Dyspepsia Flashcards

1
Q

what is dyspepsia

A

bad digestion
epigastric pain lasting a month
can be associated wiht other upper GI symptoms as long as epigastric pain is the primary concern

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2
Q

2 main dyspepsia categories

A

organic - peptic ulcer disease, gerd, barretts esophagus, cancer
functional - no cause we can find

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3
Q

what is peptic ulcer disease

A

group of ulcerative disorders that are dependent on acid and pepsin for their production

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4
Q

common symptoms of peptic ulcer disease

A

episodic epigastric pain

heartburn

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5
Q

cause of PUD

A

imbalanc ebetween mechanisms of ijury and protection

could be injured by acid, enzymes, toxins, drugs, bacteria

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6
Q

complications of PUD

A

perforation
penetration
hemorrhage
gastric outlet obstruction

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7
Q

risk factors for PUD

A

hpylori

nsaids

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8
Q

PUD and GERD treatment goals

A

symptom relief
accelerate healing
prevent and treat complications
prevent recurrence

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9
Q

PUD non pharms

A

avoid large bedtime meals (increases acid)

avoid nsaids, smoking alcohol, caffiene affect healing

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10
Q

use of antacids in PUD

A

symptomatic relief due to compliance issues

give 1 and 3 hr post meals and at night

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11
Q

cautions with antacids

A

sodium bicarb in CHF/cirrhosis
magnesium based in dialysis
constipation, diarrhea, drug interactions

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12
Q

role for H2 blockers

A

take long to work so not much use PPI much better

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13
Q

should you bother increasing dose of omeprazole

A

no only decreases acid by further 6%

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14
Q

efficacy of proton pump inhibitors

A

gold standard for ulcers

also role in hpylori eradication

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15
Q

what is considered refractory PUD

A

fail 8 week therapu in dunodenal
12 week in gastro
usually on BID PPI for recurrence

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16
Q

new recommondations for eradication of hpylori is

A

quad based therapy becuase of clarithromycin resistance in manitoba (PPI +amox/bismuth + metronidazole + tetracycline)

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17
Q

use for chronic prophylaxis of PUD

A

maybe in patients with severe PUD complication or significant comorbidity
if another blled could be catastrophic

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18
Q

PPI chronic use has what effect

A

increases gastrin level 2x which has proliferative effects on both ECL and parietal cells causing hyperplasia and hypertrophy(rebound hypersecretion)
cancres not seen in humans

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19
Q

PPI adverse effects

A

infections - cdiff, pneumonia
fractures
interaction with clopidogrel?

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20
Q

what is GERD

A

retrograde spilling of the gastric contents into the esophagus
chronically relapsing disorder

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21
Q

classical symptoms of gerd

A

regurgitation
heartburn
dysphagia
odynophagia ( pain when swallowing)

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22
Q

atypical gerd symptoms

A
coughing 
wheezing 
globus sensation 
laryngitis
chest pain 
dental erosions
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23
Q

gerd risk factors

A

pregnnacy
obesity
increased age
hiatus hernia

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24
Q

complications of gerd

A

esophagitis and esophageal bleeding
esophageal stricture
barretts esophagus - very rare
esophageal cancer - very rare

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25
Q

what is non erosive reflux disease

A

symptoms but no active imflammation

26
Q

GERD and functional dyspepsia non pharms

A
smaller more frequent meals 
avoid smoking 
reduce alcohol and caffiene 
obtain ideal weight 
stress reduction 
blocks of wood at the head of the bed
27
Q

use of antacids in gerd

A

symptom relief, breakthrough

give 1 and 3 hours post meals and at night as needed

28
Q

how do prokinetics work

A

increase LESP and accelerate gastric emptying

29
Q

recommendation for prokinetics in gerd

A

best agent cisapride but risk of cardiac arrythmias

metoclopramide good for nause but long term AE

30
Q

gold standard for gerd

A

PPI

31
Q

what is functional dyspepsia

A

dyspepsia for 3 months with no clearly identifiable pathogen
motor and sensitivity changes in GI tract?

32
Q

symptom subgroups of dyspepsia

A

ulcer like
dysmotility like
reflux like

33
Q

functional dyspepsia GOT

A

symptom relief

prevent recurrence

34
Q

role of antacids in functional dyspepsia

A

limited to no benefit

35
Q

role of PPI in functional dyspepsia

A

little more of an effect than placebo

limit to once daily dosing

36
Q

best evidence for treatment of functional dyspepsia

A

TCAs

consider if no benefit from PPI

37
Q

prokinetic role in functional dyspepsia

A

found more effective than placebo but risk with long term use

38
Q

how long to determine benefits of therapy in functional dyspepsia

A

4 weeks

39
Q

signs of serious GI disease

A
over 50 
vomit, bleeding
anemia
weight loss
dysphagia
anorexia
jaundonce
cancer history 
multiple treatment failures
recent dramatic changes in symptoms
40
Q

cancer risk is higher where

A

SE asia

south america

41
Q

recommend endoscopy for who

A

> 60 higher risk of malignancy

<60 with alarm features not recommended

42
Q

treatment duration fo r h pylori

A

14 days

43
Q

recommendation for <60with dyspepsia

A

test and treat for hpylori

44
Q

who should be tested for hpylori eradication and how

A

serious GIi bleeding or other complications

urea breath test or stool antigen test

45
Q

on demand dosing benefit

A

therapy that meets patients needs
obtain a similar outcome at less cost
potential for reduced adverse effects

46
Q

on demand dosing risk

A

under treatment of disease (symptoms dont corelate with endoscopic findings)
long term risk of complications unknown

47
Q

4 things that warrant continuing a PPI

A

barretts esophagus
chronic NSAID user with bleeding risk
severe esophagitis
documented history of bleeding GI ulcer

48
Q

in which situations would you recommend deprescribing (decrease dose, use on demand, or stop)

A

mild-mod esophagitis
GERD treated for 4-8 weeks
peptic ulcer disease treated 2-12wks
ICU stress ulcer prophylaxis beyond ICU admission
uncomplicated hpyolri treated 2 wks and asymptomatic
upper GI symptoms without endoscopy asymptomatic for 3 days

49
Q

what do you monitor for at 4 and 12 weeks of deprescribing

A

heartburn, regurgitation, dyspepsoa, epigastric pain

loss of appetite, weight loss, agitation

50
Q

non drug options to assist in deprescribing

A

avoid meals 2 hours before bedtime
elevate head of bed
weight loss
avoid dietary triggers

51
Q

alternative way to manage occasional symptoms

A

antacid, H2blocker

PPI, aliginate prn

52
Q

what to do is symptoms relapse after deprescribing

A

if persist 3-7days test and treat for hpylori and consider return to previous dose

53
Q

what is rebound hypersecretion

A

compensatory effect from PPIs blocking the proton pump
stimulastes gastrin inducing ECL and parietal cells to try produce acid
was linked to cancer in rats

54
Q

how to manage rebound hypersecretion

A

wean over 1-3 months

55
Q

are all PPIs equally effective

A

yes

56
Q

causes of drug induced esophagitis

A
tetracycline 
doxycycline 
slow release potassium 
quinidine
ASA and NSAIDs
alendronate
57
Q

treatment algorithm for functional dyspepsia hpylori negative

A

PPI —- TCA —- prokinetic —- pharmacotherapy

58
Q

typical resolution of ulcer symptoms

A

1 week

59
Q

how can nsaid use be continued after an ulcer

A

if duodenal can put back on NSAID after health but with gut protection
gastric ulcer try to keep off as long as possible
celecoxib and a PPI the best protection

60
Q

why do we take a PPI before food

A

proton pumps are normally sitting back but when we eat they get to the wall of the stomach and start pumping out acid, want the PPI in board when they are in this state