Homework

1.Currently favoured regimens for eradication of Helicobacter pylori are

triple therapy with a proton pump inhibitor along with two antibiotics

for 1 week. For example:

Omeprazole 20 mgmetronidazole 400 mg and clarithromycin

500 mg (all twice daily).

Omeprazole 20 mgclarithromycin 500 mg and amoxicillin 1 g (all

twice daily).

Resistance to amoxicillin has not yet been demonstrated.

Previously, regimens such as omeprazole, metronidazole, amoxicillin

and clarithromycin were recommended; are these regimens no longer used?

The reason behind this question is the 'sky-high' cost of clarithromycin in

Pakistan, which is inversely proportional to patient compliance (that is,

low-cost regimens tend to have a higher rate of compliance).

2.What is the difference between the management of a gastric and of a

duodenal ulcer?

3.How does omeprazole suppress Helicobacter pylori?

4.Does omeprazole cause rebound hyperacidity? Does this also apply to

H2-blockers?

5.On (K&C 7e, p. 249), you state that the postsynaptic neurotransmitter that

inhibits the relaxation of lower oesophageal sphincter (LOS) is nitric

oxide (NO). I have understood NO to promote relaxation of LOS by

acting on the non-adrenergic, non-cholinergic (NANC) inhibitory

neurones, which inhibits the action of cholinergic excitatory neurones.

Could you please explain this paradox?

6.It is stated that nitric oxide (NO) inhibits the relaxation of the lower

oesophageal sphincter (LOS) and that sildenafil is given for treating

achalasia. As far as I know, sildenafil acts to increase the guanine

monophosphate (GMP), just as NO uses the same mechanism to relax the

LOS. Could you explain this paradox?

7.In Kumar and Clark Clinical Medicine you mention that auscultation

is not important in cases of gastrointestinal disorders, but Harrison's

Principles of Internal Medicine gives this as being of equal importance

because succussion splash and bowel sounds can help in presumptive

diagnosis. Succussion splash indicates gastric obstruction (e.g.

gastroparesis) and likewise bowel sounds can help determine the status

of developing ileus. Would you agree that this is therefore a diagnostic

tool?

8.Is it hazardous to give aspirin in the antiplatelet doses (75-325 mg/day)

to a patient with a past history of haematemesis proved to be from a

peptic ulcer?

9.How can upper gastrointestinal (GI) bleeding be distinguished from

lower GI bleeding by using faecal analysis?

10.In upper gastrointestinal bleeding, without knowing the cause or

source of bleeding, why do we give proton pump inhibitors (PPIs,

e.g. omeprazole)? What is the role of these, if the source of bleeding is

not peptic or duodenal ulcer?