Absorption and Elimination PDF

Absorption and Elimination Cynthia Lasman, RNC-OB, MSN, CNE, C-EFM [email protected] Objectives  Review anatomy and physiology of the lower GI system  Discuss common laboratory tests and diagnostic tools for lower GI system  Consider the etiology and incidence of lower GI dis...

Absorption and Elimination Cynthia Lasman, RNC-OB, MSN, CNE, C-EFM [email protected] Objectives  Review anatomy and physiology of the lower GI system  Discuss common laboratory tests and diagnostic tools for lower GI system  Consider the etiology and incidence of lower GI disease and dysfunction  Describe common assessment ndings with lower GI disease and dysfunction  Describe select conditions of the lower GI system  Explain appropriate nursing care and rationales for the care of patients experiencing lower GI disease and dysfunction A&P: Lower GI  Mind and emotions play a role in function  Small Intestine  Longest segment of the GI tract (2/3 of total)  Primary function is absorption  3 sections  Duodenum (ampulla of Vater – opening from the common bile duct)  Jejunum  Ileum (ends with the ileocecal valve – prevents bacteria from ascending)  Large Intestine  Ascending (right side)  Transverse (right to left across the upper abdomen  Descending (left side)  Sigmoid Colon  Rectum  Anus (internal and external sphincters to regulate output) Waste Products  Fecal matter should be 75% 2uid and 25% solid  Brown color is from breakdown of bile by gut bacteria  GI tract contain gases formed from digestion  Absorbed by portal circulation  detoxied by the liver  Expelled from the rectum as 2atus  Process of elimination  Rectal distention causes contractions of the musculature and relaxes the internal anal sphincter  External anal sphincter is under voluntary control  Contracting the abdominal muscles can aid in defecation Gut Microbiome  Breakdown waste  Vitamin synthesis  Immune functions (protective and in2ammatory)  Colonization begins at birth and is established by 2 years old  Factors that in2uence the gut microbiome  Age  Genetics  Diet  Personal hygiene  Infection  Vaccinations  Chronic disease  Medication (especially antibiotics) Laboratory Studies  Serum laboratory studies  Stool tests  Ultrasonography  Genetic testing  Imaging studies: CT, PET, MRI, scintigraphy, virtual colonoscopy  Lower GI tract study  GI motility studies  Sigmoidoscopy / Colonoscopy Question Is the following statement true or false? When a colonoscopy is performed, the 2exible scope is passed through the rectum and sigmoid colon into the descending, transverse, and ascending colon. Answer to Question True Rationale: When a colonoscopy is performed, the 2exible scope is passed through the rectum and sigmoid colon into the descending, transverse, and ascending colon. When a 2exible beroptic sigmoidoscopy is performed, the 2exible scope is advanced past the proximal sigmoid and then into the descending colon. Constipation  Constipation  Fewer than three bowel movements weekly  bowel movements that are hard, dry, small, or di3x upper limit  Usually elevated within 24 hours of onset of symptoms  Amylase returns to normal within 48-72 hours, lipase takes longer  Abnormal imaging (CT, MRI, or ultrasound)  Treatment - Relieve symptoms and prevent complications  NPO  Feeding by enteral route (parenteral only if feeding is not tolerated)  Nasogastric suction to relieve N/V and abdominal distention (not routine use)  Analgesia (suLcient to minimize restlessness)  Often opioids – Avoid NSAIDS!  Removal of blockage Chronic Pancreatitis  Progressive in5ammatory condition  Pancreatic cells are replaced by brous tissue  Increases pressure within the pancreas leads to  obstruction of pancreatic and common bile ducts  Atrophy of the epithelium of the ducts  Most often caused by excessive alcohol consumption in the U.S.  Malnutrition is also a common cause worldwide  Typical patient is 40-60 years old  Assessment  May be asymptomatic  Usually recurrent attacks of upper abdominal and back pain accompanied by vomiting  So painful even opioids do not give relief (risk for opioid dependence)  Attacks become more frequent, severe and last longer with disease progression  Weight loss and anorexia  Frothy, frequent, foul stools, steatorrhea  Calcium stones within the ducts (advanced disease) Chronic Pancreatitis  Management  Prevention of acute attacks  Pain management  Nonsurgical (2/3 of patients)  Endoscopy (stone removal, widen strictures with stents, drain cysts)  Medication management (pain ladder)  Surgical (1/3 of patients)  Pancreaticojejunostomy (Roux-en-Y)  Allows drainage of pancreatic secretions into the jejunum  Pain relief occurs within 6mo for most patients  Other surgeries including Whipple’s resection  Many patients with sx intervention continue to have some symptoms and complications Knowledge Check What is a major symptom of chronic pancreatitis? A. Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting B. Fever, jaundice, confusion, and agitation C. Ecchymosis in the 5ank or umbilical area D. Abdominal guarding ANSWER A. Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting Rationale: Chronic pancreatitis is characterized by recurrent attacks of severe upper abdominal and back pain accompanied by vomiting. Acute pancreatitis presents with fever, jaundice, confusion, agitation, ecchymosis in the 5ank or umbilical area, and abdominal guarding. Knowledge Check Is the following statement true or false? Patients with acute pancreatitis require a high- carbohydrate, low-protein, and low-fat diet. ANSWER True Rationale: In patients with acute pancreatitis, a high-carbohydrate, low-protein, and low-fat diet increases caloric intake without stimulating pancreatic secretions beyond the ability of the pancreas to respond. Review of Objectives Review anatomy and physiology of the biliary system Discuss common laboratory tests and diagnostic tools for biliary system dysfunction Consider the etiology and incidence of biliary system dysfunction Describe common assessment ndings with biliary system dysfunction Describe select conditions of the biliary system Explain appropriate nursing care and rationales for the care of patients experiencing biliary system dysfunction Alternative Nutrition Objectives  Discuss enteral and parenteral feeding  Describe methods for safely providing nutrition to patients  Explain nursing care for the patient receiving enteral and/or parenteral feeding Click icon to add picture Delivering Nutrition Enterally Meet nutritional requirements when oral intake is inadequate or not possible, and the GI tract is functioning Advantages Safe and cost eGective Preserve GI integrity Preserve the normal sequence of intestinal and hepatic metabolism Maintain fat metabolism and lipoprotein synthesis Maintain normal insulin and glucagon ratios Enteral feeding routes  Temporary  Nasogastric  Nasoduodenal or nasojejunal  Used when the stomach needs to be bypassed for a short time (less than 4 weeks) or for a patient with a high risk of aspiration  Long-term  Gastrostomy (G-tube)  Percutaneous endoscopic gastrostomy (PEG)  Jejunostomy (J-tube) Click icon to add picture Enteral Feeding Routes Temporary Nasogastric Nasoduodenal Nasojejunal Used when the stomach needs to be bypassed for a short time (usually less than 4 weeks) or for a patient with a high risk of aspiration Typically < 12-Fr Click icon to add picture Enteral Feeding Routes Long-term Gastrostomy (G- tube) Percutaneous endoscopic gastrostomy (PEG) Jejunostomy (J-tube)  Formulas  Varity of preparations  Caloric density  Osmolality  Fiber  Minerals,  Electrolytes  Cost  Formula does not include all water needed Bolus or Continuous  Bolus  Divide total daily feeding volume in 4-6 feeds (typically 200- 400 mL)  Feeding given by syringe (>50 mL) by gravity  Relatively quick (15-60 minutes)  Start feeding slowly  Raise or lower syringe to control rate  Continuous or cyclic (over 8-18 hours)  Used for critically ill patients, high aspiration risk, risk for intolerance, small bowel placements  Pump used to control rate Administering Tube Feedings  Dependent on location  Patient education and preparation  Tube insertion  Conrming placement  Clearing tube obstruction  Monitoring the patient  Maintaining tube function  Oral and nasal care  Monitoring, preventing, and managing complications  Tube removal Assessment of the Patient Receiving an Enteral Feeding Tube placement   Patient’s ability to tolerate formula and amount  Clinical response  Signs of dehydration  Elevated blood glucose level, decreased urinary output, sudden weight gain, and periorbital or dependent edema  Signs of infection  Check gastric residual volume  I&O, weekly weights, dietician consult Enteral Feeding  Administer feeding at prescribed rate and method and according to patient tolerance  Administer water before and after each medication and each feeding, every 4 to 6 hours, and whenever the tube feeding is discontinued or interrupted  Do not mix medications with feedings  Maintain delivery system as required. To avoid bacterial contamination, do not hang more than 4 to 8 hours of feeding in an open system (manufacturer’s recommendations)  Maintain normal bowel elimination  Refer to Table 39-3  Maintain hydration by supplying additional water and assessing for signs of dehydration  Promote coping by support and encouragement; encourage self-care and activities  Patient education Question #2 Is the following statement true or false? Measuring gastric residual volumes by removing gastric contents with a large syringe at routine intervals is common practice and recommended nursing management for patients receiving enteral nutrition. Answer to Question #2 False Rationale: Assessment of gastric residual volume has not been substantiated by research and may cause clogging of gastric tubes. This practice is not usually recommended. Question #3 What position should the patient’s head be in when receiving a tube feeding to prevent aspiration? A. Flat B. 10 degrees of elevation C. 30 degrees of elevation D. 45 degrees of elevation Answer to Question #3 C. 30 degrees of elevation Rationale: The semi-Fowler position is necessary for an NG feeding with the patient’s head elevated at least 30 degrees to reduce the risk of aspiration. The nurse must assess external tube marking to avoid drift in placement and observe the patient for signs and symptoms of nausea that could lead to gastric re5ux and aspiration. Parenteral Nutrition  Assist in identifying patients who are candidates for PN  Nutrition status; decreased oral intake >1 week  Weight loss 10% or more of usual weight  Muscle wasting, decreased tissue healing  Persistent N&V  Monitor  Hydration status  Electrolytes  Caloric intake  Complications Major goals include:  Pneumothorax, air embolism Attaining an optimal level of nutrition  Clotted or displaced catheter Absence of infection  Sepsis Adequate 5uid volume  Hyperglycemia Optimal level of activity  Rebound hypoglycemia Knowledge of self-care  Fluid overload Absence of complications  Refer to Table 41-7 Parenteral Nutrition Nursing Interventions Maintaining optimal nutrition Maintaining 5uid balance  Daily weight at same time of day infusion pump  Accurate I&O do not increase or decrease 5ow rate  Caloric count rapidly  Trace elements included in solution I&O Weights  Preventing infection Monitor blood glucose levels  Appropriate catheter and IV site care  Strict sterile technique for dressing changes  Wear mask when changing the dressing  Assess insertion site  Assess for indicators of infection  Proper IV and tubing care Hepatic System Professor Rose Frowd MS, RN BC-PMH, CASAC [email protected] Objectives  Review anatomy and physiology of the hepatic system  Discuss common laboratory tests and diagnostic tools for hepatic dysfunction  Consider the etiology and incidence of liver dysfunction  Describe common assessment ndings with liver dysfunction and liver failure  Describe select conditions of the hepatic system  Explain appropriate nursing care and rationales for the care of patients experiencing liver dysfunction  Consider alternative and complimentary medications as they relate to the hepatic system A&P: Anatomy of the Liver  Largest gland in the body  Located right upper quadrant (RUQ)  Not palpable (usually)  Highly vascular  Blood supply from GI tract via the Portal Vein and Hepatic Artery  A&P: Metabolic Function Glucose metabolism Ammonia conversion Protein metabolism Vitamin and iron storag Drug metabolism Bile formation Bilirubin excretion Drug metabolism Liver Function Studies Serum Pigment studies: aminotransferases: direct and indirect serum AST bilirubin ALT urine bilirubin GGT urobilinogen GGTP Prothrombin time LDH Serum alkaline phosphatase Serum protein studies Serum ammonia Cholesterol  Diagnostic Studies  Ultrasound  Computed Telemetry (CT)  Magnetic Resonance Imagery (MRI)  Endoscopy  Liver Biopsy  Left side or supine for procedure  Right side for recovery Physical Assessment  Physical Assessment  Pallor or Jaundice  Muscle atrophy  Edema  Skin excoriation (from scratching)  Petechiae, ecchymosis, spider angiomas  Palmar erythema  Change in cognitive status  Fluid in the abdomen  Palpable liver  Tenderness with palpation Liver Dysfunction: Etiology  Alcoholism  Infection  Anorexia  Metabolic Disorder  Nutritional Deciencies Liver Dysfunction: Bilirubin  Bilirubin is produced in the liver, spleen, and bone marrow  Results from hemoglobin metabolism and is a byproduct of hemolysis  Liver removes bilirubin from blood and excretes bilirubin in bile  Two types of bilirubin Conjugated Unconjugated  Direct bilirubin  Indirect bilirubin  Circulates in the blood  Binds with protein in the blood  Direct byproduct of  Converted by liver for hemolysis excretion Liver Dysfunction: Jaundice  Also called Icterus  Skin  Mucous membranes  Sclera  Sign of dysfunction (not a disorder)  Yellow discoloration of tissue  Result from high serum concentration of bilirubin  Normal bilirubin: 0.2-1.3 mg/dL  Serum bilirubin > 2.5 mg/dL = jaundice  Varies for individual with dark skin tones  Liver Dysfunction: Types  Three types  Hemolytic  Excessive destruction of RBCs  Elevated serum unconjugated bilirubin  Hepatocellular  Liver disease  Elevated serum conjugated and unconjugated bilirubin  Obstructive  Caused by blockage of bile from the liver to the intestinal tract  Elevated serum conjugated bilirubin  Fulminate Hepatic Failure  Sudden and severe  Liver failure within 8 weeks of appearance of jaundice Liver Dysfunction: Hemolytic Jaundice  Increased destruction of RBCs  Pale or Jaundice  Dark-colored urine  Weakness  Dizziness  Activity Intolerance Liver Dysfunction: Hepatocellular Jaundice  Loss of appetite  Nausea  Weight loss  Malaise  Fatigue  Weakness  Headache  Chills  Fever (if infectious etiology) Liver Dysfunction: Obstructive Jaundice  Dark orange-brown urine  Light clay-colored stools  Dyspepsia  Intolerance of fats  Impaired digestion  Pruritus Hepatitis: Types  A systemic infection that causes necrosis and inBammation of liver cells with characteristic symptoms and cellular and biochemical changes  Two types: Infectious and Toxic  Viral Hepatitis  A  B  C  D  E  G, GB virus-C  Nonviral Hepatitis  Toxin (chemical substances, poisons)  Drug-induced (medications)  Hepatitis: Phases All types of Hepatitis have three phases (Pre-Icteric, Icteric, Post-Icteric)  Pre Icteric Phase  Icteric Phase  Post Icteric Phase  1-3 weeks before jaundice  lasts 2-6 weeks  lasts 2-12 weeks appears  Begins with appearance of  Recovery  Fatigue jaundice  Clinical  Anorexia  Discomfort in RUQ due to manifestations enlargement of liver disappear  Taste and smell changes  Dark urine  Jaundice subsides  Nasal inflammation and discharge  Light clay colored stools  Continued  Pruritis malaise  Low grade temperature  Anorexia  Easily fatigued  Mild flu-like symptoms  Fatigue  Abdominal discomfort  Depression  Joint pain  Elevated direct bilirubin  Weight loss  Elevated AST, ALT and urinary bilirubin Hepatitis: A (HAV)  Transmission: Fecal-oral (poor hygiene; hand-to-mouth contact, close contact, or through food and fluids)  Incubation: 15-50 days  Acute Illness: 4-8 weeks.  Mortality:  0.5% for younger than age 40  1-2% for those over age 40  Assessment:  mild flu-like symptoms  low-grade fever  Anorexia  later jaundice and dark urine  indigestion and epigastric distress  enlargement of liver and spleen Hepatitis: A (HAV)  Interventions:  Prevention!  Good handwashing  Safe water  Proper sewage disposal  Vaccine  Immunoglobulin for contacts to provide passive immunity  Bed rest during acute stage  Nutritional support Hepatitis: B (HBV)  Transmission: blood, saliva, semen, and vaginal secretions (sexually transmitted, transmitted to infant at the time of birth)  Incubation: 1-6 months  Long Term Complications:  Cirrhosis and liver cancer (major cause worldwide)  May become chronic  Assessment:  insidious and variable  similar to hepatitis A  Antigenic particles that elicit specic antibody markers during diHerent stages of the disease  Hepatitis: B (HBV)  Treatment:  Medications for chronic hepatitis type B include alpha interferon and antiviral agents  Interventions:  Prevention!  Vaccine: for persons at high risk (healthcare workers, routine vaccination of infants  Passive immunization for those exposed  Standard precautions/infection control measures  Screening of blood and blood products  Bed rest  Nutritional support Hepatitis: C  The most common blood borne infection  Transmission: blood and sexual contact  Incubation: Variable  Long Term Complications:  Causes 1/3 of liver cancer  Most common reason for liver transplant  Frequently becomes chronic  Assessment:  Symptoms are usually mild Hepatitis: C  Treatment:  Direct Acting Antiviral (DAA) agents  Curable for most patients  Interventions:  Prevention!  Screening of blood  Prevention of needle sticks for health care workers  Measures to reduce spread of infection as with hepatitis B  Hepatitis: D (HDV) & E (HEV) Hepatitis D   Superinfection (or co-infection)  Only persons with hepatitis B are at risk for hepatitis D  Transmission is through blood and sexual contact  Symptoms and treatment are similar to hepatitis B  More likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis  Hepatitis E  Transmitted by fecal-oral route  Incubation period 15-65 days  Resembles hepatitis A and is self-limited, with an abrupt onset  No chronic form. Cirrhosis  Obstructive liver disorder  Non-brous connective scar tissue replaces normal liver cells  Irreversible partial or complete occlusion of blood Bow through the liver  Types  Laennec’s (alcoholic)  Most common  Caused by excessive alcohol consumption or malnutrition  Post Necrotic  Secondary to infection (Hepatitis)  Biliary  Scarring around bile ducts  Biliary obstruction and/or infection  Cirrhosi s  Signs/Symptoms of Complication  Change in mental status  DiKculty with ADLs, maintain a job/social relationships  Anatomic distortion  Indicators of bleeding (shock/melena/hematemesis)  Fluid volume changes (shock/ascites)  Changes in lab data  Jaundice  Complications  Portal Hypertension  Ascites  Esophageal/gastric varices Cirrhosis: Interventions  Imbalanced Nutrition  Monitor I&O  Encourage adequate intake  Small frequent meals  Patient preferences  Supplements (especially B complex, water-soluble forms of fat- soluble vitamins if pt has steathorrhea)  High calorie diet  Sodium Restriction (if ascites is present)  Protein Restriction (if at risk for hepatic encephalopathy)  Risk for injury  Prevent falls (side rails, clear pathway, adequate lighting…)  Prevent trauma related to increased risk for bleeding  Carefully evaluate any injury for excessive bleeding Cirrhosis: Interventions  Activity Intolerance  Encourage rest  Position for respiratory eKciency  Administer oxygen  Plan mild exercise with rest periods  Address nutritional status  Interventions to prevent hazards of immobility  Impaired Skin Integrity  Frequent position changes  Gentle skin care  Consider interventions for itching  Emollient cream  Cholestyramine Resin as ordered  Keep nails short Liver Dysfunction: Portal Hypertension  Results in increased pressure throughout the portal venous system  Complications  Ascites  Esophageal Varices  Treatment - Portal systemic shunt  Decrease portal pressure  Can prevent portal hypertension  Decreases risk for esophageal varices  TIPS Transjugular Intrahepatic Portosystemic Shunt  Creation of a tract from the hepatic to the portal vein  A cannula with expandable stent is inserted in the portovenous system through the jugular vein  The stent serves as the intrahepatic shunt between the hepatic vein and portal circulation to relieve portal hypertension  May be carried out using  Ascites  Collection of Buid in the peritoneal cavity  Etiology:  Portal Hypertension  increased capillary pressure  obstruction of venous blood Bow  Vasodilation of splanchnic circulation  blood Bow to the major abdominal organs increases  Changes in the ability to metabolize aldosterone  increases Buid retention  Albumen  Decreased synthesis of albumen decreases serum osmotic pressure  Movement of albumen into the peritoneal cavity Ascites: Assessment  Abdominal girth  Daily weights  Inspect  Striae  Distended veins  Umbilical hernia  Percussion  Monitor I&O  Monitor Buid/electrolyte balance  Fluid wave Ascites: Treatment  Low sodium diet  Foods to avoid: smoked, cured, salted, canned foods, cold cuts, ham, frankfurters (hot dogs), sausage, sardines, caviar, anchovies, frozen dinners, canned soups, salted nuts  Medication  Diuretics  Albumin  Ambulation as tolerated  Paracentesis  Transjugular intrahepatic portosystemic shunt (TIPS)  Paracentesi  s Procedure to remove ascitic Buid  Needle is introduced through the abdominal wall  Relieves discomfort from distention  Relieves breathing diKculty from Buid pressing up on the diaphragm  Make sure patient voids before procedure  Up to 6-8L of Buid may be removed over 60-90 minutes  Record volume of Buid withdrawn  IV albumin is simultaneously infused to pull Buid back into the vascular space  Monitor BP and urine output to evaluate Buid shifts  Too much Buid removed can cause patient to go into hypovolemic shock Hypovolemic Shock  Signs and Symptoms  Rapid, thready (weak) pulse  Rapid breathing  Anxiety  Decreased BP  Increased HR  Decreased urine output  Cool clammy skin  Weakness  Pallor  Diaphoresis   Confusion Unconsciousness SHOCK Esophageal /Gastric Varices Etiology: Cirrhosis causes Portal Hypertension which increases pressure on vessels in the esophagus causing the veins to bulge Incidence: Bleeding occurs in 1/3 of patients with cirrhosis and varices Mortality: First bleeding episode has 30-50% mortality rate Esophageal /Gastric Varices: Assessment Hematemesis – vomit stained red (E) or black (G) Melena - black, tarry stools (G) General deterioration / Shock (loss of Buids, blood) Esophageal Varices: Treatment  ENDOSCOPIC SCLEROTHERAPY  Injection of a sclerosing agent into the esophageal varices through and endoscope  Promotes thromboses and eventual sclerosis  Obliterates the varices  ESOPHAGEAL BANDING  A rubber band like ligature is slipped over an esophageal varix via an endoscope  Necrosis results  The varix eventually sloughs off Esophageal Varices: Treatment BALLOON TAMPONADE: Sengstaken-Blakemore tube Intubated patient Three separate openings  One lumen inBates the gastric balloon  Another inBates esophageal balloon  Third aspirates blood Esophageal Varices: Interventions  Patients with cirrhosis should undergo screening endoscopy q 2 years  Monitor for associated complications such as hepatic encephalopathy resulting from blood breakdown in the GI tract and delirium related to alcohol withdrawal Esophageal Varices: Interventions  Active bleeding:  Monitor patient’s condition frequently, including emotional responses and cognitive status  With balloon tamponade  Monitor treatments, including tube care and GI suction  Monitor respiratory status (sudden deBation can cause obstruction)  Auscultate for aspiration  Oral care  Quiet, calm environment and reassuring manner / reduce anxiety  Monitor for Hypovolemic shock (Buid loss from bleeding varices)  Oxygen  IV Buids, electrolytes, volume expanders  Blood and blood products  Teaching and support of patient and family Hepatic Encephalopathy: Assessment  A life-threatening complication of liver disease  May result from accumulation of ammonia and other toxic metabolites in blood  Assessment:  EEG  Neuro status  Changes in LOC  Asterixis (involuntary Bapping movements of hands)  Potential seizures  Fetor hepaticus (sweet, slightly fecal odor to breath) Hepatic Encephalopathy: Stage 1  Stage One  Normal LOC  Lethargy  Euphoria  Reversal of day-night sleep patterns  Asterixis  Impaired writing and ability to draw line gures  Normal EEG Hepatic Encephalopathy: Stage 2  Stage Two  Increased drowsiness  Disorientation  Inappropriate behavior  Labile mood  Agitation  Asterixis  Fetor hepaticus  Abnormal EEG with generalized slowing Hepatic Encephalopathy: Stage 3  Stage Three  Stuporous  DiKcult to arouse  Sleeps most of the time  Marked confusion  Incoherent speech  Asterixis  Increased deep tendon reflexes  Rigidity of extremities  EEG markedly abnormal Hepatic Encephalopathy: Stage 4  Stage Four  COMATOSE  May not respond to painful stimuli  ABSENCE of Asterixis  ABSENCE of Deep Tendon ReBexes  Flaccidity of extremities  EEG markedly abnormal Hepatic Encephalopathy: Medication Medication   Lactulose to reduce serum ammonia level  Detoxies the ammonium  Acts as osmotic agent to draw water into the bowel  Causes diarrhea in some patients  Dose should be adjusted so patient has 2-3 soft stools per day  IV glucose to minimize protein catabolism  Cholestyramine Resin (Questran)  Urodoxycholic Acid(Actigall) - Promotes bile Bow from liver  Antacids - Decrease gastric disturbances and potential for GI bleeding  Potassium-sparring diuretics (aldactone) - For ascites  Emollient creams (for pruritis) Hepatic Encephalopathy: Management  Transfusion of Platelets and PRBCs  Diet  Protein restriction  Sodium Intake Restricted  Reduction of ammonia from GI tract Alternative Herbal Treatments  Kava Kava  Can cause or worsen liver disease  Patients should check with provider if taking possibly hepatoxic medications  Milk Thistle  May improve liver enzyme levels  May benet patients with chronic liver disease Review of Objectives Review anatomy and physiology of the hepatic system Discuss common laboratory tests and diagnostic tools for hepatic dysfunction Consider the etiology and incidence of liver dysfunction Describe common assessment ndings with liver dysfunction and liver failure Describe select conditions of the hepatic system Explain appropriate nursing care and rationales for the care of patients experiencing liver dysfunction Consider alternative and complimentary medications as they relate to the hepatic system NUR 144 Adult Health/Mental Health Rose Frowd, RN, MSPH, CASAC Christina Haggarty, RN, MSN, CASAC Cynthia Lasman, RNC-OB, MSN, CNE, C-EFM FAQ: Fall 2024  Clinical groups will have some meetings on campus, in the hospital, independent rotation, and/or online learning.  Things can change and we will adjust.  PLEASE reach out to your clinical instructor or to me with your questions and concerns!!  Exams will use ExamSoft on campus.  Alternate clinicals will use Vsims (you must purchase this) Test Dates Unit 1 (Gastrointestinal) – 10/10/24 @ 3:00 pm Unit 2 (Psychiatric) – 12/5/24 @ 3:00 pm Comprehensive – 12/19/24 @ 3:00 pm Refer to Nursing Program 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Inez Rivera [email protected] Unit one Gastrointesti nal System Lecture 1 GI assessment Gastric Duodenal Lecture 2 Hepatic Lecture 3 Biliary Alternative nutrition Lecture 4 Colon Lecture 5 Alternative elimination Gastrointestinal Assessment Professor Rose Frowd MS, RN BC-PMH, CASAC [email protected] Adapted from Wolters Kluwer Objectives  Review anatomy and physiology of the GI system  Discuss terms related to the GI system  Describe common assessments of the GI system  Organs of the Digestive System Functions of the Digestive Tract  Breakdown of food for digestion  Absorption into the bloodstream of small nutrient molecules produced by digestion  Elimination of undigested unabsorbed foodstu6s and other waste products Terms  Digestion: begins with the act of chewing, in which food is broken down into small particles that can be swallowed and mixed with digestive enzymes  Absorption: Absorption is the major function of the small intestine. Vitamins and minerals absorbed are essentially unchanged. Absorption begins in the jejunum and is accomplished by active transport and di6usion across the intestinal wall into the circulation  Elimination: phase of the digestive process that occurs after digestion and absorption when waste products are eliminated from the body  Major Enzymes and Secretions  Chewing and swallowing COLOR KEY  Saliva (mechanical breakdown)  Salivary amylase Starch / Sugar Protein  Gastric function  Hydrochloric acid Fat  Pepsin  Intrinsic factor (absorption of vitamin B12)  Small intestine (via the common bile duct)  Amylase  Lipase  Trypsin  Bile Knowledge Check Is the following statement true or false? Lipase is an enzyme that aids in the digestion of protein. ANSWER False Rationale: Lipase is an enzyme that aids in the digestion of fats. Trypsin is an enzyme that aids in the digestion of protein.  Knowledge Check What is ingestion? A. Occurs when food is taken into the GI tract via the mouth and esophagus B. Occurs when enzymes mix with ingested food and when proteins, fats, and sugars are broken down into their component molecules C. Occurs when small molecules, vitamins, and minerals pass through the walls of the small and large intestine and into the bloodstream D. Occurs after digestion and absorption when waste products are eliminated from the body ANSWER A. Occurs when food is taken into the GI tract via the mouth and esophagus Rationale: Ingestion occurs when food is taken into the GI tract via the mouth and esophagus. Digestion occurs when enzymes mix with ingested food and when proteins, fats, and sugars are broken down into their component molecules. Absorption occurs when small molecules, vitamins, and minerals pass through the walls of the small and large intestine and into the bloodstream. Elimination occurs after digestion and absorption when waste products are eliminated from the body.  Assessment of the GI System  Health history:  Information about abdominal pain, dyspepsia, gas, nausea and Common Sites of vomiting, diarrhea, constipation, Referred Abdominal fecal incontinence, jaundice, and Pain previous GI disease is obtained  Pain:  Character, duration, pattern, frequency, location, distribution of referred abdominal pain, and time of the pain vary greatly depending on the underlying cause Assessment of the GI System Dyspepsia (Indigestion)  Upper abdominal discomfort associated with eating  Pain, fullness, bloating, early satiety, belching, heartburn, regurgitation  Most common symptom of patients with GI dysfunction  Increased symptoms with fatty foods, coarse vegetables, highly seasoned foods  Intestinal gas  Bloating, distention, or feeling “full of gas”  Belching and/or excessive @atulence  Often a symptom of food intolerance or gallbladder disease Assessment of the GI System  Nausea  Vague, uncomfortable sensation of sickness or “queasiness” that may or may not be followed by vomiting  Often with distention of the duodenum or upper GI tract  Vomiting (emesis)  Forceful emptying of stomach and intestinal contents through the mouth  Causes  Visceral pain, motion, anxiety, medication, torsion, trauma, metabolic abnormalities, toxins, chemotherapy, radiation, inner ear disorders, anticipatory Assessment of the GI System  Change in bowel habits and stool characteristics  May signal colonic dysfunction or disease  Constipation, diarrhea  Other common abnormal stool characteristics  Bulk, greasy foamy stools – foul smelling (may or may not @oat)  Light gray or clay colored stool (absence of conjugated bilirubin)  Stool with mucus threads or pus (visible on gross inspection)  Loose, watery stool (may or may not be streaked with blood) Assessment of the GI System  Past health, family and social history  Oral care and dental visits  Lesions in mouth  Discomfort with certain foods  Use of alcohol and tobacco  Dentures  Previous diagnostic studies, treatments, or surgery  Weight gain or loss  Medications  Dietary intake Physical Assessment of the GI System  Oral cavity  Lips  Color, hydration, texture, symmetry, ulcerations, Cssures  Gums  In@ammation, bleeding, retraction, discoloration, odor  Tongue  Texture, color, lesions, symmetry  A thin white coat and large “V” on the distal tongue are normal Cndings Physical Assessment of the GI System  Abdominal assessment  Position Dorsal Recumbent  Inspection  Auscultation  Percussion  Palpation  Rectal inspection  Position lithotomy or side-lying  Note abnormalities and hygiene Knowledge Check Which is the correct order to complete an abdominal assessment? A. Inspection, auscultation, percussion, and palpation B. Auscultation, inspection, palpation, and percussion C. Percussion, palpation, inspection, and auscultation D. Palpation, percussion, auscultation, and inspection ANSWER A. Inspection, auscultation, percussion, and palpation Rationale: The correct order for an abdominal assessment is inspection, auscultation, percussion, and palpation. Auscultation must be completed before manipulation of the abdomen because it has an impact on motility and can lead to an inaccurate interpretation of bowel sounds. Gastric and Duodenal Disorders Cynthia Lasman, RNC-OB, MSN, CNE, C-EFM [email protected] Adapted from Wolters Kluwer Objectives  Review anatomy and physiology of the upper GI tract  Discuss common laboratory tests and diagnostic tools for upper GI dysfunction  Consider the etiology and incidence of upper GI dysfunction  Describe common assessment Cndings with upper GI dysfunction  Describe select conditions of the upper GI dysfunction  Explain appropriate nursing care and rationales for the care of patients experiencing upper GI dysfunction A&P: UPPER GI  Esophagus  In the mediastinum  Anterior to the spine  Posterior to the trachea and heart  Hollow 10” muscular tube  Passes through the diaphragm at an opening called the diaphragmatic hiatus Stomach In the peritoneum Left upper quadrant Capacity of approximately 1500 mL Stores food during eating, secretes digestive @uids, and propels the partially digested food, or chyme, into the small intestine Gastroesophageal junction is the inlet Pyloric sphincter is the outlet Laboratory and Diagnostic Studies  Serum laboratory studies  Stool tests  Breath tests  Abdominal ultrasonography  Genetic testing  Upper GI tract study  GI motility studies Laboratory and Diagnostic Studies  Endoscopic Procedures  Esophagogastroduodenoscopy (EGD)  Gastroscopy  Manometry and electrophysiologic studies  Ultrasound  Computed Telemetry (CT)  Magnetic Resonance Imagery (MRI) Disorders of the Oral Cavity  Periodontal disease  Includes gingivitis – in@ammation of the gums  Common cause of tooth loss  Dental plaque and Caries  Tooth decay – erosive process  Prevention includes cleaning teeth several times a day (brushing and @ossing), use of @uoride toothpaste and @uoridated community water sources  Nursing Implications  Poor oral intake reduces saliva production – increased oral care is required  Soft bristle brush is best, wipe with gauze pad if unable to tolerate brushing  Oral in@ammatory disease is linked to cardiovascular disease, diabetes, rheumatoid disease, premature birth, low birth weight, stroke  Encourage adequate food intake  Minimize mouth pain  Support positive self-image Disorders of the Esophagus  Achalasia – absent or ine6ective peristalsis  Dysphasia with solid food, regurgitation,  Diagnosed with x-ray  Teach patient to eat slowly and drink @uids with meals  Dilation can be done, or surgery if severe  Esophageal Spasm – muscular spasm interrupting normal peristalsis  Dysphasia, pyrosis, regurgitation, chest pain  Diagnosed with esophageal manometry  Treated with muscle relaxants and proton pump inhibitors Disorders of the Esophagus (cont.)  Diverticulum  Outpouching of mucosa through the musculature  Most common is Zenker diverticulum (ZD)  Dysphasia, fullness in the neck, belching, regurgitation, gurgling noises, halitosis  Diagnosed with barium swallow or manometric studies  Avoid NG tube insertion!  Perforation  Excruciating retrosternal pain and dysphasia  Life-threatening disorder, requires immediate surgical intervention, antibiotics  Diagnosed with xray, barium swallow, chest CT  NPO Post-op Hiatal Hernia  The opening for the esophagus becomes enlarged and the upper stomach moves into the lower chest  Assessment  Dysphagia, pyrosis, regurgitation, intermittent epigastric pain, fullness after eating, nausea/vomiting, may be asymptomatic  Diagnosis is made with x-ray studies, barium swallow, EGD, esophageal manometry, CT  Medical Management  Used to treat if the patient is symptomatic (for example, GERD)  Surgery (usually laparoscopic)  Patient Teaching  Frequent small meals  Do not recline for 1 hour after eating  Elevate HOB (4-8 in)  If post-op, advance diet slowly Gastroesophageal Re=ux Disease (GERD)  Common disorder  Back@ow of gastric or duodenal contents into the esophagus  Troublesome symptoms and/or mucosal injury to the esophagus  Excessive re@ux may occur because of an incompetent lower esophageal sphincter, pyloric stenosis, hiatal hernia, or a motility disorder  Incidence: increases with age; irritable bowel syndrome and obstructive airway disorders (asthma, COPD, cystic Cbrosis); Barrett esophagus, peptic ulcer disease, and angina  Other risk factors: tobacco use, co6ee drinking, alcohol consumption, gastric infection with Helicobacter pylori Gastroesophageal Re=ux Disease (GERD)  Back@ow of gastric/duodenal contents into the esophagus and can lead to mucosal injury  Assessment  Pyrosis and regurgitation (hallmark of GERD)  Dyspepsia, dysphagia, hypersalivation, esophagitis  pH monitoring (gold standard diagnosis)  Endoscopy, barium swallow to evaluate for complications  Complications  Dental erosion, ulcerations in the pharynx/esophagus, laryngeal damage, esophageal strictures, adenocarcinoma, pulmonary complications Gastroesophageal Re=ux Disease (GERD)  Medical Management  Medications  Surgery  Teaching  Low-fat diet  Avoid ca6eine, tobacco, beer, milk, foods containing peppermint or spearmint, and carbonated beverages  Avoid eating or drinking 2 hours before bedtime  Elevate the head of the bed by at least 30 degrees  Tobacco cessation  Limit alcohol  Maintain healthy weight Gastritis  Disruption of the mucosal barrier that normally protects the stomach tissue from digestive juices  Acute  rapid onset of symptoms  usually caused by dietary indiscretion  self-limiting  other causes; medications, alcohol, bile re@ux, and radiation therapy, ingestion of strong acid or alkali (may cause serious complications)  Chronic  prolonged in@ammation  atrophy of gastric tissue  benign or malignant ulcers of the stomach  Helicobacter pylori  Other causes; autoimmune diseases (Hashimotos, Addison, Graves), dietary factors, medications, alcohol, smoking, or chronic re@ux of pancreatic secretions or bile  Acute Gastritis  Can be classiCed as erosive or nonerosive Image reproduced with permission from Strayer, D. S., SaItz, J. E., & Rubin, E. (2015). Rubin’s pathology: Mechanisms of human disease (8th ed., Fig. 19-15).  Erosive Philadelphia, PA: Lippincott Williams & Wilkins.  Local irritants (aspirin, NSAIDS, corticosteroids, alcohol, radiation)  Severe – caused by ingestion of strong acid or alkali  Nonerosive  Helicobacter pylori (H. pylori)  Can cause peptic ulcers  Stress-related  severe burns, infection, lack of perfusion, surgery  Complications – perforation, scarring, pyloric stenosis, tissue atrophy, hemorrhage Manifestation of Gastritis  Acute: epigastric pain, dyspepsia, anorexia, hiccups, nausea, vomiting. Erosive gastritis can lead to melena, hematemesis or hematochezia  Chronic: fatigue, pyrosis, belching, sour taste in the mouth, halitosis, early satiety, anorexia, nausea and vomiting, pernicious anemia due to malabsorption of B12.  Some are asymptomatic  Mild epigastric discomfort with intolerance of spicy or fatty food, relieved by eating  DeCnitive diagnosis by endoscopy and histologic examination of biopsy specimen  Medical Management of Gastritis  Acute  Recovery in 1-3 days  Refrain from alcohol and food until symptoms subside  Supportive therapy: IV @uids, nasogastric intubation, antacids, histamine-2 receptor antagonists, proton pump inhibitors  Chronic  Modify diet, promote rest, reduce stress, avoid alcohol and NSAIDs  Pharmacologic therapy including a variety of medications  Tx may include placement of NG tube, endoscopy, surgery (perforation or hemorrhage) Nursing Management of Gastritis  Reduce anxiety; use calm approach and explain all procedures and treatments  Promote optimal nutrition; for acute gastritis, the patient should take no food or @uids by mouth. Introduce clear liquids and solid foods as prescribed. Evaluate and report symptoms. Discourage ca6einated beverages, alcohol, cigarette smoking. Refer for alcohol counseling and smoking cessation  Promote @uid balance; monitor I&O, for signs of dehydration, electrolyte imbalance, and hemorrhage  Measures to relieve pain: diet and  Peptic Ulcer Disease  Erosion of a mucous membrane forms an excavation in the stomach, pylorus, duodenum (more common), or esophagus  Most often cause by infection of H. pylori  Less often stress ulcer from burn, shock, sepsis, MODS, TBI, mechanical ventilation (probably from tissue ischemia)  Risk factors include excessive secretion of stomach acid, dietary factors, chronic use of NSAIDs, alcohol, smoking, and familial tendency, blood type O, COPD, liver cirrhosis, chronic kidney disease, autoimmune disorders Peptic Ulcer Disease  Assessment  May be asymptomatic (silent peptic ulcer)  Symptoms may come  Manifestations include a dull gnawing pain or burning in the midepigastrium; sour eructation (burping), heartburn and vomiting (undigested food in emesis, relieves pain)  Duodenal ulcers – symptoms occur 2-3 hours after eating (often pain will occur at night, waking patient), eating may relieve symptoms  Sudden onset of severe pain (especially sharp upper abdominal pain referred to the shoulder), hypotension and tachycardia may indicate perforation  Diagnosis with physical exam, upper endoscopy (with histologic exam), urea breath test Peptic Ulcer Disease  Treatment includes medications (includes antibiotics if H. pylori is present), lifestyle changes, and occasionally surgery if wounds don’t heal in 12-16 Reprinted with permission from Strayer, D. S., SaItz, J. E., & Rubin, E. (2015). Rubin’s pathology: Mechanisms weeks of human disease (8th ed., Fig. 19-23). Philadelphia, PA: Lippincott Williams & Wilkins.  Teaching  Tobacco cessation  Dietary modiCcation  Avoid extremes in temperature, alcohol, co6ee, ca6eine  Regular meals Knowledge Check Is the following statement true or false? The most common site for peptic ulcer formation is the pylorus. ANSWER False Rationale: The most common site for peptic ulcer formation is not the pylorus. The most common site for peptic ulcer formation is the duodenum.  Assessment for Gastritis or Peptic Ulcer Disease  History including presenting signs and symptoms  Dietary history and dietary associations with symptoms such as predictable time for pain  72-hour diet; diary may be helpful  Abdominal assessment, vital signs  Medications; include use of NSAIDs  Sign and symptoms of anemia or bleeding  Abdominal assessment Goals for Patient with Gastritis or Peptic Ulcer  Major goals may include:  Relief of pain  Reduced anxiety  Maintenance of nutritional requirements  Absence of complications Nursing Interventions  Relieving pain  Reducing anxiety  Maintaining optimal nutritional status  Monitoring and managing potential complications  Hemorrhage  Perforation and penetration  Gastric outlet obstruction  Patient education Knowledge Check What is the duration of treatment for proton pump inhibitors in a patient diagnosed with peptic ulcer disease? A. 1–2 weeks B. 7 days C. At least 2 years based on risk factors D. 4–8 weeks ANSWER D. 4–8 weeks Rationale: Proton pump inhibitors should be used for 4–8 weeks to allow complete peptic ulcer heading. Patients at high risk require a maintenance dose for 1 year. Review of Objectives  Review anatomy and physiology of the upper GI tract  Discuss common laboratory tests and diagnostic tools for upper GI dysfunction  Consider the etiology and incidence of upper GI dysfunction  Describe common assessment Cndings with upper GI dysfunction  Describe select conditions of the upper GI dysfunction  Explain appropriate nursing care and rationales for the care of patients experiencing upper GI dysfunction  Review anatomy and physiology of the GI system  Discuss terms related to the GI system  Describe common assessments of the GI system