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Pharm 3 Module 2: GI > drugs to treat GERD, PUD, IBD and h.pylori > Flashcards

drugs to treat GERD, PUD, IBD and h.pylori Flashcards

1
Q

what are the different treatment options for GERD

A

lifestyle modifications
antacids
surface agents
H2receptor antagonists (H2RAs)
proton pump inhibitors (PPI)

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2
Q

what is the MOA of Antacids

A

neutralize acid (raise pH)

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3
Q

what are the uses of antacids

A

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

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4
Q

what is the PK of antacids

A

onset: 5 min
duration: 30-60 minutes

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5
Q

what are the types of Antacids

A

calcium hydroxide (tums, maalox)
aluminum hydroxide (mylanta, gaviscon)
magnesium hydroxide (mylanta, gaviscon)

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6
Q

what are the SE of calcium hydroxide antacids

A

constipation
hypercalcemia
alkalosis
acute or chronic renal injury

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7
Q

what are the SE of aluminum hydroxide antacids

A

constipation
hypophosphatemia
*caustion with renal failure

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8
Q

what are SE of magneisum hydroxide antacids

A

diarrhea,
hypermagnesemia
*caution with renal failure

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9
Q

what is the MOA of surface agents

A

coats esophageal/gastric mucosa, creates physical barrier between mucosa and acid

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10
Q

what are the uses of surface agents

A

short-term management of GERD symptoms (4-8 weeks for duodenal ulcer)
swallow after meals, avoid drinking/eating afterwards

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11
Q

what is the PK of surface agents

A

onset: 5 minutes
duration: 30-60 minutes

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12
Q

what are the types of surface agents

A

sucralfate
sodium alginate
bismuth

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13
Q

what are the SE of sucralfate

A

constipation
aluminum toxicity
*caution with: renal failure, DM

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14
Q

What is the MOA of H2RAs

A

blocks stimulation of gastric parietal cells by competing with histamine H2 receptor

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15
Q

what are the uses of H2RAs

A

GERD, dyspepsia, PUD
-less effective than PPI, may be useful as adjunct
-not effective for H/pylori

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16
Q

what is the PK of H2RAs

A

onset: 2 hours
Duration: 4-10 hours

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17
Q

what are H2RA durgs

A

cimetidine, famotidine

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18
Q

what are the SE of H2RAs

A

HA, dizziness, diarrhea, constipation
cimetidine: gynecomastia
prolonged use(>2yrs) may lead to B12 deficiency

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19
Q

what is the MOA of PPIs

A

block gastric H/K-ATPase, inhibiting gastric acid secretion

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20
Q

what is the uses of PPIs

A

GERD, dyspepsia, PUD, H.pylori
-most effective acid suppressing med

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21
Q

what is the PK of PPIs

A

onset: 1 hour
duration: ~24 hours
admin: 30-60 min before first meal of the day

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22
Q

what are the PPI medications

A

Omeprazole
Pantroprazole
Lansoprazole
Esomeprazole

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23
Q

what are the risks of PPIs

A

available for >25 yo. may double blinded RCTs over years have not supported initial safety concerns
longer term: malabsorption of some minerals and vitamins, increased risk of some diarrheal illnesses, bacterial pneumonia, acute interstitial nephritis (AIN), CKD, gastric polyps

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24
Q

what are the SE of PPIs

A

HA
nausea
abdominal pain
diarrhea

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25
Q

what are drug interactions with PPIs

A

decreased absorption of certain HIV protease inhibitors
increased concentration of digoxin, carbamazepine, theophylline; warfarin, diazepam, phenytoin
Increased MTX concentration/toxicity
decrease anti-platelet effect of Plavix
decrease absorption of PO iron

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26
Q

what is the Tx of PUD

A

avoid offending agents
anti-seretory agent (PPI) = mainstay of tx
test for and treat h.pylori if present

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27
Q

what is the tx regimen for H/pylori

A

2 week duration
Triple therapy: Clarithromycin + amoxicillin + PPI
Quadruple therapy: bismuth subsalicylate + tetracycline + metronidazole + PPI

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28
Q

what is the MOA for Busmuth

A

stimulates prostaglandin/mucous/bicarb production in the stomach
mild antimicrobial activity, specifically against H.pylori
reduces inflammation

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29
Q

what is the SE of bismuth subsalicylate

A

black stools, black tongue (reversible)
bismuth neurotocixity: encephalopathy, asepctic meningitis, seizures

30
Q

what needs to be cautioned with bismuth use

A

other salicylates/ASA/NSAIDs
increased risk of bleeding
neurotoxicity
tinnitus

31
Q

what is the MOA of Misoprostol

A

synthetic prostaglandin E1 analog. Prostaglandins inhibit acid secretion by reducing the ability of parietal cells to respond to histamine

32
Q

what is the use of Misoprostol

A

prevention of NSAID-induced gastric ulcers

33
Q

what is the PK of Misoprostol

A

onset: 30 min
duration: 3 hours

34
Q

what are the SE of misoprotol

A

diarrhea
abd pain
HA
avoid with magnesium containing antacids

35
Q

what are the contraindications with misoprotol

A

caution: can induce uterine contractions
BBW: contraindicated in pregnancy or women of childbearing age. may cause birth defects, premature birth, abortion, uterine rupture

36
Q

what are the Prokinetic agents

A

Metoclopramide, doperidone, erythromycin

37
Q

what is the MOA of Metoclopramide

A

dopamine antagonist (primarily). enhances upper GI tract response to Ach to enhance motility; increases colon motility and shortens transit time

38
Q

what is the use of Metocloramide

A

gastroparesis, peristent GERD, N/V
can be useful for diabetic patients
short term use only given risk of TD: <12 weeks

39
Q

what is the PK of Metoclopramide

A

onset: 30-60 min
duration: 1-2 hours

40
Q

what are the SE of metoclopramide

A

drowsiness
dystonia
HA

41
Q

what are the contraindications with metoclopramide

A

BBW: can cause tardive dyskinesia (irreversible)
CI: Gi hemorrhage, mechanical obstruction, perforation

42
Q

what is the MOA of Domperidone

A

peripheral dopamine antagonist (does not cross BBB). increase esophageal peristalsis, gastric motility and gastric emptying; decreases small bowel transit time

43
Q

what is the use of Domperidone

A

gastroparesis/motility disorders, N/V
-not available in US

44
Q

what are the SE of Domperidone

A

HA, migraines, xerostomia
may increase prolactin levels -galactorrhea, gynecomastia

45
Q

what is the MOA of erythromycin

A

macrolide antibiotic. Motilin agonist - increases gastric contractions (prokinetic)

46
Q

what is the use of Erythromycin

A

gastroparesis (primarily used as antibiotic)
used for max 4 weeks duration d/t tachyphylaxis

47
Q

what are the SE of erythromycin

A

cardiovascular arrhythmias, QTc prolongation
superinfection (C.diff)
major inhibitor of CYP3A4
myasthenia gravis - may exacerbate or cause symptoms

48
Q

what is the MOA of Neostigmine

A

acetylcholinesterase inhibitor

49
Q

what is the use of Neostigmine

A

acute colonic pseudo-obstruction (primarily used for M. gravis, also post-op bladder distention/urinary retention)

50
Q

what are the SE of neostigmne

A

Cardiac arrhythmias - especially bradycardia
dizziness, drowsiness, diarrhea
*caution with CVD

51
Q

what are the treatment options for IBD

A

flares: glucocorticoids, aminosalicylates(5-ASAs)
maintenacne: biologics, immunomodulatiors, aminosalicylates

52
Q

what is the MOA of 5-ASAs

A

work topically on affected/inflamed areas of mucosa; anti-inflammatory and immunosuppresive activity

53
Q

what is sulfasalazine and Mesalamine

A

aminosalicylate (5-ASA)

54
Q

what is the use of 5-ASAs

A

generally used for mild-moderate UC (flares and maintenace) - can be used for mild colonic Crohn’s disease (distal)

55
Q

what are the SE of Sulfasalzine

A

Nausea
HA
rash
arthralgia
bone marrow suppression
oligospermia in men (infertility) - reversible

56
Q

what are the SE of Mesalamine

A

nausea
HA
diarrhea
abdominal pain
nephrotoxicity/interstitial nephritis - rare

57
Q

what are the drug interactions iwth mesalamine

A

antacids, H2RAs, PPIs can diminish efficacy of mesalamine

58
Q

what is the use of immunosuppresants

A

induce and maintain remission in both UC and Crohn’s. good for pts who can not maintain remission when steroids are tapered down/off, can help reduce steroid dose
-slow acting drug. can take ~3-6 montsh to observe effect

59
Q

what are the immunosuppresant medicatiosn

A

Azathioprine, methotrexate, Adalimumab/ Infliximab

60
Q

what is the SE of Azathioprine

A

N/V
bone marrow suppression (anemia, leukopenia, thrombocytopenia)
liver toxicity

61
Q

what medications should be avoided with azathioprine

A

avoid with allopurinol (gout med) - leukopenia

62
Q

what is the MOA of methotrexate

A

immunosuppressant, anti-inflammatory for IBD
one of first antineoplastic drug developed. acts as folate antagonist, inhibiting DNA syntheses, repair and cellular replication

63
Q

what is the USE of methotrexate

A

induce and maintain remission of Crohn’s disease (less commonly used for UC)

64
Q

what are the SE of methotrexate

A

diarrea
n/v
alopecia
bone marrow suppression
mucositis
severe possibly fatal skin reactions, SJS, TEN

65
Q

what are BBW with methotrexate

A

severe toxic/fatal SE
hepatotoxicity
potentially fatal opporunisitic infections
lung disease
teratogen

66
Q

what is the MOA of biologics

A

bind and sequester TNF to decrease inflammatory response

67
Q

what is the use of biologics

A

maintenance for moderate to severe IBD (mostly for Crohns disease. infliximab also used for UC)

68
Q

what are the biologic medications

A

Adalimumab/ Infliximab

69
Q

what is the SE of infliximab

A

injection site reaction/infusion reaction
HA, abdominal pain, liver toxicity, heart failure, infections, URI
risk of infection worse with concomitant immunosuppression
no live vaccines while on therapy

70
Q

what is the MOA of glucocorticoids

A

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

71
Q

what is the use of glucocorticoids

A

moderate-severe Crohn’s and UC; helpful in early tx and during flares

72
Q

what are the common glucocorticoids we use with IBD

A

PO: prednisone/prednisolone : Budesonide/entocort
Rectal: hydrocortisone

Pharm 3 Module 2: GI (4 decks)

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