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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
What are some long term risks associated with PPIs
Increased risk for CDiff bacterial pneumonia acute intestinal nephritis CKD Gastric polyps
26
what complications are associated with PUD
bleeding perf obstruction
27
What is the mainstay treatment for PUD
omeprazole
28
What is the triple therapy for H. Pylori and how long is it given
Clarithromycin +Amox (metronidazole if PCN allergy) +PPI 2 week duration
29
What is a quadruple therapy for H. Pylori
Bismuth subsalicylate + tetracycline + Metronidazole + PPI
30
When should H. Pylori eradication be confirmed
at least 2 weeks off of PPI
31
What is the MOA of Bismuth
stimulates prostaglandin/ mucus /bicarb production in the stomach reduces inflammation mild antimicrobial activity against H. Pylori
32
When is Bismuth used with H.Pylori
component of the quadruple therapy
33
What is the combo Bismuth therapy
bismuth metronidazole tetracycline
34
What are the side effects of the bismuth combo therapy
Diarrhea/ abnormal stools/ nausea/ headache photosensitivity
35
What are the side effects associated with Bismuth
Black stools & black tongue (reversible) Bismuth neurotoxicity
36
What is Bismuth neurotoxicity
encephalopathy aseptic meningitis seizures
37
What is the BBW with the bismuth combo therapy
Metronidazole is carcinogenic in mice/rats... unknown in humans
38
What is the MOA for Misoprostol
Synthetic prostaglandin E1 analog that inhibits acid secretion by reducing the ability of the parietal cells to respond to histamine
39
What is misoprostol used for
prevention of NSAID induced gastric ulcers
40
What is the BBW with misoprostol
contraindicated in pregnancy / women of child bearing age. May cause birth defects, premature birth, abortion, uterine rupture
41
What are pro kinetic agents for the GI system
Metoclopramide dompreidone erythromycin
42
What is the MOA of metoclopramide
Dopamine antagonist. Enhances upper GI tract response to Ach to enhance motility, increase colon motility, and shorten transit time
43
When is metoclopramide indicated
gastroparesis persistent GERD N/V
44
What is the BBW associated with metoclopramide
irreversible tardive dyskenesia
45
What is the MOA of Domperidone
peripheral dopamine agonist (does not cross BBB) increases esophageal peristalsis, gastric motility, and gastric emptying decreases small bowel transit time
46
When is domperidone utilized
motility disorders N/V gastroparesis
47
When is domperidone contraindicated
Pt. on other QT prolonging agents prolactinomas
48
What is the MOA of erythromycin
macrolide motilin agents and increases gastric contraction
49
When is erythromycin used with GI issues
gastroparesis as an abx *4 week max d/t tachyphylaxis
50
When is erythromycin contraindicated with GI disorders
Myasthenia gravis CYP3A4 enhancers
51
What is the MOA of neostigmine
acetylcholinesterase inhibitor
52
When is neostigmine used with the GI system
acute colonic pseudo-obstruction *primarily myasthenia gravis urinary retention post op bladder distention
53
How do you treat an IBD flare up
glucocorticoids aminosalicylates
54
What glucocorticoids can be used for IBD exacerbation
prednisone budesonide hydrocortisone
55
How do you maintain mild IBD
aminosalicylates -sulfasalazine mesalamine 5-ASA *specifically for UC)
56
Which IBD patients need biologics for IBD treatment
Severe IBD (CD+UC)
57
What biologics are used for IBD
azathiopring adalimumab inflixumab
58
What immunomodulators can be used for IBD and who uses them
azathioprine 6-MP methotrexate *moderate maintenance therapy for crohns (+/- UC)
59
What is the MOA for aminosalicylates (5-ASA)
Work topically on affected/inflamed areas of mucosa *anti-inflammatory and immunosuppressive activity
60
What is the precursor of 5-ASA
Sulfasalazine *originally an RA treatment
61
When are 5-ASAs typically used
mild-moderate UC (flares and maintenance mild colonic crohns disease (distal)
62
How do AZO work
azo bond prevents absorption of the drug when it reaches lower GI, bacteria cleave the molecule and release the 5-ASA
63
How do mesalamine compounds work
Has special resins/coatings to release the active form once in the lower GI tract
64
What are some side effects of AZO compounds
oligospermia in men (reversible) bone marrow suppression impairs folate absorption **need folate supp
65
What are the side effects of mesalamine
nephrotoxicity/ interstitial nephritis
66
What is the MOA for Thiopurines
immunosuppression
67
When are thiopurines used
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
What is the BBW for thiopurines
chronic immunosuppression increases the risk of malignancy
69
What can you not take azathioprine with and why
allopurinol because it can lead to leukopenia
70
What is the MOA of methotrexate
immunosuppressant and anti-inflammatory for IBD *cytotoxic in high doses and immunosuppressive in low doses
71
When is methotrexate used with IBD
to induce and maintain remission in crohns
72
What is the BBW with methotrexate
Malignancy lymphomas, lung disease, PJP, hepatotoxicity, teratogenic, unexpected severe bone marrow suppression and aplastic anemia
73
What are side effects of methotrexate
alopecia bone marrow suppression mucositis SJS/TEN
74
How do TNF inhibitors help with IBD
help mitigate overactive immune response in crohns and UC
75
What is the MOA of biologics for IBD
bind and sequester TNF to decrease inflammatory response
76
What BBW is associated with biologics
serious infections from immunosuppression
77
What biologics for IBD are administered SQ
certolixumab adalimumab
78
What is the MOA of glucocorticoids for IBD
inhibits production of inflammatory cytokines and inhibits migration of inflammatory cells to affected area

Pharm 3 module 2 (2 decks)

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