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ICOM- GI system > GI- Pharmacology- Drugs impacting Acid and H. Pylori > Flashcards

GI- Pharmacology- Drugs impacting Acid and H. Pylori Flashcards

1
Q

What is the most useful tool in diagnosing GERD?

A

patient history

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2
Q

Other than patient history, what are 2 other diagnostic tests for GERD?

A

endoscopy

ambulatory esophageal pH test

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3
Q

How can we distinguish GERD from heart attack?

A

in GERD: Symptoms do not worsen with physical activity

in Heart attack: precipitatio of pain by exertion

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4
Q

What population of people tend to have GERD?

A

asthmatics

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5
Q

Proton pump inhibitors typically end with what suffix?

A

-prazole

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6
Q

What is the common suffix for H2 receptor antagonists?

A

-tidine

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7
Q

What are the 4 single agent antacids (acid neurtalizers)?

A

aluminum and magnesium hydroxide

calcium carbonate and sodium bicarbonate

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8
Q

What are the mixed antacid preparations and why are they mixed?

A

They are mixed to prevent diarrhea and constipation as calcium carbonate aluminum hydroxide causes constipation and magnesium hydroxide causes diarrhea

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9
Q

omeprazole, esomeprazole, lansoprazole are the 3 main:

A

PPIs

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10
Q

Describe the MOA of PPIs:

MOA: Prodrugs that are activated in environment. bind to and irreversibly inhibits the parietal cell H+/K+-ATPase proton pump

A

acidic

Covalently

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11
Q

Why are the pharmacokinetics of PPIs longer in duration <3 days and what are the pregnancy recommendations?

A

because they irreversibly covalently bind and no adequate studies for pregnant women

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12
Q

What are the indications for PPIs?

A

Peptic Ulcer Disease,

Gastroesophageal reflux disease,

esophagitis,

gastric hypersecretion,

gastritis

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13
Q

What is the first and second line treatment for GERD?

A

PPIs then H2 receptor antagonists

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14
Q

What are some adverse side effects for PPIs and some considerations for long-term therapy?

• Adverse Side effects • Common:

• Headache, abdominal pain, nausea, vomiting, diarrhea, and flatulence

• Considerations for Long-term therapy

  • Vitamin B12 deficiency (monitor every 1 to 2 years)
  • Hypomagnesemia
  • Osteoporosis-related fractures – reduced calcium absorption
  • Clostridium difficile infections
  • Acute and Chronic Kidney Disease – subclinical acute interstitial nephritis
  • Community acquired pneumonia
  • Need to taper to avoid acid rebound hypersecretion
A
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15
Q

Why does one need to taper used of PPIs?

A

to avoid acid rebound hypersecretion

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16
Q

What is a consideration about other medications and medicines that reduce gastric acid?

A

• Have patient take other medications 2 hours prior

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17
Q

PPIs decrease the effectivness of which drug?

A

clopidogrel

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18
Q

PPIs decrease the absorption of which 4 medicines/supplements?

A
  • Cephalosporin antibiotics
  • Vitamin B12
  • Ketoconazole
  • Iron salts
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19
Q

PPIs increase levels of which 2 medications?

A
  • Digoxin
  • Voriconazole
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20
Q

What is the MOA of H2 receptor antagonists and which is the most potent of it’s class?

A

: Reversibly and competitively inhibit the binding of histamine to the H2 receptor

Famotidine is the most potent of the class

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21
Q

What are the indications for H2 receptor antagonists?

A

Peptic Ulcer Disease,

Gastroesophageal reflux disease,

esophagitis,

gastric hypersecretion,

gastritis,

indigestion,

heartburn

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22
Q

What ADE is unique about H2 receptor antagonists?

A

• Tolerance and loss of efficacy occurs with prolonged use (after 4 to 6 weeks)

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23
Q

Which H2 receptor antagonist has the most ASE and what are the 2 main worrisome effects?

A

cimetidine

1. gynecomastia and impotence due to decreased conversion of testosterone to dihydrotestosterone

unconverted testosterone converted to estrogen instead

  1. inhibits CYP P450 isoforms
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24
Q

Like PPIs, what should one consider if taking other medications?

A

Have patient take other medications 2 hours prior to taking H2 Blocker

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25
Q

H2 blockers decrease the absorption of which 4 medications/supplements?

A
  • Atazanavir
  • Vitamin B12
  • Ketoconazole
  • Iron salts
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26
Q

H2 blockers increase the levels of which 2 medicines?

A
  • Warfarin
  • Procainamide
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27
Q

Which 3 signalling molecules increase acid secretion and what are there receptors?

A

Histamine - H2 receptor

Ach - Muscarininc receptor

Gastrin - CCK2 receptor

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28
Q

What is the MOA of acid neutralizers?

A

Weak bases that neutralize the acid and form salt and water

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29
Q

What are the indications for acid neutralizers?

A

esophagitis,

indigestion,

heartburn,

calcium prophylaxis treatment for osteoporosis in postmenopausal women

note: not for GERD or PUD

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30
Q

What are the ADEs of the acid neutralizer sodium bicarbonate?

A
  • Flatulence/bloating – CO2 generation
  • NaCl absorption can result in fluid retention (caution heart failure and hypertension)
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31
Q

Which acid neutralizer is the fastest reacting?

A

sodium bicarbonate

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32
Q

Which acid neutralizer has the following ASEs?

  • Flatulence/bloating –CO2 generation
  • Constipation
  • Milk-alkali syndrome (access of calcium and unreacted alkali)
A

calcium carbonate

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33
Q
  • Aluminum hydroxide – Fastest/Slowest reaction • Causes what ASE?
  • Magnesium hydroxide – Fastest/Slowest reaction • Causes osmotic diarrhea
A

slowest reactions

Aluminum hydroxide causes constipation

slowest reactions

Magnesium hyproxide causes osmotic diarrhea

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34
Q

As with other gastric medications, patients should take other medications hours prior to taking Antacid

A

2

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35
Q

Acid neutralizers decrease levels of which 3 drugs:

A
  • Eltrombopag
  • Ketoconazole
  • Clofazimine
36
Q

Acid neutralizers decrease the effectiveness by poor absorption of which 3 drugs:

A
  • Tetracyclines
  • Levothyroxine
  • Allopurinol
37
Q

What is the MOA of the GABA-B Agonist – Baclofen?

A

suppresses transient lower esophageal sphincter relaxations

38
Q

What is the refractory GERD treatment after antacid treatments have failed?

A

GABA-B Agonist – Baclofen

39
Q

What are the indications for GABA-B Agonist – Baclofen?

A

Used in patients with GERD that have failed antacid treatment

40
Q

What are the side effects of Baclofen?s

A

sedation

skeletal muscle relaxation

41
Q

What are the considerations of GABA-B Agonist - Baclofen?

A

Use in refractory GERD with lack of response with PPIs and antacids

dose adjust with renal disease

42
Q

Which type of PUD is being described:

  • Pain occurs at any time during the day
  • Food may precipitate or accentuate the pain
  • Will cause weight loss, nausea, vomiting, diffuse epigastric pain
A

Gastric Ulcer

43
Q

Which type of PUD is being described:

A

Duodenal Ulcer

  • Pain occurs at night and will cause awaken from sleep
  • Pain occurs 1-3 hours after a meal (empty stomach)
  • Pain is relieved by food
  • Will cause weight gain and pinpoint epigastric burning pain
44
Q

What are the 2 types of cytoprotectant agents as concerning peptic ulcers?

A

Prostaglandin Analog

• Misoprostol (Cytotec)

Surface Protectant

  • Sucralfate
  • Colloidal bismuth
45
Q

In what way do NSAIDs damage the stomach mucosal barrier?

A

NSAIDs ihib COX-1 which inhibs prostaglandins and leads to

decreased mucus, bicarbonate, and blood flow

46
Q

• Prostaglandin (PGE2 & PGI2)

  • Arachidonic acid is converted via to PGE2 & PGI2
  • PGE2 & PGI2 bind to the prostaglandin receptor and inhibit/activate H+ secretion from the parietal cell
A

Cox-1

inhibit

47
Q

• Somatostatin

  • Released from cells
  • Binds to the receptor on the and inhibit H+ secretion
A

D

parietal cell

48
Q

What is the main action of Prostaglandin (PGE2 & PGI2) and Somatostatin?

A

inhibit H+ secretion

49
Q

What is the MOA of Prostaglandin Analog - Misoprostol?

A

increases bicarbonate and mucus release and reduces acid secretion

50
Q

Which gastric medication for PUD has a black box warning for pregnancy?

A

Prostaglandin Analog - Misoprostol

51
Q

What are the 2 indications for Misoprostol?

A

NSAID-induced Peptic Ulcer Disease

Termination of pregnancy

52
Q

Prostaglandin Analog - Misoprostol

• Adverse Side effects • Common:

• and abdominal pain

• Considerations

• Concurrent use with may result in decreased misoprostol effectiveness

A

Diarrhea

antacids

53
Q

Which PUD medication is considered an internal bandaid?

A

Surface Protectant - Sucralfate

54
Q

Which medication is a complex of sucrose sulfate and aluminum hydroxide that is activated in an acidic environment. Forms a sticky polymer in acidic environment and adheres to the ulcer site, forming a barrier that coats the gastric epithelial cells?

A

Surface Protectant - Sucralfate

55
Q

The only indication for Surface Protectant - Sucralfate is:

A

PUD

56
Q

What is the commin side effect of Surface Protectant - Sucralfate?

A

constipation

57
Q

Like other gastric medications, Surface Protectant - Sucralfate if mixed with will result in decreased effectiveness and may interfere with other drug

A

antacids

absorption

58
Q

Which PUD medication is poorly absorbed, has poor solubility, and therefore has no systemic toxicity?

A

Surface Protectant - Sucralfate

59
Q

Surface Protectant – Colloidal bismuth (pepto bismol)

Bismuth salts combine with mucus to form a barrier.

Stimulate production of mucosal and prostaglandin E2.

Has some activity against

A

glycoproteins

bicarbonate

H. pylori.

60
Q

What surface protectant has some activity against H. Pylori?

A

Colloidal bismuth

61
Q

Which surface protectant has constipation and at high doses: black stools, and darkening of tongue?

A

Colloidal bismuth

62
Q

Which pathogen is being described:

Gram-negative, helically-shaped, microaerophilic bacterium usually found in the stomach. Helical shape allows to penetrate the mucoid lining of the stomach and establish infection

A

H. Pylori

63
Q

H. pylori attaches to the cells of the stomach and duodenum

  • Live in low/high pH because of the production of urease
  • Urease converts urea to
  • Ammonia buffers the H+ and forms creating an alkaline cloud around the bacterium
  • is a damaging factor because it causes a strong immune response
  • Ammonium hydroxide causes gastric epithelial cell injury
A

epithelial

low

ammonia

ammonium hydroxide

Urease

64
Q

Why is acid secretion increased in patients with H. Pylori infection?

Due to increased levels of circulating , causing parietal cell proliferation and increased acid production

A

gastrin

65
Q

Why is gastrin increased in H. Pylori infection?

A

Ammonia generated by H. pylori produces alkaline environment near the G cells and causes gastrin release, increases parietal cells, results in increased acid secretion

• Number of D cells decreases in H. pylori-infected patient, resulting in decreased somatostatin production and increased gastrin release

66
Q

What is the action of H. Pylori in the duodenum?

H. pylori increase/decrease duodenal bicarbonate secretion and strengthens/weakens the protective mechanism of the duodenal mucosa, leading to ulceration

A

decrease

weakens

67
Q

What is the first line treatment of an active H. pylori infection with a penicillin allergy and with no penicillin allergy with no prior exposure to macrolides or clarithromycin resistance?

A

no penicillin allergy:

  • clarithromycin based triple therapy with amoxicillin

with penicillin allergy:

  • with recent metronidazole use—–> Bismuth quadruple therapy
  • no recent metronidazole use———> clarithromycin based triple therapy with metronidazole or Bismuth quadruple therapy
68
Q

What is the first line treatment of active infection if on has prior exposure to macrolides or evidence of clarithromycin resistance?

A

Bismuth quadruple therapy

69
Q

What is included in Bismuth quadruple therapy?

A

bismuth, metronidazole, tetracycline, and PPI

70
Q

What is included with clarithromycin based triple therapy?

A

clarithromycin, amoxicillin or metronidazole (depending if penicillin allergy), and PPI

71
Q

What is the treatment for persistant H. Pylori infection if the clarithromycin triple based therapy did not work and there is and is not a penicillin allergy?

A

Penicillin allergy—> Bismuth quadruple therapy

No penicillin allergy—> Bismuth quadruple, Levofloxacin triple therapy, or high dose dual therapy

72
Q

What is the treatment for persistant H. Pylori infection if the Bismuth quadruple based therapy did not work and there is and is not a penicillin allergy?

A

Penicillin allergy——-> Bismuth quadruple therapy with high dose PPI or

Levocloxacin triple therapy

No Penicillin allergy—–> Levofloxacin triple therapy,

high dose dual therapy, or clarithromycin quadruple therapy

73
Q

What is the last ditch treatment of H.Pylori?

A

rifabutin triple therapy

74
Q

What does the Levofloxacin triple therapy consist of:

A

levofloxacin, amoxicillin/metronidazole, and PPI

75
Q

What is high dose dual therapy?

A

amoxicillin and PPI

76
Q

What is Rifabutin triple therapy?

A

rifabutin, amoxicillin, and a PPI

77
Q

What is the second-line salvage therapy for persistent H. Pylori?

A

PPI or H2A, bismuth, metronidazole, and tetracycline (same as the quadruple bismuth therapy)

or

PPI, amoxicillin, levofloxacin

78
Q

Which antibiotic ulcer therapy is being described?

Macrolide antibiotic that inhibits bacterial RNA- dependent protein synthesis, active against many gram-positive and some gram-negative aerobic bacteria including H. pylori

A

clarithromycin

79
Q

Which antibiotic ulcer therapy is being described?

– Penicillin antibiotic that inhibits cell wall biosynthesis, a broad-spectrum bactericidal agent

A

amoxicillin

80
Q

Which antibiotic ulcer therapy is being described?

– Nitroimidazole used often due to bacterial resistance to amoxicillin and tetracycline, or due to intolerance to other agents, generates free radicals inside the cytoplasm of anaerobic bacteria and inhibits DNA synthesis, has activity against H. pylori

A

metronidazole

81
Q

What antibiotic ulcer therapy is being described?

A bactericidal agent inhibits bacterial protein and cell wall biosynthesis

A

Bismuth subsalicylate

82
Q

What antibiotic ulcer therapy is being described?

Tetracycline antibiotic that inhibits bacterial protein synthesis, a broad-spectrum bacteriostatic agent

A

tetracycline

83
Q

Acid reducers are ranked in order of efficacy by the following:

A

• PPI> H2 antagonists > antacids

84
Q

Sodium bicarbonate and calcium carbonate result in the generation of?

A

gas (CO2).

85
Q

Calcium carbonate reactions result in excess that can react with calcium to cause milk-alkali syndrome.

Milk-alkali syndrome is characterized by high blood and metabolic

A

alkali

calcium

alkalosis.

86
Q
A

ICOM- GI system (12 decks)

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