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MS2 GI > 10/5- Peptic Ulcer Disease and Helicobacter Pylori > Flashcards

10/5- Peptic Ulcer Disease and Helicobacter Pylori Flashcards

1
Q

What is dyspepsia?

A

Epigastric pain or discomfort

  • Recurrent
  • Relief obtained by eating or taking antacids
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2
Q

What is the DDx for dyspepsia?

A
  • Peptic disease
  • Gastroesophageal reflux disease (GERD)
  • Unknown (Non-ulcer dyspepsia)
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3
Q

What is peptic ulcer disease?

  • Symptoms
  • Prognosis
A
  • Abdominal pain
  • Reduced quality of life
  • Risk of complications (~25%)
  • Costs (drugs, doctor visits, tests, lost time from work, etc)
  • Increased mortality compared to those without ulcer disease
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4
Q

What characterizes:

  • Erosion
  • Ulcer
  • Penetrating ulcer
A
  • Erosion: into mucosa
  • Ulcer: into muscularis mucosa
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5
Q

What is seen here?

A

Chronic gastric ulcer

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6
Q

Describe ulcer pain

  • Location
  • Timing
A
  • Epigastric
  • Relates to acid cycle
  • Episodic, recurrent
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7
Q

Describe the pain and acid cycle

A
  • Low acid in the morning
  • Acid rises after meal, and brings pain
  • About 1 hr after meals, pt will feel pain
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8
Q

What is the most common cause of upper GI bleeding?

A

Peptic ulcer

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9
Q

What are the main locations of peptic ulcers?

A
  • Pyloric valve (near duodenum)
  • Stomach (typically along minor curvature)
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10
Q

What is seen here?

A

Peptic ulcer near pyloric valve?

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11
Q

What is seen here?

A

Peptic ulcer on minor curvature of stomach?

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12
Q

What is seen here?

A

From left to right:

  • Active gastric ulcer
  • Healing
  • Healed
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13
Q

What is the treatment for ulcers?

A

Heal the ulcer, relive pain

  • Antisecretory therapy (proton pump inhibitor or H2-receptor antagonist)

Eliminate the cause

  • Cure H. pylori infection
  • Stop NSAIDs (e.g., ibuprofen)
  • Control tumor-produced excess acid secretion (Zollinger-Ellison Syndrome)
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14
Q

What are common causes of ulcers?

A
  • H. pylori infection
  • Drug use (esp NSAIDs)
  • Pathologic hypersecretory states (Zollinger-Ellison syndrome)
  • Rare causes (Herpes simplex, tumors, Crohn’s disease…)
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15
Q

What is H. pylori infection?

  • When acquired
  • Prognosis
A
  • Transmissible infectious disease
  • Acquired in childhood
  • Disease manifestations usually in adults with variable latent periods
  • High morbidity, Modest mortality
  • Curable
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16
Q

What is this?

Describe the causative agent.

A

H. Pylori infection

  • Gm
  • spiral bacteria
  • Niche: human stomach

Causes inflammation:

  • Atrophic gastritis
  • Peptic ulcer
  • Gastric cancer
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17
Q

Outcomes of H. pylori infection?

A

Atrophic gastritis

  • > Gastric cancer
  • > Gastric ulcer

Acute gastritis

Acute on chronic gastritis

  • > Antral Predominant gastritis
  • > duodenal ulcer
  • > Lymphoma
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18
Q

What are causative associations of H. pylori?

A

Progressive gastro-duodenal damage

  • Disordered regulation of acid secretion

Diseases: gastric adenocarcinoma, peptic ulcer (gastric and duodenal), gastric lymphoma, atrophic gastritis, gastric atrophy, vitamin B12 malabsorption (pernicious anemia), iron deficiency anemia, idiopathic thrombocytopenia (ITP), dyspepsia, etc.

19
Q

Risk factors for Hp infection

A
  • Low socio-economic status
  • Birth in a developing country
  • Crowded living conditions
  • Sharing a bed as a child
  • Absence of hot water tap in home
  • Poor sanitary conditions
20
Q

How is H pylori transmitted?

A

“Situational Opportunistic transmission”; any method of gaining access to the stomach will do

  • Gastro-oral (e.g. vomit)
  • Fecal-oral
  • Contaminated water or food
21
Q

Who should be tested for Hp?

A
  • Dyspepsia
  • Ulcer disease
  • Present/past history
  • 1st degree relatives
  • Gastric cancer
  • Family history of gastric cancer
  • After endoscopic resection of gastric cancer
  • If you plan to start therapy with: chronic NSAIDs or chronic PPI therapy (for GERD)
  • Evaluate Hp eradication
  • Pt desires to be tested
22
Q

What are tests for finding/treating H. pylori?

A
  • Serologic (ELISA): lab based or office urine (IgG antibody tests)
  • Endoscopic
  • Breath tests: measure change in concentration of urea (urease converts urea -> CO2 + NH3)
  • Stool antigen tests
23
Q

How good is serology for the diagnosis of H pylori?

A
  • Specificity and Sensitivity good but not excellent
  • Antibodies can remain for years after elimination of the infection
  • Can not be used to confirm eradication
  • Not generally recommended unless high pretest probability (eg, DU)
24
Q

What diagnostic methadologies are preferred for diagnosing Hp?

A

Non invasive:

  • Breath tests
  • Stool antigen tests
25
Q

What is seen here?

A

See hyperplasia of folia (?)

  • Chemical cause (think NSAIDs)
26
Q

What is seen here?

A

H. pylori infection

27
Q

What is seen here?

A

H. pylori infection

28
Q

When should endoscopy be done for Dx of Hp?

A
  • Geographic (Korean, Japanese)
  • Alarm features present: weight loss/mass, bleeding, advanced age, long history, significant anorexia, UGI bleeding/anemia, significant vomiting, x-ray suggests ‘cancer’

NOT:

  • Classic Hx GERD
  • Lack of alarm features
29
Q

So if pt presents with dyspepsia, what are treatment options for their answer to “are serious signs/symptoms present” or “does pt have long hx GERD”?

A

Yes symptoms/GERD:

  • Endoscope to rule out gastric CA or Barrett’s

No symptoms/GERD:

  • Non-invasive Hp testing
  • If test +, give multidrug Hp and confirm cure after 4 wks
  • If test -, give anti-secretory drug to treat symptoms
30
Q

What are the rules of thumb for Hp therapy?

A
  • 2+ antibiotics; any PPI + any 2 (best with all 4):
  • Clarithromycin
  • Amoxicillin
  • Metronidazole
  • Acid suppression
  • Duration: 14 days
  • Confirm cure (UBT or stool antigen test)
31
Q

3 areas of choices for Hp eradication?

A
  • Treat with antibiotics
  • Vaccine: therapeutic or preventative
  • Improve the environment (good housing, sanitation, food, clean water, no crowding…)
32
Q

What are characteristics of complicated PUD?

A
  • Bleeding
  • Perforation
  • Obstruction
  • Penetration
33
Q

__% of people with peptic ulcers develop a potentially life-threatening complication

What is the most common complication?

A

25% of people with peptic ulcers develop a potentially life-threatening complication

  • Bleeding is most common (and more frequent with NSAID users)
34
Q

What are signs/symptoms of free perforation?

A
  • Acute onset of severe pain
  • Board like rigidity of abdomen
  • Absent bowel sounds
  • Free air in abdomen

Call surgeon!

35
Q

What is seen here?

A

Contained perforation/perforation

36
Q

What surgery can be done for PUD?

A

Attacked acid secretion physiologically

  • Cephalic phase -> cut vagus
  • Gastric phase -> remove antrum (gastrin)
  • Remove acid cells -> gastrectomy
37
Q

What is a Billroth I procedure?

A

Removal of stomach antrum and sewn directly onto duodenum

38
Q

What is a Billroth II?

A
39
Q

What is Zollinger Ellison Syndrome?

A

Gastrin-producing tumor

  • Non-beta cell tumor of the pancreas that produces gastrin (malignant >benign).
  • Gastrin secretion is not responsive to the normal down-regulatory events and thus causes sustained high levels of acid secretion
  • Gastric acid hypersecretion
  • Ulcers in unusual locations
  • Diarrhea
  • Parathyroid adenomas
40
Q

What are clues to Zollinger-Ellison syndrome?

A
  • Non-H. pylori, non-NSAID duodenal ulcer disease
  • Ulcers beyond the duodenal bulb (post-bulbar ulcers)
  • High rates of secretion of concentrated (>100 mmol/L) acid
  • High serum gastrin levels
41
Q

What is therapy for Zollinger-Ellison syndrome?

A
  • Search for the tumor (often in duodenal wall). Remove if possible (benign)
  • Control acid secretion with sufficient doses of proton pump inhibitor medications orally
42
Q

What are the main conditions associated with elevated gastring composition?

How are they distinct?

A

Atrophic gastritis or PPI therapy

  • No acid
  • High gastrin (normal regulation)

ZE syndrome

  • High acid
  • High gastrin (abnormal regulation; b/c of ectopic production of gastrin)
43
Q

Describe the circuit of acid secretion/inhibition in the stomach?

A

Cells:

  • G cell- secrete gastrin
  • D cell- secrete somatostatin (inhibits gastrin)
  • Parietal cells- secrete acid

Process:

  • Food and high pH stimulate antral gastrin release which travels via the blood to the produce acid by the parietal cells
  • High acid then interacts with the antral D cells which make somatostatin and turn down gastrin and thus acid secretion
44
Q

Summary: Peptic Ulcer Disease in the 21st century

  • The focus is on prevention, cure and treatment based on etiology.
  • The most common causes are infection with H. pylori and use of NSAIDs
  • NSAID use has rapidly become the most common cause of ulcer disease and ulcer complications
A

(:

MS2 GI (26 decks)

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