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wvc GI lecture Phil
| Question | Answer |
|---|---|
| Upper GI- | oral cavity, esophagus, stomach, small intestine |
| Lower GI- | large intestine, rectum, anal sphincter |
| Accessory Organs of the GI | - Liver, pancreas and gallbladder |
| Blood supply originates in the aorta and branches through arteries along the length of the GI tract these include | the celiac, gastric, splenic, common hepatic, internal/ external iliac/ superior/inferior iliac arteries. |
| The venous system of the GI tract | carries nutrients from the GI tract into the gastric vein, splenic vein and veins draining into the portal vein of the liver. Blood circulates through the liver and returns via the hepatic vein to the inferior vena cava. |
| The Oral Cavity | lips; Buccal mucosa; Tongue; Hard palate; Soft palate; Teeth; Salivary glands |
| Mastication | breaks food into smaller pieces |
| Salivary glands (submandibular, sublingual and parotid) secrete | saliva |
| Once a bolus is formed (oral preparatory phase), the food is | moved to the back of the mouth (oral phase), the swallowing reflex is triggered (pharyngeal phase) and food passes into the esophagus to move to the stomach (esophageal phase) |
| What digestive enzyme is a constituent of saliva? | Consists of water, mucous, sodium, bicarbonate, chloride, potassium and salivary a-amalase (pytalin). Pytalin is an enzyme that initiates carbohydrate digestion in the mouth. Saliva ph=7.4 |
| Swallowing- The bolus of food moves from the mouth, the constrictor muscle of the pharynx contracts and epiglottis slides down to prevent movement of food into the larynx; | Waves of relaxation and peristalsis move food down the esophagus; The esophageal (cardiac) sphincter is relaxed allowing food to move into the stomach. This takes 5 to 10 seconds |
| Esophagus | Muscular canal from the phaynx to the stomach (approx. 10 inches long); Propels food and fluid to the stomach and prevents reflux of stomach contents; Secretes mucus to lubricate food bolus |
| Upper esophageal sphincter prevents | air from entering the esophagus during respiration |
| Lower esophageal sphincter (cardiac sphincter) prevents | regurgitation of stomach contents up into esophagus |
| Chemical digestion | enzymes and bile |
| Mechanical Digestion | Oral Cavity- teeth, tongue; Stomach- gastric peristalsis or motility, retropulsion ; Intestine- Haustal segmentation, peristalsis |
| Anatomy of the Stomach | Located in left upper quadrant of the abdomen; Digestive and glandular organ; Consists of three major regions: Fundus (upper portion), Corpus (body) and Antrum (lower portion); Both ends are guarded by sphincters to prevent backflow |
| Three areas of the stomach are | the fundus or upper portion, the body or middle portion, and the antrum or lower portion |
| The churning of food into chyme takes several hours. Peristaltic contractions are about 3 per minute but are influenced by nerves and hormones. | There are actually a type of pacemaker cells in the stomach that initiate depolarization of muscle cells and moves food from the upper stomach to the pylorus or pyloric sphincter at the bottom of the stomach. |
| Swallowing causes the fundus to | relax to accommodate a bolus of food; Gastric motility sweeps along the body of the stomach toward the fundus; Food is mixed with stomach acid and enzymes; Peristalsis and retropulsion churn the food into chyme |
| Function of the Stomach | Food reservoir; Gastric secretion of acids and enzymes to aid digestion: cephalic, gastric and intestinal phases; Churns the food to form chime; Motility increases or decreases in response to need |
| Cephalic phase | stimulated by thought and smell of food |
| gastric phase | stimulated by the stretch of stomach |
| intestinal phases | stimulated by histamines and digestive protien |
| The Stomach Structure and Function: muscular | Layers of muscle become progressively thicker in the body and antrum of the stomach. |
| The Stomach Structure and Function: | vascular The stomach’s blood supply is so abundant, that nearly all arterial vessels must be occluded before ischemic changes occur in the stomach. |
| The Stomach Structure and Function: secreation | pH around 1-3; gastrin is a hormone that stimulates secretion of gastric acid by the stomach; released by G cells in the stomach & duodenum. Gastrin stimulates parietal cells to secrete HCl. |
| Delta cells (δ-cells) are somatostatin producing cells. | They can be found in the stomach, intestine and the Islets of Langerhans in the pancreas. |
| Which cells (in the gastric mucosa) are responsible for the production of gastric acid? | Parietal cells |
| Acid secretion is stimulated by | (acetylcholine), gastrin (a hormone), and histamine (a biologic chemical mediator), and is inhibited by somatostatin (a hormone). |
| Somatostatin is classified as inhibitory hormone, main actions: Inhibit release of GH) (opposing (GHRH)); Inhibit release of (TSH); Suppress GI hormones: Gastrin, Cholecystokinin (CCK), Secretin, Motilin, Vasoactive intestinal peptide (VIP), & more | V rate of gastric emptying, & reduces smooth muscle contractions & blood flow within intestine, Suppress release of pancreatic hormones, Inhibit the release of insulin, Inhibit the release of glucagon, Suppress the exocrine secretory action of pancreas. |
| somatostatin Synthetic substitutes | Octreotide (brand name Sandostatin, Novartis Pharmaceuticals) is an octopeptide that mimics natural somatostatin pharmacologically, though is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone. |
| Pepsinogen to Pepsin | Acetocholine, gastrin & secretin stimulate chief cells to release pepsinogen during eating; Pepsinogen is converted to pepsin (in an acid environment) (pH of 2.0 is optimal) Pepsin is proteolytic (breaks down protien and forms polypeptides in the stomach. |
| Once chyme has entered the duodenum, | the alkaline environment inactivates pepsin. |
| Gastric mucosa is protected from the digestive actions of acid and pepsin | by a coatin of mucus. (mucosal barrier) |
| Phases of Gastric Secretion | Cephalic phase ; Gastric phase ; Intestinal phase |
| The iliocecal valve (sphinchter) controls | the flow of digested material from the ileum into the large intestine and prevents reflux into the small intestine. |
| Haustral segmentation - | localized rhythmic contractions of circular smooth muscles that divide and mix the chyme, bringing it into contact with the absorbent mucosal surface an propelling it toward the large intestine. |
| Peristalsis - | Waves of contraction along short segments of longitudinal smooth muscle that allow time for digestion and absorption; sequential contraction & relaxation of outer longitudinal & inner circular layers of muscles. 3 per min (neural & hormonal activity) |
| Swallowing is mediated primarily by the | swallowing center in the medulla. |
| Duodenum The is first segment of the small bowel. This is the area where bile from the pancreas/ liver and other enzymes enter the digestive tract at the sphincter of Oddi. A large volume of food in the stomach usually increases the peristaltic activity | The highly acid stomach contents need to be neutralized by sodium bicarbonate and other enzymes from the pancreas, liver and duodenal mucosa. (about 10 inches long) |
| **the bodies main defense against aspiration is | gravity (keep the head of the bed up). |
| Jejunum- This is the longest section of the small intestine. | starts after the sphincter of Oddi & becomes the ileum after about 8 feet. |
| The ileum | is the last 8 to 12 feet before the large intestine begins at the ileocecal valve. The chyme or partially digested food is mixed, moved and absorbed through the villi in the plicae ciculares |
| Villi (Villus) cover mucosal folds and are the functional unit of the small intestine. | have occasional goblet cells for secreation & the villi provide a large area for digestion and absorption. |
| The duodenum & jejunum act as a major secretory region of the gut, the duodenum also receives secretory products from other organs to aid in digestion | digestion & absorption are maximized by the large surface area conferred by the presence of villi. The villi are composed mainly of columnar epithelial cells, each of which is covered w/ microvilli to increase cell absorption. |
| Globlet cells are present among the epithelial cells | They secrete mucus that lubricates the lining of the intestine. |
| Sloughed epithelium replace themselves about every | 4-7 days |
| Large Intestine Extends from ileocecal valve to the anus, approx. 5 to 6 feet long; Begins with the cecum, where the appendix is located; | Four divisions of the colon: Ascending colon, Transverse colon, Descending colon and Sigmoid colon, Rectum, Anal canal and sphincters (internal and external) |
| Large Intestine | Absorbs some water and electrolytes to reduce the fluid volume of chyme and make formed feces; Eliminates waste using strong peristaltic movements to move the feces toward the anus |
| Large intestine function | No real nutritive absorption takes place in this region. Water and electrolytes are absorbed; rapid movement, such as diarrhea would cause this water and electrolytes to be eliminated rather than absorbed. |
| Aldosterone & the large intestine | increases the permeability of the membrane to sodium, allowing it to be absorbed. Where else does aldosterone work to increase sodium absorption? Do you remember the regulation of fluid homeostasis from fluids and electrolytes? |
| How does aldosterone work to keep the sodium and water in balance? | Aldosterone secreted in response to decreased serum Na level or increased urine Na level. Na exerts an osmotic pressure as water tends to follow Na. This keeps Na in balance & indirectly regulates water balance. |
| Liver: Second largest organ of the body, located in the right upper quadrant of the abdomen | Consists of large right lobe and smaller left lobe; Functions are storage, protection and metabolism. Has over 400 functions; Secretes bile via the common bile duct into the duodenum- used in breakdown of fats |
| What accounts for the yellow tinge of jaundice? | elevated levels of Bilirubin |
| Gallbladder | Located on the anterior surface of the liver; Concentrates and stores the bile from the liver; Releases bile for fat metabolism; is a pear-shaped organ that stores about 50 ml of bile (or "gall") until the body needs it for digestion. |
| Cholestasis | is blockage in supply of bile into digestive tract. It can be "intrahepatic" (obstruction is in liver) or "extrahepatic" (outside the liver). It can lead to jaundice, and is identified by the presence of elevated bilirubin level that is mainly conjugated. |
| Biliary colic | is when a gallstone blocks either the common bile duct or the duct leading into it from the gallbladder. |
| Up to 25% of all people have gallstones (cholelithiasis), composed of lecithin and bile acids. | These can cause abdominal pain, usually in relation with the meal, as the gallbladder contracts and gallstones pass through the bile duct. |
| Acute or chronic inflammation of the gallbladder (cholecystitis) | causes abdominal pain. 90% of cases of acute cholecystitis are caused b presence of gallstones. The actual inflammation is due to secondary infection with bacteria of an obstructed gallbladder, with the obstruction caused by the gallstone. |
| When gallstones obstruct the common bile duct (choledocholithiasis), | the patient develops jaundice and liver cell damage. It is a medical emergency, requiring endoscopic or surgical treatment such as a cholecystectomy. |
| Polyps (growths) are sometimes detected during diagnostic tests for gallbladder disease. Small gallbladder polyps (up to 10 mm) pose little or no risk, but large ones (greater than 15 mm) pose some risk for cancer, so the gallbladder should be removed. | Patients with polyps 10 mm to 15 mm have a lower risk but they should still discuss removal of their gallbladder with their physician. |
| Pancreatic juice is composed of two secretory products critical to proper digestion: digestive enzymes (pancreatic lipase & amylase)and bicarbonate. | The enzymes are synthesized and secreted from the exocrine acinar cells, whereas bicarbonate is secreted from the epithelial cells lining small pancreatic ducts. |
| Digestive Enzymes the pancreas secretes | a battery of enzymes that reduce virtually all digestible macromolecules into forms that are capable of, or nearly capable of being absorbed. Three major groups of enzymes are critical to efficient digestion: protease, Pancreatic Lipase, amylase |
| Proteases- | Digestion of proteins is initiated by pepsin in stomach, but bulk of protein digestion is d/t pancreatic proteases. Several proteases are synthesized in pancreas & secreted into small intestine. 2 major pancreatic proteases are trypsin & chymotrypsin. |
| Pancreatic Lipase | triglycerides cannot be directly absorbed across the intestinal mucosa. Rather, it must first be digested into a 2-monoglyceride and two free fatty acids. The enzyme that performs this hydrolysis is pancreatic lipase. |
| Pancreatitis which values will be out of range? | elevated lipase and elevated amylase |
| Sufficient quantities of bile salts must also be present in the lumen of the intestine in order for lipase to efficiently digest dietary triglyceride and for the resulting fatty acids and monoglyceride to be absorbed. | This means that normal digestion and absorption of dietary fat is critically dependent on secretions from both the pancreas and liver. |
| Amylase is the enzyme that hydrolyses starch to maltose (a glucose-glucose disaccharide), as well as the trisaccharide maltotriose and small branchpoints fragments called limit dextrins. | The major source of amylase in all species is pancreatic secretions, although amylase is also present in saliva of some animals, including humans. |
| Serum test- | CBC, Electrolytes, Clotting factors, Liver Function, Amylase, Lipase, Alkaline Phosphatase, Tumor markers (CA 19-9, CEA) |
| Albumin low | indicates liver disease |
| ALT increased | indicate liver disease/ hepatitis or cirrhosis |
| AST increased | may indicate liver damage/ hepatitis or cirrhosis |
| Increased bilirubin | hemolysis; biliary obstruction, hepatic damage |
| Elevated ammonia | hepatic disease such as cirrhosis |
| Urine test- | Urinalysis, Amylase, Urobilinogen |
| Stool test- | Occult blood, Ova & Parasites |
| Radiographic GI tests | Flat plate abdomen; Upper GI and small bowel series; Barium enema; Percutaneous Transhepatic cholangiography; Gallbladder series; IV Cholangiography |
| Upper GI Barium & Enema, Use | barium to visualize the structure and function of areas of the GI tract (Client is NPO for 8 hours) (some type of bowel cleansing) (barium can be very constipating, push fluid and fiber when they are no longer NPO) |
| The upper GI and small bowel series visualizes the barium as it moves down the GI tract. It looks at | motility, structures of the esophagus, stomach, duodenum. Small bowel follow through watches the barium through the remainder of the small bowel to the ileoceccal valve. |
| The barium enema or lower GI series visualizes the large intestine. | Barium is instilled & films are taken w/ the client in various positions, prone, supine and lateral. Can be uncomfortable. Takes 45 min.-1 hour. Laxative helps to remove barium from GI tract after exam |
| Percutaneous Transhepatic Cholangiography | Studies the biliary duct system; Uses iodine dye; Dye instilled via percutaneous catheter inserted into the hepatic ducts of the liver; Post-procedure the patient is kept to bed rest for 6 hours |
| Gallbladder Series | Visualization of gallbladder; Oral ingestion of iodine-based radiopaque contrast medium; Eats fat-free diet for evening meal; Take tablets 2 hours after meal; Then NPO after midnight; After first films taken, clt. is given meal high fat and 2nd films done |
| Intravenous Cholangiography | Visualizes the gallbladder and biliary ducts; NPO after midnight the night before; Iodine IV contrast given; Test may take 2 to 4 hours; X-rays taken at 20 minute intervals. |
| Endoscopy | Direct visualization of the GI tract using a flexible fiber optic endoscope; Used to evaluate bleeding, ulceration, inflammation, masses, tumors and cancerous lesions; Used to obtain biopsy and cytologic specimens |
| Esophagogastroduodenoscopy (EGD) | Visualization of esophagus, stomach and duodenum; NPO after midnight; Conscious sedation; Sims position, dentures removed; Post-procedure care involves monitoring while sedation wears off; May have a sore throat for several days |
| Endoscopic Retrograde Cholangiopancreatography (ERCP): Visualizes liver, gallbladder & pancreas w/ common bile duct; | Cannula inserted into the main duct; NPO; Conscious sed.; Use of contrast medium to evaluate biliary tract; Can remove some gallstones via papillotomy of the ampulla of Vater |
| Colonoscopy | Endoscopic exam of the entire large bowel; Liquid diet 24 hrs before, NPO after midnight, bowel prep; Conscious sedation; May need Atropine for vagal-induced bradycardia; Post-procedure care includes monitoring while sedation wears off |
| Proctosigmoidoscopy | Visualization of rectum and sigmoid colon using a flexible or rigid scope; Screen for colon cancer, GI bleeding or inflammatory bowel disease; Liquid diet for 24 hrs before, cleansing enema, laxative; Knee-chest position; No conscious sedation used |
| Gastric Analysis | Measures HCl & pepsin content for eval. of gastric & duodenal disorders; NPO, avoid alcohol, tobacco & meds that affect gastric secretions before; Insert NG tube’ Collect samples at 15 min. intervals for 1 hr; |
| Ultrasound | High-frequency vibratory sound waves via transducer gives images of internal organs, soft tissues; NPO 12 hrs before; Want to fill bladder to better visualize underlying structures; Can be used in conjunction with endoscopy to diagnose certain tumors |
| Liver-Spleen Scan | Use of IV radioactive colloid that is taken up by liver & spleen; Evaluates tumors, abscesses, organ size, location & vascularity; Eliminated from body via the urine |
| Nasogastric Tubes (NG) | nasogastric tube is indicated to: Decompress stomach by aspiration of gastric contents (fluid, air, blood); Introduce fluids (lavage fluid, tube feedings, activated charcoal into stomach; Assist in diagnosis through analysis of substances in stomach. |
| Stomatitis | inflammation of the mouth/ oral mucosa; Primary; Herpes Simplex; Candidiasis; Vincent’s; Traumatic ulcers; Lichen Planus; |
| Tumors of the Mouth | Premalignant lesions- leukoplakia and erythroplakia ; Squamous cell carcinoma-most common, 90%; risk factor is tobacco use; Basal cell carcinoma- occurs mainly on the lips; risk factor is sun exposure; Kaposi’s sarcoma – associated with AIDS |
| **Signs and Symptoms; Cancer of the Oral Cavity: A lump in the cheek ; A sore throat or constant feeling that something is caught in the throat; Difficulty chewing and/or swallowing; Numbness of the tongue or other area of the mouth; Loose teeth; | Changes in voice; A lump in the neck; Difficulty moving the tongue or jaw; Continuous bad breath; A sore in the mouth that will not heal (most common symptom); Perpetual pain in the mouth (another very common symptom); Leukoplakia or erythroplakia |
| Care of the Patient with Problems of the Oral Cavity | See Chart 56-2, page 1233 |
| ***The Patient with Oral Cancer | See Chart 56-3, page 1236 |
| Acute Sialadenitis (Inflammation of a salivary gland) Causes | Bacterial or viral etiology; Radiation treatment – xerostomia; HIV infection; Sjogren’s syndrome; Dehydration |
| Interventions for Clients with Esophageal Problems | Iggy; Chapter 57 |
| Gastroesophageal Reflux Disease (GERD) | Backflow of gastric contents into the esophagus; Caustic irritation of the esophagus; Esophagitis; anytime there is chronic inflammation there is a greater risk for cancers or other complications. |
| Symptoms of GERD | Water brash - production of excessive saliva; Dysphagia ; Odynophagia (painful swallowing); chest pain, errectaion, burping, gas, regurgitation; dyspepsia, coughing at night, |
| Diagnostic for GERD | Barium swallow (ruling out other problems); Endoscopy; Laryngoscopy; 24 hour pH monitoring |
| Interventions for GERD | Diet & drug therapy; education; Lifestyle changes; Surgical management; Limit spicy, fatty & acidic foods; Limit tobacco & alcohol use; Carbonated, caffeinated beverages; Light meal in evening; Sleep w/ head elevated & left lateral position |
| Treatment for GERD: Antacids- | Maalox, Mylanta, Gaviscon |
| Treatment for GERD: Histamine receptor antagonists- | Famotidine, ranitadine, cimetadine, nizatidine |
| Treatment for GERD: Proton pump inhibitors- | Omeprazole, lansoprazole, rabeprazole, pantoprazole |
| Classes of GERD Drugs | Inhibition of gastric acid secreation; acceleration of gastric empting step; medications that protect the gastric mucosa |
| Treatment for GERD: Mucosal cytoprotectants- | Sucralfate (Carafate) |
| Treatment for GERD: Prokinetic drugs- | Metoclopramide |
| Treatment for GERD: Cholinergics- | Bethanecol |
| Fundoplication- | tightens and reinforces the LES area (a fold of stomach wrapped around the esophagus) |
| Placement of Angelchik | prosthesis around the distal end of the esophagus; an incomplete "doughnut" shaped ring of silicon around the gastro-oesophageal junction: the Angelchik prosthesis. |
| Hiatal Hernias | The protrusion of the stomach through the esophageal hiatus of the diaphragm into the thorax. Two types; Sliding hernia -Rolling hernia (chest pain/ dysphagia/ belching) |
| **Barrett's esophagus | is the abnormal growth of intestinal-type cells above the esophogeal border, into the esophagus. These tissue changes are a forerunner to cancer of the lower esophagus (adenocarcinoma). Regular program of EGD & biopsy; risk factors GERD/ smoking/ alcohol |
| Cancer of the Esophagus (Can be benign or malignant) | Squamous cell carcinomas are usually located in the upper 2/3 of the esophogus (account for approx. 50% of cancers); Adenocarcinomas are usually located in the lower 2/3 of the esosphogus (account for approx. 50% of all tumors). |
| Risk factors for cancer of the esophagus | are tobacco & alcohol use and GERD; Five year survival rate is 5%; monitor with Regular program of EGD & biopsy |
| Signs and Symptoms; Cancer of the Esophagus | Persistent dysphagia; Significant weight loss (>20 pounds); Painful swallowing (odynophagia) ; Hoarseness; Chronic cough; Nausea and vomiting; Hiccups; Pneumonia; changes in bowel habits; Melena (discoloration of the stool) |
| Associated Nursing Diagnoses associated with cancer of the esophagus | Risk for Aspiration, r/t impaired swallowing secondary to esophageal strictures; Impaired Swallowing r/t obstruction by esophageal tumor or the effects of radiography; Acute Pain (or Chronic Pain…) |
| Managing the Client with a Nasogastric Tube After Esophageal Surgery | See Iggy, Chart 58-10; page 1279 (make sure that the tube remains in place, tube is patent, secure tube well; |
| Esophageal Diverticula | Herniation of the esophageal mucosa and submucosa, into surrounding tissue. Creates a small pouch or sac. |
| Esophageal Diverticula Symptoms | Dysphagia; Regurgitation; Nocturnal cough; Halitosis |
| Common Causes of Esophageal Perforation (Iggy, Table 58-2; page 1281) | Straining; Seizures; Trauma; Foreign objects; Instrument or tubes; chemical injury |
| Gastritis | Inflammation of gastric mucosa; Erosive- acute gastritis, stress ulcers; Nonerosive- chronic gastritis>> Prostaglandin protective barrier is breached; HCl acid injures the lining; Hemorrhage and stomach cancer are risks of long-term inflammation |
| Peptic Ulcer Disease (PUD) Gastric acid erodes the mucosa; | Duodenal bile can reflux through pyloric incompetent sphincter which breaks down protective barrier;; Incompetent pyloric sphincter can allow gastric acid to irritate the duodenum, causing duodenal ulcers |
| Gastric Ulcers | Complications of Ulcers; Hemorrhage; Perforation; Pyloric obstruction; Intractable disease |
| PUD Assessment & Symptoms | Dyspepsia; Burning, gnawing pain in the upper epigastrium, left of midline; Associated with eating or after taking ASA, NSAIDS; Vomiting; Hematemesis or black, tarry stools; Hematocult |
| PUD Diagnostics | Lab – CBC, Stool occult blood; Radiographic – Upper GI; Endoscopy- esophagogastroduodenoscopy; Testing for H. pylori |
| Drug Therapy for PUD | Antacids; H2 receptor antagonists; Proton pump inhibitors; Mucosal barrier fortifier; Prostaglandin analogs; Antimicrobials |
| PUD Complication Management | Hemorrhage- NG tube, Acid suppression, Saline lavage, Endoscopy; Hypovolemia- IV isotonic crystalloid, bld replacement, frequent monitoring; Surg= (Vagotomy, Gastroenterotomy, Bilroth I, (gastroduodenostomy), Bilroth II (gastrojejunostomy), Pyloroplasty |
| Dumping Syndrome | Vasomotor symptoms that may result from rapid emptying of gastric contents into the small intestines |
| Gastric Carcinoma (Adenocarcinoma 85-95%; non-Hodgkins lymphoma and leiomyosarcoma are 15%) | Onset is insidious and often advanced when detected; H. Pylori infection is strongly linked w/ gastric CA; Strongly linked w/ ingestion of pickled, salted meats, nitrates-irritates the stomach |
| Early Signs and Symptoms; Cancer of the Stomach | Indigestion or a burning sensation (heartburn) ; Loss of appetite, especially for meat; Epigastric, back or retrosternal pain |
| Late Signs & symptoms of caner of the stomach | Abdominal pain or discomfort in the upper abdomen; Nausea and vomiting ; Diarrhea or constipation ; Bloating of the stomach after meals; Weight loss; Weakness and fatigue; Melena |
| Melena | dark tarry appearance in the stool |
| Erythroplakia | is be premalignant lesion in the mouth |
| Hematochezia | passage of red blood through rectum; usually bleeding in colon or rectum, but it may result from the loss of blood higher in the digestive tract although blood passed from the stomach or small intestine generally loses its red coloration |
| Achalasia | esophageal motility disorder involving smooth muscle layer of esophagus & lower esophageal sphincter .[1] Its cause is unknown. characterized by incomplete LES relaxation, increased LES tone, and inability of smooth muscle to move food down the esophagus. |
| Dumping Syndrome | Vasomotor symptoms that may result from rapid emptying of gastric contents into sm. intest. (managed w/ small meals w/ no fluids, high protein high fat, low carb; pectin; Octreotide (Sandostatin). No milk products, no sweets, liquid between meals only. |
| Dumping Syndrome:When symptoms of dumping syndrome occur during a meal or within 15 to 30 minutes following a meal, they may include: | nausea; Vomiting; Abdominal pain, cramps; Diarrhea; Dizziness, lightheadedness; Bloating, belching; Fatigue; Heart palpitations, rapid heart rate |
| Dumping syndrome: When signs and symptoms develop later, usually one to three hours after eating, they may include: | Sweating; Weakness, fatigue; Dizziness, lightheadedness; Shakiness; Feelings of anxiety, nervousness; Heart palpitations, rapid heart rate; Fainting; Mental confusion; Diarrhea; Low blood sugar (hypoglycemia) |
| Octreotide (Sandostatin) | synthetic GI hormone suppresses gastric acid secretion, by reducing gastrin secretions (Treatment of severe diarrhea & flushing episodes in pts w/ GI endocrine tumors, including metastatic carcinoid tumors & vasoactive intestinal peptide tumors (VIPomas) |
| Anemia | identify source of the anemia |
| Patients (especially elderly population)can become severely anemic overtime with a very small blood loss daily | chronic blood loss of 3-5 mls is all it can take.. |
| Intractable disease | (disease becomes more chronic) |
| Drug Therapy for PUD | Antacids (Mylanta, Tums)); H2 receptor antagonists (Zantec); Proton pump inhibitors (priloset) ; Mucosal barrier fortifier (carafate); Prostaglandin analogs( ; Antimicrobials |
| Symptoms of gastric ulcer will present before a | duodenum ulcer |
| Acute gastritis can happen during a hospital stay, often they are put on H2 blockers and proton pump inhibitors prophylactically because | the length of hospital stay without these meds can be extended and there is a correlation between poor outcomes and these stress ulcers. |
| Causes of Constipation | Frequent use of laxatives; Advanced age; Inadequate fluid intake; Inadequate fiber intake; Immobilization; A sedentary lifestyle, medications, Irritable bowel syndrome |
| Causes of Diarrhea | Viral gastroenteritis; Overuse of laxatives; Use of certain antibiotics or long term use of antibiotics (C. diff); Inflammatory bowel disease; Irritable bowel syndrome; Food borne pathogens |
| Complications with Constipation | Fecal impaction; Hemorrhoids or rectal fissure; Hypotension or bradycardia with Valsalva maneuver |
| Complications with Diarrhea | Dehydration and electrolyte imbalances; Skin breakdown; hypokalemia; |
| Interventions for diarrhea & constipation | fluid I&O; monitor hypotension; monitor elimination pattern; monitor skin integrity; adequate fluid intake; abdominal assessment; observe and document stools; administer laxatives or enemas |
| Rectal fissue | small tears form in the rectum, with another bowel movement the tear re-opens |
| Irritable Bowel Syndrome | non-inflammatory, chronic gastrointestinal GI disorder: presence of chronic or recurrent diarrhea, constipation, &/or abdominal pain & bloating. Most common digestive disorder; A functional disorder (constipation predominant or diarrhea predominant) |
| Symptoms of IBS (a non inflammatory disorder) | chronic or recurrent diarrhea, constipation and/or abdominal pain and bloating; Usually starts in young adulthood; Diagnosed by r/o other disorders; Exacerbated by stress, diet or anxiety; No change in bowel mucosa; Women 2x likely to have IBS |
| IBS treatment based on symptomology | fiber, |
| dicyclomine (Bentyl) | slows the GI tract (May have a direct and local effect on GI smooth muscle, reducing motility and tone- Therapeutic Effect(s): Decreased GI motility |
| Herniation | A hernia is a weakness in the abdominal muscle wall through which a segment of the bowel or other abdominal structure protrudes. |
| Most common types: Hernias | Might also be classified as reducible, irreducible (incarcerated) or strangulated |
| Reducible hernia | – contents of the abdominal sac can be placed back into the abdominal cavity by gentle pressure. |
| An Irreducible (incarcerated) hernia | cannot be reduced |
| A hernia is considered strangulated when blood supply to the herniated segment of the bowel is cut off by pressure from the hernial ring (the band of muscle around the hernia). | If a portion of the bowel is strangulated, there is ischemia and obstruction of the bowel loop.This can lead to necrosis of the bowel and possibly bowel perforation. |
| Signs of strangulation hernia are | Abdominal distension; Nausea; Vomiting; severe Pain; Fever and tachycardia |
| Colorectal Cancer (Third most common cancer) | 95% are adenocarcinomas; Age is a risk factor – 95% occur in persons over age 50; Metastasis occur in 15% to 30% of cases, even with surgical resection; Often not detected until advanced stage |
| Risk Factors for colorectal cancer | Age; Genetic predisposition; High fat, refined food diet; Inflammatory bowel disease; Screening Recommendations: fecal occult blood test; sigmoidoscopy or double contrast barium enema; colonoscopy |
| Interventions for colorectal cancer | Early detection (fecal occult blood test; sigmoidoscopy or double contrast barium enema; colonoscopy); Radiation; Chemotherapy; Surgical excision; Hemicolectomy and colon resection; Colostomy or anastomosis; Abdominoperineal resection |
| Types of Colostomies | See Iggy, Figure 59-5, page 1299 |
| Bowel Obstruction partial or complete obstruction of small or large bowel that impedes digestion- | Mech. obst. – adhesions (scar tissue), hernias, blockages (stool, cancer, fibroid), intussusceptions (part of bowel slips over bowel), volvulus (twisting of the bowel) //Nonmechanical obstruction - adynamic (stops or slows digestion)or paralytic ileus |
| Don’t give Metoclopramide (Reglan) (pro-kenetic) to a patient with a | mechanical bowel obstruction, can result in bowel perforation |
| Physiology of bowel Obstruction Intestinal contents accumulate above area of obstruction; Peristalsis tries to move obstruction causing increased distention & more secretions; Bowel Edema results Decreased absorption of F&E into vascular space>> | Obstruction high in small intestines results in metabolic alkalosis; Obstruction at end of small intestine or in large intestine results in metabolic acidosis; Hypovolemia can result, renal insufficiency & peritonitis |
| Signs and Symptoms of Bowel Obstruction | abdominal cramping & pain (severe), N&V in small bowel obstruction; obstipation (cannot have BM); SBO severe F&E imbalances; bloating; diarrhea, constipation; distention |
| NG tube & NPO must also ask for | iv FLUIDS! |
| Management of Bowel Obstruction | Laboratory assessment; Radiographic assessment; NG tubes; Fluid and electrolyte replacement; Pain management; Drug therapy; Surgical management |
| Polyps | Small growths attached to the mucosa; Most benign but adenomas can pose a cancer risk |
| Hemorrhoids | Swollen or distended veins in anorectal area; Can be internal or external; Caused by ^ ab. pressure (pregnant jet fighters are a high risk group) Hemorrhoids symptoms= persistent itching ; anal bleeding ; pain ; blood clots (thrombosis of the hemorrhoids) |
| Hemorrhoids Treatments include | banding; surgical ligation; injection of sclerosing agents; topical meds; cold packs, sitz baths; Diets high in fiber & fluid to promote regular BM; Stool softeners; Surgeries; Sclerotherapy ; Ligation; Cryosurgery; hemorrhoidectomy |
| Malabsorption Syndrome | Abnormalities which interfere w/ GI tract’s ability to absorb nutrients; Generalized flattening of the mucosa in the small intestine; The nutrient involved depends on type and location of the abnormality |
| Malabsorption Abnormalities | Bile salt deficiencies; Enzyme deficiencies (lactase deficiencies, carb digestion effected) common; Bacterial infection; Disruption of mucosal lining of small intestine; Altered lymphatic and vascular circulation; V in gastric or intestinal surface area |
| Pancreatic enzymes involved in the breakdown of vitamin | B12 |
| Celiac sprue Celiac disease | is a condition that damages the lining of the small intestine and prevents it from absorbing parts of food that are important for staying healthy. The damage is due to a reaction to eating gluten |
| Appendicitis | Acute inflammation of the appendix, Opening is obstructed and inflammation occurs; Swelling, infection; Can progress to gangrene and perforation within 24 to 36 hours; |
| Peritonitis | is acute inflammation of the lining of the abdominal cavity |
| Symptoms of Appendicitis | Pain in RLQ; rebound tenderness at McBurney’s; temp normal or mildly febrile; lab test do not establish diagnosis. |
| Symptoms of Peritonitis (PERITONITIS IS LIFE THREATENING!) (sign of abdominal infection/ inflammation) | Ab. pain (local or diffuse), Rigid, distended abdomen; N & V, anorexia; Diminished bowel sounds; Rebound tenderness; ^ fever; Dehydration, V urine output; ^ WBCs; Tachycardia; Hiccups; Possible respiratory compromise |
| Interventions for peritonitis | IV fluids, IV antibiotics, surgical treatment of the cause |
| Gastroenteritis | Acute N & V in response to inflammation of mucous membranes of intes. tract; viral or bacterial; Most common cause of morbidity & mortality in Asia, Africa and Latin America; Good assessment! Fluid replacement, diet & drug therapy & health teaching… |
| Ulcerative Colitis | Chronic inflammation of mucosal lining in colon or rectum; Starts at the rectum and progresses toward the cecum; Loose stools containing blood and mucous; Poor absorption of nutrients and thickening of colon wall; Multiple complications |
| Symptoms of Ulcerative Colitis (Vary with acuity and complications) | Abdominal pain; Bloody diarrhea; Tenesmus – (uncontrolled straining); Low grade fever; Decreased Hgb & Hct, increased WBCs & ESR, decreased Na, K & Cl and decreased albumin |
| Interventions for colitis | Diarrhea management; Drug Therapy; Low-fiber diet; Rest; Surgical management: Proctocolectomy with ileostomy; Colectomy with continent ileostomy; Colectomy with ileoanal anastomosis |
| proctocolectomy, | large intestine & rectum are removed, leaving the lower end of the small intestine (the ileum). The doctor sews the anus closed and makes a stoma in the skin of the lower abdomen. The surgical procedure to create the stoma is called an ostomy. |
| An ileostomy | end of small intestine (the ileum) out onto the surface of the skin. Intestinal waste passes out of the ileostomy and is collected in an external bag stuck to the skin. Ileostomies are usually sited above the groin on the right hand side of the abdomen. |
| Crohn’s Disease (Can affect any part of the intestinal tract; Some possible genetic predisposition) | Regional enteritis or granulomatous colitis; Defect in immunoregulation of inflammation in presence of bacteria or viruses; Deep fissures & ulcerations develop; Severe malabsorption; Fistula formation is common; Over time fibrosis develops & obstruction |
| Symptoms of Crohn’s Disease | Abdominal pain; Diarrhea or frequent soft, loose stools – blood in stools is rare; Steatorrhea; Low grade fever; Decreased bowel tones; Guarding; |
| Interventions for Crohn’s disease | Drug therapy; Nutritional management; Complications management; Electrolyte replacement; Prevent infection; Surgical removal of affected bowel |
| Diverticulitis Symptoms | Abdominal pain, usually localized to lower quadrants; Low grade fever; Nausea and vomiting; Tenderness to palpation; Perforation or hemorrhage will result in more severe symptoms: Dehydration, fever, hypovolemia, shock |
| Interventions for diverticulitis | Low fiber diet or clear liquids during the acute phase; Antibiotics; Rest, refrain from coughing, straining or bending; Surgical intervention (May end up with colostomy) |
| Anal abscess, fissure, fistula | Abscesses result from obstruction of some of the ducts in the anorectal area; Fissures are superficial erosions of the anal canal; Fistulas are abnormal tracts from the anal canal to perianal skin |
| Anal Fistula | Extend from the anorectal canal to the outer skin (Drainage, foul odor; Hard to heal, require surgical intervention) |
| Ulceration | erosion of the tissue |
| Cirrhosis (major types) | Portal Hypertension; Ascites; Varices; Encephalopathy; Hepatitis; Viral; Toxic, drug-induced |
| Liver diseases range in severity | from mild hepatic inflammation to chronic end-stage cirrhosis. |
| Cirrhosis | Progressive, inflammatory liver condition; Insidious, prolonged and destructive; Diffuse bands of fibrotic connective tissue that distort the livers normal architecture. Blood flow & mucus systems of the liver are upset |
| Cirrhosis Common Causes (etiologies): | alcohol liver disease; viral hepatitis; biliary disease; cardiovascular related liver disease. |
| Alcoholic Liver Disease (Laennec’s Cirrhosis) Alcohol has direct toxic effect on hepatocytes & causes liver inflammation | Liver becomes enlarged w/ fatty deposits, leukocytes & lymphocytes; Over time, inflammatory phase decreases, & the destructive phase increases; Cellular (hepatic) necrosis & hepatic failure. |
| Signs and symptoms of cirrhosis | Fatigue, weight loss, anorexia, in acute illness (nausea, anorexia, fever, ab. Pain, jaundice.) Screen for liver function tests |
| Viral Hepatitis | Infection causes scarring over a period of time, which leads to progressive scarring of the liver (usually over decades). |
| Biliary Cirrhosis | Develops as a result of chronic biliary obstruction, bile stasis, inflammation, or diffuse hepatic fibrosis. |
| Cardiac Cirrhosis | Occurs with right-sided heart failure, Cor Pulmonale, constrictive pericarditis or valvular insufficiency (liver becomes congested with venous blood, becomes anoxic and necrosis results) |
| Cirrhosis: Hepatic cell degeneration may lead to one or more of the following conditions… | Portal hypertension; Ascites; Bleeding esophageal varices; Coagulation defects; Jaundice; Portal-systemic encephalopathy (PSE) w/ hepatic coma; Hepatorenal syndrome; Spontaneous bacterial peritonitis; |
| Portal Hypertension | abnormally high bp pressure in portal venous system (resistance and reduced compliance in liver); most commonly caused by cirrhosis; also caused by obstruction of portal vein, pancreatitis, thrombotic event, ab. trauma, |
| Patients with impaired liver function can have | prolonged bleeding time (greater risk for bleeding and take associated nursing interventions for these patients) |
| Ascites | Third space fluid in the abdominal cavity; Caused by increased pressure in mesenteric tributaries of the portal vein; Hydrostatic pressure forces water out of vessels & into peritoneal cavity. Dehydration is a major concern. |
| Esophageal Varices: These blood vessels then continue to dilate until they become large enough to rupture. When esophageal varices rupture, patients become acutely ill. | In fact, 50 percent of patients with esophageal varices will eventually bleed from the varices. The mortality rate for esophageal variceal bleeding, on the first event, is between 40 and 70 percent. |
| Splenomegaly | Increased pressure in the splenic vein from prolonged portal hypertension; Causes increase in size of spleen; May require splenectomy |
| Coagulation Anomalies | Decrease in ability to absorb fat soluble vitamins (Vitamin K); Vitamin K is necessary for production of clotting factors; Impaired clotting ability make hemorrhage a risk; Also prone to anemia, DIC and thrombocytopenia |
| Jaundice (Yellowing of skin and sclera (icterus) | Caused by hyperbilirubinemia; Bilirubin accumulates in the liver and enters the bloodstream |
| **Portal-Systemic Encephalopathy | Also called hepatic encephalopathy or hepatic coma; End stage hepatic failure or cirrhosis; Stages I thru IV; Progresses from subtle personality changes to coma; Probably result of impaired ammonia metabolism |
| lactulose | In treating hepatic encephalopathy, lactulose helps "draw out" ammonia (side effect diarrhea) |
| carefate- | treatment for peptic ulcer disease (Sucralfate is used to treat ulcers. It adheres to damaged ulcer tissue and protects against acid and enzymes so healing can occur) |
| Acute | (abnormalities present for less than six months) |
| Chronic | ( more than six months) |
| Fulminant | (disease process that has progressed rapidly, usually over less than 4 weeks |
| A liver biopsy | is a procedure whereby small pieces of liver tissue are removed in order to be sent to a laboratory for examination. It is very helpful in the diagnosis of diseases that affect the liver. |
| Percutaneous Liver Biopsy | A needle the diameter of a pen refill is then passed through the skin and into the liver, where a specimen is obtained. |
| Percutaneous Image-Guided Liver Biopsy | the needle is guided by CT scan or ultrasound images. This is often helpful when the disease process is localized to discrete spots in the liver. |
| Laparoscopic Liver Biopsy | done solely for the purpose of obtaining the biopsy specimen or may be part of another operative procedure. Small incisions are made in the ab. & instruments are introduced through trocars to obtain the biopsy. |
| Open Surgical Liver Biopsy | rarely performed, unless they are part of another operative procedure. When an open biopsy is done, the surgeon may choose to use a biopsy needle or may surgically excise a small wedge of liver tissue. |
| Acute cholecystitis | caused by obstruction of the cystic duct. This starts an inflammatory process. Bile is trapped and reabsorbed into the wall of the gallbladder where it acts as an irritant. There is edema and distention of the gallbladder and ischemia. |
| Cholecystits left untreated | gallbladder tissue may begin sloughing & become necrotic. A perforation of gallbladder may cause peritonititis or abscess. Episodic, vague ab. pain that is triggered by a high-fat or high volume meal, |
| symptoms of cholecystitis | flatulence, eructation and bloating, fever and/or jaundice, Episodic, vague ab. pain that is triggered by a high-fat or high volume meal |
| Portal-Systemic Encephalopathy Grade 1 - | Trivial lack of awareness; Euphoria or anxiety; Shortened attention span; Impaired performance of addition |
| Portal-Systemic Encephalopathy Grade 2 – | Lethargy; Minimal disorientation for time or place; Subtle personality change; Inappropriate behavior; Impaired performance of subtraction |
| Portal-Systemic Encephalopathy Grade 3 – | Somnolence; semi-conscious, but responsive to verbal stimuli; Confusion; Gross disorientation |
| Portal-Systemic Encephalopathy Grade 4 - | Coma (unresponsive to verbal or noxious stimuli) |
| Hepatorenal Syndrome | Hepatic failure can lead to renal failure; Elevated BUN, Creatinine, Ammonia, Bilirubin and Sodium levels in the blood; Decreased sodium levels in urine; Can follow GI bleed; May be precipitated by medications |
| Diagnostics for Hepatorenal Sydrome | Laboratory- CBC, BUN, Creatinine, Ammonia, Urine osmolarity, urine sodium and creatinine clearance; Radiographic studies- Abdominal x-ray, GI series, CT; Oscopy- EGD; Liver scan using radioactive isotope |
| Interventions cirrhosis | Diet therapy- low sodium, fluid restriction; Drug therapy- Diuretics(care not to dehydrate) , antacids, lactulose, neomycin; Paracentesis; F&E management; Surgical intervention- shunt; Esophageal balloon tamponade |
| Viral Hepatitis A to E | Widespread inflammation of liver cells by a viral agent; Can be acute or chronic; Five major categories |
| Hepatitis A virus (HAV) | Spread via oral-fecal route; Symptoms of typical viral infection; jaundice; Incubation period is 15 to 50 days |
| Hepatitis B (HBV) (Also called serum hepatitis) | transmission through skin/mucous membranes contaminated w/ blood/serous fluid.; mild symptoms but result in serious complications; Incubation period is 45 -180 days; Chronic Hep. develops in 1%-10% |
| Hepatitis C (HCV) | associated with people who share needles or health care workers that get exposed. Pain in upper right quadrant; N&V, loss of appetite; jaundice; fatigue; associated latter with high risk of cancer. |
| Hepatitis D | Usually spread by parenteral route (IV fluids); Can co-infect a person with HBV, it needs the HBV as a helper to replicate; Can act as a super infection for a client with HBV; Incubation is 14 to 56 days |
| Hepatitis E | Waterborne epidemics after flooding; Clinical course resembles HAV; Found in travelers returning from endemic areas; Incubation period is 15 to 64 days; No known chronic form |
| Toxic or Drug-induced Hepatitis | Systemic poisons converted by the liver into toxic metabolites; Cause necrosis & fatty infiltration of liver; Tylenol (large doses), industrial toxins. |
| Idiosyncratic Toxic Hepatitis | Drug reaction that causes morphologic changes in liver similar to viral hepatitis; May occur during or shortly after exposure to the drug; Isoniazid and dilantin are known to cause ITH; Stop drug, supportive treatment, possible transplantation |
| Tumors of the Liver | Primary hepatocellular carcinoma is one of the leading causes of death in the world; Higher in African-American males; Metastasis is common due to high vascularity of the liver; Between 30% and 70% also have cirrhosis |
| Liver Transplantation | End stage liver disease that has not responded to conventional treatment; Better survival rate due to immunosuppressive drugs: Cyclosporine, Asathioprine and Prednisone |
| Liver Diagnostics | Lab: Liver function tests (AST, ALT, LDH, Bilirubin, Urobiligen), Total Protein, Albumin, Globulin, Ammonia; Abdominal x-ray, CT, EGD; Liver-Spleen Scan |
| Problems of the Gallbladder & Pancreas | Cholecystitis; Cholelithiasis; Pancreatitis; Malignancy |
| Cholelithiasis | presence of one or more gallstomes (bile can harden into stones) most often caused by bilestasis; symptoms (pain, N&V,) |
| * Cholecystitis | Cholecystitis or a gall bladder attack is inflammation of the gall bladder. chronic or acute; can be associated with gallstones or often due to bacterial infection. Pain can correlate w/ high fat meal. |
| Cholecystitis Diagnostics | Laboratory: Alkaline Phosphatase (ALK), AST, LDH, Direct & Indirect; Bilirubin, CBC; Ultrasound; Cholecystogram or Gallbladder series; IV Cholangiogram |
| Cholecystitis Interventions | Cholecystectomy- traditional or laparoscopic; Dietary restriction of fats and amount of food for clients with chronic cholecystitis; Medications- Analgesics, Anti-cholinergics |
| Tumors of the Gallbladder (Primary cancer is rare) | Chronic cholecystitis or cholelithiasis increases risk; SX are similar to other conditions and insidious; Often discovered during procedures to diagnose cholecystitis or lithiasis |
| Pancreatitis (Can be Acute or Chronic) (acute pancreatitis is serious and can be life-threatening) | Inflammation from increased pancreatic enzymes destroys ductal tissue(trypsinogen); Autodigestion & fibrosis of the pancreas; Severity depends on the extent of inflammation and tissue destruction |
| Pancreatitis signs & symptoms | Severe pain, diarrhea, N&V, altered lab values( lipase, amylase); alchoholism is a risk factor for chronic pacreatitis. |
| Treatment for pancreatitis | NPO (ingetstion of food triggers pain); PCA pump (severe pain) |
| Pancreatic Carcinoma | Account for 2% to 3% of new cancer each year; Usually found in the late stages; Can be primary or metastasis; Primary adenocarcinoma is highly metastatic; Treatment is surgical, chemotherapy, radiation |
| Enteral Feedings Persons who are not able to take oral nutrition due to swallowing issues or decreased ability to eat | Feedings via feeding tubes, PEG, PEJ; Feedings can be continuous, nocturnal cyclic) or bolus; Complications are tube blockage, fluid & electrolyte imbalance, dehydration |
| Parenteral Feedings (If the GI system is not functioning effectively, can use parenteral feeding) | Partial parenteral nutrition- can use peripheral IV line; Total parenteral nutrition- must use a central IV line due to higher concentration of dextrose & proteins; Very expensive and less effective than using the GI tract |
| Roux-en-Y Bypass | more radical stomach by pass procedure. Most of stomach and deuodumem is removed |
| Malabsorbtive Procedure | completely by-pass deuodumem and jejeunum |
| *Salivary glands | ptyalin; amylase |
| * Stomach; | gastric pepsin; lipase |
| *Liver; | bile |
| *Pancreas; | trypsin; amylase; lipase |
| *Intestine | peptidases, lactase, maltase |
| Healthy color of stoma | bright or cherry red or pink |
| Diverticulitis (can be in small or large bowel) | inflammation or infection of the Diverticula (patients may be on both gram negative and gram positive bacteria to address infection) |
| Fissures | superficial erosion of the tissue; very painful for patients (cracks in intestinal wall) |
| Fistula | unnatural opening between two different structures; inflammation and erosion of the tissue can result in fistula (pathogenic specific and patient specific) (caner or inflammatory disease process) |
| Perforation | opening from GI tract into peritoneal |
| Reasons for blood in stool | Hemorrhoid; bleeding from polyps or cancer; ulcerative colitis; esophageal varicies; |
| Ulcerative clolitis labs | Increased sed rate (indicator for inflammation), decreased sodium, reduce hct & hemoglobin, low potassium (cardiac issues), low albumin; stool hemocult; or frank blood |
| Drug therapy for ulcerative colitis | steroids for inflammatory process; Imodium; low fiber diet; |
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