Peptic Ulcer Disease (PUD) ES

Symptoms of PUD

- dyspepsia and mild epigastric pain (burning, gnawing, aching)

- epigastric pain w/ DUs normally happen 1-3 hours after a meal and is relieved by food

- Pain w/ GUs aggravated by food

- pain severity fluctuates

- heartburn, belching, bloating, N/V

Complications of PUD

- bleeding

- perforation

- obstruction

Alarm findings of PUD

- family hx of upper GI malignancy

- unintentional weight loss

- overt GI bleeding

- iron deficiency anemia

- progressive dysphagia or odynophagia

- early satiety

- persistent vomiting

- palpable mass

- lymphadenopathy

GU

gastric ulcer

DU

duodenal ulcer

Non-pharm treatments for PUD

- risk factor avoidance

- reduce physiologic stress

- avoid cigarette smoking, alcohol

- avoid NSAID or aspirin use

How do people usually contract helicobacter pylori?

first few years of life, transmitted through fecal-contaminated food or water

What kind of ulcer is most common in PUD caused by helicobacter pylori?

duodenal ulcer

Mechanism of damage for H. pylori in PUD

- must get into cell for active infection

- direct mucosal damage

- alterations in host inflammatory response

- hypergastrinemia and elevated acid secretion

Clarithromycin triple therapy components

1. clarithromycin 500 mg BID

2. amoxicillin 1 g BID OR metronidazole 500 mg TID

3. PPI BID

Clarithromycin triple therapy duration

14 days

Bismuth quadruple therapy components

1. bismut subsalicylate 300 mg QID

2. metronidazole 250-500 mg QID

3. tetracycline 500 mg QID OR amoxicillin 1 g BID

4. PPI BID

Bismuth quadruple therapy duration

10-14 days

Concomitant therapy components

1. clarithromycin 500 mg BID

2. amoxicillin 1 g BID

3. nitroimidazole 500 mg BID

4. PPI BID

Concomitant therapy duration

10-14 days

Sequential therapy components

1. amoxicillin 1 g BID + PPI BID followed by

2. clarithromyin 500 mg BID

3. nitroimidazole 500 mg BID

4. PPI BID

Sequential therapy duration

both phases 5-7 days

Hybrid therapy components

1. amoxicillin 1 g BID + PPI BID followed by

2. amoxicillin 1 g BID

3. clarithromycin 500 mg BID

4. nitroimidazole 500 mg BID

5. PPI BID

Hybrid therapy duration

7 days

Levofloxacin triple therapy components

1. levofloxacin 500 mg daily

2. amoxicillin 1 g BID

3. PPI BID

Levofloxacin triple therapy duration

10-14 days

Levofloxacin sequential therapy components

1. amoxicillin 1 g BID + PPI BID followed by

2. amoxicillin 1 g BID

3. levofloxacin 500 mg

4. nitroimidazole 500 mg BID

5. PPI BID

Levofloxacin sequential therapy duration

5-7 days for both phases

High dose dual therapy components

1. amoxicillin 1 g TID or 750 mg QID

2. PPI TID or QID

High dose dual therapy duration

14 days

Prevpac (combo therapy)

1. clarithromycin 500 mg BID

2. amoxicillin 1 g BID

3. lansoprazole 30 mg BID

Prevpac duration

10-14 days

Risk factors for NSAID induced PUD

- age > 65 y/o

- concomitant anticoagulant use

- preexisting coagulopathy

- concomitant corticosteroid use

- previous PUD or PUD complications

- CV disease and other comorbid conditions

- multiple NSAID use

- longer duration NSAID use

- high dose NSAID use

What kind of ulcers are more common in PUD caused by NSAIDs?

gastric ulcers (in stomach)

Mechanism of damage of NSAIDs in PUD

- direct irritation of gastric epithelium

- systemic inhibition of endogenous mucosal prostaglandin synthesis

How do NSAIDs cause PUD in regards to inflammatory molecule?

block COX-2, which is responsible for analgesic and anti inflammatory effects of NSAIDs, but will also block COX-1, which produces PGs that provide gastric protection

True or false: NSAIDs given parenterally and rectally have similar incidence of PUD to oral NSAIDs

true-- systemic COX inhibition

Which main classes of meds are used to treat NSAID induced PUD?

H2RAs, PPIs, sucralafate

If someone is on chronic NSAIDs, what can they be given prophylactically to reduce risk of peptic ulcers?

PPIs**, misoprostol

MOA: sucralafate

forms complexes by binding to positively charged proteins in exudates --> forms paste-like adhesive that protects ulcerated areas of gastric mucosa

A/E: sucralafate

constipation, nausea, metallic taste, possibility for Al toxicity in pts w/ renal failure

Are PPIs or H2RAs more effective for PUD?

PPIs