GI Flashcards
T106 What is an aphthous ulcer?
A painful ulcer in the oral mucosa with a grayish base and erythematous rim. Self-resolving in a few days, but tends to recur. Linked to inflammatory bowel disease or Behçet syndrome.
What causes herpes simplex in the oral cavity?
Caused by HSV1 (most common) or HSV2, presenting as grouped vesicles on an erythematous base. Reactivates from the trigeminal ganglion following stress or illness.
Describe oral candidiasis
Caused by Candida albicans in immunosuppressed patients or those with disrupted flora. Appears as a gray to white pseudomembrane that can be scraped off. Early sign of AIDS.
What is a fibroma?
A submucosal nodular fibrous tissue mass caused by chronic irritation, commonly found on the buccal mucosa. Appears as a smooth pink nodule.
What is a pyogenic granuloma?
An erythematous, hemorrhagic, exophytic mass usually found on the gingiva of children and young adults. Richly vascular and often ulcerated.
Define leukoplakia.
A white plaque that cannot be scraped off, often caused by hyperkeratosis. Associated with tobacco use and may transform into squamous cell carcinoma.
Define erythroplakia.
Red, granular, circumscribed areas with marked epithelial dysplasia. Has a high risk of malignant transformation, with over 50% of cases becoming cancerous.
What are the risk factors for oral squamous cell carcinoma?
Leukoplakia, erythroplakia, tobacco use, alcohol abuse, chronic irritation, HPV16 and HPV18, and immune suppression.
Where are squamous cell carcinomas most commonly found in the oral cavity?
The ventral surface of the tongue, floor of the mouth, and lower lip.
Describe the morphology of oral squamous cell carcinoma.
White to gray circumscribed thickenings of the mucosa, developing from dysplastic precursor lesions. Histologic patterns range from well-differentiated keratinizing neoplasms to anaplastic tumors.
What are the clinical features of oral squamous cell carcinoma?
50% mortality rate within 5 years. Causes local pain or difficulty in chewing, may be asymptomatic, and can metastasize to cervical nodes, mediastinal nodes, lungs, and liver.
What are the major and minor salivary glands?
Major salivary glands are the parotid, submandibular, and sublingual glands. Minor salivary glands are distributed throughout the mucosa.
What is xerostomia?
Xerostomia is defined as a dry mouth resulting from decreased production of saliva. It is a major feature of Sjögren syndrome and can lead to increased dental caries, candidiasis, and difficulty swallowing and speaking.
What causes sialadenitis?
Sialadenitis is inflammation of the major salivary glands due to trauma or infections. It can be viral (e.g., mumps affecting the parotid gland), bacterial (e.g., S. aureus), or autoimmune (e.g., Sjögren syndrome).
What are the complications of mumps in adults?
In adults, mumps can cause pancreatitis or orchitis (inflammation of the testis).
Describe a mucocele.
A mucocele is a cyst-like space resulting from blockage or rupture of a salivary gland duct, leading to saliva leaking into surrounding tissue. It is lined by inflammatory granulation tissue or fibrous connective tissue and filled with mucin and inflammatory cells.
What is bacterial sialadenitis, and what causes it?
Bacterial sialadenitis is inflammation of the salivary glands occurring secondarily to ductal obstruction due to stone formation (sialolithiasis) or after retrograde entry of oral cavity bacteria (e.g., S. aureus, S. viridians).
How common are salivary gland neoplasms, and where do they most often occur?
Salivary gland neoplasms are relatively uncommon, representing less than 2% of all human tumors. About 80% of these tumors occur within the parotid glands, usually in individuals aged 60-70 years.
What is the relationship between the size of the salivary gland and the likelihood of malignancy?
The likelihood that a salivary gland tumor is malignant is inversely proportional to the size of the gland. Smaller glands have a higher likelihood of malignancy (e.g., sublingual glands).
What is the most common tumor of the parotid gland, and what is the most common malignant salivary gland tumor?
The most common tumor of the parotid gland is pleomorphic adenoma, while the most common malignant tumor of the salivary glands is mucoepidermoid carcinoma.
Describe pleomorphic adenoma
Pleomorphic adenoma arises at the superficial parotid, causing a painless, mobile swelling at the angle of the jaw. It consists of a mixture of ductal (epithelial) and myoepithelial cells, exhibiting both epithelial and mesenchymal differentiation, hence the name “mixed tumor.” It appears as a rounded, well-demarcated mass with a characteristic heterogeneity of epithelial cells or myoepithelial cells within a mesenchyme-like background.
Describe mucoepidermoid carcinoma
Mucoepidermoid carcinoma is the most common primary malignant tumor of the salivary glands, composed of variable mixtures of squamous cells and mucus-secreting cells. Morphologically, it is a well-circumscribed, gray tumor often containing small cysts with mucin. Microscopically, it shows clusters of mucous, squamous, and intermediate cells.
T107 What are the causes of mechanical obstruction in the esophagus?
Mechanical obstruction in the esophagus can be caused by developmental abnormalities, fibrotic stricture, or tumors. Common conditions include atresia and esophageal stenosis.
Describe esophageal atresia.
Esophageal atresia is a condition where a thin, noncanalized cord replaces a segment of the esophagus. It most commonly occurs at or near the tracheal bifurcation and is often associated with a fistula connecting the esophagus and the bronchus/trachea.
What is esophageal stenosis, and what causes it?
Esophageal stenosis is generally caused by fibrous thickening of the submucosa, atrophy of the muscularis propria, and secondary epithelial damage. It often results from chronic gastroesophageal reflux, irradiation, or caustic injury, leading to inflammation and scarring.
What is functional obstruction in the esophagus, and what causes it?
Functional obstruction is caused by esophageal dysmotility characterized by discoordinated contraction or spasm of the muscularis propria, resulting in impaired forward movement of food to the stomach.
What is achalasia, and what are its characteristics?
Achalasia is the incomplete relaxation of the lower esophageal sphincter in response to swallowing, causing obstruction and dilation of the proximal esophagus. It is characterized by esophageal aperistalsis, incomplete relaxation of the lower esophageal sphincter, and increased tone of the lower esophageal sphincter.
What are the differences between primary and secondary achalasia?
Primary achalasia is idiopathic, caused by the failure of distal esophageal inhibitory neurons and damage to myenteric ganglions. Secondary achalasia is caused by pathological processes that impair esophageal function.
What are the clinical features and risks associated with achalasia?
Achalasia presents with dysphagia and stasis of food, which can lead to inflammation and ulceration. There is also a 5% risk of developing squamous cell carcinoma in patients with achalasia.
What is ectopia in the esophagus?
Ectopia is the presence of ectopic gastric mucosa, usually asymptomatic. The most frequent site is the upper third of the esophagus.
Describe a hiatal hernia and its types.
A hiatal hernia involves the separation of the diaphragmatic crura and the esophageal wall, allowing a segment of the stomach to protrude above the diaphragm. There are two types: sliding hernia (95% of cases, bell-shaped dilation) and paraesophageal hernia (a separate portion of the stomach enters the thorax through a widened foramen).
What is esophagitis?
Esophagitis is an injury to the esophageal mucosa with subsequent inflammation.
What are Mallory-Weiss tears and their pathogenesis?
Mallory-Weiss tears are longitudinal tears at the esophagogastric junction, often caused by severe vomiting with inadequate relaxation of the lower esophageal sphincter. They can result in hematemesis.
What is Boerhaave syndrome?
Boerhaave syndrome is characterized by transmural esophageal tears and mediastinitis. It is a rare but catastrophic event.
What is reflux esophagitis and its contributing factors?
Reflux esophagitis, often due to gastroesophageal reflux disease (GERD), is caused by impaired anti-reflux mechanisms, sliding hiatal hernia, increased gastric volume, obesity, pregnancy, alcohol, and tobacco use.
What are the clinical features and complications of reflux esophagitis?
Symptoms include heartburn, chest pain, and sour-tasting regurgitation. Complications can include esophageal ulceration, stricture development, and Barrett esophagus.
What causes chemical esophagitis?
Chemical esophagitis is caused by irritants such as alcohol, acids or alkalis, excessively hot fluids, and heavy smoking, leading to pain, particularly odynophagia (pain with swallowing).
What are common infectious causes of esophagitis?
Esophageal infections are common in immunosuppressed patients and can be caused by herpes simplex virus, cytomegalovirus (CMV), or fungal organisms like Candida.
What are the characteristics of eosinophilic esophagitis?
Eosinophilic esophagitis is an allergic inflammatory condition with infiltration by large numbers of eosinophils, particularly away from the gastroesophageal junction. It is often linked to food allergies and may present with other atopic conditions.
What are esophageal varices, and what conditions cause them?
Esophageal varices are abnormally dilated veins in the submucosal venous plexus of the distal esophagus, commonly caused by portal hypertension due to conditions like cirrhosis or hepatic schistosomiasis.
What are the clinical implications of esophageal varices?
Esophageal varices often produce no symptoms until they rupture, leading to massive hemorrhage into the esophageal lumen and wall. They are found in about 90% of cirrhotic patients and are associated with a high risk of bleeding and potential hepatocellular carcinoma.
T108 What is Barrett esophagus and how does it develop?
Barrett esophagus is a complication of long-standing gastroesophageal reflux disease (GERD) where chronic acid reflux causes metaplasia of the esophageal squamous epithelium to nonciliated columnar epithelium with goblet cells. This metaplasia occurs through the reprogramming of stem cells and can theoretically be reversed with treatment of GERD.
Who is more affected by Barrett esophagus and what risk does it pose?
Barrett esophagus affects males more than females and significantly increases the risk of developing esophageal adenocarcinoma.
What is the morphology of Barrett esophagus?
In Barrett esophagus, endoscopy reveals red mucosa extending from the gastroesophageal junction upward, correlating with the microscopic appearance of metaplastic columnar epithelium replacing the normal squamous epithelium.
What are the two major variants of esophageal carcinoma?
The two major variants of esophageal carcinoma are adenocarcinoma, which is common in Western countries and affects the lower third of the esophagus, and squamous cell carcinoma, which is the most common worldwide and involves the middle third of the esophagus.
What are the risk factors for squamous cell carcinoma of the esophagus?
Risk factors for squamous cell carcinoma of the esophagus include irritation from alcohol and tobacco use, obstructive esophageal diseases like achalasia, severe chemical injury, and chronic esophagitis.
It affects men more than women and has a higher prevalence in non-Western countries. It is also associated with HPV and abnormalities in the p16 and p53 genes.
What is the morphology of squamous cell carcinoma of the esophagus?
Squamous cell carcinoma of the esophagus tends to appear in the upper and middle thirds. Early lesions appear as small, gray-white plaques that can grow into tumor masses.
These masses can be polypoid exophytic, ulcerating, or diffuse infiltrative neoplasms causing wall thickening and lumen narrowing.
Microscopically, these carcinomas are composed of nests of malignant cells that partially recapitulate the stratified organization of squamous epithelium.
What are the clinical features of squamous cell carcinoma of the esophagus?
The first symptoms of squamous cell carcinoma of the esophagus include weight loss, difficulty swallowing, and hoarseness due to invasion of the recurrent laryngeal nerve.
At diagnosis, tumors are usually large and have invaded the esophageal wall, potentially extending into adjacent structures like the respiratory tree, aorta, mediastinum, and pericardium, causing further complications.
What is the origin of most esophageal adenocarcinomas?
Most adenocarcinomas arise from Barrett metaplasia or from glandular metaplasia in the esophageal mucosa.
What genetic mutations are involved in the progression from Barrett esophagus to adenocarcinoma?
Mutations in p53 gene, HER2/c-ERB-B2, cyclin D1, RB, and p16 genes.
Which demographic is more commonly affected by esophageal adenocarcinoma?
It is 7 times more common in men and has higher prevalence in western countries.
Where in the esophagus are adenocarcinomas usually located?
Usually in the distal 1/3 of the esophagus and may invade the gastric cardia.
What are the morphological characteristics of esophageal adenocarcinoma?
Moderate or well-differentiated mucin-producing tumors, often seen adjacent to Barrett mucosa with high-grade dysplasia.
What are the clinical features of esophageal adenocarcinoma?
Dysphagia to solids, then all food; weight loss, fatigue, weakness, and pain related to swallowing.
How does esophageal adenocarcinoma typically metastasize?
Metastasis occurs early due to the extensive lymphatic network, involving gastric and celiac lymph nodes. Recurrences are common.
T109 What is pyloric stenosis and how does it present clinically?
Pyloric stenosis is a congenital disorder caused by hypertrophy and hyperplasia of the pylorus muscle, leading to functional gastric outlet obstruction. It presents clinically around 2 weeks after birth with non-bilious vomiting, visible peristalsis on the abdominal surface, and is corrected by surgical incision of the hypertrophied muscle.
What are the two main causes of chronic gastritis and their complications?
Chronic gastritis is mainly caused by Helicobacter pylori infection and autoimmune gastritis. H. pylori infection can lead to peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and increased risk of gastric adenocarcinoma.
Autoimmune gastritis can cause loss of parietal cells, achlorhydria, hypergastrinemia, antral endocrine cell hyperplasia, vitamin B12 deficiency, megaloblastic anemia, and increased risk of adenocarcinoma.
Describe the pathogenesis and morphology of H. pylori-induced chronic gastritis.
H. pylori colonizes the mucus layer of the stomach, using urease to produce ammonia, increasing acid production. It manifests as antral gastritis with high acid production, potentially causing peptic ulcers, MALT lymphoma, and intestinal metaplasia. Morphologically, it involves superficial mucus colonization, neutrophils in the lamina propria and epithelium, lymphoid aggregates, and intestinal metaplasia.
What are the clinical features and complications of H. pylori-induced chronic gastritis?
Clinical features include nausea, vomiting, and a urea breath due to ammonia production by urease. Hematemesis is uncommon. Complications include peptic ulcer disease, MALT lymphoma, and increased risk for gastric adenocarcinoma.
How does autoimmune gastritis differ from H. pylori-induced gastritis in terms of location and effects on gastric physiology?
Autoimmune gastritis typically affects the body and fundus, sparing the antrum, and causes hypergastrinemia due to loss of parietal cells.
This leads to achlorhydria, hyperplasia of antral G cells, and vitamin B12 deficiency causing pernicious anemia. In contrast, H. pylori-induced gastritis often affects the antrum, increasing acid production without hypergastrinemia.
What are the morphological features of autoimmune gastritis?
Autoimmune gastritis shows diffuse atrophy of the mucosa in the body and fundus, an inflammatory infiltrate primarily composed of lymphocytes, macrophages, and plasma cells, and is deep and centered on the gastric glands.
There is extensive loss of parietal and chief cells, leading to increased risk of intestinal metaplasia and adenocarcinoma.
What are the complications of autoimmune gastritis?
Complications include achlorhydria, hypergastrinemia, hyperplasia of antral endocrine cells, vitamin B12 deficiency, megaloblastic anemia (pernicious anemia), and increased risk for developing gastric adenocarcinoma.
What is acute gastritis and what are its potential symptoms?
Acute gastritis is an acute mucosal inflammatory process that can be accompanied by nausea, vomiting, and pain. In severe cases, it may cause mucosal erosion, ulceration, hemorrhage, hematemesis (vomiting blood), and melena (black, tarry stools).
What causes acute gastritis?
Acute gastritis is caused by increased stomach acidity or reduced protective mechanisms of the mucosa. Risk factors include heavy use of NSAIDs (which inhibit prostaglandin formation), excessive alcohol consumption, ingestion of harsh chemicals, cancer chemotherapy drugs, increased intracranial pressure (leading to increased vagal stimulation and acid production), and severe shock or burns (causing decreased blood flow to organs).
What are the morphological features of mild and severe acute gastritis?
Mild gastritis shows intact surface epithelium with scattered neutrophils above the basement membrane. Severe acute gastritis features erosion and hemorrhage, known as acute erosive hemorrhagic gastritis.
What is an acute peptic ulcer and how does it differ from a chronic ulcer?
An acute peptic ulcer is characterized by a lack of mucosal layer, appearing as a depression with necrotic debris and neutrophils at the bottom. Unlike chronic ulcers, acute ulcers do not show granulation tissue and fibrosis underneath upon healing.
Chronic ulcers have granulation tissue and fibrosis due to ongoing repair.
What are the specific causes of acute peptic ulcers and their clinical presentation?
Acute peptic ulcers can be caused by:
- NSAIDs, which inhibit prostaglandin production, reducing bicarbonate secretion and blood perfusion.
- Curling ulcers, which occur due to hypoxia from shock or burns, often presenting as multiple ulcers in the stomach and proximal duodenum.
- Cushing ulcers, which are associated with increased intracranial pressure (IICP).
Clinically, acute peptic ulcers present with hematemesis (coffee-ground vomit) and nausea. Treatment involves addressing the underlying cause and administering proton pump inhibitors.
T110 What is an ulcer, and where are peptic ulcers most commonly found?
An ulcer is a focal lack of mucosa. Peptic ulcers are most commonly found in the stomach and duodenum.
What are the causes of acute peptic ulceration?
Acute peptic ulceration can be caused by acute peptic injury, NSAID therapy, and severe physiological stress such as shock. Other contributing factors include excessive alcohol consumption, ingestion of harsh chemicals, and cancer chemotherapy.
What are the three types of acute ulcers and their associated conditions?
- Stress ulcers: Affect patients with shock, sepsis, or severe trauma, often presenting as multiple ulcerations.
- Curling ulcers: Occur in the stomach and proximal duodenum in severe burn victims.
- Cushing ulcers: Arise in the stomach, duodenum, or esophagus in persons with increased intracranial pressure (IICP), associated with increased vagal stimulation and elevated gastric acid secretion.
How do NSAIDs contribute to acute peptic ulceration?
NSAIDs prevent prostaglandin synthesis, eliminating the protective effects of prostaglandins, which include enhanced bicarbonate secretion and increased vascular perfusion. This increases the risk of mucosal injury and ulceration.
What is the morphology of acute gastric ulcers?
Acute gastric ulcers range from shallow erosions to deeper lesions that penetrate the mucosa. They are typically small (<1 cm in diameter), sharply demarcated, with normal adjacent mucosa.
The ulcer base is often stained brown to black by acid-digested extravasated red cells. There is no scarring, granulation tissue, or fibrosis under the ulcer, but necrotic debris and neutrophils are present
What are the clinical features and potential complications of gastric ulcers?
Clinical features of gastric ulcers include nausea, vomiting, and coffee-ground hematemesis.
Potential complications include bleeding (which may be massive and require transfusion in 1-4% of patients), perforation, obstruction, and loss of function due to scarring.
What are the primary causes of peptic ulcer disease (PUD)?
Peptic ulcer disease (PUD) is most often associated with Helicobacter pylori infection or NSAID use.
What is the pathogenesis of peptic ulcer disease (PUD)?
PUD is caused by imbalances of mucosal defenses and damaging forces, often developing on a background of chronic gastritis.
Key factors include gastric hyperacidity, H. pylori-induced hyperchlorhydric chronic gastritis, chronic NSAID use, parietal cell hyperplasia, excessive secretory response, and impaired inhibition of stimulatory mechanisms like gastrin release.
Zollinger-Ellison syndrome, caused by a gastrin-secreting tumor, also leads to PUD.
What are the common locations and histological features of peptic ulcers?
Peptic ulcers commonly appear in the proximal duodenum near the pyloric valve and in the stomach on the small curvature in the antrum.
- Histologically, they show a base with necrotic debris, underlying granulation tissue rich in blood vessels, and fibrosis beneath.
What are the clinical features of peptic ulcer disease?
Peptic ulcer disease presents with epigastric pain that resolves after a meal in the case of duodenal ulcers and worsens after a meal in the case of gastric ulcers.
What are the complications of chronic peptic ulcer disease?
Complications include:
Upper gastrointestinal bleeding due to arterial erosion.
Perforation, leading to communication between the stomach and peritoneal space.
Penetration into adjacent organs (liver, pancreas, greater omentum) without peritoneal cavity communication.
Gastric stenosis from extensive fibrosis.
Rare malignant transformation with irregular, anfractuous ulcer borders.
T111 What is the most common type of primary malignant tumor in the stomach?
The most common type of primary malignant tumor in the stomach is gastric adenocarcinoma, accounting for about 90% of cases.
What are the types of gastric adenocarcinoma according to the Lauren classification?
The Lauren classification of gastric adenocarcinoma includes three types: intestinal type, diffuse type, and mixed type.
What is the key genetic mutation associated with diffuse-type gastric adenocarcinoma?
The key genetic mutation associated with diffuse-type gastric adenocarcinoma is the loss of the CDH1 gene, which encodes E-cadherin.
What role does the CDH1 gene play in diffuse gastric cancer?
The CDH1 gene encodes E-cadherin, a cell adhesion molecule crucial for normal cell differentiation and tissue architecture. Its mutation leads to loss of cell adhesion, contributing to the development of diffuse gastric cancer.
What is the progression sequence for developing gastric cancer?
The progression sequence for developing gastric cancer includes atrophic gastritis, followed by dysplasia, adenoma, and then adenocarcinoma. This process involves multiple genetic mutations, including mutations to the p53 tumor suppressor gene.
What are the environmental risk factors associated with intestinal-type gastric cancer?
Environmental risk factors for intestinal-type gastric cancer include diets high in nitrosamines (e.g., smoked foods), low consumption of fresh fruits, leafy vegetables, ascorbic acid, and beta-carotene. There is an increased prevalence in regions like Japan and Eastern Europe.
What condition is associated with the development of intestinal-type gastric adenocarcinoma?
Intestinal-type gastric adenocarcinoma often arises in the setting of atrophic gastritis, a condition characterized by chronic inflammation and destruction of stomach glands, leading to intestinal metaplasia.
How does Helicobacter pylori infection contribute to gastric adenocarcinoma?
Helicobacter pylori infection can cause chronic atrophic gastritis, leading to the destruction of stomach glands and the development of intestinal metaplasia, which increases the risk of gastric adenocarcinoma.
What are gastric polyps, and how are they related to gastric cancer?
Gastric polyps are growths on the lining of the stomach. Hyperplastic polyps, which are the most common, have increased malignant potential if larger than 0.5 cm. Adenomatous polyps also have a significant risk of cancer and require endoscopic follow-up after removal.
What percentage of gastric adenocarcinomas is associated with Epstein-Barr virus (EBV) infection, and what is the characteristic morphology?
About 10% of gastric adenocarcinomas are associated with Epstein-Barr virus (EBV) infection. EBV-positive tumors tend to occur in the proximal stomach, have a diffuse morphology, and are characterized by a marked lymphocytic infiltrate.
What are the two types of gastric adenocarcinoma according to the Lauren classification?
The Lauren classification separates gastric adenocarcinomas into intestinal and diffuse types.
Describe the macroscopic appearance of intestinal-type gastric adenocarcinoma.
Intestinal-type gastric adenocarcinoma typically presents as an elevated mass with heaped-up borders and central ulceration, usually involving the lesser curvature of the antrum.
What histological features characterize intestinal-type gastric adenocarcinoma?
Histologically, intestinal-type gastric adenocarcinoma displays irregular tubular structures with stratification and multiple lumens surrounded by reduced stroma, invading the gastric wall, and often associated with intestinal metaplasia in adjacent mucosa.
Describe the macroscopic appearance of diffuse-type gastric adenocarcinoma.
Diffuse-type gastric adenocarcinoma presents as “linitis plastica,” with a markedly thickened gastric wall due to desmoplasia and partially lost rugal folds.
What histological features characterize diffuse-type gastric adenocarcinoma?
Histologically, diffuse-type gastric adenocarcinoma consists of discohesive tumor cells that secrete mucus, forming “signet-ring cells,” and lacks glandular structures. The mucus may accumulate in the interstitium, producing large pools of mucus/colloid.
What are the common clinical features of gastric adenocarcinoma?
Gastric adenocarcinomas are generally asymptomatic initially but can present with abdominal discomfort, weight loss, early satiety, and anemia as they advance.
What is the most significant prognostic factor for gastric adenocarcinoma?
The most significant prognostic factor for gastric adenocarcinoma is the depth of tumor invasion at the time of diagnosis.
Describe the TNM classification used for staging gastric adenocarcinoma.
The TNM classification reflects the depth of tumor infiltration (T), lymph node involvement (N), and the presence of distant metastases (M). Early stages are confined to the mucosa and submucosa, while advanced stages extend into the muscularis propria and serosa, with potential invasion of adjacent organs.
What is Virchow node, and why is it significant in gastric adenocarcinoma?
Virchow node is the earliest lymph node metastasis involving the supraclavicular lymph nodes, significant in gastric adenocarcinoma for indicating regional and distal lymph node spread.
What is a Krukenberg tumor, and how is it related to gastric adenocarcinoma?
A Krukenberg tumor is a metastasis of gastric adenocarcinoma to the ovaries, characterized by signet-ring cells and desmoplasia.
What other types of tumors can arise in the stomach besides adenocarcinoma?
Other types of tumors that can arise in the stomach include extranodal lymphoma (e.g., marginal zone B-cell lymphoma, EBV-derived B-cell lymphoma) and carcinoid tumors (malignant proliferation of neuroendocrine cells).
What is a polyp?
A polyp is any nodule or mass that originates from the mucosa and projects above its level.
How common are gastric polyps, and what can cause their development?
Gastric polyps are uncommon. They may develop due to epithelial or stromal cell hyperplasia, inflammation, ectopia, or neoplasia.
What are hyperplastic polyps, and what causes them?
Hyperplastic polyps (80%-85%) arise in response to chronic gastritis and are composed of hyperplastic mucosal epithelium and inflamed edematous stroma. They are not true neoplasms.
What are fundic gland polyps, and what causes them?
Fundic gland polyps (~10%) occur sporadically and in persons with familial adenomatous polyposis (FAP). They are associated with the use of proton pump inhibitors, which reduce acidity, leading to increased gastrin secretion and glandular hyperplasia.
Where are fundic gland polyps typically located, and what are their characteristics?
Fundic gland polyps are typically located in the gastric body and fundus. They are well-circumscribed, often multiple, and composed of cystically dilated, irregular glands lined by flattened parietal and chief cells.
What are gastric adenomas, and what background do they commonly occur on?
Gastric adenomas (10%) almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia.
What is the risk associated with gastric adenomas, and where are they commonly located?
The risk for developing adenocarcinoma in gastric adenomas is related to the size of the lesion. They are commonly located in the antrum.
What type of epithelial change is exhibited by gastrointestinal adenomas?
Gastrointestinal adenomas exhibit epithelial dysplasia.
T112 What is atresia and how does it differ from stenosis?
Atresia is the complete failure of development of the intestinal lumen, most commonly affecting the duodenum (associated with Down syndrome). Stenosis is the narrowing of the intestinal lumen with incomplete obstruction.
What is intestinal duplication?
Duplication refers to saccular to tubular cystic structures pinched off from the intestine, which may or may not communicate with the lumen of the small intestine. Tubular duplication communicates with the lumen, while cystic duplication is completely pinched off.
What is Meckel diverticulum and what are its complications?
Meckel diverticulum results from failure of involution of the omphalomesenteric duct, creating a blind-ended tubular protrusion in the ileum. Complications include bleeding (especially if ectopic gastric mucosa is present), volvulus, infection, intussusception, and pernicious anemia if bacterial overgrowth depletes vitamin B12.
What is an omphalocele and how does it differ from gastroschisis?
Omphalocele is a congenital defect of the periumbilical abdominal musculature that creates a membranous sac into which the intestines herniate. Gastroschisis is the lack of formation of part of the abdominal wall, causing herniated intestines to be exposed to the external environment without a sac.
What is malrotation of the intestine and its potential complications?
Malrotation is the abnormal rotation of the developing bowel, preventing the intestine from assuming its normal intra-abdominal position. This can lead to volvulus or misdiagnosis of appendicitis, as pain may present in an atypical location.
What causes Hirschsprung disease and what are its key characteristics?
Hirschsprung disease is caused by the disrupted migration of neural crest cells to the lower rectum, resulting in an aganglionic segment that lacks the Meissner submucosal and Auerbach myenteric plexuses. This leads to a lack of peristaltic contractions and functional obstruction, causing dilation of the proximal, normally innervated colon.
What are the morphological features of Hirschsprung disease?
The aganglionic region may appear normal or contracted, while the proximal colon undergoes dilation due to distal obstruction. The critical lesion is the absence of ganglion cells and ganglia in both the muscle wall and submucosa.
What is megacolon?
Megacolon is the distension of the colon to a diameter greater than 6-7 cm. It can be either congenital or acquired.
What is Hirschsprung disease and what are its clinical features?
Hirschsprung disease is a congenital megacolon caused by the absence of the Meissner and Auerbach plexuses in segments of the colon (aganglionic segments). Clinical features include delayed passage of meconium, vomiting within 48-72 hours, and the principal threat of superimposed enterocolitis with fluid and electrolyte disturbances.
What are the causes of acquired megacolon?
Acquired megacolon may result from:
Chagas disease (Trypanosoma cruzi invasion destroys plexuses)
Organic obstruction (e.g., neoplasm or inflammatory stricture)
Toxic megacolon (complication of ulcerative colitis or Crohn disease)
Functional psychosomatic disorder (stool retention due to psychological reasons or long-term laxative abuse)
What is an abdominal hernia?
An abdominal hernia is a weakness or defect in the wall of the peritoneal cavity, allowing protrusion of a serosa-lined pouch of peritoneum called a hernia sac.
Where do acquired hernias most commonly occur?
Acquired hernias most commonly occur anteriorly through the inguinal and femoral canals, umbilicus, or at sites of surgical scars.
What complications can arise from a hernia?
Visceral protrusion into the hernia sac can lead to external herniation, which may become entrapped, impair venous drainage causing stasis and edema, leading to permanent entrapment (incarceration), and potentially resulting in arterial and venous compromise and infarction.
T113 What is the main blood supply to the intestines and how do collaterals help?
The main blood supply to the intestines comes from the celiac, superior mesenteric, and inferior mesenteric arteries. Collaterals from the proximal celiac, distal pudendal, and iliac circulations make it possible to tolerate the loss of blood supply from one artery.
What are the different extents of ischemic bowel disease?
Ischemic bowel disease can range from:
Mucosal infarction (extending no deeper than the muscularis mucosa)
Mural infarction (involving the mucosa and submucosa)
Transmural infarction (involving all three layers of the wall)
What typically causes mucosal or mural infarctions versus transmural infarctions?
Mucosal or mural infarctions are often secondary to acute or chronic hypoperfusion (e.g., cardiac failure, shock, dehydration, or vasoconstrictive drugs). Transmural infarction is generally caused by acute vascular obstruction (e.g., thromboembolism, vasculitis, thrombosis due to lupus anticoagulant or polycythemia vera).
What are the two phases of intestinal responses to ischemia?
Initial hypoxic injury: Occurs at the onset of vascular compromise; intestinal epithelial cells are relatively resistant to transient hypoxia.
Reperfusion injury: Initiated by the restoration of blood supply, associated with the greatest damage involving free radical production, neutrophil infiltration, and release of inflammatory mediators like complement proteins and cytokines.
What are watershed zones in the context of ischemic bowel disease?
Watershed zones are intestinal segments at the end of their respective arterial supplies that are particularly susceptible to ischemia due to their limited collateral blood supply.
What is the morphologic signature of ischemic intestinal disease?
The morphologic signature of ischemic intestinal disease is surface epithelial atrophy or necrosis with sloughing, accompanied by normal or hyperproliferative crypts.
What are the morphological characteristics of mucosal and mural infarctions in ischemic bowel disease?
Mucosal and mural infarctions may involve any level of the gut from the stomach to the anus. The disease frequently is segmental and patchy in distribution. The mucosa is hemorrhagic and often ulcerated, and severe disease includes extensive mucosal and submucosal hemorrhage and necrosis.
Describe the morphology of transmural infarction in ischemic bowel disease
Transmural infarction is characterized by coagulative necrosis of the muscularis propria within 1 to 4 days, often associated with purulent serositis and perforation.
What are the microscopic features of ischemic bowel disease?
Microscopic examination shows atrophy or sloughing of surface epithelium with hyperproliferative crypts. Reperfusion leads to acute inflammatory infiltrate, edema, and hemorrhage in the lamina propria. Chronic ischemia is accompanied by fibrous scarring, and acute ischemia may induce pseudomembrane formation due to superinfection and enterotoxin release.
What are the predisposing conditions for ischemic bowel disease?
Predisposing conditions include:
- Arterial thrombosis: Atherosclerosis, hypercoagulable states, aortic reconstructive surgery.
- Arterial embolism: Cardiac vegetations, myocardial infarction with mural thrombosis.
- Venous thrombosis: Hypercoagulable states induced by oral contraceptives or antithrombin III deficiency, cirrhosis, abdominal trauma.
Who is most at risk for ischemic bowel disease, and what are the acute clinical features?
Ischemic bowel disease tends to occur in older persons with coexisting cardiac or vascular disease. Acute transmural infarction typically manifests with sudden, severe abdominal pain and tenderness, and may progress to shock and vascular collapse within hours as a result of blood loss. Bacteria can enter the circulation as the mucosal barrier breaks down, potentially leading to sepsis. The mortality rate may exceed 50%.
What are the clinical implications of mucosal and mural infarctions in ischemic bowel disease?
Mucosal and mural infarctions may not be fatal by themselves but can progress to transmural infarctions, which are more severe. These types of infarctions can also result in radiation enterocolitis, where radiation-induced vascular injury produces changes similar to those seen in ischemic disease.
What is angiodysplasia, and how does it typically present?
Angiodysplasia is characterized by acquired structural abnormalities of submucosal and mucosal blood vessels, leading to tortuous dilation.
It is usually seen in the cecum and ascending colon due to high wall tension and typically presents after the sixth decade of life.
It often manifests as hematochezia, which is the passage of fresh blood through the anus.
What are the risk factors for angiodysplasia?
Risk factors for angiodysplasia include Osler-Weber-Rendu syndrome (autosomal dominant hereditary hemorrhagic telangiectasia) and CREST syndrome of scleroderma.
What are hemorrhoids, and how do they develop?
Hemorrhoids are variceal dilations of the anal and peri-anal submucosal venous plexuses.
They develop due to elevated venous pressure within the hemorrhoidal plexus, commonly after the age of 50.
Predisposing conditions include straining upon defecation, chronic constipation, venous stasis, pregnancy, and hypertension due to liver cirrhosis.
How are hemorrhoids classified, and what are their characteristics?
Hemorrhoids can be classified as:
External: Varices of the inferior hemorrhoidal plexus that occur outside the anus, covered by anal mucosa; more prone to thrombosis and very painful.
Internal: Varices of the superior and middle hemorrhoidal plexuses that occur inside the rectum; non-painful but may prolapse outside the anus.
What is the histological appearance of hemorrhoids?
On histologic examination, hemorrhoids consist of thin-walled, dilated, submucosal vessels that protrude beneath the anal or rectal mucosa.
T114 What are the two major entities of Inflammatory Bowel Disease (IBD)?
- Ulcerative colitis: Inflammation limited to the mucosa and submucosa, usually extending to the distal colon and rectum.
- Crohn disease: Transmural inflammation, usually found in the ileum and proximal colon but can affect any part of the gastrointestinal tract from mouth to anus.
What is indeterminate colitis?
Indeterminate colitis refers to the histopathologic and clinical overlap between ulcerative colitis and Crohn disease.
What are the demographics of IBD?
IBD is more common in young females, typically presenting in teenage years to 30s. It is more prevalent in Western countries, especially North America, Europe, and among Ashkenazi Jews.
What genetic predispositions are associated with Crohn disease?
First-degree relatives have a 13-18% increase in incidence.
Concordance rates of 50% in monozygotic twins.
NOD2 gene is a susceptibility gene in Crohn disease, encoding a protein that binds to intracellular bacterial peptidoglycans and activates NF-κB.
What is the role of mucosal immune response in IBD pathogenesis?
T-helper cell type 1 (TH1) polarization is a feature of Crohn disease.
TH1 cells produce interferon-gamma, IL-2, and TNF-beta, activating macrophages and cell-mediated immunity.
TH17 cells also contribute to disease pathogenesis.
Ulcerative colitis involves TH-2 and polymorphisms of the IL-10 gene.
What epithelial defects are associated with Crohn disease?
Defects in intestinal epithelial tight junction barrier function, leading to increased permeability and inflammation. Paneth cell granules, which contain antimicrobial materials, may also alter microbiota composition, linking to IBD development.
How does microbiota contribute to IBD pathogenesis?
Transepithelial flux of luminal bacterial components activates innate and adaptive immune responses. In genetically susceptible individuals, TNF and other inflammatory cytokines increase epithelial permeability, creating a cycle of inflammation.
What environmental factors are involved in IBD?
Cigarette smoking and diet are significant environmental factors.
Tobacco smoking doubles the risk of Crohn disease but appears to have a protective effect in ulcerative colitis.
What is Crohn disease and where is it usually found?
Crohn disease is a chronic inflammatory condition characterized by transmural inflammation, usually found in the ileum and cecum (proximal colon) but has the potential to affect any part of the gastrointestinal tract from mouth to anus.
What are the extra-intestinal complications associated with Crohn disease?
Extra-intestinal complications of immune origin include uveitis, sacroilitis, migratory polyarthritis, erythema nodosum, bile duct inflammatory disorders, and obstructive uropathy.
What is the macroscopic morphology of Crohn disease?
-Patchy lesional distribution with sharply delineated areas of disease surrounded by normal mucosa.
-Transmural involvement with thickening of the mucosal wall, resulting in a rubbery and thick intestinal wall due to edema, inflammation, fibrosis, and hypertrophy of
muscularis mucosae.
-Cobblestone appearance of the mucosal surface.
- “Creeping fat” formation within the fissures.
- Focal ulceration in early stages, progressing to elongated linear ulcers
What is “creeping fat” in Crohn disease?
“Creeping fat” refers to the formation of granulation tissue within the fissure that involves the stricture of the fissure, pulling up the fat of the mesentery.
What are the microscopic features of Crohn disease?
-Transmural inflammation with inflammatory cells extending from mucosa through submucosa and muscularis.
-Presence of non-caseating granulomas.
- Crypt abscesses with clusters of neutrophils and associated crypt
destruction. - Epithelial metaplasia including pseudo pyloric metaplasia and Paneth cell metaplasia.
What are the clinical features of Crohn disease?
Recurrent episodes of diarrhea, cramps with abdominal pain, fever (lasting days to weeks), and malabsorption with nutritional deficiency.
What are the potential consequences of Crohn disease?
Fistula formation to other segments of the bowel, urinary bladder, vagina, or perianal skin.
Abdominal abscesses or peritonitis.
Intestinal stricture or obstruction.
Perforations and peritoneal abscesses.
Increased risk for colonic adenocarcinoma.
What is Ulcerative Colitis and where is it typically found?
Ulcerative Colitis is an ulcero-inflammatory disease limited to the colon and rectum, affecting only the mucosa and submucosa. It begins in the rectum and extends proximally, potentially involving the entire colon (pancolitis).
Describe the macroscopic morphology of Ulcerative Colitis.
No skip lesions, meaning colonic involvement is continuous.
Mucosal ulcers rarely extend beyond the submucosa.
Mural thickening is absent.
Serosal surface appears normal.
Strictures do not occur.
Isolated islands of regenerating mucosa bulge upward, forming pseudopolyps.
What are the microscopic features of Ulcerative Colitis?
Inflammatory infiltrates, crypt abscesses, crypt distortion, and epithelial metaplasia.
Ulcers extending to the submucosa.
Absence of granulomas.
What are the clinical features of Ulcerative Colitis?
Attacks of bloody mucoid diarrhea that can persist for days, weeks, or months, then subsides only to recur after an asymptomatic interval.
- Risk of developing toxic megacolon due to inflammation and damage to the muscularis propria, causing neuromuscular damage.
- High risk of carcinoma development, which depends on the extent of colonic involvement and the duration of the disease.
T115 What is Enterocolitis?
Enterocolitis is an inflammation of the colon (colitis) and small intestine (enteritis).
What is Infectious Enterocolitis?
Infectious Enterocolitis is an intestinal inflammatory disease of microbial origin, presented by diarrhea and ulcero-inflammatory changes in the small or large intestine.
How significant is Infectious Enterocolitis in global child mortality?
Infectious Enterocolitis is responsible for approximately half of the deaths before the age of 5 worldwide.
What factors influence the prevalence and severity of Infectious Enterocolitis?
The prevalence and severity of Infectious Enterocolitis are influenced by the sanitary conditions and the host’s immune defense system
What are the three mechanisms of bacterial infection in the intestines?
- Ingestion of preformed toxin (e.g., S. aureus, Vibrio, Clostridium perfringens).
- Infection by toxigenic organisms (adhere to mucosa, proliferate, and release enterotoxins).
- Infection by enteroinvasive organisms (proliferate, invade, and destroy mucosal epithelial cells).
What are the bacterial virulence factors involved in intestinal infections?
Adherence to epithelial cells (via fimbriae or pili, e.g., C. jejuni, E. coli).
Enterotoxins (e.g., cholera toxin, enterotoxigenic E. coli).Invasion factors (e.g., enteroinvasive E. coli).
Cytotoxicity (e.g., Shiga toxin, enterohemorrhagic E. coli).
What are the morphological features of bacterial enterocolitis?
Hyperemia, edema, erosion, and ulceration of the lamina propria.
Lamina propria and intraepithelial neutrophil infiltrates.
Cryptitis (neutrophil infiltration of the crypts) and crypt abscesses (crypts with luminal neutrophils).
Preservation of crypt architecture, distinguishing from inflammatory bowel disease.
What are the clinical features of bacterial origin enterocolitis?
More severe than viral or parasitic enterocolitis.Acute self-limited colitis (ASLC) with diarrhea and abdominal distress.
Complications include massive fluid loss, dehydration, and intestinal mucosa destruction leading to perforation.
Diagnosed by stool culture.
What is the pathogenesis of cholera?
Caused by Vibrio cholerae, transmitted primarily by contaminated water.Noninvasive, remains in the intestinal lumen.
Cholera toxin (A and B subunits) causes disease by ADP ribosylation of G protein, activating adenylate cyclase, increasing cAMP, and opening CFTR channels, leading to chloride and water secretion (excretory diarrhea).
What are the clinical features of cholera?
Asymptomatic in most cases.
Severe cases present with massive watery diarrhea leading to hypovolemia.
What causes Campylobacter enterocolitis and how is it transmitted?
Caused by Campylobacter jejuni.
Transmitted through undercooked chicken, unpasteurized milk, or contaminated water.
What are the four main virulence factors of Campylobacter jejuni?
Motility (flagella).
Adherence factor.
Toxin production (cholera-like toxin, cytotoxins).
Invasion.
What are the potential complications of Campylobacter enterocolitis?
Dysentery, enteric fever, reactive arthritis, erythema nodosum, Guillain-Barré syndrome.
What are the clinical features of Campylobacter enterocolitis?
Watery diarrhea, which may progress to dysentery in 15-50% of patients.
What is Shigellosis and its primary cause?
Caused by Shigella, gram-negative bacilli, transmitted via fecal-oral route.Most common cause of bloody diarrhea.
What is the pathogenesis of Shigellosis?
Shigella is acid stable, invades via M cells, infects epithelial cells, and can produce Shiga toxin leading to dysentery
What are the different types of pathogenic Escherichia coli and their features?
Enterotoxigenic E. coli (ETEC): Causes traveler’s diarrhea, produces heat-labile (LT) and heat-stable (ST) toxins.
Enterohemorrhagic E. coli (EHEC): Produces Shiga-like toxins, can cause dysentery and hemolytic-uremic syndrome.
Enteroinvasive E. coli (EIEC): Invades gut epithelial cells, produces bloody diarrhea.
Enteroaggregative E. coli (EAEC): Adheres to enterocytes with fimbriae, produces LT and Shiga-like toxins, minimal histologic damage.
What is the impact of viral infection on the small intestine’s superficial epithelium?
Viral infection leads to the destruction of enterocytes, reducing absorptive function. This causes repopulation of villi with immature enterocytes and relative preservation of crypt secretory cells, leading to net secretion of water and electrolytes into the lumen and osmotic diarrhea from incompletely absorbed nutrients.
What are the most common viral agents causing enterocolitis?
The most common viral agents are rotavirus, calicivirus, and adenovirus.
What is the most common cause of severe childhood diarrhea and diarrhea-related deaths worldwide?
Rotavirus is the most common cause of severe childhood diarrhea and diarrhea-related deaths worldwide.
Which age group is most vulnerable to rotavirus infection, and why is there protection in certain age groups?
Children between 6 and 24 months of age are most vulnerable. Protection in the first 6 months of life is likely due to antibodies in breast milk, while immunity beyond 2 years develops after the first infection.
How does rotavirus affect the small intestine?
Rotavirus selectively infects and destroys mature absorptive enterocytes in the small intestine, leading to repopulation of villi by immature secretory cells. This results in a loss of absorptive function and net secretion of water and electrolytes.
Why are oral rotavirus vaccines less effective in developing countries?
For unknown reasons, oral rotavirus vaccines have been less effective in developing countries where they are most needed.
What is a diverticulum, and where is it most commonly located in the colon?
A diverticulum is a blind outpouching in the wall of the gut. It is most commonly located in the sigmoid colon (95% of cases).
What are the differences between congenital and acquired colonic diverticula?
Congenital diverticula (e.g., Meckel diverticulum) include all layers of the bowel wall (mucosa, submucosa, muscularis externa) and are uncommon. Acquired diverticula usually lack the muscularis mucosae or have a thin muscularis mucosae and are often pseudodiverticula of mucosa and submucosa penetrating the muscularis propria.
Why are diverticula most common in the colon?
Diverticula are most common in the colon due to its structure. The outer longitudinal layer of muscularis externa (teniae coli) creates focal defects when nerves and blood vessels penetrate to reach the inner layer of circular muscles.
What factors may contribute to the formation of diverticula?
Factors contributing to diverticula formation include constipation (often from a low-fiber diet leading to reduced stool bulk and increased difficulty in passage) and other conditions that increase intraluminal pressure.
Describe the morphology of diverticula in the colon.
Diverticula are small, spherical outpouchings (0.5-1cm in diameter) that penetrate between fibers of the circular muscle.
They are composed of atrophied, flattened mucosa and submucosa pushed into the circular layer. Inflammation can lead to diverticulitis, with the thin wall of the diverticulum potentially rupturing and causing peridiverticulitis, abscess formation, or peritonitis.
What are the clinical features of diverticulitis?
Diverticulitis produces continuous left-sided lower quadrant discomfort, a sensation of never being able to empty the rectum, left lower quadrant tenderness, and fever.
Less common complications include bleeding (hematochesia), perforation, and fistula formation.
T116 What are the main manifestations of malabsorption conditions?
Defective absorption of fat, carbohydrates, proteins, vitamins, electrolytes, and water. It commonly results in chronic diarrhea, with a hallmark of steatorrhea (fatty feces). The three most common chronic malabsorptive disorders in the US are pancreatic insufficiency, celiac disease, and Crohn disease.
How is diarrhea defined and what are its potential severities?
Diarrhea is defined as an increase in stool mass, frequency, or fluidity, typically to volumes greater than 200 mL per day. In severe cases, it can become life-threatening due to hypovolemia. It can be classified as secretory, osmotic, malabsorptive, or exudative.
What are the four primary digestive functions involved in malabsorption?
Intraluminal digestion: Enzymatic digestion of nutrients beginning in the mouth and continuing in the stomach and duodenum.
Terminal digestion: Hydrolysis of carbohydrates and peptides in the brush border of the small intestine.
Transepithelial transport: Transport of nutrients, fluid, and electrolytes across the epithelium.
Lymphatic transport: Transport of absorbed lipids.
How does cystic fibrosis cause intraluminal digestion defects?
Cystic fibrosis involves a defect in the CFTR gene, leading to defective intestinal and pancreatic chloride secretion. This results in exocrine pancreatic insufficiency, affecting intraluminal digestion due to the lack of pancreatic enzymes, and meconium ileus in newborns due to defective hydration.
What triggers celiac disease, and what genetic predispositions are associated with it?
Celiac disease is triggered by the ingestion of gluten-containing cereals in genetically predisposed individuals, particularly those of European origin. It is associated with HLA-DQ2 and HLA-DQ8 genotypes.
Describe the pathogenesis of celiac disease
Gluten is digested into gliadin peptides, which are transported across the epithelium.
In genetically predisposed individuals, gliadin is presented by antigen-presenting cells, leading to an inflammatory response involving CD8+ T cells and B cells.
This causes villous atrophy, loss of brush borders, increased turnover of enterocytes, and malabsorption.
What are the histopathological features of celiac disease?
Biopsy from the duodenum and proximal jejunum shows increased intraepithelial CD8+ T lymphocytes, intraepithelial lymphocytosis, crypt hyperplasia, and villous atrophy.
What are the clinical features and risks associated with celiac disease?
Histological features similar to other diseases; diagnosis is confirmed with biopsy and serum antigens. Treatment involves a gluten-free diet.
There is an increased risk of malignancy, including enteropathy-associated T cell lymphoma and small intestinal adenocarcinoma.
What is environmental (tropical) enteropathy and what are its impacts?
A syndrome of stunted growth and impaired intestinal function common in developing countries due to frequent intestinal infections. It leads to chronic nutrient absorption problems, malnutrition, and growth stunting in children, particularly during the first 2-3 years of life, critical for growth and brain development.
What is the histological appearance of environmental enteropathy?
The intestine in environmental enteropathy appears similar to that of celiac disease, making supplementary diets and vitamin administration insufficient to completely overcome the syndrome.
What causes lactose intolerance and what are its types?
Lactose intolerance is due to lactase deficiency, impairing terminal digestion of lactose and causing osmotic diarrhea. It has two types: congenital lactase deficiency (autosomal recessive mutation in the lactase gene) and acquired lactase deficiency (downregulation of lactase gene expression).
What is abetalipoproteinemia and what are its effects?
Abetalipoproteinemia is a deficiency of apoprotein B, which is required for chylomicron formation. Mucosal cells cannot export lipids, leading to diarrhea and steatorrhea. Microscopically, lipid vacuoles may be seen in enterocytes.
What characterizes irritable bowel syndrome (IBS)?
IBS is characterized by chronic and relapsing abdominal pain, bloating, and changes in bowel habits (diarrhea and constipation). Its pathogenesis involves psychological stressors, diet, and abnormal gastrointestinal motility, typically affecting individuals aged 20-40 with a female predominance.
What is microscopic colitis and its types?
Microscopic colitis causes chronic watery diarrhea with a normal macro appearance but identifiable by histology:
Collagenous colitis: Dense subepithelial collagen layer, increased intraepithelial lymphocytes, mixed inflammatory infiltrate in the lamina propria.
Lymphocytic colitis: Similar histology, normal thickness of the subepithelial collagen layer, and greater increase in intraepithelial lymphocytes.
What are the general symptoms and signs of malabsorption?
Symptoms and signs include diarrhea, flatus, abdominal pain, and weight loss due to nutrient malabsorption and excessive intestinal secretion.
What are the hematopoietic system effects of malabsorption?
Anemias result from deficiencies in iron and/or vitamin B12, and bleeding disorders result from vitamin K deficiency.
What are the musculoskeletal system effects of malabsorption?
Defective absorption of calcium, magnesium, vitamin D, and proteins results in osteopenia and tetany.
What are the endocrine system effects of malabsorption?
Amenorrhea, impotence, and infertility result from generalized malnutrition, and hyperparathyroidism results from prolonged calcium and vitamin D deficiencies.
What are the skin-related effects of malabsorption?
Purpura and petechiae from vitamin K deficiency, edema due to protein deficiency, and hyperkeratosis due to vitamin A deficiency
What are the nervous system effects of malabsorption?
Peripheral neuropathies due to deficiencies in vitamins A and B12.
T117 What is the most commonly affected part of the bowel in obstruction?
The small intestine is most commonly affected due to its small lumen, with about 80% of obstructions occurring there.
What is a hernia and how does it cause bowel obstruction?
A hernia is a weakness in the peritoneal wall that allows a serosa-lined sac of peritoneum to protrude. External herniation occurs when viscera intrude through the weakened wall, and incarceration happens when the herniated viscera become permanently trapped, impairing venous drainage and causing stasis and edema.
What are intestinal adhesions and how do they cause bowel obstruction?
Intestinal adhesions are fibrous bridges formed during healing after surgery or infection. The intestine can slide and become trapped by these adhesions, leading to internal herniation and obstruction.
What is intussusception and how does it cause bowel obstruction?
Intussusception occurs when a segment of the intestine telescopes into an adjacent distal segment, often due to peristalsis. This can lead to obstruction, compression of mesenteric vessels, and infarction. In adults, it may indicate an intraluminal mass such as a tumor.
What is volvulus and how does it cause bowel obstruction?
Volvulus is the twisting of a loop of bowel (or other structures like the ovary) around its base of attachment. This twisting constricts venous outflow and may also damage the arterial blood supply, leading to obstruction and infarction.
Which part of the digestive system hosts the most primary neoplasms?
The colon and rectum host more primary neoplasms than any other organ, while the small intestine is an uncommon site for benign or malignant tumors.
What are the two major types of polyps found in the intestine?
The two major types of polyps are sessile polyps (without a stalk) and pedunculated polyps (with stalks).
What are hyperplastic polyps and where are they commonly found?
Hyperplastic polyps are the most common polyps of the colon and rectum, typically found in the distal colon and rectum, and usually have no malignant potential.
What is a juvenile polyp and who does it typically affect?
A juvenile polyp is a hamartomatous polyp that usually arises in children under the age of 5.
What is Peutz-Jeghers syndrome?
Peutz-Jeghers syndrome is an autosomal dominant inherited syndrome characterized by hamartomatous polyps in the GI tract and hyperpigmented macules on the lips and oral mucosa.
What type of polyp is associated with inflammatory bowel disease?
Inflammatory polyps occur with acute or chronic inflammation and may be present in conditions such as ulcerative colitis.
What are adenomas and what is their malignant potential?
Adenomas are benign polyps with glandular origin. Although benign, they have the potential to become malignant (adenocarcinoma).
What are the classifications of GI stromal tumors?
GI stromal tumors can be classified as:
Tumors that show smooth muscle cell differentiation.
Tumors with neural differentiation.
Tumors with smooth muscle/neural dual differentiation.
Tumors lacking differentiation towards these lineages.
What is a carcinoid tumor?
Carcinoid tumors are neoplasms that arise from endocrine cells of the GI tract.
How can lymphomas involve the GI tract?
Lymphomas can involve the GI tract due to secondary spreading of non-Hodgkin lymphomas (extra-nodal location) or can arise as primary tumors in gastric MALT (mucosa-associated lymphoid tissue).
Are neoplasms of the small intestine common?
Neoplasms of the small intestine are uncommon. The most common neoplasm in the small bowel is metastasis, often from nearby organs such as the colon, ovary, pancreas, and stomach.
What are some benign tumors of the small intestine?
Benign tumors of the small intestine can include leiomyomas, fibromas, and lipomas. Most benign tumors are incidental submucosal lesions, though rarely they can be large enough to obstruct the lumen
What percentage of small-bowel tumors are malignant?
Approximately 64% of all small-bowel tumors are malignant.
What is the most common malignant tumor of the small intestine?
The most common malignant tumor of the small intestine is adenocarcinoma, particularly in the region of the papilla of Vater.
How do small-bowel adenocarcinomas resemble large-bowel adenocarcinomas?
Small-bowel adenocarcinomas share a similar geographic distribution with large-bowel adenocarcinomas, predominating in Western countries, and tend to co-occur in the same individuals.
They arise from premalignant adenomas, accumulate genetic mutations, and progress to carcinomas in situ and invasive adenocarcinomas, similar to the process in the colon.
What genetic mutations are common in small-bowel adenocarcinomas?
Kras mutation and p53 overexpression are common in small-bowel adenocarcinomas, similar to colorectal carcinomas.
However, mutation of the APC tumor suppressor gene, which is characteristic of colorectal carcinoma, does not commonly occur in small-bowel adenocarcinoma.
What percentage of small-bowel malignancies are sarcomas?
Sarcomas account for approximately 15% of small-bowel malignancies in the United States.
What are GI stromal tumors (GISTs)?
GI stromal tumors (GISTs) are mesenchymal neoplasms believed to be derived from the interstitial cells of Cajal in the GI tract.
They may exhibit partial differentiation with incomplete expression of muscle-associated antigens, and the term GIST is a more general term used for these tumors.
What are some histologic features of small-bowel sarcomas?
While some small-bowel sarcomas may exhibit clear histologic features of smooth muscle origin, many tumors display only partial differentiation with incomplete expression of muscle-associated antigens.
How can GI stromal tumors (GISTs) be classified?
GI stromal tumors can be classified as:Tumors that show smooth muscle cell differentiation.Tumors with neural differentiation.Tumors with smooth muscle/neural dual differentiation.Tumors lacking differentiation towards these lineages.
T118 What is a polyp and where are they most commonly found?
A polyp is a mucosal outward raised protrusion, commonly found in the colon. They can be sessile (without a connecting stalk, broad-based) or pedunculated (with a connecting stalk).
