Differential Diagnosis of Anal Pain: Understanding the Causes

Anal pain can be a distressing symptom that can have various underlying causes. One of the most common causes is an anal fissure, which is a painful tear in the anal canal. This condition is often caused by trauma from hard or painful bowel movements and is associated with low-fiber diets.

Patients with anal fissures typically experience severe pain during bowel movements, which can lead to constipation and worsening symptoms. However, medical therapy with stool-bulking agents and fiber supplementation can help resolve acute anal fissures in most cases.

Other potential causes of anal pain include distal colonic polyps, anal warts, hemorrhoids, and rectal carcinoma. Distal colonic polyps are slow-growing overgrowths of the colonic mucosa that carry a small risk of becoming malignant. Anal warts are caused by the human papillomavirus (HPV) and can present as painless bumps or eruptions in the anogenital area.

Hemorrhoids are swollen blood vessels in the lower rectum that can cause rectal bleeding, pain, pruritus, or prolapse. Rectal carcinoma is a rare but serious condition that can cause bleeding, change in bowel habits, abdominal pain, and malaise.

In summary, understanding the differential diagnosis of anal pain is crucial for accurate diagnosis and appropriate treatment. A thorough physical examination and medical history can help identify the underlying cause and guide management.

The primary management approach for NAFLD is weight loss, achieved through diet and exercise. Medications have not shown to be effective in improving the condition’s outcome.

Non-Alcoholic Fatty Liver Disease: Causes, Features, and Management

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disease in developed countries, primarily caused by obesity. It encompasses a range of conditions, from simple steatosis (fat accumulation in the liver) to steatohepatitis (fat with inflammation) and may progress to fibrosis and liver cirrhosis. Insulin resistance is believed to be the primary mechanism leading to steatosis, making NAFLD a hepatic manifestation of metabolic syndrome. Non-alcoholic steatohepatitis (NASH) is a type of liver damage similar to alcoholic hepatitis but occurs in the absence of alcohol abuse. It affects around 3-4% of the general population and may be responsible for some cases of cryptogenic cirrhosis.

NAFLD is usually asymptomatic, but hepatomegaly, increased echogenicity on ultrasound, and elevated ALT levels are common features. The enhanced liver fibrosis (ELF) blood test is recommended by NICE to check for advanced fibrosis in patients with incidental NAFLD. If the ELF blood test is not available, non-invasive tests such as the FIB4 score or NAFLD fibrosis score, in combination with a FibroScan, may be used to assess the severity of fibrosis. Patients with advanced fibrosis should be referred to a liver specialist for further evaluation, which may include a liver biopsy to stage the disease more accurately.

The mainstay of NAFLD treatment is lifestyle changes, particularly weight loss, and monitoring. Research is ongoing into the role of gastric banding and insulin-sensitizing drugs such as metformin and pioglitazone. While there is no evidence to support screening for NAFLD in adults, NICE guidelines recommend the management of incidental NAFLD findings.

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.

If a patient with mild-moderate ulcerative colitis does not respond to topical or oral aminosalicylates, the next step is to add oral corticosteroids. In the case of this patient, who is experiencing five episodes of diarrhea and some blood but is otherwise stable, oral prednisolone is the appropriate treatment option. Intravenous ceftriaxone, intravenous hydrocortisone, and oral amoxicillin with clavulanic acid are not indicated in this situation. Oral azathioprine may be considered after the flare is controlled to prevent future exacerbations.

Ulcerative colitis can be managed through inducing and maintaining remission. The severity of the condition is classified as mild, moderate, or severe based on the number of stools and presence of systemic upset. Treatment for mild-to-moderate cases of proctitis involves using topical aminosalicylate, while proctosigmoiditis and left-sided ulcerative colitis may require a combination of oral and topical medications. Extensive disease may require a high-dose oral aminosalicylate and topical treatment. Severe colitis should be treated in a hospital with intravenous steroids or ciclosporin. Maintaining remission can involve using a low maintenance dose of an oral aminosalicylate or oral azathioprine/mercaptopurine. Methotrexate is not recommended, but probiotics may prevent relapse in mild to moderate cases.

Understanding the Association between H. pylori Infection and Gastric Diseases

H. pylori infection is a common bacterial infection that affects approximately 50% of the global population. While it is primarily associated with peptic ulcer disease, it can also lead to other gastric diseases. Gastric malignancies, for instance, are often caused by chronic inflammation of MALT from H. pylori infection. MALTomas, which are extranodal marginal zone B-cell lymphomas, are the most common type of gastric lymphoma and are associated with H. pylori infection in over 90% of cases.

However, not all gastric diseases are associated with H. pylori infection. Coeliac disease, for example, is an autoimmune disorder related to gluten sensitivity. Non-ulcer dyspepsia, a group of upper gastrointestinal symptoms, is not generally associated with H. pylori infection. Reflux oesophagitis, a condition caused by the failure of relaxation of the lower end of the oesophagus, is also not associated with H. pylori infection.

It is important to note that the development of gastric malignancies from H. pylori infection is a slow process that may stop at any step. The disease process starts with chronic gastritis, followed by atrophic gastritis, intestinal metaplasia, dysplasia, and eventually gastric malignancy (Correa’s cascade). However, other factors are also required for gastric cancers to develop, not just H. pylori infection.

In conclusion, understanding the association between H. pylori infection and gastric diseases is crucial in the diagnosis and treatment of these conditions. While H. pylori infection is a common cause of gastric malignancies, it is not associated with all gastric diseases.

Management of Dyspepsia and Referral for Possible Cancer

Dyspepsia is a common symptom that can be caused by various factors, including medication and lifestyle choices. However, it can also be a sign of underlying conditions such as stomach or oesophageal cancer. The 2015 NICE guidelines provide updated advice on when urgent referral for endoscopy is necessary. Patients with dysphagia or an upper abdominal mass consistent with stomach cancer should be referred urgently. Patients aged 55 years or older with weight loss and upper abdominal pain, reflux, or dyspepsia should also be referred urgently. Non-urgent referrals include patients with haematemesis or those with treatment-resistant dyspepsia, upper abdominal pain with low haemoglobin levels, or raised platelet count with other symptoms.

For patients with undiagnosed dyspepsia, a step-wise approach is recommended. First, medications should be reviewed for possible causes. Lifestyle advice should also be given. If symptoms persist, a trial of full-dose proton pump inhibitor for one month or a ‘test and treat’ approach for H. pylori can be tried. If symptoms persist after either approach, the alternative should be attempted. Testing for H. pylori infection can be done using a carbon-13 urea breath test, stool antigen test, or laboratory-based serology. If symptoms resolve following test and treat, there is no need to check for H. pylori eradication. However, if repeat testing is required, a carbon-13 urea breath test should be used.

Acute mesenteric ischaemia (AMI) is a rare but potentially life-threatening condition caused by inadequate blood flow through the mesenteric vessels, leading to ischaemia and gangrene of the bowel wall. It can be classified as either arterial or venous, with embolic phenomena being the most common cause. Symptoms include sudden and severe abdominal pain, vomiting, and diarrhoea, with physical signs developing late in the disease process. Early and aggressive diagnosis and treatment are crucial to reduce mortality, but once bowel wall infarction has occurred, the mortality rate may be as high as 90%. Appendicitis, diverticulitis, pseudomembranous colitis, and ruptured AAA are important differential diagnoses to consider.

Understanding and Managing Irritable Bowel Syndrome (IBS)

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder that affects 10-20% of the population, with women being more likely to develop it than men. It is characterized by abdominal pain, bloating, and altered bowel habits without any specific organic pathology.

Diagnosis of IBS is based on the presence of symptoms such as abdominal pain or discomfort, bloating, and change in bowel habit for at least 6 months. Physical examination and further investigations are necessary to exclude other differential diagnoses.

Management of IBS primarily involves psychological support and dietary measures such as fiber supplementation, low FODMAP diets, increased water intake, and avoiding trigger foods. Pharmacological treatment is adjunctive and should be directed at symptoms. Anti-spasmodics, anti-diarrheals, and antidepressants may have a positive effect on symptoms.

It is important to note that symptoms not consistent with IBS, such as rectal bleeding, anorexia/weight loss, nocturnal symptoms, or fecal incontinence, should alert the clinician to the possibility of an organic pathology. Referral for psychological therapies should be considered for patients who do not respond to pharmacological treatments after 12 months and who develop a continuing symptom profile.

The elevated ferritin level can be attributed to the patient’s excessive alcohol consumption, as the typical transferrin saturation rules out iron overload as a potential cause.

Understanding Ferritin Levels in the Body

Ferritin is a protein found inside cells that binds to iron and stores it until it is needed in other parts of the body. When ferritin levels are increased, it is usually defined as being above 300 µg/L in men and postmenopausal women, and above 200 µg/L in premenopausal women. However, it is important to note that ferritin is an acute phase protein, meaning that it can be produced in higher quantities during times of inflammation. This can lead to falsely elevated results, which must be interpreted in the context of the patient’s clinical picture and other blood test results.

There are two main categories of causes for increased ferritin levels: those without iron overload (which account for around 90% of cases) and those with iron overload (which account for around 10% of cases). Causes of increased ferritin levels without iron overload include inflammation, alcohol excess, liver disease, chronic kidney disease, and malignancy. Causes of increased ferritin levels with iron overload include primary iron overload (hereditary hemochromatosis) and secondary iron overload (such as from repeated transfusions). To determine whether iron overload is present, the best test is transferrin saturation, with normal values being less than 45% in females and less than 50% in males.

On the other hand, reduced ferritin levels can indicate a deficiency in iron, which can lead to anemia. When iron and ferritin are bound together, a decrease in ferritin levels can suggest a decrease in iron levels as well. Measuring serum ferritin levels can be helpful in determining whether a low hemoglobin level and microcytosis are truly caused by an iron deficiency state.

For a mild-moderate flare of distal ulcerative colitis, the recommended first-line treatment is rectal aminosalicylates. This is particularly effective if the inflammation is limited to the rectum. If rectal aminosalicylates are not effective, oral aminosalicylates may be used in combination with or instead of the topical treatment. However, if the patient has contraindications or intolerances to aminosalicylates, topical or oral steroids may be preferred. Intravenous steroids are typically reserved for severe flares of colitis with symptoms such as frequent bloody stools, systemic upset, anemia, or elevated inflammatory markers.

Ulcerative colitis can be managed through inducing and maintaining remission. The severity of the condition is classified as mild, moderate, or severe based on the number of stools and presence of systemic upset. Treatment for mild-to-moderate cases of proctitis involves using topical aminosalicylate, while proctosigmoiditis and left-sided ulcerative colitis may require a combination of oral and topical medications. Extensive disease may require a high-dose oral aminosalicylate and topical treatment. Severe colitis should be treated in a hospital with intravenous steroids or ciclosporin. Maintaining remission can involve using a low maintenance dose of an oral aminosalicylate or oral azathioprine/mercaptopurine. Methotrexate is not recommended, but probiotics may prevent relapse in mild to moderate cases.

The M rule for primary biliary cholangitis includes the presence of IgM and anti-Mitochondrial antibodies, specifically the M2 subtype, in middle-aged women.

Primary Biliary Cholangitis: A Chronic Liver Disorder

Primary biliary cholangitis, previously known as primary biliary cirrhosis, is a chronic liver disorder that is commonly observed in middle-aged women. The exact cause of this condition is not yet fully understood, but it is believed to be an autoimmune disease. The disease is characterized by the progressive damage of interlobular bile ducts due to chronic inflammation, leading to cholestasis and eventually cirrhosis. The most common symptom of primary biliary cholangitis is itching in middle-aged women.

This condition is often associated with other autoimmune diseases such as Sjogren’s syndrome, rheumatoid arthritis, systemic sclerosis, and thyroid disease. Early symptoms of primary biliary cholangitis may be asymptomatic or may include fatigue, pruritus, and cholestatic jaundice. Late symptoms may progress to liver failure. Diagnosis of primary biliary cholangitis involves immunology tests such as anti-mitochondrial antibodies (AMA) M2 subtype and smooth muscle antibodies, as well as imaging tests to exclude an extrahepatic biliary obstruction.

The first-line treatment for primary biliary cholangitis is ursodeoxycholic acid, which slows down the progression of the disease and improves symptoms. Cholestyramine is used to alleviate pruritus, and fat-soluble vitamin supplementation is recommended. In severe cases, liver transplantation may be necessary, especially if bilirubin levels exceed 100. However, recurrence in the graft can occur, but it is not usually a problem. Complications of primary biliary cholangitis include cirrhosis, portal hypertension, ascites, variceal hemorrhage, osteomalacia, osteoporosis, and an increased risk of hepatocellular carcinoma.

The three main symptoms of Charcot’s cholangitis are fever, jaundice, and pain in the upper right quadrant. This type of cholangitis is known for causing these three symptoms, which are collectively referred to as Charcot’s triad. When there is inflammation in the gastrointestinal tract, amylase levels may be slightly elevated. While cholecystitis can lead to jaundice, it is usually not severe. On the other hand, pancreatitis typically does not cause jaundice, and amylase levels are typically much higher.

Understanding Ascending Cholangitis

Ascending cholangitis is a bacterial infection that affects the biliary tree, with E. coli being the most common culprit. This condition is often associated with gallstones, which can predispose individuals to the infection. Patients with ascending cholangitis may present with Charcot’s triad, which includes fever, right upper quadrant pain, and jaundice. However, this triad is only present in 20-50% of cases. Other common symptoms include hypotension and confusion. In severe cases, Reynolds’ pentad may be observed, which includes the additional symptoms of hypotension and confusion.

To diagnose ascending cholangitis, ultrasound is typically used as a first-line investigation to look for bile duct dilation and stones. Raised inflammatory markers may also be observed. Treatment involves intravenous antibiotics and endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction.

Overall, ascending cholangitis is a serious condition that requires prompt diagnosis and treatment. Understanding the symptoms and risk factors associated with this condition can help individuals seek medical attention early and improve their chances of a successful recovery.

The presence of fever, jaundice and right upper quadrant pain is known as Charcot’s cholangitis triad, which indicates an infection of the bile ducts. This patient is likely suffering from ascending cholangitis. Cholecystitis, which is inflammation of the gallbladder, can also cause right upper quadrant pain and may precede ascending cholangitis. While gallstones are a common cause of cholangitis, they can be asymptomatic and are not a diagnosis on their own. Pregnancy is not a likely cause of right upper quadrant pain. Gilbert’s syndrome typically causes mild jaundice only during times of stress and is usually asymptomatic.

Understanding Ascending Cholangitis

Ascending cholangitis is a bacterial infection that affects the biliary tree, with E. coli being the most common culprit. This condition is often associated with gallstones, which can predispose individuals to the infection. Patients with ascending cholangitis may present with Charcot’s triad, which includes fever, right upper quadrant pain, and jaundice. However, this triad is only present in 20-50% of cases. Other common symptoms include hypotension and confusion. In severe cases, Reynolds’ pentad may be observed, which includes the additional symptoms of hypotension and confusion.

To diagnose ascending cholangitis, ultrasound is typically used as a first-line investigation to look for bile duct dilation and stones. Raised inflammatory markers may also be observed. Treatment involves intravenous antibiotics and endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction.

Overall, ascending cholangitis is a serious condition that requires prompt diagnosis and treatment. Understanding the symptoms and risk factors associated with this condition can help individuals seek medical attention early and improve their chances of a successful recovery.

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.

Paracetamol overdose leads to a liver disease characterized by hepatocellular symptoms. This type of liver disease is different from cholestatic (obstructive) or mixed liver diseases, which have distinct laboratory test results. Hepatocellular disease is indicated by raised ALT levels, while cholestatic disease is indicated by raised ALP levels. Mixed liver disease has raised levels of both ALT and ALP. AST and ALT are both produced by hepatocytes, and in hepatocellular disease, these enzymes are released into the bloodstream, causing raised ALT levels. ALP, on the other hand, is produced by the cells lining the bile ducts, and its levels rise in obstructive liver disease.

Understanding Drug-Induced Liver Disease

Drug-induced liver disease is a condition that occurs when certain medications or drugs cause damage to the liver. This condition is generally divided into three categories: hepatocellular, cholestatic, or mixed. However, there is often overlap between these categories, as some drugs can cause a range of changes to the liver.

Hepatocellular drug-induced liver disease is characterized by damage to the liver cells. Some of the drugs that tend to cause this type of damage include paracetamol, sodium valproate, phenytoin, MAOIs, halothane, anti-tuberculosis medications, statins, alcohol, amiodarone, methyldopa, and nitrofurantoin.

Cholestatic drug-induced liver disease, on the other hand, is characterized by a reduction in bile flow from the liver. Some of the drugs that tend to cause this type of damage include the combined oral contraceptive pill, antibiotics such as flucloxacillin, co-amoxiclav, and erythromycin, anabolic steroids, testosterones, phenothiazines such as chlorpromazine and prochlorperazine, sulphonylureas, fibrates, and rare reported causes such as nifedipine. Methotrexate, methyldopa, and amiodarone can cause both hepatocellular and cholestatic damage.

It is important to note that drug-induced liver disease can be a serious condition and can lead to liver cirrhosis if left untreated. Therefore, it is important to be aware of the potential risks associated with certain medications and to seek medical attention if any symptoms of liver damage occur.

Understanding Primary Sclerosing Cholangitis

Primary sclerosing cholangitis is a condition that affects the bile ducts, causing inflammation and fibrosis. The cause of this disease is unknown, but it is often associated with ulcerative colitis, with 4% of UC patients having PSC and 80% of PSC patients having UC. Crohn’s disease and HIV are also less common associations. Symptoms of PSC include cholestasis, jaundice, pruritus, right upper quadrant pain, and fatigue. Diagnosis is typically made through endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP), which show multiple biliary strictures giving a ‘beaded’ appearance. A liver biopsy may also be performed, but it has a limited role in diagnosis. Complications of PSC include cholangiocarcinoma in 10% of cases and an increased risk of colorectal cancer.

Overall, understanding primary sclerosing cholangitis is important for early diagnosis and management of the disease. With proper treatment and monitoring, patients can manage their symptoms and reduce the risk of complications.

Acute cholangitis is a serious infection of the biliary tract that can lead to significant health complications. Symptoms typically include fever, abdominal pain (specifically in the upper right quadrant), and jaundice, which is known as Charcot’s triad. This patient is displaying all of these symptoms and has a history of gallstones, making acute cholangitis the most likely diagnosis. Treatment for acute cholangitis depends on the severity of the infection, as determined by the TG13 guideline. Patients will require intravenous fluids and antibiotics, and may need biliary drainage or intensive care support if the disease is severe. Influenza, acute cholecystitis, acute viral hepatitis, and biliary colic are all potential differential diagnoses, but do not match this patient’s symptoms and medical history.

Irritable bowel syndrome (IBS) is a gastrointestinal disorder that causes abdominal pain, bloating, and changes in bowel habits without any identifiable organic pathology. It is more common in women and can be worsened by stress and the perimenstrual period. Diagnosis is made by ruling out other potential causes of symptoms. Management includes dietary changes, such as increasing fiber intake and avoiding trigger foods, as well as psychological support. Medications may also be used to alleviate symptoms. This patient’s symptoms are not consistent with chronic pancreatitis, ulcerative colitis, peptic ulcer disease, or diverticulitis.

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.

Cholestyramine is an effective treatment for bile-acid malabsorption. It functions by binding to bile acids in the small intestine and facilitating their reabsorption into the bile acid production cycle. This approach addresses the root cause of diarrhea in patients with this condition. In the case of the patient described, the removal of her gallbladder likely disrupted the normal cycle of bile release and reabsorption, leading to excessive bile in the large intestine and resulting in increased water and salt loss in the stool and faster transit time of stool through the intestines. While bismuth may be useful in preventing symptoms during infectious diarrhea, it is not a long-term solution. Creon is typically used to replace pancreatic enzymes in conditions such as cystic fibrosis, where there is a reduction in pancreatic enzymes reaching the intestine. Loperamide may be effective in preventing diarrhea in the short term, but it does not address the underlying cause of the patient’s condition.

Understanding Bile-Acid Malabsorption

Bile-acid malabsorption is a condition that can cause chronic diarrhea. It can be primary, which means that it is caused by excessive production of bile acid, or secondary, which is due to an underlying gastrointestinal disorder that reduces bile acid absorption. This condition can lead to steatorrhea and malabsorption of vitamins A, D, E, and K. Secondary causes are often seen in patients with ileal disease, such as Crohn’s disease, as well as those who have undergone cholecystectomy, have coeliac disease, or have small intestinal bacterial overgrowth.

To diagnose bile-acid malabsorption, the test of choice is SeHCAT, a nuclear medicine test that uses a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid. Scans are done 7 days apart to assess the retention or loss of radiolabeled 75SeHCAT.

The management of bile-acid malabsorption involves the use of bile acid sequestrants, such as cholestyramine. These medications work by binding to bile acids in the intestine, preventing their reabsorption and promoting their excretion. With proper management, the symptoms of bile-acid malabsorption can be controlled, and patients can lead a normal life.

The sole recommended test for H. pylori after eradication therapy is the urea breath test. It should be noted that H. pylori serology will still show positive results even after eradication. In such cases, a stool antigen test, rather than culture, may be a suitable alternative.

Tests for Helicobacter pylori

There are several tests available to diagnose Helicobacter pylori infection. One of the most common tests is the urea breath test, where patients consume a drink containing carbon isotope 13 (13C) enriched urea. The urea is broken down by H. pylori urease, and after 30 minutes, the patient exhales into a glass tube. Mass spectrometry analysis calculates the amount of 13C CO2, which indicates the presence of H. pylori. However, this test should not be performed within four weeks of treatment with an antibacterial or within two weeks of an antisecretory drug.

Another test is the rapid urease test, also known as the CLO test. This involves mixing a biopsy sample with urea and a pH indicator. If there is a color change, it indicates the presence of H. pylori urease activity. Serum antibody tests can also be used, but they remain positive even after eradication. Culture of gastric biopsy can provide information on antibiotic sensitivity, while histological evaluation alone can be done through gastric biopsy. Lastly, the stool antigen test has a sensitivity of 90% and specificity of 95%.

Overall, these tests have varying levels of sensitivity and specificity, and the choice of test depends on the patient’s clinical presentation and the availability of resources.

It is not recommended to use faecal occult blood testing for colorectal cancer screening in symptomatic patients who are under the age of 60. This woman is displaying symptoms of irritable bowel syndrome and has normal blood results, without any red flag symptoms. Repeating the full blood count is unlikely to provide any additional information. The use of steroids and azathioprine is not appropriate for treating irritable bowel syndrome, as they are typically used for ulcerative colitis, which is not likely in this case.

Colorectal Cancer Screening: Faecal Immunochemical Test (FIT)

Colorectal cancer is often developed from adenomatous polyps. Screening for this type of cancer has been proven to reduce mortality by 16%. The NHS offers a home-based screening programme called Faecal Immunochemical Test (FIT) to older adults. A one-off flexible sigmoidoscopy was trialled in England for people aged 55 years, but it was abandoned in 2021 due to the inability to recruit enough clinical endoscopists, which was exacerbated by the COVID-19 pandemic. The trial, partly funded by Cancer Research UK, showed promising early results, and it remains to be seen whether flexible sigmoidoscopy will be used as part of a future bowel screening programme.

Faecal Immunochemical Test (FIT) Screening:
The NHS now has a national screening programme that offers screening every two years to all men and women aged 60 to 74 years in England and 50 to 74 years in Scotland. Patients aged over 74 years may request screening. Eligible patients are sent FIT tests through the post. FIT is a type of faecal occult blood (FOB) test that uses antibodies that specifically recognise human haemoglobin (Hb). It is used to detect and quantify the amount of human blood in a single stool sample. FIT has advantages over conventional FOB tests because it only detects human haemoglobin, as opposed to animal haemoglobin ingested through diet. Only one faecal sample is needed compared to the 2-3 for conventional FOB tests. While a numerical value is generated, this is not reported to the patient or GP. Instead, they will be informed if the test is normal or abnormal. Patients with abnormal results are offered a colonoscopy. At colonoscopy, approximately 5 out of 10 patients will have a normal exam, 4 out of 10 patients will be found to have polyps that may be removed due to their premalignant potential, and 1 out of 10 patients will be found to have cancer.

Gastroenteritis can occur either at home or while traveling, known as travelers’ diarrhea. This condition is characterized by at least three loose to watery stools in 24 hours, accompanied by abdominal cramps, fever, nausea, vomiting, or blood in the stool. The most common cause of travelers’ diarrhea is Escherichia coli. Acute food poisoning is another pattern of illness that results in sudden onset of nausea, vomiting, and diarrhea after ingesting a toxin. Staphylococcus aureus, Bacillus cereus, or Clostridium perfringens are typically responsible for acute food poisoning.

There are several types of infections that can cause gastroenteritis, each with its own typical presentation. Escherichia coli is common among travelers and causes watery stools, abdominal cramps, and nausea. Giardiasis results in prolonged, non-bloody diarrhea, while cholera causes profuse, watery diarrhea and severe dehydration leading to weight loss. Shigella causes bloody diarrhea, vomiting, and abdominal pain, while Staphylococcus aureus results in severe vomiting with a short incubation period. Campylobacter typically starts with a flu-like prodrome and progresses to crampy abdominal pains, fever, and diarrhea, which may be bloody and mimic appendicitis. Bacillus cereus can cause two types of illness, vomiting within six hours, typically due to rice, or diarrheal illness occurring after six hours. Amoebiasis has a gradual onset of bloody diarrhea, abdominal pain, and tenderness that may last for several weeks.

The incubation period for gastroenteritis varies depending on the type of infection. Staphylococcus aureus and Bacillus cereus have an incubation period of 1-6 hours, while Salmonella and Escherichia coli have an incubation period of 12-48 hours. Shigella and Campylobacter have an incubation period of 48-72 hours, while Giardiasis and Amoebiasis have an incubation period of more than seven days.

Taking Omeprazole may heighten the possibility of experiencing severe diarrhoea, specifically Clostridium difficile infections. Omeprazole is a type of proton pump inhibitor that can lead to side effects like abdominal pain, flatulence, nausea/vomiting, and diarrhoea. The risk of contracting severe infections like clostridium difficile is higher, especially if the patient has received antibiotics, particularly broad-spectrum agents, for their spontaneous bacterial peritonitis.
Propranolol, a beta-blocker, can cause side effects such as a slow heart rate, dry eyes, tiredness, and nausea, but it may also result in abdominal discomfort with altered bowel habit.
Allopurinol is known to cause a rash or nausea and vomiting.

Understanding Proton Pump Inhibitors and Their Adverse Effects

Proton pump inhibitors (PPIs) are medications that block the H+/K+ ATPase of the gastric parietal cell, leading to irreversible effects. Common examples of PPIs include omeprazole and lansoprazole. While these medications are effective in treating conditions such as gastroesophageal reflux disease (GERD) and peptic ulcers, they can also have adverse effects on the body.

One of the potential adverse effects of PPIs is hyponatremia, which is a condition characterized by low levels of sodium in the blood. PPIs can also lead to hypomagnesemia, which is a deficiency of magnesium in the blood. Additionally, long-term use of PPIs has been linked to an increased risk of osteoporosis and fractures. Another potential adverse effect is microscopic colitis, which is inflammation of the colon that can cause diarrhea and abdominal pain. Finally, PPIs have been associated with an increased risk of C. difficile infections, which can cause severe diarrhea and other gastrointestinal symptoms.

To prevent spontaneous bacterial peritonitis, it is recommended to administer oral ciprofloxacin or norfloxacin as prophylaxis to patients with ascites and protein concentration of 15 g/L or less.

Understanding Spontaneous Bacterial Peritonitis

Spontaneous bacterial peritonitis (SBP) is a type of peritonitis that typically affects individuals with ascites caused by liver cirrhosis. The condition is characterized by symptoms such as abdominal pain, fever, and ascites. Diagnosis is usually made through paracentesis, which involves analyzing the ascitic fluid for a neutrophil count of over 250 cells/ul. The most common organism found on ascitic fluid culture is E. coli.

Management of SBP typically involves the administration of intravenous cefotaxime. Antibiotic prophylaxis is also recommended for patients with ascites who have previously experienced an episode of SBP or have a fluid protein level of less than 15 g/l and a Child-Pugh score of at least 9 or hepatorenal syndrome. NICE recommends prophylactic oral ciprofloxacin or norfloxacin until the ascites has resolved.

Alcoholic liver disease is a significant predictor of poor prognosis in SBP. Understanding the symptoms, diagnosis, and management of SBP is crucial for healthcare professionals to provide appropriate care and improve patient outcomes.

When dealing with a severe flare of ulcerative colitis, it is important to evaluate the severity of the condition. In this case, the patient is experiencing more than six bloody stools per day, as well as systemic upset indicated by raised inflammatory markers and anaemia. This places him in the severe category. The first line of treatment would be IV corticosteroids, with IV ciclosporin as a second-line option if the steroids do not induce remission. Hospital admission for IV steroids is the appropriate course of action to induce remission, after which maintenance treatment can be assessed. For moderate extensive disease, oral aminosalicylate and oral steroids can be used. It would be inappropriate to send this patient home without any treatment, as he is clearly unwell and experiencing a flare of UC.

Ulcerative colitis can be managed through inducing and maintaining remission. The severity of the condition is classified as mild, moderate, or severe based on the number of stools and presence of systemic upset. Treatment for mild-to-moderate cases of proctitis involves using topical aminosalicylate, while proctosigmoiditis and left-sided ulcerative colitis may require a combination of oral and topical medications. Extensive disease may require a high-dose oral aminosalicylate and topical treatment. Severe colitis should be treated in a hospital with intravenous steroids or ciclosporin. Maintaining remission can involve using a low maintenance dose of an oral aminosalicylate or oral azathioprine/mercaptopurine. Methotrexate is not recommended, but probiotics may prevent relapse in mild to moderate cases.

When a patient with type 2 diabetes and obesity presents with abnormal liver function tests, the most probable diagnosis is non-alcoholic fatty liver disease. To confirm this diagnosis, the patient will need to undergo a liver screen, ultrasound, and liver biopsy. While haemochromatosis should be considered in patients with both abnormal LFTs and diabetes, a normal ferritin level makes this diagnosis less likely.

Non-Alcoholic Fatty Liver Disease: Causes, Features, and Management

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disease in developed countries, primarily caused by obesity. It encompasses a range of conditions, from simple steatosis (fat accumulation in the liver) to steatohepatitis (fat with inflammation) and may progress to fibrosis and liver cirrhosis. Insulin resistance is believed to be the primary mechanism leading to steatosis, making NAFLD a hepatic manifestation of metabolic syndrome. Non-alcoholic steatohepatitis (NASH) is a type of liver damage similar to alcoholic hepatitis but occurs in the absence of alcohol abuse. It affects around 3-4% of the general population and may be responsible for some cases of cryptogenic cirrhosis.

NAFLD is usually asymptomatic, but hepatomegaly, increased echogenicity on ultrasound, and elevated ALT levels are common features. The enhanced liver fibrosis (ELF) blood test is recommended by NICE to check for advanced fibrosis in patients with incidental NAFLD. If the ELF blood test is not available, non-invasive tests such as the FIB4 score or NAFLD fibrosis score, in combination with a FibroScan, may be used to assess the severity of fibrosis. Patients with advanced fibrosis should be referred to a liver specialist for further evaluation, which may include a liver biopsy to stage the disease more accurately.

The mainstay of NAFLD treatment is lifestyle changes, particularly weight loss, and monitoring. Research is ongoing into the role of gastric banding and insulin-sensitizing drugs such as metformin and pioglitazone. While there is no evidence to support screening for NAFLD in adults, NICE guidelines recommend the management of incidental NAFLD findings.

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.

Understanding Coeliac Disease: Symptoms, Diagnosis, and Treatment

Coeliac disease (CD) is a common autoimmune disorder that affects almost 1% of individuals in developed countries. It is triggered by gluten and related prolamins present in wheat, rye, and barley, and primarily affects the small intestine, leading to flattening of the small intestinal mucosa. CD can present in various ways, including typical GI symptoms, atypical symptoms, or no symptoms at all. Diagnosis is made through serology tests for specific autoimmune markers, and treatment involves a lifelong avoidance of gluten ingestion.

Other potential diagnoses, such as travellers’ diarrhoea, growth hormone deficiency, hypothyroidism, and severe combined immunodeficiency, have different clinical presentations and are not consistent with this patient’s symptoms. Understanding the symptoms, diagnosis, and treatment of CD is crucial for proper management and improved quality of life for affected individuals.

The patient’s symptoms of dull, central abdominal pain that worsens after meals and radiates to the back, along with a history of regular alcohol consumption, suggest a diagnosis of chronic pancreatitis. Imaging studies, such as an abdominal X-ray or CT scan, may reveal pancreatic calcifications, which are a common finding in chronic pancreatitis. If imaging is inconclusive, a faecal elastase test may be used to assess pancreatic exocrine function. The presence of the football sign, air under the diaphragm, dilated loops of small bowel, or the Rigler sign on an abdominal X-ray would suggest other conditions such as gastrointestinal perforation or bowel obstruction, which do not fit the patient’s presentation.

Non-Alcoholic Fatty Liver Disease: Causes, Features, and Management

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disease in developed countries, primarily caused by obesity. It encompasses a range of conditions, from simple steatosis (fat accumulation in the liver) to steatohepatitis (fat with inflammation) and may progress to fibrosis and liver cirrhosis. Insulin resistance is believed to be the primary mechanism leading to steatosis, making NAFLD a hepatic manifestation of metabolic syndrome. Non-alcoholic steatohepatitis (NASH) is a type of liver damage similar to alcoholic hepatitis but occurs in the absence of alcohol abuse. It affects around 3-4% of the general population and may be responsible for some cases of cryptogenic cirrhosis.

NAFLD is usually asymptomatic, but hepatomegaly, increased echogenicity on ultrasound, and elevated ALT levels are common features. The enhanced liver fibrosis (ELF) blood test is recommended by NICE to check for advanced fibrosis in patients with incidental NAFLD. If the ELF blood test is not available, non-invasive tests such as the FIB4 score or NAFLD fibrosis score, in combination with a FibroScan, may be used to assess the severity of fibrosis. Patients with advanced fibrosis should be referred to a liver specialist for further evaluation, which may include a liver biopsy to stage the disease more accurately.

The mainstay of NAFLD treatment is lifestyle changes, particularly weight loss, and monitoring. Research is ongoing into the role of gastric banding and insulin-sensitizing drugs such as metformin and pioglitazone. While there is no evidence to support screening for NAFLD in adults, NICE guidelines recommend the management of incidental NAFLD findings.

To avoid the possibility of masking serious underlying pathology like gastric cancer, patients who are taking proton pump inhibitors or H2 receptor blockers should discontinue their use at least two weeks before undergoing an endoscopy.

Management of Dyspepsia and Referral for Possible Cancer

Dyspepsia is a common symptom that can be caused by various factors, including medication and lifestyle choices. However, it can also be a sign of underlying conditions such as stomach or oesophageal cancer. The 2015 NICE guidelines provide updated advice on when urgent referral for endoscopy is necessary. Patients with dysphagia or an upper abdominal mass consistent with stomach cancer should be referred urgently. Patients aged 55 years or older with weight loss and upper abdominal pain, reflux, or dyspepsia should also be referred urgently. Non-urgent referrals include patients with haematemesis or those with treatment-resistant dyspepsia, upper abdominal pain with low haemoglobin levels, or raised platelet count with other symptoms.

For patients with undiagnosed dyspepsia, a step-wise approach is recommended. First, medications should be reviewed for possible causes. Lifestyle advice should also be given. If symptoms persist, a trial of full-dose proton pump inhibitor for one month or a ‘test and treat’ approach for H. pylori can be tried. If symptoms persist after either approach, the alternative should be attempted. Testing for H. pylori infection can be done using a carbon-13 urea breath test, stool antigen test, or laboratory-based serology. If symptoms resolve following test and treat, there is no need to check for H. pylori eradication. However, if repeat testing is required, a carbon-13 urea breath test should be used.

Treatment Options for Primary Biliary Cholangitis

Primary biliary cholangitis (PBC) is a liver disease that can lead to cirrhosis if left untreated. Ursodeoxycholic acid (UDCA) is the main treatment for PBC, as it can prevent or delay the development of cirrhosis. UDCA increases bile flow, inhibits toxic bile acid production, prevents hepatocyte apoptosis, and reduces the liver’s immune response. However, UDCA may cause side effects such as diarrhea, nausea, and thinning hair.

Spironolactone is a diuretic that can be useful for end-stage liver disease with ascites, but it is not indicated for treating fatigue in PBC patients. Aspirin and ibuprofen should be avoided by PBC patients, as they can worsen liver disease. Cholestyramine is used for cholestatic itching, but it should not be taken with UDCA as it can prevent UDCA absorption.

In summary, UDCA is the primary treatment for PBC, and other medications should be used with caution and only for specific symptoms or complications.

Cyclizine is a recommended first choice anti-emetic for nausea and vomiting caused by intracranial or intra-vestibular issues. It is also useful in palliative care for managing gastrointestinal obstruction and vagally-mediated nausea or vomiting caused by mechanical bowel obstruction, movement disorders, or raised intracranial pressure. Domperidone is effective for gastro-intestinal pain in palliative care, while metoclopramide is used for acute migraine, chemotherapy or radiotherapy-induced nausea and vomiting. Ondansetron is indicated for chemotherapy-related nausea and vomiting. Dexamethasone is a steroid that may be used in palliative care for treating nausea, anorexia, spinal cord compression, and liver capsule pain. If the cause of nausea is suspected to be raised intracranial pressure, cyclizine should be the first-line option, and dexamethasone may be considered as an additional treatment.

Managing Nausea and Vomiting in Palliative Care: A Mechanistic Approach

Nausea and vomiting are common symptoms in palliative care, often caused by multiple factors. Identifying the primary cause is crucial in selecting the appropriate anti-emetic therapy. Six broad syndromes have been identified, with gastric stasis and chemical disturbance being the most common. In palliative care, pharmacological therapy is the first-line method for treating nausea and vomiting. Two approaches can be used in selecting drug therapy: empirical or mechanistic. The mechanistic approach matches the choice of anti-emetic drug to the likely cause of the patient’s symptoms.

The mechanistic approach involves selecting medication based on the underlying cause of the nausea and vomiting. For example, pro-kinetic agents are useful in scenarios where reduced gastric motility is the primary cause. First-line medications for this syndrome include metoclopramide and domperidone. However, metoclopramide should not be used in certain situations, such as complete bowel obstruction or gastrointestinal perforation. If the cause is chemically mediated, correcting the chemical disturbance should be the first step. Key treatment options include ondansetron, haloperidol, and levomepromazine. Cyclizine and levomepromazine are first-line for visceral/serosal causes, while cyclizine is recommended for nausea and vomiting due to intracranial disease. If the oral route is not possible, the parenteral route of administration is preferred, with the intravenous route used if access is already established.

In summary, a mechanistic approach to managing nausea and vomiting in palliative care involves selecting medication based on the underlying cause of the symptoms. This approach can improve the effectiveness of anti-emetic therapy and reduce the risk of adverse effects.

Autoimmune Diseases: Understanding the Causes and Symptoms

Autoimmune diseases are conditions where the body’s immune system mistakenly attacks its own tissues. Here are some examples of autoimmune diseases and their causes and symptoms:

Coeliac Disease: This disease is caused by gluten sensitivity and results in chronic diarrhoea, weight loss, and fatigue. It is caused by an autoimmune reaction to glutenin or gliadin, which are gluten proteins found in wheat.

Pemphigus Vulgaris: This rare autoimmune disease causes blistering to the skin and mucosal surfaces. It is caused by autoantibodies against desmoglein.

Graves’ Disease: This autoimmune disease of the thyroid results in hyperthyroidism. It is associated with anti-thyroid-stimulating hormone receptor antibodies.

Systemic Lupus Erythematosus (SLE): SLE is a multisystem autoimmune disease associated with a wide number of autoantibodies, including anti-nuclear antibody (ANA), anti-double-stranded (ds) DNA, anti-Smith, anti-SSA, anti-ribosomal P, anti-RNP, and anti-histone antibodies.

Type I Diabetes Mellitus (T1DM): T1DM is an autoimmune disease resulting in destruction of the islet cells. Islet cell autoantibodies and antibodies to insulin have been described.

Understanding the causes and symptoms of autoimmune diseases can help with early diagnosis and treatment.

The latest recommendations state that individuals should limit their alcohol consumption to no more than 14 units per week, regardless of gender. Additionally, it is suggested that individuals should spread out their drinking over a minimum of three days if they regularly consume 14 units per week.

Alcohol consumption guidelines were revised in 2016 by the Chief Medical Officer, based on recommendations from an expert group report. The most significant change was a reduction in the recommended maximum number of units of alcohol for men from 21 to 14, aligning with the guidelines for women. The government now advises that both men and women should not exceed 14 units of alcohol per week, and if they do, it is best to spread it evenly over three or more days. Pregnant women are advised not to drink alcohol at all, as it can cause long-term harm to the baby. One unit of alcohol is equivalent to 10 mL of pure ethanol, and the strength of a drink is determined by its alcohol by volume (ABV). Examples of one unit of alcohol include a 25ml single measure of spirits with an ABV of 40%, a third of a pint of beer with an ABV of 5-6%, and half a 175ml standard glass of red wine with an ABV of 12%. To calculate the number of units in a drink, multiply the number of millilitres by the ABV and divide by 1,000.

Patients who have ascites due to liver cirrhosis should receive an aldosterone antagonist, such as spironolactone, as it helps to counteract the secondary hyperaldosteronism that occurs in cirrhosis. This condition attempts to increase intravascular volume, which is lost into the abdomen as ascites. Amiloride is not effective in treating ascites as it does not lead to significant diuresis and has no effect on the aldosterone pathway. Eplerenone is an alternative to spironolactone for patients who cannot tolerate its adverse effects. Furosemide is useful in treating ascites but should be used in conjunction with spironolactone due to the additional benefits of aldosterone blocking. Bendroflumethiazide is not useful in managing or preventing fluid overload conditions such as ascites.

Understanding Ascites: Causes and Management

Ascites is a medical condition characterized by the accumulation of abnormal fluid in the abdomen. The causes of ascites can be classified into two groups based on the serum-ascites albumin gradient (SAAG) level. A SAAG level greater than 11g/L indicates portal hypertension, which is commonly caused by liver disorders such as cirrhosis, alcoholic liver disease, and liver metastases. On the other hand, a SAAG level less than 11g/L is caused by hypoalbuminaemia, malignancy, infections, and other factors such as bowel obstruction and biliary ascites.

The management of ascites involves reducing dietary sodium and fluid restriction, especially if the sodium level is less than 125 mmol/L. Aldosterone antagonists like spironolactone and loop diuretics are often prescribed to patients. In some cases, drainage through therapeutic abdominal paracentesis is necessary. Large-volume paracentesis requires albumin cover to reduce the risk of paracentesis-induced circulatory dysfunction and mortality. Prophylactic antibiotics are also recommended to prevent spontaneous bacterial peritonitis. In severe cases, a transjugular intrahepatic portosystemic shunt (TIPS) may be considered.

Understanding the causes and management of ascites is crucial in providing appropriate medical care to patients. Proper diagnosis and treatment can help alleviate symptoms and improve the patient’s quality of life.

The appropriate surgical procedure for a patient with rectal cancer on the anal verge is abdominoperineal excision of the rectum. This procedure involves the removal of the anus, rectum, and a section of the sigmoid colon. Symptoms of rectal cancer include blood mixed with stools, changes in bowel habits, and copious mucus in stools. Haemorrhoidectomy is not the correct choice for this patient as the diagnosis is unlike. High anterior resection is used for upper rectal tumours, while low anterior resection is used for low rectal tumours, but not for anal verge tumours. Rubber band ligation is used to treat haemorrhoids in outpatient clinics, which is not the diagnosis for this patient.

Colorectal cancer is typically diagnosed through CT scans and colonoscopies or CT colonography. Patients with tumors below the peritoneal reflection should also undergo MRI to evaluate their mesorectum. Once staging is complete, a treatment plan is formulated by a dedicated colorectal MDT meeting.

For colon cancer, surgery is the primary treatment option, with resectional surgery being the only cure. The procedure is tailored to the patient and tumor location, with lymphatic chains being resected based on arterial supply. Anastomosis is the preferred method of restoring continuity, but in some cases, an end stoma may be necessary. Chemotherapy is often offered to patients with risk factors for disease recurrence.

Rectal cancer management differs from colon cancer due to the rectum’s anatomical location. Tumors can be surgically resected with either an anterior resection or an abdomino-perineal excision of rectum (APER). A meticulous dissection of the mesorectal fat and lymph nodes is integral to the procedure. Neoadjuvant radiotherapy is often offered to patients prior to resectional surgery, and those with obstructing rectal cancer should have a defunctioning loop colostomy.

Segmental resections based on blood supply and lymphatic drainage are the primary operations for cancer. The type of resection and anastomosis depend on the site of cancer. In emergency situations where the bowel has perforated, an end colostomy is often safer. Left-sided resections are more risky, but ileo-colic anastomoses are relatively safe even in the emergency setting and do not need to be defunctioned.

There is insufficient evidence to support the use of PPIs in stopping bleeding, as in most cases, bleeding ceases without their administration. Administering IV proton pump inhibitors and fresh frozen plasma prior to endoscopy is incorrect, as PPIs should not be given and fresh frozen plasma should only be given to patients with specific blood clotting abnormalities.

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.

Primary biliary cholangitis is a likely diagnosis for a middle-aged female patient with an obstructive liver injury picture and positive anti-mitochondrial antibodies, M2 subtype. This differential is important to consider, as alcohol abuse may not always be obvious and gallstones could produce a similar result on liver function tests. However, the absence of pain and positive anti-mitochondrial antibodies make these less likely. Paracetamol overdose is also a potential differential, but the liver function profile in this case is more consistent with an obstructive picture, with a higher ALP and bilirubin and a modest increase in ALT. Additionally, anti-mitochondrial antibodies are not associated with paracetamol overdose.

Primary Biliary Cholangitis: A Chronic Liver Disorder

Primary biliary cholangitis, previously known as primary biliary cirrhosis, is a chronic liver disorder that is commonly observed in middle-aged women. The exact cause of this condition is not yet fully understood, but it is believed to be an autoimmune disease. The disease is characterized by the progressive damage of interlobular bile ducts due to chronic inflammation, leading to cholestasis and eventually cirrhosis. The most common symptom of primary biliary cholangitis is itching in middle-aged women.

This condition is often associated with other autoimmune diseases such as Sjogren’s syndrome, rheumatoid arthritis, systemic sclerosis, and thyroid disease. Early symptoms of primary biliary cholangitis may be asymptomatic or may include fatigue, pruritus, and cholestatic jaundice. Late symptoms may progress to liver failure. Diagnosis of primary biliary cholangitis involves immunology tests such as anti-mitochondrial antibodies (AMA) M2 subtype and smooth muscle antibodies, as well as imaging tests to exclude an extrahepatic biliary obstruction.

The first-line treatment for primary biliary cholangitis is ursodeoxycholic acid, which slows down the progression of the disease and improves symptoms. Cholestyramine is used to alleviate pruritus, and fat-soluble vitamin supplementation is recommended. In severe cases, liver transplantation may be necessary, especially if bilirubin levels exceed 100. However, recurrence in the graft can occur, but it is not usually a problem. Complications of primary biliary cholangitis include cirrhosis, portal hypertension, ascites, variceal hemorrhage, osteomalacia, osteoporosis, and an increased risk of hepatocellular carcinoma.