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Y2 Pharm (LCRS1) > Anti-Ulcer Drugs > Flashcards

Anti-Ulcer Drugs Flashcards

1
Q

What are the two types of peptic ulcer?

A
  • Gastric ulcer
  • Duodenal ulcer
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2
Q

What are the protective factors that protect the stomach lining from damage?

A

Mucous lining the stomach Bicarbonate produced by cells in the stomach Prostaglandins facilitate a good blood flow in the stomach, increase mucous and bicarbonate production and inhibit acid secretion

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3
Q

Which cells produce stomach acid?

A

Parietal cells

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4
Q

Which cells produce pepsinogens?

A

Gastric chief cells

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5
Q

State some factors that could contribute to the pathogenesis of ulcers.

A

Increase in acid production Decrease in bicarbonate production Decreased thickness of mucosal layer Increase in pepsin Decreased mucosal blood flow Increase in H. pylori

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6
Q

Explain the ways of testing for H pylori

A
  1. Carbon urate breath test Give a urate mixture that contains a distinctive isotope of carbon H. pylori has enzymes that can break down the urate mixture and liberate the carbon isotope This carbon isotope is then incorporated into carbon dioxide and is breathed out – this can then be detected to confirm high levels of H. pylori 2. Stool antigen test Test for antigens of H. Pylori and urease
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7
Q

What treatments can be put together to form the best practice ‘Triple Therapy’?

A

Antibiotics Drugs that reduce gastric acid secretion Drugs that promote healing

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8
Q

Where are parietal cells found in the stomach?

A

Fundus

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9
Q

Which cells in the stomach produce histamine?

A

H cells

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10
Q

Which cells in the stomach produce gastrin and where are these cells found?

A

G cells Located in the antrum

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11
Q

What triggers gastrin release from G cells?

A

The breakdown of food in the stomach and the liberation of amino acids stimulate gastrin release

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12
Q

What do D cells release?

A

Somatostatin

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13
Q

What are the effects of somatostatin?

A

It is inhibitory – it decreases the release of histamine and gastrin

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14
Q

What type of ion transporter is the proton pump found in parietal cells?

A

H+/K+ ATPase

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15
Q

Which cells produce bicarbonate?

A

Superficial epithelial cells

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16
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

17
Q

What is the mechanism of action of PPIs?

A

Irreversible inhibitors of H+/K+ ATPase

18
Q

What are the effects of PPIs?

A

Inhibits basal and stimulated gastric acid secretion from the parietal cells by >90%

19
Q

What features of PPIs limits its action on other proton pumpsaround the body?

A

Inactive at neutral pH It is a WEAK BASE so it accumulates in the cannaliculi of the parietal cells – this concentrates its actions in the cannaliculi

20
Q

Describe the pharmacokinetics of omeprazole.

A

Orally active Enteric-coated slow release formulation

21
Q

Give an example of a histamine receptor antagonist.

A

Ranitidine

22
Q

What are the effects of histamine receptor antagonists?

A

Inhibits gastric acid secretion from the parietal cells by about 60%

23
Q

What is the drug of choice for gastroesophageal reflux disease?

A

Proton pump inhibitors e.g. omeprazole

24
Q

What is the presentation of a H. Pylori infections causing peptic ulcers?

A

Uncomplicated infection: Epigastric pain and a burining sensation that occurs after eating a meal Complicated infection: Constant epigastric pain and burning sensation

25
Q

What is the treatment for H. Pylori infection?

A
  1. Antibiotics:
  • Amoxicillin
  • & Clarithromycin/Metronidazole
  1. Proton Pump Inhibitor (PPI) :
  • Omeprazole
  • Reduces acid production
26
Q
A
27
Q

What is H Pylroi?

A
  • Gram negative
  • motile
  • microaerophilic bacterium
28
Q

Where does H Pylori live?

A
  • Normally a commensal
  • Resides in human GI tract – exclusively colonising gastric-type epithelium
29
Q

How does H Pylori form Peptic ulcers?

A
  1. Increased gastric acid formation
    * increased­ gastrin or decreased somatostatin
  2. Gastric metaplasia
    * Cell transformation due to excessive acid exposure
  3. Downregulation of defence factors
  • Reduced epidermal growth factor (stimulates epithelial cell growth
  • Reduced bicarbonate production - reduced mucus layer
  1. Urease enzyme
  • Catalyses urea into ammonium chloride & monochloramin - damage epithelial cells
  • It’s antigenic - evokes immune response -> inflammation and associated damage of epithelial cells
30
Q

What is the difference in treatment for a complex H Pylori infection over a simple infection?

A
  1. Quinolone and Tetracycline administered
  2. Omeprazole
  • Given for 7 days in a simple infection
  • Given for 4-12 weeks in a complex infection
31
Q

What are the specific virulence factors for H Pylori?

A
  • CagA - antigenic
  • VacA - cytotoxic
32
Q

How does the H+-K+-ATPase get to the apical membrane of the parietal cell?

A
  • Normally found in vesicles inside the cell
  • Increased Ca2+ -> Increased cAMP
  • Causes increased translocation of secretory vesicles to the apical membrane
  • More ATPase in the membrane -> more H+ excretion
33
Q

What are the 2 most common causes of a peptic ulcer?

A
  • H Pylori. infection
  • NSAID use - particularly aspirin
34
Q

Why do NSAIDS cause peptic ulcers?

A
  • Directly cytotoxic
  • Reduces mucus production
  • Increases likelihood of bleeding
  • Increased acidity à peptic ulcer
35
Q

What is the treatment for NSAID induced peptic ulcer?

A
  • Removal of NSAID
  • Proton Pump Inhibitor or histamine H2 receptor antagonist (Ranitidine) – 4-8 weeks
36
Q

What are the 4 receptors that stimulate gastric acid production and how do they do this?

A
  1. Muscarininc (M3) receptor
  • ACh from vagus or enteric nerves
  • Increases parietal cell Ca2+ levels
  1. EP3 receptors
  • Prostaglandins from local cells
  • increased cAMP
  1. Histamine (H2) receptors
    * Released from enterochromaffin-like cells (ECL)
    * Increase ­cAMP
  2. Cholecystokinin B (CCKB) receptors
  • Gastrin from the blood stream
  • Increased intracellular Ca2+
37
Q

How does asprin increase gastric acid production?

A
  • Main effect is on increasing histamine release
  • Also increases prosta glandin release

Y2 Pharm (LCRS1) (34 decks)

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