10/5- Peptic Ulcer Disease and Helicobacter Pylori Flashcards

(44 cards)

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
What is seen here?
See hyperplasia of folia (?) - Chemical cause (think NSAIDs)
26
What is seen here?
H. pylori infection
27
What is seen here?
H. pylori infection
28
When should endoscopy be done for Dx of Hp?
- **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
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"?
_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
What are the rules of thumb for Hp therapy?
- 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
3 areas of choices for Hp eradication?
- Treat with antibiotics - Vaccine: therapeutic or preventative - Improve the environment (good housing, sanitation, food, clean water, no crowding...)
32
What are characteristics of complicated PUD?
- Bleeding - Perforation - Obstruction - Penetration
33
\_\_% of people with peptic ulcers develop a potentially life-threatening complication What is the most common complication?
25% of people with peptic ulcers develop a potentially life-threatening complication - Bleeding is most common (and more frequent with NSAID users)
34
What are signs/symptoms of free perforation?
- Acute onset of severe pain - Board like rigidity of abdomen - Absent bowel sounds - Free air in abdomen Call surgeon!
35
What is seen here?
Contained perforation/perforation
36
What surgery can be done for PUD?
Attacked acid secretion physiologically - Cephalic phase -\> cut vagus - Gastric phase -\> remove antrum (gastrin) - Remove acid cells -\> gastrectomy
37
What is a Billroth I procedure?
Removal of stomach antrum and sewn directly onto duodenum
38
What is a Billroth II?
39
What is Zollinger Ellison Syndrome?
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
What are clues to Zollinger-Ellison syndrome?
- 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
What is therapy for Zollinger-Ellison syndrome?
- 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
What are the main conditions associated with elevated gastring composition? How are they distinct?
**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
Describe the circuit of acid secretion/inhibition in the stomach?
_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
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
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