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pathopharm exam 4
chapter 78
| Question | Answer |
|---|---|
| Peptic Ulcer Disease | upper gastrointestinal (GI) disorders erosion of the gut wall(LINING OF GI TRACK-NON-STERILE) Severe erosion can be complicated by hemorrhage and perforation |
| what are the cause of peptic ulcer disease? | Imbalance between mucosal and aggressive factors |
| WHAT ARE THE Pathogenesis of Peptic Ulcers? | Mucus •Secreted cells of the GI mucosa(LINING) •Forms a barrier to protect underlying cells from acid and pepsin |
| WHAT ARE THE Pathogenesis of Peptic Ulcers? DEFENSIVE FACTORS | Bicarbonate PH-BASES Secreted by epithelial cells of stomach and duodenum •Most remains trapped in mucous layer to neutralize hydrogen ions that penetrate the mucus |
| WHAT ARE THE Pathogenesis of Peptic Ulcers? | Blood flow •Poor blood flow can lead to ischemia(LIMITED BLOOD FLOW), cell injury, and vulnerability to attack Prostaglandins •Stimulate the secretion of mucus and bicarbonate |
| Aggressive factors ARE? | HelicobacteR PYLORI •Gram-negative bacillus (3 LAYERS W/THICK CELL WALLS) = colonize the stomach and duodenum •Lives between epithelial cells and the mucous barrier Escapes destruction by acid •Can remain in the GI tract for decades |
| Pathogenesis of Peptic Ulcers AGGRESSIVE FACTORS? PT W/ H.P MIGHT NOT HAVE ULCERS | •60% to 70% of patients with PUD have H. pylori infection •Half of the world is infected, but most people do not develop symptomatic peptic ulcer disease (PUD) *50% harbor H. pylori, but only 10% develop PUD •H. pylori CAUSES gastric cancer |
| AGGRESSIVE FACTORS | H.P= CAUSES Duodenal ulcers •Eradication of H.P promotes healing of the PUD and minimized recurrence of PUD |
| OTHER CONTRIBUTING FACTORS Zollinger-Ellison syndrome -HYPER SECRETION OF ACID=INCREASE PUD | NSAID Reduce blood flow, mucus, and bicarbonate AS IT Inhibit the biosynthesis of prostaglandins(P CAUSE ULCER=DIRECTLY INJURES CELL OF MUCOSA, INdirectly activating pepsin ALONE DOESNT INCREASE ULCER, BUT IT IS A FACTOR IN PUD |
| OTHER FACTORS | SMOKING Delays ulcer healing and increases risk for recurrence VASOCONSTRICTION-DECREASE BLOOD FLOW TO STOMACH-INCREASE RISK FOR PUD PEPSIN Proteolytic enzyme in gastric juice-STOMACH LINING |
| WHAT ARE THE TREATMENT? GOALS OF DRUG THERAPY EXCEPT ANTIBIOTIC DRUG TO NOT ALTER A DISEASE PROCESS BUT CREATE A CONDUCIVE HEALING | Alleviate symptoms Promote healing Prevent complications(BLEEDING AND PERFORATION-HOLE IN STOMACH Prevent recurrence |
| WHAT ARE Classes of Antiulcer Drugs? | Antibiotics Antisecretory agents-DECREASE SECRETION OF ACID Mucosal protectants-PROTECT LINING OF GI Antisecretory agents that enhance mucosal defenses Antacids |
| HOW DO ANTIBIOTICS HELP W/ PUD? | GIVEN FOR gastric/duodenal ulcers and documnted H. pylori infection Not given to those who are asymptomatic ALTER DISEASE PROCESS |
| NSAID-Induced Ulcers-GOOD DEFENCE PT W/ NSAID-DISCONTINUE -DECREASE DOSE | Prophylaxis HIGHER RISK 4 ULCER Age over 60 years history of ulcers, high-dose NSAID therapy |
| TREATMENT? | Proton pump inhibitors (PPIs) are preferred (eg, omeprazole) Misoprostol is also effective( diarrhea) Histamine blockers+PPI Antacids, sucralfate, and histamine2 receptor blockers are not recommended |
| Pepsin | Proteolytic(BREAKDOWN) enzyme = ulcer formation; it promotes ulcers by breaking down protein in the gut wall ACT ON GUTT WALL=PROTECTIVE MECHANISM ARE BROKEN DOWN |
| PEPSIN=PH DEPENDENT=1.3 PH IN STOMACH | Activity of pepsin is pH dependent= ANTACID, PPPI, HISTAMINE BLOCKER DECREASE ACIDITY=HIGH PH=MORE PEPSIN=MORE DESCTRUCTION PH ABOVE 5, KEEPSTEADY PEPSIN LEVEL TO AVOID INCREASE PEPSIN(DESTROY GI MUCOSA) |
| NON-DRUG THERAPY=DIET? | ULCER DIET DOESN'T HEAL CAFFEINE DOESN'T PROMOTE ULCER HEALING Change in eating pattern to five or six small meals a day , THAN HUGE MEALS reduces pH fluctuations AVOID NSAIDS-ASPIRIN-ALCOHOL-SMOKING REDUCE STRESS |
| Evaluation of Therapy | MONITOR PAIN RELIEF PAIN LEVEL AND DISSAPEARENCE OF ULCER DO NOT POSITIVELY CORRELATE Pain may subside before complete healing or may continue after healing H.PYLORI TESTS-PRE, POST TREATMENTS Radiologic or endoscopic examination of ulcer site |
| H. pylori Tests | NON-INVASIVE Breath test-BREATH IN BAG THEN SEAL; DRINK SMALL LIQUID SPECIFIC TO H.P=SEND TO LAB Serologic test-BLOOD TEST Stool test-STERILE COLLECTION CUP-USE URINE COLLECTION CONTAINER |
| H.PYLORI TESTS Endoscopic specimen obtained and evaluated-LIGHT DOWN THROAT-GET SPECIMEN= DONE W/ PT W/ GASTRIC PAIN | INVASIVE •Stained and viewed under microscope to see if H. pylori is present •Assayed for presence of urease (a marker enzyme for H. pylori) •Cultured and then assayed for presence of H. pylori |
| H. pylori Treatment | NOT EFFECTIVE ALONE Minimum of two antibiotics prescribed (up to three may be used) to reduce risk of resistance developing ESPECIALLY FOR NON-COMPLIANT PATIENTS=ANTIBIOTIC BACTERIA GIVE ANTABIOTIC FROM DIFFERENT CLASSES |
| Antibiotic Regimen-MAIN ANTIBIOTICS FOR H.P | Clarithromycin, amoxicillin, bismuth, metronidazole, and tetracycline If these drugs are used alone, the risk of resistance developing increases |
| Clarithromycin [Biaxin]? | Suppresses growth of H. pylori BY inhibiting protein synthesis In the absence of resistance, treatment is highly effective rate of resistance is rising, exceeding 20% in some areas S/E=NauseaDiarrheaDistortion of taste |
| Amoxicillin-GOOD COMBINATION | H. pylori is highly sensitive to amoxicillin Rate of resistance is low, only about 3% Amoxicillin kills bacteria by disrupting cell wall WORKS BEST AT NEUTRAL PH=DECREASE SECRETION OF GASTRIC ACID REDUCE ACID W/Antisecretory agent(PPI) S/E=DIARRHEA |
| Bismuth Compounds(PEPTO-BISMAL) | Act topically to disrupt the cell wall of H. pylori, causing lysis and death inhibit urease activity and may prevent H. pylori from adhering to the gastric surface ADR=TONGUE ANDSTOOL(UP GI BLDG 2) Long-term therapy: Possible risk of neurologic injury |
| Metronidazole [Flagyl] | Very effective against sensitive strains of H. pylori Over 40% of strains are now resistant S/E nausea and headache CONTRAINDICATION alcohol: Disulfiram-like reaction Avoid use during pregnancy |
| Tetracycline | Inhibitor of bacterial protein synthesis Highly active against H. pylori Resistance is rare (less than 1%) CONTRAINDICATION pregnant patients and young children = can stain developing teeth |
| Antibiotic Regimens -Minimize emergence of resistance; guidelines using at least two antibiotics, preferably three | Antisecretory agent: PPI or histamine2 receptor antagonist (H2RA) also should be used Eradication rates are good with a 10-day course and slightly better with a 14-day course |
| Histamine2 Receptor Antagonists Ranitidine [Zantac] +Nizatidine [Axid] PROMOTE DEVELOPMENT OF GASRIC CANCER | FIRST CHOICE DRUGS=DUODENAL AND GASTRIC CANCER (Cimetidine [Tagamet +Famotidine [Pepcid]) Promote healing by suppressing secretion of gastric acid |
| Cimetidine [Tagamet] ADR=likely to occur in elderly patients who have renal or hepatic impairment. Patients may experience confusion, hallucinations, lethargy, restlessness, and seizures. | Pharmacokinetics Absorption is slowed if taken with meals Crosses the blood-brain barrier with difficulty May cause some CNS side effects |
| THERAPEUTIC USE-PROTOTYPE DRUG | Gastric and duodenal ulcers Gastroesophageal reflux disease (GERD) Zollinger-Ellison syndrome Aspiration pneumonitis Heartburn, acid indigestion, sour stomach |
| Adverse effects - Antiandrogenic effects-enlarged breast tissue (gynecomastia), reduced libido, and impotence Cimetidine and antacids should be administered at least 1 hour apart | Antiandrogenic effects CNS effects Pneumonia IV bolus: Can cause hypotension and dysrhythmias interactions=Warfarin, phenytoin, theophylline, lidocaine Antacids can reduce absorption of cimetidine |
| Proton Pump Inhibitors-Most effective drugs for suppressing secretion of gastric acid Selection of PPI is based on cost and prescriber’s preference suppress acid secretion by inhibiting gastric H＋,K＋-ATPase, the enzyme that makes gastric acid | uses: Short term Gastric/duodenal ulcers GERD Well toleratedCan increase the risk of serious adverse events, including fracture, pneumonia, acid rebound, and possibly intestinal infection with Clostridium difficile OTC |
| Omeprazole [Prilosec]=PROTOTYPE NO HX OF ULCER, BUT GIVEN TO PT AT RISK FOR ULCER PROPHYLAXIS | First available PPI Inhibits gastric secretion Short half-life Used for short-term therapy Ulcer prophylaxis PT in ICU W/ additional risk factors = multiple trauma, spinal cord injury, or prolonged mechanical ventilation (longer then 48 hours) |
| Adverse effects | Usually inconsequential with short-term use Pneumonia Fractures -OSTEOPOROSISHypomagnesemia GI effectsRebound acid hypersecretion Gastric cancer C. difficile infection- S/E=Headache CONTRAINDICATION=REDUCE EFFECT OF CLOPIDOGREL- |
| Other Antiulcer Drugs | Sucralfate [Carafate] Misoprostol [Cytotec] Antacids |
| SUCRALFATE- 1OES1HR-AC -NO CRUSHING, CAN SPLIT IN HALF Increased barrier to pepsin NOT EAT OR DRINK ALOT=WASHE COATING ON SIDE OF ESOPHAGUS-WAIT A WHILE B4 EATING, TO GET THE COATING Sucralfate can impede the absorption of phenytoin; | Creates a protective barrier for up to 6 hours GIVEN MULTIPLE TIMES A DAY Therapeutic uses - Acute ulcers and maintenance therapy ADR=Constipation (only 2% of patients) Drug interactions-Minimal Antacids AND PHENYTOIN(SPRATE 2HRS) |
| Misoprostol [Cytotec] stimulating the secretion of mucus and bicarbonate to maintain submucosal blood flow. | Therapeutic uses prevention of gastric ulcers caused by long-term NSAID therapy ADR-Dose-related diarrhea and abdominal pain Contraindicated- pregnancy: Category X=UNLESS TRYING TO INITIATE LABOR |
| Antacids-CHANGE PH OF STOMACH NEUTRALIZE absorbing, or buffering gastric acid, which raises the gastric pH above 5. | React with gastric acid to produce neutral salts or salts of low acidity Reduce destruction of gut wall by neutralizing acid enhance mucosal protection by stimulating production of prostaglandins |
| ANTACIDS-TUMS | Except for sodium bicarbonate, antacids do not alter systemic pH CONTRAINDICATED= renal impairment |
| Adverse effects | Constipation: Aluminum hydroxide Diarrhea: Magnesium hydroxide Sodium loading Drug interactions = Cimetidine-Ranitidine-Sucralfate |
| Antacid Families | Aluminum compounds Magnesium compounds Calcium compounds Sodium compounds-AVOID IN RENAL IMPARIMENT |
| Magnesium Hydroxide [Milk of Magnesia] | FIRST CHOICE TO PROMOTE BOWEL MOVEMENT(NOT IN ABDOMINAL PAIN) Rapid acting, high acid-neutralizing capacity (ANC), produces long-lasting effects ADR= diarrhea TAKEN W/ aluminum hydroxide, LAXATIVES Use with caution in patients with renal failure |
| Aluminum Hydroxide PROMOTE CONSTIPATION | Relatively low ANC, slow acting Effects have long duration Rarely used alone Widely used in combination with magnesium hydroxide Caution: Significant amounts of sodiumConstipationDrug interactions: Tetracyclines, warfarin, digoxin |
| A patient is prescribed cimetidine [Tagamet] and aluminum hydroxide [Maalox] for the treatment of peptic ulcer disease. What should the nurse teach the patient to do? | Cimetidine and antacids should not be administered together. The patient should be instructed to take the medications at least 1 hour apart. |
| A patient is prescribed amoxicillin and tetracycline to treat peptic ulcer disease. The nurse will instruct the patient that these medications will do what? | Destroy the bacteria in the stomach that are causing ulceration. |
| Which medication is used to promote gastric ulcer healing by providing a protective barrier? | Sucralfate promotes ulcer healing by creating a protective barrier against acid and pepsin. |
| pathophysiology of peptic ulcer disease Prostaglandins are needed to stimulate mucus and bicarbonate to maintain mucosal blood flow. | Sufficient bl. flow to cells of the GI mucosa is needed to maintain integrity. In Zollinger-Ellison syndrome, hypersecretion of acid alone causes ulcers by overcoming mucosal defenses. Bicarbonate is needed to neutralize hydrogen ions. |
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Seka_nurse
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