Psych 211 Pharmacology

Front 1

Dose-response curve

Back 1

the magnitude of an effect of a drug as a function of how much administered. higher the dose, the greater the effect, UNTILL the point of maximum effect
morphine ex- has two effects- stops pain and depresses. a low does relieves pain, a high dose causes depressant and the dif between these is the 'margin of safety'

Front 2

why do drugs vary in efficacy?

Back 2

1) different sites of action (direct to cns is best)
2) They have different affinities for the molecules to which they attach. a drug with a high affinity will produce an effect on a very low dose. A drug may have a high affinity at one site of action and low at another.

Front 3

sensitization vs tolerance

Back 3

1) tolerance- drugs effects diminish because of repeated use, it is the bodes attempt to compensate for drugs effect

2) Sensitization- drug becomes more and more effective through repeated use. is barbiturates have sedative and depressive effects and the sedative effect shows tolerance while depressive does not.

Front 4

direct vs indirect agonist/antagonist

Back 4

direct agonist/ antagonist= competitive binding - mimics neurotrans, attaches to binding site of neurotrans causing ion channels to open (agonist) or close (antagonist)
indirect= incompetitive binding - attaches to site other than that of neurotrans. and cause the ion channels to open/close

Front 5

cocaine, meth

Back 5

catecholamine agonist that is highly addictive and increases dopamine and norepinephrine activity by blocking reuptake

Front 6

benzodiazepines

Back 6

acts as GABA agonist BUT doesn't mimic the action of GABA (don't bind to same site), reduces anxiety, induces sleep

Front 7

botox

Back 7

nicotinic antagonist which blocks acetylcholoine release

Front 8

curare

Back 8

cholinergic receptor, paralyzes because blocks muscarinic receptors of ACh

Front 9

routes of administration (10)

Back 9

intraperitoneal (stomach), IV (vein), intramuscular (slow), oral, sublingual, interectal, inhalation, topical, intracerebral (brain), intracerebroventivular (into cerebral ventricle)

Front 10

this type of drug easily passes through blood brain barrier:

Back 10

lipid soluble

Front 11

therapeutic index

Back 11

the margin of safety. for example 5.0 means the toxic dose is five times higher than that go the desired effects

Front 12

pharmacokinetics

Back 12

process by which drugs are absorbed and distributed in body

Front 13

Botulinium toxin (AChl)

Back 13

produced by a bacteria that can grow in improperly canned food- inhibits ACh!

Front 14

Black widow spider venom

Back 14

stimulates ACh release

Front 15

neostigmine (ACh)

Back 15

drug which inhibits Acetylcholinesterase (thus gives more ACh) often for muscular dystrophy patients

Front 16

Atrophine (ACh)

Back 16

blocks muscarinic receptors of ACh

Front 17

the Monoamines, which are catecholaminases?

Back 17

Dopamine, Epinephrin and norepinephrine (cate)
serotonin, histamine

Front 18

What are the three Dopaminergic areas?

Back 18

NIGROSTRATAL SYSTEM (in substantia nigra and project to Striatum), MESOLIMBIC SYSTEM (in tegmentum and go to limbic system), MESOCORTIAL SYSTEM ( also in tegmentum but project to prefrontal cortex)

Front 19

Dopamine is made from___, serotonin from___

Back 19

tyrosine; tryptophan hydroxylase

Front 20

reserpine (monoamines)

Back 20

drug that interferes with storage of monamines in vesicles

Front 21

types of dopamine receptors, which are most common?

Back 21

most common D1, D2 ; D3 and D4 are less common

Front 22

Apomorphine (dopamine)

Back 22

blocks dopamine autoreceptors at low doses and at higher doses blocks postsynaptic, too

Front 23

methlphenidate (dopamine)

Back 23

inhibits reuptake of dopamine

Front 24

Two types of ACh receptors

Back 24

A) Metatrophic (Muscarinic)
B) Ionotrophic (Nicotinic) (on muscle fibres)

Front 25

MOA; Deprenly

Back 25

destroy monoamines; blocks MOAs

Front 26

Chloropromazine (dopamine)

Back 26

reduces schizophrenia by blocking dopamine D2 receptors

Front 27

Fusaric Acid (nor.)

Back 27

inhibits production of norepin.

Front 28

Mocluobemide

Back 28

blocks MOA-A (destroys specifically norepinephrine)

Front 29

Axonal varicosity

Back 29

enlarged part of axon that contains vesticles and releases a neurotrans.

Front 30

idoazoxan ( nor.)

Back 30

facilitates release of norepinephrine

Front 31

serotonin also called...

Back 31

5- HT

Front 32

PCPA blocks...

Back 32

tryptophan hydroxylase thus is an serotonergenic antagonist

Front 33

Fluoxetine (prozac) and Fenflramine

Back 33

SSRI to treat depression

Front 34

MDMA and LSD are...

Back 34

seretonergenic agonists

Front 35

What are the 4 glutamate receptors?

Back 35

NMDAm(controls na and ca channel), AMPA (controls na) ,= most common, ionotrophoc receptor
Kainate= ionotropic receptor
metabotropic glutamate = metabotropic (clearly)

Front 36

PCP binds with...

Back 36

the PCP binding site of the NMDA receptor

Front 37

AP5 blocks...

Back 37

the glutamate binding site on NMDA

Front 38

GABA is made from

Back 38

GAD enzyme

Front 39

allyglycine (GABA)

Back 39

inhibits GAD and synthesis of GABA

Front 40

What are the 2 receptors of GABA?

Back 40

GAGAa and GABAb

Front 41

Benzodiazepines like Valium bind with...

Back 41

GABAa receptor and incude sleep or reduce seizures

Front 42

Anxiolytic means

Back 42

anxiety-reducing effect

Front 43

see chart ' neurotransmitters and drugs '

Back 43

see notes

Front 44

what are the types of norepinephrine receptors?

Back 44

alpha 1, alpha 2
beta 1, beta 2
adrenergenic receptors

Front 45

histamine receptors, what is histamine involved in?

Back 45

H1, H2, H3- sleep, itching

Front 46

what are the serotonin receptors? (9)

Back 46

5-HT 1A, 1B, 1D, 1E, 1F
5-HT 2A, 2B, 2C
5- HT 3

Front 47

Autoreceptors vs heteroreceptors?

Back 47

auto- preynaptic, sensitive to only the neruotrans from its neuron
hetero- presynaptic also but sensitive only to neurotrans other than its own

Front 48

Why does caffeine have the effect that it does?

Back 48

Adenosine is an inhibitor nerurotransmitter in CNS and caffeine acts as an antagonist for it, causing stimulation

Front 49

Why do people form dependence on nicotine?

Back 49

imitates ACh and binds to its nicotinic receptor. Some of these are located in the tegmentum where dopaminergic areas are. So dopamine is released when these areas are stimulated and = rush. This shows tolerance and the rush reduces with chronic smoking. In chronic smokers, the nicotine causes a desensitization of the nicotinic receptor chronically. When they stop smoking overnight for example, this regains sensitivity and much ACh is there, causing agitation and discomfort.