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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

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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
H2 blockers decrease the absorption of which 4 medications/supplements?
* Atazanavir * Vitamin B12 * Ketoconazole * Iron salts
26
H2 blockers increase the levels of which 2 medicines?
* Warfarin * Procainamide
27
Which 3 signalling molecules increase acid secretion and what are there receptors?
Histamine - H2 receptor Ach - Muscarininc receptor Gastrin - CCK2 receptor
28
What is the MOA of acid neutralizers?
Weak bases that neutralize the acid and form salt and water
29
What are the indications for acid neutralizers?
esophagitis, indigestion, heartburn, **calcium prophylaxis** treatment for osteoporosis in postmenopausal women note: not for GERD or PUD
30
What are the ADEs of the acid neutralizer sodium bicarbonate?
* **Flatulence/bloating** – CO2 generation * NaCl absorption can result in **fluid retention** (caution heart failure and hypertension)
31
Which acid neutralizer is the fastest reacting?
sodium bicarbonate
32
Which acid neutralizer has the following ASEs? * Flatulence/bloating –CO2 generation * Constipation * **Milk-alkali syndrome** (access of calcium and unreacted alkali)
calcium carbonate
33
* Aluminum hydroxide – **Fastest/Slowest** reaction • Causes what ASE? * Magnesium hydroxide – **Fastest/Slowest** reaction • Causes osmotic diarrhea
slowest reactions Aluminum hydroxide causes constipation slowest reactions Magnesium hyproxide causes osmotic diarrhea
34
As with other gastric medications, patients should take other medications hours prior to taking Antacid
2
35
Acid neutralizers decrease levels of which 3 drugs:
* Eltrombopag * Ketoconazole * Clofazimine
36
Acid neutralizers decrease the effectiveness by poor absorption of which 3 drugs:
* Tetracyclines * Levothyroxine * Allopurinol
37
What is the MOA of the GABA-B Agonist – Baclofen?
suppresses transient lower esophageal sphincter relaxations
38
What is the refractory GERD treatment after antacid treatments have failed?
GABA-B Agonist – Baclofen
39
What are the indications for GABA-B Agonist – Baclofen?
Used in patients with **GERD that have failed antacid treatment**
40
What are the side effects of Baclofen?s
sedation skeletal muscle relaxation
41
What are the considerations of GABA-B Agonist - Baclofen?
Use in refractory GERD with lack of response with PPIs and antacids dose adjust with renal disease
42
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
Gastric Ulcer
43
Which type of PUD is being described:
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
What are the 2 types of cytoprotectant agents as concerning peptic ulcers?
**Prostaglandin Analog** • Misoprostol (Cytotec) **Surface Protectant** * Sucralfate * Colloidal bismuth
45
In what way do NSAIDs damage the stomach mucosal barrier?
NSAIDs ihib COX-1 which inhibs prostaglandins and leads to decreased mucus, bicarbonate, and blood flow
46
**• 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
Cox-1 inhibit
47
**• Somatostatin** * Released from cells * Binds to the receptor on the and inhibit H+ secretion
D parietal cell
48
What is the main action of Prostaglandin (PGE2 & PGI2) and Somatostatin?
inhibit H+ secretion
49
What is the MOA of Prostaglandin Analog - Misoprostol?
increases bicarbonate and mucus release and reduces acid secretion
50
Which gastric medication for PUD has a **black box** warning for pregnancy?
Prostaglandin Analog - Misoprostol
51
What are the 2 indications for Misoprostol?
NSAID-induced Peptic Ulcer Disease Termination of pregnancy
52
**Prostaglandin Analog - Misoprostol** _• Adverse Side effects • Common:_ • and abdominal pain _• Considerations_ • Concurrent use with may result in decreased misoprostol effectiveness
Diarrhea antacids
53
Which PUD medication is considered an internal bandaid?
Surface Protectant - Sucralfate
54
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?
Surface Protectant - Sucralfate
55
The only indication for Surface Protectant - Sucralfate is:
PUD
56
What is the commin side effect of Surface Protectant - Sucralfate?
constipation
57
Like other gastric medications, Surface Protectant - Sucralfate if mixed with will result in decreased effectiveness and may interfere with other drug
antacids absorption
58
Which PUD medication is poorly absorbed, has poor solubility, and therefore has no systemic toxicity?
Surface Protectant - Sucralfate
59
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
glycoproteins bicarbonate H. pylori.
60
What surface protectant has some activity against H. Pylori?
Colloidal bismuth
61
Which surface protectant has constipation and at high doses: **black stools, and darkening of tongue**?
Colloidal bismuth
62
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
H. Pylori
63
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
epithelial low ammonia ammonium hydroxide Urease
64
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
gastrin
65
Why is gastrin increased in H. Pylori infection?
**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
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
decrease weakens
67
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?
**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
What is the first line treatment of active infection if on has prior exposure to macrolides or evidence of clarithromycin resistance?
Bismuth quadruple therapy
69
What is included in Bismuth quadruple therapy?
bismuth, metronidazole, tetracycline, and PPI
70
What is included with clarithromycin based triple therapy?
clarithromycin, amoxicillin or metronidazole (depending if penicillin allergy), and PPI
71
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?
Penicillin allergy---\> Bismuth quadruple therapy No penicillin allergy---\> Bismuth quadruple, Levofloxacin triple therapy, or high dose dual therapy
72
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?
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
What is the last ditch treatment of H.Pylori?
rifabutin triple therapy
74
What does the Levofloxacin triple therapy consist of:
levofloxacin, amoxicillin/metronidazole, and PPI
75
What is high dose dual therapy?
amoxicillin and PPI
76
What is Rifabutin triple therapy?
rifabutin, amoxicillin, and a PPI
77
What is the second-line salvage therapy for persistent H. Pylori?
PPI or H2A, bismuth, metronidazole, and tetracycline (same as the quadruple bismuth therapy) or PPI, amoxicillin, levofloxacin
78
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
clarithromycin
79
Which antibiotic ulcer therapy is being described? **– Penicillin** antibiotic that **inhibits cell wall biosynthesis**, a broad-spectrum bactericidal agent
amoxicillin
80
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
metronidazole
81
What antibiotic ulcer therapy is being described? A bactericidal agent **inhibits bacterial protein and cell wall biosynthesis**
Bismuth subsalicylate
82
What antibiotic ulcer therapy is being described? Tetracycline antibiotic that **inhibits bacterial protein synthesis**, a broad-spectrum **bacteriostatic agent**
tetracycline
83
Acid reducers are ranked in order of efficacy by the following:
• PPI\> H2 antagonists \> antacids
84
Sodium bicarbonate and calcium carbonate result in the generation of?
gas (CO2).
85
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
alkali calcium alkalosis.
86

ICOM- GI system (12 decks)

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