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What are the 3 types of dyspepsia?
  • Ulcer-like or acid dyspepsia ("classic" symptoms)
    -Epigastric hunger pain relieved with food 
  • Functional dyspepsia (Indigestion)
    -Belching, bloating
    -Early satiety
    -Anorexia, nausea, vomiting 
  • Gastroesophageal ("Reflux type") dyspepsia 
True or False:
  • GI symptoms correlate well with physical findings
  • Clasically, when do symptoms occur due to a duodenal ulcer (DU)? (2)
  • Classically, what provides relief to a duodenal ulcer (DU)? (3)
  • 2-3 hours after meals
  • At night
  • Alkali
  • Food
  • Anti-secretory agents 
The "classic" DU symptoms occur how much of the time?
  • Ulcer-like epigastric hunger pain relieved with food/antacids
  • What is it important to rule out when assessing peptic ulcer disease (PUD)?
  • Name 4 alarm symptoms
Must rule out gastric carcinoma

Alarm symptoms: 
  • Weight loss
  • GI bleeding
  • Anemia
  • Dysphagia
True or false:
  • Pain felt due to ulcers is always as a result of acid bathing the ulcer crater. 
  • Pain due to ulcers is more complicated than just acid bathing a crater 
What are 2 major causes of PUD?
  • H. pylori
  • NSAIDs
What is the prevalence of H. pylori in duodenal ulcers (DU)?
Up to ~95%
Name 4 normal processes that H. pylori interferes with.
  • Gastric acid secretion
  • Gastric metaplasia
  • Immune responses
  • Mucosal defense mechanisms
Only 15% of people with H. pylori get ulcer disease. This is because not all people have the most disease-causing strain, which is what?
CagA+ strain
Besides H. pylori, NSAIDs and smoking, what is another significant risk factor for PUD?
  • Some people have higher parietal cell mass
H. pylori is responsible for approximately what proportion of ulcer disease?
How do you diagnose peptic ulcer disease? (2)
  • Endoscopy
  • Upper GI radiography

Empiric therapy can be justified without firm diagnosis in many cases.
Patients with ulcer symptoms, under 45 years of age, without alarm symptoms should receive what?
  • What if older than 45? 

Under 45, do H. pylori test:
  • Stool antigen
  • Breath test

If older than 45, refer to GI (due to small risk of gastric cancer)
If H.pylori test is positive, is eradiation therapy indicated?
Yes, in all patients
Compare endoscopy vs radiography
  • Endoscopy: Sensitive, specific, allows for direct inspection and biopsy
  • Radiography: Sensitive
What is the preferred H. pylori eradication regime? (3)
  • PPI
  • Clarithromycin
  • Amoxicillin
Describe indications for surgery in PUD (3)
Surgery not normally needed, however:
  • Failure to treat complication of ulcer
  • Failure of medical therapy for ulcer
  • Suspicion of malignancy 
What are 3 surgical techniques for fixing ulcers? (performed laparoscopically)
  • Sectioning the vagus
  • Resecting antrum (reduces hormones)
  • Resecting parietal cells (reduces acid)
  • What is hematochezia?
  • What can it mean? (2)
Maroon or bright red blood clots per rectum (usually a sign of lower GI source, but can be due to massive upper GI bleed)
How do the majority of GI bleeds resolve?
On their own
  • However, endoscope can be used to stratify risk of rebleed
How can GI bleeds be treated endoscopically? (5)
  • Thermal coagulation
  • Injection therapy
  • Hemostatic clips
  • Sealant
  • Argon plasma coagulation
What is the ideal pharmacological therapy for a patient with an acute bleeding ulcer?
PPI via IV
  • Obviously need to stabilize patient too if acute 
When do you call a surgeon for an upper GI bleed?
  • Hemodynamically unstable despite resuscitation
  • Recurrent hemorrhage after initial stabilization
  • Shock (due to hemorrhage)
  • Continued slow bleeding needing more than 3 units per day of blood
What 2 ways does upper GI bleed commonly present (in terms of blood)?
  • Hematemesis (vomiting of blood or coffee-ground material)
  • Melena (black, tarry stools)
Describe the contents of gastric juice in terms of organics (4) and ions (5)
  • Water
  • Organics
  • Ions
Describe what happens when a parietal (oxytnic) cell is activated (3)
  • Tubulovesicles containing H+/K+ ATPase proton pumps and intrinsic factor (IF) fuse with lumenal membrane
  • Membrane size increases, and leads to formation of microvilli, generating cannaliculi
  • Proton pumps facilitate HCl production in canaliculi, and IF is also released

Note: The H+ is derived from H2O using carbonic anhydrase, and HCO3- is pumped into the blood.
Give 4 functions of gastric acid
  • Bacteriostatic
  • Activates pepsinogen
  • Initiates protein denaturation
  • Facilitates absorption of iron, calcium and vitamin B12
Summarize what parietal cells produce? (2)
  • HCl
  • IF
Summarize what chief cells produce? (2)
  • Pepsinogen
  • Lipase
What catalyzes the conversion of pepsinogen to pepsin? (2)
  • HCl (low pH induces conformational change)
  • Pepsin itself (autocatalysis)
What does pepsin do?
Enzymatically digest peptides to peptones
What does gastric lipase do?
Enzymatically cleaves 1 fatty acid from a TAG
What cells secrete the gastric mucus? (2)
  • Mucus neck cells
  • Superficial epithelial cells
What is contained in the mucosal barrier? (2)
  • Hydrated glycoproteins/mucins
  • HCO3- ions
What does the mucosal barrier protect the gastric epithelium from? (3)
  • Acid
  • Pepsin
  • Microorganisms
What holds mucus in place on the gastric epithelium?
Surface active phospholipids
  • Mucus is released by exocytosis 
Is the mucosal barrier acidic?
No. HCO3- is secreted into the mucus (after being imported from the bloodstream). It can then neutralize acid at the luminal surface.
Where in the stomach is HCl released?
Gastric glands
What are the 3 major secretagogues for pepsinogen and HCl?
  • Gastrin (hormone)
  • Histamine (paracrine)
  • Acetylcholine (neurotransmitter)
  • What cells produce gastrin?
  • Where are these cells found
  • G cells
  • Found deep in gastric pits in the antrum of the stomach

GRP stimulates release of gastrin from G Cells
What cell type produces histamine in the stomach?
ECL cells (enterochromaffin-like cells)
  • What 2 things stimulate histamine production in the stomach?
  • What type of drug inhibits histamine production in the stomach? 
  • Stimulate:

    Acetylcholine (directly)
    Gastrin (indirectly)
  • Inhibit:

    H2 receptor blockers 
Summarize how the parietal cells are stimulated to secrete HCl.
Acetylcholine, gastrin and histamine all induce secretion of HCl.
  • Acetylcholine and gastrin also increase histamine production. 
Describe the cephalic phase of stimulation of gastric secretion (1 mechanism, 3 cell types)
Senses (thought, smell, taste) cause brain to stimulate:
  • Parietal cells
  • Chief cells
  • G cells
via vagus nerve
Describe the gastric phase of stimulation of gastric secretion (2)
  • 1. Stretch/mechanoreflex acts both locally and via vagus nerve to stimulate secretion (via nodose ganglion)
  • 2. Feedback to parietal cells (food buffering gastric juice) and G cells (due to peptones)
Describe intestinal phase of stimulation of gastric secretion (1)
Peptones in chyme (in the proximal small intestine) stimulate G cells to produce gastrin that then acts on stomach
Describe the cephalic phase of inhibition of gastric secretion (2)

via vagus nerve:
  • Stomach filling (reflex)
  • Feeling of satiety

lead to inhibition
Describe the gastric phase of inhibition of gastric secretion (1)
Reduced pH in antrum causes D cells to release somatostatin which inhibits G cell production of gastrin
Desribe the intestinal phase of inhibition of gastric secretion (2)
  • Passage of chyme into duodenum stimulates a short neuronal "enterogastric reflex arc" through the sympathetic celiac ganglion
  • Stimulates production of enterogastrones, which are hormones that feedback to inhibit G cells, parietal cells, chief cells and smooth muscle contraction
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