Session 13 Flashcards Preview

Han's Pharmacology > Session 13 > Flashcards

Flashcards in Session 13 Deck (36):
1

What is the role of the parietal cells?

Secrete hydrochloric acid, a component of gastric juice, into large canaliculi.

2

Describe the mechanism of acid secretion.

H+ ions generated in parietal cell from dissociation of water.
OH- ions combine with CO2 to form HCO3-.
Bicarbonate transported out in exchange for chloride.
Cl- and K+ transported into the canaliculi lumen.
H+ pumped into the canaliculi lumen, in exchange for K+, via H+K+ATPase.
Accumulation of H+ generates an osmotic gradient across the membrane, resulting in outward diffusion of water.

3

Give three stimulators of acid secretion.

ACh, gastrin, histamine.

4

Describe the role of H2 receptor antagonists.

E.g. ranitidine, cimetidine. Blocks the parietal cell receptor for histamine.

5

Describe the role of PPIs

Non-competitively bind and inactivate H+K+ATPase, located in the cannalicular membrane of the parietal cell. Strong inhibition of acid secretion. E.g. Omeprazole, Lansoprazole.

6

Describe the step-up process to manage GORD/oesophagitis.

Lifestyle modification, antacids/alginates, H2 receptor blockers, then PPIs.

7

Give three ADRs of H2 receptor blockers.

Hypotension, headache, tiredness, dizziness, confusion, diarrhoea, constipation.

8

How does Cimetidine affect CYP metabolism?

It is a CYP inhibitor.

9

Give three ADRs of PPIs.

Headache, nausea, diarrhoea, fatigue, dizziness, rash, itch, flatulence, constipation.

10

Describe the myogenic control of gastric motility.

Rhythmic contraction, passive current spread through gap junctions and interstitial cells of Cajal act as a pacemaker.

11

Describe the neuronal control of gastric motility.

Stimulation of post-ganglionic cholinergic enteric nerves increases force of contraction of the gut. Stimulation of non-adrenergic inhibitory nerves inhibits contraction.

12

Where is Auerbach's plexus located?

Between circular and longitudinal muscle layers.

13

What is the intestino-intestinal inhibitory reflex?

Distension of one intestinal segment causes complete intestinal inhibition.

14

What is the anointestinal inhibitory reflex?

Distension of the anus causes intestinal inhibition.

15

What are the gastocolic and duodenocolic reflexes?

Stimulate motility after material has entered the stomach or duodenum.

16

Give three neurotransmitters involved in controlling gastric motility.

Gastrin, secretin, CCK, motilin and paracrine transmitters (histamine, somatostatin and prostaglandins).

17

How does gut motility differ in the fed and fasting state?

Fasted: motility is highly organised into a distinct and cyclic recurring or peristalsis.
Fed: pattern is temporarily abolished and replaced by a band of random contractions.

18

How can gastrointestinal motility be measured?

Manometry. Uses various pressure sensors to measure contractility.

19

What is emesis?

Phyloric sphincter closes while the cardia and oesophagus relaxes. Gastric contents propelled by contraction of abdominal wall and diaphragm. Glottis closes with elevation of the soft palate preventing entry of vomitus into the trachea and nasopharynx.

20

Describe the role of dopamine D2 receptor antagonists in anti-emesis medication.

E.g. Domperidone. Increases rate of gastric emptying. Does not cross the BBB. Also stimulates prolactin release (galactorrhoea).

21

Describe the role of 5-HT3 antagonists in anti-emesis medication.

E.g. Ondansteron. Works against vagal afferent nerves in the GI, hence reduced vagal stimulation.

22

Describe the role of Metoclopramide in anti-emesis medication.

D2 antagonist, anti-cholinergic effects and blocks vagal afferent 5-HT3.

23

When should Metoclopramide be avoided?

In Parkinson's due to extra-pyramidal reactions.

24

Describe the role of anti-muscarinics in anti-emesis medication.

E.g. Hyoscine. Antagonist of muscarinic cholinergic receptors. Used to treat motion sickness.

25

Describe the role of Histamine H1 receptor antagonists in anti-emesis medication.

E.g. Cyclizine. Also has anti-muscarinic effects. Can cause QT prolongation. Crosses the BBB.

26

Describe the role of bulk laxatives.

E.g. Ispaghula. Vegetable fibre in attempt to re-establish normal bowel habits. Relieves constipation.

27

Describe the role of faecal softeners.

Arachis oil and glycerol lubricate and soften stool.

28

Describe the role of magnesium and sodium salts.

Osmotically active laxatives. Cause water retention in bowel to increase peristalsis. Act quickly and are severe.

29

Describe the role of irritant/stimulant laxatives.

Excitation of sensory nerve endings leads to water and electrolyte retention and thus peristalsis. Used for rapid treatment. E.g. castor oil, bisacodyl, anthraquinones.

30

Which type of laxative would you give if the history revealed hard faeces?

Osmotic laxatives or bulk-forming laxatives.

31

Which type of laxative would you give if the history revealed soft faeces?

Stimulant laxatives (senna, bisacodyl, glycerol).

32

Describe the role of anti-motility drugs for managing diarrhoea?

Act via opioid receptors in the bowel. Reduce bowel motility, increase anal tone and reduce sensory defecation reflex.

33

Describe the role of bulk-forming drugs for managing diarrhoea?

Drugs such as ispaghula act via water absorption. Useful for patients with IBS.

34

Describe the role of fluid absorbents for managing diarrhoea?

Kaolin acts as a fluid absorbent, therefore producing a more formed stool.

35

Describe the role of Mebeverine for the treatment of IBS.

Direct effects on hypermotility and relieves spasms of intestinal muscle. Useful when combined with a bulk forming agent.

36

Give three examples of drugs that cause diarrhoea?

Laxatives, antibiotics, chemo, lansoprazole, opiates, diuretics, iron preparations, anticholinergic drugs, calcium/aluminium antacids, verapamil etc.