Peptic Ulcer disease and Gastritis Flashcards
1
Q
mucosal defect in the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion
A
peptic ulcer disease
2
Q
Epithelial cell damage and regeneration with or no associated inflammation
- secondary to endogenous or exogenous irritants
A
Gastropathy
3
Q
precursor to PUD and it is clinically difficult to differentiate the two. it denotes inflammation assoicated with mucosal injury
- Histologic diagnosis
- usually due to H.pylori (infectious) or other conditions
A
Gastritis
4
Q
cuases of non H.pylori gastritis
A
Chemical gastritis (acute and chronic)
- alcohol-induced gastritis
- drug-induced gastritis (e.g, NSAID)
- reflux (due to duodenal juice or bile) gastritis
- other chemical gastritis
Radiation
allergic
autoimmune
duodenitis
5
Q
Prostaglandins- the primary factor mediating cytoprotection
- Stimulate bicarbonate and mucus production
- help maintain adequate mucosal blood flow
Prostaglandin deficiency is final common pathway to injury
A
Mucosal cytoprotection
6
Q
- Ulcerated lesion in the mucosa of the stomach or duodenum
- types: Gastric, duodenal
A
Peptic Ulcers
7
Q
signs and symptoms of PUD?
A
- Epigastric pain is most common symptom
- pain described as gnawing or burning
- may radiate to the back (consider penetration)
- occurs 1-3 hours after meals or at night
- relieved by food, antacids (duodenal) or vomiting (gastric)
- dyspepsia including belching/bloating
- hematemesis or melena with GI bleeding
8
Q
alarm symptoms of PUD?
A
require early/urgent endoscopy
- > 50 yrs old
- bleeding
- anemia
- early satiety
- unexplained weight loss
- dysphagia or odynophagia
- recurrent vomiting
- family hx of GI cancer
9
Q
Complications of PUD?
A
- bleeding- most common complication
- gastric outlet obstruction
- perforation- may lead to free perforation or posterior perforation into pancreas with secondary pancreatitis #1 cause of pneumoperitoneum
10
Q
- More common than gastric ulcers
- always non-malignant
- almost always in bulb (except for hypersecretory states (zollinger ellison syndrome or gastrinoma)
- patient will report feeling better after eating= weight gain
A
Duodenal ulcer considerations
11
Q
- although almost always benign, has malignant potential
- therefore, repeat endoscopy recommended after course of acid suppresion
- document healing, biopsy for malignancy
- patient feel worse with eating= weight loss
A
gastric ulcer
12
Q
NSAID induced gastritis or ulcers are frequently?
A
“silent”
13
Q
which NSAIDs is considered High risk for development of PUD?
A
- Piroxicam/ Feldene
- ketorolac/ toradol
- indomethacin/ indocin
14
Q
Patients at risk for NSAID-induced PUD
A
- Prior hx of an adverse GI event (ulcer hemorrhage) increase risk four to five fold
- age > 60 increases risk five to sixfold
- high (more than twice normal) dosage of a NSAID increases risk 10fold
- concurrent use of glucocorticoids increases risk four to fivefold
- concurrent use of anticoagulants increases risk 10-15fold
15
Q
- Spiral shaped, gram (-) rod with flagella
- most common cause of PUD
- transmission route fecal-oral
- secrets urease–> convert urea to ammonia
- produces alkaline environment enabling survival in stomach
A
H. Pylori
15
Q
Differentiating between H.pylori and NSAID- induced ulcer
A
Ulcers associated with H.pylori
- More oftne in duodenum
- often superficial
- less severe GI bleeding
Ulcers associated with NSAIDS
- More often in stomach
- often deep
- more severe GI bleeding
- sometimes asymptomatic
16
Q
Physical exam findings in PUD?
A
Uncomplicated
- epigastric tenderness
- bowel sounds -normal
- rectal exam may show melena/ guaiac +stoll from occult blood loss
- signs of peritonitis with perforation
GI bleed
- look for signs of volume depeletion: tachycardia, hypotenstion, orthostatics, skin tugor, MM appearance
- look for signs of anemia: conjunctiva or skin pallor, new heart murmur
17
Q
diagnosis of peptic ulcer disease?
A
- Upper endoscopy with biopsy: diagnostic test of choice
- endoscopy with biopsy: gold standard in diagnosing H. pylori infection
- urea breath test: noninvasive. H.pylori converts labeled urea into labeled carbon dioxide
- H.pylori stool antigen: useful in diagnosing H.pylori & confirming eradication after therapy
- serologic antibodies: only useful in confirming H.pylori infection not eradication (antibodies can stay elevated long after eradication
18
Q
- Endoscopy indicated in the following high risk patients?
A
- > 50 years old with new onset dyspepsia
- dyspepsia with dysphagia and/or weight loss
- evidence of GI bleeding
- failed appropriate trial of empiric therapy
- using NSAIDs or other high risk meds
- signs of UGI tract obstruction (early satiety, vomiting)
- genetic background assoc. with increased UGI malignancies
19
Q
- useful for intial diagnosis + confimation of eradication
- sensitivity and specificity over 90% (false positives are rare)
- urease activity iis present in the stomach in those infected with H. pylori
- ingest urea labeled with radioactive carbon
- hydrolysis or urea–> labeled carbon dioxide
- rapidly absorbed into bloodstream and within a few minutes, appears in breath
- false negative with PPI, bismuth, antibiotics
A
Urea breath test
20
Q
- Useful in initial diagnosis + confirmation of eradication
- test requires collection of stool samply- size of acorn
- performed in lab
- requires little preparation, however patients may not be compliant with collecting sample
- false negative PPI, bismuth, antibiotics
- test 4 weeks after treatment
A
H. pylori stool antigen test
21
Q
- office based test that is faster but less acurate than lab-based Elisa tests
- sensitivity and specificity of approx 90%
- not useful for evaluating eradication- antibody levels can persist for long time, need serial titers to evaluate
- ELISA to detect IgG antibodies to H.pylori (does not determine if active H.pylori infection)
A
serology
22
Q
when is serology testing useful?
A
- patients who never received H.pylori treatment
- symptomatic patients not using NSAIDS- if negative serology- unlikely PUD
not useful in elderly populations to detect active disease prevalence; populations with low disease prevalence
23
Q
treatment for non H.pylori PUD?
A
OTC neutralizers
- Aluminum and magnesium hydroxide salt (Maalox, mylanta) - not used in treatment but pts may have used them
- calcium carbonate
- bismuth subsalicylate (binds to ulcer base forming a protective coat, has anti-inflammatory and bacteriocidal properties- can cuase dark stools
H2 blockers
PPIs
Surgery
24
Q
- Selectively block receptors on parietal cells reducing acid secretion
- used primarily in ulcer disease not associated with H. pylori
- famotidine, cimetidine
- treatment duration is 6-8 wk
- not #1 treatement option (that PPI)
A
H2 blockers (most OTC)
25
Q
Side effects of Cimetidine
A
- Elderly patients- confusion
- young males- impotence +/- gynecomastia
- may alter levels of other drug- warfarin
- may alter renal function requiring lower doses
- likely not a first choice but is available otc
26
Q
- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump
- relieve pain and heal peptic ulcers more rapidly than H2 blockers
- drugs in this class are equally effective
- treatment length depends on location, etiology and complications
- omeprazole, lansoprazole, pantoprazole
A
Proton pump Inhibitors
PPI> H2 blocker in efficacy for NSAID related PUD
27
Q
what if you can’t d/c the NSAIDs in PUD?
A
- try to get to the lowest dose that is tolerable
- sucralfate: binds proteins in exudates and forms viscous adhesive that protects GI lining
- misoprostol: prostaglandin analog- protects lining of GI tract by replacing depleted prostaglanding E1. Prevents peptic ulcers in patients taking NSAIDs
- misoprostol and lansoprazole for high risk patients taking nonselective NSAIDS
28
Q
Surgical options for non-H.pylori PUD?
A
- antrectomy with vagotomy
- truncal vagotomy with pyloroplasty
- highly selective vagotomy
29
Q
H.Pylori triple therapy treatment? Quadruple therapy?
A
- triple therapy for 14 days is treatment of choice
- clarithromycin based triple therapy (PPI + clarithromycin +amoxicillin) substitute metronidazole in pen allergic
* bismuth based quadruple= bismusth subsalicylate+tetracycline +metronidazole +PPI
30
Q
why doesn’t treatment?
A
- # 1 =adequate patient compliance
31
Q
failure treatment for PUD?
A
- Retest for presence of H.pylori (can’t use serology)
- retreat if positive
- reinforce compliance and education
- switch treatment if you trust they took the previous treatment correctly (treat with PPI, lefofloxacin and amoxicillin- 10 days)
32
Q
Subsequent management of DU, GU?
A
- DU: don’t repeat EGD unless symptoms persist
- GU: surveillance EGD in 8-12 weeks
33
Q
- Neuroendocrine tumors that produce gastrin
- symptoms similar to typical peptic ulcer
- symptoms may be controlled by standard doses of antisecretory drug
- patients may not be tested for hypergastrinemia
- most patients are diagnosed between the ages of 20 and 50
- gastrinomas can be sporadic or associated with multiple endocrine neoplasia type 1
A
Zollinger Elison Syndrome
34
Q
red flags of ZES?
A
- multiple ulcers
- diarrhea (significant diarrhea)
- ulcer in atypical site (usually in the bulb and antrum of stomach; Would see in body, lower abdomen)
- resistant ulcer
- enlarged folds
- severe esophagitis
- family hx of MEN 1
35
Q
diagnosis ZES?
A
- fasting gastrin level (usually 3x higher than normal level)
- secretin stimulation test (secretin will normally suppress gastrin release, in ZES, gastrinoma cells are stimulated by secretin)
- imaging
36
Q
ZES treatment
A
Omeprazole effectively controlled acid output in all patients
