Oesophageal candidiasis, a known complication of inhaled steroid therapy, often presents with pain while swallowing (odynophagia).

Understanding Dysphagia and its Causes

Dysphagia, or difficulty in swallowing, can be caused by various conditions affecting the esophagus, such as oesophageal cancer, oesophagitis, oesophageal candidiasis, achalasia, pharyngeal pouch, systemic sclerosis, and myasthenia gravis. Each condition has its own characteristic features, which can help in identifying the underlying cause of dysphagia. For instance, dysphagia associated with weight loss, anorexia, or vomiting during eating may indicate oesophageal cancer, while dysphagia of both liquids and solids from the start may suggest achalasia.

To determine the cause of dysphagia, patients usually undergo an upper GI endoscopy, which allows doctors to examine the esophagus and detect any abnormalities. Fluoroscopic swallowing studies may also be done to evaluate motility disorders. Additionally, a full blood count and ambulatory oesophageal pH and manometry studies may be required for certain conditions.

It’s important to note that new-onset dysphagia is a red flag symptom that requires urgent endoscopy, regardless of age or other symptoms. Therefore, understanding the different causes of dysphagia and their characteristic features can aid in prompt diagnosis and treatment.

According to NICE, the initial serological test for coeliac disease should be tissue transglutaminase antibodies.

Investigating Coeliac Disease

Coeliac disease is a condition caused by sensitivity to gluten, which can lead to villous atrophy and malabsorption. It is often associated with other conditions such as dermatitis herpetiformis and autoimmune disorders. Diagnosis of coeliac disease is made through a combination of serology and endoscopic intestinal biopsy. The gold standard for diagnosis is the biopsy, which should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis. The biopsy traditionally takes place in the duodenum, but jejunal biopsies are also sometimes performed. Findings supportive of coeliac disease include villous atrophy, crypt hyperplasia, an increase in intraepithelial lymphocytes, and lamina propria infiltration with lymphocytes. Serology tests for coeliac disease include tissue transglutaminase antibodies and endomyseal antibodies, while anti-gliadin antibodies are not recommended. Patients who are already on a gluten-free diet should reintroduce gluten for at least six weeks prior to testing. Rectal gluten challenge is not widely used. A gluten-free diet can reverse villous atrophy and immunology in patients with coeliac disease.

Barrett’s oesophagus is most strongly associated with the presence of GORD as a risk factor.

Understanding Barrett’s Oesophagus

Barrett’s oesophagus is a condition where the lower oesophageal mucosa is replaced by columnar epithelium, increasing the risk of oesophageal adenocarcinoma by 50-100 fold. It is typically identified during an endoscopy for upper gastrointestinal symptoms such as dyspepsia. The length of the affected segment correlates strongly with the chances of identifying metaplasia, with the overall prevalence estimated to be around 1 in 20. Risk factors include gastro-oesophageal reflux disease (GORD), male gender, smoking, and central obesity. Interestingly, alcohol does not seem to be an independent risk factor for Barrett’s. Management includes high-dose proton pump inhibitors and endoscopic surveillance with biopsies every 3-5 years for patients with metaplasia. If dysplasia of any grade is identified, endoscopic intervention such as radiofrequency ablation or endoscopic mucosal resection is offered.

Barrett’s oesophagus is a condition where the lower oesophageal mucosa is replaced by columnar epithelium, increasing the risk of oesophageal adenocarcinoma. It is typically identified during an endoscopy for upper gastrointestinal symptoms such as dyspepsia. The length of the affected segment correlates strongly with the chances of identifying metaplasia, with the overall prevalence estimated to be around 1 in 20. Risk factors include GORD, male gender, smoking, and central obesity. Interestingly, alcohol does not seem to be an independent risk factor for Barrett’s. Management includes high-dose proton pump inhibitors and endoscopic surveillance with biopsies every 3-5 years for patients with metaplasia. If dysplasia of any grade is identified, endoscopic intervention such as radiofrequency ablation or endoscopic mucosal resection is offered.

The most appropriate way to provide nutritional support for patients with motor neuron disease is through the insertion of a percutaneous gastrostomy (PEG) tube. If a patient is struggling to feed themselves, they may initially benefit from smaller, more liquid-like meals, but if this is not sufficient, a PEG tube is a definitive long-term management option. Continuing with their current diet regimen is not recommended as it may lead to poor nutrition and a risk of aspiration. Total parenteral nutrition is only used as a last resort when there is impaired nutrient absorption. Inserting a nasogastric tube is not a suitable option as it must be removed after a few weeks to avoid adverse effects. A percutaneous jejunostomy tube is also not recommended as it is less commonly used and harder to maintain than a PEG tube.

Managing Motor Neuron Disease

Motor neuron disease is a neurological condition that affects both upper and lower motor neurons. It typically presents after the age of 40 and can manifest in different patterns, such as amyotrophic lateral sclerosis, progressive muscular atrophy, and bulbar palsy. The cause of the disease is unknown.

One medication used in the management of motor neuron disease is riluzole, which works by preventing the stimulation of glutamate receptors. It is mainly used in cases of amyotrophic lateral sclerosis and has been shown to prolong life by approximately three months.

Respiratory care is also an important aspect of managing motor neuron disease. Non-invasive ventilation, usually in the form of BIPAP, is used at night and has been associated with a survival benefit of around seven months.

Nutrition support is also crucial in managing motor neuron disease. The preferred method is percutaneous gastrostomy tube (PEG), which has been linked to prolonged survival.

Unfortunately, the prognosis for motor neuron disease is poor, with 50% of patients dying within three years.

Hepatocellular carcinoma is primarily caused by hepatitis B worldwide, while in Europe, hepatitis C is the most common cause.

Hepatocellular carcinoma (HCC) is a type of cancer that ranks as the third most common cause of cancer worldwide. The leading cause of HCC globally is chronic hepatitis B, while chronic hepatitis C is the most common cause in Europe. The primary risk factor for developing HCC is liver cirrhosis, which can result from various factors such as hepatitis B and C, alcohol, haemochromatosis, and primary biliary cirrhosis. Other risk factors include alpha-1 antitrypsin deficiency, hereditary tyrosinosis, glycogen storage disease, aflatoxin, certain drugs, porphyria cutanea tarda, male sex, diabetes mellitus, and metabolic syndrome.

HCC tends to present late, and patients may exhibit features of liver cirrhosis or failure such as jaundice, ascites, RUQ pain, hepatomegaly, pruritus, and splenomegaly. In some cases, decompensation may occur in patients with chronic liver disease. Raised AFP levels are also common. Screening with ultrasound and alpha-fetoprotein may be necessary for high-risk groups, including patients with liver cirrhosis secondary to hepatitis B and C or haemochromatosis, and men with liver cirrhosis secondary to alcohol.

Management options for early-stage HCC include surgical resection, liver transplantation, radiofrequency ablation, transarterial chemoembolisation, and sorafenib, a multikinase inhibitor. It is important to note that Wilson’s disease is an exception to the typical causes of liver cirrhosis and HCC.

In elderly patients, constipation is a frequent cause of heightened confusion and is the most probable reason for the symptoms described in this case. The patient’s confusion, slight abdominal discomfort, and palpable mass can all be attributed to constipation. While a colonic tumor could explain the discomfort and fullness on palpation, it is unlikely that its metastases would cause a sudden increase in confusion without a prior diagnosis. Constipation is a common presentation in elderly patients, and it is important to consider it as a potential cause of confusion. Mild cognitive impairment does not typically progress rapidly to dementia with disorientation to time and place. A urinary tract infection or acute diverticulitis would not account for the fullness in the left iliac fossa or the other symptoms described.

Acute confusional state, also known as delirium or acute organic brain syndrome, is a condition that affects up to 30% of elderly patients admitted to hospital. It is more common in patients over the age of 65, those with a background of dementia, significant injury, frailty or multimorbidity, and those taking multiple medications. The condition is often triggered by a combination of factors, such as infection, metabolic imbalances, change of environment, and underlying medical conditions.

The symptoms of acute confusional state can vary widely, but may include memory disturbances, agitation or withdrawal, disorientation, mood changes, visual hallucinations, disturbed sleep, and poor attention. Treatment involves identifying and addressing the underlying cause, modifying the patient’s environment, and using sedatives such as haloperidol or olanzapine. However, managing the condition can be challenging in patients with Parkinson’s disease, as antipsychotics can worsen Parkinsonian symptoms. In such cases, careful reduction of Parkinson medication may be helpful, and atypical antipsychotics such as quetiapine and clozapine may be preferred for urgent treatment.

Overall, acute confusional state is a complex condition that requires careful management and individualized treatment. By addressing the underlying causes and providing appropriate sedation, healthcare professionals can help patients recover from this condition and improve their overall quality of life.

Esophageal cancer is unlikely due to the individual’s good health and two-year history.

Understanding Pharyngeal Pouch or Zenker’s Diverticulum

A pharyngeal pouch, also known as Zenker’s diverticulum, is a condition where there is a posteromedial diverticulum through Killian’s dehiscence. This triangular area is found in the wall of the pharynx between the thyropharyngeus and cricopharyngeus muscles. It is more common in older patients and is five times more common in men.

The symptoms of pharyngeal pouch include dysphagia, regurgitation, aspiration, neck swelling that gurgles on palpation, and halitosis. To diagnose this condition, a barium swallow combined with dynamic video fluoroscopy is usually done.

Surgery is the most common management for pharyngeal pouch. It is important to address this condition promptly to prevent complications such as aspiration pneumonia. Understanding the symptoms and seeking medical attention early can help in the proper management of pharyngeal pouch.

Treatment and Diagnosis of Acute Pancreatitis

Acute pancreatitis can lead to systemic inflammatory response syndrome and multiple organ dysfunction syndromes. The mainstay of treatment is supportive measures such as fluid resuscitation and oxygen supplementation. Abdominal ultrasound can be useful to identify gallstones as the cause of pancreatitis, but fluid resuscitation takes priority. IV antibiotics are not indicated unless complications occur. Enteral feeding is preferred over nil by mouth, and parenteral feeding should be considered if enteral feeding is not tolerated. Urgent CT of the abdomen is not necessary in the acute stage unless complications are suspected. However, for severe pancreatitis, contrast-enhanced CT may be indicated four days after initial symptoms to assess for complications.

If a person with Addison’s disease experiences vomiting, they should take IM hydrocortisone until the vomiting stops. This is especially important if the vomiting is caused by food poisoning from undercooked meat. IM hydrocortisone is a glucocorticoid steroid hormone that is used to manage Addison’s disease and prevent an Addisonian crisis. It is important to note that doubling the fludrocortisone dose or pausing hydrocortisone is not the correct approach in this situation. The patient requires extra hydrocortisone to prevent an Addisonian crisis, not extra fludrocortisone. While drinking plenty of fluids is generally good advice for someone who is vomiting, it is not sufficient for a person with Addison’s disease in this situation.

Addison’s disease is a condition that requires patients to undergo both glucocorticoid and mineralocorticoid replacement therapy. This treatment usually involves taking a combination of hydrocortisone and fludrocortisone. Hydrocortisone is typically given in 2 or 3 divided doses, with patients requiring 20-30 mg per day, mostly in the first half of the day. Patient education is crucial, and it is essential to emphasize the importance of not missing glucocorticoid doses. Additionally, patients should consider wearing MedicAlert bracelets and steroid cards, and they should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis.

During an intercurrent illness, it is crucial to manage the glucocorticoid dose properly. In simple terms, the glucocorticoid dose should be doubled, while the fludrocortisone dose should remain the same. The Addison’s Clinical Advisory Panel has produced guidelines that detail specific scenarios, and patients should refer to these guidelines for more information. It is essential to discuss how to adjust the glucocorticoid dose during an intercurrent illness with a healthcare professional. Proper management of Addison’s disease is crucial to ensure that patients can lead healthy and fulfilling lives.

A temporary and disproportionate increase in blood urea can be caused by an upper gastrointestinal bleed, which can function as a source of protein.

Acute upper gastrointestinal bleeding is a common and significant medical issue that can be caused by various conditions, with oesophageal varices and peptic ulcer disease being the most common. The clinical features of this condition include haematemesis, melena, and a raised urea level due to the protein meal of the blood. The differential diagnosis for acute upper gastrointestinal bleeding includes oesophageal, gastric, and duodenal causes.

The management of acute upper gastrointestinal bleeding involves risk assessment using the Glasgow-Blatchford score, which helps clinicians decide whether patients can be managed as outpatients or not. Resuscitation is also necessary, including ABC, wide-bore intravenous access, and platelet transfusion if actively bleeding platelet count is less than 50 x 10*9/litre. Endoscopy should be offered immediately after resuscitation in patients with a severe bleed, and all patients should have endoscopy within 24 hours.

For non-variceal bleeding, proton pump inhibitors (PPIs) should not be given before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding. However, PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy. If further bleeding occurs, options include repeat endoscopy, interventional radiology, and surgery. For variceal bleeding, terlipressin and prophylactic antibiotics should be given to patients at presentation, and band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices. Transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures.