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GI Liver Pharmacology > The Pharmacotherapy of Peptic Ulcer Disease & other GI disorders > Flashcards

The Pharmacotherapy of Peptic Ulcer Disease & other GI disorders Flashcards

1
Q

The most common GI disorders are the result of

A 
Chronic inflammation:
Gastric ulcers
Duodenal ulcers
Gastritis
Dysepepsia
Gastroesophageal reflux disorder (GERD)
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2
Q

Etiology of Gastric Ulcers

A
  • Associated with normal or reduced gastric acid output.

* Altered mucosal resistance may be a primary factor.

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3
Q

Etiology of Duodenal Ulcers

A
  • Associated with high gastric acid output, especially at night.
  • Inadequate duodenal bicarbonate secretion and insufficient
  • acid neutralization are significant contributing factors.
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4
Q

Etiology Gastroesophageal Reflux Disease (GERD)

A

Caused by insufficient constriction of the esophageal sphinctor, resulting in exposure of esophagus to gastric acids

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5
Q

Major causes of PUD

A

H. pylori is a gram-negative, spiral-shaped flagellated bacterium.

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6
Q

H. pylori is resistant to the harmful effects of the acidic environment because

A

they produce the enzyme urease which converts urea in stomach juice into ammonia & bicarbonate.

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7
Q

H. pylori Diagnosis:

A

Blood antibody test: To detect if antibodies to H. Pylori are present. It means either you are currently infected or have been infected.
Urea breath test: checks to find out if you currently have H. Pylori bacteria in the stomach.

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8
Q

H. pylori infection has been linked with the

development of

A

gastric cancer
• Include adenocarcinoma of corpus & antrum, & MALT lymphoma
• Labelled as a class I carcinogen.

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9
Q

Overall Goals for the Treatment of Peptic Ulcer Disease

A

Eradication of H. pylori Administration of antibiotics:
Tetracycline, clarithramycin, metronidazole
Relief of symptoms Antisecretory agents, antacids
Healing of ulcerations Prostaglandin agonists, bismuth compounds, sucrasulfate

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10
Q

Drug Treatment of PUD

A
  • Antacids
  • Histamine2-receptor blockers
  • Proton pump inhibitors
  • Mucosal Protective agents
  • Antibiotics
  • Multi-drug regimen in the management of H. Pylori
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11
Q

Antacids Mechanism of action:

A

• NaHCO3 + HCl = NaCl + CO2 + H20
• Antacids NEUTRALIZE gastric acid in the stomach.
• pH from 1.3 to 1.6 neutralizes 50%
• pH from 1.3 to 2.3 neutralizes 90%
• prevent the transformation of pepsinogen to
pepsin. Goal to raise gastric pH >4.

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12
Q

Ingredients in Antacids

A
  • Aluminum hydroxides—constipation
  • Magnesium hydroxides— diarrhea
  • combinations of Al and Mg are popular.
  • Calcium carbonate (Tums™) gas ad acid reflux.
  • Simethicon—surfactant.
  • Anti reflux antacids, they usually contain alginic acid (floating gel) to prevent regurgitation ex. Gaviscon™.
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13
Q

H2 Histamine Receptor Antagonists

Mechanism of action:

A
  • Bind to & block H2 receptor stimulation by histamine.
  • Inhibit basal, food-stimulated, & nocturnal gastric acid secretion.
  • Reduce both the volume & H+ concentration of gastric acid secretion
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14
Q

H2 Histamine Receptor Antagonists

Side Effects:

A
  • Specificity for the H2 receptor & secondary importance of H2 receptors outside the stomach results in infrequent & mild adverse effects—minimal side effects (OTC).
  • The four H2 antagonists are equally efficacious but differ in potency
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15
Q

CIMETIDINE

Relative potency

A

1

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16
Q

RANITIDINE

Relative potency

A

4-10

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17
Q

NIZATIDINE

Relative potency

A

4-10

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18
Q

FAMOTIDINE

Relative potency

A

20-50

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19
Q

Cimetidine inhibits

A

The activity of cytochrome p450 & thus slows the metabolism of many drugs. If drugs interactions are to be avoided, choose an H2 blocker other than cimetidine.

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20
Q

Proton pump inhibitors

Pharmacological effects:

A

These drugs inhibit the hydrogen ion pump that is responsible for secreting HCl into the gastric lumen. They can inhibit HCL secretion by more than 90%

21
Q

Omeprazole and Esomeprazole: Inhibit/duration

A

These drugs inhibit acid secretion & are effectively orally. They have a long duration of action & are more powerful than H2 blockers in inhibiting HCl secretion.

22
Q

Lansoprazole: less effective?

A

This compound has similar indication to Omeprazole, except that it is less effective in severe esophagitis.

23
Q

Rabeprazole: metabolized

A

This drug is metabolized to a much lower extent by the cytochrome P450 system.

24
Q

Mechanism of action of PPI

A

• Enteric coating allows release of prodrug in the intestine.
• In neutral pH environment of the intestine, the PPI prodrug is stable.
• Lipid solubility of PPIs permits absorption into the bloodstream.
• PPIs are then carried by the blood to the parietal cells & diffuse into the secretory canaliculi, where the acid pH causes protonation & trapping of the
drug near the proton pump.

25
Q

Protonated PPI is active and permits

A

irreversible binding to H+/K+ ATPase enzyme molecules. This bond prevents the movement of hydrogen ions from the parietal cell into the stomach.

26
Q

PPI Result in:

A

Achlorhydria - ALL gastric acid secretion is blocked. In order to return to normal acid secretion, the parietal cell must synthesize new H+/K+ ATPase.

27
Q

Clinical uses of proton pump inhibitors:

A

—Short-term treatment of active PUD, for the management of Zollinger-Ellison syndrome & in refractory gastric, esophageal & duodenal ulcers.
—Management of the symptoms of GERD.
—A single daily dose is safe and effective even for long term (> 2 years) use.

28
Q

Cytoprotective agents

A

Bismuth subsalicylate
Sucralfate
Misoprostol

29
Q

Bismuth subsalicylate

Mechanism/treatment for:

A

Enhances secretion of mucus and HCO3-.
– Inhibits pepsin activity.
– Chelates with proteins at the base of the ulcer
crater & forms a protective barrier against acid & pepsin.
– Inhibits H. Pylori.
– An effective adjunct for treatment & prophylaxis of duodenal & gastric ulcers, GERD & diarrhea.

30
Q

Sucralfate

Mechanism/treatment for:

A
  • Forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid & pepsin.
  • Is the only agent in its class that requires an acid pH for its maximal activity.
  • Has special value in H2-blocker or PPI-induced pneumonia in bedridden patients.
31
Q

Misoprostol

Mechanism/treatment for:

A
  • Slowly metabolized analog of PGE1.
  • Stimulates mucus and HCO3- production.
  • Has intolerable side effects; Causes diarrhea in 40% of patients.
  • Primarily used for patients who must use NSAIDs.
  • Off label use.
32
Q

ANTIBIOTIC TERAPY IN THE TREATMENT OF PUD

A

(a) Clarithromycin
(b) Amoxicillin
(c) Tetracycline
(d) Metronidazole
(e) Furazolidine (FZD)

33
Q

Clarithromycin is

A

a macrolide that inhibits protein synthesis in microbes.

34
Q

Amoxicillin is

A

Effective against gram negative bacilli. This drug is contraindicated in patients allergic to penicillin.

35
Q

Tetracycline is

A

a second line drug, which may be used instead of
amoxicillin in patients allergic to penicillin. It is necessary to stagger its dose when it is given in conjunction with Bismuth.

36
Q

Metronidazole is

A

a synthetic antibiotic that is active against obligate anaerobes.

37
Q

Furazolidine (FZD) a

A

nitrofuran antibacterial & antiprotozoal.

38
Q

Antibiotic Therapies for Treatment of H. Pylori Induced PUD

A

Antibiotics are given as multi-drug regimen to reduce the incidence of resistance & to increase the efficacy of these drugs.

39
Q

Gastroesophageal reflux disease (GERD)

Definition:

A

GERD is defined as conditions associated with involuntary regurgitation of gastric contents particularly at night (nocturnal) or when the stomach is full.

40
Q

Gastroesophageal reflux disease (GERD)

Two conditions cause a reflux episode to occur:

A
  1. Gastrointestinal contents must be ready to reflux.

2. The anti-reflux mechanism at the LES is compromised.

41
Q

Postural & dietary therapy of GERD [condition 1]:

A
  1. Decrease gastric contents, i.e. decrease size of meal.
  2. Weight reduction.
  3. Bed elevation
  4. Low fat diet
  5. Avoid agents that decrease LES, coffee, peppermint.
42
Q

DRUGS USED IN THE TREATMENT OF GERD

Classes

A
  1. Prokinetic Drugs (gastric motility enhancing drugs)

2. Antisecretory Drugs

43
Q

Prokinetic Drugs perform:

A
  • Target the physiology of GERD.
  • Improve LES tone & competence.
  • Enhance esophageal clearance.
  • Improve delayed gastric emptying.
44
Q

Prokinetic Drugs Examples:

A

—Metoclopramide
—Domperidone
—Cisapride

45
Q

Metochloparmide & Domperidone:

Mechanism of action:

A

They are Dopamine2 receptor blockers. Within the GI tract blockade of D2 receptors increases the local release of acetyl choline via 5HT4-R agonism.

46
Q

Metochloparmide & Domperidone:

Pharmacological actions

A
  • Stimulates GI smooth muscle
  • Increases amplitude of esophageal contractions
  • Accelerates gastric emptying
  • Increases LES pressure
  • Therefore, the main anti-reflux is enhanced gastric emptying.
47
Q

Metochloparmide & Domperidone:

Side effects:

A

High incidence of side effects related to central dopaminergic antagonism such as tardive dyskinesia. Therefore, prescribed for short periods of time (1-2 weeks).

48
Q

DRUGS USED IN THE TREATMENT
OF GERD
Antisecretory Drugs Examples:

A
  1. H2-receptor blockers:

2. Proton pump inhibitors:

GI Liver Pharmacology (9 decks)

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