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PHAR 255 > Peptic Ulcer > Flashcards

Peptic Ulcer Flashcards

1
Q

Main causes of peptic ulcers?

A

NSAID induced
H. pylori

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2
Q

Main alarm sx of peptic ulcers?

A

VBAD

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3
Q

WHo needs an endoscopy?

A

new onset of sx, >50yrs
any VBAD sx
refractory sx
at risk for barrett’s esophagus

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4
Q

What is peptic ulcer disease?

A

any breach in mucosa of digestive tract, majority are in gastric and duodenal ulcers

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5
Q

Difference between ulcer and gastric erosion?

A

gastric erosion is first step of ulcer formation; erosion is damage but isn’t through mucosa fully whereas ulcers are.-

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6
Q

Causes of an Ulcer?

A

imbalance of aggressive and protective factors;
aggressive facotr incluce:
- NSAIDs*
- H pylori*
- Pepsin
- Physiologic stress
- acid
- ethanol
- smoking?
- psychological stress?
Protective factors include:
- Gastric mucosa
- HCO3
- prostaglandins
- mucosal blood flow
- epithelial cell regenration

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7
Q

How do NSAIDs cause peptic ulcers?

A

decrease COX1 therfore decrease prostiglandins –> predispose mucosa to injury

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8
Q

Do the presence of dyspeptic sx and severity correlate to peptic ulcers?

A

poorly correlate –> can be on NSAID for years and have nothing then ulcer forms or damages enough to have complications

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9
Q

What is important when determining risk of NSAID induced peptic ulcers?

A

dose and duration, but a short therapy can still cause an ulcer

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10
Q

How does mucosa injury progress?

A

positive feedbackloop ish;
mucosa damage –> microscopic damage –> tissue damage
erosions –> ulcers –> perforation

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11
Q

WHich NSAIDs induce ulcers?

A

ALL can trigger; potent COX1 highest risk
COX2 selective may have protective role in stomach so, COX2 selective can be harmful as well

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12
Q

Highest risk NSAIDs for peptic ulcers?

A

Piroxicam
Ketorolac

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13
Q

Low risk NSAIDs for peptic ulcers?

A

Celecoxib (very low)
Ibuprofen

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14
Q

NSAID induced peptic ulcer risk factors?

A

history of uncomplicated ulcer
age> 60 (+++risk of >70)
high dose or multiple NSAID use
Concomitant ASA, GCs, anticoagulants, antiplatlets, SSRIs (each drug counts as 1 risk factor)
History of CVD

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15
Q

High risk NSAID induced PUD?

A

complicated ulcer history or >=3 risk factors

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16
Q

Moderate risk NSAID induced PUD?

A

1-2 risk factors

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17
Q

Low risk NSAID induced PUD?

A

No risk factors

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18
Q

H. pylori bacteria type?

A

gram negative rod

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19
Q

How is H. pylori spread?

A

fecal-oral route

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20
Q

Risk factors of H. pylori colonization?

A

crowded living conditions
unclean water
raw veggies

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21
Q

H. pylori enzymes produced?

A

urease –> converts urea to ammonia
phospholipase and catalase –> antioxidant effect preventing immune system from detecting bacterium

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22
Q

How does H. pylori end up causing damage to gastric epithelium?

A

direct cytotoxic effect of bacteria
renders udnerlying mucosa more vunerable to acid damage
high level of ammonia:
- prevents detection of acidity
- direct toxic effect on epithelial cells
Promotes cytokines and inflammation –> increases permeability of cells –> acid more easily able to cause damage to tissues

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23
Q

what % of ulcers are asymptomatic?

A

70%

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24
Q

Symptoms of peptic ulcers?

A

dyspeptic sx
duodenal ulcer –> food intially relieves pain, then 2-5 hrs after meal pain and at night
Gastric –> immediately worsened by food

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25
Q

Complications of an ulcer?

A

QoL decrease
GI bleeds
perforations and fistulations
gastric outlet obstruction
mortality increase

26
Q

Symptoms of PUD complications of bleeding?

A

N&V
Hematemesis
Melena
orthostatic Hypotension
RBCs in stool if massive bleed (very red flag)

27
Q

Symptoms of PUD complications of obstruction?

A

N&V
early satiety
bloating
indigestion
anorexia
wt loss

28
Q

Symptoms of PUD complications of perforation or fistula occurs?

A

Sudden change in sx pattern
halitosis ( bad breath)
post-prandial diarrhea
wt loss

29
Q

How to diagnose PUD?

A

endoscopy gold standard but, remember who is indicated, cost on HC system

30
Q

Who should be tested for H. pylori?

A

active or past history of PUD
history of H. pylori and recurrent sx
uninvestigated dyspepsia sx otehr than GERD or no NSAID use (guidlines could be changing)
Unexplained iron defeciency
ongoing dyspeptic sx despite PPI use
Potentially if considering chronic NSAID use (including ASA)

31
Q

What must be done before H. pylori testing?

A

d/c of PPI x 2 weeks
d/c of bismuth and antibiotics x 4 weeks

32
Q

Most common H. pylori testing?

A

urea breath test; accurate and cheap

33
Q

Risk that increase recurrence of H. pylori PUD?

A

NSAIDs
smoking
alcohol use
long standing PUD
H. pylori suboptimal eradication or reinfection

34
Q

Goals of tehrapy for PUD treatment?

A

relieve dyspepsia
heal ulcer
prevent complications
pevent recurrence
implement lifestyle changes

35
Q

Treatment of NSAID induced PUD?

A

d/c NSAID if possible
begin ulcer healing therapy;
- PPI standard dose***
- H2RA high dose
- Misoprostol
H. pylori testing
Consider secondary prevention for some pts

36
Q

Duration of therapy for NSAID induced PUD therapy?

A

Gastric ulcer: 8-12 weeks
Duodenal ulcer: 4-8 weeks

37
Q

Strategies for secondary prevention for NSAID induced ulcer?

A

lower NSAID dose
switch to celecoxib
add long-term PPI
add misoprostol (limited b/c poor efficacy)

38
Q

Efficacy of secondary prevention strategies for NSAID induced PUD?

A

Celecoxib + PPI > NSAID + PPI = celecoxib alone > NSAID + misoprostol > NSAID + H2RA

39
Q

Secondary prevention of NSAID induced PUD indicated for?

A

Continued NSAID use
Giant ulcer(>1cm diameter) and age > 50
H. pylori resistance
refractory peptic ulcer
recurrent peptic ulcer

40
Q

Primary prevention of NSAID induced PUD indicated for?

A

High risk or past complicated ulcer
strongly considered if moderate risk

41
Q

Primary prevention strategies?

A

Same as secondary except Misoprostol is = PPI

42
Q

Misoprostol MOA?

A

prostaglandin analogue –>
increases gastric mucous,
bicarb secretion,
inhbition of basal and nocturnal gastric acid secretion

43
Q

Misoprostol indications for PUD?

A

treatment of duodenal ulcer
Primary prevention of NSAID induced ulcers

44
Q

WHy is misoprostol’s use limited?

A

QID dosing (poor adherence)
SEs of diarhea, abdominal pain, and dyspepsia

45
Q

H. pylori ulcer treatment?

A

Quadruple therapy
Longer duration favoured over short durations

46
Q

Drugs used in H. pylori eradication treatment?

A

PPI standard doses
Bismuth (pepto)
Amoxicillin
Metronidazole
tetracycline
clarithromycin
levofloxacin
rifabutin

47
Q

First line H. pylori options?

A

PPI + Bismuth + Metronidazole + tetracycline

PPI + amoxicillin + metronidazole + clarithromycin

48
Q

Second line treatment of H. pylori?

A

PPI + amox + Levofloxacin +/- bismuth

49
Q

Last line treatment of H. pylori?

A

PPI + amox + rifabutin

50
Q

PBMT advantages? Disadvantages? duration? dosing sig?

A

ADvantages:
- highly effective
- ovecomes resistance
- preferred if penicillin allergy
similar tolerability to triple therapy
Disadvantages:
- high pill burden
- Metronidazole interacts w/ alcohol
14 day duration
PPI - BID
Bismuth - QID
Metro - TID or QID
tetra - QID

51
Q

Main benefit to taking PAMC?

A

simplified more adherence b/c all drugs are BID

52
Q

Disadvantages of PAMC?

A

previous use of antibiotic may impact efficacy/ resistance (clarithromycin***)
more GI AEs
Penicillin allergies

53
Q

Why are triple therapy options restricted?

A

b/c ony to be used in >15% resistance which is not known so Quad therapy should be recommended b/c less failure rate

54
Q

Sequential therapy regiment?

A

PPI BID + Amox BID x 5 days
PMC x 5 days

55
Q

How to choose a regiment for H. pylori treatment?

A

use local resistance rates (usually not known)
follow guideline recommendations
pt factors:
- allergies**
- recent antibiotic use**
- alcohol use
- DIs
- adherence/ pill burden
- anticoagulants or antipaltelets use if consideringbismuth (low risk can still be used)

56
Q

SE of H. pylori treatment?

A

GI
Diarrhea
Headache
Dizziness
(each antibiotic has unqiue SEs)

57
Q

What is one of the most important things to discuss w/ a pts when counseling quad therapy for H. pylori?

A

ADHERENCE
–> missing even a few doses can cause treatment failure resulting in 14 days of another quad therapy

58
Q

H. pylori canadian guidelines flow of treatment?

A
  1. PAMC –> PAL –> PBMT –> PAR
  2. PBMT –> PAL –> Optimized PBMT –> PAR
59
Q

Causes of H. pylori treatment failure?

A

Poor adherence***
incorrect regiment used
high local resistance

60
Q

Who is recommended to get confirmation of eradication testing for H. pylori? When tested and what test?

A

complciated duodenal ulcer
gastric ulcer
gastric cancer
persistent sx
Test 4 weeks after therapy completion, fecal stool antigen test is optimal for confirmation

61
Q

Use of PPI after H. pylori eradication?

A

duodenal ucler: genrally not indacted, possibly 2 weeks
gastric ulcer: continue PPI for 8 weeks
Continued PPI should be reduced to once daily

62
Q

Probiotics place in P. pylori ulcer management?

A

meh; wont hurt to try

PHAR 255 (14 decks)

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