Nutrition Notes - Nutrition-Metabolic Problems...

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Unformatted text preview: Nutrition-Metabolic Problems Gastritis (1011-1014) - inflammation of gastric mucosa (stomach), in which the mucosa becomes edematous and hyperemic (congested with fluid and blood), leading to superficial erosion - gastritis may be the 1st sign of acute systemic infection Acute Gastritis - inflammation of the superficial lining (top layer) of the gastric mucosa (doesn't not affect muscle layers) and may last several hourseveral days. usually recover in 1 day - Causes of acute gastritis: local irritants like caffeine, stress, smoking, alcohol, excess aspirin intake, bacterial endotoxins (H Pylori), bile reflux, highly seasoned foods, and radiation therapy. Risk of perforation s/s: abd. Discomfort, anorexia, headache, lassitude (tiredness, lethargic), mild epigastric distress, belching, heartburn after eating, N/V, hematemesis (blood), hiccupping o Some have no symptoms. Can lead to peritonitis if it perforates o scaring can cause stenosis, resulting in GERD (impaired emptying) - - Diagnosis of acute gastritis is made by endoscopy (can biopsy), upper GI series (biopsy), H Pylori test, 1 min. ultra rapid urease test, breath test, serum test for H plyori - Treatment of acute gastritis: mucosal protect agents (Cytotec, Carafate), antacids (Aluminum Hydroxide); avoid alcohol and food until symptoms subside. Patient may need to be NPO if bad enough. o When able to eat again, begin with bland diet (noodles, mashed potatoes, fruit cocktail) o If bleeding occurs (ulcer formation), NG tube may be needed to decompress stomach. Get dr. order first o Analgesics, IV fluids, monitor electrolytes and I&O o If there are multiple attacks of acute gastritis (in 1 year), scar formation and stenosis can occur in pylorus, which can lead to GERD Chronic Gastritis - Causes: may be due to infections (H Pylori treatment = antibiotics) or an autoimmune disorder (Pernicious anemia because stomach atrophies and fails to secrete intrinsic factor responsible for absorption of Vit B12), dietary factors such as caffeine, use of meds (NSAIDS), alcohol, smoking, tumors, or reflux There is a link between H Pylori and adenocarcinoma of the stomach. Erosion of stomach lining causes the mucous protection of the stomach to be gone. Progressive thinning and degeneration of the gastric mucosa irritates the muscular layer (may lead to ulcer formation) S/S: ; epigastric discomfort, anorexia, anemia (from bleeding), B 12 def (may need B12 injections), sour taste in mouth, heartburn, N/V Treatment of chronic gastritis o Treat the cause (H Pylori) with antibiotics (tetracycline or amoxicillin combined with clarithromycin. Teach to complete full course of therapy) o Promote rest/ teach patient how to reduce stress (imagery, deep breathing) o Change diet. Stop smoking. Avoid alcohol and caffeine o Proton Pump Inhibitors(prevacid and pecid, Aciphex) o Bismuth (Pepto) - 1 o AVOID ASPIRIN o May need B 12 injections for Pernicious Anemia - Diagnosis of chronic gastritis: Altered Nutrition (from nausea and irritation): less than. Pain. Knowledge def. Anxiety, risk for imbalanced fluid volume Assessment: ask pt what triggers it, s/s, family history of GI disease, heartburn, indigestion, N/V, or constipation and for how long?, specific time of day, B4 or after meals, recent change in weight, anxiety, stress, how are symptoms relieved, history of previous gastric disease or surgery, food diary (past 72 hours), last BM (listen to bowel sounds) Nursing management of Chronic Gastritis o Reduce anxiety answer questions, therapeutic touch, teach relaxation, prepare for diagnostic studies, explain all procedures - o Manage symptoms N/V, and heartburn o Promote fluid balance monitor fluid and electrolytes and I&O, detect early signs of dehydration. If food and fluids withheld, IV fluids. Minimal urine output of 30 ml/hr and minimal intake of 1.5L/day o Teach to avoid irritating food/fluids by mouth for a few days until symptoms subside o Pain relief (Table 371, pp 10131014) o Antibiotics and Bismuth salts o Tagament, Zantac, Pepcid, Prilosec (to decrease acid) o ALWAYS DOCUMENT TEACHING! GERD - excessive backflow of gastric or duodenal content into the esophagus - Causes: decreased lower esophageal sphincter pressure (normally, pressure increases when food passes through. With lower pressure, food refluxes), incompetent sphincter, pyloric stenosis (due to scarring) Risk factors: alcohol, overweight, pregnancy, smoking S/S: dental erosion, pyrosis (heartburn), dyspepsia (indigestion), regurgitation, dysphagia, esophagitis, heartburn and chest pain (mimics heart attack), hypersalivation, Management of GERD: o Low fat diet. Maintain normal weight o Teach to avoid situations that decrease lower esoph. Sphincter pressure or cause esoph. Irritation (alcohol, caffeine, tobacco, beer, milk, food containing spearmint or peppermint, carbonated drinks, eating 2 hours before sleep, tight fitting clothing o Elevate HOB with 68" block. Remain upright at least 1 hour after eating. Eat sm. Freq. meals. Elevate upper body with pillows Meds for GERD o Antacids and histamine blockers o Prevacid, Aciphex (PPI's that decreases gastric acid; also predisposes you for infection because of decreased acid) o Reglan and Urecholine (prokinetic agents that accelerate gastric emptying). Reglan has CNS complications with long term use. - - Surgery for GERD : Fundoplication wrapping of a portion of the gastric fundus around the sphincter of the esophagus to increase pressure (done by laparoscopy). This decrease the risk of reflux. Patient comes back with several abdominal incisions! - TEACH MEDS! 2 Peptic Ulcer Disease - Excavation (hollowed out area) that forms in mucosal wall of the stomach in the fundus, pylorus, duodenum or esophagus. Damaged mucosa cannot secrete enough mucous to act as a barrier against HCL. Can lead to bleeding and perforation (leads to peritonitis med emergency!) - Causes of PUD: erosion caused by increased concentration or activity of the acid Pepsin, or by decreased resistance of the mucosa. Most ulcer occur in the duodenum because bile and pancreatic enzymes are released here Contributing factors: stress/anxiety (teach ways to destress), H. Pylori, chronic use of NSAIDS (inhibits mucosal secretions, decreasing protection and predisposing pt. to ulcers), family history, excessive secretion of HCL(milk, caffeine, smoking (decreases secretion of HCO3 from pancreas into duodenum area will be more acidic), alcohol (increases HCL), Type O blood, ages 4060 (most common), least common in women in childbearing ages because of estrogen and progesterone (decreases acidic secretions) - - S/S: dull, gnawing pain or burning in midepigastrium or in the back (referred pain experienced in area that is not the source). Pyrosis (heart burn), vomiting (if GI bleed from severe erosion), constipation/diarrhea (because of meds and change in diet), belching, dark, tarry stools (the darker the color the higher up the bleed) Nursing Management of ulcers o If bleeding ulcer, insert NG to decompress (NPO). Get Dr. order first. Highfowlers if awake and alert; side lying for coma o Start IV, fluids o Monitor H&H (very impt. to refer to most recent) o Urinary catheter (monitor I&O) o Vitals (look for decrease in BP and increase in HR for signs of bleeding) - - Major goals of treatment with ulcers: o Prevent aspiration o Monitor for hemorrhagic shock (pale, cool, moist skin, decrease BP, increased HR). **report tachycardia, hypotension o Monitor I and O - Diagnosis of PUD made by endoscope Nursing Dx: pain, anxiety, imbalanced nutrition (more or less depending on type) Complications of PUD o Hemorrhage correct blood loss to prevent shock o Perforation erosion of ulcer thru gastric serosa into peritoneal cavity without warning (persistent pain followed by dysphagia. Possible fever, leukocytosis, and severe hypotension may occur) Tx of perforation: antibiotics to decrease risk of infection, NG tube (may need parenteral nutrition), and NPO o Penetration erosion of ulcer thru gastric serosa into adjacent structures (pancreas) o Pyloric obstruction s/s include N/V, distended abd with abd pain Interventions for PUD: relieve pain, reduce anxiety, maintain nutrition Medical management of PUD: o Eradicate H pylori with antibiotics 3 o Manage gastric acidity with Histamine blockers and Antacids (Zantac, Tagament, Pepcid, Axid) - S/S of gastric ulcer: burning in epigastric area that usually occur 30 min1 hr after eating, food worsens symptoms, vomiting may ease discomfort (may lose weight), pyrosis (heart burn); heal slower because of position o Causes of gastric ulcer: H pylori, gastritis, alcohol, smoking NSAIDS, stress S/S of duodenal ulcer: cramp like pain on empty stomach (usually 23 hours after eating), food relieves symptoms because it neutralizes acid, often occurs at night with gastric pain, may gain weight, pyrosis (heart burn) more likely to perforate (risk for peritonitis). May complain of sharp, localized tenderness when applying pressure to Right Midline o Causes of duodenal ulcer: H pylori, alcohol, smoking, cirrhosis, stress Tx of ulcers caused by H pylori: antibiotics, PPI's, bismuth salts. All other ulcers and NSAID induced ulcers: H 2 antagonists and PPI's Patient Education for Peptic Ulcer Disease: o Adhere to med regiment. o Teach to rest and reduce stress. o Stop smoking o Diet: NPO during acute attack, then clear liquids, then bland diet (mashed potatoes, noodles, fruit cocktail). Teach to eat 3 meals per day. o Avoid extremes in temp, meat extracts, alcohol, caffeine, milk, chocolate, or tea. Eat small, frequent meals o May be on maintenance dose of H2 antagonist for 1 year - Surgical Management of Peptic Ulcers: recommended when ulcer fail to heal after 1216 wks of medical treatment o Vagotomy sever vagus nerve to decrease acid production o Pyloroplasty incision made in pylorus to enlarge/widen outlet and relax muscle (usually done in conjunction with Vagotomy) o Bilroth I removal of antrum of stomach (the eroded part), then reanastomose small portion left with the duodenum (sm. Intest) o Bilroth II same as Bilroth 1, except reanastomose with jejunum in both I and II, the pt is left with small stomach (gets full quicker, small meals) Complications of Gastric Surgery: o Hemorrhage assess pt frequently. Monitor vitals. Look for s/s of shock (major drop in BP, tachycardia, tarry stools). Monitor H and H, test stool for occult blood, I and O hourly Management of GI Bleed: - insert IV for fluid and/or blood monitor H&H insert NG admin. Room temp lavage of saline or water insert indwelling urinary cath monitor vitals and o2 sat and administer oxygen 4 - place patient in recumbent position with legs elevated to prevent hypotension, or to prevent aspiration, place on left side treat hemorrhagic shock Complications of Gastric Surgery Continued o Perforation and penetration requires immediate surgery o Pyloric obstruction N/V, constipation, epigastric fullness, anorexia, and later, weight loss 1st insert NG. aspirate fluid (more than 400 greatly suggest obstruction). Upper GI study or endoscopy to confirm. Balloon dilation may be needed o Bile Reflux burning epigastric pain and vomiting of bilious material Treated with Questran, antacids, and/or Reglan Teach to eat small, frequent meals with HOB elevated. Sit up after o Dumping Syndrome fullness, weakness, fainting, dizziness, palpitations, diaphoresis, cramping and diarrhea. Later, rapid increase in blood glucose (increased insulin eventually leads to hypoglycemia) food goes straight thru pt. To delay stomach emptying, low fowlers during mealtime, after lie down 2030 min, antispasmodics, fluid intake with meals is discouraged (make have fluids 1 hour before or after meals), meals should contain more dry items than liquid items, eat fat as tolerated but keep carb intake low, - eat small frequent meals, and dietary supplements and vitamins, vit. B 12 injections may be prescribed Nursing Management of PUD o Pain management (teach how to use PCA pump) o Teach med reg and how to splint with pillow when coughing (always treat pain first). Encourage family to let patient control pump. Teach dietary restrictions and smoking cessation. o Monitor for complications. Monitor Bowel sounds (usually hypoactive postop. make sure to listen 35 min. may be absent for 48 hours. After 48 hours, abnormal. report o Do not palpate abdomen! o Monitor incision site for infection. Makes sure edges are approximated Hiatal Hernia - opening of diaphragms where esophagus passes becomes enlarged (normally is tightly closed) and part of upper stomach moves up into lower portion of thorax. Weakness in muscle allows stomach to budge - Risk Factors: more in women, overweight, smoking, trauma, straining, increased abd. Pressure from coughing, pregnancy and delivery, excessive weight gain, over 50 (the aging process in general) - Potential complications: o Strangulation tissue death due to lack of oxygen o N/V, unable to have BM Diagnostic studies: confirmed by Xray, barium swallow under fluoroscopy - Sliding Hiatal Hernia (at least 50% asymptomatic) - Upper stomach and gastro esophageal junction are displaced upward and slide in and out of the thorax. The sphincter no longer is in tact. There is decreased sphincter pressure because it is displaced. 5 - S/S: heartburn, regurgitation, reflux, dysphasia Reflux can be treated with meds Treatment: like GERD (sm. Freq. Meals. Elevate HOB on 48" blocks. Don't recline 1 hr after eating) - Para esophageal Hiatal Hernia - More of a concern than sliding (risk of hemorrhage, obstruction, and strangulation pain and tissue death), but less common. Occurs when all or part of the stomach pushes through diaphragm beside the esophagus. The sphincter remains in place (so there is not reflux), but the stomach is pushed upwards - S/S: sense of fullness after eating (may be asymptomatic b/c part of stomach is displaced) Treatment: Emergency Surgery to correct twisting/strangulation (leads to restriction of blood flow) Peritonitis - inflammation of peritoneum (thin membrane lining abd wall and covering most organs) - Causes: stomach perforation, ruptured appendix, bacterial infection (E Coli), peritoneal dialysis, anything that causes rupture or leak of bacteria into peritoneal cavity Risk Factors: liver disease, kidney or lung damage, fluid in abd, compromised immunity, pelvic inflamm disease, appendicitis, stomach ulcers, torn or twisted intestine, inflamed gallbladder, trauma S/S: tender, rigid abd; extreme pain, tender to touch (rebound tenderness), pallor, cold, clammy skin, sweating, elevated temp, decreased BP, and tachycardia (from infection can become septic). Absent or diminished bowel sounds (may be hypoactive early). o Put NG to decompress anything in the stomach (decreases risk for infection) o Observe for N/V and foul smelling emesis (signs that indicate need for NG) o Observe for s/s of dehydration (oliguria, thirst, dry, swollen tongue) - Complications: sepsis (priority), shock, wound evisceration (apply moist, sterile dressings, stay with patient, monitor, have another nurse call DR), abscess formation - Treatment of Peritonitis o Fluid and electrolyte replacement are the major focuses of management. Of peritonitis. o Analgesics and antiemetics. DO NOT PALPATE ABDOMEN! o Side lying position is the best for comfort (have them bend knees to decrease stress on stomach) o Monitor I&O and vitals. o NG tube to suction: o Massive Antibiotic therapy to treat infection o Listen to bowel sounds (should return in 48 hours, but may be hypoactive) o Oxygen therapy o Surgery (Incision and Drainage) to drain and repair. Come back with drains o NPO until bowel sounds return. Once returned, start on clear liquids, then progress according to pt. tolerance Nursing Management of Peritonitis o Position: side lying (fetal) or semifowlers. o Assess pain and GI function, vitals, and F/E balance (I and O) 6 o Not amount and character of drainage form drains (document). Postop drainage expected to be serous (bloody). As healing begins, it becomes more serosangeneous (pinkish). Amount should decrease daily. If any abnormal drainage, take a specimen (don't need Dr. order for this) o Monitor H&H for signs of bleeding o Make sure pt is passing gas. Abdomen should return to soft and nontender within 48 hours o Signs that indicate peritonitis is subsiding: decrease temp and pulse, softening of abd., return of peristaltic sounds, passing of flatus, and bowel movement. o Increase fluids and food gradually and reduced parenteral fluids as ordered. Gall Bladder - located under right lobe of liver' active storage shed and digestive organ that absorbs mineral salts and water from liver and converts it to bile (holds about 50 mL of bile) - Role: stores bile, emulsifies fat, and releases bile when food passes to duodenum to help aid digestion. Also aids in absorp of fatsol vit. (A D E K) When food enters duodenum and mixes with chyme, the sphincter of Oddi relaxes, allowing bile to enter intestines. This response is mediated by secretion of CCKPZ (bile breaks down fat) If the flow of bile is impeded, bilirubin does not enter the intestines. As a result, bilirubin levels increase When stone becomes lodged in gall bladder, bile can't leave and the gall bladder becomes inflamed. Bile returns back to liver where it is produced, and it begins to circulate in the blood (pt. appears jaundice and has clay colored stool) Cholecystitis inflamm of gallbladder that can result in edema and perforation Cholelithiasis gallstones (pigment or cholesterol) See risk factors (p 1127 chart) Choledocholithiasis stones in common bile duct Risk factors for Gallbladder Disease - obesity, multiple pregnancies, frequent changes in weight, high or low dose estrogen therapy, such as oral contraceptives (increase biliary cholesterol saturation), rapid weight loss, cystic fibrosis, diabetes, ileal resection or disease Manifestations of GB disease: jaundice, bulky, foul smelling, clay colored stool, steatorrhea, steady pain in upper abd (usu. After fatty meal), referred pain between shoulder blades (biliary colic), pain under right shoulder, attacks often occur at night, vit K def (risk for bleeding), abd bloating, colic (N/V), belching, gas, indigestion, Diagnostic Studies for GB disease: - Ultrasound diagnostic procedure of choice; detects stones and clogged bile duct. NPO after midnight to give gallbladder time to fill (more visible). When we eat, the gallbladder is stimulated and it empties. o Can be used in pts with liver dysfunction and jaundice - Radionuclide imaging or cholescintigrapy diagnosis of acute Cholecystitis; radioactive agent admin. IV, biliary tract scan; expensive, takes longer; cannot detect gall stones - Cholecystography not useful in jaundice b/c pt can't rid of dye (check iodine allergies); contrast agent admin. Orally 1012 hour before. Assess allergies. 7 - Endoscopic retrograde cholangiopancreatography (ERCP) dye injected into biliary tract by needle inserted into liver (biliary tree); bile is aspirated. o Liver is highly vascular so watch for bleeding**look at bleeding studies (PT, PTT, and INR) before procedure o Multiple position changes - Percutaneous Transhepatic Cholangiography dye injected into biliary tract; the entire length of common bile duct, cystic duct and gallbladder is outline clearly; can be used with liver dysfunction and jaundice; moderate sedation, NPO. ASSESS BLEEDING STUDIES BEFORE. BROAD SPEC ANTIBIOTICS ADMINS. BEFORE - WBC elevated and ph elevated (alkaline) Medical Management of GB disease: - Ursodeoxycholic Acid and Chenodeoxycholic Acid/chenodiol inhibit synthesis and secretion of cholesterol (612 mo of therapy are required usually) - Lithotripsy repeated shock waves break up stones; fragments removed by endoscopy, or are dissolved by bile acid orally. Particles are excreted as waste in the stool Dissolution therapy meds to break up/dissolve gallstones ERCP direct visualization by endoscope inserted into esophagus to descending duodenum. (bleeding studies before) o NPO, moderate sedation, can extract stones if present o Multiple position changes o Pigment stones cannot be dissolved. Only cholesterol stones Surgical Management of GB Disease - Lap Cholecystetomy small incision thru abd wall into umbilicus; cavity filled with CO2 to assist in insertion; several additional punctures are made (lap sites X 45) - T Tube inserted along bile tract when gall bladder is removed to drain into a bag (dark green in color). Acts as a stint (left in place until bile excess is out). o Make sure tube is patent; meticulous skin care around site (bile is alkaline, but can eat way skin). Record output. Encourage pt not to touch site. Physician removes T tube - Open cholecystectomy removal of gallbladder (bile salts will not go straight to duodenum) Nursing Care after Gall Bladder Surgery - pain relief. Demerol is drug of choice. Comfortable positioning focus on bowel sounds (expect to be absent or hypoactive initially) Assess lap sites. Monitor for infection. Will have sutures. Do not palpate abd! Antibiotics Monitor urine color (improvement if urine not green) and stool (improvement if not clay colored, should be brown) Encourage pt to TC and DB (teach how to splint and give pain meds before Diet: low fat (cooked fruits, rice or tapioca, lean meats, mashed potatoes, non gas forming veg., bread, coffee, or tea as tolerated. Avoid eggs, cream, pork, fried foods, cheese, and rich dressings, gasforming veg. and alcohol Avoid smoking, Aspirin and herbs before surgery (alter coagulation) - 8 - Post op: low fowlers, IV fluids, NG suction, TC, DB, monitor drainage and skin around drains Encourage pt not to flush toilet. Nurse needs to observe urine and stool Pancreas - Exocrine pancreas o Secretes digestive enzymes (amylase, lipase, and trypsin to aid in digestion). Enzymes are high in protein and electrolyte rich fluid. The secretions are alkaline because of their high concentration of bicarb and are capable of neutralizing highly acidic gastric juice that enters duodenum o secretin major stimulus for increased bicarb secretion (smoking decreases bicarb) o cholecystokinin (CCKPZ) major stimulus for digestive enzyme secretion o gastrin regulator of gastric acid secretion Endocrine Pancreas o Responsible for secretion of insulin (beta cells; lowers BS, stores fat, synthesizes protein), glucagon (alpha cells; increase BS) and somatostatin (inhibits release of insulin and gastrin If blood sugar is stable) Pancreatitis - Inflamm. of pancreas, from destructive effects of pancreatic enzymes; increases with age Pancreas secretes digestive enzymes into sm. Intestines thru the pancreatic duct. Normally, digestive enzymes do not become active until they reach the small intestines, where they begin digesting food. But, if these enzymes become active inside the pancreas, they start digesting the pancreas (Auto digestion). The pancreas becomes inflamed and can hemorrhage. Classic signs of pancreatic hemorrhage o Cullen's sign ecchymosis around umbilicus o Grey Turner's sign ecchymosis in flank area Causes of Pancreatitis: alcoholism and gallstones are resp for 80% (alcohol causes hypersecretion of protein in pancreatic secretions, which leads to protein plugs, which clog the pancreatic duct (forms stones and calculi). Other causes may include trauma. Renal failure, cystic fibrosis, shock, and lupus Acute Pancreatitis - Sudden mild to severe pain in upper abd that may radiate to back and occasionally the chest. Pain may be nearly constant for hours or days and typically worsens when consuming alcohol or eating **completely avoid alcohol and remain NPO during acute pancreatitis Bending forward or curling into fetal position may provide temp relief (allow them to position self for comfort) S/S: N/V, fever, rapid pulse, swollen, tender abd. In severe cases, dehydration and low BP, internal bleeding and shock can occur - Chronic Pancreatitis 9 - ongoing damage to pancreas can lead to chronic condition that destroys pancreas and nearby tissues symptoms may not appear for year or may never experience discomfort drinking alcohol or eating worsens symptoms S/S of Chronic Pancreatitis: N/V, fever, bloating and gas, weigh loss (not digesting properly), oily, malodorous stool resulting from poor digestion and malabsorption of nutrient, particularly fats (steatorrhea). Can't break down fats - Diagnostic Studies for Pancreatitis: - ERCP (check coagulation studies before) Blood test o H&H o Amylase/lipase will be 3X normal in 1st 24 hours o Calcium (hypercalcemia is the cause, hypocalcemia is the result (stones build up from too much calcium and calcium cannot be absorbed) o WBC elevated o CT scan (if pt. claustrophobic, admin. Sedative) Management of Pancreatitis - attempt to alleviate fear; administer sedative drug therapy: NPO. Avoid alcohol Avoid morphine! Demerol (meperdine) is drug of choice give antacids low fat diet after surgery give calcium if decreased (monitor for signs of hypocalcemia EKG changes, arrythmias, seizures, + Tross. And Chov signs) IV fluids - - Management of Pancreatitis - attempt to alleviate fear; administer sedative drug therapy: NPO (eating stimulates pancreas) Avoid alcohol. Monitor closely. Gradually put on diet. Check tolerance to diet before discharge. Avoid morphine (causes spasms in sphincter of Oddi)! Demerol (Meperdine) is drug of choice for pain give antacids low fat diet after surgery give calcium if decreased (tetany, arrythmias (EKG changes), + Trosseaus and + Chovecks sign, seizures (signs of hypocalcemia) 0. IV fluids Surgical Treatment for Pancreatitis Laparotomy-surgical opening of the abdomen (cut away necrotic tissue). Pt will come back with TTube (make sure it's patent. Monitor output. Physician will have us clamp tubing when ready to take Ttube out. If patient tolerates meal with T tube clamped, it can be d/c. If N/V occurs, unclamp it. Cholecystectomy removal of gallstones (Taber's pg.404) - 1. 2. 10 3. Transduodenal Sphincterotomy-removal of gall stones in the pancreatic ampula in case of biliary pancreatitis to relieve pancreatic duct; unblock it. ampula 4. 5. 6. Nursing Management with Pancreatitis Pain Management (Demerol) Monitor blood sugars as ordered (endocrine fx of pancreas) 7. Patient Teaching Avoiding alcohol and foods high in fat that cause pain (low fat diet) Overview of the Liver (P1075-1121) The liver is the largest internal organ; very vascular (watch for bleeding with procedures. Check coagulation studies Located in right upper quadrant of the abdomen, beneath the diaphragm It weighs about 3 lbs in the adult It is covered by a connective tissue, known as Glisson's Capsule 8. 9. 10. 11. before!) 12. Dual Blood Supply About 400cc of blood per min enters the liver through the hepatic artery. Another 1000cc per min enters the liver via the valveless portal vein. The hepatic duct from the liver & cystic duct from the gallbladder join to for the common bile duct. This empties into the small intestine. The sphincter of Oddi controls the flow. Major Functions of the Liver Digestive Organ manufactures & secretes bile 13. 14. 15. Endocrine Organregulates glucose & protein metabolism Hematologic Organ iron storage Excretory Organ removes waste from blood stream & secretes them into bile Functions of Liver 1. 2. 3. 4. 5. 6. 7. 8. glucose metabolism ammonia conversion protein metabolism fat metabolism vit & iron storage drug metabolism bile formation bilirubin excretion Digestive Organ Degrades excess nutrients and converts them into substances essential to the body Builds carbohydrates from proteins (carb metab) Converts sugars to fat to be stored 16. 17. 18. 11 19. 20. Stores excess Vit. A, D, E, K and B 12 Secretes bile salts for fat digestion Process and stores fats, carbohydrates and proteins that are absorbed by the intestines. 21. 22. 23. 24. Endocrine Organ Metabolizes glucocorticoids, mineralocoticoids and sex hormones Metabolizes lipid soluble substances that can't be directly excreted by the kidneys toxicity is a potential complication of many medications if liver dysfunction is present, be careful with drugs. Risk for toxicity (Tylenol) Regulates carbohydrates, fat and protein metabolism Because the liver is central to metabolic disposition of virtually all drugs and foreign substances, drug induced liver 25. 26. 27. 28. makes bilirubin soluble, which is then excrete through bile and exits body through stool. If disease is presence, the pt may appear jaundice Hematopoiesis in certain disease states Synthesis of blood clotting factors Hematologic Organ Responsible for temporary storage of blood Synthesis of bilirubin from breakdown products (by product of Hgb). Not soluble when entering liver. But liver acts as a filter and cleanses bacteria that is absorbed through the GI tract Excretory Organ Responsible for detoxification of drugs and other foreign substances Responsible for excretion of bile pigment, excretion of cholesterol via bile, and urea synthesis 29. 30. Urea excreted through kidneys (urea is a by product of ammonia, which comes from protein) Protein is broken down into ammonia in intestines, the liver then converts it to urea...if there is no conversion to urea,then there is an increase in ammonia levels. 31. In this respect, the bile, which carries the end product of substances metabolized by the liver, is much like urine, which carries the body waste filtered by the kidneys. Gerontologic Considerations Steady decrease in size and weight of the liver, particularly in women Decrease in blood flow (doesn't function as well) Decrease in replacement/repair of liver cells after injury Reduced drug metabolism 32. 33. 34. 35. 36. 37. 38. Decline in drug clearance capability (may be incoherent for a longer period of time) Disorders of the Liver Hepatitis A, B, & C (p10941099) Cirrhosis of the Liver 12 Type Incubation period (dormant) Transmission Hep A (most common) 1550 days Fecal/oral Occurs in crowded conditions; poor hygiene, contaminated food, water, or shellfish; oralanal, sex; poor sanitation Signs in restaurant bathrooms to wash hands! Stress hand hygiene, Hep B (vaccine) 28160 days Blood/body fluids Saliva, semen, vaginal secretions; contaminated needles; IV drug abusers; intimate sexual contact; perinatal transmission. Hep B is a major cause of cirrhosis Hep C 15160 days Parental route Through blood & blood products, needles, syringes, sex with infected partner, blood transfusions before 1992, needle sticks. Don't recap needles except when preparing med, not after administering to patient safe handling of food 1) Hepatitis *CAN BE TRANSMITTED DURING THE INCUBATION PERIOD!!! **LAB TESTS: Are the ONLY real distinguishable thing b/t Hepatitis types 39. Hepatitis is defined as an inflammation of the liver, usually viral in nature. Pathophysiology of Hepatitis Widespread Inflammation of liver tissue cause hepatic cell degeneration and necrosis. Distortion of the normal structure of the liver interferes with the flow of blood & bile. Complications of Hepatitis Fulminant hepatitis (page 1101) Necrosis and shrinking of the liver, possibly resulting in liver failure. It is the sudden and severely impaired liver function in a previously healthy person. Viral hepatitis is the most common cause. Will see jaundice and profound anorexia. 40. 41. 42. elderly pt with Hep B are at major risk for fulminant hepatitis. (restricted protein diet) 43. (b/c ammonia (CNS depressant) levels increase), and coma develops.(Fmly. is best to ask about any change) 44. Mortality rate is high. Treatment of fulminate septicemia= liver transplant Develops 68 weeks after initial symptoms, anorexia, and vomiting, abdominal pain, progressive jaundice followed by ascites, GI bleeding, lethargy (due to increased ammonia, causing change in CNS), disorientation, personality changes, confusion Take ALL protein out of diet b/c liver is not metabolizing the protein. **Protein is broken down to ammonia in intestines, then to urea & excreted to kidneys. Diagnostic Test for Hepatitis Preicteric stage (pre-jaundice) 45. Electrolytes: abnormal 46. *anorexia,N/V,fatigue, constipation or diarrhea, weight loss ; RUQ hepatomegaly/splenomegaly 47. 48. Virus and antibodies present in serum. Liver Function Studies 49. (AST, ALT, alkaline phosphatase): elevated 13 Icteric stage (Jaundice) *fatigue, weight loss, lightcolored stools, dark urine (bilirubin circulating in blood), hepatomegaly w/ tenderness;splenomegaly 50. Total, conjugated, and unconjugated serum bilirubin: elevated (liver not conjugating unconjugated hemoglobin) 51. pruritus (itchy skin waste product circulating in blood) pruritus (itchy skin 52. Urinalysis: bilirubinuria (kidney compensates) Encourage pt to get plenty of rest (get bathroom privlidges) 53. 54. 55. 56. Posticteric (After jaundice) *fatigue, but increased sense of wellbeing, hepatomegaly gradually decreasing Serum bilirubin and enzymes: normal or returning to normal Serum antibodies elevated Complications of Hepatitis/jauncice o increased ammonia in circulation (CNS changes, behavior changes, confusion) o enc. Pt. to eat foods low in protein (if liver dysfunction is present, protein cannot be metabolized) Nursing Management with Hepatitis *ENCOURAGE REST* 57. Administer medications: antiemetics & antihistamines (b/c itching/pruritus) 58. Prevent skin breakdown (turn Q2H; enc pt not to scratch!) apply topical antihistamine cream. 59. 60. 61. Avoid drugs detoxified in the liver: (Tylenol)(Herbs) Monitor fluid and electrolytes and I&O 62. Supportive care with rest and gradual return to normal activities Refrain from alcohol @ least 6 months after jaundice 64. 65. In fulminant hepatitis,protein is restricted Use of Standard Universal Precautions Discuss Dietdecrease protein; frequent, small, freq meals of choice b/c anorexia; possible calorie counter; low fat diet (liver can't break down fat) 68. 66. Good handwashing TEACH (Hep A) Protected sex Hepatitis VaccinesHep B (ESP FOR HEALTHCARE PROVIDERS) DOCUMENT TEACHING Tx= depending on cause, antibiotics, rest, fluids Scenario You are taking care of a 46 year old male with a health history which includes DM, alcohol and drug abuse. He has Hepatitis B & C. It is noted that several times during the shift he requests Tylenol, which is ordered prn. The order reads: Tylenol 650mg po q4hrs prn for temp >101.1 or pain. Not to exceed 4000mg in 24 hrs. What should be the concerns of the nurse? and why? Tylenol b/c metabolized by liver *DON'T give, call DR. ( question order). If the order stands (if pt complains of pain, don't keep giving Tylenol, go on nursing judgement) 14 69. most common cause as well as protein deficiency. Liver bile ducts become inflamed and occluded with thickened bile and pus. The liver attempts to form new bile; hence, there is an overgrowth and it's surrounded by scar tissue. *Don't see fat; Hypertension Etiology of Cirrhosis Alcoholism major cause; alcohol injures the liver by blocking the normal metab or protieins, fats, and carbs Viral Hepatitis (Chronic) Toxic reactions to drugs or chemicals Biliary Obstruction CIRRHOSIS (P1101) A chronic, progressive disease characterized by inflammation, fibrosis, and degeneration of the liver tissue. (As a result, the tissue degenerates and the lobules are infiltrated with fat.). the liver is is not functioning. Alcohol consumption is 70. 71. 72. 73. 74. Cardiac Disease (lack of circulation to liver) poor perfusion Types of Cirrhosis Early Clinical Manifestations of Cirrhosis 75. GI disturbancesb/c carbs, fats and proteins are not metabolized; N/V, loss of appetite, irregular bowel habits flatulence, indigestion; also GI varices can occur b/c of back up of blood into other areas 76. 77. 78. 79. 81. Hepatomegaly fatty liver is enlarged; blood starts to back up Hepatomegaly Pain from hepatomegaly Slight weight loss (poor metabolism of nutrients) Fever infection and peritonitis, inflammation Splenomegaly backflow of blood Splenomegaly Fatigue Pruritus waste products circulating in blood Pruritus 80. 82. Late Signs of Cirrhosis Portal obstruction and ascites late manifestation; blood backs up into the spleen and FI and cannot function properly. Indigestion and altered bowel function result. Fluid rich in protein may accumulate in the peritoneal cavity, producing ascites. Edema late symptom; a reduced plasma albumin concentration predisposes the patient; over production of aldosterone causes sodium and water retention and K excretion. (put patient in upright position. Elevate edematous extremities) Vitamin deficiency and Anemia Mental deterioration hepatic encephalopathy and coma Would expect decrease albumin, increased ALT, GGT, AST, and bilirubin levels, and PTT is prolonged. Treat with antacids, vitamin and nutritional supplements, diuretics, and avoid alcohol. Complication of Clients with Liver Disorders 87. Jaundice 88. Portal Hypertension 15 89. Etiology of Jaundice (P1081) Jaundice results from functional derangement of liver cells and compression of the bile duct by connective tissue overgrowth. Billirubin is not removed from blood (serum bilirubin exceeds 2.5mg/dL). In darker person, observe the sclerea, mucous membranes, and nailbeds for jaundice. 90. 91. 92. 93. Pathogenesis of Jaundice Destruction of red blood cells Impaired uptake of bilirubin by liver cells Decreased ability to conjugate or excrete bilirubin into the biliary system Obstruction of bile flow in the channel of the hepatic duct Portal Hypertension (P1082) Portal Hypertension is an abnormally high blood pressure in the portal venous system The most common cause of portal hypertension is obstruction caused by cirrhosis of the liver. Blood pools and backs up to organs b/c the liver is pressure within the veins are increased; so veins in other organs engorge (=varices). 94. 95. may have hemorrhoids, esophageal varices (engorged veins in esophagus) Two major consequences are ascites and varices. Complications of Portal Hypertension 97. Esophageal Varicesveins engorge from pooling of blood 98. Peripheral Edema 99. Ascites (swelling of abdomen) 100. 101. Hepatic Encephalopathy (Coma)due to increased ammonia circulating Hepatorenal Syndrome 102. 103. 104. Large collateral channels develop between the portal and systemic veins that supply the lower rectum, esophagus and umbilicus veins... Esophageal Varices (P1085) 105. Enlarged and swollen veins of the esophagus caused by portal hypertension as a result resistance of normal venous drainage of the liver from the portal vein. Bleeding esophageal varices are lifethreatening and can result in hemorrhagic shock. This patient may present with hematemesis, melena, or deterioration in mental status. Pathology of Portal Hypertension With gradual obstruction of venous blood flow in the liver... The pressure in the portal vein increases... Diagnosis of Esophageal Varices 106. Esophagoscopy/endoscope the examination of the esophagus using an endoscope to search for esophageal varices and abnormalities 107. Nursing Management of Esophageal Varices The goal of treatment of esophageal varices is avoidance of bleeding and hemorrhage. Teach not to do anything that 16 would increase intraabdominal pressure so no coughing (meds to suppress cough) or straining (stool softeners; teach not to do Valsalver maneuver) 108. 109. Rest is indicated because it reduces the metabolic demands of the liver and promotes liver cell regeneration. Teach patient about factors that produce ulceration and irritation to esophagus (spicy foods. Bland diet Contributing Factors to Bleeding Esophageal Varices 110. Ingestion of course food 111. Alcohol ingestion. Avoid alcohol. 112. 113. 114. 115. Avoid aspirin (NSAIDS) (thins blood increases risk for bleed) Avoid aspirin (NSAIDS) (thins blood Increased intraabdominal pressure (coughing, straining) Avoid spicy foods Decrease risk of acid regurgitation from the stomach 116. Medical Management of Bleeding Esophageal Varices (increased ammonia levels blood breaks levels down to ammonia from protein in the blood) 1st step is to stabilize and manage pt airway. Must suction and intubate. (risk for aspiration) Balloon tamponade (SengstakenBlakemore tube) inserted (2 balloons); will be intubated; has 4 openings (one for gastric aspiration, esophageal aspiration, gastric balloon, esophageal balloon); check placement via chest xray; there has to be traction (to anchor football facemask)inflate with air...this should put pressure on esophagus to stop bleeding. Risk for breakdown (At least 812 hours, deflate balloons to prevent necrosis). Monitor patient for bleeding when deflating balloon. MUST be down in stomach NOT ESOPHAGUS 118. Supportive measures during bleeding includes initiating IV therapy (losing fluid volume), & administration of blood products 119. Drug therapy Vasopressin (causes vasoconstriction, decreases blood loss), beta blockers (propanolol decreases Drug therapy Vasopressin (causes vasoconstriction, decreases blood loss), beta blockers (propanolol pressure in the veins) Dangers of Balloon Tamponade Displacement of tube (check where tape is on tube) 120. 121. Obstruction of airway (keep scissors at bedside. Cut tube if airway becomes obstructed) NEVER LEAVE PATIENT ALONE (prob need restraints) Rupture of gastric balloon (100200 ml of air can be inflated don't exceed this amt. or u could rupture balloon) Rupture of gastric balloon (100200 ml of air can be inflated Obstruction of airway, aspiration of GI content (most common complication) 122. 123. 124. Necrosis of the nose, mucosa of stomach, or the esophagus (deflate balloon Q 812 hours; skin care at insertion site; keep sciccors at bedside) Nursing Measures for Bleeding Esophageal Varices Frequent mouth & nasal care 126. Oral suction to keep airway open 125. 17 127. 128. Ensure that patient is not left alone (may need restraints) Frequent assessment of patient Ascites & Peripheral Edema (P1082) 129. Ascites The accumulation of fluid in the peritoneal cavity. The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney. 130. Edema results from decreased colloidal osmotic pressure due to impaired liver synthesis of albumin. Tx of ascites= spironolactone (aldactone) teach pt to avoid table salt, salted butter or margarine, canned/frozen foods. May use salt substitutes (contraind. In renal dx (contain K+), liberal use of powerdered, low sodium milk. If this does not work, diet is restricted to < 500 mg Na and diuretics given Mechanisms of Ascites Portal Hypertension pooling of blood Hypoalbumemia (liver not synthesizing albumin) 131. 132. 133. Hyperaldosteronism retention of Na and H2O (liver metabolizes aldosterone, but liver is not functioning, so there is an increased amt. of aldosterone) Fluid seeps from intravascular to peritoneal cavity. Where sodium goes, water follows Fluid seeps from intravascular to peritoneal cavity Clinical Manifestations of Ascities 134. Umbilicus may be everted, increased abd. circumference 135. Abdominal Striae (stretch marks) 136. 137. 138. 139. 140. Caput Medusaea plexus of dilated veins around the umbilicus Weight gain Abdominal distention Dyspnea (fluid puts pressure on diaphragm) most comfortable position = upright Bulging Flanks 141. 142. 143. 144. 145. 146. 147. 148. Nursing Management of Ascites Daily weights Measuring abdominal girth daily (mark where you measure) Promote skin integrity Administer Diuretics as ordered Accurate I & O's Monitoring electrolyte balance when pt taking diuretics Provide comfort. Position upright Reinforce Sodium & Fluid Restriction 149. Medical Intervention for Ascites Paracentesis (done when breathing is compromised; severe ascities)A needle puncture in the abdominal cavity to remove ascitic fluid and relieve respiratory distress. need to be upright, measure abd girth before and after procedure. During procedure (fluids high in protein and pt is at risk for drastic VS changes), monitor Vitals (esp. BP which can drop drastically). Document how much physician drained, the color and odor of drainage, how pt. tolerated procedure. After procedure, put pressure on site. Bedrest. 18 150. cavity. Complication of Paracentesis Peritonitis inflammation of the peritoneum caused by bacteria or irritating substances introduced into the abdominal HYPOTENSION 151. Signs and Symptoms of peritonitis include fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid. 152. 153. 154. Complications of Ascites Respiratory Compromise Rupture of Umbilicus in massive ascites Infections 155. Hepatic Encephalopathy (P1090) Hepatic Encephalopathy (HE) or Coma is a manifestation of liver damage caused by chronic or acute liver disease, waste toxic to the brain is not neutralized in the liver before being shunted back into peripheral circulation of the blood. Protein is not being metabolized increased ammonia (CNS depressant) is not being metabolized 156. 157. 158. Any process that increases protein in the intestine, such as increased dietary intact or GI bleeding, causes elevated blood ammonia levels. Contributing Factors to Increased Ammonia Levels Ammonia is produced in the gastrointestinal tract when protein is broken down by bacteria. The digestion of blood from leaking or ruptured varices adds to the amount of ammonia present in the systemic blood. 159. Ammonia is absorbed into the portal circulation and transported to the liver, where it is converted to urea before being released into the blood. 160. The diseased liver is unable to convert ammonia to urea, so that large quantities remain in the systemic circulation and cross the blood/brain barrier, producing neurologic toxic symptoms. Factors of Hepatic Encephalopathy 161. Ammonia that reaches the brain may alter cerebral energy metabolism or interfere with neurotransmitters. high mortality rate. Support family 164. 165. 166. Ammonia is increased as a result of GI bleeding, highprotein diet, bacterial infections, and uremia. In the presence of alkalosis or hypokalemia, increased amounts of ammonia are absorbed from the GI tract. Ammonia is a CNS Depressant HE is characterized by increased levels of ammonia in the blood and cerebrospinal fluid. There is a high mortality rate associated with HE. 167. 168. 169. Clinical Manifestations of Hepatic Encephalopathy Memory loss Irritability Sleep disturbances 19 170. 171. 172. 173. 174. Confusion Impaired judgment Subtle changes in personality (ask family) Slight tremor Seizures Apraxia inablility to perform purposive movements (deteriation in handwriting have pt draw star or write their inablility to perform purposive movements (deteriation in handwriting Asterixis abnormal muscle tremor consisting of involuntary jerking movements (hands) (have pt extend hand out, Fetor Hepaticus sweet, fecal odor to the breath (smells like aged wine or acetone, smells book says it smells sweet, fecal odor to the breath (smells like aged wine or acetone, smells 175. 176. 177. name) and it drop. Pt loses control of hand reflex) like freshly mowed grass! WOW!!) **Pt goes from confusion, disorientation, ultimately to coma 178. Principle Interventions in Hepatic Encephalopathy The goal of management includes reduction and elimination of ammonia. The drug of choice is lactulose (binds with ammonia allows to be excrete in stool. Pad bed well. pt c//o diarrhea, but explain that this is what we want) ammonia 179. This consist mainly of protein restriction 180. 181. reduction of ammonia formation in the intestines sterilization of the intestines with antibiotics (neomycin) 182. Medical Management ofHepatic Encephalopathy Neomycin reduces the bacterial flora of the colon. Bacterial action on protein in the feces results in ammonia production. 183. **Lactulose (drug of choice)traps ammonia in the gut, the laxative effect of the drug expels the ammonia from **Lactulose the colon. This prevents ammonia from entering portal circulation. Nursing Considerations of Hepatic Encephalophathy Conduct ongoing neurological assessments and report deteriorations. The nurse who is with the client over time is usually the best person to assess a change in level of mental functioning. Protect client from injury (pt confused) (pad side rails, bed in low position, get family member to stay at all times or a 184. 185. 186. nurse or aid or sitters, orient frequently, offer bedpan often, bed in low position, document) 187. Maintain bed rest. Turn and provide skin care q2 hours. low protein, low fat, low sodium diet 188. 189. Avoid administration of drugs detoxified in the liver. (can't metabolize them) The prognosis for the client with hepatic Encephalopathy is poor. Support family. Hepatorenal Syndrome 190. Because a dysfunctional liver can't detoxify waste, drugs, metabolites, they accumulate in the body. The kidneys try to alleviate the buildup of waste products, but compensation is only temporarily effective, and renal failure frequently occurs. 20 191. 192. 193. 194. Characteristics of Hepatorenal Syndrome Characterized by functional renal failure with advancing: Azotemia Presence of excessive urea (waste) in blood. Caused by failure of kidneys to remove urea from blood Oliguria decreased urine Oliguria Intractable ascites not relived by paracentesis Intractable ascites Serum Enzyme Test (*table P1078-1079) Alanine Aminotransferase (ALT) or Serum Glutamate Pyruvate Transaminase (SGPT)nonspecific markers of liver necrosis if elevated Aspartate Aminotransferase (AST) or Serum GlumtamicOxaloacetic Transaminase (SGOT) elevated with liver cell o 195. damage 196. 197. Alkaline Phosphatase (ALP) measures bilary tract obstruction (cholelithisasis) common bile duct Y Glutamyltranferase (GGT) elevated in alcohol abuse; indicates liver dysfunction Unconjugated bilirubin increased because it is not being metabolized, conjugated bilirubin will also be increased because there is a decrease amt of bilirubin excreted in stool 198. 199. Diagnostic Test Ultrasound shows size of abd. organs and presence of masses. Shows enlarged liver Liver Scan (CT Scan) Liver scan shows size & shape of liver, scars, cysts, tumors CT scan shows hepatic neoplasms, cysts, abscesses, hematomas, cerebral atrophy (shows areas of scarring) 200. Blood Test normal PTT is 1216 sec. will detect liver dysfunction and the cause of cirrhosis Liver Biopsy always look at bleeding studies before Liver Biopsy Liver Biopsy The removal of a small amount of liver tissue usually through needle aspiration to permit examination of liver cells. 201. 202. Liver Biopsy Procedure 203. Preprocedure coagulation, studies ultrasound Liver Biopsy Procedure 204. During procedure the pt lies supine with the rt arm over the head. The pt is instructed to (take a deep breath and hold) expire fully and not breathe while needle is inserted. Usually sedated before, if doesn't have cirrhosis. Monitor vitals 205. Post procedure keep pt lying flat on right side for a minimum of 2 hours (put pressure on site for at least 2 hours) to splint the incision. Check vital signs as ordered 21 206. 207. and other assessments are confusing. 208. Allow a recommendation for treatment. 209. Determine if you have a medication induced liver disease. Risk of Liver Biopsy 210. Bleedingobtain bleeding studies 211. Puncture of Organ 212. Pain Benefits of Liver Biopsy Determine the severity of liver disease (inflammation). Assess the amount of liver scar tissue Change or finalize the diagnosis of the cause of liver disease if the blood tests 213. 214. 215. 216. 217. 218. 219. 220. Nursing Diagnosis Impaired gas exchange related to increased abdominal pressure from ascitic fluid Altered nutrition related to abdominal distention, discomfort and anorexia Impaired skin integrity related to jaundice and edema Fluid Volume Excess related to ascites and edema Knowledge deficit Risk for injury Activity intolerance Altered thought process 22 ...
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This note was uploaded on 05/04/2008 for the course NURS 210 taught by Professor Jones-thomas during the Spring '08 term at Lady of the Lake.

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