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Drugs & Behavior > Cumulative Info (w/o Unit 4) > Flashcards

Cumulative Info (w/o Unit 4) Flashcards

1
Q

what is pharmacology?

A

the study of drug

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2
Q

what is psychopharmacology?

A

drugs that effect thinking, mood, and Bx

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3
Q

what is neuropharmacology?

A

drugs that effect neurons and the NS

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4
Q

what is neuropharmacology?

A

drug interaction with neurons and their effect of mood, thinking, and bx

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5
Q

what are psychoactive drugs?

A

biologically active substances that chemically alters cell structure or function of neurons that effect mood, thinking, and bx

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6
Q

what are three functions of neurons?

A

transmit, intergrate, store

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7
Q

what is the neural model?

A

sensory cell -> sensory neuron -> interneuron -> motor neuron -> effector

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8
Q

what do sensory cells do?

A

transduction (turn environ. signal into a biochemical signal)

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9
Q

what to effectors do?

A

muscles and glands that produce bx and excite/inhibit motor neurons

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10
Q

what is specific drug effect?

A

drug-receptor interaction (alc binds to GABA-R and causes sleepiness)

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11
Q

what is nonspecific drug effect?

A

environmental effects, individual differences (sex, weather, diet)

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12
Q

what are the four different names for a drug?

A

chemical
generic
trade
street

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13
Q

what do each of the four names for drugs describe?

A

chemical: IUPAC ID, molecular structure
generic: official name after paten, not capitalized
trade: paten name, capitalized
street: societal name that changes generation to generation

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14
Q

what are the five different drug types?

A

CNS stimulants (cocaine)
CNS depressants (alcohol)
Analgesics (sleepy, morphine)
Hallucinogens (distort perception and mood)
Psychotherapeutics (help with depression, anxiety)

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15
Q

what are the three different drug equivalences?

A

chemical
biological
clinical

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16
Q

what is chemical equivalence?

A

same chemical compound
same drug effect
same systems

different drug names

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17
Q

what is biological equivalence?

A

different chemical compound
same drug effect
same systems

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18
Q

what is clinical equivalence?

A

different chemical compound
same drug effect
different systems

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19
Q

Drugs are ____ and have ____ effects

A

variable, multiple

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20
Q

how many drug schedules are there and what are they used to determine?

A

5 schedules
-determines abuse potential and medicinal value

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21
Q

Schedule 1

A

-high abuse
-no medicinal value
-not prescribed
-heroin

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22
Q

Schedule 2

A

-high abuse
-accepted medicinal value
-prescribed, but no refills
-cocaine

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23
Q

Schedule 3, Schedule 4, Schedule 5

A

3: moderate abuse
4: low abuse
5: lowest abuse

5 refills over 6 months

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24
Q

how long does it take for a drug to get approved? how long does the patent last?

A

-takes 10yrs for approval
-patent lasts 20 yrs

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25
Q

what two things does animal testing test?

A

-carcinogenicity (cancer risk)
-teratogenicity (embryo affects)

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26
Q

how many human phases does a drug go through to get approved?

A

4 phases

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27
Q

what is phase 1 of human clinical trials? (years it takes, size of group, what is being tested)

A

safety & dosage
-1.5 yrs
-sm. group (20-100) healthy people
-how drug effects body

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28
Q

what is phase 2 of human clinical trials? (years it takes, size of group, what is being tested)

A

efficacy and side effects
-2 yrs
-medium group (100-1,000) diagnosed people

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29
Q

what is phase 3 of human clinical trials? (size of group, what is being tested)

A

efficacy and adverse rxns
-lg. group (1,000-3,000) diagnosed people
-appropriate dosage

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30
Q

what is phase 4 of human clinical trials? (years it takes, size of group, what is being tested)

A

real world impact
-ongoing and never stops
-safety monitoring

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31
Q

after which phase does the drug get approval?

A

after phase 3

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32
Q

what is pharmacokinetics?

A

what body does to drug (absorption, administration)

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33
Q

what is pharmacodynamics?

A

what drug does to body (drug effects)

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34
Q

what does is the difference between enteral and parenteral administration methods?

A

enteral: GI tract
parenteral: all other routes

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35
Q

what is the per Os (PO) administration method? (include kinetics)

A

-1st pass metabolism
-absorbed through gut membranes
-slow onset, low magnitude, long duration

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36
Q

what is the sublingual administration method? (absorption)

A

absorb through mucous membranes and glands (LSD)

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37
Q

what is the transbuccal administration method? (absorption)

A

absorb through mouth lining (chewing tobacco)

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38
Q

what is IV injection administration method? (include kinetics)

A

-does not cross membranes
-fastest onset, high magnitude, short duration

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39
Q

what is IM injection administration method? (include kinetics)

A

-deltoid and glute muscle injections (deltoid is faster)
-has two solutions it is mixed with (aqueous is faster than oil)
-faster onset than PO, slower onset than IV

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40
Q

what is the SC injection administration method? (include kinetics)

A

-under skin (insulin)
-slow onset

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41
Q

what is the IP injection administration method? (include kinetics)

A

-abdomen
-similar kinetics to IM (fairly fast onset)

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42
Q

what is inhalation administration method? (include kinetics)

A

-passes through capillary membrane in lungs (smoking)
-slower onset than IV (fairly fast onset though)

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43
Q

what is intranasal administration method? (include kinetics)

A

-passes through mucous membranes
-no 1st pass metabolism (bypasses BBB)
-slower onset than inhalation

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44
Q

list the onset peaks from highest to lowest (inhalation, SC, PO, IV, (IM,IP,intranasal))

A

IV (highest peak, highest magnitude, shortest duration)
Inhalation
IM,IP,Intranasal
SC
PO (lowest peak, lowest magnitude, longest duration)

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45
Q

when is absorption complete?

A

when concentration at target area = concentration at administration site

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46
Q

what are capillaries and what do they do?

A

-one cell thick w/ pores and spaces b/w cells
-exchange materials b/w blood and cells
-typically leaky

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47
Q

what is the blood-brain-barrier and what does it do?

A

-barrier b/w blood and brain
-selectively permeable
-water soluble molecules need active transport to enter
-maintains stable CNS environment
-incomplete at birth until 2 yrs old

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48
Q

what happens when toxic neurons enter the BBB at the area postrema CTZ (chemical trigger zone)?

A

vomitting

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49
Q

what does ionization do to molecules?

A

decrease lipid solubility
-dependent on pH (acidic)

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50
Q

what does ion trapping do?

A

-traps drugs so it can’t cross membranes
-prolongs drug effects (creates ‘free’ drug)

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51
Q

what are the characteristics of molecules best at absorption? (size, polarity, pKa/pH, ionization)

A

-small molecules
-lipid soluble (non-polar)
-low in ion-trapping
-pKa matches fluid pH

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52
Q

what is depot binding?

A

similar to ion trapping EXCEPT
-no ionization
-still decreases bioavailability of drug and creates more ‘free’ drug

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53
Q

what is nonselective binding?

A

competition for sites
-increases bioavailability of drug

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54
Q

what is half-life? what are the two types (describe them)?

A

-time drug decreases by 1/2
-types (1st-order and 0-order)

1st-order: constant fraction eliminated, small % of clearance sites occupied, decreasing exponential line
0-order: constant amount eliminated, all clearance sites occupied, decreasing linear line

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55
Q

what are the two phases of biotransformation?

A

Phase 1: non-synthetic modification (reduction, oxidation, hydrolysis)

Phase 2: synthetic modification / adding something (conjugation, ion trapping, acetylation)

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56
Q

where does biotransformation take place?

A

liver

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57
Q

what are cytochrome P450’s?

A

detoxification enzymes that oxidizes psychoactive drugs during phase 1 of biotransformation

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58
Q

what is enzyme induction?

A

creates more enzymes to reestablish homeostasis
-tolerance, brussel sprouts

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59
Q

what is enzyme inhibition?

A

lessens the effect of enzymes
-creates more ‘free’ drug

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60
Q

what does the kidney do to molecules?

A

ionizes them to be released as urine
-pH 4.5-7.5

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61
Q

what is the antidiuretic hormone (AHD)? what inhibits ADH?

A

ADH inhibits water excretion
-alc and caffeine inhibit ADH (causing more urination)

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62
Q

what is the effective dose? threshold dose?

A

dose that produces a biological response
-threshold dose: minimum response

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63
Q

what are the two types of dose-response curves?

A

% of population responding
response magnitude (mean response)

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64
Q

what is potency?

A

drug A has same effect as drug B but at a lower dose
-drug A is more potent

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65
Q

what is maximum efficacy?

A

drug B has a higher maximum efficacy due to a higher y-axis point

66
Q

what is the equation for the therapeutic index? do bigger or small numbers mean it is more safe

A

LD50/ED50
-bigger number means it is more safe

67
Q

what are three different things that can affect dose-response curves?

A

sex, age, tolerance

68
Q

what are cumulative effects?

A

single drug
-repeated administration before drug is completely eliminated
-the effect decreases before drug is completely eliminated

69
Q

what are additive effects?

A

multiple drug
-drugs with same effects (add together)

70
Q

what are physiological effects?

A

multiple drug
-drugs with opposing effects (the difference)

71
Q

what are potentiation effects?

A

multiple drug
-the whole is greater than the sum of products
-bigger than additive effects

72
Q

what is tolerance?

A

decrease in response to same dose of drug

73
Q

what is metabolic tolerance?

A

production of more enzyme (enzyme induction)

74
Q

what is pharmacodynamic tolerance?

A

decreased NT synthesis

75
Q

what is behavioral tolerance?

A

conditioned response (pavlovian conditioning)

76
Q

what is acute tolerance?

A

decrease of effect b/w doses (nic hits)

77
Q

what is cross tolerance?

A

tolerance to drugs that work by same mechanism (alc and phenobarbital)

78
Q

what is sensitization?

A

increase response to same dose of drug
-due to repeated exposure to a stimulus

79
Q

what is rate dependency?

A

interaction of drug and the baseline rate of bx
-different effects produced due to initial activity of system
-low dose: increases affects
-high dose: decreases affects
-EX: ADHD

80
Q

what are the 6 steps of the synaptic transmission model?

A
  1. precursor transport
  2. synthesis
  3. storage
  4. release
  5. activation
  6. termination
81
Q

what occurs during precursor transport (1)

A

NT at axon terminal
sm. peptide at soma

82
Q

what occurs during synthesis (2)

A

enzymes and cofactors are loaded into axon terminal

83
Q

what occurs during storage (3)

A

NT, ATP, GTP, Ca2+ stored in synaptic vesicles

84
Q

what occurs during release (4)

A

exocytosis
-anchored to axon terminal by synapsin-actin linkages
-vesicle is next to synapse and action potential reaches vesicle
-Ca2+ influx to release NT and open voltage gate
-Ca2+ bind calmodulin to activate CaMK2
-CaMK2 phosphorylated synapsin to release vesicle

membrane fusion
-vesicle diffuses toward synaptic membrane
-SNAPs and NSFs primes for fusion (alpha, gamma, beta)
-SNAREs open configuration and intertwine (synaptobrevin, syntaxin, SNAP-25)
-synaptotagmin binds Ca2+ and fuses everything together

85
Q

what occurs during activation (5)

A

NT binds to receptor and changes conformation

86
Q

what occurs during termination (6)

A

4 different ways
-diffusion
-enzymatic degradation
-reuptake
-autoreceptors

87
Q

what is diffusion termination (6)

A

receptor becomes inactive

88
Q

what is enzymatic degradation termination (6)

A

cuts up NT

89
Q

what is reuptake termination (6)

A

active transport of NT out
-goes back to vesicle it came from
-OR degraded by an astrocyte / glial cell

90
Q

what is autoreceptor termination (6)

A

binds NT on presynaptic cell
-decreases depolarization
-decreases NT release

91
Q

what occurs at presynaptic facilitation? (K+, Ca2+ channels, NT release)

A

decreases K+ efflux so Ca2+ channels stay open, increase NT release

92
Q

what occurs at presynaptic inhibition? (K+, Ca2+ channels, NT release)

A

increases K+ efflux so Ca2+ channels close, decreases NT release

93
Q

what is affinity?

A

ability to bind to receptor

94
Q

what is efficacy?

A

ability to activate receptor

95
Q

what are some characteristics of ligand binding?

A

-lock and key model but has the ability to change structure of drug to fit
-still specific!
-L and D isomers (levo is more active)
-ligand binds and activated 2d messenger systems (EPSP, IPSP)

96
Q

what does direct mean?

A

at NT postsynaptic R

97
Q

what does indirect mean?

A

at sites other than NT’s binding site

98
Q

what is an agonist?

A

mimics or increases NT effect
-affinity and efficacy

99
Q

what is an antagonist?

A

blocks or decreases NT effect
-affinity, NO EFFICACY

100
Q

what are competitive antagonists?

A

competes for same R site
-decreases potency (takes more of drug to produce same effect)

101
Q

what are noncompetitive antagonists?

A

binds at different site but same R (allosteric binding)
-effects maximum response

102
Q

what is an ionotropic receptor?

A

channel and binding site on same protein
-NT directly controls channel
-acute tolerance

103
Q

what is a monotropic receptor?

A

channel and binding site in different proteins
-GTP required
-neuromodulation

104
Q

explain the 2d messenger system of NE

A

beta adrenergic R
Gs
increases adenyly cyclase
increases cAMP
increases protein kinase A

105
Q

explain the 2d messenger system of DA

A

D2 R
Gi
decreases adenylyl cyclase
decreases cAMP
decreases protein kinase A

106
Q

where are monoamines found, released by, and the two types?

A

-found at axon terminals that bind at postsynaptic R
-released by action potentials
-types: catecholamines (1 ring) & indolamines (2 rings)

107
Q

what are the catecholamine NT?

A

DA, NE, EPI

108
Q

what are the indolamine NT?

A

5-HT, melatonin

109
Q

how are all monoamines terminated?

A

monamine oxidase (MAO)

110
Q

how are only catecholamines terminated?

A

catechol-O-methyltransferase (COMT)

111
Q

what does reserpine do to monoamines?

A

blocks monoamine transporters
-decreases NT storage
-indirect ANT

112
Q

where is DA found?

A

midbrain

113
Q

what are the DA receptors?

A

D1: Gs proteins
D2: Gi proteins

114
Q

what are the three ascending pathways in DA?

A

nigrostriatal (substantia nigra -> striatum) parkinson’s disease
mesolimbic (VTA -> limbic)
mesocortical (VTA -> cortex)

115
Q

how is DA synthesized? what is the major metabolite?

A

tyrosine –(tyrosine hydroxylase)–> DOPA –(AADC)–>DA
-homovanillic acid

116
Q

where is NE found?

A

adrenal glands, locus coeruleus

117
Q

what are the NE receptors?

A

alpha: 1(Gq=increases Ca2+), 2(Gi)
beta: 1&2 (Gs)

118
Q

how is NE synthesized? what are the major metabolites?

A

tyrosine –(tyrosine hydroxylase)–>DOPA –(AADC)–> DA –(dopamine beta hydroxylase)–> NE
-MHPG, VMA

119
Q

where is 5-HT found?

A

raphe nucleus

120
Q

are the 5-HT receptors ionotropic or metabotropic?

A

all metabotropic
-EXCEPT 5-HT3

121
Q

how is 5-HT synthesized? what is the major metabolite?

A

tryptophan –(tryp. hydroxylase)–> 5-HTP –(AADC)–> 5-HT
-5-HIAA

122
Q

what degrade ACh?

A

acetylcholinesterase

123
Q

how is ACh synthesized?

A

choline + acetyl CoA –(choline acetyltransferase)–> ACh

124
Q

what are the two types of receptors for ACh?

A

nicotinic
muscarinic

125
Q

what are nicotinic receptors? (characteristics, location)

A

found in PNS (skeletal muscle, autonomic ganglia)
-excitatory: Na+ and Ca2+ channels
-desensitizes: makes channel inactive
-depolarization block: R reaches a maximum efficacy

126
Q

what are muscarinic receptors? (characterisitics, location)

A

-excite and inhibit 2d messenger systems
-increases cAMP
-decreases phosphoionsitide activity
-G protein: K+ efflux

127
Q

what are two excitatory AAs?

A

glutamate
aspartate

128
Q

what are two inhibitory AAs?

A

GABA
glycine

129
Q

where is glutamate found?

A

cerebral cortex, hippocampus, cerebellum

130
Q

what can an increase of glutamate lead to?

A

excitotoxicity = cell death

131
Q

what is GABA degraded by?

A

aminotransferase
-through presynaptic and glial reuptake

132
Q

what are the two GABA receptors? what do they do, and are they ionotropic or metabotropic?

A

GABA(A): ionotropic, Cl- influx, allosteric binding
GABA(B): metabotropic, decreases cAMP, opens K+ channel

133
Q

how is GABA synthesized?

A

glutamine –(glutaminase)–> glutamate –(glutamic acid decarboxylase)–> GABA

134
Q

what are two types of neuropeptides?

A

substance P
endorphins

135
Q

what is substance P?

A

pain transmission, slow & long enduring pain

136
Q

what are endorphins?

A

bind at opioid receptors (mu, delta, kappa)
-enkephalins, naloxone insensitive

137
Q

what do antihistamines do?

A

stop the inflammatory response

138
Q

what NT is responsible for the sympathetic NS?

A

NE

139
Q

what are the lengths of the pre- and post- ganglia for the sympathetic NS? where are the ganglia located (near spinal cord or effector)?

A

short preganglia, long postganglia
-near the spinal cord

140
Q

what outflow does the sympathetic NS have? what is the strength and rapidity of the activation?

A

thoracolumbar outflow (lateral horns)
-strong and fast activation

141
Q

what NT is responsible for the parasympathetic NS?

A

ACh

142
Q

what are the lengths of the pre- and post- ganglia for the parasympathetic NS? where are the ganglia located (near spinal cord or effector)?

A

long preganglia, short postganglia
-near the effector

143
Q

what outflow does the parasympathetic NS have? what is the strength and rapidity of the activation?

A

craniosacral outflow
-slow and discrete activation (not all activate at same time)

144
Q

how many neurons do the adrenal glands have?

A

one neuron!

145
Q

what does the reticular activating system do? where does it get its signal from?

A

activates alertness
-inputs come from classical sensory afferents (sensory info)

146
Q

what are the cortical arousal streams of the reticular activating system? describe the process

A

Vental Stream (RF -> BF)
Dorsal Stream (RF -> thalamus -> BF)

147
Q

what increases arousal in the reticular activating system?

A

ACh and NE

148
Q

what decreases arousal in the reticular activating system?

A

5-HT

149
Q

what does GABA do to arousal in the reticular activating system?

A

can increase or decrease
-high GABA = low arousal

150
Q

what are nociceptors?

A

free nerve endings used in pain signaling
-three types (mechanical, thermal, chemical)

151
Q

what is the anterolateral system? names the two branches

A

the pathways of pain
-Two Branches: Sensory-discriminative (locus, intensity, type), Affective-motivational (emotion, Bx)

152
Q

what do 1st order sensory neurons do?

A

release glutamate and substance P
-dorsal root ganglia neurons

153
Q

what do 2nd order sensory neurons do?

A

send signal to anterolateral branches (PAG & thalmus->cortex)
-gray matter of dorsal horn

154
Q

what is behavioral analgesia?

A

decreases perceived pain, decrease in nociception
-in the supra-spinal!

155
Q

what receptors mediate analgesia?

A

opioid and non-opioid receptors

156
Q

what is a direct ANT of analgesia?

A

naloxone

157
Q

what is the descending analgesia circuit?

A

anterolateral branches -> PAG -> RN or LC -> spinal cord

158
Q

what neurons does PAG contain?

A

GABA, ACh, opioid

159
Q

what neurons does the spinal cord contain?

A

5-HT, NE, enkephalin

160
Q

what neurons directly inhibit neurons in pain circuits?

A

enkephalin
GABA

Drugs & Behavior (5 decks)

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