Margaret Denise P. del Rosario2308190682Sec. AJuly 3, 2015

A 55 year-old male presents with a three year history of on and off localized burning epigastric pain associated with occasional nausea, initially relieved by food and MgAlOH antacid. Two months PTC, pain became more frequent and severe, with early satiety and fullness. A few hours PTC, he passed out black tarry stools associated with vomiting once of coffee ground material. Questions:1. What additional data will you elicit and why?History of Present Illness Is there fever, weight loss, and easy fatigability? Have you had pallor, dizziness or loss of consciousness? Does the pain radiate to other areas? Is there dysphagia? What are the aggravating factors? Experience of passing out of black tarry stools or stools with fresh blood before? How much food causes satiety and fullnesscompare with past normal consumptions. Has he been diagnosed with H. pylori infection?Past Medical History Are there prior surgeries or diagnostic procedures done? Any other admissions? Presence of DM, HTN, etcFamily History Is there a history of cancer?specifically cancers affecting the GI Are there other family members who present with the same symptoms? Is there a family history of PUD?Personal-social History Smoking Alcohol consumption NSAID useif so, what specific medications2. What are the expected PE findings?Inspection Increased or Decreased HR, Increased RR, Decreased BP PallorAuscultation Hyperactive bowel sounds because of the bleedingPalpation Board-like rigid abdomen Direct and rebound tenderness Percussion Tympanitic 3. Explain the pathophysiologic disease mechanisms underlying the symptoms three years, two months PTC and a few hours PTCThree years PTCon and off localized burning epigastric pain associated with occasional nausea, initially relieved by food and MgAlOH antacid It is presumably the start of the defense mechanism failure caused by aggressive factors. Aggressive factors such as pepsin and hydrochloric acid start breaching the defensive mucosal barrier, bicarbonate ions are unable to neutralize these aggressive factors as well as prostaglandins. This may be caused by intake of NSAIDs that are non-selective. COX-1 is responsible in keeping the integrity of the gastric mucosa, inhibition of this will cause a decrease of defensive mechanisms allowing aggravating factors to cause damage. H. pylori infection also causes ammonia production that is toxic to epithelial cells, this toxic effect causes chronic inflammation that later on allows gastric acid to cause damage in the mucosa. Smoking is also a factor because it causes vasoconstriction causing less perfusion to the stomach impairing its gastric emptying abilityTwo months PTCpain became more frequent and severe, with early satiety and fullness Longer period of exposure of gastric mucosa causes further damage leading to the formation of an ulcer. The ulcer inhibits gastric emptying because of its lack of ability to cause peristalsis that leads to early satiety and fullness. Few hours PTCpassed out black tarry stools associated with vomiting once of coffee ground material. More injury to the gastric mucosa has probably lead to a perforation causing bleeding. Melena and the coffee ground material passed upon vomiting can be explained by the blood reacting to gastric acids. 4. How will you approach the diagnosis? State expected findings. DiseaseRule InRule Out

Peptic Ulcer Disease--perforationEpigastric painBurning in characterRelieved by meals and antacidEarly Satiety and fullnessMelena and hematemesisSudden onset of symptomsRule out through endoscopy with H. pylori testingAsk for history of NSAID consumption

Chronic GastritisEpigastric painVomitingEarly satiety and fullnessWeight loss is commonRule out through endoscopy

Gastric malignancyPossible presence of ulcerMelena and hematemesisEarly satiety and fullnessIf ulcer is found at lesser curvatureIf >2cm in sizeRule out through biopsy

Acute CholangitisAbdominal painUsually presents with RUQ pain and jaundice

CholecystitisEpigastric painVomitingLocalized pain to the RUQPain is colicky not burning

Diagnosis: Peptic Ulcer Disease Thorough History takingexpect consumption of NSAIDs, past diagnosis of H. pylori infection, smoking or excessive alcohol intake, possibly a strong family history of PUD or Gastric cancer Test for H. pylori infection through endoscopic biopsytested for urease Confirmatory if there is (+) urease Endoscopydiscrete mucosal lesions with a punched out smooth ulcer base filled with whitish fibrinoid exudate at the junction of the fundus and antrum or along the lesser curvature (possible malignancy) RadiographyFree abdominal air if perforated; contrast study will show extravasation of contrast outside the perforation

5. Given the differential diagnoses in Question 4, discuss the therapeutic plans. Surgical Endoscopic therapy such as coagulation therapy, hemoclips and thermal endoscopic therapy Obtain a biopsy to rule out gastric malignancy Pharmacological Proton Pump Inhibitorsto decrease the activity of receptors responsible for aggressive factors Histamine-2-receptor antagoniststo decrease gastric acid secretion If using NSAIDs prescribe a COX-2 selective NSAID and warn against unnecessary use of it can still aggravate ulcer in the long run If positive for H. pyloriPPI-based triple therapy: PPI + amoxicillin + clarithromycin for 7 to 14 daysDiet and lifestyle Avoid fatty food that may delay gastric emptying time Avoid carbonated beverages Avoid alcohol consumption Quit smoking