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1 Upper GI Disorders Peptic Ulcer Disease. 2 3 PUD Extremely common disorder  4 million people, 350,000 new cases/year  >100,000 hospitalizations/year.

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Presentation on theme: "1 Upper GI Disorders Peptic Ulcer Disease. 2 3 PUD Extremely common disorder  4 million people, 350,000 new cases/year  >100,000 hospitalizations/year."— Presentation transcript:

1 1 Upper GI Disorders Peptic Ulcer Disease

2 2

3 3 PUD Extremely common disorder  4 million people, 350,000 new cases/year  >100,000 hospitalizations/year and 3000 deaths/year Ulcer  Disruption in bowel wall extending deep to the muscular mucosa  Resulting from imbalance of mucosal injury, protection and repair

4 4 Stomach and Duodenum: Normal Anatomy and Histology The major regions: Fundus, Cardia, Body Transitional Zone Antrum, Pylorus, Sphincter Duodenum

5 5 In the body & fundus region:  Deep within the glands – are parietal cells (oxyntic cells) which secrete HCl, and – chief cells – which secrete pepsinogen  Mucous cells Cells in the Antrum:  Mucous cells, gastrin-releasing cells ( no parietal or chief cells)

6 6 Normal Gastric Physiology Human stomach secretes ~ 2L of HCl every day Parietal (oxyntic) cells in the stomach mucosa  When stimulated secrete acid into the gastric lumen  In resting state: secrete intrinsic factor (carrier protein for Vit B12) Three substances that stimulate parietal cells: Acetylcholine, Gastrin, Histamine

7 7 Agonist binds to a specific parietal cell receptor  S econd messenger systems activate the gastric proton pump (H+/K+ -ATPase )  one-to-one exchange of intracellular H+ for luminal K+ ions (terminal step in acid secretion ) Basal Acid Secretion: The usual circadian rhythm – higher acid secretion in afternoon (2 to 11pm) lower rates in the morning (5 to 11 am)

8 8 Meal Stimulated Acid secretion: 3 Phases Cephalic – Sensory input initiates acid secretion (vagus nerves stimulate nerves in gut wall → ACh is released, → stimulates acid secretion) Gastric – Activated by stimuli within the stomach (acid secretion is controlled by distension → change in acidity, & chemical constituents of food  activate vagal nerves to stimulate gastrin release) Intestinal – Amino acids stimulate parietal cells to release acid → intraluminal acid, fat, and hyperosmolar solutions inhibit acid

9 9 Pepsin and Pepsinogen: Gastric mucosal cells secrete proenzymes: pepsinogen I &II During the cephalic, gastric, & intestinal phases, the factors which stimulate or inhibit acid exert the same effects on pepsinogen secretion. Pepsin is activated by acid pH ( ), inactivated at pH 4.0, destroyed at pH 7.0 High acidity is required for the activation & activity of pepsin. PGI secretion is directly proportional to the rate of acid suppression.

10 10 Contraction of gastric smooth muscle :  by: ACh (parasympathetic) & by gastrin  by: NE (sympathetic) & by secretin

11 11 Pepsinogens – secreted throughout the stomach & duodenum HCl – released in the fundus & body Gastrin – released in the antrum

12 12 Cotran: Robbins Pathologic Basis of Disease, 6th ed., Copyright © 1999 W. B. Saunders Company

13 13 Protective Mechanisms Within the Gut Wall

14 14 Protective Mechanisms Within the Gut Wall

15 15 The protective factors are balanced with the presence of aggressive factors.

16 16 Helicobacter pylori. -colonizes the gastric mucosa (normally a harsh environment for bacteria) -adapted itself to establish colonization

17 17

18 18 Adaptive mechanisms: Uses flagella to hide in mucous layer away from acid Produces urease – hydrolyzes urea into CO2 & ammonia (creates an alkaline microenvironment) Produces mucinase – thins viscous mucous & allows bacteria to burrow into mucous layer Provides a passageway for hydrogen ions to enter epithelium. Not all people infected with H pylori develop ulcers. The only relatively absolute requirements are: 1) Secretions of acid & pepsin, 2) H. pylori infxn 3) NSAID use

19 19 Definitions Peptic Ulcer Disease : A group of disorders characterized by erosion of the mucosa anywhere in the GI tract that is exposed to the erosive action of acid and pepsin Erosions (more superficial) may be reepithelialized rapidly by a process called restitution. Ulcers extend into the deeper layers of the mucosa and require a more complex healing process.

20 20 Definitions Duodenal  Associated with acid output  usually seen in the proximal duodenum [the 1st few cm past pyloric sphincter] Increased pepsinogen I (parietal cell mass) Gastric ( in Stomach)  Usually not associated with acid output  occur mainly in the antrum of the stomach

21 Etiology and Pathophysiology 21

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25 25 Types of PUD 1-Non ulcer dyspepsia Dyspepsia: an imprecise symptom complex that includes: epigastric pain or discomfort, Nausea, belching, bloating. There is over lap between the symptoms reposted by patients diagnosed with peptic ulcer and dyspepsia

26 26 2-NSAID-Induced Ulcers Symptomatic ulcers occur in only 1% of patients after 3-6 months of NSAIDs This type of ulcer does not correlate with pain because analgesic action may mask ulcer pain Mechanisms of Injury: Produce gastric damage by two mechanisms  Direct irritant effect  Systemic effect → inhibition of cyclooxygenase COX-1 → ↓ PG synthesis

27 27 PG protect the GI mucosa by maintaining blood flow & stimulating bicarbonate & mucus Low PG impair the ability of the gastric mucosa to withstand aggressive factors COX –2 inhibitions is responsible for anti- inflammatory and analgesic effects Ulcers occur more frequently in the stomach than in the duodenum. Many are painless acute, low-dose NSAID-induced lesions usually heal spontaneously

28 28 Risk factors Age > 60 yrs, High-NSAID dose OR Use of multiple NSAIDs, Hx of ulcer/complication, Co-morbid illness, Concurrent steroid use, GI sx in past 6 mos requiring discontinuation of the NSAID or the addition of another drug. Patients taking anticoagulants High surgical risk or Debilitated patients

29 29 Association of steroids and PUD is controversial. Steroids may induce ulcers : ↑ gastric acid secretion, ↓ PG production May delay or inhibit healing of ulcers caused by NSAIDs. Patients taking steroids considered at high risk Recent studies: elderly taking both steroids and NSAIDs are at much higher risk of PUD than those receiving either agent alone (related to dose & duration of therapy) 3-Adrenocorticosteroids

30 30 Increased basal & postprandial acid secretion Mechanisms:  Enhanced sensitivity of the parietal cell to vagal stimulation,  Impaired acid inhibitory mechanisms Zollinger-Ellison Syndrome: caused by a gastrin- secreting tumor of the duodenum or pancreas → marked gastric acid hypersecretion & recurrent peptic ulceration. 2/3 of tumors are malignant. Found in ~ 0.1% of patients with duodenal ulcers. 4-Disorders of Acid Hypersecretion

31 31 Risk Factors for PUD Cigarette smoking Genetic factors Psychological & physiological stress - multiple trauma, sepsis, neurosurgical problems, ICU stresses Dietary factors

32 Clinical Presentation 32

33 33 Chief complaint : Pain (25% are painless) doesn’t always correlate w/presence of acid or ulcer craters Duodenal UlcerGastric UlcerMost common symptom Sharp, burning, or gnawingLess typical & predictable Occurs 1-3 hrs after mealsMay occur during a meal Relieved by alkali & foodFood offers little/no relief; may precipitate it Usually located in RUQMay extend over a wide area of epigastrum Nocturnal; awakens patient (1-2am)

34 34 Clinical Manifestations Symptom analysis of the chief complaint : PQRSTA P recipitating factors – what brings on the problem? Q uality – describe what the problem is like. R adiating/ R elief factors – does the problem start in one place in your body, then move elsewhere? What have you done to make it better (did it work)? S everity – try to rate how bad the problem is right now on a scale from 1-10, with “10” being the absolute worst. T emporal factors – does the problem seem to occur at a particular time of the day or with a specific activity? A ssociated symptoms – do you have any other sensations, feelings around the same time as this problem?

35 35

36 36 Clinical presentation of ZE Syndrome Similar to sever PUD More persistent Less responsive to standard therapy Abdominal pain; most common Sx Diarrhea: because gastrin inhibits sodium and water reabsorption from intestine

37 37 Complications Three Major Complications Hemorrhage Perforation Gastric outlet obstruction  Initially treated conservatively  May require surgery at any time during course of therapy

38 38 Hemorrhage Most common complication of peptic ulcer disease Develops from erosion of  Granulation tissue found at base of ulcer during healing  Ulcer through a major blood vessel

39 39 Perforation Most lethal complication of peptic ulcer Commonly seen in large penetrating duodenal ulcers that have not healed and are healed and are located on posterior mucosal wall Occurs when ulcer penetrates serosal surface Size of perforation directly proportional to length of time patient has had ulcer

40 40 Gastric Outlet Obstruction Active ulcer formation is associated with edema, inflammation Duodenum can predispose to gastric outlet obstruction ↑ contractile force needed to empty stomach results in hypertrophic stomach wall Obstruction is not totally due to fibrous scar tissue Short duration or absence of pain indicative of a malignant obstruction Vomiting and Constipation are a common complaint

41 41 Diagnosis Visualization of the ulcer defines the disease 1-Barium Upper GI Study (X-rays) Can show obstruction, perforation, or penetration Cannot show bleeding 30-60% of ulcers can be detected

42 42 2-Endoscopy Most often used Superior test for diagnosis More costly & less patient acceptance Can visualize the ulcer Can visualize any bleeding Can treat bleeding Determines degree of ulcer healing after treatment Tissue specimens can be obtained to identify and to rule out gastric cancer

43 43 Indications for Endoscopy: New onset dyspepsia in pts > 45 yrs old (to rule out gastric cancer) Patients with “alarm” symptoms:  Evidence of GI bleeding, anemia, unexplained weight loss, recurrent  vomiting, decreased appetite, easy fullness, dysphagia, abdominal mass,  lymphadenopathy Patients whose symptoms have failed to respond to initial therapy Patients with recurrent or difficult to control disease

44 44 Laboratory tests Guaiac test on stool sample CBC should be done if the patient’s stool is guaiac positive Acute blood loss :  Red cell indices:  RBC,  Hct,  Hgb,  Normocytic (MCV), Normochromic (MCH) Chronic blood loss :  Iron deficiency:  RBC,  Hct,  Hgb,  MCV,  MCH

45 45 Tests for GUT Blood Very important tool for screening in the clinic setting Hemoccult (stool) Gastroccult (stomach) Both are based on the catalytic activity of hemoglobin during the conversion of guiac into a blue pigment in the presence of peroxide

46 46 Diagnosis of ZE syndrome Measurement of gastric acid secretion >15 mmol/hr in patients with no prior gastric surgery > 5 mmol/hr in patients with prior gastric surgery fasting gastrin level > 1000 pg/ml secretin provocative test: secretion will cause a marked increase in serum gastrin

47 47 H. pylori Testing Indications for H. pylori testing: New onset dyspepsia in patients < 45 years old (with no alarm symptoms) Active peptic ulcer disease PMH of documented peptic ulcer, which has not been tested for H. pylori Gastric lymphoma

48 48 Methods of diagnosis for Helicobacter pylori

49 49 13 C Breath Test + + Can be used multiple times; noninvasive; Non radioactive May not be widely available; requires expensive equipment (cost ~ $300) 14 C Breath Test + Good for follow- up; noninvasive; rapid (60 min), Less expensive than 13 C test (cost ~ $50) Small radiation exposure; not able to repeat test multiple times Serology+Noninvasive; least expensive; rapid; simplest Look for IgG antibodies to H. pylori Not useful for short-term f/u of antimicrobial therapy, preferred when endoscopy not done Not useful for pts s/p H. pylori Tx

50 50 Stool Antigens A stool antigen enzyme immunoassay has a sensitivity of about 94% and specificity of about 90%. It should not be used to test for eradication of H. pylori until 6- 8 weeks after therapy.

51 51 Testing for H. Pylori UREASE breath test kits : Urea pill with labeled 13 C or 14 C Measuring CO 2 10 minutes later Must be off of antibiotics before taking the test. Gastric biopsy: Special histologic stains for identification Cotran: Robbins Pathologic Basis of Disease, 6th ed., Copyright © 1999 W. B. Saunders Company

52 52 Gold Standard: Gastric biopsy The Rapid UreaseTest is the most popular and recommended because of its excellent sensitivity & low cost. The labeled C breath tests utilize H pylori’s ability to hydrolyze urea into ammonia. Urea labeled with carbon isotope is administered orally If organism is present, urea is hydrolyzed & pt will exhale labeled Co 2 which can be quantified. 14 C is radioactive – not recommended for children, pregnant women, or for multiple uses in the same person. 13C is non-radioactive

53 53 The Serological Test An excellent initial screen to determine infection because the result is known in 20 min. H. pylori infection elicits an immune response with an increase in IgG and IgA antibodies. There are commercially available tests that measure IgG antibody. All of the tests – with the exception of serological testing – may be falsely negative in pts who have taken antibiotics, bismuth compounds, or omeprazole in the recent past.

54 54 Therapy Therapeutic Objectives Relieve pain; control symptoms Prevent pain recurrence Prevent further irritation while healing occurs Remove or treat cause if possible Promote healing Prevent complications Maintain the healed ulcer condition Indices of Therapeutic Effect: A.Pain relief/Absence of pain B.Frequency of antacid use C. Endoscopy (to confirm healing – if symptom response is inadequate

55 55 General Treatment Principles : Establish diagnosis with certainty (poor symptom correlation) Utilize non-drug modalities, removing potential exacerbating factor Non-drug Therapy: Avoid alcohol Stop smoking Avoid caffeine Avoid aggravating foods Reduce stress Eliminate drug- induced causes (NSAIDs, ASA)

56 56

57 Action of Anti-Ulcer drug groups

58 58 H 2 -blockers MOA Selectively and competitively Inhibit the action of histamine on H 2 receptors of the parietal cells → reducing basal and stimulated secretion of gastric acid Efficacy Equally Effective for: Treatment of acute ulcers in the absence of H. pylori Treatment of NSAID-induced ulcers Maintenance therapy in patients unable to tolerate a course of antimicrobial therapy to eradicate H. pylori

59 59 1-H 2 -blockers Efficacy 70-95% heal rate in 4-8 weeks Standard doses inhibit % of 24-hour acid secretion Equal in efficacy to antacid, and sucralfate therapy Effective as single therapy in pts with no H pylori infection

60 60 Side effects Safe, Frequency of SE is low Common SE:  Diarrhea, constipation, Mental confusion, headache, dizziness, drowsiness, and rashes  Confusion/agitation occurs more frequently in elderly, renal & hepatic dysfxn Similar profile (reported more frequently with cimetidine) Mental status changes, diarrhea, headache (2-3%) Rare: bone marrow suppression (thrombocytopenia, agranulocytosis)

61 61 Cimetidine : Prolonged use – gynecomastia, erectile dysfxn,  sperm ct (anti-androgen) Ranitidine : Hepatitis Famotidine :CNS, headache Nizatidine :Sweating, itching, hepatic

62 62 Table 27-4 Cimetidine inhibits oxidative metabolism CYP450 Magnitude of interaction varies from patient to patient Generally it will reduce clearance of another drug by 20-30% Clinically significant in drugs with narrow therapeutic window Addition of cimetidine may require ↓ dosage of the object drug to avoid increased serum concentration lidocaine, valium, propranolol, metoprolol, warfarin, phenytoin, theophylline Drug Interaction Profile

63 63 Other H 2 -blockers have lower affinity for p450 system; fewer drug interactions: Cimetidine > ranitidine, nizatidine > famotidine Cimetidine and ranitidine inhibit renal tubular secretion of procanamide and its metabolite All 4 drugs can affects absorption and reduce bioavailability of some drugs by requiring gastric PH Cimetidine ↑ PH → slows dissolution of ketoconazole → ↓ absorption Cimetidine, ranitidine, nizatidine ↑ absorption of ethanol

64 64 See Table 27-1 and Table 1 Control of night time acid secretion is more effective in healing ulcers May be given as a single bedtime dose for treatment of DU For ZES: Not totally effective, require large doses and more frequent dosing The dose to heal an ulcer – DU=GU The dose to maintain a healed ulcer –DU=GU Maintenance dose is cut in half, single daily dose Route of Administration and Dosing

65 65 2-Sucralfate MOA Protects ulcerated mucosa from aggressive factors It binds to damaged tissue forming a physical barrier to injury Efficacy 1 gm 4 times daily as effective as 2 gms twice daily Requires acid medium to work (don’t combine with H2-blocker) As effective as H2-blockers in promoting DU healing

66 66 Side effects Not absorbed systemically Constipation, xerostomia, skin eruptions, nausea, indigestion, dizziness Contains aluminum (Al); accumulates in pts with renal dysfxn; Neuro toxicity; seizures Drug Interaction profile Al dissociates from sucralfate:  absorption of TCN, phenytoin, warfarin Chelation with other drugs given simultaneously

67 67 Dosing: 1 gram, four times daily, before meals & at bedtime (compliance) For duodenal ulcer, 2 grams bid (before breakfast & at bedtime) may be as effective Large tablet size – may be difficult to swallow Route of Administration and Dosing Frequency

68 68 3-Antacids MOA Relive pain and promote healing by providing a cytoprotective effect through stimulation of PG Neutralizing gastric acid Stimulating restitution of the gastric mucosa Efficacy Low to moderate doses may be as effective in healing duodenal ulcers as H 2 blockers if taken multiple times a day neutralize acid; inhibit pepsinogen to pepsin, bile salts

69 69 Antacids High dose as effective as H 2 -blockers May provide less symptom relief than H 2 -blockers High dose: 30 cc po 1hr before & 3 hrs after each meal & at bedtime (7 doses) May accelerate healing of GU (lack of data to confirm it, but likely) Currently used for symptomatic relief in addition to H 2- blockers or sucralfate Primarily used on as PRN for pain Liquid formulation are more rapid acting

70 70 Side Effects Aluminum antacids Reacts with intestinal bicarbonate low alkalosis risk Constipation, hypophosphatemia, renal accumulation Magnesium antacids : Reacts with intestinal bicarbonate - low alkalosis risk, Diarrhea (dose-related), avoid in CRF Combination (Al/Mg )Less ADRs; lower doses used Sodium bicarb : Patients with poor renal fxn –metabolic alkalosis, Sodium overload – 12 Meq/g (edema, CHF, CRF, HTN)

71 71 Calcium antacids Constipation, rebound hyperacidity (may not be clinically signif.) More potent & prolonged neutralization, Systemic alkalinization, milk alkali syndrome, pH ,  Ca++  kidney stones Malgaldrate: chemical entity composed of aluminum & magnesium hydroxides (not a physical mixture & lower neutralizing capacity)

72 72 Drug Interaction Profile Chelation – divalent/trivalent cations bind drugs &  absorption e.g ciprofloxacin, TCN Gastric pH – interfere w/drugs requiring low pH for absorption e.g digoixn, phenytion, isoniazid Urinary pH – may affect drugs requiring acidic/basic urine for elimination May reduce absorption of tetracyclines, iron, digoxin, & many other drugs Can reduce absorption of H2-blockers, may  effect of sucralfate Avoid taking other meds 1-2 hrs before & after taking an antacid

73 73 Route of Administration and Dosing frequency Tablets: chewed/dissolved, palatable. Suspensions work faster; more surface area

74 74 4-Proton Pump Inhibitors : PPI MOA: Specific inhibitors of gastric acid secretion by irreversible biding to K+-H+ - ATPase ( enzyme which transports acid across parietal cells) Inhibit basal and stimulated acid secretion Indicated for short-term treatment of DU Indicated for long-term treatment of ZES

75 75 PPI Efficacy Absolute healing rates are similar Superior to H 2 -blockers with regard to onset of healing & pain relief Effective in patients refractory to H 2 -blockers. may be more efficacious than H 2 -blockers for the prevention of recurrent GU and DU in patients who must continue on NSAID therapy.

76 76 PPI Efficacy Standard doses inhibit more than 90% of 24-hour acid secretion. For DU: Omeprazole 20 mg qd  90 –100% healing in 4 weeks Lansoprazole 30 mg qd  90 – 100% healing in 4 wks For GU: As effective as H2-blockers for healing ulcer Higher doses may provide faster relieof pain,  recurrence

77 77 For ZES : Long-term efficacy has been observed Decreases diarrhea, heals ulcers Daily dose of 120 mg (mean daily dose 60-70mg) controls symptoms in > 90% of pts Side Effects May cause headache, diarrhea, abdominal pain, nausea, dizziness. Concern over long-term use & development of carcinoid tumors Treatment:  acid will  pH; which  gastrin secretion – possible ECL cell hyperplasia (recommended to check serum gastrin levels annually in pts on long-term therapy )

78 78 PPI : Drug Interaction Profile All agents are extensively metabolized by cytochrome p450 Omeprazole : Inhibitor of oxidative metabolism by p450 system May  diazepam, phenytoin, warfarin, etc. Omeprazole and Clarithromycin →  concentration of both drugs Lansoprazol e Metabolized through p450 system: may  clearance of theophylline (10%) Sucralfate Reduces absorption of PPIs Drugs whose absorption may be impaired from reduced acidity: Ketoconazole, iron, ampicillin, etc.

79 79 Route of Administration and Dosing See table 1 & 2 Rabeprazole is available as a 20mg enteric-coated tablet; dosed once daily. Pantoprazole is dosed 40mg po qd For ZES: Longer duration of action so require less frequent dosing Large doses are necessary Start at 60mg lansoprazole or 80mg omeprazole po qd

80 80 5-Prostaglandin E1 Analog MOA Inhibits basal & nocturnal gastric acid secretion; Enhances mucous & bicarb secretion; Reduces pepsin concentration but does not affect histamine stimulated secretion.

81 81 Prostaglandin E1 Analog Efficacy For prevention of NSAID-induced gastric ulcers in patients at high risk. Superior to sucralfate in preventing NSAID-induced gastric ulcers Superior to H2-blockers in reducing mucosal injury, but may relieve pain less rapidly (H2-blockers more effective for inhibiting gastric acid output, especially at night) May be effective in healing H2 blocker-resistant ulcers

82 82 Side Effects : Diarrhea, abdominal pain, nausea, headache, flatulence, constipation Can  GFR and improve renal function Contraindicated in women of childbearing age unless effective contraceptive measures are used (may cause uterine contractions; abortifacient). Take with or after meals and at bedtime to reduce ADRs

83 83 Drug Interaction Profile No effect on cytochrome p450 system Use of Mg-containing antacids can worsen misoprostol-induced diarrhea (use an Al-antacid) Dosing : 200  g qid If patient unable to tolerate: can be given 100  g qid OR 200  g bid or tid (also a small  in effectiveness at lower doses)

84 84 6-Bismuth Subsalicylate MOA Direct mucosal protective effect; anti-infective actions, weak antacid properties It complexes deposit on the surface of H. pylori, diminishing its ability to adhere to the gastric epithelium. The end result is lysis of the organism within min. The addition of an antimicrobial agent produces a synergistic effect. May also stimulate production of prostaglandins & modulate the immune response. Side Effects Abdominal pain, constipation, headache, confusion, anxiety, tinnitus, tremor.

85 85 Drug Interaction Profile Anticoagulants (plt fxn), May potentiate hypoglycemic effects of diabetic agents May displace other drugs from protein binding sites May form complexes with other drugs (TCN, quinolones) May  effects of uricosuric agents, use with omeprazole may  systemic absorption of bismuth (unknown significance) Dosing 2 tablets QID (1 tablet = 262mg bismuth subsalicylate; equiv to 100mg salicylate)

86 86 7-Prokinetic Agents: Metoclopramide MOA Increases GI motility and peristalsis Increases LES tone Antagonizes dopamine receptors. Side Effects Extrapyramidal symptoms Drug Interaction Profile Increased sedative effect of benzodiazepines or alcohol. Dosing Metaclopramide 5-15 mg dose, up to 4 times a day (take 30 min before meals). Single dose of 20 mg may be needed in a provoking situation

87 87 Treatment of NSAID induced ulcer 1-Stop NSAIDs when possible. 2- Treat with low dose H-2 antagonist for 8 weeks Prophylactic therapy In patients unable to discontinue NSAIDs and have risk factors for development of ulcer 1-PPIs: they are preferred if NSAIDs are to be continued 2-Misoprostol 3-H 2 antagonist are more effective in healing duodenal ulcer than gastric ulcer

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89 Treatment plan & Monitoring 1. Assess risk factors for NSAID-induced ulcers and ulcer-related complications, and when indicated 2.recommend appropriate strategies for reducing ulcer risk (see Table 35-10). 3. Recommend eradication treatment for H. pylori-positive patients taking NSAIDs. 89

90 Treatment plan & Monitoring 4. Monitor patients for signs and symptoms of NSAID-related upper GI complications. 5. Assess and monitor patients for potential drug interactions and adverse effects (especially misoprostol). 90

91 Treatment plan & Monitoring 6. Provide patient education to patients who are at risk of NSAID-induced ulcers or GI-related complications, including why cotherapy is used with nonselective NSAIDs; when and how to take medications; adverse effects; alarm symptoms; when to contact their healthcare provider; the importance of adherence to drug treatment. 91

92 92 Eradication of Helicobacter pylori In the past, PUD was considered a chronic disorder because the ulcer tended to recur. Eradication of H. pylori dramatically reduces ulcer recurrence & cures many patients of their disease. Advantages of eradication: Inflammatory changes return to normal Restoration of microvilli by 4 months Decrease in disease recurrence Problems: Eradication may be difficult; resistance to antibiotics Adverse reactions to antibiotics

93 93 Who should be treated for H. pylori? All pts with established duodenal ulcers with H. pylori. All pts with gastric ulcers with H. pylori. First or recurrent H. pylori infection Who should not be treated for H. pylori Asymptomatic (H. pylori positive or negative) Non-ulcer dyspepsia* (H. pylori positive or negative) Gastric ulcer (H. pylori negative) Duodenal ulcer (H. pylori negative) Gastroesophageal reflux disease Gallbladder or pancreatic disease Irritable bowel or inflammatory bowel disease

94 94 Disadvantages of Maintenance Treatment: recurrence despite long-term treatment doesn’t change H. pylori colonization long-term drug exposure increased cost potential for disease complications from recurrence

95 95 H. pylori Eradication Regimens Monotherapy with antibiotics or acid suppressants have not been optimal Combination of acid suppressants with antibiotics Should contain one anti-secretory agent & at least 2 antibiotics) Dosing Clarithro 500 mg bid, Amoxil 1000mg bid, Metronidazole 500mg bid, Tetracycline 500mg bid BMT-1: Bismuth 525mg qid + Metronidazole 500mg tid + Tetracycline 500mg qid BMT-2: Bismuth 525mg qid + Metronidazole 250mg qid + Tetracycline 500mg qid

96 96

97 Treatment plan & Monitoring 1. Assess patient allergies to determine if allergic to penicillin (or other antibiotics) so that drug regimens that contain penicillin (or other antibiotics) can be avoided. 2. Assess patient use of alcohol or alcohol-containing products with metronidazole and oral birth control medications with antibiotics and counsel appropriately. 3. Assess likelihood of nonadherence to the drug regimen as a cause of treatment failure. 97

98 Treatment plan & Monitoring 4. Recommend a different antibiotic combination if H. pylori eradication fails and a second treatment is planned. 5. Inform the patient of change in stool color when bismuth salicylate. 6. Assess and monitor patients for potential adverse effects, especially those associated with metronidazole, c1arithromycin, and amoxicillin. 98

99 Treatment plan & Monitoring 7. Assess and monitor patients for potential drug interactions, especially those receiving metronidazole, clarithromycin, or cimetidine. 8.Monitor patients for salicylate toxicity, especially patients receiving cotherapy with other salicylates, anticoagulants, and patients with renal failure. 9.Monitor patients for persistent or recurrent symptoms within 14 days after completion of a course of therapy. 99

100 Treatment plan & Monitoring 10. Provide patient education to patients including why antibiotic and antiulcer combinations are used; when and how to take medications; adverse effects; the importance of adherence to the entire course of drug treatment; to contact their healthcare provider if alarm symptoms develop (e.g., blood in the stools, black tarry stools, vomiting, severe abdominal pain), or if symptoms persist or return. 100

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