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PHAR255 > Peptic Ulcer Disease > Flashcards

Peptic Ulcer Disease Flashcards

1
Q

What is peptic ulcer disease?

A

any breach in the mucosa of the digestive tract

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2
Q

True or false: peptic ulcers are the same as gastric erosions

A

false

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2
Q

What is the pathophysiology of PUD?

A

caused by imbalance of aggressive and protective factors
aggressive factors:
-H.pylori
-NSAIDs
-pepsin
-physiologic stress
-acid
-ethanol
-smoking
-psychologic stress
protective factors:
-gastric mucous
-HCO3
-prostaglandins
-mucosal blood flow
-epithelial cell regeneration

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2
Q

What are the most common types of peptic ulcers?

A

gastric or duodenal ulcers

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3
Q

Is NSAID-induced PUD due to a topical effect of NSAIDs on gastric mucosa?

A

no, its a systemic effect

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4
Q

How do NSAIDs cause PUD?

A

decrease COX-1 activity=decreased PGs=predispose mucosa to injury
acid and pepsin triggers mucosal injury

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5
Q

What is an important determinant of risk of NSAID-induced PUD?

A

dose and duration

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6
Q

True or false: presence of dyspeptic symptoms and severity are well correlated to NSAID-induced PUD

A

false
many cases are asymptomatic

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7
Q

Which NSAIDs can cause PUD?

A

all NSAIDs can be a trigger
-even low dose ASA
-potent COX-1 inhibition has highest risk
-COX-2 may have protective role as well

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8
Q

Which NSAIDs have the lowest GI risk?

A

celecoxib
ibuprofen

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9
Q

Which NSAIDs have average GI risk?

A

ASA low dose
diclofenac
meloxicam
indomethacin
naproxen
ketoprofen

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10
Q

Which NSAIDs have the highest GI risk?

A

piroxicam
ketorolac

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11
Q

Which NSAID is thought to be the safest for GI?

A

celecoxib
-long term use > 6 months shows slight risk increases
-concomitant ASA or anticoagulant increases ulcer risk
-high doses (>400mg/d) reduces COX-2 selectivity

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12
Q

What are the risk factors for NSAID-induced ulcers?

A

history of an uncomplicated ulcer
age > 60 (++ risk > 70)
high dose or multiple NSAID use
concomitant ASA, glucocorticoids, anticoagulants, antiplatelets, SSRI
history of CVD

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13
Q

Differentiate between high, moderate, and low risk of NSAID-induced ulcers.

A

high: complicated ulcer history or > 3 risk factors
moderate: 1-2 risk factors
low: no risk factors

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14
Q

What kind of bacteria is H.pylori?

A

gram negative rod

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15
Q

Where does H.pylori colonize?

A

exclusively colonizes gastric epithelium

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16
Q

What are the risk factors for H.pylori colonization?

A

croweded living conditions
unclean water
raw vegetables

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17
Q

How is H.pylori spread?

A

fecal-oral route

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18
Q

What are the pathogenic mechanisms of H.pylori?

A

direct cytotoxic effect of bacteria
renders underlying mucosa more vulnerable to acid damage
high levels of ammonia:
-prevents detection of acidity
-direct toxic effect on epithelial cells
promotion of cytokines and inflammation

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19
Q

What is responsible for most duodenal and gastric ulcers?

A

H.pylori

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20
Q

Asides from ulcers, what else is H.pylori a common cause of?

A

chronic gastritis
gastric cancer
mucosal-associated lymphoma tissue

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21
Q

What are the clinical symptoms of PUD?

A

70% of peptic ulcers asymptomatic
dyspeptic symptoms
symptoms in relation to food:
-duodenal ulcer: food initially relieves pain, then pain 2-5h after a meal and at night
-gastric ulcer: immediately worsened by food

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22
Q

What are the complications of PUD?

A

quality of life decrease
GI bleeds
perforations or fistulation
gastric outlet obstructions
mortality increase

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23
What are the symptoms of PUD complications if bleeding?
nausea and vomiting hematemesis melena orthostatic hypotension red blood in stool if massive bleed (hemtochezia)
24
What are the symptoms of PUD complications if there is an obstruction?
NV early satiety bloating indigestion anorexia and weight loss
25
What are the symptoms of PUD complications if there is a perforation or fistula?
sudden change in symptom pattern halitosis post-prandial diarrhea weight loss
26
What is the gold standard for diagnosis of PUD?
endoscopy
27
When is endoscopy indicated?
new onset symptoms (other than reflux/heartburn) > 50 (>60) or red flag symptoms any alarm features refractory GERD at risk for Barretts esophagus
28
What are the testing methods for H.pylori?
endoscopy -biopsy urease -histology -bacterial culture urea breath testing stool antigen assay serology
29
What must be done prior to testing for H.pylori?
d/c PPI x 2 weeks; bismuth and antibiotics x 4 wks
30
What are the recurrence rates of PUD?
10%
31
What are the indications for H.pylori testing?
active or past history of PUD history of H.pylori infection and recurrent sx uninvestigated dyspepsia if sx other than GERD or no NSAID use unexplained iron deficiency ongoing dyspeptic sx despite PPI use potentially if considering chronic NSAID use (including ASA)
32
What are the goals of therapy for PUD?
relieve dyspepsia heal the ulcer prevent complications prevent recurrence implement lifestyle changes (trigger foods, alcohol, smoking)
33
What is the treatment of an NSAID-induced ulcer?
1. discontinue the NSAID if possible; consider alternatives 2. begin ulcer healing therapy -PPI standard dose -H2RA high dose -misoprostol 3. H.pylori testing should be done 4. consider on-going secondary prevention for some pts
34
What is the duration of treatment with a PPI, high dose H2RA or misoprostol for an NSAID-induced ulcer?
gastric ulcer: 8-12 weeks duodenal ulcer: 4-8 weeks
35
What are the strategies for secondary prevention of NSAID-induced PUD?
lower NSAID dose switch to celecoxib add long-term PPI add misoprostol
36
What is the order of efficacy for the secondary prevention strategies of NSAID-induced PUD?
celecoxib + PPI > NSAID + PPI = celecoxib mono > NSAID + misoprostol > NSAID + H2RA
37
What are the indications for secondary prevention of NSAID-induced PUD?
continued NSAID use giant ulcer and age > 50 years H.pylori resistance refractory peptic ulcer recurrent peptic ulcer
38
When is primary prevention of NSAID-induced PUD indicated?
high risk (> 3 risk factors) or past complicated ulcer strongly considered if moderate risk (1-2 risk factors) not indicated for low risk
39
What are the strategies for primary prevention of NSAID-induced PUD?
same as secondary, but misoprostol = PPI
40
What is the MOA of misoprostol?
a prostaglandin analogue leading to an increase in: -gastric mucous -bicarbonate secretion -inhibition of basal and nocturnal gastric acid secretion
41
What are the PUD indications for misoprostol?
treatment of duodenal ulcer prevention of NSAID-induced ulcers (mostly primary)
42
How many times a day is misoprostol dosed for PUD?
QID
43
What is a warning of misoprostol?
occupational hazard
44
What are the common side effects of misoprostol?
diarrhea and abdominal pain dyspepsia
45
What are the drug interactions of misoprostol?
Mg+ antacids enhance GI ADRs of misoprostol
46
Who should be offered treatment for H.pylori?
all patients testing positive for H.pylori
47
What are the drugs used in eradication regimens for H.pylori?
PBAMTCLR PPIs standard doses bismuth (subsalicylate, subcitrate not available) amoxicillin metronidazole tetracycline clarithromycin levofloxacin rifabutin
48
What are the first line options for H.pylori eradication?
PBMT - bismuth quadruple therapy PAMC - non-bismuth quadruple therapy
49
What are the second line options for H.pylori eradication?
used if treatment failure or intolerant to 1st line -PAL or PABL -PBMT if not already attempted
50
What is the last line option for H.pylori eradication?
PAR
51
What are the restricted options for H.pylori eradication?
triple therapy, only use if local resistance < 15% -PAC -PMC -PAM
52
Which form of therapy is not recommended for H.pylori eradication?
sequential therapy
53
What is the role of bismuth in PBMT?
can decrease resistance
54
What are the advantages of PBMT?
highly effective overcomes resistance preferred if penicillin allergy similar tolerability to triple therapy
55
What are the disadvantages of PBMT?
high pull burden metro and alcohol *regimen needs proper adherence to work*
56
What are the advantages of PAMC?
highly effective simplified regimen (BID compared to QID in PBMT)
57
What are the disadvantages of PAMC?
more GI ADRs clarithromycin resistance may impact efficacy penicillin allergy metro and alcohol *no bismuth = more likely for resistance*
58
What are the advantages of PAC, PMC, and PAM?
best compliance PAC available as Hp-PAC
59
What are the disadvantages of PAC, PMC, and PAM?
high failure rates cost if Hp-PAC used metro and alcohol penicillin allergy (except PMC)
60
What are the advantages of PAL and PABL?
important option for previous failure
61
What are the disadvantages of PAL and PABL?
lower eradication rates vs 1st line penicillin allergy
62
What are the advantages of PAR?
important option for previous failure low resistance rates
63
What are the disadvantages of PAR?
lower eradication rates vs 1st line rifabutin expensive myelotoxicity use may increase rates of mycobacterium resistance
64
What are the advantages of sequential therapy?
may reduce GI ADRs
65
What are the disadvantages of sequential therapy?
complexity high failure rates similar to triple therapy
66
What does sequential therapy look like?
PA --> PMC
67
In general, how long is H.pylori eradication therapy?
14 days
68
What are some general considerations when selecting a regimen for H.pylori eradication?
follow local resistance rates if known follow guidelines recommendations patient factors -allergies, recent abx use, alcohol use, DI potential, adherence, anticoag/plat if bismuth use
69
What are the expected side effects of the medications used in H.pylori eradication?
metronidazole: metallic taste, alcohol issue tetracycline: photosensivity, esophagitis bismuth: darkening of tongue/stool levofloxacin: CNS, peripheral neuropathy, photosensitivity, tendon rupture, QT prolongation rifabutin: urine discolouration, myelotoxicity
70
What are the common reasons for treatment failure of H.pylori eradication regimens?
poor adherence incorrect regimen used high local resistance
71
When is confirmation of H.pylori eradication recommended?
complicated duodenal ulcer gastric ulcer gastric cancer persistent symptoms *four weeks after completion of therapy using fecal stool antigen*
72
Are PPIs used as maintenance therapy after H.pylori eradication?
duodenal ulcer: generally not indicated, possibly 2 weeks gastric ulcer: continue PPI for 8 weeks if continuing, reduce PPI to once daily
73
How frequently are PPIs dosed for H.pylori eradication?
BID
74
What is the use of probiotics for H.pylori eradication?
may be helpful --> improves efficacy and tolerability optimal dose, strains and administration not known not harmful to try
75
What is the MOA of sucralfate?
binds to ulcers and forms a protective barrier
76
What is the use of sucralfate for H.pylori?
inferior to H.pylori eradication and PPI use not commonly recommended

PHAR255 (24 decks)

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