Gastro Notes PDF

**Osmotic and Secretory Diarrhea** **Osmotic diarrhea** occurs when a nonabsorbable substance in the intestine draws excess water into the intestinal lumen by osmosis, increasing stool weight and volume. This results in **large-volume diarrhea.** Some causes of osmotic diarrhea include: - Large...

**Osmotic and Secretory Diarrhea** **Osmotic diarrhea** occurs when a nonabsorbable substance in the intestine draws excess water into the intestinal lumen by osmosis, increasing stool weight and volume. This results in **large-volume diarrhea.** Some causes of osmotic diarrhea include: - Large oral doses of poorly absorbed ions such as magnesium, sulfate, and phosphate. - Excessive ingestion of synthetic, nonabsorbable sugars. - Introduction of full-strength tube feeding formulas. - Dumping syndrome. - Lactase deficiency. - Pancreatic enzyme or bile salt deficiency. - Small intestine bacterial overgrowth. - Celiac disease. **Secretory diarrhea** is a form of **large-volume diarrhea** caused by excessive mucosal secretions of chloride or bicarbonate-rich fluid or the inhibition of sodium absorption. Some infectious causes of secretory diarrhea include: - Viruses (e.g., rotavirus). - Bacterial enterotoxins (e.g., *Escherichia coli*, *Vibrio cholerae*). - Exotoxins (e.g., overgrowth of *Clostridioides difficile* following antibiotic therapy). - Small bowel bacterial overgrowth. These infections cause the secretion of transmitters from enteroendocrine cells, activation of afferent neurons that stimulate submucosal secretomotor neurons, and altered sodium and chloride transport, all of which results in decreased water absorption. Certain neoplasms, such as gastrinoma and thyroid carcinoma, also produce hormones that stimulate intestinal secretion, causing diarrhea. **Small-volume diarrhea** is usually caused by an inflammatory bowel disorder, such as **ulcerative colitis** or **Crohn\'s disease.** **Constipation** **Constipation** is difficult or infrequent defecation. It is defined as a decrease in the number of bowel movements per week, hard stools, straining, abdominal pain, and difficult evacuation. Constipation can be **primary** or **secondary.** - **Chronic idiopathic or primary constipation** is generally classified into three categories: - Functional defecation disorder - Slow transit constipation - Constipation-predominant irritable bowel syndrome (IBS-C) These classifications are not mutually exclusive and there may be overlap between them. - **Secondary constipation** can be caused by: - Diet - Medications - Neurogenic disorders - Rectal fissures, strictures, or hemorrhoids - Endocrine or metabolic disorders - Pelvic hiatal hernia - Diverticula - Irritable bowel syndrome (constipation predominant) - Pregnancy - Aging - Pain or weakness of the abdominal muscles - Depression **Irritable Bowel Syndrome (IBS)** **Irritable bowel syndrome (IBS)** is a disorder of brain-gut interaction characterized by recurrent abdominal pain with altered bowel habits. Although the pathophysiology of IBS is unknown, several mechanisms may be involved: - **Visceral hypersensitivity:** This means that the nerves in the gut are more sensitive to stimuli, such as stretching or gas, than they are in people without IBS. - **Abnormal GI motility:** Individuals with diarrhea-predominant IBS have rapid colonic transit times, while those with constipation-predominant IBS have delayed transit times. - **Altered gut microbiota:** The composition of the bacteria in the gut may be different in people with IBS. - **Immune activation:** There is evidence that the immune system may be involved in IBS, although the exact role is not clear. - **Psychosocial factors:** Stress and anxiety can worsen IBS symptoms. **Clinical manifestations** of IBS vary from mild to debilitating and can be grouped into three categories: diarrhea-predominant IBS (IBS-D), constipation-predominant IBS (IBS-C), and mixed IBS (IBS-M). **Gastroesophageal Reflux Disease (GERD)** **Gastroesophageal reflux disease (GERD)** is the reflux of acid and pepsin or bile salts from the stomach into the esophagus, causing esophagitis. It occurs when gastroesophageal reflux causes troublesome symptoms or complications that affect daily functioning. The **pathophysiology** of GERD involves abnormalities in lower esophageal sphincter (LES) function, esophageal motility, and gastric motility or emptying. **Risk factors** for GERD include: - - - - - - - - - - - - **Clinical manifestations** of GERD in adults include: - - - - - - - - - **Clinical manifestations** of GERD in infants include: - - - - - - - - **Clinical manifestations** of GERD in children include: - - - - - **Gastritis and Peptic Ulcer Disease (PUD)** **Gastritis** is a nonspecific inflammatory disorder of the gastric mucosa. It can be acute or chronic. **Peptic ulcer disease (PUD)** is the ulceration of the lower esophagus, stomach, or duodenum and can be acute or chronic. **Characteristic** **Gastritis** **Peptic Ulcer Disease (PUD)** -------------------- ------------------------------------------------------------------------------------------------------------------------------------------ -------------------------------------------------------------------------------------------------------------------------------------------------------------------- **Causes** Medications (NSAIDs), excessive alcohol use, chemotherapy, *Helicobacter pylori*infections, autoimmune reactions, chronic use of alcohol Medications (NSAIDs and *H. pylori*), corticosteroids, bisphosphonates, potassium chloride, fluorouracil, smoking, alcohol consumption, Zollinger-Ellison syndrome **Mechanism** Injury to the protective mucosal barrier (acute gastritis), Chronic inflammation that causes mucosal atrophy and metaplasia Imbalance between the gastric mucosal protective factors and destructive factors leading to breaks or ulcerations in the protective mucosal lining **Symptoms** Epigastric discomfort, nausea, vomiting, belching, loss of appetite, acute abdominal pain Abdominal pain, heartburn, nausea, vomiting, bloating, feeling full quickly after eating, weight loss, poor appetite **Crohn\'s Disease and Ulcerative Colitis** **Crohn\'s disease** and **ulcerative colitis** are the two most common types of inflammatory bowel disease (IBD), characterized by chronic, debilitating relapsing and remitting inflammation of the gastrointestinal tract. **Characteristic** **Crohn\'s Disease** **Ulcerative Colitis** ----------------------------------- --------------------------------------------------------------------------------------------------------------------- ----------------------------------------------------------------------------------------------------------------------------------------------------------------- **Location of lesions** Any portion of the GI tract from mouth to perianal area, typically occurs in the terminal ileum and proximal colon Limited to the colon and rectum **Nature of inflammatory damage** Transmural inflammation that affects the entire thickness of the GI wall Affects only the mucosal layer of the colon and rectum **Clinical manifestations** Abdominal pain, diarrhea, rectal bleeding, weight loss, fever, fatigue, anemia, malabsorption, fistulae, strictures Abdominal pain, diarrhea, rectal bleeding, tenesmus, urgency, weight loss, fever, fatigue, anemia, dehydration, toxic megacolon, extraintestinal manifestations **Diverticulitis and Diverticulosis** **Diverticula** are herniations or sac-like outpouchings of the mucosa and submucosa through the muscle layers, usually located in the wall of the sigmoid colon. - **Diverticulosis** is asymptomatic diverticular disease. - **Diverticulitis** represents inflammation of the diverticula. **Appendicitis** **Appendicitis** is an inflammation of the **vermiform appendix**, a projection from the apex of the cecum. It is the most common surgical emergency of the abdomen. While the exact mechanism of appendicitis is not understood, it is believed to be caused by obstruction of the lumen with stool, tumors, or foreign bodies. This leads to bacterial infection, increased intraluminal pressure, and decreased mucosal blood flow, eventually resulting in inflammation and gangrene. **Clinical manifestations** of appendicitis include: - Vague abdominal symptoms, often with a tender or nontender mass in the lower right quadrant - Mild fever - Leukocytosis **Clinical Course of Viral Hepatitis** The clinical course of viral hepatitis usually consists of three phases, preceded by an incubation phase. - **Incubation phase:** The length of this phase varies depending on the virus. - **Prodromal (preicteric) phase:** - Begins approximately 2 weeks after exposure and ends with the appearance of jaundice - Symptoms include fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade fever - The infection is highly transmissible during this phase. - **Icteric phase:** - Begins 1 to 2 weeks after the prodromal phase and lasts 2 to 6 weeks - Jaundice, dark urine, and clay-colored stools are common - The liver is enlarged, smooth, and tender - Fatigue and abdominal pain may persist or become more severe - **Recovery phase:** - Begins with the resolution of jaundice - Symptoms gradually improve and liver function tests return to normal - Can take several months for complete recovery **Hepatitis Virus Transmission** **Virus** **Transmission** ----------- ---------------------------------------------------------------------------------- HAV Fecal-oral route HBV Blood-borne pathogen; direct exposure to contaminated blood, sexual transmission HCV Blood-borne pathogen; direct exposure to contaminated blood HDV Coinfection with HBV; depends on the viral coat of HBsAg molecules on HBV **Acute and Chronic Pancreatitis** **Pancreatitis** is an inflammation of the pancreas. It can be acute or chronic. **Risk factors** for pancreatitis include: - Obstructive biliary tract disease (particularly cholelithiasis) - Alcoholism - Obesity - Peptic ulcers - Trauma - Hyperlipidemia - Hypercalcemia - Smoking - Certain drugs - Genetic factors (hereditary pancreatitis, cystic fibrosis) **Acute pancreatitis** develops due to obstruction of pancreatic digestive enzyme outflow caused by bile and pancreatic duct obstruction. This is most commonly caused by gallstones. Direct cellular injury from alcohol, drugs, or viral infection can also cause acute pancreatitis. The **pathophysiology** of acute pancreatitis is unclear, but it is believed to be triggered by both intracellular and systemic events, including reflux of bile acids into the pancreatic duct, ethanol metabolites within the pancreas, and calcium overload. These triggers lead to inappropriate intracellular trypsin activation, impaired fluid and bicarbonate secretion in ductal cells, activation of the pro-inflammatory NF-kB pathway, and cell necrosis. **Clinical manifestations** of acute pancreatitis include: - - - - - - - - - - - - - - - - - **Chronic pancreatitis** occurs when repeated episodes of acute pancreatitis or other triggers cause irreversible damage to the pancreas. This damage leads to fibrosis, strictures, and duct obstruction. **Clinical manifestations** of chronic pancreatitis include: - - - - - - - **Cholelithiasis and Cholecystitis** **Cholelithiasis** is the presence of gallstones, which form in the biliary tract as a result of impaired metabolism of cholesterol, bilirubin, and bile acids. **Cholecystitis** is inflammation of the gallbladder. It typically develops after a gallstone becomes lodged in the cystic duct, causing the gallbladder to become distended and inflamed. **Causes** of cholelithiasis include: - Impaired metabolism of cholesterol, bilirubin, and bile acids - Hypomotility of the gallbladder **Consequences** of cholelithiasis and cholecystitis include: - Epigastric and right hypochondrium pain - Intolerance to fatty foods - Biliary colic - Jaundice - Fever - Leukocytosis - Rebound tenderness - Abdominal muscle guarding - Ischemia - Necrosis - Perforation - Acute pancreatitis **Sliding and Paraesophageal Hiatal Hernias** A **hiatal hernia** is characterized by a protrusion or bulging of an abdominal structure into the thoracic cavity. **Sliding hiatal hernia (type 1)**: - - - - **Paraesophageal hiatal hernia (type 2)**: - - - **Gastrointestinal Cancers** Risk factors, pathophysiological mechanisms, and clinical manifestations of gastrointestinal (GI) cancers, focusing on cancers of the colon and rectum: **Organ** **Percentage of Cancer Deaths** **Risk Factors** **Pathophysiological Mechanisms** **Clinical Manifestations** ------------------ --------------------------------- ------------------------------------------------------------------------------------------------------------------------- ----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- ----------------------------------------------------------------------------------------------------------------- **Esophagus** 2.6% Malnutrition, alcohol, tobacco, chronic reflux Squamous cell carcinomas are associated with smoking tobacco and chronic alcohol consumption. Adenocarcinomas are associated with chronic GERD. Barrett esophagus is a precursor to adenocarcinoma. Chest pain, dysphagia **Stomach** 1.8% Salty food, fried red meat, nitrates-nitrosamines Gastric adenocarcinomas are associated with *H. pylori* infection and progress from chronic gastritis to atrophic gastritis, intestinal metaplasia, dysplasia, and intestinal-type gastric cancer. Anorexia, malaise, weight loss, upper abdominal pain, vomiting, occult blood **Colon/rectum** 8.7% Polyps, long-term inflammatory bowel disease, diverticulitis, diets high in fat and refined carbohydrates; low in fiber Adenocarcinomas arise from the glandular epithelium of the colon. Left-sided tumors tend to grow as constricting rings, while right-sided tumors grow as polypoid masses. Pain, mass, anemia, bloody stool, obstruction, distention, change in bowel habits, narrow, pencil-shaped stools Percentages for cancer deaths refer to the proportion of deaths from that specific cancer out of all cancer deaths. Ex. esophageal cancer accounts for 2.6% of all cancer deaths.