Gastrointestinal ulcers Flashcards

1
Q

Example of a systemic antacid

A

Sodium Bicarbonate NaHCO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA of NaHCO3

A
  • dissociates in the stomach
  • the bicarbonate ion is absorbed into the blood and slightly increases pH
  • increases the pH of the stomach
  • quick, easy and effective SHORT TERM Tx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Problems with NaHCO3

A
  • alkalotic urine can increase the deposition of Ca+ and P to form a kidney stone
  • this increases blood Na levels, thus exacerbating HTN
  • acid rebound due to feedback regulation (aka stomach’s response to rising pH is to make more acid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List 3 examples of non-systemic antacids. How do they differ from NaHCO3 (bicarbonate)?

A
  • CaCO3, Al(OH)3, Mg(OH)2

- they do NOT effect extracellular or blood pH; however, they have the same problem with rebound acidity as bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can you counteract the constipation often seen with Al and Ca antacids?

A

Combine them with magnesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MOA of anticholinergic drugs to treat ulcers

A
  • Muscarininc ACh receptors in parietal cells stimulate HCl secretion from these cells
  • inhibition of these receptors reduces acid secretion (but not by much)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List an example of a muscarinic type 1 receptor blocker

A

Pirenzipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Side effects of anti-cholinergic drugs

A

dry mouth, vision problems, sedation, etc.
Anticholinergics are very non-selective
- thus, lots of side effects and limited acid reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are cytoprotectives?

A

Drugs which protect cells from acidic damage, either directly or through stimulation of mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List the two major cytoprotective drugs

A
  • Sucralfate

- Misoprostol (taken if patient is on long-term NSAIDs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe sucralfate and its MOA

A
  • Aluminum base salt
  • binds to H+ ions to increase pH
  • also binds to degenerating cells, forming a protective layer of ‘artificial’ mucus
  • works for 8-12h and specifically protects damaged tissue as well as reduces acidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Problem with sucralfate

A

Can inhibit absorption of other drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Misoprostol MOA

A
  • Cytoprotectant (recall)
  • given w/ NSAIDs because COX inhibition causes PGE inhibition. PGE is critical for mucus production to protect the stomach.
  • Misoprostol stimulates production of the mucosal barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do H2 blockers work?

A
  • stimulation of H2 receptors in parietal cells increases HCl production
  • inhibition of H2 is highly effective in a number of acid-related disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List 3 H2 blockers

A
  • Cimetidine
  • Ranitidine
  • Famotidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe Cimetidine

A
  • 50-60% reduction in acidity
  • binds to CYP 450 so can cause drug interactions
  • can cause SE’s due to binding to androgen receptors (reduced libido, impotence, etc)
17
Q

Describe Ranitidine

A
  • More effective than Cimitidine (reduces acid by 65-70%)
  • less drug interaction
  • does NOT bind androgen receptors
18
Q

Describe Famotidine

A
  • H2 blocker that is most effective (best at reducing acid secretion)
  • very few adverse effects (does not bind P450 at all)
19
Q

MOA of PPIs

A
  • Inhibits the gastric H+/K+ ATPase (proton pump)
  • especially good for rapid reduction of acid
  • bind to H+ extrusiion sites and block the release of H+ and Cl-

Pathway:

  • PPIs go to the small intestine and enter the parietal cell after absorption
  • the prodrug is converted to the active drug by the acidity
  • active drug binds very tightly to the pump
  • long half life
20
Q

List two PPI drug examples

A
  • omeprazole

- esomeprazole

21
Q

What additional benefit does the PPI Rabeprazole have?

A

also increases mucus secretion

22
Q

H. Pylori is present in what % of ulcers?

A
  • 95% of duodenal ulcers

- 80% of gastric ulcers

23
Q

Pathogenesis of H. Pylori

A
  • H. Pylori burrows into the gastric mucosa to escape the stomach acid
  • It then produces urease, the enzyme that converts urea to ammonia and CO2
  • this kills mucosal epithelial cells, leaving the gut unprotected
24
Q

Testing for H. pylori infection

A
  • breath test for urea
  • serological
  • culture
  • histology
25
Q

Describe effective Tx for H. Pylori

A

Triple therapy: A PPI to control acid, and 2 effective antibiotics to kill the bacteria
- for quadruple therapy, add bismuth

26
Q

Describe GERD

A
  • most prevalen type of ulceration; 5X mroe common than gastric ulcers
  • LES defect allows acidic contents to contact the esophageal lining
27
Q

What type of drugs can be effective in reducing LES pressure?

A
  • beta blockers
  • Ca channel blockers
  • nicotine
28
Q

Describe GERD Tx

A
  • Drug options (PPIs) are not nearly as effective as behaviour change
  • avoid fat, caffeine, chocolate, peppermint, alcohol
  • avoid large meals at night
  • stop smoking