0133427269 Module10 Inflammation LectureOutline

Module 10 Inflammation  The Concept of Inflammation A nonspecific, complex response to reduce effects of what the body sees as harmful May result from injury, infection Inflammation acts as a protective process ( stimulates healing, prevent further damages, progressive deterioration Normal presentation Inflammation( adaptive response to injury, illness, that brings fluid, dissolved substances, blood cells into interstitial tissues where invasion, damage has occurred Nonspecific ( same events occur regardless of the inflammatory process Invader neutralized, eliminated, destroyed tissue is removed, process of healing, repair initiated Phagocytosis debridement, prepares room for healing Adequate nutrition essential for healing to proceed Adapted mechanism ( destroys, dilutes injurious agent, prevents further spread of injury, promotes repair of damaged tissue Physiology review Five signs Pain Swelling Redness Heat Impaired function of the part Suffix -itis describes inflammatory process Injurious agents Physical agents mechanical objects causing trauma, excessive heat, cold, radiation Chemical agents ( external irritants, internal irritants Microorganisms ( bacteria and viruses The inflammatory process Inflammation ( contains injury or destroys microorganisms Allows repair to injured area to proceed at a faster pace Acute or chronic Stages of inflammation ( three stages Stage 1 ( vascular and cellular responses Blood vessels at site of injury, infection constrict Injured tissue releases substances ( chemical mediators to dilate blood vessels, contract smooth muscle Histamines Kinins Prostaglandins Causes increased blood flow to injured area ( hyperemia Vascular permeability increases at site ( fluid, proteins, leukocytes leak into the interstitial spaces Blood flow slows in dilated vessels ( more leukocytes to injured tissues Emigration ( leukocytes move into the tissue spaces Stage 1 injuries ( sprains, broken bones, minor blunt-force injuries Stage 2 ( exudate production Exudate fluid that escaped from blood vessels, dead phagocytic cells, dead tissue cells, products they release Major types of exudate Serous ( typically accompanies mild inflammation Clear or straw colored, thin, watery Purulence, or pus ( usually opaque, milky Normally indicates presence of infection, contains large quantity of cells and necrotic debris Hemorrhagic ( blood from ruptured blood vessels, red and thick Stage 3 ( reparative phase ( repairs injured tissues Regeneration ( replacement of destroyed tissue cells by cells that are identical or similar in structure and function Fibrous (scar) tissue formation ( damaged tissues replaced with connective tissue elements Early stages ( tissue called granulation tissue As tissue shrinks, collagen fibers contract, leaves cicatrix Mediators of inflammation Histamine and heparin work together to increase blood flow to the injured tissue Heparin prevents blood clotting Histamine ( key chemical mediator of inflammation, stored in mast cells Detects foreign agents, injury and responds by releasing histamine Also directly stimulates pain receptors Histamine dilates nearby blood vessels ( capillaries become more permeable Anaphylaxis ( rapid release of chemical mediators of inflammation on large scale throughout body See Table 101 CHEMICAL MEDIATORS OF INFLAMMATION, p. 635 See Box 101 SYMPTOMS, TREATMENT OF ANAPHYLAXIS, p. 636 See Figure 101 STEPS IN ACUTE INFLAMMATION, p .635 Histamine receptors ( histamine combined with cellular histamine receptors Four classified receptors of two types H1 receptors ( in smooth muscle of vascular system, bronchial tree, digestive tract H2 receptors ( primarily in stomach Genetic and lifespan considerations Several differences in anatomy and physiology influence effects of inflammation in children Structural differences in airway increase risk for obstruction Fewer and smaller alveoli ( reduction in surface area available for gas exchange Glomerular filtration not fully developed in infants Absolute volumes of fluid loss represent larger proportion of total body fluid Changes in excitation-contraction coupling, left ventricular mass, and high contractile state of the heart reduce sympathetic nervous system response to changes in blood volume abd stress Gastrointestinal inflammation that reduces nutrient absorption affects children more than adults Immune system response to insult differs from that of adults Alterations Inflammation can occur in any tissue, organ, system Common diseases ( appendicitis, Crohn disease, arthritis, nephritis, peptic ulcers, systemic lupus erythematosus, and more Alterations and manifestations Classic signs of inflammation ( redness, swelling Prevalence Millions of adults and children in U.S. have inflammatory disorders Rheumatoid arthritis ( 1.3 million adults Asthma ( 24.6 million Appendicitis ( 80,000 children/year Genetic considerations and nonmodifiable risk factors Vary depending on the inflammatory disorder Native and Mexican Americans ( increased risk for gallstones African Americans ( increased risk for nephritis as complication of SLE Family history ( peptic ulcer disease See CONCEPTS RELATED TO INFLAMMATION, pp. 637-638 See ALTERATIONS AND THERAPIES INFLAMMATION, p. 639 Case Study Part 1 ( Ryan Blake is a 29-year-old African American male. Prevention Preventing excessive inflammatory response involves avoidance Individuals with hypersensitivity should avoid triggers Those with inflammatory bowel disease or peptic ulcer disease should avoid foods that trigger inflammation Handwashing is primary method of preventing infection that can result in inflammation Modifiable risk factors Crohn disease ( lower risk of flare-ups with diet, increased fiber, no smoking Gallstone formation ( maintain appropriate weight, consume diet high in fiber, low in fat Diabetes ( follow treatment protocols, maintain healthy diet Screening Acute disorders ( no screening possible Allergic rhinitis ( skin testing Assessment Nursing assessment History Assess degree to which client at risk of developing inflammation Client self-report that suggests presence of inflammation Physical assessment Sign and symptoms vary according to body area involved Appendicitis versus arthritis Widespread inflammation may cause diverse symptoms See ASSESSMENT INTERVIEW Inflammation, p. 641 Lifespan and cultural considerations Children Less invasive tests are often used in children Exhaled breath condensates rather than bronchoscopy Fecal microbial sequencing rather than colonoscopy Ultrasound rather than endoscopy Older adults Inflammatory markers may be increased More susceptible to chronic diseases Diagnostic tests Primary laboratory test ( erythrocyte sedimentation rate (ESR) Measures how far erythrocyte settles in tube over given period of time Normal sedimentation rate for males 015 mm/hr, females 025 mm/hr C-reactive protein (CRP) test Protein found in blood in response to inflammatory process Can also be used to assess risk of cardiac disease Other laboratory tests based on cause, location, type of inflammation WBC with differential Serum protein electrophoresis Routine chemistry panels See Table 102 THE WHITE BLOOD CELL COUNT AND DIFFERENTIAL, p. 642 Case Study Part 2 ( After experiencing a flare-up of his symptoms, Mr. Blake returns to see his gastroenterologist Interventions and therapies Generally aimed at reducing mobility, elevation to reduce edema, antipyretics are involved, anti-inflammatory medication Independent Emphasize client teaching Importance of preventing further injury Taking medications as prescribed Maintaining adequate nutrition and fluids Teaching family how to assist with caregiving Alleviate discomfort and reduce inflammation( positioning, applying heat or cold Promote coping Collaborative Chronic inflammatory state often associates with aging and obesity Nutritionist ( clients benefit from balanced diet Physical therapy ( clients benefit from exercise Surgery, for example Appendectomy for appendicitis Removal of colon and rectum ( ulcerative colitis Pharmacologic therapy Aimed at reducing inflammatory response and reducing pain See MEDICATIONS Inflammatory Diseases, p. 643 Review The Concept of Inflammation Relate Link the Concepts Ready Go to Companion Skills Manual Refer Go to Student Nursing Resources Reflect Case Study Part 3 ( Mr. Blakes condition worsens and he goes to the emergency room. Exemplar 10.1 Appendicitis Overview Appendicitis ( inflammation of the vermiform appendix Common cause of acute abdominal pain Can occur at any age, but most common in adolescents and young adults Pathophysiology and etiology Appendix ( tubelike pouch attached to cecum just below ileocecal valve Usually located in the right iliac region ( area designated as McBurney point See Figure 102 A MCBURNEY POINT, p. 645 Obstruction of proximal lumen of appendix is apparent in most acutely inflamed appendices After obstruction ( appendix becomes distended Pressure increases, impairing blood supply ( leading to inflammation, edema, ulceration, infection Tissue necrosis, gangrene results ( perforation Contents of GI tract flow into peritoneal space ( peritonitis Etiology Caused by obstruction in appendiceal lumen ( fecalith (hard mass of feces) Risk factors Adolescent males at greatest risk Diet low in fiber, high in carbohydrates at greater risk Prevention Cannot be prevented Reduce risk by eating foods high in fiber content Clinical manifestations Continuous, mild generalized, upper abdominal pain Pain intensifies, localizes right lower quadrant Aggravated by moving, walking, coughing Rebound tenderness on palpation May be less acute in older adults ( delay diagnosis Complications Perforation, peritonitis, abscess Chronic appendicitis Lifespan and cultural considerations Infants and children Manifestations in infants include listlessness, inconsolability, vomiting, distended abdomen Uncommon for children under age 4 to develop appendicitis Appendicitis in young children often progresses to rupture because they cannot accurately tell their parents where it hurts Ethnicity plays a role in progression of appendicitis in children ( Black and Latino children have a higher rate of perforation than White children Older adults In older adults, less than 30 present with classic symptoms ( half are afebrile, half have no rebound or involuntary guarding, one quarter have no lower right quadrant pain Instead, older adults present with confusion Collaboration Acutely inflamed appendix can perforate within 24 hours Diagnostic tests Abdominal ultrasound Abdominal x-rays Intravenous pyelogram Urinalysis Pelvic examination WBC with differential Surgery Treatment of choice ( appendectomy Laparoscopic approach Direct visualization of appendix allows definitive diagnosis Postoperative hospitalization is short Postoperative complications are infrequent Recovery, resumption of normal activities rapid Laparotomy Small transverse incision made at McBurney point Appendix isolated, ligated, and removed Pharmacologic therapy IV fluids Antibiotic therapy with third-generation cephalosporin Repeated during surgery, continued for at least 48 hours postoperatively Nursing process Assessment Health history Current manifestations including onset, duration, progression, aggravating or relieving factors Most recent food/fluid intake Known allergies Current medications History of chronic diseases Physical examination Vital signs Apparent general health Abdominal shape, contour, bowel sounds, tenderness light palpation Diagnosis Risk for Impaired Gas Exchange Acute Pain Risk for Deficient Fluid Volume Anxiety Fear Risk for Infection Planning Developed in collaboration with client, family Client will articulate concerns about surgery prior to event Client will articulate understanding of procedure, reasons for it, preoperative instructions prior to arrival for surgery Client will verbalize relief from pain following administration of pain management Client will receive appropriate postoperative wound care Client will verbalize instructions for self-care prior to being discharged Implementation Promote effective respiratory gas exchange Encourage client should turn, cough, and breathe deeply Encourage client to get out of bed and walk two or three times/day Teach client to splint incision area with a pillow when coughing Encourage incentive spirometry ( for children, give the child bubbles to blow Promote fluid volume balance Monitor and continue IV infusion until bowel function returns after surgery Once bowel sounds return, NG tube (if needed) removed ( offer water in small amounts, then other clear fluids Closely monitor client for nausea after giving oral fluids Monitor intake and output Prevent infection Monitor vital signs, including temperature Maintain IV infusion until oral intake is adequate Assess wound, abdominal girth, postoperative pain Provide effective pain management Assess pain ( character, location, severity, duration Administer analgesics as ordered Assess effectiveness of medication 30 minutes after administration Promote psychosocial well-being Elicit history, perform physical exam, coordinate diagnostic tests, prep client for surgery Provide emotional support for client, family Provide good preoperative education to reduce anxiety Encourage and answer any questions the client or family may have Provide effective client teaching Give instructions on slowly reestablishing a nutritious diet as tolerated Teach client or parents to recognize signs, symptoms of infection ( seek early treatment Ruptured appendix ( several days in hospital for IV antibiotics If wound open, generally closed after a few days prior to discharge Provide teaching How to care for the wound Signs, symptoms of wound infection, when to call physician Method and frequency of taking temperature Activity limitations, restrictions, return to work, school Pain management Evaluation Clients pain is managed effectively Client will not develop secondary infection Client and family verbalize understanding of condition, treatment Effective airway clearance is maintained Adequate hydration is achieved and maintained Restoration of normal nutritional intake will occur Client experiences decreased fear and anxiety associated with the hospitalization and procedures Review Appendicitis Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 10.2 Gallbladder Disease Overview Altered bile flow through hepatic, cystic, common bile duct a common problem Cholelithiasis ( formation of stones in gallbladder, or biliary duct system Pathophysiology and etiology Most gallstones formed in gallbladder ( migrate into ducts, leads to cholangitis Early manifestations may be vague Stones that obstruct cystic duct or common bile duct may cause biliary colic Severe, steady pain in epigastric region or right upper quadrant (RUQ) of abdomen May radiate Cholecystitis ( inflammation of gallbladder Acute cholecystitis usually follows obstruction of cystic duct by stone Usually begins with attack of biliary colic Pain usually lasts longer than biliary colic Chronic cholecystitis ( may result from repeated bouts of acute cholecystitis, persistent irritation of gallbladder wall by stones Complications Empyema ( collection of infected fluid in gallbladder Gangrene and perforation with resulting peritonitis or abscess formation Formation of fistula in adjacent organ Obstruction of small intestine by large gallstone (gallstone ileus) Etiology Gallstones form when with several factors interact Abnormal bile composition Biliary stasis Inflammation of gallbladder Most consist of cholesterol When bile supersaturated with cholesterol ( can precipitate out to form stones Risk factors Incidence rates vary among ethnicities Native Americans and Mexican Americans at greater risk Age, family history of gallstones, obesity, rapid weight loss, and being female are all risk factors Biliary status ( pregnancy, fasting, prolonged TPN Certain diseases/conditions ( cirrhosis, sickle cell disease, hyperlipidemia Prevention Modifiable risk factors include obesity, certain medications, high-fat diet, rapid weight loss, dyslipidemia Clinical manifestations See Table 103 MANIFESTATIONS AND COMPLICATIONS OF CHOLELITHIASIS AND CHOLECYSTITIS, p.651 Collaboration Treatment depends on acuity of condition, clients overall health status Diagnostic tests Serum bilirubin (see Box 103 SORTING OUT TOTAL, DIRECT, AND INDIRECT BILIRUBIN LEVELS, p. 651) CBC Serum amylase, lipase Abdominal x-ray Ultrasonography of the gallbladder Oral cholecystogram Gallbladder scan Surgery Laparoscopic cholecystectomy ( minimally invasive, low risk of complications, hospital stay of less than 24 hours Stones lodged in ducts ( cholecystectomy with common bile duct exploration T-tube inserted to maintain patency of duct, promote bile passage while edema decreases See Figure 104 T-TUBE PLACEMENT, p. 652 See Box 104 NURSING CARE OF THE CLIENT WITH A T-TUBE, p. 652 Poor surgical risks may have cholecystotomy to drain gallbladder, choledochostomy to remove stones, position T-tube in common bile duct (CBD) Shock wave lithotripsy may be used with drug therapy Extracorporeal shock wave therapy ( ultrasound used to align stones Mild sedation during approximately 1-hour procedure Percutaneous cholecystostomy ( ultrasound-guided drainage of gallbladder Pharmacologic therapy Clients who refuse surgery, inappropriate for surgery ( drug to dissolve gallstones Act by reducing cholesterol content of bile ( best with stones with high cholesterol content May take 2 years or more High incidence of recurrent stone formation Ursodiol ( well tolerated Chenodiol ( hepatotoxic If infection suspected ( antibiotics Nonpharmacologic therapy Food intake may be eliminated during acute attack of cholecystitis ( NG tube inserted to relieve nausea and vomiting Dietary fat intake may be limited If bile flow is obstructed, fat-soluble vitamins and bile salts may need to be administered Nursing process Assessment Health history Current manifestations, nausea/vomiting, other symptoms, duration of symptoms, risk factors, chronic diseases, current diet, use of contraceptives, possibility of pregnancy Physical assessment Weight, color of skin and sclera, abdominal assessment, color of urine and stool Diagnosis Pain Imbalanced Nutrition Less Than Body Requirements Risk for Infection Planning Client will obtain adequate pain relief to allow for comfort Client will demonstrate understanding of low-fat diet with adequate intake of fat-soluble vitamins Client will verbalize symptoms to report immediately Client will not contract infection Implementation Prevent infection Acutely inflamed gallbladder ( may become necrotic and rupture Open cholecystectomy ( client at higher risk for pulmonary infection (high abdominal incision) Monitor vital signs Assess abdomen every 4 hours and as indicated Assist with coughing and deep breathing, incentive spirometry Place in Fowler position, encourage ambulation Administer antibiotics as ordered Provide effective pain management Discuss relationship between intake and pain Teach ways to reduce fat intake Withhold oral food and fluids during episodes of acute pain For severe pain, administer narcotic analgesia Place in Fowler position ( decreases pressure on inflamed gallbladder Promote balanced nutrition Client may develop nutritional imbalance related to anorexia, pain, nausea, impaired bile flow Assess nutritional status, including diet history, height, weight, skinfold measurements Evaluate laboratory results Report abnormal to primary care provider Refer to dietitian, nutritionist for diet counseling to promote healthy weight loss, reduce pain episodes Administer vitamin supplements as ordered Evaluation Client reports adequate pain control to maintain comfort Client demonstrates food choices( diet low in fat, high in fat-soluble vitamins Client has normal temperature, displays no symptoms of infection Review Gallbladder Disease Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 10.3 Inflammatory Bowel Disease Overview Inflammatory bowel disease (IBD) ( chronic inflammation of the bowel Ulcerative colitis ( chronic inflammatory bowel disorder that affects the mucosa and submucosa of the colon, rectum Chronic intermittent colitis (recurrent ulcerative colitis) most common form Distal colon affected, few systemic manifestations of the disease 15 of people with ulcerative colitis develop fulminant colitis ( acute form of disease that involves entire colon Manifestations include bloody diarrhea, acute abdominal pain, fever Crohn disease ( chronic, relapsing inflammatory disorder Also known as regional enteritis Affects terminal ileum, ascending colon (can affect any portion of GI tract from mouth to anus) See Table 104 CHARACTERISTICS OF ULCERATIVE COLITIS AND CROHN DISEASE, p. 657 Pathophysiology and etiology Inflammatory process of ulcerative colitis Begins at rectosigmoid area of anal canal, progresses proximally Begins with inflammation at the base of crypts of Lieberkhn in distal large intestine and rectum See Figure 105 A PHOTOMICROPHGRAPH OF THE MUCOSA, p. 658 Crypt abscesses form ( penetrate superficial submucosa ( lead to necrosis, sloughing of bowel mucosa Further tissue damage is caused ( mucosa becomes edematous, friable Chronic inflammation leads to atrophy, narrowing, shortening of colon Crohn disease Typically begins as small inflammatory aphthoid lesion (shallow ulcer) Can progress to involve all layers of intestinal wall Deeper ulcerations, fissures may develop Lumen of affected bowel assumes cobblestone appearance Lesions not continuous ( some normal-looking bowel Fibrotic changes ( bowel wall thickens, loses flexibility ( inflammation, edema, fibrosis leads to local obstruction, abscesses, formation of fistulas See Figure 106 THE PROGRESSION OF CROHN DISEASE, p. 658 Malabsorption, malnutrition may develop ( ulcers prevent absorption of nutrients Ulcerations can lead to protein loss, chronic slow blood loss Etiology Unknown Genetic, environmental factors, autoimmunity, lifestyle factors may affect development Risk factors IBD occurs more frequently in United States, northern European nations American Jews of European descent 4 to 5 times more likely to develop IBD African Americans and Whites are more likely to develop IBD than Hispanics or Asians Smoking may increase risk of Crohn disease Use of NSAIDS may increase risk of IBD Prevention Avoidance or cessation of smoking is major factor in preventing IBD Clinical manifestations Ulcerative colitis Diarrhea predominant manifestation Stool contains blood, mucus Severe ulcerative colitis( more than 6 to 10 bloody stools per day Left lower quadrant (LLQ) cramping relieved by defecation ( common Clients with severe disease may have systemic manifestations Arthritis, skin and mucous membrane lesions, uveitis Complications Hemorrhage Toxic megacolon ( acute motor paralysis and dilation of colon to greater than 6 cm Colon perforation Increased risk for colorectal cancer Crohn disease Manifestations vary ( majority experience persistent diarrhea Abdominal pain, tenderness are common Right lower quadrant (RLQ) pain relieved by defecation Complications Intestinal obstruction ( caused by repeated inflammation and scarring Abscess Fistula ( may be asymptomatic, may cause abscess Perforation uncommon See CLINICAL MANIFESTATIONS AND THERAPIES Inflammatory Bowel Disease, p. 661 See MULTISYSTEM EFFECTS OF INFLAMMATORY BOWEL DISEASE, p. 659 Lifespan and cultural considerations Occurrence of IBD peaks at 15 30 years of age But it does occur in children Pediatric differences More males than females Children suffer from Crohn more than ulcerative colitis Location of disease differs Malabsorption causes failure to grow Collaboration Interdisciplinary care begins with diagnosis Treatment is supportive ( medications, dietary measures to decrease inflammation, promote intestinal rest and healing, reduce intestinal motility Diagnostic tests Sigmoidoscopy, colonoscopy, barium upper/lower x-ray series Laboratory tests include stool examination Also CBC, sedimentation rate, serum levels of vitamins, liver function tests Surgery Generally performed only when necessitated by complications of disease Bowel obstruction Perforation Internal or external fistula Abscess Perianal complications Resection of the affected portion with end-to-end anastomosis is usual treatment Increased risk of fistulas Bowel strictures may be treated with strictureplasty Colectomy to treat disease itself, eliminate complications Surgical procedure of choice ( total colectomy with an ileal pouch-anal anastomosis (IPAA) see Figure 107, p. 30 Temporary or loop ileostomy generally performed to allow anal anastomosis to heal Ostomy Surgically created opening between intestine and abdominal wall that allows passage of fecal material Surface opening called the stoma (see Figure108 A HEALTHY-APPEARING STOMA, p. 662) Name depends on location of stoma Ileostomy ( ostomy made in the Ilium of the small intestine Colon, rectum, anus usually completely removed (total proctocolectomy with permanent ileostomy) Loop ileostomy may be formed to eliminate feces, allow tissue healing for 23 months Continent ileostomy (see Figure 109 CONTINENT (KOCK) ILEOSTOMY on p. 663) ( intra-abdominal reservoir constructed, nipple valve formed Stool collects in internal pouch Nipple valve prevents it from leaking through stoma Catheter inserted into pouch to drain stool Pharmacologic therapy Ultimate goal to terminate acute attacks quickly, reduce incidence of relapse Locally acting, systemic anti-inflammatory drugs are primary medications Sulfasalazine acts topically on colonic mucosa to inhibit inflammatory process Corticosteroids given for acute exacerbations Mercaptopurine, other immunosuppressive agents can be used to treat clients who have not responded to other treatments Other immune response modifiers Remicade Mesalamine Antibiotic therapy Antidiarrheal agents ( loperamide, diphenoxylate Reinforce importance of adhering to strict medication regimen even when asymptomatic See MEDICATIONS Inflammatory Bowel Disease, p. 664-665 Nonpharmacologic therapy Antigens in diet may stimulate immune response( exacerbating IBD Dietary management should be individualized Increased dietary fiber may reduce diarrhea, but contraindicated for clients with intestinal strictures Acute exacerbation of Crohn disease may require withholding food Total parenteral nutrition (TPN) Elemental diet such as Ensure Complementary and alternative therapy Lack of research determining efficacy of alternative therapies Clients should discuss all potential therapies with their healthcare provider Nursing process Assessment Health history Current manifestation ( onset, severity, number of stools, presence of blood Diet Associated manifestations Physical examination Appearance, weight, vital signs Abdominal assessment Diagnosis Diarrhea Constipation Risk for Deficient Fluid Volume Acute Pain Chronic Pain Disturbed Body Image Imbalanced Nutrition Less Than Body Requirements Planning Client will achieve resolution of discomfort from symptoms Client will maintain adequate hydration Client will maintain optimal nutritional status Client will demonstrate positive, healthy coping skills Client will describe appropriate home self-care, including administering medications, making dietary choices, and preventing exacerbations Implementation Teaching major aspect of care Monitor fluid volume Acute exacerbation ( diarrhea can be frequent, painful Use stool chart to record frequency, amount, color of stools Monitor vital signs every 4 hours Weigh daily and record Assess for other indications of fluid deficit Maintain bowel rest by keeping NPO or limiting oral intake to elemental feedings as indicated Administer anti-inflammatory, antidiarrheal medications as indicated Maintain fluid intake by mouth or IV as indicated Provide good skin care Assess perianal area for irritation, denuded skin Promote healthy body image May experience frustration at lack of control over fecal elimination ( interfering with ability to complete tasks Major concern for children, adolescents Accept clients feelings and perception of self Encourage discussion of physical changes and consequences as they relate to self-concept Encourage discussion about concerns regarding effect of disease or treatment on close personal relationships Encourage client to make choices and decisions regarding care Discuss possible treatment options, effects openly, honestly Involve client in care, teaching and demonstrating as needed Provide care in accepting, nonjudgmental manner Arrange for interaction with clients, groups of people with IBD or ostomies Teach coping strategies and support their use Promote adequate nutritional intake IBD ( malabsorption, nutrient losses, multiple nutrient deficits can affect growth, development, healing, muscle mass, bone density, electrolyte imbalance Monitor laboratory results Provide the prescribed diet high-kilocalories, high-protein, low-fat, restricted dairy if lactose intolerant Provide parenteral nutrition as necessary Arrange for dietary consultation Provide or administer elemental enteral nutrition, supplements as ordered Include family members, including primary food preparer in particular, in teaching and dietary discussions See CLIENT TEACHING Dietary Instructions for Children with Inflammatory Bowel Disease, p. 667 See COMMUNITY-BASED CARE Home Care for the Client with IBD, p. 667 Evaluation Client demonstrates absence of GI distress Client, family demonstrate successful management of medication without side effects Client remains free from infection due to central line Positive body image is achieved Client demonstrates integration of relaxation techniques into daily life Review Inflammatory Bowel Disease Relate Link the Concepts and Exemplars Ready Go to Companion Skill Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 10.4 Nephritis Overview Nephritis is inflammation of kidney Classifications based on areas of involvement or etiology Glomerulonephritis Acute postinfectious glomerulonephritis (APIGN) Pathophysiology and etiology Acute proliferative glomerulonephritis ( glomerular damage occurs as result of immune complex reaction that is localized on glomerular capillary wall, leading to inflammation and obstruction See Figure 1010 INFECTION FROM GROUP A BETA-HEMOLYTIC STREPTOCOCCUS , p. 670 Chronic glomerulonephritis ( typically end stage of other glomerular disorders Slow progressive destruction of glomeruli, gradual decline in renal function Lupus nephritis ( consequence of systemic lupus erythematosus (SLE) Manifestations range from microscopic hematuria to massive proteinuria May be slow and chronic or fulminant Goodpasture syndrome ( rare autoimmune disorder of unknown etiology Formation of antibodies to the glomerular basement membranes May also bind to alveolar membranes causing pulmonary hemorrhage Manifestations include hematuria, proteinuria, edema Rapid progression to renal failure may occur Etiology ( distinct for each form of nephritis Autoimmune, such as SLE Infection Diabetes mellitus Risk factors Diabetes mellitus and/or hypertension Prematurity, trauma, familial history Other diseases Prevention Preventing viral infections with good hygiene Maintaining adequate diabetes and blood pressure control Quitting smoking Maintaining healthy body weight Clinical manifestations Asymptomatic to abrupt onset Flank, midabdominal pain Irritability, malaise, fever Microscopic hematuria in nearly all cases Gross hematuria ( tea-colored urine in up to 50 of cases Mild periorbital edema, dependent edema Edema may progress Acute post infection glomerulonephritis ( abrupt onset of hematuria, proteinuria, salt and water retention, evidence of azotemia 1014 days after initial infection Older adult may have fewer apparent symptoms See CLINICAL MANIFESTATIONS AND THERAPIES Nephritis, p.672 Collaboration Includes nephrologists, primary care provider, nurses, pharmacists, dietitians, possibly parents, teachers, school nurse Nurses role includes teaching, follow-up, coordination of referral services, communication between team members Diagnostic tests Throat or skin cultures Antistreptolysin O (ASO) titer ESR Kidney, ureter, bladder (KUB) abdominal x-ray Kidney scan Biopsy Blood urea nitrogen (BUN) Serum creatinine Urine creatinine Creatinine clearance Serum electrolytes Urinalysis Pharmacologic therapy Treat underlying disorders Antibiotics ( postinfection glomerulonephritis Aggressive immunosuppressive therapy for acute inflammatory processes Prednisone ( 1 mg/kg/day Cyclophosphamide Azathioprine Oral glucocorticoids also used in high doses to induce remission of nephritic syndrome Angiotensin-converting enzyme (ACE) inhibitors reduce protein loss associated with nephritic syndrome Antihypertensives may be prescribed to maintain blood pressure within normal limits Nonpharmacologic therapy Bed rest during acute phase Carefully monitor urinary output, weight, blood pressure, serum electrolytes Sodium and potassium restriction Dietary protein restricted Plasma exchange therapy (plasmapheresis) removes damaging antibodies from plasma used in rapidly progressing glomerular nephritis (RPGN) and Goodpasture syndrome RBCs returned to client with albumin or human plasma to replace plasma removed Complications include those associated with IV catheters, fluid volume shifts, altered coagulation Nursing process Assessment Health history Current manifestations Edema, weight gain, malaise, pain, cough or shortness of breath, changes in urine History of skin or pharyngeal streptococcal infection Diabetes SLE Kidney disease Medications Physical examination Appearance Vital signs Weight Edema Infection Skin, throat for lesions, infection Diagnosis Risk for Infection Excess Fluid Volume Risk for Impaired Skin Integrity Imbalanced Nutrition Less Than Body Requirements Fatigue Ineffective Role Performance Planning Client maintains, regains normal urine output Client is able to meet nutritional needs Client avoids infections Client maintains skin integrity Additional goals for pediatric clients Clients maintains education to remain current with classmates Client participates in diversional activities during period of bed rest Implementation Prevent infection Impaired renal function puts client at risk for infection Monitor for signs of infection Avoid, minimize invasive procedures Instruct family in good hand hygiene Limit visitors Protect skin integrity Dependent areas prone to pressure vulnerable Turn client frequently Pad body prominences Keep bed free of crumbs Keep sheets tight, free of wrinkles Promote nutritional balance Team approach No added salt and low-protein diet Client often anorexic ( encourage family to bring clients favorite foods Serve age-appropriate quantities Allow client to eat with other clients, family members Monitor and maintain fluid volume balance Monitor vital signs, fluid and electrolyte status, and intake and output Monitor degree of ascites Maintain fluid restriction as ordered Prevent unnecessary fatigue Common ( anemia, loss of plasma proteins, anorexia Schedule activities, procedures to provide adequate rest, energy conservation Assist with ADLs as needed Reduce energy demands with frequent small meals, short periods of activity Limit number of visitors, visit length Discuss with client, family relationship between fatigue and disease process Promote healthy self-esteem Manifestations, treatment of nephritis can affect ability to maintain usual roles, activities Encourage client self-care and participation in decision making Support coping skills Discuss effect of disease and treatments on roles, relationships Help client, family develop plan for alternative behaviors and relationships Provide accurate, optimistic information about disorder Evaluate need for additional support, social services ( provide referrals as needed Evaluation Client receives appropriate fluid volume each day and maintains or regains normal urine output Client develops no areas of redness, abrasions, skin breakdown Clients temperature remains within normal limits, client remains free of secondary infection Client maintains pre-illness weight, tolerates daily intake to meet nutritional requirements Client administers medications as prescribed Clients sodium and potassium levels reflect adherence to dietary restrictions Review Nephritis Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study Exemplar 10.5 Peptic Ulcer Disease Overview Peptic ulcer disease (PUD) ( break in lining of GI tract where it comes into contact with gastric juice ( chronic problem Ulcer is break in GI mucosa Peptic ulcers ( occur in any area of GI tract exposed to acid-pepsin secretions Esophagus Stomach Duodenum Duodenal ulcers ( most common Men more than women Gastric ulcers ( older clients, stomach More common in smokers, NSAID users See Figure 1011 COMMON SITES AFFECTED BY PUD, p. 677 Pathophysiology and etiology Innermost layer of stomach gastric mucosa Columnar epithelial cells supported by middle layer of blood vessels, glands, thin outer layer of smooth muscle Mucosal barrier protects the gastric mucosa Helicobacter pylori infection is unique in colonizing stomach Bacteria produces enzymes that reduce efficacy of mucus gel Inflammatory response to H. pylori contributes to gastric epithelial cell damage NSAIDs ( systemic, topical mechanisms Interrupt prostaglandin synthesis by disrupting action of enzyme cyclooxygenase (COX) Ulcers may affect esophagus, stomach, duodenum See Figure 1012 A SUPERFICIAL PEPTIC ULCER, p. 677 Sharply demarcated, less than 1 cm in diameter Etiology Often caused by H. pylori Risk factors Chronic H. pylori Aspirin and NSAID use Familial pattern suggests genetic factor Smokers Prevention Etiology determines what actions will minimize risk Prevention of H. pylori infection ( meticulous hand hygiene and food preparation NSAID use ( add or change medications to reduce occurrence of peptic ulcers Clinical manifestations Pain is classic symptom Gnawing, burning, aching, hunger-like Epigastric region, sometimes radiating to the back Relieved by eating Presentation in older adult often less clear Complications Hemorrhage as result of ulceration, erosion into blood vessels of gastric mucosa Gastric outlet obstruction may result from edema surrounding ulcer, smooth muscle spasm, scar tissue Perforation ( penetration of ulcer through mucosal wall Chemical peritonitis Bacterial peritonitis within 612 hours Immediate severe upper abdominal pain radiating throughout abdomen, possibly to shoulder Zollinger-Ellison syndrome ( form of peptic ulcer disease caused gastrinoma Secretes gastrin 5070 malignant Characteristic ulcerlike pain common High levels of hydrochloric acid entering duodenum may cause diarrhea, steatorrhea from impaired fat digestion and absorption Collaboration Treatment for PUD focuses on cause Diagnostic tests Upper GI series Gastroscopy Biopsy specimens obtained during gastroscopy ( tested for H. pylori Noninvasive methods of detecting H. pylori ( serologic testing, fecal antigen immunoassays, urea breath test If Zollinger-Ellison syndrome suspected ( gastric analysis performed to evaluate gastric acid secretion Surgery Not often with identification of H. pylori Older adults may have had gastric resection in past Pharmacologic therapy Combination therapies to eradicate H. pylori Two antibiotics with proton-pump inhibitor (PPI) Clarithromycin amoxicillin PPI Bismuth subsalicylate tetracycline metronidazole PPI NSAID-induced ulcers Discontinue NSAID if possible If not possible ( twice daily PPI PPIs bind acid-secreting enzyme that functions as proton pump Histamine2 (H2) receptor blockers inhibit histamine binding to receptors on gastric parietal cells ( reduces acid secretion Mucosal protectors Sucralfate binds to proteins in ulcer base ( forming protective barrier Bismuth compounds stimulate mucosal bicarbonate and prostaglandin production to promote ulcer healing ( antibacterial action against H. pylori Antacids stimulate gastric mucosal defenses Prostaglandin analogs (misoprostol) ( stimulate mucous and bicarbonate secretions, inhibit acid secretions Nonpharmacologic therapy Maintain good nutrition Bland, restrictive diets no longer necessary Mild alcohol intake is not harmful Smoking discouraged ( slows rate of healing, increases frequency of relapses Nursing process Assessment Health history Complaint of pain Relief measures Nausea, vomiting Mediations Cigarette smoking, alcohol use Physical examination General appearance, including heightweight relationship Vital signs including orthostatic measurements Abdominal examinations Diagnosis Risk for Bleeding Chronic Pain Disturbed Sleep Pattern Imbalanced Nutrition Less than Body Requirements Risk for Deficient Fluid Volume Planning Client will reduce risk factors to prevent recurrence Client will experience a reduction in discomfort related to PUD Client will maintain adequate nutritional intake Client will maintain hydration Implementation Restore and maintain fluid volume balance Monitor stools, gastric drainage for overt, occult blood Maintain IV therapy with fluid volume, electrolyte replacement solutions Administer blood products as ordered Insert NG tube, maintain position, patency Monitor hemoglobin, hematocrit, serum electrolytes, BUN, creatinine values Assess abdomen, including bowel sounds, distention, girth, tenderness every 4 hours and record Maintain bed rest with head of bed elevated Ensure safety Manage pain Assess pain, including location, type, severity, frequency, duration Typically experienced 24 hours after eating Administer PPIs, H2-receptor antagonists, antacids or mucosal protective agents as ordered Teach relaxation, stress reduction, lifestyle management techniques Facilitate adequate rest Nighttime ulcer pain typically occurs between 1 and 3 a.m. Emphasize importance of taking medications as prescribed Instruct client to limit food intake after evening meal, eliminating bedtime snack Encourage use of relaxation techniques, comfort measures as needed to promote sleep Promote balanced nutrition Anorexia, early satiety are associated with PUD Client may gradually reduce food intake to avoid discomfort Assess current diet, including pattern of food intake, eating schedule, foods that precipitate pain, being avoided in anticipation of pain Refer to dietitian for meal planning to minimize PUD symptoms, meet nutritional needs Monitor for complaints of anorexia, fullness, nausea, vomiting Monitor laboratory values for indications of anemia, other nutritional deficits Evaluation Client experiences no complications realted to PUD Client obtains pain control adequate to promote rest, sleep Client describes actions that will reduce risk of recurrence of PUD Client maintains fluid volume homeostasis Client obtains adequate rest, sleep to promote health Review Peptic Ulcer Disease Relate Link the Concepts and Exemplars Ready Go to Companion Skills Manual Refer Go to Nursing Student Resources Reflect Case Study 2015 by Education Lecture Outline for Nursing A Concept-Based Approach to Learning, 2e, Volume 1 PAGE PAGE MERGEFORMAT 39 Y, dXiJ(x(I_TS1EZBmU/xYy5g/GMGeD3Vqq8K)fw9 xrxwrTZaGy8IjbRcXI u3KGnD1NIBs RuKV.ELM2fiVvlu8zH (W uV4(Tn 7_m-UBww_8(/0hFL)7iAs),Qg20ppf DU4p MDBJlC5 2FhsFYn3E6945Z5k8Fmw-dznZxJZp/P,)KQk5qpN8KGbe Sd17 paSR 6Q