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MD3002 Pharmacology > Treatment of peptic ulceration and Inflammatory Bowel disease > Flashcards

Treatment of peptic ulceration and Inflammatory Bowel disease Flashcards

1
Q

What are gastric acid secretions required for?

A
  • Digestion of food
  • Iron absorption
  • Killing pathogens
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2
Q

What are the protective mechansims against gastric acid?

A 
Mucous secreting cells 
- Trap bicarbonate ions (alkaline)
- Creates gel like barrier 
- Important protective layer 
Prostaglandins locally produced
- Stimulates secretion of mucus and bicarbonate 
- Dilate mucosal blood vessels 
- Cytoprotective
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3
Q

How much gastric juice is produced per day?

A

2.5L

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4
Q

What are proenzymes e.g. prorennin and pepsinogen produced by?

A

Chief / peptic cells

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5
Q

What cells produce HCL and intrinsic factor

A

Oxyntic / parietal cells

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6
Q

What is intrinsic factor?

A

a substance secreted by the stomach which enables the body to absorb vitamin B12. It is a glycoprotein.

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7
Q

What does the production of HCl involve?

A

Proton pump (K+H+ATPase)

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8
Q

What does inhibition of the proton pump result in?

A

Less HCl being secreted by cheif cells therefore increased pH

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9
Q

What are the 3 endogenous secretagogues? (3 substances which increase HCl production)

A
  • Gastrin
  • Acetylcholine
  • Histamine
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10
Q

What is gastrin produced by?

A

Gastrin cells (G cells)

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11
Q

What kind of substance is gastrin?

A

Polypeptide hormone

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12
Q

Where are gastrin cells located?

A

Gastric antrum and duodenum

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13
Q

What have a strong effect on the G cells?

A

Proteins in food

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14
Q

How does gastrin work?

A
  • Secreted by G cells into blood
  • Stimulates secretion of acid by parietal cells (thro the proton pump)
  • Also increases pepsinogen secretion - stimulates blood flow and increases gastric motility
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15
Q

How does acetylcholine increase gastric acidity?

A
  • Released from neurons to stimulate muscarinic receptors on surface of parietal cells and histamine containing cells
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16
Q

What does histamine act on to increase gastric acidity?

A
  • Parietal cell H2 receptors
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17
Q

What cells release histamine?

A
  • Mast cells lying close to parietal cell
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18
Q

What substances increase histamine release?

A
  • Gastrin

- Acetylcholine

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19
Q

How does Helicobacter pylori damage the stomach?

A
  • Damages mucosal barrier

- Creates inbalance between protective and destructive factors

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20
Q

What percentage of the population are infected in Helicobacter pylori?

A

Roughly 50% (30% in UK)

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21
Q

Where can peptic ulcers be found?

A
  • Stomach or duodenum

- Gastric and duodenal ulcers = peptic ulcers

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22
Q

What can H pylori infection increase the chances of?

A
  • Gastric cancer (adenocarcinoma)
  • Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma
  • GORD, Dyspepsia, Atrophic gastritis, iron deficiency anaemia, idiopathic thrombocytopenic Purpura
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23
Q

What is dyspepsia?

A

Indegestion

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24
Q

What is the clinical name for bad breath?

A

Halitosis

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25
Q

What symptoms can an H pylori infection present with?

A
  • Nausea
  • Dyspepsia
  • Malaise
  • Halitosis
    Acute infection lasts about 2 weeks
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26
Q

What happens to the mucosa as a result of H pylori infection?

A
  • Gastric mucosa becomes inflammed with neutrophils and inflammatory cells with marked persistant lymphocyte penetration
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27
Q

What does the outcome of H pylori infection depend on?

A
  • Pattern of inflammation
  • Host response
  • Bacterial virulence
  • Enviromental factors
  • Patient age
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28
Q

What does a h pylori chronic infection result in?

A

Local inflammation and gastritis

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29
Q

What are the tests used to diagnose H pylori infection?

A
  • Urea breath test
  • Stool antigen
  • CLO test (rapid urease test)
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30
Q

What test would be used to diagnose H pylori infection in primary care?

A
  • Urease breath test or stool antigen test as they are non-invasive
  • Stool antigen test cannot be undertaken to check eradication
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31
Q

WHat is the problem associated with stool antigen test for diagnosing H pylori?

A

Antigen will stay positive even if infection cleared (n

32
Q

What test can be done simulatneously with an endoscopy?

A
  • Biopsy based diagnostic test: Rapid urease test CLO test
33
Q

What does the urea breath test really test for?

A
  • Isotope labelled carbon dioxide
  • Fromed from C-urea which is broken down by Urease (produced by H pylori) into the NH3 and isotope labelled carbon dioxide
34
Q

What should patients who test positive for H pylori be treated with? (non-penicillin allergic)

A
  • 7-day, twice-daily course of treatment with:
  • PPI
  • Amoxicillin
  • Clarithromycin or Metronidazole
35
Q

Name some proton pump inhibitors used for the first-line treatment of H pylori infection

A
  • Esomeprazole
  • Lansoprazole (common)
  • Omeprazole (common)
  • Pantoprazole
  • Rabeprazole
36
Q

What diseases can Proton pump inhibitors be used to treat?

A
  • Peptic ulcer disease
  • Dyspepsia
  • GORD
  • Treatment and prevention of NSAID associated ulcers
  • Reflux oesophagitis
  • Zollinger-Ellison syndrome
37
Q

How does omeprazole work?

A
  • Inhibits K+H+ATPase irreversibly (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
38
Q

What are the unwanted side-effects and cautions of ppis?

A
  • Relatively uncommon
  • Headaches
  • Diarrhoea
  • Rashes
  • Dizziness
  • Somnolence
  • Confusion
  • Impotence
  • Gynaecomastia
  • Pain in muscles / joints
  • Caution in:
  • Liver disease
  • Pregnancy
  • Breast feeding
  • May mask the symptoms of gastric cancer
39
Q

Give some examples of Histamine H2 Receptor Antagonists?

A
  • Ranitidine

- Cimetidine

40
Q

What are Histamine H2 Receptor Antagonists used to treat?

A
  • Peptic ulcers

- Reflux oesophagitis

41
Q

What do Histamine H2 Receptor Antagonists inhibit?

A
  • Histamine
  • Gastrin
  • Ach stimulated acid production
  • Pepsin secretion also falls with reduction in volume of gastric juice
42
Q

What are some of the differences between Ranitidine and Cimetidine?

A 
- Bioavailability 
Ranitidine ~ 50%
Cimetidine > 60%
- Half-life (renal excretion)
Ranitidine 2.5 hrs 
Cimetidine 2 hrs
43
Q

What drugs which reduce gastric acid secretions can be bought over the counter?

A

Histamine H2 Receptor Antagonists

44
Q

What is the better tolerated Histamine H2 Receptor Antagonist Ranitidine or Cimetidine?

A

Ranitidine

45
Q

What are the side-effects of Histamine H2 Receptor Antagonists?

A 
Rare 
- Diarrhoea 
- Dizziness 
- Muscle pains
- Alopecia 
- Transient rashes 
- Hypergastrinaemia 
Can mask symptoms of gastric cancer
46
Q

What are some of the unwanted side-effects specific to Cimetidine and why is this?

A 
- Can interact with androgen receptors 
Gynaecomastia 
Decreased sexual function 
- Inhibits cytochrome P450 
Slows metabolism (and potentiates action) of range of drugs e.g oral anticoagulants and tricyclics 
- Confusion in elderly
47
Q

What differntiates dyspepsia from GORD?

A
  • Dyspepsia = pain or discomfort centered in upper abdomen exac by food
  • GORD = acid reflux, assoc with waterbrash
48
Q

What is waterbrash?

A

A sudden flow of saliva (watery acidic taste) associated with indegestion

49
Q

How is dyspepsia and GORD treated in adults?

A
  • Stop NSAIDs where applicable
  • OTC Remedies e.g antacids, Alignates and Simeticone
  • Consider PPI for symptomatic treatment
  • H2 receptor antagonist potential alternative
  • Consider H pylori testing -> treat if positive
50
Q

What are antacids?

A
  • OTC medication used to treat Dyspepsia + GORD
  • Directly neutralise acid + inhibit the activity of peptic enzymes
  • Salts of magnesium and aluminium (gaviscon, alka-seltzer)
51
Q

What are Alignates?

A
  • OTC medication used to treat GORD + dyspepsia

- Increase viscosity and adherence of mucus to oesophageal mucosa

52
Q

What is Simeticone?

A

Antifoaming agent (helps bloating, flautulence)

53
Q

What are the mucosal-damaging factors?

A
  • Acid

- Pepsin

54
Q

What are the mucosal-protecting factors?

A
  • Mucus
  • Bicarbonate
  • Prostaglandins
  • Nitric oxide
55
Q

What simply can be used to treat dyspepsia and GORD in the absence of red flag symptoms?

A

Dietary and lifestyle advice

56
Q

How are peptic ulcers treated when H pylori positive?

A

Offer H pylori eradication if peptic ulcer disease and H pylori +ve

57
Q

How are NSAID associated peptic ulcers treated?

A

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

58
Q

How is peptic ulcer disease treated when H pylori negative; no NSAID?

A

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

59
Q

What do PPIs usually end in?

A

-prazole

60
Q

What do H2 Receptor Antagonists usually end in?

A

-idine

61
Q

When should a repeat endoscopy be done?

A
  • 6 - 8 wks later depending on size of lesion

- Perform re-testing for H pylori using carbon-13 urea breath test if no peptic ulcer

62
Q

What should be done with an individual with an unhealed ulcer?

A
  • Exclude non-adherence, malignancy, failure to detect H pylor, inadverent NSAID use, other ulcer-inducing medication and rare causes such as Zollinger-Ellison syndrome or Crohn’s disease
63
Q

What should be done if symptoms continue to recur after peptic ulcer treatment?

A
  • Offer a PPI to be taken at the lowest possible dose to control symptoms
  • Discuss using the treatment on an as-needed basis with people to manage own symptoms
64
Q

What is Zollinger-Ellison syndrome?

A

a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers

65
Q

What are the 2 types of Inflammatory Bowel Disease?

A
  • Ulcerative colitis

- Crohn’s disease

66
Q

Where does Ulcerative colitis affect?

A

Colon and rectum, inner lining

67
Q

Where can Crohn’s disease affect?

A

Any part of GI tract, through whole wall

68
Q

How prevelant is UC and Crohn’s in the UK?

A
  • UC: 1 in 400

- Crohn’s: 1 in 700

69
Q

What is the age of onset usually of UC and Crohn’s?

A

Peaks at 15-30 and 50-70

70
Q

What are the symptoms of IBDs?

A
  • Abdo pain
  • Diarrhoea
  • PR blood
  • Weight loss
  • Systemic upset
  • Ulcers
  • Fever
    Very variable prognosis
71
Q

What kind of lesions are usually present in Crohn’s disease?

A

Skip lesions

72
Q

What can the complications of IBDs be?

A
  • Stoma
  • Anaemia
  • Perforation
  • Obstruction/stricture
  • Fistulae
  • Toxic megacolon
  • malnutrition
  • Increased risk of bowel cancer
73
Q

What tests would be carried out to test for IBD?

A
  • FBC, CRP
  • Stool MCS
  • Faecal calprotectin
  • CT scan/MRI
  • Endoscopy (sigmoidoscopy, colonoscopy) + biopsies
74
Q

What can differentiate IBS from IBD?

A

IBS does not have any inflammatory markers

75
Q

What are the treatments availabke for IBDs?

A
  • Aminosalicylates e.g. mesalazine
  • DMARDS e.g azathioprine, methotrexate decrease immune response
  • Biologics e.g inflixamab
  • Corticosteroids
  • Symptomatic relievers (analgesics, lazxatives, “constipators”)
  • Surgery

MD3002 Pharmacology (7 decks)

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