Week 1 Digestive System PDF

Week 1: Digestive System Gastroesophageal reflux disease Syndrome characterized by reflux of gastric contents into lower esophagus Affects 1/6 canadians Can be normal – happens after large/fatty meals When it’s more pervasive → GERD GERD The lower esophageal sphincter (...

Week 1: Digestive System Gastroesophageal reflux disease Syndrome characterized by reflux of gastric contents into lower esophagus Affects 1/6 canadians Can be normal – happens after large/fatty meals When it’s more pervasive → GERD GERD The lower esophageal sphincter (LES) is a ring of muscle at the bottom of the esophagus that acts like a valve between the esophagus and stomach Incompetent LES allows stomach content to reflux back into the esophagus Predisposing conditions Lower esophageal sphincter (LES) dysfunction → stomach acid able to flow back into esophagus Impaired esophageal motility → allows some acid to remain longer in the esophagus o May be d/t neuro conditions, inflammation, meds o In diabetes – damage to vagus nerve (responsible for controlling esophageal muscles) o Vagus nerve can be impaired by opioids Delayed gastric emptying → if stomach is not able to empty quick enough, there is inc vol and inc pressure o Can be caused by high bp meds, antidepressants, opioids Increased intra-abdominal pressure → pregnancy, obesity, chronic coughing can push stomach contents higher up into esophagus Hiatal hernia → upper part of stomach pushes into diaphragm into chest cavity, disrupting normal pressure barrier b/w stomach and esophagus which will facilitate reflux o Often seen in age-related changes Diaphragm can weaken as ppl age – makes it easier for stomach to push up into diaphragm Lifestyle factors and diet o Foods that decrease LES pressure → chocolates, etc. o Anticholinergic meds Pregnant women at inc risk d/t hormone change (progesterone relaxes smooth muscle) Pathogenesis - Number of factors that contribute to development of GERD Defective mucosal defence: esophagus has defence mechanisms to protect it from stomach acid o Esophagus has mucus secreting glands that protects against gastric acid o Reflux, infections, meds, etc. can cause these defence mechanisms to become ineffective Reflux of gastric contents: something like lying down after large meal can cause this Small intestine reflux of bile: when bile refluxes into stomach, it can go into esophagus and cause inflammation and damage to esophageal lining o Caused by damage to pyloric valve (separates stomach from duodenum), surgeries (especially anything around the stomach or gall bladder) LES dysfunction: refer to above Delayed gastric emptying: refer to above Impaired esophageal motility: refer to above Pathophysiology Regurgitation of acid contents from stomach into the esophagus → esophageal irritation & inflammation; may see corrosion of the mucosa o Esophagus cannot withstand prolonged exposure to stomach acid o In addition to stomach acid, gastric enzymes can further contribute to the damage being caused to esophageal lining Clinical Manifestations Heartburn (pyrosis): burning sensation in chest or upper central abdo o Need to consider cardiac cause of symptoms – rule out cardiac issue first o Mild symptoms: occurs once a week May have respiratory symptoms – wheezing, coughing, dyspnea Regurgitation Early satiety, bloating, N&V Dysphagia (difficulty swallowing), odynophagia (painful swallowing) Complications Esophagitis: inflammation of esophagus o Frequent complication/can lead o other complications  Dysphagia: difficulty swallowing o Secondary to esophageal strictures; occurs from esophagitis o Strictures can form overtime when repeated exposure to stomach acid, scar tissue forms in esophagus which can narrow esophagus Barrett’s esophagus: esophagitis + esophageal ulceration = changes to esophageal lining o Squamous mucosa gradually replaced by columnar epithelium o Inc risk of esophageal cancer Respiratory complications Dental erosion: may lead to diagnosis of GERD Evaluation Symptoms Medical Hx: frequency, duration, diet, lifestyle, meds, previous surgeries Diagnostics: barium swallow, paper endoscopy, biopsy/cytology, esophageal manometry, pH monitoring, radionuclide tests o Barium swallow: protrusion of the stomach o Biopsy/cytology: Barrett’s esophagus o Manometry: measure pressure in the esophagus and in LES pH monitoring ▪ Normal pH around LES is 4-6 (if higher indicates GI problem) o Radionuclide: location/movement of things in the esophagus How to manage GERD Avoiding foods that lead to symptoms – eating small, frequent meals may be helpful Losing weight may improve symptoms by decreasing intra-abdominal pressure Elevating HOB 10-15 cm to promote esophageal emptying Stopping smoking – nicotine relaxes LES and irritates and decreases saliva production Avoiding alcohol – alcohol impairs peristalsis, promotes acid secretion, affects LES Nutrition management o Avoiding high fat foods: associated with dec LES pressure o Avoiding chocolate, peppermint, caffeine: decrease LES pressure o Avoiding dairy products: associated with inc gastric acid secretion Pharmacotherapy o Antacids – first line PRN o H2R (Histamine-2-Receptor) blockers decrease acid production – reduce Cl- release o Proton pump inhibitors Peptic Ulcer Disease PUD: Defensive vs Aggressive Factors Aggressive Factors Defensive Factors  Helicobacter Pylori: releases a toxin that destroys gastric & Protect stomach & duodenum from self-digestion: duodenal mucosa, reducing the epithelium’s resistance to Mucus: forms protective barrier against attack by acid & acid/pepsin pepsin NSAIDs: inhibit the biosynthesis of prostaglandins; can also Bicarbonate: neutralizes H+ ions irritate the mucosa directly Blood flow: maintains mucosal integrity; dec blood flow Gastric acid: can cause direct injury; activates pepsin causes local ischemia & cell injury Pepsin: can cause direct injury Prostaglandins: stimulate secretion of mucus & bicarb, Smoking: may contribute by accelerating gastric acid promote vasodilation & suppress gastric acid secretion emptying and reduced secretion of bicarbonate Risk Factors of PUD H. Pylori o Most common cause (but not all ppl with H. pylori will develop PUD) o Secretes an enzyme called urease that creates a protective barrier around the bacteria, which makes it harder to eradicate o Urease generates ammonia in the mucous layer which damages the mucosa and creates a condition of chronic inflammation o This inflammation also makes the mucosa more vulnerable to other noxious substances o Risk factor for gastric carcinoma ▪ If presented with PUD, test for H. Pylori and eradicate NSAIDs (non-steroid anti-inflammatory drugs) o second most common cause o includes aspirin Steroids Cytotoxic drugs o Examples: chemotherapy, agents used in treatment of rheumatoid arthritis Alcohol, smoking & drug use Diet Genetics o Examples: blood group O at increased risk Chronic diseases Psychological stress Age A viscous cycle that lead to worsening erosions and damage to blood vessels Clinical Manifestations Pain Gastric Duodenal Location High in the epigastrium Mid-epigastric region, possibly back Description Burning or gassy Burning or cramp-like Timing Occurs about 1-2 hours after eating, but can also Usually occurs 2-4 hours after meals. occur on an empty stomach Often occurs at night. May be relieved by eating. Complications Hemorrhage o Most common  o May present with hematemesis (vomiting blood) or melena (tarry stool) o Signs: tacky & hypo, pale & clammy, dec RBC, altered LOC Perforation o Sudden onset of abdominal pain, Abdomen is rigid, board-like, Tachycardia, Shallow, rapid respirations Peritonitis and septic shock o Tachycardia & hypo, Threads pulse, Cold and clammy, Altered LOC Gastric outlet obstruction o early satiety, bloating, N&V, epigastric pain after eating, weight loss o obstruction can be caused by edema, spasms, etc. Evaluation endoscopy & biopsy (biopsy can identify H. pylori) H. Pylori break down urea and release nitrogen urea breath test (can detect H. pylori) stool antigen test (can detect H. pylori) Note: prior to testing for H. pylori, ideally PPI therapy should be stopped 1-2 weeks Barium studies – lack accuracy o Swallowing barium and x-ray to visual stomach and duodenum Labs: CBC, LFTs, amylase, fecal occult blood o CBC – may be increased WBC d/t ulcers, dec RBC o Liver Function Tests – rule out other diseases o Amylase – lipase (pancreatic enzyme) – elevated can be pancreatitis (can mimic peptic ulcer signs) o Fecal occult blood for bleeding ulcers How to manage PUD Treat the underlying cause (e.g. H. pylori, discontinue NSAIDs) In addition to pharmacotherapy: o Adequate rest o Dietary changes may be needed o Smoking cessation – smoking irritates mucosa, delays healing o Complete healing (with pharmacotherapy) may take 3-9 weeks Pharmacotherapy: antacids o Short-lasting relief of heartburn o Work by neutralizing hydrochloric acid o Taken 1-3 hours after meals and at bedtime o Not beneficial with moderate-severe symptoms o Examples: aluminum hydroxide, calcium carbonate, magnesium hydroxide o Avoid magnesium preparations with renal insufficiency – inc risk of electrolyte imbalance and kidney failure o Antacids may interfere with absorption of many medications – check timing H2R blockers o Block the action of histamine on the histamine2 receptors of the parietal cells o This decreases the secretion of hydrochloric acid by the stomach o Decreases conversion of pepsinogen to pepsin, and helps ulcer healing o Examples: cimetidine, famotidine ▪ Cimetidine is used less often due to multiple side effects & drug interactions Proton pump inhibitors (PPIs) o Gastric proton pump is made up of H+/K+/ATPase ▪ Hydrogen ion, potassium ion, adenosine triphosphate enzyme o This gastric proton pump is in the parietal cells of the stomach, and is needed to produce hydrochloric acid o PPIs block this pump o Most effective drug for suppressing gastric acid secretion o Examples: Lansoprazole, omeprazole, pantoprazole o Treatment should be limited to 4-8 wks o However, there are patients who require long-term therapy o Adverse effects: incl, dec absorption of calcium & magnesium, inc risk of C. diff, vitamin B12 and iron malabsorption o drug interactions: can dec levels of anticoagulants, dec absorption of protease inhibitors (for HIV) Treatment of H. Pylori o Triple medication therapy: Proton pump inhibitor, amoxicillin, clarithromycin  o Quadruple medication therapy: PPI, Bismuth subsalicylate, Tetracycline, Metronidazole (created to maximize eradication of H. pylori) Other anti ulcer medications o Sucralfate: forms a barrier over the erosion that protects against gastric acids, enzymes and bile salts ▪ this protective barrier promotes healing ▪ can decrease absorption of other drugs o Misoprostol: used with NSAIDs to prevent ulcers ▪ Contraindicated in pregnancy – causes uterine contraction and leads to miscarriages (also used in abortions) Biliary disorders: Cholelithiasis & Cholecystitis Cholelithiasis o Refers to stones in the gallbladder o Most common disorder of the biliary system Cholecystitis o Inflammation of the gallbladder o Usually associated with cholelithiasis Store 30-60 ml of bile →concentrated as water is being absorbed by cells of gall bladder – contract to force the bile to the duodenum after eating Gallstones Can form if the bile being stored has: o Too much cholesterol o Too much bilirubin o Not enough bile salts Bile hardens into small hardened deposit or stones No direct reasoning Suspect of high cholesterol and abnormal metabolism Most stones are made of cholesterol Cholelithiasis Most individuals with cholelithiasis are asymptomatic Obstruction can cause spasms (biliary colic) Obstruction of common bile duct may cause: o Bleeding tendencies o Clay-coloured stools o Dark amber urine o Inability to tolerate foods that are fatty o Jaundice o Pruritus o Steatorrhea (fatty stools bc no bile to absorb dietary fats)  o Malabsorption of vitamin K (important for clotting) – bc bile is important for absorption of fat (and fat soluble vitamin, aka Vit K) Bile gives stool its colour Pruritus (itchiness) bc of build up of bilirubin Cholecystitis (inflammation of the gall bladder) Most commonly associated with gallstones or biliary sludge o Often caused when gallstones are blocking the gallbladder – biliary sludge can contribute Symptoms range from none to severe Clinical manifestations o Indigestion o Acute pain at RUQ, may radiate to right shoulder and scapula (d/t phrenic nerve from diaphragm to neck) o May have positive Murphy’s sign on exam – pt has pain on palpation around gallbladder area, they abruptly stop breathing o Nausea & vomiting – d/t inflammation in gallbladder, severe pain, or obstruction o Fever – d/t inflammation or infection (not common) Evaluation Ultrasound ERCP (endoscopic retrograde cholangiopancreatography): used to diagnose conditions of the bile duct and pancreas; flexible tube w endoscope and camera is inserted to visualize and sometimes treat blockages Labs: o bilirubin (high bili → jaundice) o LFTs – assess liver function and detect any abnormalities + elevated liver enzymes , o CBC (to assess for leukocytosis) – look for signs of infection and inflammation Cholelithiasis management Laparoscopic cholecystectomy: most commonly used for symptomatic cholelithiasis Extracorporeal shock-wave lithotripsy – using high energy sound waves to break up the stones. Can be painful. Once broken up, the stones can pass on their own through biliary system ERCP: can remove stones Medications o Ursodeoxycholic acid (Ursodiol) can be used to dissolve stones ▪ For pts who can’t tolerate or undergo surgery, and prevents gallstones long term o Pain management → key part of management For acute cholecystitis: o Admission to hospital & placed on bed rest o Pain management o If vomiting, N/G suction, NPO & IV fluids o Broad-spectrum parenteral antibiotics o The definitive treatment is a cholecystectomy (timing depends on risk factors) For chronic cholecystitis: o Laparoscopic cholecystectomy – to prevent symptom recurrence and further complications o Conservative interventions (e.g. low-fat diet, weight reduction, anticholinergics, pain meds & antacids) Acute Pancreatitis Pancreas secretes enzymes to help digestion (lipase, amylase, trypsin) o Important for breaking down fats, carbs, and proteins o Also important for producing insulin and glucagon  Other causes include trauma, infection, post-op complications, medications Pancreatic enzymes Pancreatic enzymes are inactive when they are secreted into the duodenum o Inactive secretion → prevents enzymes from digesting the pancreas itself They are only activated once they reach the duodenum In pancreatitis, the enzymes return to the pancreas in their activated form and cause auto digestion of the pancreas Enzymes include: trypsin, phospholipids A2, and elastase Can cause severe inflammation leading to necrosis and bleeding Gallstone can travel and block ampulla of voter → block pancreatic enzymes’ exit → back up into pancreas, becoming activated within pancreas Pancreatitis: Alcohol use disorder Pathophysiology is not completely understood Binge drinking increases the release of pancreatic enzymes and plays a role in the activation of the enzymes Chronic alcohol use thought to possibly lead to formation of protein plugs that block pancreatic ducts Clinical manifestations of pancreatitis LUQ, mid-epigastric pain that can radiate to the back (worse with eating) o Typically sudden onset o Abdo tenderness with muscle guarding N&V Weakness Fever, leukocytosis Jaundice, if there is obstruction of the bile duct Shock secondary to hemorrhage Grey-turner’s sign: ecchymosis in the flanks, discolouration of the flank (retroperitoneal hemorrhage)  Cullen’s sign: peri-umbilical ecchymosis, jaundice or necrosis around the umbilical → signs of pancreatitis o Both are associated with hemorrhagic pancreatitis – worry about bleeding – severe pancreatitis + poor prognosis Autodigestion of pancreas – pancreatic enzymes digest the pancreas itself Inflammation Vascular damage Necrosis Formation of pseudocyst within the pancreas (which are collections of leaked pancreatic fluids) – as a result of inflammation and damage that’s happening Complication Pseudocyst Abscess Description Accumulation of fluid, pancreatic Infected pseudocyst, associated with enzymes, tissue debris, inflammatory extensive necrosis in the pancreas exudate Clinical Abdominal pain, palpable mass, N&V Abdo pain, abdo mass, high fever, manifestations leukocytosis Course without May resolve spontaneously or May rupture or perforate into other organs management perforate (leading to peritonitis) Management Watchful waiting (if small and Requires surgical drainage asymptomatic); drainage (if larger or causing symptoms) Evaluation Labs: o amylase, lipase ▪ key indicators for acute pancreatitis: lipase is more specific for acute – will remain elevated longer o LFTs, bilirubin ▪ Assess liver involvement and potentially bile duct obstruction o Calcium ▪ Hypocalcemia can be assoc with acute pancreatitis Imaging: abdo U/S, CT scan (to check extent of inflammation and damages) Management of acute pancreatitis Supportive care Ensuring hydration Pain management Treatment of shock if present  Bowel rest to decrease enzyme secretion: use of NG suction Monitoring for infection Treating cause if indicated (gallstones) Nutrition therapy o May require enteral feeds (via jejunal feeding tube or TPN) o When food is allowed – small, frequent meals, high carbohydrate REVIEW QUESTIONS WEEK 1 1. Where is the antrum of the stomach located? a. Near the esophagus b. In the middle of the stomach c. Near the pylorus d. In the duodenum 2. Where is bile released during digestion? a. Duodenum b. Esophagus c. Stomach d. Large intestine 3. What is the name of the sphincter that separates the esophagus from the stomach? a. Pyloric sphincter b. Lower esophageal sphincter c. Ileocecal valve d. Urethral sphincter 4. The most common site for peptic ulcers is? a. Duodenum b. Antrum (of the stomach) c. Fundus (of the stomach) d. Esophagus 5. What is the most common complication of PUD? a. Esophageal stricture b. Hemorrhage c. Perforation d. Pyloric obstruction 6. GERD is a result of: a. Excessive production of hydrochloric acid b. A zone of low pressure of the LES c. Presence of H. pylori in the esophagus d. Reverse muscular peristalsis of the esophagus 7. In managing the symptoms with GERD, the nurse should assign the highest priority to which of the following interventions? a. Decrease daily intake of vegetables and water, and ambulate frequently b. Drink coffee diluted with milk at each meal, and remain in an upright position for 30 mins c. Eat small, frequent meals, and remain in an upright position for at least 30 mins after eating d. Avoid over-the-counter drugs that have antacids in them 8. The most common cause of duodenal ulcers is: a. Hypersecretion of gastric acid b. Hyposecretion of pepsin c. H. pylori d. E. Coli 9. A client with cholelithiasis has a gallstone lodged in the common bile duct. When assessing this client, the nurse expects to note:  a. Yellow sclerae b. Light amber urine c. Circumoral pallor d. Black, tarry stools 10. Which of the following best describes Murphy’s sign? a. Periumbilical ecchymosis exists b. On deep palpation and release, pain is elicited c. On deep palpation, pain is elicited and breathing stops d. Abdominal muscles are tightened in anticipation of palpation 11. Which of the following is a common clinical manifestation of acute pancreatitis? a. Right lower quadrant pain b. Mid-epigastric pain radiating to the back c. Pain relieved by eating d. Chronic cough 12. Which laboratory test is most specific for diagnosing acute pancreatitis? a. Serum amylase b. Serum lipase c. Liver function tests d. Complete blood count (CBC) 13. What is the preferred initial imaging modality for evaluating suspected acute pancreatitis? a. MRI b. Abdominal ultrasound c. Chest x-ray d. PET scan