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last minute revision GIT pathology.pdf

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PreciousField

Uploaded by PreciousField

Ibn Sina National College for Medical Studies

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pathology gastrointestinal esophagus anatomy

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LAST MINUTE REVISION OF GIT PATHOLOGY Esophagus Mechanical Obstruction Atresia and fistulas can lead to regurgitation during feeding, most commonly at or near the tracheal bifurcation. Stenosis in adults can cause progressive dysphagia to solids and fluids, caused by fibrous thic...

LAST MINUTE REVISION OF GIT PATHOLOGY Esophagus Mechanical Obstruction Atresia and fistulas can lead to regurgitation during feeding, most commonly at or near the tracheal bifurcation. Stenosis in adults can cause progressive dysphagia to solids and fluids, caused by fibrous thickening of the submucosa due to inflammation and scarring. Functional Obstruction Achalasia is characterized by incomplete LES relaxation, increased LES tone, and esophageal aperistalsis. Hiatal hernia can lead to symptoms such as heartburn, regurgitation, mucosal ulceration, bleeding, and perforation. Lacerations (Mallory Weiss Syndrome) Longitudinal tears in the esophagus at the esophagogastric junction can occur in chronic alcoholics after severe vomiting, leading to hematemesis. Esophageal Varices Portal hypertension can lead to the formation of dilated vessels called varices, which may produce no symptoms until they rupture, causing massive hematemesis and death. Esophagitis Chemical esophagitis can be caused by irritants including alcohol, corrosive acids or alkalis, excessively hot fluids, heavy smoking, and iatrogenic factors. Infectious esophagitis can be caused by viruses and is most frequent immunosuppressed individuals. Reflux Esophagitis Reflux of gastric contents is the most frequent cause of esophagitis and may lead to complications such as esophageal ulceration, hematemesis, melena, stricture development, and Barrett esophagus. Barrett Esophagus It is a complication of chronic GERD, characterized by intestinal metaplasia within the esophageal squamous mucosa and presents with areas of mucosal erythema of the lower esophagus and islands of normal pale esophageal squamous mucosa. Esophageal Tumors Risk factors for squamous cell carcinoma include alcohol and tobacco use, poverty, caustic esophageal injury, achalasia, frequent consumption of very hot beverages, previous radiation therapy to the mediastinum. Adenocarcinoma risk factors include Barrett esoph,-standing GER, tobacco use, obesity, and previous radiation therapy to the mediastinum. Adenocarcinoma Risk Factors Diets rich in fresh fruits and vegetables show reduced adenocarcinoma risk. Inc is seven times higher in men than in women, with variations different countries. Clinical Presentation and Survival Rates features include pain, difficulty swallowing, weight loss, chest pain, and vomiting. Overall 5-year survival rate is less than 25%, but adenocarcinomas limited to mucosa or submucosa have an 80% survival rate. Stomach Mechanisms of Gastric Mucosa Protection The mucus layer safeguards the gastric epithelium. Bicarbonate ion secretion maintains a neutral pH in the mucosa. Vascular Support to Gastric Mucosa Rich vascular supply delivers oxygen, bicarbonate, and nutrients. Helps wash away excess acid, contributing to mucosal protection. Protective Effects of Prostaglandins Enhanced bicarbonate secretion and increased vascular perfusion aid in mucosal defense. Congenital Disorders - Pyloric Stenosis Characterized by abnormal muscle hypertrophy at the pylorus. Presents with projectile vomiting and is more common in males. Inflammatory Diseases of the Stomach Includes acute gastritis, a transient inflammatory process with various causes. Involves acute peptic ulceration with erosions penetrating the mucosa. Helicobacter pylori Gastritis 90% associated with chronic gastritis affecting the antrum. Infection may lead to peptic ulcer disease and increased cancer risk. Autoimmune Gastritis Characterized by antibodies to parietal cells and intrinsic factor. Can induce hypergastrinemia and lead to Vitamin B12 deficiency. Peptic Ulcer Disease Mostly associated with H. pylori infection or NSAIDs. More prevalent in gastric antrum and first part of duodenum. Peptic Ulcers Heal by epithelial regeneration and fibrosis, with potential complications like pyloric stenosis or hourglass deformity. Clinical features include epigastric burning or aching pain, nausea, vomiting, bloating, and belching. Neoplastic Disease of the Stomach Gastric Adenocarcinoma is the most common stomach malignancy, influenced by mutations, chronic gastritis, and specific risk factors. Classified based on gross and histologic morphology, with clinical features like dyspepsia, dysphagia, and lymph node metastasis. Pathogenesis of Gastric Adenocarcinoma Involves mutations in CDH1, loss of E cadherin function, chronic gastritis, and H. pylori infection. Classifications into intestinal and diffuse types based on morphology, each with distinct clinical features. Clinical Features and Prognosis Features include dyspepsia, weight loss, anemia, and lymph node metastasis. 5-years survival rate for early gastric cancer post-surgical resection can exceed 90%, emphasizing early detection's importance. Small and large intestines Developmental Anomalies of Small and Large Intestines Atresia, particularly duodenal atresia, represents a common complete lumen development failure in the small and large intestines. Meckel diverticulum, often found in the ileum, features a blind-ended tubular protrusion with all bowel wall layers, which may contain functioning gastric mucosa. Hirschsprung Disease This disease is characterized by an aganglionic segment that lacks essential plexuses, leading to colon obstruction. Symptoms include delays in meconium passage, vomiting, and potential enterocolitis. Bowel Obstruction - Mechanical Causes Common mechanical causes of bowel obstruction may include hernias, adhesions, intussusception, and volvulus. Hernias involve protrusion through weak abdominal walls, while intussusception refers to telescoping of bowel segments. Volvulus twisting of a loop of bowl Malabsorption Syndromes Causes of malabsorption syndromes may encompass defective digestion, mucosal abnormalities, and reduced small intestinal surface area, infections , lymphatic obstruction May be lead into consequences (Endocrine system , skin , nervous system , MSK , hematopoietic system ) Symptoms of malabsorption syndromes can include steatorrhea, weight loss, and musculoskeletal issues. Celiac Disease This is characterized by an immune reaction to gluten affecting and reduction in small intestine absorption, with diagnosis involving villous atrophy on biopsy. Complications of celiac disease may include lymphomas, skin disorder called dermatitis herpetiformis Inflammatory Bowel Disease - Crohn's Disease Crohn's disease is defined by transmural inflammation, noncaseating granulomas, and fistula formation, most commonly located at terminal ileum Symptoms of Crohn's disease include diarrhea, abdominal pain, and extra-intestinal complications such as uveitis. Consequences of Crohn's Disease Debilitating effects of Crohn's disease may involve fistula formation, abscesses, intestinal strictures, and increased carcinoma risk. The disease can lead to complications affecting other organs and systems. Genetic and Immunologic Factors in IBD Genetic predisposition and aberrant immune responses play crucial roles in inflammatory bowel diseases. While Crohn's disease can affect any bowel level, ulcerative colitis is associated with specific HLA genes. Ulcerative Colitis An Ulceroinflammatory disease affecting the colon, limited to the mucosa and submucosa. Possible associations with migratory polyarthritis, sacroiliitis, ankylosing spondylitis, uveitis, erythema nodosum, and hepatic involvement. Clinical Features of Ulcerative Colitis Key clinical features include attacks of bloody mucoid diarrhea, cramps, tenesmus, and colicky lower abdominal pain. Fever, weight loss, serious bleeding, and fluid and electrolyte imbalance can also occur. Microscopic Features of Ulcerative Colitis Notably, well-formed granulomas are absent, and mucosal ulcers rarely extend below the submucosa. Comparison: Crohn Disease vs. Ulcerative Colitis Distinguishing macroscopic and microscopic features can differentiate Crohn Disease from Ulcerative Colitis. Tumors of the Small and Large Intestines Various types of polyps, including adenomas with the potential to progress to cancer, are noted. Familial polyposis syndromes, such as Familial Adenomatous Polyposis (FAP), are mentioned along with associated risks. Colorectal Carcinoma Factors influencing the development of colorectal carcinoma include environmental, dietary, and genetic factors. Two distinct pathways for colon cancer development, namely the APC/catenin pathway and mismatch repair pathway, are highlighted. Molecular Pathways in Colorectal Carcinoma Differences in clinical phenotypes, histopathology, and genetics are associated with adenocarcinoma sequence and microsatellite instability. Diagnosis and Staging Methods for diagnosing colorectal tumors, such as digital rectal examination and colonoscopy with biopsy, are discussed. Utilization of Duke's classification for staging to determine the extent of the tumor is also mentioned. Colon Cancer Findings Barium enema and colonoscopy revealed multiple instances of adenocarcinoma in the rectosigmoid region and rectum. Additionally, diverticula were found in the sigmoid colon, indicating a common condition in developed nations with low-fiber diets. Hepatobiliary system Hepatitis Classification and Causes Hepatitis is characterized by patterns of hepatocyte injury with inflammation and scarring. Causes encompass hepatitis viruses, autoimmune factors, drugs, and toxins. Morphological Changes in Hepatitis Morphological alterations vary from mild mottling to massive hepatic necrosis. Patterns include ballooning degeneration, apoptosis, necrosis, and intracellular accumulation. Clinical Manifestations of Liver Disease Clinical signs of hepatic failure entail jaundice, encephalopathy, and respiratory failure. Autoimmune hepatitis shares similarities with chronic viral hepatitis but responds to immunosuppressive therapy. Alcoholic and Nonalcoholic Fatty Liver Disease Alcohol and nonalcoholic fatty liver diseases can lead to steatosis, steatohepatitis, and cirrhosis. Excessive ethanol consumption is linked to various liver conditions in alcoholic liver disease. Mechanisms and Clinical Features Alcoholic liver diseases involve acetaldehyde-induced lipid peroxidation and inflammation mediated by cytokines. Patients with alcoholic cirrhosis may display malaise, weight loss, hepatomegaly, and liver dysfunction. Prognosis and Treatment Alcohol abstinence is essential for treating alcoholic liver disease. Survival rates significantly improve with abstinence but decline with continued alcohol consumption. Nonalcoholic Fatty Liver Disease (NAFLD) NAFLD is correlated with insulin resistance, obesity, and the metabolic syndrome. It can progress to steatohepatitis and cirrhosis, often asymptomatic until advanced stages. Diagnostic Techniques Diagnosis of liver diseases involves serum testing, autoantibody screening, liver biopsy, and imaging. Progression from steatosis to advanced liver disease generally occurs slowly, underscoring the importance of early detection. Jaundice Normal bilirubin production primarily from red cell breakdown and liver uptake for excretion. Gut bacteria degrade bilirubin, leading to yellow discoloration of skin and sclerae, Occurs when systemic retention of bilirubin produces serum level above 2.0 mg/dl ( normal adults below 1.2mg/dl) , in sever reach 30 to 40 mg/dl Commonly results in elevated bilirubin levels and compromised liver function. Cholestasis Systemic retention of bilirubin and other solutes (particularly but also salts and cholesterol) due to conditions like hepatitis or bile flow obstruction. Hepatic Encephalopathy Range of brain dysfunction from behavioral changes to deep coma, often linked to liver disease. Features may include rigidity, seizures, hyperreflexia, and asterixis. Liver Cirrhosis A diffuse liver process with fibrosis and abnormal nodules, caused by various factors like chronic infections or autoimmune diseases. Clinical features range from anorexia and weight loss to potential hepatic failure.

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