Pharmacology Weeks 1-3 Flashcards
pharmacokinetics vs pharmacodynamics
pharmacokinetics: what body does to drugs
pharmacodynamics: what drugs do to body
List various types of receptors and describe the fundamental differences between them
ion channel: fastest, ligand causes to open. ex. ACh
G-protein coupled:second messengers ex Epi
R couples to enzyme: membrane tyr kinases. ex GFs
Intracellular: slowest, gene expression, ex steroids
agonist
affinity and intrinsic activity (exerts an effect)
- partial agonist: has affinity but less than full intrinsic activity and given receptor
- inverse agonist: inactivates constitutively active receptors (rare)
antagonist
affinity but lacks intrinsic activity
- reversible and irreversible
- chemical antagonist: drug that inhibits action of another drug
- phyl antagonist: counteracts physiological effects of another compound via DIFFERENT receptor
graded dose reponse curve
Plot réponse vs log[dose]
- assess efficacy (Emax=max response) and potency (50% Emax=measure of how much drug is needed)
- steep slope=more potent
quantal dose response curves
- assess all or none response: what percentage responds at a given dose?
- used to assess relationship btw efficacy and safety
- steep slope=less population variability
TD50
dose where 50% of individuals will have a toxic response
Therapeutic index
TD50/ED50
margin of safety
effect of reversible/irreversible antagonist on dose response curve of given agonist
- reversible: Lower potency, same Emax
- irreversible: lower Emax
antisense
- complementary strand of mRNA blocks transcription of DNA
- cancer
- RNAi marks mRNA for destruction
- names end in -sen
monoclonal antibodies
- highly specific antagonist, or bind ligand
- inflammatory disorders (chron’s), neurological disorders (MS), visual (mac degen), cancer
- names end in -mab
fusion proteins
- receptor fused to antibody, binds ligans and prevents it binding real receptor
- inflammatory disorders
- names end -cept
aptamers
- oligonucleotides that bind target protein, prevet receptor interaction
- cancer, viruses
- names include -apt-
tolerance
reduction in response over time
- receptor downregulation: fewer on cell surface
- desensitiaion: receptors less responsive (attenuated signalling)
- Tachyphylaxis: tolerace develops rapidly (min-hrs) due to desensitizaion
Rebound
- receptor upregulation can occur with chronic use of antagonist
- stop meds=exaggerated opposite response
- prevent by weaning off meds slowly
Law of Mass action
More drugs means more binding means greater response
spare receptors
receptors that are not bound when maximal response achieved
side effects
- effect continues longer
- receptor at unwanted region
- lack of sensitivity
-dose is main determinant
