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Gastrointestinal > Drugs Impacting Acid And H. Pylori > Flashcards

Drugs Impacting Acid And H. Pylori Flashcards

1
Q

Chest pain: GERD vs. MI

A

GERD:

  • Heartburn, belching, chest pain
  • Worse after eating
  • Worse at night when lying down
  • NOT worse with physical activity

MI:

  • Chest pain, nausea, dyspnea, diaphoresis, radiating pain to jaw/left extremity
  • Pain precipitated by and WORSE WITH exertion
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2
Q

Proton Pump Inhibitor (PPI) Drugs (first and second generation: 6)

A

First generation:
1. Omeprazole

Second generation:

  1. Esomeprazole
  2. Lansoprozole
  3. Pantoprozole
  4. Rabeprozole
  5. Dexlansoprazole
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3
Q

H2 Receptor Antagonists (first and second generation: 4)

A

First generation:
1. Cimetidine

Second generation:

  1. Famotidine
  2. Nizatidine
  3. Ranitidine - REMOVED FROM MARKET DUE TO PRESENCE OF CARCINOGEN (NDMA)
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4
Q

Antacids/Acid Neutralizers (single agents and mixed preparations: 6)

A

Single agents:

  1. Aluminum hydroxide
  2. Calcium carbonate
  3. Magnesium hydroxide
  4. Sodium bicarbonate

Mixed preparations:

  1. Aluminum hydroxide/magnesium hydroxide (Mylanta)
  2. Calcium carbonate/magnesium hydroxide (Rolaids)
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5
Q

Proton Pump Inhibitors (MOA, PK, Pregnancy, Indications)

A

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

PK: Onset 1 hour. t1/2: 30-60 minutes. Duration: less than 3 days

Pregnancy: N/A

Indications: PUD, GERD, esophagitis, gastric hypersecretion, and gastritis

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6
Q

Proton Pump Inhibitors (ADRs, Considerations, DDIs)

A

ADRs: headache, abdominal pain, nausea, vomiting, diarrhea, flatulence

Considerations: may cause B12 DEFICIENCY and hypomagnesemia. Increases FRACTURE risk. Need to taper to avoid rebound acid hypersecretion. Ask patient to take other meds 2 hours prior to PPI.

DDIs:
Decreases: cephalosporin abx, B12, ketoconazole, iron salts
Increases: digoxin, voriconazole

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7
Q

H2 Receptor Antagonists (MOA, PK, Pregnancy, Indications)

A

MOA: Reversibly and competitively inhibits the binding of histamine to the H2 receptor. Stops H+ secretion. Famotidine is the most potent of the class.

PK: Onset 1 hour. t1/2: 2-3 hours. Duration: 13 hours.

Pregnancy: N/A

Indications: PUD, GERD, esophagitis, gastric hypersecretion, indigestion, gastritis, heartburn

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8
Q

H2 Receptor Antagonist (ADRs, Considerations, DDIs)

A

ADRs: headache, dizziness, diarrhea, TOLERANCE.
Cimetidine- GYNECOMASTIA, inhibits CYP P450.

Considerations: Have patients take other meds 2 hours before H2 receptor antagonist.

DDIs:
Decreases: Atazanavir, B12, ketoconazole, iron salts
Increases: Warfarin, procainamide

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9
Q

Acid Neutralizers (MOA, PK, Pregnancy, Indications)

A

MOA: Weak bases neutralize HCl to salt and water

PK: Onset variable. t1/2: 2-4 hours. Duration: 20-180 minutes.

Pregnancy: N/A

Indications: esophagitis, indigestion, heartburn, calcium prophylaxis treatment for OSTEOPOROSIS/OSTEOPENIA in postmenopausal women

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10
Q

Acid Neutralizers (ADRs, Considerations, DDIs [levels and effectiveness])

A

ADRs: can cause rebound acid
Sodium bicarbonate - fastest reaction: flatulence/bloating from CO2 generation, NaCl absorption can result in fluid retention (caution in CHF and HTN)
Calcium carbonate: flatulence/bloating from CO2 generation, CONSTIPATION, MILK-ALKALI SYNDROME- excess calcium and metabolic alkalosis
Aluminum hydroxide - slow reaction: CONSTIPATION
Magnesium hydroxide - slow reaction: DIARRHEA

Considerations: Ask patients to take other meds 2 hours before antacid.

DDIs:
Decreases levels: eltrombopag, ketoconazole, clofazimine
Decreases effectiveness: tetracyclines, levothyroxine, allopurinol

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11
Q

GABA-B Agonist - Baclofen (MOA, PK, Pregnancy, Indications)

A

MOA: GABA- B agonist suppresses transient LES relaxation and prevents reflux at rest by inducing inhibitory interneuron. Inhibits transmission of monosynaptic and polysynaptic reflexes at the spinal cord level by hyperpolarization and induces resultant relief of muscle spasticity.

PK: Onset 1 hour. t1/2: 3-4 hours. Duration: 4-8 hours.

Pregnancy: C

Indications: REFRACTORY GERD that has failed antacid treatment

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12
Q

GABA-B Agonist - Baclofen (ADRs and Considerations)

A

ADRs: sedation, muscle relaxation

Considerations: Used in refractory GERD- patients with lack of response when adhering to twice daily PPI even after dose adjustment and alignments with meals (10-40% of patients). Dose adjustment needed for pts with renal disease. Not to be confused with Bactroban.

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13
Q

Gastric Ulcer vs. Duodenal Ulcer

A

Gastric ulcer:

  • Pain occurs any time during day
  • Food precipitates pain or worsens pain
  • Causes weight loss, nausea, vomiting, and diffuse gastric pain

Duodenal ulcer:

  • Pain occurs at night and will cause awakenings from sleep
  • Pain occurs 1-3 hours after a meal (empty stomach)
  • Pain is relieved by food
  • Causes weight gain and pinpoint epigastric burning pain
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14
Q

Cytoprotectant Agents (Classes and Agents; 2 and 3)

A

Prostaglandin analog:
- Misoprostol

Surface protectant:

  • Sucralfate
  • Colloidal bismuth
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15
Q

How do NSAIDs damage the mucosal barrier?

A

NSAIDs decrease prostaglandin synthesis (E2 and I2), which decreases gastric mucus secretion, bicarbonate secretion, and blood flow (healing)

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16
Q

Molecules that inhibit gastric acid secretion (2)

A
  1. Prostaglandin (E2 and I2): bind to the prostaglandin receptor on the parietal cell and inhibits H+ secretion by decreasing intracellular cAMP.
  2. Somatostatin: Released from D cells. Binds to the somatostatin receptor on parietal cell and inhibits H+ secretion by decreasing intracellular cAMP.
17
Q

Prostaglandin Analog - Misoprostol (MOA, PK, Pregnancy, Indications)

A

MOA: Prostaglandin analog binds to PGE receptor on parietal cell and reduces acid secretion. Increases bicarbonate and mucus release.

PK: Onset 30 minutes. t1/2: 20-40 minutes. Duration: 3 hours.

Pregnancy: BLACK BOX WARNING- causes birth defects, abortion, premature birth, or uterine rupture

Indications: NSAID-induced PUD, termination of pregnancy

18
Q

Prostaglandin Analog - Misoprostol (ADRs and Considerations)

A

ADRs: diarrhea and abdominal pain

Considerations: Cocurrent use with antacids may result in decreased misoprostol effectiveness.

19
Q

Surface Protectant - Sucralfate (MOA, PK, Pregnancy, Indications)

A

MOA: Complex of sucrose sulfate and aluminum hydroxide is activated in acidic environment. Forms sticky polymer and adheres to the ulcer site, forming a barrier that coats the gastric epithelial cells.

PK: Onset 1-2 hours. Duration 6 hours.

Pregnancy: B

Indications: PUD

20
Q

Surface Protectant - Sucralfate (ADRs, Considerations, DDIs)

A

ADRs: constipation

Considerations: no risk of systemic toxicity due to poor solubility. Cocurrent use with antacids may result in decreased effectiveness.

DDIs: may bind with other drugs and interfere with absorption

21
Q

Surface Protectant - Colloidal Bismuth (MOA, PK, Pregnancy, Indications)

A

MOA: Bismuth salts combine with mucus glycoproteins to form a barrier. Stimulates production of mucosal bicarbonate and prostaglandin E2. Some activity against H. pylori.

PK: Onset 4 hours. Duration 6 hours.

Pregnancy: B

Indications: PUD with H. pylori, diarrhea, heartburn, indigestion, nausea, upset stomach

22
Q

Surface Protectant - Colloidal Bismuth (ADRs and DDIs)

A

ADRs: constipation, black stools, DARKENING OF TONGUE

DDIs: N/A

23
Q

H. pylori characteristics and infection in the stomach (7)

A
  1. Gram negative and helically-shaped
  2. Attaches to epithelial cells of stomach and duodenum
  3. Able to live in low pH due to production of UREASE
  4. Urease converts urea to ammonia
  5. Ammonia buffers H+ and forms ammonium hydroxide; creates alkaline cloud around bacteria
  6. Urease also induces strong immune response that is damaging to host
  7. Ammonium hydroxide causes gastric epithelial cell injury
24
Q

H. pylori in duodenal PUD (4)

A
  1. Acid secretion is INCREASED in patients with H. pylori infection
  2. Ammonia generated by H. pylori produces alkaline environment near G cells, causing them to secrete more gastrin, increase parietal cell proliferation, and increase H+ secretion
  3. The number of D cells is also decreased in infected patients as a result of inflammatory mediators, resulting in decreased somatostatin release and increased gastrin
  4. H. pylori decreases bicarbonate secretion in the duodenum and weakens the protective mechanism of duodenal mucosa
25
Q

Drug regimens to eradicate H. pylori (3)

A

90% effective

  1. PPI-based Triple Therapy: PPI 1-2x daily + clarithromycin 500mg 2x daily + amoxicillin 1g 2x daily OR metronidazole 500mg 2x daily
  2. Bismuth-based Quadruple Therapy: PPI OR H2RA 1-2x daily + Bismuth subsalicylate 525mg 4x daily +metronidazole 250-500mg 4x daily + tetracycline 500mg 4x daily
  3. Second-Line Salvage Therapy for Persistent Infections: PPI 1-2x daily + amoxicillin 1g 2x daily + levofloxacin 250mg 2x daily
26
Q

Antibiotic Ulcer Therapy [used in combination] (5)

A
  1. Clarithromycin: Macrolide abx that inhibits bacterial RNA-dependent protein synthesis. Active against many G+ and G- aerobic bacteria, including H. pylori.
  2. Amoxicillin: Penicillin abx that inhibits cell wall biosynthesis. Broad-spectrum bactericidal.
  3. Metronidazole: Nitroimidazole used often due to bacterial resistance to amoxicillin and tetracycline, or intolerance of other agents. Generates free radicals inside cytoplasm of anaerobic bacteria and inhibits DNA synthesis. Active against H. pylori.
  4. Bismuth subsalicylate: Bactericidal agent that inhibits bacterial protein and cell wall biosynthesis.
  5. Tetracycline: Inhibits bacterial protein synthesis. Broad-spectrum bacteriostatic.
27
Q

Acid reducers in order of efficacy:

A

PPI > H2RA > Antacids

Gastrointestinal (7 decks)

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