Metabolism And Elimination

METABOLISM AND ELIMINATION Marcus Rowell Cueno, RN

DISORDERS OF THE PANCREAS •

Pancreatitis - inflammatory process of the pancreas o May be acute or chronic o Severity depends on extent of inflammation and tissue destruction o Range from edema and inflammation to necrotizing hemorrhagic pancreatitis with fibrosis and tissue death Acute Pancreatitis

•

Major Pathophysiologic Processes Are: o Lypolysis o Proteolysis o Necrosis of Blood Vessels o Inflammation Etiology of Pancreatitis

• • • •

Contributing factors may be alcoholism and biliary tract disease with gallstones Trauma, surgical minipulation, the Whipple procedure, and partial gastrectomy Viral infections, gactric or duodenal ulcers, tumors, cysts, abcesses, Drug toxicities and oral contraceptives Incidence

• • • •

Middle-aged males after heavy alcohol consumption Females after biliary tract disturbances Prognosis better if unrelated to alcohol 10% die, 60% if alcohol related Nursing Care

•

Assessment - History very important; ask re: abdominal pain, alcohol consumption, high fat meals, family history, biliary or pancreatic problems, abdominal surgery, other contributing causes previously listed Physical Assessment/Clinical Manifestations

•

• • • •

Abdominal pain; mid or ULQ area; radiates to back, left flank or left shoulder and aggravated by alcohol, fatty meal, lying in recumbent position; relieved with fetal position or sitting upright and bending forward Weight loss, N&V, jaundice, gray-blue discoloration of abdomen (Cullen’s sign) and the flanks (Turner’s sign) Bowel sounds absent or decreased (paralytic ileus), abdominal tenderness, rigidity, and guarding (peritonitis); palpable mass Elevated temp, tachycardia, decreased BP, decreased or abnormal breath sounds, dyspnea or orthopnea Changes in behavior and sensorium

Diagnostic Assessment • • • • • • •

Elevated serum amylase, lipase, glucose, bilirubin, alkaline phosphatase, WBC Elevated urine amylase Decreased serum calcium CT Chest x-ray Ultrasound and MRI Bentiromide test to assess pancreatic functioning Nursing Diagnoses (Analysis)

• • •

Pain related to the effects of pancreatic inflammation and enzyme leakage AEB___ Altered nutrition: Less than body requirements related to the effects of pancreatic dysfunction, N&V, and anorexia AEB____ Others??? Planning/Expected Outcomes

• •

The client will experience relief of abdominal pain by_____ The client will have sufficient nutritional intake to maintain body weight with a decrease in pancreatic stimulation by___ Non-Surgical Management

• • •

Fasting to rest pancreas and reduce enzyme secretion IV fluids, NG tube (must have bowel sound before removed) Drug therapy and comfort measures Drug Therapy

• • • • • • •

Meperidine Nitroglycerine Antispasmodics Carbonic anhydrase inhibitor Antacids Histamine H2-receptor antagonists Calcium gluconate

• • • • • •

Adrenocortical steroids Aprotinin Glucagon Somatostatin Albumin (if shock present) Chronic Pancreatitis - Pancreatin and Insulin used Comfort Measures

• • •

Fetal position Oral hygiene -NG tube Lower anxiety level - explain procedures, diversional activities, encourage visitors, encourage expression of emotions Surgical Management

•

Usually not indicated

• • •

Complications such as cyst and abcess may necessitate surgical drainage General pre-op measures, NG- tube, IV fluids, teaching re: pancreatic drainage tube and what to expect Drainage tubes may be connected to low suction (80mmHg or less) Postoperative Care-Interventions

• • • • • • •

`Monitor drainage tubes for patency, kinks, ordered suction pressure, integrity Record intake and output, character of drainage Meticulous skin care and dressing changes Skin barriers -Stomahesive wafer, aluminum paste; ET nurse NPO, TPN Begin with small frequent, moderate to high carbohydrate, high-protein, low-fat meals; bland; no caffeine Ensure, Isocal to supplement diet, fat-soluable and other vitamin/mineral supplements Continuing Care

• • • •

Health teaching to avoid further episodes Acute pain, jaundice, clay-colored stools, dark urine call Dr. Limit physical activity Home visits, AA, family support (Al-Anon) Evaluation

•

Expected outcomes from nursing diagnoses should be evaluated as well as nursing interventions. Chronic Pancreatitis

• • •

Chronic Calcifying Pancreatitis (CCP) - alcohol induced; protein plugs ducts causing inflammation and fibrosis Chronic Obstructive Pancreatitis - develops from inflammation, spasm, and obstruction of the sphincter of Oddi Review Patho notes for other changes! Key Features of Chronic Pancreatitis

• • • • • •

Intense burning or gnawing abdominal pain Abdominal tenderness; ascites; LUQ mass (cyst or abscess) Respiratory compromise Steatorrhea; clay-colored stools Weight loss; jaundice; dark urine Polyuria, polydipsia, polyphagia (diabetes) Nursing Care/Interventions

• • •

Same as with acute Analgesia important for pain Enzyme replacement essential - give before or with meals, swallow without chewing, mix with applesauce or fruit juice, not protein-containing foods, wipe lips after taking meds, monitor serum uric acid levels for increase (caused by pancrelipase)

Surgical Invervention • • • •

Not a primary intervention Done for abscess, cyst, or underlying cause Pancreaticojejunostomy to relieve obstruction Whipple procedure for pancreatic cancer

BILIARY DISORDERS DISORDERS OF THE GALLBLADDER • • •

• • •

CHOLECYSTITIS - inflammation of the gallbladder Acute - usually associated with cholelithiasis (gallstones); may be caused by bacteria in absence of stones Trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall having a toxic effect Bile, impaired circulation, edema, and distention cause ischemia, resulting in tissue sloughing with necrosis and gangrene Perforation may occur causing an abcess or peritonitis Interfere with bile for fat digestion Chronic Cholecystitis

• • • •

• •

Results with persistent inefficient emptying of bile by the gallbladder May be caused by or lead to the formation of gallstones Gallbladder becomes fibrotic and contracted which results in decreased motility and deficient absorption Pancreatitis and cholangitis (inflammation of the common bile duct) can occur as complications due to back up of bile Bile obstruction leads to jaundice which may be extrahepatic or intrahepatic Circulating levels of bilirubin are increased, and jaundice occurs if more than 2 mg/dL Cause of Cholecystitis

• •

Exact etiology unknown Formation of gallbladder calculi, trauma, decreased blood supply, prolonged anesthesia/surgery, adhesions, edema, neoplasms, long-term fasting, prolonged dehydration, prolonged immobility, excessive opioid use, anatomic problems sedentary lifestyle, familial tendency, obesity, and diabetes INCIDENCE

• • • • •

Sedentary life style Familial tendancy Obesity Diabetes White women Symptoms and Assessment

• • •

Episodic or vague abdominal pain or discomfort that may radiate to right shoulder Pain after high fat or high volume meal Anorexia

•

Nausea or vomiting

• • • • • • • •

Dyspepsia Eructation Flatulence Feeling of abdominal fullness Pruritis (itching) or burning sensation of skin Rebound tenderness (Blumberg’s sign) Fever Jaundice, clay-colored stools, dark urine, steatorrhea (most common with chronic cholecystitis) Diagnostic Assessment

•

• • • • •

Elevated serum levels of alkaline phosphatase, aspartate aminotransferase (AST), Lactate dehydrogenase (LDH), direct and indirect bilirubin, WBC, and amylase Oral cholecystogram (OCG) Gallbladder (GB) radiographic series Upper GI radiographic series Technetium-labeled acetanilido iminodiacetic acid (99mTc HIDA) Ultrasonography of gallbladder (has replaced OCG) Interventions

• • •

Non-surgical initially to rest inflammed gallbladder and relieve pain Diet Therapy - avoid high fat and high volume meals, NG tube to decompress stomach, smaller more frequent meals Drug Therapy, - opioid analgesics (Demerol), antispasmodic agents, and antiemetics Surgical Management

• • •

CHOLECYSTECTOMY - removal of the gallbladder Pre-op Care - teaching re: deep breathing, coughing, splinting, early ambulation, NPO Operative Procedure - T-tube, Penrose or Jackson-Pratt drain for serosanguineous, bile stained drainage. Postoperative Nursing Care

• • • • • •

Incisional pain relief (PCA pump) Coughing and deep breathing Antiemetics Wound and T-tube care; drainage irritating NPO or NG tube 4-6 weeks recovery Nursing Care: T-Tube

• • • •

Assess drainage; bloody, green-brown; report more than 1000ml/day Administer bile salts (Decholin) Inspect skin around T-tube insertion; keep dressing dry Keep drainage system below level of gallbladder

• •

Never clamp, irrigate, or aspirate a T-tube without a physician’s order Assess drainage system for kinks, pulling, or tangling of tubing

•

When ordered, raise the drainage bag to level of abdomen (4th or 5th postop day) and assess client for feelings of fullness, nausea, or pain

•

Clamp T-tube for 1-2 hours before and after meals as ordered; assess for tolerance of food Observe stools for return of brown color 7-10 days post-op

•

Laparoscopic Cholecystectomy • • •

• • • • •

Treatment of choice since 1989 10 mm incision at umbilicus, abdominal cavity insufflated with 3-4L carbon dioxide Trocar catheter inserted and laparoscope is passed through it and attached to a video camera so abdominal organs can be viewed on monitor; laser used to dissect. Reduces risk of wound complications Early ambulation promotes absorption of carbon dioxide and decreased "free air pain" Requires less pain med Return to usual activities, including work, much sooner (1-3 weeks) SEE CLINICAL PATHWAY CHOLELITHIASIS

• •

•

The presence of one or more gallstones in biliary tract; most common disorder Contributing factors: excessive bile salt losses, decreased gallbladderemptying rates, supersaturation of bile with cholesterol, changes in bile concentration or bile stasis within the gallbladder Causes cholecystitis Composition of Gallstones

• • • • • •

Substances normally found in bile such as: Cholesterol Bilirubin Bile salts Calcium Proteins Types of Gallstones

• • •

Cholesterol Stones Result of metabolic imbalances of cholesterol and bile salts Most common type in U.S.

• • • •

Pigment Stones Result of metabolic imbalances of unconjugated bilirubin Small, brown or black Black stones composed of calcium bilirubinate; most common Etiology

• •

Familial tendency related to dietary habits, excessive cholesterol intake, and sedentary lifestyles Seen more frequently in obese clients with impaired fat metabolism

•

Low-calorie or liquid diets cause liberation of cholesterol from tissues and excretion as crystals in bile Women’s Health Considerations

• • • • • •

Incidence of gallbladder disease is higher in women, especially European American women. By age 60, nearly one-third of obese women develop biliary disease Pregnancy tends to increase gallstone formation Pregnancy and estrogen cause delayed muscular contraction of gallbladder which decrease rate of bile emptying Incidence of gallstones higher in women who have had multiple pregnancies Cholelithiasis seen with hemolytic blood disorders, bowel disease, and after jejunoileal bypass surgery for obesity, and diabetes Incidence of Cholelithiasis

• • • • •

Higher in women; males 50 and older Caucasians and Native Americans (Navajo and Pima tribes) have higher incidence Prevalent in Asian-Americans and African-American More than 20 million diagnosed in U.S. One million cases reported yearly Assessment and Symptoms

• • •

Severity of pain and presentaion depend on mobility, size, location, obstruction, and inflammation Initially a steady, mild ache in mid-epigastric area; may radiate to right shoulder or back; RUQ pain of abdomen Biliary colic may include tachycardia, pallor, diaphoresis, and prostration; N &V Diagnosis

• • • • •

Same lab tests as cholecystitis Abdominal x-ray Oral or IV cholecystogram Ultrasound (test of choice); 95% accurate Percutaneous transhepatic cholangiography Nonsurgical Interventions

• • • • • •

Rest inflammed gallbladder Diet Therapy - low fat, vitamins A, D, E, K, bile salts Drug Therapy - same as before; Questran Bile acid therapy (Ursodiol - Actigall) Extracorporeal shock wave lithotripsy; 3 or fewer stones Percutaneous transhepatic biliary catheter insertion Surgical Intervention

• •

Cholecystotomy - opening made and stones removed Choledocholithotomy - incision into common bile duct to remove stones Nursing Care: Same as with Cholecystectomy and T-Tube

•

The nurse also instructs the client to report symptoms of biliary tract disease, including jaundice, darkened urine, light-colored stools, pain, fever, or chills

HEPATIC DISORDERS Jaundice • • • •

Associated with liver disorders Yellowish coloration visible when bilirubin levels in the blood 3x normal alteration in bilirubin metabolism or obstruction to flow of bile into the duct system first seen in sclera and skin Types of Jaundice

• • •

Hemolytic - increased RBC breakdown, blood transfusion, sickle cell crisis, hemolytic anemia Hepatocellular - Hepatic carcinoma or hepatitis; alteration in bilirubin uptake, conjugation or excretion Obstructed - impeded flow of bile through liver; liver tumors, hepatitis or cirrhosis Jaundice and Hyperbilirubinemia

• • • • •

Refer to Patho notes for forms of bilirubin (unconjugated and conjugated) Excess production of bilirubin Impaired uptake of unconjugated bilirubin Impaired conjugation of bilirubin Decreased excretion of conjugated bilirubin HEPATITIS

•

Primarily viral in origin but can be caused by bacteria, drugs, and chemicals (toxic) Viral Hepatitis - A,B,C,D,E; cytomegalovirus, Epstein-Barr herpes, coxsackievirus, and rubella Many cases asymptomatic - undiagnosed

• • •

Up to 50% of adults in U.S. have been infected with Type A virus Diagnosis based on presence of antigens and antibodies Infection with one type provides immunity to that type but not to others

• •

HEPATITIS A • • • • •

Occurs worldwide in children fecal-oral route, contaminated food or water Incubation of 15-50 days Found in feces before and after symptoms In blood only briefly

HEPATITIS B • • •

Transmitted through exposure to blood/products, sexual & perinatal contact Incubation 45-180 days Complex DNA structure with 3 antigens HEPATITIS C

• • •

Transmitted by exposure to blood/products, sexual contact Incubation 14-180 days RNA virus

HEPATITIS D • • • •

Delta virus always follows HBV Chronic carriers of HBV at risk Incubation period not known Routes of transmission same as HBV HEPATITIS E

• • • •

Fecal-oral transmission Mostly in underdeveloped countries with poor sanitation Incubation 15-64 days Based on diagnosis of exclusion - no serologic tests Hepatitis and Liver Damage

• • • •

Inflammation causes liver tissue damage Bile flow may be interrupted & inflammation of the gall bladder may occur Without complications, liver cells will regenerate & normal function returns Systemic effects are: immune reactions (rash, angioedema, arthritis, fever, malaise, glomerulonephritis, vasculitis; many asymptomatic, especially children Phases of Hepatitis

•

Pre-icteric Phase: 1-2 days before onset of jaundice, anorexia, nausea, vomiting, RUQ pain, constipation or diarrhea, malaise, headache, fever, joint pain, urticaria, weight loss, liver and spleen enlargement

•

Icteric Phase: 2-4 weeks, jaundice, pruritis, dark urine, bilirubinuria, light stools, fatigue, liver enlargement, tenderness, and weight loss

•

Post-icteric Phase: convalescent or recovery phase, lasts weeks to months, fatigue, general malaise, spleen returns to normal before liver, relapses may occur

•

Hepatitis mortality rate low, high in elderly Complications

• • •

Can become chronic persistent with delayed convalescence Chronic active - idiopathic, may lead to cirrhosis, persistent Fulminant - severe necrosis, liver failure and death

Diagnosis of Hepatitis • •

Liver studies, serologic tests, biopsy Liver tenderness, hepatomegaly, myalgia, splenomegaly, arthralgia, abdominal pain, fever, irritability, lethargy, malaise, N&V Nursing Diagnoses/Analysis

• • • • • • •

Altered nutrition Activity intolerance Anxiety Pain Body image disturbance Fatigue Knowledge deficit Management

• • • • •

Usually at home Rest Adequate diet, high protein and carbohydrate, vitamins Avoid alcohol and drugs (detoxified in liver), fatty foods Vaccine, gamma globulin, interferon Nursing Care/Interventions

• • • • • •

UNIVERSAL PRECAUTIONS! Comfort measures Small frequent feedings; adequate fluid intake;, oral hygiene Antiemetics (Tigan, Dramamine) Monitor activities; weak, build strength Promote return of normal liver function Other Types of Hepatitis

•

•

Toxic and Drug-Induced: may occur after injection, ingestion, inhalation of chemical substances, systemic poisons, drugs (acetaminophen), drug sensitivity; liver necrosis occurs within days Idiopathic: Autoimmune form; usually affects women; treated with corticosteroids and immunosuppressive agents HEPATITIS CASE STUDY

• • • •

Winningham, GI Disorders, Case Study 8: Hepatitis A Work in groups Critical thinking activity Be thorough! CIRRHOSIS

• • • • •

Chronic, progressive disease; long, tortuous Extensive cell destruction Disorganized regrowth with fibrous distortion of blood vessels and bile ducts Lobes become irregular in shape and size, impeding vascular flow Alcohol most common cause; men 40-60; high death rate; unpleasant disease course TYPES OF CIRRHOSIS

• • • •

Alcoholic (Laennec’s) -early changes reversible, fat accumulation; later scar tissue forms and irreversible; alcohol or malnutrition cause Postnecrotic - complication of viral, toxic, idiopathic; scar tissue Cardiac - chronic right sided heart failure with cor pulmonale, constrictive pericarditis, and tricuspid insufficiency Biliary - chronic biliary obstruction and infection; scar tissue Early Manifestations

• •

GI disturbances, anorexia, flatulence, N&V, changes in bowel habits d/t alterations in metabolism Abdominal pain, fever, lassitude, weight loss, liver and spleen enlargement Late Manifestations

•

•

Jaundice, peripheral edema, ascites, skin lesions, hematologic disorders, endocrine disturbances, peripheral neuropathies; liver becomes small and nodular; bile salts collect under the skin causing severe pruritus, anemia, clotting disorders Every body system affected! (See picture in textbook.)

Complications of Cirrhosis • • • • • • • •

Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal-systemic encephalopathy (PSE) with hepatic coma Hepatorenal syndrome KNOW WHAT CAUSES EACH ONE! Diagnosis

• • • • • • • • • • • •

Serum enzymes Bilirubin Serum Proteins Serum Ammonia Prothrombin time ALL ELEVATED! Serum protein & albumin decreased in chronic/severe liver disease Abdominal x-ray Upper GI series CT of abdomen Esophagogastroduode-noscopy(EGD) Injection sclerotherapy Portal Hypertension & Esophageal Varices

• • •

Compression and destruction of portal & hepatic veins cause obstruction to blood flow causing portal hypertension Collateral circulation develops as a compensatory mechanism particularly in esophageal area Varicosities also develop where systemic and collateral circulations join, causing esophageal and gastric varices/hemorrhoids

• • •

Collateral vessels are fragile, fairly non-distensible, so they don’t tolerate high pressure; bleed easily The bigger and more tortuous the vessel, the more it will bleed; mortality rate high Reoccurrence of bleeding high; precipitated by alcohol, coarse food, straining, vomiting, sneezing, lifting Peripheral Edema & Ascites

• • • •

• • • •

Caused by change in osmotic pressure due to impaired synthesis of albumin and increased portacaval pressure from PHT Edema at ankles and presacral areas Ascites: fluid collection in peritoneal cavity results in increased abdominal girth and weight gain ADH, water & sodium retention cause K+ loss, decreased output & dehydration Decreased blood flow and other problems cause renal damage Increased levels of ammonia in blood cause hepatic encephalopathy, lethargy, coma progressive disorientation, impaired judgement, and confusion occur Asterixis, liver flap etc.