Peptic disease Flashcards
If all peptic ulcers were biopsied, 70% would reveal:
H. pylori
(Spiral shaped, gram -)
A patient presents with epigastric pain that worsens with meals. Biopsy of the body of the stomach would reveal:
Normal histology!
(H. pylori resides in antrum only; this presentation suggests gastric ulcer)
What substances are elevated in duodenal ulcer patients compared with normal patients? Reduced?
Basal and peak acid output and [gastrin] elevated
Basal and acid-induced HCO3- secretion from mucus cells reduced
Chronic diseases associated with PUD
- ICU patients on ventilators (think stress ulcer due to hypoperfusion)
- Cirrhosis
- COPD
- Organ transplantation
Dx of this stomach biopsy?
Chronic gastritis with metaplasia
(Notice the appearance of intestinal epithelium with goblet cells + inflammatory cells in lamina propria)
Dx?
Alcoholic hemorrhagic gastritis
(Multiple subepithelial hemorrhages without breaks in mucosa)
Epigastric pain relieved by eating
Duodenal ulcer
(Duodenum begins secreting protective factors against the acid load it would receive from stomach)
Epigastric pain worse with eating
Gastric ulcer
(Stomach produces HCl)
A patient presents with N/V and a succussion splash. Barium x ray yields this results. What is the cause of this in a patient with an acute vs chronic ulcer?
Gastric outlet obstruction due to edema (acute) or fibrosis (chronic)
A patient with known duodenal ulcer presents with the sudden onset of severe abdominal pain radiating to the back and N/V. CT scan is below. What is the cause of his symptoms?
Perforated posterior duodenal ulcer causing acute pancreatitis due to activation of pancreatic enzymes
G cell hyperplasia
Autoimmune chronic gastritis
(ABs against parietal cells = no HCl = gastrin trying to stimulate HCl production so G cells increase in number)
How can H. pylori lead to gastric adenocarcinoma?
CagA protein causes degradation of p53 which leads to cell proliferation and altered cellular polarization
The symptoms of the patient from whom this immunoflourescence with anti-parietal cell antibodies was taken would have been:
Abd pain, N/V, hematemesis due to gastritis caused by achlorhydria
Fatigue, parasthesias, weakness due to pernicious anemia caused by lack of intrinsic factor for B12 absorption in ileum
(Autoimmune gastritis)
Biopsy of the lamina propria of the antrum of the stomach in H. pylori infection would reveal:
Primarily PMNs but NOT THE BUG!!
(H. pylori doesn’t invade but release chemotactic peptide + LPS)
What are some causes of acute gastritis?
NSAIDs, alcohol, bile reflux, Cushing ulcer, Curling ulcer, chemo/radiation, shock/stress, ingesting corrosives
(Anything that increases acid or decreases mucosal barrier)
Curling vs. Cushing ulcer
Curling = severe burn causes hypovolemia which reduces blood flow to gastric mucosa, reducing protective barrier
Cushing = increased intracranial pressure causes vagal stimulation which increases ACh which increases HCl production)
Dx?
Chronic lymphocytic gastritis secondary to H. pylori
(Notice the germinal centers)
List 4 ways to diagnose H. pylori
- Urea breath test
- Fecal antigen test
- Serological testing
- Biopsy of gastric ulcers (urea tests, histological tests)
Which artery is the most common culprit in bleeding from a gastric ulcer? From a duodenal ulcer?
Left gastric artery (runs along lesser curvature of stomach where most gastric ulcers are)
Gastroduodenal ulcer (if duodenal ulcer is posterior)
Dx?
Endoscopic gastritis
(Radial streaks of erythema)
Describe the pathogenesis of H. pylori-induced peptic ulcers
- H. pylori resides in proximal duodenum &/or antrum of stomach
- H. pylori produces LPS and a peptide
- LPS and peptide are chemotactic
- Inflammatory cells release IL-1, TNF, ROS, and prostaglandins that promote further inflammation
- Defect in mucosa extending through muscularis mucosa
Histology of a chronic peptic ulcer reveals:
Necrosis
Inflammation (mostly PMNs)
Granulation tissue
Scar (fibrosis)
What are some causes of chronic gastritis?
H. pylori, autoimmune disease, bile reflux
(AI = ABs against parietal cells)
List the 3 ways in which NSAIDs cause peptic ulcers
- Decrease PG inhibition of HCl production
- Decrease HCO3- and mucin production
- Decrease glutathione (free radical scavenger) production
A patient with a history of duodenal ulcer presents with sudden onset of severe abdominal pain and left shoulder pain. What do you expect to see on x ray?
Air under diaphragm
(Presentation is classic for perforated duodenal ulcer, which will leak air into the peritoneal cavity)
Dx?
Benign gastric ulcer
(Protrudes away from lumen, no mass effect)
Which H. pylori test should not be used to monitor recurrence?
Serology; only tells you if you have ever had H. pylori
Biopsy of this stomach would reveal:
PMNs infiltrating the gastric mucosa
What is T4SS?
Type 4 secretion system of H. pylori that injects CagA protein into cells
How could a peptic ulcer be present two feet distal to the iliocecal valve?
Meckel’s diverticulum containing ectopic gastric mucosa
(Remember Meckel’s diverticulum is generally 2 feet from iliocecal valve)
How could a peptic ulcer be present in the jejunum?
ZE syndrome
(Also suggested by multiple ulcers)
Benign or malignant?
Benign
(Round, small, flat margins)
Benign or malignant?
Malignant
(Heaped up border, irregular shape, very large, necrotic)
A patient presents to your office complaining of headache and abdominal pain. He hit a tree while skiing about a week ago but felt fine so did not seek medical attention. He reports throwing up what looked like blood. Explain the etiology of these findings.
Cushing ulcer (stress ulcers)
May have concussion/intracranial bleed (cause of HA)= increased ICP = increased vagal stimulation = increased ACh = increased HCl production = stress ulcers (usually hemorrhagic = cause of hematemesis)
