NSG 531 Advanced Pharmacology Exam 3 Study Guide with Verified Answers
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NSG 531 Advanced Pharmacology Exam 3 Study Guide with Verified Answers
thrombogenesis and selective cox-2 inhibitors - ANS cox-1 found in platelets makes TXA2 which causes vasoconstriction and platelet aggregation
cox-2 found in endothelial cells - makes prostacyclin which causes vasodilation ...
NSG 531 AdvANced PhArmAcoloGy exAm 3
Study Guide with verified ANSwerS
thrombogenesis and selective cox-2 inhibitors - ANS cox-1 found in platelets makes TXA2
which causes vasoconstriction and platelet aggregation
cox-2 found in endothelial cells - makes prostacyclin which causes vasodilation and inhibits
platelet aggregation
people that were taking cox-2 were having thrombotic effects and having heart attacks
cox 1 platelets cox2 immune cells
cox 1 acts on arachidonic acid and it makes TXA2 which is stronger
cox-2 inhibitrs platelelt aggregation
if you selectively inhibit cox-2 you are tipping the balance in favor of TXA 2 vasoconstriction
and platelelt aggregation
cytokine inhibitors - ANS humira, remicaid
antigen presenting cell presents the antigen to the T cell, activates macrophages, releases
inflammatory cytokines such as tumor necrosis factor alpha
those durgs are TNF alpha monochromal antibodies - bind to the TNF alpha released by the
antibodies and prevent it from producing inflammatory effects
anakirna blocks action of IL1 antagonist receptor for cytokines
the problem with this is that you could inhibit your immune system by blocking those binding
sites
leukotriene inhibitors - ANS drugs that bind to the receptor for leukotriene and lock those sites
up - or we can give a drug that blocks the LOX enzyme itself
flag inhibitors - inhibits the formation of leukotriene
statins as anti-inflammatory drugs - ANS inhibit the cholesterol synthesis pathway
,HMG CoA is inhibited by the statins blocking the pathwya
by blocking that early in the pathway you also inhibit isoprenoids which are inflammatory
byproducts
pediatric issues of GI absorption - ANS gastric pH at birth is 6-8 gradually declines until adult
values reached by 2-3 years of age
evidence that active and passive transport do not fully develop until four months
not known when efflux pumps or intestinal P450 enzymes develop
slowed gastric emptying
evidence that switch from breast milk to formula induces hepatic P450 enzymes
what does a high gastric pH at birth effect? - ANS base drugs will be better absorbed and acidic
drugs will not - kids are the opposite of adults
describe issues of GI transport in pediatrics - ANS because of the transporter proteins not being
developed in infants a drug will struggle if it is dependent on transportation across the gut into
the circulation via transporter proteins
describe issues of efflux pumps in GI for pediatrics - ANS pumps develop at different ages -
depending on whether that drug is able to bind to the efflux pump and back into the intestine will
effect whether or not it will end up in circulation
pediatric issues of intramuscular absorption - ANS decreased skeletal muscle blood flow and
inefficient movement may decrease absorption
may be offset by increased capillary density
skeletal muscle mass is still relatively low and they can't make the same efficient movements as
adults - this decreases absorption
pediatric issues of percutaneous absorption - ANS increased percutaneous absorption d/t thin
stratum corneum and increased skin hydration
increased percutaneous absorption also r/t higher body surface area
, describe issues of ratio of body surface area to weight between infants to adults - ANS covering
a similar percentage of the newborn's body with a skin absorbable substance will lead to a larger
dose per unit of body weight compared to an adult
ratio of body surface area to weight is 3x higher in infant - example if you cover a similar
percentage of a newborn's body when compared to adults with an absorbable substance you
could be giving a higher dose 2 fold
pediatric issues of drug distribution - ANS increased TBW as percent weight and increased ECF
increased weight-adjusted Vd and relatively increased loading
decreased plasma protein concentration - contributes to increased Vd
Increased bilirubin due to increased RBC turnover and immature liver
why does decreased plasma protein concentration lead to increased volume of distribution in
peds - ANS because less drug is binding to plasma proteins because the children are relatively
hypoalbuminemic compared to adults
why do peds have increased bilirubin - ANS because the liver is not mature enough they can't
always convert RBC to conjugated bilirubin that can be eliminated
they tend to have unconjugated non water soluble bilirubin that hangs around longer - it can then
bind to plasma proteins so bilirubin will then comptete with drugs for plasma protein binding
sites
if the bilirubin has a higher affinity for the plasma protein you see jaundice
if the drug has higher affinity for the plasma protein then you have higher plasma concentrations
of the drug
pediatric issues of biotransformation - ANS reduced phase I and phase II reactions
reduced glucuronidation - cause of chloramphenicol-induced gray baby syndrome
with phase II we get concerned about being able to conjugate glucoronic acid to a drug - major
phase II reaction
pediatric issues of elimination - ANS reduced GFR in neonates and premmies
tubular secretion is 20-30% of adult values and reaches adult levels at 30-40 weeks
, reduced tubular reabsorption
don't eliminate as well as adults due to lower kidney function
if you have reduced GFR you are going to filter less and therefore reabsorb less
clinical implications of pediatric issues - ANS clearance determines maintenance doses - lower
maintenance doses than adults
hepatic and renal function mature with age need to increase daily doses to prevent subtherapeutic
concentrations
regular clinical assessment and TDM
if a child is going to be on a drug for a very long time over time that dose is going to have to be
titrated up as they mature due to growth and development
Geriatric issues of absorption - ANS increased gastric pH (promotes base and inhibits acid
absorption)
slower rate of absortpion
variable changes in bioavailability:
decreased gut active transport - transporters slow down with age
decreased first pass effect - liver function slows with age - they don't absorb as much but what
they do absorb is less susceptible to first pass which will effect dose
decreased gut P450
Geriatric issues of distribution - ANS TBW and lean body mass decrease - reduced volume of
distribution
reduced albumin concentration - increase the distribution of the drug because less will be bound
to albumin
reduced loading doses
geriatric issues of biotransformation - ANS liver mass and blood flow decrease with aging
phase I declines
little change in phase II
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