Pharmacology - Gi Tract

Front 1

What balance is damaged in peptic ulceration?

Back 1

Between mucosal-damaging processing mechanism (secretion of acid and pepsin) and mucosal-protective mechanisms (secretion of bicarbonate and muscus

Front 2

What organism is implicated in causing peptic ulceration? How does it do it (briefly)?

Back 2

bacillus Helicobacter pylori

Front 3

What drugs can also cause peptic ulceration?

Back 3

NSAIDs

Front 4

What cell secret gastric acid?

Back 4

parietal cells

Front 5

What is the pH of the stomach?

Back 5

about 1

Front 6

What is the action of H2 receptor stimulation?

Back 6

Stimulation of gastric acid secretion, via increasing cAMP levels

Front 7

Other than histamine what stimulates the secretion of gastric acid?

Back 7

ACh>muscarinic receptors, Gastrin>gastrin receptors.

Front 8

By what mechanisms do ACh and gastrin increase the secretion of gastric acid?

Back 8

One cell hypothesis>Act directly on the parietal cell>increasing Ca2+.
Two cell hypothosis>stimulate release of histamine from mast cells

Front 9

What does increasing levels of cAMP and Ca2+ in parietal cells do?

Back 9

It activated a proton pump, moving H+ into the lumen in exchange for K+,
a cotransporter then moves Cl- into the lumen with K+.

Front 10

What physiological mechanism can decrease gastric acid secretion?

Back 10

PGE2 acting on EP3 prostaglandin receptor

Front 11

What kind of muscarinic receptor are found in the gut?

Back 11

M1

Front 12

What are the types of treatment for reducing gastric acid secretion?

Back 12

H2 antagonists, proton pump inhibitors (these two are the most effective), M1 selective antagonists, Antacids, PGE2 analogue.

Front 13

Give an example of a H2 antagonists?

Back 13

Cimetidine

Front 14

Give an example of a proton pump inhibitor?

Back 14

Omeprazole

Front 15

Give an example of a selective M1 antagonist?

Back 15

Prienzepine

Front 16

What are the clinically useful gastrin inhibitors?

Back 16

There are none.

Front 17

Give an example of an antacid?

Back 17

magnesium trisilicate

Front 18

Give an example of a PGE2 analogue?

Back 18

Misoprostol

Front 19

Other than decreasing gastric acid secretion what other actions does Misoprostol have?

Back 19

increase bicarbonate and mucus secretions.

Front 20

What is the main use of Misoprostol?

Back 20

counteracting the use of NSAIDs

Front 21

What are the three treatment roots when treating peptic ulcers?

Back 21

Reduce gastric acid secretion
Trea Heliobacter Pylori
Protect gastric mucosa

Front 22

What is the drug treatment of Heliobacter Pylori infection?

Back 22

Proton pump inhibitor/H2 antagonist
2 antibiotics (ampacillin + metronidazole/clarithromycin)
Bismuth (antibacterial action + mucos protecting effect)

Front 23

What drugs are used to protect gastric mucosa?

Back 23

Sucralfate (complex of aluminium hydroxide and sulphate sucrose) forms complex gels with mucus-enhances protection.

Front 24

How are H2 antagonist administered?

Back 24

Orally

Front 25

What are the unwanted effects of H2 antagonists?

Back 25

Inhibit renal secretion of basic drugs. Cimetidine inhibis P450 an so potentiates many drugs (oral anticoagulants, phenytoin, aminophylline)

Front 26

What are the unwanted effects of sucralfate?

Back 26

Can inhibit uptake of drugs for the gastric (digoxin, tetracycline, theophylline)

Front 27

What two centres of the CNS are involved in the control of vomiting, where are they found?

Back 27

Vomiting centre and the chemoreceptor trigger zone. found in the medulla.

Front 28

List the stimuli that can give rise to emesis (5) ?

Back 28

1) input form higher centres: repulsive sights and signs
2) impulse from versibuar/labyrinth nuclei
3) endogenous blood-borne factors
4) drugs
5) stimuli acting in the pharynx or stomach

Front 29

What are the main receptors involved in the control of vomiting?

Back 29

H1, muscarinic, dopamine, 5-HT, Opioid, neurokinin-1, endocannabinoids.

Front 30

What two drugs act on vestibular and local gut stimuli but not CTZ? Give examples

Back 30

H2 antagonists=promethazine
Antimuscarinics =hyoscine

Front 31

What 3 types of drugs act on CTZ (two of which don't work against local gut stimuli)?

Back 31

D2 antagonist=domperidone
5-HT3 antagonist=ondansetron
Cannabinoids = nabilone

Front 32

What drugs are used to control chemotherapy emesis (example)?

Back 32

neurokinin antagonists=aprepitant
given with 5-HT3 antagonist=ondanstron or decamethasone

Front 33

How can hyoscine be give when vomiting prevents normal oral root?

Back 33

transdermal patch

Front 34

What are the unwanted effects of D2 antaognists?

Back 34

Extrapyramidal effects and incresed prolectin released can cause galactorrhoea.

Front 35

Why might domperidone be preferential to prochlorperazine?

Back 35

Less extrapyramidal effects as it crosses the blood brain less well.

Front 36

What is the treatment roots for Diarrhoea?

Back 36

Fluid and electrolytes replacement, antibiotics if appropriate, Opiates to decease motility.

Front 37

What opiates are chosen for use in diarrhoea?

Back 37

Loperamide as it has less CNS effects

Front 38

What is the drug treatment for gallstones?

Back 38

ursodeoxycholic acid-reduces synthesis and secretion of cholesterol

Front 39

Other than decreasing motility what other effects do opiates have on the GI tract?

Back 39

Decrease secretions.

Front 40

What are the three classes of drugs for constipation?

Back 40

Bulk laxatives, osmotic purgatives, stimulant purgatives.

Front 41

Give an example and method of bulk laxatives?

Back 41

methycellulose. not digested so increase bulk in gut and stimulate peristalsis.

Front 42

Give an example and method of osmotic purgatives?

Back 42

lactulose, not absorbed and increase what in gut by osmosis and thus stimulate peristalsis.

Front 43

Give an example and method of stimulant purgatives?

Back 43

Senna (metabolised by gut to produce active stimulants). work by increasing secretions by stimulating enteric nerves.