Solution 2024/2025
Pepper
NURO 545 Exam 1 Questions And Answers
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Van der Waals
shifting of electrons between different molecules, weakest bond
Hydrogen bond
H+ bound to nitrogen or oxygen and become positively polarized; slightly
stronger bond
ionic bond
atoms with excess electrons share with atoms with electron deficiency;
stronger bond
Covalent Bond
2 bonding atoms share electrons; strongest bond
Pharmacodynamics
what the drug does to the body' body biological response to drugs
Pharmacokinetics
what the body does to the drug; movement of drugs through the body
(absorption, distribution, metabolism, excretion)
Efficacy
the ability of a drug to achieve its desired effect
Potency
drugs have the same efficacy but stronger ; will need a smaller dose
Therapeutic Window
toxic effect vs effective dose; we need enough of a drug to have an effect
but not too much where there is a toxic effect
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Effective dose 50
the point where 50% of individuals may experience an efficacious impact
Toxic dose 50
Dose toxic to 50% of population
Lethal dose
the point where there is a lethal effect
pKa
pH where 50% of the drug is ionized (means it can diffuse across the
membrane)
Agonist
drug that binds to a receptor, produces similar response to the intended
chemical receptor by activating the receptor
Full Agonist
give a drug, that drug binds to receptor
Partial agonist
not the full effect of drug, there is an effect but not the full potential
Inverse Agonist
inactivates free active receptors; a receptor is actively turned on, drug
binds to receptor --> turns off the receptor; has opposite effect of an
agonist
Antagonist
inhibits agonist activity, drug binds to receptor and stops receptors from
producing a response; blocker
Competitive antagonist
knock something off a receptor that is already there and replace; reversible
binding block agonist at an active site
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Non-competitive antagonist
irreversible binding blocks agonist at active or allosteric; bonds and stays
there until effects wears off
Active Site
Receptor
Allosteric site
another site where drug binds to it and morphs the site into a shape where
lock and key wont fit
Hydrophilic
water loving, ionized, requires transport mechanism to cross membranes,
forms H+ bonds, renal excretion
hydrophobic/lipophilic
water-fearing, insoluble, passively diffuse across cell membrane, non-polar,
usually not ionized
ways drugs cross cell membranes
passive diffusion, facilitated diffusion, active transport, endocytosis, CNS
penetration
Absorption
getting into body (PO, IV, transdermal, SL), rate and extent to which a drug
leaves its site of admin
Bioavailability
the amount of drug that reaches systemic circulation (that is the amount
that becomes active)
Factors that modify absorption
higher concentration, circulation, drug solubility, surface area
Advantages of PO administration
safe, convenient, economical painless, systemic infection less likely
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Disadvantages of PO admin
destruction in harsh GI environment, passage along GI tract, slow delivery,
first pass metabolism, non-ionized, lipophilic drug favored
Advantage of parenteral route
rapid delivery, high bioavailability, no hepatic first pass, no harsh GI
environment
disadvantage of parenteral route
irreversible, pain/fear, increased risk of infection
Advantages of mucous membrane
rapid, no hepatic first pass, no harsh GI environment
disadvantages of transdermal
requires drugs with lipophilicity, slow delivery, irritation
advantages of transdermal
simple, convenient, painless, no hepatic first pass, no harsh GI environment,
continuous admin
Distribution
drugs going from blood into target tissue
Factors affecting distribution
cardiac output, local blood flow, capillary permeability, tissue volumes,
degree of binding of the drug to plasma and tissue proteins
Vd
volume of distribution (the larger VD the farther the extent of distribution)
Metabolism
how the body breaks down the drug; inactivating the drugs
Site of metabolism