Breaks up food particles. Assists in producing spoken language. Formed by the hard and soft palate, cheeks, teeth, and lips, lined with mucosal membranes.

Mastication: process of mechanical digestion (food is chewed). Chemical digestion: food is broken down by saliva.

Movements of the GI tract are due to contraction of two layers of smooth muscle (i.e., the longitudinal and circular layers). Smooth muscle exhibits two types of electrical potentials: basic oscillations (slow waves), which do not result in contraction, and action potentials (spikes), which trigger calcium entry and result in contraction. Contraction of smooth muscle results in two types of intestinal motility: propulsive (peristalsis) and mixing (segmental). Regulated by the enteric nervous system, the autonomic nervous system, and hormonal mediators. The enteric nervous system has two branches- myenteric and submucosal- that coordinate reflexive contraction and relaxation along the entire GI tract. Luminal distention is an important stimulus for reflexive motility. Sympathetic nervous system activity is generally inhibitory to GI motility (and secretion). Parasympathetic nervous system activity generally enhances motility. Regulatory hormones include gastrin (increases gastric motility), Gastric inhibitory polypeptide (decreases gastric motility), cholecystokinin (gallbladder contraction), and secretin (decreases GI motility).

Swallowing is a complex function coordinated by a swallowing center in the medulla. Swallowing is partially voluntary and partially involuntary. Cranial nerves IX, X, and XI mediate the various stages of swallowing.

Regulation of gastric emptying involves gastric and duodenal factors. Gastric distention and the release of gastrin from gastric mucosa promote gastric emptying. Duodenal distention, acidity, hypertonicity, and high protein and fat concentrations inhibit gastric emptying.

Chyme remains in the small intestine for 3 to 5 hours. There it is continually mixed by segmental contractions and slowly propelled toward the ileocecal valve by peristalsis. Distention of the terminal ileum results in relaxation of the ileocecal sphincter, which allows contents to enter the large bowel.

Segmental contractions in the large intestine promote water absorption. About 18 hours is required for the contents to traverse the large intestine and reach the distal end of the colon. Three to four times a day a peristaltic mass movement sweeps fecal material along the colon. Mass movements may be initiated by entry of food into the stomach and duodenum.

An urge to defecate occurs when feces enters the rectum. Contraction of the distal end of the colon and relaxation of the internal anal sphincter occur involuntarily as feces enter the rectum. The external anal sphincter is under voluntary control and inhibits defecation until voluntarily relaxed.

Major secreting glands and secretions in the GI tract can be summarized as follows:

• Salivary gland: Salivary amylase.

• Gastric glands: Chief cells secrete pepsinogen; parietal cells secrete HCl and intrinsic factor. HCl activates pepsinogen to pepsin, and intrinsic factor enhances vitamin B₁₂ absorption. Parietal cell secretion is stimulated by acetylcholine, histamine, and gastrin. G cells secrete gastrin into the bloodstream. Gastrin increases gastric motility and stimulates chief and parietal cell secretion.

• Intestinal epithelium: Secretes brush border enzymes (peptidases, lipases, sucrase, lactase); secretin, which stimulates pancreatic secretion; and cholecystokinin, which stimulates gallbladder contraction.

• Pancreas: Secretes bicarbonate-rich fluid containing amylase, trypsin, chymotrypsin, and lipase into the duodenum when stimulated by secretin.

• Gallbladder: Secretes concentrated bile salts into the duodenum when stimulated by cholecystokinin.

Digestion, the process of converting large molecules to simpler forms, is accomplished by mechanical and enzymatic processes. Digestion is a necessary prelude to absorption because only simple molecules can cross the intestinal epithelia.

Digestion of complex carbohydrates is initiated in the mouth, where salivary amylase begins to cleave large molecules into disaccharides. Pancreatic amylase continues this process in the small intestine. Disaccharides (maltose, sucrose, lactose) are cleaved into monosaccharides (glucose, fructose, galactose) by brush border enzymes (maltase, sucrase, lactase) on the intestinal epithelia. Glucose and galactose are absorbed across the intestinal epithelia by a sodium-dependent cotransporter. Fructose is absorbed passively by facilitated diffusion. Monosaccharides then travel via the bloodstream to the liver.

Lipid digestion begins in the small intestine, where bile salts from the gallbladder mix and emulsify the fatty substances. Emulsification mechanically separates the lipids into small drops that are more accessible to enzymatic digestion. Pancreatic lipase and brush border lipases digest the fats into free fatty acids and glycerol, which remain associated with the bile salts and form micelles. Cholesterol is digested by pancreatic esterase. Fatty acids are transported to the intestinal epithelia by micelles. Free fatty acids diffuse out of the micelle and into the epithelial cell passively. Epithelial cells synthesize large protein-lipid complexes (chylomicrons) that enter the lymphatic system.

Protein digestion begins in the stomach, where HCl from parietal cells activates pepsinogen to pepsin. Pepsin cleaves proteins into smaller polypeptides. Pepsin is neutralized in the duodenum, and pancreatic trypsin, chymotrypsin, and carboxypeptidase take over protein digestion. Brush border peptidases split tripeptides and dipeptides into single amino acids. Amino acid transport into intestinal epithelial cells is mediated by a sodium-dependent cotransport system similar to monosaccharide transport. Small peptides may also undergo endocytosis and be cleaved into amino acids within the epithelial cells.

Amino acids pass into the bloodstream and travel to the liver.

Absorption of water occurs passively by osmosis. An osmotic gradient for water absorption is created as electrolytes are absorbed.

Affects one or all layers of the stomach or duodenum.

Causes:

H. pylori

Use of aspirin/NSAIDS.

Symptoms:

Discomfort and pain

Pain (burning, gnawing or cramplike) occurs with empty stomach. Located in the midline in the epigastrium may radiate to back and right shoulder.

Complications- hemorrhage, perforation and penetration and gastric outlet obstruction

Rare.

Causes:

A gastrin-secreting tumor (gastrinoma). Tumor may be single or multiple. It is a malignant tumor.

Discomfort and pain

Pain (burning, gnawing or cramplike) occurs with empty stomach. Located in the midline in the epigastrium may radiate to back and right shoulder.

Complications- hemorrhage, perforation and penetration and gastric outlet obstruction

Usually found in the fundus of the stomach and proximal duodenum

Cushing (gastric, duodenal, esophageal) occurs in patients with intracranial injury, post surgical procedure or certain types of tumors

Causes:

Physiologic stress-trauma, sepsis, acute respiratory distress syndrome, severe liver failure, major surgery, intensive care patients and large-surface-area burns.

Due to ischemia, tissue acidosis and bile salts entering the stomach of critically ill patients with decreased gastric motility

Symptoms:

Painless upper GI bleed

Curlings Ulcer: Develop in response to severe physiological stress.

Risk for development: shock, burns, trauma, sepsis, acute respiratory distress syndrome, severe liver failure, major surgery. Most often in fundus of stomach. Due to ischemia, tissue acidosis, and bile salts entering the stomach in critically ill pts with reduces GI motility.

Cushing's ulcer: gastric ulcer produces by elevated intracranial pressure usually from traumatic brain injury, strokes, or neurosurgeries.

S/S: 5-10% of pts admitted to intensive care units develop stress ulcers; manifested by painless upper GI tract bleeding; prevention is the key, give them IV Protonix; may still develop ulcer despite the use of prophylaxis.

Chronic inflammatory diseases of the bowel exist in two different forms:

Ulcerative colitis and Crohn’s disease

• The etiology is unknown for both conditions. Both are believed to have an autoimmune basis, especially ulcerative colitis (often accompanies other autoimmune conditions such as thyroid disease and pernicious anemia).
• There is a strong genetic relationship for both diseases; both diseases may appear within a given family. Two related inflammatory bowel disorders. Have many things in common but are distinguishable. Familial tendency.

Normally a balance of bile salts and cholesterol keep gallstones from forming. If there are abnormally high levels of bile salts or, more commonly, cholesterol, stones can form. Factors that contribute to gallstones are abnormalities in the composition of bile, stasis (inactivity or staying) of bile and inflammation of the gallbladder.

Also, age, obesity and some medications are associated with gallstones. Gallstones may be asymptomatic. Colicky pain occurs due to intermittent obstruction of the cystic duct by a stone. Colicky pain is located in the upper right quadrant or epigastric pain and may be referred to the upper back, the right shoulder or midscapular region. Nausea, vomiting, sweating, fatty food intolerance and flatus may also occur. Symptoms may be precipitated by a meal.

Vagus nerve: parasympathetic innervation to the stomach, small intestine, secum, ascending colon, and transverse colon.

Pelvic nerves: remainder of the colon innervated by parasympathetic fibers that exit the sacral segments of the spinal cord.

Most parasympathetic innervation is excitatory. Vagovasal influence motility and secretions.

Sympathetic innervation: controls the extent of mucus secretion by the mucosal glands, reduces motility by inhibiting the activity of interamural plexus neurons, enhances sphincter function, and increased the vascular smooth muscle tone of the blood vessels that supply the GI tract.

Types of movement: mixing, propulsion

Five major activities: secretions of electrolytes, hormones, and enzymes; movement of ingested products; digestion of foods and liquids; absorption of end products into the bloodstream; elimination

GI secretions: mucous- produced throughout the GI tract; digestive- produced in mouth, stomach, duodenum, and jejunum.

Diverticulosis: condition which the mucosal layer of colon herniates through the muscularis layer; most occur in sigmoid colon; usually due to- lack of fiber, poor bowel habits, effects of aging.

Diverticulitis: complications of diverticulosis; inflammation and microscopic perforation of diverticulum; pain in LLQ; N/V, fever, elevated WBC; can last for several days with formation of abscesses. Complications: peritonitis, hemorrhage, bowel obstruction, fistulas.

Inflammation of the liver. Due to reactions to drugs, toxins. Infectious Hepatitis due to: malaria, infectious mononucleosis, salmonella. Hepatotropic viruses: a virus that primarily affects the liver, such as the hepatitis viruses.

Mechanisms of injury: direct cellular injury. induction of immune responses: acute inflammation necrosis with prompt immune response will eliminate the virus; milder symptoms with marginal immune response don't eliminate virus and then becomes carrier.

Phases: 1st-Prodromal: malaise, myalgia, arthralgia, fatigue, n/v/a, right-sided abd pain; 2nd-Icterus: 5-10d after prodromal, jaundice, increase in prodromal symptoms, pruritis and liver tenderness; 3rd-Convalescent: increased well-being, fadin jaundice, subsides 2-3 wks with complete recovery 9-16wks.

Causes: impaired synthesis of plasma proteins- decreased levels of serum albumin with development of edema and ascites, decreases carriers proteins for hormone and drugs; decreased synthesis of blood clotting factors- bleeding tendencies; failure to remove and conjugate bilirubin from blood-jaundice; impaired bile synthesis- malabsoprtion of fats and fat-soluble vitamins; impaired metabolism of drugs cleared by liver- drug reactions and toxicity; impaired gluconeogenesis- abnormal glucose tolerance; decreased ability to convert ammonia to urea- elevated ammonia levels, encephalopathy.

S/S: early-wt loss, weakness, anorexia, diarrhea, constipation, hepatomegaly, jaundice, pain in RUQ; late- splenomegaly (pancytopenia), ascites-up to 15L can accumulate, obstruction of venous blood flow (shunts)-esophageal varices, hemorrhoids

Associated with obstruction that causes inflammation. Due to chemical irritation from bile. Mucosal swelling and ischemia due to venous congestion and lymphatic stasis (necrosis and sloughing, possible perforation). Distention of gallbladder. Secondary bacterial infection.

S/S: precipitated by fatty meal causing indigestion that doesn't subside. Responds poorly to analgesics. Pronounced pain in RUQ (tender to touch, spasm of muscle at that area). Vomiting (75%). Jaundice (25%). Fever, elevated WBC, elevated serum bilirubin, aminotransferase, and alkaline

Results from repeated episodes of acute type. Can be from chronic irritation by stones. Can be associated with common duct stone, pancreatitis, and carcinoma of the gallbladder.

S/S: intolerance to fatty foods, belching, biliary colic- episodes of colicky pain abrupt in onset, increase intensity for 30-60 minutes, and last for 2-8 hrs. Pain can radiate to back, above the waist, the right shoulder, right scapula.