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Clin Med II > Peptic Ulcer Disease > Flashcards

Peptic Ulcer Disease Flashcards

1
Q

H. pylori pathophysiology

A

Colonizes the mucus layer of the gut

H. Pylori is adapted survive in low gastric pH via production of urease

Eventually penetrates mucus layer to adhere to gastric epithelial cells

Years of chronic inflammation → damaged gastric epithelium → normal gastric tissue replaced by intestinal-type mucosa (intestinal metaplasia) - thought to be a precursor to gastric adenocarcinoma

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2
Q

H. pylori causes the majority of ______

A

Duodenal and gastric ulcers

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3
Q

H. pylori also associated with

A

Chronic gastritis
Mucosa-associated lymphoid tissue lymphoma (MALToma)
Gastric adenocarcinoma

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4
Q

Indications for testing for H. pylori

A

Current guidelines recommend treatment for H. pylori whenever it is detected – so only test if you plan to treat if positive

Indications for Testing:
Patients with MALToma of Malt lymphoma
Active peptic ulcer disease
H/o peptic ulcer without documented cure of H. pylori infection
Early gastric cancer
Patients with dyspepsia
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5
Q

When should you test vs empiric treatment for H. pylori

A

Testing: Dyspepsia in patients <60* yo without alarm sxs (pts with alarm symptoms or ≥60* yo with new onset dyspepsia should have EGD)

Unexplained iron deficiency

Recurrent idiopathic thrombocytopenia

Empiric treatment: Peptic ulcer disease

MALToma

Atrophic gastritis

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6
Q

H. pylori alarm symptoms

A 
Unexplained weight loss
Dysphagia
Recurrent vomiting
Early satiety 
Digestive bleeding
Anemia
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7
Q

H. pylori referral for endoscopy

A

Patients ≥60* with dyspepsia (*previously 55)

Pts with alarm symptoms (unexplained weight loss, dysphagia, recurrent vomiting, early satiety or digestive bleeding or anemia)

Biopsy specimens can then be tested for urease and also examined histologically for H. pylori infection and its lesions

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8
Q

H. pylori testing for patients NOT undergoing EGD

A

Urea breath test

Stool antigen assay: Patient should be off acid supression for at least 2 weeks prior

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9
Q

H. pylori first line treatment

**Need to know

A

Triple therapy

PPI BID + clarithromycin + amoxicillin for 7-14 days (in PCN allergic pts, substitute metronidazole for amoxicillin)

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10
Q

H. pylori second line
treatment
**Need to know

A 
Quadruple therapy (reserved for patients that fail first line treatment)
(After first-line failure; patients who fail first-line treatment should have H. pylori susceptibility testing done prior to starting second-line treatment)

This regimen is also used as first line Rx in areas of high clarithromycin resistance and in pts with recent or repeated exposure to clarithromycin

PPI BID + metronidazole + bismuth subsalicylate (Pepto-Bismol) + tetracycline for 14 days

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11
Q

H. pylori follow up treatment

A

All patients should receive follow up to confirm eradication. (At least 4 weeks after starting treatment and remember to d/c PPI 2 weeks before)

Urea breath test is preferred but can also do stool antigen.

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12
Q

Gastritis

A

Inflammation of the gastric mucosa; can be acute or chronic

Etiologies: 
H. pylori and other infections
NSAIDs
Drinking alcohol
Autoimmune disorders
Critical illness
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13
Q

Peptic ulcer disease (PUD)

A

Refers to both gastric or duodenal ulcers

Ulcer is a disruption in the mucosal integrity of the stomach and or duodenum > 5mm in size due to inflammation.

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14
Q

What are the two major factors associated with PUD?

A
  1. H. Pylori infection

2. Consumption of NSAIDs

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15
Q

PUD: NSAIDs

A

Associated with increased risk of complications from PUD

Mucosal damage by ASA and NSAIDs due to inhibition of COX-1 in upper GI tract

COX-1 is an enzyme that plays a key role in the protection of the gastrointestinal tract from the acidic environment of the stomach

Cox-1 is responsible for production of prostaglandins

Prostaglandins (such asPGE2) are in turn responsible for production of mucus and bicarbonate by the gastric cell lining

COX-1 inhibition reduces mucosal generation of protective prostaglandins

This can lead to formation of ulcers. Development of GI symptoms in patients taking NSAIDs should prompt evaluation.

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16
Q

Patients at increased risk for NSAID GI toxicity

A

High risk: Hx of previous ulcer
Multiple risk factors

Moderate risk: Age > 65
High dose NSAID
Hx of uncomplicated ulcer
Concurrent use of ASA, steroids, and anticoagulants.

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17
Q

Stress ulcers

A

Severe physiologic stress can lead to the development of PUD

Stress ulcers commonly seen in patients hospitalized for acute medical or surgical illnesses – especially in the ICU and on ventilator

Etiology is unclear

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18
Q

PUD: Progression of ulcers

A

(Gastritis) Inflammation –> Erosions –> ulceration

19
Q

Types of ulcers: Clean based ulcers

A

White shiny base without signs of active or recent bleeding

Some of the most common

20
Q

Types of ulcers: ulcers with flat pigmented spots

A

These are more suggestive of sites of recent bleeding.

Usually treated endoscopically

21
Q

Types of ulcers: Ulcers with nonbleeding visible vessel

A

Serious lesions - very likely to bleed unless treated endoscopically
Blood vessel can be seen in the ulcer bed

22
Q

Types of ulcers: actively bleeding

A

Require immediate endoscopic treatment

23
Q

PUD: Clinical presentation

A

80-90% of dyspepsia
Postprandial fullness, early satiety, epigastric pain or burning

Hallmark is epigastric pain that is gnawing/hungerlike

24
Q

What are the three types of dyspeptic patterns

A

Ulcer-like or acid dyspepsia:
burning pain; epigastric hunger-like pain; relief with food, antacids

Food-provoked dyspepsia or indigestion: postprandial epigastric discomfort and fullness, belching, early satiety, nausea and occasional vomiting

Reflux dyspepsia: frequently associated with gastroesophageal reflux

25
Q

Duodenal ulcer clinical presentation

A

Pain improves with food (buffer to acid secretion) but returns 1-2 hours later.

symptoms typically ~2-5 hrs after meals and at night and ~11pm – 2am
Can result in RUQ pain and mimic acute cholecystitis or biliary colic

26
Q

Gastric ulcer clinical presentation

A

Pain worsening with food (indigestion) typically withing 5-15 minutes.
Relieved by fasting which can lead to associated weight loss.

27
Q

Silent ulcer clinical presentation

A

43-87% of pts with bleeding ulcers present without antecedent dyspepsia or other GI symptoms

Ulcer perforation frequently occurs without preceding symptoms

May be more frequent in elderly pts and pts on NSAIDs

28
Q

PUD symptoms suggesting complications

A

Change in pain location and character

No longer relieved by food or antacids

Sudden development of severe diffuse abdominal pain that may indicated perforation

Vomiting may suggest gastric outlet obstructions

Nausea, hematemesis, melena, or dizziness

29
Q

PUD differential diagnosis

A 
Functional dyspepsia (diagnosis of exclusion)
Gastric carcinoma
Drug induce dyspepsia
Granulamotous disease
Crohn's disease
Zollinger-Ellison syndrome (ZES)
30
Q

Gastric carcinoma alarm symptoms

A 
Unintended weight loss
Bleeding
Anemia
Dysphagia
Odynophagia
Palpable abdominal mass
Persistent vomiting
Hematemesis
Unexplained iron def. anemia
Family hx
Previous gastric surgery
Jaundice
31
Q

Zollinger-Ellison syndrome

A

The classic triad of involves:

  1. peptic ulcers in unusual locations (i.e., the jejunum)
  2. massive gastric acid hypersecretion
  3. gastrin-producing islet cell tumor of the pancreas (gastrinoma)
32
Q

When should you consider ZES?

A 
Patients will present with PUD symptoms but consider ZES with
recurrent disease
chronic diarrhea
multiple GI tract ulcers
Development of ulcers at a young age
Ulcers distal to the duodenal bulb

It is important to think about this because most gastrinomas are malignant.

33
Q

ZES diagnosis

A

Diagnosis is based on elevated fasting gastrin levels in presence of elevated basal gastric acid output.

34
Q

ZES treatment

A

PPIs
Excision of the gatrinoma (can be located in pancreas, stomach, and duodenum) which can be curative if it is a single lesion with no metastases.

35
Q

ZES: Multiple endocrine neoplasia syndrome Type 1 (MEN1)

A

Autosomal dominant disorder with tumors of the parathyroid glands, anterior pituitary, duodenum, pancreatic islet cells

36
Q

PUD diagnosis

A

Definitive diagnosis by endoscopy

Labs: CBC, CMP, LFTs, Calcium
H. pyloria testing in all pts with PUD

If ZES is possible test serum gastrin levels

37
Q

PUD: H pylori testing

A

For pts not having endoscopy (i.e. <60yo, no alarm symptoms or UGIB), test for H. pylori

Noninvasive testing – urea breath or stool antigen testing

Invasive testing – urease testing on biopsy at endoscopy; histologic examination of gastric mucosa

PPIs, bismuth, many Abx and UGIB lead to false negative tests. Have to be free of these factors for at least 2 weeks before testing

If pt with known ulcer tests negative (invasive or noninvasive), must confirm with additional testing

38
Q

PUD treatment goals

A

relief of sxs, promote ulcer healing, prevent recurrence & complications

All on PPI therapy
PPI + Abx for positive h pylori
Discontinue etiological or contributing agents (NSAIDs, cigarettes, etc)

39
Q

PUD duodenal vs gastric ulcer

A

Difference in timing of treatment
Duodenal= 4 weeks PPI treatment
Gastric= 8 week PPI treatment

40
Q

PUD prognosis

A

~60% of peptic ulcers heal spontaneously but with eradication of H. pylori infection, ulcer healing rates are ~ >90%

Even with continued PPI use, ~5-30% of peptic ulcers recur within 1st year based on whether H. pylori has been successfully eradicated

~5-10% of ulcers are refractory to antisecretory therapy with a PPI

Risk of complications in patients with chronic peptic ulcer disease is 2-3% per year – complications – bleeding, perforation, obstruction

41
Q

Types of endoscopic therapy

A
  1. Injection therapy
  2. Thermal therapy
  3. Mechanical therapy
42
Q

Endoscopic therapy: Injection therapy

A

Most commonly used with diluted epinephrine solution

Injected around base of ulcer to produce a mechanical tamponade of any nearby vessels via creation of a submucosal fluid collection that compresses the vessel

Typically results are short-lived and rarely used alone – used along with a sclerosant agent

Stops bleeding acutely so underlying ulcer can be washed and visualized more clearly in preparation for more definitive therapy

43
Q

Endoscopic therapy: Thermal therapy

A

Local heating of tissue in an attempt to cauterize the bleeding or nonbleeding vessels in the ulcer

Many devices available and most of these rely on electrocautery

Most of the time coaptation (compression of the vessel in question by the endoscopic probe before and during application of the heat) is used in an attempt to seal the vessel in a compressed/closed position

44
Q

Endoscopic therapy: Mechanical therapy

A

Use of deployable objects to physically compress or close the vessel in an ulcer
Endoscopic clips are most commonly used
Endoscopic loops or bands also used

Clin Med II (7 decks)

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