PUD Flashcards
Etiologies of PUD
H pylori
NSAID induced
Stress ulcers
Site for H pylori induced PUD
Duodenum > stomach
Site for NSAID induced PUD
Stomach > duodenum
Site for stress induced PUD?
Stomach > duodenum
What are the sx of h. pylori
Epigastric pain common
What are the sx of NSAID/stress induced PUD?
Asymptomatic
H pylori ulcer depth
Superficial
NSAID induced ulcer depth
Deep
Duodenal ulcer time for pain
Worse at night
How does food affect duodenal ulcer
Relieved by food
How does food affect gastric ulcers
Made worse by eating
Associated sx of PUD
Heartburn, belching, nausea, bloating and anorexia
Nationalities most affected by H pylori
Africans
Latin Americans
Gen propreties of H pylori
Spiral shaped
pH-sensitive
G-
Where is H pylori typically found
Between the mucus layer and surface epithelial cells in the stomach
How does H pylori survive in the stomach
Urease production - neutralizes acid
Adherence pedestals - prevent being shed with the GI lining
How does H pylori cause GI injury
Direct damage
Altering host response
Causing hypergasterinemia which leads to increased acid secretion
Who do we test for H pylori?
Active peptic ulcer disease History of PUD Gastric lymphoma After resection for gastric cancer Starting chronic NSAID therapy Iron deficiency anemia Idiopathic thrombocytopenic purpura Long term low dose ASA
Diagnostic test for H pylori
Endoscopic
Urea breath test
Fecal antigen
Ab testing
What is tested in endoscopic exams
Histology
Rapid urease testing
Culture
Polymerase chain rxn
What Antibodies are being tested for in non-endoscopic tests for H pylori
Serum IgG to H pylori
Serum Ab to H pylori
When is it acceptable to test for H pylori eradications
Sx despite treatment
H pylori associated ulcer or MALT lymphoma
Resection for early gastric cancer
Test 4 weeks after the end of treatment
Eradication rates lower with 7 day regimens
No PPI for at least 1-2 weeks and no bismuth or abx for at least 4 weeks
First line treatment recommendations for H pylori
Clarithromycin Triple therapy
Bismuth Quadruple Therapy
Concomitant Quadruple therapy
Antisecretory therapy is generally continued at standard dose after initial 10-14 days of therapy
Clarithromycin triple therapy
PPI + Amox/flagyl + Clarithromycin x 14 days
Clarithromycin resistance < 15%
Bismuth Quadruple therapy
PPI + Bismuth + Flagyl + tetracycline x 10-14 days
Concomitant Quadruple therapy
PPI + Amox + Flagyl + Clarithromycin x 10-14 days
Can use prevpac + flagyl
Preferred over quadruple regimen because all medications are dosed twice daily
How does Bismuth help?
Healing d/t antibacterial and local protective effect, also stimulates PGs
What are the salvage therapies?
Bismuth quadruple therapy
Levaquin triple therapy
Concomitant quadruple therapy
Rifabutin triple therapy
Levaquin triple therapy
PPI + Levaquin + Amox x 10-14 days
Rifabutin triple therapy
Reserved for pts with multiple (> 3) treatment failures
PPI + Rifabutin + amox x 10 days
NSAID ulcers
Dose dependent
Use of chronic non-selective NSAIDs (also ASA)
What is mucosal injury a result of
Direct topical irritation (drugs are acidic in nature)
Inhibition of protective effects of mucosal PGs
What does COX-1 do
Produces PG involved in maintaining GI mucosal integrity and platelet homeostasis
What does COX-2 do
Produces PG involved in inflammation
Risk factors for NSAID ulcers
Age > 65 Previous peptic ulcer NSAID use or NSAID related dyspepsia ASA including cardioprotective dosages Concomitant use of NSAID + low dose ASA Concomitant use of anticoagulant or antiplatelet agents Concomitant use of oral bisphosphoantes Concomitant use of SSRIs Chronic or debilitating disorders H pylori infection Smoking/EtOH consumption
Complications of NSAID ulcers
GI bleeds
Perforation into peritoneal cavity
Gastric outlet obstruction
non-pharm treatment of NSAID ulcers
Reducing psychosocial stress
Avoid aggravating foods
Smoking cessation
Pharm treatment of NSAID-induced ulcers
STOP NSAID if possible and treat with PPI qd for 4 weeks
Most ulcers will health with standard doses of PPI, H2RA or sucralfate
PPI + NSAID - when NSAID must be continued - PPI for 8-12 weeks
Pharm prevention of NSAID ulcers
Misoprostol or PPI with NSAID or COX-2
COX-2 alone
Why are H2RAs not used for NSAID ulcers?
Only prevent duodenal ulcers
Non-salicylates that are non-selective?
Indomethacin Piroxicam Ibuprofen Naproxen Sulndac Ketoprofen Ketoralac Flurbiprofen
Non-salicylates that are partially selective
Etodolac
Nabumetone
Meloxicam
Diclofenac
Non-salicylates that are cox-2 selective
Celebrex
Salicylates that are acetylated
ASA
Salicylates that are non-acetylated
Salsalate
Trisalicylate
What happens when cox-2s are taken with low dose ASA
Lose gastroprotective effect
What is the max total daily dose of celebrex to minimize CV risk?
400mg/d
What do the guidelines recommend for patients on low dose ASA and at low-mod risk for GI toxicity
misoprostol or PPI
Which drugs decrease plavix effectiveness?
Nexium and prilosec
inhibit 2C19
Which type of ulcers are sucralfate used for
Duodenal ulcers
What are the ADRs for sucralfate
Constipation, nausea, dry mouth, dizziness and metallic taste
How is sucralfate taken
On empty stomach
What drugs have a reduced bioavailability when taken with sucralfate
Warfarin Dig Synthroid Phenytoin Tetracycline Quinolones Theophylline
What is misoprostol
Synthetic PG
Misoprostol ADRs
Diarrhea Ab cramping Nausea Flatulence HA
Intra-abdominal infection
Peritoneal inflammation in response to micro-organisms resulting in purulence in the peritoneal cavity
Uncomplicated intra-abdominal infection
Intramural inflammation of the GI tract without anatomic disruption
Complicated intra-abdominal infection
Expands beyond the source organ into the peritoneal space
Types of complicated intra-abdominal infection
Primary peritonitis
Secondary peritonitis
Primary peritonitis
Also known as spontaneous bacterial peritonitis (SBP)
Bacterial translocation across the gut wall from the bloodstream, lymphatic system, indwelling peritoneal dialysis catheter, or fallopian tubes
Secondary peritonitis
Microbial contamination through a perforation, laceration or necrotic segment of the GI tract
Which peritonitis is often monomicrobial
Primary
Patients with cirrhosis
Patients on peritoneal dialysis
Which bugs affect patients with cirrhosis?
G-
Enterococcal
Which bugs affect patients on peritoneal dialysis
S aureus
Which peritonitis is commonly polymicrobial
Secondary
Which bugs are common for secondary peritonitis in the stomach and duodenum?
Strep
Lactobacillus
Which bugs are common for secondary peritonitis in biliary infections
E coli
Klebsiella
Enterococcus
Which bugs are common for secondary peritonitis in the small intestine
E coli Klebsiella Lactobacillus Strep Diptheroids Enterococcus
Which bugs are common for secondary peritonitis in distal ileum and colon
Bacteroides fragillis Clostridium E col Enterobacter Klebsiella Peptostreptococci Enterococcus
Examples of secondary peritonitis
Appendicitis (most common) Diverticulitis IBD Salpingitis Biliary tract infections Necrotizing pancreatitis Neoplasms causing intestinal obstruction or perforation Mechanical GI obstructions (hernias, adhesions) Blunt abdominal trauma with rupture of intestine Penetrating abdominal trauma Endoscopy induced intestinal perforation Abdominal surgery complications
Tertiary
A persistent or recurrent infection at least 48 hours after appropriate management of a primary OR secondary peritonitis
Clinical presentation of intra-abdominal infections
Non-specific physical findings Ab pain Constipation Diarrhea Ab distention
Management of intra-abdominal infections
Resuscitation
Source control
Abx treatment
Resuscitation in intra-abdominal infections
Fluid replacement with isotonic IV fluids or blood products (if needed)
hemodynamic support
Source ontrol in intra-abdominal infections
Drainage of abscess
Debridement if necessary
Intra-abdominal infections abx treatment approaches
Treat until resolution of fever, leukocytosis, and/or ileus
Fixed duration 3-5 days
Which abx have we seen icnreasing resistance?
Bacteroides fragillis and E coli to clindamycin and cefotetan
When should empiris FQs and 1st and 2nd gen ceph be avoided until?
Antibiograms show > 80-90% susceptibility
What is the DOC for pathogens producing extended spectrum beta-lactamases?
Carbapenems
What is the most common intra-abdominal surgical emergency?
Appendicitis
How is appendicitis diagnosed?
Diagnosed with physical s/sx and CT imaging
What is surgical intervention for appendicitis reserved for?
Complicated infections with abscess or rupture
Abx for appendicitis
Pip/tazo
Cefepime plus metro
Carbapenem
Duration of abx in appendicitis
3-5 days
Diverticulitis treatment
Bowel rest
Abx
Diverticulitis abx for mild cases
PO abx (7-14 days)
Cipro (or levaquin) + metro
Bactrim plus metro
Diverticulitis abx for severe cases
Pip/tazo
Carbapenem
Spontaneous bacterial peritonitis (SBP) in peritoneal dialysis diagnosis
Clinical features and analysis of dialysate
Presume pt is infected if clinical features present
Should be treated empirically while waiting for results of dialysate analysis
SBP in peritoneal dialysis treatment
Empiric treatment should cover G+ (vanc or 1st gen ceph) and G- (AGs) organisms
SBP in peritoneal dialysis route of administration
Intraperitoneal
Give continuous or intermittent
Abx are stable for variable times after being added to the PD solution
Some abx can be mixed in the bag but not the same syringe
Treatment for small/large bowel perforation
Pip/tazo
Cefepime plus metro
Carbapenem
Treatment for rupture spleen
3rd or 4th generation cephalosporin
Vanc if MRSA suspected
