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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
Q

What are the symptoms of PUD complications if bleeding?

A

nausea and vomiting
hematemesis
melena
orthostatic hypotension
red blood in stool if massive bleed (hemtochezia)

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24
Q

What are the symptoms of PUD complications if there is an obstruction?

A

NV
early satiety
bloating
indigestion
anorexia and weight loss

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25
Q

What are the symptoms of PUD complications if there is a perforation or fistula?

A

sudden change in symptom pattern
halitosis
post-prandial diarrhea
weight loss

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26
Q

What is the gold standard for diagnosis of PUD?

A

endoscopy

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27
Q

When is endoscopy indicated?

A

new onset symptoms (other than reflux/heartburn) > 50 (>60) or red flag symptoms
any alarm features
refractory GERD
at risk for Barretts esophagus

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28
Q

What are the testing methods for H.pylori?

A

endoscopy
-biopsy urease
-histology
-bacterial culture
urea breath testing
stool antigen assay
serology

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29
Q

What must be done prior to testing for H.pylori?

A

d/c PPI x 2 weeks; bismuth and antibiotics x 4 wks

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30
Q

What are the recurrence rates of PUD?

A

10%

31
Q

What are the indications for H.pylori testing?

A

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
Q

What are the goals of therapy for PUD?

A

relieve dyspepsia
heal the ulcer
prevent complications
prevent recurrence
implement lifestyle changes (trigger foods, alcohol, smoking)

33
Q

What is the treatment of an NSAID-induced ulcer?

A
  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
Q

What is the duration of treatment with a PPI, high dose H2RA or misoprostol for an NSAID-induced ulcer?

A

gastric ulcer: 8-12 weeks
duodenal ulcer: 4-8 weeks

35
Q

What are the strategies for secondary prevention of NSAID-induced PUD?

A

lower NSAID dose
switch to celecoxib
add long-term PPI
add misoprostol

36
Q

What is the order of efficacy for the secondary prevention strategies of NSAID-induced PUD?

A

celecoxib + PPI > NSAID + PPI = celecoxib mono > NSAID + misoprostol > NSAID + H2RA

37
Q

What are the indications for secondary prevention of NSAID-induced PUD?

A

continued NSAID use
giant ulcer and age > 50 years
H.pylori resistance
refractory peptic ulcer
recurrent peptic ulcer

38
Q

When is primary prevention of NSAID-induced PUD indicated?

A

high risk (> 3 risk factors) or past complicated ulcer
strongly considered if moderate risk (1-2 risk factors)
not indicated for low risk

39
Q

What are the strategies for primary prevention of NSAID-induced PUD?

A

same as secondary, but misoprostol = PPI

40
Q

What is the MOA of misoprostol?

A

a prostaglandin analogue leading to an increase in:
-gastric mucous
-bicarbonate secretion
-inhibition of basal and nocturnal gastric acid secretion

41
Q

What are the PUD indications for misoprostol?

A

treatment of duodenal ulcer
prevention of NSAID-induced ulcers (mostly primary)

42
Q

How many times a day is misoprostol dosed for PUD?

A

QID

43
Q

What is a warning of misoprostol?

A

occupational hazard

44
Q

What are the common side effects of misoprostol?

A

diarrhea and abdominal pain
dyspepsia

45
Q

What are the drug interactions of misoprostol?

A

Mg+ antacids enhance GI ADRs of misoprostol

46
Q

Who should be offered treatment for H.pylori?

A

all patients testing positive for H.pylori

47
Q

What are the drugs used in eradication regimens for H.pylori?

A

PBAMTCLR
PPIs standard doses
bismuth (subsalicylate, subcitrate not available)
amoxicillin
metronidazole
tetracycline
clarithromycin
levofloxacin
rifabutin

48
Q

What are the first line options for H.pylori eradication?

A

PBMT - bismuth quadruple therapy
PAMC - non-bismuth quadruple therapy

49
Q

What are the second line options for H.pylori eradication?

A

used if treatment failure or intolerant to 1st line
-PAL or PABL
-PBMT if not already attempted

50
Q

What is the last line option for H.pylori eradication?

A

PAR

51
Q

What are the restricted options for H.pylori eradication?

A

triple therapy, only use if local resistance < 15%
-PAC
-PMC
-PAM

52
Q

Which form of therapy is not recommended for H.pylori eradication?

A

sequential therapy

53
Q

What is the role of bismuth in PBMT?

A

can decrease resistance

54
Q

What are the advantages of PBMT?

A

highly effective
overcomes resistance
preferred if penicillin allergy
similar tolerability to triple therapy

55
Q

What are the disadvantages of PBMT?

A

high pull burden
metro and alcohol
regimen needs proper adherence to work

56
Q

What are the advantages of PAMC?

A

highly effective
simplified regimen (BID compared to QID in PBMT)

57
Q

What are the disadvantages of PAMC?

A

more GI ADRs
clarithromycin resistance may impact efficacy
penicillin allergy
metro and alcohol
no bismuth = more likely for resistance

58
Q

What are the advantages of PAC, PMC, and PAM?

A

best compliance
PAC available as Hp-PAC

59
Q

What are the disadvantages of PAC, PMC, and PAM?

A

high failure rates
cost if Hp-PAC used
metro and alcohol
penicillin allergy (except PMC)

60
Q

What are the advantages of PAL and PABL?

A

important option for previous failure

61
Q

What are the disadvantages of PAL and PABL?

A

lower eradication rates vs 1st line
penicillin allergy

62
Q

What are the advantages of PAR?

A

important option for previous failure
low resistance rates

63
Q

What are the disadvantages of PAR?

A

lower eradication rates vs 1st line
rifabutin expensive
myelotoxicity
use may increase rates of mycobacterium resistance

64
Q

What are the advantages of sequential therapy?

A

may reduce GI ADRs

65
Q

What are the disadvantages of sequential therapy?

A

complexity
high failure rates similar to triple therapy

66
Q

What does sequential therapy look like?

A

PA –> PMC

67
Q

In general, how long is H.pylori eradication therapy?

A

14 days

68
Q

What are some general considerations when selecting a regimen for H.pylori eradication?

A

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
Q

What are the expected side effects of the medications used in H.pylori eradication?

A

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
Q

What are the common reasons for treatment failure of H.pylori eradication regimens?

A

poor adherence
incorrect regimen used
high local resistance

71
Q

When is confirmation of H.pylori eradication recommended?

A

complicated duodenal ulcer
gastric ulcer
gastric cancer
persistent symptoms
four weeks after completion of therapy using fecal stool antigen

72
Q

Are PPIs used as maintenance therapy after H.pylori eradication?

A

duodenal ulcer: generally not indicated, possibly 2 weeks
gastric ulcer: continue PPI for 8 weeks
if continuing, reduce PPI to once daily

73
Q

How frequently are PPIs dosed for H.pylori eradication?

A

BID

74
Q

What is the use of probiotics for H.pylori eradication?

A

may be helpful –> improves efficacy and tolerability
optimal dose, strains and administration not known
not harmful to try

75
Q

What is the MOA of sucralfate?

A

binds to ulcers and forms a protective barrier

76
Q

What is the use of sucralfate for H.pylori?

A

inferior to H.pylori eradication and PPI use
not commonly recommended

PHAR255 (24 decks)

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