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Pharmacology > L10 Therapeutics of Peptic Ulcer Disease > Flashcards

L10 Therapeutics of Peptic Ulcer Disease Flashcards

1
Q
  1. What is a peptic ulcer?
  2. What causes it?
A
  1. Defect in the gastric or duodenal mucosa
  2. Due to an imbalance in the peptic acid secretion and gastroduodenal mucosal defence
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2
Q
  1. What is the drug target for Peptic Ulcer Therapy?
  2. What do these cells normally secrete?
A
  1. Parietal Cells in the lumen of the stomach
  2. Gastric acid (HCl) and Intrinsic Factor (Ca2+ absorption)
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3
Q

What do the following cells secrete?

  1. Mucous neck cell
  2. Parietal cells
  3. Enterochromaffin-like cell
  4. Chief cells
  5. D cells
  6. G cells
A
  1. Mucous (protects lining) and Bicarbonate
  2. Gastric acid (HCl) and intrinsic factor (Ca2+absorption)
  3. Histamine (stimulates acid)
  4. Pepsinogen and Gastric Lipase
  5. Somatostatin (inhibits acid)
  6. Gastrin (stimulates acid)
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4
Q

Outline the physiological control of acid secretion in the parietal cell

A

ACH, Histamine and Gastrin all have an inductive effect

PGE2 (Prostaglandin E2) has an inhibitory effect

all act on the H+/K+ ATPase Pump (PROTON PUMP)

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5
Q

What are the principles of Peptic Ulcer Disease (PUD) therapy?

A
  • Relief of pain
  • Ulcer Healing
  • Prevention of Relapse and Complications
  • Must investigate anyone at increased risk of gastric carcinoma as treatment may mask early symptoms.
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6
Q

Clinically, how is PUD treated?

A
  • Removal of the irritants - especially NSAIDs, Helicobacter if present
  • Antacids
  • Proton Pump Inhibitors
  • H2 Receptor Antagonists
  • Misoprostol
  • Antibiotics
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7
Q
  1. What are the main irritants in PUD?
  2. How do they act?
  3. What are other drugs that can act as aetiological factors in PUD?
A
  1. NSAIDs (Non-Steroidal Anti-inflammatory Drugs eg ibruprofen, naproxen) and Helicobacter Pylori infection
  2. Reduce prostaglandin formation, blocking the PGE2 protective signal in the parietal cell acting on the H+/K+ ATPase pump. Acid secretion isn’t inhibited.
    1. Aspirin/Corticosteroids
    2. Bisphosphonates (used to treat osteoporosis to prevent loss of bone mass - when taking, not allowed food, must sit upright for half an hour)
    3. Nicotine (smoking)
    4. Alcohol
    5. Caffeine
    6. Severe Physiological Stress
    7. Hypersecretory States (uncommon)
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8
Q

Antacids

  1. Why are they used for PUD?
  2. What are they most commonly made up of?
  3. What is a rapidly acting antacid? What are the problems with it?
A
  1. Produce symptomatic relief by raising gastric pH and reducing proteolytic activity
  2. ALUMINIUM and MAGNESIUM SALTS often in combination
  3. Sodium Bicarbonate - well absorbed and can cause a metabolic alkalosis, sodium and water retention and renal stone formation

Milk isnt a good anatcid – sometimes the pH can be slightly acidic.

Stimulates gastrin within a short period of going into the stomach – will get a rebound effect even if initial benefit

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9
Q

Proton Pump Inhibitors

  1. Give 4 exampes of PPIs
  2. What is their mechanism of action?
  3. Give some general properties

(particular care with azoles and myocins in exam)

A
  1. •Omeprazole
  • Lansoprazole
  • Pantoprazole
  • Esomeprazole
  1. Inhibit the H+/K+ ATPase (proton) pump in the parietal cell of the gastric muscosal lining, resulting in less gastric acid secretion.
  2. •Very effective
  • Side effects uncommon
  • Care with regard to masking Gastric Cancer symptoms
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10
Q

Omeprazole

  1. What is it’s mechanism of action?
  2. What are it’s clinical indications?
  3. What are the common adverse reactions?
  4. What are the important adverse reactions?
A
  1. Targeted irreversible proton pump inhibitor.
  2. PUD, Reflux Oesophagitis (GORD)
  3. •GI disturbance e.g. nausea, vomiting, abdominal pain, flatulence, diarrhoea, constipation

•Headache

  1. •Increased risk of Clostridium difficile infection,
  • Hyponatraemia, Hypomagnesaemia,
  • Hepatitis, Interstitial nephritis, Blood disorders – leucopenia, leucocytosis, pancytopenia, thrombocytopenia,
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11
Q

Omeprazole Continued

  1. What are common interactions, and why?
  2. What are the current debates on PPIs?
A
  1. Warfarin (Omeprazole and esomeprazole are weak CYP450 enzyme inhibitors, therefore they can increase anticoagulant effect)

Clopidogrel (Pro-drug) (Omeporazole and esomeprazole are weak CYP450 enzyme inhibitors reduce antiplatelet effect)

  1. •Probable reduction in efficacy of Clopidogrel when PPI used prophylacticly in cardiac patients on dual anti-platelet therapy

•Possible rebound effect after stopping treatment after >8/52 – Rebound acid hypersecretion syndrome (RAHS)

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12
Q

Histamine2 Receptor Antagonists

  1. Name two H2RAs
  2. What is their mechanism of action?
  3. When are they used?
A
  1. Cimetidine, Ranitidine
  2. Competitive antagonist at the H2 (histamine) receptor in gastric parietal cells, less H+ secretion as a result
  3. 2nd line agent for peptic ulcer disease and reflux oesophagitis. (PUD and GORD)
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13
Q

Cimetidine

  1. What type of drug is it?
  2. What is it’s mode of action?
  3. When is it indicated?
  4. What are the adverse effects?
  5. What interactions can it have?
A
  1. Histamine2 Receptor Antagonist
  2. Competitive antagonist at the H2 (histamine) receptor in gastric parietal cells
  3. 2nd line agent for peptic ulcer disease and reflux oesophagitis.
  4. Diarrhoea, confusion, gynaecomastia.
  5. A potent inhibitor of cytochrome P450 dependent metabolism.

(Don’t prescribe cimetidine until you really have to)

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14
Q

Ranitidine

  1. What type of drug is it?
  2. What is it’s mode of action?
  3. When is it indicated?
  4. What are the adverse effects?
  5. What interactions can it have?
A
  1. Histamine2 Receptor Antagonist
  2. Competitive antagonist at the H2 (histamine) receptor in gastric parietal cells
  3. 2nd line agent for peptic ulcer disease and reflux oesophagitis.
  4. Diarrhoea (fewer than cimetidine)
  5. A mild inhibitor of cytochrome P450 dependent metabolism, of little clinical importance
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15
Q

Prostaglandin Analogues

  1. Name a prostaglandin analogue
  2. What is it’s mode of action?
  3. When is it indicated?
  4. Give some adverse effects
  5. What might some interactions be?
  6. What is an important contraindication?
A
  1. Misoprostol
  2. A prostaglandin E2 analogue. Binds at PGE2, enhancing the protective inhibitory effect upon the K+/H+ ATPase pump (proton pump)
  3. 2nd Line - to prevent peptic ulceration in patients taking long term non-steroidal anti- inflammatory drugs (PPI 1st line).
  4. Diarrhoea, abdominal pain, nausea, flatulence and abnormal vaginal bleeding.
  5. Additive effects with drugs causing gastrointestinal intolerance.
  6. Women of child bearing age because of increased risk of abortion.
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16
Q

Helicobacter Pylori

  1. Describe it’s appearance
  2. What is it a risk factor for?
  3. How?
A
  1. gram negative bacillus
  2. Recurrence of peptic ulcers, Gastric cancer, Mucosa-associated lymphoid tissue (MALT) lymphoma
  3. Mucus layer : secrete inflammatory proteins, toxins. Urease producing - urea to NH4 and CO2. Undermines the mucosal protection system
17
Q

Helicobacter Pylori

  1. How is it tested for?
  2. What is the C13 breath test based upon?
  3. What do H.Pylori eradication regimes involve?
A
  1. Initially detected by Carbon-13 urea breath test, Upper GI endoscopy with biopsy and rapid urease test useful. (Serology (IgG) not currently recommended by NICE due to inadequate performance)
  2. The ability of H.pylori to convert urea to ammonia and CO2
  3. •PPI (or H2 blocker)

•Clarithromycin

•Amoxicillin (or Metronidazole if penicillin allergic)

•<strong>Triple therapy for 7 – 14 days</strong>

•If there is an ulcer will need PPI daily for 1-2 months

•Use a different antibiotic if requiring a second treatment course

18
Q

Ulcers Induced by Non-Steroidal Anti-Inflammatory Drugs

  1. What do you do in the case of a high-risk patient requiring a NSAID?
  2. What about for H.Pylori positive patients who are about to start an NSAID?
  3. What should patients with NSAID induced ulcers revieve?
A
  1. prescribe PPI, misoprostol or an H2 antagonist
  2. should receive eradication therapy
  3. a proton pump inhibitor
19
Q

When is URGENT upper GI endoscopy required?

A
  • Acute bleeding suspected
  • Chronic bleeding / Fe def Anaemia
    • Upper and Lower as 10% dual pathology
  • Weight loss
  • Dysphagia
  • Persistent vomiting
  • Anyone with unexplained, persistent dyspepsia
    • Especially if 55+ years
20
Q

Summarise the treatment of gastric ulcers

A
  • Remove gastric irritants especially NSAIDs
  • Test and treat for H Pylori infection
  • 1st Line – Proton pump inhibitors
  • 2nd Line – H2 antagonist

Must investigate anyone at increased risk of gastric carcinoma as treatment may mask early symptoms.

Pharmacology (26 decks)

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