case 1: peptic ulcer Flashcards

Question

risk factors of hypochlorhydria

Answer 1

– Age – people over the age of 65 have the highest risk – Medications – proton pump inhibitors, antacids or heart burn medications – Helicobacter pylori infection

Answer 2

– Gastrointestinal infections, bloating, burping, gas, diarrhea – Undigested food in the stool – Nutrient deficiencies

Answer 3

mucosal layer is damaged

Answer 4

mucosal, submucosal and/or muscle layers are damaged

Answer 5

all four layers are damaged → stomach contents leak into abdominal cavity →peritonitis

Answer 6

gastric, duodenal, esophageal

Answer 7

* Imbalance between the aggressive and defensive factors in the gastroduodenal mucosa – Aggressive factors – gastric acid, pepsin, Helicobacter pylori infection & NSAIDs – Protective factors – mucin, HCO3-, prostaglandins (epithelial cell replenishment) – PUD patients → ↑ gastric emptying rate → ↑ duodenum acidification → gastric metaplasia → ↑ H. pylori colonization in duodenum

Answer 8

* Epidemiology – lifetime prevalence – 5-10% * Helicobactor pylori infection (~85%) – Only infects gastric mucosa – Found in 80-95% of duodenal ulcers, due to gastric metaplasia (change in duodenal mucosa to gastric mucosa → decreases HCO3- production → decreases acid neutralization – Found in 70-90% of gastric ulcer * Non-steroidal anti-inflammatory drug (NSAIDs) (10-15%) * Overproduction of gastrin (Zollinger-Ellison syndrome) – 0.1% * “Myth” risk factors (not an initiator) – Cigarette smoking, stress, personality & occupation – Diet (spicy food, neutral fats), alcohol consumption

Answer 9

– Gram-negative, curved, with 4-6 flagella, rod – Resides in gastric-type epithelium within mucosal layer (protects the bacteria from acid) – Is the main cause of peptic ulcers (85%) – Can also cause gastritis and stomach cancer

Answer 10

* The causative role of H. pylori infection in PUD was first elucidated by Barry J. Marshall and J. Robin Warren in 1984. * To prove the causative role, Marshall ingested inoculum of H. pylori and confirmed the presence of its infection. * Marshall and Warren received Nobel Prize for Medicine and Physiology in 2005. * H. pylori is now classed by WHO as a class 1 carcinogen. * H. pylori uses its flagella to penetrate gastric mucus layer to reach gastric epithelial cells (more neutral pH)

Answer 11

* H. pylori harm gastric epithelium by: – Producing urease to convert urea into ammonia * (NH2)2CO + H2O → CO2 + 2 NH3 * NH3 + H+ → NH4+ – NH3 is toxic to gastric epithelium – Produce proteases and other chemicals disrupts tight junctions and causes apoptosis * Mode of transmission – Likely oral-oral/fecal-oral – Age of acquirement – childhood

Answer 12

* Function of cyclooxygenase (COX) – COX-1 – constitutively active, catalyzes production of gastric prostaglandins * Support blood flow in stomach wall * Enhance mucus and HCO3- production * Mediate somatostatin (from gastric D cells) suppression of acid secretion – COX-2 – induced as part of an immune response, inflammatory prostaglandins contribute to pain, heat, swelling * NSAIDs (non-steroidal anti-inflammatory drugs) – most widely used classes of drugs, non-selective – Ibuprofen (Advil), naproxen (Alleve), sulindac (Clinoril), aspirin, indomethacin (Indocin) – Baby aspirin (81 mg daily) → decrease gastric mucosal PGE2 → gastric lesions

Answer 13

* NSAIDs → decrease gastric prostaglandins secretion → decrease mucin secretion → weaken the mucosal barrier → acid can directly injure the mucosa → causes gastric ulcers * Risk of NSAID-induced ulceration – Age > 60; increasing duration & dose of therapy – Concurrent steroid or anticoagulant use * Symptoms (quite variable) – Asymptomatic – Vague abdominal discomfort – Classical symptom – dyspepsia * Pain centered in the upper abdomen * Discomfort in the form of fullness, bloating, distention or nausea * 1-3 hr post-meal or midnight; relieved by food or antacid

Answer 14

* Severe physiologic stress → (fight or flight) → splanchnic hypoperfusion → ischemic → a cascade of inflammatory responses are the key causes – In this sense, stress does cause stress ulcers – Acid alone does not cause stress ulcers * Splanchnic circulation – the blood flow to abdominal GI organs ( stomach, liver, spleen, pancreas, small intestine & large intestine * Cushing ulcer – ↑ intracranial pressure → vagus nerve → ↑ parietal cells → increase acid secretion * Curling ulcer – severe burn (>35%) → decrease gastric ischemia

Answer 15

* Caused by tumors * Most often found in the head of the pancreas and the upper small intestine * Produce the hormone gastrin and are called gastrinomas * Stimulates the parietal cells to secrete gastrin * → HCl secretion to maximal activity * → Gastrointestinal mucosal ulceration

Answer 16

* Immediate endoscopy, X-ray or CT scan * Noninvasive test for H. pylori – Serological testing for IgG, can remain “+” for 3 yr after therapy – Urea breath test – use C13 or C14 labeled urea * (NH2)2CO + H2O → HCO3- + 2 NH3 → CO2 + 2 NH3 * Detect level of CO2 – Stool H. pylori antigen test * Invasive test for H. pylori – Biopsy for H. pylori culture or histology – Rapid urease test

Answer 17

1. * decrease HCl secretion by parietal cells – Proton pump inhibitors (PPI, most effective) * Drugs ending in "prazole“ – omeprazole, esomeprazole – Histamine (H2) blockers (very safe) * Competitive antagonists at H2 receptors, e.g. ranitidine, cimetidine * decrease Basal & meal-stimulated HCl * H1 antagonists – anti-allergy, anti- vomiting, motion sickness – Anticholinergic drugs * Eradicate H. pylori – antibiotics (clarithromycin, amoxicillin, or metronidazole) * Mucosal protectants such as sucralfate require acidic environment for activation. As such, does not work with H2 blockers or antacids (decrease acidity) 2. * Mucosal protectants (protect mucosa) – Sucralfate (disaccharide-SO3-Al) * The negatively charged sucrose sulfate binds to positively charged proteins in the base of ulcers or erosions * → form a cross-linking, viscous, paste-like material * → physical barrier that restricts further caustic damage – Bismuth subsalicylate – like sucralfate, bismuth coats ulcers and erosions, creating a protective layer against acid and pepsin – Side effects – constipation & black stool * Re-establish mucosal barrier – prostaglandins (PGE & PGI) * Acidity – buffering acid & decrease acid secretion – Antacids – aluminum or magnesium hydroxide * Al(OH)3 + 3 HCl <--> AlCl3 + 3 H2O

Answer 18

* Acute gastritis – submucosa inflammation * Causes – Non-steroidal anti-inflammatory drugs (NSAIDs) – Mast cells tumor (most common skin tumor in dogs) → ↑ histamine production → ↑ H+ production from parietal cells – Helicobacter pylori – humans, rare in cats, not in dogs

Answer 19

* Normally lower esophageal sphincter (LES) closes to prevent acidic chyme from reflux * Reflux occurs when the LES is weak or relaxes inappropriately → GERD (heart burn) * Treatment – Antacids (neutralize HCl), mucosal protectants, reducing HCl production Gastroesophageal Reflux Disease (GERD)

case 1: peptic ulcer Flashcards

(43 cards)