Cumulative Info (w/o Unit 4) Flashcards
(160 cards)
1
Q
what is pharmacology?
A
the study of drug
2
Q
what is psychopharmacology?
A
drugs that effect thinking, mood, and Bx
3
Q
what is neuropharmacology?
A
drugs that effect neurons and the NS
4
Q
what is neuropharmacology?
A
drug interaction with neurons and their effect of mood, thinking, and bx
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
6
Q
what are three functions of neurons?
A
transmit, intergrate, store
7
Q
what is the neural model?
A
sensory cell -> sensory neuron -> interneuron -> motor neuron -> effector
8
Q
what do sensory cells do?
A
transduction (turn environ. signal into a biochemical signal)
9
Q
what to effectors do?
A
muscles and glands that produce bx and excite/inhibit motor neurons
10
Q
what is specific drug effect?
A
drug-receptor interaction (alc binds to GABA-R and causes sleepiness)
11
Q
what is nonspecific drug effect?
A
environmental effects, individual differences (sex, weather, diet)
12
Q
what are the four different names for a drug?
A
chemical
generic
trade
street
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
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)
15
Q
what are the three different drug equivalences?
A
chemical
biological
clinical
16
Q
what is chemical equivalence?
A
same chemical compound
same drug effect
same systems
different drug names
17
Q
what is biological equivalence?
A
different chemical compound
same drug effect
same systems
18
Q
what is clinical equivalence?
A
different chemical compound
same drug effect
different systems
19
Q
Drugs are ____ and have ____ effects
A
variable, multiple
20
Q
how many drug schedules are there and what are they used to determine?
A
5 schedules
-determines abuse potential and medicinal value
21
Q
Schedule 1
A
-high abuse
-no medicinal value
-not prescribed
-heroin
22
Q
Schedule 2
A
-high abuse
-accepted medicinal value
-prescribed, but no refills
-cocaine
23
Q
Schedule 3, Schedule 4, Schedule 5
A
3: moderate abuse
4: low abuse
5: lowest abuse
5 refills over 6 months
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
25
what two things does animal testing test?
-carcinogenicity (cancer risk)
-teratogenicity (embryo affects)
26
how many human phases does a drug go through to get approved?
4 phases
27
what is phase 1 of human clinical trials? (years it takes, size of group, what is being tested)
safety & dosage
-1.5 yrs
-sm. group (20-100) healthy people
-how drug effects body
28
what is phase 2 of human clinical trials? (years it takes, size of group, what is being tested)
efficacy and side effects
-2 yrs
-medium group (100-1,000) diagnosed people
29
what is phase 3 of human clinical trials? (size of group, what is being tested)
efficacy and adverse rxns
-lg. group (1,000-3,000) diagnosed people
-appropriate dosage
30
what is phase 4 of human clinical trials? (years it takes, size of group, what is being tested)
real world impact
-ongoing and never stops
-safety monitoring
31
after which phase does the drug get approval?
after phase 3
32
what is pharmacokinetics?
what body does to drug (absorption, administration)
33
what is pharmacodynamics?
what drug does to body (drug effects)
34
what does is the difference between enteral and parenteral administration methods?
enteral: GI tract
parenteral: all other routes
35
what is the per Os (PO) administration method? (include kinetics)
-1st pass metabolism
-absorbed through gut membranes
-slow onset, low magnitude, long duration
36
what is the sublingual administration method? (absorption)
absorb through mucous membranes and glands (LSD)
37
what is the transbuccal administration method? (absorption)
absorb through mouth lining (chewing tobacco)
38
what is IV injection administration method? (include kinetics)
-does not cross membranes
-fastest onset, high magnitude, short duration
39
what is IM injection administration method? (include kinetics)
-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
40
what is the SC injection administration method? (include kinetics)
-under skin (insulin)
-slow onset
41
what is the IP injection administration method? (include kinetics)
-abdomen
-similar kinetics to IM (fairly fast onset)
42
what is inhalation administration method? (include kinetics)
-passes through capillary membrane in lungs (smoking)
-slower onset than IV (fairly fast onset though)
43
what is intranasal administration method? (include kinetics)
-passes through mucous membranes
-no 1st pass metabolism (bypasses BBB)
-slower onset than inhalation
44
list the onset peaks from highest to lowest (inhalation, SC, PO, IV, (IM,IP,intranasal))
IV (highest peak, highest magnitude, shortest duration)
Inhalation
IM,IP,Intranasal
SC
PO (lowest peak, lowest magnitude, longest duration)
45
when is absorption complete?
when concentration at target area = concentration at administration site
46
what are capillaries and what do they do?
-one cell thick w/ pores and spaces b/w cells
-exchange materials b/w blood and cells
-typically leaky
47
what is the blood-brain-barrier and what does it do?
-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
48
what happens when toxic neurons enter the BBB at the area postrema CTZ (chemical trigger zone)?
vomitting
49
what does ionization do to molecules?
decrease lipid solubility
-dependent on pH (acidic)
50
what does ion trapping do?
-traps drugs so it can't cross membranes
-prolongs drug effects (creates 'free' drug)
51
what are the characteristics of molecules best at absorption? (size, polarity, pKa/pH, ionization)
-small molecules
-lipid soluble (non-polar)
-low in ion-trapping
-pKa matches fluid pH
52
what is depot binding?
similar to ion trapping EXCEPT
-no ionization
-still decreases bioavailability of drug and creates more 'free' drug
53
what is nonselective binding?
competition for sites
-increases bioavailability of drug
54
what is half-life? what are the two types (describe them)?
-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
55
what are the two phases of biotransformation?
Phase 1: non-synthetic modification (reduction, oxidation, hydrolysis)
Phase 2: synthetic modification / adding something (conjugation, ion trapping, acetylation)
56
where does biotransformation take place?
liver
57
what are cytochrome P450's?
detoxification enzymes that oxidizes psychoactive drugs during phase 1 of biotransformation
58
what is enzyme induction?
creates more enzymes to reestablish homeostasis
-tolerance, brussel sprouts
59
what is enzyme inhibition?
lessens the effect of enzymes
-creates more 'free' drug
60
what does the kidney do to molecules?
ionizes them to be released as urine
-pH 4.5-7.5
61
what is the antidiuretic hormone (AHD)? what inhibits ADH?
ADH inhibits water excretion
-alc and caffeine inhibit ADH (causing more urination)
62
what is the effective dose? threshold dose?
dose that produces a biological response
-threshold dose: minimum response
63
what are the two types of dose-response curves?
% of population responding
response magnitude (mean response)
64
what is potency?
drug A has same effect as drug B but at a lower dose
-drug A is more potent
65
what is maximum efficacy?
drug B has a higher maximum efficacy due to a higher y-axis point
66
what is the equation for the therapeutic index? do bigger or small numbers mean it is more safe
LD50/ED50
-bigger number means it is more safe
67
what are three different things that can affect dose-response curves?
sex, age, tolerance
68
what are cumulative effects?
single drug
-repeated administration before drug is completely eliminated
-the effect decreases before drug is completely eliminated
69
what are additive effects?
multiple drug
-drugs with same effects (add together)
70
what are physiological effects?
multiple drug
-drugs with opposing effects (the difference)
71
what are potentiation effects?
multiple drug
-the whole is greater than the sum of products
-bigger than additive effects
72
what is tolerance?
decrease in response to same dose of drug
73
what is metabolic tolerance?
production of more enzyme (enzyme induction)
74
what is pharmacodynamic tolerance?
decreased NT synthesis
75
what is behavioral tolerance?
conditioned response (pavlovian conditioning)
76
what is acute tolerance?
decrease of effect b/w doses (nic hits)
77
what is cross tolerance?
tolerance to drugs that work by same mechanism (alc and phenobarbital)
78
what is sensitization?
increase response to same dose of drug
-due to repeated exposure to a stimulus
79
what is rate dependency?
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
what are the 6 steps of the synaptic transmission model?
1. precursor transport
2. synthesis
3. storage
4. release
5. activation
6. termination
81
what occurs during precursor transport (1)
NT at axon terminal
sm. peptide at soma
82
what occurs during synthesis (2)
enzymes and cofactors are loaded into axon terminal
83
what occurs during storage (3)
NT, ATP, GTP, Ca2+ stored in synaptic vesicles
84
what occurs during release (4)
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
what occurs during activation (5)
NT binds to receptor and changes conformation
86
what occurs during termination (6)
4 different ways
-diffusion
-enzymatic degradation
-reuptake
-autoreceptors
87
what is diffusion termination (6)
receptor becomes inactive
88
what is enzymatic degradation termination (6)
cuts up NT
89
what is reuptake termination (6)
active transport of NT out
-goes back to vesicle it came from
-OR degraded by an astrocyte / glial cell
90
what is autoreceptor termination (6)
binds NT on presynaptic cell
-decreases depolarization
-decreases NT release
91
what occurs at presynaptic facilitation? (K+, Ca2+ channels, NT release)
decreases K+ efflux so Ca2+ channels stay open, increase NT release
92
what occurs at presynaptic inhibition? (K+, Ca2+ channels, NT release)
increases K+ efflux so Ca2+ channels close, decreases NT release
93
what is affinity?
ability to bind to receptor
94
what is efficacy?
ability to activate receptor
95
what are some characteristics of ligand binding?
-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
what does direct mean?
at NT postsynaptic R
97
what does indirect mean?
at sites other than NT's binding site
98
what is an agonist?
mimics or increases NT effect
-affinity and efficacy
99
what is an antagonist?
blocks or decreases NT effect
-affinity, NO EFFICACY
100
what are competitive antagonists?
competes for same R site
-decreases potency (takes more of drug to produce same effect)
101
what are noncompetitive antagonists?
binds at different site but same R (allosteric binding)
-effects maximum response
102
what is an ionotropic receptor?
channel and binding site on same protein
-NT directly controls channel
-acute tolerance
103
what is a monotropic receptor?
channel and binding site in different proteins
-GTP required
-neuromodulation
104
explain the 2d messenger system of NE
beta adrenergic R
Gs
increases adenyly cyclase
increases cAMP
increases protein kinase A
105
explain the 2d messenger system of DA
D2 R
Gi
decreases adenylyl cyclase
decreases cAMP
decreases protein kinase A
106
where are monoamines found, released by, and the two types?
-found at axon terminals that bind at postsynaptic R
-released by action potentials
-types: catecholamines (1 ring) & indolamines (2 rings)
107
what are the catecholamine NT?
DA, NE, EPI
108
what are the indolamine NT?
5-HT, melatonin
109
how are all monoamines terminated?
monamine oxidase (MAO)
110
how are only catecholamines terminated?
catechol-O-methyltransferase (COMT)
111
what does reserpine do to monoamines?
blocks monoamine transporters
-decreases NT storage
-indirect ANT
112
where is DA found?
midbrain
113
what are the DA receptors?
D1: Gs proteins
D2: Gi proteins
114
what are the three ascending pathways in DA?
nigrostriatal (substantia nigra -> striatum) parkinson's disease
mesolimbic (VTA -> limbic)
mesocortical (VTA -> cortex)
115
how is DA synthesized? what is the major metabolite?
tyrosine --(tyrosine hydroxylase)--> DOPA --(AADC)-->DA
-homovanillic acid
116
where is NE found?
adrenal glands, locus coeruleus
117
what are the NE receptors?
alpha: 1(Gq=increases Ca2+), 2(Gi)
beta: 1&2 (Gs)
118
how is NE synthesized? what are the major metabolites?
tyrosine --(tyrosine hydroxylase)-->DOPA --(AADC)--> DA --(dopamine beta hydroxylase)--> NE
-MHPG, VMA
119
where is 5-HT found?
raphe nucleus
120
are the 5-HT receptors ionotropic or metabotropic?
all metabotropic
-EXCEPT 5-HT3
121
how is 5-HT synthesized? what is the major metabolite?
tryptophan --(tryp. hydroxylase)--> 5-HTP --(AADC)--> 5-HT
-5-HIAA
122
what degrade ACh?
acetylcholinesterase
123
how is ACh synthesized?
choline + acetyl CoA --(choline acetyltransferase)--> ACh
124
what are the two types of receptors for ACh?
nicotinic
muscarinic
125
what are nicotinic receptors? (characteristics, location)
found in PNS (skeletal muscle, autonomic ganglia)
-excitatory: Na+ and Ca2+ channels
-desensitizes: makes channel inactive
-depolarization block: R reaches a maximum efficacy
126
what are muscarinic receptors? (characterisitics, location)
-excite and inhibit 2d messenger systems
-increases cAMP
-decreases phosphoionsitide activity
-G protein: K+ efflux
127
what are two excitatory AAs?
glutamate
aspartate
128
what are two inhibitory AAs?
GABA
glycine
129
where is glutamate found?
cerebral cortex, hippocampus, cerebellum
130
what can an increase of glutamate lead to?
excitotoxicity = cell death
131
what is GABA degraded by?
aminotransferase
-through presynaptic and glial reuptake
132
what are the two GABA receptors? what do they do, and are they ionotropic or metabotropic?
GABA(A): ionotropic, Cl- influx, allosteric binding
GABA(B): metabotropic, decreases cAMP, opens K+ channel
133
how is GABA synthesized?
glutamine --(glutaminase)--> glutamate --(glutamic acid decarboxylase)--> GABA
134
what are two types of neuropeptides?
substance P
endorphins
135
what is substance P?
pain transmission, slow & long enduring pain
136
what are endorphins?
bind at opioid receptors (mu, delta, kappa)
-enkephalins, naloxone insensitive
137
what do antihistamines do?
stop the inflammatory response
138
what NT is responsible for the sympathetic NS?
NE
139
what are the lengths of the pre- and post- ganglia for the sympathetic NS? where are the ganglia located (near spinal cord or effector)?
short preganglia, long postganglia
-near the spinal cord
140
what outflow does the sympathetic NS have? what is the strength and rapidity of the activation?
thoracolumbar outflow (lateral horns)
-strong and fast activation
141
what NT is responsible for the parasympathetic NS?
ACh
142
what are the lengths of the pre- and post- ganglia for the parasympathetic NS? where are the ganglia located (near spinal cord or effector)?
long preganglia, short postganglia
-near the effector
143
what outflow does the parasympathetic NS have? what is the strength and rapidity of the activation?
craniosacral outflow
-slow and discrete activation (not all activate at same time)
144
how many neurons do the adrenal glands have?
one neuron!
145
what does the reticular activating system do? where does it get its signal from?
activates alertness
-inputs come from classical sensory afferents (sensory info)
146
what are the cortical arousal streams of the reticular activating system? describe the process
Vental Stream (RF -> BF)
Dorsal Stream (RF -> thalamus -> BF)
147
what increases arousal in the reticular activating system?
ACh and NE
148
what decreases arousal in the reticular activating system?
5-HT
149
what does GABA do to arousal in the reticular activating system?
can increase or decrease
-high GABA = low arousal
150
what are nociceptors?
free nerve endings used in pain signaling
-three types (mechanical, thermal, chemical)
151
what is the anterolateral system? names the two branches
the pathways of pain
-Two Branches: Sensory-discriminative (locus, intensity, type), Affective-motivational (emotion, Bx)
152
what do 1st order sensory neurons do?
release glutamate and substance P
-dorsal root ganglia neurons
153
what do 2nd order sensory neurons do?
send signal to anterolateral branches (PAG & thalmus->cortex)
-gray matter of dorsal horn
154
what is behavioral analgesia?
decreases perceived pain, decrease in nociception
-in the supra-spinal!
155
what receptors mediate analgesia?
opioid and non-opioid receptors
156
what is a direct ANT of analgesia?
naloxone
157
what is the descending analgesia circuit?
anterolateral branches -> PAG -> RN or LC -> spinal cord
158
what neurons does PAG contain?
GABA, ACh, opioid
159
what neurons does the spinal cord contain?
5-HT, NE, enkephalin
160
what neurons directly inhibit neurons in pain circuits?
enkephalin
GABA
