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GI II: Test 1 > GERD/PUD tx > Flashcards

GERD/PUD tx Flashcards

1
Q

dexlansoprazole

A

PPI

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2
Q

Esomeprazole

A

PPI

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3
Q

Lansoprazole

A

PPI

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4
Q

Omeprazole

A

PPI

** may inhibit metabolism of warfarin, diazepam, phnytoin

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5
Q

Pantoprazole

A

PPI

** use this one if using clopidogrel

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6
Q

Rabeprazole

A

PPI

** use this one if using clopidogrel

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7
Q

Cimedtidine

A

H2RA
** has most DDI’s

see gynecomastia or impotence in men, galactorrhea in women

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8
Q

Famotidine

A

H2RA

** has least amount of DDI’s

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9
Q

Nizatidine

A

H2RA

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10
Q

Ranitidine

A

H2RA

- has moderate amount of DDIs

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11
Q

Sodium bicarbonate

A

Antacid
“baking soda”
- has high amount of CO2 production –> gas, belching, distension

  • can cause metabolic alkalosis and fluid retention, may pose risk for pts. w/ HF, HTN and renal insuffiecncy

Sodium bicarbonate + HCl –> NaCl and CO2
CO2 (distension and belching)
Alkali absorption (metabolic alkalosis)
NaCl absorption (fluid retention)

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12
Q

Calcium carbonate

A

Antacid = “tums”

Calcium carbonate + HCl –> CaCl2 and CO2

  • has high amount of CO2 production –> gas, belching, distension
  • can lead to hypercalcemia, renal insufficiency, metabolic alkalosis
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13
Q

Magnesium hydroxide/aluminum hydroxide

A

Antacid

no gas generated so belching doesn’t occur, metabolic alkalosis is also uncommon

however,
Mg2+ salts – osmotic diarrhea
Al3+ salts – constipation

watch out for renal insufficiency

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14
Q

Bismuth Subcitrate

A

agent w/ mucosal protection

Bismuth coats ulcers and erosions; stimulates intestinal prostaglandin, mucus, and bicarbonate secretion

ADRs:
Harmless blackening of stool and tongue
Salicylate toxicity (high doses)

Therapeutic use:
Dyspepsia and acute diarrhea
Traveler’s diarrhea
H. pylori

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15
Q

Bismuth Subsalicylate

A

“pepto-bismol” : agent w/ mucosal protection

Bismuth coats ulcers and erosions; stimulates intestinal prostaglandin, mucus, and bicarbonate secretion

Salicylate (like ASA) inhibits intestinal prostaglandin and chloride secretion

ADRs:
Harmless blackening of stool and tongue
Salicylate toxicity (high doses)

Therapeutic use:
Dyspepsia and acute diarrhea
Traveler’s diarrhea
H. pylori

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16
Q

Misoprostel

A

agent w/ mucosal protection

MOA: prostaglandin analog

** useful in prevention of NSAID induced ulcers

** not wel tolerated - see diarrhea and cramping/ ab pain

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17
Q

Sucralfate

A

agent w/ mucosal protection

MOA: unknown - forms viscous paste in water/acid sol’n which binds ulcers for up to six hours

** use: stress-related mucosal injury (slightly less effective than H2RA’s IV) - used preferentially over acid-inhibitory therapies due to concern of increased risk of pneumonia created by alkaline envirnment

18
Q

AB tx for H. pylori?

A

PPI or H2RA w/ two or more Abs:

  • amoxicillin
  • clarithromycin
  • metronidazole
  • tetracycline
19
Q

physio of acid secretion?

A

ACh - attaches to M3 receptors:

  • stimulates Gastrin to be released from G cells
  • directly stimulates parietal cells –> acid
  • stimulates Histamine to be released from ECL cells

Gastrin (from G cells): binds CCKB-R of parietal cells –> stimulates acid secretion

Histamine (from ECL cells): binds H2R on Parietal cells–> acid section
(is stimulated by both ACh and Gastrin)

THus - ACh provides direct parietal stimulation while gastrin effects are primarily mediated through indirect release of histamine from ECL cells

20
Q

role of prostaglandins?

A

inhibit the proton pump by reducing cAMP –> result in stimulation of protective factors (mucus and bicarb)

21
Q

NSAIDS

A

block PG production –> more acid secretion, less mucus and bicarb production and diminished blood flow –> thus NSAIDs are ulcerogenic and should be avoided in ulcer pts.

22
Q

tx of mild GERD

A

antacid or H2RA as needed

23
Q

NERD

A

antacid or H2RA

24
Q

Erosive esophagitis GERD tx?

A

PPI for 8 weeks

25
Q

Duodenal ulcer tx?

A

H2RA or PPI for 4 weeks

26
Q

Gastric ulcer tx?

A

PPI for 8 weeks

27
Q

PPI’s

A

they are lipophilic prodrugs that readily cross lipid membrane and are protonated and activated in parietal cells –> forms a covalent disulfide bond w/ H+/K+ ATPase –> irreversibly inactivating the enzyme

** they have short half life and longer duration! :)

** they are well tolerated and work to inhibit 90% of all total acid secretion

used for tx of GERD, PUD (better sx control than H2RA), H. pylori infection, NSAID ulcers, ZE syndrome

28
Q

AEs of PPIs?

A

handled well for the most part

diarrhea, h/a, ab pain

** increased risk of C. diff

** decreased vit B12 absorption –> increased risk of pneumonia

29
Q

DDI’s of PPIs?

A

must dose adjust for hepatic fn.

30
Q

what to watch out for w/ warfarin?

A

omeprazole

31
Q

what to watch out for clopidogrel

A

PPI’s: omeprazole, lansoprazole, dexlansoprazole

*** use Pantoprazole or Rabeprazole

32
Q

H2RA’s

A

Histamine2 receptor antagonists - tidine

MOA: competitively inhibit parietal cell H2 receptors and block histamine released from ECL cells

** suppresses basal more than meal stimulated acid secretion ** thus most useful for nocturnal acid secretion (only modest effect for meal inhibited acid)

** must be dosed multiple times per day - and dose adjust for BOTH hepatic and renal fn

tx: used for GERD, PUD (largely replaced by PPI’s except for DU’s), NSAID ulcers, stress injury

DDI’s: Cimetidine»>rantidine&raquo_space;»»>famotidine/nizatidine

competes with creatinie and other drugs for renal secretion

33
Q

AE’s of H2RA’s

A

Diarrhea, headache, fatigue, myalgia (< 3%)

Mental status changes (ICU patients, elderly, renal or hepatic impairment)

Nosocomial pneumonia, rare blood dyscrasias, bradycardia/hypotension (rapid IV infusion)

inhibits gastric acid (except famotidine) first-pass metabolism of alcohol - dont use w/ alcoholics!!!

34
Q

antacids

A

react with HCl to form a salt and water

used for dyspepsia and intermittent heart burn

35
Q

NSAID ulcers tx?

A

Discontinue ASA or NSAID (faster healing)

PPIs - Preferred if ASA or NSAID must be continued (pantoprazole, rabeprazole)

H2RAs - May be used if ASA or NSAID discontinued

36
Q

tx for stress ulcers?

A

use PPIs for stress ulcer prophylaxis : Omeprazole sodium bicarbonate only PPI FDA approved – given per tube

H2RA’s Preferred IV over PPI IV if no nasoenteric tube present or with significant ileus

37
Q

fastest onset?

A

antacids > H2RA’s > PPis

38
Q

efficacy of acid prevention?

A

PPIs > H2RA’s

H2RA’s inhibit fasting (basal) acid secretion ; PPI’s block both fasting and food stimulated secretion

39
Q

tolerance?

A

repeated admin. of H2RA’s –> reduced effectiveness

tolerance with PPI’s doesn’t occur

40
Q

14 day triple therapy for H. pylori?

A
  1. PPI
  2. Clarithromycin
  3. Amoxicillin or Metronidazole (for penicillin-allergic individs)
41
Q

14 day quadruple therapy for H. pylori?

A
  1. PPI or H2RA
  2. Metronidazole
  3. Tetracycline/doxycycline
  4. Bismuth subsalicylate
42
Q

AE’s of antibiotics?

A

Clarithromycin: GI upset, diarrhea, altered taste

Amoxicillin: GI upset, headache, diarrhea

Metronidazole: metallic taste, intolerance to alcohol

Tetracycline: GI upset, photosensitivity

GI II: Test 1 (6 decks)

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