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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 - 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.
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Pathology - Pathologies of the salivary glands
Mucocele • Accumulation of salivary mucus resulting from obstruction of a salivary duct. • Primarily occurs on the lower lip. Histology reveals a cystic lesion filled with mucus and bordered by epithelium (retention mucocele) or granulation tissue (extravasation mucocele).
Pleomorphic adenoma • The most prevalent neoplasm of the salivary glands. The majority manifests in the parotid gland as a painless, gradually enlarging mass. Fine needle aspiration (FNA) cytology reveals a cellular composition characterized by a plethora of epithelial and myoepithelial cells, together with fibrous stromal fragments. Histological analysis reveals a well-defined tumor consisting of a combination of ductal epithelium, myoepithelial cells, and a myxochondroid stroma. • Benign neoplasm, although may return after insufficient resection.
Warthin's tumor • The second most prevalent neoplasm of the salivary glands. • Nearly all instances arise in the parotid gland, presenting as a painless, gradually enlarging mass. • Fine needle aspiration cytology reveals clusters of oncocytic epithelial cells accompanied by a substantial presence of lymphoid cells in the background. Histology reveals a confined tumor consisting of a bilayer of oncocytic epithelium accompanied by a thick lymphoid stroma beneath. • Benign neoplasm, although may return after insufficient resection
.
Mucoepidermoid carcinoma • The most prevalent malignant tumor of the salivary glands. • Exhibits a painful tumor associated with a principal salivary gland. FNA cytology reveals the presence of mucus, intermediate cells, and mucous cells. Histology reveals an infiltrative tumor comprised of a combination of intermediate, squamoid, and mucous cells. Cystic alterations may be observed. Most tumors are low-grade and exhibit favorable behavior, with a survival rate exceeding 95%. High-grade tumors exhibit aggressive behavior, with a survival rate of approximately 45%.
Acinic cell carcinoma • Malignant salivary gland neoplasm predominantly originating in the parotid gland. • Exhibits a bulk that may be painful. Histology reveals a tumor comprised of serous acinar cells exhibiting granular cytoplasm, which may develop in various architectural configurations. • Five-year survival rate approximately 80%.
Adenoid cystic carcinoma • Malignant salivary gland neoplasm predominantly originating in small salivary glands. • Manifestations include a gradually enlarging lump that may be uncomfortable. Histology reveals an infiltrative tumor comprised of basaloid epithelial and myoepithelial cells, typically organized into cribriform sheets. Perineural invasion is commonly observed. • Five-year survival rate around 60%
Mucocele • Accumulation of salivary mucus resulting from obstruction of a salivary duct. • Primarily occurs on the lower lip. Histology reveals a cystic lesion filled with mucus and bordered by epithelium (retention mucocele) or granulation tissue (extravasation mucocele).
Pleomorphic adenoma • The most prevalent neoplasm of the salivary glands. The majority manifests in the parotid gland as a painless, gradually enlarging mass. Fine needle aspiration (FNA) cytology reveals a cellular composition characterized by a plethora of epithelial and myoepithelial cells, together with fibrous stromal fragments. Histological analysis reveals a well-defined tumor consisting of a combination of ductal epithelium, myoepithelial cells, and a myxochondroid stroma. • Benign neoplasm, although may return after insufficient resection.
Warthin's tumor • The second most prevalent neoplasm of the salivary glands. • Nearly all instances arise in the parotid gland, presenting as a painless, gradually enlarging mass. • Fine needle aspiration cytology reveals clusters of oncocytic epithelial cells accompanied by a substantial presence of lymphoid cells in the background. Histology reveals a confined tumor consisting of a bilayer of oncocytic epithelium accompanied by a thick lymphoid stroma beneath. • Benign neoplasm, although may return after insufficient resection
.
Mucoepidermoid carcinoma • The most prevalent malignant tumor of the salivary glands. • Exhibits a painful tumor associated with a principal salivary gland. FNA cytology reveals the presence of mucus, intermediate cells, and mucous cells. Histology reveals an infiltrative tumor comprised of a combination of intermediate, squamoid, and mucous cells. Cystic alterations may be observed. Most tumors are low-grade and exhibit favorable behavior, with a survival rate exceeding 95%. High-grade tumors exhibit aggressive behavior, with a survival rate of approximately 45%.
Acinic cell carcinoma • Malignant salivary gland neoplasm predominantly originating in the parotid gland. • Exhibits a bulk that may be painful. Histology reveals a tumor comprised of serous acinar cells exhibiting granular cytoplasm, which may develop in various architectural configurations. • Five-year survival rate approximately 80%.
Adenoid cystic carcinoma • Malignant salivary gland neoplasm predominantly originating in small salivary glands. • Manifestations include a gradually enlarging lump that may be uncomfortable. Histology reveals an infiltrative tumor comprised of basaloid epithelial and myoepithelial cells, typically organized into cribriform sheets. Perineural invasion is commonly observed. • Five-year survival rate around 60%
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Pathology - Coeliac disease
Definition: An autoimmune condition resulting from an aberrant immunological response to dietary gluten.
Epidemiology • Prevalent, impacting approximately 1% of the population.
Aetiology: Dietary gluten and associated proteins. Pathogenesis The offending proteins are inadequately degraded by intestinal proteases. Intact peptides penetrate the lamina propria and undergo deamidation by tissue transglutaminase, resulting in a negative charge. Negatively charged peptides bind more efficiently to HLA receptors on antigen-presenting cells, which are detected by intestinal T lymphocytes. Activated T-cells elicit an immunological response in the gut wall.
Presentation • Symptoms associated with the gastrointestinal tract may include weight loss, stomach pain, and diarrhea. Many individuals, however, are asymptomatic and are detected solely during the study of iron deficiency anemia. Serology • The detection of serum IgA endomysial or transglutaminase antibodies is very specific and sensitive for celiac disease.
Macroscopy • Villi may exhibit blunting and flattening when observed under a dissecting microscope.
Histopathology • Advanced cases have elevated intraepithelial lymphocytes, many lymphocytes and plasma cells in the lamina propria, villous atrophy, and crypt hyperplasia. • Less severe cases may present solely with increased intraepithelial lymphocytes in the absence of villous atrophy. 2 It is important to recognize that these alterations are not exclusive to celiac disease; similar modifications can be observed in several other illnesses. Biopsy findings must be analyzed in conjunction with the clinical and serological context.
Prognosis: • Rigorous compliance with a gluten-free diet results in symptom relief and histological normalization. • Elevated risk of type 1 diabetes, autoimmune thyroid disease, dermatitis herpetiformis, oropharyngeal and esophageal cancer, small bowel adenocarcinoma, and a rare, although very aggressive, variant of T-cell lymphoma referred to as enteropathy-associated T-cell lymphoma
Definition: An autoimmune condition resulting from an aberrant immunological response to dietary gluten.
Epidemiology • Prevalent, impacting approximately 1% of the population.
Aetiology: Dietary gluten and associated proteins. Pathogenesis The offending proteins are inadequately degraded by intestinal proteases. Intact peptides penetrate the lamina propria and undergo deamidation by tissue transglutaminase, resulting in a negative charge. Negatively charged peptides bind more efficiently to HLA receptors on antigen-presenting cells, which are detected by intestinal T lymphocytes. Activated T-cells elicit an immunological response in the gut wall.
Presentation • Symptoms associated with the gastrointestinal tract may include weight loss, stomach pain, and diarrhea. Many individuals, however, are asymptomatic and are detected solely during the study of iron deficiency anemia. Serology • The detection of serum IgA endomysial or transglutaminase antibodies is very specific and sensitive for celiac disease.
Macroscopy • Villi may exhibit blunting and flattening when observed under a dissecting microscope.
Histopathology • Advanced cases have elevated intraepithelial lymphocytes, many lymphocytes and plasma cells in the lamina propria, villous atrophy, and crypt hyperplasia. • Less severe cases may present solely with increased intraepithelial lymphocytes in the absence of villous atrophy. 2 It is important to recognize that these alterations are not exclusive to celiac disease; similar modifications can be observed in several other illnesses. Biopsy findings must be analyzed in conjunction with the clinical and serological context.
Prognosis: • Rigorous compliance with a gluten-free diet results in symptom relief and histological normalization. • Elevated risk of type 1 diabetes, autoimmune thyroid disease, dermatitis herpetiformis, oropharyngeal and esophageal cancer, small bowel adenocarcinoma, and a rare, although very aggressive, variant of T-cell lymphoma referred to as enteropathy-associated T-cell lymphoma
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Pathology - Peptic duodenitis
Definition • Inflammation and ulceration of the duodenal mucosa resulting from excessive stomach acid.
Epidemiology • Prevalent, impacting up to 10% of the populace. • Predominantly observed in male patients over 40 years of age. The primary aetiological component is believed to be chronic H. pylori infection. • Tobacco use and nonsteroidal anti-inflammatory drugs (NSAIDs) are significant risk factors. Recurrent numerous duodenal ulcers, especially if located beyond the initial segment of the duodenum, should prompt consideration of potential Zollinger–Ellison syndrome.
Pathogenesis Increased stomach acid production results in damage to the duodenal mucosa, ranging from moderate erosions to severe ulceration.
Presentation: • Epigastric pain characterized by a burning sensation, alleviated by food intake. • Severe instances result in enduring epigastric discomfort, nausea, and emesis.
Macroscopy • Peptic duodenitis exhibits mucosal erythema with possible superficial erosions. • Peptic ulcers present as well-defined, punched-out mucosal defects featuring granulation tissue at the base.
Histopathology: Peptic duodenitis exhibits acute inflammation, edema, and hemorrhage in the lamina propria. The surface epithelium generally exhibits regions of gastric metaplasia. H. pylori organisms may be detected on the metaplastic gastric epithelium. Peptic ulcers exhibit a total loss of the mucosal layer, which is replaced by granulation tissue and underlying scar tissue.
Prognosis: The elimination of H. pylori and the administration of acid suppressive medication enhance symptoms and promote healing. Scarring of ulcers may result in stricture development and blockage. A perforation of a major vessel due to a peptic ulcer is a prevalent cause of sudden upper gastrointestinal hemorrhage. Free perforation results in acute widespread peritonitis, requiring immediate surgical intervention.
Definition • Inflammation and ulceration of the duodenal mucosa resulting from excessive stomach acid.
Epidemiology • Prevalent, impacting up to 10% of the populace. • Predominantly observed in male patients over 40 years of age. The primary aetiological component is believed to be chronic H. pylori infection. • Tobacco use and nonsteroidal anti-inflammatory drugs (NSAIDs) are significant risk factors. Recurrent numerous duodenal ulcers, especially if located beyond the initial segment of the duodenum, should prompt consideration of potential Zollinger–Ellison syndrome.
Pathogenesis Increased stomach acid production results in damage to the duodenal mucosa, ranging from moderate erosions to severe ulceration.
Presentation: • Epigastric pain characterized by a burning sensation, alleviated by food intake. • Severe instances result in enduring epigastric discomfort, nausea, and emesis.
Macroscopy • Peptic duodenitis exhibits mucosal erythema with possible superficial erosions. • Peptic ulcers present as well-defined, punched-out mucosal defects featuring granulation tissue at the base.
Histopathology: Peptic duodenitis exhibits acute inflammation, edema, and hemorrhage in the lamina propria. The surface epithelium generally exhibits regions of gastric metaplasia. H. pylori organisms may be detected on the metaplastic gastric epithelium. Peptic ulcers exhibit a total loss of the mucosal layer, which is replaced by granulation tissue and underlying scar tissue.
Prognosis: The elimination of H. pylori and the administration of acid suppressive medication enhance symptoms and promote healing. Scarring of ulcers may result in stricture development and blockage. A perforation of a major vessel due to a peptic ulcer is a prevalent cause of sudden upper gastrointestinal hemorrhage. Free perforation results in acute widespread peritonitis, requiring immediate surgical intervention.
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Pathology - Gastrointestinal stromal tumors
Definition: Mesenchymal tumors with varying degrees of malignancy that originate in the gastrointestinal tract wall and mimic the phenotype of interstitial cells of Cajal, the pacemaker cells of the Auerbach plexus.
Epidemiology • Incidence is approximately 15 cases per million people annually. • Predominantly occurs in adults with a median age of 50 to 60 years
. The aetiology of occasional occurrences remains unidentified. A minor percentage occurs in conjunction with neurofibromatosis type 1, Carney's triad, and families possessing germline KIT mutations.
Genetics • The majority exhibit activating mutations in the oncogene KIT. • The remainder display activating mutations in the related gene PDGFRA.
Presentation • Noticeable upper abdominal mass, discomfort, or hemorrhage. • Malignant neoplasms may manifest with symptoms associated with metastasis. Locations of engagement • Can manifest throughout the gastrointestinal tract, from the esophagus to the rectum. • The majority originate in the stomach (60–70%) or small intestine (20–30%). A little quantity seems to originate predominantly in the omentum.
Macroscopy • Clearly delineated tumor mass located inside the submucosal, muscular, or serosal layer of the bowel. • Size varies from 1 to over 20 cm.
Histopathology • Characterized by spindle cells, frequently exhibiting paranuclear vacuoles. • More robust epithelioid cells may also be observed, and certain tumors may be exclusively epithelioid. Small intestinal tumors may also exhibit so-called 'skeinoid' fibers. Nearly all exhibit the markers CD117 (c-kit) and DOG-1.
Prognosis: All cases should be regarded as potentially malignant. They are categorized into extremely low-risk, low-risk, intermediate-risk, and high-risk classifications for malignancy based on location, size, and mitotic activity.
Definition: Mesenchymal tumors with varying degrees of malignancy that originate in the gastrointestinal tract wall and mimic the phenotype of interstitial cells of Cajal, the pacemaker cells of the Auerbach plexus.
Epidemiology • Incidence is approximately 15 cases per million people annually. • Predominantly occurs in adults with a median age of 50 to 60 years
. The aetiology of occasional occurrences remains unidentified. A minor percentage occurs in conjunction with neurofibromatosis type 1, Carney's triad, and families possessing germline KIT mutations.
Genetics • The majority exhibit activating mutations in the oncogene KIT. • The remainder display activating mutations in the related gene PDGFRA.
Presentation • Noticeable upper abdominal mass, discomfort, or hemorrhage. • Malignant neoplasms may manifest with symptoms associated with metastasis. Locations of engagement • Can manifest throughout the gastrointestinal tract, from the esophagus to the rectum. • The majority originate in the stomach (60–70%) or small intestine (20–30%). A little quantity seems to originate predominantly in the omentum.
Macroscopy • Clearly delineated tumor mass located inside the submucosal, muscular, or serosal layer of the bowel. • Size varies from 1 to over 20 cm.
Histopathology • Characterized by spindle cells, frequently exhibiting paranuclear vacuoles. • More robust epithelioid cells may also be observed, and certain tumors may be exclusively epithelioid. Small intestinal tumors may also exhibit so-called 'skeinoid' fibers. Nearly all exhibit the markers CD117 (c-kit) and DOG-1.
Prognosis: All cases should be regarded as potentially malignant. They are categorized into extremely low-risk, low-risk, intermediate-risk, and high-risk classifications for malignancy based on location, size, and mitotic activity.
