Flashcards in pharm - GI drugs Deck (53)
what stimulates chief cells ? result?
ACh, CCK, gastrin --> release of pepsinogen
prostaglandins in the stomach
are protective! stimulate mucous cell secretion (reduce inflammation)
vs rest of body where they cause inflammation
ECL cell secrete
major stimulatory mechanism for HCl secretion from parietal cells?
paracrine - histamine from ECL cells --> H2 receptor
imbalance between aggressive and defensive stomach mechanisms
peptic ulcer disease
neutralization of the HCl
4 --> aluminum hydroxide, magnesium hydroxide, calcium carbonate, and sodium bicarbonate
sodium bicarbonate/ca carbonate
may increase gassiness and bloating due to CO2 product
antacids w effects on gastric motility
aluminum hydroxide --> DECREASE motility
magnesium hydroxide --> INCREASE motility
tums --> no effect
which antacid INCREASES gastric motility?
mucosal protective drugs
sucralfate (aluminum sucrose sulfate)
aluminum sucrose sulfate
forms a water insoluble viscous layer over ulcer tissue - maintenance therapy
**give on empty stomach!
-few side effects (constipation/dry mouth)
(pepto) does NOT neutralize acid --> binds to ulcer and
1) absorbs bile acids
2) stimulates mucous secretion
3) antibacterial effect on H pylori
**aspirin sensitive people might be sensitive
**turns stool black
what drug forms a viscous water insoluble layer over ulcer; non curative just maintenance
dicyclomine and hycosamine
dicyclomine and hycosamine use?
antimuscarinic agents ----UNPLEASANT, bad side effects, rarely used to treat PUD
H2 receptor antagonists
*used to treat ulcers
mech: structural analogs to histamine --> competitively inhibit histamine binding to H2 receptors
----REDUCE ACID SECRETION
Do H2 receptor antagonists have CNS side effects?
**they are hydrophilic so NO CNS side effects
H2 receptor antagonists have a ____ half life.
why is this not an issue?
short (2-3 hrs)
lack of significant side effects allow high/multiple dosages
which H2 receptor antagonist is the least ideal (most side effects)?
what are its negative effects?
-enhances prolactin and binds androgen receptos leading to gynecomastia, impotence and lactation issues
-inhbits cyt P450s --> prolongs half life of other drugs
proton pump inhibitors - used to treat ulcers
omeprazole, esomeprazole, lansoprezole, pantoprazole
mech: inhibit the H K ATPase of gastric parietal cells with an irreversible covalent bond(kills the pump)
how PPIs get to the ATPase
prodrug as delayed release/enteric coated capsules--> absorbed as prodrug in duodenum --> circulation --> reaches parietal cell and is pumped into the acidic caniculi --> protonated by low pH --> active drug --> inactivates that same atpase
PPIs are most effective when...
how long is the effect?
-->taken 30-60 minbefore eating
when you are hungry the pumps begin pumping
they have half life of 1 hr, but since the ATPases are irreversibly inhibited, effect lasts days until new ones can be made
treatment of choice for zollinger ellison syndrome?
what is more effective for GERD: PPI or H2 antagonists?
do PPIs have CNS effects?
PPIs side effects
*CNS, nausea, diarrhea
*prolonged suppression of acid secretion may increase c dificile colonization in stomach --> risk of pneumonia
*risk of spinal/hip fracture
*inhibits clopidrogel activation
prostaglandin analog that inhibits gastric acid secretion and stimulates mucin secretion (protective just like PGE2)
why is misoprostol not used often?
1) PPIs are more effective and getting cheaper
2) potential abortifacient --> doesnt allow/aborts pregnancies
antimicrobial therapy for peptic ulcers
many ulcers have H pylori infection
Quadruple therapy - PPI + 2 antibiotics (tetracycline and metronidazole) + busmuth-subsalicylate
Concomittant therapy - PPI + 3 antibiotics (clarithromycin, metronadizole/tinidazole, and amoxicillin)