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Pharm > GI: GERD & PUD > Flashcards

GI: GERD & PUD Flashcards

1
Q

Pathophys of GERD (6)

A
  • decreased salivation
  • decreased basal LES pressure
  • LES relaxation
  • impaired esophageal clearance
  • dec acid clearance
  • delayed gastric emptying
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2
Q

Severity of GERD is related to:

A

amount of time esophagus is exposed to acid and pepsin

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3
Q

aggravating factors for GERD (6)

A 
diet
exercise
pregnancy
tight clothing
cigarettes
alcohol
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4
Q

substances which “cause” GERD

A 
nicpotine
iron
potassium
alcohol
narcotics
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5
Q

complications of GERD (4)

A

Erosive esophagitis
strictures
barrett’s esophagus
esophageal adenocarcinoma

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6
Q

Peptic ulcer disease consists of

2

A

gastric ulcers

duodenal ulcers

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7
Q

duodenal ulcers may result from

A

h pylori

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8
Q

3 common forms of PUD

A

H pylori
NSAID induced
stress related

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9
Q

non pharm therapy for PUD

A

dietary change

lifestyle change

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10
Q

pharmacologic goals for PUD

A

eradicate h pylori
relieve pain
heal ulcers/erosions

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11
Q

how to “heal” ulcers and erosions of PUD

A

PPI

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12
Q

step up management for PUD/GERD

A

treat with OTC antacids and escalate to rx H2 blockers and PPIs

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13
Q

step down treatment for PUD/GERD

A

starting with highest treatment and going down

Rx H2 blockers or PPI first, de escalate.

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14
Q

when is metocloperamide prescribed for GERD?

A

only after confirmed diagnosis

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15
Q

follow up for GERD/PUD

A

additional drugs and lifestyle changes like PPIs or misoprostol

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16
Q

MoA Antacids

3

A
  • neutralize acid by increasing intragastric pH
  • inhibits conversion of pepsinogen to pepsin
  • may also stimulate production of mucosal prostaglandins and LES tone
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17
Q

stimulating prostaglandins: antacids

A

protective to GI mucosa

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18
Q

types of antacids (4)

A

aluminum
magnesium
calcium
bismuth

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19
Q

antacids for ulcers

A

symptomatic relief but do not provide healing

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20
Q

antacid suspensions vs pills

A

suspensions are better

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21
Q

AE aluminum based antacid

A

constipation

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22
Q

AE of magnesium based antacid

A

diarrhea

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23
Q

antacids decrease absorption of drugs which require

A

an acidic environment to work

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24
Q

solution for antacid drug interactions

A

separate drugs and antacids by 2 hours

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25
Q

aluminum plus magnesium

A

maalox

mylanta

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26
Q

calcium carbonate

A

tums

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27
Q

sodium bicarb / bismuth

A

peptic bismol

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28
Q

ae pepto bismol

A

black tongue

dark stool

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29
Q

antacid duration/dosing

A

quick onset, short duration, many doses per day

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30
Q

antacids in renal disease

A

watch for accumulation

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31
Q

histamine-2 receptor antagonists MoA

A

inhibit histamine receptors on parietal cells in stomach, decreasing secretion of H+ ions

32
Q

MoA PPI

A

allow acid to be made but inhibit the final step of secretion by inhibiting H+/K+ ATPase on parietal cells

33
Q

H2 blockers are 1st line for

A

mild to moderaste PUD or GERD

34
Q

H2 blockers/PPI may be used for (6)

A 
tx of ulcers
maintenance of remission
tx of h pylori
tx of nsaid ulcers
erosive/non erosive esophagitis
PUD/GERD
35
Q

h2 blockers or PPI for duodenal ulcer duration of therapy

A

4-8 wks

36
Q

h2 blockers/PPI for gastric ulcers: duration of therapy

A

4-8 wks

37
Q

h2 blockers/PPI for GERD: duration of therapy

A

8 weeks

38
Q

monitoring parameters for h2 blockers (4)

A

relief of symptoms
healing of ulceration
adverse effects
renal function

39
Q

4 common h2 blockers

A

cimetidine
nizatidine
ranitidine
famotidine

40
Q

cimetidine interacts c

A

warfarin
lidocaine
theophylline

41
Q

ranitidine interacts with

A

warfarin

diazepam

42
Q

H2 blockers are first line for _, while PPIs are first line for _

A

h2: mild to mod PUD/GERD
ppi: mod to severe PUD/GERD

43
Q

patient teaching for PPI

A

do not chew or crush

take before 1st meal of day

44
Q

risks in long term use of PPI

A

fractures
hypomagnesemia
c diff

45
Q

short term risk of PPI

A

CAP

46
Q

pt with osteoporosis who needs a PPI

A

limit dose/duration
ensure adequate ca/vit d
bone density screening

47
Q

hypomagnesemia with PPIs

A

comes into play with patients who are on meds which also waste mag

48
Q

PPI drug examples

A 
dexlansoprazole
lansoprazole
omeprazole
rabeprazole
pantoprazole
esomeprazole
49
Q

safest PPI in terms of drug interactions

A

pantoprazole

50
Q

common AE of PPIs (3)

A

nausea
diarrhea
HA

51
Q

metoclopramide MoA

A

stimulates motility of upper GI and increases LES tone

52
Q

metoclopramide increases

A

anal contractions and peristalsis

53
Q

dosing time: metoclopramide

A

30 min before meals and sleep

54
Q

AE of metoclopramide

A 
galactorrhea
diarrhea
EPS
depression
drowsiness
55
Q

metoclopramide is contraindicated with

A

parkinsons

bowel obstruction

56
Q

monitoring for metoclopramide

A

renal function

57
Q

metoclopramide interacts with

A

anti cholinergics
MAOI
levodopa

58
Q

sucralfate MoA

A

promotes mucosal defenses by reacting with HCl in stomach to form a paste and bind to ulcer, allowing it to heal.

59
Q

sucralfate does not

A

have acid-reducing capacity

60
Q

sucralfate should be given as

A

adjunct, not on its own

61
Q

NSAID induced ulcers

A

adverse effect related to inhibition of COX 1 or seen dose dependently with cox 2 inhibitors

62
Q

cox sites

A

cox 1: GI, kidney

cox 2: inflammation sites

63
Q

tx of nsaid induced ulcer

A

dc nsaid, start PPI or H2 blocker.

64
Q

nsaid induced ulcer in the pt who needs to continue nsaid

A

use PPI and see if the NSAID can be changed to either celecoxib or meloxicam

65
Q

prevention of NSAID induced ulcers:

A

misoprostol

PPI

66
Q

using misopristol prophylactically is indicated for patients who are

A

> 60 y/o
prior hx GIB
high dose NSAID therapy
receiving anticoags/steroids

67
Q

MoA misoprostol

A

prostaglandin E1 analog
stimulates production of mucous/HCO3
cytoprotective

68
Q

AE misoprostol (4)

A

diarrhea
abd pain
spontaneous abortion
postmenopausal bleeding

69
Q

Misoprostol is CI in

A

women of childbearing age

70
Q

h pylori and nsaid induced ulcers

A

tx of h pylori is recommended for pts taking NSAIDs who have ulcers and h pylori

71
Q

tx of h pylori (2 options)

A

clarithromycin, amoxicillin, PPI
clarithromycin, metronidazole, PPI

depending on previous hx of macrolide exposure (resistance)

72
Q

if you can’t use clarithromycin in triple therapy, what are your next 3 options for h pylori tx?

A

bismuth quadruple therapy:
bismuth, metronidazole, tetracycline, PPI

concomitant: ppi/clarith/amox/metro

levo triple therapy:
PPI, levo, amoxicillin

73
Q

bismuth quadruple therapy

A

bismuth/metro/tetra/ppi

74
Q

concomitant therapy for h pylori in areas where clarithro resistance is high

A

PPI, clarithro, amox, metro

75
Q

levo triple therapy for H pylori

A

PPI, levo, amox

Pharm (31 decks)

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