PK/PD/etc! Flashcards
Hydrogen Bond
H atoms bound to Nitrogen or O2 become more + polarized, allowing them to bond to more (-) polarized atoms such as O2, Nitrogen or Sulfer. Strength: Second Weakest
Covalent Bond
Two bonding atoms share electrons - Strongest bond - often irreversible
Example: ASA
Ionic Bond
Atoms with an excess of electrons (imparting overall (-) charge on the atom) are attracted to atoms with a deficiency of electrons (imparting an overall (+) charge on the atom. Third strongest bond.
Van der wals
Shifting electron density in areas of a molecule, or in a molecule as a whole, results in the generation of transient (+) or (-) charges - these areas interact with transient areas of opposite charge on another molecules
Define PD
what the drug does to the body
Define PK
What the body does to the drug
Efficacy vs. potency
Potency: Strength (amt of drug needed to achieve intended effect.
Efficacy: ability of drug to produce same response:
NOTE: Drugs can have the same efficacy but different potency (i.e. statins).
Characteristics of HYDOPHILIC
Water loving
Polar, usually ionized
Renal excretion
Requires transport mech to x cell membranes and BBB
Forms H= bonds (ionized = (-) charge somewhere)
Can penetrate CNS via active transport, facilitated transport, intrathecal admin.
Characteristics of HYDOPHOBIC
Think Oil/Vinegar LIPOphilic Fat Loving/water insoluble Passively diffuses across cell membranes and BBB (d/t lipid bilayer so fat soluble will go through) Non-polar, usually NOT-ionized
Core of a cell is what: hydrophilic or phobic?
Hydrophobic lipid core
Membrane of a cell is what: hydrophilic or phobic?
Hydrophilic
“D+R DR DR* “ means what?
Empty drug + empty rc (does nothing)
DR = drug bound to rc
DR* activated drug/rc (activity taking place).
Agonists : Full
Elicit max. result
Stabilize DR*
Think “Full faucet”
i.e. ACH binds to nicotinic rc and induces conformational change from nonconducting to fully conducting state.
Partial Agonist
Activates rc w/o max efficacy
Stabilizes DR and DR*
i.e. Beta Blockers
Typically this is an intended design ie. CNS meds when you do not want full firing or full activity.
Inverse agonists
Inactivates free active rc’s (which is active at BSL)
Stabilizes DR in the case of R* (which is the natural state of the enzyme).
Example: inactivate an overactive enzyme in CA pt.
Example: Diphenhydramine: inverse agonist when need histamine to be turned OFF.
Competitive Antagonists
Reversible binding blocks agonist at ACTIVE SITE
Stabilizes DR, PREVENTS DR*
Agonist can bump antagonist off which would lead to DR* therefore, need more agonist on board to out compete the antagonist.
Noncompetitive Antagonist
Irreversible binding
Blocks agonist at Active or Allosteric site
Can reach plateau b/c agonist is taken out of play or antag prevents it from doing anything.
TI: What and how calculated
TI = TD50/ED50
Want higher TI for low toxicity and high efficacy; high TD and low ED
High TI: wide therapeutic window with TD much > ED
pKa and why do we care?
pH at which 50% of drug is ionized, ph at which 50% of a drug can passively diffuse across membranes. Want to know if a drug can cross membrane or not and NOT GET TRAPPED as it needs to be WITHOUT a charge to passively diffuse.
What is the MOST desirable PD for a medication:
a. Low LD50
b. Low TI
c. High TI
d. Low TD50
C: high efficacy and low toxicity
Absorption: where
GI tract, parenteral, Skin/Membranes