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Yr 2 Gastrointestinal > Wk 1 - Pharmacology: Anti-Ulcer Drugs > Flashcards

Wk 1 - Pharmacology: Anti-Ulcer Drugs Flashcards

1
Q

List the symptoms of indigestion (ie dyspepsia).

A

Very generalised - very difficult to pin down to dyspepsia

  1. Upper abdominal pain (above the navel)
  2. Belching (generating gas)
  3. Nausea (with or without vomiting)
  4. Abdominal bloating (the sensation of abdominal fullness without objective distention)
  5. Early satiety and, possibly, abdominal distention
    (swelling)

Most often provoked by eating

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2
Q

What is the ratio of duodenal ulcers to gastric ulcers?

A

Ratio of duodenal:gastric ulcer is 4:1 –> i.e. duodenal ulcers are more common

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3
Q

What are the THREE goals of ulcer therapy?

A
  1. Relieve symptoms (via antacids, prostaglandins, gel formers)
  2. Repair damage (via PPI and H2 antagonists)
  3. Eradicate bacteria (via antimicrobials)
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4
Q

Which type of ulcer is more likely to become malignant?

A

Stomach (gastric) ulcers

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5
Q

List the main risks associated with ulcer development.

A
  1. H. pylori bacteria (found in 50% of pts but ‘dormant’) - MAIN RISK FACTOR
  2. Lifestyle and individual-related - smoking, predisposition (eg blood type O, Zollinger-Ellison Syndrome, RA, liver disease), stress
  3. Medications esp NSAIDs
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6
Q

Why do ulcers develop?

A
  • Acid and pepsin secretion increases (due to risk factors and H.pylori mainly) –> presence of bacteria - gastritis - increased acid secretion to get rid of bacteria
  • Impaired mucosal defence (via NSAIDs)

–> damage to GI lining - ulceration

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7
Q

List the symptoms of a peptic gastric ulcer.

A
  1. Vomit
  2. Upper abdominal pain
  3. Appetite loss
  4. Weight loss
  5. Anaemia
  6. Blood is stool
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8
Q

List the symptoms of a peptic duodenal ulcer.

A
  1. Weight gain
  2. Relieved by eating: milk, eating, rest and antacids
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9
Q

What does a stomach ie gastric ulcer affect?

A
  • Nerve agitation - Pain
  • Erosion of blood vessels - Hemorrhages
  • Stomach or intestine wall tear – Peritonitis
  • Spasm or swelling - Obstruction
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10
Q

What is gastro-oesophageal reflux disease (GORD/GERD)?

A
  • Gastro-oesophageal reflux disease (GORD) is a common condition, where acid from the stomach leaks up into the oesophagus (gullet).
  • It usually occurs as a result of the ring of muscle at the bottom of the oesophagus (lower oesophageal sphincter) becoming weakened.
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11
Q

What is one possible complication of GORD?

A

Barrett’s oesophagus ie metaplasia of oesophageal epithelium to stomach/gastric epithelium

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12
Q

List the three main therapy goals when treating GORD.

A
  1. Relieve symptoms (PPI work really well for GORD)
  2. Repair oesophagus (in oesophagitis)
  3. Prevent relapse and complications (e.g. Barrett’s oesophagus)
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13
Q

List the symptoms associated with GORD.

A
  1. Heart burn
  2. Pain on swallowing
  3. Bleching
  4. Waterbrash
  5. Throat irritation
  6. Morning hoarseness
  7. Sour taste
  8. Bad breath
  9. Enamel erosion
  10. Gum inflammation
  11. Laryngitis
  12. Chronic sore throat
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14
Q

List some risk factors in GORD.

A
  1. Spicy food
  2. Mint flavouring
  3. Garlic/onions
  4. Caffeine
  5. Chocolate
  6. Citrus fruit
  7. Smoking
  8. Pregnancy
  9. Overweight
  10. Fatty/fried food
  11. Alcohol
  12. Tomato-based foods
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15
Q

What are the TWO most common/important risk factors for peptic ulcers?

A
  1. H.pylori bacteria
  2. NSAIDs
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16
Q

How is acid secretion controlled in the stomach?

A

Stimulates acid secretion:

  • Gastrin (feedback mechanism when pH is at 2 gastrin release inhibited) - generated by the pancreas
  • Histamine (via enterochromaffin cells)
  • Acetylcholine (via vagus stimulation)

All acts directly on gastrin, ACh muscarinic, and H2 receptors + ACh and gastrin stimulate histamine secretion from ECL.

Inhibits acid secretion:

  • PGE2 (prostaglandins) - could be why NSAIDs affect gut – these are removed by NSAIDs so increase acid secretion

All four control proton pump (H/K ATPase)

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17
Q

What classes of drugs are used to inhibit stomach acid secretion?

A
  • Proton pump inhibitors (PPI)
  • Histamine (type-2) receptor antagonist
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18
Q

List some PPIs.

A
  • Omeprazole
  • Lansoprazole
  • Pantoprazole
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19
Q

Remember PPIs are prodrugs, so what is the active enzyme PPIs are converted into?

A

Active metabolite is sulfenamide

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20
Q

How long does a PPI effect last for?

A

1 dose lasts 24 hours as it causes irreversible inhibition of PP and would require PP resynthesis

21
Q

How do PPIs work?

A

They suppress gastric acid secretion due to direct inhibition of the proton pump (H/K ATPase) - irreversible inhibition

22
Q

List some S/E of omeprazole and pantoprazole (specifically to do with other drug used with it).

A

May enhance warfarin effect via inhibition of Cytochrome P450. So can use lansoprazole as metabolised by different Cytochrome P450 (Cyt450 B vs Cyt450 A for warfarin and omeprazole).

23
Q

What’s the risk associated with using PPIs and anti-histamines to inhibit acid secretion?

A

It can mask gastric cancer

24
Q

What are histamine (type 2) receptor antagonist?

A

The are a class of drugs used to inhibit acid secretion via H2 receptor antagonism on parietal cells. COMPETITIVE INHIBITION of H2 receptors on parietal cells.

25
Q

Why are anti-histamines (H2 antagonist) less effective than PPIs?

A

Because they are competitive inhibitors - so can be over-ridden if enough histamine is released via gastrin stimulation of ECL cells

26
Q

Give some example histamine (H2) receptor antagonists used to inhibit acid secretion.

A
  • Cimetidine
  • Ranitidine

Both are OTC

27
Q

What is one S/E of Cimetidine?

A

Inhibition of P450 so potential for drug interactions (warfarin and theophylline)

28
Q

What class of drugs are used to neutralise released gastric acid?

A

Antacids

29
Q

Give some examples of antacids.

A
  • Aluminium hydroxide
  • Magnesium trisilicate
  • Calcium
  • Sodium bicarbonate
30
Q

What is the mechanism of action of antacids?

A
  • Simple acid-base chemistry. H + OH = H2O
  • Fast-acting (lasts longer after food due to slower gastric emptying) about 1hr
  • Need high doses for ulcer healing
31
Q

What are the S/Es of antacids?

A
  • Constipation with Aluminum salts, diarrhoea with Magnesium (therefore a combination of salts balance each other out)
  • Not taken with other drugs due to risk of malabsorption e.g. ketoconazole (antifungal)
  • Blocks Calcium – hypercalcaemia (then how hypercalcaemia? bc of initial high intake of Ca), alkalosis (if overdose on atnacids)
32
Q

What drug class protect the GI mucosa?

A
  • Prostaglandin analogues
  • Gel formers
33
Q

Give an example of a prostaglandin analogue used in GI mucosa protection.

A

Misoprostol

34
Q

How does Misoprostol work?

A

Increased mucous secretion and blood flow (helps with buffering)

35
Q

When is Misoprostol use C/I?

A

Pregnant woman as risk of abortion (it stimulates uterus contraction)

36
Q

List some gel formers.

A
  • Sulcrafate/alginate
37
Q

What are gel formers used for?

A

In GI, to protect mucosa

38
Q

How do gel formers work?

A

Form gel at low pH and buffers acid

39
Q

When are gel formers usually given?

A

Before food

40
Q

What is bismuth subsalicylate (pepto-bismol)?

A
  • Drug used to protect GI mucosa
  • Potential barrier effects in ulcers
  • Potential antibacterial effect
41
Q

List some S/E of Pepto-bismol.

A
  • Greying of teeth enamel
  • Blackening of stool (melaena)
  • Reyes syndrome (v rare) - a flu-like disease that could lead to encephalopathy esp in children
42
Q

How is indigestion managed?

A
  • OTC antacids and alginates
  • Initial PPI
  • Test and treat for H.pylori
  • 2 week wash out of PPi before PPI test
  • Lifestyle changes + avoid triggers!
43
Q

How is indigestion treated?

A
  • If H.pylori +ve –> (1) antibiotics + PPI, (2) if PPI does not work switch to H2 antagonists and antacids for symptomatic relief
    • NEED to eradicate H.pylori as recurrence of ulcer within one year
  • If H.pylori -ve –> (1) PPI, then (2) H2 antagonist and antacids for symptomatic relief
    • If NSAIDs taken, STOP
44
Q

What are the possible complications of untreated/managed indigestion?

A
  • Anaemia
  • Perforation
  • Stomach cancer
45
Q

How is GORD/GERD managed?

A
  • Antacids
  • Foaming agents
  • PPI
  • H2 antagonist
  • If due to hiatal hernia –> surgery
  • Lifestyle changes
46
Q

In a 60-year-old patient, why is it important to examine further underlying cause of dyspepsia?

A

Bc there is an increased risk of gastric cancer as cause of elevated acid secretion in over 50s

47
Q

Why do antacids interfere in the absorption of some drugs?

A

Due to alteration (increase pH) of stomach

48
Q

What are the drug targets of the parietal cell (acid-secreting cells)? Give one example of each.

A
  1. PPI - Omeprazole
  2. H2 antagonist - Ranitidine
  3. Prostaglandin analogue - Misoprostol

Yr 2 Gastrointestinal (37 decks)

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