Pharmacology (Intro)

drugs

treat, cure, mitigate, prevent, diagnose disease

tensilon test

used for myasthenia gravis

pharmacodynamics

what the drug does to the body

receptors

undergoes a conformational change which activates signaling pathway to bring a cellular response

Ionotropic or Ligand-gated ion channel Receptors

type 1 receptor

g-protein coupled

type 2 receptor

enzyme linked

type 3 receptor

nuclear

type 4 receptor

ligand-gated

aka inotropic receptors

ionotropic receptor

GABA receptor increases chloride influx resulting a hyperpolarization

7-TM receptor

G protein coupled receptor is known as

inc cAMP

adenylyl cylcase when activated by Gs it results to

phospholipase C

it is activated by Gq which produces a PAG and IP3

tyrosine kinase receptor

Enzyme-linked receptor is known as

enzyme linked receptor

insulin receptors activates tyrosine kinase resulting to increase glucose uptake is an example of:

nuclear receptor

receptor that the drug must be lipophilic

GPCR

its main action is activating 2nd messengers (cAMP, DAG, IP3)

TKR

phosphorylation process can occur in

NR

gene transcription where sex hormones are targeted can occur in

milliseconds

response of LGIC

seconds

response of GPCR

mins

response of TKR

hours or days

response of NR

Gs that activates AC

beta 1 and 2

agonist

it mimics the activity of endogenous compound

chemical bond

strong bond involved in DR interaction

ionic bond

When two ions of opposite charge are attracted to each other through electrostatic forces

hydrogen bond

Hydrogen that is linked via a covalent bond to a strongly electronegative atom

Van der Waals

interactions between nonpolar organic molecules

phentolamine

drug that is reversible alpha blocker

phenoxybenzamine

drug that is irreversible alpha blocker

pharmacopore

main binding of receptors is

active site

main binding of enzyme is

conformational change

it initiates the activation of response and dissociation of D-R complex

lock and key theory

enzyme active site is able to accept only specific type of substrate

occupancy theory

Increased # of receptor occupied = increased intensity of effect

induced-fit theory

as the drug approaches the receptor, a conformational change occurs in the receptor to allow effective binding

rate theory by paton

the intensity of response depends on the number of encounters of a drug with its receptor

Diastereomer

not mirror image, not super imposable, and different physicochemical properties

chemical bonding

irreversible bond

racemate

mixture of 2 enantiomeric compounds

antagonist

has affinity but no intrinsic activity

antidote

blocks the effect of agonist refers to:

full agonist

100% maximal response refers to

partial agonists

full agonist + partial agonist

inverse agonist

provide paradoxical effect

pharmacologic antagonists

2 drugs binding to the same receptor

reversible competitive antagonists

atropine + ACh

irreversible competitive antagonists

PPI + hyperacidity

non competitive antagonist

aka allosteric antagonist

physiologic antagonist

aka functional antagonist

functional antagonist

two drugs acting on different receptors

histamine + epinephrine

most common example of physiologic antagonist

chemical antagonist

MOA: neutralization, chelation, and complexation

chemical antagonist

protamine sulfate + heparin

efficacy, biologic activity, pharmacologic response

intrinsic activity refers to

constitutive activity

activity of a receptor in the absence of a ligand

graded dose response curve

relationship between dose and magnitude of effect

potency

dose required to produce 50% effect

ceiling dose

minimal dose that produces maximal 100% response

quantal dose-response curve

relationship between dose and frequency of effect

therapeutic index

measure of drug’s relative safety

less safe

narrow therapeutic index means

therapeutic window

dosage range at which a drug is both safe and effective

the lower the potency

the higher the dose means