Upper GI conditions

Question 1

What is the potential problem with self-medicating in Gi conditions?

Answer 1

Could potentially be masking more serious conditions e.g. Gastric cancer

Question 2

What are the risk factors for gastric cancer?

Answer 2

Smoker
Alcohol intake
H.pylori infection
Salt intake
risk is decreased in vegetarians
family history
nearly 2 times more common in males
Age- biggest diagnosis group is 75-79 years

Question 3

What do chief cells secrete?

Answer 3

They secrete pepsinogen- which is a precursor of pepsin that is needed for hydrolysis of proteins

Question 4

What do parietal cells secrete?

Answer 4

Parietal cells in the fundus secrete hydrochloric acid and intrinsic factor.
HCL- activates pepsinogen and kills bacteria
Intrinsic factor- aids vitamin b12 absorption

Question 5

What are the 3 phases of acid activity involved with eating?

Answer 5

• Cephalic phase (Nervous control)- PNS by vagus nerve due to thought/smell/sight of food- prepares for eating
• Gastric phase (local control)- Distension of the stomach causes release of gastrin
• Intestinal phase (hormonal control)- Food in the duodenum (chyme) causes secretion of somatostatin which inhibits acid production- negative feedback reflex

4th phase- basal state, in-between meals

Question 6

Discuss how parietal cells secrete gastric acid?

Answer 6

LOOK AT DIAGRAM- GO OVER AND MAKE THIS A PROPER PROCESS

Parietal cells secrete hydrogen ions via a proton pump exchange:
H+ out and k+ into the parietal cell
- It is stimulated by histamine, gastrin and acetylcholine
- is produced in response to vagus stimuli, rise in pH, ingested protein and calcium

Vagus nerve stimulation- release acetylcholine which acts at M3 receptors on the parietal cell surface to activate it

Histamine acts at h2 receptor on parietal cell surface

Gastrin acts on CCK2 receptors of parietal cells

Question 7

What 3 things stimulate parietal cells to secrete gastric acid?

Answer 7

It is stimulated by histamine, gastrin and acetylcholine

Question 8

What suppresses gastric acid production from parietal cells?

Answer 8

Somatostatin binding to PGE2 receptor on parietal cells

Question 9

What is the role of prostaglandins in gastric cytoprotection and what drugs threaten this?

Answer 9

Gastric cytoprotection prevents auto-digestion of the stomach
- Prostaglandins e.g. somatostatin help this by increasing mucus and bicarbonate ions - together maintain neutral pH even in acidic environment and also increases blood flow (if blood flow decreases causes necrosis of mucosa)

BUT NSAIDs decrease production of prostaglandins via COX pathway hence how NSAIDs cause gi side effects and ulcers

Question 10

What is gastritis?

Answer 10

Inflammation of the gastric mucosa

Question 11

Symptoms of gastritis?

Answer 11

Dyspepsia
Indigestion
Nausea and vomitting
stomach pain

Question 12

What is the most common cause of gastritis?

Answer 12

80% of cases are caused by the bacteria H.pylori (Heliobacter pylori)

Question 13

How does H.pylori survive in the acidic environments of the GI tract?

Answer 13

• H.pylori secretes urease which hydrolyses urea to ammonia. This creates a buffer around itself
• Has flagella so can bury itself into the mucosa
• Also prefers the acidic environment generally as It can colonise beneath the mucus layer causing chronic inflammation

Question 14

How is h.pylori spread?

Answer 14

Through kissing
Ingestion of contaminated vomit, saliva, stool

Question 15

How is a H.pylori infection identified?

Answer 15

• Via a stool sample- avoid antibiotics for 4 weeks prior, hand in a stool sample that is tested
• Breath test- given a drink that contains radiolabelled urea as h.pylori in the stomach breaks down urea. The CO2 breathed out after ingestion will show

Question 16

What are the causes of peptic ulcer disease (PUD)?

Answer 16

• Gastric hyper secretion- caused by a genetic predisposition
• Reduced mucosal resilience e.g. smoking damages mucosa

Duodenal ulcer= increased acid output
Gastric ulcer = decreased mucosal resistance

Question 17

Risk factors for PUD?

Answer 17

H.pylori infection
Use of nsaids
smokers- no of cigarettes per day increased PUD
genetic link
salt intake
stress-related

Question 18

What is the safest NSAID for use in patients at risk of PUD (e.g. 1/3 of RA patients develop PUD)?

Answer 18

ibuprofen - less inhibitory effects on cox-1 so decrease in prostaglandin synthesis is inhibited

Question 19

What are the symptoms of peptic ulcer disease?

Answer 19

GASTRIC ULCER:
Epigastric pain- below sternum and above naval
pain on eating

DUODENAL ULCER:
Pain between meals and at night
Localised, dull pain
Pain in upper abdomen, slightly to the right

BOTH
bloating
nausea
anorexia
belching
blood in vomit
dark stick faces (melaena)

Question 20

What type of drugs are responsible for 50% of drug induced oesophageal ulceration?

Answer 20

antibiotics- especially clindamycin

Question 21

How are gastric and duodenal ulcers treated?

Answer 21

Not treated otc!
- Identify if there is a h.pylori infection
if so, eradicate:
7 day triple therapy with:
- PPI
- 2 X antibiotics e.g. amoxicillin and clarithromycin

• Stop any innapropriate therapy e.g. NSAIDs
• Reduce acid production via e.g. PPI or H2 antagonists for 8 weeks, this should heal ulcer and then eradicate h.pylori if there

Question 22

How do we eradicate H.pylori infection?

Answer 22

7 day triple therapy with:
- PPI
- 2 X antibiotics e.g. amoxicillin and clarithromycin

Question 23

What non-pharmacological advice should be offered to GORD patients?

Answer 23

Smaller meals
Avoid fatty foods
Avoid eating 4 hours before bed
avoid tight clothing
weight loss
don’t lay down after eating
decrease alcohol
raised bed by 15-23 cm

Question 24

How do antacids work?

Answer 24

Neutralises the stomach acid by combining with HCl to release co2 as a biproduct to give a sense of relief (burp)

Question 25

Antacid examples

Answer 25

Rennies (magnesium and calcium carbonate)
Tums

Question 26

Alginate examples

Answer 26

Gaviscon

Question 27

How do alginates work?

Answer 27

Form a raft in the stomach to trap air bubbles and co2 from reacting with the stomach contents and protects the oesophagus from the stomach contents

Question 28

H2 receptor antagonist examples

Answer 28

Cimetidine
Famotidine
Ranitidine

Question 29

How do H2 antagonist work?

Answer 29

decrease gastric acid secretion by reversibly binding to histamine H2 receptors located on gastric parietal cells, thereby inhibiting the binding and activity of the endogenous ligand histamine

Question 30

Which H2 antagonists can be bought OTC and how are they taken?

Answer 30

Ranitidine
max dose of 2 tablets in 24 hours and should only be used for 6 days

Question 31

PPI examples

Answer 31

Omeprazole, lansoprazole, esomeprazole

Question 32

Why are PPIs enteric coated?

Answer 32

to allow them to reach the small intestine without being degraded in the stomach

Question 32

What PPIs can be bought OTC and how should they be taken?

Answer 32

Omeprazole and esomeprazole (Nexium)
for reflux in >18 years old
20mg OD until symptoms improve, then 10mg OD

Question 33

Can H2 antagonists be given in GORD?

Answer 33

NO they should not be given- use PPIs or alginates
only if these are inadequate, h2 antagonists may be considered