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S2 Case 1 - IBD > Treatment of Dyspepsia, Peptic Ulcer Disease + GORD > Flashcards

Treatment of Dyspepsia, Peptic Ulcer Disease + GORD Flashcards

1
Q

What are the 3 main treatments?

A

Neutralisation
Reduction of acid secretion
Prokinetics

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2
Q

What are the treatments for neutralisation?

A

Antacids
Alginates
Sucralfate (mucosal protectants)

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3
Q

What are the treatments for reduction in acid production?

A

Proton pump inhibitors
Histamine H2 receptor antagonists

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4
Q

What are antacids?

A

Weak bases
Neutralise excess acid in stomach

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5
Q

Describe treatment of antacids

A

Quick BUT short term
Increase pH

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6
Q

What do antacids not do?

A

Prevent over-production of acid

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7
Q

What is an example of antacid?

A

Gaviscon
Has foaming agent = stops acid damaging mucosa

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8
Q

What are antacids normally combined with?

A

Alginates + foaming agents

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9
Q

Describe systemic antacids

A

Useful in short term therapy
Rapid onset
BUT prolonged = overload to kidney

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10
Q

Describe non-systemic antacids

A

Useful in long term
Most doses remain in GI tract
eg. Tums, Rennies

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11
Q

What are the interactions of antacids?

A

Bind to other drugs = reduce bioavailability
Chemical inactivation of drugs
Increase gastric pH = decrease drug absorption + excretion

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12
Q

What can be the adverse effects of antacids?

A

Mg(OH)2 = laxative properties
Al(OH)3 = constipation
CaCO3 = renal calculi (stones)
CO3 = bloating + flatulence

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13
Q

Describe alginates

A

Forms protective barrier on top of gastric contents
Usually combined with antacid

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14
Q

What do muscarinic receptor antagonists do?

A

Block competively

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15
Q

What do H2 receptor antagonists do?

A

Block competively

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16
Q

What do PPIs do?

A

Block by covalent modification

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17
Q

What do NSAIDs do?

A

Block irreversibly

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18
Q

What do PPIs do?

A

Act upon parietal cells

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19
Q

What are PPIs?

20
Q

What are examples of PPIs?

A

Omeprazole
Lansoprazole

21
Q

What does it mean that PPIs are prodrugs?

A

Inactive at neutral pH
BUT active in acidic conditions

22
Q

What do PPIs have?

A

Enteric coating to resist gastric metabolism

23
Q

How do PPIs work?

A

Activated form binds irreversibly to cysteines of H+/K+-ATPase
= inhibits active proton pump
= prevents movement of H+

24
Q

What is achlorhydria?

A

All gastric acid secretion blocked

25
Q

Describe omeprazole activation + activity

A

Diffuse into parietal cells
Activated by proton-catalysed formation of sulfenic acid
Active drug irreversibly binds sulfhydryl group of cysteines of H+/K+ pump
Irreversible inactivation of proton pump

26
Q

Why is timing of dosing important for PPIs?

A

Drug must be present in plasma at effective conc whilst proton pumps are active
Before food (30-60mins)

27
Q

When is full effect of PPI achieved?

A

After repeated dosing

28
Q

What does histamine do?

A

Stimulate acid production by parietal cells

29
Q

What does gastrin do?

A

Stimulate ECL cells to release high levels of histamine

30
Q

What are the 2 H2 receptor blockers?

A

Cimetidine
Ranitidine = fewer side effects

31
Q

How do H2 receptor antagonists work?

A

Act as competitive antagonists
Block histamine-mediated component of acid secretion
+ reduce secretion evoked by Ach + gastrie

32
Q

When is H2 receptor antagonists effective?

A

Once/twice daily by oral administration

33
Q

What are the pharmacokinetics of H2 antagonists?

A

Rapidly absorbed after oral administration
Conc peak 1-3hrs
Therapeutic levels maintained up to 12hrs

34
Q

What does cimetidine inhibit?

A

Hepatic P450s = which modulate drug metabolism

35
Q

What decreases effectiveness of H2 antagonists?

36
Q

What does PGE + PGI do?

A

Synthesized by gastric mucosa
Bind to EP3 receptors = decrease acid production

37
Q

What are the cytoprotective effects of PGE + PGI?

A

Stimulate mucin + bicarbonate production

38
Q

What are the adverse effects of PGE + PGI?

A

Diarrhoea + abdominal cramps
Exacerbate inflammatory bowel disease

39
Q

What is sucralfate?

A

Complex of aluminium hydroxide + sucrose octasulphate

40
Q

What does sucralfate do?

A

Dissociates in gastric acid environment to anionic form
Forms complex gel with mucus
+ forms cross-linked viscous polymer

41
Q

What is the mechanism for sucralfate?

A

Acts as acid buffer + impairs diffusion of H+
Stimulates PG-synthesis + bicarbonate secretion

42
Q

What are the pharmacokinetics for sucralfate?

A

Only slightly absorbed from gut
Essentially free of side effects
Absorbed fraction excreted unchanged by kidney

43
Q

What is an example of prokinetic?

A

Dopamine receptor antagonist

44
Q

What does dopamine receptor antagonist do?

A

Enhance gastric motility
Increase rate of gastric emptying
Increase gastro-oesophageal tone

45
Q

Why are prokinetics rarely used?

A

Severe side effects
eg. fatigue, tremors , cardiac events

S2 Case 1 - IBD (18 decks)

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