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MD3002 - GI Pharmacology > Treatment of Peptic Ulceration and Inflammatory Bowel Disease > Flashcards

Treatment of Peptic Ulceration and Inflammatory Bowel Disease Flashcards

1
Q

Why does the digestive system need acid?

A

o Digestion of food o Iron absorption o Killing pathogens

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2
Q

What is the function of mucous secreting cells as a protective mechanism against acid?

A

o Trap bicarbonate ions (alkaline) o Creates gel like barrier o Important protective layer

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3
Q

What is the action of prostaglandins are locally produced in the stomach?

A

o Stimulates secretion of mucus and bicarbonate

o Dilate mucosal blood vessels

o Cytoprotective

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4
Q

What increases the risk of GORD and ulcers?

A
  • If disturbance in protective layer/secretions PLUS acid
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5
Q

What is likely to disturb protective functions of the stomach?

A
  • Many NSAIDs disturb these protective functions (Inhibit COX-1, enzymes responsible for synthesis of prostaglandins)
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6
Q

What are the 2 main cells involved in gastric acid production?

A

oxyntic/parietal cells chief/peptic cells

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7
Q

What is the action of oxyntic cells?

A

form HCl and release intrinsic factor

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8
Q

What is the function of intrinsic factor?

A

absorb Vitamin B12

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9
Q

Draw a diagram illustrating the secretion of HCl by the gastric parietal cells

A
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10
Q

What are the three endogenous secretagogues?

A

Gastrin, Acetylcholine and Histamine

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11
Q

Describe the action of Gastrin

A
  • Gastrin is a polypeptide hormone
  • Gastrin is secreted by gastrin cells; G Cells
  • Located in the gastric antrum and duodenum
  • Proteins in food have a strong effect in the gastrin cells
  • Stimulates secretion of acid by parietal cells (through the proton pump)
  • Also increases pepsinogen secretion – stimulates blood flow and increases gastric motility
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12
Q

Describe the function of ACh

A
  • Released from neurons
  • Stimulates muscarinic receptors on surface of parietal cells and histamine containing cells
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13
Q

Describe the function of histamine

A
  • Mast cells lying close to parietal cell release histamine
  • Histamine release increased by gastrin and acetylcholine
  • Acts on parietal cell H2 receptors
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14
Q

What is a secretagogue?

A

substances that promote the production and secretion of acid

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15
Q

What are the main associations of H.pylori with stomach problems?

A
  • Causative factors in gastric and duodenal ulcers
  • Risk factor for gastric cancer (adenocarcinoma)
  • Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma
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16
Q

What are the additional associations of H.pylori with stomach problems?

A
  • Gastro-oesophageal reflux disease
  • Dyspepsia
  • Atrophic gastritis
  • Iron deficiency anaemia
  • Idiopathic Thrombocytopenia Purpura
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17
Q

What type of infection can H.pylori cause?

A

Can cause acute infection with symptoms that include nausea, dyspepsia, malaise and halitosis

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18
Q

How long does acute infectoon by H pylori tend to last?

A

Acute infection tends to last about two weeks

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19
Q

What is the damage to the gastric mucosa in acute infection caused by H pylori?

A

Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

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20
Q

What does the outcome of chronic infection by H pylori depend on?

A
  • Pattern of inflammation
  • Host response
  • Bacterial virulence
  • Environmental factors
  • Patient age
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21
Q

What is the pathogenesis of chronic infection caused by H pylori?

A

Local inflammation and gastritis

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22
Q

What is the first line treatment of Helicobacter pylori?

A
  • First line = offer people (non-penicillin allergic) who test positive for H. pylori a 7-day, twice-daily course of treatment with:
  • A PPI and amoxicillin and either clarithromycin or metronidazole
23
Q

What are the main proton pump inhibitors and what is their action?

A

reduce gastric acid secretion

  • Esomeprazole
  • Lansoprazole
  • Omeprazole
  • Pantoprazole
24
Q

What are the main indications for a proton pump inhibitor?

A
  • Helicobacter pylori eradication
  • Peptic ulcer disease
  • Dyspepsia
  • GORD
  • Treatment and prevention of NSAID associated ulcers
  • Reflux oesophagitis
  • Zollinger-Ellison syndrome
25
Q

Describe the action of omeprazole

A
  • inhibits K+H+ATPase irreversibly (the proton pump)
  • Basal and simulated gastric acid secretion reduced
  • Drug is weak base and accumulates in acid environment of the canaliculi of the stimulated parietal cell
  • Usually oral administration
26
Q

Describe the unwanted effects of PPIs

A
  • Relatively uncommon
  • Includes:
    • Headache
    • Diarrhoea
    • Rashes
    • Dizziness
    • Somnolence
    • Confusion
    • Impotence
    • Gynaecomastia
    • Pain in muscles/joints
27
Q

When should proton pump inhibitors be used with caution

A

liver disease, pregnancy, breast feeding

28
Q

What may a PPI mask the symptoms of?

A

gastric cancer

29
Q

What are histamine H2 receptor antagonists used for?

A

peptic ulcers and reflux oesophagitis

30
Q

What is the mechanism of action of Histamine H2 receptor antagonists?

A
  • Competitively inhibit histamine actions at all H2 receptors
  • Inhibit histamine, gastrin and acetylcholine stimulated acid production
  • Pepsin secretion also falls with reduction in volume of gastric juice
31
Q

What are the main examples of Histamine H2 receptor antagonists?

A

Ranitidine (approximately 50% bioavailability, half-life 2-2.5hrs, renal excretion)

Cimetidine (>60% bioavailability, half-life = 2hrs, renal excretion

32
Q

What are the unwanted effects of Histamine H2 Receptor Antagonists?

A
  • Diarrhoea
  • Dizziness
  • Muscle pains
  • Alopecia
  • Transient rashes
  • Hypergastrinemia
33
Q

What are the cautions of Histamine H2 receptor antagonists?

A

can mask symptoms and signs of gastric cancer

34
Q

What are the specific unwanted effects of Cimetidine?

A
  • Can interact with androgen receptors:
    • Gynaecomastia in men
    • Decreased sexual function
  • Inhibits cytochrome P450
    • Slows the metabolism (and potentiates action) of range of drugs e.g. oral anticoagulants and tricyclics
  • Confusion in elderly
35
Q

Dyspepsia =

A

pain or discomfort in upper abdomen exacerbated by food

36
Q

GORD =

A

acid reflux, associated with water brash

37
Q

What is the lifestyle advice when treating dyspepsia and GORD?

A
  • Healthy eating
  • Weight reduction
  • Smoking cessation
38
Q

What are the known precipitants of dyspepsia and GORD?

A
  • Alcohol
  • Coffee
  • Chocolate
  • Fatty foods
39
Q

What is the main advice offered prior to pharmacological intervention for dyspepsia and GORD?

A
  • Raise the head of the bed and have a main meal well before going to bed
  • Stop NSAIDs where appropriate/applicable
40
Q

What are the main iver the counter remedies for dyspepsia and GORD?

A
  • Antacids; directly neutralise acid and inhibit activity of peptic enzymes
    • Salts of magnesium and aluminium
  • Alignates; increases viscosity and adherence of mucus to oesophageal mucosa
  • Simeticone; antifoaming agent (helps bloating, flatulence)
41
Q

What is a peptic ulcer?

A

gastric or duodenal ulcer

42
Q

Genesis of peptic ulcers

A
  • Can be associated with infection and gastric mucosa with H pylori
  • Imbalance between:
    • Mucosal-damaging and mucosal protecting
43
Q

Initial treatment for peptic ulcer disease if H pylori positive

A

Offer H pylori eradication if peptic ulcer disease and H pylori positive

44
Q

Initial treatment for NSAID associated ulcers

A

Stop the used of NSAIDs where possibly. Offer full-dose PPI or H2RA therapy for 8 weeks and, if H pylori is present, subsequently offer eradication therapy

45
Q

Initial treatment of peptic ulcer if H pylori negative and no NSAID

A

Offer full-dose PPI or H2RA therapy for 4 to 8 weeks

46
Q

What should people with a gastric ulcer and H pylori be offered?

A

repeat endoscopy after 6-8 weeks

Perform re-testing for H pylori using carbon 13 urea breath test

47
Q

What should be excluded if a person has a non-healed ulcer?

A

non-adherence, malignancy, failure to detect H pylori, NSAID use, other ulcer inducing medication and rare causes such as Zollinger-Ellison syndrome or Crohn’s disease

48
Q

What is inflammatory bowel disease an umbrella term for?

A

ulcerative colitis and crohn’s disease

49
Q

Symptoms of inflammatory bowel disease

A

abdominal pain, diarrhoea, PR blood, weight loss, systemic upset, ulcers, fever

50
Q

What are the main differences between UC and Crohn’s

A
51
Q

What are the main complications of inflammatory bowel disease

A
  • Stoma
  • Anaemia
  • Perforation
  • Obstruction/stricture
  • Fistulae
  • Toxic megacolon
  • Malnutrition
  • Increased risk of bowel cancer
52
Q

What are the main invetsigations for inflammatory bowel disease?

A
  • RBC, CRP
  • Stool MCS
  • Faecal calprotein
  • CT scan/MRI
  • Endoscopy (sigmoidoscopy, colonoscopy) + biopsies
53
Q

What are the main treatments for inflammatory bowel disease?

A
  • Aminosalicylates e.g. mesalazine
  • DMARDs e.g. azathioprine, methotrexate
  • Biologics e.g. infliximab
  • Corticosteroids
  • Symptomatic relivers (analgesics, laxatives, “constipators”)
  • Surgery
54
Q
A

MD3002 - GI Pharmacology (4 decks)

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