GASTROINTESTINAL NURSING DIAGNOSTIC TESTS: PATIENT PREPARATION /CARE Fecal Studies to detect blood, fat and infectious organisms

s Collect stool in a clean and dry container. Dont use stool that has been in contact with toilet bowl water and urine For fat or infectious organisms, collect 3 separate specimen and label day 1, 2, 3 Hematologic Studies: Hgb, hct, WBC Serologic tests: Carcinoembryonic antigen (CEA) Hepatitis and associated antigens Radiography- abdominal X-Ray, also called flat plate of the abdomen- helps detect tumors, abnormal gas collections, stones and other abdominal disorders. X- ray appears black, fat looks gray and bones look white Nsg. Care- no special pre and post test care Ultrasonography- this techniques uses a focused beam high frequency sound waves to create echoes Upper GI Series (UGIS) or Barium SwallowFlouroscopic examination of the upper GI tract to determine structural problems and gastric emptying time. Client must swallow barium sulfate or other contrast medium, sequential films taken as it moves through the system. Nsg care pre test a. Keep patient NPO pmn or 6-8 hrs pre test b. Explain that the barium will taste chalky Nsg care post test ADMINISTER LAXATIVES TO ENHANCE ELIMINATION OF BARIUM Lower GI Series (LGIS) or Barium Enema

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Barium is instilled in the colon by enema, client retains the contrast medium while xrays are taken to identify structural abnormalities of the colon Nsg. Care- pre test Keep patient NPO pmn Give enema in the morning of test Administer laxative or suppository Explain that cramping may occur during procedure Post test- administer laxatives and fluid to assist in expelling the barium Endoscopy (Esophagogastroduodenoscopy) Direct visualization of the esophagus, stomach and duodenum by insertion of a lighted fluoroscope to observe strictures, ulcerations, inflammations and tumors Nsg care pre test- NPO 6-8 hrs Explain that local anaesthesia will be used to ease discomfort and that speaking during the procedure is not allowed Colonoscopy Visualization of the large intestines and may include biopsy and removal of foreign substances Nsg Care pre testNPO for 8 hrs Administer laxatives for 1-3 days Explain that an instrument is inserted in the rectum Sigmoidoscopy Visualization of the sigmoid colon Nsg care pre testOffer a light supper and light breakfast Do bowel prep Explain to client that the sensation of urge of discomfort and abdominal cramping might be experienced Post test- assess for bleeding and perforation Gastric analysis Insertion of NGT to examine gastric content for acidity and volume Nsg care pre test Keep patient NPO 6-8 hrs pre test

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Advise client about smoking, anti cholinergic and ulcer medications for 24 hrs prior the test Esophageal manometry Measures the intraluminal pressure of the esophagus Also evaluates the quality of the esophageal peristaltic actions Patient swallows manometric catheter containing transducer Interpretations Normal LES pressure- 15-25 mmHg Incompetent sphincter 0-5mmHg GERD, hiatal hernia, esophagitis High Esophageal LES pressure- up to 50mmHg Hypertensive sphincter- achalasia. Esophageal spasm, diverticula and CA Oral Cholecystogram Injection of radiopaque dye and x-ray examination to visualize the gallbladder Nsg care pre test1. Offer a low fat meal in the evening before the test 2. Check for iodine sensitivity and administer dye tablets as ordered Nsg care post test Observe for side effects of the dye tablets like nausea, vomiting and diarrhea Liver Biopsy Invasive procedure where a specially designed needle is inserted into the liver to remove a small piece of tissue for study Nsg Care Pre test Keep NPO 6-8 hrs Instruct the patient to hold breath during biopsy Nsg Care post testAssess vital signs every hour for 8-12 hours Place patient on right side for few hrs, with a pillow against the abdomen to provide pressure on the liver Observe puncture site for hemorrhage Assess for complications like pneumothorax

Nursing Procedures for Gastrointestinal System Total Parenteral Nutrition It is indicated in clients who need extensive nutritional support over an extended period like major G.I. Diseases, severe malnutrition and cancer. The primary purpose is to provide glucose . The usual site is subclavian vein. The clavicle provides good support to catheter Nursing Responsibilities Trendelenburg position during insertion Administer at room temperature Consume TPN formula within 24 hours Monitor urine and blood glucose levels Prevent infection of the catheter Gastric and Intestinal Decompression Removal of fluid and gas to prevent gastric and intestinal distention Miller abbott tube Enemas Cleansing enema- stimulates peristalsis by irritating the colon and rectum by distending the intestine with fluid 500-1000 ml of fluid Carminative enema- to expel flatus 60-180 ml of fluid Retention enema- introduces oil in the rectum and sigmoid colon and is being retained for 1-3 hrs to soften the feces Return flow enema-/colonic irrigation Used to expel flatus Used 100-200 ml of fluid and is introduced in and out of the large intestines for 5 times Non retention enema Tap water- 500-1000ml Soap suds- 20 ml of castile soap in 5001000ml of water Fleet enema-90-20ml

Height of solution 18 inches above the rectum ORAL DISORDERS cheilitis Causes= exposure to sun, radiation May lead to squamous cell carcinoma Assessment findings- scaling. Fissuring, painful crusting and it usually involves the lower lip Treatment management- protect lips using lip ointment or balm, electro or cryo surgery to reduce inflammation Cheilosis or Angular Stomatitis Causes: Mechanical trauma of poorly fitting dentures Overclosure of the mouth Poor oral hygiene stress Assessment findings: softening of the skin at the angles of the mouth, followed by fissuring or cracking Often leading to secondary infection like moniliasis and bacteria Treatment/management Oral hygiene, good nutrition, soft bland diet, antibiotics Herpes simplex clinical signs - Cold Sores, herpes labialis, blister, fever opportunistic infection common in immuno-supressed patients recurrent- which appears to lie dormant after primary herpes infection lesions are contagious coated tongue -> foul breath clinical signs - Cold Sores, herpes labialis, blister, fever opportunistic infection common in immuno-supressed patients recurrent- which appears to lie dormant after primary herpes infection lesions are contagious coated tongue -> foul breath

Conservative management focus in relief of symptoms pain may be treated with analgesics Acyclovir (drug of choice], healing is 10-14 days Apply cold soaks to the lips for 20 minutes Refrain from direct contact or kissing Avoidance of spicy foods Chancre sore Hard papule as a primary lesion of syphilis Very contagious Reddened circumscribed lesion that ulcerates and become crusted Antibiotics, analgesics, cold compress to relieve pain leukoplakia Painless white thickened patches adherent to mucous membrane Appearance is likened to a dry, white paint Common to smokers May progress to Ca see doctor if persists for 2 wks Management Avoid tobacco , biopsy if the lesion is more than 2 weeks CANDIDIASIS Monilial thrush Caused by Candida Albicans yeast like fungus common in immuno-suppressed pts Immuno suppressed decrease levels of normal flora> leads to overgrowth of rest normal flora common in intubated patients White patches on tongue, palate and mucosa Lesions difficult to remove referred to as milk curds APTHOUS STOMATITIS Canker sores

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Shallow ulcers with white or yellow

eating

No heavy lifting or exercise after Avoid alcohol and tobacco Drink adequate fluid to enhance passage Surgery - NISSENS FUNDOPLICATION, hill repair, angel chick

With red border Starts with burning, tingling, sensation and slight swelling Pain last 4-7 days and heals without a scar Cause unknown- related to stress, trauma, food drug allergy, vit deficiency, endocrine imbalances Management Oral hygiene Soft, bland diet Topical antibiotics and steroids VINCENTS ANGINA Trench mouth/Necrotizing gingivitis Sudden onset of painful superficial bleeding, gingival ulcers covered with grey white membrane Ulcers become punched out lesions after a slight pressure or irritation Malaise, fever, excessive salivation, bad breath, pain while talking or eating Removal of devitalized tissue using an ultrasonic scaler Antibiotics, analgesic Hourly mouth rinses(equal amount of water and hydrogen peroxide) Soft, non irritating diet Esophageal Disorders GERD Management PPI, ANTACIDS, H2BLOCKERS AVOID DRUGS THAT DECREASE THE LES, ex. Anticholinergics, xanthine derivatives, diazepam and calcium channel blockers Small, frequent feedings avoid eating before sleeping High fowlers position or upright up to 2 hrs after eating Lose weight if obese Elevate head of the bed8-12 inches No constrictive clothing

Achalasia-progressive increasing dysphagia Cause- unknown Increased basal tone of LES and fails to relax Resulting to impaired propulsion and accumulation of food Bougienage- temporary relief (balloon tamponade) Surgery- ESOPHAGOMYOTOMY Hiatal or diaphragmatic hernia Sliding hernia- upper stomach and parasesophageal junction are displaced upward the thorax ROLLING HERNIA/paraesophageal hernia Gastroesophageal junction stays below the diaphragm but all parts of the stomach pushes through into the thorax SLIDING/ROLLING HERNIA Management PPI, ANTACIDS, H2BLOCKERS Surgery- Nissen Fundoplication, Hill repair ESOPHAGEAL DIVERTICULA Sac like outpouchings in one or more layers of the esophagus Food can be trapped in the diverticulum and can be later regurgitated Hypopharynx or Zenkers- most common Midpoint- caused by scar adhesion, chronic irritation Epiphrenic Signs and symptoms-

Halitosis, dysphagia, regurgitation, aspiration, fullness in the neck, sour taste in the mouth Diagnosis: Barium swallow ENDOSCOPY IS CONTRAINDICATED BECAUSE IT MAY PERFORATE THE DIVERTICULUM!!!!!!!!! Surgery- diverticulum is excised and esophageal mucosa is anastomosed GASTRIC DISORDERS PEPTIC ULCER DISEASE It is circumscribed break in the mucosa occurring in the duodenum, stomach and less common in esophagus and jejunum Thought to be caused by H. Pylori usually due by eating raw or improperly cooked food Hydrochloric acid and pepsin serve as aggressors to GI mucosa Contributing factors: Altered gastric acid levels Smoking and alcohol use- nicotine stimulates increased HCL secretion and vasoconstriction Caffeine- increased HCL secretion and vasoconstriction resulting to decreased blood flow to the GI mucosa that causes decreased mucous secretion NSAIDS, Aspirin Genetic predisposition Medications- antacids, PPI, ANTIBIOTICS TO TREAT H.PYLORI Surgeries- antrectomy BILROTH 1 and BILROTH II vagotomy , pyloroplasty Post op complications Hemorrhage Pyloric stenosis Pernicious anemia- Vit B 12 deficiency Perforation Dumping syndrome- rapid emptying of hyperosmolar fluid into the

jejunum. Rapid emptying causes fluid shift from bloodstream into the jejunum resulting to decreased blood volume Dumping Syndrome INTESTINAL DISORDERS APPENDICITIS Pathophysiology Inflammation accompanies the ulceration and temporarily obstruct the appendix Obstruction if present is usually caused by stool accumulation around the vegetable fibers(fecalith) The abdominal pain usually occurs suddenly, often causing a person to wake up at night begins near the periumbilical area and then descends to right lower quadrant gets worse in a matter of hours gets worse when moving around, taking deep breaths, coughing, or sneezing Assessment Vague epigastric pain sometimes described as cramping, then localized at the right lower abdominal area N/V Low grade fever Either diarrhea or constipation Elevated WBC In case of RUPTURE, spasm will occur followed by a BRIEF CESSATION of abdominal pain DX- X-ray with radiographic contrasts Special Abdominal Examinations Guarding. Guarding occurs when a person subconsciously tenses the abdominal muscles during an examination. Rebound tenderness. applying hand pressure to a patients abdomen and then letting go. INTENSIFICATION OF PAIN WHEN PRESSURE IS RELEASED Rovsings sign. applying hand pressure to the lower left side of the

abdomen. Pain felt on the lower right side of the abdomen upon the release of pressure on the left side Psoas sign. applying resistance to the right knee as the patient tries to lift the right thigh while lying down. Alternately do it on the left side increased abdominal pain on either maneouver means irritation of the psoas muscle by the inflamed appendix Obturator sign. Flex the patients right thigh at the hip, when the knee bent, rotate the leg internally at the hip. This maneuver stretches the obturator muscle. Right hypogastric pain means positive obturator sign When the appendix is inflamed, tenderness can be noted in the RLQ at the Mc Burneys point Management Place patient on NPO, Start IVF Do not give pain medications Place ice pack for 20 minutes Place on right side lying or low fowlers position to relieve pain No hot water compresses/applications Avoid enemas/ suppositories Monitor for changes in pain level Monitor for changes in temperature PERITONITIS Most common complication of ruptured appendix Localized or generalized inflammation of part or all the parietal and visceral surfaces of the abdominal cavity It caused by a leakage of contents from abdominal organs to abdominal cavity usually as a result of inflammation, infection, ischemia, trauma Intestinal motility gradually decreases that will result to paralytic ileus Assessment Findings Severe abdominal pain, rebound tenderness, muscle rigidity (boardlike)

because of the reflex muscle guarding, absent bowel sounds, abdominal distention Anorexia, n/v Shallow respirations- the patient is trying to avoid pain caused by body movement Patient lies still because any movement aggravates the pain Decreased urinary output, weak rapid pulse and elevated temperature Diagnostic tests will reveal elevated WBC, HCT ( if there is hemoconcentration) decreased electrolytes management NPO with fluid replacement Assess respiratory status and provide O2 supplementation, Assess characteristic of pain Monitor and maintain F&E balance, monitor for signs of septic shock Administer analgesics and antibiotics as ordered Sx- Laparotomy- opening made through the abdominal wall into the peitoneal cavity Bowel resection depending on the cause DIVERTICULAR DISEASES Diverticulum- saclike herniation of the lining of the bowel that extends through a defect in the muscle coat of the large intestine It may occur anywhere but most common site is sigmoid colon Diverticulosis if there are multiple diverticula without inflammation or symptoms Diverticulitis- when becomes infected and inflamed that impedes drainage and leads to perforation and abscess formation Incidence- more common in men, 45 years and above and obese Risk factors- chronic constipation due to low fiber diet

Pathophysiology Atrophy or weakness of the bowel muscle Mucosal and submucosal layer of the colon herniate through muscular wall because of high intraluminal pressure, decreased muscle strength in the colon caused by hardened fecal mass secondary to low fiber diet Signs and symptoms Mild episodic dull, steady left quadrant or mid abdominal pain Rectal bleeding in 15% of patientsanemia In mild diverticulosis- bowel irregularity, nausea, vomiting, bloating and abdominal distention Diverticulitis- LLQ pain, narrow stool, leukocytosis, fever, weakness and may lead to septicemia Urinary frequency if the site is proximal to the bladder Diagnostic exams Radiographic studies- narrowing of the colon and thickened mucus layers Sigmoidoscopy, colonoscopy, barium enema, CT scan Management Diverticulosis- high fiber diet BULK FORMING LAXATIVEMETAMUCIL, drink at least 8 glasses of water Diverticulitis- NPO,IVF, broad spectrum antibiotic, corticosteroids, anti spasmodics, NGT suctioning to rest the bowel Meperidine or demerol for pain Avoid morphine because it can increase intraluminal pressure in the colon, exacerbating symptoms Avoid activities that increase intra abdominal pressure Reduce weight if obese Surgery is done if complication develops like hemorrhage, obstruction, abcesses and perforation

Total colectomy, ileorectal/ileoanal anastomosis (entire colon is removed and the end of the small intestine is joined to the rectum or anus) MALABSORPTION SYNDROME Inability of the digestive system to absorb one or more of the major nutrients, minerals and nutrients Interruptions of the complex digestive process may occur anywhere but the most common site is small intestine. Celiac or non tropical sprueaccumulation of amino acid glutamine which is toxic to intestinal mucosal cells Intolerance to gluten an protein component of Barley Rye Oats Wheat (BROW) Tropical sprue- associated with folic acid deficiency Lactose intolerance- absence or deficiency in lactase required for the digestion of lactose Signs and symptoms Foul smelling, bulky diarrhea with increased fat content- steatorrhea Malnutrition- weight loss, anemia, easy brusing, osteoporosis IRRITABLE BOWEL SYNDROME used to describe a functional G.I. disorder characterized by a combination of chronic and recurrent intestinal symptoms not explained by structural and biochemical abnormalities More common in women Exact cause remains unknown but can be linked to STRESS Pathophysiology IBS results from a functional G.I. disorder of intestinal motility May be a result of diverticular disease, ingestion of irritants, abuse of laxatives, food poisoning and colon cancer Change may be from neuroendocrine dysregulation, infection or irritation or metabolic disturbance that

affects the peristaltic waves of the intestines Signs and symptoms Alternate diarrhea or constipation or combination of both Abdominal pain and bloating Diagnostic exams- stool exam, Barium enema, colonoscopy, x-ray Inflammatory Bowel Diseases Causes unknown Can affect the entire GI tract Chronic relapsing disease that may develop discontinuously in any segment of the alimentary canal Inflammation extends through all the layers of the intestinal wall and may involve lymph nodes Regional enteritis- when it affects small intestines Crohns disease of the colon or granulomatous colitis- colon Pathophysiology Lymph nodes enlarge and lymph flow in submucosa is blocked edema, ulcerations (skipping lesions) fissures, granulomas, abcesses development of oval elevated patches of closely pacled lymph follicles(peyers patch) on the small intestine Fibrosis occurs that causes thickening and shortening of the bowel resulting to stenosis and narrowing of the lumen loops adhere to other diseased or normal loops that will eventually become thicker and shorter Cobblestone appearance in Crohns disease Signs and symptoms RLQ Abdominal pain Chronic diarrhea from bile salts malabsorption and bacterial growth Stool- soft semi fluid consistency, fat malabsorption(steatorrhea) may be bloody Malaise and weight loss, fever Complications

Severe diarrhea and corrosion of perianal area can cause fistula(most common complication) Intestinal obstruction Nutrient deficiency VIT B12, fluid imbalance Ulcerative Colitis Causes Unknown Signs and Symptoms Abdominal Cramping, Nausea, Vomiting, Diarrhea Fever or Weight Loss Treatment Follow general treatment guidelines. An inflammatory disease that spans the entire length of the colon. It starts from the rectum spreads upward to involve the sigmoid and descending colon Etiology is unknown but may be related to immune response in the GI tract genetics Pathophysiology Starts from the rectum and lower colon proximally affecting the mucosa to submucosal layer mucosa develops diffuse ulceration with hemorrhage, congestion and edema inflammation causes pinpoint mucosal bleeding and suppurate(crypt abcesses) becomes necrotic and denuded areas as a result of inflammatory process, tongue like projections that resembles into polyps repeated episodes will result to thickening of the bowel and loss of the haustral folds Signs and symptoms recurrent bloody diarrhea with pus and mucus with tenesmus- 20x/day LLQ colicky pain N/V, Anemia, Fever Diagnostic exams FOBT Small bowel x-ray- ulceration, stiffening, irregular mucosa Barium enema- strictures, narrowing Biopsy- granulomas

Decreased hemoglobin, K, Ca, Mg, Elevated WBC Treatment Corticosteroids to reduce inflammation Sulfasalazine- has anti inflammatory and antimicrobial properties Anti diarrheals like diphenoxylate Iron supplements Anti spasmodics Nursing interventions Provide appropriate nutrition while reducing bowel motility Provide TPN HIGH CHON, CALORIC DIET Low residue diet(low fiber, no milk products Omit gas producing foods Weigh patient daily Monitor and record stool characteristics Surgeries repair bowel perforation, fistula and intestinal obstruction Crohns- colectomy with ileostomy Ulcerative colitis- performed when patient has massive dilatation of the colon (toxic megacolon), does not respond to drugs or the symptoms are unbearable Proctocolectomy with ileostomy, pouch ileostomy KOCK POUCH Intestinal obstructions Interference with the normal peristaltic movement of intestinal contents due to the neurogenic or mechanical impairment Types of intestinal obstructions mechanical- physical blockage of the passage of intestinal contents with the subsequent distention by fluid and gas caused by adhesion, hernias, volvulus, intussusception, IBD, foreign bodies, strictures, fecal impaction Post-op adhesion- after abdominal surgery, when some area of the abdomen may not completely healed and loops of the intestine become adherent and may

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cause kinking of an intestinal loop-3rd-4th day post-op Intussusception- condition in which one part of the intestines slips into another part located below (telescoping) Volvulus- life threatening obstruction in which the bowel is twisted upon itself and the intestinal lumen is obstructed. The accumulation of gas and fluid in the trapped bowel leads to necrosis, perforation and necrosis 2. Paralytic ileus- neurogenic/adynamic ileus- obstruction results from neurogenic or muscular impairment of the peristalsis which results to inability to propel the contents along the bowel in the interference of the blood supply to the intestine resulting to dcreased or absence of peristalsis Causes: abdominal surgery, peritonitis, shock, burn, toxic conditions 3. Vascular obstruction- interference with the blood supply to a portion of the intestines resulting in ischemia or gangrene of the bowel Causes: embolus, atherosclerosis The major effects of intestinal obstructions are abdominal distention, loss of F&E , strangulation, gangrenous changes and ultimately perforation of the bowel Signs and symptoms 1. Small intestines- non fecal vomiting, colicky intermittent abdominal pain 2. Large intestines- cramp like abdominal pain, occasional fecal type vomitus, unanble to pass flatus or stool 3. Abdominal distention- rigidity, high pitched bowel sound above the level of obstruction, decreased or absent bowel sound distal the obstruction Dx exams Flat plate xray of abdomenpresence of gas and fluid Increased hct- dehydration Decreased serum Na, K, Cl- may indicate small bowel obstruction Management

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Decompression Monitor F&E balance NPO with IVF replacement Fowlers position to alleviate pressure in the diaphragm and encourage nasal breathing to minimize swallowing of air and further abdominal distention Measure abdominal girth and assess signs of peritonitis Surgery- incision of the cause to relieve obstruction and remove ischemic bowel to reestablish bowel patency (bowel resection and colostomy) HERNIAS Abnormal protrusion of an organ or structure, fissure, part of an organ from its normal cavity through an abnormal opening/weakened area/congenital/acquired weakness of abdominal musculature Types of hernias reducible- can be manually placed back into the abdominal cavity Irreducible/incarcerated- cannot be manually reduced and which the intestinal flow may be obstructed completely Strangulated- not only are the contents irreducible but the blood and intestinal flow through the intestine in the hernia is stopped completely 4. Inguinal hernia direct- passes through the posterior inguinal wall. More common in males and harder to repair than indirect hernia. Believed to be hereditary Indirect- most common type of hernia. Due to the weakness of the abdominal wall where the spermatic cord in men and round ligament in women, through this opening, the hernia extends down the inguinal canal into the scrotum or the labia 5. Umbilical hernia- most found in children but also common in obese women as the protrusion in the umbilicus. Result of the failure of the umbilical orifice to close. 6. Ventral or incisional hernis- occurs at the site of previous surgical incision in

which the drainage is necessary resulting to inadequate healing. Weakened by infection, a slight bulge will result to a definite hernial sac 7. Femoral hernia- appears below the pouparts ligament below the groin as a round bulge. More common in women due to the changes in pregnancy Signs and symptoms 1. vomiting, protrusion of involved area (more obvious when coughing or straining or lifting) and discomfort at the site of protrusion 2. Crampy abdominal pain and abdominal distention if it is strangulated with a bowel obstruction Management 1. Manual reduction- use of truss 2. Bowel surgery if strangulated 3. Herniorrhaphy- surgical repair of the hernia by suturing the defect Postpone the operation if the patient has cough or colds Post op- elevate the scrotum by a rolled towel and ice pack for 20 minutes to relieve swelling and pain Use of jock strap for support and comfort Splint the incision when coughing Report any drainage from incision Diet modification- high fiber diet Limit activities for 7 days and no heavy lifting for 6 weeks Intussusception Volvulus Adhesions HERNIAS Abdominal truss Umbilical hernia Anorectal Disorders Hemorrhoids Pathophysiology Mass of swollen veins in anus or rectum Idiopathic Signs and Symptoms Limited bright red bleeding and painful stools

Consider lower GI bleeding Rectal Fissure Ulceration or tear of the lining of the anal canal usually on the posterior wall Acute fissures occur as a result of excessive stretching and possibly from the passage of hard stool through the area Management Keep the stool soft by using Metamucil, mineral oil or Colace as prescribed Clean the area after defecation Hot sitz bath to aid healing and relieve pain Suppositories with local anesthesia Rectal abcess With Most abcesses starts as cryptitis with the formation of cysts that extends though the tubular ducts into the submucosal space May also originate from the abrasions of local tissues with the entry of virulent organisms MANAGEMENT- draining the abcess Rectal Fistula A sinus tract that develops between two body cavities or between a body cavity and external environment A chronic condition where a rectal fistula develops a tract that leads from the anal canal to the skin outside the anus . Management- Surgery is the only cure leaving it open to heal by granulation Colon Cancer Usually caused by adenocarcinomas Most tumors are found in rectal area, sigmoid and descending colons Risk factors Family hx of colon cancer, familial polyposis Age greater than 40 Hx of IBD High fat, low residue, high refined foods

Living in industrialized, urban societies Signs and symptoms Ascending colon (right)- occult blood in stool, anemia, anorexia and weight loss Abdominal pain above umbilicus, palpable mass in the area Distal colon and rectal area Hematochezia, change in bm, pencil or ribbon shaped stool, tenesmus, pain below the umbilicus Dukes classification of colon CA STAGE A- confined to bowel mucosa- 80-90%, 5 year survival rate STAGE B- invades muscle wall of the colon STAGE C- lymph node involvement STAGE D- metastasis , less than 5%- 5 year survival rate Surgeries Hemicolectomy for ascending and transverse colon APR or Miles Surgery For recto sigmoid cancer- this surgery involves 2 incisions to remove the sigmoid, perineal incision to remove the rectum T-binder to secure perineal dressing Requires permanent colostomy Pre op Bowel prep by administering oral cathartics, antibiotics like neomycin or sulfonamides 24 hrs pre op Low residue diet for 3-5 days, clear liquid 24 hrs pre op Administration of bowel enema Correction of anemia Post op Kinds of colostomies Ascending colostomy- stoma is on the right side Fecal drainage is watery Transverse or double barrelled colostomy-

Two stomas- right side or proximal stoma drains semi formed stool Left side or distal stoma drains mucus Descending or sigmoid colostomy Stoma is on the left side of the abdomen Fecal drainage is well formed COLOSTOMY SITES Monitor the stoma- it must be red and moist Report immediately if it turns dusky or dark It should protrude - inch over the abdomen Monitor colostomy output and care for the incision site Patient may remain in gastric suction for several days until peristalsis returns Flatus and fecal drainage usually begins 3-7 days Empty the pouch when 1/3 to full of stool to prevent leakage Use skin barrier like karaya powder Colostomy irrigation It is being done to promote peristalsis initially then to promote evacuation of feces on a regular interval Irrigating solution should be 12-18 inches above the stoma using 500-1000ml NSS OR warm tap water Lubricate catheter before inserting it 2-4 inches without force and allow it 510 minutes while massaging abdomen gently for better cleansing Foods that reduce odor- yogurt, parsley, green beets Foods that form foul odor- dairy products, fish, cabbage, celery, cauliflower, nuts, highly seasoned foods Place deodorant tablet or mouthwash or charcoal in the pouch Rinse pouch in weak vinegar solution A colostomy pouch is normally emptied one or more times daily.

The pouch itself usually needs to be changed every four to six days The stoma and surrounding skin need to be kept clean and sanitary Colostomy pouches may be either open ended or closed. Open-ended pouches require a clamp for closure. They can be drained simply and reused after they are emptied. Closed pouches are sealed at the bottom and are usually used by patients who irrigate their colostomies or who have a regular bowel elimination pattern Functions of the liver Glucose metabolism Ammonia conversion Protein metabolism Synthesizes almost all plasma proteins except gamma globulin Needs Vit K in synthesis of prothrombin and some clotting factors Amino acids are building blocks for protein synthesis Fat metabolism Vitamin and Iron storage Vitamin A, B and D Vitamin B complex vitamins Iron Drug metabolism May affect activity of the medication may need conjugation with some compounds to become more soluble. *Liver function is complex and any dysfunction affects all systems of functioning in the body * It is considered a chemical factory where it manufactures, stores, synthesize, stores substances needed in metabolism Liver disorders Result of viral infection Exposure to toxic substances

 Biliary Obstruction Assessment Health history Exposure of patient to hepatotoxics or infection Occupation, social activities family lifestyle/background and Travel history Hx of Alcohol or drug abuse/medications Past medical history Diagnostics Liver function tests serum enzyme activity serum concentration of proteins * serum aminotransferases- denotes injury to liver cells, and hepatitis ALT, AST, GGT most common C T Scan, MRI Ultrasonography, Liver biopsy Physical assessment Pallor Jaundice (skin, mucosa, sclera) Muscle atrophy ( extremities) Skin excoriations, itching, ecchymosis, palamar erythema, spider angiomas Male patient assessed for testicle atrophy Mental clarity (recall, memory Neurologic (tremor, slurred speech, asterixis) Hepatic dysfunction Maybe acute or chronic, chronic more common (cirrhosis 40% related to alcohol)

Disease process leading to hepatocellular dysfunction may be caused by infectious agents, medications, metabolic disorders etc. most common to tissue damage is malnutrition especially related to alcoholism Parenchymal cells protective response is replacing glycogen with lipids resulting to fatty infiltration Resulting into shrunken, fibrotic liver if not necrosis. signs and symptoms: Jaundice = bilirubin concentration in the blood Portal hypertension, ascites, and Varices due to circulatory changes w/in the diseased liver Nutritional difficiencies due to inability of the liver cells to metabolize Hepatis encepalopathy ammonia HEPATITIS Inflammation > Liver damage Caused by infection, drugs, alcohol Chronic, Acute Hepatitis A (infectious hepatitis) Most common Fecal oral route Contaminated food, water Oral anal sexual practices S/s low grade fever, nausea, fatigue, hepatomegaly Tx rest, ^ CHO diet HEP B (serum hepatitis) DNA virus, contaminated blood, Semen saliva Tendency to go chronic > cirrhotic > Ca s/s jaundice, hepatomegaly, pale stools, lethargy, nausea Tx rest, nutrition, no alcohol Hep C Extra hepatic disease Transfer from mother to baby

IV drug use, multiple blood transfusion Tendency to go Chronic > CA Hep D IV drug use Transmission parenteral co infects with HVB to replicate Hep E Water borne Fecal oral Resemble HVA No chronicity Drug Induced Hepatitis Adverse reaction to drugs > damage of hepatocytes Fulminant Hepatic Failure Massive liver death following acute hepatitis Confusion, ascites, coagulation problem, shrinking of liver Mx liver transplant CIRRHOSIS extensive scarring - caused by irreversible reaction to inflammation Degeneration > destruction of hepatocytes tissue becomes nodular > blocks bile ducts and blood flow. Flow alteration caused by compression and proliferation of fibrous tissue Types: Alcoholic scar tissue surrounding the portal areas. Caused by alcoholism (most common type of cirrhosis) Post necrotic caused by previous bouts of acute viral hepatitis. Broad bands of scar tissue Biliary Cirrhosis scarring occurs around bile ducts .. May be caused by chronic biliary obstruction or biliary infection Medical management Antacids, H2 R antagonist minimize gastric distress spironolactone ascites

sylimarin anti oxydant- improve liver function Nursing Rest reduce demands on the liver > increase blood supply. May resume after nutritional status improves Hi protein diet ?? High CHO, restricted sodium Skin care no soap, no tapes..lotion Risk of injury Complications (liver disease) Manifestations Portal Hypertension Ascites Esophageal/Gastric Varices Hepatic Encephalopathy hemorrhoids Jaundice Hi bilirubin concentration in the blood Obstructive Jaundice- caused by an occlusion in the bile duct with stones, inflammation, tumor, pressure from another organ. Portal hypertension ascites Increased girth Increased weight Striae , distended veins fluid electrolyte imbalance Presence of fluid wave Medical management Dietary modification ( sodium restriction) Use of diuretics Bed rest Paracentesis PVS Nursing management Teaching patient self care Diet (low sodium) Abstinence from alcohol Medications (diuretics)

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Weights and girth Skin care, Bed rest Esophageal varices Medical Sclerotherapy injecting an sclerosing agent to promote thrombosis and eventual sclerosis via endoscopy Esophageal Banding Bleeding varices: balloon tamponade Hepatic encephalopathy (PSE) Life threatening complication of liver failure associated with accumulation of ammonia and other toxic metabolites in the blood Onset is insidious and subtle asterixis (flapping tremor) liver flap Fetur hepaticus sweet, slightly fecal odor acetone breath Management: Medical eliminating precipitating cause (lactulose ) via NGT or rectal - IV glucose , antibiotics Nursing- monitor mental status I & O, watch out for dehydration Vital signs low protein diet

Bile enters the Gall Bladder in between meals when the sphincter of Oddi is closed People at Risk (4 Fs) Female Fat Forty and above Fertile Clinical Manifestations Presence of murphys sign Pain and biliary colic Jaundice and pruritus Changes in urine and stool color Vitamin deficiency due to interference of absorption of fat soluble vitamins A,D.E.K Cholecystitis Pathophysiology Inflammation of the Gallbladder Cholelithiasis Bacterial infection Acalculus Cholecystitis Burns, sepsis, diabetes Multiple organ failure Gall Stones Pigment stones Cholesterol stones Management ESWL ERCP with Basketting Cholecystectomy CBDE with T-Tube LAP CHOLE T-tube Pancreas Has exocrine as well as endocrine functions Acinar cells -exocrine portion of the organ.(99%) secrete pancreatic juice consisting of digestive enzymes, sodium bicarbonate and water

Gall Bladder Pear shaped sac like located in a depression in the posterior surface of the liver 3-4 in. long (7.5-10cm) Can hold 30 50 mls of bile Connects to the CBD thru the cystic duct functions A storage reservoir for bile

The remaining 1% make up the endocrine portion cell clusters are called Islets of Langerhands composed of alpha, beta, and delta cells. beta cells - secreting insulin Alpha cells - glucagon, Delta cell - somatostatin, Neural and hormonal stimulation of pancreatic juice secretion Pancreatitis Signs & Symptoms Mild Pancreatitis Epigastric Pain, Abdominal Distention, Nausea/Vomiting Elevated Amylase and Lipase Levels Severe Pancreatitis Refractory Hypotensive Shock and Blood Loss Respiratory Failure Common causes: Alcohol abuse, gallstone Assessment LUQ Pain- starts with midepigastrium with radiation to the back, flanks and substernal area Nausea and vomiting Severe dehydration Steatorrhea due to excretion of undigested fats Elevated serum amylase and lipase Hypocalcemia- Ca binds with undigested fats and it is lost in steatorrhea Hyperglycemia Post hemorrhagic necrosis- purplish discoloration- cullens sign-{ periumbilical area} and turners sign {flanks} Management Relieve pain NPO during acute phase, then bland low fat diet Antimicrobials to prevent infections, PPI, H2Blockers, antacids Ca supplement Insulin

Eliminate alcohol pancrelipase (Creon-10, Pancreatin,Pancrease, Viokase) Pancreatic enzyme replacement Treatment of malabsorption Often used with cystic fibrosis patients Can be taken before or with meals