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  • 1. Eat smaller meals at more frequent intervals / adherence to six,small,dry, meals per day. 2. Avoid high-carbohydrate intake and concentrated sweets. 3. Consume liquids only between meals or refraining from taking fluids during meals but rather 2 hours after meals. 4. Lie down or rest after eating or on a recumbent position for ½ hour after meals. 1. Eat smaller meals at more frequent intervals / adherence to six,small,dry, meals per day. 2. Avoid high-carbohydrate intake and concentrated sweets. 3. Consume liquids only between meals or refraining from taking fluids during meals but rather 2 hours after meals. 4. Lie down or rest after eating or on a recumbent position for ½ hour after meals.
  • Abdominal cramps and spasms after meals Chronic diarrhea / steatorrhea Fever Flatulence Nausea Pain in the lower right quadrant Weight loss 3-4 semisoft stools / day with mucus and pus.
  • 1. Subjective: indigestion after eating fatty or fried foods; pain, usually in the right upper quadrant of the abdomen, which may radiate to the back, nausea. 2. Objective: a. Vomiting; elevated temperature and WBC; jaundice may be present b. Diagnostic tests - Serum bilirubin is elevated - Ultrasonography determines the presence of gallstones; - Endoscopic retrograde cholangiopancreatography (ERCP) reveals presence of gallstones
  • 1. Secure the drainage bag; avoid kinking of the tube 2. Measure drainage at least every shift; drainage during the first day may reach 500 to 1000 ml and then gradually decline 3. Apply ordered protective ointments around tube to prevent excoriation 4. When the tube is removed, usually in 7 days, observe stool for normal brown color, which indicates bile is again entering the duodenum T-tube tract removal – threaded catheter with basket ERCP removal – cut papilla of sphincter of Oddi enlarge opening, threaded cath with basket
  • Pain – meperidine, NG sxn, oral care, bedrest Nutrition – IVF, BT, wt, I/O, abd. Girth Respi – position, cough, deep breath Teaching – biliary dse, alcohol Goals: control pain, rest pancreas, support nutrition/hydration
  • Goals: Eliminate cause, Rest, Nutritional/Fluid support, liver transplant
  • Subjective: anorexia; nausea; weakness; fatigue; abdominal discomfort; pruritus Objective: Weight loss; ascites; esophageal varices resulting from portal hypertension; hemorrhoids; edema of extremities; hematemesis; hemorrhage resulting from decreased formation of prothrombin; jaundice; delirium caused by rising blood ammonia levels Elevated liver enzymes (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) Decreased serum albumin; elevated serum bilirubin
  • Rest- wt, I/O, position, O2 Nutrition – early-CHON, B complex, Vit ACK, small freq, NGT/TPN, Aquasol ADE Late – adeq CHON – encephalopathy – (-) nitrogen balance mm wasting Skin care- SQ edema, immobility, jaundice, infxn, position, lotion Bleeding- pad rails, pressure injection site, melena, v/s, stool softeners Teaching- Alco Anon, low Na
  • varicesSengstaken - Blakemore tube for bleeding esophageal varices to apply direct pressure to the varices; vasopressin may be administered IV to control GI bleeding; plasminogen inhibitors to limit fibrinolysis

Gastrointestinal Gastrointestinal Presentation Transcript

  •  
  • Gastrointestinal System
    • Anatomy and Physiology
  •  
    • The Mouth
    • Important for the mechanical digestion of food
    • The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of carbohydrates
    • The Esophagus
    • A hollow collapsible tube
    • Length- 10 inches
    • The upper third contains skeletal muscles
    • The middle third contains mixed skeletal and smooth muscles
    • The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here
    • Functions to carry or propel foods from the oropharynx to the stomach
    • The stomach
    • J-shaped organ in the epigastrium
    • Contains four parts- the fundus, the cardia, the body and the pylorus
    • The esophageal sphincter prevents the reflux of the contents into the esophagus
    • The pyloric sphincter regulates the rate of gastric emptying into the duodenum
    • Capacity is 1,500 ml!
    • The functions of the stomach are generally to digest the food and to propel the digested materials into the SI for final digestion
    • The Glands and cells in the stomach secrete digestive enzymes:
    • 1. Parietal cells- HCl acid and Intrinsic factor
    • 2. Chief cells- pepsin digestion of PROTEINS!
    • 3. Antral G-cells- gastrin
    • 4. Argentaffin cells- serotonin
    • 5. Mucous neck cells- mucus
    • The Small intestine
    • Grossly divided into the Duodenum, Jejunum and Ileum
    • The duodenum contains the two openings for the bile and pancreatic ducts
    • The ileum is the longest part (about 12 feet)
    • The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff
    • Enzymes for carbohydrates
    • - disaccharidases
    • Enzymes for proteins
    • -dipeptidases and aminopeptidases
    • Enzyme for lipids
    • - intestinal lipase
    • The Large intestine
    • Approximately 5 feet long, with parts:
    • 1. The cecum - widest diameter, prone to rupture
    • 2. The appendix
    • 3. The ascending colon
    • 4. The transverse colon
    • 5. The descending colon
    • 6. The sigmoid - most mobile, prone to twisting
    • 7. The rectum
    • Absorbs water
    • Eliminates wastes
    • Bacteria in the colon synthesize Vitamin K
    • Appendix participates in the immune system
  • Accessory Organs
    • The Liver
    • The largest internal organ
    • Located in the right upper quadrant
    • Contains two lobes- the right and the left
    • The hepatic ducts (right and left) join together with the cystic duct to become the common bile duct
    • Functions to store excess glucose, fats and amino acids
    • Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
    • Produces the BILE for normal fat digestion
    • The Von Kupffer cells remove bacteria in the portal blood
    • Detoxifies ammonia into urea
    • The gallbladder
    • Located below the liver
    • The cystic duct joins the hepatic duct to become the bile duct
    • The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum
    • Stores and concentrates bile
    • Contracts during the digestion of fats to deliver the bile
    • Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi
    • The pancreas
    • A retroperitoneal gland
    • Functions as an endocrine and exocrine gland
    • The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi
  • The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats and proteins Pancreatic amylase - carbohydrates Pancreatic lipase (steapsin) - fats Trypsin, Chymotrypsin and Peptidases - proteins Bicarbonate - to neutralize the acidic chyme.
  • Diagnostics
  • Guaiac Test - detects the presence of fecal occult blood . Positive guaiac test shown on right, as would be seen for this patient. Negative result (on left) included for comparison.
    • Fecal Occult Blood Testing-FOBT (Guaiac Test)
    • Instruct the patient to adhere to a 3-day meatless diet (avoid any blood-containing food, cantaloupe, uncooked broccoli, turnip, radish, or horseradish)
    • No intake of NSAIDS, aspirin and anti-coagulant
    • Avoid citrus fruits and vitamin C supplements
    • Screening test for colonic cancer
    • Barium swallow :
    • A series of x-rays of the esophagus and stomach. The patient drinks a liquid that contains barium (a silver-white metallic compound). The liquid coats the esophagus and x-rays are taken. This procedure is also called an upper GI series
    • Upper GIT study: barium swallow
    • Pre-test : NPO post-midnight; 6-8 hours before procedure
    • Post-test : Laxative is ordered, increase pt fluid intake, instruct that stools will turn white, monitor for obstruction
    • Barium enema procedure. The patient lies on an x-ray table. Barium liquid is put into the rectum and flows through the colon. X-rays are taken to look for abnormal areas.
    • Lower GIT study: barium enema
    • Examines the lower GI tract
    • Pre-test : Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test
    • Lower GIT study: barium enema
    • Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction
  •  
    • EGD
    • (esophagogastroduodenoscopy)
    • Visualization of the upper GIT by endoscope
    • Pre-test : ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
    • Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access
    • Post-test : NPO until gag reflex returns, place patient in SIMS position until he awakens , monitor for complications, saline gargles for mild oral discomfort
    • ULTRASONOGRAPHY
    • 1. A noninvasive test focuses high-frequency sound waves over an abdominal organ to obtain an image of the structure.
    • 2. Ultrasound can detect small abdominal masses, fluid-filled cysts, gallstones, dilated bile ducts, ascites, and vascular abnormalities.
    • 3. Ultrasound with Doppler may be ordered for vascular assessment.
    • COMPUTED TOMOGRAPHY (CT) SCAN
    • 1. This is an x-ray technique that provides excellent anatomic definition and is used to detect tumors, cysts, and abscesses.
    • 2. The CT can also detect dilated bile ducts, pancreatic inflammation, and some gallstones.
    • ENDOSCOPIC PROCEDURES
    • Endoscopy is the use of a flexible tube (the fiberoptic endoscope) to visualize the GI tract and to perform certain diagnostic and therapeutic procedures. Images are produced through a video screen or telescopic eyepiece. The tip of the endoscope moves in four directions, allowing for wide-angle visualization.
  • Customizable to meet specific surgical needs, endoscopes can be fitted with scissors, knives, lasers, or cameras. Here, the endoscope is fitted with a small grasping tool to remove a toy lodged in the esophagus of an infant
    • PROCTOSIGMOIDOSCOPY AND COLONOSCOPY
    • 1. Proctosigmoidoscopy (rectosigmoidoscopy) is the visualization of the anal canal, rectum, and sigmoid colon through a fiberoptic sigmoidoscope.
    • 2. Colonoscopy is the visualization of the entire large intestine, sigmoid colon, rectum, and anal canal.
    • 3. Sigmoidoscopy or colonoscopy can be used to diagnose malignancy, polyps, inflammation, or strictures.
  •  
  • 34 yr old female. She also had an endoscopy first. (bleeding and/or pain was the reason she came in.) That pinkish/white mass is cancer. It's right by/on the valve between the ileum (small intestine) and cecum (large intestine.)
  • TREATMENTS
    • gastrointestinal
    ENEMA NASOGASTRIC INTUBATION TOTAL PARENTERAL NUTRITION
  • PURPOSES OF ENEMA ADMINISTRATION
    • 1. Bowel preparation for diagnostic tests or surgery to empty the bowel of fecal content.
    • 2. Delivery of medication into the colon ( such as enemas containing neomycin to decrease the bowel’s bacteria count or a kayexalate enema to decrease the serum potassium level)
  • PURPOSES OF ENEMA ADMINISTRATION
    • 3. To soften the stool ( oil-retention enemas)
    • 4. To relieve gas( tidal,milk and molasses,or fleet enemas)
    • 5. Promote defecation and evacuate feces from the colon for patients with constipation or an impaction
  • PURPOSES OF NASOGASTRIC INTUBATION
    • Remove fluid and gas from the stomach (decompression).
    • Prevent or relieve nausea and vomiting after surgery or traumatic events by decompressing the stomach.
    • Irrigate the stomach (lavage) for active bleeding or poisoning.
  • PURPOSES OF NASOGASTRIC INTUBATION
    • Administer medications and feeding (gavage) directly into the GI tract.
    • Obtain a specimen of gastric contents for laboratory studies when pyloric or intestinal obstruction is suspected.
  • Nasogastric intubation
    • Ensuring proper NG tube placement:
    • examine the patient’s mouth and throat for signs of a coiled section of tubing.
    • watch for respiratory distress signs
    • try to aspirate stomach contents
    • auscultate for air sounds with your stethoscope (should hear a whooshing sound in the epigastric region)
    • Secure the NG tube to the patient’s nose with hypoallergenic tape
  • TOTAL PARENTERAL NUTRITION
    • TPN is administered to meet a client’s total nutritional needs when oral feedings, tube feedings, and standard IV feedings are contraindicated.
    • It’s used for client’s with various GI problems or other conditions that necessitate nutritional support such as some oncology clients.
  • IMPORTANT POINTS:
    • In most cases, administer TPN through a central vein such as subclavian. The fluid is highly concentrated to provide rapid dilution and thus decrease the risks of peripheral inflammation and thrombosis
  •  
  • GASTROINTESTINAL DISORDERS
  • HIATAL HERNIA
    • A. ETIOLOGY
    • 1. Portion of the stomach protruding through a hiatus (opening) in the diaphragm into the thoracic cavity.
    • 2. May result from a congenital weakness of the diaphragm or from injury, pregnancy, or obesity.
    • 3. Function of the cardiac sphincter is lost, gastric juices enter the esophagus causing inflammation.
  •  
    • B. CLINICAL FINDINGS:
    • 1. Subjective: substernal burning pain or fullness after eating; dyspepsia in the recumbent position; nocturnal dyspnea .
    • 2. Objective: GI series and endoscopy show protrusion of the stomach through the diaphragm; regurgitation
    • C. THERAPEUTIC INTERVENTIONS:
    • 1. Small, frequent, bland feedings.
    • 2. Pharmacologic management: antacids, antisecretory agents, antiemetics, especially those that promote gastric emptying
    • 3. Surgical repair (done infrequently)
    • Fundoplication
  • Nissen fundoplication. The fundus of the stomach is wrapped around the lower esophagus and the edges are sutured together.
    • NURSING CARE:
    • 1. Teach the client and family about the dietary regimen.
    • 2. Encourage attempts at weight loss.
    • 3. Avoid constricting clothing and heavy lifting.
    • 4. Encourage the client to sit up for at least 1 hour after eating.
    • 5. Encourage the client to eat slowly and avoid drinking fluids with meals to limit the volume in the stomach.
  • Gastroesophageal reflux disease
    • Backflow of gastric contents, doudenal contents, or both past the lower esophageal sphincter (LES) into the esophagus without associated belching or vomiting.
    • Usually occur after a meal
    • Occurs when LES is deficient or pressure in stomach exceeds LES pressure.
  •  
  •  
  • Gastroesophageal reflux disease
    • Causes:
    • Food, alcohol, or cigarette that lower LES pressure
    • Increased abdominal pressure
    • Hiatal hernia
    • Weakened esophageal sphincter
    • Assessment:
    • Burning pain in epigastric area/ heartburn
    • Pain after meals or when lying down
  • Gastroesophageal reflux disease
    • Decrease LES pressure
    • LES relaxes
    • Gastrc contents regurgitates into the esophagus
    • Irritation of LES
    • Inflammation and injury
    • Reflux esophagitis
  • Gastroesophageal reflux disease
    • Nursing care:
    • Frequent, small meals
    • Avoidance of eating before going to sleep
    • Sitting upright during and after meals
    • Sleeping with head elevated
    • Antacid to neutralize acidic content of the stomach and minimize irritation.
    • H2 blocker to inhibit gastric acid secretion
    • Proton pump inhibitor to reduce gastric acidity
    • Smoking cessation to improve LES pressure ( nicotine lowers LES pressure)
    • Surgery (if hiatal hernia is the source.)
  • GASTRITIS
    • GASTRITIS is an inflammation of the gastric mucosa (the stomach lining).
    • It may be acute or chronic. Acute gastritis produces mucosal reddening, edema, hemorrhage, and erosion. Chronic gastritis is common among elderly people and people with pernicious anemia. In chronic atrophic gastritis, all stomach mucosal layers are inflamed.
    • POSSIBLE CAUSES:
    • Acute gastritis
    • Chronic ingestion of irritating foods, spicy foods or alcohol
    • Drugs, such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)(in large doses), cytotoxic agents, caffeine, corticosteroids, antimetabolites, phenylbutazone, and indomethacin
    • Ingestion of poisons, especially dichlorodiphenyltrichloroethane (DDT), ammonia, mercury, carbon tetrachloride, and corrosive substances
    • Endotoxins released from infecting bacteria, such as staphylococci, Escherichia coli, and salmonella, viruses (gastroenteritis)
  • GASTRITIS
    • Break in the protective barrier of stomach lining(prostaglandin)
    • Autodigestion
    • HCL diffuses back to mucosa & injure small vessels
    • The walls & lining of stomach atrophy
    • Destruction of the gastric glands
    • Hemorrhage & forms ulcer
    • DIAGNOSTIC EVALUATION:
    • Fecal occult blood test can detect occult blood in stools if the client has gastric bleeding.
    • Blood studies show low Hgb level and Hct when significant bleeding has occurred.
    • Upper GI endoscopy with biopsy confirms the diagnosis when performed within 24hrs of bleeding.
    • Upper GI series may be performed to exclude serious lesions.
    • TREATMENT:
    • Blood transfusion
    • I.V. fluid therapy
    • NG lavage to control bleeding
    • Oxygen therapy, if necessary
    • Partial or total gastrectomy (rare)
    • IMPLEMENTATION :
    • If the client is vomiting, give antiemetics and I.V. fluids to prevent dehydration and electrolyte imbalance.
    • 2. Monitor fluid intake and output and electrolyte levels.
    • 3. Offer smaller, more frequent meals to reduce irritating gastric secretions. Eliminate foods that cause gastric upset.
    • 4. If surgery is necessary, prepare the client preoperatively and provide appropriate postoperative care to decrease preoperative anxiety and prevent intraoperative and postoperative complications.
    • 5. Administer antacids and other prescribed medications
  • PEPTIC ULCER DISEASE (PUD)
    • A. ETIOLOGY:
    • 1. Ulcerations of the gastrointestinal mucus and underlying tissues caused by gastric secretions that have a low pH (acid)
    • 2. Causes include conditions that increase the secretion of hydrochloric acid by the gastric mucosa or that decrease the tissue’s resistance to the acid.
  • PUD
    • h.pylori, acid & pepsin damages the barrier
    • Autodigestion of acids
    • Inc.production of of acid
    • Dysfunction of the pyloric sphincter
    • Large acid bolus into the doudenum
    • Mucosal inflammation & injury
    • Insufficient bile & p. enzymes to control the acid
    • ulceration
  •  
  •  
    • THERAPEUTIC INTERVENTIONS:
    • 1 . Bland foods, and restriction of irritating substances.
    • 2. Antibiotic therapy if microorganism is identified; tetracycline, metronidazole, and bismuth
    • 3. Histamine H2 receptor antagonists or proton pump inhibitors, antacids
    • 4. Sedatives, tranquilizers, anticholinergics, and analgesics
    • 5. Antiemetics
  • . Surgical intervention:
    • Billroth I: removal of the lower portion of the stomach and attachment of the remaining portion to the duodenum.
    • . Billroth II: removal of the antrum and distal portion of the stomach and subsequent anastomosis of remaining section to the jejunum.
    • Vagotomy – surgical cuttting of any of the branches of the vagus nerve.
    • Antrectomy: removal of the antral portion of the stomach.
    • Gastrectomy: removal of 60%-80% of the
    • stomach.
    • Esophagojejunostomy (total gastrectomy): removal of the entire stomach with a loop of jejunum anastomosed to the esophagus
  • Total gastrectomy
  • dumping syndrome
  • The pathogenesis and manifestations of dumping syndrome
  •  
  • APPENDICITIS
  •  
    • MEDICAL DIAGNOSIS AND TREATMENT
    • Surgical removal of the appendix
    • Management of peritonitis, shock, dehydration, and infection
    • Chest x-ray to differentiate appendicitis from pneumonia(pneumonia may cause referred pain in the right lower quadrant and thus may be misdiagnosed as appendicitis)
    • Barium GI series and ultra-sonography to differentiate appendicitis from other abdominal problems
  • DIVERTICULAR DISEASE
  • DIVERTICULAR DISEASE
    • Diverticular disease has 2 clinical forms: DIVERTICULOSIS and DIVERTICULITIS.
    • Diverticulosis occurs when the intestinal mucosa protrudes through the muscular wall. The common sites for diverticula are in the descending and sigmoid colon, but they may develop anywhere from the proximal end of the pharynx to the anus.
    • Diverticulitis is an inflammation of the diverticula that may lead to infection, hemorrhage, or obstruction.
  •  
    • POSSIBLE CAUSES:
      • Age (most common in people over age 40)
      • Chronic constipation, more common in obese individuals
      • Congenital weakening of the intestinal wall
      • Low intake of roughage and fiber
      • Straining during defecation
      • Stress
      • Men affected more than women
  • DIVERTICULAR DISEASE
    • Low fiber diet, constipation
    • Musculature of the colon hyper trophies
    • Herniation of the mucosa & submucosa
    • Muscle weakness
    • Diverticula (diverticulosis)
    • Trapped undigested food, fecal materials
    • Bacteria builds up & impede blood flow
    • Inflammation (diverticulitis)
    • ASSESSMENT FINDINGS:
    • - Anorexia
    • - Stool with blood and mucus
    • - Change in bowel habits
    • - Constipation and diarrhea
    • - Fever
    • - Flatulence
    • - Nausea
    • - Rectal bleeding
    • TREATMENT:
    • - Generally no treatment for asymptomatic diverticulosis
    • - Colon resection (for diverticulitis refractory to medical treatment)
    • - High residue diet with no seeds for diverticulosis
    • - Low residue diet with diverticulitis
    • - high fiber diet
      • - Temporary colostomy possible for perforation, peritonitis, obstruction, or fistula that accompanies diverticulitis.
      • .
  • CROHN’s DISEASE ( Regional Enteritis)
  • CROHN’s DISEASE ( Regional Enteritis)
    • CROHN’s DISEASE is a chronic inflammatory disease of the small intestine, usually affecting the terminal ileum. It also sometimes affects the large intestine, usually in the ascending colon. It’s slowly progressive with exacerbations and remissions.
    • POSSIBLE CAUSES:
    • Emotional upsets
    • Fried foods
    • Milk and milk products
    • Unknown
  • CROHN’s DISEASE
    • Acute inflammation of entire intestines
    • Deep fissures & ulceration develops
    • Loss of healthy intestinal surface area & bacterial growth
    • Chronic changes include thickening of the bowel wall
    • Narrowing and strictures of bowel lumen
    • Formation of fistula, perforation, hemorrhage, obstruction, & abscess
  •  
    • TREATMENT:
    • DRUG THERAPY OPTIONS:
    • Analgesic: meperidine (Demerol), morphine
    • Antianemic: ferrous sulfate (Feosol), ferrous gluconate (Fergon)
    • Antibiotic: sulfasalazine (Azulfidine), metronidazole (Flagyl)
    • Anticholinergic: propantheline (Pro-Banthine), dicyclomine (Bentyl)
    • Antidiarrheal: diphenoxylate (Lomotil)
    • Antiemetic: prochlorperazine (Compazine)
    • Anti-inflammatory: olsalazine (Dipentum)
    • Corticosteroid: prednisone (Deltasone)
    • Immunosupressant: mercaptopurine (Purinethol), azathioprine (Imuran)
    • Potassium supplement: potassium chloride (K-Lor) administered with food, potassium gluconate (Kaon)
    • IMPLEMENTATION:
    • Bedrest, weigh daily
    • NPO in acute stage, TPN as ordered.
    • High CHON, calorie, bland, low residue diet.
    • Avoid gas-producers, irritating food, and milk products.
    • Offer small frequent feedings.
    • Vitamin replacement ADEK.
    • IVF, I/O, tepid fluids up to 3L/day.
    • Perianal care with lubricants and ointments.
    • Hot sitz baths, monitor stools.
    • Emotional support esp. family members.
  • ULCERATIVE COLITIS
    • ULCERATIVE COLITIS is a major health problem and a potentially debilitating disease. It’s a type of inflammatory bowel disease that produces lesions primarily confined to the large bowel, with ulcerations of the large bowel’s mucosa and submucosa .
    • POSSIBLE CAUSES:
    • Genetics
    • Idiopathic
    • Allergies
    • Autoimmune disease
    • Emotional stress
    • Viral and bacterial infections
  • ULCERATIVE COLITIS
    • Inflammation of the intestinal mucosa (rectum sigmoid entire colon)
    • Inflammation
    • Loss epithelium with erosion
    • Ulceration
    • Exudate edema with henorrhage
    • Abscess & mucupurulent exudate
    • Necrosis and scarring
    • Tissue replacement will narrow the colon
    • Loss characteristics of epithelium
    • ASSESSMENT FINDINGS:
    • Abdominal cramping, distention, and tenderness
    • Anorexia
    • Bloody, purulent, mucoid, watery stools (15 to 20 per day)
    • Dehydration
    • Fever
    • Hyperactive bowel sounds
    • Nausea and vomiting
    • Weakness
    • Weight loss
    • DIAGNOSTIC EVALUATION:
    • Barium enema shows ulcerations.
    • Blood chemistry shows decreased potassium level and increased osmolality.
    • Hematology shows decreased Hgb level and Hct.
    • Intestinal biopsy helps to differentiate between ulcerative colitis and regional enteritis.
    • Stool specimen is positive for blood and mucus.
    • Urine chemistry displays increased urine specific gravity.
    • TREATMENT:
    • Colectomy or ileostomy
    • IMPLEMENTATION:
    • Assess GI status and fluid balance to determine deficient fluid volume.
    • Monitor and record vital signs, intake and output, laboratory studies, daily weight, urine specific gravity, calorie count, and fecal occult blood to determine deficient fluid volume.
    • Monitor the number, amount, and character of stools to determine status of nutrient absorption.
    • Maintain the client’s diet; withhold food and fluid as necessary to prevent nausea and vomiting.
    • Administer I.V. fluids and TPN to maintain hydration and improve nutritional status
  • Types of Ostomy
    • Ostomy = opening made to allow passage of urine or stool
      • Piece of intestine is brought out onto the client’s abdomen.
      • Lacks nerve endings
      • Doesn’t hurt to touch but has other implications
    • Stoma = mouth like opening in the abdominal wall to drain urine or stool
    • Effluent – drainage from stoma
    • Ileostomy
      • End of small intestine
      • By passes large intestine = frequent liquid stools
    • Colostomy
      • Large intestine
      • More solid stool
    • OSTOMY CARE
    • Referral to enterostomal therapist.
    • Encourage verbalization of fears/concerns.
    • Teach character of drainage: ileostomy – liquid 4-6x/day, transverse colostomy – mushy OD, descending/sigmoid – soft formed q 2-3 days
    • Skin care – nystatin, karaya powder, soap/H2O pat dry
    • Odor control – deodorant drops, bismuth tabs, mouthwash solutions, spinach, parsley added to ostomy bag.
    • Odor – avoid gas-formers (cabbage, beans, broccoli, cauliflower, corn, onions, eggs, fish, condiments.
  • Differential features of colitis & crohn’s disease
    • Location : (UC)
    • Rectum-sigmoid-cecum
    • Etiology :
    • Unknown
    • Peak incidence:
    • 15-25 or 55-65 y.o.
    • Stool :
    • 10-20 liquid bloody stools per day
    • Location : ( crohn’s)
    • Terminal ileum
    • Etiology :
    • Unknown
    • Peak incidence:
    • 15-40 y.o.
    • Stool :
    • 5-6 soft loose rarely bloody stools per day
    Common complications: Hemorrhage, perforation, fistula, nutritional deficiency
  • INTESTINAL OBSTRUCTIONS
  • Strangulated hernia adhesions tumor intussusceptions Volvulus or twisting
  • INTESTINAL OBSTRUCTIONS
  • INTESTINAL OBSTRUCTIONS
    • Complications:
    • Infection/septicemia
    • Gangrene of the bowel
    • Perforation of the bowel
    • Fluid imbalances
  • INTESTINAL OBSTRUCTIONS
    • Treatment:
    • Mechanical and vascular intestinal obstructions are generally treated surgically; ileostomy or colostomy may be necessary.
    • Intestinal intubation and decompression
    • Maintain fluid and electrolyte balances and adequate nutrition.
  • CHOLELITHIASIS / CHOLECYSTITIS
    • A. ETIOLOGY AND PATHOPHYSIOLOGY:
    • cholecystitis is the Inflammation of the gallbladder; usually caused by the presence of stones (cholelithiasis), which are composed of cholesterol, bile pigments, and calcium.
  • Common locations of gallstones Abnormal metabolism of cholesterol & bile salts Gallstone fromation Gallstones may obstruct gall bladder Stasis of bile Autodigestion Migration of gallstones to ducts Inflammatory response Iiritation & impaired blood flow Ischemia of the gallbladder wall Necrosis & gangrene Perforation Abscess & peritonitis
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    • C. THERAPEUTIC INTERVENTIONS:
    • Medical management
    • - Nasogastric suctioning to reduce nausea and eliminate vomiting
    • - Narcotics to decrease pain
    • - Antispasmodics and anticholinergics to reduce spasms and contractions of the gallbladder
    • - Antibiotic therapy if infection is suspected
    • - cholecystectomy- removal of the gallbladder
  • T-tube placement in the common bile duct. Bile fluid flows with gravity into a drainage collection device below the level of the common bile duct.
  • T tube care:
    • Semi fowlers position
    • Ensure that t-tube is connected to close gravity drain
    • Avoid kinks, clamping & pulling
    • MIO q shift
    • Expect 300-500ml bile colored drainage (1 st 24H) 200ml/ 24H (3-4 days)
    • Light colored stool
    • Skin care around the tube
    • TREATMENT OF STONES:
    • CHOLESTEROL DISSOLVENT:
    • Moctanin is administered through a nasal biliary catheter to dissolve stones left in the bile duct after cholecystectomy. Dissolution may take 1 to 3 weeks. Observe the client for anorexia, nausea, vomiting, and abdominal pain.
    • ORAL BILE ACIDS:
    • Chenodiol ( chenix ) and ursodiol ( actigall ) are administered to dissolve small stones. Side effects include diarrhea ( especially with chenodiol ), elevation of hepatic enzymes,gastritis, and gastric ulcers. Dissolution takes between 6 months and 2 years, and the success rate is only about 30 %
    • Percutaneous transhepatic dissolution
  • Endoscopic sphincterotomy/retrograde cholangio-pancreatography
  • ESWL
    • Lithotripsy is the use of high-energy shock waves to fragment and disintegrate biliary stones. ESWL
    • (Extracorporeal Shock-wave Lithotripsy) – uses soundwaves to pulverize gallstones (30-40mins)
    • - suitable only for radiolucent stones
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  • PANCREATITIS
    • PANCREATITIS is the inflammation of the pancreas. In acute pancreatitis, pancreatic enzymes are activated in the pancreas rather than the duodenum, resulting in tissue damage and autodigestion of the pancreas.
    • In chronic pancreatitis, chronic inflammation resu lts in fibrosis and calcification of the pancreas, obstruction of the d ucts, and destruction of the secreting acinar cells.
    • POSSIBLE CAUSES:
    • 1. Alcoholism - chronic
    • 2. Bacterial or viral infection
    • 3. Biliary tract disease - acute
    • 4. Blunt trauma to the pancreas or abdomen
    • 5. Drugs: steroids, thiazide diuretics, oral contraceptives
  • Inflammation caused premature acvtivation of enzymes Causes tissue damage Enzymes back up and spill out into pancreatic tissue Auto digestion Acute pancreatitis: Hemorrhagic necrotising pancreatitis Cell death & tissue damage Hemorrhage Multi organ failure Shock Chronic pancreatitis: Repeated attacks Cell replacement of fibrous tissue Inc.pressure & obstruction Inflammation & destruction Necrosis attack
    • ASSESSMENT FINDINGS:
    • Abrupt onset of pain in the epigastric / LUQ area that radiates to the shoulder , substernal area, back, and flank
    • Abdominal tenderness and distention
    • Aching, burning, stabbing, pressing pain
    • Knee-chest position, fetal position , or leaning forward for comfort d/t abdominal pain
    • Mental confusion, hypocalcemia – irritability
    • Nausea and vomiting
  • TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY
    • g. Tachycardia, shock, hypotension
    • h. Dyspnea
    • i. Low grade fever
    • j. Elevated serum amylase / lipase / glucose
    • k. Grey Turner’s, Cullens’s sign
    • l. Chronic steatorrhea
    • m. Jaundice
    • o. Hyperglycemia
    • TREATMENT: PANCREATITIS
    • NPO, TPN, Bland, low-fat, high-protein diet of small, frequent meals with restricted intake of caffeine, alcohol, and gas-forming foods
    • Bed rest
    • 3. I.V. fluids (vigorous replacement of fluids and electrolytes) BT: packed RBC, FWB
    • Surgical intervention to treat the underlying cause, if appropriate
    • Maintain position, patency, and low suction of NG tube to prevent nausea and vomiting.
    • Monitor I/O, wt OD, abd girth, electrolytes.
    • Monitor blood glucose levels.
    • Meds: meperidine, H2 blockers, anticholinergics, antacids, Ca gluconate, pancreatic enzyme replacements (Viokase, Pancreatin, Pancrease)
  • 24–7 Pancreatoduodenectomy (Whipple’s procedure). A , areas of resection; B , appearance following resection.
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  • Cirrhosis of the liver
  • Lets go back to the function of the liver…
    • a. Carbohydrate metabolism by liver cells
    • -glycogenesis- glucose converted into glycogen
    • -glycogenolysis- glycogen is broken down into glucose
    • -gluconeogenesis- glucose into energy
    • b. Fat metabolism by liver cells
    • c. Storing reserves of nutrients (ADEK & B12)
    • d. Filtering poisons and wastes from blood
    • e. Production and synthesize variety of proteins.
    • Ex. Albumin (helps regulate the movement of water from the bloodstream)
    • globin- components of Hg (02 carrying substance in RBC)
    • globulin- group of protein that includes antibodies
    • fibrinogen & prothrombin- blood coagulation that helps heal wound
    • f. Regulating many chemicals found in the blood stream
    • g. Can regenarate or grow back
    • h. Bile production
    • Damaged repeatedly can cause irreversible changes that interfere function.
    • j. Conversion of ammonia to urea
  • HEPATIC CIRRHOSIS
    • A. ETIOLOGY AND PATHOPHYSIOLOGY
      • 1. Irreversible fibrosis and degeneration of the liver
      • 2. Several types of cirrhosis; La ënnec’s (alcoholic cirrhosis, nutritional cirrhosis) most common, biliary cirrhosis, & post necrotic cirrhosis
      • 3. Incidence higher in alcoholics, who are often malnourished, and in those who have had hepatitis
    • Chronic alcoholism
    • Toxic effect on hepatocytes
    • Liver inflammation (alcoholic hepatitis)
    • Destructive phase
    • Fibrosis or scar formation
    • Necrosis
    • Hardened and lumpy liver
    • Liver Shrinks
    • Liver failure
  • Hepatic circulation
  • inc. hydrostatic pressure in portal circulation Dec.plasma osmotic pressure Inc.serum aldosterone & ADH Upward pressure on diaphragm impairs respiration inc. risk for peritonitis Impaired digestion & absorption
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  •  
  •  
    • C. THERAPEUTIC INTERVENTIONS:
    • Rest
    • Restriction of alcohol, hepatotoxic drugs.
    • Vitamin therapy: especially the fat soluble vitamins A, D, E and K and vitamin B (thiamine chloride and nicotinic acid); zinc and calcium supplements
    • Diuretics to control ascites and edema
    • 5. Neomycin and lactulose may be prescribed for elevated blood ammonia levels (2-4 soft stools)
    • 6. Paracentesis if respiratory distress occurs as a result of ascites
    • Paracentesis is a procedure to take out fluid that has collected in the belly ( peritoneal fluid ). This fluid buildup is called ascites
  • Paracentesis Sites
  • Sites and position for paracentesis. A , Potential sites of needle or trocar insertion to avoid abdominal organ damage. B , The client sits comfortably; in this position, the intestines float back and away from the insertion site.
  • 7. Surgical intervention to decrease portal hypertension: a portacaval shunt or TIPS
    • 8. Esophageal varices management
    • Sengstaken-Blakemore tube:
    • 9. Dietary modification:
    • a. Cirrhosis:
    • 1. Protein as tolerated (80-100g); with increasing liver damage, protein metabolism is hindered
    • 2. High carbohydrate , moderate fat; provides for energy ; vitamin, mineral , and electrolyte supplements
    • 3 . Low sodium (500-1000mg daily); helps control increasing ascites
    • 4. Soft foods if esophageal varices are present; prevents danger of rupture and bleeding
    • 5. Alcohol contraindicated to avoid irritation and malnutrition
    • b. Hepatic coma
    • 1. Protein : reduced according to tolerance; 15-30g
    • 2. High calorie (1500-2000g) to prevent catabolism and liberation of nitrogen
    • 3 . Fluid carefully controlled according to output
  • Peritonitis
    • Peritonitis is the generalized inflammation of the peritoneal cavity. Leading intraabdominal infection.
    • Intestinal motility is decreased, and fluid accumulates as a result of the inability of the intestine to reabsorb fluid.
    • Fluid will leak into the peritoneal cavity, precipitating fluid, electrolyte, and protein losses, as well as fluid depletion.
  • Inc. permeability Intestinal bacteria leak out into peritoneal cavity Bacterial peritonitis Constant severe pain Reflex contrxn of abdominal muscle Hypovolemicshock Dec. peristalsis adhesion
  • PYLORIC STENOSIS
    • Pyloric stenosis is the obstruction of the pyloric sphincter by hypertrophy and hyperplasia of the circular muscle of the pylorus.
    • Assessment
    • Risk factors/etiology
    • 1. Occurs most often in firstborn, term infants (infantile hypertrophic stenosis)
    • 2. More common in male infants.
    • 3. Seen more frequently in white infants.
    • Clinical manifestations
    • 1. Onset of vomiting may be gradual, occurring in first few weeks; or forceful, projectile vomiting may develop at 4 to 6 weeks of age.
    • 2. Emesis is not bile stained but may be curdled from length of time in stomach.
    • 3. Vomiting occurs shortly after feeding.
    • 4. Infant is hungry and nurses well.
    • 5. Infant does not appear to be in pain or acute distress.
    • 6. Weight loss occurs, if untreated.
    • 7. Stools decrease in number and in size.
    • 8. Dehydration occurs as condition progresses; hypochloremia and hypokalemia as vomiting continues.
    • 9. Upper abdomen is distended, and an “olive-shaped mass may be palpated in the right epigastric area.
    • Diagnostics
    • 1. Palpation of abdominal mass.
    • 2. Prolonged vomiting.
    • 3. X-ray film and ultrasound examination of abdomen.
    • Treatment; surgical release of the pyloric muscle (pyloromyotomy)
    • Celiac disease is also known as sprue, gluten enteropathy , and malabsorption syndrome. This disease is an inborn error metabolism of rye, wheat, barley, and oat products. 
    Celiac disease
    • Symptoms generally begin between the ages of 1 year and 5 years, but they may also occur in those 50 to 60 years.
    • Severe malnutrition results from a loss of nutrients via the stool.
    • Atrophy of villi of intestines
    • Decrease absorptive surface
    • Decrease absorption of fats
    • Malabsorption of fat soluble vitamins
    • Severe malnutrition
    Intolerance of gluten (BROW) steatorrhea
    • Assessment
    • Cause: congenital defect in metabolism.
    • Clinical manifestations
    • 1. Symptoms begin when child has increased intake of gluten-type foods: cereals, breads, pastas, etc.
    • 2. Watery, pale diarrhea; steatorrhea.
    • 3. Vomiting, anorexia.
    • 4. Poor weight gain, failure to thrive.
    • 5. Constipation, vomiting, and abdominal pain may be the initial presenting signs/symptoms.
    • 6. Abdominal distention
    • Diagnostics
    • 1. Stool analysis
    • 2. Jejunal biopsy.
    • Treatment
    • Primarily dietary management; gluten-free diet
  • HIRSCHSPRUNGS'S DISEASE
    •   - Hirschsprungs's disease (congenital aganglionic megacolon) absence of innervations in a segment of colon wall. Absent of ganglion cells needed for peristalsis.
    • Assessment
    • Risk factors/etiology; congenital, may be associated with Down syndrome.
    • Clinical manifestations
    • 1. varies according to age and amount of colon involved.
    • 2. Inadequate or absent peristalsis.
    • 3. Newborn.
    • a. Failure to pass meconium within 24 to 48 hours after birth.
    • b. Vomiting
    • c. Abdominal distention.
    • d. Reluctance to take fluids.
    • 4. Older infant.
    • a. Passage of watery stools and diarrhea, ribbon like stools
    • b. failure to thrive.
    • c. Lack of appetite.
    • d. Persistent constipation, impactions.
    • Diagnostics
    • 1. Rectal biopsy.
    • 2. Barium enema.
    • Treatment
    • Surgical correction usually involves creation of a temporary colostomy, then a pull-through of the colon to a point near the rectum. After the reanastomosis has healed, the temporary colostomy is closed.
  • CLEFT LIP AND PALATE
    • Cleft lip- failure of maxillary and median nasal processes to fuse.
    • - 7-8 weeks lip closes at age of gestation.
    • Cleft palate- midline fissure of the palate
    • - 7-12 weeks palate closes at AOG
  • Types of cleft lip & cleft palate
  • CLEFT LIP AND PALATE
    • Manifestation:
    • Difficulty swallowing
    • Distended abdomen
    • Feeding difficulty
    • Complication:
    • Malnutrition
    • Speech impediment
    • Possible aspiration
    • Impaired self-esteem
  • CLEFT LIP AND PALATE
    • Mgt/ Interventio n:
    • Surgery:
    • Cheiloplasty (6-12 weeks old)
    • Uranoplasty- (4-6 weeks) to save speech
    • Palatoplasty (12-18 months old)
    • Feeding should be done in an upright position
    • Special nipples on feeding devices:
    • Lamb’s nipple, flanged nipple, rubber-tipped medicine dropper, asepto syringe
    • Bubble and burp frequently
  • CLEFT LIP AND PALATE
    • Post-op care (cleft lip)
    • Metal appliance/ adhesive strips are taped to cheeks “logans bar”
    • Elbow restraints
    • Clear liquids initially, then formula feeding as tolerated
    • Oral hygiene
    • Meticulous care on suture line
    • Suctioning PRN
    • Maintain upright position
  • CLEFT LIP AND PALATE
    • Post-op care ( cleft palate)
    • Lie on abdomen
    • Fluids best taken from the cups
    • Avoid use of suction or other objects in the mouth
    • Elbow restraints
    • Soft diet
    • Analgesic PRN- prevent crying of the patient
  • TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
    • TEF- An abnormal opening in esophagus and trachea
    • EA- blind pouch or no continuous passage of esophagus and stomach
    • Causes: unknown cause, malformation idiopathic
    • Diagnostic: x-ray of abdomen
  • TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
  • TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
    • Assessment:
    • Excessive salivation and drooling
    • 3 C’s of TEF
    • Coughing
    • Choking
    • Cyanosis
    • Apnea
    • Respiratory distress
    • Abdominal distension
  • TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
    • Surgical intervention:
    • Division and ligation of TEF
    • Anastomosis of esophagus
    • Age of surgery- 16-24 months
    • Temp. esophagostomy
    • Temp. gastostomy
    • Post-op care: gastrostomy feeding
    • No oral intake 10-14 days post-op
  • Gastrostomy . A , Gastrostomy tube placement. B , The tube is fixed against both the abdomen and stomach walls by cross bars.
  • TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
    • Nursing care:
    • On NPO upon diagnosis, IV fluids
    • Frequent suctioning
    • 02 administration
    • Supine position with head elevated at least 30 degrees
    • Pacifier periodically
    • Complication after surgery: leak of anastomosis, strictures, esophageal motility disorder
    • GOOD LUCK AND GOD BLESS!!!!
    • Post test after 10 minutes…