GI Flashcards
What are the four sets of GI drugs?
- Acidity, ulcers GERD
- Bowel motility, water flux
- Reduce prevent nausea
- IBD
What stomach cells secret HCl?
parietal
What increases acidity production in the stomach 3 Receptors?
ACh receptors
gastrin receptors
histamine receptors
What happens to HCO3 from its dissociation from H+ in the stomach epithelial?
exported into blood in exchange for Cl-
What nerve begins cephalic response? acts on what cells?
vagus- M receptors of parietal cell and ECL cells (Fundus) which release histamine in a long term manner
Where is G cell located? What cells does gastrin work on?
antrum, Parietal and ECL cells
What stims Gastrin release?
Increase pH and stretch
How does PGE2 and PGI2 promote protection from gastric acidity?
activate Gi and decrease cAMP to decrease acid
also same receptor in epithelial cell causes increased mucus and bicarb secretion
What pumps protons out of the parietal cell?
H/K ATPase. K is recycled with Cl antiporter
Does a PPI stop working after its 2 hour activity window (acid labile)? What activates them?
No because of irreversible binding
Stomach acid activates
Where does PPI reach the cell?
Through blood. It is acid labile and therefore must be protected as it passes through stomach.
What is Zollinger Ellison Syndrome?
secretion of Gastrin from tumors of pancreas and intestine.
Where are PPIs cleared? CYP influences?
Liver- increase serum warfarin, decrease activation of clopidogrel
What is useful to block for nocturnal acid secretion?
H2 receptors blockers (24 hour effectiveness 70%)
How are H2 blockers secreted?
Renal- organic cation system
How long does it take tolerance to develop with H2 blockers?
3 days–> increased Gastrin
Does sucralfate stick better to gastric or duodenal ulcers? how is it activated?
duodenal, acid activated
Is Mg or Al fast acting as an antacids? What is added to reduce case?
- Mg (stimulates gastric emptying and motility while Al slows)
- Surfactant simethicone
Where does muscaranic antagonists work?
M1 intramural ganglia!!!!!!
What determines if the H. pylori infection will be pathogenic?
Vacuolating endotoxin A
What are the 3 types of therapy for H Pylori?
triple-PPI+clarithromycin+metronidazole/amoxi/tetra
Quadruple- PPI+metro+ bismuth+ tetra
Quadruple- H2 blocker+bismuth+metro+tetra
mechanical stim of Enterochromaffin cells release what?
serotonin–> primary afferent–>reflex contracts orally and relax anally
Does dopamine generally decrease or increase ACh release?
decreasses
What cells secrete motilin?
enterochromaffic cells and M cells in upper small bowel
What are 60% of constipated patients actually complaining about? How to treat?
stool hardness (normal transit times) Increase fiber
T-F–laxatives are really cathartics at lower dosages but act as laxatives when the dose is increased
False- opposite is true- cathartic means to purge
What type of drugs are best for constipation with associated opioid use?
osmotic laxatives
Do stool wetting agents increase frequency of defecation?
No– just soften the stool
Does castor oil actually stimulate smooth muscle? Is the castor bean toxic?
Yes, yes due to soluble Ricin fraction
How is glycerin administered?
rectal suppository- increases water retention and stimulates peristalsis
What is one bad thing about fiber laxatives?
absorb other drugs
Can bulk forming agents be used as a laxative and as antidiarrheal agents?
Yes- can be a sponge for antidiarrheal
[colloids or polymères polycarbophil derivatives]
Is loperamide more potent than morphine”?
yes 40x
How do you administer somatostatin or octreotide?
parenteral–> combats secretorial diarrhea of tumors, post-surgical gastric dumping
What happens to salicylate found in pep to bismol? leads to what?
is released in the stomach and is absorbed systemically leading to increased prostanoids and decreased motility
T-F– emesis has many inputs? What is it controlled by? What is special about this area?
- True- CNS, memory, environment, sensors of toxins, gut sensation and movement sensation
- Chemoreceptor Trigger Zone in the area postrema at bottom of 4th ventricle & NTS of Vagus nerve
- Crosses the BBB and senses blood and CSF
Does serotonin promote motility? Is it widely used for chemotherapy induced emesis and nausea? Where are the serotonin receptors located for this ability?
- Yes
- Most widely Used
- peripheral small intestine and CTZ and NTS
Most serotonin antagonists are secreted by the liver except for which one?
Palonosetron which is secreted by kidney
Dopamine receptor antagonists block D2 and H1 receptors. Blocking H1 gives what benefit? H1 receptors are found primarily where for anti-emesis effects?
- anti- motion sickness
2. brainstem and vestibular apparatus
How is scopolamine usually administered? What does the drug particular act on for its anti motion sickness effects? Is it effective for chemotherapy induced nausea?
- Transdermal patch
- vestibular apparatus
- No, minimal CTZ effects
Why is charcoal used more than emetic drugs for poisoning/
Danger of aspirating
Does syrup of ipecac and apomorphine acton on the CTZ?
Yes
Is ulcerative colitis or crohns confluent lesions? What are the 3 aims of therapy for these conditions?
- ulcerative colitis (and is only in anal verge/colon)
2. a. treat acute symptoms b. maintain remissions c. treat super infections.
Does TH1 contribute for to Chrons or UC?
Crohn’s……UC is TH2
What activates sulfasalazine, olsaalazine and balsaalazide? what is the outcome?
cleaved by colonic bacterial enzymes at diazo bond to yield mesalamine
In Crohn’s is it necessary to select dosage forms that target part of bowel involved?
Yes
Where are sulfasalazine and olsalazine activated? Where is pH sensitive mesalamine capsules released? what about delayed capsules?
In the colon
ileum
jejunum
When is cyclosporine used for inflammatory BD?
patients failing glucocorticoid therapy [parenteral]
Is IBS and IBD the same? What does Tx focus on?
No, IBS is alternating constipation and diarrhea with bloating. Tx focuses on motility of the gut
