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The Approach to Upper GI Bleeding

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1 The Approach to Upper GI Bleeding
Group D – Analyst Grp Vigilia, Patrice Villaflor, Irene Villafuerte, Marc Villar, Cherry Villasis, Ramon Vistal, Kristine Yap, Margaux

2 Presentation Objectives
Review of the anatomy and physiology of the digestive tract. Presentations of GI bleeding, its classifications, and its sources. Approach to a patient with Upper GI bleeding. Enumerate the different tools used in the evaluation and diagnosis of patients presenting with GI bleeding.

3 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.

4 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.

5 Functions of the GI Tract
Two main functions: Assimilation of nutrients 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.

6 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.

7 GI Bleeding Classification
Acute vs Chronic UGI Bleeding vs LGI Bleeding

8 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

9 UGI Bleeding vs LGI Bleeding
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 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 Harrison’s Principle of Internal Medicine, 17th ed.

10 The remaining portion of the Small Intestines
Sources of GI Bleeding Upper GI Esophagus Stomach Duodenum Lower GI The remaining portion of the Small Intestines Colonic Source Harrison’s Principle of Internal Medicine, 17th ed.

11 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.

12 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.

13 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.

14 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.

15 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.

16 Endoscopy Risks of procedure: risk of bleeding
gastrointestinal perforation Harrison’s Principle of Internal Medicine, 17th ed.

17 Algorithm for patients with acute upper gastrointestinal bleeding
IV PPI therapy + endoscopic therapy ICU for 1-2 days; ward for 2-3 days Endoscopic therapy No endoscopic therapy Ward for 1-2 days Discharg e ICU for 1 day; ward for 2 days IV PPI therapy +/- endoscopic therapy No IV PPI or endoscopic therapy Ward for 3 days Discharge Active bleeding or visible vessel Ligation (preferred) or sclerotherapy + IV octreotide Clean base Adherent Clot Flat, pigmented spot Active bleeding No active bleeding Acute Upper GI Bleeding Ulcer Esophageal Varices Mallory-Weiss Tear Harrison’s Principle of Internal Medicine, 17th ed.

18 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.

19 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

20 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]

21 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

22 Clinical Impression: Acute Upper GI bleeding secondary to PUD (to rule out Gastric CA)

23 Hemorrhagic or Erosive gastropathy
Peptic Ulcer Causes of Upper GI Bleeding Esophageal Varices Mallory Weiss Tears Hemorrhagic or Erosive gastropathy Gastric CA Differential Diagnosis

24 Peptic Ulcer Disease Siy, Jeniffer, So, Roizza, Solang, Jenifer, Soriano, Whitney, Soto, Ian, Suelto, Jeremy, Suero, Diane


26 Incidence and Epidemiology
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

27 Incidence and Epidemiology
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. The reason for the reduction in the frequency of DUs is likely related to the decreasing frequency of Helicobacter pylori. Before the discovery of H. pylori, the natural history of DUs was typified by frequent recurrences after initial therapy. Eradication of H. pylori has greatly reduced these recurrence rates. Harrisons principles of internal madicine 17th ed p1838

28 Incidence and Epidemiology
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

29 Incidence and Epidemiology
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 In contrast, in the United States this organism is rare in childhood. The overall prevalence of H. pylori in the United States is ~30%, with individuals born before 1950 having a higher rate of infection than those born later. About 10% of Americans <30 are colonized with the bacteria. The rate of infection with H. pylori in industrialized countries has decreased substantially in recent decades. The steady increase in the prevalence of H. pylori noted with increasing age is due primarily to a cohort effect, reflecting higher transmission during a period in which the earlier cohorts were children. It has been calculated through mathematical models that improved sanitation during the latter half of the nineteenth century dramatically decreased transmission of H. pylori. Moreover, with the present rate of intervention, the organism will be ultimately eliminated from the United States. The risk of H. pylori infection is declining in developing countries. Harrisons principles of internal madicine 17th ed p1838

30 Incidence and Epidemiology
Helicobacter pylori The rate of infection in the United States has fallen by >50% when compared to 30 years ago. Transmission of H. pylori occurs from person to person, following an oral-oral or fecal-oral route Harrisons principles of internal madicine 17th ed p1838

31 Incidence and Epidemiology
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. Two factors that predispose to higher colonization rates include poor socioeconomic status and less education. These factors, not race, are responsible for the rate of H. pylori infection in blacks and Hispanic Americans being double the rate seen in whites of comparable age. Other risk factors for H. pylori infection are (1) birth or residence in a developing country, (2) domestic crowding, (3) unsanitary living conditions, (4) unclean food or water, and (5) exposure to gastric contents of an infected individual. Harrisons principles of internal madicine 17th ed p1838

32 Clinical Presentation of Upper GI Bleeding due to PUD
History PE

33 History Abdominal or Epigastric pain Duodenal Ulcer
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

34 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

35 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.

36 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.


38 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

39 Film reveals a small duodenal ulcer crater on the inferior aspect of the bulb with a moderately severe cloverleaf deformity of the bulb. Benign duodenal ulcer appears as a well demarcated crater, seen at the bulb

40 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 Benign. lesser curvature gastric ulcer. Red arrows point to Hampton's Line, a thin, straight line at neck of ulcer in profile view which represents the thin rim of undermined gastric mucosa. The blue arrows point to the ulcer mound, a smooth, sharply delineated soft-tissue mass surrounding a benign ulcer. Note how the ulcer projects beyond the confines of the expected wall of the stomach.

41 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

42 Duodenal ulcer Gastric ulcer A B


44 GOALS in treating PUD Provide relief of symptoms (pain or dyspepsia)
Promote ulcer healing Prevent ulcer recurrence and complications

45 Drugs used in the Treatment of PUD
Drug Type Examples Dose Acid-suppressing (Antacids) Mylanta, Maalox, Tums, Gaviscon meq/L 1-3 h after meals and hs H2 receptor antagonists Cimetidine 400 mg bid Ranitidine 300 mg hs Famotidine 40 mg hs Nizatidine Proton Pump inhibitors Omeprazole 20 mg/d Lansoprazole 30 mg/d Rabeprazole Pantoprazole 40 mg/d Esomeprazole Harrison’s Principle of Internal Medicine 17th edition

46 Mucosal Protective Agents
Drugs used in the Treatment of PUD Drug Type Examples Dose Mucosal Protective Agents 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

47 Drugs used in the Treatment of PUD
Acid neutralizing/inhibitory drugs (Antacids) MOA: neutralize secreted acids Often used by patients for symptomatic relief of dyspepsia Antacids Side effects Maalox 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 Combination of Mg and Al OH avoid the side effects. Maalox contraindicated in chronic renal failure patients because of possible hyperphosphatemia (Mg) and neurotoxicity (Al)

48 Drugs used in the Treatment of PUD
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

49 Drugs used in the Treatment of PUD
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 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) Lanoprazole Pantoprazole Enteric-coated tablet, Parenteral Rabeprazole Enteric-coated tablet

50 Drugs used in the Treatment of PUD
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

51 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 Azithromycin or Metronidazole 400 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

52 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

53 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


55 Harrison’s Principles of Internal Medicine 17th edition
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

56 Pathophysiology

57 Pathophysiology Schematic 1. Possible Pathogenesis of NSAID Induced Small Bowel Damage. J Pharm Pharmaceut Sci ( 3(1): , 2000

58 Harrison’s Principles of Internal Medicine 17th edition
Symptoms: dyspepsia nausea, vomiting diarrhea gastric and duodenal ulceration upper GI bleeding Harrison’s Principles of Internal Medicine 17th edition

59 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

60 Diagnosis and treatment

61 Treatment of NSAID-related mucosal injury
CLINICAL SETTING RECOMMENDATION Active Ulcer NSAID discontinued NSAID continues H2 receptor antagonist / PPI PPI Prophylactic Therapy Misoprostol 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

62 Guide to NSAID therapy NO or LOW NSAID GI Risk NSAID GI Risk
NO Cardiovascular Risk (no Aspirin) 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. Harrison’s Principles of Internal Medicine 17th edition

63 Gastric Adenocarcinoma
Group C Trias - Ventura

64 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

65 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

66 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)

67 Unusual clinical features:
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

68 Risk Factors high concentration of nitrates smoked, dried, salted food
Diet high concentration of nitrates smoked, dried, salted food Environment lower socioeconomic classes bacterially-contaminated food exogenous source of nitrate-converting bacteria Kasama pa ba age and gender dito? (m>f, elderly  >65???) Or is it under epidemiology?

69 Risk Factors Medical Conditions Menetrier’s disease pernicious anemia atrophic gastritis hx of gastric ulcer Genetic blood type A adenomatous polyps mutation in E-cadherin gene Menetrier’s dse – extreme hypertrophy of gastric rugal folds Pernicious anemia – vitamin B12 deficiency Atrophic gastritis – chronic inflammation of the stomach; intestinal metaplasia  cellular atypia  neoplasia Under medical conditions, not sure if included: hx of gastric ulcer (possible risk factor, cause-effect not yet established, more data needed) Pernicious anemia, atrophic gastritis seen in elderly accdg to Harrison? Genetic Type A – may be related to differences in mucous secretion, leading to altered mucosal protection from carcinogens HNPCC – hereditary nonpolyposis colorectal cancer FAP – familial adenomatous polyposis

70 Risk Factors + Hypothesis
Acquired decreased gastric acidity H. pylori infection prior gastric surgery (antrectomy) prolonged exposure to histamine H2-receptor antagonists ↑ Nitrate-converting Bacteria Conversion of dietary nitrates to carcinogenic nitrites Hypothesis: nsa baba… should we include??

71 Diagnosis Double-Contrast Radiographic Examination Gastroscopy
Gastroscopic Biopsy and Brush Cytology Endoscopic Biopsy

72 Diagnosis Simplest diagnostic procedure
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

73 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

74 Diagnosis Gastroscopic Biopsy and Brush Cytology Endoscopic Biopsy
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.

75 Staging system for gastric ca
Stage TNM Features No. of Cases % 5 year survival, % TisN0M0 Node negative; Limited to mucosa 1 90 IA T1N0M0 Invasion of lamina propria or submucosa 7 59 IB T2N0M0 Invasion of muscularis propria 10 44 II T1N2M0 T2N1M0 Node positive; invasion beyond mucosa but within wall 17 29 T3N0M0 Node negative, extension through wall IIIA T2N2M0 T3N1-2M0 Node positive; invasion of muscularis propria or through wall 21 15 IIIB T4N0-1M0 Node negative; adherence to surrounding tissue 14 9 IV T4N2M0 Node positive; adherence to surrounding tissue 30 3 T1-4N0-2M1 Distant metastases

76 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

77 TREATMENT PROGNOSIS depends on 5 year survival probability
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

78 TREATMENT Radiotherapy Chemo + Radio therapy 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 GASTRIC ADENOCARCINOMA – relatively radioresistant tumor; adequate tumor control requires doses of irradiation exceeding the tolerance of surrounding structures (ie bowel mucosa and spinal cord) therefore, radiotherapy is mainly for PALLIATION

79 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 Perioperative treatmetn

80 Thank You!

81 Analysis

82 Gastrointestinal Bleeding
Upper - Refers to bleeding from esophagus, stomach, duodenum (above the Ligament of Treitz) Lower - Refers to bleeding from distal small bowel, colon, rectum, and anal canal (below the Ligament of Treitz) Fauci et al Harrison’s Principles of Internal Medicine (17th ed)

83 Clinical Presentation
Upper GI Bleeding Hematemesis Melena Hematochezia (associated with hemodynamic instability and dropping hemoglobin) Hyperactive bowel sounds Elevated BUN Lower GI Bleeding Hematochezia Fauci et al Harrison’s Principles of Internal Medicine (17th ed)

84 Mallory Weiss Tears Hx: vomiting, retching, coughing preceding hematemesis especially in alcoholics Stops spontaneously (80-90%) Fauci et al Harrison’s Principles of Internal Medicine (17th ed)

85 Esophageal Varices 4-31% of causes
Most often it is a consequence of portal hypertension Fauci et al Harrison’s Principles of Internal Medicine (17th ed)

86 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 Harrison’s Principles of Internal Medicine (17th ed)

87 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 Harrison’s Principles of Internal Medicine (17th ed)

88 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 Harrison’s Principles of Internal Medicine (17th ed)

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