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Samenvatting Cursusmateriaal WC 4 FA-Ba101
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De verplichte opgaven van week 4 inleiding farmacie
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Voorbereidende opdracht voor WC4Onderwerp:
Wat bepaalt welk middel je krijgt voorgeschreven bij maagklachten (indicatie). Hoe werkt het en hoe
krijg je het op de plek waar werking vereist is?
Leren om specifieke formatie te vinden over geneesmiddelen bij maagaandoeningen en hierbij de NGH-
standaard, Zelfzorgstandaard maagklachten en Informatorium Medicanmentum - middelen bij peptische
aandoeningen te leren gebruiken.
Zelfstudie: voorbereidende opdrachten voor WC4
1. Hoe wordt een maagzweer als gevolg van een H.Pylori-infectie behandeld? Verklaar de
keuze van de geneesmiddelen.
2. Geef in je mindmap/schema aan hoe de maagwand zichzelf beschermt tegen zuur en hoe H.
Pylori de bescherming van de maagwand aantast. (zie bijv. Boron en filmpje:
https://www.sumanasinc.com/scienceinfocus/sif_helicobacter.html)
3. Waarom krijgt niet iedereen met een H. Pylori infectie een maagzweer?
Lees onderstaand gedeelte uit het reviewartikel van Lahner et al (2014): Helicobacter pylori
infection and drugs malabsorption, en maak de onderstaande vragen 9 en 10:
POSSIBLE MECHANISMS FOR A LINK BETWEEN H. PYLORI INFECTION AND IMPAIRED DRUGS
ABSORPTION. The exact mechanisms forming the basis of the relationship between H. pylori infection
and impaired drugs absorption and/or bioavailability are not yet established. In general, characteristics
of the drug, as molecular size and shape, ionization degree, and lipid solubility of its ionized and
nonionized forms may affect drug absorption.Noticeably, motility of the stomach as well as volume and
modifications of gastric juice may influence the pharmacokinetics of a drug.
H. pylori infection acts as a trigger to chronic inflammation of gastric mucosa, causing an impairment of
gastric physiology: gastric motility may be affected by inducing myoelectrical activity variations which in
turn bring about an impaired gastric emptying.
Also an impaired gastric acid secretion often follows H. pylori induced gastritis, being the degree of
impairment closely related with the wideness and the severity of the damage.
In fact, when H. pylori gastritis involves the corporal mucosa, which contains the oxyntic glands, a
diminished acid secretion may ensue. At an early stage of infection, a direct inhibition of the parietal cells
secretion may be exerted by products of inflammation. Interleukin 1β, a proinflammatory cytokine and a
key mediator in H. pylori associated disease, inhibits gastric acid secretion in vitro and in vivo. Gastric
hypoaciditiy may be partly or fully reversed upon H. pylori eradication, without losing the bulk of parietal
cells.
A massive loss of parietal cells, as a consequence of long-standing H. pylori injury, may ensue atrophy of
oxyntic glands and, thus, hypoacidity of gastric juice. In such a case, whether the cure of infection might
reverse the impaired acid secretion is, as yet, controversial.
The process of drug absorption may be potentially affected by these pathological changes of the
intragastric environment during H. pylori infection. The consequences of this infection may explain the
proposed link between H. pylori-related gastritis and reduced bioavailability of some drugs. In particular,
the reduced gastric acid secretion seems to be relevant in the process of impaired drug absorption
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