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30 Cards in this Set

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DOC to cause bulimia
ipecac
moa~ Stimulates the CTZ (chemoreceptor trigger zone & causes local irritation of the stomach & upper duodenum
"If I eat a cac ("penis") I would want to throw up!!!!" (ipe-cac
Prophylaxis for motion sickness
Scopolamine
moa~ Blocks muscarinic receptors in the vestibular nuclei & reticular formation (anticholinergic)
antiemetic (for chemo)
1. dexamethasone-very powerful
2. ondansetron-moa: -block 5-HT3 rec at vagal afferent nerve endings and/or CTZ
Say “X” (deXa) to chemo-induced V.
N/V from radiation (advanced CA
dronabinol
“Radiation is a “drone.” “
~ Prophylaxis for motion sickness
~ Prophylaxis for N/V during pregnancy
dimenhydrinate &
diphenhydramine (Benadryl) &
meclizine

moa-Antihistamine/anticholinergic

Hint:
“2 men (dimen) hydrate (hydrinate) themselves to prevent motion sickness and vomiting in their pregnant wives.”)

-The “2 men” (dimen) are named “mec” and “liz”.”
~ Tx for motion sickness
~ Tx associated N/V with diarrhea
promethazine
moa-Antihistamine/anticholinergic
“PRO at Tx motion sickness.”
1. n/v, anti-emetic
2. Clears stomach prior to GI endoscopy or surgery
3. Diabetic gastroparesis
Metoclopramide
moa~
1.Serotonin/dopamine receptor blocker; Blocks 5-HT3 recptors (vagal afferent fibers & CTZ) and D2-dopamine receptors (CTZ)

2 & 3.~ Enhance release of ACh by stimulating prejunctional 5-HT4 receptors on cholinergic fibers

NOTE: blocks 5HT3 (Serotonin)-->anti-emetic

stim 5HT4 (Ach)-->clears stomach
~ Prophylaxis for N/V during pregnancy
ondansetron
moa~ Block 5-HT3 receptors at vagal afferent nerve endings and/or the CTZ
~ GERD
1. cisapride
2. tegaserod
pharm: ~ Incr LES pressure
~ Tx of irritable bowel syndrome primarily associated w/ constipation
tegaserod
moa-Enhance release of ACh by stimulating prejunctional 5-HT4 receptors on cholinergic fibers

~ Tegaserod also stimulates the release of calcitonin gene-related peptide (CGRP) from sensory neurons in the GI tract
Tx of constipation
-maintain a soft stool in patients who should avoid straining during defecation (patients w/ hemorrhoids,
1. methylcellulose
2. psyllium
3. Ca polycarbophil
4. lactulose
5. docusate sodium

1&2.moa****"Bulk laxatives"****~ Attract water to form a HYDROGEL w/ feces in the large bowel--hydration incr the bulk by 30x
~ Psyllium also binds to bile acids (more are excreted in feces…lowers Tc & LDL)???
4. lactulose moa-Bacteria in bowel degrade lactulose into lactic, acetic & organic acids which exert an osmotic effect drawing H2O
pharm-bowel distention
~ Acidification of the colonic contents also causes NH3 in blood to be trapped & excreted as NH4+
5. =soap;
~ An anionic surfactant: the detergent action lowers surface tension of feces to allow penetration of water
add to Fe supplements
docusate sodium
GI exam
Evacuate the bowel prior to radiological or sigmoidoscopic exam
1.Bisacodyl 2.magnesium (hydroxide, citrate & sulfate)
3.polyethyleneglycol

1. moa~ (“bis brings water into the colon (codyl) only.”)
Irritant action increases the accumulation of water & electrolytes in lumen of colon (ONLY)
~ Keeton: don’t use much!! "Bad"

2&3.~ Hypertonic solutions that create osmotic forces which draw water into large bowel

pharm~ Bowel distention activates stretch receptors, which increases peristalsis

s/e=* Laxative
dependence!!!
irritable bowel syndrome (IBS)
1. bulk laxatives:
methylcellulose
psyllium
Ca polycarbophil
lactulose
docusate sodium

Bulk laxatives MOA-Expands the large bowel via * & thus prevents the alternating segmental contractions of vsm--antegrade peristalsis is restored
*Attract water to form a HYDROGEL w/ feces in the large bowel--hydration incr the bulk by 30x
2. dicyclomine (musc rec -), moa-prevent bowel spasm
3. tegaserod (prokinetic)
IBD (UC and CD)
1. methylprednisone-
*moa-corticosteroid, inhibits syn of PGs and LTs & locally alters immune fxn

2,3,4 are NSAIDS:

Keeton: "5-ASA (5-aminosalicylic acid) is used as po therapy to tx UC & CD (bc inhibits PGs & LTs (5-ASA inhibits COX 1,2 & lipooxygenase, which are precursors for PG and LT, respectively)) - I expect you to know that!"

2. sulfaSALazine=DOC, conjugate of SULFApyridine and 5-aminoSALIcylic acid (5-ASA)

3. meSALamine-capsule slowly releases 5-ASA as move thru bowel

4. oSALazine: two 5-ASA mcs joined by azo bond (conjugate) that is cleaved by bact enzymes in lg bowel
diarrhea (non-bacterial)
*loperamide (Imodium)=DOC
-diphenoxlate

moa-opiates!
-Slow colonic transit rate by direct/indirect inhibition of GI motility
bacterial diarrhea
1. kaopectate
moa**** Absorbent Powder ****
~ A hydrated aluminum silicate CLAY ("kao") + a complex carbohydrate PECTIN ("pectate")
~ Large SA of the clay (which has a negative charge) absorbs bacterial toxins & the pectin becomes hydrated to form a viscous colloid solution, which helps consolidate stool

2. Bismuth subsalicylate
(Pepto-Bismol)
moa-**** Coating Agent ****
~ Bismuth is not absorbed, but 90% of the salicylate is absorbed
Anti-bact: * Binds to -SH groups of microbial proteins to destroy their 3° structure

Anti-ulcer:
Incr PG synthesis & alkali secretion
* Anti-proteolytic action counteracts breakdown of mucus coat by pepsin & H.pylori protease (preserves mucus coat)

S/E: salicylate toxicity
kaopectate
moa**** Absorbent Powder ****
~ A hydrated aluminum silicate CLAY ("kao") + a complex carbohydrate PECTIN ("pectate")
~ Large SA of the clay (which has a negative charge) absorbs bacterial toxins & the pectin becomes hydrated to form a viscous colloid solution, which helps consolidate stool
Bismuth subsalicylate
(Pepto-Bismol)
moa-**** Coating Agent ****
~ Bismuth is not absorbed, but 90% of the salicylate is absorbed
Anti-bact: * Binds to -SH groups of microbial proteins to destroy their 3° structure

Anti-ulcer:
Incr PG synthesis & alkali secretion
* Anti-proteolytic action counteracts breakdown of mucus coat by pepsin & H.pylori protease (preserves mucus coat)

S/E: salicylate toxicity
octreotide
Tx:
-reduce D d/t metastatic carcinoid syndrome & VIPomas
-stop bleeding d/t esoph varices

moa-SMS +
pharm-constricts splanchnic arterioles to DEC splanchnic BF & thus portal venous press
Donna: "I want a Treo, STAT!!!" (octreotide, somatostatin agonist)
PUD
*Abx triple therapy (2 Abx + PPI)

1. Clarithromycin
2. Amoxicillin
3. OmePRAZOLE (PPI)
PUD
Stress ulcers
Heartburn
GERD
Al hydroxide
S/E: constipation

Mg hyroxide
S/E: diarrhea
Al/Mg hydroxide

**** Antacids **** (makes sense that antacids are hydroxides b/c hydroxides neutralize gastric acids

-temporarily raises pH of gastric contents to 3-4
~ Zollinger-Ellison syndrome (drug tolerance & 25%-50% failure rate)
~ PUD
~ Stress ulcers
~ Heartburn
~ GERD
"Every girl wants TO DINE w.a guy who drives an H2!"
*H2 Rec (-)
1. cimeTIDINE
2. raniTIDINE
3. famoTIDINE

s/e: inhibit CYP450-->
*inc half-life of Rx like warfarin
*gynecomastia (b/c dec estrogen metabolism)
*Pregnancy Category B
~ Zollinger-Ellison syndrome (no drug tolerance)
~ PUD
~ GERD
*PPI
*Inhibits gastric H+-K+ ATPase (proton pump) to block acid secretion

1. esomePRAZOLE
2. lansoPRAZOLE

pharm-inc gastric pH to 4-5
-partially - abs of Vit B12
~ NSAID induced gastropathy
misoprostol
(stable analog of PGE1)
"Me so prostaglandin" (misoprostol, PG agonist)

*** NSAID induced gastrophay has Nothing to do w/ H. pylori--so DONT TX w/ antibiotics

moa-**** PGE1 Agonist ****
~ Stimulates PGE1 receptors on gastric parietal cells to inhibit acid secretion
~ PUD
~ Stress ulcers in ventilated pts (bc elevated gastric pH may incr risk of nosocomial pnia in ventilated pts since low pH has antibiotic action--sucralfate prevents ulcers w/o changing gastric pH)
~ NSAID induced gastropathy ~ GERD
SucrALfate (AL=AL OH; sucralfate=sucrose sulfate)
“S(tress) UCRAL (ulcers)”
moa-**** Coating Agent **** (protective barrier)
pharm-Water insoluble complex of AlOH & sucrose sulfate which polymerizes (when pH <4) to form sticky viscous gel which forms a protective layer on the ulcer (coats ulcer)
~ The gel binds tightly to ulcerated gastric mucosa, & gel refluxed into the lower
esophagus aids in the tx of GERD
~ Does NOT neutralize stomach acid or inhibit acid secretion
-dissolving gallstones (but you do need a functioning GB)
~ Primary biliary cirrhosis
Ursodiol
"Hey gallstones, ur so die!" (dead)--ursodiol
DOC for dissolving gallstone

~ Increases the ratio of (bile acids & phospholipids) : cholesterol by:
* Decreasing cholesterol synthesis (inhibits HMG CoA reductase)
* Decreasing the GI absorption of cholesterol
* Decreasing the biliary secretion of cholesterol
~ Hyperlipoproteinemia
Psyllium
hyperlipoproteinemia
Psyllium
(works same as resins did!!)
~ Psyllium binds bile acids-->Fecal excretion of bile acids
~ This loss of bile acids decreases the intrahepatic concentration of the "sterol" pool leading to upregulation of hepatic LDL receptors via the "sterolstat"
DOC for IBD (CD and UC)
DOC=sulfasalazine

*conjugate of SULFApyridine and 5-aminoSALIcylic acid (5-ASA)