Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Group D – Analyst Grp Vigilia, Patrice Villaflor, Irene Villafuerte, Marc Villar, Cherry Villasis, Ramon Vistal, Kristine Yap, Margaux Presentation Objectives 1. Review of the anatomy and physiology of the digestive tract. 2. Presentations of GI bleeding, its classifications, and its sources. 3. Approach to a patient with Upper GI bleeding. 4. Enumerate the different tools used in the evaluation and diagnosis of patients presenting with GI bleeding. The Anatomy GI Tract extends from the mouth to the anus, and comprises several organs with distinct functions separating the organs are specialized independently controlled thickened sphincters that assist in the gut compartmentalization gut wall: is organized into well- defined layers that contribute to the functional activities in each region Harrison’s Principle of Internal Medicine, 17th ed. Important Point: The anatomic cut-off for upper GI is the Ligament of Treitz It is located in the fourth portion of the duodenum (the last 2 inches). It connects the fourth portion of the duodenum to the diaphragm near the splenic flexure of the colon. Snell’s Clinical Anatomy, 7th ed. Functions of the GI Tract • Two main functions: o Assimilation of nutrients o Elimination of wastes ORGANS FUNCTION Esophagus Propels the bolus of food to the stomach Stomach Furthers food preparation by triturating and mixing the bolus with pepsin and acid. Small Intestines Site of major nutrient absorption. Large Intestines Prepares the waste materials for controlled evacuation. Harrison’s Principle of Internal Medicine, 17th ed. GI Bleeding Presentation Hematemesis - vomitus of red blood or coffee-grounds material Melena – black, tarry, foul-smelling stool Hematochezia – passage of bright red or maroon blood from the rectum Occult GI Bleeding – identified through fecal occult blood test or the presence of iron deficiency Systemic signs of Blood Loss or Anemia – lightheadedness, syncope, angina, dyspnea Harrison’s Principle of Internal Medicine, 17th ed. GI Bleeding Classification Acute vs Chronic UGI Bleeding vs LGI Bleeding Acute vs Chronic Acute - typically presents with overt blood loss that can be readily recognized by the patient or treating physician Chronic - long-term GI bleeding may go unnoticed or may cause fatigue, anemia, black stools, or a positive test for microscopic blood Washington manual of medical therapeutics, 32nd edition emedicinehealth.com UGI Bleeding vs LGI Bleeding UGI Source of bleeding is ABOVE the ligament of Treitz • Usually presented as: – HEMATEMESIS – MELENA, indicates that blood has been present in the GI tract for at least 14 hrs – May also present as HEMATOCHEZIA if an upper lesion bleeds briskly that blood does not remain in the bowel long enough for melena to develop. – May be occult Harrison’s Principle of Internal Medicine, 17th ed. LGI • Source of bleeding is BELOW the LIGAMENT of TREITZ • Usually presented as – HEMATOCHEZIA – passage of bright red or maroon blood from the rectum. – May be occult Esophagus Upper GI Stomach Duodenum Sources of GI Bleeding Lower GI The remaining portion of the Small Intestines Colonic Source Harrison’s Principle of Internal Medicine, 17th ed. Approach to the patient Measurement of the heart rate and blood pressure is the best way to assess the patient. Clinically significant bleeding leads to postural changes in HR or BP, tachycardia and recumbent hypotension. Approach to the patient Hemoglobin Determination Does not fall immediately with acute GIB: this is due to the proportionate reduction in plasma and red cell volumes. As extravascular fluid enters the vascular space to restore volume, the hemoglobin falls. UPPER GI BLEEDING History and PE in not usually diagnostic. Upper endoscopy is the test of choice and should be performed urgently in patients with hemodynamic instability. Harrison’s Principle of Internal Medicine, 17th ed. Endoscopy • procedure is the best method for examining upper GI • • • • mucosa minimally invasive diagnostic medical procedure used to assess interior surfaces of organs by inserting a tube into the body instrument may have a rigid or flexible tube & not only provide an image for visual inspection and photography, but also enable taking biopsies & retrieval of foreign objects sedatives may be given so as to relieve discomfort Harrison’s Principle of Internal Medicine, 17th ed. Endoscopy • Used to determine the cause of bleeding, pain, nausea and vomiting, weight loss, altered bowel function and fever • Upper endoscopy – evaluates the esophagus, stomach and duodenum – initial test performed in patients with suspected ulcer disease, esophagitis, neoplasm, malabsorption and Barrett's metaplasia because it directly visualizes abnormality Harrison’s Principle of Internal Medicine, 17th ed. Endoscopy Risks of procedure: risk of bleeding gastrointestinal perforation Harrison’s Principle of Internal Medicine, 17th ed. Algorithm for patients with acute upper gastrointestinal bleeding Acute Upper GI Bleeding Ulcer Esophageal Varices Active bleeding or visible vessel Adherent Clot Flat, pigmented spot Clean base IV PPI therapy + endoscopic therapy IV PPI therapy +/- endoscopic therapy No IV PPI or endoscopic therapy No IV PPI or endoscopic therapy ICU for 1 day; ward for 2 days Ward for 3 days Ward for 3 days Harrison’s Principle of Internal Medicine, 17th ed. Discharge Mallory-Weiss Tear Ligation (preferred) or sclerotherapy + IV octreotide Active bleeding No active bleeding ICU for 1-2 days; ward for 2-3 days Endoscopic therapy No endoscopic therapy Ward for 1-2 days Discharg e Other tests that may be performed: Laboratory Tests (CBC, Serum Electrolyte, Fecal Occult Blood, BUN/Crea Ratio) Radiography (Barium Swallow, CT Scan) Harrison’s Principle of Internal Medicine, 17th ed. Summary Assess the patient by doing History and PE Heart Rate and Blood Pressure Do an Endoscopic Exam Perform other laboratory and radiographic exams if necessary Salient Features 55 y/o female History of vague epigastric discomfort hematochezia [2 episodes of melena (2 cupfuls/episode)] hematemesis [1 episode of coffee ground vomiting] cold clammy sweats and dizziness intake of Diclofenac Na intermittently regular medications: clopidogrel (anticoagulant) (+) DM overweight [BMI = 26.5] 10 kg weight loss for the past 6 months orthostatic hypotension (BP 120/80 when supine, 100/60 at sitting) PR 105/min RR 22/min Pale palpebral conjuctiva and anicteric sclera no cervical lymphadenopathy lung and heart sounds are normal apex beat at 6th LICS Abdomen with hyperactive bowel sounds, soft non tender, without palpable mass or organomegaly DRE maroon colored stools Clinical Impression: Acute Upper GI bleeding secondary to PUD (to rule out Gastric CA) Peptic Ulcer Mallory Weiss Tears Causes of Upper GI Bleeding Esophageal Varices Hemorrhagic or Erosive gastropathy Gastric CA Differential Diagnosis Siy, Jeniffer, So, Roizza, Solang, Jenifer, Soriano, Whitney, Soto, Ian, Suelto, Jeremy, Suero, Diane Acid peptic disorders - 4 million individuals (new cases and recurrences) affected per year Lifetime prevalence of PUD in the United States ▪ ~12% in men and 10% in women an estimated 15,000 deaths per year - as a consequence of complicated PUD estimated burden on direct and indirect health care costs of ~$10 billion per year in the United States Harrisons principles of internal madicine 17th ed p1838 Duodenal Ulcers occur in 6–15% of the Western population incidence of DUs declined steadily from 1960 to 1980 and has remained stable since then. death rates, need for surgery, and physician visits have decreased by >50% over the past 30 years Eradication of H. pylori has greatly reduced recurrence rates. Harrisons principles of internal madicine 17th ed p1838 Gastric Ulcers occur later in life than duodenal lesions (peak incidence reported in the sixth decade) More than half occur in males less common than Duodenal Ulcers Autopsy studies suggest a similar incidence of DUs and GUs. Harrisons principles of internal madicine 17th ed p1838 Helicobacter pylori Prevalence : developing parts of the world (80% of the population by age of 20) industrialized countries (20 – 50 %) United States (~30%) About 10% of Americans <30 are colonized with the bacteria Harrisons principles of internal madicine 17th ed p1838 Helicobacter pylori The rate of infection in the United States has fallen by >50% when compared to 30 years ago. Harrisons principles of internal madicine 17th ed p1838 Helicobacter pylori Risk Factors : (1) birth or residence in a developing country (2) domestic crowding (3) unsanitary living conditions (4) unclean food or water (5) exposure to gastric contents of an infected individual. Harrisons principles of internal madicine 17th ed p1838 History PE History Abdominal or Epigastric pain Described as burning, gnawing, aching sensation or hunger pain Important to know the temporal pattern Duodenal Ulcer • Occurs 90 mins to 3 h after a meal • Relieved by antacids or food • Pain that awakes the patient fr sleeping (bet. midnight & 3 am) Gastric Ulcer • Discomfort precipitated by food • Nausea & weight loss occur here more commonly NSAID induced mucosal disease • Can present with complications like bleeding, perforation, and obstruction without antecedent symptom History Penetrating ulcer (pancreas) • Constant dyspepsia , no longer relieved by food or antacids, radiates to the back Perforation • Sudden onset of severe, generalized abdominal pain Gastric outlet obstruction • Pain worsening with meals, nausea & vomiting of undigested food Bleeding • Tarry stools or coffee ground emesis Physical Examination Epigastric tenderness is the most frequent finding in patients with GU or PU Pain may be found at the right side of the midline. Tachycardia and orthostasis may be suggestive of dehydration secondary to vomiting or active gastrointestinal blood loss. Physical Examination Perforation is possible if patients manifest severely tender broad like abdomen Presence of succussion splash indicated retain fluid in the stomach suggestive of intestinal obstruction. Radiographic Procedure (Barium Study) Commonly used as a first test for documenting an ulcer Sensitivity: 80% (single contrast barium meals); 90% (double contrast) Sensitivity is decreased in small ulcers (<0.5cm), presence of previous scarring, postoperative patients Benign duodenal ulcer appears as a well demarcated crater, seen at the bulb Benign gastric ulcer Ulcer crater-collection of barium on dependent surface which usually projects beyond anticipated wall of stomach in profile (penetration) Hampton’s line-1 mm thin straight line at neck of ulcer in profile view which represents the thin rim of undermined gastric mucosa Ulcer collar-smooth, thick, lucent band at neck of ulcer in profile view representing thicker rim of edematous gastric wall Ulcer mound-smooth, sharply delineated tissue mass surrounding a benign ulcer Ring shadow-thin rim of contrast which represents an ulcer on the non-dependent surface of an air-contrast study Thickened folds radiating directly to the base of the ulcer en face Endoscopy Provides the most sensitive and the most specific approach for examining the upper GI Permits direct visualization of the mucosa Facilitates photographic documentation of mucosal defect and tissue biopsy to rule out malignancy or H. pylori Helpful in identifying lesions too small to detect by radiographic examination, for evaluation of atypical radiographic abnormalities, determine if ulcer is source of loss of blood A B GOALS in treating PUD Provide relief of symptoms (pain or dyspepsia) 2. Promote ulcer healing 3. Prevent ulcer recurrence and complications 1. Drugs used in the Treatment of PUDDrug Type Examples Dose Acid-suppressing (Antacids) H2 receptor antagonists Proton Pump inhibitors Mylanta, Maalox, Tums, Gaviscon 100-140 meq/L 1-3 h after meals and hs Cimetidine 400 mg bid Ranitidine 300 mg hs Famotidine 40 mg hs Nizatidine 300 mg hs Omeprazole 20 mg/d Lansoprazole 30 mg/d Rabeprazole 20 mg/d Pantoprazole 40 mg/d Esomeprazole 20 mg/d Harrison’s Principle of Internal Medicine 17th edition Mucosal Protective Agents Drug Type Examples Dose Sucralfate Sucralfate 1 g qid Prostaglandin analogue Misoprostol 200 ug qid Bismuth-containing compounds Bismuth subsalicylate (BSS) See anti-H. pylori regimen Harrison’s Principle of Internal Medicine 17th edition Acid neutralizing/inhibitory drugs (Antacids) MOA: neutralize secreted acids Often used by patients for symptomatic relief of dyspepsia Antacids Maalox Side effects Magnesium OH Diarrhea and hypermagnesemia Aluminum OH Constipation and phospahte depletion Calcium carbonate Milk alkali syndrome – hypercalcemia, hyperphosphatemia, renal calcinosis renal insufficiency (long term use) Sodium bicarbonate Systemic alkalosis H2 receptor antagonists MOA: Competitive inhibitors of the action of histamine at H2 receptors Healing in 80-90% of cases after 4-8 weeks of therapy Cimetidine has an anti-androgenic effect due to cytochrome p450 enzyme inhibition reversible gynecomastia and impotence Harrison’s Principle of Internal Medicine 17th edition Proton Pump (H+,K+ ATPase) inhibitors MOA: Covalently bind and irreversibly inhibit H+K+ ATPase Given before meal, activation in acidic environment Examples of drugs Omeprazole Lanoprazole Administered as enteric-coated grabules in a sustained-release capsule that dissolves in SI at pH 6, Lanoprazole can be taken in an orally disintegrating tablet (with or w/out water) Pantoprazole Enteric-coated tablet, Parenteral Rabeprazole Enteric-coated tablet Cytoprotective agents Drugs MOA Sucralfate Physicochemical barrier, promote trophic action by binding to growth factors, enhance prostaglandin synthesis, stimulate mucous and HCO3 secretion, enhance mucosal defense and repair Colloidal bismuth subcitrate and bismuth subsalicylate Prevention of further pepsin/HCl-induced damage, stimulation of prostaglandin, HCO3 and mucous secretion Prostaglandin analogue Maintain mucosal integrity and repair, enhance mucous and HCO3 secretion, stimulate mucosal blood flow, decrease mucosal cell turnover Harrison’s Principle of Internal Medicine 17th edition Regimens recommended for eradication of H. pylori infection TRIPLE THERAPY Dose Bismuth salicylate Metronidazole Tetracycline 2 tablets qid 250 mg qid 500 mg qid Ranitidine bismuth citrate Tetracycline Azithromycin or Metronidazole 400 mg bid 500 mg bid 500 mg bid Omeprazole (lansoprazole) Clarithromycin Metronidazole or Amoxicillin 20 mg (30 mg) bid 250 or 500 mg bid 500 mg bid or 1 g bid Harrison’s Principle of Internal Medicine 17th edition Regimens recommended for eradication of H. pylori infection QUADRUPLE THERAPY Dose Omeprazole (Lansoprazole) Bismuth subsalicylate Metronidazole Tetracycline 20 mg (30 mg) daily 2 tablets bid 250 mg bid 500 mg bid ** combination therapy for 14 days provides greatest efficacy Harrison’s Principle of Internal Medicine 17th edition SURGICAL THERAPY Surgical intervention in PUD 1. elective for treatment of medically refractory disease 2. urgent/emergent for the treatment of ulcer-related complications ( hemorrhage, perforation and obstruction) Pharmacologic and endoscopic approaches for treatment of PUD and its complications decreased number of operations NSAID Gastropathy Pathophysiology NSAIDs decrease mucosal defense and repair through prostaglandin depletion HCl secretion Mucin secretion Bicarbonate secretion Surface active phospholipid secretion Epithelial cell proliferation Direct toxicity “ion trapping” Endothelial effects causing stasis Harrison’s Principles of Internal Medicine 17th edition Pathophysiology Symptoms: • dyspepsia • nausea, vomiting • diarrhea • gastric and duodenal ulceration • upper GI bleeding Harrison’s Principles of Internal Medicine 17th edition Risk Factors: • • • • • • • • advanced age (>60 y/o) History of ulcer Concomitant use of glucocorticoids Multiple, high-dose NSAIDs Corticosteroids Concomitant anticoagulation or coagulopathy Serious or multisystem disease Potential risk factors: smoking, alcohol, H. pylori infection Harrison’s Principles of Internal Medicine 17th edition Treatment of NSAID-related mucosal injury CLINICAL SETTING RECOMMENDATION Active Ulcer NSAID discontinued NSAID continues H2 receptor antagonist / PPI PPI Prophylactic Therapy Misoprostol PPI Selective COX-2 Inhibitor H. Pylori infection Eradication if active ulcer present or there is a past history or peptic ulcer disease Harrison’s Principles of Internal Medicine 17th edition Guide to NSAID therapy NO Cardiovascular Risk (no Aspirin) NO or LOW NSAID GI Risk NSAID GI Risk Traditional NSAID Traditional NSAID / Coxib plus PPI Consider non-NSAID therapy WITH Cardiovascular Risk (consider Aspirin) Traditional NSAID plus PPI if GI risk warrants gastroprotection A gastro-protective agent must be added if a traditional NSAID is prescribed. Consider non-NSAID therapy Consider non-NSAID therapy Harrison’s Principles of Internal Medicine 17th edition Group C Trias - Ventura Epidemiology Incidence and mortality decreased markedly for the past 75 years, worldwide Remains high in Japan, China, Chile & Ireland Risk is greater among lower socioeconomic classes • Environmental exposure (begins in early life) Migrants (high low) maintain their susceptibility, while the risk of offspring approximate the homeland Dietary carcinogens – most likely factors Clinical Features of Gastric Carcinoma Superficial & surgically curable – no symptoms More extensive – insidious upper abdominal discomfort Anorexia with slight nausea – very common but is not the usual presenting complaint Weight loss - observed Nausea and vomiting – prominent with tumors of the pylorus Dysphagia and early satiety – symptoms caused by diffuse lesions originating in the cardia No early physical signs Palpable abdominal mass – long standing growth and regional extension Gastric CA spread by: Direct extension through the gastric wall to the perigastric tissues, adhering to adjacent organs (pancreas, colon, or liver). Liver is most common site for hematogenous spread. Lymphatics Seeding of peritoneal surfaces • Metastases that occur frequently: intraabdominal and supraclavicular nodes Krukenberg’s tumor – metastatic nodules to the ovary “Sister Mary Joseph node” – periumbilical region Peritoneal cul-de-sac (Blumer’s shelf palpable on rectal/vaginal exam) Presence of Iron deficiency anemia in men and occult blood in stool for both sexes mandates a search for occult GI tract lesion Careful assessment is of particular importance in patients with atrophic gastritis or pernicious anemia Unusual clinical features: Migratory thrombophlebitis Microangiopathic hemolytic anemia Acanthosis nigricans Risk Factors Diet Environment • high concentration of nitrates • smoked, dried, salted food • lower socioeconomic classes • bacterially-contaminated food • exogenous source of nitrateconverting bacteria Risk Factors Medical Conditions Genetic • • • • Menetrier’s disease pernicious anemia atrophic gastritis hx of gastric ulcer • blood type A • adenomatous polyps • mutation in E-cadherin gene Risk Factors •+decreased Hypothesis gastric acidity Acquired • H. pylori infection • prior gastric surgery (antrectomy) • prolonged exposure to histamine H2-receptor antagonists ↑ Nitrate-converting Bacteria Conversion of dietary nitrates to carcinogenic nitrites Diagnosis Double-Contrast Radiographic Examination Gastroscopy Gastroscopic Biopsy and Brush Cytology Endoscopic Biopsy Diagnosis Double-Contrast Radiographic Examination Simplest diagnostic procedure Evaluates patient with epigastric complaints Helps detect small lesions by improving mucosal detail Stomach should be distended every radiographic examination, decrease distensibility is the only indication of a diffuse infiltrative carcinoma Diagnosis Gastroscopy Diagnostic method of choice Involves insertion of a fibre optic camera into the stomach to visualize it Not a mandatory if the radiographic features are typically benign Diagnosis Gastroscopic Biopsy and Brush Cytology Recommended to all patient with gastric ulcer in order to exclude a malignancy Endoscopic Biopsy done with the help of a fiber-optic endoscope which is inserted into the gastrointestinal tract Since gastric carcinomas are difficult to distinguish clinically or radiographically from gastric lymphomas, endoscopic biopsy should be made as deeply as possible due to the submucosal location of lymphoid tumors. TREATMENT Complete surgical removal of the tumor + resection of adjacent lymph nodes -only chance for cure Subtotal gastrectomy Treatment of choice for distal tumors Total / Near-Total gastrectomy Treatment for proximal tumors • Extended lymph node dissection • Added risk of complications w/o enhancement of survival • Reduction of tumor bulk is the best form of palliation • May enhance benefit from subsequent therapy TREATMENT • PROGNOSIS depends on • Degree of tumor penetration into gastric wall • Regional lymph node involvement • Vascular invasion • Abnormal DNA content (aneuploidy) 5 year survival probability ~20% for distal tumors <10% for proximal tumors Recurrences for ≥ 8 years post surgery TREATMENT Radiotherapy Palliation of pain Radiotherapy alone after complete resection does not prolong survival Chemo + Radio therapy 5FU combined with radiation therapy slightly improved survival 5FU may function as a radiosensitizer TREATMENT Cytotoxic Drugs Cisplatin + epirubicin or 5FU (infusional) or irinotecan Associated with partial responses in 30-50% of cases Minimal improvement of survival with adjuvant chemotherapy alone ff. complete resection Perioperative treatment and post-op chemotherapy + radiotherapy reduces recurrence rate and prolongs survival Thank You! Analysis Gastrointestinal Bleeding Upper Lower - Refers to bleeding from esophagus, stomach, duodenum (above the Ligament of Treitz) - Refers to bleeding from distal small bowel, colon, rectum, and anal canal (below the Ligament of Treitz) Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Clinical Presentation Upper GI Bleeding Lower GI Bleeding - Hematemesis - Hematochezia - Melena - Hematochezia (associated with hemodynamic instability and dropping hemoglobin) - Hyperactive bowel sounds - Elevated BUN Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Mallory Weiss Tears Hx: vomiting, retching, coughing preceding hematemesis especially in alcoholics Stops spontaneously (80-90%) Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Esophageal Varices 4-31% of causes Most often it is a consequence of portal hypertension Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Hemorrhagic or Erosive gastropathy 3-11% (less common) mucosal lesions and thus do not cause major bleeding. Risk factors for NSAID-induced gastroduodenal ulceration: old age,high dose/multiple NSAID use, concomitant use of anticoagulant (clopidogrel), serious or multisystem disease (DM, HPN) Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Gastric CA 1-4% of causes (rare) risk factors present in our patient: old age and overweight Presents with significant weight loss, progressive epigastric pain and GI bleeding Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed) Peptic Ulcer 35-62% (most common),1/3 of patients w/ active bleeding abdominal or epigastric pain is described as burning, gnawing, aching sensation or hunger pain Risk Factors present in our patient: age, NSAID use , anticoagulant use (clopidogrel) Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)