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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 - Gastric carcinoma
Definition • A malignant epithelial neoplasm originating in the stomach.
Epidemiology • Significant geographical diversity in incidence attributable to dietary variables. Changes in diet in nations with a historically high incidence are resulting in a consistent decrease in global incidence.
Aetiology: Diet is the most consistent determinant. Excessive salt consumption is a significant risk factor, whereas fresh fruits and vegetables offer protection due to their antioxidant properties. H. pylori and autoimmune gastritis are significant risk factors, as they facilitate a progression from chronic gastritis to gastric atrophy, then to intestinal metaplasia, followed by epithelial dysplasia, and ultimately cancer.
Carcinogenesis • Free radicals, oxidants, and reactive oxygen species generated by H. pylori infection and dietary carcinogens induce DNA damage. Common genetic targets encompass TP53 and KRAS. Diffuse-type carcinomas frequently exhibit a lack of E-cadherin.
Presentation • Early gastric cancer may be asymptomatic or elicit nonspecific symptoms such as dyspepsia. • Advanced cases result in chronic stomach pain accompanied by weight loss. • Tumors may also hemorrhage, resulting in hematemesis, or impede the gastric exit, leading to emesis.
Macroscopy • A tumor mass within the gastric wall that may present as exophytic or diffusely infiltrative.
Histopathology: Predominantly adenocarcinomas. Intestinal-type adenocarcinoma has infiltrating malignant epithelial cells that create discernible glandular structures. Diffuse-type adenocarcinoma is characterized by infiltrating malignant epithelial cells that exhibit weak cohesion and minimal to no glandular development. Malignant cells may possess intracytoplasmic vacuoles filled with mucin. Cells engorged with mucin, causing the nucleus to be shifted to one side, are referred to as 'signet ring' cells. Tumors characterized by a high prevalence of signet ring cells are typically extensively infiltrative.
Prognosis • Varies with stage, but typically manifests late with an unfavorable prognosis
Definition • A malignant epithelial neoplasm originating in the stomach.
Epidemiology • Significant geographical diversity in incidence attributable to dietary variables. Changes in diet in nations with a historically high incidence are resulting in a consistent decrease in global incidence.
Aetiology: Diet is the most consistent determinant. Excessive salt consumption is a significant risk factor, whereas fresh fruits and vegetables offer protection due to their antioxidant properties. H. pylori and autoimmune gastritis are significant risk factors, as they facilitate a progression from chronic gastritis to gastric atrophy, then to intestinal metaplasia, followed by epithelial dysplasia, and ultimately cancer.
Carcinogenesis • Free radicals, oxidants, and reactive oxygen species generated by H. pylori infection and dietary carcinogens induce DNA damage. Common genetic targets encompass TP53 and KRAS. Diffuse-type carcinomas frequently exhibit a lack of E-cadherin.
Presentation • Early gastric cancer may be asymptomatic or elicit nonspecific symptoms such as dyspepsia. • Advanced cases result in chronic stomach pain accompanied by weight loss. • Tumors may also hemorrhage, resulting in hematemesis, or impede the gastric exit, leading to emesis.
Macroscopy • A tumor mass within the gastric wall that may present as exophytic or diffusely infiltrative.
Histopathology: Predominantly adenocarcinomas. Intestinal-type adenocarcinoma has infiltrating malignant epithelial cells that create discernible glandular structures. Diffuse-type adenocarcinoma is characterized by infiltrating malignant epithelial cells that exhibit weak cohesion and minimal to no glandular development. Malignant cells may possess intracytoplasmic vacuoles filled with mucin. Cells engorged with mucin, causing the nucleus to be shifted to one side, are referred to as 'signet ring' cells. Tumors characterized by a high prevalence of signet ring cells are typically extensively infiltrative.
Prognosis • Varies with stage, but typically manifests late with an unfavorable prognosis
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Pathology - Gastric polyps
Hyperplastic polyp • A prevalent polyp primarily found in the antrum or body. • A non-neoplastic reactive lesion believed to signify an amplified regenerative reaction to mucosal damage. • Typically linked to underlying stomach conditions, including Helicobacter infection or autoimmune gastritis. • Histological examination reveals a polyp characterized by dilated, elongated, convoluted foveolar epithelium inside an edematous, inflamed lamina propria.
Fundic gland polyp • A prevalent polyp that is found exclusively in the body or fundus. • May manifest spontaneously or in conjunction with familial adenomatous polyposis (FAP). FAP-associated polyps tend to be numerous and manifest at an earlier age. Sporadic polyps are typically not linked to any underlying mucosal condition. • Certain articles have indicated a correlation with proton pump inhibitors; however, this assertion has been contested thereafter. Histological examination reveals a polyp characterized by cystically dilated fundic glands, which are bordered by flattened parietal and chief cells.
Gastric adenoma • Rare neoplastic polyp that may arise in various regions of the stomach. • Microscopically characterized by dysplastic glands featuring stratified hyperchromatic nuclei. • Two variants are identified: intestinal and foveolar kinds. Intestinal forms are significantly more prone to exhibit high-grade dysplasia or contain gastric cancer compared to the foveolar type.
Gastric xanthoma: An uncommon polyp that can manifest in any region of the stomach. • Exhibits a pale yellow nodular owing to its lipid composition. • Histological examination reveals an abundance of lipid-laden macrophages within the lamina propria.
Inflammatory fibroid polyp • Uncommon lesion primarily located in the antrum. • Histological examination reveals a submucosal lesion consisting of innocuous spindle cells organized around prominent arteries, embedded in a loose myxoid stroma including notable eosinophils.
Hyperplastic polyp • A prevalent polyp primarily found in the antrum or body. • A non-neoplastic reactive lesion believed to signify an amplified regenerative reaction to mucosal damage. • Typically linked to underlying stomach conditions, including Helicobacter infection or autoimmune gastritis. • Histological examination reveals a polyp characterized by dilated, elongated, convoluted foveolar epithelium inside an edematous, inflamed lamina propria.
Fundic gland polyp • A prevalent polyp that is found exclusively in the body or fundus. • May manifest spontaneously or in conjunction with familial adenomatous polyposis (FAP). FAP-associated polyps tend to be numerous and manifest at an earlier age. Sporadic polyps are typically not linked to any underlying mucosal condition. • Certain articles have indicated a correlation with proton pump inhibitors; however, this assertion has been contested thereafter. Histological examination reveals a polyp characterized by cystically dilated fundic glands, which are bordered by flattened parietal and chief cells.
Gastric adenoma • Rare neoplastic polyp that may arise in various regions of the stomach. • Microscopically characterized by dysplastic glands featuring stratified hyperchromatic nuclei. • Two variants are identified: intestinal and foveolar kinds. Intestinal forms are significantly more prone to exhibit high-grade dysplasia or contain gastric cancer compared to the foveolar type.
Gastric xanthoma: An uncommon polyp that can manifest in any region of the stomach. • Exhibits a pale yellow nodular owing to its lipid composition. • Histological examination reveals an abundance of lipid-laden macrophages within the lamina propria.
Inflammatory fibroid polyp • Uncommon lesion primarily located in the antrum. • Histological examination reveals a submucosal lesion consisting of innocuous spindle cells organized around prominent arteries, embedded in a loose myxoid stroma including notable eosinophils.
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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.
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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 - 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 - Gastrointestinal infections
Campylobacter, Salmonella, Shigella, Escherichia coli • Prevalent bacterial etiologies of gastrointestinal infections. Mucosal biopsies typically reveal acute colitis characterized by the presence of neutrophils in the lamina propria and inside crypts.
Enterotoxigenic E. coli (ETEC) is a prevalent etiological agent of diarrhea in travelers. ETEC has fimbriae that enable the bacteria to attach to small bowel epithelial cells and secrete toxins, resulting in significant fluid loss.
Enterohaemorrhagic E. coli synthesizes a cytotoxin, resulting in haemorrhagic necrosis of the intestinal mucosa and bloody diarrhea. Vulnerable individuals, especially children, are at risk of developing thrombotic microangiopathy, resulting in hemolysis and acute renal failure (hemolytic uremic syndrome).
Clostridium difficile • A significant etiology of colitis frequently linked to the administration of broad-spectrum antibiotics in hospitalized individuals. The clinical presentation is diverse, spanning from mild diarrhea to severe colitis with potential for perforation and mortality. • Macroscopically, colitis results in the development of cream-colored pseudomembranes on the colonic mucosal surface. • Microscopically, crypts filled with neutrophils and mucus are enveloped by pseudomembranes consisting of fibrin and neutrophils.
Mycobacterium avium • Notable opportunistic pathogen in immunocompromised individuals. • A disseminated infection affecting the small and large intestine results in persistent diarrhea. Mucosal biopsy reveals significant infiltration of the lamina propria by macrophages with acid-fast bacilli.
Rotavirus is the predominant etiological agent of severe diarrhea in newborns and young children. • Transmission occurs via the faecal-oral route. • Immunity is acquired in childhood, rendering adult infections uncommon.
Norovirus • A prevalent etiological agent of epidemic gastroenteritis outbreaks. • Highly contagious, transmitted via contaminated food or drink, direct person-to-person interaction, and surface contamination. • Frequently observed in confined populations such as institutions, hospitals, and cruise ships.
Cytomegalovirus • Typically linked to immunocompromised states. Cytomegalovirus (CMV) infection significantly contributes to abrupt clinical decline in immunosuppressed individuals with inflammatory bowel disease. • Microscopically, the alterations range from modest inflammation to profound ulceration. CMV inclusions are present in endothelial and stromal cells.
Giardia lamblia • Protozoan transmitted through the use of water contaminated with the organism's cysts. The developed pathogen adheres to the brush edge of the epithelial cells of the upper small intestine. The inflammatory response induces a mild diarrheal condition that persists for approximately one week before resolution. Immunocompromised persons may experience persistent infections.
Entamoeba histolytica • Prevalent protozoal infection impacting around 10% of the global population. • Symptoms vary from mild diarrhea and stomach discomfort to severe fulminant colitis. The infection may spread to several areas, including the liver, and, infrequently, massive inflammatory tumors known as amoebomas may develop. • Mild instances exhibit neutrophilic infiltration only, but more severe cases are linked to profound ulceration of the gut. The organisms are spherical entities featuring a bean-shaped nucleus and a frothy cytoplasm that contains engulfed red blood cells.
Enterobius vermicularis Nematode pinworm transmitted via hand-to-mouth transfer of ova. • Larvae develop into adult organisms, primarily inhabiting the caecum. During nocturnal hours, female organisms travel to the anus to lay eggs, resulting in significant perianal pruritus.
Necator americanus with Ancylostoma duodenale Nematode hookworms that adhere to the jejunal mucosa. A pump mechanism is employed to extract blood and interstitial fluid from the host. Elevated worm burdens can result in substantial cumulative blood loss. Hookworm infection is the predominant cause of iron deficiency anemia globally.
Campylobacter, Salmonella, Shigella, Escherichia coli • Prevalent bacterial etiologies of gastrointestinal infections. Mucosal biopsies typically reveal acute colitis characterized by the presence of neutrophils in the lamina propria and inside crypts.
Enterotoxigenic E. coli (ETEC) is a prevalent etiological agent of diarrhea in travelers. ETEC has fimbriae that enable the bacteria to attach to small bowel epithelial cells and secrete toxins, resulting in significant fluid loss.
Enterohaemorrhagic E. coli synthesizes a cytotoxin, resulting in haemorrhagic necrosis of the intestinal mucosa and bloody diarrhea. Vulnerable individuals, especially children, are at risk of developing thrombotic microangiopathy, resulting in hemolysis and acute renal failure (hemolytic uremic syndrome).
Clostridium difficile • A significant etiology of colitis frequently linked to the administration of broad-spectrum antibiotics in hospitalized individuals. The clinical presentation is diverse, spanning from mild diarrhea to severe colitis with potential for perforation and mortality. • Macroscopically, colitis results in the development of cream-colored pseudomembranes on the colonic mucosal surface. • Microscopically, crypts filled with neutrophils and mucus are enveloped by pseudomembranes consisting of fibrin and neutrophils.
Mycobacterium avium • Notable opportunistic pathogen in immunocompromised individuals. • A disseminated infection affecting the small and large intestine results in persistent diarrhea. Mucosal biopsy reveals significant infiltration of the lamina propria by macrophages with acid-fast bacilli.
Rotavirus is the predominant etiological agent of severe diarrhea in newborns and young children. • Transmission occurs via the faecal-oral route. • Immunity is acquired in childhood, rendering adult infections uncommon.
Norovirus • A prevalent etiological agent of epidemic gastroenteritis outbreaks. • Highly contagious, transmitted via contaminated food or drink, direct person-to-person interaction, and surface contamination. • Frequently observed in confined populations such as institutions, hospitals, and cruise ships.
Cytomegalovirus • Typically linked to immunocompromised states. Cytomegalovirus (CMV) infection significantly contributes to abrupt clinical decline in immunosuppressed individuals with inflammatory bowel disease. • Microscopically, the alterations range from modest inflammation to profound ulceration. CMV inclusions are present in endothelial and stromal cells.
Giardia lamblia • Protozoan transmitted through the use of water contaminated with the organism's cysts. The developed pathogen adheres to the brush edge of the epithelial cells of the upper small intestine. The inflammatory response induces a mild diarrheal condition that persists for approximately one week before resolution. Immunocompromised persons may experience persistent infections.
Entamoeba histolytica • Prevalent protozoal infection impacting around 10% of the global population. • Symptoms vary from mild diarrhea and stomach discomfort to severe fulminant colitis. The infection may spread to several areas, including the liver, and, infrequently, massive inflammatory tumors known as amoebomas may develop. • Mild instances exhibit neutrophilic infiltration only, but more severe cases are linked to profound ulceration of the gut. The organisms are spherical entities featuring a bean-shaped nucleus and a frothy cytoplasm that contains engulfed red blood cells.
Enterobius vermicularis Nematode pinworm transmitted via hand-to-mouth transfer of ova. • Larvae develop into adult organisms, primarily inhabiting the caecum. During nocturnal hours, female organisms travel to the anus to lay eggs, resulting in significant perianal pruritus.
Necator americanus with Ancylostoma duodenale Nematode hookworms that adhere to the jejunal mucosa. A pump mechanism is employed to extract blood and interstitial fluid from the host. Elevated worm burdens can result in substantial cumulative blood loss. Hookworm infection is the predominant cause of iron deficiency anemia globally.
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Pathology - Intestinal blockage
Definition: A mechanical obstruction in a section of the intestine.
Epidemiology • Prevalent.
Aetiology • Small bowel obstruction: adhesions, hernias, intussusception, volvulus. • Large bowel obstruction: neoplasms, sigmoid volvulus, diverticular strictures.
Pathogenesis • Mechanical obstruction of the bowel inhibits normal peristaltic activity.
Presentation • Small bowel obstruction: severe colicky stomach pain, abdominal distension, initial vomiting, followed by complete constipation (absence of both flatus and feces). • Large bowel obstruction: severe colicky stomach pain, abdominal distension, initial absolute constipation, followed by subsequent vomiting.
Macroscopy The bowel anterior to the obstruction is typically distended. The primary reason of the obstruction is typically evident, such as adhesions, tumors, or intussusception.
Histopathology • Ischemic alterations may occur in extended cases. • Characteristics of the fundamental cause may also be observed.
Prognosis is contingent upon the underlying etiology. Benign causes of blockage typically exhibit a favorable prognosis with either spontaneous resolution or surgical intervention. Large intestinal obstruction resulting from colorectal cancer typically indicates advanced disease and a diminished prognosis.
Definition: A mechanical obstruction in a section of the intestine.
Epidemiology • Prevalent.
Aetiology • Small bowel obstruction: adhesions, hernias, intussusception, volvulus. • Large bowel obstruction: neoplasms, sigmoid volvulus, diverticular strictures.
Pathogenesis • Mechanical obstruction of the bowel inhibits normal peristaltic activity.
Presentation • Small bowel obstruction: severe colicky stomach pain, abdominal distension, initial vomiting, followed by complete constipation (absence of both flatus and feces). • Large bowel obstruction: severe colicky stomach pain, abdominal distension, initial absolute constipation, followed by subsequent vomiting.
Macroscopy The bowel anterior to the obstruction is typically distended. The primary reason of the obstruction is typically evident, such as adhesions, tumors, or intussusception.
Histopathology • Ischemic alterations may occur in extended cases. • Characteristics of the fundamental cause may also be observed.
Prognosis is contingent upon the underlying etiology. Benign causes of blockage typically exhibit a favorable prognosis with either spontaneous resolution or surgical intervention. Large intestinal obstruction resulting from colorectal cancer typically indicates advanced disease and a diminished prognosis.
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Pathology -Small Bowel Infarction
Definition: Ischaemic necrosis of a section of the small intestine. Epidemiology • Typically observed in those over 50 years of age.
Aetiology • Thrombosis associated with an unstable atherosclerotic plaque in the superior mesenteric artery. • Thromboemboli originating from the left ventricle or left atrium. • Hypovolemia.
Pathogenesis A sudden decrease in blood flow through the superior mesenteric artery results in ischemic necrosis of a portion of the small intestine. Massive hemorrhage into the infarcted colon results in hypovolemia. Bacteria swiftly infiltrate the necrotic gut wall, resulting in sepsis.
Presentation: • Sudden onset of intense stomach pain accompanied by hematochezia and hypovolemia.
Macroscopy The infarcted small intestine exhibits a dusky purple hue. Upon incision of the intestinal segment, substantial quantities of blood are observed within the lumen, and the mucosal surface appears fragile and necrotic. Histopathology • Complete thickness necrosis of the intestinal wall
.
Prognosis • Timely laparotomy is crucial for the resection of the infarcted bowel segment. • Prognosis is typically unfavorable due to the swift onset of hypovolaemia and sepsis, leading to multiorgan failure.
Definition: Ischaemic necrosis of a section of the small intestine. Epidemiology • Typically observed in those over 50 years of age.
Aetiology • Thrombosis associated with an unstable atherosclerotic plaque in the superior mesenteric artery. • Thromboemboli originating from the left ventricle or left atrium. • Hypovolemia.
Pathogenesis A sudden decrease in blood flow through the superior mesenteric artery results in ischemic necrosis of a portion of the small intestine. Massive hemorrhage into the infarcted colon results in hypovolemia. Bacteria swiftly infiltrate the necrotic gut wall, resulting in sepsis.
Presentation: • Sudden onset of intense stomach pain accompanied by hematochezia and hypovolemia.
Macroscopy The infarcted small intestine exhibits a dusky purple hue. Upon incision of the intestinal segment, substantial quantities of blood are observed within the lumen, and the mucosal surface appears fragile and necrotic. Histopathology • Complete thickness necrosis of the intestinal wall
.
Prognosis • Timely laparotomy is crucial for the resection of the infarcted bowel segment. • Prognosis is typically unfavorable due to the swift onset of hypovolaemia and sepsis, leading to multiorgan failure.
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Pathology – Pneumothorax
Definition • The accumulation of air in the pleural cavity.
Epidemiology: Prevalent. • Males are impacted more significantly than females.
Aetiology
Spontaneous pneumothorax generally manifests in slender, tall young males. The phenomenon is believed to originate from the rupture of small, fragile apical blebs in lung tissue caused by lung expansion. • Preexisting pulmonary conditions, such as COPD, asthma, pneumonia, tuberculosis, cystic fibrosis, sarcoidosis, lung cancer, and idiopathic pulmonary fibrosis (IPF). Uncommon disorders frequently linked to pneumothorax encompass pulmonary Langerhans cell histiocytosis, pulmonary lymphangioleiomyomatosis, and thoracic endometriosis. • Trauma, such as penetrating thoracic injury and rib fractures. • Iatrogenic, for instance, subclavian vein cannulation and lung biopsy.
Pathogenesis
Air escapes from the compromised lung into the pleural cavity until the pressures equilibrate. The lung collapses to a varying extent, contingent upon the magnitude of the pneumothorax. • Infrequently, the tissues next to the pulmonary lesion function as a unidirectional valve, obstructing pressure equalization. The persistent accumulation of pressure and volume in the pleural cavity displaces mediastinal structures, resulting in cardiorespiratory arrest (tension pneumothorax).
Presentation:
• Abrupt onset of unilateral pleuritic thoracic discomfort. • Breathlessness may occur, contingent upon the magnitude of the pneumothorax. Individuals with preexisting pulmonary conditions typically observe an exacerbation of their symptoms.
Radiology
• Air is present in the pleural space alongside various degrees of lung collapse. Histopathology: Apical lung tissue removed from patients with spontaneous pneumothoraces has one or more bullae linked to subpleural alveolar collapse and fibrosis. The superficial visceral pleura exhibits reactive mesothelial hyperplasia and inflammation, frequently characterized by an abundance of eosinophils.
Prognosis: Approximately one-third of patients with spontaneous pneumothorax experience recurring episodes, typically on the same side.
Definition • The accumulation of air in the pleural cavity.
Epidemiology: Prevalent. • Males are impacted more significantly than females.
Aetiology
Spontaneous pneumothorax generally manifests in slender, tall young males. The phenomenon is believed to originate from the rupture of small, fragile apical blebs in lung tissue caused by lung expansion. • Preexisting pulmonary conditions, such as COPD, asthma, pneumonia, tuberculosis, cystic fibrosis, sarcoidosis, lung cancer, and idiopathic pulmonary fibrosis (IPF). Uncommon disorders frequently linked to pneumothorax encompass pulmonary Langerhans cell histiocytosis, pulmonary lymphangioleiomyomatosis, and thoracic endometriosis. • Trauma, such as penetrating thoracic injury and rib fractures. • Iatrogenic, for instance, subclavian vein cannulation and lung biopsy.
Pathogenesis
Air escapes from the compromised lung into the pleural cavity until the pressures equilibrate. The lung collapses to a varying extent, contingent upon the magnitude of the pneumothorax. • Infrequently, the tissues next to the pulmonary lesion function as a unidirectional valve, obstructing pressure equalization. The persistent accumulation of pressure and volume in the pleural cavity displaces mediastinal structures, resulting in cardiorespiratory arrest (tension pneumothorax).
Presentation:
• Abrupt onset of unilateral pleuritic thoracic discomfort. • Breathlessness may occur, contingent upon the magnitude of the pneumothorax. Individuals with preexisting pulmonary conditions typically observe an exacerbation of their symptoms.
Radiology
• Air is present in the pleural space alongside various degrees of lung collapse. Histopathology: Apical lung tissue removed from patients with spontaneous pneumothoraces has one or more bullae linked to subpleural alveolar collapse and fibrosis. The superficial visceral pleura exhibits reactive mesothelial hyperplasia and inflammation, frequently characterized by an abundance of eosinophils.
Prognosis: Approximately one-third of patients with spontaneous pneumothorax experience recurring episodes, typically on the same side.
