PUD Flashcards
(92 cards)
1
Q
Etiologies of PUD
A
H pylori
NSAID induced
Stress ulcers
2
Q
Site for H pylori induced PUD
A
Duodenum > stomach
3
Q
Site for NSAID induced PUD
A
Stomach > duodenum
4
Q
Site for stress induced PUD?
A
Stomach > duodenum
5
Q
What are the sx of h. pylori
A
Epigastric pain common
6
Q
What are the sx of NSAID/stress induced PUD?
A
Asymptomatic
7
Q
H pylori ulcer depth
A
Superficial
8
Q
NSAID induced ulcer depth
A
Deep
9
Q
Duodenal ulcer time for pain
A
Worse at night
10
Q
How does food affect duodenal ulcer
A
Relieved by food
11
Q
How does food affect gastric ulcers
A
Made worse by eating
12
Q
Associated sx of PUD
A
Heartburn, belching, nausea, bloating and anorexia
13
Q
Nationalities most affected by H pylori
A
Africans
Latin Americans
14
Q
Gen propreties of H pylori
A
Spiral shaped
pH-sensitive
G-
15
Q
Where is H pylori typically found
A
Between the mucus layer and surface epithelial cells in the stomach
16
Q
How does H pylori survive in the stomach
A
Urease production - neutralizes acid
Adherence pedestals - prevent being shed with the GI lining
17
Q
How does H pylori cause GI injury
A
Direct damage
Altering host response
Causing hypergasterinemia which leads to increased acid secretion
18
Q
Who do we test for H pylori?
A
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
19
Q
Diagnostic test for H pylori
A
Endoscopic
Urea breath test
Fecal antigen
Ab testing
20
Q
What is tested in endoscopic exams
A
Histology
Rapid urease testing
Culture
Polymerase chain rxn
21
Q
What Antibodies are being tested for in non-endoscopic tests for H pylori
A
Serum IgG to H pylori
Serum Ab to H pylori
22
Q
When is it acceptable to test for H pylori eradications
A
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
23
Q
First line treatment recommendations for H pylori
A
Clarithromycin Triple therapy
Bismuth Quadruple Therapy
Concomitant Quadruple therapy
Antisecretory therapy is generally continued at standard dose after initial 10-14 days of therapy
24
Q
Clarithromycin triple therapy
A
PPI + Amox/flagyl + Clarithromycin x 14 days
Clarithromycin resistance < 15%
25
Bismuth Quadruple therapy
PPI + Bismuth + Flagyl + tetracycline x 10-14 days
26
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
27
How does Bismuth help?
Healing d/t antibacterial and local protective effect, also stimulates PGs
28
What are the salvage therapies?
Bismuth quadruple therapy
Levaquin triple therapy
Concomitant quadruple therapy
Rifabutin triple therapy
29
Levaquin triple therapy
PPI + Levaquin + Amox x 10-14 days
30
Rifabutin triple therapy
Reserved for pts with multiple (> 3) treatment failures
| PPI + Rifabutin + amox x 10 days
31
NSAID ulcers
Dose dependent
| Use of chronic non-selective NSAIDs (also ASA)
32
What is mucosal injury a result of
Direct topical irritation (drugs are acidic in nature)
| Inhibition of protective effects of mucosal PGs
33
What does COX-1 do
Produces PG involved in maintaining GI mucosal integrity and platelet homeostasis
34
What does COX-2 do
Produces PG involved in inflammation
35
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
```
36
Complications of NSAID ulcers
GI bleeds
Perforation into peritoneal cavity
Gastric outlet obstruction
37
non-pharm treatment of NSAID ulcers
Reducing psychosocial stress
Avoid aggravating foods
Smoking cessation
38
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
39
Pharm prevention of NSAID ulcers
Misoprostol or PPI with NSAID or COX-2
| COX-2 alone
40
Why are H2RAs not used for NSAID ulcers?
Only prevent duodenal ulcers
41
Non-salicylates that are non-selective?
```
Indomethacin
Piroxicam
Ibuprofen
Naproxen
Sulndac
Ketoprofen
Ketoralac
Flurbiprofen
```
42
Non-salicylates that are partially selective
Etodolac
Nabumetone
Meloxicam
Diclofenac
43
Non-salicylates that are cox-2 selective
Celebrex
44
Salicylates that are acetylated
ASA
45
Salicylates that are non-acetylated
Salsalate
| Trisalicylate
46
What happens when cox-2s are taken with low dose ASA
Lose gastroprotective effect
47
What is the max total daily dose of celebrex to minimize CV risk?
400mg/d
48
What do the guidelines recommend for patients on low dose ASA and at low-mod risk for GI toxicity
misoprostol or PPI
49
Which drugs decrease plavix effectiveness?
Nexium and prilosec
| inhibit 2C19
50
Which type of ulcers are sucralfate used for
Duodenal ulcers
51
What are the ADRs for sucralfate
Constipation, nausea, dry mouth, dizziness and metallic taste
52
How is sucralfate taken
On empty stomach
53
What drugs have a reduced bioavailability when taken with sucralfate
```
Warfarin
Dig
Synthroid
Phenytoin
Tetracycline
Quinolones
Theophylline
```
54
What is misoprostol
Synthetic PG
55
Misoprostol ADRs
```
Diarrhea
Ab cramping
Nausea
Flatulence
HA
```
56
Intra-abdominal infection
Peritoneal inflammation in response to micro-organisms resulting in purulence in the peritoneal cavity
57
Uncomplicated intra-abdominal infection
Intramural inflammation of the GI tract without anatomic disruption
58
Complicated intra-abdominal infection
Expands beyond the source organ into the peritoneal space
59
Types of complicated intra-abdominal infection
Primary peritonitis
| Secondary peritonitis
60
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
61
Secondary peritonitis
Microbial contamination through a perforation, laceration or necrotic segment of the GI tract
62
Which peritonitis is often monomicrobial
Primary
Patients with cirrhosis
Patients on peritoneal dialysis
63
Which bugs affect patients with cirrhosis?
G-
| Enterococcal
64
Which bugs affect patients on peritoneal dialysis
S aureus
65
Which peritonitis is commonly polymicrobial
Secondary
66
Which bugs are common for secondary peritonitis in the stomach and duodenum?
Strep
| Lactobacillus
67
Which bugs are common for secondary peritonitis in biliary infections
E coli
Klebsiella
Enterococcus
68
Which bugs are common for secondary peritonitis in the small intestine
```
E coli
Klebsiella
Lactobacillus
Strep
Diptheroids
Enterococcus
```
69
Which bugs are common for secondary peritonitis in distal ileum and colon
```
Bacteroides fragillis
Clostridium
E col
Enterobacter
Klebsiella
Peptostreptococci
Enterococcus
```
70
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
```
71
Tertiary
A persistent or recurrent infection at least 48 hours after appropriate management of a primary OR secondary peritonitis
72
Clinical presentation of intra-abdominal infections
```
Non-specific physical findings
Ab pain
Constipation
Diarrhea
Ab distention
```
73
Management of intra-abdominal infections
Resuscitation
Source control
Abx treatment
74
Resuscitation in intra-abdominal infections
Fluid replacement with isotonic IV fluids or blood products (if needed)
hemodynamic support
75
Source ontrol in intra-abdominal infections
Drainage of abscess
| Debridement if necessary
76
Intra-abdominal infections abx treatment approaches
Treat until resolution of fever, leukocytosis, and/or ileus
| Fixed duration 3-5 days
77
Which abx have we seen icnreasing resistance?
Bacteroides fragillis and E coli to clindamycin and cefotetan
78
When should empiris FQs and 1st and 2nd gen ceph be avoided until?
Antibiograms show > 80-90% susceptibility
79
What is the DOC for pathogens producing extended spectrum beta-lactamases?
Carbapenems
80
What is the most common intra-abdominal surgical emergency?
Appendicitis
81
How is appendicitis diagnosed?
Diagnosed with physical s/sx and CT imaging
82
What is surgical intervention for appendicitis reserved for?
Complicated infections with abscess or rupture
83
Abx for appendicitis
Pip/tazo
Cefepime plus metro
Carbapenem
84
Duration of abx in appendicitis
3-5 days
85
Diverticulitis treatment
Bowel rest
| Abx
86
Diverticulitis abx for mild cases
PO abx (7-14 days)
Cipro (or levaquin) + metro
Bactrim plus metro
87
Diverticulitis abx for severe cases
Pip/tazo
| Carbapenem
88
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
89
SBP in peritoneal dialysis treatment
Empiric treatment should cover G+ (vanc or 1st gen ceph) and G- (AGs) organisms
90
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
91
Treatment for small/large bowel perforation
Pip/tazo
Cefepime plus metro
Carbapenem
92
Treatment for rupture spleen
3rd or 4th generation cephalosporin
| Vanc if MRSA suspected
