Peptic Ulcer Diseases and Its Medicines

Dr. apt. Nunuk Aries Nurulta, M.Si.

Faculty of Pharmacy
Universitas Muhammadiyah Purwokerto

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 Peptic Ulcer Diseases (PUD)

• Peptic ulcer disease (PUD) is characterized by discontinuation in the inner

lining of the gastrointestinal (GI) tract because of gastric acid secretion or
pepsin.
• Today, testing for Helicobacter pylori is recommended in all patients with
peptic ulcer disease.
• Endoscopy may be required in some patients to confirm the diagnosis,
especially in those patients with sinister symptoms.

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 Peptic Ulcer Diseases (PUD)
• The two m ost com m on types
of peptic ulcer:
- Gastric ulcers
(Stomach)
- Duodenal ulcers
(Beginning of small
intestine/small
bowel/duodenum )
• A person may have both
gastric and duodenal ulcers
at the same time.
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 Sympthoms
• Many people with ulcers have no symptoms at all.
• Some people with an ulcer have belly pain, often in the upper abdomen.
• Sometimes food makes the pain better, and sometimes it makes it worse.
• Other symptoms include nausea, vomiting, or feeling bloated or full.
• It is important to know that there are many causes of abdominal pain, so not all pain in the
abdomen is an “ulcer”.
• The most important symptoms that ulcers cause are related to bleeding.
• Bleeding from an ulcer can be slow and go unnoticed or can cause life-threatening
hemorrhage.
• Ulcers that bleed slowly might not produce the symptoms until the person becomes anemic.
• Symptoms of anemia include fatigue, shortness of breath with exercise and pale skin color.

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 Causes/Risk Factors
• The two most important causes of ulcers are infection with Helicobacter pylori
and a group of medications known as NSAIDs.
• People infected with H. pylori are at increased risk of developing peptic ulcers.
• NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are a group of medications
typically used to treat pain.
• NSAID use is very common because many are available over the counter without
a prescriptionand therefore they are a very common cause of peptic ulcers.
• NSAIDs cause ulcers by interrupting the natural ability of the stomach and the
duodenum to protect themselves from stomach acid.
• NSAIDs also can interfere with blood clotting, which has obvious importance
when ulcers bleed.
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 Helicobacter pylori Infection

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 Virulence Factors of Helicobacter pylori

• Urease:
The secretion of urease breaks down urea into ammonia and
protects the organism by neutralizing the acidic gastric environment.
• Toxins:
CagA/VacA protein is associated with stomach mucosal inflammation
and host tissue damage.
• Flagella:
Provides motility and allows movement toward the gastric epithelium.

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 Virulence Factors of Helicobacter pylori

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 NSAID and PUD

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 NSAIDs MoA

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 Stomach Homeostasis

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 PUD Treatment

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 PUD Treatment
• First-line treatment for H. pylori-induced PUD is a triple regimen comprising two
antibiotics and a proton pump inhibitor (Pantoprazole, clarithromycin, and metronidazole
or amoxicillin are used for 7 to 14 days).
• If first-line therapy fails, quadruple therapy with bismuth and different antibiotics is used.
• Antisecretory drugs: 1) H2-receptor antagonists and 2) the proton pump inhibitor (PPIs).
• PPIs have largely replaced H2 receptor blockers due to their superior healing and efficacy.
• PPIs block acid production in the stomach, providing relief of symptoms and promote
healing.
• Treatment may be incorporated with calcium supplements as long-term use of the PPIs
can increase the risk of bone fractures.
• Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-
induced peptic ulcers.
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 Pharmacology Intervention

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 Drug Mechanism Scheme

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 Drug Mechanism Scheme
• A model of the regulation of gastric acid secretion
showing the actions of antisecretory drugs and
antacids.
• Production of gastric acid is stimulated by three
endogenous compounds: (1) acetylcholine (ACh) acting
at muscarinic (M) receptors; (2) histamine (Hist) acting
at histamine2 (H2) receptors; and (3) gastrin (Gast)
acting at gastrin (G) receptors.
• As indicated, all three compounds act through
intracellular messengers—either calcium (Ca++) or
cyclic AMP (cAMP)—to increase the activity of H+,K+-
ATPase, the enzyme that actually produces gastric acid.
• Prostaglandins (PG) decrease acid production, perhaps
by suppressing production of intracellular cAMP.
• The actions of histamine2 receptor antagonists
(H2RAs), proton pump inhibitors (PPIs), and other
drugs are indicated.
Fakultas Farmasi Fakultas Farmasi Fakultas Farmasi • (P = prostaglandin
Fakultas Farmasi receptor.)
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 H2 Blocker and Proton Pump Inhibitor

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 H2 Receptor Blockers

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 Proton Pump Inhibitors

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 Proton Pump Inhibitors

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 Antacids

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 Sucralfate
• The affinity of sucralfate for defective mucosa is
explained by the drug's viscous adhesiveness and the
formation of polyvalent bridges between the
negatively charged sucralfate polyanions and positively
charged proteins present in high concentrations in
mucosal lesions.
• Sucralfate also buffers acid, inhibits the action of
pepsin, and adsorbs bile salts.
• These properties of sucralfate enable the drug to act as
an effective barrier to the penetration of acid, pepsin,
and bile salts.
• Animal data show that the action of sucralfate is
sustained because of its viscous adhesiveness, slow
reaction with acid, and high affinity for defective
mucosa.
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 Anticholinergic

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 Terima Kasih

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