2. constipation & diarrhea

7/29/2019 2. Constipation & Diarrhea

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PepticPepticPepticPeptic ulcerulcerulcerulcer diseasediseasediseasedisease ((((PUDPUDPUDPUD)))) refers to a group of

ulcerative disorders of the upper gastrointestinal

(GI) tract that require acid and pepsin for their

.

UlcersUlcersUlcersUlcers differ from gastritis and erosions in that

they extend deeper into the muscularis mucosa.


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Helicobacter pylori (HP)-associated ulcers,

nonsteroidal anti-inflammatory drug (NSAID)-

,

stress-related mucosal damage (also called stress

ulcers).


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Factors that

Increase Acidity

Factors that

Protect Against

Acidity


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Factors IncreasingFactors IncreasingFactors IncreasingFactors Increasing

H. pylori

NSAIDs

Factors DecreasingFactors DecreasingFactors DecreasingFactors Decreasing

Mucus production

Buffers

Pepsin

Smoking

Prostaglandins


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Most peptic ulcers occur in the presence ofacid and pepsin when H. pylori, NSAIDs, or

other factors disrupt normal mucosal defenseand healing mechanisms.

to disruption of mucosal integrity.

Alterations in mucosal defense induced by

H.Pylori or NSAIDs are the most importantcofactors in peptic ulcer formation.


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Mucosal defensemechanisms include mucusand bicarbonate secretion, intrinsic epithelial

cell defense, and mucosal blood flow.

Maintenance of mucosal inte rit and re air

is mediated by endogenous prostaglandinproduction.

H. pylori infection causes gastritis in allinfected individuals and is causally linked toPUD.


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Most non-NSAID ulcers are infected with HP,

and HP eradication markedly decreases ulcerrecurrence.

. direct mucosal damage,

impairing mucosal defense via elaboration of toxinsand enzymes( urase),

altering the immune/inflammatory response, and

increasing antral gastrin release, which leads toincreased acid secretion.


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Nonselective NSAIDs (including aspirin) cause

gastric mucosal damage.

Use ofcorticosteroids alone does not increase

the risk of ulcer or complications, but ulcer

risk is doubled in corticosteroid users taking

NSAIDs concurrently.


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Epidemiologic evidence links cigarette smoking to

PUD, impaired ulcer healing, and ulcer-related GI

complications.

oug c n ca o serva on sugges s a u cerpatients are adversely affected by stressful life

events, controlled studies have failed to document

a cause-and-effect relationship.


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Coffee, tea, cola beverages, beer, milk, and spices

may cause dyspepsia but do not increase PUD risk.

Ethanol ingestion in high concentrations is

assoc a e w acu e gas r c mucosa amage anupper GI bleeding but is not clearly the cause of

ulcers.


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Abdominal pain is the most frequent symptom ofPUD.

The pain is often epigastric and described asburning but can present as vague discomfort,abdominal fullness, or cramping.

a n rom uo ena cer o en occurs o oursafter meals and is usually relieved by food,

whereas food may precipitate or accentuate ulcerpain in Gastric Ulcer.

Antacids provide rapid pain relief in most ulcerpatients


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Heartburn, belching, and bloating oftenaccompany the pain.

Nausea, vomiting, and anorexia are morecommon in GU.

NSAIDs include :upper GI bleeding,

perforation into the peritoneal cavity,

penetration into an adjacent structure (e.g., pancreas,biliary tract, or liver), and

gastric outlet obstruction.


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Physical examination may reveal epigastric

tenderness between the umbilicus and the xiphoidprocess that less commonly radiates to the back.

, ,

detect bleeding.

The diagnosis of HP infection can be made using

endoscopic or non-endoscopic tests.


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Non-endoscopic tests include serologic antibody

detection tests, the urea breath test (UBT), and the stoolantigen test.

The dia nosis of PUD de ends on visualizin the ulcer

crater either by upper GI radiography or endoscopy.

Radiographymay be the preferred initial diagnostic

procedure in patients with suspected uncomplicated

PUD.


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Ifcomplications are thought to exist or if an

accurate diagnosis is warranted upper

endoscopy should be performed.

If a gastric ulcer is found on radiography,

malignancy should be excluded by direct

endoscopic visualization and histology.


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The goals of treatment are:

Relieving ulcer pain, healing the ulcer, preventing

ulcer recurrence, and reducing ulcer-related

complications. In HP-positive patients, the goals are to eradicate

the organism, heal the ulcer, and cure the disease

with a cost-effective drug regimen.


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NonpharmacologicNonpharmacologicNonpharmacologicNonpharmacologic TreatmentTreatmentTreatmentTreatment

Patients with PUD should eliminate or reducepsychological stress, cigarette smoking, and

.

Patients should avoid foods and beveragesthat cause dyspepsia or exacerbate ulcer

symptoms (e.g., spicy foods, caffeine, andalcohol).


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Eradication of HP is recommended for HP-infected patients with GU, DU, ulcer-relatedcomplications, and in some other situations.

, ,easy to comply with, and cost-effective.

First-line eradication therapy is

o a proton pump inhibitor (PPI)-based three-drugregimen containing two antibiotics.


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The PPI should be taken 15 to 30 minutes beforemeals along with the two antibiotics.

Although an initial 7-day course provides

minimally acceptable eradication rates, longertreatment periods (10 to 14 days) are associatedwith higher eradication rates and less

.

First-line treatment with quadruple therapy usinga PPI (with bismuth, metronidazole, andtetracycline) achieves similar eradication rates asPPI-based triple therapy and permits a shortertreatment duration (7 days).


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If the initial treatment fails to eradicate HP,

second-line empiric treatment should:

(1) use antibiotics that were not included in the initial

regimen;

problems;

(3) use a drug that has a topical effect (e.g., bismuth);

(4) be extended to 10 to 14 days.


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Conventional treatment with standard dosages of

H2RA or sucralfate alone (without antibiotics) relievesulcer symptoms and heals most gastric and duodenalulcers in 6 to 8 weeks.

PPIs provide comparable healing rates over 4 weeks.

Maintenance therapy with a PPI, low-dose H2RA, orsucralfate may be indicated for :

patients who have a history of ulcer-related complications,

a healed refractory ulcer, failed HP eradication therapy, or who are heavy smokers or NSAID users.


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Most uncomplicated NSAID-induced ulcersheal with standard regimens of an H2RA, PPI,or sucralfate if the NSAID is discontinued.

If the NSAID must be continued, considerationshould be given to:

reducing the NSAID dose or

switching to acetaminophen, a nonacetylated

salicylate, a partially selective COX-2 inhibitor, or aselective COX-2 inhibitor.


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PPIs are the drugs of choice when NSAIDsmust be continued because potent acidsuppression is required to accelerate ulcerhealing.

If HP is present, treatment should be initiated

PPI.

Patients at risk of developing serious ulcer-

related complications while on NSAIDs shouldreceive prophylactic cotherapy withmisoprostol or a PPI.


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Patients with ulcers refractory to treatmentshould undergo upper endoscopy to confirma nonhealing ulcer, exclude malignancy, andassess HP status.

HP-positive patients should receive eradicationthera .

In HP-negative patients, higher PPI doses (e.g.,omeprazole 40 mg/day) heal the majority of ulcers.Continuous PPI treatment is often necessary to

maintain healing.


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Patients should be monitored for symptomaticrelief of ulcer pain as well as potential adverse

effects and drug interactions related to drugtherapy.

NSAIDs are discontinued and within 7 days uponinitiation of antiulcer therapy.

Most patients with uncomplicated PUD will besymptom-free after treatment with any one ofthe recommended antiulcer regimens.


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High-risk patients on NSAIDs should be closely

monitored for signs and symptoms ofbleeding,

obstruction, penetration, and perforation.

Follow-up endoscopy is justified in patients with

frequent symptomatic recurrence, refractory

disease, complications, or suspected

hypersecretory states.

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