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104 Cards in this Set

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pharmacodynamics
the effects of a drug on the body, relates the drug concentration to its effect
pharmacokinetics
relationship bet. drug dose and tissue concentration, involve ADME processes, how the drug get into tissue
agonist
a substance which interacts at a receptor to elicit a response
antagonist
a substance which blocks the response of an agonist at a receptor
receptor locations
cell memb, cell cytoplasm, nuclear envelope
association constant
kA, the affinity of drug binding, kA= kon/koff
dissociation constant
kD, the concentration at which 50% of the receptors are occupied, kD=1/kA=koff/kon
clearance
the removal of a drug in units of volume/time
intensity of effect
relate to drug concentration at receptor sites
duration of action
r/t how long drug concentration at receptor site remains high enough to provide response
mathematical model
encompassing known factors about drug, hypothesized first, them proven by real-life observation
one-compartment model
assumes a single compartment which is in equilibrium which accounts for drug in plasma and various tissues
two-compartment model
seen when drug moves into tissues and is handled at different rates than central plasma compartment
kCp
kCp=dCp/dt
Cp
Cp=C0*e-kt
logCp
logCp=logC0-kt/2.303
Vd
volume of distribution
Vd=D0/C0
elimination half life
t1/2=0.693/k
(0.693=ln2)
zero-order kinetics
rate is independent of the concentration
bioavailability
% of a drug or drug product that enters the general systemic circulation
includes not only amount entering body but also rate of entry
fructions of admi. drug that gains access to the syst. circulation in a chemically unchanged form
specific receptor
act at receptor site inside on the ribosomes to change the way proteins are synthesized
ex. Neuroleptics, Aminoglycoside antibiotics
semispecific
anesthetics
heavy metals
nonspecific
mannitol
acidifying drugs
affinity
strength to bind at site
intrinsic activity
response that elicited by the binding
Atropine
blocks muscarinic Ach receptors (on smooth muscle and glands)
nicotinic receptors
on skeletal muscle
ionophore
ion channels
receptor site coupled with proteins
exclude/include only certain ions
metabophore
causes metabolic process
ex. Adenylate cyclase & GTP
bioavailability
F=AUC(oral)/AUC(IV)
total body clearence
Cltot=kVd
Cltot=D/AUC(IV)
Q
Q=amount of drug supplied per unit time
Q=kVd*Cpss
Q=Cltot*Cpss
loding dose
L=Vd*Cpss
average Cpss
average Cpss=(Dm/Tm)/Cl
Dm=maintenance dose
Tm=maintenance dose interval
Cl=kVd
ideal doseing regimen
maintenance dose
Dm=(Cptox-Cpther)Vd
ideal dose regimen
maintenance dose interval
Tm=(ln Cptox- ln Cpther)/k
=(2.3/k)log (Cptox/Cpther)
=3.32t1/2 log (Cptox/Cpther)
high extraction ratio
ClH controled by flood flow rate only
strong first-pass effect
plasma protein binding may facilitate clearance
extraction ratio=1
Cv=0
when the entire drug is removed during one pass through the organ
if hepatic blood flow increased
ER hep is decreased since the transit time of the drug through the liver is shortened, and hepatic uptake is reduced
low extraction ratio
does not depend on hepatic perfusion, but rather dep. on plasma protein binding and intrinsic clearance
renal clearance
rate of renal excretion=rate of filtration + rate of secretion - rate of reabsorption
ClR
ClR=(excreted amount/time interval)/plasma concentration
biliary excretion
ClB=(D concentration in bile/ D concent. in plasma)*bile flow
normal bile flow
0.5-0.8ml/min.
clearance
is additive
Cltot=ClH + ClR + ....
extraction ratio
E=(Ca-Cv)/Ca
Ca=D concent. in arterial inflow
Cv=D concent. in venous outflow
E=0-1
therapeutic equivalence
comparable clinical effectiveness and safety bet. similar drugs
zero-order kinetics
rate is independent of the concent.
Cl tissue
Cl tissue= Q tissue*E
Q tissue= tissue blood flow
first pass effect
FH=1-E
FH= the bioavailability fraction due to first pass
E=extraction ratio
bioequivalence
comparable bioavailability bet. drugs
enantiomers
are pairs of molecules existing in forms that are mirror images of each other but that cannot be superimposed
Henderson-Hasselbach equation
pH=pKa+log[protonated]/[unprotonated]
drug absorption
depend on route, MW (size), solubility, and availability of carrier molecules
tissue permeability
GI mucose, skin, cornea, lung, urinary bladder
barrier: occluding zonulae
permeability: complete blockage of intercellular spaces; drugs must permeate cell memb.
CSF/plasma equilibrium
more lipid-soluble drugs ex. thiopental, equilibrate more readily bet. CSF and plasma
CSF to brain
no barrier, very easy passage
CSF barriers
Chorold plexus cells to CSF
B: occluding zonulae
P: difficult passage
BBB
B: occluding zonulae
P: drugs permeate memb.
Glomeruli, excretory and secretory organs
B: Fenestrae
P: free passage of MW < 45,000
placenta
B: limited by blood flow
P: slow equilibrium
distribution
phase following absorption
describes how a drug gets to it's target tissue for action
incluenced by solubility, body water, protein binding, tissue binding, specific carriers
total body water
intracelluler -40%
extracelluler -20% (interstitial 15%, vascular 5%)
peritoneum
B: Maculae
P: free passage
prodrugs
utilize metabolism to form active compounds
phase 1 metabolism
breakdown
involves oxidation, reduction, and/or hydrolysis
large # of these reactions are catalyzed by cytochrome P450 dependent enzmes
CYP 3A4
isoenzyme in liver and GI wall
phase 2 metabolism
synthetic
involves conjugation reaction
ex. addition of glucuronic acid, sulfonic acid, or acetylation
morphine-6-glucuronide
phase 2 metabolite of morphine
competitive antagonist
cause a shift of the agonist dose-response curve to the right
have no intrinsic activity
both the antagonist and the agonist bind to the same site on the receptor
non compeitive antagonist
"allosteric"
the antagonist binds to a site other than where the agonist binds
negative antagonist
inverse agonist
partial agonist/antagonist
have efficacies (intrinsic activities)greater than zero but less than that of a full agonist
compounds act less
get less effect
pharmacogenetics
single gene differences among population groups and the effects on pharmacodynamics
pharmacogenomics
genome-wide varietions in DNA sequences responsible for pharmacodynamic differences
human genome
comprised of ?
approximately 30,000 genes from a total of 3 billion base pairs
different base-pair combinations
result in?
different proteins produced
single base mutation
can alter?
a produced protein (enzyme) significantly
different population groups have?
somewhat different proteins and enzymes
Multidrug Resistance Gene
can cause differences in?
absorption of some drugs (digoxin) by altering carrier proteins or barrier compounds in the GI tract
5-hydroxytrypamine transporter polymorphisms
can affect the neuronal reuptake of serotonin, an important neurotransmitter
plasma cholinesterase
breaks down succ, tetracaine, mivacurium
is seen in some individuals to have reduced activity, which can cause increased duration of these compounds
different CYP genes
different metabolic rates of some drugs by individuals
CYP 2D6
shows widest known differences
responsible for appro. 25% of all drug metabolism
drugs meta. by CYP 2D6
analgesics
neuroleptics
antiarrhythmics
amide-type LA's
beta-blockers
TCA's
antiemetics
CYP 2C9 metabolises?
warfarin
phenytoin
NSAIDS
NAT metabolises?
isoniazid (INH)
sulfonamides
procainamide
NAT polymorphisms
fast (Asian)
slow (European)
CYP 3A4
female clear drugs oxidized by CYP3A4 40% faster than male
conjugation metabolic reactions
occur at a faster rate in males than females
females
lower pain tolerance
greater opioid sensitivity
higher risk of Halothane toxicity than males
females with anesthesia
awaken 50% faster from propofol, alfenta, N2O than men
require greater doses to reach proper anes. levels
why has pharmacogenetics not become more important in practice of anesthesia?
require genetic testing, which concerns prople
costs and time of screening
physiochemical interaction
=drug incompatiblilities
physical properties of different drugs are sometimes incompartible
pharmacokinetic interaction
occurs when one drug alters the way another drug is handled by the body
example of enzyme induction
enhanced metabolism of neuromascular blockers by pts taking anticonvulsants chronically
pharmacodynamic
occurs when a drug increases or decreases the effect of another drug
additive drug interaction
involves two drugs that act by the same mecanism (sometimes different mecha.)
the effect is equal to what would be expected by direct summation of each effect
synergistic drug interaction
involves effects of two drugs acting by different mechcanisms (sometimes the same mecha.)
the effect is greater than the simple sum of each drug effect
antagonistic drug interaction
effect of two drugs where the observed effect is less than additive
common causes of drug interactions
1)additive, synergestic, antagonistic actions
2)enzyme induction
3)enzyme inhibition
4)displacement
5)absorption interference
6)water and ionic disturbances
giving two synergistic drugs
allow decreased doses of each and minimize potential toxicity
volatile anesthetics (or propofol) and opioid interactions
giving together, a synergistic interaction occurs, allowing lower doses of each to be used and provide good overall anesthetic and pain blocker
ultra-short acting opioids (Remifentanil) together with propofol
provide excellent short acting synergistic anesthesia