GI System & its Disorders By, Aswathy Krishnan, 1st Yr M Sc. Nursing(2008-2010) Bombay Hospital College of Nursing
GI System –
Structure & Functions
Oral cavity Pharynx esophagus stomach small intestine large intestine rectum
Propulsion
Peristaltic contractions
Digestion Mixing Enzymatic breakdown
Absorption of nutrients Defecation
GI System
- Anatomy
Mouth Anterioly bounded by lips Posteriorly bounded by the oropharynx Mechanical and chemical digestion (secretion of saliva by salivary glands)
Pharynx & Esophagus
The pharynx is the common passageway for both food and air. Contracts when food enters. Forces food into the esophagus. The esophagus is the passageway that connects mouth to the stomach. Cardiac Sphincter muscle.
Stomach
Fundus (top) body pylorus Pyloric sphincter Mechanical and chemical digestion: Mixing food and acid and enzymes to create chyme. Goblet Cells Parietal Cells Chief Cells G Cells Blood supply : Celiac artery Venous drainage in to portal vein
GI System
Small intestine
- Anatomy
~ 5m (~16.7’) tube From Pyloris to Ileocecal Valve Duodenum jejunum ileum Circular folds and villae to increase surface area Most digestion and absorption takes place here via intestinal enzymes and exocrine secretions from the liver and pancreas (which enter the duodenum via ducts)
Large intestine: extends from terminal ileum to rectum
Ascending colon, transverse colon descending colon, sigmoid colon and the rectum Appendix extends from the lower portion of the cecum and is a blind sac chyme generated ends up entering the colon Water and electrolytes are absorbed out of the chyme
Absorbs 1.5 L of water per day Also absorbs Na, K & Cl
Blood Supply: superior & inferior mesenteric arteries
Accessory organs: pancreas and liver
Liver
Located in the upper rt. Abdomen Rt, Lt.& caudate lobes ,subdivided into segments Blood supply: Portal Vein, Hepatic Artery Roles of the liver:
Conjugation of billurubin Synthesis and deactivation of clotting factors Phagocytosis Detoxification Processes nutrients
Gallbladder Sac like organ attached to Liver Storage facility for bile(50ml.) CCK stimulates contraction of Gall bladder Bile composition: water, bile salts (emulsify lipids), bile pigments] Blood Supply: Cystic & hepatic artery Biliary Ducts Ducts of the Billiary tract very imp in proper functioning of GIS Bile Calculli Left, Right Hepatic duct Common hepatic duct Cystic Duct + Common hepatic duct Common Bile Duct duodenum
Accessory organs: pancreas and liver
Pancreas Endocrine Functions
Exocrine Function
Production of Insulin, glucagon, somatostatin Pancreatic enzymes: Trypsin, lipase and amylase Bicarbonate: help neutralize the acidity of the chyme
Blood Supply: Hepatic and cystic artery
Health Assessment- History Taking
Dietary habits
Personal Habits
Use of Tobacco, alcohol
Past History
The number of meals ate per day. Meal times. Food restrictions or special diets followed. Changes in appetite. Increased? Decreased? No appetite? What foods, if any, have been eliminated from the diet? Why? What foods are not well tolerated? Alterations in taste.
Previous GI disease? Past treatment and surgery? Medications used. Dosage and frequency
Bowel patterns
Frequency of bowel movements. Use of laxatives and/or enemas. Changes in bowel habits. Stool Description. (a) Constipation. (b) Diarrhoea. (c) Blood in stool. (d) Mucous in stool. (e) Black, tarry stools. (f) Pale or clay colored stools. (g) Foul smelling stools. (h) Pain with stool
Abdominal Pain
Indigestion
Frequency? Duration? Associated with specific foods? Relieved by?
Gas (belching and flatus).
Location? Frequency? Duration? Character of the pain? Pattern? distribution of reffered pain & associated factors
Frequency? Associated with specific foods? Relieved by?
Nausea, Vomiting
Frequency? Duration? Associated with meals? Character of emesis? Relieved by?
Health Assessment- Physical
Perform a brief, general head-to-toe visual inspection of the patient. Are height and weight within normal range for the patient's age and body type Observe the skin for Color (pale, jaundiced), Surgery scars, Bruises, Rashes, Lesions, Turgor and moisture content, Edema. Examine the mouth and throat. Look at the lips, tongue, and mucous membranes, noting abnormalities such as cuts, sores, or discoloration. Observe the condition of the teeth.. Observe the gums. Are they healthy and pink? Examination of the abdomen
Physical examination of the abdomen involves visual inspection, auscultation, and palpation patient is resting in a supine position, knees slightly flexed to relax the abdominal muscles abdomen is viewed as four quadrants
AUSCULTATION • Ausculate all four quadrants •Listen for bowel sounds. The best location is below and to the right of the umbilicus. • Describe the sounds heard according to location, frequency, and character of the sound. • Abnormalities include absent bowel sounds and the peristaltic rush of a hyperactive bowel.
PALPATION • Palpate all four quadrants •used to detect muscle guarding, tenderness, and masses. • Record Rigidity or Guarding, Pain or Tenderness, Rebound Pain Masses.
Diagnostics Laboratory Tests Blood Test
Complete blood count RBC, Hb, HCT Electrolytes
Sodium, Pottasium
CEA : Blood tumor marker
Serum enzymes
amylase, lipase, alkaline phosphatase, SGOT, SGPT, and LDH Check liver function
Pancreatic function
Colon cancer
Eval serum protein levels, clotting times, serum liver enzymes, bilirubin levels Serum enzyme levels
Faecal Analysis
occult blood, lipids, urobilinogen, ova, parasites, and other substances consider the patient's diet when assessing and documenting the character of a patient's stool.
Gastric analysis
presence, amount, or absence of hydrochloric acid presence of cancer cells types and amounts of enzymes present.
Abdominal Ultrasonography Radiographic Test
upper GI Series ( Barium swallow)
normally held NPO gum chewing, smoking discouraged as it stimulates gastric action.
Lower GI Series ( Barium Enema)
patient is held NPO Constipation a side effect of the contrast medium
Endoscopy Upper GI endoscopy
Upper Gastrointestanal Fibroscopy/ Esophagogastrodeodenoscopy patient must be fasting
Lower GI endoscopy
proctoscopy, sigmoidoscopy and colonoscopy Bowel should be free of stool to enhance visualization
Endoscopy through Ostomy Laproscopy
Computer Tomography & MRI Liver and pancreatic abnormalities
Gastrointestinal Disorders - Disorders of Mouth
Includes inflammation, infection, neoplastic lesions
Pathophysiology Causes include mechanical trauma, irritants such as tobacco, chemotherapeutic agents Oral mucosa is relatively thin, has rich blood supply, exposed to environment
Manifestations
Visible lesions or erosions on lips or oral mucosa Pain
Collaborative Care Direct observation to investigate any problems; determine underlying cause and any coexisting diseases Any undiagnosed oral lesion present for > 1 week and not responding to treatment should be evaluated for malignancy
General treatment includes mouthwashes or treatments to cleanse and relieve irritation
Alcohol bases mouthwashes cause pain and burning Sodium bicarbonate mouthwashes are effective without pain Fungal (candidiasis): nystatin “swish and swallow” or clotrimazole lozenges Herpetic lesions: topical or oral acyclovir
Nursing Care Goal: to relieve pain and symptoms, so client can continue food and fluid intake
Impaired oral mucous membrane
Assess clients at high risk Assist with oral hygiene post eating, bedtime Teach to limit irritants: tobacco, alcohol, spicy foods
Imbalanced nutrition: less than body requirements
Assess nutritional intake; use of straws High calorie and protein diet according to client preferences
Oral Cancer Uncommon (5% of all cancers) but has high rate of morbidity, mortality Highest among males over age 40 Risk factors include smoking and using oral tobacco, drinking alcohol, marijuana use, occupational exposure to chemicals, viruses (human papilloma virus) Pathophysiology Squamous cell carcinomas Begin as painless oral ulceration or lesion with irregular, ill-defined borders Lesions start in mucosa and may advance to involve tongue, oropharynx, mandible, maxilla Non-healing lesions should be evaluated for malignancy after one week of treatment Collaborative Care Elimination of causative agents Determination of malignancy with biopsy Determine staging with CT scans and MRI Based on age, tumor stage, general health and patients preference, treatment may include surgery, chemotherapy, and/or radiation therapy Advanced carcinomas may necessitate radical neck dissection with temporary or permanent tracheostomy; Surgeries may be disfiguring Nursing Care Health promotion: Teach risk of oral cancer associated with all tobacco use and excessive alcohol use Need to seek medical attention for all non-healing oral lesions (may be discovered by dentists); early precancerous oral lesions are very treatable Nursing Diagnoses
Ineffective airway clearance Acute pain Impaired oral mucous membrane Altered Nutrition: Less than body requirements Impaired Verbal Communication: establishment of specific communication plan and method should be done prior to any surgery Knowledge deficit about disease process & treatment plan Risk for infection
Gastroesophageal Reflux Disease (GERD) Gastric contents flow back in to the oesophagus due to incompetent oesophageal sphincter Pathophysiology Gastroesophageal reflux results from transient relaxation or incompetence of lower esophageal sphincter, or increased pressure within stomach Prolonged reflux –oesophigitis Clinical Manifestations Heartburn, dysphagia. Diagnostic Tests Barium swallow (evaluation of esophagus, stomach, small intestine) Upper endoscopy: direct visualization; biopsies may be done Esophageal manometry, which measure pressures of esophageal sphincter and peristalsis Esophageal motility studies Medications Antacids for mild to moderate symptoms H2-receptor blockers: decrease acid production; given BID or more often, e.g. cimetidine, ranitidine, famotidine, nizatidine Proton-pump inhibitors: reduce gastric secretions, promote healing of esophageal erosion and relieve symptoms, e.g. omeprazole; lansoprazole initially for 8 weeks; or 3 to 6 months Promotility agent: enhances esophageal clearance and gastric emptying, e.g. metoclopramide
Gastroesophageal Reflux Disease (GERD)
Dietary and Lifestyle Management Elimination of acid foods (tomatoes, spicy, citrus foods, coffee Avoiding food which relax esophageal sphincter or delay gastric emptying (fatty foods, chocolate, alcohol) Eat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to bed Elevate head of bed to decrease reflux No smoking Surgical Management Laparoscopic procedures to tighten lower esophageal sphincter Open surgical procedure: Nissen fundoplication - upper portion of the stomach is wrapped around the distal oesophagus and sutured, creating a tight LES Nursing Care Pain usually controlled by treatment Assist client to institute home plan
Complications Esophageal stricture , ulceration of the esophagus, Barrett’s oesophagus
Hiatal Hernia A condition in which cardiac sphincter becomes enlarged allowing the stomach to pass in to the thoracic cavity
Sliding hernia More common
Upper portion of stomach and gastro esophageal junction are displaced upward into the thorax Esp. when supine Standing herniated portion slides down into abdominal cavity Rolling Hernia the gastro esophageal junction is in normal place but part of stomach herniates through esophageal hiatus; hernia can become strangulated; client may develop gastritis with bleeding
Predisposing factors
Increased intra-abdominal pressure Increased age Trauma Congenital weakness
Manifestations
Heartburn
Brief substernal burning sensation
Freq belching Discomfort when lying supine
Diagnostic Tests
Barium swallow Endoscopy
Treatment
Similar to GERD
NSG Management
Gastritis Inflammation of stomach lining from irritation of gastric mucosa (normally protected from gastric acid and enzymes by mucosal barrier) Acute Gastritis
Disruption of mucosal barrier allowing hydrochloric acid and pepsin to have contact with gastric tissue: leads to irritation, inflammation, superficial erosions Gastric mucosa rapidly regenerates; self-limiting disorder
Causes of acute gastritis
Irritants include aspirin and other NSAIDS, alcohol, caffeine Ingestion of corrosive substances: alkali or acid Effects from radiation therapy, certain chemotherapeutic agents Erosive Gastritis: form of acute which is stress-induced, complication of life-threatening condition (Curling’s ulcer with burns); gastric mucosa becomes ischemic and tissue is then injured by acid of stomach
Manifestations
Mild: anorexia, mild epigastric discomfort, belching More severe: abdominal pain, nausea, vomiting, hematemesis, melena Diaehoea, the contaminated food is the cause of gastritis
Treatment
NPO status to rest GI tract for 6 – 12 hours, reintroduce clear liquids gradually and progress; intravenous fluid and electrolytes if indicated Medications: proton-pump inhibitor or H2-receptor blocker; sucralfate acts locally; coats and protects gastric mucosa If gastritis from corrosive substance: immediate dilution and removal of substance by gastric lavage (washing out stomach contents via nasogastric tube), no vomiting
Gastritis - Chronic
Superficial Gastritis Atrophic Gastritis
Type A: Parietal cells normally secrete intrinsic factor needed for absorption of B12, when they are destroyed by gastritis pts develop pernicious anemia
Type B: more common and occurs with aging; caused by chronic infection of mucosa by Helicobacter pylori; associated with risk of peptic ulcer disease and gastric cancer
Hypertrophic Gastritis Manifestations
Treatment
Vague gastric distress, epigastric heaviness not relieved by antacids Fatigue associated with anemia; symptoms associated with pernicious anemia Type B: eradicate H. pylori infection with combination therapy of two antibiotics (metronidazole (Flagyl) and clarithomycin or tetracycline) and proton–pump inhibitor (Prevacid or Prilosec) Bland Diet Small Frequent meals Antacids Administer vitamin B12
Diagnostic Tests
Gastric analysis: assess hydrochloric acid secretion (less with chronic gastritis) Hemoglobin, hematocrit, red blood cell indices: anemia including pernicious or iron deficiency Serum vitamin B12 levels: determine pernicious anemia Upper endoscopy: visualize mucosa, identify areas of bleeding, obtain biopsies; may treat areas of bleeding with electro or laser coagulation or sclerosing agent
Peptic Ulcer Disease (PUD) refers to ulcerrations in the mucosa of the lower oesophagus , stomachor dueodenum Incidence Duodenal ulcers: most common; affect mostly males ages 30 – 55; ulcers found near pyloris Gastric ulcers: affect older persons (ages 55 – 70); found on lesser curvature and associated with increased incidence of gastric cancer Pathophysiology ACTH & Cortisone
Structure of mucosa Amount of Mucous produced
Trauma, infection, physical or psychological stress can cause increase in gastric secretion, blood supply and gastric motility by way of thalamus stimulus to vagal nerve Use of NSAIDS: interrupts prostaglandin synthesis which maintains mucous barrier of gastric mucosa
Types Duodenal Ulcers
Ususlly occur 1.5 cm. from pylorus Hypersecretion of acid Protien rich meals, Calcium, vagal stimulation
Gastric ulcers
Junction of fundus and pylorus Caused by break in mucosal barrier due to incompetent pylorus
Peptic Ulcer Disease (PUD) Manifestations Pain: gnawing, burning, aching, cramplike
Gastric
Duodenal
when stomach is full and relieved by vomiting Upper epigastric region when stomach is empty and relieved by food Left epigastric region
Nausea and vomiting
generally associated with Gastric ulcers
Treatment Rest and stress reduction Nutritional management Pharmacological management
Antacids (Mylanta)
Proton pump inhibitors (Prilosec, Prevacid)
Histamine blockers (Tagamet, Zantac, Axid)
Block gastric acid secretion Blocks gastric acid secretion
Carafate
Mucosal barrier enhancers (colloidal bismuth, prostoglandins)
Antibiotics (Amoxicillin, Ampicillin)
Neutralizes acids
Forms protective layer over the site Protect mucosa from injury Treat H. Pylori infection
Surgical intervention Minimally invasive gastrectomy
Partial gastric removal with laproscopic surgery
Bilroth I and II
Vagotomy
Pyloroplasty
Removal of portions of the stomach Cutting of the vagus nerve to decrease acid secretion Widens the pyloric sphincter
Nursing Management Administer medication as ordered Client Teaching & discharge plan
Medical regimen Diet Avoidance of stress producing situations
Complications Hemorrhage: frequent in older adults Gastric outlet (pyloric sphincter) obstruction: edema surrounding ulcer blocks GI tract from muscle spasm or scar tissue Perforation: ulcer erodes through mucosal wall and gastric or duodenal contents enter peritoneum leading to peritonitis; chemical at first (inflammatory) and then bacterial in 6 to 12 hours
Cancer of Stomach Malignant neoplasms found in the stomach,usually Adenocarcinoma
Etiology and risk factors Presence of H pylorai inf. in the stomach Chronic atrophic gastritis, adenomatous polyps, pernicious anemia Increase in absorption of carcinogens from diet Genetic factors Pathophysiology Adenocarcinoma most common form involving mucus-producing cells of stomach in distal portion Begins as localized lesion (in situ) progresses to mucosa; spreads to lymph nodes and metastasizes early in disease to liver, lungs, ovaries, peritoneum Manifestations Disease often advanced with metastasis when diagnosed Early symptoms are vague: early satiety, anorexia, indigestion, vomiting, pain after meals not responding to antacids Later symptoms weight loss, cachexia (wasted away appearance), abdominal mass, stool positive for occult blood Presence of lactic acid and LDH Diagnostic tests Upper GI tract X ray exam Upper endoscopy: visualization and tissue biopsy of lesion Medical Management Client may receive Chemotherapy or radiation therapy Primary treatment is surgical management Surgery, if diagnosis made prior to metastasis
Partial gastrectomy with anastomosis to duodenum: Bilroth I or gastroduodenostomy Partial gastrectomy with anastomosis to jejunum: Bilroth II or gastrojejunostomy Total gastrectomy (if cancer diffuse but limited to stomach) with esophagojejunostomy
Appendicitis
It is an inflammation of the vermiform appendix that develops most commonly in adolescents and young adults Etiology A
fecalith which occludes the lumen of appendix Kinking Swelling of the bowel wall External occlusion of the bowel
Pathophysiology Appendix
obstructed > intrlumunar pressure increases > Venus drainage decreases > thrombosis, edema bacterial infection > hyperaemia of appendix
Manifestations Surgical Management Complictions Perforation
of the bowel
Colon Cancer Pathophysiology
Most malignancies begin as adenomatous polyps and arise in rectum and sigmoid Spread by direct extension to involve entire bowel circumference and adjacent organs Metastasize to regional lymph nodes via lymphatic and circulatory systems to liver, lungs, brain, bones, and kidneys
Manifestations
Often produces no symptoms until it is advanced Presenting manifestation is bleeding; also change in bowel habits (diarrhea or constipation); pain, anorexia, weight loss, palpable abdominal or rectal mass; anemia
Complications
Bowel obstruction Perforation of bowel by tumor, peritonitis Direct extension of cancer to adjacent organs; reoccurrences within 4 years
Diagnostic Tests
CBC: anemia from blood loss, tumor growth Fecal occult blood (guiac or Hemoccult testing): all colorectal cancers bleed intermittently Carcinoembryonic antigen (CEA): not used as screening test, but is a tumor marker and used to estimate prognosis, monitor treatment, detect reoccurrence may be elevated in 70% of people with CRC Colonoscopy or sigmoidoscopy; tissue biopsy of suspicious lesions, polyps Chest xray, CTscans, MRI, ultrasounds: to determine tumor depth, organ involvement, metastasis
Pre-op care
Consult with ET nurse if ostomy is planned Bowel prep with GoLytely NPO NG
Surgery
Surgical resection of tumor, adjacent colon, and regional lymph nodes is treatment of choice Whenever possible anal sphincter is preserved and colostomy avoided; anastomosis of remaining bowel is performed Tumors of rectum are treated with abdominoperineal resection (A-P resection) in which sigmoid colon, rectum, and anus are removed through abdominal and perineal incisions and permanent colostomy created
Colostomy
Ostomy made in colon if obstruction from tumor
Temporary measure to promote healing of anastomoses Permanent means for fecal evacuation if distal colon and rectum removed
Named for area of colon is which formed
Sigmoid colostomy: used with A-P resection formed on LLQ Double-barrel colostomy: 2 stomas: proximal for feces diversion; distal is mucous fistula Transverse loop colostomy: emergency procedure; loop suspended over a bridge; temporary Hartman procedure: Distal portion is left in place and oversewn; only proximal colostomy is brought to abdomen as stoma; temporary; colon reconnected at later time when client ready for surgical repair
Post-op care
Pain NG tube Wound management
Stoma
Should be pink and moist Drk red or black indicates ischemic necrosis Look for excessive bleeding Observe for possible separation of suture securing stoma to abdominal wall
Evaluate stool after 2-4 days postop
Ascending stoma (right side)
Transverse stoma
Descending stoma
Liquid stool Pasty Normal, solid stool
Radiation Therapy
Used as adjunct with surgery; rectal cancer has high rate of regional recurrence if tumor outside bowel wall or in regional lymph nodes Used preoperatively to shrink tumor Provides local control of disease, does not improve survival rates
Chemotherapy:
Used postoperatively with radiation therapy to reduce rate of rectal tumor recurrence and prolong survival
Nursing Care Prevention is primary issue Client teaching Diet: decrease amount of fat, refined sugar, red meat; increase amount of fiber; diet high in fruits and vegetables, whole grains, legumes Screening recommendations Seek medical attention for bleeding and warning signs of cancer Risk may be lowered by aspirin or NSAID use Nursing Diagnoses for post-operative colorectal client Pain Imbalanced Nutrition: Less than body requirements Anticipatory Grieving Alteration in Body Image Risk for Sexual Dysfunction