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GI > Acid Peptic Drugs > Flashcards

Acid Peptic Drugs Flashcards

1
Q

What are the aggressive factors in peptic ulcer disease? (6)

A

HCL, pepsin, H Pylori, NSAIDs, caffeine/alcohol/tobacco, bile

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2
Q

What are the protective factors in peptic ulcer disease? (5)

A

Bicarbonate, gastric mucous, postaglandins, mucosal blood flow, mucosal integrity

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3
Q

What are three receptors on parietal cells? Is there cross-reactivity?

A

H2 receptor
mAChR
Gastrin/CCK-B receptor

No cross-reactivity

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4
Q

Which receptors do ECL cells have? What do they release in turn?

A

mAChR and gastrin receptors–>secrete histamine when stimulated

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5
Q

What is effect of pepsin on GI tract? How is effect altered?

A

Pepsin is a protease that can damage GI tract, but it is pH dependent.
It is inactivated at pH>4 and irreversibly inactivated at pH>6

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6
Q

What is mechanism of injury of NSAIDs

A

Systemic: reduce PGE1 synthesis, anti platelet effect
Direct: Toxic resulting in erosion, reducing protect factors

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7
Q

Who tends to sustain bile related injury to upper GI tract?

A

Patients who have had surgery where anatomy of pylorus has been disrupted (i.e pylorotomy/pyloroplasty)

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8
Q

What are effects of caffeine, alcohol and tobacco on upper GI?

A

Caffeine: enhances acid secretion, lowers LES pressure
Alcohol: Directly toxic to UGI
Tobacco: impairs mucosal protective factors

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9
Q

Where is bicarbonate secreted? What is its protective role?

A

Secreted by stomach, duodenal surface epithelium mucus neck cells, brunner’s glands

Bicarbonate neutralizes HCl

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10
Q

Where is gastric mucous secreted? What is its protective function?

A

Secreted by stomach/dudoenal epithelium, mucous neck cells, Brunner’s glands

Lubricant/discrete layer that establishes gradient between acidic lumen and neutral cell surface– prevents autodigestion

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11
Q

What are 5 broad approaches to PUD treatment?

A
  1. Inhibit acid production
  2. Acid neutralizers
  3. Treatment for H Pylori
  4. Avoidance of NSAID therapy
  5. Enhance protective mechanisms
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12
Q

How do we inhibit acid production? (2)

A

H2-receptor antagonist

Proton-pump inhibitors

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13
Q

Describe pharmacokinetics for H2-receptor antagonists: Metabolism, dosing

A

Rapidly absorbed with quick onset
Hepatic metabolism via p450 and renal excretion

Continuous dosing keeps gastric pH>4, which inactivates pepsin

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14
Q

What are the clinically significant drug interactions of H2 receptor antagonists?

A

Warfarin, phenytoin theophylline, diazepam

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15
Q

Names of PPIs end in ____

A

____prazole: omeprazole (prilosec), lansoprazole, rabeprazole

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16
Q

What is the MOA of PPIs? Describe their efficacy

A

Irreversibly block H/K ATPase– results in more effective and longer lasting reduction of gastric acid production

17
Q

Describe the activation process of PPIs

A

Administered as a prodrug that is protonated and sulfonated before it can bind proton pump

18
Q

What is the effect of the unique properties of PPIs?

A

Although it’s half life is only 1-2 hours, it has a duration of action of 24-36 hours due to its prodrug requirements

19
Q

What was the largest theoretical concern of PPI use?

A

Gastrinomas due to hypergastrinemia secondary to lack of somatostatin…though there is no real evidence in humans of gastrinomas

20
Q

What are AEs of PPIs

A

Hip fractures in long-term use due to reduced osteoclast acid production and reduced calcium absorption

21
Q

What is MOA of antacids?

A

neutralize acid via sodium bicarbonate (alka seltzer), calcium carbonate (tums) or mylanta

22
Q

What are adverse effects of antacids?

A

Toxicity due to taking large doses
Mg: diarrhea/muscle weakness
Al: constipation
Ca: nephrocalcinosis, rebound acid

23
Q

What are the antimicrobial therapies used for H pylori?

A

Triple or quadruple regimens: CLAMP

Clarithromycin, levofloxacin, amoxicillin, metronidazole + PPI

24
Q

What is a natural PGE2 analogue?

A

Misprostol

25
Q

When can you not use misoprostol?

A

Women of child-bearing age

26
Q

How does sucralfate work?

How does it affect acid secretion?

A

Binds to GI mucosa and stimulates mucus, HCO3, PGE2 production and increases resistance to pepsin

It does not decrease gastric acid secretion

GI (41 decks)

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