Gastritis and Peptic Ulcer Pharm Flashcards by Wei Shynn Tan

What are 5 factors that promote the formation of peptic ulcers?

1) H. pylori
2) NSAIDs
3) Acid
4) Pepsin
5) Smoking

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What are 4 endogenous factors that prevent the formation of peptic ulcers?

1) Prostaglandins → →
2) HCO3-
3) Mucous
4) Blood flow

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How do NSAIDs promote the formation of peptic ulcers?

NSAIDs inhibit COX → ↓prostaglandins
→ ↓mucus, HCO3-, blood flow

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What type of receptors are responsible for the activation of protons pumps in parietal cells?

H2 receptors (GPCR)

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What are 3 drug classes that reduce gastric acidity?

1) Antacids
2) H2-blockers
3) PPIs

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(Strong/weak) bases are used as antacids.

Weak

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What are 4 examples of antacids in decreasing rates of neutralisation?

NaHCO3 > CaCO3 > Mg(OH)2 > Al(OH)3

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Liquid antacids have a (faster/slower) onset than tablet formulations.

Faster (faster rate of dissolution)

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What are the clinical indications for antacids?

Non-prescription (OTC) remedy for heartburn and dyspepsia

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Some antacids preparations contain simethicone as a ___________.

Anti-foaming agent (eases gas release in the GIT via burping/flatulence)

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True or False: Large and frequent doses are sufficiently potent to treat peptic ulcers or GERD.

False

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What are 3 AEs of antacids?

1) Na+:
- fluid retention, HTN, CHF,

2) Ca2+:
- HyperCa2+, Rebound acid secretion

3) Na/Ca:
- Metabolic alkalosis
- Milk-alkali syndrome

4) HCO3/CO3
- CO2 gas formation → gastric distention, belching, flatulence

5) Mg2+:
- Osmotic diarrhoea

6) Al2+:
- Constipation

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Which 2 salts are often combined in formulation to minimise their impact on bowel function?

Mg(OH)2 and Al(OH)3

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In which px should long-term use of antacids be avoided?

px with renal insufficiency (need to secrete out)

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Why should antacids not be taken within 2 hours of other medication?

Alter stomach/GIT pH → affect absorption of other medications

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What is the moa of antacids?

Neutralise gastric acid to form salt and water

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What is the moa of H2-receptor antagonists?

Competitively inhibit H2 receptor on parietal cells → suppress acid secretion by parietal cells

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True or false: H2-receptor antagonists inhibit 60-70% of total 24hr gastric acid secretion.

True

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H2-receptor antagonists are (more/less) effective at inhibiting nocturnal acid secretion than meal-induced acid secretion.

More effective for nocturnal acid secretion (histamine)

Modest effect of meal-induced (gastrin and ACh)

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What are 3 examples of H2-receptor antagonists (in order of decreasing potency)?

Famotidine > Ranitidine > Cimetidine

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True or false: H2 antagonists are relatively safe drugs with high TI.

True

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What are 4 AEs of H2 antagonists?

Famo/Ranitidine:
1) Headache, nausea, xerostomia
2) Rare: tachycardia, blood dyscrasia, blurred vision, MSK pain

Cimetidine:
3) Headache, nausea, constipation, fatigue
4) Mental confusion (critically ill/renal or hepatic dysfunction)
5) Anti-androgenic: gynecomastia, impotence, galactorrhea (inhibits estradiol metabolism, ↑serum prolactin)

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What is the moa of PPIs?

Study These Flashcards

Irreversibly block H+/K+-ATPase in parietal cells

some anti-microbial activity against H. pylori

What are 2 examples of PPIs?

Study These Flashcards

1) Omeprazole (Racemic mixture)
2) Esomeprazole (S/L-isomer)

PPIs are administered as (active/inactive) forms.

Inactive pro-drugs (active drug very poorly absorbed)

PPIs are administered in a _________-coated formulation which protects against activation by stomach acidity. - absorbed in the _________ - protonated, activated and concentrated in _________ - forms reactive thiophilic sulphenamide active drug with forms _________ bonds with H+/K+-ATPase to inhibit gastric acid secretion

Enteric-coated formulation Absorbed in intestines Protonated, activated and concentrated in parietal cell canaliculi Forms irreversible covalent disulphide bonds with H+/K+-ATPase

Where are PPIs activated?

Parietal cell canaliculi

What time are PPIs supposed to be taken?

On an empty stomach (usually before breakfast) - 1hr before meal (so present when pumps are active) (Oral F ↓50% by food)

Why can't PPIs be chewed or cut for easier swallowing?

Break enteric-coating → premature-activation in stomach → does not reach target parietal cell canaliculi (where H+/K+ ATPase are)

PPIs block (active/quiescent pumps).

Active pumps (must be present during mealtime)

True or false. PPIs have a long duration of action and thus once daily dose is sufficient to reach maximal acid secretion inhibition regardless of duration of course.

True but takes 3-4 days/doses to fully inhibit acid secretion

True or false: Mean 24hr intra-gastric pH is increased to pH3-4 by PPIs.

True

What are 4 AEs of PPIs?

1) Headaches 2) Nausea 3) Flatulence 4) Diarrhoea 5) Dizziness 6) Rash 7) ↑risk of C. diff and MDR infections 8) HypoMg 9) ↑risk of microscopic colitis 10) Rare: acute interstitial nephritis, ↑CKD risk, CLE/SLE

What are 3 cytoprotective agents used for gastric mucosal protection?

1) Sucralfate 2) Bismuth compounds 3) Misoprostol

Why does sucralfate have little to no systemic effects?

Highly insoluble

What is the moa of sucralfate?

1) Broken down → -ve sucrose sulphate → binds to +ve proteins @ ulcer → forms viscous, tenacious gel (prevents further attack) 2) Stimulates mucosal prostaglandin → HCO3 and mucous secretion

What are 2 AEs of sucralfate?

1) Constipation (contains Al(OH)3) 2) Impairs other drug absorption (bind to +ve drugs)

When are sucralfate adminstered?

Empty stomach (at least 1hr before meals)

True or false: Sucralfate are most commonly used for ulcers and preventing stress-related bleeding in critically-ill px.

False Used as adjunct for preventing stress-related bleeding in critically-ill px Limited use for ulcers (H2 antagonist and PPIs more effective)

What is the moa of bismuth?

1) form protective layer to protect ulcers 2) Stimulates mucus and HCO3 secretion 3) Directly anti-microbial activity against H. pylori

Why are bismuth compounds only used for short periods and avoided in px with renal insufficiency?

Prolonged use: bismuth toxicity → encephalopathy (ataxia, headaches, confusion, seizures) (<1% that is absorbed is eliminated by slow renal excretion)

How is bismuth eliminated?

>99% in stools <1% absorbed then slow renal excretion

Blackening of stools and reversible darkening of the tongue is caused by what class of peptic ulcer drugs?

Bismuth compounds

What is the clinical indication for misoprostol?

Preventing NSAID-induced peptic ulcers

What is the moa of misprostol?

Synthetic PGE1 analogue - binds to PGE2 receptors - low dose (cytoprotective): ↑HCO3, mucus and blood flow - high dose (antisecretory): inhibit gastric acid secretion

Misoprotol is given (oral/IV/IM/Subcut) and has a (short/long) T1/2.

Oral and short T1/2: 30mins (given 4x/day)

What are 4 AEs of misoprostol?

1) Abdominal pain 2) Diarrhoea 3) Abortion (uterine contraction) 4) Bone pain, hyperostosis

Why is misoprostol rarely used today?

1) COX-2 selective NSAIDs 2) Non-compliance (Multiple daily dosing) 3) AEs 4) Abuse as abortifacient

Why is a double antibiotic therapy needed for H. pylori infections?

R to metronidazole and clarithromycin when given alone

What is the first and second line therapy for H. pylori infections?

1st line (7-14 days): CAO 1) Clarithromycin 2) Amoxicillin/Metronidazole 3) Omeprazole/Esomeprazole 2nd line (10-14days): 1) Clarithromycin 2) Amoxicillin/Metronidazole 3) Omeprazole/Esomeprazole/H2 antagonist 4) + Bismuth

How does first line therapy against H. pylori change when the px is allergic to penicillin?

Change amoxicillin to metronidazole CAO → CMO

True or false: The therapeutic goal of H. pylori therapy is to promote the repair of peptic ulcers through anti-secretory therapy.

False. Need anti-secretory (PPI/H2 antagonists) + Antimicrobials (recurrence is 60-100% w/o eradication.

In H. pylori triple therapy: ABs are administered ____/day within ________ of food to reduce GI AEs PPIs are administered ___/day within ________ of food

AB: 2x/day, within 1hr of food PPIs: 2x/day, 30min-1hr before food with >2hrs of fasting

How do PPIs aid in the eradication of H. pylori in triple therapy?

1) Direct (minor) antimicrobial properties 2) ↑intragastric pH → ↓symptoms of peptic ulcers and ↑healing → ↓MIC of ABs (more effective)

After completion of H. pylori triple therapy, ___________ are continued for _____________________.

PPIs continued for: Duodenal: 4-8 wks Gastric: 8-12 wks

What are 3 common AEs of H. pylori triple therapy?

1) Diarrhoea 2) Nausea 3) Vomiting

Gastritis and Peptic Ulcer Pharm Flashcards

(56 cards)