Gi- Upper Pharm

Front 1

PPI- Omeprazole, esomeprazole

Back 1

MOA: blocks end point of acid secretion, enteric coated to get thru stomach, released in basic SI and act on parietal stomach cells
ASE: HA and B12 def
associated w/ hip fractures hosp aquired pneumonin
changes ph may not kill some org.
Also blocks Ca absorption
admin: give 1 hr prior to food

Front 2

omprezole drug interacitons:

Back 2

inhib diazepam via cyp2c19
inhib clopidogrel via:
cyp2c19 or incre gastic ph, reduce absorpt

Front 3

which ppi do you use if pt is a bleeding risk and is taking clopridogrel?

no risk?

Back 3

esomeprazole or pantoprazole (not omeprazole)

if not risk, give H2 antagonist to avoid interaciton

Front 4

H2 antagonist: cimetidine, RANITIDINE, famotidine

how are they excreted?

Back 4

only blocks histamine stim of parietal cells. other pathways (gastrin and ACh)
can develop tolerance
renal excretion: dose based on creatinine

Front 5

cimetidine drug interactions:

Back 5

cyp450, incr warfain and amiodarone

Front 6

which drug is the safest H2 inhib in terms of DI?

Back 6

famotidine

Front 7

sodium bicar

Back 7

may drastially affect acid base balance
risk for caridac and renal pts
co2 can cause bloat and flatulence

Front 8

calcium car

Back 8

may induce acid rebond
co2 bloat flatulence

Front 9

magnesium/Al hydroxide

Back 9

mg rapid, Al slow gives sustained neutralizing capacity, poorly absorberd, sustained effect
mg-diarrhea, al constipation

Front 10

antacids drug interactions

Back 10

dec absorption of weakly acidic drugs
VINDS TETRACYCLINE AND FLUORO
avoid by taking 2 hrs before or after

Front 11

misopstol:

Back 11

cytoprotective
MOA: prostaglandin analogue blocks acid secretion and help lay down bicarb layer
bind to rectpor on pairetal cells seimulate Gi, dec cAMP dec acid secretion
ASE: diarrhea and ab pain: not compliant

Front 12

should you ever give misoprostol to preggers?

Back 12

HELL NO

Front 13

sulcrafate

Back 13

MOA: reacs with HCL to make paste substance varier that adheres to ulcers (active ulcer)
ASE: constipation aluminum absortpion

Front 14

sulcrafate drug interactions:

Back 14

aluminum can bind drugs and reduce bioavailability

Front 15

NSAIDS:

Back 15

MOA 1: cross gastric mucosas (not ionized) direct effect on cells
MOA 2: main way; cyclooxy inhib Cox1

Front 16

what is the standard of care for h pylori and acid?

Back 16

2 abx and ppi
tripple thearpy, more compliant than others

Front 17

5 HT3 recpetor antagonists

Back 17

ondansetron, granisetron, dolasetron (-setron)
MOA: block 5HT3 recep found centrally in CTZ and vagal visceral afferents
for: chemo and post op naseua

Front 18

ASE of 5HT3 block

Back 18

H, malaise/fatigue, constipation
QT prolongation (higher doess)

Front 19

drug Inter of 5ht3 blockers:

Back 19

icreaese apomorphine (don't use)

Front 20

dopamine recetor antagomists

Back 20

metoclopramide, trimethobenzamamide

Front 21

metoclopramide

Back 21

MOA: dop recp antag that alos blosck serotinin recp in CTZ
increase LES tone, aids gastric empty, accelerates transit through sb
For: gastric motility N/V (diabetics)

Front 22

ASE of metoclopramide:

Back 22

Cns effects that are dose related
chroinc use: EPs-->tardive dyskinesia (involuntary repetitive movemetns)

Front 23

drug inter of metoclopramide:

Back 23

incre levels of cyclosporine, sertaline venlafaxine

Front 24

phenothiazines

Back 24

useful for simple n/v
sedation due to dopa blck
gangrene from IV
give deep IM, or find a big vein

Front 25

cyclizine hydroxzine diphenhydramine

Back 25

MOA: act on vestibular afferent w/in rainstem
For : H1 for motion sickness tleated to inner ear
ASE: cosntipation dry mouth drowsi urinary retein dry eyes
Meclizine does not cross BBB

Front 26

antivcholinergics:

Back 26

scopalamine
MOA: bolck neural path from vesitbular nuclie in ear to bain and from teicular form to vom center
for : motin sick preven and tx and post op n/v
not demo

Front 27

aprepitant (sub p recep antag)
MOA
combo?

Back 27

MOA: antagonize NK1 recep for sub p- acute and delayed effect; good for chemo
combo w/5ht3 recp antag and corticosteroids
ASE: fatigu dizzi diarrhea
DI: cypsa4 may inhib chemo drugs

Front 28

5ASA

Back 28

MOA: in hib IL1 and TNF alpha, scavneg free radicals inbi inflam path
formulated with azole link to prevent absortpitno unitl colon (may protect v cancer)
PROVEN FOR UC
differ formuation to release in different parts of bowel
pentasa:everywhere
olsalazin: colon
ph tablet: ileum for CD

Front 29

DI of 5ASA

Back 29

anything that changes ph changes where absorbed

Front 30

corticosteroids

Back 30

mainstay of therapy for IBD used in all pts
MOA: decre inflam by inhib cytokines and pmn migra
ASE: all, HPA suppr, infection, insomia htn
longer taper with IBD
IV steroids for acute flare

Front 31

budesonide

Back 31

oral steriod; released in terminal ileum, less ASE a lot not absorbed

Front 32

thiopurines

Back 32

MOA: in hib DNA RNA and protin synthese supres t cells
monitor 6TG can cause bone marrow suppressinon
monitor TMPT activity
ASE: inc risk of infection, hepatotoxi, pancreatitis

Front 33

di of thiopurines

Back 33

allopurinaol inhibit XO: more bone marrow suppression

Front 34

TNF alpha inhib

Back 34

MOA: block Tnf alpha, proinflamcytokine block IL1 and 6
infliximab:most likely to have Ab formation
ASE: nause infusion sit rxn, flu like symp. Lympohona, TB reactive, Hep B

Front 35

di for tnfa inhib

Back 35

anakinra and abatacept fro RA or MS cum immuno suppres, live vacine

do chest xr before treat, monitor EF

Front 36

natlizumab

Back 36

humanized monoclonal ab
MOA: prevent ranmiario of leuko across endo blocks inflam process (a4 integrin recep antag)

Front 37

ASE for natilizumab

Back 37

nasuea infusion sit rxn PML (brain rot)
TOUCH program

Front 38

Methotrexate

Back 38

primarily used for CD
MOA: blocks dihydrofolate reductase; interfesr with IL-1
ASE: ha vom htn hyperuicemia,leucopenia reanl failure liver fail
DI: anthing that interferes iwt folat emetabolism bactim
must give folate supplements

Front 39

cyclosporine
moa
ase
di

Back 39

MOA: in hib lymphocyte acivatio an dingib prod of IL2
ASE: htn tremor nephrotox
DI:always have drug interaction

Front 40

metronidazole= flagyl

Back 40

used for moderate c diff
MOA: interacts w/ bac DNA, inhib prot synthises
ASE: metalic taste
DI: warfarin alcohol use
cheapre than oral vanco

Front 41

oral vanco

Back 41

used for severe C diff
MOA: inhib cell wall synthesi
DI: contra for corn allergy
consider: large molecul, little absorption
no ASE, cost is expensive

Front 42

fidaxomicin

Back 42

used for c diff refractory to oral vanco
MOA: inhib RNA synthesis selec for C idff anaerob g pos

Front 43

anion binding resins colestipol cholestryamine

Back 43

MOA bind toxin and other things including vanco

Front 44

loperamide:

Back 44

MOA: inhib peristalisis dec diarrhea
ASE: cosntip
cannot exceed cerain dose

Front 45

diphenosylate/ atropine

Back 45

moa in hib GI motility and proulsion
ASE: andti cholingergic SE, on purpose

Front 46

aoili and pectin

Back 46

binda toxin decres fluid

Front 47

bismuth subsalicylate

what DI?

Back 47

MOA: anti secretory, anti microbial; anti infalmamaroty (h pylori)
ASE: dark stoolds
DI: tetracyclines
contra w/flu chicken pox gi bleed

Front 48

when do you want to avoid lomitl and paragoric?

Back 48

if pt has dependence issues

Front 49

osmotic laxitives

Back 49

saline lax,
MOA: mg and sodium cause osmotically mediate water retneion sim peristlasis lactulose and sorbitol are hydrolyzed in colon and draw in water
can cause cramp dehydration

Front 50

stool wetting lax

Back 50

MOA: lower surface tension and allsow stool to mix with aueous and fatty subs softens sotll
mineral oil can impari asorptio of fat solubel vitamins

Front 51

stim lax

Back 51

MOA: direct effect on enterocytes and GI SM, forece peristalsi
fluid def electolyt issues ab crapm durg abuse

Front 52

chloride channel activator lubiprostone

Back 52

MOA: acitbates cl channesl bings water into stoll imporves consistnecy icrease fequency