Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Digestive > 33 - Drugs and the Gut > Flashcards

33 - Drugs and the Gut Flashcards

1
Q

What 2 types of drugs inhibit gastric secretion?

A
  • H2 (histamine 2) receptor antagonists

- proton pump inhibitors

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

Who invented the first H2 receptor antagonist?

A

Sir James Black

- before this they did surgery/resection of vagus nerve

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

Most common gut disease?

A

Gastro-oesophageal reflux disease (GORD)

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

What do I need to know?

A
  1. the problems with the delivery of drugs to the appropriate region of the GI tract
  2. understand the appropriate treatment for gastric acid suppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histamine is involved in both … and …

A

Allergic reaction and gastric acid secretion

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

What 3 receptors are on parietal cells in the stomach?

A
  1. histamine receptors
  2. ACh/vagus nerve receptor
  3. Gastrin Receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How many histamine receptors are there and what are they?

A

2
H1 receptor - on smooth muscle and endothelial cells, responsible for allergy

H2 receptor - on parietal cells and responsible for acid secretion

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

What do anti-histamines work on?

A

They are H1 receptor antagonists

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

Anti-acid medications act on

A

H2 receptor

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

How do H1/2 medicines work

A

The drug and histamine COMPETE for the receptor binding site (competitive antagonist)

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

H2 receptor drugs are

A

competitive antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the consequences of the H2 receptor antagonists being competitive antagonists?

A
  • can be overcome by a strong agonist
  • increasing the dose has a less additive dose
  • there is a tolerance/trachyphylaxis
  • rapid action and can saturate receptors in 6-8 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is tachyphylaxis?

A

tolerance
Can be receptor saturation and so tolerance to the medicine - first dose response good but subsequent doses are less effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some problems with H2 competitive antagonists?

A
  • not effective for many patients with heartburn
  • is unable to heal moderate to severe reflux oesophagitis
  • needs multiple doses 4 times a day for severe symptoms
  • the maximum acid suppression for H2 antagonists is 50%
  • okay for peptic ulcers given as a single night dose BUT they reoccur on stopping the treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Are H2 antagonists effective for people with heartburn?

A

not effective for many

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the maximum acid suppression for people taking H2 antagonists?

A

50% - not great

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Do H2 antagonists cure peptic ulcers?

A

Work well when taken once nightly but once you stop taking it they reoccur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How long does the medicine last and what does this mean?

A

last 4-6 hours means you have to take it several times a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is there only max 50% acid suppression?

A

gastrin and Ach also stimulate parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do you use after H2 antagonists are ineffective?

A

Proton pump inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why are proton pumps so important?

A

They are the final common pathway before acid secretion

22
Q

Example of proton pump inhibitor?

A

Omeprazole

23
Q

How does omeprazole work?

A
  • absorbed into blood and travels to parietal cell
  • in the presence of acid omeprazole is converted to sulphonamide
  • sulphonamide reacts with the sulphydryl group of cysteine at the proton pump
  • blocks entire pump resulting in 90% acid secretion suppression
24
Q

Simply, what does omeprazole do?

A

Irreversible blockage of activated proton pump for a long duration/whole day

25
Q

Perk of proton pump inhibitors compared to H2 inhibitors

A
  • long lasting
  • 90% suppression
  • blockage CANT be over-ridden by an increased stimulation by histamine OR gastrin or ACh
26
Q

What are proton pump inhibitors largely used for and not so much for?

A
  • GORD
  • ulcer disease CAUSED by NSAIDs (non-steroidal anti-inflam drugs) like aspirin
  • useful in acute ulcer bleeding
  • not so much peptic ulcer disease due to the improved treatment of H pylori infection
27
Q

Why is omeprazole effective for acute ulcer bleeding?

A

Pepsin usually dissolves fibrin clot trying to form at ulcer - is inactive in higher pH, so blocking proton pumps increases pH and decreases pepsin activity

28
Q

Who discovered H.pylori?

A

only treatment was H2 receptor antagonists
Barry Marshal
Proved by drinking H pylori to prove caused peptic ulcer disease (even though no treatment!!)

29
Q

When should you use H2 receptor antagonists?

A
  • one off heart burn
  • good for nocturnal symptoms
  • rapid onset and good first dose effect
  • not as good for food stimulated acid secretion
30
Q

When use proton pump inhibitors

A
  • takes 4-6 weeks/10 days to see impact/several days for maximal effect
  • good for maintenance treatment
  • give empty stomach/30 min before meal as need to stimulate proton pumps
31
Q

Long term problem with long term acid suppression?

A
  • in ICU population can cause bacterial overgrowth of stomach
    > aspirate stomach contents with bacteria causing pneumonia
  • malabsorption of B12/calcium/iron
  • potential formation of carcinogenic compounds
  • decreased sterilisation of food
  • ECL hyperplasia (see as polyps) to compensate
32
Q

What are 5 effects of the gut on drug delivery

A
  1. Acid can degrade drugs - need to be enteric coated
  2. Acid can enhance absorption
  3. Effect of rate of gastric emptying
    > matching insulin and meals
  4. Hepatic enzyme function
  5. Enterohepatic circulation/biliary secretion
33
Q

Give an example of how gastric emptying can effect drug delivery?

A

i.e. matching insulin and meals. If you give insulin but have no rush of glucose in blood it will empty blood of the little BG it has > hypoglycemic. Need gastric emptying for food absorption and blood glucose for insulin to act on
> need a meal within 30 min of insulin dose

34
Q

What are the problems and solutions of supplementing someone with pancreatic enzymes due to pancreatic insufficiency? patient has steatorrhea

A
  • large vol of enzymes needed
  • they are degraded by the gastric acid as require a neutral pH as is in the duodenum naturally
  • enzymes need to be released/active in the proximal SI as this is where fats are absorbed
35
Q

Possible solutions to supplementing pancreatic enz?

A
  • enteric coated capsules. Means they are protected from the acid but their release will be delayed
  • give proton inhibitor to decrease acid and increase pH to stop degradation
36
Q

What is enteric coating?

A

acid resistant coating. Protected in stomach and delayed release in the small intestine

37
Q

Creon =

A

pancreatic enzyme supplement

38
Q

How does creon supplementation work?

A

Enteric coated minimicrospeheres in gelatin capsules

  • the gelatin capsule dissolves in stomach release the 100s of minimicrospheres that are acid resistant
  • the enteric coating of the minimicrospheres dissolves in a pH greater than 5.5 i.e. SI to release enzymes for fat digestion
39
Q

Treatment for ulcerative colitis?

A

5 - ASA

40
Q

Problem with 5-ASA?

A

5-ASA is the drug used to treat IBD BUT is degraded by gastric acid and needs to get to LI and terminal ileum (areas of inflam)

41
Q

How to solve problem of acid degradable 5-ASA?

A
  1. Join 2 5-ASA molecules together with an AZO bond which needs colonic bacteria to BREAK
  2. Enteric coating to resist gastric breakdown
  3. Time dependent release
  4. pH dependent release (neutral/alkaline)
42
Q

What is sulpasalazine?

A

5-ASA linked to sulphapyridine

needs colonic bacteria to cleave to be active

43
Q

What are the limitations of sukpasalazine?

A
  • adverse affects in 20% of people can include hypersensitivity or intolerance due to sulphur
  • only successful in colon disease i.e. can’t give to CHRONS patient
  • higher doses are more effective BUT cause more side effects
44
Q

How can you target delivery of 5-ASA for IBD treatment?

A
  • azo bond cleaved only by bacteria in colon
  • moisture dependent release
  • pH dependent release
  • apply topically

= site specific delivery

45
Q

What is the diagnosis - ibuprofen for 6 weeks > melaena

A

NSAID > gastric ulcers > omeprazole

46
Q

NSAIDs cause .. from …

A

GI bleeding from gastric ulceration

47
Q

How do NSAIDs work????

A
  • arachidonic acid forms COX-1 (NSAID)
  • COX-1 inhibits prostaglandin 2 which is primarily involved in cytoprotection
  • results in decreased mucus secretion, HCO3- secretion and mucosal blood flow
  • the alkaline mucus layer usually protects the gastric mucosa from acid
  • results in injury to epithelium that can’t heal
  • peptic ulcers and GI bleeding
  • melaena
48
Q

What 2 functions do prostaglandins have?

A

Cytoprotection (protects cells)

Inflammatory

49
Q

What is the main mechanism of NSAIDs?

A

Inhibition of COX 1

50
Q

What does COX 1 do usually?

A

Important in producing prostaglandins - inflam AND cytoprotection via stomach coating

51
Q

How can you reduce the risk of GI bleeding from NSAIDs?

A
  • stop NSAIDs; are they needed
  • alternatives (panadol)
  • use lowest dose
  • use a protective drug AS well i.e. proton pump inhibitor/omeprazole
  • COX2 inhibitor
52
Q

Why use COX 2 inhibitor rather than COX 1

A

Cox 2 acts most for inflam while COX 1 is cytoprotective
risk of bleeding is halved
more expensive and ^ risk of myocardial infarction and stroke (work of platelet aggregation)

Digestive (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions