Peptic Ulcers PDF

Peptic ulcers GNT Block Editing File Color index : Main text ( black) Female Slides (Pink) Male Slides (Blue) Important ( Red) Dr’s note (Green) Extra Info ( Grey) OBJECTIVES Deine ulcer & erosion Describe the pathogenesis and pathology, clinical features of both Acute gastric ulcers & chronic pe...

Peptic ulcers GNT Block Editing File Color index : Main text ( black) Female Slides (Pink) Male Slides (Blue) Important ( Red) Dr’s note (Green) Extra Info ( Grey) OBJECTIVES Deine ulcer & erosion Describe the pathogenesis and pathology, clinical features of both Acute gastric ulcers & chronic peptic ulcers Describe the complications of chronic peptic ulcers This lecture was presented by Dr.Maha Arafah & Dr.Ahmed Alhumaidi If You want to read the lecture from Robbins If You want to read the lecture from First aid If You want to watch Dr.Fouda Explanation (till min 34) If You want to read osmosis summary Introducing Definition - Erosion: a breach in the epithelium of the mucosa only - Only a small part-. - Ulcer: a breach in the mucosa of the alimentary tract extending through muscularis mucosa into submucosa or deeper . Ulcers Acute/stress Acutely developing gastric mucosal defects that may appear after severe stress e.g. intracerebral hemorrhage Multiple - Small - Superficial Chronic/peptic Solitary/single - Deep If I said peptic ulcer without acute or chronic, then it is chronic Acute Peptic Ulcers More than 75% of critically ill patients develop endoscopically visible gastric lesions during the first 3 days of their illness Pathophysiology A result of extreme hyperacidity Complication of a severe stress response Part of an acute gastritis Acute response to an irritant chemical injury by drugs: ● Severe burns ( Curling ulcers) ● NSAIDs ● Major trauma (stress / Cushing ulcer) ● Cerebrovascular accidents ( Cushing ulcer ) ● Alcohol Zollinger-Ellison syndrome it’s a tumor that produce more gastrin hormone = ++ Acidity. Female Slides Prognosis: Gastric mucosa can recover completely it the person does not die from the primary disease Prophylaxis: Proton pump Inhibitors 01 Morphology: Range in depth very superficial lesions (erosion) deeper lesion that involve entire mucosal thickness (true ulceration) 02 03 Location: Anywhere in the stomach 04 05 Clinical feature: ● Melena ● Hematemesis ● Pertoration ● Iron deficiency Chronic Peptic Ulcer ● Chronic ulcers , recurring lesions that occur most often in middle-aged to older aD. adults without obvious precipitating conditions, other than chronic gastritis. ● Often solitary Chronic peptic ulcer Location Gastric peptic ulcers: in stomach, mainly the interface of body + antrum at lesser curvature. 98% located in first portion of duodenum or stomach. Duodenal ulcers: in the first portion of duodenum, usually within a few centimeters of pyloric valve at the anterior duodenal wall. 4:1 Ratio duodenal is 4 times more than gastric. ● ● ● ● Esophagus, as a result of GERD or acid secretion by ectopic gastric mucosa Gastric mucosa within a Meckel diverticulum can result in peptic ulceration of adjacent mucosa. Meckel diverticulum: most common congenital abnormality of small intestine caused by an incomplete obliteration of the vitelline duct. -team 41: Simply it is normal tissue at abnormal location, so if Gastric tissue in the small intestine it will cause peptic ulceration of of adjacent mucosa. A congenital anomaly in which there is a diverticulum/in the small intestine (ilium) Zollinger-Ellison syndrome: Multiple peptic ulcerations in the stomach, duodenum, and even the jejunum Gross morphology Diameter: usually <20 mm, they may reach > 100 mm - Usually 2 cm.Duodenal ulcers: never malignant → reason for not taking a biopsy Classic Benign Peptic Ulcer (mostly): round to oval, shallow, clean, sharply demarcated punched-out defect, with straight walls, surrounded by hyperemia. Malignant Peptic Ulcer (Cancer, rare): heaped-up margins, requires biopsy.Most gastric ulcers are benign. Small percentage may be malignant, reason for biopsy Microscopy: Base: necrotic tissue and polymorph exudate overlying inflamed granulation tissue which merges with mature fibrous (scar) tissue Neutrophils within gastric glands → active inflammation + presence of H pylori (mostly) Chronic Peptic Ulcer Clinical feature -for duodenal ulcerRelieved by food or antacids -‫ﻓوار‬- Gnawing-‫ﻋﺿﮫ‬-or burning sensation. 01 02 Epigastric pain (Most common symptom). 03 04 Occurs 2-3 hours after meals 05 Patient awakens from pain at night Complication Frank hemorrhage that will lead to iron deficiency anemia Penetration ،The ulcer penetrates the full thickness of duodenal wall or stomach, Progression into adherent underlying tissue (pancreas or liver). Perforation = peritonitis. Fibrous stricture in stomach: ulcers may cause pyloric stenosis Malignant change ( extremely uncommon). Extra table Treatment ● ● H.pylori eradication by antibiotics . Acid suppression by proton pump inhibitors or H2 blockers. Duodenal Ulcer Gastric Ulcer Food relieves pain Food aggravates pain Epigastric pain 2-3 hours after meal Epigastric pain shortly after meal Vomiting not common Vomiting Is common Patient awakens with pain at night Rarely occurs at night Chronic peptic ulcer Pathophysiology Gastric Ulcers Duodenal Ulcers H. pylori (70% of patients) ✓ 75% of patients ✓ All patients NSAIDs ✓ ✘ Duodeno-ga stric reflux (bile) ✓ ✘ Hyperacidity ✘ ✓ H. pylori infection of the pyloric antrum is present in nearly all patients with chronic duodenal ulcer and approximately 75% of patients with chronic gastric ulcer. Although more than 70% of individuals with PUD are infected by H. pylori, fewer than 20% of H. pylori–infected individuals develop peptic ulcer. Imbalance between aggressive factors & defensive factors: Aggressive Factors Defensive Factors H. pylori Mucus Drugs (NSAIDs) Bicarbonate (HCO3-) Acid Blood flow & Cell renewal Pepsin Prostaglandins Bile salts Phospholipid Chronic gastric ulcer Pathophysiology The mucosal defenses against acid attack consist of: 1 The surface epithelium A. B. NSAIDs (blocking the synthesis of the prostaglandins) H. pylori infection (cytotoxins, phospholipases and urease with ammonia production) Mucus-bicarbonate barrier ….2 A. Duodeno-gastric reflux ( bile ) In Peptic ulcers of the stomach, breakdown of mucosal defense is much more important than excessive acid production. Other causes: NSAID and aspirin stop prostaglandin synthesis The protective effects of prostaglandins: enhanced bicarbonate secretion and increased vascular perfusion. High-dose corticosteroids, which suppress prostaglandin synthesis and impair healing. Cigarette smoking: impairs mucosal blood flow and healing Chronic renal failure, and hyperparathyroidism: associated with hypercalcemia: stimulates gastrin production and therefore increases acid secretion Psychological stress (can increase gastric acid secretion) Chronic peptic ulcer Helicobacter pylori infection H. pylori infection of gastric mucosa is present in 100% of patients with duodenal ulcer and 70% of those with gastric ulcer. H pylori infection is a major factor in the pathogenesis of peptic ulcer. Possible mechanisms of peptic ulcer by H. pylori: 01 H. pylori does not invade the tissue. It induces an intense inflammatory and immune response and increased production of proinflammatory cytokines such as ● IL-1 ● IL-6 ● Tumor necrosis factor (TNF) ● and most notably IL-8. This cytokine(IL-8) is produced by the mucosal epithelial cells, and it recruits and activates neutrophils. 02 H. pylori secretes: ● Phospholipases: Damage surface epithelial cells. ● Urease: Breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. 03 H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. This altered milieu seems to favor gastric metaplasia (the presence of gastric epithelium) in the first part of the duodenum. Such metaplastic foci provide areas for H. pylori colonization. 04 H. pylori lead to thrombotic occlusion of surface capillaries (promoted by a bacterial platelet-activating factor)and produce agents, including lipopolysaccharides, recruit inflammatory cells to the mucosa. The chronically inflamed mucosa is more susceptible to 01 acid-peptic injuries and peptic ulceration. Chronic peptic ulcer Possible mechanisms of peptic ulcer by H. pylori: (cont’d) 05 In addition, chronic inflammation of the mucosa is possibly important in the pathogenesis of gastric adenocarcinoma and a low-grade gastric lymphoma, also known as MALToma (MALT: Lymphoma of Mucosa-Associated Lymphoid Tissue) Pathophysiology of duodenal ulcers Increased production of acid assumes more importance in the pathogenesis of duodenal ulceration. H. pylori-infected individuals secrete 2-6 times as much acid as non-infected controls. H. pylori does not colonise normal duodenal epithelium. H. pylori is involved in duodenal ulceration because there is gastric metaplasia in response to excess acid. Gastric metaplasia paves the way for colonisation by H. pylori. Increased production of acid + Helicobacter P (H. Pylori) = Duodenal ulcers Clinical Note Gastric ulcers occur in the alkaline-producing mucosa of the stomach, usually on or close to the lesser curvature. A chronic ulcer invades the muscular coats and, in time, involves the peritoneum so that the stomach adheres to neighboring structures. An ulcer situated on the posterior wall of the stomach may perforate into the lesser sac or become adherent to the pancreas. Erosion of the pancreas produces pain referred to the back. The splenic artery runs along the upper border of the pancreas, and erosion of this artery may produce fatal hemorrhage. A penetrating ulcer of the anterior stomach wall may result in the escape of stomach contents into the greater sac, producing diffuse peritonitis. The anterior stomach wall may, however, adhere to the liver, and the chronic ulcer may penetrate the liver substance. Chronic peptic ulcer Female Slides Pathophysiology of chronic peptic ulcers in stomach Acquisition of H. Pylori Chronic H. pylori infection in stomach CagA+ tox+ CagA- tox- Intense gastritis (↑IL-8, neutrophil infiltration), epithelial damage Gastric ulceration Pathophysiology of chronic peptic ulcers in Duodenum Multiple factors (smoking, age at acquisition of infection) Acquisition of H. Pylori Chronic H. pylori infection in stomach Somatostatin/ Gastrin dysregulation Increased acid secretion Gastric metaplasia in duodenum H. Pylori colonization in duodenum ↓ Bicarbonate secretion in duodenum ↑ Inflammation (duodenitis) Duodenal ulceration Dr. Maha Case & Questions click here Keywords Acute Peptic Ulcer ● ● ● ● ● ● ● consumption of NSAID (block PG synthesis) , Alcohol Stress Severe burns (Curling ulcer) Cerebrovascular accidents (Cushing ulcer) Zollinger-Ellison syndrome Iron deficiency Melena ● Gastric peptic ulcers: interface of body + antrum at lesser curvature. Duodenal ulcers: first portion of duodenum ( more common) Meckel diverticulum Benign Peptic Ulcer : sharply demarcated punched-out defect, with straight walls, surrounded by hyperemia. Malignant Peptic Ulcer (Cancer, rare): heaped-up margins Epigastric pain (can be seen in acute) Dyspepsia Radiology : free air in left dome of diaphragm Occurs 2-3 hours after meals Relieved by food or antacids (Especially duodenal) iron deficiency anemia Patient with rheumatoid arthritis (prolong NSAIDs use) Bleeding Aggressive Factors : H. pylori , Drugs (NSAIDs) , Acid , Pepsin , bile salt ● ● ● Chronic ● ● ● ● ● ● ● ● ● ● Gastric Ulcers ● ● ● ● H. pylori In 70% of patient associated with use of NSAIDS associated with Duodeno-gastric relux (bile) Not associated with Hyperacidity Duodenal Ulcers ● ● ● ● H. pylori In all patient Not associated with use of NSAIDS Not associated with Duodeno-gastric relux (bile) associated with Hyperacidity If You want A summary click here YOU MCQs Which syndrome is characterized by increased gastrin production and multiple peptic ulcers? A- Zollinger-Ellison syndrome B- Cushing syndrome C- Curling syndrome D- Meckel diverticulum syndrome Which of the following is a complication of chronic peptic ulcers? A- Perforation B- Iron deficiency anemia C- Malignant change D- all the above Which of the following is NOT a defensive factor against peptic ulcers? A- Mucus B- Acid C- Prostaglandins D- Good blood flow What is the main cause of peptic ulcers in patients taking NSAIDs? A- Increased acid production B- Decreased mucus production C- Reduced blood flow D- Inhibition of prostaglandin synthesis 1-A / 2-D / 3-B / 4-D YOU MCQs What is the most common location for duodenal ulcers? A- Stomach B- First portion of the duodenum C- Pyloric valve D- Anterior duodenal wall What is the characteristic symptom of a duodenal ulcer? A- Hematemesis B- Melena C- Epigastric pain relieved by food D- Malignant Which factor is responsible for the breakdown of mucosal defense in gastric ulcers? A- Excessive acid production B- NSAIDs stoppage C- PPI use D- Duodeno-gastric reflux What is the gross feature of benign peptic ulcer? A- On greater curvature B- heaped-up margins C- Punched out appearance D- more than 2 cm diameter 5-B / 6-C / 7-D / 8-C CASES YOU 1. A 50-year-old woman with long-standing rheumatoid arthritis complains of weakness and fatigue. She states that her stools have recently become black after taking a new nonsteroidal anti-inflammatory drug (NSAID). Gastroscopy shows numerous superficial, bleeding mucosal defects. Which of the following is the most likely diagnosis? A.Acute erosive gastritis B.Early gastric cancer C.Helicobacter pylori gastritis D.Ménétrier disease 2.A 40-year-old woman presents with a 2-month history of burning epigastric pain that usually occurs between meals. The pain can be relieved with antacids or food. The patient also reports a recent history of tarry stools. She denies taking aspirin or NSAIDs. Laboratory studies show a microcytic, hypochromic anemia (serum hemoglobin = 8.5 g/dL). Gastroscopy reveals a bleeding mucosal defect in the antrum measuring 1.5 cm in diameter. An endoscopic biopsy shows that the lesion lacks mucosal lining cells and is composed of amorphous, cellular debris and numerous neutrophils. Which of the following is the most important factor in the pathogenesis of this patient’s disease? A.Achlorhydria B.Autoimmunity C.Gastrinoma D.Helicobacter pylori infection 3.A 58-year-old woman suffers a massive stroke and expires.The stomach at autopsy is shown in the image. Prior to her death, this patient would most likely have exhibited which of the following? A.Dysphagia B.hyposecretion of gastric acid C.Melena 1-A / 2-D / 3-C D.Steatorrhea Need explanation ? Click here YOU CASES Extra Cases May Require extra info 1.A 37-year-old man presents to the primary care physician with a several month history of burning epigastric pain approximately 3 hours after eating. The patient reports he is often woken up at night with abdominal discomfort and nausea. He does not have any previous medical problems and does not take any medications. The patient undergoes endoscopy, which demonstrates the following pathologic lesion. Which of the following is the most likely complication of this disease process? A.Diffuse lesion with raised margins and distant metastasis B.Postprandial pain C.Gastric outlet obstruction due to scarring D.Grossly thickened stomach wall 2.A 37-year-old woman presents to the primary care clinic due to three days of severe abdominal pain, bloating, and increased belching. The pain has a burning sensation and is located in the upper abdomen. It is the worst in the morning and after meals. No family members have similar symptoms. Past medical history is significant for recurrent migraines, for which the patient takes high-dose naproxen several times per week. Vital signs are unremarkable. On physical examination, there is moderate tenderness to palpation in the epigastrium. Stool antigen testing is negative for Helicobacter pylori infection. Which of the following medications should be given at this time? A.Omeprazole B.Calcium carbonate C.Amoxicillin, clarithromycin, and pantoprazole D.Calcium carbonate and tramadol for migraines 1-C / 2 - A ‫‪Pathology Team‬‬ ‫زﻳﺎد اﻟﻌﺘﻴﱯ‬ ‫ﻋﺎﺋﺸﺔ إﺑﺮاﻫﻴﻢ‬ ‫اﻟﺪاﻧﺔ ﻋﺒﺪهللا‬ ‫‪er‬‬ ‫‪ad‬‬ ‫‪Le‬‬ ‫ﻟﻤﻰ اﻟﻌﺘﻴﱯ‬ ‫ﻋﺒﺪاﻟﺮﺣﻤﻦ اﻟﻤﺴﻠَّﻢ‬ ‫‪r‬‬ ‫‪de‬‬ ‫‪a‬‬ ‫‪Le‬‬ ‫ﻧﻮرة اﻟﻤﺤﻴﻤﻴﺪ‬ ‫رﻏﺪ اﻟﻤﺼﻠﺢ‬ ‫ﻟﻴﺎن اﻟﺮوﻳﲇ‬ ‫رﻳﻤﺎ اﻟﻤﻄﲑي‬ ‫ﻓﻴﺼﻞ اﻟﺸﻮﻳﻌﺮ‬ ‫رﻳﻤﺎز اﻟﻤﺤﻤﻮد‬ ‫زﻳﺎد ﺣﻜﻤﻲ‬ ‫ﺳﻠﻄﺎن اﻟﺒﻘﻤﻲ‬ ‫ﻋﺮوب اﻟﻤﺤﻤﻮد‬ ‫ﺧﺎﻟﺪ اﻟﺮﺷﻴﺪ‬ ‫ﻋﺒﺪهللا اﻟﻀﻮﻳﺤﻲ‬ ‫اﻟﺠﻮﻫﺮة اﻟﻮﻫﻴﱯ‬ ‫ﻟﺆي اﻟﺤﺪﻳﱻ‬ ‫ﻫﻴﺎ اﻟﺰﻳﺮ‬ ‫ﻋﺒﺪهللا اﻟﻜﻮدري‬ ‫ﻣﺤﻤﺪ اﻟﺴﻼﻣﻪ‬ ‫ﻣﻌﺎذ اﻟﺤﻀﻴﻒ‬ ‫إﻳﻼف ﻣﻌﺘﱯ‬ ‫ﻳﻮﺳﻒ ﺑﺎدﻏﻴﺶ‬ ‫ﺳﺎره اﻟﻌﺠﺎﺟﻲ‬ ‫ﻳﺰﻳﺪ ال ﻃﻠﺤﻪ‬ ‫أﻓﻨﺎن اﻷﺣﻤﺮي‬ ‫رﻧﺪ اﺑﺎ اﻟﺨﻴﻞ‬ ‫رزان اﻟﺴﻄﻴﺤﻲ‬ ‫ﻫﺪى ﺑﻦ ﺟﺪﻋﺎن‬ ‫ﻣﻨﺼﻮر اﻟﻌﺘﻴﱯ‬ ‫زﻳﺎد اﻟﺴﻮﻳﻠﻢ‬ ‫ﻣﺤﻤﺪ اﻟﻌﺮﻓﺞ‬ ‫داﻧﻪ اﻟﻤﺤﻴنس‬ ‫ﻋﺒﺪاﻟﺮﺣﻤﻦ اﻷﺣﻴﺪب‬ ‫ﻧﻮره اﻟﻤﺎﻟﻚ‬ ‫دﻳﻨﺎ اﻟﻤﻬﻮس‬ ‫ﻋﺒﺪاﻟﻤﺤنس اﻟﺪاﻳﻞ‬ ‫ﺷﻮق اﻟﺨﻠﻴﻔﺔ‬