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  1. 1. Gastrointestinal System Disorders
  2. 2. Gastrointestinal System
  3. 3. Gastrointestinal Tract Upper GIT • • consists of structures that aid in the ingestion and digestion of food includes the mouth, esophagus, stomach, duodenum Hypothalamus – satiety center  is responsible for notifying the body that it is satisfied or has received sufficient food Lower GIT • • • consists of the small and large intestines digestion is completed in the small intestine , and most nutrients are absorbed in this part of the GIT the large intestine serves primarily to absorb water and electrolytes and to eliminate the waste products of digestion through the feces
  4. 4. Gastrointestinal Tract Mouth •Salivation  the “thought” of food initiates saliva production a.) serous secretions  contain ptyalin for starch digestion – produced by parotid and submaxillary glands b.) mucous secretions - for lubrication of food – produced by the buccal, sublingual and submaxillary glands •Mastication    chewing of food teeth - for initial breakdown of food to small particles it helps prevent excoriation of the lining of the tract and increase rate of digestion Major Structures in the Mouth • • teeth – to grind the food salivary glands – moisten food and mucous membranes and begin carbohydrate digestion
  5. 5. Gastrointestinal Tract Esophagus     is a hollow tube, the upper 1/3 is composed of skeletal muscles, the rest is smooth muscle lined with mucous membrane – secretes mucoid substance for protection the bolus of food arrives at the cardiac sphincter of the stomach w/in 5-10 secs. after ingestion the lower esophageal sphincter (LES) prevents reflux of food in the stomach back into the lower esophagus Swallowing (deglutition) 3 phases: 1.) tongue forces the bolus of food into the pharynx 2.) the food moves into the upper esophagus 3.) the food moves down into the stomach * Food is prevented from passing into the trachea by closing of the
  6. 6. Gastrointestinal Tract Stomach  made up of 5 layers of smooth muscle 2 types of contractions: 1.) tonus contractions – continuous contractions 2.) rhythmic contractions – may be slow ( q2-3 mins.) or fast – responsible for the mixing of food and peristaltic movement Vagus nerve – supplies the nervous stimulation for the stomach - has both symphathetic and parasymphatetic fibers movement of food through the stomach and intestines is by peristalsis  the alternate contraction and relaxation of the muscle fibers that propels the food in a wave-like motion chyme – food in the stomach - is pumped through the pyloric sphincter into the duodenum
  7. 7. Gastrointestinal Tract Digestive Function of the Stomach: Pepsin – needed for protein digestion HCL acid – aids in pre-digestion of food
  8. 8. Gastrointestinal Tract Intestines Small Intestine  2.5 cm. (1 inch) wide and 6 meters (20 feet) long – fills most of the abdomen 3 parts : a.) duodenum – which connects to the stomach (10 inches) b.) jejunum – middle portion (8 feet long) c.) ileum – with connects to the large intestine (12 feet long) Large Intestine  6 cm. (2 ½ in.) wide and 1.5 meters (5 feet long) 3 parts : a.) cecum – which connects to the small intestines b.) colon – 4 parts (ascending, transverse, descending, sigmoid colon) c.) rectum – 17-20 cm. (7-8 inches) long,  anal canal
  9. 9. Gastrointestinal Tract       ileocecal valve – prevents backward flow of fecal contents from the large intestine to the small intestine vermiform appendix – has no function , near the ileocecal valve anus – anal opening, is controlled by a smooth muscle internal sphincter and a striated muscle external sphincter chyme is propelled toward the anus by peristalsis, also mixes the intestinal contents in the colon, the feces is pushed forward by mass movements – stimulated by gastrocolic reflexes initiated when food enters the duodenum from the stomach Defecation reflex  when feces enter the rectum and cause distention of wall of the rectum  send impulses to the sacral segment of the spinal cord – then back to the colon, sigmoid and rectum  initiate
  10. 10. Gastrointestinal Tract Secretion and Digestion  major portion of digestion occurs in the small intestines by the action of pancreatic and intestinal secretions (enzymes) and bile a.) Carbohydrate digestion start in the mouth  Ptyalin – breakdown polysaccharides to disaccharides intestinal enzymes (maltase, lactase, sucrase) 🡲 breakdown disaccharides to monosaccharides (glucose, galactose fructose) b.) Protein digestion - start in the stomach  pepsin – breakdown of proteins to polypeptides - small intestines  trypsin – breakdown of polypeptides into peptides and amino acids c.) Fat digestion - fats require emulsification into small droplets before it can be broken down into glycerol and fatty acids
  11. 11. Gastrointestinal Tract Absorption the intestinal wall has many folds which are covered by fingerlike projections called (villi)  increase the absorptive area of the small intestines in the center of the villi are capillaries, veins, small arteries for absorption of nutrients into the blood vessel system 90% of absorption occurs within the small intestines by active transport or diffusion amino acids, monosaccharides, Na+, Ca++ are transported by active transport w/ the expenditure or use of energy other nutrients, fatty acids and H2O – diffuse passively across the cell membrane reabsorption of H2O, electrolytes and bile occurs mainly in the ascending colon
  12. 12. Gastrointestinal Tract GIT role in Fluid and Electrolytes Balance   GIT secretions contain electrolytes severe fluid and electrolyte imbalance may occur with excessive losses of gastrointestinal fluids Ex. 1.) Na+ and K+ deficits : vomiting, diarrhea, gastric suctioning, intestinal fistula 2.) Ca++ & Mg++ deficits: malnutrition, malabsorption, intestinal fistula 3.) Metabolic alkalosis : loss of gastric acid by suctioning or persistent vomiting 4.) Metabolic acidosis : loss of bicarbonate-rich intestinal secretions by severe diarrhea or fistula Other functions of the GIT   the GIT supports bacterial growth and has a role in antibody formation intestinal bacteria synthesize Vit. K  required for production of clotting factors II (Prothrombin), VII, IX,X
  13. 13. Assessment of the GIT Nursing History : Subjective Data 1. General Data a. presence of dental prosthesis, comfort of usage b. difficulty eating or digesting food c. nausea or vomiting d. weight loss e. pain – may be caused by distention or sudden contraction of any part of the GIT - specify the area, describe the pain 2. Specific data if symptoms are present • situations or events that effect symptoms • onset, possible cause, location, duration, character of symptoms • relationship of specific foods, smoking or alcohol to severity
  14. 14. Assessment of the GIT 3. Normal pattern of bowel elimination a. frequency and character of stool b. use of laxatives, enemas 4. Recent changes in normal patterns • • changes in character of stool (constipation, diarrhea, or alternating constipation and diarrhea) changes in color of stool melena - black tarry stool (upper GI bleeding) hematochezia – fresh blood in the stool (lower GI bleeding) c. drugs /medications being taken d. measures taken to relieve symptoms
  15. 15. Assessment of the GIT B. Physical Examination : Objective Data a.) Mouth and Pharynx 1. lips – color, moisture, swelling, cracks or lesions 2. teeth – completeness (20 in children, 32 in adults), caries, loose teeth, absence of teeth  impair adequate chewing 3. gums – color, redness, swelling, bleeding, pain (gingivitis) 4. mucosa – color (light pink)  examine for moisture, white spots or patches, areas of bleeding, or ulcers  white patches – due to candidiasis (oral thrush)  white plaques w/in red patches may be malignant lesions • tongue – color, mobility, symmetry, ulcerations / lesions or nodules • pharynx – observe the uvula, soft palate, tonsils, posterior pharynx  signs of inflammation (redness, edema, ulceration, thick yellowish secretions), assess also for symmetry of uvula and
  16. 16. Assessment of the GIT b.) Abdomen - assess for the presence or absence of tenderness, organ enlargement, masses, spasm or rigidity of the abdominal muscles, fluid or air in the abdominal cavity Anatomic Location of Organs RUQ – liver, gallbladder, duodenum, right kidney, hepatic flexure of colon RLQ - cecum, appendix, right ovary and fallopian tube LUQ – stomach, spleen, left kidney, pancreas, splenic flexure of colon LLQ – sigmoid colon, left ovary and tube
  17. 17. Assessment of the GIT
  18. 18. Assessment of the GIT 1. Inspection  assess the skin for color, texture, scars, striae, engorged veins, visible peristalsis (intestinal obstruction), visible pulsations (abdominal aorta), visible masses (hernia)  assess contour (flat, protuberant, globular)  abdominal distension, measure abdominal girth or circumference at the level of umbilicus or 2-5 cm. below
  19. 19. Assessment of the GIT 2. Auscultation  presence or absence of peristalsis or bowel sounds  Normoactive – every 5-20 secs.  Hypoactive – 1 or 2 sounds in 2 mins.  Absent – no sounds in 3-5 mins.  peritonitis, paralytic ileus,  Hyperactive – 5-6 sounds in less than 30 sec. 🡲 diarrhea, gastroenteritis, early intestinal obstruction
  20. 20. Assessment of the GIT 3. Percussion     done to confirm the size of various organs to determine presence of excessive amounts of air or fluid Normal – tympany dullness or flatness – area of liver and spleen, solid structure – tumor 4. Palpation    to determine size of liver, spleen, uterus, kidneys – if enlarged determine presence and chac. of abdominal masses determine degree of tenderness and muscle rigidity (rebound or direct) c.) Rectum   perineal skin and perianal skin assess for presence of pruritus, fissures, external hemorrhoids, rectal prolapse
  21. 21. Diagnostic Tests A. Laboratory tests 1. Stool examination (fecalysis)  Stool for occult blood o GI bleeding o No red meat, turnips, horseradish, steroids, NSAIDS, iron  Stool for Ova and parasites  proper collection of specimen  should not be mixed with water or urine, should be sent immediately to the laboratory
  22. 22. Diagnostic Tests 2. CEA (Carcinoembryonic antigen)  (+) colon cancer and other forms of cancer  it is useful as in indicator of the effects of therapy  🡲 CEA - recurrence or spread of tumor  🡲 effectiveness of therapy  A blood sample is withdrawn or sent to laboratory
  23. 23. Diagnostic Tests 3. Exfoliative Cytology  Detect malignant cells  Liquid diet  UGI: NGT insertion – saline lavage  LGI: laxative, enema, proctoscope
  24. 24. Radiologic Tests  visualization of the GIT by barium swallow, upper GI series or barium enema  Barium – is a radiopaque substance that when ingested or given by enema in solution, outlines the passage ways of the GIT for viewing by x-ray or fluoroscopy
  25. 25. Radiologic Tests 1. Barium swallow/UGIS  for identification of disorders of esophagus, stomach, duodenum – esophageal lesions, hiatal hernia, esophageal reflux, tumors, ulcers, inflammation  Pt. swallows a flavored barium solution and the radiologist observes the progress of the barium through the esophagus and take x-ray films  NPO for 6-8 hrs  Post procedure: o Increase fluid intake o Laxative o Stool – white for 24-72 hrs. o Observe for: impaction, distended abdomen,
  26. 26. Radiologic Tests 2. Barium Enema/LGIS Purpose : to visualize the colon to detect tumors, polyps, inflammation, obstruction  Prep. o low residue diet (1-2 days), clear liquid diet (evening meal) o Laxative, cleansing enema in AM  Post o Laxative or enema o Same as UGIS
  27. 27. Other Tests a.) Gastric analysis  to quantify gastric acidity Normal 1-5 mEq / L 🡲 gastric acid : gastric cancer, pernicious anemia 🡲 gastric acid : duodenal ulcer Normal gastric acid : gastric ulcer   NPO for 12 hours an NGT is inserted and gastric contents are aspirated, connected to suction
  28. 28. Other Tests b.) Biopsy  Upper GI biopsy – biopsy of the oral cavity or tongue, or any lesion or ulcerated area - local anesthesia  assess site for bleeding , give oral hygiene  Biopsy of stomach - done during endoscopy  Rectal biopsy – biopsy of lesions, polyps, tumors of the lower sigmoid colon, rectum and anal canal  during sigmoidoscopy - monitor for signs of bleeding
  29. 29. Endoscopy  directly visualize the GIT by the use of a fiberscape  fiberscope – has a thin, flexible shaft that can pass through and around bends in the GIT, transmit light and the image can be seen in the monitor
  30. 30. Endoscopy 1. Upper GI endoscopy  Esophagoscopy, Gastroscopy and Duodenoscopy  To identify upper GI bleeding, gastric cancer, gastric ulcers, duodenal ulcers  useful in detecting tumor, hernia, esophageal strictures Preparation : o o o o o NPO 6-8 hrs prior to procedure Anticholinergics(atropine), sedatives are given Remove dentures Lidocaine spray – depress gag reflex Place on left side lying position Post-procedure : NPO until gag reflex returns (2-4 hrs.) o o monitor vital signs, assess for dyspnea, dysphagia, abdominal
  31. 31. Endoscopy 2. Colonoscopy  to visualize the colon  useful to identify tumors, colonic cancer, colonic polyps  not done when there is active bleeding or inflammatory disease Preparation :  clear liquid diet 24 hrs. before  fleet or cleansing enema  dulcolax tabs  NPO 8 hrs. prior to procedure  Position: left side, knees flexed Post-procedure :   provide rest, monitor VS (vasovagal response- 🡲 HR,🡲BP) assess for sudden abdominal pain (perforation), fever, active bleeding
  32. 32. Endoscopy 3. Sigmoidoscopy – examination of sigmoid colon, rectum and anus Proctoscopy – examination of rectum and anus  used as a screening test for persons 40 yrs old and above, with history of colonic cancer  used for pt with lower GI bleeding or inflammatory disease - Preparation :  light dinner and light breakfast  dulcolax tab.  Fleet enema or cleansing enema Post-procedure :  provide rest period  assess for sudden abdominal pain, bleeding
  33. 33. Alternative Feeding: 2. Enteral hyperalimentation- delivery of nutrients directly to the GI tract. • Short- term- esophagostomy; nasogastric tube • Long- term- gastrostomy; jejunostomy Indications of NGT: • Gavage- to deliver nutrients; for feeding purposes • Lavage- to irrigate the stomach • Decompression- to remove stomach contents or air
  34. 34. • Hyperalimentation (total parenteral nutrition)- method of giving highly concentrated solutions intravenously to maintain a patient’s nutritional balance when oral or enteral nutrition is not possible Nursing Managements: • Filter is used in the IV tubing to trap bacteria • Solution and administration equipment should be changed every 24 hours • Dressing changes every 48-72 hrs with antibiotic ointment to catheter insertion • Medication is never administered in a TPN line • Observe for complications • Infection • Venous thrombosis
  35. 35. Esophageal Disorders Dysphagia  problem in ingesting necessary nutrients because of difficulty in swallowing Causes : 1) pharyngeal muscle weakness   disease or trauma of glossopharyngeal nerves neuromuscular disorders (poliomyelitis, multiple sclerosis, myasthenia gravis 2) esophageal disorders   obstruction caused by enlarged thyroid, tumors, strictures  narrowed opening absence of peristalsis of the esophagus Pathophysiology Weak pharyngeal/esophageal muscles  difficulty moving the food from the oropharynx into the esophagus  immediate regurgitation of fluids into the nasal passages  aspiration of feedings may occur from failure of the glottis to close
  36. 36. Esophageal Disorders Assessment history of difficulty in swallowing   assess for gag reflex – touching the posterior tongue or pharynx with a tongue depressor  ask the pt to swallow and observe movement of the larynx Nsg. Management Pts. with pharyngeal weakness:      can tolerate solids more easily than liquids teach “double-swallow” technique – 1) inhale, 2) put food in pharynx and swallow 3) exhale 4) swallow again helps minimize the possibility of aspiration closely supervise the pt during feeding, suction equip. shld. be ready elevate head of bed during feeding or position on the unaffected side - to ensure better control  if the ability to swallow is absent  NGT or gastrostomy feeding Pts. With esophageal weakness:  small-frequent feedings are advised to pts
  37. 37. Gastroesophageal Reflux Disease (GERD)  refers to a group of conditions that cause reflux of gastric and duodenal contents back to the esophagus Causes : - idiopathic incompetent lower esophageal sphincter (LES) - pregnancy - obesity - surgical removal lower esophagus due to cancer - ascites - hiatal hernia 🡲 major cause Hiatal hernia – refers to protrusion of part of the stomach, through the diaphragmatic hiatus into the thoracic cavity  caused by obesity, trauma, weakening of muscles
  38. 38. Gastroesophageal Reflux Disease (GERD) Pathophysiology Lower esophageal sphincter (LES) – muscle at the junction between esophagus and stomach  When food enters the pharynx and esophagus  LES relaxes to permit or allow food to enter into the stomach  LES is usually contracted to prevent reflux of gastric material back to the esophagus  🡲 LES pressure  reflux can occur  caused by anticholinergics, caffeine, alcohol, smoking, when the person is lying down
  39. 39. Gastroesophageal Reflux Disease (GERD) S/SX :  heartburn (pyrosis) – major symptom of GERD  burning sensation below the sternum that may be referred or radiate to the back or neck if severe  frequently accompanied by a sour regurgitation of gastric contents into the mouth but is not accompanied by nausea Hiatal hernia – may be diagnosed by x-ray, upper gastrointestinal series (UGIS)
  40. 40. Gastroesophageal Reflux Disease (GERD) Medical Mgt. Liquid antacids (ex. Maalox) – 30 ml taken 1 hr. and 3 hrs. after meals and at bedtime or whenever heartburn occurs  to decrease gastric acidity Medications that increase LES contraction  Urecholine, Metoclopramide HCL (reglan, plasil)  to be taken 30 mins. before meals and at bedtime  Cimetidine, Ranitidine, Famotidine (histamine H2 receptor blockers) – used for severe reflux, acts by reducing gastric secretions, thereby decreasing irritating effects Surgery for hiatal hernia Ex. Posterior gastropexy – returning the stomach to the abdomen and suturing it in place Nissen fundoplication – wrapping the fundus of the stomach around the lower part of the esophagus to restore sphincter competence and prevent reflux
  41. 41. Gastroesophageal Reflux Disease (GERD) Nsg. Intervention Patient teaching for GERD: 3.high-protein, low-fat diet ( to stimulate release of gastrin and cholecystokinin  🡲 LES pressure) 4.avoidance of foods containing caffeine (coffee, tea, colas), theobromine (chocolate) and alcohol 🡲 🡲 LES pressure 5.small, frequent meals ( to prevent gastric distention with resulting gastric acid secretion) 6.avoidance of : • smoking – it 🡲 LES pressure • supine position for 2-3 hrs after eating • bending over (🡲 intraabdominal pressure) • lifting heavy objects and wearing tight belts or girdles after eating ( to prevent 🡲 abdominal pressure) •sleeping with the head slightly elevated  to prevent regurgitation while pt is sleeping
  42. 42. Achalasia     also called cardiospasm or aperistalsis there is absence of peristalsis in the esophagus and in which the esophageal sphincter fails to relax after swallowing cause is unknown little or no food enters the stomach S/Sx:     gradual onset of dysphagia for both fluids and solids loss of weight substernal chest pain regurgitation of esophageal contents onto pillow at night Diagnostic tests : Barium swallow, esophagoscopy
  43. 43. Achalasia Medical Mgt: Medications – Nitrates, Nifedipine – to decrease LES pressure Forceful dilation of the LES by pneumatic dilators  a balloon is inserted and inflated for 1 min., 2-3 times - opens the sphincter and relieves the dysphagia Nsg. Interventions: encourage pt. to drink fluids with meals and use the valsalva maneuver (bearing down with a closed glottis) while swallowing  to help push the food advise soft diet elevate head during sleeping to prevent regurgitation after esophageal surgery, monitor for signs of esophageal perforation as evidenced by chest pain, shock, dyspnea and fever
  44. 44. Esophageal Strictures  narrowing of the lumen of the esophagus Causes : ingestion of corrosive substances (alkaline or acid) reflux esophagitis - prolonged NGT irritation of the esophageal walls lead to formation of a stricture that 🡲 the esophageal lumen and leads to dysphagia food may collect and partially or totally obstruct the esophagus fluids are easier to swallow than solids Interventions : gradual dilation by mechanical dilators or balloons rubber or metal mechanical dilators of increasing sizes are passed through the area of strictures, producing mild discomfort the balloon is inflated to create pressure dilation procedure is done every 3-4 wks for 4-6 months monitor pt for signs of esophageal perforation
  45. 45. Esophageal Carcinoma  most common cause of obstruction of the esophagus  Risk factors – chronic GERD, achalasia, smokers, alcoholics  tumor occur commonly in the middle and lower third of esophagus  common type is squamous cell carcinoma, occur in ages 40-70 y.o  early diagnosis and treatment is important for treatment to be successful  report and consult to the doctor for any sign of dysphagia S/Sx     progressive dysphagia – 1st w/ solid food  then w/ liquids regurgitation may occur, aspiration  coughing and pneumonitis foul breath and foul taste in the mouth metastasis rapidly occurs to the pulmonary system,
  46. 46. Esophageal Carcinoma Medical Mgt. Surgery : o Esophagogastrostomy (removal of the lower part of the esophagus and part of the stomach) o Esophagectomy o Radical neck dissection Radiation and chemotherapy – done 3-4 wks before surgery, reduces tumor size and facilitates surgery and length of survival
  47. 47. Nurs E ing sM oa p na h ge a me g nt e : a Po lst C -op ac r ar c e inoma  Fowler’s position – to prevent reflux  observe for regurgitation and dyspnea  prevent aspiration pneumonia – turn to sides  w/ NGT attached to low intermittent suction (for decompression); do not manipulate bec. damage to the anastomosis may occur; removed after 5-7 days  Feeding through tube jejunostomy  Start oral feeding w/ small sips of water 🡲 soft diet (after 1-2 wks)  Remain upright for at least 2 hours after each meal
  48. 48. Gastric Disorders
  49. 49. Structural Layers of the GIT 1. Mucosa – mucous membrane composed of three layers a. Epithelium b. Lamina propria – connective tissue containing blood vessels, lymph nodes and glands:      cardiac glands – secrete mucus chief (peptic) cells – secrete mucus and pepsinogen  pepsin parietal cells – secrete hydrochloric acid (HCL) and water, also produce intrinsie factor neck cells - secrete mucus pyloric glands – secrete gastrin and mucus • Muscularis mucosa – thin layer of smooth muscle between mucosa and submucosa • Submucosa – connective tissue containing blood vessels, lymph channels, nerves and glands • Tunica muscularis – layers of smooth muscle  produce peristaltic activity of the stomach as it mixes food during digestion
  50. 50. Stomach Gastric Secretion    The stomach secretes 1500 to 3000 ml of gastric juice per day. Major secretions are HCL, pepsin and mucus HCL and pepsin provide the corrosive power of gastric secretion Pepsin is the most active factor in the digestive processes of the stomach, acting to break proteins into polypeptides  Mucus has a neutralizing effect which protects the stomach mucosa 3 Phases of Gastric Secretion 1. Cephalic Phase    is stimulated by hunger, food odors, sight and smell, taste it begins before food enters the stomach is mediated by the vagus nerve, releasing acetylcholine which stimulates the parietal cells and chief cells to secrete acid, pepsin and mucus
  51. 51. Gastric secretion 2. Gastric Phase     begins with the arrival of food in the stomach distention of the stomach and presence of digested proteins stimulate gastrin hormone secretion Gastrin stimulates the parietal cells of the stomach to secrete HCL this phase continues for several hours, until the acidity of gastric contents reaches pH of 1.5 3. Intestinal Phase    is stimulated by food entering the duodenum a substance similar to gastrin is released from the intestines  it stimulates gastric secretion of pepsin and mucus when the pH in the duodenum decreases (🡲 acidity) this results to release of Secretin hormone – w/c inhibit gastric acid secretion and slows gastric motility and gastric emptying
  52. 52. Acute Gastritis  transient inflammation of the gastric mucosa  char. by erosion of the surface epithelium in a diffuse or localized pattern, that are usually superficial Causes / precipitating factors :  injury of the protective mucosal barrier by drugs or chemicals  anti-inflammatory drugs ex. Aspirin, NSAIDs  inhibit prostaglandin which normally stimulate mucus secretion  steroids ex. Prednisone  food or substance poisoning  bacterial infection (staphylococcus organism)  alcohol abuse  extreme physical stress or prolonged emotional tension  excessive amounts of coffee, tea, pepper, spices  stimulate acid secretion
  53. 53. Acute Gastritis Clinical Manifestations:  epigastric pain or discomfort  abdominal tenderness  cramping  severe nausea and vomiting  eructation (belching / burping)  anorexia  sometimes gastrointestinal bleeding – hematemesis  Healing usually occurs spontaneously within a few days Discontinuing injurious drugs, using antacids (ex. Maalox), decreasing acid secretion using Histamine receptor blockers (ex. Ranitidine, Cimetidine) facilitates healing Provide bed rest Eat non-irritating bland diet ( avoid highly seasoned, greasy or
  54. 54. Peptic Ulcer Disease  Normally, the gastric and duodenal mucosa is protected from acid and pepsin by mucus and bicarbonate (base) that are secreted by surface epithetical cells Peptic ulcer • is a sharply defined break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum which may involve the submucosa and muscular layers • such breaks may expose the submucosal layers to gastric acid secretions and pepsin and cause Autodigestion • True ulcers extend through the muscularis mucosa and damage blood vessels, causing bleeding or may lead to perforation of the GIT wall
  55. 55. Peptic Ulcer Disease Predisposing Factors  excessive use of aspirin, non-steroidal anti-inflammatory drugs (NSAID’s) (ex. Mefenamic, Ibuprofen), steroids (ex. Prednisone)  cause mucosal injury, 🡲 gastric acid secretion, and 🡲 gastric mucus secretion  cigarette smoking  genetic predisposition  dietary indiscretion – not eating on time  severe physiological / psychological stress – stimulation of the vagus nerve  alcohol abuse  infection of the gastric and duodenal mucosa with Helicobacter pylori  caffeine – stimulate acid production
  56. 56. Predisposing factors (cont.)  prolonged stress from severe burns, injuries, severe trauma, infection, head injury  may cause “stress ulcer” – due to sympathetic response  vasoconstriction of blood vessels of the GIT  🡲 perfusion of the mucosal lining and ischemia 🡲 🡲mucosal secretion, 🡲protective ability of the mucosa 🡲 damage of mucosal barrier by acids & pepsin 🡲 Ulcer and bleeding Peptic Ulcer Disease
  57. 57. Pathophysiology of Peptic Ulcers Gastric acid  is secreted in parietal cells of the fundus of the stomach Gastric acid secretion is stimulated by: •acetylcholine (from the vagus nerve) •gastrin (secreted by cells in the pyloric area of stomach) •histamine (found in cells throughout the gastric mucosa) - H2 receptors found in the cells of the stomach  mediate HCL acid secretion
  58. 58. Pathophysiology of Peptic Ulcers Gastric Ulcers
  59. 59. Pathophysiology of Peptic Ulcers Duodenal Ulcers
  60. 60. Gastric ulcer Duodenal Ulcer
  61. 61. Clinical Manifestations
  62. 62. Clinical Manifestations  nausea and vomiting – occurs more often in gastric ulcer  anorexia  eructation (belching)  weight loss  bleeding – when an ulcer erodes through a blood vessel    Hematemesis caffe-ground emesis melena (black, tarry stool) Diagnostic tests: - Endoscopy (gastroscopy) - Barium swallow - UGIS - stool exam for occult blood
  63. 63. Complications of Ulcers 2. Bleeding and Hemorrhage (more common in gastric ulcers) due to perforation of a blood vessel Mild bleeding  less than 500ml - may result to weakness and diaphoresis  seen as melena or coffee-ground emesis Massive bleeding   bright red blood vomitus (hematemesis) severe blood loss over 1 liter per 24 hrs 🡲 hypovolemic shock  weak pulse, hypotension, tachycardia, cold clammy skin 5.Perforation – when ulcer penetrates entire stomach or duodenum wall, releasing stomach contents into the peritoneal cavity  peritonitis  more common in duodenal ulcers and in long-term disease states S/Sx: sudden onset of severe abdominal pain, diffuse abdominal tenderness     diminished or absent bowel sounds abdominal distention rigid or board-like abdomen may result to shock – rapid, weak pulse, hypotension, 🡲LOC, diaphoresis
  64. 64. Complications of Ulcers (cont.) 3. Obstruction of the GIT (Gastric Outlet Obstruction)   repeated cycles of ulceration and healing in the pyloric region may cause scar tissue build-up and cause an obstruction or narrowing of the lumen of the GIT result to obstruction or blockage in the flow of GI contents S/Sx :      nausea abdominal distention feeling of fullness abdominal pain profuse vomiting of undigested food
  65. 65. Medical Management 1. Providing rest – physical and mental rest, sedative, mild tranquilizer, ensure calm, peaceful environment 2. Protecting the mucosa:    by neutralizing acid content eliminating sources of irritation by slowing down gastric motility Medications: • Antacids      🡲 pain by reducing gastric acid activity by physical absorption or by chemical neutralization of acid given 1 hr after meals and at bedtime (severe pain, give every 30 mins) ex. MgAlHydroxide (Maalox), Simethicone, Amphogel, Calcium carbonate liquid antacids are more effective than solid antacids tablets must be chewed thoroughly
  66. 66. Medical Management (cont.) 2. Anticholinergics    🡲 gastric motility and delay gastric emptying, 🡲gastric acid secretion ex. Probanthine, Bentyl S.E. – dryness of the mouth, drowsiness, constipation 3. H2 Receptor Blockers reduce the onset of pain and hasten healing of duodenal ulcers inhibit acid secretion - blocks the effect of histamine    given with meals and at bedtime 4. Su  cra elx f. at Ce im –em tiu d c in oe sa , lRp ar no iti e d c it no er ,,F c a o m ao ts tid th in e eulcer, prevents action of acid and pepsin on ulcer prevent further irritation and promote mucosal healing heals ulcer in 4-6 wks Ex. Iselpin    should be given 1 hr before meals and at bedtime 5. Gastric acid pump inhibitor   Ex. Omeprazole (Losec) given 30 mins. before breakfast
  67. 67. Management for Peptic Ulcers Diet  Bland diet, small frequent feedings (5x or more per day)  avoid foods that cause increase pain  avoid stimulants of gastric acid secretion (coffee, alcohol, spicy foods, caffeine, cola drinks)  raw fruits, whole grain cereals, fried or greasy foods are also avoided  Milk is also avoided bec. it can also stimulate gastric acid secretion Health Teachings:       Stop smoking Dietary modifications eliminate caffeine and alcohol intake teach about medications that irritate ulcer (aspirin, NSAIDs, steroids) - shld. be taken w/ meals or antacids Stress management, relaxation techniques Regular exercise program
  68. 68. Management of Perforation and Bleeding  Monitor VS, I/O  Control bleeding   insertion of NGT – irrigate stomach (gastric lavage) w/ cold saline solution until return flow is clear; connect to suction machine give antacid or mucosal protector (sucralfate) after acute bleeding has stopped  Replace blood loss – blood transfusion  Minimize consequences of perforation   give antibiotics as ordered keep pt. on Fowler’s position to localize gastric contents to one area of the peritoneum  Surgery
  69. 69. Surgical Interventions A. Gastrectomy  total removal of the stomach  result to no gastric juice for digestion, malnutrition, pernicious anemia, weight loss B. Subtotal Gastrectomy  removal of a part of the stomach and the remaining stomach is anastomosed to the intestine Billroth I (Gastroduodenostomy) – removal of the distal ½ of the stomach w/ anastomosis to the duodenum Billroth II (Gastrojejunostomy) – removal of the lower stomach and antrium w/ anastomosis to the jejunum C. Vagotomy – resection of the vagus nerve thus decreasing motility and gastric secretions
  70. 70. Surgical Interventions (cont.) Post-op Care:          bloody drainage from NGT normal during 1st 12 hrs. 🡲 eventually dark green color indicating presence of bile & intestinal secretion Turn, cough, deep breathe q 2-4 hrs. to prevent atelectasis and hypostatic pneumonia Pain medications, splint the incision insertion of NGT for gastric decompression, connected to drainage bottle or to intermittent suction tube may be irrigated w/ 30 ml. of NSS to keep the tube patent Keep pt. on Fowler’s position to promote lung expansion and gastric drainage Pt. is kept on NPO for 5-7 days to allow incision to heal TPN while on NPO, provide oral care Monitor for return of peristalsis, progress to clear liquids then DAT
  71. 71. Post-op Care
  72. 72. Dumping Syndrome  may occur following subtotal or total gastrectomy  food enters duodenum rapidly 🡲 hyperosmolarity of intestinal contents 🡲 pulls H2O from the vascular bed resulting to rapid fluid shift (intestines swell) 🡲 🡲 circulating blood volume S/Sx: vertigo, dizziness, nausea weakness, diaphoresis tachycardia, orthostatic hypotension cold clammy skin Abdominal cramping and pain
  73. 73. Dumping Syndrome (cont.) Interventions:  Eat frequent small meals that are dry and contain moderate protein, fat and reduced carbohydrate  Blood glucose levels can rise rapidly after a meal containing simple sugars, triggering a reactive hypoglycemia several hours after the meal  Do not take fluids with meals to slow gastric emptying (take fluids in between meals)  Rest or lie down on the left side for 30 mins. after meals if possible to slow down gastric emptying
  74. 74. Gastric Cancer  May develop in any part of the stomach but is found commonly at the distal third  More common in men and in age 50-70 years old Causes: heredity, chronic gastric ulcer, chronic gastritis S/Sx:  Gastric distress  Flatulence  Early satiety  Loss of appetite, anorexia  Loss of strength and weight loss Dx: UGIS, absence of HCL – due to destruction of parietal cells by cancer cells Tx: Gastrectomy, chemotherapy
  75. 75. Gastric Cancer
  76. 76. Acute Abdominal Inflammations A pa pn ei n nf l da m im ca it to r iy sl e s i o n of the vermiform appendix, located near the ileocecal valve   can be caused by occlusion of the lumen of the appendix by hardened feces (fecaliths), by foreign objects, or by kinking of the appendix may impair circulation and lower resistance to organisms such as bacilli or streptococci a small part of the appendix may be edematous or necrotic or entire appendix may be involved  abscess formation  may lead to rupture and peritonitis S/Sx:  pain on the umbilical area and throughout the abdomen then become localized at the RLQ  specifically at the McBurney’s point  nausea, vomiting  direct tenderness and rebound tenderness in the RLQ  abdominal muscle rigidity  🡲WBC, Neutrophil count above 75%
  77. 77. Appendicitis (cont.) Med. Mgt. surgery – Appendectomy – as soon as possible to prevent rupture with subsequent peritonitis Antibiotics Nsg. Mgt. e.Preoperative Care     bed rest placed pt on NPO – in preparation for surgery intravenous fluids – to maintain F/E balance ice bag may help relieve pain, no heat is applied because this may 🡲 circulation and congestion to the appendix and lead to rupture •Post-operative care   general post-op care food permitted when peristalsis returns
  78. 78. Peritonitis  is an inflammation of the peritoneum caused by trauma or by rupture of an organ containing bacteria, which are then introduced into the abdominal cavity  ex. of organisms – E-coli, streptococci, staphylococci, gonococci  can also be caused by rupture of the fallopian tube in ectopic pregnancy, perforation of a gastric ulcer, traumatic rupture of the spleen or liver Pathophysiology:    inflammation causes adhesions, abscess formation peritoneum  there is redness, edema and production of large amounts of fluid containing electrolytes and proteins  hypovolemia, electrolyte imbalance, dehydration hypovolemic shock cessation of peristalsis occurs due to severe peritoneal infection and lead to acute intestinal obstruction
  80. 80. S/S P x:eritonitis (cont.)  abdominal pain and tenderness (local or diffuse, often rebound) abdominal rigidity (board-like abdomen)  nausea, vomiting  high fever, high leukocytosis  weakness, diaphoresis, pallor, tachycardia, shock  later signs : paralytic ileus, abdominal distention Medical Mgt. Surgery – depending on underlying cause , peritoneal lavage Post-operative medical mgt.  1) NGT insertion – to prevent GIT distention 2) IV fluids and electrolytes 3) antibiotics – to control infection 4) maintain drains – to remove abscesses Nsg. Mgt. bed rest in semi-fowler’s position  to help localize pus in lower abdomen give mouth care – prevent drying of mucous membranes and cracking of lips maintain F/E replacement encourage deep breathing exercises use measures to reduce the pts anxiety