Exam 1 Flashcards
semiantagonism
the idea that partial agonists can act as antagonists because they can bind and reduce the Emax of the endogenous drug
inverse agonists
they bind to the receptor site preferentially in the inactivate state to lower basal activity
THESE ARE NOT ANTAGONISTS
spare receptors
the idea that only a fraction of the total receptors are needed to yield a 100% response. EC50<Kd HERE. think of insulin
therapeutic index
calculated by ld50/ed50
downregulation
a decrease in the number of receptors typically when they are overstimulated
tachyphylaxis
acute tolerance build up
competitive agonist
type of agonist that shifts curve right
noncompetetive antagonists
type of agonist that shift curve down
mdr1
the most important drug transporter
first pass effects
in oral consumption of drugs, it causes a loss of much of the dose
bioavailability
auc(drug given as tablet)/auc(drug given as IV)
loading dose equation
Co(plasma drug concentration at time 0)= X(total amount of drug in body)/[volume of distribution *patient weight]
target mediated drug disposition
the process of eliminating monoclonal antibodies(fast, mAb specific)
half time for drug elimination
T1/2=.693/first order elimination rate constant
hepatic metabolism
the dominant elimination mechanism for lipophilic drugs
phase 1 of hepatic metabolism
the oxidization of lipophilic drugs into polar molecules by cytochrome p450
phase 2 of hepatic metabolism
the addition of groups to a drug to make it more water soluble and therefore more easy to excrete in urine
renal elimination
the primary mechanism of elimination for hydrophilic drugs. filtration secretion reabsorption and excretion in the nephron
bile excretion
main elimination mechanism for large hydrophilic molecules (can be slow because some drugs may go through enterohepatic circulation)
maintenance dose
Css(steady state plasma drug concentration)= infusion rate/ CI(drug clearance total)
beta lactam antibiotics
penicillins and cephalosporins
penicillin prototype drugs
G, V and amoxicillin. cell wall moa. treats otitis media, bronchitis, and pneumonia. can cause anyphlyacti shock but its very rare
cephalosporins
proto drug= cephalexin. cell wall moa. crosses bbb. treats meningitis. can cause anaphylactic shock but rare
cell membrane antibiotics
daptomycin. cell membrane moa. interactions with statins cause muscle toxicity
ribosomal antibiotics
tetracyclines, aminoglycosides, microlides, chloramphenicol
tetracyclines
doxycycline. mechanism through 30 s ribosome. reversible. impaired by food. tooth coloration bone deposition and growth inhibition. no children or pregos. interacts negatively with dairy and antacids
aminoglycosides
tobramycin, 30s ribosome irreversible, treats eye infection, but is ototoxic(hearing/balance)
macrolides
azithromycin, 50s ribosome, treats gram positive and negative bacteria, disturbed by food, interactions inhibit CYP450
Chloramphenicol
proto drug same, 50 s reversible, causes bone marrow bad and gray baby syndrome. interactions inhibit cyp 450
folic acid antibiotics (antimetabolites)
sulfonamides
sulfonamides(trimethoprim)
synergistic with trimethoprim, sulfamethizole, inhibit folate synthesis, cause photosensitivity and stevens johnson syndrome
dna gyrase inhibitors
ciprofloxacin
ciprofloxacin
dna gyrase topoisomerase 2 inhibition, damage growing cartilage, no kids or pregos
antimycobacterial antibiotics
isoniazid and rifampin
isoniazid
cell wall moa of mycolic acids, treats tb (mycobacteria)
rifampin
inhibits rna synthesis, treats tb, orange urine sweat and tears (harmless) cyp inducer
ergosterol synthesis antifungals
Imidazoles: ketoconazole, moa disrupts ergosterol synthesis by binding to fungal cyt p450, fungistatic
antimitotic antifungals
griseofulvin: slowly disrupts mitosis, only effective when used against dermatophytes, fungistatic
antiinfluenza antiviral
oseltamivir: for influenza a and b and avian flu. Neuraminidase inhibitor
antihepatitis antivirals
sofosbuvir(harvoni), boceprevir, entecavir
sofosbuvir
hep c drug. (eradication)
boceprevir
for hep c(eradication) protease inhibitor
entecavir
hep b (suppression) dna polymerase inhibitor
antihiv antiviral
abacavir, rilpivirine, darunavir
abacavir
Nucleoside reverse transcriptase inhibitor. competitive inhibition of hiv reverse trasncriptase and acts to block dna chain elongation
rilpivirine
nonnucleoside rti. allosteric inhibition of reverse transcriptase
darunavir
protease inhibitor that blocks post translational modificatio of viral proteins. cyp3a4 inhibitor
non cell cycle specific chemo
cyclophosphamide: transfers alkyl groups to dna
s phase chemo
methotrexate, 5-fluorouacil, hydroxyurea, etopside
methotrexate
inhibits dihydrofolate reductase
5-fluorouracil
inhibits pyrimidine synthesis
hydroxyurea
inhibits dna (not RNA) synthesis by blocking ribonucleotide reductase
etoposide
blocks topoisomerase II
g2/m phase chemo
bleomycin: causes oxidative damage to dna
m phase chemo
vincristine, paclitaxel, ixabepilone
vincristine
vinca alkaloid that inhibits tubulin polymerization, preventing mitosis
paclitaxel
taxane that targets microtubules and stabilizes them, preventing mitosis
ixabepilone
antimicrotubule inhibitor. like taxanes they stabilize microtubules to prevent mitosis
hormone chemo
tamoxifen, letrozole, leuprolide, degarelix, flutamide
tamoxifen
binds to estrogen binding site on hormone binding receptor. antagonist in breast tissue, agonist in bone and endometrium. cancer must be er positive
letrozole
inhibits aromatase
leuprolide
GnRH agonist, overstimulates and desensitizes the anterior pituitary
degarelix
GnRH antagonist, prevents pituitary response to GnRH
flutamide
Blocks androgen receptor to prevent testosterone effect
receptor tyrosine kinaseinhibitor chemo
nilotinib and erlotinib
nilotinib
inhibits tyrosine kinase domane of bcr abl oncroprotein and prevents phosphorylation by atp
erlotinib
inhibits tyrosine kinase domane of edfr rtk oncroprotein and prevents phosphorylation by atp
