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1. Pharmacology > Pharmidynamics > Flashcards

Pharmidynamics Flashcards

1
Q

Molecular response

A

Modulation of enzyme activity/movement of ions across the plasma membrane

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2
Q

Cellular response

A

Modulation of secretion of hormone or NT or the modulation of cell motility

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3
Q

Organ response

A

Smooth muscle contraction (ACH)

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4
Q

Whole animal response

A

Behavior changes/ response can be lethal

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5
Q

Therapeutic range

A

Dose/ response curve
Dose range expected to achieve desired therapeutic effects

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6
Q

Therapeutic Index (TI)

A

TI= TD50 (toxic dose)/ ED50 (effective dose)
Or
TI = LD50 / EC50

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7
Q

Efficacy

A

Expresses level of response with a maximal possible effect (y, Emax)

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8
Q

Potency

A

Strength related to dose
Function of drugs affinity for receptor and ADME factors (x)
EC50 measure drug potency
(Closer to the y axis)

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9
Q

Full agonist

A

Greatest possible response
IA=1
Ex: isoprenalin

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10
Q

Partial Agonist

A

Partial response
IA<1
Ex; buprenorphine

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11
Q

Antagonist

A

Inhibit action of an agonist
IA=0
Also called blockers because they bind to receptor so agonist won’t
Ex: ranitidine, H2 antagonist

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12
Q

Inverse Agonist

A

Produces opposite response to that of an agonist
IA=0 to -1

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13
Q

Agonist- Antagonist

A

Acts simultaneously as an agonist on one set and as an antagonist on another set of receptors
Ex: nalorphine activates K opioid receptor but blocks mu-opioid receptor

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14
Q

Types of Antagonism

A

Chemical (antacids)
Functional/ physiological (insulin and glucagon on blood sugar)
Dispositional
Receptor (competitive and non competitive)

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15
Q

Competitive Antagonism

A

Reversible receptor binding
Antagonist will bind with the same receptor site as the agonist
Antagonist usually resembles in structure with the agonist

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16
Q

Non competitive antagonist

A

Irreversible receptor binding
Antagonist could bind with the same receptor site as the agonist or to an allosteric site
Efficacy and slope will decrease

17
Q

Terms for drug interaction

A

Potentiation (increased drug response, drug A enhancing activity of drug B)
Additivity
Synergism (2 active drugs enhancing each other)

18
Q

5 major cross-membrane signaling mechanisms (receptors)

A

Steroid
Tyrosine kinase
JAK-STAT
Ion channel
GPCR

19
Q

Ionotropic-Receptors Ligan Gated Ion-channels

A

Ligand binds to ion channel for ions to pass inside cell
Cationic channels: K, Na and Ca, excitatory
Anionic: Cl, Inhibitory
Quick response

20
Q

G-protein coupled receptor

A

Membrane bound, regulates effector proteins through mediation of tranducers (nucleotides like GTP and GDP- G-proteins)
Medium response

21
Q

G-proteins

A

Heterotrimerica molecules with 3 subunits: a, b, g attached to the inner surface of plasma membrane
They have homologous guanine nucleotide binding domain

22
Q

Effector systems

A

Adenylate cyclase:cAMP system
Phospholipase C: IP3-DAG system
Phospholipase A2: AA system

23
Q

Tyrsoine Kinase receptor

A

Ligand binds to both binding sites and forms a dimer –> TK activated inside the cell –> ATP converted to ADP –> Phosphorylation –> activated other down stream signaling proteins –> activate transduction signals
Ex: growth hormone, cytokines, insulin

24
Q

Nuclear receptors

A

Intranuclear receptors are located in the cytoplasm or nucleus
Signal molecule lipophilic to cross membrane
Long lasting effect

25
Q

Up-regulation

A

Body increases the # of receptors
Seen when receptors are continuously deprived of their ligand or continued use to antagonist (continuously blocked) —> supersensitization

26
Q

Down-regulation

A

Cell decreases the quality of receptor or protein population
Causes diminished drug effects
When tissue continuously exposed to agonist –> over-activation

27
Q

What does down-regulation lead to?

A

Desensitization/ refractioness
Won’t get the desired effect

1. Pharmacology (29 decks)

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