Nursing Care of Patients with Alterations in the GI tract

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  • Slide 54. I was under the impression that Duodenal ulcers are relieved with food. Gastric Ulcers are aggravated by food.
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  • This is a child.***Acquired umbilical hernia may be seen if patient is 50 pounds above ideal body weight**With complaint of abd pain, nausea, vomiting and hypoactive BS consider intestinal obstruction
  • Minimally invasive commonly used**Will have an NG tube post-op—usually dark brown (old blood) for first 8 hours—just document**Keep head of bed elevated 30 degrees in the immediate post-op periodPost opSoft foods for one week, stay on antireflux meds, no driving, report fever > 101, nausea vomiting or bloating. Walk daily **otify provider if develops signs of a cold**Gas bloat is common—avoid gasy foods and eat small frequent meals.
  • A Colostomy is when only part of the large intestine is removed whereas an Ileostomy involves the removal of the whole of the large intestine and often the rectum as well. The distinguishing feature between a colostomy and an ileostomy is that in a colostomy, the stoma is made out of the large bowel and the stoma is therefore a little bigger than for an ileostomy where the stoma is made from the small intestine. Both colostomies and ileostomies can either be permanent or temporary. A Urostomy is when the bladder is bypassed or removed
  • Historically, the standard operation for ulcerative colitis has been removal of the entire colon, rectum, and anus. This operation is called a proctocolectomy (Illustration A) and may be performed in one or more stages. It cures the disease and removes all risk of developing cancer in the colon or rectum. However, this operation requires creation of a Brooke ileostomy (bringing the end of the remaining bowel through the abdomen wall, Illustration B) and chronic use of an appliance on the abdominal wall to collect waste from the bowel

Transcript

  • 1. Nursing Care of Patients with Alterations in the GI tract
    C. Cummings RN,EdD
  • 2. A & P of GI system
  • 3. GI tract
    Hollow muscular tube, lumen surrounded by 4 tissue layers:
    Mucosa- innermost, thin layer of smooth muscle and exocrine cells
    Submucosa- connective tissue
    Muscularis- smooth muscle
    Serosa- outermost, connective tissue
  • 4. GI tract
    Function:
    Secretion- secretes HCL acid, digestive enzymes
    Digestion- mechanical and chemical, food is broken down to chyme
    Absorption- from GI tract to blood supply
    Motility
    Elimination
  • 5. GI tract
    Nerve Supply
    Intrinsic stimulation by myenteric plexus in smooth muscle and submucosa plexus in inner layer
    Autonomic system- Parasympathetic stimulation by vagus nerve, connects with intrinsic system
    Vagus-stimulates motor and secretory activity and relaxes spinchters
    Sympathetic system- thoracic and lumbar splanchnic nerves slows movement, inhibits secretions and contracts spinchters
  • 6. Nerves of GI tract
  • 7. Mouth
    Function:
    Mastication, taste, begin movement
    Glands produce 1 L of saliva/day
    Saliva contains mucin and salivary amylase with begins to break down CHO
    Oral preparatory phase- food is softened, made into a “bolus” and tongue moves to the back of the mouth
    Oral phase- tongue presses bolus against hard palate, elevates the larynx and forces the food bolus to the pharynx, triggering swallowing
    Pharyngeal phase- soft palate elevates and seals nasal cavity, inhibits respirations and allows esophagus to open
    Esophageal phase- is when bolus enter at cricopharyngeal juncture, peristalsis now takes food to the stomach
    All this takes about 10 seconds !
  • 8. Esophagus
    Canal about 10 in long, passes through the center of the diaphragm
    Upper end is the upper esophageal sphincter, at rest it is closed to prevent air from entering the esophagus
    Lower end is the lower esophageal sphincter, it sits at the gastroesophageal junction, at rest it is closed to prevent reflux of gastric contents, this is where GERD occurs
    Function- to propel food and fluids and prevent reflux
    Mucous is secreted to move the food along
    Cardiac sphincter of the stomach opens to allow the food to enter
  • 9. Stomach
    Digestive and endocrine organ, in midline and LUQ
    Four regions:
    Cardia- narrow part that is distal to the gastroesophageal junction
    Fundus- left above the GE junction
    Body or corpus- largest area
    Antrum- pylorus, is the distal portion and is separated from the duodenum by the pyloric sphincter, prevents backflow from the duodenum
    Surface is covered in rugae or folds and have smooth muscle for motility
    Has intrinsic and extrinsic nerves
  • 10. Stomach
    • Function:
    • 11. Parietal cells secrete HCL acid and intrinsic factor, which absorbs B 12, without it, what anemia can occur?
    • 12. Chief cells secrete Pepsinogenpepsin
    • 13. Cephalic phase- sight, smell and taste of food, regulated by vagus, begin secretory and contractile activity
    • 14. Gastric phase- G cells in the antrum secrete gastrin, which causes HCL and pepsinogen to be released. HCL changes pepsinogen to pepsin, which digest proteins. Mucous and Bicarb are secreted to protect the stomach wall
    • 15. Intestinal phase- chyme produced empties into the duodenum and causes distention, this produces secretin, which stops the acid production and gastric motility !
  • Stomach
  • 16. Small Intestine
    Longest portion of the GI tract, 16-19 ft.
    Made up of 3 sections:
    Duodenum- first 12” and is attached to the pylorus. The CVD and pancreatic duct join to form the ampulla of Vater and empty into the duodenum at the duodenal papilla. This surrounded by a muscle, called the Sphincter of Oddi
    Jejunum- middle 8 ft portion
    Ileum- last 8-12 ft. The ileocecal valve separates the ileum form the cecum of the large intestine
    Inner lining is made up of intestinal villi and folds of mucosa and submucosa for digestion.
  • 17. Small Intestine
    3 main functions:
    Movement- mixing and peristalsis
    Moves chyme by segmental contractions and mixes with enzymes
    Digestion- enzymes produced by the intestinal cells make:
    Enterokinase, peptidases, lactase, maltase and sucrase
    Help to digest, CHO, proteins and lipids
    Absorption- absorbs most of the nutrients from food, takes 3-10 hours for the contents to pass through
    Major organ for absorption
  • 18. Small intestine
  • 19. Large Intestine
    Ileocecal valve to the anus, 5-6’, lined with columnar epithelium tha thas absorptive and mucous cells.
    Cecum- is the beginning, dilated pouch like structure, appendix is attached to the base
    Colon has 4 divisions:
    Ascending, transverse, descending and sigmoid
    Rectum- last 6-8” to the sphincter muscles and anus
  • 20. Large Intestine
    Function:
    Movement- segmental contractions, to allow time for the water and electrolytes to be absorbed
    Absorption- absorbs most of water and electrolytes, reduces fluid volume of chyme and creates a more solid mass for elimination
    Elimination- 3-4 strong peristaltic contraction /day triggered by colonic distention in proximal large intestine to propel contents to rectum, until urge to defecate.
  • 21. Nursing Assessment
    Family history- GI disorders, cancer
    Personal history- what kinds of things?
    Diet history- anorexia, dyspepsia- what is that? What should you question them on for diet history?
    Health history- diarrhea, constipation, # and color of stools, change in wt. or appetite
    Abdominal pain-
    P- precipitating
    Q-quality- how intense, severe, type
    R-region or radiation
    S- severity scale- 0-10
    T-timing- when did it first occur, duration and frequency
  • 22. Physical Assessment
    Abdomen:
    Inspection- skin, symmetry, rashes, lesions, scars
    Auscultation- all four quadrants, normally heard in 5-15 seconds, normal, hypoactive or hyperactive, listen 1 full minute. What is borborygmus? Why would bruits be heard? Why would there not be bowel sounds heard?
    Percussion- tympanic- air filled, dull- organ
    Palpation- light and deep palpation, masses, tenderness, look for guarding
  • 23. Lab tests
    CBC- anemia
    Oncofetal antigens- CA19-9 and CEA, used to monitor for cancer in the GI tract
    Ca- decreased in malabsorption
    K – decreased with vomiting, diarrhea
    Xylose absorption- decreased indicates possible malabsorption in the small intesting
    Stool for Occult blood
    Stool for ova and parasite- infection
    Stool for fecal fat- increased with Crohn’s disease and malabsorption
  • 24. Radiology
    Abdominal films- air in bowel and masses
    Upper GI and small bowel- pharynx to duodenojejunal junction, barium swallow and SBFT
    NPO 8 hours before, drink barium, then lie, stand and turn in multiple directions to view movement of barium
    SBFT- drink more barium and view passage
    After drink fluids to pass barium
    Barium enema
    Large intestine, done for obstructions, masses, not done is perforated colon or fistulas
    Only clear liquids for 12-24 hours prior, NPO, given bowel prep like Golytely
    Insert rectal catheter with a balloon and give 500-1500 ml of barium and hold
    Can be uncomfortable, must take a laxative after
  • 25. UGI exam
  • 26. Diagnostic Tests
    EGD- esophagogastroduodenoscopy
    Visualize esophagus to duodenum, NPO prior, given versed and fentanyl, maybe cetacaine to inhibit gag reflex, pass tube and visualize structures, can take biopsies
    Gag reflex may not return for 1-2 hours after, so no eating or drinking until then
    Colonoscopy- large bowel, take biopsies and remove polyps, have a bowel prep prior, given versed and fentanyl prior; Capsule enteroscopy is now done to visualize, apply a data recorder to the abdomen and the patient swallows the capsule
    Proctosigmoidoscopy- like colonoscopy, only a rigid tube, less invasive and does not require the cleansing of the colonoscopy
  • 27. Colonoscopy
  • 28. Case Study
    72 year old male admitted with chest pain and nausea. He states that he awakens in the night with pain in his chest and nausea.
    What would you do first to evaluate his condition?
    What diseases could he have?
    What kind of lab work would you like to obtain?
    What past medical history do you need?
  • 29. Case Study
    Your patient starts to have hematemesis.
    What does this mean?
    Is this life-threatening?
    What interventions should be done?
    What could have caused this condition?
  • 30. Case Study
    It is determined that your patient can be treated non-surgically. What medications would be given? (should have 3)
    What type of teaching would be done for prevention?
    If he needed surgery, what could have been done?
  • 31. Esophageal Problems
    GERD- gastroesophageal reflux disease
    Reflux causes esophageal mucosa to be irritated by the effects of gastric and duodenal contents, results in inflammation
    Causes:
    Inappropriate relaxation of the LES, sphincter tone is decreased
    Irritation from refluxed material
    Delayed gastric emptying, gastric volume or intra-abdominal pressure is increased
    Abnormal esophageal clearance
  • 32. GERD
    Refluxed material has a pH of 1.5-2, whereas the esophagus normally has a pH of 6-8 erosive esophagitis, once inflammed, the mucosa can’t eliminate the material as quickly. This leads to increased blood flow and more erosion. Gastric acid and Pepsin cause the tissue injury.
    Can lead to Barrett’s epithelium- thicker, but can be cancerous, can also cause hemorrhage, aspiration pneumonia, asthma, laryngitis and dental deterioration.
  • 33. GERD
  • 34. GERD
    Physical Manifestations:
    Dyspepsia- heartburn, substernal or retrosternal burning that moves up and down in wavelike fashion, pain may radiate to neck or jaw or back, worsens when bends over, strains or lies on their back, occurs after meals and last 1-2 hours, helped by fluids and staying upright
    Regurgitation- food entering throat without nausea, watch for cough, hoarseness or wheezing
    Hypersalivation- water brash in response to reflux, fluid without sour or bitter taste
  • 35. GERD
    Physical Manifestations
    Dysphagia and Odynophagia- difficulty swallowing, esophagus may be narrowed by inflammation or tumor, odynophagia- means what?
    Chronic cough, mostly at night
    Atypical chest pain
    Belching and flatulence or bloating
    Diagnosis:
    Endoscopy, 24 hour ambulatory pH monitoring- pass a small tube into esophagus and monitor pH levels
  • 36. GERD
    Nursing Diagnoses:
    What diagnoses would apply to these patients?
    1.
    2.
    3.
    Interventions:
    Diet therapy- what type of dietary modifications would be appropriate?
    Certain foods decrease LES pressure- chocolate, fat and mints. Also, smoking and alcohol decrease
    Spicy foods irritate the esophagus and Carbonated can increase gastric pressure
  • 37. GERD
    Lifestyle changes:
    How should they sleep?
    What things increase intra-abdominal pressure?
    Drug therapy:
    Goal is to inhibit gastric acid secretion, accelerate gastric emptying and protect the gastric mucosa
    Antacids:
    Elevate the pH and deactivate pepsin, good for heartburn, take 1 hour before and 2-3 hr after a meal
    Name 2 antacids.
  • 38. GERD
    Drug therapy:
    Histamine Receptor Antagonists
    Decrease acid, help promote healing of the esophagus
    Name 2 common ones sold OTC (generic ends in “dine”)
    Proton Pump Inhibitors
    Main treatment for GERD, long acting inhibition of gastric acid secretions by inhibiting protom pump of parietal cell, can reduce by 90%/ day
    Name 2 proton pump inhibitors (generic ends in “zole”)
  • 39. GERD
    Other therapies:
    Consider medications that may lower LES pressure- oral contraceptives, anticholinergics, sedative, tranquilizers, B-adrenergic agonists, nitrates and Ca channel blockers
    Prokinetic drugs- for emptying and peristalsis- metoclopramide (reglan)
    Endoscopic:
    Enteryx procedure- spongy material in LES to tighten it Stretta procedure- radiofrequency energy through needles to inhibit the vagus nerve
    Surgical:
    Laparoscopic Nissen Fundoplication
    Angelchik esophageal antireflux- anchors the LES in the abdomen to increase sphincter pressure
  • 40. Hiatal Hernia
    Protrusion of stomach through the esophagus
    Sliding or Rolling hernias
    Symptoms are similar to GERD patient
    Nonsurgical management is like GERD
    Surgical:
    Lap Nissen Fundoplication- reinforces the LES, wraps a portion of the stomach around the distal esophagus to anchor it
    Post op- risk for bleeding, infection and respiratory complications
    Have an NGT, begin PO once BS return
    Watch for gas-bloat syndrome and air swallowing
  • 41.
  • 42.
  • 43.
  • 44.
  • 45. Nursing Diagnosis: GERD
    Impaired Nutrition: less than body requirements
    What things can be done to improve their intake and decrease pain?
    What would be the expected outcomes?
    How would you monitor their progress?
    Acute Pain r/t irritation of the esophagus
    What interventions can be performed?
    Risk for aspiration r/t reflux of gastric contents
    How can you determine that this does not occur?
  • 46. Peptic Ulcer Disease
    Mucosal lesion of the stomach or duodenum
    Peptic can be gastric or duodenal
    PUD- gastric mucosal defenses become impaired and they can no longer protect the epithelium from acid and pepsin
    Three main types of ulcers:
    Gastric
    Duodenal
    Stress
  • 47. Peptic Ulcers
  • 48. Gastric Ulcers
    Gastric mucosa is protected by mucous and bicarbonate that maintain a normal pH on the gastric tissue and protects it from acid
    Gastromucosal prostaglandins increase the barrier’s resistance to ulceration by producing mucous
    Integrity is improved by a rich blood supply to the mucosa
    If there is a break in the mucosal barrier, HCL acid damages the epithelium. Gastric ulcers result from back-diffusion of acid or dysfunction of the pyloric sphincter.
  • 49. Gastric Ulcers
    If the pyloric sphincter doesn’t function, bile backs up into the stomach, produces H+ ion back diffusion and  mucosal inflammation
    Toxic agents and bile destroy the lipid plasma membrane of the mucosa. Delayed gastric emptying also affects. What drug can be given to improve emptying?
    Gastric Ulcers are deep and penetrating and usually are in the lesser curvature of the stomach, near the pylorus
  • 50. Duodenal Ulcers
    Occur in the first portion of the duodenum.
    Deep lesions that penetrate through the mucosa and submucosa into the muscle layer. The floor of the ulcer consists of a necrotic area on granulation tissue and surrounded by fibrosis
    High gastric acid secretion, pH levels are low for long periods
    Protein rich meals, calcium and vagal excitation stimulate acid secretion
    Hypersecretion, rapid emptying of food from stomach reduces the buffering effect of food and delivers a large acid bolus to the duodenum
    Inhibitory secretory mechanisms and pancreatic secretion may be insufficient to control the acid
    Many patients have H. pylori infection. H. pylori produces urease changes urea to ammonia, H+ ions released contribute to damage
  • 51.
  • 52. Stress Ulcers
    Acute gastric mucosal lesions occurring after and acute medical crisis or trauma
    Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis
    Bleeding is the principle manifestation
    Multifocal areas often in the proximal portion of the stomach and duodenum
    Usually elevated HCL acid levels and hospital stay longer than 11 days
  • 53. Complications of Ulcers
    Hemorrhage:
    15-25% of patients with PUD, most serious complication
    Most often with gastric ulcers and elderly
    After initial bleed, 40% have a recurrence if untreated, especially if H. pylori untreated and no H2 antagonist
    Have Hematemesis- bleeding at or above the duodenojejunal junction
    Smaller amounts of bleeding are seen as melena, more often seen in duodenal ulcers, stool may appear black.
  • 54. Complications of Ulcers
    Perforation
    Gastric or duodenal may perforate or bleed
    Stomach or duodenal contents can leak into the abdomen, acid peptic juice, bile and pancreatic juice empty through the anterior wall of the stomach into the peritoneal cavity
    Sudden, sharp pain in midepigastric region and spread over the abdomen
    Amount of pain correlates with the amount and type of GI contents spilled
    Abdomen is tender, rigid and boardlike, go into a fetal position to decrease tension of abdomen
    Chemical peritonitis, bacterial septicemia and hypovolemic shock follow paralytic ileus and possible death
  • 55. Perforated ulcer
  • 56. Complications of Ulcers
    Pyloric obstruction
    Small number of patients, vomiting caused by stasis and gastric dilation
    Obstruction occurs at the pylorus and is caused by scarring, edema, and/or inflammation
    Gastric outlet obstruction abdominal bloating, nausea and vomiting
    May go into metabolic alkalosis from loss of large quantities of acid gastric juice (H+ and Cl-)
    Hypokalemia may result from the vomiting
  • 57. Complications of Ulcers
    Intractable disease
    Disease may recur throughout life, stressors, inability to adhere to therapy, no longer responds to management
    Cause:
    Use of NSAID’s- break down the mucosal barrier and disrupt the protection by COX inhibition. Cause the depletion of prostaglandins, have a high rate of recurrence
    Drugs such as Theophylline, corticosteroids and caffeine stimulate HCL acid production
    H pylori infection is transmitted person to person
    50% of people with PUD have a first or second line relative with PUD, usually the same type of ulcer
  • 58. Physical Manifestations
    Epigastric tenderness, midline between the umbilicus and xiphoid process
    May begin as hyperactive BS, then diminish if perforation
    Dyspepsia- discomfort around the epigastrium, sharp, burning or gnawing
    Gastric- occurs in upper epigastrium with localization to the left of the midline and may be relieved by food
    Duodenal- located to the right of the epigastrium, occurs 90 min to 3 hours after eating and awaken at night, may be aggravated by spicy foods, onions, alcohol, caffeine and ASA, NSAIDS
  • 59. Physical Manifestations
    Vomiting may occur
    Appetite is maintained, unless pyloric obstruction occurs
    Fluid volume deficit, if bleeding, take orthostatic BPs
    Watch for Hematemesis and melena
    Monitor H & H
    Dx- barium swallow and EGD
    Test for H. pylori is IgG serologic testing and urea breath testing
  • 60. Nursing Diagnoses
    Name 5 diagnoses r/t PUD
    1.
    2.
    3.
    4.
    5.
    What would be an expected outcome for this disorder?
  • 61. Nursing Interventions
    Drug Therapy
    Goals: Provide pain relief, eradicate H. pylori, heal ulcerations, prevent recurrence
    Eliminate H. pylori- triple treatment:
    Bismuth product (pepto-bismol) or a a proton pump inhibitor and two antibiotics (metronidazole (Flagyl) and tetracycline or amoxicillin)
    May have to take medications 4 x’s/day for 14 days and often they don’t complete the series
  • 62. Nursing Interventions
    Drug therapy:
    Hyposecretory drugs- reduce gastric acid secretions
    Antisecretory agents- proton pump inhibitors, “zole” ending, suppress H, K-ATP ase enzyme system of gastric acid production, can be given IV or PO
    H2 receptor antagonists- block histamine-stimulated gastric secretions, “dine” ending
    Prostaglandin analogues- reduce gastric acid secretion and enhance gastric mucosal resistance to tissue injury, Misoprostol (Cytotec) helps prevent NSAID induced ulcers, does cause uterine contraction and can not be given to pregnant women
  • 63. Nursing Interventions
    Antacids
    Buffer gastric acid and prevent formation of pepsin, heal duodenal ulcers
    Aluminum hydroxides and magnesium hydroxide, may affect those with renal impairment
    Take 2 hours after meals to reduce the H+ion load
    Calcium carbonate (TUMS) is an antacid, but it triggers gastrin release and causes a rebound acid secretion
    Antacids can interact with other drugs- tetracycline, dilantin, also may have a high sodium content
    Mucosal Barrier fortifiers- sucralfate (Carafate) supplies a protect coating by forming a complex with proteins, binds with bile acids and pepsin, should be given on an empty stomach and not within 1 hour of eating or taking antacids
  • 64. Nursing Interventions
    Diet therapy
    Bland diet may help to relieve symptoms
    Food may help to neutralize acids, rebound may follow when more acid is released
    Avoid foods that stimulate gastric acid release
    They are??
    Yoga for stress relief, herbals, such as licorice and vitamins may help
  • 65. Gastrointestinal Bleeding
    What would be a nursing diagnosis for GI Bleeding?
    1.
    2.
    What would be the expected outcome and how would you know that this was met?
  • 66. GI bleeding
  • 67. Gastrointestinal Bleeding
    Hypovolemia Management
    Monitor vital signs and I&O, assess for bleeding and vomiting, monitor CBC
    Fluid and electrolyte replacement is necessary, usually NSS or LR, may give PRBC’s or FFP
    Watch for signs of shock, what are they??
    Bleeding reduction
    Monitor labs, insert and NGT to decompress the stomach, give an H2 blocker, may need gastric lavage, what is that??
  • 68. Nursing Interventions for GI bleeding
    Endoscopic therapy
    EGD, can do:
    cautery on the bleeding sites
    inject a sclerosing agent with diluted epipherine
    Laser therapy
    Clip the bleeding vessel
    Somastatin Analogue- Sandostatin may be used to suppress gastric acid secretion on parietal and chief cells, vasoconstricts the splanchnic arteries which reduce hemorrhage
  • 69. Surgical management of GI bleeding
    MIG- minimally invasive gastrectomy- laproscopic to remove chronic gastric ulcer or treat hemorrhage, make several small incisions, may partially remove the stomach and/or vagotomy to control acid secretion
    Gastroenterostomy- creates a passage between the body of the stomach and jejunum, reduces motor activity in the pyloroduodenal area, diverts acid, a vagotomy may be done with it to decrease secretion. Can do truncal, selective or proximal. Billroth I- connect to duodenum, Billroth II connects to jejunum
    Pyloroplasty- widens the exit of the pylorus and empties the stomach
  • 70. Billroth 1
  • 71. Postop care for GI surgery
    NGT management
    Monitor for complications of:
    Dumping syndrome- vasomotor symptoms, rapid emptying of gastric contents into the small intestine, shifts fluid into the gut and cause abdominal distention, 30 min after eating have vertigo, tachycardia, syncope, sweating, pallor, palpitations. 90 min later have excessive amount of insulin released, this dizziness, palpitations, diaphoresis and confusion
    Should eat smaller amounts, take less liquid with food, high protein and fat, low CHO diet, sandostatin may be given and pectin with food
  • 72. Postop Care of GI surgery
    Reflux gastropathy- bile reflux, when pylorus is bypassed, bile in stomach and have abdominal discomfort and vomiting
    Delayed gastric emptying- usually resolves in 1 week, edema at the anastomosis or adhesions may occur, hypokalemia, hypoproteinemia and hyponatremia may also cause
    Afferent loop syndrome- duodenal loop is partially obstructed, pancreatic and biliary secretions fill the intestinal loop, it becomes distended painful contractions, bloating and pain 20-60 min after eating
  • 73. Post op GI surgery
    Recurrent ulceration- occurs in 5% of patients, may have ulcers at the anastomosis
    Nutritional management:
    Deficiencies of B12, folic acid and iron
    Impaired Ca metabolism and reduced absorption of Ca and vitamin D
    Shortage of intrinsic factor, r/t the resection and rapid emptying of the food
     pernicious anemia- weak, anemic, atrophic glossitis- beefy shiny tongue
    Give back B12 and folic acid
  • 74. Pernicious anemia
  • 75. Irritable Bowel Syndrome
    Chronic GI disorder, with chronic or recurrent diarrhea, constipation, abdominal pain and bloating
    Spastic colon, impairment of the motor/sensory function diarrhea alternating with constipation
    Usually begin as a young adult
    Stress, anxiety and familial factors may predispose patient
  • 76. IBS
    Assessment:
    History of bowel pattern
    Manning criteria- abdominal pain relieved by defection, abdominal distention, sensation of incomplete evacuation of stool, presence of mucus with the stool
    Pain in LLQ and cramps, may be tenderness and air in bowels
    Dx- flexible sigmoidoscopy or colonoscopy if >40
    Barium enema
  • 77. IBS
    Interventions
    Diet therapy- limit caffeine, alcohol, beverages with sorbitol, take in fiber and bulk, 30-40 gm/day
    Drug therapy:
    Bulk forming laxatives (Metamucil)
    antidiarrheals (loperamide)
    anticholinergics (bentyl)
    antidepressants (elavil)
    5-HT4 agonists(Zelnorm) for prokinetic activity, imitates serotonin to stimulate peristalsis
    Stress management- relaxation techniques
  • 78. Nursing Diagnoses
    Constipation r/t low residue diet and stress
    What can be done to manage this?
    Diarrhea r/t increased motility of intestines
    How can this be corrected or treated?
    What can be done to correct constipation and impaction?
    What role may analgesics play in constipation?
  • 79. Colorectal Cancer
    95% are adenocarcinomas, most come from adenomatous polyps
    2/3 occur in rectosigmoid region
    Can metastasize through blood and lymph, liver most common site with 15-30% spread there, can also go to the lungs, brain, bones and adrenals
    May form fistulas into bladder and vagina
    Genetics- autosomal dominant disorder- familial adenomatous polyposis only 1%, 100% malignant, usually starting at age 20. Also, hereditary nonpolyposis colorectal cancer- autosomal dominant, 10% of cancers, develop by age 45
  • 80. Colorectal cancer
    75% have no known cause
    Age is a risk factor
    Dietary- decreased bowel emptying time, foods with carcinogens- red meat, fatty food, fried meats and fish, concentrated sweets
    High fat diet increases bile acid secretion and anaerobic bacteria
    Irritable bowel diseases
    Third most common malignancy
  • 81. Colorectal Cancer
  • 82. Colorectal cancer
    Manifestations:
    Rectal bleeding, anemia and change in stool
    Gas pains, cramping or incomplete evacuation
    Hematochezia- bright red blood when in rectum
    Tumors can grow large when in upper abdomen, mostly liquid stool, more pain when in lower
    Tests- stool for occult blood, CEA, barium enema, CT of abdomen
    Colonoscopy or sigmoidoscopy
  • 83. Colorectal cancer
    Nursing Diagnoses- Name 4 diagnoses, associated with colorectal cancer
    1.
    2.
    3.
    4.
    What would be the expected outcomes?
  • 84. Colorectal cancer
    Nonsurgical management:
    Duke’s staging classification
    A- tumor has penetrated into, but not through the bowel wall
    B- tumor has penetrated through the bowel wall
    C-tumor has penetrated through the bowel wall and there is lymph node involvement
    D- tumor has metastasized to distant sites
    Radiation therapy
    Drug therapy-chemotherapy IV 5-FU and leucovorin, side effects are diarrhea, mucositis, leucopenia and mouth ulcers
    Eloxatin, Camptosar, Avastin are also being used, along with monoclonal antibodies- cetuximab
  • 85. Colorectal cancer
    Surgical management:
    Colon resection- removal of tumor and lymph nodes
    Colectomy- colon removal
    Abdominal perineal resection- removes sigmoid colon, rectum and anus, colostomy is performed
    Colostomies may be ascending, descending, sigmoid, transverse or double barreled
    Stool returned depends on the site of the colostomy
  • 86. Colostomy
  • 87. Colorectal cancer
    Postoperative Care:
    Colostomy management
    What types of nursing diagnoses may accompany this procedure?
    How should the stoma appear?
    Report any bleeding, breakdown of the sutures from the wall and signs of ischemia or necrosis
    Wound care management- JP drains, monitor for infection
    Fluid volume deficit and electrolyte imbalance
  • 88. Colorectal cancer
    Teaching:
    Colostomy care- what kinds of things should be covered?
    Dietary measures to control stool and gas, what would they be?
    Psychological adjustment to the colostomy, what diagnosis relates to this?
    Grief and family coping- what resources may be needed?
    Genetic testing if familial type
  • 89. Intestinal Obstruction
    Partial or complete
    Mechanical- bowel is physically obstructed by adhesions, tumors
    Nonmechanical- paralytic ileus or adynamic ileus, neuromuscular distrubance- slow movement or backup
    Contents accumulate at or above the obstruction distention, peristalsis increases to aid movement, stimulates more secretions more distention edema of the bowel, increased capillary permeability
  • 90. Intestinal Obstruction
    Plasma leaks into the peritoneal cavity and trapped fluid decreases the absorption of fluid and electrolytes into the vascular space reduced blood volume and electrolyte imbalances, can  hypovolemic shock
    Can also lead to metabolic alkalosis if high and there is a loss of gastric acid, if low, metabolic acidosis occurs with the loss of alkaline fluids
    Bacterial peritonitis and septic shock can also occur from the release of endotoxins
  • 91. Intestinal obstruction
  • 92.
  • 93. Intestinal Obstruction
    Adhesions account for 45-60%, r/t scar tissue
    Intussusception- telescoping bowel and volvulus- twisting of the bowel
    Paralytic ileus- decreased peristalsis from trauma, toxin or autonomic, can result from surgery, MI’s, rib fracture, pneumonia, peritonitis and vascular insufficiency from heart failure or shock
  • 94. Intestinal Obstruction
    Assessment:
    History of symptoms and occurrence
    Abdominal pain and cramping
    Obstipation, vomiting with brown and foul smelling
    Borborygni above the obstruction, then absent
    Abdominal distention and tympanic abdomen
    Abdominal films and CT of abdomen
    WBC elevated in some cases
  • 95. Intestinal Obstruction
    Nonsurgical management:
    NGT to decompress to LCS
    Nasointestinal tubes- Miller-Abbott, mercury balloons and migrate down the intestine by peristalsis, don’t irrigate with fluid- it will increase edema at the obstruction
    Fluid and electrolyte replacement- NPO, give NSS or LR, replace K
    Pain control- not normally given opioids, mask pain and peritonitis
    Antibiotics if suspect perforation
    Surgical management:
    Exploratory laparotomy
  • 96. Case Study
    24 year old female admitted with frequent bloody diarrhea stools, weight loss and anemia.
    What do you suspect?
    What labwork should you do?
    What treatment may be needed?
  • 97. Case Study
    Your patient tells you that the diarrhea has been occurring for months.
    How do you differentiate between U.C. and Crohn’s disease?
    What may be her treatment options?
  • 98. Case Study
    How do you help your patient decide about a colostomy?
    If she does want a colostomy, what type of teaching needs to be done?
  • 99. Chronic Inflammatory Bowel Disease
    Ulcerative Colitis and Crohn’s
    Ulcerative Colitis:
    Remissions and exacerbations
    Loose stools with blood and mucous 10-20/day
    Poor absorption of nutrients and thickening of the colon wall
    Abdominal distention and cramping
    Complications are: hemorrhage, perforation, fistulas and nutritional deficiencies
    May be familial tendency, inflammation r/t response to normal flora
  • 100. Ulcerative Colitis
  • 101. Chronic Inflammatory Bowel Disease
    Crohn’s disease
    Terminal ileum, patching involvement through all layers of the bowel
    Deep fissures and ulcers occur
    5-8 loose stools/day, rarely bloody
    Complications are:
    Fistulas, nutritional deficiencies
    Cause is thought to be mycobacterium paratuberculosis, genetic predisposition
  • 102. Crohn’s Disease
    Garrard
    Crohn's story
  • 103. Ulcerative Colitis
    Manifestations:
    Abdominal pain, bloody diarrhea, tenesmus- uncontrolled straining
    Dx- barium enema
    Nursing Diagnoses:
    Diarrhea r/t inflammation of the bowel
    Acute and chronic pain
    Imbalance nutrition: less than body requirements
    Disturbed body image
  • 104. Ulcerative Colitis
    Diarrhea management-
    Drugs- salicylate compounds- Sulfasalazine (Azulfidine) inhibits prostaglandins to reduce inflammation, also use Asacol, Pentasa
    Corticosteroids- Prednisone to decrease edema
    Immunosuppressive- cyclosporine
    Antidiarrheals
    Monoclonal antibody- Remicade neutralizes the activity of tumor necrosis factor and prevents toxic megacolon
  • 105. Ulcerative Colitis
    Diet therapy:
    NPO at first, then TPN, may have low fiber or low residue, what foods would be included?
    Surgical management:
    Total Proctocolectomy with permanent Ileostomy
    Total colectomy with a continent ileostomy
    Total colectomy with ileoanal anastomosis and ileoanal reservoir or pouch
    Postop- teaching for ostomy, pain control and monitoring for GI bleeding and fluid volume deficit
  • 106.
  • 107.
  • 108. Crohn’s Disease
    Aggravated by bacterial infection, inflammation and smoking
    History of fever, abdominal pain and loose stools, weight loss
    Steatorrhea is common- fatty stools
    Fistulas may occur between bladder and vagina
    Drug therapy- same as UC, except may take metronidazole if fistulas and imuran as an immunosuppressant
    Diet therapy- may be on TPN, supplements like ensure, vivonex
  • 109. Crohn’s Disease
    Monitor for fistulas- infections, skin problems, malnutrition, fluid and electrolyte imbalances
    Fluid and electrolyte therapy- what would this entail?
    Name one antidiarrheal.
    Surgical management:
    Bowel resections
    Fistula repairs
    Ileostomies may also be required to rest the bowel or repair damaged areas.