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Drugs & Behavior > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

what is the liver the main site for?

A

site of metabolism of nutrients (phase 1&2 of biotransformation)
-DETOXIFICTATION
-1st pass metabolism occurs here

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2
Q

what does 1st pass metabolism occur through in the liver?

A

through hepatic portal vein
-GI –> Liver

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3
Q

what type of enzymes does the liver contain to help maintain homeostasis?

A

microsomal enzymes

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4
Q

what do microsomal enzymes do?

A

-all-purpose binding sites (can bind several molecules in binding sites, not specific)

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5
Q

what family are the microsomal enzymes in the liver apart of?

A

cytochrome 450 super family
-over 50 different types

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6
Q

what does the cytochrome 450 family do?

A

oxidized psychoactive drugs in phase 1 of biotransformation
-antidepressants, morphine

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7
Q

what is enzyme induction?

A

creation of MORE enzymes to reestablish homeostasis
-with repeated use, it increases enzyme synthesis
-can be effected by diet

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8
Q

what type of food can create enzyme induction?

A

brussel sprouts

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9
Q

what is enzyme inhibition?

A

things that LESSEN the effectiveness of the enzyme
-decrease metabolism
-creates more ‘free’ drug
-can be effected by diet

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10
Q

what type of food can create enzyme inhibition?

A

grapefruit

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11
Q

which can contribute to tolerance, enzyme inhibition or enzyme induction?

A

enzyme induction

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12
Q

what is drug competition?

A

multiple drugs ‘fight’ for same sites and increase drug effects
-more ‘free’ drug

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13
Q

what do the kidneys do?

A

filters blood and removes toxins as urine (pH 4.5 - 7.5)

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14
Q

what is required for biotransformation and ion-trapping to occur in the kidneys?

A

ionization

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15
Q

what does the Koryak tribesman w/ Amanita muscaria mushroom proove?

A

proves that you can feel the effects of the drug a second time after being excreted as urine

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16
Q

how can ‘free’ drug stop someone from smoking?

A

when the compounds aren’t ionized (can be done through diet), the nicotine keeps circulating as the ‘free’ drug
-you don’t feel the effects but the drug is still circulating, lessening the cravings
-stress can stop the ‘free’ drug from being free and increase cravings

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17
Q

what does ADH (antiduretic hormone) do and what is a common every-day example with ADH?

A

inhibits excretion of water
-alc and caffeine INHIBIT ADH causing you to pee more and become dehydrated

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18
Q

how else can a drug be excreted besides through the kidneys?

A

-lungs (breathing alc)
-breast milk (acidic so it ion traps alkaloids)
-skin
-salvia
-bile in feces

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19
Q

what is the general relationship between dose and effects?

A

increasing dose, increases effects
-only to a max, then it decrease due to toxicity
-deals with pharmacodynamics (drug interaction w/ target)

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20
Q

what are 3 common factors that can impact the dose and effect relationship?

A

size/weight
pharmacokinetics
pharmacodynamics

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21
Q

how does pharmacokinetics impact the dose and effect relationship?

A

-protein binding
-cyt 450 differences
-acetylation in phase 2 (rats > humans > dogs)
-conjugation in phase 2 (humans > cats)

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22
Q

how does pharmacodynamics impact the does and effect relationship?

A

-NT and receptor distributions vary

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23
Q

how does weight impact the dose and effect relationship?

A

-amount of drug per body weight (mg/kg)
-how much it takes to achieve equal blood conc/

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24
Q

what does an effective dose produce?

A

produces a biological response

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25
Q

what is threshold in dose?

A

minimum biological response

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26
Q

what are the two types of group-dose relationship curves?

A

-% of pop. responding
-response magnitude

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27
Q

when graphing side effects, are they all together on the same curve?

A

no, each side effect has its own curve

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28
Q

which is greater, % of population affected or threshold response?

A

% population affected

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29
Q

what is the response magnitude?

A

the mean % of max response

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30
Q

what is the symbol for effective dose?

A

EDn
n=% of pop. with effective dose

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31
Q

what is the symbol for lethal dose?

A

LDn
n=% of pop.with lethal dose

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32
Q

what is potency?

A

measured amount needed to produce a certain response
-relative term
-Drug A has the same effect as Drug B but at a lower dose

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33
Q

what happens when more of drug is added after max response?

A

no increase of effects
-might create more side effects

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34
Q

what curve would have a higher potency?

A

lower drug dose with a lower % responding

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35
Q

what curve would have greater max efficacy?

A

higher % responding at a high dose

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36
Q

what does the dose-response curve look at?

A

represent mean for a group

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37
Q

what is standard error?

A

gives an idea of response range for magnitude of response curve
-PROBABILITY not exactness

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38
Q

what is the therapeutic index?

A

effect of dose and % of population responding
-margin of safety

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39
Q

what is the equation for therapeutic index?

A

LD50 / ED50

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40
Q

should a big or small number be calculated when the drug is safe when using the therapeutic index?

A

big number
~100

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41
Q

when graphing therapeutic index, do you want the LD and ED lines close together or far apart?

A

far apart
-you want LD (lethality) to occur at much higher dose

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42
Q

what does the slope tell you?

A

how big the change in effects are when you increase dose

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43
Q

what does a steep slope tell you?

A

large y-axis (R) change

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44
Q

what is the type of single drug interaction?

A

cumulative effects

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45
Q

what are the types of multiple drug (2+) interactions?

A

additive
physiological antagonism
potentiation

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46
Q

what is a cumulative single drug interaction?

A

repeated administration before drug is completely eliminated
-increase of drug in blood conc.
-half life is very relevant
-subjective effects

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47
Q

what are subjective effects?

A

effect goes away but drug is still high in blood conc.

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48
Q

what are additive effects?

A

two different drugs with same effect
-add effects of drugs together

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49
Q

what category of drugs are commonly associated with additive effects?

A

CNS depressants

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50
Q

what is physiological antagonism?

A

two different drugs with opposing effects

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51
Q

what is a common example of physiological antagonism?

A

alc and caffeine

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52
Q

what is potentiation in multiple drug interactions?

A

synergistic (the whole is more than the sum of its parts)
-bigger than additive effects
-hepatoxicity

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53
Q

what is hepatoxicity?

A

nontoxic + toxic = very toxic
toxic + toxic = super duper toxic

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54
Q

what causes potentiation in multiple drug interactions?

A

due to a change in metabolism (biotransformation) or depot binding

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55
Q

what is tolerance?

A

repeated use of same dose of drug (chronic use) decreases the response
-compensatory and homeostatic responses

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56
Q

what is metabolic tolerance (drug disposition)?

A

enzyme induction: more enzyme produced to break down drug
-creates a smaller response

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57
Q

what is pharmacodynamic tolerance (neuronal)?

A

modifications of NT or the NT receptor
-decreases NT synthesis and down-regulates receptors

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58
Q

what is behavioral tolerance (associative)?

A

Pavlovian (classical) conditioning
-conditioned compensatory responses

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59
Q

what is acute tolerance (tachyphylaxis)?

A

occurs b/w 1st and 2nd dose (first nic hit is better than 2nd hit)
-rapid and transient (brief)
-due to NT depletion and the receptors being occupied

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60
Q

what is cross tolerance?

A

tolerance to drugs that work by the same mechanism

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61
Q

what category of drugs is tolerance associated with?

A

depressants

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62
Q

what is sensitization?

A

increase response to same dose of drug
-opposite of tolerance

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63
Q

cocaine and amphetamine in sensitization

A

increase motor activation, reward/motivation

64
Q

what is sensitization NOT explained by?

A

homeostasis

65
Q

what are nonspecific drug factors?

A

things that influence drug effects based on individual differences other than drug action

66
Q

what are the four classes nonspecific drug factors?

A

organism
environment
psychological
task (rate-dependent effects)

67
Q

what are nonspecific factors based on organisms?

A

weight, sex, age, disease, nutrition, biological rhythms, hormonal states, intraspecies differences, interspecies differences

68
Q

what is a synapse and what are the two types?

A

communication b/w neurons
-electrical and chemical

69
Q

what are the four types of chemical synapse and what are they?

A

ligand/receptor
axodendritic: b/w axon terminal and dendrite
axosomatic: axon directly on soma
axoaxonic: involves a third neuron

70
Q

what are the six parts to the synaptic transmission model?

A

precursor transport
NT synthesis
storage
release
activation
termination

71
Q

what happens at precursor transport?

A

-NT is loaded into axon terminal
-peptide NT at soma

72
Q

what drives precursor transport?

A

active transport

73
Q

what happens during NT synthesis?

A

enzymes and cofactors are loaded into axon terminal
-peptide still at soma
-NT still at axon terminal

74
Q

what are enzymes?

A

protein that catalyzes a rxn

75
Q

what are cofactors?

A

donate a portion of itself to the process and becomes apart of NT

76
Q

during storage, where are the molecules stored in and how are they loaded?

A

stored in synaptic vesicles and loaded by active transport

77
Q

what are the molecules in the synaptic vesicles?

A

NT, nucleotides (ATP, GTP), and Ca2+

78
Q

what are the synaptic vesicles made out of?

A

the same lipid bilayer as the cell membrane

79
Q

what are the membrane proteins of synaptic vesicles?

A

transporter proteins, docking proteins, and ATPase

80
Q

what molecules does a cholinergic vesicle contain?

A

ATP, GTP, acetylcholine, and Ca2+

81
Q

what process occurs during release?

A

exocytosis

82
Q

what initiates exocytosis?

A

action potential

83
Q

how are the reserve pools anchored?

A

anchored to axon terminal by synapsin-actin linking

84
Q

what is the step by step of release?

A

-vesicle next to synapse
-action potential reaches vesicle
-Ca2+ INFLUX occurs
-Ca2+ opens voltage-gated channels
-Ca2+ binds to calmodulin
-this activates CaMK2
-CaMK2 phosphorylates synapsin
-synapsin dissociates from vesicle
-vesicles are now free floating and diffuse toward synaptic membrane

85
Q

what fuses the vesicles to the postsynaptic membrane?

A

SNAPs/NSF
SNARES
Synaptotagmin

86
Q

what do SNAPs and NSF do?

A

prime for fusion and make sure everything is ready

87
Q

what are the types of SNAPs and NSFs?

A

SNAPS: alpha, beta, gamma
NSF: ATPase

88
Q

what do SNAREs do?

A

it is the SNAP receptor that pulls membranes together and intertwines

89
Q

type of vesicle and membrane SNARE?

A

vesicle: synaptobrevin
membrane: syntaxin, SNAP-25 (not a SNAP)

90
Q

what does synaptotagmin do?

A

binds Ca2+ and fuses it all together?

91
Q

what are the steps of release when the vesicle fuses with membrane?

A

-SNAPs/NSF ensure the membrane is ready
-vesicle docks
-SNAREs pull membranes together and intertwine
-Ca2+ binds to synaptotagmin
-Ca bound synaptotagmin fuses with membrane by binding to SNAREs and plasma membrane

92
Q

what occurs at activation?

A

-NT binds to receptor by diffusing from high conc/ to low con.
-binding changes the conformation of the receptor which changes the post synaptic cell (open/close channel, activate 2d messenger)

93
Q

what are the two types of receptors that a NT binds to a the post synaptic cell?

A

ionotropic
metatropic

94
Q

what are ionotropic receptors?

A

channel and binding sites are integrated in same protein
-changes EPSP or IPSP
-rapid desensitization
-acute tolerance (tachyphylaxis)

95
Q

what are metabotropic receptors?

A

channel and binding sties are in different proteins
-G protein-coupled receptors
-requires GTP
-has neuromodulation (after the NT isn’t binding, it makes adjustments over time)

96
Q

which receptor, ionotropic or metabotropic, is fast and transient (brief)?

A

ionotropic receptors

97
Q

what are the four ways of termination?

A

diffusion
enzymatic degradation
reuptake
autoreceptors

98
Q

what is diffusion termination?

A

-ligand and receptor are bound for temporary amount of time
-receptor becomes inactive and can associate with other ligands

99
Q

what is enzymatic degradation?

A

cuts up NT so it can’t fit in binding sites

100
Q

what is reuptake termination?

A

-metabolic pumps pump NT back into axon terminal to possibly go back to a vesicles or a glial cell
-if it enters a glial cell (astrocyte) it degrades the NT to be recycled

101
Q

what is autoreceptor termination?

A

binds same NT they release on the presynaptic cell
-different receptor type and affinity though

102
Q

what are the two types of autoreceptors?

A

terminal autoreceptor
somatodendritic autoreceptor

103
Q

what is a terminal autoreceptor?

A

on the presynaptic terminal
-decrease depolarization by manipulating Ca and K channels
-creates an EFFLUX of K+
-decreases NT release

104
Q

what is a somatodendritic autoreceptor?

A

decreases action potential rate
-decreases NT release

105
Q

for termination to occur, you must have a ___ signal

A

discrete

106
Q

what happens if channels are continually open during termination?

A

the ions are at equilibrium
-membrane is no longer polarized and no EPSP/IPSP

107
Q

what does a depolarization block do?

A

disrupts neural communication and makes the synapse nonfunctional

108
Q

what are heteroreceptors and which type of synapse are they found in?

A

involving a third neuron
-in axoaxonic synapses

109
Q

what two functions can axoaxonic synapses do?

A

presynaptic facilitation
presynaptic inhibition

110
Q

what is presynaptic facilitation?

A

keeps membrane depolarized
-decreases K+ efflux so the K+ molecules can’t escape
-axon terminal stays depolarized and Ca2+ channels open
-increasing NT release

111
Q

what is presynaptic inhibition?

A

-increases K+ efflux
-Ca2+ channels close due to Ca2+ influx
-decreasing NT release

112
Q

what is a binding site?

A

ligand and receptor interaction

113
Q

what is affinity?

A

attraction and ability to bind receptor
-physically and electrically

114
Q

what is efficacy?

A

ability to activate receptor and initiate a biological action

115
Q

drugs can ___ or ___ a NT message

A

mimic, block

116
Q

what is direct action?

A

what happens at NT postsynaptic receptor

117
Q

what is indirect action?

A

what happens at sites other than the NT binding site

118
Q

what is an agonist?

A

mimics or increases NT effects
-AFFINITY and EFFICACY (binds receptor and activates)

119
Q

what is an antagonist (ANT)?

A

blocks or decreases NT effects
-only AFFINITY (only binds to receptor)

120
Q

what is a direct agonst?

A

binds to NT receptor and activates it

121
Q

what is a direct antagonist?

A

binds to same NT site and takes up a spot so an agonist can’t bind
-does not activate receptor

122
Q

what is an indirect agonist/antagonist?

A

affects NT metabolism, storage, release, reuptake, etc.

123
Q

what is a competitive antagonist?

A

competes for same site and whoever gets their first gets to bind
-decreases potency
-takes more drug to produce same effect

124
Q

what is a noncompetitive antagonist?

A

binding occurs at a different site on the receptor (allosteric binding)
-disturbs membrane or other intracellular effects
-example of indirect antagonists

125
Q

what does noncompetitve antagonist affect on a curve?

A

the max. response produced

126
Q

what is allosteric interactions?

A

binds at a different site but on same receptor
-potentiation opens the channel more

127
Q

what is a partial agonist?

A

channel opens part way producing a weaker NT effect
-still activates receptor

128
Q

what is an inverse agonist?

A

creates opposite effect of NT and completely closes channel
-still activates receptor

129
Q

what is activated when a ligand binds a receptor?

A

activates EPSP / IPSP or a 2nd messenger

130
Q

can the same NT bind a physically different receptor?

A

yes!
-it has multiple it can bind to
-it binds on a different part of the NT
-it still is specific for certain ones though

131
Q

what determines how well the receptor can be activated?

A

the physical fit

132
Q

which form is more active, levo or dextro?

A

LEVO (left)

133
Q

what is affected when you change the structure of the drug?

A

affinity, potency, and which receptors it can bind to

134
Q

why can drugs have multiple effects?

A

it can bind to a variety of receptors

135
Q

what does SSRI stand for?

A

selective serotonin reuptake inhibitor

136
Q

what does more plus signs mean when talking about a drug and its SSRI ability?

A

the more active and stronger affinity

137
Q

what are G-proteins?

A

G-proteins are a transducer

138
Q

what are the two types of G-proteins and what do they do?

A

Gs: activate/increase activity
Gi: inhibit/decrease activity

139
Q

what are G protein-gated ion channels?

A

receptor is separate from the effector and indirectly controls the channel

140
Q

what is the speed of G protein-gated ion channels?

A

relatively fast
-slower than ionotropic though

141
Q

what are 2nd messenger systems?

A

-effects are slow but long lasting
-converts molecule to make the 2nd messenger (extracellular signal)

142
Q

what is the 1st messenger?

A

NT
-external signal

143
Q

what are the membrane associated proteins/components?

A

-receptor proteins
-transducer (transfers)
-primary effector

144
Q

what is an example of an intracellular messenger?

A

2d messenger
-communicates with a protein kinase or another effector (secondary effector)

145
Q

what are the 2d messengers?

A

cyclic nucleotides
phosphoinositol
Ca2+ (CaMK)

146
Q

what are the cyclic nucleotides and what is their secondary effector?

A

cAMP -> PKA
cGMP -> PKG

147
Q

what are the phosphoinositol 2d messengers and what is their secondary effector?

A

DAG and IP3 -> PKC
-increases Ca2+ inside the cell

148
Q

what is the beta-adrenergic transducer?

A

G2

149
Q

what is the beta-adrenergic primary effector?

A

increase of adenylyl cyclase

150
Q

what is the secondary messenger and secondary effector of beta-adrenergic receptor?

A

increase of cAMP -> increase of PKA

151
Q

what is the transducer of the D2 receptor?

A

Gi

152
Q

what is the primary effector of the D2 receptor?

A

decrease of adenylyl cyclase

153
Q

what is the secondary messenger and secondary effector of the D2 receptor?

A

decrease cAMP -> decrease of PKA

154
Q

what do protein kinases do?

A

phosphorylates

155
Q

what do protein phosphatases do?

A

dephosphorylates

156
Q

how does the cell modulate gene expression?

A

through transcriptional factors
-can increase or decrease transcription

Drugs & Behavior (5 decks)

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