Peptic Ulcer Disease Flashcards
H. pylori pathophysiology
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
H. pylori causes the majority of ______
Duodenal and gastric ulcers
H. pylori also associated with
Chronic gastritis
Mucosa-associated lymphoid tissue lymphoma (MALToma)
Gastric adenocarcinoma
Indications for testing for H. pylori
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
When should you test vs empiric treatment for H. pylori
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
H. pylori alarm symptoms
Unexplained weight loss Dysphagia Recurrent vomiting Early satiety Digestive bleeding Anemia
H. pylori referral for endoscopy
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
H. pylori testing for patients NOT undergoing EGD
Urea breath test
Stool antigen assay: Patient should be off acid supression for at least 2 weeks prior
H. pylori first line treatment
**Need to know
Triple therapy
PPI BID + clarithromycin + amoxicillin for 7-14 days (in PCN allergic pts, substitute metronidazole for amoxicillin)
H. pylori second line
treatment
**Need to know
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
H. pylori follow up treatment
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.
Gastritis
Inflammation of the gastric mucosa; can be acute or chronic
Etiologies: H. pylori and other infections NSAIDs Drinking alcohol Autoimmune disorders Critical illness
Peptic ulcer disease (PUD)
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.
What are the two major factors associated with PUD?
- H. Pylori infection
2. Consumption of NSAIDs
PUD: NSAIDs
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.
Patients at increased risk for NSAID GI toxicity
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.
Stress ulcers
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
PUD: Progression of ulcers
(Gastritis) Inflammation –> Erosions –> ulceration
Types of ulcers: Clean based ulcers
White shiny base without signs of active or recent bleeding
Some of the most common
Types of ulcers: ulcers with flat pigmented spots
These are more suggestive of sites of recent bleeding.
Usually treated endoscopically
Types of ulcers: Ulcers with nonbleeding visible vessel
Serious lesions - very likely to bleed unless treated endoscopically
Blood vessel can be seen in the ulcer bed
Types of ulcers: actively bleeding
Require immediate endoscopic treatment
PUD: Clinical presentation
80-90% of dyspepsia
Postprandial fullness, early satiety, epigastric pain or burning
Hallmark is epigastric pain that is gnawing/hungerlike
What are the three types of dyspeptic patterns
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
Duodenal ulcer clinical presentation
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
Gastric ulcer clinical presentation
Pain worsening with food (indigestion) typically withing 5-15 minutes.
Relieved by fasting which can lead to associated weight loss.
Silent ulcer clinical presentation
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
PUD symptoms suggesting complications
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
PUD differential diagnosis
Functional dyspepsia (diagnosis of exclusion) Gastric carcinoma Drug induce dyspepsia Granulamotous disease Crohn's disease Zollinger-Ellison syndrome (ZES)
Gastric carcinoma alarm symptoms
Unintended weight loss Bleeding Anemia Dysphagia Odynophagia Palpable abdominal mass Persistent vomiting Hematemesis Unexplained iron def. anemia Family hx Previous gastric surgery Jaundice
Zollinger-Ellison syndrome
The classic triad of involves:
- peptic ulcers in unusual locations (i.e., the jejunum)
- massive gastric acid hypersecretion
- gastrin-producing islet cell tumor of the pancreas (gastrinoma)
When should you consider ZES?
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.
ZES diagnosis
Diagnosis is based on elevated fasting gastrin levels in presence of elevated basal gastric acid output.
ZES treatment
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.
ZES: Multiple endocrine neoplasia syndrome Type 1 (MEN1)
Autosomal dominant disorder with tumors of the parathyroid glands, anterior pituitary, duodenum, pancreatic islet cells
PUD diagnosis
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
PUD: H pylori testing
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
PUD treatment goals
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)
PUD duodenal vs gastric ulcer
Difference in timing of treatment
Duodenal= 4 weeks PPI treatment
Gastric= 8 week PPI treatment
PUD prognosis
~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
Types of endoscopic therapy
- Injection therapy
- Thermal therapy
- Mechanical therapy
Endoscopic therapy: Injection therapy
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
Endoscopic therapy: Thermal therapy
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
Endoscopic therapy: Mechanical therapy
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
