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89 Cards in this Set
- Front
- Back
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Peptic Ulcer Disease
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acid related disease of the upper GI tract characterized by lesions that extend deeper into the muscularis mucosa
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Causes of PUD
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1) TYPICAL (H pylori, NSAID-induced, Stress related)
2) ATYPICAL (idiopathic, hypersecretion, viral infections) |
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Risk Factors of PUD
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1) H. pylori
2) NSAIDS (chronic use) 3) Smoking (can impair healing, exact MOA unknown) 4) Psychological stress 5) Diet (caffeine, spicy foods) |
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Pathophys of PUD
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1) Imbalance between mucosal defense factors (bicarb, mucin, prostaglandins, NO)
2) Injurious Factors (acid, pepsin) 3) Alteration of mucosal defense mechanisms (H. pylori, NSAIDS) |
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Complications of PUD
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1) Upper GI bleed and perforations
2) GI obstruction |
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Symptoms of PUD
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1) epigastric ab pain (mild-moderate)
2) nocturnal pain (in the evening, over night) 3) severity may be seasonal (with stress) 4) Heartburn, belching, bloating 5) Nausea, vomiting, anorexia 6) weight loss |
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Goals of treatment for PUD
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1) Relieve pain
2) heal ulcer 3) prevent recurrence 4) reduce complications |
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Non-pharm treatment of PUD
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1) reduce stress
2) smoking cessation 3) reduce use of NSAIDS 4) avoid spicy foods 5) avoid caffeine 6) avoid alcohol |
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Proton Pump Inhibitors for PUD
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inhibit H+/K+ ATPase and inhibit actively secreting acid
take 30-60 minutes before meals acid suppression increases over the first 3-4 days ADRs: nausea, ab pain, constipation/diarrhea, flatulence |
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H2RAs for PUD
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inhibit acid production by reversibly competing with histamine for binding to H2 receptors on parietal cells
Smokers: higher doses/longer duration Mod-Severe renal failure: dose reduction ADRs: GI, headache, fatigue, drowsiness, muscle pain |
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Sucralfate for PUD
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Mucosal protectant - protective coating on gastric lining
multiple doses/day ADRs: constipation, seizures, hypophosphatemia Interactions: fluoroquinolones |
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Dosing of Sucralfate for PUD
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Duodenal/gastric: 1g QID or 2g BID
Maintenance: 1-2g BID or 1 g QID |
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Antacids for PUD
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Neutralize gastric acids, inactivate pepsin and bind bile salts
Interactions: iron, warfarin, tetracyclines, dig, fluroquinolones (separate by 2 hours) |
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Aluminum Antacids for PUD
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suppress H. pylori, enhance mucosal defense
ADR: constipation interfere with phosphorus (care with sucralfate) |
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Magnesium Antacids for PUD
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ADR: diarrhea
caution in CrCl < 30 (CKD, AKI, elderly Mg excretion impaired |
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Misoprostol for PUD
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synthetic prostaglandin E1 analog - inhibits acid secretion and enhances mucosal defense
DOSE: 200mcg QID or 400mcg BID ADRs: diarrhea!!! |
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Bismuth for PUD
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antibacterial, gastroprotective effect and prostaglandin stimulation
Caution: older patients with renal failure, salicylate sensitivity ADRs: black stool, black tongue |
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Causes of H. Pylori PUD
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1) Geographic location
2) Socioeconomic status (developing countries) 3) Ethnicity (AA > Hispanic > Caucasion) 4) Age (elderly) |
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Trasmission of H. pylori PUD
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Person-to-person
1) Gastro-oral (vomit) 2) Fecal-oral (Diarrhea) 3) inadequately sterilized endoscopes |
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Goals of treatment for H. pylori PUD
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1) eradicate bacteria
2) heal ulcer 3) Cure the disease |
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Duration of therapy for H. pylori PUD
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10-14 days
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Types of therapy for H. pylori PUD
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1) Triple Therapy - most common!
2) Quadruple Therapy 3) Sequential Therapy - not used in US |
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Triple Therapy for H. Pylori PUD
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PPI BID
+ Clarithromycin 500mg BID + Amoxicillin 1g BID |
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Quadruple Therapy for H. pylori PUD
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PPI or H2RA
+ Bismuth 525mg QID + Metronidazole 500mg QID + Tetracycline 500mg QID |
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medication for treatment of H. pylori PUD with PCN allergy
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Lose Amox
Use Metronidazole 500mg BID |
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Reasons for Treatment Failure for PUD
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1) Antibiotic resistance
2) Adherence 3) Short duration of therapy 4) Low intragastric pH 5) High bacterial load |
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ADRs of PUD medications
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1) nausea, vomiting, diarrhea
2) ab pain 3) taste disturbances 4) Disulfiram-like reaction 5) tooth discoloration 6) darkening of stool and tongue |
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Risk Factors for NSAID-induced ulcers
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1) >65 years old
2) previous peptic ulcer 3) high dose NSAIDS 4) NSAID selection 5) Multiple NSAIDS 6) ASA 7) NSAID + low dose ASA 8) Bisphos 9) corticosteroids 10) SSRIs 11) antiplatelet therapy |
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Treatment of NSAID-induced ulcers
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1) discontinue NSAID ASAP (if possible)
2) Start *PPI*, H2RA, Sucralfate |
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Signs/Symptoms of GI Bleeding
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1) weakness/fatigue
2) hematemesis (vomiting of blood/coffee-ground like) 3) melena (black colored stool) 4) hematochezia (bright red/maroon blood from rectum) 5) positive fecal occult blood test 6) epigastric or RUQ pain 7) elevated BUN 8) hemodynamic instability |
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Types of Upper GI bleed
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1) Non-variceal
2) Variceal |
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Causes of Non-Variceal Upper GI bleed
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1) PUD
2) Stress related mucosal disease 3) gastroduodenal erosions 4) esophagitis 5) mallory weiss tear 6) upper GI cancer 7) vascular malformations |
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Peptic Ulcer Bleeds
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Risk: H. pylori, NSAID use, stress
Single vessel S/Sx: hematemesis, weakness/fatigue Location: any part of stomach |
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Stress Related Mucosal Disease Bleeds
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Risk: Critical illness
Multiple capillaries S/Sx: asymptomatic Location: proximal stomach |
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Treatment of Non-Variceal Upper GI Bleed: Step 1
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Assess hemodynamic status and resuscitate as needed
1) Correct fluid loss 2) intubate 3) PRBCs 4) Classify risk for rebleeding/mortality |
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Classifying risk for Rebleed/mortality on non-variceal GI bleed
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Risks: age > 65, hemodynamic status (shock), comorbid disease states, low Hbg, melena, fresh blood
Blatchford score: before endoscopy Preendoscopi Rockell score |
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Treatment of Non-Variceal Upper GI Bleed: Step 2
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correct any coagulopathy in patients recieving anticoagulants
Don't delay endoscopy Give FFP if INR > 1.5 |
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Treatment of Non-Variceal Upper GI Bleed: Step 3
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consider NG tube
suction aspirate from stomach clear blood/clots to allow better visualization from endoscopy |
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Treatment of Non-Variceal Upper GI Bleed: Step 4
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consider preendoscopic medical therapy
PPIs - continuous infusion, do not delay endoscopy, can reduce further bleeding Pro-motility agents (IV erythromycin) |
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Treatment of Non-Variceal Upper GI Bleed: Step 5
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Endoscopy
within 24 hours of presentation, after resuscitations can perform biopsy |
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Treatment of Non-Variceal Upper GI Bleed: Step 6
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Pharmacological therapy
Goal: decrease acid production AFTER endoscopic intervention = IV PPI IV pantoprazole, esomeprazole: 80mg bolus, continuous infusion 8mg/hr x72 hrs |
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Treatment of Non-Variceal Upper GI Bleed: Step 7
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Discharge medications
1)daily PPI for as long as indicated by underlying cause 2) restart ASA as soon as risk of cardiac complications outweigh risk of rebleeding |
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7 steps of treatment of Non-Variceal Upper GI bleed
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1) Assess hemodynamic status and resuscitate as needed
2) Correct coagulopathy 3) consider placement of NG tube 4) consider preendoscopic medical therapy 5) Endoscopy 6) Pharmacological Therapy (PPI) 7) Discharge Meds (PPI) |
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Causes of Variceal Upper GI Bleed
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1) cirrhosis - development of fibrous tissue and regenerative nodules
2) structural resistance to blood flow and intrahepatic vasoconstriction 3) portal hypertension 4) formation of port-systemic collaterals (include gastroesophageal and gastric varices) 5) rupture results in a variceal hemorrhage |
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6 steps for tretament of Variceal Upper GI bleed
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1) assess hemodynamic status and resuscitate as needed
2) Correct coagulopathy 3) Short term antibiotic prophylaxis for spontaneous bacterial peritonitis 4) Splanchic Vasoconstriction 5) Endoscopy within 12 hours 6) bleeding continues - additional therapy |
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Treatment of Variceal Upper GI bleed: Step 1
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Assess hemodynamic status and resuscitate as needed
1) Intubate if needed 2) CAREFULLY transfuse PRBC as required (Hgb >8) 3) AVOID IV fluid resuscitation if possible |
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Treatment of Variceal Upper GI bleed: Step 2
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correct any coagulopathy in patients receiving anticoagulants
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Treatment of Variceal Upper GI bleed: Step 3
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Short term antibiotic prophylaxis for SBP
1) infection lead to early recurrence of hemorrhage 2) Empiric coverage for Gram-Neg **Norfloxacin 400mg PO BID x7d **Ciprofloxacin 400mg IV q12h x7d |
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Treatment of Variceal Upper GI bleed: Step 4
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Splanchic Vasoconstrictors
1) Octreotide (Sandostatin) - 50mcg IV bolus, then continuous infusion at 50mcg/hr for 3-5 days **use only in combo** 2) Vasopressin - continuous infusion at 0.2-0.4 units/min for 24 HOURS ONLY **Always give with continuous infusion of Nitroglycerin 40-400mcg/min titrated to SBP >90) |
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Treatment of Variceal Upper GI bleed: Step 5
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Endoscopy within 12 hours (or ASAP)
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Treatment of Variceal Upper GI bleed: Step 6
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If bleeding continues or recurs early, additional therapy may be required
1) Transjugular intrahepatic portsystemic shunts 2) Shunt surgery 3) Balloon tamponade |
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Causes of Lower GI Bleed
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1) diverticular disease
2) angiodysplasia 3) Neoplasm 4) Anorectal causes (hemorrhoids, rectal varices) 5) Colitis |
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6 step treatment for Lower GI bleed
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1) Assess hemodynamic status and resuscitate as needed
2) Place NG tube 3) Correct any coagulopathy 4) If bleeding is stopped provide colon cleanse prior to colonoscopy 5) Endoscopy (preferred) 6) Alternatives to Endoscopy - no source of bleeding found |
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Treatment of Lower GI bleed: Step 1
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Asses hemodynamic status and resuscitate as needed
1) Correct fluid loss with IV fluids 2) Transfuse PRBCs as required |
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Treatment of Lower GI bleed: Step 2
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Place NG tube (nasogastric)
1) suction aspirate from stomach |
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Treatment of Lower GI bleed: Step 3
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Correct coagulopathy in patients receiving anticoagulants
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Treatment of Lower GI bleed: Step 4
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If bleeding is stopped, provide colon cleanse prior to colonoscopy either PO or per NG tube
Purpose: cleanse the colon and allow better visualization of bleeding source Polyethylene Glycol over >2 hours until effluent is clear Max 4 liters total = 240mL PO q10 minutes or thru NG |
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Treatment of Lower GI bleed: Step 5
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Endoscopy (preferred)
1) colonoscopy or sigmoidoscopy 2) localize the site of bleeding |
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Treatment of Lower GI bleed: Step 6
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Alternatives to Endoscopy - no source of bleeding is found
1) arteriography 2) nuclear scan 3) surgery 4) evaluation of small bowel |
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Treatment of Non-Variceal Upper GI bleed - transfuse PRBCs maintain Hgb
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7 mg/dl
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Blatchford Score
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allows some patients to be managed as outpatients
how severe is GI bleed |
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Non-Variceal Upper GI bleed - active bleeding or non-bleeding visible vessel
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Endoscopic Therapy
IV PPI bolus + continuous infusion for 72 hours |
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Non-Variceal Upper GI bleed - adherent clot
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May consider endoscopic therapy
IV PPI bolus + infusion |
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Non-Variceal Upper GI bleed - flat spot or clean base
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No endoscopic therapy
Oral PPI |
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Dose of PPI in Non-Variceal Upper GI bleed
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80mg bolus followed by continuous infusion of 8mg/hr for 72 hour
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Major problem associated with Variceal Upper GI bleed
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Portal Hypertension
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Short Term antibiotic prophylaxis for spontaneous bacterial (SBP)
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1) Norfloxacin 400mg PO BID x7d
2) Ciprofloxacin 400mg IV q12h x7d 3) Ceftriaxone 1g IV daily x7d |
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Dose of Octreotide (Sandostatin) in Variceal Upper GI bleed
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50 mcg IV bolus, then continuous IV infusion at 50 mcg/hr for 3-5 days
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Indications for Prophylaxis in GI bleed
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1) NSAID induced peptic ulcer disease
2) Stress related mucosal damage 3) Variceal bleeding in cirrhosis |
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Treatment approach for NSAID induced peptic ulcer prophylaxis
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1) Identify high risk patients
2) test for/treat H. pylori 3) choose appropriate prevention strategy based on CV risk 4) risk factors no longer present, discontinue |
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High Risk patients for NSAID induced GI complications
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1) history of previously complicated ulcer (recent
2) multiple (>2) risk factors |
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Moderate Risk patients for NSAID induced GI complications (1-2 risk factors)
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1) > 65 years old
2) high dose NSAID therapy 3) previous history of uncomplicated ulcer 4) concurrent use of ASA, corticosteroids, or anticoagulants |
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NSAID induced:
CV risk low/ GI risk low |
Lowest dose NSAID
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NSAID induced:
CV risk Low/ GI risk Moderate |
NSAID PLUS PPI / misoprostol
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NSAID induced
CV risk Low / GI risk high |
Alternative treatment
OR COX2 + PPI or misoprostol |
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NSAID induced
CV risk high / GI risk low |
Naproxen + PPI / misoprostol
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NSAID induced
CV risk high / GI risk moderate |
Naproxen plus PPI / misoprostol
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NSAID induced
CV risk high / GI risk high |
Alternative treatment
(no COX2/NSAID) |
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Treatment Options for NSAID induced prophylaxis
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1) H2RA - double the dose
2) Misoprostol - 200mcg PO QID; BBW, not commonly used 3) PPIs - most common (primary/secondary prevention) |
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Concerns about prolonged PPI use
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1) rebound hypersecretion upon discontinuation
2) hypomagnesemia 3) Drug interactions 4 increased risk of bone fractures 5) C. diff 6) pneumonia 7) decreased absorption of iron and B12 |
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When is Stress Ulcer Prophylaxis recommended
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IN THE ICU
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Risk Factors for Stress Ulcer Prophylaxis: 1 of the following
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**IN ICU**
1) Mechanical ventilation >48 hours 2) Coagulopathy (platelet <50000, INR > 1.5 3) history of GI ulceration or bleeding within 1 year 4) Head injury 5) Burn injury |
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Risk Factors for Stress Ulcer Prophylaxis
2 of the following: |
**IN ICU**
1) sepsis 2) ICU admission > 1 week 3) Occult GI bleed ing >/= 6 days 4) Glucocorticoid therapy >250mg |
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Treatment options for Stress Ulcer Prophylaxis
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1) H2RAs - first line; IV/PO (famotidine/ranitidine)
2) PPIs - recommended by new ASHP guidelines **Continuous infusion** 3) Sucralfate - not commonly recommended 4) Antacids - not commonly recommended |
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Variceal GI Bleed primary prophylaxis
No varices |
1) Surveillance endoscopy every 2-3 years
2) No pharmacotherapy indicated |
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Variceal GI bleed Primary Prophylaxis
Small, nonbleeding varices |
High Risk of Hemorrhage: non-selective beta blocker
Low risk of Hemorrhage: non-selective beta blocker or surveillance endoscopy |
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Variceal GI bleed Primary Prophylaxis
Medium-large, nonbleeding varices |
High risk of Hemorrhage: non selective beta blocker OR EVL
Low risk of Hemorrhage: non-selective beta blocker (preferred) or EVL + EGD periodically |
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non-selective beta blockers used in primary prophylaxis of Variceal GI bleed
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1) Propranalol 20mg PO BID
2) Nadalol 40mg PO daily 3) Carvedilol 3.125mg PO BID **Goal heart rate = 55-60 |
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Secondary Prophylaxis of Variceal GI bleed
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**Experienced a Bleed and recovered**
FIrst Line: combo of non-selective beta blocker + EVL |
