[PPT] Gastrointestinal Disorders

IBS is a common disorder that affects the gut, causing symptoms like abdominal pain, cramping, bloating, diarrhea, constipation, and gas. However, the exact cause is unknown.

The disruption of the normal balance of bacteria in the gut. This can lead to inflammation and other symptoms.

The connection between the brain and the gut. Changes in this communication can affect digestion and cause IBS symptoms.

Excess gas production in the intestines.

An increased sensitivity to stretching and pressure in the gut, leading to pain.

Abnormal muscle contractions in the gut, affecting the speed and efficiency of digestion.

Sac-like pouches that bulge outward from the wall of the colon, usually in the sigmoid colon.

The condition of having diverticula, often asymptomatic.

Inflammation and infection of the diverticula, leading to pain, fever, and other symptoms.

Inflammation of the appendix, a small pouch attached to the colon.

A chronic condition where stomach acid flows back into the esophagus (food pipe).

A bacterium known for its role in peptic ulcers, but also impacts GERD by influencing gastric acid levels and influencing the environment for GERD.

A therapy that is unconventional, newer, or outside the usual methods for treating a disease.

Conventional therapy for IBD can be ineffective for some patients and have side effects, so novel treatments are explored to address these limitations.

It is a type of immune cell involved in IBD. Th17 cells are involved in both Crohn's disease and ulcerative colitis.

A type of hepatitis virus that requires the presence of hepatitis B virus for infection. It can only infect a person who already has Hep B.

A general term for inflammation of the liver, often caused by viral infections.

An antibody produced by the body in response to hepatitis B infection. It indicates immunity to hepatitis B.

A blood test that detects the presence of hepatitis B surface antigen, indicating an active hepatitis B infection.

A general term for a group of blood tests that assess the functions of the liver. These tests measure the levels of different enzymes and proteins produced by the liver.

A scale used to assess the severity of liver fibrosis, ranging from F0 (no fibrosis) to F4 (cirrhosis).

A condition characterized by irreversible scarring of the liver, hindering its normal function.

A non-invasive method that uses ultrasound to assess liver stiffness, providing information about fibrosis and steatosis.

Presence of gallstones in the gallbladder.

Inflammation of the gallbladder.

Presence of gallstones in the common bile duct.

Intermittent pain in the upper right abdomen caused by gallstones blocking the bile ducts.

A condition where there is a build-up of cholesterol within the gallbladder.

Gallstones formed primarily from bilirubin, a waste product of red blood cell breakdown.

A state where bile flow is obstructed, which can contribute to gallstone formation.

A thick, sticky substance that can form in the gallbladder and contribute to gallstone formation.

An enzyme found primarily in the liver that helps convert proteins into energy for liver cells. Elevated levels may indicate liver damage or disease.

An enzyme found in the liver, bone and other tissues. Elevated levels may indicate liver damage or disease (e.g., blocked bile duct), bone diseases, or even muscle damage.

An enzyme present in the blood. Higher-than-normal levels often suggest liver or bile duct damage.

A protein produced by the liver. Low levels can indicate liver damage or disease.

A breakdown product of heme, the iron-containing portion of hemoglobin. Elevated levels can indicate liver damage or disease.

A measure of how long it takes for blood to clot. Prolonged clotting times may indicate liver damage or disease.

Inflammation of the pancreas, caused by premature activation of digestive enzymes. It can be acute (sudden) or chronic (long-lasting).

Stones formed in the gallbladder, usually made of cholesterol. They can block the bile duct, leading to pain and inflammation.

A screening program for colorectal cancer in people with no family history of the disease. Individuals between 50 to 74 years old and without pre-cancerous polyps or inflammatory bowel disease are eligible.

A screening program for colorectal cancer in people with a family history of the disease. Screening begins either at age 50 or 10 years earlier than the relative's diagnosis, whichever comes first.

A stool test that checks for the presence of blood in the stool, which can be a sign of polyps or colorectal cancer. This test is recommended every two years for average-risk individuals.

A procedure that examines the lower part of the colon with a flexible tube and has a higher detection rate compared to stool tests.

The benefits of regular stool tests include early detection of pre-cancerous polyps, reassurance for those with negative results, and potentially preventing cancer by finding it early.

Limitations of stool tests include false positive results, false negative results, overdiagnosis, and the need for further investigation with colonoscopy after a positive result.

A colonoscopy is a procedure that examines the entire colon with a long, flexible tube fitted with a camera. This is considered the gold standard for colorectal cancer screening.

This program discourages the use of blood tests for early detection of colorectal cancer, since they can be misleading and ineffective.

The lower esophageal sphincter (LES) is a muscular valve that prevents the reflux of stomach contents into the esophagus. In patients with GERD, this sphincter often relaxes more frequently, allowing acidic chyme to back up into the esophagus.

Barrett's Esophagus is a condition where the normal squamous epithelium in the esophagus is replaced by metaplastic columnar epithelium, often due to chronic exposure to acidic chyme. This change increases the risk of developing esophageal adenocarcinoma.

GERD is characterized by reflux of chyme from the stomach to the esophagus or higher regions of the digestive system. This can cause noticeable symptoms, like heartburn, and complications over time.

Gastritis is an inflammation of the stomach's inner lining (gastric mucosa). It can be either acute, usually temporary, or chronic, which is long-term.

Acute gastritis is a temporary inflammation caused by things like NSAID medications, excessive alcohol, chemotherapy, or H. pylori infections. It often leads to superficial lesions in the stomach lining.

Chronic gastritis is a long-term inflammation of the stomach lining, commonly occurring in older adults. It is often linked to H. pylori infections.

The pancreas has both an endocrine function (hormone secretion) and an exocrine function (digestive enzyme production). In its endocrine role, the Islets of Langerhans secrete glucagon (α cells) and insulin (β cells) into the bloodstream.

Chyme is the partially digested food mixture that leaves the stomach and enters the small intestine. In GERD, this acidic mixture can flow backwards into the esophagus, causing irritation and damage to the esophageal lining.

The esophagus does not have the same protective mucus layer as the stomach, making it vulnerable to damage from acidic chyme. This can lead to inflammation (reflux esophagitis), heartburn, and other complications.

GERD can cause a variety of symptoms beyond heartburn, including hoarseness, chronic cough, throat clearing, dysphagia (difficulty swallowing), and even aspiration of acid into the airways.

GERD risk factors include sliding hiatal hernia, obesity, smoking, alcohol consumption, medications that relax the LES, certain foods, and conditions or activities that increase abdominal pressure.

H. pylori infections are a common cause of acute gastritis, leading to superficial lesions in the stomach lining. It can also play a role in chronic gastritis and other stomach disorders.

Both acute and chronic gastritis can lead to various symptoms like epigastric discomfort, nausea, vomiting, belching, loss of appetite, and even acute abdominal pain.

In severe GERD cases, repeated acid exposure can cause ulcers or strictures in the esophagus. These complications can lead to further complications like difficulty swallowing, bleeding, or even esophageal cancer.

The ongoing inflammation leads to a thinning of the stomach lining (atrophy) and changes in the cell type (metaplasia). It can increase the risk of gastric cancer.

An autoimmune reaction against the stomach's parietal cells. These cells produce intrinsic factor, crucial for vitamin B12 absorption.

Autoantibodies target intrinsic factor and proton pumps, leading to destruction of the parietal cells. This can result in pernicious anemia.

Ulceration of the lower esophagus, stomach, or duodenum. It can be acute or chronic and can lead to bleeding or perforations in severe cases.

While the exact cause is unclear, major risk factors include NSAIDs and H. pylori infections.

H. pylori is a spiral-shaped bacterium with flagella that infects approximately half the world's population. It thrives in the acidic environment of the stomach, secreting urease to neutralize acid. It also produces mucinase to break down mucus and adheres to the epithelial lining.

Non-steroidal anti-inflammatory drugs (NSAIDs) reduce inflammation by inhibiting cyclo-oxygenase enzymes. These enzymes are essential for producing prostaglandins, which protect the stomach lining by promoting bicarbonate secretion, mucin production, and inhibiting acid secretion. NSAIDs expose the stomach to a more acidic environment without these protective factors, leading to damage and ulceration.

H. pylori is a leading cause of peptic ulcers. It is an aggressive bacterium that survives in the stomach's acidic environment and secretes urease to neutralize acid, allowing it to colonize the mucosal lining.

Urease is an enzyme produced by H. pylori that breaks down urea into ammonia and bicarbonate. Ammonia neutralizes the stomach's acid, creating a more hospitable environment for the bacteria to thrive.

H. pylori burrows into the stomach lining (mucosa) and secretes mucinase, an enzyme that breaks down the protective mucus layer. This allows the bacteria to adhere to the epithelial cells and damage the stomach lining, contributing to ulcer formation.

H. pylori infection is a major risk factor for peptic ulcer disease. The bacteria disrupts the stomach's protective mechanisms, making it more susceptible to ulcers.

H. pylori is often implicated in the development of gastritis, a common condition characterized by inflammation of the stomach lining. The bacteria disrupt the stomach's normal balance, leading to inflammation and potential ulcers.

H. pylori is a common bacterium found in stomach infections. It can affect the stomach lining, leading to inflammation and ulcers. Treatment often involves antibiotics to eradicate this bacteria.

A common symptom of peptic ulcer disease, characterized by intermittent pain in the middle upper abdomen, often starting 2-3 hours after eating and worsening at night.

A type of peptic ulcer that occurs in the stomach lining, often caused by Helicobacter pylori infection, increased acid production or certain medications.

A type of peptic ulcer that occurs in the duodenum, the first part of the small intestine. It's often associated with H. pylori infection, increased acid production, and rapid gastric emptying.

A bacterium that commonly infects the stomach and is a major cause of peptic ulcers. It disrupts the stomach's protective lining, allowing acid to damage the tissue.

A group of medications used to reduce stomach acid production. Examples include H2 receptor inhibitors and proton pump inhibitors.

H. pylori can lead to peptic ulcer disease, which is a condition marked by sores in the lining of the stomach or duodenum. It is a major contributor to these ulcers, especially when the use of NSAIDs is ruled out.

If treated and eradicated, H. pylori infections significantly reduce the chance of ulcers coming back. This makes treatment crucial for managing peptic ulcer disease.

H. pylori infections typically begin early in life and can persist throughout a person's life unless treated. This emphasizes the importance of early detection and treatment.

While not all infected individuals develop ulcers, approximately 15% of those with H. pylori infection are at risk of developing peptic ulcer disease. It is a significant factor in the development of ulcers.

H. pylori infections are strongly linked to the development of gastric cancers, including adenocarcinoma and lymphoma. These cancers often occur alongside or before H. pylori infection.

VacA is a toxin produced by H. pylori that weakens the stomach lining, making it more vulnerable to damage. It disrupts the cell membrane, leading to inflammation.

A chronic, inflammatory disease of the gastrointestinal tract characterized by relapsing and remitting inflammation.

Affects any part of the GI tract, from mouth to anus, most commonly the terminal ileum and proximal colon. Inflammation is discontinuous, meaning it skips parts, and transmural, affecting the entire wall thickness.

A key genetic marker linked to Crohn's Disease, located on chromosome 16. This gene plays a role in immune response against bacteria.

Inflammation starts in the rectum and spreads proximally, affecting only the mucosa, the innermost layer of the large intestine.

Chronic inflammation of the liver, with many causes including viruses, alcohol abuse, drugs, toxins, trauma, and autoimmune disorders.

A viral form of hepatitis transmitted through the fecal-oral route, typically through contaminated food or water.

Spread through contact with infected blood, commonly from sharing needles or multiple sexual partners. It can cause chronic hepatitis in a significant portion of infected individuals.

Spread through infected blood, especially through contaminated needles. It often becomes chronic, leading to liver damage and cirrhosis in many patients.

Gallstones are formed in bile that is supersaturated with cholesterol, leading to crystallization and aggregation into stones.

Inflammation of the gallbladder, commonly caused by gallstones obstructing the flow of bile.

Inflammation of the pancreas, caused by premature activation of digestive enzymes within the pancreas itself. This can be acute (sudden) or chronic (long-lasting).

A predominantly Th1 T helper cell-mediated immune response is characteristic of Crohn's disease.

A predominantly Th2 T helper cell-mediated immune response is characteristic of Ulcerative Colitis.

Premature activation of pancreatic enzymes can cause tissue destruction, leading to inflammation. The enzymes are normally activated in the duodenum, not inside the pancreas.

Obstruction to the outflow tract of pancreatic enzymes can lead to acute pancreatitis. This is a common cause, often stemming from gallstones or chronic alcoholism.