What Is Carbohydrate Malabsorption? Carbohydrate malabsorption is a digestive disorder characterized by the inability to properly digest and absorb carbohydrates within the small intestine to supply needed energy to the body. Q: What carbohydrates should be normally…
What Is Chronic Or Recurrent Abdominal Pain? Abdominal pain is characterized by pain anywhere in the abdominal cavity between the chest and groin. This region is often referred to as the belly. Abdominal pain, or…
What Is Chronic Abdominal Distention?Abdominal distention, or bloating, is characterized by enlargement in normal size of abdomen not due to fatty tissue.
Q: Why does the abdomen enlarge?
A: The abdomen enlarges because the bowel is dysfunctional. Loops of bowel usually lack normal peristalsis (rhythmic wave-like muscle movement) trapping gas in stagnant loops of bowel, inflammation swells loops of bowel also trapping gas, and dysbiosis overproduces gas. All these factors distend the abdomen.
Primary sclerosing cholangitis (PSC) is an uncommon, slowly progressive bile duct disease that results in stagnation or build-up of bile in the liver, called cholestasis.
Primary sclerosing cholangitis is characterized by sclerosis, or scarring inflammation in bile ducts both within the liver (intra-hepatic ducts), and outside the liver (extra-hepatic ducts), causing progressive narrowing and, eventually, obliteration of the bile ducts.
Primary sclerosing cholangitis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1
Q: What happens when scarred bile ducts can no longer transport bile out of the liver?
A: Bile that cannot be removed from the liver by the biliary duct system backs up and damages the liver, causing cirrhosis.
Bile is continually made by the liver from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation to be carried out of the liver. Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. As such, bile must continually flow out of the liver to prevent build-up in the liver.
Bile is a greenish brown liquid made by the liver. Bile ducts carry it out of the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components.
The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.
Build-up of bile in the liver is the end result of the inflammatory process in primary sclerosing cholangitis, that by swelling and scarring of bile ducts impedes and eventually prevents bile flow out of the liver, leading to liver failure. There is no curative treatment available for primary sclerosing cholangitis, besides liver transplantation.2
The appearance of the intrahepatic and extrahepatic biliary ducts can be assessed by use of cholangiography, and magnetic resonance (MR) imaging is the best way to identify patients. See image above.3
MR cholangiography offers a noninvasive method of obtaining images of the biliary system without the use of a contrast agent. There is no radiation exposure. Pulse sequences can be chosen to obtain bright bile or black bile cholangiograms. Image processing algorithms can be selected to obtain a three-dimensional representation of biliary anatomy and pathology, and those images can be rotated in any plane so that ductal anatomy and pathology can be seen to best advantage.4
There is no cure for primary sclerosing cholangitis but there are symptom treatments one of which is supplementation for low levels of vitamins A,D,E, and K. Liver transplant is the only effective option.
What Is Primary Biliary Cirrhosis?Primary biliary cirrhosis (PBC) is a biliary tract disease characterized by chronic cholestasis (build-up of bile) and gradual destruction of bile ducts within the liver, called intrahepatic bile ducts, caused by chronic inflammation.
Primary biliary cirrhosis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1
Q: What is the end result of destruction of bile ducts?
A: The end result of destruction of bile ducts is liver damage.
Injured liver tissue from chronic inflammation and the buildup of bile leads to cirrhosis, a condition in which the liver slowly deteriorates and malfunctions.
Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver’s normal ability to control infections, remove bacteria and toxins from the blood, process nutrients, hormones, and drugs, make proteins that regulate blood clotting, produce bile, and effectively replace its own cells when they become damaged.2
The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.
Bile ducts carry bile, a greenish brown liquid made by the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat and fat-soluble vitamins A, D, E, and K from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components which can then be absorbed into the body.
Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. Bile is continually made by the liver from phospholipids, bile acids, cholesterol, and aging blood cells it removes from circulation. As such, bile must continually flow out of the liver to prevent build-up in the liver.
There is no cure for primary biliary cirrhosis.
Autoimmune cholangitis is a rare inflammatory self-targeted disease of the biliary tract produced by high levels of immunoglobulin G (IgG) antibodies and antinuclear antibodies (ANA).
Autoimmune cholangitis is characterized by progressive inflammation and scarring that leads to narrowing and destruction of the bile ducts and development of biliary cirrhosis of the liver.
Autoimmune cholangitis is also termed anti-mitochondrial antibody-negative primary biliary cirrhosis because there is no production of anti-mitochondrial antibodies.
Q: What happens when bile ducts can no longer transport bile out of the liver?
A: Bile that cannot be removed from the liver by the biliary tract backs up and damages the liver, causing cirrhosis. In Figure 1, bile back up would directly damage the hepatic (liver) cells seen here as grey “blocks.”
Bile is a greenish brown liquid continually made by the liver cells (hepatocytes) from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation.
Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. As such, bile must continually flow out of the liver to prevent build-up in the liver.
Bile from the hepatic cells drains into small tubes called canniculi and then into larger bile ducts to be carried out of the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components.
Unfortunately, autoimmune cholangitis is difficult to diagnose because it mimics many other diseases such as primary sclerosing cholangitis, sarcoidosis, cancer and lymphoma.
Collagenous gastritis is a rarely reported stomach disorder characterized by the deposition of a subepithelial collagen band and accompanying inflammatory infiltrate in the stomach wall.
A subepithelial collagen band means that collagen, a tough fibrous protein, has abnormally accumulated under the surface layer of epithelial cells which form the mucosa lining the stomach.
The surface mucosa may remain intact and not show lymphocytosis and/or gastritis on endoscopic examination or it may become stripped off and bleed from entrapped capillaries. Biopsy is necessary to diagnose collagenous gastritis.1
Q: Why does collagen become deposited under the surface lining of the stomach?
A: It is thought that collagen deposition is preceded by inflammation and tissue damage. However, the natural history and pathogenesis of collagenous gastritis remain unclear.2
Multiple gastric ulcerations denote a stomach disorder that involves damage to the superficial mucosa characterized by many sores of the stomach antrum that are marked by inflammation, necrosis (death of the affected cells) and sloughing of destroyed tissue.
Q: Where is the stomach antrum?
A: The antrum is the lower region of the stomach before the pylorus which is nearest the duodenum (first part of the small intestine). The stomach and duodenum are separated by the powerful pyloric sphincter.
The stomach antrum propels food in the stomach against the pylorus which resists passage of food until it is turned into chyme. Chyme is highly acidic liquified food that has been thoroughly mixed with stomach juices.
Gastric ulcerations are typically associated with widespread gastritis (inflammation), inflammatory involvement of acid producing cells, and atrophy of acid and pepsin producing cells.1
The primary causes of gastric ulcerations are H. pylori infection, use of Aspirin and non-steroidal drugs (NSAIDS), and stress.1
Geographic tongue is a painful alteration in tongue tissue that is characteristic of riboflavin (vitamin B2) deficiency.1
Q: How does the tongue surface appear?
A: Areas of inflamed tissue with flattened papillae develop among areas of normal tissue, giving a map-like appearance to the tongue surface. There are often swollen papillae that hurt or sting, such as is seen in the photo to the left.
A diet that does not provide adequate amounts of riboflavin and any condition that 1) interferes with riboflavin absorption from the gut, 2) depletes the vitamin from the body, 3) overuses the vitamin in the body, or 4) adversely affects its use in the body will result in riboflavin deficiency causing geographic tongue.
Riboflavin is essential for converting foodstuffs into energy, maintaining the normal lifespan of red blood cells and maintaining healthy skin, eyes, hair, and nervous system. Riboflavin is converted into its active forms, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). These enzymes are primarily involved as co-factors in oxidation reduction reactions that are essential for cellular energy production and respiration.
Riboflavin is required for the conversion of pyridoxine (vitamin B6) to its functional form and the production of niacin (vitamin B3) from the amino acid tryptophan. Riboflavin has a role in antioxidant status by activating glutathione reductase, which regenerates used glutathione, a powerful antioxidant.
Respiratory infection, exercise, certain diseases, drugs and hormones can adversely influence riboflavin status.2 Stress is a major depleter of riboflavin.
Chronic lesions of the oral mucosa are disorders of the mouth that are characterized by soreness and sores of the soft mucosal lining of the mouth.