Week 9 - Alterations in Gastrointestinal Function - Student PDF

Alterations in Gastrointestinal Function KARA SEALOCK EdD MEd BN RN CNCC (C) CCNE NOVEMBER 1 S T AND 3 R D , 2022 By the End of this Lecture You Will: Critically reflect upon the overall anatomy and physiology of the gastrointestinal system and how dysfunction leads to significant changes system...

Alterations in Gastrointestinal Function KARA SEALOCK EdD MEd BN RN CNCC (C) CCNE NOVEMBER 1 S T AND 3 R D , 2022 By the End of this Lecture You Will: Critically reflect upon the overall anatomy and physiology of the gastrointestinal system and how dysfunction leads to significant changes systemically Explain pathophysiology and effects on the body related to:  Gastritis Stomach and  Gastroesophageal Reflux Disease (GERD) Intestinal  Peptic Ulcer Disease (PUD) Dysfunction  Gastrointestinal (Upper and Lower) Bleed  Obstruction/Ileus  Hepatitis Liver and  Acute Liver Dysfunction  Hepatic Encephalopathy Gall Bladder  Cholelithiasis and Cholecystitis  Fulminant Hepatic Failure Begin to prioritize patient conditions related to nursing assessment and clinical manifestations Objectives for this lecture: By the end students will be able to identify at least 5 common issues that occur in the gastrointestinal system Students will be able to explain dysfunction associated with the stomach, intestine and liver Students will be able to explain at least 3 differences in pathophysiology and assessment of the stomach/intestinal system, and liver Students will continue to apply previously learned concepts associated with gastrointestinal/ liver dysfunction through critical thinking exercises  Abdominal Assessment Objective Data: Subjective Data:  Appetite Inspect  Dysphagia (contour, symmetry, umbilicus, skin, hair, movement and  Food intolerance demeanor)  Abdominal pain Ausculate  Nausea/vomiting (hyperactive, hypoactive and  Bowel habits absent)  Past abdominal history Percuss  Medications Palpate  Nutritional assessment Objective Data Figure 35-1, p. 863, Power-Kean et al., (2023) Stomach and Intestinal Dysfunction  Gastritis Inflammation of the stomach May have many causes: acute or chronic  Acute is usually due to local irritants  May or may not be symptomatic  Chronic leads to atrophy of the glandular epithelium of the stomach  H. pylori gastritis is most common  Autoimmune and multifocal least common but increases risk of carcinoma  Chemical from reflux of duodenal contents, pancreatic secretions, bile  Gastritis Pathophysiology:  Occurs as a result of the breakdown of the normal gastric mucosal barrier  Hydrochloric acid moves back into the mucosa  Results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen and possible hemorrhage Clinical Manifestations:  Anorexia, nausea and vomiting, epigastric tenderness and a feeling of fullness  Hemorrhage is commonly associated with alcohol abuse  Acute gastritis is self limiting, lasting from a few hours to days with complete healing  Chronic gastritis, patients lose intrinsic factor (a substance secreted by gastric mucosa that is essential for absorption of cobalamin (vitamin B12) leading to cobalamin deficiency  changes in RBC production anemia and neurological complications Nursing Assessment:  GI: Nausea/vomiting, pain, blood noted in stool or emesis, nutritional intake, ETOH, Causes of Gastritis Table 44- 13, p. 1011, Tyerman & Cobbett (2023) http://library.med.utah.edu/WebPath/GIHTML/ GI016.html  Gastroesophageal Reflux Disease Acronym GERD Backwards movement of stomach contents into esophagus Pathophysiology:  Backflow regulated by a sphincter at stomach entrance; transient relaxation common after meals, especially fatty foods Clinical Manifestation:  Most common symptom epigastric pain or heartburn, sometimes belching, chest pain  Respiratory symptoms include: wheezing, coughing, and dyspnea  Otolaryngologic symptoms include: hoarseness, sore throat, lump in the throat (globus sensation), and choking  Gastroesophageal Reflux Disease Nursing Assessment:  NEURO: dysphagia, pain (PQRST); CV: identify if chest pain is cardiac in nature or a result of GERD, tachypnea, changes in BP; RESP: sore throat, lump in throat, hoarseness of cords, wheezing, coughing, dyspnea, crackles if aspiration pneumonia has occurred; GI: nutritional status, odynophagia (painful swallowing), heartburn, nausea/vomiting, weight loss https://www.choc.org/programs-services/gastroenterology/gerd/  Gastroesophageal Reflux Disease Complication: Barrett esophagus -scarring, edema, spasm (strictures) https://www.mayoclinic.org/ diseases-conditions/barretts- esophagus/symptoms-causes/ syc-20352841  Peptic Ulcer Disease  Group of disorders resulting from exposure of upper GI tract to acid- pepsin secretions. Mostly duodenal and gastric; duodenal much more common. Men 55-70 most commonly affected  Caused often by H. pylori, Non-Steriodal Anti-Inflammatory Drugs (NSAIDs)  Pathophysiology:  Only develop in the presence of an acid environment  Mucosa barrier becomes impaired, and back-diffusion of acid lead to PUD  Can affect all layers of mucosa and eventually penetrate through  Clinical Manifestations:  Primary symptom is pain usually on empty stomach; relieved by food http://www.medicinenet.com/peptic_ulcer/page2.htm  Peptic Ulcer Disease Complications include hemorrhage, gastric outlet obstruction (from edema, spasm, contraction of scar tissue), perforation (which can lead to peritonitis) Fig 36-6, p. 893, Power- Kean et al., (2023) https://www.healthclop.com/differences-of- peptic-gastric-and-duodenal-ulcer/  Gastrointestinal Bleed Can happen anywhere in GI tract- (UGIB or LGIB) Site of bleeding indicated by colour and texture: bright red to tarry black (melena)  Upper GI often coffee-ground material (partially digested) or bright red  Brighter red means bleeding closer to the source; darker means further from source (e.g. source is duodenum, which is high up, blood in stools will be dark; hemorrhoids often produce bright red blood)  May be hard to pinpoint source; e.g. with hypermotility blood may be bright red even if source is high in GI tract Think EMERGENCY Situation!!! Patients may also develop lower GI bleeding where primary symptom is frank red blood Fig 36-1, pg. 887, Power-Kean et al., (2023)  Gastrointestinal Bleed Nursing Assessment (IPAP’s): NEURO: LOC, alert, orientated, lethargic, dizziness, light headedness, anxiety, confusion, stupor, coma (due to low cerebral blood flow); CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, low CO, low BP, tachycardia, changes in perfusion, capillary refill, cool to touch, changes in pulses especially in lower extremities, chest pain or angina present, dysrhythmias (AF); RESP: tachypnea, dyspnea, cyanosis, crackles due to pulmonary edema or heart failure; GI: absent of hypoactive bowel sounds, epigastric tenderness, anorexia; RENAL: urine output, < or > 30 cc/hr (due to decreased blood flow to kidneys), monitoring for tubular necrosis, colour, consistency, frequency, 24 hour fluid balance LAB Values: CBC (Hgb, platelets, hematocrit), All electrolytes with careful attention to potassium, creatinine, BUN, GFR  Obstruction/Ileus What is an obstruction?  Any condition that prevents normal flow of chime through intestine  Loss of intestinal motility in the absence of an ileus  Classified as simple or functional Primary Cause of Small Primary Cause of Large Bowel Obstruction: Bowel Obstruction: Adhesions * Malignancy Hernia Volvulus Tumors Strictures related to diverticulitis Pathophysiology of Intestinal Obstruction Figure 36-5, p. 892, Power-Kean et al., (2023)  Intestinal Obstruction Clinical Manifestations:  Symptoms based on degree and duration of obstruction  May be sudden and dramatic symptoms of pain (intermittent), vomiting, distention, borborygmus**, peristaltic rushes, restlessness and awareness of peristaltic movements Treatment based on cause. May respond to decompression, but may require surgery  Stomach and Intestinal Dysfunction Key Assessment Points Changes or Absent Bowel Sounds Complaints of Nausea, Vomiting, Anorexia and Distention Abnormalities noted in Lab Values GI Pain  Usually sharp or burning  May be steady or intermittent  May be referred  As with all pain, assessment of timing, quality, and intensity of pain is key Liver and Gallbladder Dysfunction  Liver and Gall Bladder Liver Structure and Function Fig 35-15, p. 874, Power-Kean et al., (2023)  Liver Structure and Function STRUCTURE FUNCTION Largest; divided into R & L Multi-skilled organ lobes Secretes bile Located RUQ Metabolism of Bilirubin Main blood supply from hepatic Hematologic(hematopoiesi artery and portal vein. Portal s, clotting, storage) vein drains from alimentary Metabolism of Nutrients canal, spleen and pancreas. Blood drains into sinusoids, and (CHO, CHON, Fat) from there into central veins Detoxifies (at risk for and then to Inferior Vena Cava further injury) Hepatic circulation important Stores Minerals (Vitamins b/c obstruction leads to portal B12, D, A, E, and K) hypertension  Hepatitis A Pathophysiology:  Widespread inflammation of the liver tissue  Liver damage is mediated by cytotoxic cytokines and natural killer cells that cause lysis of infected hepatocytes  Damage results from liver necrosis  Inflammation of periportal areas may interrupt flow of bile  Hepatitis A is transmitted through feces (fecal-oral route; contaminated water and food; blood)  Hepatitis A has an incubation period of 2-7 weeks. Clinical Manifestations: Fatigue, nausea vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, rash, but is usually a mild disease  Fulminant Viral Hepatitis  Clinical syndrome that results in severe impairment or necrosis of the liver cells May occur with Hepatitis B or C virus Tylenol overdoses are common to cause this severe syndrome  Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma Acute liver failure develops within 6-8 weeks after initial symptoms of hepatitis Clinical Manifestations:  Anorexia, vomiting, abdominal pain, progressive jaundice, followed by ascites and gastrointestinal bleed  Jaundice  May occur as a result of liver dysfunction Results from 1. extrahepatic (post-hepatic) obstruction to bile flow, 2. intrahepatic obstruction, 3. prehepatic excessive production of unconjugated bilirubin Conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts stools become light or clay coloured Pruritis can occur due to bile salts accumulating under the skin Urine may become dark brown or brownish red Mechanis ms of Jaundice Fig 36-14, pg. 909, Power-Kean et al., (2023)  Portal Hypertension Abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow Pathophysiology:  Intrahepatic result from vascular remodelling with intrahepatic shunts, thrombosis, inflammation or fibrosis such as in cirrhosis of the liver, viral hepatitis, or schistosomiasis (parasitic infection)  Posthepatic causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart (RV HF); blood backs up and there is increased pressure in the portal system  Prehepatic causes occur with narrowing of the hepatic portal vein  Long term complications include: varices, splenomegaly, hepatopulmonary syndrome and portopulmonary hypertension Clinical Manifestations:  Most common clinical manifestation is vomiting of blood from bleeding esophageal varices, then slow, chronic bleeding from varices causes anemia or melena  Portal Hypertension  Backup leads to varices, ascites and right sided heart failure  Varices can result in profound bleed: melena, frank red blood, vomiting  Rapid treatment needed - volume replacement, drugs, endoscopy, balloon tamponade, surgery  (portacaval shunt) Fig 35-6, pg. 865, Power- Kean et al., (2023)  Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH) Nonalcoholic Fatty Liver Disease(NAFLD)  Hepatocytes are infiltrated with fat (triglycerides)  Occurs in absence of alcohol  Associated with obesity, high levels of cholesterol and triglycerides, metabolic syndrome and type 2 diabetes  May develop NASH Nonalcoholic Steatohepatitis (NASH)  Hepatocellular injury, inflammation and fibrosis  May progress to cirrhosis and end-stage liver disease https://www.stockwinners.com/ blog/tag/nonalcoholic-fatty-liver- disease-nafld/  Cirrhosis of the Liver Pathophysiology:  Irreversible inflammatory, fibrotic liver disease  Fibrosis occurs when the liver tries to regenerate after an injury but the regenerative process is disorganized  Overgrowth of new and fibrous tissue distorts the structure, resulting in lobules of irregular size and shape impeding blood flow  Leads to poor cellular nutrition, and hypoxia causing inadequate flow and scar tissue decreasing the function of the liver  Cirrhosis of the Liver  Clinical Manifestations:  Abnormal liver function tests; AST, ALT, GGT, Alk Phos,  Normal blood values; Albumin, Bilirubin (initially but then increases as the disease progresses), PTT  Initially, patient’s complain of abdominal pain, fatigue, slight weight loss, and enlargement of the liver and the spleen  As the illness progresses, patients develop: jaundice, skin lesions, peripheral neuropathy, portal hypertension, esophageal and gastric varices, peripheral edema and ascites, hepatic encephalopathy, hepatorenal syndrome  Ascites Sodium, water and protein accumulate in peritoneal cavity due to pressure changes in lymph system, capillaries. Oncotic and osmotic pressures rise May require paracentesis as pressures in abdomen increase Sodium restriction, diuretics Colloids to increase oncotic pressure Fig 36-12, p. 907 Power-Kean et al (2023)  Ascites Accumulation of fluid in the peritoneal cavity reducing amount of fluid available for normal physiological functions Most common complication of cirrhosis but can also occur with right sided heart failure, abdominal malignancies, nephrotic syndrome, and malnutrition Pathophysiology:  Contributing factors include: portal hypertension, decreased synthesis of albumin by the liver, splanchnic arterial vasodilation, and renal sodium and water retention Clinical Manifestations:  Increased abdominal distention, increased abdominal girth, and weight gain  Dyspnea caused by decreased lung capacity leading to increase in respiratory rate  Peripheral edema  May develop bacterial peritonitis (fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid) Fig 36-15, p. 911, Power-Kean et al., (2023) Fig 34-14, p.Fig 36-13, p. 907, 917 Power-Kean et al., (2023)  Hepatic Encephalopathy AKA portosystemic encephalopathy Pathophysiology:  Complex neurologic syndrome characterized by impaired cognitive function, asterixis, and EEG changes  May develop rapidly and become an EMERGENCY situation quickly  Increased amounts of Ammonia and GABA (inhibitory transmitter) may contribute to reduced LOC Clinical Manifestations:  subtle changes in personality, memory loss, irritability, lethargy and sleep disturbances are common. Symptoms can progress to confusion, flapping tremor of the hands, stupor, convulsions and coma Treatment: lactulose, lactulose, lactulose http://www.youtube.com/watch?v=atvlbGXlUU4 Anatomy of the Gallbladder http://www.cancer.gov/cancertopics/pdq/treatment/gallbladder/ Patient/page1  Gallbladder: Structure and Function Saclike organ Primary function is to store and concentrate bile between meals Bile is an alkaline, bitter tasting, yellowish green fluid that contains bile salts, cholesterol, bilirubin, electrolytes, and water Aids in digestion of fats Bile is released in response to food Conditions slowing or obstructing flow of bile out of the gallbladder lead to gallbladder disease  Disorders of the Gallbladder Cholelithiasis (Gallstones) Pathophysiology  Gallstones are formed from impaired metabolism of cholesterol, bilirubin, and bile salts  3 types of gallstones: cholesterol (most common), pigmented (black-hard, brown- soft), and mixed  Form when there is decreased motility and biliary stasis  Stones may lay dormant and silent until they become lodged in the cystic or common duct, causing pain when the gallbladder contracts Clinical Manifestations:  Often asymptomatic  Epigastric and RUQ pain and intolerance to fatty foods are cardinal manifestations  Vague symptoms include heartburn, flatulence, epigastric discomfort, pruritus, jaundice, and foot intolerances particularly to fats and cabbage  Biliary colic (pain) occurs 30 to several hours after eating a fatty meal  Disorders of the Gallbladder Cholecystitis Pathophysiology:  Can be acute or chronic  Caused by the lodging of a gallstone in the cystic duct  Gallbladder becomes distended and inflamed  Colic pain but decreased blood flow can result in ischemia, necrosis, and perforation of the gallbladder Clinical Manifestations:  Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding  Serum bilirubin and alkaline phosphatase (ALP) may be elevated Fig 36-16, p. 915, Power-Kean et al., (2023)  Gallbladder Disorder Nursing Assessment:  RUQ or epigastric pain may be referred  May be severe- peak in 30 minutes and can last for several hours  Pain may be dull, constant and radiate to back, waist, shoulder, and scapula  Lab tests with cholelithiasis and biliary colic often normal  Monitor for high WBC in cholecystitis  AST, ALT may be elevated with CBD stone  Serum amylase may be elevated  Increased bilirubin  Urine culture and sensitivity to rule out pyelonephritis or renal stones Diagnostic Tests Associated with Gallbladder Disorder ERCP (Endoscopic Plain x-rays (show calcium Retrograde ring on some stones, air in Cholangiopancreatography biliary tree, other sources of ) obstruction) Radiographic and Ultrasound most common endoscopic; diagnosis & and probably most reliable with least risk (90-95% treatment sensitive for cholecystitis) Computed Tomography Scintigraphy (HIDA) (nuclear Scan (CT misses 20%) scanning)  Endoscopic Retrograde Cholangiopancreatography  Key Points to Remember Can you perform a full abdominal assessment with knowledge of physiological landmarks and anatomy and physiology related to GI assessment? Explain the “why” associated with GI assessment and connections to other systems Identify and apply concepts of V/Q mismatching related to multiple respiratory conditions  Do you understand the pathophysiology, clinical manifestations and nursing assessment related to :  Dysfunction of the Stomach and Intestines  Gastritis, GERD, PUD, UGIB, LGIB, Obstruction/Ileus  Dysfunction of the Liver and Gall Bladder  Hepatitis, Acute Liver Dysfunction, Hepatic Encephalopathy,