Differential diagnosis of obstructive liver function tests

Obstructive liver function tests, characterized by elevated conjugated bilirubin and alkaline phosphatase, can be caused by various conditions. Here are some possible differential diagnoses:

– Stone in common bile duct: This can obstruct the flow of bile and cause jaundice, as well as dilate the bile duct. The absence of urobilinogen in urine and the correction of prothrombin time with vitamin K support the diagnosis.
– Haemolytic anaemia: This can lead to increased breakdown of red blood cells and elevated unconjugated bilirubin, but usually does not affect alkaline phosphatase.
– Hepatitis: This can cause inflammation of the liver and elevated transaminases, but usually does not affect conjugated bilirubin or alkaline phosphatase.
– Liver cirrhosis: This can result from chronic liver damage and fibrosis, but usually does not cause obstructive liver function tests unless there is associated biliary obstruction or cholestasis.
– Paracetamol overdose: This can cause liver damage and elevated transaminases, but usually does not affect conjugated bilirubin or alkaline phosphatase unless there is associated liver failure or cholestasis.

Therefore, a careful clinical evaluation and additional tests may be needed to confirm the underlying cause of obstructive liver function tests and guide appropriate management.

Angiodysplasia

Angiodysplasia is a condition where previously healthy blood vessels degenerate, commonly found in the caecum and proximal ascending colon. The majority of angiodysplasias, around 77%, are located in these areas. Symptoms of angiodysplasia include maroon-coloured stool, melaena, haematochezia, and haematemesis. Bleeding is usually low-grade, but in some cases, around 15%, it can be massive. However, bleeding stops spontaneously in over 90% of cases.

Radionuclide scanning using technetium Tc99 labelled red blood cells can help detect and locate active bleeding from angiodysplasia, even at low rates of 0.1 ml/min. However, the intermittent nature of bleeding in angiodysplasia limits the usefulness of this method. For patients who are haemodynamically stable, a conservative approach is recommended as most bleeding angiodysplasias will stop on their own. Treatment is usually not necessary for asymptomatic patients who incidentally discover they have angiodysplasias.

Overall, angiodysplasia and its symptoms is important for early detection and management.

The knife likely cut the right gastro-omental artery, which is a branch of the gastroduodenal artery. This artery runs along the greater curvature of the stomach within the superior border of the greater omentum and anastomoses with the left gastro-omental artery, a branch of the splenic artery. The coeliac trunk, which supplies blood to the foregut, is not related to the greater omentum but to the lesser omentum. The hepatic artery proper, one of the terminal branches of the common hepatic artery, courses towards the liver in the free edge of the lesser omentum. The splenic artery, a tortuous branch of the coeliac trunk, supplies blood to the spleen and gives off the left gastro-omental artery. The short gastric artery, on the other hand, supplies blood to the fundus of the stomach and branches off the splenic artery.

Understanding Liver Function Tests: Indicators of Synthetic and Parenchymal Function

Liver function tests are crucial in determining the nature of any liver impairment. The liver is responsible for producing vitamin K and albumin, and any dysfunction can lead to an increase in prothrombin time, indicating acute synthetic function. Albumin, on the other hand, provides an indication of synthetic liver function over a longer period due to its half-life of 20 days in serum.

While prothrombin time is a reliable indicator, alkaline phosphatase (ALP) would be raised in obstructive (cholestatic) disease. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) represent liver parenchymal function, rather than synthetic function. It’s important to note that both can be normal despite significantly decreased synthetic function of the liver.

While albumin does give an indication of liver function, it can be influenced by many other factors. ALP, on the other hand, would be raised in cholestatic disease. It’s important to consider all these factors when interpreting liver function tests, as neither ALT nor ALP would indicate synthetic function of the liver.

Effects of Aspirin on Gastric Mucosal Lining

Aspirin is a commonly used medication for pain relief and anti-inflammatory purposes. However, it can have adverse effects on the gastric mucosal lining. One of the effects of aspirin is the reduction of surface mucous secretion, which normally protects the gastric mucosal lining. This is due to the inhibition of PGE2 production. To prevent gastrointestinal bleeding and peptic ulceration, patients taking aspirin should consider taking a proton pump inhibitor alongside it.

Aspirin has no effect on gastric motility, but it causes a reduction in PGI2, resulting in reduced blood flow to the gastric lining and mucosal ischaemia. This prevents the elimination of acid that has diffused into the submucosa. Aspirin also causes decreased surface bicarbonate secretion and increased acid production from gastric parietal cells, as prostaglandins normally inhibit acid secretion.

It is important to note that the risk factors for aspirin and non-steroidal anti-inflammatory drug (NSAID)-induced injury include advanced age, history of peptic ulcer disease, concomitant use of glucocorticoids, high dose of NSAIDs, multiple NSAIDs, and concomitant use of clopidogrel or anticoagulants. Therefore, patients should be cautious when taking aspirin and consult with their healthcare provider if they have any concerns.

The Adverse Effects of Aspirin on Gastric Mucosal Lining

Differential Diagnosis for a Patient with Alcohol Withdrawal Symptoms

Delirium Tremens, Korsakoff’s Psychosis, Wernicke’s Encephalopathy, Hepatic Encephalopathy, and Focal Brain Infection: Differential Diagnosis for a Patient with Alcohol Withdrawal Symptoms

A patient presents with agitation, hyperthermia, and visual hallucinations after acute cessation of alcohol. What could be the possible diagnoses?

Delirium tremens is the most likely diagnosis, given the severity of symptoms and timing of onset. It requires intensive care management, and oral lorazepam is recommended as first-line therapy according to NICE guidelines.

Korsakoff’s psychosis, caused by chronic vitamin B1 deficiency, is unlikely to have caused the patient’s symptoms, but the patient is susceptible to developing it due to alcohol dependence and associated malnutrition. Treatment with thiamine is necessary to prevent this syndrome from arising.

Wernicke’s encephalopathy, also caused by thiamine deficiency, presents with ataxia, ophthalmoplegia, and confusion. As the patient has a normal neurological examination, this diagnosis is unlikely to have caused the symptoms. However, regular thiamine treatment is still necessary to prevent it from developing.

Hepatic encephalopathy, a delirium secondary to hepatic insufficiency, is unlikely as the patient has no jaundice, abnormal LFTs, or hemodynamic instability.

Focal brain infection is also unlikely as there is no evidence of meningitis or encephalitis, and the full blood count and urinalysis provide reassuring results. The high MCV is likely due to alcohol-induced macrocytosis. Although delirium secondary to infection is an important diagnosis to consider, delirium tremens is a more likely diagnosis in this case.

Magnetic resonance defecography is the most appropriate investigation for a patient with abnormal pelvic floor muscle tone, perineal descent, and symptoms of incomplete evacuation during defecation. This test evaluates global pelvic floor anatomy and dynamic motion, identifying prolapse, rectocele, and pelvic floor dysfunctions. Other tests, such as abdominal ultrasound, barium enema, colonoscopy, and CT abdomen, may not provide sufficient information on the underlying pathology of the patient’s symptoms.

Management of Mallory-Weiss Tear: A Case Study

A Mallory-Weiss tear is a longitudinal mucosal laceration at the gastro-oesophageal junction or cardia caused by repeated retching. In a stable patient with a Hb of 145 g/l, significant blood loss is unlikely. Observation overnight is recommended, and if stable, the patient can be discharged the following morning. Further endoscopic investigation is not necessary in this case. Intravenous pantoprazole is not indicated for a Mallory-Weiss tear, and antacid treatment is unnecessary as the tear will heal spontaneously. Urgent endoscopic investigation is not required if the patient remains clinically stable and improves.

Hormones and Enzymes: Their Effects on Gastrin Secretion

Gastrin secretion is regulated by various hormones and enzymes in the body. One such hormone is somatostatin, which inhibits the release of gastrin. In the treatment of gastrinomas, somatostatin analogues like octreotide can be used instead of proton pump inhibitors (PPIs).

Aldosterone, on the other hand, is a steroid hormone that is not related to gastrin and has no effect on its secretion. Similarly, glycogen synthase and hexokinase, which play regulatory roles in carbohydrate metabolism, do not affect gastrin secretion.

Another steroid hormone, progesterone, also does not play a role in the regulation of gastrin secretion. Understanding the effects of hormones and enzymes on gastrin secretion can help in the development of targeted treatments for gastrointestinal disorders.

Giardia Lamblia and its Treatment

Giardia lamblia is a common cause of traveller’s diarrhoea and intestinal malabsorption, along with E. coli. The most effective treatment for this condition is metronidazole. However, detecting cysts and oocysts in stool microscopy is laborious and lacks sensitivity. The current test of choice is the detection of antigens on the surface of the organisms in the stool specimen. A single stool examination can identify about 50% of cases, while three stool samples can identify about 90%. It is important to note that blood loss is not a feature of this condition. HUS, on the other hand, may be caused by E. coli 0157 infection, but not giardiasis.

Liver Tumours: Types, Risk Factors, and Diagnostic Methods

Liver tumours are abnormal growths that develop in the liver. The most common primary liver tumour is hepatocellular carcinoma (HCC), which is often associated with hepatitis B infection, cirrhosis, male gender, and increasing age. Chronic hepatitis B is the major risk factor worldwide, while hepatitis C is the major risk factor in Europe. Patients with underlying cirrhosis may present with decompensation of liver disease, such as ascites, jaundice, worsening liver function tests, and variceal haemorrhage. Examination may reveal hepatomegaly or a right hypochondrial mass. Vascularity of the tumour may result in an audible bruit on auscultation.

Diagnostic methods for liver tumours include increased α-fetoprotein, which is produced by 60% of HCCs. Ultrasound scanning will reveal focal lesions and may also show involvement of the portal vein. Helical triple-phase computed tomography (CT) scanning will identify HCC due to its hypervascular nature. Alternatively, magnetic resonance imaging (MRI) may be used.

Other types of liver tumours include fibrosarcoma, which is an extremely rare primary tumour of the liver, cholangiocarcinoma, which are usually adenocarcinomas and are the second most common primary tumour of the hepatobiliary system, affecting biliary ducts, hepatoblastoma, which is a liver tumour that typically presents in childhood, in the first 3 years of life, and leiomyosarcoma, which is another rare primary tumour of the liver. Leiomyosarcoma is thought to affect women more than men and typically seems to present later in life, in the fifth and sixth decades of life. However, greater understanding of the epidemiology of these rare tumours is required.

Diagnosing and Managing Complications of ERCP: A Case Study

A patient presents with abdominal pain, hypocalcaemia, and a pleural effusion several hours after undergoing an ERCP. The most likely diagnosis is pancreatitis, a known complication of the procedure. Immediate management includes confirming the diagnosis and severity of pancreatitis, aggressive intravenous fluid resuscitation, oxygen, and adequate analgesia. Severe cases may require transfer to intensive care. Intestinal and biliary perforation are unlikely causes, as they would have presented with immediate post-operative pain. A reaction to contrast would have occurred during the procedure. Another possible complication is ascending cholangitis, which presents with fever, jaundice, and abdominal pain, but is unlikely to cause hypocalcaemia or a pleural effusion. It is important to promptly diagnose and manage complications of ERCP to prevent severe complications and improve patient outcomes.

Differentiating Autoimmune Liver Disease: Antibody Tests

When a patient presents with abnormal liver function tests and a young age, autoimmune liver disease is a possible diagnosis. To confirm this, the most specific antibody test is for anti-smooth muscle antibodies, which are positive in about 80% of patients with autoimmune liver disease.

On the other hand, anti-mitochondrial antibodies are the hallmark of primary biliary cholangitis, with over 95% of patients being subtype M2 positive. Hepatitis A IgM antibodies are elevated in patients with acute hepatitis A infection, but not in autoimmune liver disease.

While raised anti-nuclear antibodies (ANAs) are seen in many autoimmune conditions, they are not very specific for autoimmune hepatitis. Positive ANAs are also seen in other diseases like systemic sclerosis, rheumatoid arthritis, and Sjögren syndrome. Similarly, anti-Smith antibodies are seen in about 20% of patients with systemic lupus erythematosus but are not specific for autoimmune liver disease.

In conclusion, antibody tests play a crucial role in differentiating autoimmune liver disease from other liver conditions.

Diuretics for Ascites in Liver Cirrhosis: Mechanisms and Options

Ascites is a common complication of liver cirrhosis, caused by both Na/water retention and portal hypertension. Spironolactone, an aldosterone antagonist, is the first-line diuretic for ascites in liver cirrhosis. It promotes natriuresis and diuresis, while also preventing hypokalaemia and subsequent hepatic encephalopathy. Furosemide, a loop diuretic, can be used as an adjunct or second-line therapy. Bumetanide and amiloride are alternatives, but less preferred. Acetazolamide and thiazide diuretics are not recommended. Common side-effects of diuretics include electrolyte imbalances and renal impairment. Careful monitoring is necessary to ensure safe and effective treatment.

The Hepatic Arteries and Their Branches

The liver is a vital organ that requires a constant supply of oxygen and nutrients. This is provided by the hepatic arteries and their branches. Here are some important branches of the hepatic arteries:

1. Right Hepatic Artery: This artery supplies the right side of the liver and is the main branch of the hepatic artery proper. It usually gives rise to the cystic artery, which supplies the gallbladder.

2. Gastroduodenal Artery: This artery is a branch of the common hepatic artery and supplies the pylorus of the stomach and the proximal duodenum.

3. Right Gastric Artery: This artery is a branch of the hepatic artery proper and supplies the lesser curvature of the stomach.

4. Hepatic Proper Artery: This artery is a branch of the common hepatic artery and divides into the right and left hepatic arteries. These arteries supply the right and left sides of the liver, respectively.

5. Left Hepatic Artery: This artery is a branch of the hepatic artery proper and supplies the left side of the liver.

In summary, the hepatic arteries and their branches play a crucial role in maintaining the health and function of the liver.

Causes of Hyperuricaemia: Understanding the Relationship between Gastrointestinal Bleeding and Urea Production

Hyperuricaemia, or elevated levels of uric acid in the blood, can be caused by various medical conditions. One of the factors that contribute to this condition is gastrointestinal bleeding, particularly in the upper part of the digestive system. When there is bleeding in the upper gastrointestinal tract, such as in cases of gastric ulcer, the blood that is excreted undergoes digestion as it passes through the small intestine. This results in an increased production of urea, a by-product of blood digestion, which is then absorbed into the bloodstream. However, reduced renal perfusion in patients with upper gastrointestinal bleeding can further exacerbate the levels of urea in the blood, as excretion becomes less effective.

It is important to note that not all types of gastrointestinal bleeding are associated with hyperuricaemia. Lower gastrointestinal bleeding, such as in cases of diverticular disease, does not cause a rise in urea levels. This is because blood released in the lumen of the large bowel does not undergo the same amount of digestion as it does in the small intestine. Instead, the large bowel primarily functions to reabsorb water and sodium.

Other medical conditions, such as intracranial haemorrhage and ulcerative colitis, are not directly linked to hyperuricaemia. However, significant bleeding in any part of the body can indirectly cause this condition by leading to kidney hypoperfusion and pre-renal acute kidney failure.

In summary, understanding the relationship between gastrointestinal bleeding and urea production can help in identifying the causes of hyperuricaemia. While upper gastrointestinal bleeding can lead to elevated levels of urea in the blood, lower gastrointestinal bleeding and other medical conditions may not have the same effect.

Autoimmune Liver Diseases: Differentiating PBC, PSC, and AIH

Autoimmune liver diseases, including primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH), can present with non-specific symptoms and insidious onset. However, certain demographic and serological markers can help differentiate between them.

PBC is characterized by chronic granulomatous inflammation of small intrahepatic bile ducts, leading to progressive cholestasis, cirrhosis, and portal hypertension. It is often diagnosed incidentally or presents with lethargy and pruritus. AMA M2 subtype positivity is highly specific for PBC, and treatment involves cholestyramine for itching and ursodeoxycholic acid. Liver transplantation is the only curative treatment.

PSC is a disorder of unknown etiology characterized by non-malignant, non-bacterial inflammation, fibrosis, and strictures of the intra- and extrahepatic biliary tree. It is more common in men and frequently found in patients with ulcerative colitis. AMA is negative, and diagnosis is based on MRCP or ERCP showing a characteristic beaded appearance of the biliary tree.

AIH is a disorder of unknown cause characterized by autoantibodies directed against hepatocyte surface antigens. It can present acutely with signs of fulminant autoimmune disease or insidiously. There are three subtypes with slightly different demographic distributions and prognoses, and serological markers such as ASMA, anti-LKM, and anti-soluble liver antigen antibodies can help differentiate them.

A hepatitis screen is negative in this case, ruling out hepatitis C. A pancreatic head tumor would present with markedly elevated bilirubin and a normal autoimmune screen.

The Origin of Hepatocytes: Understanding the Different Germ Layers

Hepatocytes are a type of cell found in the liver that play a crucial role in metabolism and detoxification. Understanding their origin can provide insight into various liver diseases and conditions.

Endoderm is the germ layer from which hepatocytes differentiate during embryonic development. Mallory bodies, intracytoplasmic inclusions seen in injured hepatocytes, are derived from cytokeratin, an intermediate cytoskeletal filament unique to epithelial cells of ectodermal or endodermal origin.

While hepatocytes and bile ducts are endodermal in origin, hepatic blood vessels and Kupffer cells (hepatic macrophages) are mesodermal in origin.

Spider angioma, palmar erythema, gynaecomastia, and dilation of the superficial abdominal veins are signs of cirrhosis or irreversible liver injury. Bridging fibrosis extending between the adjacent portal systems in the liver is the precursor of cirrhosis.

It is important to note that hepatocytes are not derived from ectoderm or neural crest cells. The yolk sac gives rise to primordial germ cells that migrate to the developing gonads.

Understanding the origin of hepatocytes and their relationship to different germ layers can aid in the diagnosis and treatment of liver diseases.

Histological Diagnoses of Gastric Conditions

Gastric lymphoma is often caused by chronic infection with H. pylori, and eradicating the infection can be curative. If not, chemotherapy is the first-line treatment. Other risk factors include HIV infection and long-term immunosuppressive therapy. In contrast, H. pylori gastritis is diagnosed through histological examination, which reveals lymphocytes and may indicate gastric lymphoma. Gastric ulcers are characterized by inflammation, necrosis, fibrinoid tissue, or granulation tissue on histology. Gastric carcinoma is identified through adenocarcinoma of diffuse or intestinal type, with higher grades exhibiting poorly formed tubules, intracellular mucous, and signet ring cells. Finally, alcoholic gastritis is diagnosed through histology as neutrophils in the epithelium above the basement membrane.

Management of Upper Gastrointestinal Bleeding: Endoscopy, Laparotomy, Sengstaken-Blakemore Tube, and IV Antibiotics

In cases of upper gastrointestinal bleeding, prompt and appropriate management is crucial. For patients with severe haematemesis and haemodynamic instability, immediate resuscitation and endoscopy are recommended by the National Institute for Health and Care Excellence (NICE) guidelines. Crossmatching blood for potential transfusion is also necessary. Urgent endoscopy within 24 hours of admission is advised for patients with smaller haematemesis who are haemodynamically stable.

Laparotomy is not necessary unless the bleeding is life-threatening and cannot be contained despite resuscitation or transfusion, medical or endoscopic therapy fails, or the patient has a high Rockall score or re-bleeding. The insertion of a Sengstaken-Blakemore tube may be considered for haematemesis from oesophageal varices, but endoscopy remains the primary diagnostic and therapeutic tool.

Prophylactic antibiotics are recommended for patients with suspected or confirmed variceal bleeding at endoscopy. However, arranging for a psychiatric consult is not appropriate in the acute phase of management, as the patient requires immediate treatment and resuscitation.