Pharmacology Flashcards
competitive inhibitors
- resemble substrate
- can be overcome by increasing substrate
- binds active site
- does not affect Vmax
- increases Km
- less potent
competitive inhibitors, irrersible
- resembles substrate
- cant be overcome by increasing substrate
- binds active site
- lowers Vmax
- unchanged Km
- less efficacious
noncompetitive inhibitors
- doesn’t resemble substrate
- cant by overcome by increasing substrate
- does not bind active site
- lowers Vmax
- does not affect Km
- less efficacious
bioavailability (F)
fraction of drug that reaches the systemic circulation
- IV dose = 100%
volume of distribution
volume occupied by total amount of drug in body relative to plasma concentration
Vd equation
Vd = amount of drug/concentration (mg/mg/ml=ml)
low Vd
stays in IV space, large/charged molecules, protein bound
high Vd
in all tissues, small lipophilic molecules
clearance
volume of drug clear per unit time
- can change based on organ function
clearance equation
Cl = rate of elimination / drug concentration (mg/min / mg/ml)
half life equation
t1/2 = Vd*0.693/Cl
loading dose equation
Cp * Vd / F
maintenance dose equation
Cp *CL * dose interval / F
additive drug interaction
A + B = sum of effects
permissive drug interactions
A is required for full B effects
synergistic drug interactions
A + B = greater than sum of parts
tachyphylactic drug interactions
acute decrease in response after administation
zero order elimination
eliminated independent of concentration (constant amount)
zero order drugs
phenytoin, ethanol, aspirin
first order elimination
eliminated dependent on concentration (constant fraction)
weak acids in urine
deprotonated form is ionized
will dissociate and stay trapped in urine
- in case of overdose, add base to remove H+ and keep drug in urine
weak bases in urine
protonated is ionized
- in case of overdose, add acid to increase protonated form
phase I drug metabolism
reduction, oxidation, hydrolysis with P450, yield slightly polar, water soluble metabolites
phase II drug metabolism
conjugation (methylation, glucuronidation, acetylation, sulfation), very polar inactive metabolites
- slow acetylators have increased side effects
efficacious drug
high Vmax, unrelated to potency
potent drug
lowest dose that still causes symptoms
- unrelated to efficacy
competitive antagonist curve
shift curve right, does not change efficacy, can be overcome
noncompetitive antagonist curve
lowers curve (efficacy), doesn’t change potency
partial agonist
acts at the same site, lower efficacy, potency is independent
sweat glands
are part of sympathetic pathway but are innervated by cholinergic fibers
nicotinic receptors
ligand gated Na/K channels
- Nn = autonomic
- Nm = neuromuscular junction
muscarinic receptors
G protein coupled receptors
- use Ach
alpha 1 effects
increase vascular smooth muscle, pupillary dilator muscle contraction, intestinal and bladder contraction
Gq pathway
receptor binding, phospholipase C converts PIP2 to IP# and DAG, activated PKC and increasing calcium
Gs pathway
receptor binding, increase in adenylyl cyclase, increase cAMP, protein kinase A, increase in calcium and blocks myosin light chain
Gi pathway
receptor binding, decrease in adenylyl cyclase, decrease cAMP, protein kinase A, decrease in calcium and activates myosin light chain
tetrodotoxin
puffer fish toxin
- binds voltage gated sodium channels preventing depolarization
ciguatoxin
reef fish toxin
- opens sodium channels causing depolarization
