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Pathology - Primary sclerosing cholangitis Definition: A chronic hepatic condition marked by inflammation and fibrosis inside the biliary tree. The entire biliary tree is typically involved; but, in some instances, just the small interlobular bile ducts are impacted, known as small duct primary sclerosing cholangitis (PSC). Epidemiology • Rare occurrence. • Primarily observed in young males with ulcerative colitis (about 70% of patients with primary sclerosing cholangitis also have ulcerative colitis). Aetiology • Unknown, though a genetic association with specific HLA types exists. Pathogenesis: Chronic biliary inflammation leads to fibrotic scarring that constricts the afflicted bile ducts. Obstruction in the biliary system results in gradual fibrosis of the liver, culminating in cirrhosis. Biliary stasis additionally facilitates infection and the production of stones. Presentation • Typically asymptomatic in first stages, but frequently detected through high alkaline phosphatase values in patients with known ulcerative colitis (UC). Radiology • The presence of strictures and dilations in the biliary tree observed on imaging is strongly indicative of primary sclerosing cholangitis (PSC). Macroscopy • Initial PSC typically results in no observable macroscopic alterations. Progressive illness results in a cirrhotic liver with bile stains. Fibrotic biliary strictures may be evident in the principal bile ducts. Histopathology • Explanted liver specimens exhibit fibrosis and inflammation in the major bile ducts, accompanied by thickened bile and calculi. A biliary pattern of cirrhosis is characterized by huge, uneven, jigsaw-like nodules of hepatocytes. Liver biopsy results exhibit varied features based on the biopsy location. If the biopsy is obtained from a region not impacted by the underlying disease, however distal to a significant duct stricture, the liver exhibits characteristics of duct obstruction (i.e., portal edema accompanied by bile ductule growth). If the biopsy is obtained from a region impacted by PSC, medium-sized bile ducts have periductal edema and concentric fibrosis, while small bile ducts are frequently entirely absent. Prognosis: Progressive hepatic illness ultimately resulting in cirrhosis. Two patients are at elevated risk for bile duct cancer, which occurs in around 20% of cases and is associated with a dismal prognosis. 
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Pathology - Primary biliary cirrhosis Definition: A chronic liver disease with autoimmune destruction of tiny intrahepatic bile ducts and anti-mitochondrial antibodies. Epidemiology • Uncommon. • Most common in middle-aged women and linked to other autoimmune disorders. The cause is unknown, but infections with organisms that resemble antigens on the biliary epithelium may be a contributing factor. Pathogenesis: • Identified as an autoimmune disease when the immune system reacts abnormally to the biliary epithelium. Early stages of the disease may be asymptomatic, but high alkaline phosphatase values may indicate a diagnosis. Patients may experience weariness or pruritus owing to bile salt buildup. More than 95% of cases have anti-mitochondrial antibodies targeting a component of the pyruvate dehydrogenase complex in the inner mitochondrial matrix. Early disease exhibits few macroscopic changes in the liver, while advanced disease causes cirrhosis and bile staining. Histopathology: • The earliest feature is the invasion and destruction of interlobular bile ducts by lymphocytes and macrophages, known as a 'fluid duct lesion'. Macrophages may form clusters and create granulomas. As the condition advances, it causes inflammation and loss of hepatocytes along the portal tract margins (interface hepatitis), leading to periportal fibrosis, portal-portal bridging, and cirrhosis. Prognosis: Gradual progression to cirrhosis over 15-20 years. Ursodeoxycholic acid therapy slows the progression.  Pathology - Autoimmune hepatitis Definition: A hepatic disorder resulting from an autoimmune reaction directed at the liver. Epidemiology: Rare occurrence. • Generally impacts middle-aged women. Aetiology • Definitively unknown, yet believed to be precipitated by infection or pharmacological agents. Pathogenesis • Contemporary understanding posits that liver injury resulting from an infection or pharmacological agent leads genetically predisposed individuals to develop sensitization to their liver, subsequently eliciting an immune response against it. Presentation • The majority of cases are asymptomatic during the initial stages, although may be identified accidentally through irregularities in liver function testing. • Certain patients exhibit delayed presentation with manifestations of chronic liver disease or end-stage cirrhosis. Approximately 25% of cases manifest abruptly with an episode of severe hepatitis accompanied by jaundice. Occasionally, significant acute liver injury manifests, resulting in abrupt hepatic failure in the patient. Serology • Serum IgG levels are typically elevated. • Various autoantibodies may be detected, including anti-nuclear antibodies, liver-kidney microsomal antibodies, and smooth muscle antibodies. Macroscopy • Limited macroscopic alterations, observed mostly in patients with cirrhosis or in instances of severe acute hepatitis characterized by extensive hepatocyte necrosis. Histopathology • Chronic hepatitis exhibits a pattern of injury characterized by portal inflammation, interface hepatitis, lobular inflammation, and variable fibrosis. • Unlike chronic viral hepatitis, interface hepatitis and lobular inflammation are typically more pronounced. Plasma cells are frequently a prominent element of the inflammatory cell infiltrate. Prognosis • The majority of cases exhibit favorable responses to immunosuppressive therapy. • The long-term prognosis is contingent upon the degree of fibrosis present in the liver at the time of diagnosis.  Pathology – Non Alcoholic Fatty Liver Disease • The metabolic syndrome's hepatic manifestation, which includes hyperlipidemia, poor glucose tolerance, and central obesity. Simple steatosis (fatty liver), non-alcoholic steatohepatitis (NASH), and cirrhosis are among the disorders that fall under the umbrella of non-alcoholic fatty liver disease (NAFLD). Epidemiology: Due to increased obesity rates, this condition is very frequent and is becoming more common. • The most frequent reason for abnormal liver function tests these days. • A large number of cirrhosis cases that were previously believed to be cryptogenic are now believed to be end-stage NAFLD. The cause • The most frequent correlations are between diabetes and obesity. • Also connected to parenteral feeding and some medications. The pathogenesis • Obesity and insulin resistance appear to be the main contributing factors. • Hepatocyte damage and fat storage are brought on by insulin resistance. • Inflammation in reaction to hepatocyte damage causes fibrosis and, in certain cases, cirrhosis. Presentation: Abnormal liver function tests are used to identify the majority of asymptomatic cases. • Cirrhosis-related problems can occasionally be seen in patients. The macroscopy • Cirrhotic livers are diffusely nodular; the liver is swollen, squishy, and greasy. The study of histopathology • NASH exhibits steatosis together with the presence of enlarged hepatocytes and neutrophils; steatosis is characterized by the buildup of fat within hepatocytes without discernible inflammatory activity. Depending on the disease's stage, there may be variable fibrosis. Keep in mind that these histology results are nearly the same as those observed in alcoholic liver disease. It can occasionally be challenging to rule out alcoholic liver disease since many individuals significantly underreport their alcohol consumption. The outlook • There is extremely little chance that steatosis may develop into chronic liver disease. • About 10–15% of NASH cases progress to cirrhosis over the course of 8 years. • Compared to individuals with cirrhosis brought on by alcoholic liver disease, those with cirrhosis brought on by nonalcoholic fatty liver disease typically have a higher survival rate.  Pathology – Alcoholic liver illness Definition: Liver disease brought on by heavy alcohol use. There are three recognized disease patterns: cirrhosis, alcoholic steatohepatitis (ASH), and steatosis. The study of epidemiology • Very prevalent. The pathogenesis • High amounts of NADH produced by the liver's breakdown of alcohol promote the synthesis of fatty acids and triglycerides, which results in steatosis. • In certain people, oxidative stress brought on by alcohol metabolism results in hepatocyte damage and necroinflammatory response (ASH). • Liver fibrosis, which can develop into cirrhosis, is brought on by persistent necroinflammatory activity. Display Although mild ASH and steatosis are typically asymptomatic, they are frequently the source of modestly abnormal liver function tests. • After binge drinking, severe alcoholic hepatitis results in fever, malaise, and a substantial increase in liver function tests. If there is a significant decline in liver function, jaundice may develop. • Alcoholic cirrhosis manifests as cirrhosis complications, such as ruptured oesophageal varices or ascites. The macroscopy Steatosis results in a mushy, greasy, swollen liver. Because of cirrhosis, the liver develops diffuse nodules, and ASH can result in a firm texture. The study of histopathology • Hepatocytes with steatosis exhibit enormous fat droplets that push the nucleus to one side (macrovesicular steatosis). • Inflammatory infiltrate rich in neutrophils and Mallory's hyaline, which are clusters of dense pink material, may be present in ASH's enlarged hepatocytes. ASH usually causes pericellular fibrosis, which eventually develops into fibrous bridges. • Nodules of regenerating hepatocytes encircled by fibrous bands diffusely replace the liver in cirrhosis. Hepatitis and background steatosis might not be present. Prognosis: If alcohol use stops, simple steatosis can be completely reversed. • Alcoholic hepatitis can either go away when alcohol use stops or it can develop into cirrhosis and fibrosis. • The 5-year survival rate for alcoholic cirrhosis is only 50%, which indicates a bad prognosis.  Pathology – Chronic Viral Hepatitis Definition of chronic viral hepatitis: Hepatitis B or C infection of the liver that lasts longer than six months. The study of epidemiology • Approximately 3% of people globally are afflicted with chronic HCV. • Chronic HBV has greater regional variance, with infection rates as high as 15% in parts of Asia and China and being less common in western nations. Immunopathogenesis • When the immune system is unable to eradicate the virus after infection, chronic viral hepatitis results. About 10% of individuals do not recover from an HBV infection. About 90% of individuals are unable to recover from an HCV infection. Presentation: Usually asymptomatic, it is discovered by chance when liver function tests show abnormalities. • Many patients do not show up until they have ascites and severe cirrhosis. The study of serology • Serum HBsAg and anti-HBcAg antibodies are indicators of chronic HBV. • Serum anti-HCV antibodies and HCV RNA detected by polymerase chain reaction (PCR) are indicators of chronic HCV. The macroscopy • Fibrosis may cause the liver to feel a little firm. The study of histopathology • The majority of the cells that make up portal inflammation are lymphocytes. • The extension of the portal inflammatory infiltrate into the hepatocytes at the limiting plate linked to hepatocyte deterioration is known as interface hepatitis (also known as "piecemeal necrosis"). • In contrast to acute viral hepatitis, when it is the predominant site, lobular inflammation is typically localized and modest in chronic viral hepatitis. • One indicator of the disease's severity is fibrosis. Cirrhosis is the result of extensive bridging fibrosis through the liver. Keep in mind that chronic liver injury can result from a variety of reasons and manifest all of these alterations. However, there may be indications of a viral aetiology, such as portal lymphoid aggregates in hepatitis C and "ground glass" hepatocytes in hepatitis B. The degree of fibrosis found during a liver biopsy is a major determinant of prognosis. • In hepatitis C, viral genotype is also significant. • Hepatocellular carcinoma is more likely, especially in cas  Pathology - Acute viral hepatitis Definition: Infection of the liver caused by hepatitis A, B, C, or E, persisting for six months or less. Epidemiology Hepatitis A virus (HAV) and hepatitis C virus (HCV) are prevalent globally. Hepatitis B virus (HBV) is prevalent in certain regions of Asia and China. • The Hepatitis E virus (HEV) is prevalent in Southeast Asia, India, and Central America. • Individuals of all ages may be impacted. Virology Hepatitis A virus (HAV) is a positive-sense, single-stranded RNA picornavirus that is spread orally through fecal contamination of food or water. HBV is a partly double-stranded DNA hepadnavirus spread via contaminated needles, sexual contact, or vertically from an infected mother to her offspring. HCV is a positive-sense, single-stranded RNA hepacivirus spread by contaminated needles, primarily through intravenous drug use. HEV is a positive-sense, single-stranded RNA hepevirus spread orally through fecal contamination of food or water. Immunopathogenesis • The viruses localize within the liver. Following a varied incubation period, a specific T-lymphocyte response to the virus is elicited. The necroinflammatory activity in the liver induces an episode of acute hepatitis. Presentation • Numerous cases are clinically asymptomatic or result in a non-specific, influenza-like illness. • Clinically evident instances induce nausea, vomiting, malaise, and jaundice. Serology • The detection of serum anti-hepatitis IgM antibodies confirms a recent infection. Macroscopy • The liver may exhibit swelling and discoloration due to bile accumulation. Histopathology: Liver lobules exhibit infiltration by mononuclear inflammatory cells. Hepatocyte damage is visually characterized by swelling ('ballooning') or shrinking and pyknosis (acidophil bodies). • Severe instances exhibit confluent regions of hepatocyte necrosis and parenchymal collapse. It is important to note that these histological alterations are not exclusive to viral hepatitis and may also occur in acute liver injury from various other etiologies. Prognosis • Acute HAV does not advance to chronic infection. Approximately 10% of acute HBV cases advance to chronic infection. Approximately 90% of acute HCV cases advance to chronic infection.  Pathology - Anal pathology Hemorrhoids • Abnormally expanded and bulging anal cushions. • Highly widespread. • Thought to arise from the disturbance of standard suspensory mechanisms caused by persistent straining during feces. • Causes pronounced red rectal bleeding and discomfort. • Microscopic analysis of removed hemorrhoids demonstrates significantly dilated blood vessels with overlying hyperplastic squamous epithelium. Anal tags are polypoid protrusions of the anal mucosa and submucosa. They are distinct from hemorrhoids, although they are occasionally misdiagnosed as such. • A microscopic structure comprising a fibrovascular core surrounded by squamous epithelium. The fibrovascular core lacks the typical ectatic vessels linked to hemorrhoids. Anal fissure: A rupture in the mucosal lining of the lower anal canal, commonly located posteriorly along the midline. The origin is unclear; however, chronic infection may lead to reduced mucosal flexibility, resulting in a tear with the passage of firm feces. • Typically presents with severe discomfort. Anorectal abscess • A purulent collection in the deep perianal tissue. • A consequence of infection in a deep anal gland. • Marked by perianal erythema, edema, and discomfort. Anorectal fistula: An abnormal epithelial-lined passage connecting the anal canal to the perianal skin. It usually develops from an infection in an anal gland that extends to the skin surface. Multiple perianal fistulas may also suggest Crohn's disease. Anal cancer is uncommon and frequently associated with HPV infection. The predominant kind is squamous cell carcinoma, which arises from areas of squamous dysplasia known as anal intraepithelial neoplasia (AIN).  Pathology - Diverticular Disease Definition: Colonic mucosa herniation through the big bowel's circular muscle layer. The great majority of instances occur in the sigmoid colon. Epidemiology • Extremely common. Mostly an illness of patients over the age of 60. A low-fiber, high-meat diet is the primary risk factor. Pathogenesis • Firm stools demand greater intraluminal pressure to propel. • High intraluminal pressure pushes pouches of colonic mucosa through a weak spot in the muscular layer, allowing blood vessels to nourish the mucosa. Presentation: Intermittent stomach pain, changed bowel habits, and iron deficiency anaemia. 2 These symptoms may closely resemble colorectal malignancy. • Acute diverticulitis causes considerable pain in the left iliac fossa. • Erosion of a big submucosal artery may result in significant rectal bleeding. During macroscopy, diverticula can be detected herniating between the sigmoid colon's taenia. • The circular muscle layer is thicker and has redundant mucosal folds that protrude into the lumen. • In acute diverticulitis, an inflamed mass may surround the diverticulum. • Diverticular strictures constrict the gut lumen, resembling stenosing cancer. Histopathology: Diverticula are found herniating through a thicker circular muscle layer. The diverticulum is separated from the pericolic fat by a thin layer of muscle. Acute diverticulitis is characterized by acute inflammation and pericolic abscess development. Prognosis: • Acute diverticulitis can lead to pericolic abscess formation, fistula formation, and free perforation. • Free perforation can result in widespread peritonitis, which can be deadly in frail elderly individuals.  Pathology - Colorectal carcinoma Definition: • A malignant epithelial tumor in the colon or rectum.Tumors that penetrate the muscularis mucosae into the submucosa are considered malignant at this site. In contrast, carcinomas at other sites just require a breach of the basement membrane directly beneath the epithelium to be classified as malignant. Epidemiology: • Third most frequent cancer in the UK, with a lifetime risk of 1 in 16 males and 1 in 20 women. • Second leading cause of cancer-related deaths. A diet high in animal fat and low in fiber, combined with a sedentary lifestyle, increases risk. Idiopathic inflammatory bowel illness (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) are also linked. Carcinogenesis: • Most cancers develop through a crypt focus (dysplasia in a single crypt), adenomatous polyp, or invasive carcinoma. • Common genetic aberrations include loss of APC, TP53, and SMAD4. • In some tumors, mismatch repair genes are inactivated, resulting in microsatellite instability. Symptoms include gastrointestinal changes, tenesmus, stomach pain, and iron deficiency anemia. Asymptomatic tumors can be detected by screening or surveillance programs. Macroscopy reveals that tumors typically develop as polypoid lumps in the gut lumen, with surface ulceration. Some tumors in the distal colon cause circumferential stenosing lesions. • The sliced surface shows a whitish tumor mass with poorly defined edges that penetrates the intestinal wall. • Mucinous carcinomas produce large pools of gelatinous material. Histopathology • Most cancers are adenocarcinomas, which are malignant epithelial tumors with glandular differentiation. • Well-differentiated tumors exhibit extensive tube formation, while poorly differentiated tumors exhibit little gland formation. • Tumors are typically moderately differentiated and include a high amount of necroinfiltrated detritus within glandular gaps, known as 'dirty' necrosis. Mucinous adenocarcinomas are characterized by significant mucin synthesis in around 10% of colonic and 30% of rectal tumors, resulting in malignant cells floating in huge pools of extracellular mucin. Prognosis: 5-year survival rate around 50%. • Prognostic markers for tumors include stage, vascular invasion, tumor differentiation, and surgical excision. National Health Service (NHS) bowel cancer screening program. • Provides screening every two years to men and women aged 60-69. • People above the age of 70 are not typically invited, but they can request screening. • Eligible patients receive a faecal occult blood test kit at home, with instructions on how to complete the test and send their sample to the nearest laboratory. • Approximately 2% of individuals have a positive result and are recommended to undergo a colonoscopy. • Of those, 50% have a normal colonoscopy, 40% have a polyp, and 10% have cancer. TNM 7 Pathological Staging of Colorectal Cancers Primary Tumor (T) pT1: The tumor invades the submucosa. pT2: The tumor invades the muscularis propria. In pT3, tumors penetrate the subserosa or non-peritonealized pericolic or perirectal tissues via the muscularis propria. pT4a: The tumor perforates the visceral peritoneum. pT4b: The tumour immediately invades another organ or structure. Regional lymph nodes. (N) pN0 indicates no regional lymph node metastasis. pN1a indicates metastases in one regional lymph node. pN1b refers to metastases in two or three regional lymph nodes. pN2a: metastases in 4-6 regional lymph nodes. pN2b: metastases in seven or more regional lymph nodes.  |
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