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GIT > Gastritis and Peptic Ulcer Pharm > Flashcards

Gastritis and Peptic Ulcer Pharm Flashcards

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1
Q

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

A

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

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2
Q

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

A

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

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3
Q

How do NSAIDs promote the formation of peptic ulcers?

A

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

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4
Q

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

A

H2 receptors (GPCR)

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5
Q

What are 3 drug classes that reduce gastric acidity?

A

1) Antacids
2) H2-blockers
3) PPIs

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6
Q

(Strong/weak) bases are used as antacids.

A

Weak

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7
Q

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

A

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

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8
Q

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

A

Faster (faster rate of dissolution)

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9
Q

What are the clinical indications for antacids?

A

Non-prescription (OTC) remedy for heartburn and dyspepsia

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10
Q

Some antacids preparations contain simethicone as a ___________.

A

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

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11
Q

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

A

False

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12
Q

What are 3 AEs of antacids?

A

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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13
Q

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

A

Mg(OH)2 and Al(OH)3

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14
Q

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

A

px with renal insufficiency (need to secrete out)

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15
Q

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

A

Alter stomach/GIT pH → affect absorption of other medications

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16
Q

What is the moa of antacids?

A

Neutralise gastric acid to form salt and water

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17
Q

What is the moa of H2-receptor antagonists?

A

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

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18
Q

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

A

True

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19
Q

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

A

More effective for nocturnal acid secretion (histamine)

Modest effect of meal-induced (gastrin and ACh)

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20
Q

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

A

Famotidine > Ranitidine > Cimetidine

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21
Q

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

A

True

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22
Q

What are 4 AEs of H2 antagonists?

A

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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23
Q

What is the moa of PPIs?

A

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

  • some anti-microbial activity against H. pylori
24
Q

What are 2 examples of PPIs?

A

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

25
Q

PPIs are administered as (active/inactive) forms.

A

Inactive pro-drugs
(active drug very poorly absorbed)

26
Q

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
A

Enteric-coated formulation

Absorbed in intestines

Protonated, activated and concentrated in parietal cell canaliculi

Forms irreversible covalent disulphide bonds with H+/K+-ATPase

27
Q

Where are PPIs activated?

A

Parietal cell canaliculi

28
Q

What time are PPIs supposed to be taken?

A

On an empty stomach (usually before breakfast)
- 1hr before meal (so present when pumps are active)

(Oral F ↓50% by food)

29
Q

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

A

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

30
Q

PPIs block (active/quiescent pumps).

A

Active pumps
(must be present during mealtime)

31
Q

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.

A

True

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

32
Q

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

A

True

33
Q

What are 4 AEs of PPIs?

A

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

34
Q

What are 3 cytoprotective agents used for gastric mucosal protection?

A

1) Sucralfate
2) Bismuth compounds
3) Misoprostol

35
Q

Why does sucralfate have little to no systemic effects?

A

Highly insoluble

36
Q

What is the moa of sucralfate?

A

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

37
Q

What are 2 AEs of sucralfate?

A

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

38
Q

When are sucralfate adminstered?

A

Empty stomach (at least 1hr before meals)

39
Q

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

A

False
Used as adjunct for preventing stress-related bleeding in critically-ill px

Limited use for ulcers (H2 antagonist and PPIs more effective)

40
Q

What is the moa of bismuth?

A

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

41
Q

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

A

Prolonged use: bismuth toxicity
→ encephalopathy (ataxia, headaches, confusion, seizures)

(<1% that is absorbed is eliminated by slow renal excretion)

42
Q

How is bismuth eliminated?

A

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

43
Q

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

A

Bismuth compounds

44
Q

What is the clinical indication for misoprostol?

A

Preventing NSAID-induced peptic ulcers

45
Q

What is the moa of misprostol?

A

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

46
Q

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

A

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

47
Q

What are 4 AEs of misoprostol?

A

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

48
Q

Why is misoprostol rarely used today?

A

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

49
Q

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

A

R to metronidazole and clarithromycin when given alone

50
Q

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

A

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

51
Q

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

A

Change amoxicillin to metronidazole
CAO → CMO

52
Q

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

A

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

53
Q

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

PPIs are administered ___/day within ________ of food

A

AB: 2x/day, within 1hr of food

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

54
Q

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

A

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

55
Q

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

A

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

56
Q

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

A

1) Diarrhoea
2) Nausea
3) Vomiting

GIT (14 decks)

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