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Pharm 3 module 2 > GERD, PUD, IBD, H.Pylori > Flashcards

GERD, PUD, IBD, H.Pylori Flashcards

1
Q

What defenses does the stomach have against gastric acid

A

mucus
bicarb
prostaglandins (stim mucus prod)

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2
Q

What medications are acid blocking

A

PPIs
H2 blockers

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3
Q

What factors contribute to acid related mucosal injury

A

NSAIDs
H. Pylori

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4
Q

What is the MOA of antacids

A

Neutralize acids (raise pH)

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5
Q

What is the indicated use for antacids

A

mild, intermittent heartburn / reflux (<1 episode/week)

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6
Q

What agents are antacids

A

Calcium carbonate
aluminum hydroxide
magnesium hydroxide

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7
Q

What are examples of calcium hydroxide antacids

A

Tums
maalox

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8
Q

What are examples of aluminum hydroxide and magnesium hydroxide

A

Mylanta
Gaviscon

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9
Q

What are the side effects of aluminum based antacids

A

constipation
hypophosphatemia

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10
Q

What are the side effects of calcium based antacids

A

constipation
hypercalcemia
alkalosis
AKI/CKD

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11
Q

What is the MOA of surface agents used in GERD

A

coats the esophageal/gastric mucosa and creates a physical barrier from the acid

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12
Q

When should surface agents be used in GERD

A

swallow after meals and avoid drinking/eating after meals

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13
Q

What agents are surface agents for GERD

A

Sucralfate
Sodium alginate
Bismuth

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14
Q

What are the uses of H2 blockers

A

GERD
Dyspepsia
PUD

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15
Q

What is the MOA for H2 blockers

A

block stimulation of gastric parietal cells by competing with H2 receptors

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16
Q

Which agents are H2 blockers

A

Cimetidine
Ranitidine
Famotidine

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17
Q

What are the side effects of H2 blockers

A

H/A, Dizziness, Diarrhea, constipation

*cimetidine: gynecomastia
*prolonged use may lead to B12 deficiency

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18
Q

What is the MOA of PPIs

A

block gastric H/K ATPase, inhibiting gastric acid secretion

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19
Q

When are PPIs used with GI issues

A

GERD, PUD, H Pylori
dyspepsia

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20
Q

What is the most effective acid suppressing medication

A

PPI

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21
Q

When should PPIs be taken

A

30-60 min before first meal of the day

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22
Q

Why should PPIs be TAPERED off if taken for longer that 6 months

A

To avoid rebound gastric hyper secretion

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23
Q

What agents are PPIs

A

Omeprazole
pantoprazole
lansoprazole
esomeprazole

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24
Q

What drug interactions occur with PPIs

A

Decrease HIV protease inhibitors
increase digoxin concentration
increased methotrexate conc
decrease platelet effect of clopidogrel
decrease PO absorption of iron

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25
Q

What are some long term risks associated with PPIs

A

Increased risk for CDiff
bacterial pneumonia
acute intestinal nephritis
CKD
Gastric polyps

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26
Q

what complications are associated with PUD

A

bleeding
perf
obstruction

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27
Q

What is the mainstay treatment for PUD

A

omeprazole

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28
Q

What is the triple therapy for H. Pylori and how long is it given

A

Clarithromycin +Amox (metronidazole if PCN allergy) +PPI

2 week duration

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29
Q

What is a quadruple therapy for H. Pylori

A

Bismuth subsalicylate + tetracycline + Metronidazole + PPI

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30
Q

When should H. Pylori eradication be confirmed

A

at least 2 weeks off of PPI

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31
Q

What is the MOA of Bismuth

A

stimulates prostaglandin/ mucus /bicarb production in the stomach

reduces inflammation
mild antimicrobial activity against H. Pylori

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32
Q

When is Bismuth used with H.Pylori

A

component of the quadruple therapy

33
Q

What is the combo Bismuth therapy

A

bismuth
metronidazole
tetracycline

34
Q

What are the side effects of the bismuth combo therapy

A

Diarrhea/ abnormal stools/ nausea/ headache
photosensitivity

35
Q

What are the side effects associated with Bismuth

A

Black stools & black tongue (reversible)

Bismuth neurotoxicity

36
Q

What is Bismuth neurotoxicity

A

encephalopathy
aseptic meningitis
seizures

37
Q

What is the BBW with the bismuth combo therapy

A

Metronidazole is carcinogenic in mice/rats… unknown in humans

38
Q

What is the MOA for Misoprostol

A

Synthetic prostaglandin E1 analog that inhibits acid secretion by reducing the ability of the parietal cells to respond to histamine

39
Q

What is misoprostol used for

A

prevention of NSAID induced gastric ulcers

40
Q

What is the BBW with misoprostol

A

contraindicated in pregnancy / women of child bearing age. May cause birth defects, premature birth, abortion, uterine rupture

41
Q

What are pro kinetic agents for the GI system

A

Metoclopramide
dompreidone
erythromycin

42
Q

What is the MOA of metoclopramide

A

Dopamine antagonist. Enhances upper GI tract response to Ach to enhance motility, increase colon motility, and shorten transit time

43
Q

When is metoclopramide indicated

A

gastroparesis
persistent GERD
N/V

44
Q

What is the BBW associated with metoclopramide

A

irreversible tardive dyskenesia

45
Q

What is the MOA of Domperidone

A

peripheral dopamine agonist (does not cross BBB)

increases esophageal peristalsis, gastric motility, and gastric emptying

decreases small bowel transit time

46
Q

When is domperidone utilized

A

motility disorders
N/V
gastroparesis

47
Q

When is domperidone contraindicated

A

Pt. on other QT prolonging agents
prolactinomas

48
Q

What is the MOA of erythromycin

A

macrolide
motilin agents and increases gastric contraction

49
Q

When is erythromycin used with GI issues

A

gastroparesis as an abx
*4 week max d/t tachyphylaxis

50
Q

When is erythromycin contraindicated with GI disorders

A

Myasthenia gravis
CYP3A4 enhancers

51
Q

What is the MOA of neostigmine

A

acetylcholinesterase inhibitor

52
Q

When is neostigmine used with the GI system

A

acute colonic pseudo-obstruction
*primarily myasthenia gravis
urinary retention
post op bladder distention

53
Q

How do you treat an IBD flare up

A

glucocorticoids
aminosalicylates

54
Q

What glucocorticoids can be used for IBD exacerbation

A

prednisone
budesonide
hydrocortisone

55
Q

How do you maintain mild IBD

A

aminosalicylates
-sulfasalazine
mesalamine
5-ASA
*specifically for UC)

56
Q

Which IBD patients need biologics for IBD treatment

A

Severe IBD
(CD+UC)

57
Q

What biologics are used for IBD

A

azathiopring
adalimumab
inflixumab

58
Q

What immunomodulators can be used for IBD and who uses them

A

azathioprine
6-MP
methotrexate
*moderate maintenance therapy for crohns (+/- UC)

59
Q

What is the MOA for aminosalicylates (5-ASA)

A

Work topically on affected/inflamed areas of mucosa
*anti-inflammatory and immunosuppressive activity

60
Q

What is the precursor of 5-ASA

A

Sulfasalazine
*originally an RA treatment

61
Q

When are 5-ASAs typically used

A

mild-moderate UC (flares and maintenance

mild colonic crohns disease (distal)

62
Q

How do AZO work

A

azo bond prevents absorption of the drug

when it reaches lower GI, bacteria cleave the molecule and release the 5-ASA

63
Q

How do mesalamine compounds work

A

Has special resins/coatings to release the active form once in the lower GI tract

64
Q

What are some side effects of AZO compounds

A

oligospermia in men (reversible)
bone marrow suppression
impairs folate absorption

**need folate supp

65
Q

What are the side effects of mesalamine

A

nephrotoxicity/ interstitial nephritis

66
Q

What is the MOA for Thiopurines

A

immunosuppression

67
Q

When are thiopurines used

A

to induce and maintain remission of both UC and Crohns

*good with patients ho cannot maintain remission
*can take 3-6 months to observe effect

68
Q

What is the BBW for thiopurines

A

chronic immunosuppression increases the risk of malignancy

69
Q

What can you not take azathioprine with and why

A

allopurinol because it can lead to leukopenia

70
Q

What is the MOA of methotrexate

A

immunosuppressant and anti-inflammatory for IBD
*cytotoxic in high doses and immunosuppressive in low doses

71
Q

When is methotrexate used with IBD

A

to induce and maintain remission in crohns

72
Q

What is the BBW with methotrexate

A

Malignancy lymphomas, lung disease, PJP, hepatotoxicity, teratogenic, unexpected severe bone marrow suppression and aplastic anemia

73
Q

What are side effects of methotrexate

A

alopecia
bone marrow suppression
mucositis
SJS/TEN

74
Q

How do TNF inhibitors help with IBD

A

help mitigate overactive immune response in crohns and UC

75
Q

What is the MOA of biologics for IBD

A

bind and sequester TNF to decrease inflammatory response

76
Q

What BBW is associated with biologics

A

serious infections from immunosuppression

77
Q

What biologics for IBD are administered SQ

A

certolixumab
adalimumab

78
Q

What is the MOA of glucocorticoids for IBD

A

inhibits production of inflammatory cytokines and inhibits migration of inflammatory cells to affected area

Pharm 3 module 2 (2 decks)

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