It is not typical for irritable bowel syndrome to cause pain that disrupts a patient’s sleep.

Diagnosis and Management of Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that affects many people. In 2008, the National Institute for Health and Care Excellence (NICE) published clinical guidelines on the diagnosis and management of IBS. According to these guidelines, a positive diagnosis of IBS should be considered if the patient has had abdominal pain, bloating, or a change in bowel habit for at least six months. Additionally, a positive diagnosis should be made if the patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to two of the following four symptoms: altered stool passage, abdominal bloating, symptoms made worse by eating, and passage of mucus. Other features such as lethargy, nausea, backache, and bladder symptoms may also support the diagnosis.

It is important to note that red flag features should be enquired about, including rectal bleeding, unexplained/unintentional weight loss, family history of bowel or ovarian cancer, and onset after 60 years of age. Primary care investigations such as a full blood count, ESR/CRP, and coeliac disease screen (tissue transglutaminase antibodies) are suggested. By following these guidelines, healthcare professionals can effectively diagnose and manage IBS in their patients.

Differential Diagnosis for a Patient with Worsening Ascites

Worsening ascites can be a sign of various underlying conditions. One possible diagnosis is hepatocellular carcinoma (HCC), which is a primary malignancy of the liver that often occurs in patients with chronic liver disease and cirrhosis. Another possible diagnosis is chronic active hepatitis, which is caused by the hepatitis C virus and can result in joint and muscle pain, nausea, and exhaustion. Superimposed hepatitis B infection can also cause liver injury and jaundice. Alcoholism, which can lead to alcoholic hepatitis, is another possible diagnosis, but it is not consistent with the clinical scenario given if there has been no further alcohol consumption. Spontaneous bacterial peritonitis is an acute bacterial infection of ascitic fluid that can cause fever, abdominal pain, and other symptoms. It is important to consider these and other possible diagnoses when evaluating a patient with worsening ascites.

The patient is displaying signs of sepsis and a developing neurological deficit in their lower limbs, which could indicate the presence of an epidural abscess. This is particularly likely given the patient’s history of diabetes, which is a known risk factor for this condition. While a diabetic foot can also cause neurological deficits and sepsis, the distribution of symptoms would be different and not affect the proximal limb on the opposite side. Discitis with a pathological fracture is also a possibility, but the absence of pain makes this less likely. Intracranial pathology is unlikely as the neurological deficit is confined to the lower limbs and there are no other systemic neurological symptoms present.

Understanding Discitis: Causes, Symptoms, Diagnosis, and Treatment

Discitis is a condition characterized by an infection in the intervertebral disc space, which can lead to serious complications such as sepsis or an epidural abscess. The most common cause of discitis is bacterial, with Staphylococcus aureus being the most frequent culprit. However, it can also be caused by viral or aseptic factors. The symptoms of discitis include back pain, pyrexia, rigors, and sepsis. In some cases, neurological features such as changing lower limb neurology may occur if an epidural abscess develops.

To diagnose discitis, imaging tests such as MRI are used due to their high sensitivity. A CT-guided biopsy may also be required to guide antimicrobial treatment. The standard therapy for discitis involves six to eight weeks of intravenous antibiotic therapy. The choice of antibiotic depends on various factors, with the most important being the identification of the organism through a positive culture, such as a blood culture or CT-guided biopsy.

Complications of discitis include sepsis and epidural abscess. Therefore, it is essential to assess the patient for endocarditis, which can be done through transthoracic echo or transesophageal echo. Discitis is usually due to haematogenous seeding of the vertebrae, which implies that the patient has had a bacteraemia, and seeding could have occurred elsewhere. Understanding the causes, symptoms, diagnosis, and treatment of discitis is crucial in managing this condition and preventing its complications.

Ankylosing spondylitis, a spondyloarthropathy associated with HLA-B27 and commonly seen in men aged 20-30, can be managed with exercise regimes and NSAIDs as the first line of treatment. Pelvic X-rays are helpful in identifying subchondral erosions and sclerosis in the commonly affected sacroiliac joints. Physiotherapy and NSAIDs like ibuprofen are recommended as the initial management. Intra-articular corticosteroid injections are useful for unilateral joint symptoms, while methotrexate may be considered for peripheral joint involvement. Paracetamol can be used in conjunction with NSAIDs if needed, but ibuprofen should be the first-line option.

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.

Antibiotics may be prescribed for acute bronchitis if the patient has co-existing co-morbidities or is at high risk of complications. NICE guidelines advise against the use of antibiotics for those who are not systemically very unwell and not at high risk of complications. However, if the patient is very unwell or at risk of complications, antibiotics should be offered. In this case, the patient’s age, diabetes, and heart failure put him at high risk, so antibiotics should be offered in accordance with NICE guidelines. While local guidelines should be consulted, NICE recommends oral doxycycline as the first-line treatment. Inhaled bronchodilators should not be offered unless the patient has an underlying airway disease such as asthma. Oral flucloxacillin is not commonly used for respiratory tract infections, and IV co-amoxiclav is not necessary in this stable patient who can be managed without admission.

Acute bronchitis is a chest infection that typically resolves on its own within three weeks. It occurs when the trachea and major bronchi become inflamed, leading to swollen airways and the production of sputum. The primary cause of acute bronchitis is viral infection, with most cases occurring in the autumn or winter. Symptoms include a sudden onset of cough, sore throat, runny nose, and wheezing. While most patients have a normal chest examination, some may experience a low-grade fever or wheezing. It is important to differentiate acute bronchitis from pneumonia, which presents with different symptoms and chest examination findings.

Diagnosis of acute bronchitis is typically based on clinical presentation, but CRP testing may be used to determine if antibiotic therapy is necessary. Management involves pain relief and ensuring adequate fluid intake. Antibiotics may be considered for patients who are systemically unwell, have pre-existing health conditions, or have a CRP level between 20-100mg/L. Doxycycline is the recommended first-line treatment, but it cannot be used in children or pregnant women. Alternatives include amoxicillin.

Unilateral nasal polyps are a cause for concern and should be promptly referred to an ENT specialist as they may indicate nasal cancer. However, they can also be caused by other factors such as nose picking, foreign bodies, misapplication of nasal spray or cystic fibrosis. Treatment with antibiotics, oral steroids, nasal drops or cautery is unlikely to be effective and may delay the diagnosis of a serious condition.

Understanding Nasal Polyps

Nasal polyps are a relatively uncommon condition affecting around 1% of adults in the UK. They are more commonly seen in men and are not typically found in children or the elderly. There are several associations with nasal polyps, including asthma (particularly late-onset asthma), aspirin sensitivity, infective sinusitis, cystic fibrosis, Kartagener’s syndrome, and Churg-Strauss syndrome. When asthma, aspirin sensitivity, and nasal polyposis occur together, it is known as Samter’s triad.

The symptoms of nasal polyps include nasal obstruction, rhinorrhoea, sneezing, and a poor sense of taste and smell. It is important to note that any unusual symptoms, such as unilateral symptoms or bleeding, require further investigation. If nasal polyps are suspected, patients should be referred to an ear, nose, and throat (ENT) specialist for a full examination.

The management of nasal polyps typically involves the use of topical corticosteroids, which can shrink polyp size in around 80% of patients. Overall, understanding nasal polyps and their associations can help with early detection and appropriate management.

Before considering thrombolysis for a patient, it is crucial to ensure that their blood pressure is well-controlled. If the patient’s blood pressure is above 200/120mmHg, thrombolysis cannot be performed. In such cases, medications like Labetalol are administered to rapidly lower the blood pressure. The other options mentioned are not suitable as the patient’s chest and BM examinations were normal. Additionally, statins do not play a role in the acute management of stroke.

The Royal College of Physicians (RCP) and NICE have published guidelines on the diagnosis and management of patients following a stroke. The management of acute stroke includes maintaining normal levels of blood glucose, hydration, oxygen saturation, and temperature. Blood pressure should not be lowered in the acute phase unless there are complications. Aspirin should be given as soon as possible if a haemorrhagic stroke has been excluded. Anticoagulants should not be started until brain imaging has excluded haemorrhage. Thrombolysis with alteplase should only be given if administered within 4.5 hours of onset of stroke symptoms and haemorrhage has been definitively excluded. Mechanical thrombectomy is a new treatment option for patients with an acute ischaemic stroke. NICE recommends thrombectomy for people who have acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography or magnetic resonance angiography. Secondary prevention includes the use of clopidogrel and dipyridamole. Carotid artery endarterectomy should only be considered if carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.

Understanding Metabolic Acidosis and Anion Gap

Metabolic acidosis is a condition that occurs when the body produces too much acid or when the kidneys are not able to remove enough acid from the body. It is commonly classified according to the anion gap, which can be calculated by subtracting the sum of chloride and bicarbonate levels from the sum of sodium and potassium levels. The normal range for anion gap is 10-18 mmol/L. If a question supplies the chloride level, it may be a clue that the anion gap should be calculated.

There are two types of metabolic acidosis based on anion gap levels. Normal anion gap or hyperchloraemic metabolic acidosis is caused by gastrointestinal bicarbonate loss, prolonged diarrhea, ureterosigmoidostomy, fistula, renal tubular acidosis, drugs, ammonium chloride injection, and Addison’s disease. On the other hand, raised anion gap is caused by lactate, ketones, urate, acid poisoning, and other factors.

Metabolic acidosis secondary to high lactate levels may be subdivided into two types: lactic acidosis type A and lactic acidosis type B. Lactic acidosis type A is caused by sepsis, shock, hypoxia, and burns, while lactic acidosis type B is caused by metformin. Understanding the different types of metabolic acidosis and anion gap levels can help in diagnosing and treating the condition.

Horner’s syndrome is a medical condition that is characterized by a set of symptoms including a small pupil (miosis), drooping of the upper eyelid (ptosis), sunken eye (enophthalmos), and loss of sweating on one side of the face (anhidrosis). The presence of heterochromia, or a difference in iris color, is often seen in cases of congenital Horner’s syndrome. Anhidrosis is also a distinguishing feature that can help differentiate between central, pre-ganglionic, and post-ganglionic lesions. Pharmacologic tests, such as the use of apraclonidine drops, can be helpful in confirming the diagnosis of Horner’s syndrome and localizing the lesion.

Central lesions, pre-ganglionic lesions, and post-ganglionic lesions can all cause Horner’s syndrome, with each type of lesion presenting with different symptoms. Central lesions can result in anhidrosis of the face, arm, and trunk, while pre-ganglionic lesions can cause anhidrosis of the face only. Post-ganglionic lesions, on the other hand, do not typically result in anhidrosis.

There are many potential causes of Horner’s syndrome, including stroke, syringomyelia, multiple sclerosis, tumors, encephalitis, thyroidectomy, trauma, cervical rib, carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis, and cluster headache. It is important to identify the underlying cause of Horner’s syndrome in order to determine the appropriate treatment plan.

This question assesses the candidate’s understanding of TIA risk stratification. The individual meets the criteria for crescendo TIAs, having experienced two TIAs within a week. This necessitates prompt evaluation and imaging. Admission is recommended for any patient with a score of more than 4 on the ABCD2 scale or crescendo TIA.

A transient ischaemic attack (TIA) is a brief period of neurological deficit caused by a vascular issue, lasting less than an hour. The original definition of a TIA was based on time, but it is now recognized that even short periods of ischaemia can result in pathological changes to the brain. Therefore, a new ’tissue-based’ definition is now used. The clinical features of a TIA are similar to those of a stroke, but the symptoms resolve within an hour. Possible features include unilateral weakness or sensory loss, aphasia or dysarthria, ataxia, vertigo, or loss of balance, visual problems, and sudden transient loss of vision in one eye (amaurosis fugax).

NICE recommends immediate antithrombotic therapy with aspirin 300 mg unless the patient has a bleeding disorder or is taking an anticoagulant. If the patient has had more than one TIA or has a suspected cardioembolic source or severe carotid stenosis, specialist review is necessary. Urgent assessment is required within 24 hours for patients who have had a suspected TIA in the last 7 days. Referral for specialist assessment is necessary as soon as possible within 7 days for patients who have had a suspected TIA more than a week previously. Neuroimaging and carotid imaging are recommended, and antithrombotic therapy is necessary. Carotid artery endarterectomy should only be considered if the carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.