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GI > drugs used in peptic ulcer and dyspepsia > Flashcards

drugs used in peptic ulcer and dyspepsia Flashcards

1
Q

Peptic ulcer by Use of Nonsteroidal anti-inflammatory drug (NSAID)
Treatment Approaches?

A

Avoidance of NSAIDs/ prevention of ulcer

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2
Q

Inadequate mucosal defense against gastric acid

Treatment Approaches?

A

Protecting the gastric mucosa from damage

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3
Q

3 Drugs Classification

A
  1. Agents that reduce intragastric secretion/acidity
  2. Agents that enhance mucosal resistance/cytoprotective agents
  3. Drugs for treatment of Helicobacter Pylori infection
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4
Q

Agents that reduce intragastric secretion/acidity

A

1.Proton pump inhibitors(PPIs):
Omeprazole, esomeprazole, lansoprazole, dexlansoprazole, rabeprazole, pantoprazole
2. H2-receptor antagonists:
Cimetidine, ranitidine, famotidine
3. Antacids:
Aluminum hydroxide, calcium carbonate, Mg(OH)2, NaHCO3
Muscarinic antagonists (pirenzepine, telenzepine, propantheline, etc.)

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5
Q

Agents that enhance mucosal resistance/cytoprotective agents

A

Prostaglandin analogs:
Misoprostol, Sucralfate
Miscellaneous: carbenoxolone, bismuth compounds

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6
Q

Drugs for treatment of Helicobacter Pylori infection

A

Antibiotics:
Amoxicillin, Bismuth compounds, Clarithromycin, Metronidazole, Tetracycline

Triple therapy :(PPI + clarithromycin + amoxicillin or metronidazole)

Quadruple therapy: (PPI + metronidazole + Bismuth subnitrate + tetracycline)

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7
Q

Effects of Drugs on Acid Secretion

  • H2 receptor antagonist
  • Proton pump inhibitor
A

H2-receptor antagonist has a marked effect upon nocturnal acid secretion

Proton pump inhibitor suppresses meal-stimulated and nocturnal acid secretion

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8
Q

Proton pump inhibitors (PPI)

  1. examples
  2. What else does this drug require?
  3. 2 MOAs
  4. ROA
  5. Therapeutic Uses
A

1.PROLED:Pantoprazole,Rabeprazole,Omeprazole, Lansoprazole,Esomeprazole, Dexlansoprazole,

  1. Prodrugs - given 30min before meal
    - After absorption into systemic circulation, the prodrug diffuses into parietal cells and activated in the acidic secretory canaliculi
  2. MOA:
    - Irreversibly binds covalently with H+ K+-ATPase ( require18 hours to resynthesize new enzyme)
  • Inhibit both basal and stimulated gastric acid secretion
    4. enteric coated capsule / tablet / powder for suspension to protect them from premature degradation by gastric acid; intravenous :pantoprazole / lansoprazole

5.For short-term treatment 4-8 weeks for GU and DU
Zollinger-Ellison Syndrome (pathologic hypersecretion)
Treatment and prevention of NSAID-associated GU, Prevention of stress related mucosal bleeding(critical illness)
Multiple endocrine hyperplasia

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9
Q

PPI PHARMACOKINETICS

  1. ABSORPTION
  2. METABOLISM- what enzyme?
    - excretion
    - how many days therapy?
  3. PROTEIN BINDING
  4. GIVEN HOW MANY TIMES DAILY?
  5. WHEN IS DOSE REDUCTION REQUIRED?
A

1.Rapid absorption from small intestine
2. Extensively metabolised by CYP2C19 (slow metabolizer)
-Metabolites excreted in urine and faeces
-Takes ~5 days of therapy to get 70% inhibition of acid secretion at once daily dose.
3Highly protein bound.
4.Usually given twice daily.
5.Dose reduction needed in liver disease, but not in chronic renal failure.

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10
Q

PPI 8 ADVERSE EFFECTS

A
  1. Headache,
  2. Abdominal pain, diarrhoea, constipation,
  3. Myopathy
  4. Arthralgia, rash
  5. Vitamin B12 /Fe deficiency
  6. Prolonged hypochlorhydria
  7. Secondary hypergastrinemia/acid rebound,
  8. Use of these drugs can “mask” the symptoms of gastric cancer
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11
Q

PPI Drug Interaction

A
  1. Omeprazole inhibits the metabolism of warfarin, phenytoin, diazepam, and cyclosporine.
  2. PPIs + Clopidogrel → ↑ risk of major cardiovascular events OR acute coronary syndrome(↓ CYP2C19/3A4)
  3. ↑Fracture risk (↓ Ca2+ absorption, impaired activity of osteoclasts)
  4. Hypomagnesemia
  5. ↑ Enteric infections
  6. ↑ Community Acquired Pneumonia
  7. ↑ Neoplasia (gastric polyps/gastric cancer/gastric carcinoids/colon cancer)
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12
Q

PPI Drug administration- when?
- what should be taken after for
best effect?
- Regimen for GERD symptoms?

A
  1. PPIs should be taken 30 minutes before breakfast or the largest meal of the day.
  2. H2-receptor antagonist (if also needed) should be taken well after the PPI for best effect.
  3. In patients with GERD, PPI twice-daily regimen or PPI in the morning and adding an H2 antagonist in the evening may improve symptom control.
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13
Q

Agents Reduce Intragastric Secretion :
H2 receptor antagonists

  1. 5 EXAMPLES
  2. 2 MOA
A
  1. EXAMPLE: Cimetidine, Ranitidine, Famotidine, Nizatidine, Roxatidine
    Cimetidinewas the prototypical histamine H2-receptor antagonist from which later drugs were developed.
  2. MOA:
    -Inhibit acid production by reversible inhibition of H2-receptors on basolateral membrane of parietal cell.
    -Mainly inhibit nocturnal acid secretion
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14
Q

H2 receptor antagonists PHARMACOKINETICS

  1. ABSORPTION
  2. HOW MANY TIMES DAILY
  3. PROTEIN BINDING
  4. METABOLISM - in liver
    - excretion
  5. DOSE REDUCTION
A

PHARMACOKINETICS:

  1. Rapid absorption, peak 1-3 hr.
  2. Can be given twice daily in doses of 400-600 mg or 800mg at bedtime
  3. Minimal protein binding.
  4. Metabolized <30% in liver. Excreted in urine (reduce dose in renal impairment).
  5. dose reduction in renal disease
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15
Q

H2 receptor antagonists SIDE EFFECTS

A
  1. In general, well tolerated, except forcimetidine
  2. Few S/E reported: Diarrhoea, headache, drowsiness, fatigue, muscle pain, confusion, hallucination, slurred speech, blood dyscrasias
  3. Crosses placenta, and Secreted in breast milk
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16
Q

3 Uses of H2 Blockers

A

DU/GU by mainly inhibit nocturnal acid secretion -The most determinant of the rate of healing of DU

treatment of GERD,

prevent occurrence of stress ulcer

17
Q 
1. DRUG INTERACTIONS OF H2 BLOCKERS 
(cimetidine and ranitidine)
2. Tolerance
3. CNS penetration
4. Excretion
A

Cimetidine –

  1. decrease testosterone binding to androgen receptor gynaecomastia (reversible),
    - Inhibits CYPs :CYP1A2, CYP2C9, CYP2D6 that metabolize estradiol and many other drugs( warfarin,phenytoin,quinidine,carbamazepine,theophyline,imipramine) —> increase drug serum level
  2. Tolerance occurs With Chronic use of H2 blockers (but not with PPIs.)
  3. Penetration of cerebrospinal fluid occurs at high dose
  4. unchanged drug and metabolites appear in urine and bile

Ranitidine
inhibits CYPs minimally. Famotidine has no significant effect.

18
Q

Agents Reduce Intragastric Acidity: Antacids

  1. 4 examples
  2. what are they?
  3. ROA
  4. Constituents
  5. Why are Mg and Al used in combinations?
A

1.Aluminum hydroxide Al(OH)3, Calcium carbonate, Mg(OH)2, NaHCO3

  1. They are weak bases that react with gastric hydrochloric
  2. Antacids are used in combination (liquid/tablet) to neutralize acid.
  3. Most antacids have principal constituent Magnesium or Aluminum alone or combination:
    -Aluminium hydroxide (usually a mixture of Al(OH)3 and aluminium oxide) and/or magnesium hydroxide [Mg(OH)2].
    - Occasionally combined with Sodium carbonate [NaCO3] or Calcium salt
  4. Mg has laxative effects (Used prior to endoscopy) and
    Al causes constipation so using both gives neither constipation or diarrhoea
19
Q

Antacids-MOA-

  1. How?
  2. Can we heal ulcer using antacids alone?
  3. Used for?
A
  1. -Ability to reduce gastric acidity
    - NaHCO3 + H ions—> H2CO3—>H20 + CO2
  • NaHCO3—> Na ions + HCO3 that are absorbed into circulation In intestine
  • Pepsin is inactive in solution above pH 4.0
    2. Ulcer healing effectiveness by antacids alone is inadequate
    3. It is for symptomatic relief and only justified for minor symptoms
20
Q

ANTACIDS: HOW LONG AFTER MEALS? WHY

DOSAGE

A

Normally given 1 hour after a meal effectively neutralizes gastric acid for 2 hours.

A second dose given 3 hours after eating – will then maintain the effect for 4 hours after meals

21
Q

Adverse effects of the 4 Antacids

A
  1. Aluminium hydroxide :hypophosphatemia, constipation,
  2. Magnesium hydroxide :diarrhoea,
  3. Calcium carbonate :hypercalcaemia and causes rebound acid secretion, chelation of drugs given together
  4. Sodium bicarbonate: sodium overload, metabolic alkalosis
22
Q

Prostaglandin analogs: Misoprostol

MOA

A

Misoprostol:

PGE2 & PGI2 synthesized by gastric mucosa & bind to EP3 receptor
Stimulate the Gi pathway decrease cAMP and gastric acid secretion.
2. Cytoprotective effect(high dose) = stimulate mucus and bicarbonate secretion & increase mucosal blood flow
Misoprostol (analog of PGE1) inhibit basal acid secretion ~90% and food-stimulated secretion ~80%.

23
Q

Adverse effects of misoprostol

A

Diarrhoea, abdominal pain & cramps

24
Q

CONTRAINDICATION of misoprostol

A
  1. Contraindicated during pregnancy
    (stimulate uterine contraction,
    2.used for therapeutic abortion
25
Q

CLINICAL USE of misoprostol

effectiveness for peptic ulcer compared to H2 antagonists and PPIs

A

To prevent or reduce NSAID induced mucosal injury(e.g. in patients with rheumatoid arthritis);
less effective than H2 antagonists and the PPIs in acute treatment of peptic ulcers)

26
Q

What is Sucralfate ?

A

Complex of aluminium hydroxide and sucrose-octasulfate

27
Q
  1. MOA of Sucralfate

2. Does it prevent NSAID-induced ulcers?

A

In acid pH, sucralfate forms viscous sticky polymer that form complex gels with mucus and adheres to epithelial cells and ulcer crater for 6 hr
Thus creates a physical barrier which prevents destruction of mucosa by pepsin, acid and bile.
Stimulates prostaglandin release as well as mucus and bicarbonate output, and it inhibits peptic digestion.

Does not prevent NSAID-induced ulcers, nor does it heal gastric ulcers.

Sucralfate effectively heals duodenal ulcers and is used in long-term maintenance therapy to prevent their recurrence.

28
Q
  1. Drug Interaction of Sucralfate

2. Sytemic Side effects?

A

1.As it requires an acidic pH for activation, sucralfate should not be administered with H2 antagonists or antacids or PPI.
Interfere with the absorption of other drugs by binding to them (quinolones, digoxin, theophylline, amitriptyline etc.)

2.Some of the drug is absorbed systemically, no systemic side effects.

29
Q

3 Therapeutic Uses of sucralfate

A
  1. Prophylaxis of bleeding from stress ulcer
  2. Oral mucositis (radiation, aphthous ulcer)
  3. As enema for radiation proctitis
30
Q

3 Therapeutic Uses of sucralfate

A
  1. Prophylaxis of bleeding from stress ulcer
  2. Oral mucositis (radiation, aphthous ulcer)
  3. As enema for radiation proctitis
31
Q

4 Adverse effects of sucralfate

  • which patient to avoid in?
A

1 .Constipation

  1. Inhibit absorption of other drugs in GIT
  2. Formation of bezoars in stomach

-Avoid in patient with renal failure

32
Q

name 2 Bismuth compounds

2 MOA

A
  1. subcitrate, subsalicylate

2-Bind to base of ulcer, coating it and protecting it from acid & pepsin
-Promote mucin and bicarbonate secretion

33
Q

Uses of Bismuth Compounds

A
  1. Have significant antibacterial effects

2. Used to eradicate H pylori infection and prevent ulcer recurrence

34
Q

4 Side effects of Bismuth compounds

A

Side effects: black stool, constipation, darkening of tongue, neurotoxicity with long term use

35
Q

Therapy of Helicobacter pylori Infection

A

Triple therapy x 10-14 days:

PPI healing dose twice/d (see lower pane) +
Clarithromycin 500 mg +
(Amoxicillin 1 g or Metronidazole 500 mg ) twice a day.
(Tetracycline 500 mg can be substituted for amoxicillin or metronidazole.)

Quadruple therapy x 7-14 days:

Proton pump inhibitor twice a day +
Metronidazole 500 mg three times daily +
Bismuth subsalicylate 525 mg four times daily +
Tetracycline 500 mg four times daily
or
H2 receptor antagonist twice a day +
Bismuth subsalicylate 525 mg four times daily +
Metronidazole 250 mg four times daily +
Tetracycline 500 mg four times daily

36
Q
  1. Normal control of acid secretion

2. How does H pylori increase gastric acid?

A

1.Normal control of acid secretion:
A low antral pH stimulates release of somatostatin from D cells in the antral glands.
Somatostatin inhibits gastrin release from adjacent G cells and acid secretion reduced.

  1. -H. pylori produces alkaline ammonia to protect itself against acidity in the stomach
    - Production of NH3 on the surface of gastric epithelium and antral gland, prevents ‘D’ cells from sensing the true level of luminal acidity
    - Somatostatin release is reduced and gastrin release is increased leading to excess acid secretion
37
Q

Synthesis of prostaglandin and function

A

slide 29

GI (5 decks)

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