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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.
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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 - 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.
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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Pathology - Crohn's disease
Definition: An idiopathic inflammatory bowel illness distinguished by multifocal regions of inflammation that can affect any segment of the gastrointestinal system.
Epidemiology • Rare. • Significant occurrence between the ages of 20 and 30 years.
Aetiology and Pathogenesis • Believed to result from an aberrant mucosal immune response to luminal bacteria in genetically predisposed individuals. Mutations in the CARD15 gene, which encodes an intracellular receptor for bacterial peptidoglycan components, have been linked to small intestinal Crohn's disease in Caucasian populations. • Smoking elevates the risk. A definitive infectious etiology remains unsubstantiated.
Presentation: • Crampy pain in the right iliac fossa accompanied by diarrhea, typically non-bloody. Fever, malaise, and weight reduction are prevalent symptoms.
Macroscopy • The disease typically affects the terminal ileum and colon. • The involved intestine exhibits thickening with infiltration of mesenteric fat surrounding the anti-mesenteric barrier, referred to as 'fat wrapping.' • Adhesions and fistulas may be observed between contiguous loops of bowel. • The mucosal surface exhibits linear ulcers and cobblestoning.
Histopathology- Mucosal biopsies exhibit diversity in inflammation both within a single biopsy and among many biopsies, which is a critical characteristic. This is usually exhibited by distinct regions of inflammation near histologically normal crypts. Surface erosions and ulcerations may be evident. Poorly formed granulomas may occur, but they are often rare. • Resection specimens: deep fissuring ulcers delineated by reasonably normal mucosa. Lymphoid aggregates are located in the submucosa and muscle layers. Granulomas of suboptimal formation may be observed.
Prognosis: • Characterized by a relapsing and remitting trajectory. • The majority of patients necessitate surgical intervention at some stage to alleviate symptoms resulting from obstruction or fistula formation. • Elevated risk of small and large bowel adenocarcinoma. Extragastrointestinal signs encompass enteropathic arthropathy,anterior uveitis, gallstones, erythema nodosum and pyoderma gangrenosum.
Definition: An idiopathic inflammatory bowel illness distinguished by multifocal regions of inflammation that can affect any segment of the gastrointestinal system.
Epidemiology • Rare. • Significant occurrence between the ages of 20 and 30 years.
Aetiology and Pathogenesis • Believed to result from an aberrant mucosal immune response to luminal bacteria in genetically predisposed individuals. Mutations in the CARD15 gene, which encodes an intracellular receptor for bacterial peptidoglycan components, have been linked to small intestinal Crohn's disease in Caucasian populations. • Smoking elevates the risk. A definitive infectious etiology remains unsubstantiated.
Presentation: • Crampy pain in the right iliac fossa accompanied by diarrhea, typically non-bloody. Fever, malaise, and weight reduction are prevalent symptoms.
Macroscopy • The disease typically affects the terminal ileum and colon. • The involved intestine exhibits thickening with infiltration of mesenteric fat surrounding the anti-mesenteric barrier, referred to as 'fat wrapping.' • Adhesions and fistulas may be observed between contiguous loops of bowel. • The mucosal surface exhibits linear ulcers and cobblestoning.
Histopathology- Mucosal biopsies exhibit diversity in inflammation both within a single biopsy and among many biopsies, which is a critical characteristic. This is usually exhibited by distinct regions of inflammation near histologically normal crypts. Surface erosions and ulcerations may be evident. Poorly formed granulomas may occur, but they are often rare. • Resection specimens: deep fissuring ulcers delineated by reasonably normal mucosa. Lymphoid aggregates are located in the submucosa and muscle layers. Granulomas of suboptimal formation may be observed.
Prognosis: • Characterized by a relapsing and remitting trajectory. • The majority of patients necessitate surgical intervention at some stage to alleviate symptoms resulting from obstruction or fistula formation. • Elevated risk of small and large bowel adenocarcinoma. Extragastrointestinal signs encompass enteropathic arthropathy,anterior uveitis, gallstones, erythema nodosum and pyoderma gangrenosum.
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Pathology - Acute appendicitis
Definition • An acute inflammatory condition of the appendix caused by blockage. Epidemiology: Peak incidence occurs between the ages of 5 and 15, although it can manifest at any age.
Aetiology • Considered to arise from the occlusion of the appendiceal lumen due to a faecolith, undigested food, or hypertrophied lymphoid tissue.
Pathogenesis: Obstruction of the appendiceal lumen results in a secondary infection within the mucosa, which then disseminates throughout the whole wall of the appendix.
Presentation: Right iliac fossa pain along with fever and malaise. • Numerous cases lack typical characteristics, potentially associated with the specific placement of the appendix within the individual.
Macroscopy • In initial situations where inflammation is restricted to the mucosal layer, the appendix may present as normal. • In advanced cases, the appendix exhibits dilation, and a fibrinopurulent discharge may be observed on the serosal surface.
Histopathology • Initial cases exhibit neutrophils within crypts (crypt abscesses) and erosion of the superficial epithelium. • Neutrophils subsequently infiltrate the lamina propria of the mucosa and accumulate within the lumen of the appendix. • Subsequent cases demonstrate the progression of the acute inflammatory response into the submucosa, muscularis propria, and serosa. Extensive necrosis of the muscularis propria may result in perforation.
Prognosis • The prognosis is favorable, contingent upon the timely execution of an appendectomy. Delayed treatment poses a danger of perforating the inflamed appendix, which may lead to complications such as intra-abdominal abscess formation or widespread peritonitis.
Definition • An acute inflammatory condition of the appendix caused by blockage. Epidemiology: Peak incidence occurs between the ages of 5 and 15, although it can manifest at any age.
Aetiology • Considered to arise from the occlusion of the appendiceal lumen due to a faecolith, undigested food, or hypertrophied lymphoid tissue.
Pathogenesis: Obstruction of the appendiceal lumen results in a secondary infection within the mucosa, which then disseminates throughout the whole wall of the appendix.
Presentation: Right iliac fossa pain along with fever and malaise. • Numerous cases lack typical characteristics, potentially associated with the specific placement of the appendix within the individual.
Macroscopy • In initial situations where inflammation is restricted to the mucosal layer, the appendix may present as normal. • In advanced cases, the appendix exhibits dilation, and a fibrinopurulent discharge may be observed on the serosal surface.
Histopathology • Initial cases exhibit neutrophils within crypts (crypt abscesses) and erosion of the superficial epithelium. • Neutrophils subsequently infiltrate the lamina propria of the mucosa and accumulate within the lumen of the appendix. • Subsequent cases demonstrate the progression of the acute inflammatory response into the submucosa, muscularis propria, and serosa. Extensive necrosis of the muscularis propria may result in perforation.
Prognosis • The prognosis is favorable, contingent upon the timely execution of an appendectomy. Delayed treatment poses a danger of perforating the inflamed appendix, which may lead to complications such as intra-abdominal abscess formation or widespread peritonitis.
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Pathology - Esophageal polyps and nodules
Squamous papilloma • An atypical lesion typically observed as a little white polyp in the distal esophagus during endoscopy. • While the association with human papillomavirus (HPV) infection has been hypothesized, the majority of investigations have failed to detect HPV material within these lesions.
Histological examination reveals non-descript squamous epithelium exhibiting papillary projections.
leiomyoma • Rare benign smooth muscle neoplasm originating from the muscular layers of the esophagus. • Typically manifests as a polypoid mass enveloped by mucosa, which may exhibit surface ulcers.
Histological examination reveals interwoven fascicles of benign smooth muscle cells.
Granular cell tumor • An infrequent neurological neoplasm that may arise throughout the gastrointestinal tract, predominantly in the tongue and esophagus. • A tiny firm mucosal nodule is present in the lower esophagus. •
Histological examination reveals clusters of large polygonal cells with prominent granular cytoplasm. • The majority are benign, while rare instances of malignancy have been documented.
Fibrovascular polyp • Uncommon oesophageal lesion that commonly manifests as dysphagia. • May attain a remarkably large size (up to 25 cm in length), perhaps resulting in regurgitation into the throat or oral cavity. • Endoscopically identifiable as a pedunculated lesion on an elongated stalk. • Histological examination reveals a polypoid lesion enveloped by squamous epithelium, with an underlying stromal core consisting of loose fibrous tissue, adipose tissue, and a conspicuous vascular network.
Squamous papilloma • An atypical lesion typically observed as a little white polyp in the distal esophagus during endoscopy. • While the association with human papillomavirus (HPV) infection has been hypothesized, the majority of investigations have failed to detect HPV material within these lesions.
Histological examination reveals non-descript squamous epithelium exhibiting papillary projections.
leiomyoma • Rare benign smooth muscle neoplasm originating from the muscular layers of the esophagus. • Typically manifests as a polypoid mass enveloped by mucosa, which may exhibit surface ulcers.
Histological examination reveals interwoven fascicles of benign smooth muscle cells.
Granular cell tumor • An infrequent neurological neoplasm that may arise throughout the gastrointestinal tract, predominantly in the tongue and esophagus. • A tiny firm mucosal nodule is present in the lower esophagus. •
Histological examination reveals clusters of large polygonal cells with prominent granular cytoplasm. • The majority are benign, while rare instances of malignancy have been documented.
Fibrovascular polyp • Uncommon oesophageal lesion that commonly manifests as dysphagia. • May attain a remarkably large size (up to 25 cm in length), perhaps resulting in regurgitation into the throat or oral cavity. • Endoscopically identifiable as a pedunculated lesion on an elongated stalk. • Histological examination reveals a polypoid lesion enveloped by squamous epithelium, with an underlying stromal core consisting of loose fibrous tissue, adipose tissue, and a conspicuous vascular network.
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Pathology - Gastritis
Acute hemorrhagic gastritis • Resulting from a sudden injury to the gastric hmucosa. Acute gastritis frequently results from a significant alcohol binge, although any acute medical condition that diminishes stomach blood flow may potentially induce it. • Endoscopy reveals many punctate erosions that exude blood. • Severe cases may result in substantial upper gastrointestinal hemorrhage. Histology reveals neutrophilic infiltration of the stomach mucosa accompanied by hemorrhage and mucosal necrosis. • Acute gastritis typically cures swiftly and without complications.
Chemical/reactive gastritis • Induced by any minor damage to the stomach mucosa. • Primarily observed in the antrum associated with bile reflux or non-steroidal anti-inflammatory medicines (NSAIDs). • Endoscopic examination reveals erythema of the stomach mucosa. • Histological analysis indicates vascular congestion, foveolar hyperplasia, and smooth muscle proliferation. Inflammation is negligible or nonexistent. Reactive gastritis typically resolves without complications upon removal of the causative agent.
Iron pill gastritis • Induced by the corrosive properties of consumed iron supplements. • Histological examination reveals acute inflammation accompanied by erosion or ulceration of the stomach mucosa. Yellow-brown iron pigment may be observed.
Helicobacter gastritis • A prevalent etiology of gastritis, typically antral-predominant. • Predominantly caused by Helicobacter (H.) pylori, a curved flagellated Gram-negative bacillus. H. heilmannii, characterized by its tighter coiling, constitutes less than 1% of instances. Histology reveals a substantial lymphoid inflammatory infiltrate in the lamina propria, accompanied by neutrophilic infiltration of the superficial mucosa. • The organisms can be identified with normal stains, but are more effectively visible with specific stains that accentuate the bacteria. In most instances, gastritis is resolved by eliminating the organism. • A minority of untreated instances may lead to complications such as peptic ulceration, gastric cancer, or gastric marginal zone B-cell lymphoma.
Autoimmune gastritis • Resulting from an autoimmune assault on parietal cells within the fundic glands. • Histological examination reveals infiltration of the mucosal tissue by lymphocytes and plasma cells. The infiltrate targets fundic glands, resulting in the loss of chief and parietal cells. Pyloric and intestinal metaplasia is prevalent. • Elevated risk of stomach neuroendocrine tumors and carcinoma. • Certain patients may also produce antibodies against intrinsic factor, resulting in vitamin B12 deficiency and megaloblastic anemia.
Acute hemorrhagic gastritis • Resulting from a sudden injury to the gastric hmucosa. Acute gastritis frequently results from a significant alcohol binge, although any acute medical condition that diminishes stomach blood flow may potentially induce it. • Endoscopy reveals many punctate erosions that exude blood. • Severe cases may result in substantial upper gastrointestinal hemorrhage. Histology reveals neutrophilic infiltration of the stomach mucosa accompanied by hemorrhage and mucosal necrosis. • Acute gastritis typically cures swiftly and without complications.
Chemical/reactive gastritis • Induced by any minor damage to the stomach mucosa. • Primarily observed in the antrum associated with bile reflux or non-steroidal anti-inflammatory medicines (NSAIDs). • Endoscopic examination reveals erythema of the stomach mucosa. • Histological analysis indicates vascular congestion, foveolar hyperplasia, and smooth muscle proliferation. Inflammation is negligible or nonexistent. Reactive gastritis typically resolves without complications upon removal of the causative agent.
Iron pill gastritis • Induced by the corrosive properties of consumed iron supplements. • Histological examination reveals acute inflammation accompanied by erosion or ulceration of the stomach mucosa. Yellow-brown iron pigment may be observed.
Helicobacter gastritis • A prevalent etiology of gastritis, typically antral-predominant. • Predominantly caused by Helicobacter (H.) pylori, a curved flagellated Gram-negative bacillus. H. heilmannii, characterized by its tighter coiling, constitutes less than 1% of instances. Histology reveals a substantial lymphoid inflammatory infiltrate in the lamina propria, accompanied by neutrophilic infiltration of the superficial mucosa. • The organisms can be identified with normal stains, but are more effectively visible with specific stains that accentuate the bacteria. In most instances, gastritis is resolved by eliminating the organism. • A minority of untreated instances may lead to complications such as peptic ulceration, gastric cancer, or gastric marginal zone B-cell lymphoma.
Autoimmune gastritis • Resulting from an autoimmune assault on parietal cells within the fundic glands. • Histological examination reveals infiltration of the mucosal tissue by lymphocytes and plasma cells. The infiltrate targets fundic glands, resulting in the loss of chief and parietal cells. Pyloric and intestinal metaplasia is prevalent. • Elevated risk of stomach neuroendocrine tumors and carcinoma. • Certain patients may also produce antibodies against intrinsic factor, resulting in vitamin B12 deficiency and megaloblastic anemia.
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Pathology - Oesophageal carcinoma
Definition • A malignant epithelial neoplasm originating in the oesophagus. • Two primary subtypes are identified: squamous cell carcinoma and adenocarcinoma.
Epidemiology • Both forms manifest at a median age of 65 years. • Oesophageal adenocarcinoma has garnered significant attention in developed nations due to its substantial and persistent increase in incidence over recent decades.
Aetiology • Significant tobacco and alcohol consumption is associated with squamous cell carcinoma. • Chronic gastro-oesophageal reflux disease resulting in Barrett’s oesophagus is the predominant precursor to adenocarcinoma. Carcinogenesis • Both forms commonly possess TP53 mutations.
Presentation: Dysphagia, retrosternal or epigastric discomfort, and weight loss. • By the time the majority of individuals seek medical attention, the tumor is typically in an advanced stage.
Macroscopy • Tumor mass in the esophagus may exhibit exophytic growth into the lumen or infiltrate the wall in a plaque-like manner. • Squamous cell carcinomas typically arise in the mid-esophagus, whereas adenocarcinomas are generally found in the lower esophagus.
Histopathology • Squamous cell carcinomas exhibit infiltrating malignant epithelial cells demonstrating squamous differentiation, characterized by intercellular bridges and/or keratinization. • Adenocarcinomas display infiltrating malignant epithelial cells evidencing glandular differentiation, indicated by tubule formation and/or mucin production. The neighboring oesophageal mucosa may exhibit high-grade dysplasia in a region of Barrett’s oesophagus.
Prognosis: Generally unfavorable due to delayed presentation. • Five-year survival rates around 10–20%
TNM 7 pathological staging of oesophageal carcinoma
Primary tumour (T)
pT1a: tumour invades no deeper than the submucosa.
pT2: tumour invades the muscularis propria.
pT3: tumour invades the adventitia.
pT4: tumour invades adjacent structures.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1: 1 or 2 regional lymph node metastases.
pN2: 3–6 regional lymph node metastases.
pN3: 7 or more regional lymph node metastases
Definition • A malignant epithelial neoplasm originating in the oesophagus. • Two primary subtypes are identified: squamous cell carcinoma and adenocarcinoma.
Epidemiology • Both forms manifest at a median age of 65 years. • Oesophageal adenocarcinoma has garnered significant attention in developed nations due to its substantial and persistent increase in incidence over recent decades.
Aetiology • Significant tobacco and alcohol consumption is associated with squamous cell carcinoma. • Chronic gastro-oesophageal reflux disease resulting in Barrett’s oesophagus is the predominant precursor to adenocarcinoma. Carcinogenesis • Both forms commonly possess TP53 mutations.
Presentation: Dysphagia, retrosternal or epigastric discomfort, and weight loss. • By the time the majority of individuals seek medical attention, the tumor is typically in an advanced stage.
Macroscopy • Tumor mass in the esophagus may exhibit exophytic growth into the lumen or infiltrate the wall in a plaque-like manner. • Squamous cell carcinomas typically arise in the mid-esophagus, whereas adenocarcinomas are generally found in the lower esophagus.
Histopathology • Squamous cell carcinomas exhibit infiltrating malignant epithelial cells demonstrating squamous differentiation, characterized by intercellular bridges and/or keratinization. • Adenocarcinomas display infiltrating malignant epithelial cells evidencing glandular differentiation, indicated by tubule formation and/or mucin production. The neighboring oesophageal mucosa may exhibit high-grade dysplasia in a region of Barrett’s oesophagus.
Prognosis: Generally unfavorable due to delayed presentation. • Five-year survival rates around 10–20%
TNM 7 pathological staging of oesophageal carcinoma
Primary tumour (T)
pT1a: tumour invades no deeper than the submucosa.
pT2: tumour invades the muscularis propria.
pT3: tumour invades the adventitia.
pT4: tumour invades adjacent structures.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1: 1 or 2 regional lymph node metastases.
pN2: 3–6 regional lymph node metastases.
pN3: 7 or more regional lymph node metastases
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Pathology - Oesophagitis
Definition • Inflammation of the esophagus.
Presentation • Retrosternal burning sensation (heartburn). • Dysphagia and singultus may also manifest.
Reflux oesophagitis • Induced by gastric acid refluxing into the lower oesophagus. • Highly prevalent. Predominantly observed in adult Caucasian males, though it can manifest in individuals of any gender, race, and age, including children. • Contributing factors encompass alcohol consumption, pharmacological agents, hypothyroidism, pregnancy, hiatal hernia, diabetes, and obesity. • Mucosal biopsy reveals regenerative alterations in the squamous epithelium, characterized by basal cell hyperplasia and the extension of vascular papillae into the upper epithelial layers. Inflammation is often modest with dispersed eosinophils. Approximately 10% of patients exhibit glandular metaplasia of the lower esophagus, identifiable during endoscopy (Barrett's esophagus). Two Barrett's oesophagus is linked to a 50-fold heightened incidence of oesophageal cancer.Individuals diagnosed with Barrett’s oesophagus ought to be evaluated for participation in a monitoring program involving routine endoscopy and biopsy to assess for glandular epithelial dysplasia.
Drug-induced (pill) esophagitis • Resulting from the direct toxicity of medications to the esophageal mucosa. • Predominantly affects the elderly population. • Frequently implicated medications include bisphosphonates and iron supplements. Mucosal biopsy reveals acute inflammation accompanied by erosion or ulceration of the surface epithelium. Encrusted golden brown iron pigment may be observed in instances attributed to iron tablets. Typically, this condition resolves following the cessation of the implicated medication.
Eosinophilic esophagitis • A rare disorder predominantly affecting atopic persons with a history of allergies, asthma, and medication sensitivities. • Mucosal biopsy reveals significant infiltration of eosinophils in the mucosa, typically forming clusters. • Favorable prognosis if discovered and treated promptly. If left untreated, it may result in significant oesophageal strictures.
Infectious esophagitis • Primarily observed in immunocompromised individuals, as the esophagus typically exhibits significant resistance to infection. • Mucosal biopsy reveals inflammation alongside pseudohyphae in Candida, multinucleation, and chromatin margination in herpes simplex, as well as inclusions in cytomegalovirus.
Definition • Inflammation of the esophagus.
Presentation • Retrosternal burning sensation (heartburn). • Dysphagia and singultus may also manifest.
Reflux oesophagitis • Induced by gastric acid refluxing into the lower oesophagus. • Highly prevalent. Predominantly observed in adult Caucasian males, though it can manifest in individuals of any gender, race, and age, including children. • Contributing factors encompass alcohol consumption, pharmacological agents, hypothyroidism, pregnancy, hiatal hernia, diabetes, and obesity. • Mucosal biopsy reveals regenerative alterations in the squamous epithelium, characterized by basal cell hyperplasia and the extension of vascular papillae into the upper epithelial layers. Inflammation is often modest with dispersed eosinophils. Approximately 10% of patients exhibit glandular metaplasia of the lower esophagus, identifiable during endoscopy (Barrett's esophagus). Two Barrett's oesophagus is linked to a 50-fold heightened incidence of oesophageal cancer.Individuals diagnosed with Barrett’s oesophagus ought to be evaluated for participation in a monitoring program involving routine endoscopy and biopsy to assess for glandular epithelial dysplasia.
Drug-induced (pill) esophagitis • Resulting from the direct toxicity of medications to the esophageal mucosa. • Predominantly affects the elderly population. • Frequently implicated medications include bisphosphonates and iron supplements. Mucosal biopsy reveals acute inflammation accompanied by erosion or ulceration of the surface epithelium. Encrusted golden brown iron pigment may be observed in instances attributed to iron tablets. Typically, this condition resolves following the cessation of the implicated medication.
Eosinophilic esophagitis • A rare disorder predominantly affecting atopic persons with a history of allergies, asthma, and medication sensitivities. • Mucosal biopsy reveals significant infiltration of eosinophils in the mucosa, typically forming clusters. • Favorable prognosis if discovered and treated promptly. If left untreated, it may result in significant oesophageal strictures.
Infectious esophagitis • Primarily observed in immunocompromised individuals, as the esophagus typically exhibits significant resistance to infection. • Mucosal biopsy reveals inflammation alongside pseudohyphae in Candida, multinucleation, and chromatin margination in herpes simplex, as well as inclusions in cytomegalovirus.
