CTB - Drugs to treat acid secretion

Question 1

Antacid - MOA + Examples?

Answer 1

• Buffers Gastric acid –> Increasing gastric pH

- Rennie + Maalox

Question 2

Alginate - MOA?

Answer 2

• Anionic polysaccharides form viscous gel upon binding water
• Increase viscosity of stomach contents
• Gel ‘raft’ floats on surface of stomach contents –> reducing reflux symptoms

Question 3

H2RA - MOA? (2)

Answer 3

• Competitively inhibit histamine @ H2 receptors

- Decrease basal + stimulated acid secretion

Question 4

PPI - MOA? Short

Answer 4

• Irreversible inhbit H+/K+ ATPase pump.
• Key step in acid secretion pathway
• Decrease both basal/stimulated acid secretion

Question 5

PPI or H2RA which is more effective?

Answer 5

PPI

Question 6

When are PPIs inactive?

Answer 6

Neutral pH

Question 7

Accumulation of PPIs?

Answer 7

• Secretory canaliculi of parietal cells

- Activated in acid environment,

Question 8

PPI - MOA? Long answer.

How long does a single dose last?

Answer 8

• From circulation, Pro drug crosses parietal cell and enters canaliculus
• Drug activated and trapped here
• Binds to H+/K+ ATPase - irreversibly inactivity it
• For acid secretion to resume, more pumps have to be synthesised.
• Single dose affects daily acid for 2-3 days

Question 9

Conditions requiring treatment of acid secretion? 2

Answer 9

• Reflux Oesophagitis

- Peptic ulcer - Zollinger-Ellison syndrome, NSAIDs, H.Pylori

Question 10

What is reflux Oesophagitis?

Answer 10

• Results from GORD - stomach acid regurgitating into oesophagus

Definition:

'’Inflammation of lower oesophagus due to persistent episodes of reflux’

Question 11

Reflux oesophagitis - Signs and complications?

Answer 11

• Heartburn
• Regurgitation
• Haematemesis
• Oesophageal ulceration
• Peptic stricture
• Barrett’s Oesophagus

Question 12

Treatments of Reflux Oesophagitis?

Answer 12

• Antacids/Alginates
• H2RA
• PPIs

Question 13

What is gastritis?

Answer 13

• Inflammation of underlying tissue of stomach

Question 14

Persistent erosion of gastric mucosa leads too…

Answer 14

Gastric ulcers

Question 15

What is gastric ulcer? What is peptic ulcer

Answer 15

Gastric = Lesion in gastric mucosa

Peptic = lesion in mucosa of digestive tract (usually stomach or duodenum)

Question 16

NSAIDS - Stomach damage mechanism?

Answer 16

• Impair gastric mucosa renewal due to interfering with PG production

NSAIDs inhibit cox –> inhibiting PG synthesis –>
Impairs gastric mucosal renewal –> Impaired gastroprotection causes gastric erosions/worsening ulcers

Arachidonic acid –> PG (COX enzyme is 1st step in this)

Question 17

What do prostaglandins E2 and I2 do?

Answer 17

• Stimulate gastric mucus production
• Stimulate bicarb production
• Inhibit gastric acid production
• Promote local healing

Question 18

Preventing GI ADRs with NSAIDs?

Answer 18

• Alternative
• Low dose, short course
• Avoid other NSAIDS
• Review often
• co-prescribe PPI

Question 19

What is Zollinger-Ellison Syndrome?

Answer 19

• Increased gastrin made (typically due to gastrinoma of duodenum or pancreas)
• Gastrin increases acid secretion –> Peptic ulcers
• Gastrin acts as Trophic factors for parietal cells –> More cells making acid at MORE rate

Question 20

Zollinger-Ellison Syndrome - Treatment?

Answer 20

• PPis and H2ra

- Remove tumour/Chemo

Question 21

H. pylori - What is it? How does it cause issue?

Answer 21

• Gram -VE, damages stomach + duodenum tissue
• Produces/Secretes Urease –> breaking down urea to C02 and NH3.
• Nh3 neutralises gastric acid
• H.Pylori –> penetrates mucus barrier, facilitating acid penetration
• NH3, other bacteria products and acid –> damage epithelial cell’s

Question 22

H.Pylori - treatment?

Answer 22

• PAC500

- Eradicating H.Pylori –> Produce long term remission of ulcers