Pharm - basics Flashcards
competitive inhibitors bind
active site
competitive inhibitors affect
potency (lower it)
non competitive inhibitors affect
efficacy (lower it)
can alter volume of distribution
liver and kidney disease
volume of distribution =
amount of drug in body/plasma drug concentration
large/charged molecules are distrubted in
the blood
small hydrophillic molecules are distributed in the
ECF
small lipophillic moclecules are distributed in
all tissues
half life =
.(07 x volume of distribution)/clearance
a drug infused at a constant rate takes how ling to reach steady state
4-5 half lives
clearance =
(rate of elimnation of drug/plasma drug concentration)
or
(volume of distribution x elimination constant)
loading dose =
target plasma concentration x (volume of distribution/bioavailability)
maintance dose =
target plasma concentration x (clearance/bioavailability)
dosage calculation that changes in renal/liver disease
maintainance dose (lower)
zero-order elimination drug examples
asprin, phenytoin, ethanol
rate of elimination is constant regardless of plasma concentration is called
zero order
rate of elimination is directly proportional to drug concentration
first order
treat OD of weak acids with
bicarb (to trap in urine)
weak acid drug ex:
phenobarbital, methotreaxate, asprin
treat OD of weak bases with
amonium cholride (traps in urine)
weak base drug ex
amphetamines
phase I metabolism results in
slightly polar slightly water souable metabolites
phase II metabolism results in
very polar, inactive metaboltes that are renally excreted
phase metabolism reactions
reduction, oxidation, hydrolysis with cytochrome P450
phase II metabolism reactions
conjugation (glucoronidation, acetylation, sulfation)
maximal effect a drug can produce
efficacy
high efficacy drug classes
pain meds, antibiotics, antihistamines, decongestants
amount of drug needed for a given effect
potency
high potency drug classes
chemo, HBP drugs, antilipid drugs
shifts dose effect curve to right and decreses potency
competive agonist
shifts dose effect curve down and decreses efficacy
noncompetetive agonist
acts at same site as full agonisyt but with reduced maximal effect
partial agonist
cannot be overcome by increasing agonist substrate concentration
noncompetitive antagonist
theraputic index=
LD50/ED50
drugs with low theraputic indexes
digoxin, lithium, theophylline, warfarin
nicotinic ACh receptors are what type
ligand gated Na/K
muscarinic ACh receptors are what type
G-protein coupled
sympathetic a1 receptor functions
increase: vascular smooth muscle tone, contraction of pupilarry dilator muscle (mydriasis), contract intestinal and bladder sphincter muscle
sympathetic a2 receptor functions
lowered: sympathetic outflow, insulin release, lipolysis
raised: platelet aggretation
sympathetic B1 receptor functions
increase: HR, contractability of heart, lipolysis, increased renin release
sympathetic B2 receptor functions
vasodilation, bronchodilation, increased HR and contractability, increased lipolysis and insulin release, lower uterine tone, cilary muscle relaxation, increased aqueous humor production
parasympathetic M2 receptor functions
lowers HR and contractability of atria
parasympathetic M3 receptor functions
increase exocrine gland secretions, increase gut peristalis, increase bladder contraction, increase bronchoconstriction, miosis, accomidation (increases ciliary muscle contraction)
D1 receptor function
relaxes renal vascular smooth muscle
D2 receptor function
modulates transmitter release, esp in brain
H1 receptor function
nasal and bronchial mucus production, contraction of bronchioles, itching and pain
H2 receotor function
gastric acid release
V1 receptor functon
vascular smooth muscle contraction
V2 receptor function
H20 permability and resbsprption in the collecting tubiles in the kidney
prevents tyrosine becoming DOPA
metyrosine
prevents dopamine from becoming NE
reserpine
prevents NE uptake
cocaine, amphetamine, TCA
prevents NE release
guanathidine, bretylium
releases extra NE
amphetamine
prevents choline uptake
hemicholinium
prevents ACh production
vesamicol
prevents ACh release
botulism toxin
ACh broken down by AChesterase into
choline and acetate