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Clinical Pharmacology & Intro to Prescribing > Session 11 - GI Pharmacology > Flashcards

Session 11 - GI Pharmacology Flashcards

1
Q

What is GORD?

A

Symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond.

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2
Q

Types of GORD.

A

Erosive

Non-erosive

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3
Q

Symptoms/Signs of GORD.

A

Heart burn

Cough

Laryngitis

Astha

Dental erosion

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4
Q

Complications of GORD

A

Oesophagitis

Ulceration

Haemorrhage

Stricture formation

Barrett’s oesophagus

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5
Q

Risk factors of GORD.

A

Older age

Hiatus hernia

Obseity

Pregnancy

Smoking

Alcohol consumption

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6
Q

Give examples of medications that can exacerbate GORD.

A

Alpha-blockers

Anticholinergics

Benzodiazepines

Beta-blockers

CCBs

Corticosteroids

NSAIDs

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7
Q

Give examples of lifestyle options in order to manage GORD.

A

Weight loss

Avoiding trigger foods

Smaller meals

Reduce alcohol and caffeine intake

Stop smoking

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8
Q

Medication pathway for GORD.

A

Proton pump inhibitor to start with.

In case it’s not enough add in H2 Receptor antagonist.

If that is not enough surgery (fundoplication)

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9
Q

Give examples of PPis

A

Omeprazole

Esomeprazole

Rabeprazole

Pantoprazole

Lansoprazole

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10
Q

What is gastritis?

A

Inflammatory changes in the gastric mucosa.

Can be either erosive or non-erosive.

Can be either acute or chronic.

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11
Q

Symptoms of gastritis.

A

Usually asymptomatic but:

Burning epigastric pain

Nausea

Vomiting

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12
Q

Complications of gastritis

A

GI tract bleeding

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13
Q

Risk factors of gastritis

A

H pylori infection

Chronic NSAID use

Bile refluxe

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14
Q

Treatment of erosive causes of gastritis, such as NSAIDs, alcohol or bile.

A

Reduce or stop the irritants

Give PPi or H2 RA.

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15
Q

Treatment of non-erosive gastritis such as H. pylori.

A

Triple therapy with PPi and 2x antibiotics

Quadruple therapy with PPi, bismuth and 2x antibiotics.

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16
Q

Treatment of autoimmune gastritis.

A

Cyanocobalamin treatment to treat the atrophy

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17
Q

State which drugs are used in triple therapy of non-erosive H. pylori gastritis.

A

PPi such as omeprazole

Amoxicillin

Clarithromycin or Metronidazole

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18
Q

What is peptic ulcer disease?

A

Defects in the gastric or duodenal mucosa that extend through the muscularis mucosa.

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19
Q

Symptoms of peptic ulcer.

A

Epigastric pain after meals

Soon after if gastric ulcer

2-3 hours after if duodenal.

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20
Q

Complications of peptic ulcers.

A

Perforation leading to peritonitis

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21
Q

Risk factors of peptic ulcers.

A

H. pylori

NSAIDs

22
Q

Treatment of peptic ulcer if H. pylori negative

A

Stop NSAIDs and give COX-2 inhibitor instead such as celecoxib.

Give PPi and consider H2 RA if PPi is not effective.

Consider misoprostol if NSAIDs need to be given.

23
Q

Treatment of peptic ulcer if H. pylori positive.

A

PPi

Amoxicillin

Clarithromycin or metronidazole

24
Q

How is H. pylori tested for?

A

Carbon-13 urea breath test

Stool antigen test

Laboratory based serology

25
Q

Luminal defences of the GI tract.

A

Acid to reduce bacterial invasion

Mucus to lubricate to reduce physical damage, traps bacteria, barrier against pepsin etc…

26
Q

Epithelial defence of GI mucosa.

A

Apical membrane of parietal and chief cells hare highly resistant to acid

Renewable every 2-4 days.

27
Q

Blood flow defence of GI mucosa

A

If epithelium is destroyed rapid repair can occur.

28
Q

Give examples of gastric prostaglandins and their effects.

A

PGE2

PGI2

They are potent vasodilators that decrease acid secretion and stimulate mucus and bicarbonate secretion in stomach.

Also reduce permeability of epithelium to back flow acid.

Reduce the release inflammatory mediators that may contribute to mucosal injury.

Promotes ulcer healing by increasing blood flow.

29
Q

Explain parietal cells in their resting/non secreting state and the transformation into secreting/stimulated state.

A

The proton pumps (H+/K+-ATPase) are located in membrane bound compartments called tubulovesicles. They lack K+ permeability and block proton pump activity.

The apical membrane of the parietal cell has K+ channels and involutions.

The tubulovesicles then fuse with the canalicular membrane and moves the proton pumps to a position where they can exchange H+ for K+.

30
Q

PPis are prodrugs. How are they activated?

A

Pro drugs that are activated by the acidic conditions of the parietal cell caniculi.

The PPis are weak bases and will accumulate in the acidic space.

31
Q

Oral forms of PPis can be activated prematurely in the stomach.

How is this prevented?

A

By an enteric coating of the PPi

32
Q

Mechanism of action of PPis.

A

Bind covalently to gastric proton pumps, irreversibly and block the function.

This leads to prologed and nearly complete suppression of acid secretion and needs de novo synthesis of pump enzyme to produce more acid

33
Q

Pharmacokinetics of PPis

A

Metabolised by CYP2C19 and CYP3A4

The metabolites are then excreted by the kidneys.

34
Q

ADRs of PPis

A

Headache

Nausea

GI tract issues

Abdo pain

Can lead to increased levels of gastrin and therefore parietal cell and ECL hyperplasia. This may leead to increased risk of gastric carcinoid tumours.

Increase risk of hip fractures

Can lead to increased risk of various infections

35
Q

How will PPIs react with clopidogrel?

A

May decrease the effectiveness of clopidogrel as both use CYP2C19. And clopidogrel use that enzyme to activate.

36
Q

Mechanism of action of H2 RAs.

A

Competitively and reversibly inhibit binding of histamine to H2 receptors.

Indirectly block the effects of gastrin and ACh on parietal cells and therefore less H+ secretion.

They are rapidly absorbed in the small intestine and then excreted by the liver and kidneys.

37
Q

Give an example of a H2 receptor antagonist.

A

Cimetidine

38
Q

ADRs of H2 RAs.

A

Diarrhoea

Constipation

Muscle ache

Fatigue

39
Q

DDIs of cimetidine.

A

Inhibits several cytochrome P450 enzymes leading to decreased metabolism of lidocaine, phenytoin, theophylline and warfarin and can potentially lead to toxic levels of these drugs.

40
Q

Give an example of a prostaglandin analogue.

A

Misoprostol

41
Q

Explain the action of misoprostol.

A

Acts of PGE2 and via the prostaglandin will inhibit seceretion of more H+.

It is used to treat NSAID induced ulcers.

42
Q

ADRs of misoprostol.

A

Diarrhoea

Abdo pain

43
Q

Contraindications of misoprostol.

A

In pregnant women it can cause uterine contractions and possible abortion.

44
Q

Mechanism of action of antacids.

A

Neutralise HCL by reacting with the acid to form water and salt.

45
Q

Give examples of antacids.

A

Aluminium hydroxide

Magnesium hydroxide

Sodium bicarbonate

Calcium bicarbonate

46
Q

ADRs of Aluminium hydroxide.

A

Can cause constipation

Can bind phosphate and result in low phosphate levels leading to malaise and weakness.

In the presence of renal failure it can cause neurotoxicity

47
Q

ADRs of magnesium hydroxide.

A

Diarrhoea

Can lead to increased magnesium levels in renal failure

48
Q

When to avoid sodium bicarbonate?

A

Since it forms water, CO2 and salt when it reacts with HCL it needs to be avoided in hypertension and fluid overload.

49
Q

How does H. pylori cause damage to GI mucosa?

A

Can attach to gastgric epithelia and produce urease.

It also produces a strong immune response and produces ammonium hydroxide that is toxic to gastric epithelia.

It also has endotoxins which are directly toxic.

50
Q
A

Clinical Pharmacology & Intro to Prescribing (24 decks)

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