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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 – 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.
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.
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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.
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.
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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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Diagnostic Tests – Persantine Thallium
What Is Persantine Thallium Testing?
Persantine thallium testing is a type of pharmacologic stress test used to evaluate myocardial perfusion in patients who cannot perform adequate physical exercise. Instead of using a treadmill or bicycle to increase the heart’s oxygen demand, this test uses medication to mimic the physiologic effects of exercise. It is noninvasive and helps determine whether areas of the heart receive sufficient blood flow under conditions that simulate stress.
How Is the Test Performed?
The test involves two major components: Persantine (dipyridamole) and thallium imaging.
Persantine is a phosphodiesterase inhibitor that causes coronary artery vasodilation, increasing blood flow to healthy myocardium. Diseased or stenotic coronary arteries, however, do not dilate as effectively, creating a “steal phenomenon” in which more blood flows to normal areas and less to ischemic areas.
After Persantine is administered, thallium, a radioactive tracer, is injected. Normal cardiac muscle takes up thallium readily, whereas ischemic or infarcted areas absorb significantly less. Imaging with a gamma camera then reveals patterns of perfusion, highlighting areas of reduced blood flow.
When Should You Choose Persantine Thallium Testing?
Persantine thallium is the correct diagnostic choice when a patient cannot exercise adequately for a standard treadmill stress test—but still requires evaluation of possible ischemic heart disease. This includes individuals with orthopedic limitations, neurologic conditions, deconditioning, or severe physical frailty.
It is also useful in preoperative cardiac risk assessment for patients with chest pain, when there is uncertainty about whether the pain represents ischemia.
When Is Persantine Thallium the Wrong Answer?
This test should NOT be selected in patients with asthma, COPD, or emphysema, because Persantine can provoke bronchospasm and worsen respiratory symptoms.
Additionally, any form of stress testing—including pharmacologic testing—is contraindicated in cases of acute myocardial infarction or unstable angina, where stressing the heart is unsafe and inappropriate.
What Is the Alternative Choice?
If Persantine cannot be used—especially due to respiratory disease—the preferred alternative is a dobutamine stress echocardiogram. Dobutamine increases myocardial oxygen demand by raising heart rate and contractility, functioning as a safe pharmacologic stress agent for patients who cannot tolerate Persantine.
What Is the Most Accurate Diagnostic Test?
Regardless of the stress modality used, the single most accurate test of myocardial perfusion and coronary anatomy is coronary angiography. It provides direct visualization of the coronary vessels, allowing clinicians to identify and quantify stenoses with precision.
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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 - 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.
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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.
