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GI > GI pharm: esophagus, stomach, and duodenum > Flashcards

GI pharm: esophagus, stomach, and duodenum Flashcards

1
Q

What antacids are used for the tx of ulcers?

A
  • aluminum salts
  • magnesium hydroxide
  • calcium carbonate
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2
Q

MOA of antacids?

A

-tx of ulcers
work by neutralizing gastric acid
- protect gastric mucosa against acute chemical injury
- bind bile acids and inhibit peptic activity
- promote angiogenesis in injured mucosa
- heavy metals suppress H. pylori

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3
Q

Antacids drug interactions?

A
  • variety of drug interactions
  • can bind with drugs taken at same time decreasing absorption of that agent
  • interact w/ many abx
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4
Q

Magnesium salts - names, SEs, caution?

A
  • magnesium hydroxide/aluminum hydroxide
  • brand names: Maalox, alamag, Mag-A1, Mag-A1 ultimate, mylanta
  • common side effects: diarrhea, constipation, abd cramps, N/V, hypermagnesemia
  • caution with renal insufficiency!!!!
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5
Q

Aluminum salts - caution, names?

A
  • caution in renal insufficiency
  • can block the intestinal absorption of phosphate
  • names:
    acid gone
    gaviscon
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6
Q

Calcium carbonate - names, indications, most common side effects, special instructions?

A
  • tums, maalox regular chewable, cclci-chew, rolaids, chooz, alka-mints
  • indications: acid indigestion, heartburn
  • most common side effects: constipation, bloating, gas, N/V, abdominal pain, xerostomia
  • separate from other meds by 2 hrs
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7
Q

Name the H2 blockers?

A
  • cimetidine (tagamet)
  • ranitidine (zantac)
  • famotidine (pepcid)
  • nizatidine (axid)
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8
Q

indications for H2 blockers?

A
  • tx and maintenance therapy of PUD
  • tx of GERD
  • management of dyspepsi
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9
Q

MOA of H2 blockers?

A
  • inhibit acid secretion by blocking histamine H2 receptors on parietal cell
  • generally dosed to take 30-60 min prior to a meal (if using for acid suppression with meals)
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10
Q

SEs of H2 blockers?

A
  • rare, severe adverse effects, such as renal and hepatotoxicity
  • myelosuppresison:
    thrombocytopenia
    neutropenia
    anemia
    pancytopenia
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11
Q

Rare CNS SEs from H2 blockers?

A
  • can cause confusion, restlessness, somnolence, agitation, HAs, dizziness, with prolonged therapy: hallucinations, focal twitching, seizures, unresponsiveness, and apnea (primarily in elderly with concomitant RENAL and/or hepatic failure)
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12
Q

Rare cardiac SEs from H2 blockers?

A
  • sinus bradycardia
  • hypotension
  • AV block
  • prolong. QT interval
  • sinus and cardiac arrest have occured with rapid infusion
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13
Q

SEs of cimetidine? Should you use it?

A
  • can rarely cause gynecomastia and impotence
  • polymyositis
  • interstitial nephritis
  • cleared through P450 system so has mult drug interactions
  • giving rapidly IV can cause cardiac arrhythmias and hypotension
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14
Q

Absorption and distribution of H2 blockers?

A
  • well absorbed after oral dosing
  • peak serum concentrations occur within 1-3 hrs
  • absorption is reduced by 10-20% if taken with antacids
  • don’t give acid suppression therapy together: will actually decrease efficacy of drugs
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15
Q

Class of PPIs?

A
  • omeprazole (prilosec, zegrid)
  • lansoprazole (prevacid)
  • pantoprazole (protonix)
  • esomeprazole (nexium)
  • dexlansoprazole (kapidex)
  • rabeprazole (AcipHex)
  • all have the same efficacy
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16
Q

Indications for PPIs?

A

tx of all acid related conditions:

  • PUD
  • GERD
  • zollinger-ellison syndrome
  • tx and preventing NSAID assoc gastroduodenal mucosal injury
  • eradication of H. pylori infection
17
Q

MOA of PPIs?

A
  • block acid secretion:
    irreversibly binds to and inhibits the H-K ATPase pump on parietal cell membrane
  • parietal cells need to be active for PPIs to work so don’t give other antisecretory meds at same time
  • the amt of H-K ATPase present in parietal cell is greatest after a prolonged fast, PPIs should be admin b/f first meal of the day
  • if on long term therapy- need to taper off
  • anticholinergics will decrease efficacy of PPI
18
Q

Onset of action for a PPI?

A
  • about an hour

- peak concentration in about 2 hrs

19
Q

SEs of PPIs?

A
  • diarrhea
  • HA
  • flatulence with protonix
20
Q

Drug interactions with PPIs? Which one has the least?

A
  • pantoprazole (protonix): lowest potential for P450 drug interactions
  • omeprazole (prilosec, zegrid) and esomeprazole (nexium): metabolized largely by CYP2C19 and the potential for interactions thus appears to be greatest among PPIs
    (omeprazole is supposed to be more powerful, probably isn’t)
21
Q

What drug does omeprazole have a significant interaction with? BBW

A
  • clopidogrel (plavix)

- decreases efficacy of antiplatelet action of clopidogrel - increased risk of clotting

22
Q

What other drugs do omeprazole have interactions with?

A
  • warfarin
  • diazepam
  • phenytoin
  • theophylline
  • digoxin
  • carbamazepine
23
Q

Long term admin of PPIs ma increase the incdience of?

A
  • infections: C diff, pneumonia
  • fractures: hip, wrist, spine
  • malabsorption of:
    B12 (check levels)
    magnesium (check levels esp with diuretics and digoxin admin)
  • iron
  • if person is anemic, ask about PPI use
24
Q

Admin of PPIs?

A
  • takes 30-60 min b/f first meal of the day

- if 2x daily dosing is needed then take 2nd dose 30-60 min prior to last meal of the day

25
Q

Use of Sulcrafate (carafate)?

A
  • sucrose octasulfate-aluminum hydroxide
  • prevents chemical induced mucosal damage
  • heals chronic ulcers
26
Q

MOA of sulcrafate?

A
  • stimulates angiogenesis and formation of granulation tissue likely due to growth factor binding
  • binds to ulcer base best at pH below 3.5 so should be admin 30-60 min prior to meals (don’t give with acid suppression therapy)
27
Q

Cautions with sulcrafate use?

A
  • due to combo with Al hydroxide don’t admin with Al containing antacids in pts with renal failure
  • don’t admin with citrate containing compounds - increases Al absorption by 50x in normal renal fxn
28
Q

Use of Bismuth?

A
  • suppresses H. pylori infection

- not helpful in tx of non H pylori induced ulcers

29
Q

MOA of Bismuth?

A
  • inhibition of peptic activity but not pepsin secretion
  • may bind to ulcer craters
  • recruits macrophages to edge of the ulcer crater to promote healing
  • may increase mucosal prostaglandin production and mucus bicarbonate secretion
30
Q

Indication of misoprostol (cytotec) use? Pregnancy category? MOA?

A
  • indicated for prevention and tx of NSAID induced ulcers
  • preg category: X
  • prostaglandin E1 analog
  • enhances mucosal defenses and promote ulcer healing
  • not a first line therapy
31
Q

BBW for misoprostol?

A
  • use during pregnancy may cause abortion, birth defects, or premature birth. It isn’t to be used to reduce NSAID induced ulcers in woman of childbearing potential unless she is capable of complying with effective contraceptive measures and is at high risk of developing gastric ulcers and/or their complications
32
Q

What is metaclopramide (reglan)? Fxn?

A
  • prokinetic
  • 1st line therapy for gastroparesis for no longer than 12 weeks unless benefits outweigh risks
  • improves gastric emptying by increasing gastric antral contractions and decreasing postprandial fundul relaxation
  • dopamine receptor antagonist (reduces vomiting)
  • 5-HT4 agonist
  • weak 5-HT3 receptor antagonist
33
Q

SEs of metaclopramide (reglan)?

A
  • anxiety
  • restlessness
  • depression
  • hyperprolactinemia
  • QT prolongation
  • extrapyramidal effects: dystonia, and tardive dsykinesia (this may not be reversible)
34
Q

What are dangerous drug interactions to avoid with metoclopramide?

A
  • antipsychotics
  • droperidol (inapsine)
  • promethazine (phenergran)
  • tetrabenazine (xenzine): huntington’s chorea
  • trimetazidine (vastarel MR): antianginal

more drugs to avoid:

  • SSRIs
  • TCAs
  • atovaquone (mepron): - antimalarial
  • metyrosine (demser): tx sxs of pheochromocytoma

GI (21 decks)

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