Day 5- PUD, GI Bleed, and IBD Flashcards
What are the 3 main causes of PUD?
What are signs and symptoms of PUD?
What is the gold standard of PUD?
H. Pylori, NSAID, SRMD(stress).
Ab pain, nocturnal pain that awakes patients, heartburn, belching, bloating, N/V and anorexia. Alarm symptoms are Hematemesis and Melena.
PPI are gold standard, Antacid can provide symptomatic relief. Relieve ulcer pain, ulcer healing, prevent recurrence.
What are signs of an H.Pylori ulcer?
What is the pathophysiology in H. Pylori?
What are your diagnostic things for H. Pylori?
chronic, Less bleeding, epigastric pain, more dependent on pH, Duodenum>stomach. NSAID and SRMD opposite and SRMD is acute.
Resides between mucus and epithelial layer and binds to epithelium to prevent organism from being shed. Produces urease and make an igloo–> recruits more H. Pylori until mucosal layer is exposed.
Histology, culture, rapid urease test, PCR(can give false positives), Antibody test, Fecal/stool antigen test. Non endoscopic is preferred.
What is 1st line treatment for H.Pylori?
What is 2nd line treatment for H.Pylori?
What are your NSAID induced risk factors?
Triple therapy: Clarithromycin, Amoxicillin, PPI or Clarithromycin(avoid in QT prolongation), Metronidazole, PPI. Last 10-14 days.
Quadruple therapy: Bismuth, Metronidazole(metallic taste, disulfiram interaction with alcohol), tetracycline, PPI. Or exact same except replace tetra with amoxicillin or clarithromycin.
Old age, you know most of it, Concomittant use with aspirin, oral bisphosphonate, corticosteroids, anticoagulant, antiplatelet, SSRI’s.
Are semi selective or non selective most damaging?
What are the semi selective NSAIDS?
How do you treat NSAID ulcers?
Non selective.
Etodolac, Meloxicam, Diclofenac, Celecoxib.
Stop NSAID and administer H2RA’s, PPI’s, or sucralfate with PPI preferred for 4 weeks or 8-12 if NSAID continued.
How to treat an NSAID ulcer if NSAID is continued?
How do you prevent an NSAID ulcer if patient is at high CV risk(aspirin required)?
How do you prevent an NSAID ulcer if patient is low CV risk(aspirin not required)?
Co-therpay with PPI or Misoprostol(watch for cramping and diarrhea and pregnancy). Do not use H2RA’s. Reduce dose, switch to more selective NSAID, switch to other analgesic.
Low and medium GI- Naproxen and PPI or Mistoprostol. High is Avoid NSAIDS and use alternative analgesic.
Low, Moderate, High–>Non selective NSAID or partially selective NSAID + (PPI or misoprostol(moderate and high)). Can avoid in high.
What are risk factors for SRMD?
How do you treat SRMD?
How do you treat GI bleeds?
Mechanical Ventilation and Coagulopathy.
Keep gastric pH >4 or provide mucosal protection. H2RA’s, PPI. Sucralfate.
Supportive care, stop bleed, prevent re bleeding(IV PPI). Watch for big drop in hGb of 2 units in more than 24 hours.
What are your two main categories of IBD?
How does smoking affect IBD?
How do UC and CD differ?
Ulcerative colitis and Chrons disease. Most prevalent in north western areas.
Decreases risk in ulcerative colitis, increases risk in chrons disease.
UC confined to rectum and colon. Affects mucosal and submucosal layers. Lots of bloody stools, tenusmus(ghost poo). CD is deeper and has a skip pattern, fistula apperance and colon takes cobblestone look, nutritional deficiency common.
What are your extraintestinal complications of CD?
What are complications of IBD?
What are your goals of therapy for IBD?
Occurs in CD only, hypercoagulability, ocular, joints, skin, stomatitis, kidney stones, liver, biliary tract.
Abscesses, Obstruction or stricture, perianal disesase and fistula.
No cure, induce remission, maintain remission, prevent surgery and complications, improve quality of life.
What is treatment for mild to moderate UC?
How do you treat severe or failure of mild to moderate UC?
When are 5-ASA’s CI’d and common ADE’s?
Oral or rectal 5-ASA/budesonide/coricosteroids with taper and then maintenance therapy is oral or rectal 5-ASA.
Steroids + thiopurine or Biologic + thiopurine/mtx. Maintenance is thiopurine or biologics + thiopurine/mtx.
Salicylate hypersensitivity, sulfasalazine(sulfa allergy). N/V, rash, diarrhea(1st-olsalazine, 2nd- balsalazide).
What are the ADE’s of sulfasalazine?
What are the drug interactions for the 5-ASA’s?
Are sulfalaslzine, olsalazine, and balsalazide all prodrugs?
Oligospermia, infertility, discoloration of urine and nephrolithiasis.
NSAIDS, Azathioprine and 6-MP, antacids and PPI’s.
Yes. Metabisulfate in sulfasalazine.
What is the most comprehensive for coverage of the 5-ASA’s? Can you use combination 5-ASA’s?
What does Rowasa cover?
What does Canasa cover?
Pentasa. YES.
Enema, get on your row boat.
Suppository.
Are systemic corticosteroids appropriate for maintenance therapy?
What special things to know about Budesonide?
What special things to know about Thiopurines?
NO.
Avoids steroid complications(not in conjunction normally), high first pass metabolism, indicated for induction, topical effect in GI tract.
Maintenance therapy only. Myelosuppresion ADR.
When do you use top down therapy in chrons disease?
What is induction therapy in low risk CD?
What is maintenance therapy in low risk CD?
Severe(biologics–> traditional therapy).
Steroid or budesonide.
Stop and observe, budesonide 6mg/day up to 3 months, AZA, 6MP, MTX.
What is induction therapy in moderate to high risk CD?
What is maintenance in moderate to high risk CD?
Which Biologic is UC only and which one is CD only?
Biologics, Anti TNF + Thiopurine. Non tnf blocker for anti-tnf failure. Mono therapy if non other available. If remission doesn’t get achieved check thiopurine levels and change biologics.
Anti TNF- Thiopurine.
Golimumab, Certolizumab pegol.
What are the big side effects in Natalizumab?
What to know about Vedolizumab?
If a patient is taking a PPI and antibiotics or bismuth, how long do you wait to test for H. Pylori?
Progressive leukoencephalopathy, severe cholastatic injury, put in CD touch program.
Preferred over Tysabri reserved for non responsive.
PPI- 2 weeks, antibiotics and bismuth- 4 weeks.
