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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.
• 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.
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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.
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.
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.
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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.
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.
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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
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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).
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).
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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.
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.
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Pathology - Colorectal polyps
Hyperplastic polyps are prevalent, predominantly found in the distal colon. • Typically little lesions, less than 1 cm in size, located on the apex of a mucosal fold. Microscopically, they consist of crypts that are dilated and serrated in the superficial region and constricted at the base. • Benign lesions devoid of any potential for development to malignancy. Adenomatous polyps • Prevalent polyps that can manifest throughout the large intestine. • They predominantly manifest sporadically, although are also linked to familial adenomatous polyposis (FAP).
Familial Adenomatous Polyposis (FAP) is a hereditary disorder characterized by the proliferation of many adenomas throughout the colon at an early age, leading to the unavoidable onset of colorectal cancer in the absence of preventive colectomy.
• Neoplastic polyps that contain prevalent mutations of APC, KRAS, and TP53. The polyps exhibit dysplastic glands, characterized by epithelial cells with stratified hyperchromatic nuclei, arranged in intricate tubules or finger-like villous extensions. The dysplasia is classified as low grade or high grade based on the extent of cytological and architectural abnormalities. Approximately 10% of adenomas progress to cancer. The probability of malignant transformation increases with larger polyps, high-grade dysplasia, and a villous architecture.
Sessile serrated adenomas • Recently identified polyps that are often greater than 1 cm and are more frequently located in the right colon. • Genetically, they typically possess mutations in mismatch repair genes. • Microscopically, they exhibit significantly dilated serrated crypts that are broadened at their base. • Correlated with a heightened risk of subsequent colorectal cancer.
Inflammatory polyps • Delicate filiform lesions arise subsequent to any mucosal injury, frequently observed in individuals with inflammatory bowel illness. • Microscopically, they are enveloped by mucosa on both sides, with minimal submucosal tissue present.
Mucosal prolapse • Prolapsed mucosal fragments manifesting as polypoid projections. • May manifest at any location within the large intestine, but is typically observed on the anterior rectal wall or in conjunction with diverticular illness. • May ulcerate and resemble colorectal malignancy. • Microscopically, they have deformed, angulated crypts embedded inside a lamina propria that contains bundles of smooth muscle.
Benign fibroblastic polyps are typically discovered during screening colonoscopy in adults. They appear as bland spindle cell growth in the lamina propria under a microscope. Immunohistochemistry analysis does not reveal a distinct differentiation line for spindle cells.
Leiomyomas are benign smooth muscle tumors that originate from the muscularis mucosae. They are often tiny polyps seen in the distal large bowel and exhibit bland smooth muscle cell bundles under the microscope.
Juvenile polyps • The most frequent colonic polyp in children. • Identified as hamartomatous. • Microscopically, they have dilated and disordered colonic glands in an oedematous stroma. Multiple juvenile polyps may indicate juvenile polyposis, an autosomal dominant disorder caused by germline mutations in SMAD4 or BMPR1A.
Hyperplastic polyps are prevalent, predominantly found in the distal colon. • Typically little lesions, less than 1 cm in size, located on the apex of a mucosal fold. Microscopically, they consist of crypts that are dilated and serrated in the superficial region and constricted at the base. • Benign lesions devoid of any potential for development to malignancy. Adenomatous polyps • Prevalent polyps that can manifest throughout the large intestine. • They predominantly manifest sporadically, although are also linked to familial adenomatous polyposis (FAP).
Familial Adenomatous Polyposis (FAP) is a hereditary disorder characterized by the proliferation of many adenomas throughout the colon at an early age, leading to the unavoidable onset of colorectal cancer in the absence of preventive colectomy.
• Neoplastic polyps that contain prevalent mutations of APC, KRAS, and TP53. The polyps exhibit dysplastic glands, characterized by epithelial cells with stratified hyperchromatic nuclei, arranged in intricate tubules or finger-like villous extensions. The dysplasia is classified as low grade or high grade based on the extent of cytological and architectural abnormalities. Approximately 10% of adenomas progress to cancer. The probability of malignant transformation increases with larger polyps, high-grade dysplasia, and a villous architecture.
Sessile serrated adenomas • Recently identified polyps that are often greater than 1 cm and are more frequently located in the right colon. • Genetically, they typically possess mutations in mismatch repair genes. • Microscopically, they exhibit significantly dilated serrated crypts that are broadened at their base. • Correlated with a heightened risk of subsequent colorectal cancer.
Inflammatory polyps • Delicate filiform lesions arise subsequent to any mucosal injury, frequently observed in individuals with inflammatory bowel illness. • Microscopically, they are enveloped by mucosa on both sides, with minimal submucosal tissue present.
Mucosal prolapse • Prolapsed mucosal fragments manifesting as polypoid projections. • May manifest at any location within the large intestine, but is typically observed on the anterior rectal wall or in conjunction with diverticular illness. • May ulcerate and resemble colorectal malignancy. • Microscopically, they have deformed, angulated crypts embedded inside a lamina propria that contains bundles of smooth muscle.
Benign fibroblastic polyps are typically discovered during screening colonoscopy in adults. They appear as bland spindle cell growth in the lamina propria under a microscope. Immunohistochemistry analysis does not reveal a distinct differentiation line for spindle cells.
Leiomyomas are benign smooth muscle tumors that originate from the muscularis mucosae. They are often tiny polyps seen in the distal large bowel and exhibit bland smooth muscle cell bundles under the microscope.
Juvenile polyps • The most frequent colonic polyp in children. • Identified as hamartomatous. • Microscopically, they have dilated and disordered colonic glands in an oedematous stroma. Multiple juvenile polyps may indicate juvenile polyposis, an autosomal dominant disorder caused by germline mutations in SMAD4 or BMPR1A.
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Pathology - Microscopic colitis
Definition • A chronic variant of colitis marked by persistent watery diarrhea, normal or almost normal colonoscopy findings, and microscopic indications of colonic inflammation. Categories Two forms are identified: lymphocytic colitis and collagenous colitis. Lymphocytic colitis has an incidence of 3 cases per 100,000 individuals.
• Equal incidence of sex.
The average age of onset is 50 years
. • Significant correlation with celiac disease. Mucosal biopsy results reveal an elevated quantity of plasma cells in the lamina propria and an increased presence of intraepithelial lymphocytes.
• The majority of patients exhibit a positive response to pharmacological treatment. Collagenous colitis • Incidence of 1 to 2 per 100,000 individuals. • Notable preference for women
The average age of onset is 60 years.
• Correlation between NSAIDs and celiac disease. Mucosal biopsy findings reveal subepithelial collagen deposition, an elevated count of plasma cells in the lamina propria, and an increase in intraepithelial lymphocytes. • The majority of patients exhibit a positive response to pharmacological treatment.
Definition • A chronic variant of colitis marked by persistent watery diarrhea, normal or almost normal colonoscopy findings, and microscopic indications of colonic inflammation. Categories Two forms are identified: lymphocytic colitis and collagenous colitis. Lymphocytic colitis has an incidence of 3 cases per 100,000 individuals.
• Equal incidence of sex.
The average age of onset is 50 years
. • Significant correlation with celiac disease. Mucosal biopsy results reveal an elevated quantity of plasma cells in the lamina propria and an increased presence of intraepithelial lymphocytes.
• The majority of patients exhibit a positive response to pharmacological treatment. Collagenous colitis • Incidence of 1 to 2 per 100,000 individuals. • Notable preference for women
The average age of onset is 60 years.
• Correlation between NSAIDs and celiac disease. Mucosal biopsy findings reveal subepithelial collagen deposition, an elevated count of plasma cells in the lamina propria, and an increase in intraepithelial lymphocytes. • The majority of patients exhibit a positive response to pharmacological treatment.
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Pathology – Ulcerative Colitis
Ulcerative colitis is an idiopathic inflammatory bowel illness defined by inflammation confined to the mucosa of the large intestine, invariably involving the rectum and extending proximally in a continuous manner across a variable distance.
Epidemiology: Rare occurrence. • Significant occurrence between the ages of 15 and 25.
Aetiology and Pathogenesis • Believed to result from an aberrant mucosal immune response to luminal microorganisms. The genetic association is less robust than that of Crohn's disease. • Smoking seems to reduce the risk of ulcerative colitis (UC). • An atypical yet frequently validated observation is the preventive influence of appendectomy on the later onset of ulcerative colitis (UC).
Presentation • Recurrent episodes of hematochezia, frequently accompanied by urgency and tenesmus.
Macroscopy • Erythematous mucosa exhibiting a friable, degraded surface accompanied by hemorrhage. Inflamed mucosa may develop polypoid projections (inflammatory polyps). The disease invariably affects the rectum and extends continually to involve a varying extent of the colon.
Histopathology • Biopsies reveal widespread mucosal inflammation accompanied by cryptitis and the production of crypt abscesses. Inflammation is typically more pronounced distally. Resection specimens exhibit widespread inflammation confined to the mucosal layer. Inflammatory polyps may be present. In cases of severe acute ulcerative colitis, inflammation may extend into the submucosa or muscular layers; however, the mucosal layer remains the site of most inflammation.
Prognosis: Generally favorable with intervention. • Elevated risk of colorectal cancer necessitates the recommendation of surveillance colonoscopy several years post-diagnosis. Extragastrointestinal manifestations encompass enteropathic arthropathy, primary sclerosing cholangitis?erythema nodosum,pyoderma gangrenosum,uveitis, and AA amyloidosis.
