03.02 Drugs for Peptic Ulcer Disease Flashcards

1
Q
Distal to the junction between antrum and acid secretory mucosa
High risk of malignancy
H. pylori, NSAID-induced
Gastric acid output normal or decreased
Burning or gnawing discomfort
Precipitated by food
A

Gastric ulcer

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2
Q

First portion of the duodenum (within 3 cm of pylorus)
Rare risk of malignancy
H. pylori, NSAIDS
High gastric acid secretion, low bicarbonate secretion
Burning or gnawing, awakens at night
90 minutes to 3 hours after a meal, relieved by antacids or food

A

Duodenal ulcer

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3
Q

Burning pain on epigastric region, often accompanied by a feeling of post-prandial fullness

A

Dyspepsia

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4
Q

Protective factors of GI mucosa

A

Bicarbonate
Gastric mucosa
Prostaglandins
Nitric oxide

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5
Q

Damaging factors of GI mucosa

A
Stress and trauma
NSAIDS
H. pylori
Caffeine
Acids
Skipping meals
Smoking, alcohol
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6
Q

Rebound acidity, diarrhea, constipation, metabolic alkalosis, abdominal distension, gas flatulence

A

Antacids

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7
Q

Dizziness, inhibition of CYP450, hormonal imbalances, Vit B12 supplementation

A

H2 receptor antagonists

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8
Q

CYP450 inhibition, rebound acidity, Vit B12 supplementation

A

PPI

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9
Q

Constipation, flatulence, dry mouth

A

Sulcralfate

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10
Q

Blackening of tongue and stool

A

Bismuth chelate

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11
Q

Empiric trial acid suppresion for ___ is the recommended line of therapy

A

4-8 weeks

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12
Q

If initial acid suppression fails after ___, it is reasonable to step up therapy

A

2-4 weeks

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13
Q

Most sensitive and specific approach for examining the upper GI tract
Direct visualization of the mucosa
Test for malignancy

A

Endoscopy

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14
Q

Other diagnostic procedures for peptic ulcer diseases

A

Barium studies

H. pylori detection (urease test)

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15
Q

Two types of antacids

A

Bicarbonates

Hydroxides

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16
Q

Acid neutralizer only
Rapidly neutralizing HCl and reducing pepsin activity
Stimulate mucosal prostaglandin production
Weak bases that react with H+ to form a salt and water
Fast onset, short duration

A

Antacids

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17
Q

Symptomatic relief of acid peptic disorders
Reduce the phosphorus levels among patients with renal insufficiency/failure
Ca2+ supplement for patients with osteoporosis or hypocalcemia

A

Antacids

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18
Q

Adverse effects of antacids

A

Metabolic alkalosis
Rebound acidity
Increased acid secretion due to negative feedback
Milk-alkali syndrome
Flatulence, abdominal distention, bloating or belching

19
Q

CI in patients with cardiac or renal problems

A

Sodium bicarbonate

20
Q

Increase acid secretion due to negative feedback

A

Calcium carbonate

21
Q

Osmotic diarrhea
Hypermagnesemia
Flatulence

A

Mg(OH)2

22
Q

Constipation
Usually combined with Mg(OH)2
Hypophosphatemia
Flatulence

A

Al(OH)3

23
Q

Cimetidine, ranitidine, nizatidine, famotidine

A

H2 receptor antagonist

24
Q

Technically an antihistamine
Block H2 receptors of the parietal cells via competitive inhibition
Reduces the direct-stimulatory effect of gastrin and acetylcholine
Suppress basal gastric acid secretion
Longer effect than antacids

A

H2 receptor antagonist

25
Q

Indications of H2 receptor antagonists

A
Nocturnal acid secretion
Stress ulcers
NSAID-induced ulcers
GERD
Erosive esophagitis
Non-ulcer dyspepsia
First-line for bleeding from stress-related gastritis
26
Q

Adverse effects of H2 receptor antagonists

A
Mental status changes among the elderly
Cross the placenta
Secreted into breast milk
Blood dyscrasias
Arrythmia
27
Q

Prototype drug of H2 receptor antagonist

Rarely used because of its side effects (gynecomastia, galactorrhea, CNS effects)

A

Cimetidine

28
Q

Commonly prescribed
Inhibit nocturnal gastric secretion
Known to prevent stress ulcers

A

Ranitidine

29
Q

Ideal drug based on guidelines
Most potent acid inhibitory agents
Inhibits meal-stimulated acid secretion during the day as well as basal secretion overnight

A

PPI

30
Q

Irreversibly inhibits proton pump
Rapid onset and duration
Prodrug that require activation in an acidic environment

A

PPI

31
Q

Clinical uses of PPI

A

Gastric and duodenal ulcers, GERD, erosive esophagitis
Zollinger-Ellison syndrome
PPIs inhibit acid-secretion during fasting and during meals
Progressive acid inhibitory effects

32
Q

Most common adverse effects of PPI

A

Headache and diarrhea

33
Q

Included in the Philippine Drug Formulary

A

Omeprazole

34
Q

Provide physical barrier over the surface of the ulcer

Increase secretion of protectant mucus, prostaglandin, bicarbonate

A

Mucosal resistance enhancers

35
Q

Combination of sulfated sucrose and aluminum
Non-absorbable drug that provides a physical barrier unto the damaged mucosa to protect it against acid and pepsin
Stimulates secretion of mucus, bicarbonate and mucosal prostaglandin
Adminster on an empty stomach (acidic)

A

Sucralfate

36
Q

Clinical uses of sucralfate

A

Peptic ulcers

Reduce incidence of GI bleeding

37
Q

Protect gastric mucosa
Important H. pylori theraphy
Coats damaged mucosa, promotes secretion of bicarbonate and prostaglandins, and reduce peptic activity

A

Bismuth chelate

38
Q

Clinical use of bismuth chelate

A

Quadruple therapy for H. pylori

Hordes iron stores

39
Q

Increase mucus secretion

Reduces peptic activity

A

Carbenoxolone

40
Q

Prostaglandin E1 analogue
Increase mucus production
Enhancement of mucosal integrity and repair

A

Misoprostol

41
Q

Adverse effects of misoprostol

A

Diarrhea
Uterine bleeding and contractions
Abortifacient

42
Q

H. pylori eradication theraphy

A

OCA (most common)
OCM (penicillin allergies)
OCA/M + B (2nd line)

43
Q

Treatment duration of H. pylori

A

10-14 days