Flashcards in Exam 1- Lectures 3 & 4 Deck (38):
#1 cause of monogenic hypercholesterolemia
familial hypercholesterolemia (FH)
FH class 1
no LDL receptors made
treatment for FH
HMG-CoA reductase inhibitors (statins)
what class can you not treat with HMG-CoA reductase inhibitors (statins) and why?
class 1- bc it requires at least some working receptors.
what kind of enzyme is NAT2?
phase II enzyme
all NAT2 mutations are
what is the function of NAT2?
detoxification/inactivation of xenobiotics by acetylation
slow acetylations due to NAT2 mutation increase risk of what cancers?
lung, liver, colon, bladder, non-hodgkin's lymphoma
decreases therapeutic effects
drug induced anemia (G6PD enzyme)
colorectal cancer (K-ras & EGFR)
what drugs can cause drug induced anemia due to GDPD
primaquine, salicylates, sulfonamides, nitrofurans, vitamin K derivatives
causes tumor proliferation if activated
what mutation can occur in tumor cells that makes it not respond to the receptor and be always activated ?
a patient would not respond to anti-EGFR therapy if
the tumor has a k-ras mutation
what the body does to the drug
route of dose
first pass metabolism
active transport systems
chemical structure changes in drug
phase I/phase II
methods in identifying drug response phenotype
biomarkers- efficacy & toxicity
major pharmacogenomic considerations
intestinal wall/drug uptake
liver, first pass metabolism
decreased first-pass metabolism often leads to
increased drug bioavailability
mainly binding of basic drugs
ORM2- most important; major source of variability in the binding of basic drugs
causes reduced levels of P-gp & higher plasma  of drugs transported through P-gp
P-gp is a biomarker for
drug resistance & prognosis in cancer patients
P-gp is a target for
novel anticancer agents
multiple drug resistance protein (MRP) transport what?
organic acid transporter (OAT) transports
Organic anion transporting polypeptide (OATP) transports
organic cation transporter (OCT) transports
efflux of cations