Peptic disease Flashcards

1
Q

If all peptic ulcers were biopsied, 70% would reveal:

A

H. pylori

(Spiral shaped, gram -)

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2
Q

A patient presents with epigastric pain that worsens with meals. Biopsy of the body of the stomach would reveal:

A

Normal histology!

(H. pylori resides in antrum only; this presentation suggests gastric ulcer)

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3
Q

What substances are elevated in duodenal ulcer patients compared with normal patients? Reduced?

A

Basal and peak acid output and [gastrin] elevated

Basal and acid-induced HCO3- secretion from mucus cells reduced

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4
Q

Chronic diseases associated with PUD

A
  1. ICU patients on ventilators (think stress ulcer due to hypoperfusion)
  2. Cirrhosis
  3. COPD
  4. Organ transplantation
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5
Q

Dx of this stomach biopsy?

A

Chronic gastritis with metaplasia

(Notice the appearance of intestinal epithelium with goblet cells + inflammatory cells in lamina propria)

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6
Q

Dx?

A

Alcoholic hemorrhagic gastritis

(Multiple subepithelial hemorrhages without breaks in mucosa)

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7
Q

Epigastric pain relieved by eating

A

Duodenal ulcer

(Duodenum begins secreting protective factors against the acid load it would receive from stomach)

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8
Q

Epigastric pain worse with eating

A

Gastric ulcer

(Stomach produces HCl)

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9
Q

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?

A

Gastric outlet obstruction due to edema (acute) or fibrosis (chronic)

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10
Q

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?

A

Perforated posterior duodenal ulcer causing acute pancreatitis due to activation of pancreatic enzymes

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11
Q

G cell hyperplasia

A

Autoimmune chronic gastritis

(ABs against parietal cells = no HCl = gastrin trying to stimulate HCl production so G cells increase in number)

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12
Q

How can H. pylori lead to gastric adenocarcinoma?

A

CagA protein causes degradation of p53 which leads to cell proliferation and altered cellular polarization

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13
Q

The symptoms of the patient from whom this immunoflourescence with anti-parietal cell antibodies was taken would have been:

A

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)

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14
Q

Biopsy of the lamina propria of the antrum of the stomach in H. pylori infection would reveal:

A

Primarily PMNs but NOT THE BUG!!

(H. pylori doesn’t invade but release chemotactic peptide + LPS)

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15
Q

What are some causes of acute gastritis?

A

NSAIDs, alcohol, bile reflux, Cushing ulcer, Curling ulcer, chemo/radiation, shock/stress, ingesting corrosives

(Anything that increases acid or decreases mucosal barrier)

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16
Q

Curling vs. Cushing ulcer

A

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)

17
Q

Dx?

A

Chronic lymphocytic gastritis secondary to H. pylori

(Notice the germinal centers)

18
Q

List 4 ways to diagnose H. pylori

A
  1. Urea breath test
  2. Fecal antigen test
  3. Serological testing
  4. Biopsy of gastric ulcers (urea tests, histological tests)
19
Q

Which artery is the most common culprit in bleeding from a gastric ulcer? From a duodenal ulcer?

A

Left gastric artery (runs along lesser curvature of stomach where most gastric ulcers are)

Gastroduodenal ulcer (if duodenal ulcer is posterior)

20
Q

Dx?

A

Endoscopic gastritis

(Radial streaks of erythema)

21
Q

Describe the pathogenesis of H. pylori-induced peptic ulcers

A
  1. H. pylori resides in proximal duodenum &/or antrum of stomach
  2. H. pylori produces LPS and a peptide
  3. LPS and peptide are chemotactic
  4. Inflammatory cells release IL-1, TNF, ROS, and prostaglandins that promote further inflammation
  5. Defect in mucosa extending through muscularis mucosa
22
Q

Histology of a chronic peptic ulcer reveals:

A

Necrosis

Inflammation (mostly PMNs)

Granulation tissue

Scar (fibrosis)

23
Q

What are some causes of chronic gastritis?

A

H. pylori, autoimmune disease, bile reflux

(AI = ABs against parietal cells)

24
Q

List the 3 ways in which NSAIDs cause peptic ulcers

A
  1. Decrease PG inhibition of HCl production
  2. Decrease HCO3- and mucin production
  3. Decrease glutathione (free radical scavenger) production
25
Q

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?

A

Air under diaphragm

(Presentation is classic for perforated duodenal ulcer, which will leak air into the peritoneal cavity)

26
Q

Dx?

A

Benign gastric ulcer

(Protrudes away from lumen, no mass effect)

27
Q

Which H. pylori test should not be used to monitor recurrence?

A

Serology; only tells you if you have ever had H. pylori

28
Q

Biopsy of this stomach would reveal:

A

PMNs infiltrating the gastric mucosa

29
Q

What is T4SS?

A

Type 4 secretion system of H. pylori that injects CagA protein into cells

30
Q

How could a peptic ulcer be present two feet distal to the iliocecal valve?

A

Meckel’s diverticulum containing ectopic gastric mucosa

(Remember Meckel’s diverticulum is generally 2 feet from iliocecal valve)

31
Q

How could a peptic ulcer be present in the jejunum?

A

ZE syndrome

(Also suggested by multiple ulcers)

32
Q
A
33
Q

Benign or malignant?

A

Benign

(Round, small, flat margins)

34
Q

Benign or malignant?

A

Malignant

(Heaped up border, irregular shape, very large, necrotic)

35
Q

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.

A

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)