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Clinical Pharmacology > 10.1 GI Pharmacology > Flashcards

10.1 GI Pharmacology Flashcards

1
Q

Why are peptic ulcers difficult to locate?

A

As visceral pain felt is not well localised - manifests as general epigastric pain
Chronic ulcers can be asymptomatic so no pain to help localise.

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2
Q

Why do asymptomatic chronic ulcers pose a difficulty in treating patients?

A

Can be a challenge as do not realise they have chronic ulceration and are mistakenly put on a drug that puts them at increased risk of bleeding.

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3
Q

What are potential complications of peptic ulceration?

A

Bleeding, perforation, scarring and possible obstruction especially if around the pyloric sphincter

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4
Q

What are risk factors of peptic ulceration?

A 
Inability of normal acid to inhibit further acid secretion
Early gastric emptying 
Helicobacter pylori 
NSAIDs
Smoking and alcohol delay healing
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5
Q

What drug class is Gaviscon?

A

Alginates and antacids

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6
Q

What is the function of antacids?

A

Buffering the stomach acid, increases the pH and therefore decreases the likelihood of ulcer formation as less damage from stomach acid

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7
Q

What is the function of alginic acid?

A

Increase stomach content viscosity and reduce reflux

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8
Q

Give an example of a alginate and antacid compound preparation

A

Sodium alginate (salt alginic acid)
+
Aluminium hydroxide/magnesium carbonate (antacid)

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9
Q

Why are antacids given as a combination of magnesium and aluminium salts?

A

Magnesium salts can cause diarrhoea and aluminium salts can cause constipation, so limits the amount of adverse effects as they’re adverse effects cancel out

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10
Q

When are antacids and alginates contraindicated?

A

Na+ and K+ containing preparations should be used with caution in renal failure
High [sucrose] in some preparations – hyperglycaemia in DM

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11
Q

What are the important drug-drug interactions of Gaviscon?

A

Can reduce absorption and therefore oral bioavailability of many drugs so dose timings should be separated
Increased urine alkalinity can increase aspirin excretion

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12
Q

What is the drug class of lansoprazole and omeprazole?

A

Proton pump inhibitors.

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13
Q

Describe the mechanism of action of lansoprazole

A

Irreversibly inhibit the H+/K+ ATPase in gastric parietal cells, reducing the amount of H+ secreted into the stomach
Final stage in the pathway – very significant reduction in acid secretion

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14
Q

What are the adverse drug reactions of lansoprazole?

A

GI disturbance - abdominal pain, constipation, diarrhoea
Headache, dizziness
Drowsiness/confusion

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15
Q

What are the warnings/contraindications of omeprazole?

A

Mask symptoms of gastro-oesophageal cancer

Osteoporosis - fracture risk

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16
Q

Why is lansoprazole preferentially prescribed instead of omeprazole on coronary intervention?

A

As omeprazole is a CYP inhibitor and reduces the action of clopidogrel ( a prodrug)
Lansoprazole is not a CYP inhibitor

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17
Q

What are the important drug-drug interactions of PPIs?

A

Omeprazole CYP inhibitor – reduced clopidogrel action

PPIs can increase effects of warfarin and phenytoin - monitor

18
Q

PPIs should be prescribed for the ‘Shortest effective duration at lowest effective dose’. Why?

A

Due to significant ADRs

19
Q

Why are PPIs prescribed alongside NSAIDs and steroids?

A

As they both are risk factors of peptic ulcers. NSAIDs and steroids cause a reduction in the potentially protective prostaglandins. PPIs help reduce this ADR.

20
Q

What drug class is ranitidine?

A

Histamine 2 receptor antagonist

21
Q

What is the mechanism of action of ranitidine?

A

Inhibition of histamine 2 receptors. This reduces the amount of stimulation of this receptor, less Gs subunits are activated and less cAMP is produced. Therefore less protein kinases are activated and there is less stimulation of the proton pump

22
Q

Why are histamine 2 receptor antagonists not as effective at reducing acid secretion as proton pump inhibitors?

A

As H2 receptor antagonists only inhibit one route of stimulation of the proton pump. Other routes are still available to stimulate the pump. Only have a partial reduction in acid secretion
As PPi’s inhibit the proton pump itself, the final stage in the pathway, they have a greater effect

23
Q

What are the ADRs of ranitidine?

A

generally well tolerated - diarrhoea, headache

24
Q

What are the contraindications of histamine 2 receptor antagonists?

A

Mask symptoms of gastro-oesophageal cancer, renal impairment

25
Q

What is the structure of Helicobacter Pylori?

A

Gram negative spiral bacterium

26
Q

When should helicobacter pylori infection be suspected?

A

Consider for all patients with duodenal or gastric ulcers not associated with NSAID or unresponsive to lifestyle PPI and antacids

27
Q

How is infection with helicobacter pylori diagnosed?

A

Clinical presentation

Urea breath test

28
Q

What is the urea breath test

A

Test to detect colonisation of stomach with H.Pylori
Patients ingest urea enriched with carbon 13
Broken down in gut to urea.
Urease released by H.Pylori breaks down urea into ammonia and carbon dioxide
High level of carbon 13 isotope detected in exhaled CO2 - much higher than normal confirms H.Pylori present.

29
Q

What is the treatment of H.Pylori infection?

A

One week of triple therapy with a PPI and 2 antibacterial agents.
E.g
Lansoprazole + clarithromycin + amoxicillin (preferred as some evidence of metronidazole resistance)
OR
Lansoprazole + clarithromycin + metronidazole (if allergic to amoxicillin)

30
Q

What drug class is mesalazine?

A

Amionsalicylates

31
Q

What is the first line treatment of ulcerative collitis?

A

Amniosalicylates e.g. mesalazine

32
Q

What is the mechanism of action of mesalazine?

A 
Causes release of 5-aminosalsylic acid, has a topical action at the colon to:
T-cell
– inhibition of proliferation
– possible T-cell apoptosis
– inhibition of IL-2 production 
• Neutrophil
– reduced  chemotaxis
– reduced degranulation
33
Q

How does the role of mesalazine differ from sulfasalazine?

A

mesalazine works in the colon/distal ileum and is the first line treatment for UC, has no role in rheumatoid arthritis
sulfasalazine has more side effects so used infrequently for UC but sulfa group good for rheumatoid arthritis, also works is colon

34
Q

What are the ADRs of mesalazine?

A

GI disturbance – nausea, dyspepsia

leukopenia

35
Q

What are the contraindications of mesalazine?

A

Hypersensitivity - similar to aspirin

36
Q

What are the important drug drug interactions of mesalazine?

A

Enteric coated tablets may break down quicker in presence of PPI (because of ↑pH)

37
Q

Which drugs are of particular concern when co prescribed with a PPI?

A

Clopidogrel if prescribed with omeprazole (CYP inhibitor would reduce clopidogrel action)
Warfarin and phenytoin - PPIs can increase their effects

38
Q

Why are aluminium and magnesium antacid compounds often co-prescribed?

A

As magnesium salts can cause diarrhoea, where as aluminium salts cause constipation. Therefore ADRs from antacids are less likey if given together as have opposing symptoms.

39
Q

Describe the triple therapy options recommended for H. pylori. When should they be varied?

A

Losaprazole +clarithromycin + amoxicillin - preferential as some evidence of resistance to metronidazole

Losarprazole +clarithromycin + metronidazole - used if allergic to amoxicillin

40
Q

Why does a PPI give greater protection against acid secretion than a H2 antagonist?

A

As PPI’s target the final stage in pathway, and H2 antagonists do not. Can still get stimulation of the PPI by ACh, Prostaglandin E2 and gastrin whilst taking H2 antagonist.

41
Q

The half life of most PPIs is only a few hours. Why is acid secretion inhibited for longer than this?

A

PPIs bind irreversibly to the H+/K+ ATPase, so takes a long time to make more channels before acid can be secreted again

Clinical Pharmacology (26 decks)

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