Pieces of monoclonal antibodies, known as light chains or Bence Jones proteins, can also lodge in the kidneys and cause permanent damage. In some cases, an increase in the viscosity of the blood may lead to headaches.