I am pharmacolising this post!
Sunday, October 03, 2010
Okay. I planned to study/cram/revise all of the GI module tonight.
1) Microbiology
2) Pharmacology
3) Pathology (this will take AGES)
4) Physiology
5) Anatomy
Microbio done. Anatomy ongoing.. therefore, considered done.
But as I am trying to revise Pharmacology now.. it is not really going into my brain :(
so i came up with the genius plan of blogging about it!!
I'll try my best to do it from memory first.. then i shall refer to the flashcards/notes!
Basically in the pharmacology vertical module of GI module, we have to learn about drugs that can target GUT MOTILITY and GUT SECRETION.
[1] GUT MOTILITY
- gut movement.. which can cause vomiting, obstruction within bowel (eg constipation) or diarrhoea. therefore! we need - ANTIEMETICS, PURGATIVES and ANTIDIARRHOEAL.
(a) ANTIEMETICS
- there are 6 kinds.
= H1 antagonists eg PROMETHAZINE
-> target the vestibular nuclei, treat vomiting that arose from motion sickness. can cause drowsiness and sedation as side effects, also slight effect at mACh receptors
= mACh antagonists eg HYOSCINE
-> target vestibular nuclei and vomiting centre - principally for prophylaxis and treatment of motion sickness. ADRs include dry mouth and -ve effect on mental alertness
= 5HT3 antagonists eg ONDANSETRON
-> target visceral afferents and CTZ thus useful for treating or preventing postoperative nausea and vomiting which are drug-induced. also treat against nausea caused by toxins eg radiation therapy or cytotoxic drug like cisplatin
= D2 antagonists eg METACLOPRAMIDE
-> target CTZ but also has peripheral action on the GI tract, which increases motility... unwanted effects like fatigue and movement disorders can occur due to blockage of dopamine receptors in CNS, will also cause prolactin release
= Nabilone
-> treat vomiting that is resistant to antiemetics! opioid receptors are involved because effects can be blocked by naloxone - can cause drowsiness, dizziness, mood changes!
= high dose dexamethasone
-> treat vomit that is caused by cytotoxics
- alter GI motility!!! but abusive use can lead to constipation
- there are 4 kinds:
= Bulk Laxatives eg METHYLCELLULOSE
-> form hydrated mass by attracting water, therefore promoting peristalsis, take several days to work though!!
= Osmotic Laxatives eg LACTULOSE
-> poorly absorbed solutes trap water in the lumen, accelerating emptying of bowel by distention and purgation. can cause diarrhoea and cramps :(
= Faecal Softener eg DOCUSATE
-> help water to penetrate feces, making it softer and easier to pass! :p
= Stimulant Laxatives eg SENNA or BISACODYL
-> increase electrolyte and water secretion and hence increase peristalsis (through the myenteric plexus!) hence lead to defecation... ooooh....
(c) ANTIDIARRHOEAL
- there are 2 types!
= Morphine/Codeine
-> need a lower dose for antidiarrhoeal effect than for analgesic effect! :) this decreases stomach emptying and contractions, overall increase in fluid and electrolyte absorption :D so therefore no diarrhoea!
= Loperamide
-> this is the drug of choice for travellers, so you out there, if you are scared of diarrhoea, bring this along! :D it is an opioid but doesnt cross BBB, so theres no CNS systemic effect - ie it selectively targets the GIT, decrease abdominal cramps and passage of feces :)
Man this is taking so long :(
[2] GUT SECRETION
- most importantly, the acid in stomach can cause problems!!
- there are 4 types:
= Antacids
->buffer gastric and esophageal contents but only short term relief :( they dont prevent overproduction of acid! includes salts like Mg, Ca, Al and Na. ADRs: Mg can cause diarrhoea, Ca and Al can cause constipation and CaCO3 can cause belching and fan pi! HAHA
Excessive use can result in metabolic alkalosis
= H2 Receptor Antagonists eg CIMETIDINE, FAMOTIDINE
->inhibits histamine action hohoho - this is good at decreasing basal rate of acid production, so this is good for nocturnal use, so its quite ineffective at daytime. some ADR that i think i will remember... all excreted in breast milk. ew.. ur baby will get a lot of it :O
= Proton Pump Inhibitor eg OMEPRAZOLE, LANSOPRAZOLE
-> AHA! this is the one i had to take when my tummy was hurting due to oversecretion of acid in my tummy as correctly diagnosed by the doctor at student health. this inhibits the H+K+ ATPase pump by binding to it covalently, so that H+ is not secreted from parietal cells. this is a prodrug though, it needs to be activated by acidic environment, so take it 30mins before meal. since it is bound covalently, this means it is irreversible, thus acid secretion can only resume when new pumps are made. hence this is prolonged suppression of acid! over 24 to 48 hours le! ADRs include headache, abdominal pain and nausea.
= Prostaglandins eg PROSTACYCLIN (PGI2)
->binds to the parietal EP3 receptor which is linked to a Gi subunit and this inhibits the adenyly cyclase, decrease cAMP and so decrease acid secretion!! eh easy la! like the GPCR ma!
some extra info: use MISOPROSTOL which is a PGE analogue to prevent gastric mucosal injury that is caused by NSAIDS that inhibits COX1, which decreases PG formation :(
ADRs include abdominal pains lo.. and also 30% ppl have diarrhoea
KAY LA FINI LIAO :(
dont feel like doing pathology now though.... aiyo
Labels: pharmacology, study, uni
2 comments:
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aaah finally something of my language! Though ive moved on from pharmacology into pharmacotheraputics...so i cant be bothered too much about MoA now hehehe. interesting to see u got a PPI before trying out antacid, hhmm....
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theres so so so so so much to remember my brain is dyinggggggggggggg :(
aaah finally something of my language! Though ive moved on from pharmacology into pharmacotheraputics...so i cant be bothered too much about MoA now hehehe. interesting to see u got a PPI before trying out antacid, hhmm....