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Year 2 - LCRS - Pharmacology > Treatment of Gastric and Duodenal Ulcers (20.02.2020) > Flashcards

Treatment of Gastric and Duodenal Ulcers (20.02.2020) Flashcards

1
Q

Acute gastric/duodenal ulcer symptoms

A
  • Epigastric pain

- burning sensation that occurs after meals

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2
Q

What are the most important tests for ulcers?

A
  • Carbon-urea breath test – positive (suggests H. pylori presence)
  • Stool antigen test – positive -> confirms H. Pylori

Diagnosis = H Pylori positive peptic ulcer

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3
Q

Pathophysiology of H. pylori

A
  • Dissolves mucus layer (in small portions) -> urease enzyme
  • Causes epithelial cell death (exotoxins, inflammation)
  • Increased acidity -> peptic ulcer

can cause upper GI blood loss

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4
Q

Treatment of an acute H Pylori positive peptic ulcer (first line)

A
  • Amoxicillin & Clarithromycin/Metronidazole – Antibiotics that are most effective against that bacterium
  • Proton Pump Inhibitor (PPI) – reduces acid production (7d)
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5
Q

Helicobacter pylori

A
  • causes mucous layer to dissolve
  • Gram negative, motile, microaerophilic bacterium
  • Resides in human GI tract – exclusively colonising gastric-type epithelium
  • generally it is a commensal bacterium, found in many people
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6
Q

How does H pylori cause ulcers?

A
  • Increased gastric acid formation – increased gastrin or decreased somatostatin
  • Gastric metaplasia – cell transformation due to excessive acid exposure
  • Downregulation of defence factors - decreased epidermal growth factor & decreased bicarbonate production
  • The Urease enzyme is very problematic, a product damages epithelial cells, evokes immune response
  • certain virulent strains produce cytotoxins

=> does several different things, multi front attack on the gastric epithelium

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7
Q

Virulence of H. pylori

A
  • Urease – catalyses urea into ammonium chloride & monochloramine -> damage epithelial cells
  • Urease – antigenic -> evokes immune response
  • Certain virulent strains produce CagA (antigenic) or VacA (cytotoxic) – more intense tissue inflammation
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8
Q

Presentation of chronic ulcers

A
  • Epigastric pain
  • burning sensation

Had an ulcer before

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9
Q

Treatment of chronic peptic ulcers

A
  • Antibiotics for H Pylori (amoxicillin & clarithromycin/metronidazole)
  • Consider quinolone, tetracycline, bismuth (peptobsimol), sucralfate -> alkalating agents, create a less acidic environment in the stomach, increase pH
  • Proton Pump Inhibitor (omeprazole) – 4-12 weeks

Triple therapy with AB, PPI and maybe bismuth/sucralfate or AB other option that first ones

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10
Q

Proton pump

A

H+-K+-ATPase (proton pump)
- Expressed on secretory vesicles within parietal cells
- increased [Ca2+]ic -> increased cAMP -> translocation of secretory vesicles to parietal cell apical surface -> H+ secretion
(- cAMP is directly linked to Gs proteins)

In ulcers: Increased activity of proton pump – increased H+ secretion -> reduction gastric pH
=> treat with PPIs

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11
Q

Are most ulcers H pylori positive or negative?

A

positive

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12
Q

What is the second most common cause of ulcers?

A

NSAID use

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13
Q

Presentation of a H. pylori negative ulcer

A

Epigastric pain

burning sensation

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14
Q

INVESTIGATIONS and diagnosis of a Hp negative ulcer

A

Carbon-urea breath test – negative
Stool antigen test – negative
NSAID use – positive

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15
Q

NSAIDS and ulcers

A
  • Directly cytotoxic
  • Reduces mucus production
  • Increases likelihood of bleeding
  • Increased acidity -> peptic ulcer

REWATCH THIS PART

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16
Q

How do you treat NSAID induced ulcers?

A
  • removal of NSAID (this is not always possible, the patient might be taking the NSAID for their heart)
  • Proton Pump Inhibitor or histamine H2 receptor antagonist (Ranitidine) – 4-8 weeks
    (- H2 receptor increases acid secretion)
17
Q

Ranitidine

A
  • histamine H2 receptor antagonist
  • effective for ulcers
  • not used that commonly because PPIs are more effective
18
Q

Give an example of an H2R antagonist

A

Ranitidine

  • effective for ulcers
  • not used that commonly because PPIs are more effective
19
Q

What can cause changes in PPIs?

A
  1. Acetylcholine (ACh) released from neurones (vagus / enteric) acts on muscarinic (M3) receptors - increases [Ca2+]i
  2. Prostaglandins (PGs) released from local cells act on EP3 receptors - ↓ cAMP => PROTECTIVE
  3. Histamine released from enterochromaffin-like cells (ECL) act on H2 receptors - increase cAMP
  4. Gastrin released from G-cells, acts on cholecystokinin B receptors - increase [Ca2+]i
20
Q

What increases / decreases PPIs?

A

Increases:

  • ACh
  • Histamine
  • gastrin

Decreases
- Prostaglandin

21
Q

What effects does ACh have of PPIs?

A

Acetylcholine (ACh) released from neurones (vagus / enteric) acts on muscarinic (M3) receptors - increases [Ca2+]i

=> increased H+ secretion

22
Q

What effects does histamine have of PPIs?

A

Histamine released from enterochromaffin-like cells (ECL) act on H2 receptors - increase cAMP
-> increased gastric acid secretion

23
Q

What effects do prostaglandins have of PPIs?

A

Prostaglandins (PGs) released from local cells act on EP3 receptors - ↓ cAMP
=> decreased H+ secretion

24
Q

What effects does gastrin have of PPIs?

A

Gastrin released from G-cells, acts on cholecystokinin B receptors - increased [Ca2+]i
=> increased H+ secretion

25
Q

MCQ 2: Which of the following drugs is not used in the treatment of peptic ulcers?

  • amoxicillin
  • aspirin
  • omperazole
  • ranitidine
  • other AB
A

Aspirin

26
Q

MCQ 3: activation of which receptor does not cause increased secretion of

A

EP3 and SS-receptor activation

27
Q

LO1: Explain the underlying pathology of peptic ulcers

A
  • Helicobacter pylori: increased gastric acid formation; gastric metaplasia; decreased defence factors
  • Proton pump: H+ secretion - activated by increased Ca2+ and increased cAMP
  • Histamine released from ECL cells act on H3 receptors - I increased cAMP
28
Q

LO2: Identify the drugs used in the treatment of peptic ulcers and their mechanisms of action

A
  • Antibiotics: removal of H pylori infection
  • Proton pump inhibitors: e.g. omeprazole – reduce acid -production from parietal cells
  • Histamine H2 antagonists: reduce acid production from parietal cells
29
Q

MCQ 3: activation of which receptor does not cause increased secretion of H+?

  • ACh
  • EP3
  • Histamine
  • Gastrin R
  • SS R
A

EP3 and SS-receptor activation

30
Q

LO1: Explain the underlying pathology of peptic ulcers

A
  • Helicobacter pylori: increased gastric acid formation; gastric metaplasia; decreased defence factors
  • Proton pump: H+ secretion - activated by increased Ca2+ and increased cAMP
  • Histamine released from ECL cells act on H3 receptors - increased cAMP

Year 2 - LCRS - Pharmacology (34 decks)

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