Management of Common GI Issues.pdf

Management of Common GI Issues Valdres Esophagus à stomach à HCL à Intrinsic Factor à Duodenum à Bile Amylase, lipase à Jejunum à Ileum à colon à Cecumà Rectum à anus Abdominal Pain • Common complaint • Acute abdominal pain must be evaluated • Numerous causes for abdominal pain • Accounts for 90% of...

Management of Common GI Issues Valdres Esophagus à stomach à HCL à Intrinsic Factor à Duodenum à Bile Amylase, lipase à Jejunum à Ileum à colon à Cecumà Rectum à anus Abdominal Pain • Common complaint • Acute abdominal pain must be evaluated • Numerous causes for abdominal pain • Accounts for 90% of all ER visits • General Assessment a. RUQ: Cholecystitis, RLL pneumonia, acute hepatitis b. RLQ: Appendicitis, diverticulitis, ureteral calculi, ovarian cyst, ectopic pregnancy c. LLQ: Diverticulitis, RLQ disease, associate the classic signs of a condition with normal physiologies d. LUQ: Gastritis, pancreatitis, LLL pneumonia and MI • Abdominal Pain DDX a. Sudden Severe Pain i. Appendicitis ii. Intestinal perforation iii. Mesenteric infection iv. Ruptured aneurysm b. Burning Pain i. GERD ii. Gastritis iii. Diverticulitis c. Crampy or colicky pain i. Intestinal obstruction ii. IBD iii. IBS iv. Salpingitis v. Urinary stones d. Ectopic pregnancy e. Constant Pain i. Pancreatitis ii. Cholecystitis iii. Cholelithiasis Constipation 1. Definition: change in bowel patterns a. Decrease in frequency or increase in difficulty of defication 2. Common in Western Society 3. Most common GI disorder in the US a. elderly b. sedentary 4. Causes a. Lack of dietary fiber b. Habitual use of laxatives c. Irritable bowel syndrome d. Sedentary lifestyle e. Change in environment or travel f. Medication g. Supressing urge to deficate h. Tumors i. Hypothyroidism j. Diabetes k. Hypercalcemia l. Pregnancy 5. DDX a. Low dietary fiber b. Functional constipation c. IBS d. Fecal impaction e. Idiopathic slow transit time f. Anal fissure g. Hemorrhoids h. Drug induced i. Bowel tumor 6. Treatment: a. Increase dietary fiber to 25-35 g/day b. Exercise c. Adequate hydration d. Medication i. Bulking agents (psyllium) ii. Methylcellulose preparations iii. Stool softeners (docusate sodium) iv. Saline laxatives (magnesium sulfate) v. Stimulating laxatives (bisocodyl, senna, sascara) vi. Lubricants (mineral oil) Diarrhea 1. Increased frequency, volume of fluid content of bowel movement 2. Average stool weight in United States is 200 g 3. Average frequency is once a day 4. Types a. Osmotic diarrhea i. Lactose deficiency ii. Ingestion of poorly absorbed solutes (Mg sulfate) iii. Small bowel injury b. Secretory diarrhea i. Bacterial enterotoxins (cholera and strains of E coli) ii. Laxative abuse iii. Bile salt malabsorption iv. Endocrine tumors c. Morphological Changes i. Inflammatory bowel disease 5. DDX a. Acute i. Abrupt onset < 1 week ii. Viral or bacterial iii. Dysentery b. Chronic i. Lasts over months ii. IBD iii. Crohn’s disease iv. Ulcerative colitis c. Drug induced (laxatives or C-deficile) d. IBS e. Celiac Sprue Nausea & Vomiting 1. Nausea a. Unpleasant sensory experience in the stomach b. Can be accompanied by diaphoresis, increased salivation, and vasovagal signs 2. Vomiting a. Forceful expulsion of gastric contents b. Reflex response to stimulation or receptor sites in the upper GI tract, inner ear, chemoreceptor trigger zone (CTZ) in the medulla oblongata 3. Assessment a. Onset and duration i. associated with meals ii. Projectile vomiting iii. Timing - early morning may indicatepregnancy b. Characteristics i. Odor, color, contents c. Associated symptoms accompanied by nausea i. Vertigo, tinnitus ii. Headache iii. Diarrhea 4. Treatments a. Treat underlying cause b. Antihistamines (Benadryl, promethazine, Loratadine, fexofenadine) c. Anticholinergic (meclizine, reglan, tigan) d. Antidopaminergics (Phenothiazine, Compazine) e. Antidopaminergics and cholinergics f. Cholinergic antagonists (scopolamine, atropine, Robinul) g. Serotonin receptor antagonists (Zofran, kytril aloxi) Dyspepsia and Heartburn 1. Dyspepsia a. Epigastric discomfort b. Postprandial fullness, early satiety c. Anorexia, belching, bloating d. Nausea/vomiting e. Dysphagia and abdominal burning 2. Causes a. Alcohol b. Drugs i. NSAIDs ii. Corticosteroids iii. Erythromycin iv. Theophylline c. Giardiasis d. H. Pylori 3. Heartburn a. Extreme pain that is difficult to distinguish from angina pectoris b. Sometimes described as radiating to back, arms, or jaw 4. Retrosternal burning a. 7% of US population has daily symptoms b. 14% has weekly symptoms c. 36% has some heartburn 5. GERD a. Most common cause of heartburn 6. Gastroenteritis a. Inflammation of the stomach and intestine b. Manifests as anorexia, nausea, vomiting, and diarrhea c. Acute form is from bacteria, viruses, parasites, injury to bowel mucosa, poisons, and drugs d. Chronic form is from good allergies, food intolerances, stress, and lactose deficiency. e. Etiology/Incidence i. Infection - fecal-oral route; possibly respiratory ii. Viruses - Most common, bacteria and parasites iii. Common in all ages and with travel to developing countries f. Risk Factors i. Improper hand washing and food preparation ii. Day care attendance (elderly) iii. Recent use of antibiotic (C-dif) iv. Lack of sanitation v. Immunocompromised patients vi. Recent travel to developing countries g. Clinical Presentation i. Nausea, vomiting, diarrhea (3 loose stools/24 hrs) ii. Fever iii. Abdominal pain and cramping iv. Associated symptoms 1. Fatigue, malaise, anorexia, tenesmus, borborygmus v. Chills and sweats, headache h. Management i. Fluids and sodium (Pedialyte or Gatorade) ii. Possible hospitalization iii. Antimotility drugs (not in febrile dysentery) iv. Antibiotics (viral NO, bacterial/parasites YES) 1. Salmonella+, E coli, Shigella-, Campylobacter & cholera) v. No solid foods vi. No dairy products vii. Avoid alcohol viii. Hydrating liquids ix. Eat fruits and vegetables i. Diagnosis to consider in the Elderly patient i. Inflammatory bowel disease ii. Malabsorption iii. Colon cancer iv. Diverticular disease j. v. Constipation with overflow diarrhea 1. NOTE: ask about recent travel, DRE if suspicious overflow, stool culture, blood test, abd X-ray, sigmoidoscopy, colonoscopy Management i. Prevention ii. Nonpharmacologic iii. Pharmacologic 1. Antiemetics 2. Selective 5HT3 receptor antagonists 3. Antibiotics GERD 1. Case Study: a. a 40 year old patient complaints of a chronic heartburn of many years duration period his symptoms are associated with large fatty meals and worsened when supine. He has a long term history of OTC antiacids and H2 blockers. May be on chronic NSAIDS, ASA or ETOH. b. Objective i. Acidic or sour odor to breath and reflux when over eating ii. Tooth enamel is thin iii. Chronic sore red throat iv. Chronic coughing 2. A long term regular occurrence of acid reflux. a. A digestive disorder that affects the lower esophageal sphincter (LES), the ring of muscle between the esophagus and stomach. b. You have back flow into the esophagus leading to the damage. c. 35 to 45% of adults have gerd. 3. Clinical presentation. a. Subjective. i. Heartburn. ii. Regurgitation. iii. Sour taste in mourning. iv. Belching. v. Coughing. vi. Hoarseness. b. Objective. i. Only sign may be occult blood in stool. 4. Precipitating or aggravating factors. a. Reclining after eating. b. Eating a large meal. c. Alcohol. d. Chocolate. e. Caffeine. f. Decaffeinated coffee. g. h. i. j. k. Fatty or spicy foods. Constrictive clothing. Heavy lifting, straining, or working in a bent over position. Peppermint or spearmint. Tomato products. Certain drugs. i. Anticholinergic agents. ii. Calcium channel blockers. iii. Diltiazem. iv. Estrogen and progesterone. v. Beta adrenergic blocking agents. vi. Nicotine, including second hand smoke. vii. The offline. 5. Diagnostic tests. a. History alone has sensitivity of 80%. b. Ambulatory esophageal pH monitoring or manometry - LES function. c. upper endoscopy with biopsy is test of choice to document type and extent of tissue damage. d. Labs: gold standard - it's official motility study/ manometry (measure the peristalsis - measure the pressure, esophageal strength and muscle coordination when swallowing) diagnosis of achalasia. 6. Management. a. Approaches to acid reducing therapy. i. Step down. 1. Begin treatment with proton pump inhibitor 2. maintain improvement with PPI. 3. Switch to H2RA. ii. Step up approach. 1. Begin treatment with H2 RA. 2. Inadequate response move towards PPI. 3. Inadequate response leads to increase PPI dose. b. Step up. i. Mild to moderate symptoms nonerosion. 1. H2 blockers, either OTC or prescribed ranitidine. 2. If no improvement, proton pump inhibitor omeprazole. a. Step up dosage to eliminate symptoms. 3. Can start at higher doses. a. step down to lower doses that suppress acid secretions. 4. Continue for six weeks and evaluate. 5. ***If no relief, patient becomes a high risk for Barrett’s esophagus.*** c. Troubling symptoms. i. Severe symptoms Warrant endoscopic evaluation. ii. PPI - eight week course of once a day treatment is 80% effective. iii. PPI - twice a day is 95 percent effective. iv. Maintenance therapy is necessary for severe erosive esophagitis. v. H2 antagonist: provide relief for 6 to 12 hours. Cimetidine, Famotidine, ranitidine. vi. antacids for mild GERD: increase PH short term up to four hours? 1. Maalox, Rolaids and tums. 7. Things to remember about GERD. a. Barrett's esophagus is a precancer condition; Esophageal cancer. Diagnose upper endoscopy and biopsy. b. Lifestyle factors to teach; No mints avoid caffeine. c. Worrisome symptoms: progressive dysphagia, iron deficiency anemia, weight loss, hemoccult positive. Peptic ulcer disease PUD 1. Middle-aged to older adult complains of episodic epigastric pain, burning, gnawing pain or ache 80%. Pain is relieved by food and Oregon antacids 50% of the time with reoccurrence 2 to three hours after a meal. Patient self-medicated with over the counter antacids and maybe taking non-steroidal anti-inflammatory drugs. 2. Abdominal exam: normal or mild epigastric tenderness; Hemoccult positive. 3. CBC shows anemia. 4. Peptic ulcer disease: PUD. a. Ulceration involving the stomach or the duodenum: H pylori, gram negative bacteria. b. Duodenal ulcer most often between 30 and 55 years of age; Four times more common than gastric. c. Gastric ulcers are more prevalent between the ages of 55 and 70 years old. 5. Risk factors. a. Cigarette smoking and excessive alcohol use. b. Use of biphosphonates. c. Family history or previous ulcer. d. H pylori. e. Over 60 years of age. 6. Clinical presentation. a. Duodenal - burning pain, awakens patient early in the morning. b. Gastric - pain in is exacerbated with eating, nausea and vomiting, early satiety. c. Acute hemorrhage - coffee ground emesis, tari, black stools. d. Iron deficiency anemia - Due to occult blood loss. e. Perforation - board like abdomen with rebound tenderness. f. Worrisome*** early satiety, anorexia, anemia, weight loss. 7. Diagnostic tests. a. Upper GI endoscopy is the gold standard. b. H pylori testing. i. ELISA test ii. Breath test. c. Fasting gastrin levels. 8. Management. a. Goals. i. Pain relief. ii. Heal ulcer. iii. Prevent complication. iv. Prevent recurrence. b. H2 receptor agonist i. treatment for H pylori negative ulcers. 1. H2 blockers/antagonist - Ranitidine 150 mg/Tagamet 400 mg qD 2. PPI’s; Omeprazole 20 milligrams daily or Nexium 40 milligrams per day. ii. Treatment for H pylori positive ulcers. 1. Triple therapy - clarithromycin plus amoxicillin 1 gram bid for 14 days; plus PPI bid for 6 to 8 weeks. 2. Quadruple therapy - Bismuth subsalicylate 600 milligrams QID plus metronidazole 250 milligrams QID plus tetracycline 500 milligrams QID for two weeks plus PPI daily for four to six weeks or longer. 9. Follow up and referral. a. If no improvements in two weeks, a referral to a gastroenterologist for endoscopy is needed. b. If suspect the gastric rather than duodenal ulcer, refer for endoscopy because of incidence of gastric cancer. c. Grow up is necessary for anyone not responding to treatment. Jaundice. 1. Yellowing of skin, mucous membranes, and sclera. 2. Accumulation of bilirubin in the blood. 3. Can be a result of; a. decreased uptake of bilirubin. b. Decrease conjugation of bilirubin. c. Decreased excretion of bilirubin. Cholecystitis 1. Acute inflammation of the gallbladder wall. 2. Usually caused by cholelithiasis. 3. If no gallstones, a calculus Cholecystitis and has high mortality rate. 4. More prevalent in western societies. 5. Affects 20 million Americans; 75% of native americans over 25 years having gallstones. 6. Clinical presentation. a. Pain. i. Colicky right upper quadrant mass and tenderness. ii. 80% have had this pain before. iii. Can be referred to middle of back to the infra scapular region. iv. Indigestion, nausea, vomiting. v. Positive Murphy's sign. vi. Fever, usually low grade. vii. Mild jaundice. viii. Elevated CRP and WBC. 7. diagnostic. a. Ultrasound is the gold standard and diagnosis. b. Radionucleotide scan. c. HIDA Scan is helpful if the ultrasound is negative but patient is suspected to have cholecystitis or gallbladder disease. 8. Management. a. Low fat diet. b. Antiemetic c. Non-surgical. i. Stone dissolution. ii. Shockwave lithotripsy. d. Surgery. Acute pancreatitis. 1. Inflammation of the pancreas and surrounding tissue secondary to alcohol abuse, gallstones, elevated triglycerides, infection: >800 mg/dl. 2. Results from pancreatic enzymes and tissue, causing chemical burns. 3. Mild. a. Usually improves within 48 to 72 hours. b. Does not involve other organs. 4. Severe. a. Often associated with complications and multi system organ failure. i. Hemodynamic instability, shock, renal failure, respiratory compromise. b. Can be life threatening. c. Pancreatic necrosis with secondary gram negative sepsis - 100% mortality rate unless surgical debridement. 5. Diagnostic criteria for acute pancreatitis. 6. Clinical presentation. a. Abrupt deep epigastric pain persisting hours to days. b. c. d. e. f. g. h. i. Intense pain. Refractory to large doses of narcotics. Aggravated by activity. Improves when patient is seated and leaning forward. Acutely ill. Nausea and vomiting. Abdominal tenderness with guarding. Tachycardia, rapid shallow respirations, normal temperature progressing to 39 degrees Celsius, blood pressure normal or low. 7. Diagnostic tests. a. History and physical. b. Serum amylase: elevated up to three times normal. c. Concurrent elevation of serum lipase and AST/ ALT. d. WBC count elevated. e. C- reactive protein elevated correlates with pancreatic necrosis. f. CT scan. g. Ultrasound if gallstone pancreatitis is suspected. 8. Ranson’s criteria for predicting the severity. a. At admission. i. 55 or older. ii. WBCS > 16,000/mcl iii. BS > 200mg/dl iv. Base deficit > 4 mEq/L v. LDH > 350 U/L vi. AST > 250 U/L b. During first 48 hours i. BUN ii. HCT rise > 5 mg/dl iii. PaO2 < 60 iv. Ca+ <8 mg/dl v. Fluid sequestration > 6 L c. < 2 signs = 5% mortality risk d. 3-4 signs = 15-20% mortality risk e. 5-6 signs = 40% mortality risk f. > 7 signs = 99% mortality rate 9. Management. a. Maintain fluid status: IV fluids. b. Pain control. c. NPO and NG tube. d. Introduction of clear liquids or fluids when pain free and amylase and lipase return to normal. e. Advanced as tolerated. Chronic pancreatitis 1. progressive inflammatory process. 2. Irreversible fibrosis of the pancreas. 3. Destruction and atrophy of exocrine and endocrine glandular tissue. 4. Management. a. Goal is to prevent further pancreatic damage manage pain, supplement exocrine and endocrine function. b. Abstinence from alcohol. c. Pancreatic enzyme supplementation may relieve pain. d. Narcotic analgesia. e. Low fat diet: less than 50g/day f. Insulin - hypertriglyceridemic pancreatitis lowers TG by triggering enzymatic activity of lipoprotein lipase. Insulin restores the energy level of pancreatic acinar cells which fuels calcium pumps on the cell membrane. g. Surgery. i. Drain pseudo assists. ii. Distal pancreatectomy. iii. Whipple procedure. iv. Puestow Procedure. 5. Case study. a. Adult patient complains of acute onset of fever, nausea, vomiting associated with rapid onset abdominal pain radiating to the midback.. On exam reveals guarding and tenderness over the epigastric area or the upper abdomen, hypo active bowel sounds. Positive Cullens’s and Grey Turner’s sign. May have an ileus and symptoms of shock. b. Cullen’s sign + bluish discoloration in the umbilical region; Grey Turner’s Sign+ bluish discoloration on the flank area 6. Acute pancreatitis. Hepatitis. 1. Viral refers t liver disease caused by: (resulting in chronic infection) a. Hep A - fecal-oral route, B - Blood borne & body fluids, C - Blood borne, D - blood borne& body fluids or infected with HBV and E - Fecal/oral route. b. Cytomegalovirus - Epstein-Barr virus, herpes virus, rubella, varicella-zoster virus, yellow-fever virus. 2. Risk Factors a. Exposure to someone with chronic infection b. Travel/living in endemic conditions c. Anal intercourse d. Poor sanitation/body tattoo e. Sex - infected partner or multiple partners & IV drug use f. Provider/caregiver to an infected person g. Blood transfusion, dialysis patients and clotting factor products 3. Common Hepatitis Markers: DX a. IgM - First one to be produced during acute infection b. IgG - Immunoglobulins; you produce after you had an infection c. Hep B surface antigens d. Hep B surface antibody e. Core antibody f. CBC, BMP, PT/INR, Ammonia, AFT & US liver 4. Diagnostic Tests a. AST/ALT - Elevations indicate liver injury (not liver function) b. Bilirubin may be elevated c. Albumin and prothrombin are indicators of liver function 5. Hep A Diagnostic Test a. IgM anti-HAV appears 4 weeks after exposure b. IgG Anti-HAV appears 2 weeks after IgM anti-HAV begins to increase c. IgG anti-HAV persists for 10 years and provides immunity d. If IgM is elevated in the absence of IgG, acute Hepatitis is suspected e. If IgG is elevated in the absence of IgM, past exposure and non-infective and immunity to Hepatitis A. 6. Hep B Diagnostic Test a. Hep B has inner core that contains a core antigen (HBcAg) surrounded by an outer capsule that contains Hep B surface Antigen (HBsAG) b. Detection of HBsAg is diagnostic for Hep B - first test to order - appears 1-10 weeks after exposure ad remains positive during acute phase. If Persists longer, suspect chronic disease c. IgM anti-Hbc appears shortly after HBsAg and persists for 3-6 months d. IgM anti-HBs diagnostic for acute Hepatitis e. IgG anti-HBs present in recovery and for life f. IBeAg is index of viral replication and infectivity - continued presence of HBeAg predicts chronic Hepatitis B 7. Hepatitis Markers? a. IgG (Antibodies present); immune b. IgM (antibodies present, no immunity yet, patient contagious) c. Hepatitis B surface antigen (screening test for Hep B); if present patient is infectious and has the virus d. Hepatitis B surface antibody (Ab is present and immune: Past infection) e. Core Ab (appears at onset of symptoms and persists for life; indicates previous or ongoing infection in undefined time) 8. Hep C Diagnostic Test a. Anti-HCV by enzyme immunoassays b. Hepatitis C RNA detects actual virus i. Example: ELISA - >90% specificity 9. Clinical presentation a. Variable presentation from asymptomatic to death. b. Prodromal. i. Anorexia, nausea, vomiting, molaise, upper respiratory infection, myalgia, arthralgia, fatigability, fever, abdominal pain. c. Enteric. i. Jaundice, dark urine, light colored stools. d. Convalescent. i. Increased sense of well-being, appetite returns. ii. Jaundice, abdominal pain, fatigability abates. 10. Chronic hepatitis. a. Characterized by elevated ALT and AST for more than six months. b. Hepatitis B&C viruses produce chronic hepatitis. c. Cirrhosis develops in 40% of patients with chronic hepatitis B. d. Hepatocellular cancer develops in 20% of patients with chronic hepatitis C. 11. Differential diagnosis. a. Other viral diseases that affect the liver. i. Infectious mononucleosis. ii. Cytomegalovirus. iii. Herpes simplex virus. b. Drug or toxin induced liver damage. 12. Management. a. Goal of management of hepatitis: prevent transmission and symptomatic relief. b. Vaccinations for hepatitis A&B. c. Balanced nutrition. d. Avoidance of alcohol. e. Activity restriction in acute phase. 13. Treatment. a. Pegylated interferon alpha 2a. b. antiviral agent, Lamivudine c. liver biopsy to determine response. d. Response rate only about 40%. 14. Follow up and referral. a. Anyone diagnosed with hepatitis C should be referred to a hematologist. b. Patients with hepatitis A usually do not require follow up. c. Patients with hepatitis B should be seen in one month and should have blood drawn for HBsAg after six months. i. Persistent elevation of HBsAg indicates A chronic state, and these patients should be referred to a hepatologist. 15. Patient education. a. Instructions about the cause of hepatitis, the mode of transmission, and measures that prevent the transmission. b. Household contacts and sexual contacts should be given passive immunity: immunoglobulin, for hepatitis A&B, as well as active immunization. c. Good hand washing and personal hygiene can prevent the spread. d. No sharing of your personal items such as toothbrushes razors and eating utensils during the period of infectivity. e. Patients with active or chronic hepatitis or a carrier state should be instructed to practice safe sex. Appendicitis 1. Appendicitis is the inflammation of the variform appendix caused by an obstruction and/or infection. 2. It is the most common cause of acute right lower quadrant abdominal pain requiring surgical intervention. 3. Acute Appendicitis results in more than 200,000 appendectomies annually. 4. Epidemiology and causes a. Occurs at any age but is most common between ages 10-30 b. Men are twice as likely to be diagnosed with appendicitis between 10 and 30 years than women, but this equalizes over the life span. c. Appendicitis will affect 10 in 100,000 people in the US, with a lifetime risk for individuals projected at 7-10%. 5. Clinical Presentation a. Acute Onset of mild to severe colicky, epigastric, or peri-umbilical pain; maximum tenderness + rigidity (McBurney’s Point). i. Vague at first, but within 24 hours it localizes over the RLQ ii. Exacerbated by walking or coughing + psoas sign iii. In male patients the pain may radiate into the testicles. iv. May be associated with abdominal muscle spasm in male or female patients v. Fever 99-101 F vi. Elderly - weakness, nausea, vomiting, tachycardia, distention. b. Nausea and anorexia after the onset of pain i. If nausea is present, the patient usually reports that abdominal pain was present before vomiting began. ii. The sensation of constipation is typical, although diarrhea is present in some patients. c. Mildly elevated Temp 999-100 F d. Positive Rovsing’s sign (when pressure is applied on the patients LLQ - causes pain in the RLQ e. (+) Mc Burney’s sign - firmly palpate RLQ, if patient has pain then it is positive f. (+) Psoas and Obturator sign - inflamed appendix. 6. Diagnostic test a. Lab findings are not diagnostic b. Made from History and physical exam c. CBC usually reveals a mild to moderate Leukocytosis (WBC 10-20,000 mcg/L) with a left shift. d. Urinalysis shows microscopic hematuria or pyuria in 25% of patients e. Urine human chorionic gonadotropin (hCG) test completed to rule out (ectopic) pregnancy. f. X-ray studies become more important as appendicitis progresses i. Plain X-ray films of the abdomen, a CT of the abdomen is helpful in ruling out other diagnostic possibilities g. Abdominal US h. Diagnostic Laparoscopy 7. Management a. Keep NPO b. Refrain from using laxatives, enemas or heat compress c. Refer to surgery (Pre-op Ab) Inflammatory Bowel Disease 1. Ulcerative Colitis (UC) a. UC involves only the mucosal surface of the colon, which ultimately results in friability, erosion and bleeding. 2. Crohn’s Disease (CD) - slow and progressive a. Can involve all or any layer of the bowel wall as well as any portion of the GI tract from the mouth to the anus. 3. Epidemiology and Causes a. Genetic predisposition for IBD. b. Ability of bacteria in the gut to cause inflammation. c. Incidence of IBD is about equal in men and women. d. Highest prevalence is in Scandinavian and northern European countries. e. The overall incidence and prevalence of both diseases is about equal worldwide, with incidence rates between 3 and 10 per 100,000 and prevalence rate between 30 and 50 per 100,000. f. The age at onset is frequently in early adulthood, but can be anywhere from the ages of 10 to 40. 4. Crohn's disease versus ulcerative colitis. a. Crohn's disease. symptoms. i. Abdominal pain. ii. Diarrhea. iii. Nausea. iv. Vomiting. v. Weight loss. vi. Can affect the entire gastrointestinal tract. vii. Has a discontinuous pattern throughout the gastrointestinal tract. b. Ulcerative colitis symptoms. i. Abdominal pain. ii. Rectal bleeding. iii. Bloody diarrhea. iv. Affects only the colon. v. Starts in the rectum vi. and progresses continuously throughout the colon. 5. Inflammatory bowel disease a. Crohn’s. i. Inflammation tends to occur in patches ii. Can affect any part of the GI tract from the anus to the esophagus. iii. Blood and mucus in the stools not as common. iv. Can also cause nausea and vomiting. v. Abdominal pain may be more severe or continuous. vi. Inflammation present and mucous and muscle tissue. vii. Granulomas (specific cell formations developed by the immune system to isolate threats to the body) usually present. viii. More likely to cause fistula (small tunnels), fissures (tears) or strictures (narrowing) in the bowel. b. Ulcerative colitis. i. Inflammation is more likely to be uniform or continuous. ii. Localized to the bowel and large bowel. iii. Blood and mucus in the stool more common. iv. Nausea and vomiting not usually seen. v. Pain is more likely to be intermittent and experienced with bowel movements. vi. Typically inflammation is confined to mucosa. vii. Not as likely to cause granulomas. viii. Fistula, fissures and strictures less common. ix. More commonly associated with non or ex-smokers. x. Treated with steroids, 5-ASAs, immunosuppressant medication and biologics. xi. Surgery to the colon (where required) resolves the disease. c. diagnostic tests. i. Definitive diagnosis is made by correlating the symptoms with the history and physical exam. ii. Colonoscopy for ulcerative colitis. iii. Small bowel series follow through contrast for Crohn's disease. iv. Stool analysis and cultures for bacterial, fungal, or parasitic infection. v. Stool culture for mucus and blood, which are normally present with ulcerative colitis. vi. Electrolytes, serum protein, BE, ultrasound of the abdomen. vii. CBC with differential. viii. Evaluation for malabsorption. 1. Anemia secondary to bleeding and iron deficiency. 2. Macrocytic anemia from inflammation of the terminal ileum and poor absorption of folate. 3. Hypocalcemia and vitamin D deficiency, hypoalbuminemia, and steatorrhea resulting from bile salt deficiency. d. UC management. i. Nutritional counseling. 1. Avoidance of caffeine, raw fruits and vegetables. 2. Bland diet high in calories and protein. ii. Antidiarrheal medications. 1. Lomotil. 2. Imodium. iii. Steroids. iv. Immunosuppressive agents. 1. Imuran 2. Cyclosporine. 3. Metabolite 6-mercaptopurine. v. 5-ASA Preparations 1. Mesalamine. 2. Sulfasalazine vi. Surgery. e. Colectomy. Patient education. i. Stress importance of adequate rest and stress reduction. ii. Educate about the disease, diagnostic and laboratory tests, and diet and lifestyle changes. iii. Provide information and addresses for national organizations such as Crohn's and colitis foundation of America incorporated. Irritable bowel syndrome (IBS) 1. It is a functional disorder of the colon marked by exacerbation and remission; Characterized by abdominal pain and discomfort. 2. common - accounts to 50% of GI complaints; Nearly 20% of adults suffer from this. 3. Absence of detectable pathology; Test lab - unrevealing. 4. Case: female complaints of intermittent episode of abdominal pain, cramping, left lower quadrant relieved with defecation. 5. Patients must also have two of these features: a. abdominal pain, cramping or discomfort that is relieved by defecation. b. Change in frequency in stool or appearance of the stool (diarrhea alternating with Constipation). c. Frequent stools (more than three per day). d. Fewer stools (less than three per week). e. Passing mucus. f. Feelings of straining, urgency, or incomplete evacuation. g. Flatulence and abdominal distinction, bloating. 6. Clinical presentation. a. Two types. i. Abdominal pain and altered bowel habits. ii. Painting this diary yeah. b. Abdominal distension. c. Gas and belching. d. Dyspepsia. e. Pyrosis. f. Nausea and vomiting. g. Urgent need to defecate. h. Physical exam is usually normal. 7. Criteria for diagnosing. a. Abdominal pain relieved by defecation or has been associated with a change in frequency or a change in consistency of stools for three months, b. AND c. two or more of the following: i. altered stool frequency. ii. Altered stool form. iii. Altered sensory act of defecation. iv. Passage of mucus. v. Varying degrees of bloating and abdominal distension. 8. Management. a. Identify the symptom pattern. b. Address precipitating factors. c. Avoiding foods that exacerbate the condition. d. High fiber diet ( 20 to 30 grams per day) e. antidiarrheal medication used only temporarily. f. Anticholinergics. g. Serotonin receptor agonists or antagonists. Diverticulitis. 1. Diverticula is the outpouching that can occur along the wall of the large intestine. 2. Etiology - aerobic and anaerobic bacteria that invades the diverticula. 3. Risk factors. a. Low fiber low residue diet. b. > 50 Years old. c. Smoking. d. NSAIDs, aspirin use. 4. Occurs most often within the descending and sigmoid colon. a. Diverticular tend to form at weakened areas of the intestinal wall, usually where arterial vessels perforate the colon. b. The thinner layer of these pouch like protrusions form a narrow neck, which is continuous with the inner layer of the colon, and the sack herniates through the muscle wall. c. Most diverticula are found incidentally with endoscopy or barium enema. 5. Clinical presentation. a. 25% with Diverticular disease develop symptoms. i. left lower quadrant pain and fever in 70% of cases. ii. Right lower quadrant pain and fever. iii. May have blood in stool and Constipation or change in bowel habits, nausea and vomiting, Constipation, diarrhea and flatulence. iv. Decreased white count, chills, tachycardia. v. Rebound tenderness. vi. Guarding and rigidity. vii. Fever, bloating, gas and abdominal distension. b. Diagnosis: local sycosis and thickened gallbladder walls on ultrasound. 6. Management. a. An incidental finding of uncomplicated diverticulosis and requires no further intervention. i. Managed with a high fiber diet or daily fiber supplementation with psyllium. b. Mild symptoms can be managed on an outpatient basis. i. Rest. ii. Oral antibiotics. iii. Clear liquid diet. c. Acute illness. i. Hospitalization. ii. IV antibiotics and hydration, analgesia, bowel rest, and positive nasal gastric tube placement. 7. Follow up and referral. a. Colonoscopy. b. Follow up barium enema can be repeated every three years. c. Patient education should emphasize the importance of a high fiber diet. Colorectal Cancer 1. colorectal tumors are both curable and preventable. 2. Can be symptomatic or asymptomatic. 3. Polyps are classified as a. hyperplastic (non neoplastic) b. Adenomatous (neoplastic) i. Adenomatous Polyps are precursors to the malignant adenocarcinomas, which comprise over 95% of all malignant tumors of the colon. c. Submucosal (lipomas). 4. Decline in mortality rates over the last 20 years attributed to improvement in screening, diagnosis, and treatment. 5. Cure rates of colorectal carcinoma are estimated to be as high as 50%. 6. Epidemiology and causes. a. 9% of all cancer deaths in the United states. b. One in 17 Americans will get colon cancer. c. 148,070 diagnosed each year. d. Risk increases with age. e. Survival rate is 50 to 55%. f. Japanese Americans who adopt the western diet have higher rates than traditional Japanese. 7. Risk factors. a. Family history. b. Diet high in fat, red meat, and refined carbohydrates, and low implant fiber. 8. Clinical presentation. a. Few early warning signs. b. Melena or bright red bleeding from the rectum. c. Change in bowel habits, including Constipation alternating with diarrhea or a change in stool caliber. d. Approximately 50% of patients with a positive fecal occult blood test have either an adenoma ( 38% ) or a neoplasm ( 12% ). e. Fecal occult blood test is positive only in 60 to 70% of patients with known large intestine cancers. 9. Diagnostic tests. a. Serum immune assay for carcinoembryonic antigen (CEA). b. Colonoscopy with a biopsy and barium enema are used to establish definitive diagnosis of colorectal cancer. c. Endoscopic ultrasound has been used to stage regional rectal cancers. 10. Follow up and referral. a. Initial assessment and screening for colorectal carcinoma is the responsibility of every primary care provider. b. Screening for high risk patients should include colonoscopy, which is best done by an experienced gastroenterologist. c. Scheduled: surveillance is required. Hemorrhoids. 1. A mass of dilated and tortuous veins that represent prolapsed submucosal tissue. 2. Classified as either internal or external. 3. Primary causes of hemorrhoids. a. Straining during defecation. b. Constipation. c. Prolonged sitting. d. Pregnancy. e. Annual infection. 4. Some hemorrhoids are asymptomatic and require no treatment. 5. Others can result in profuse bleeding, requiring emergent ligation. 6. Clinical presentation. a. Abrupt onset of pain that is associated with a perianal lump. b. Intense pain after defecation or other straining maneuvers. c. Pruritis. d. External hemorrhoids may not be visible at rest but usually protrude on standing or with the Valsalva maneuver. e. Internal hemorrhoids most often present with rectal bleeding. 7. Management. a. Oral analgesia. b. Sits baths c. bulk forming laxative. d. increase daily fiber intake slowly to 25 - 35 grams. e. Topical hydrocortisone creams for pruritus. f. Surgical excision. g. Sclerotherapy or infrared coagulation. Bye bye we'll see you later bye right see you later buddy OK That I don't know