The Digestive System
The system that takes the nutrients from the food you eat :)
WHAT IS IT?
The digestive system is made up of the digestive tract—a series of hollow organs joined in a long, twisting tube from the mouth to the anus—and other organs that help the body break down and absorb food.
Organs that make up the digestive tract are the mouth, esophagus, stomach, small intestine, large intestine—also called the colon—rectum, and anus. Inside these hollow organs is a lining called the mucosa, which produces juices to help digest food, and smooth muscles that help move the food along.
The liver and the pancreas produce digestive juices that reach the intestine through small tubes called ducts. The gallbladder stores the liver's digestive juices until they are needed in the intestine. Parts of the nervous and circulatory systems also play major roles in the digestive system.
Why is digestion important?
When you eat foods—such as bread, meat, and vegetables—they are not in a form that the body can use as nourishment. Food and drink must be changed into smaller molecules of nutrients before they can be absorbed into the blood and carried to cells throughout the body. Digestion is the process by which food and drink are broken down into their smallest parts so the body can use them to build and nourish cells and to provide energy.
How is food digested?
Digestive juices move it through the digestive tract, and breaking down large molecules of food into smaller molecules. Digestion begins in the mouth, when you chew and swallow, and is completed in the small intestine.
THE LONG PROCESS. Here's how it goes down.
Muscles propel food and liquid through the system and mix the contents within each organ. Food moves from one organ to the next through muscle action called peristalsis.
The first step is swallowing the food/drink. Although you are able to start swallowing by choice, once the swallow begins, it becomes involuntary and proceeds under the control of the nerves.
Then the food is pushed into the esophagus, which connects the throat above with the stomach below. As food approaches the closed sphincter, an involuntary muscle, relaxes and allows the food to pass through to the stomach.
The stomach then stores the swallowed food and liquid, mixes up the food, liquid, and digestive juices by its muscle action, then lastly it slowly emptys its contents into the small intestine.The kind of food and the degree of muscle action can affect this process.
Finally, the digested nutrients are absorbed through the intestinal walls and transported throughout the body. The waste products of this process include undigested parts of the food, known as fiber, and older cells that have been shed from the mucosa. These materials are pushed into the colon, where they remain until the feces are expelled by a bowel movement.
Ahh. You gotta love em Nutrients :)
Most digested molecules of food are absorbed through the small intestine. The mucosa of the small intestine contains many folds that are covered with tiny fingerlike projections called villi, which are covered with microscopic projections called microvilli. These structures create a vast surface area through which nutrients can be absorbed. Specialized cells allow absorbed materials to cross the mucosa into the blood, where they are carried off in the bloodstream to other parts of the body for storage or further chemical change. This part of the process varies with different types of nutrients.
WAIT A MINUTE! How does this happen?
Hormone Regulators that are produced and released by cells in the mucosa of the stomach and small intestine control the functions of the digestive system. These hormones are released into the blood of the digestive tract, travel back to the heart and through the arteries, and return to the digestive system where they stimulate digestive juices and cause organ movement.
The main hormones that control digestion are gastrin, secretin, and cholecystokinin (CCK):
Additional hormones in the digestive system regulate appetite:
Both of these hormones work on the brain to help regulate the intake of food for energy. Researchers are studying other hormones that may play a part in inhibiting appetite, including glucagon-like peptide-1 (GPL-1), oxyntomodulin (+ ), and pancreatic polypeptide.
DISEASES
Jaundice Disease
Yellowing of the skin and whites of the eyes due to a backup of bile metabolic by-products from the blood into body tissues, which is the result of blockage in the ducts draining bile from the liver into the intestines or excessive breakdown of red blood cells. Hemoglobin from destroyed RBCs is broken down, and in part, ends up in bile secretions.
Cause and Pathogenesis
Excess amounts of bilirubin in the body can be caused by the overproduction of bilirubin, the failure of the liver cells to metabolize or excrete the bilirubin produced, or a blockage of the bile ducts. Overproduction of bilirubin may be caused by the destruction of an unusually large number of red blood cells, which occurs in a condition known as hemolytic anemia. In this condition the liver cannot excrete the bilirubin which is formed more rapidly. This may occur in diseases such as malaria, thalassemia, and haemolytic disease (due to destruction of the red blood cells) of the new-born . Often, mild jaundice occurs as a common and normal condition in new-born babies because at birth there is both a deficiency in the enzyme that helps to eliminate bilirubin and also an increased breakdown of red blood cells (RBC) in the body. In babies, the condition generally disappears within a few days after birth as the enzyme is formed in the body. Sometimes, deficiency of this enzyme can also cause jaundice in adults. Jaundice may also result from various diseases or conditions that can affect the liver, such as hepatitis, cirrhosis, or cancer. A blockage of the bile ducts, may cause jaundice. The ducts may be blocked by various factors including inflammation and infection (cholangitis), gallstones (cholelithiasis), or cancer of the pancreas or the common bile duct.
The clinical types of jaundice include haemolytic jaundice which is due to the breakdown of RBC; hepatocellular jaundice caused by hepatic pathology due to viruses, drugs, alcohol abuse, etc; and Cholestatic jaundice due to biliary tract obstruction.
There are various strains of hepatitis viruses including hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV). Viruses F and G also exist and may cause primary hepatitis. HAV is transmitted by contaminated food and water and by the faecal-oral route; HBV and HDV are transmitted by contact with bodily fluids, HCV by percutaneous exposure to blood, and HEV, by contaminated water and by the faecal-oral route. Hepatitis A is seen most often in children and young adults, but the incidence is rising among those who are HIV positive. Hepatitis B affects all age groups and is associated with blood transfusion. Hepatitis C accounts for most transfusion-related cases. It is seen in all age groups. Hepatitis D is seen in individuals who are susceptible to HBV or may be HBV carriers, such as haemophiliacs and IV drug users. The disease manifestation is severe in children. Hepatitis E is seen primarily among young adults in developing countries. It is most severe in pregnant women. Congenital non-haemolytic hyperbilirubinemia such as Gilbert's Syndrome also causes jaundice. Sometimes certain drugs such as chlorpromazine (an anti-psychotic drug) may inhibit bilirubin excretion by the liver, causing jaundice.
Symptoms and Signs
The main symptoms of jaundice are the characteristic yellowish colour of the skin, sclera (whites) of the eyes, nail beds and tongue. Other symptoms usually depend on the actual cause of the jaundice. In some types of jaundice, bilirubin is excreted in the urine, which becomes yellowish brown in colour. If the excretion of bile is obstructed, stools are almost white and the digestion of fat is consequently impaired. If the jaundice has been present for a long time, pruritis (intense itching) may occur. In jaundice, due to obstruction, lipid deposits on the skin such as xanthelesmas on the eyelids or xanthomas can develop. Some patients with jaundice may also have vomiting, and abdominal pain, malaise, severe weakness etc. Complications include hepatic failure with its attendant complications such as bleeding, vomiting of blood, accumulation of fluid in the abdomen (ascites), and a condition called hepatic encephalopathy where the patient has altered consciousness and later coma. Fulminant hepatic failure and hepatic coma may often be fatal even with treatment. Another complication of hepatitis is the development of cirrhosis (due to destruction of the liver cells) and also conditions such as chronic active hepatitis wherein the jaundice may persist for several months. The prognosis in these conditions may be poor although the results are better with prompt and effective treatment.
Investigations and Diagnosis
Diagnosis of jaundice requires blood tests, which determine whether the liver is diseased, whether the bilirubin is metabolised normally by the liver cells, and if there is any abnormal breakdown and destruction of the red blood cells. Blood tests will also indicate any obstruction present. Hyperbilirubenaemia (increased serum levels of bilirubin) is present. The normal total of serum bilirubin is about 2-17 micro-mol/l(<1 mg/dl). The urine is examined for the presence of bile salts, bile pigments and urobilinogen. The faeces is examined for pale colouration, which usually indicates an obstruction to bile excretion. The diagnosis of hepatitis is based on the clinical history and various laboratory tests. In HAV, the stool is positive for the virus two to four weeks after exposure, and the enzyme-linked immunosorbent assay (ELISA) shows a rise in HAV antibodies. In HBV, serum antigen tests detect HBsAg, as well as a series of antibodies such as anti-HBe. A serum test for HCV can also be done. A liver biopsy may be done, for indications of cellular changes or pathology. Ultrasonogram can be done to examine the liver, gallbladder, and bile ducts to detect obstructions and locate gallstones. ERCP is done to detect abnormalities in the biliary tract and pancreas. Liver function tests are done to detect hepatic abnormalities. For some pancreatic pathologies, abdominal CT Scans or MRIs may be required.
Treatment and Prognosis
Treatment consists mainly of treating the underlying cause (if treatable) and in providing supportive therapy. The basic pathology or disease responsible for the jaundice should be diagnosed and treated. Obstructive jaundice can be relieved by removing the cause of the blockage such as gallstones, by surgical intervention. Haemolytic jaundice is treated by drugs that target the cause of the haemolysis (e.g., malaria), and by other therapy such as blood transfusion. It is important to stop the intake of the drugs or toxic chemicals or alcohol that may be responsible for the jaundice. Proper diet and nutritional supplements are also important in preventing the condition from worsening. Vitamin K injections may need to be given to prevent bleeding.
Prevention
The most important step in prevention of Hepatitis B infection is vaccination. Three doses of the vaccine need to be given at intervals of one month each or alternately two doses may be given at monthly intervals followed by the third dose at the sixth month. The immunity lasts for five years and booster doses are required after that period. It is important to avoid causes of liver disease such as alcohol abuse, drugs, and toxins. Prompt treatment of underlying hepatic disorders or pathology is essential to prevent or minimise permanent damage to the liver
gastritis
Gastritis occurs when the lining of the stomach becomes inflamed or swollen.
Gastritis can last for only a short time (acute gastritis), or linger for months to years (chronic gastritis).
Causes, incidence, and risk factors
The most common causes of gastritis are:
Certain medications, such as aspirin, ibuprofen, or naproxen, when taken over a longer period of time
Drinking too much alcohol
Infection of the stomach with a bacteria called Helicobacter pylori
Less common causes are:
Autoimmune disorders (such as pernicious anemia)
Backflow of bile into the stomach (bile reflux)
Cocaine abuse
Eating or drinking caustic or corrosive substances (such as poisons)
Extreme stress
Viral infection, such as cytomegalovirus and herpes simplex virus, especially in people with a weak immune system
Trauma or a severe, sudden illness such as major surgery, kidney failure, or being placed on a breathing machine may cause gastritis.
Symptoms
Many people with gastritis do not have any symptoms.
Symptoms you may notice are:
Nausea and vomiting
Pain in the upper part of the belly or abdomen
If gastritis is causing bleeding from the lining of the stomach, symptoms may include:
Black stools
Vomiting blood or coffee-ground like material
Signs and tests
Tests that may be needed are:
Complete blood count (CBC) to check for anemia or low blood count
Examination of the stomach with an endoscope (esophagogastroduodenoscopy or EGD)
H. pylori tests
Stool test to check for small amounts of blood in the stools, which may be a sign of bleeding in the stomach
Treatment
Treatment depends on the specific cause. Some of the causes will disappear over time.
You may need to stop taking aspirin, ibuprofen, naproxen, or other medicines that may be causing gastritis, but only after you talk with your health care provider.
You may use other over-the-counter and prescription drugs that decrease the amount of acid in the stomach, such as:
Antacids
H2 antagonists: famotidine (Pepsid), cimetidine (Tagamet), ranitidine (Zantac), and nizatidine (Axid)
Proton pump inhibitors (PPIs) -- omeprazole (Prilosec), esomeprazole (Nexium), iansoprazole (Prevacid), rabeprazole (AcipHex), and pantoprazole (Protonix)
Antacids may be used to treat chronic gastritis caused by infection with Helicobacter pylori bacteria.
Expectations (prognosis)
The outlook depends on the cause, but is usually good.
Complications
Blood loss and increased risk of gastric cancer are possible complications.
Calling your health care provider
Call for an appointment with your health care provider if you develop:
Pain in the upper part of the belly or abdomen that does not go away
Black or tarry stools
Vomiting blood or coffee-ground-like material
Prevention
Avoid long-term use of irritants (such as aspirin, anti-inflammatory drugs, or alcohol).
Cirrhosis
Causes, incidence, and risk factors
Cirrhosis is the end result of chronic liver damage caused by chronic liver diseases. Common causes of chronic liver disease in the United States include:
Hepatitis C infection (long-term infection)
Long-term alcohol abuse (see alcoholic liver disease)
Other causes of cirrhosis include:
Disorders of the drainage system of the liver (the biliary system), such as primary biliary cirrhosis andprimary sclerosing cholangitis
Hepatitis B (long-term infection)
Medications
Metabolic disorders of iron and copper (hemochromatosis and Wilson's disease)
Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)
Symptoms
Symptoms may develop gradually, or there may be no symptoms.
When symptoms do occur, they can include:
Confusion or problems thinking
Impotence, loss of interest in sex, and breast development (gynecomastia) in men
Loss of appetite
Nausea and vomiting
Nosebleeds or bleeding gums
Pale or clay-colored stools
Small, red spider-like blood vessels on the skin
Swelling or fluid buildup of the legs (edema) and in the abdomen (ascites)
Vomiting blood or blood in stools
Weakness
Weight loss
Yellow color in the skin, mucus membranes, or eyes (jaundice)
Signs and tests
During a physical examination the health care provider may find:
An enlarged liver or spleen
Excess breast tissue
Expanded (distended) abdomen, as a result of too much fluid
Reddened palms
Red spider-like blood vessels on the skin
Small testicles
Widened (dilated) veins in the abdomen wall
Yellow eyes or skin (jaundice)
Tests can reveal liver problems including:
Anemia (detected on a complete blood count test)
Clotting problems
Liver function problems (detected on liver function tests)
Low blood albumin
The following tests may be used to evaluate the liver:
Endoscopy to check for abnormal veins in the esophagus or stomach
A liver biopsy confirms cirrhosis.
Some patients will be screened for liver cancer. Your doctor will use a blood test to check for levels of alpha fetoprotein and will do an imaging test (ultrasound, MRI, or CT scan).
Treatment
All patients with cirrhosis can benefit from certain lifestyle changes, including:
Stop drinking alcohol.
Limit salt in the diet.
Eat a nutritious diet.
Get vaccinated for influenza, hepatitis A and hepatitis B, and pneumococcal pneumonia (if recommended by your doctor).
Tell your doctor about all prescription and nonprescription medications, and any herbs and supplements you take now or are thinking of taking.
Other treatment options are available for the complications of cirrhosis:
Bleeding varices -- upper endoscopy with banding and sclerosis
Excess abdominal fluid (ascites) -- take diuretics, restrict fluid and salt, and remove fluid (paracentesis)
Coagulopathy -- blood products or vitamin K
Confusion or encephalopathy -- lactulose medication and antibiotics
Infections -- antibiotics
A procedure called transjugular intrahepatic portosystemic shunt (TIPS) is sometimes needed for bleeding varices or ascites.
When cirrhosis progresses to end-stage liver disease, patients may be candidates for a liver transplant.
Support Groups
You can often ease the stress of illness by joining a support group whose members share common experiences and problems. See liver disease - support group.
Expectations (prognosis)
Cirrhosis is caused by irreversible scarring of the liver. Once cirrhosis develops, it is not possible to heal the liver or return its function to normal. It is a serious condition that can lead to many complications.
A gastroenterologist or liver specialist (hepatologist) should help evaluate and manage complications. Cirrhosis may result in the need for a liver transplant.
Complications
Bleeding disorders (coagulopathy)
Buildup of fluid in the abdomen (ascites) and infection of the fluid (bacterial peritonitis)
Enlarged veins in the esophagus, stomach, or intestines that bleed easily (esophageal varices)
Increased pressure in the blood vessels of the liver (portal hypertension)
Kidney failure (hepatorenal syndrome)
Liver cancer (hepatocellular carcinoma)
Mental confusion, change in the level of consciousness, or coma (hepatic encephalopathy)
Calling your health care provider
Call your health care provider if:
You develop symptoms of cirrhosis
Call your provider, go to the emergency room, or call the local emergency number (such as 911) if you have:
Abdominal or chest pain
Abdominal swelling or ascites that is new or suddenly becomes worse
A fever (temperature greater than 101 °F)
Diarrhea
New confusion or a change in alertness, or it gets worse
Rectal bleeding, vomiting blood, or blood in the urine
Shortness of breath
Vomiting more than once a day
Yellowing skin or eyes (jaundice) that is new or suddenly becomes worse
Prevention
Don't drink alcohol heavily. If you find that your drinking is getting out of hand, seek professional help.
Measures for preventing the transmission of hepatitis B or C include:
Avoid sexual contact with a person who has acute or chronic hepatitis B or C.
Use a condom and practice safe sex.
Avoid sharing personal items, such as razors or toothbrushes.
Do not share drug needles or other drug paraphernalia (such as straws for snorting drugs).
Clean blood spills with a solution containing 1 part household bleach to 10 parts water.
Portal hypertension
A potential complication of chronic alcoholism resulting in liver damage and obstruction of venous blood flow through the liver. The rising blood pressure in the veins between the gastrointestinal tract and liver causes engorgement of veins around the umbilicus .
FOR MORE INFORMATION . . .
National Digestive Diseases Information Clearinghouse
Bethesda, MD 20892–3570
Phone: 1–800–891–5389
TTY: 1–866–569–1162
Fax: 703–738–4929
Email: nddic@info.niddk.nih.gov
Internet: www.digestive.niddk.nih.gov
American Dietetic Association
120 South Riverside Plaza, Suite 2000
Chicago, IL 60606–6995
Fax: 312–899–4739
Email: hotline@eatright.org
Internet: www.eatright.org