Flashcards
DBB Midterm Review - Important Terms part 1
Cards in this deck (200)
- 1neuronnerve cell
- 2glia(glial cells)
support cells
speed up neuronal communication without any electrical signals
~100-300 billion
2 main types in CNS: astrocytes and oligodendrocytes - 3CNSCentral Nervous System
(counterpart of Peripheral NS)
where the action happens --> primary drug effects
brain + spinal cord - 4PNSPeripheral Nervous System
everything (all nerves/parts of cells) the CNS is NOT
more than in the CNS
many in gut
live in gangs (ganglia) - 5Spinal cordbody part (spine) part of the CNS
sends sensory information from body to brain
sends motor information from brain to body - 6nerveneuron
building block of nervous system - 7ganglionnerve cell cluster in ANS
- 8somatic NS1/2 of division of PNS
sensation from muscles, skin, sensory organs + voluntary movement - 9autonomic NS2/2 of division of PNS
regulates the internal environment (digestion, blood pressure, temperature; intestines, heart, glands)
serve most organs of the body - 10sympatheticpart of autonomic division of PNS
energy expenditure
"fight or flight"
prepare for action
acetylcholine + adrenaline (epinephrine) - 11—sympathetic NS
part of autonomic division of PNS - 12parasympatheticpart of autonomic division of PNS
dominant during REST
conserves and stores energy
always acetylcholine (NT) - 13—parasympathetic NS
part of autonomic division of PNS
- 14dorsaltop of head
back of spine - 15ventralbottom of head
front of spine - 16anteriorfront of brain
- 17posteriorback of brain
- 18superiortop of brain
- 19inferiorbottom of brain
- 20lateralaway from spine
- 21medialcenter/toward spine
- 22dorsal root of spinal cordcontain cell bodies of sensory neurons
located in posterior root of spinal cord - 23ventral root of spinal cordefferent motor root of spinal cord
found w/in gray matter - 24brain stem1/3 division of brain
organized in nuclei (neuron clusters)
imp. nuclei produce NTs
made of medulla, pons, and midbrain (relay station of spinal cord)
control many basic reflexes
Heart rate/Blood pressure/Breathing rate Gastrointestinal functioning/vomiting
Sleep/wakefulness/alertness - 25ponscontains Raphe nuclei
produces Serotonin (affected by mdma, SSRIs, LSD)
contains Locus Coeruleus
produces Norepinephrine (aka noradrenaline; affected by stimulants) - 26midbraincontains Substantia Nigra/Ventral Tegmental Area
reward center
produces Dopamine (affected by cocaine, meth, all others)
Movement vs. REWARD - 27ventral tegmental area/substantia nigrareward center of brain
produce DA
located in midbrain
movement & reward - 28cerebellum2/3 of major division of brain
heavily connected to brain stem
sensorimotor coordination
integration of movement & stability/posture
affected by alcohol - 29forebrain3/3 of major division of brain
made up of 4 parts
cerebral cortex
limbic system
basal ganglia
diencephalon - 30diencephalon1/4 of forebrain
contains hypothalamus and thalamus - 31hypothalamus1/2 of diencephalon
Internal environment (control ANS)
Drives (hunger/satiety)
Pituitary gland (hormonal output) - 32thalamus2/2 part of diencephalon
Receives all sensory & motor input
Processes, and sends to cortex (e.g., vision) - 33basal ganglia2/4 of forebrain
contains Globus pallidus
contains Striatum:
– Putamen
– Caudate
– Dorsal vs. VENTRAL
– Motion vs. REWARD
– Targets of dopamine (VTA/SN) - 34limbic system3/4 of forebrain
contains Amygdala and Hippocampus - 35amygdala1/2 of limbic system
Emotion/mood, alerting, salience and fear
– Ex: beta-blockers, alcohol - 36hippocampus2/2 of limbic system
Long term and spatial memory
Rich in receptors for THC - 37cerebral cortex4/4 of forebrain
contains 4 lobes/cortexes: frontal, parietal, occipital, and temporal
Conscious experience!!
Receive sensory from thalamus
“Primary” sensory area - 38frontal cortex/lobe1/4 of cerebral cortex
Higher cognition: Language, control,
working memory, decision making - 39temporal cortex/lobe2/4 of cerebral cortex
hearing and some sight - 40parietal cortex/lobe3/4 of cerebral cortex
process sensory information (taste, temp, touch) - 41occipital cortex/lobe4/4 of cerebral cortex
processes visual information - 42sulcusa groove or furrow on the surface of the brain
Gyri and sulci create the folded appearance of the brain - 43cortical layers(related to cerebral cortex)
differ in type, density, arrangement
Functional significance? Probably complexity - 44gyrusa ridge on the cerebral cortex
Gyri and sulci create the folded appearance of the brain - 45astrocytesstar-shaped glial (support) cells in the CNS
concerned w/ the maintenance of the blood–brain barrier - 46oligodendrocytesglial (support) cell that produces myelin in the CNS
- 47myelinwhite matter that surround neurons and improves the speed of impulses
- 48somacell body of neuron
- 49axoncontain vesicles at axon terminal that are full of NTs which are sent to other neurons
surrounded by glial cells (myelin sheath, nodes of ranvier [gap b/w sheaths], white matter) - 50dendritepart of neuron that receives NTs
- 51axon hillockwhere summation/integration happens
until membrane threshold at AH crosses -50mV (then all-or-none action potential w/in cell happens) - 52nodes of ranviergap b/w myelin sheaths
- 53synapsegap b/w neurons that NTs cross
where most drugs exert their action - 54gray matternuclei that perform the processing role of the brain stem
- 55white matterconducts nerve signals within the brain stem and to the spinal cord and other regions of the brain
carry nerve impulses b/w neurons - 56axodendritic synapsewhere the pre-synaptic neuron releases NTS onto the dendrite of the post-syn neuron
- 57axosomatic synapsewhere the pre-synaptic neuron releases NTS onto the soma of the post-syn neuron
- 58axoaxonic synapsewhere the pre-synaptic neuron releases NTS onto the axon of the post-syn neuron
less common than axodendritic or axosomatic - 59presynaptic cell/neuronthe one that releases the NTs onto the next cell
- 60post-synaptic cell/neuronthe one that receives the NTS released from the previous cell
- 61synaptic cleftthe gap b/w neurons
where drug action happens - 62membraneneuron's skin/coat
the lipid bilayer that is selectively permeable
stops ions from passing freely in/out of neuron - 63ionscharged particles that affect mechanisms in and out of the cell
- 64resting membrane potentialthe state of a neuron's membrane at rest
neuron is polarized
charge inside is ALWAYS more (-) than outside
charge = -65 to -70 mV
Membrane doesn’t let particles move freely = keeps them at a disequilibrium - 65polarizationthe difference between the negatively charged neuron and the more positively charged outside
When a neuron is not stimulated — it's just sitting with no impulse to carry or transmit — its membrane is polarized - 66ion channelone of the mechanisms by which ions travel in/out of neuron --> selective permeability
protein that lives in the membrane
allow ions to diffuse down conc. gradient
closed = no ion flow
open = ion flow
has 3 types (resting, voltage-dependent, ligand-dependent) - 67transporter/pumpspecific proteins in the cell membrane that transport molecules into and out of the cell
e.g., proteins that remove NTs from the synaptic cleft following their release
3 Na+ out, 2 K+ in - 68voltage-dependent2/3 of ion channels/gates
type of ion channel that opens if at a certain voltage - 69resting channels1/3 of ion channels/gates
open at resting membrane potential
open to K+ only - 70ligand-dependent ("receptors")3/3 of ion channels/gates
needs NTs to bind to it for it to open - 71concentration gradientdifference in the amt. or conc. of a substance on each side of a bio barrier, such as the cell membrane
- 72electrostatic pressure (opposites attract)force drawing an ion to either side of the cell membrane in an attempt to balance or neutralize ionic charges
- 73depolarizationchange in membrane potential making the inside of the cell more positive
- 74hyperpolarizationact of making the inside of a cell more negative relative to the resting potential, reducing the likelihood that the cell will fire an action potential
- 75IPSPinhibitory post-synaptic potential
hyperpolarizing responses of a postsynaptic cell that result from NTs binding to specific receptors on the cell.
IPSPs move the membrane potential farther from the threshold for firing, hence decrease the likelihood of an action potential - 76EPSPexcitatory post-synaptic potential
small localized membrane depolarization of a postsynaptic neuron that results from NTs binding to specific receptors on the cell
EPSPs move the membrane potential closer to the threshold for firing - 77summation/integrationprocess at the axon hillock whereby several small depolarizations or hyperpolarizations will add together to create one large change in membrane potential
simultaneous depolarizations and hyperpolarizations will cancel each other out - 78thresholdmembrane potential, typically -50mV, at which voltage-gated Na+ channels will open, generating an action potential
- 79action potentialrapid change in electrical signal that is transmitted down the axon
how information is sent within the neuron
once the threshold is met at -50mV an all or none response is initiated
Na+ ion channels open and Na+ rushes in, depolarizing the neuron
peak reached at +40mV.
then Na+ channels close and experience refractory period
then K+ channels open and the cell becomes negative again - 80saltatory conductionmode of action potential conduction along a myelinated neuron characterized by jumps from one node of Ranvier to the next
where voltage-gated Na+ channels open initiating Action Potential.
Na+ spreads rapidly to the NEXT NODE – rapidly depolarizing it to threshold – opening Na+ channels, triggering the Action Potential - 81synaptic vesiclessac-like structures located in the axon terminal that are filled with molecules of NT
- 82exocytosiswhen synaptic vesicles fuse with the membrane, causing a release of NTs into the synaptic cleft
- 83neurotransmitterchemical substance released by a neuron to comm with another cell, which may be a different neuron, a muscle cell, or a hormone-producing cell in an endocrine gland
synthesized in neurons
packaged in vesicles in axon terminal
CENTRAL TO DRUG ACTION - 84neuropeptidepart of 1/2 of structural class of NT
(non-classic NT)
small proteins (3-40 amino acids long) in the NS that act as NTs - 85classic/small molecule1/2 of structural class of NT
acetylcholine, amino acids, purines, monoamines
DA, 5-HT, ACh, glutamate, GABA, ATP - 86acetylcholinea type of classic NT
affected by nicotine/cigarettes - 87amino acidsa type of classic NT
also essential building blocks of proteins
glutamate - Special K, DXM
GABA - alcohol
aspartate, glycine - 88purinea type of classic NT
ATP - coffee, chocolate - 89monoaminea type of classic NT
DA - stimulants, all drugs abused by ppl
5-HT - SSRIs, MDMA, LSD
norepinephrine, epinephrine - 90small vesicleswhere small molecules, such as acetylcholine (ACh) or dopamine are packaged
released by exocytosis at active zones associated with Ca2+ channels - 91big (or large) vesicleswhere large molecules made up of chains of amino acids are packaged
can also contain small molecules
released by exocytosis generally anywhere from the presynaptic membrane - 92excitatory NTNTs that are more likely to make the postsynaptic cell fire
NT action depends on receptor beh - 93inhibitory NTNTs that are less likely to make the post synaptic cell fire
NT action depends on receptor beh - 94neuromodulatorchemicals that don't follow the typical NT model
they may regulate NT activity or act at distant sites from their point of release
e.g., 5-HT - 95ionotropic receptor1/2 of type of receptors
shares def. w/ ligand-gated ion channels
--> open an ion channel thru which an ion can flow
have 4-5 subunits
Form an an ion channel (Na+, Ca2+, CI-)
– Channel is closed until NT binds [1]
– NT binding opens ion channel RAPIDLY [2]
effects = depolarization
faster than metabotropic - 96metabotropic receptors2/2 of type of receptors
not made of sub units like ionotropic Rs
made of long chain that spirals in and out
and has parts in and out of membrane
linked to a G protein (G protein can detach from receptor and indirectly open
ion channels that are ligand-gated [g protein ligand gated channel])
slower and more long-lasting than ionotropic - 97G proteinspecific membrane proteins that are necessary for NT signaling by metabotropic receptors.
regulate ion channels or effector enzymes involved in the synthesis or breakdown of second messengers, ultimately causing biochemical or physiological changes in the postsynaptic cell
once NT binds to receptor, there is a change in the receptor that results
in the detachment of the G protein (due to chemical changes in receptor).
the effect of the receptor depends on which ion channel its G protein act
upon (inside the neuron) - 98second messengerssubstance that, when activated by signaling molecules bound to receptors in the cell membrane, will initiate biochemical processes within the cell
Ca2+ often acts as second messenger - 99autoreceptorsOn presynaptic neuron
For the NT produced by it
Negative feedback (when the release turns too high, then autoR turns off its own release of NT)
Reduce own synthesis and release - 100reuptakewhere NT is taken up by neuron that released it
typically back to presynaptic neuron
reuptake transporters - proteins on the membrane
Just move NTs into cell - always outside to inside, but no other changes
then Repackaged and enzymatically broken down - 101enzymatic degradationNT meets enzyme molecules
Lead to chemical breakdown of NT
Create inactive metabolites/by products
Metabolites may be resynthesized into NTs - 102agonistsubstances that activate a receptor like a NT
enhance/mimic NT action - 103antagonistsubstances that block receptors
block NT action - 104glutamatemajor EXCITATORY NT --> EPSPs
amino acid NT
Critical roles in sensory, motor, cognitive function, learning, SYNAPTIC PLASTICITY, LTP, cell death
increase glutamate = stimulation
decrease glutamate = sedation - 105gluta-"mate"glutaMATE is stimulatory
important for synaptic plasticity and LTP
- 106glutamate affecting drugsAlcohol
DXM
PCP
Ketamine
Memantine
others - 107Doogie mice experimentmice genetically engineered to overexpress NMDA receptor subunits
More efficient NMDA receptor
more glu-based excitation
1. Mice see objects A & B
2. After delay, see objects A & C
(FYI: Mice look at objects longer when they are new)
3. Measure looking time (DV)
4. If good memory – A is old, look at C more
5. If bad memory – both seem new, look at both - 108—Results: Doogie mice have better memory!
Remember A for a full week! (look at A less than they look at C)
Increased glu binding @ NMDA = better memory
mice are smart but more PAIN-SENSITIVE
Too much glu is toxic –> “excito-toxicity”
- 109Dangers of glutamateincreased Pain-sensitivity
excito-toxicity
responsible for alcohol withdrawal symptoms
--> most dangerous form of drug w/drawal - 110Gamma Aminobutyric Acid – GABAmajor INHIBITORY NT --> IPSPs
amino acid NT
Synthesized from glutamate
pro GABA = inhibitory
block GABA = excitatory
10-40% of neurons produce/release GABA
e.g., cerebral cortex, hippocampus, substantia nigra - 111GABA-ergic drugsALCOHOL (alc = GABA agonist)
Valium, Xanex, Ativan, Klonopin
Anesthetics - 112—represents effects of pro-GABA drugs
sedation
- 113GABA(B) receptormetabotropic
opens K+ channels, lets K+ out -->
hyperpolarization
Inhibits second messenger (G protein) formation
SLOWWWW - 114GABA(A) receptorionotropic
allows CI- in --> FAST hyperpolarization
(even more when already depolarized)
Subunit have several locks (binding sites)
ALL modulate the effect of GABA at GABA(A)
Effects: Anxiolytic, sedative, relaxant, hypnotic... - 115—Drugs can bind to GABA(A) receptor subunits
Don’t activate -- they modulate
Enhance GABA @ GABA(A) = increase inhibition
- 116glutamate elimination methodRe-uptake into glutamate-producing neurons (transporter in axon terminal takes up glutamate)
Enzymatic degradation
Uptake by ASTROCYTES into glial cells
(enzymatic transformation)
1. Astro takes glutamate
2. Turns glutamate to glutamine
3. Pumps glutamine out
4. Neurons takes glutamine
5. Turns it into glutamate
6. Neuron repackages glutamate
7. Etc. - 117glutamineprecursor of the transmitter-related glutamate
part of the process for glutamate elimination - 118receptor subtypesgroup of RECEPTORS that RESPOND to the SAME NT but that differ from each other to varying degrees with respect to their structure, signaling mechanisms, and pharmacology
- 119AMPA receptoran ionotropic glu receptor selective for the synthetic amino acid agonist AMPA
allow Na+ into cell - 120Kainate receptorionotropic glu receptor selective for the agonist kainic acid
allow Na+ into cell - 121NMDA receptorionotropic glu receptor selective for the agonist NMDA
To open:
1. Requires Glu binding
2. Requires CO-AGONIST Glycine/D-Serine
3. Requires depolarization in post-syn
THEN: Mg2+ block moves out of receptor
Channel allows Na+ & Ca2+
– Second messenger - 122—resting state of NMDA glu receptor
To open:
1. Requires Glu binding
2. Requires co-agonist Glycine/D-Serine
3. Requires depolarization
- 123—depolarized state of NMDA glu receptor
after it's depolarized,
THEN: Mg2+ moves out of receptor
Channel allows Na+ & Ca2+
– Second messenger
- 124secondary siteswho knows???
- 125acetylcholine (cholinergic)classic NT involved w/ CNS and PNS
localized production, wide distribution
Mostly excitatory
Burst of Ach @ neuromuscular junction --> muscle contraction in SNS
– Parasympathetic activation (rest and digest) in ANS
– In brain: Sensory perception; learning, MEMORY, and ATTENTION; behavioral AROUSAL, and REM
synthesized by the cholinergic neurons
target of many of the deadliest neurotoxins - 126nicotinic receptor1/2 of ACh receptors
nicotine also binds to it - 127muscarinic receptor2/2 of ACh receptors
muscarine also binds to it - 128acetylcholinesterase (AChE)primary way ACh is eliminated
AChE = OFF command for muscle contraction
In presynaptic cell (excess)
On post-synaptic cell (release)
Choline is reuptaken (choline = byproduct of degradation)
Target of action of several drugs - 129what happens if you degrade AChE?you have more ACh
- 130if you degrade AChE, would you have less ACh binding or more ACh binding?more ACh binding
- 131is it dangerous for too much AChE to be broken down? why or why not?too much binding = dangerous b/c
ACh is too excitatory and muscles don’t
stop contracting - 132sarin gassarin inhibits the break down of ACh, which overstimulates parasympathetic nerves
- 133monoamines (classic)MODULATORY NTs made of a single amine group
NE/E
DA
5-HT
(histamine)
Classic Monoamines: Catecholamines (DA & NE/E) + indolamines (5-HT) - 134Catecholaminestype of classic monoamine
DA and NE/E - 135Indolaminetype of classic monoamine
5-HT - 136monoamine oxidaseenzyme responsible for metabolic breakdown of catecholamines and 5-HT
- 137dopamine (DA)Synthesized from dietary tyrosine
Proteins, seeds, nuts, bananas, avocado
L-DOPA = precursor for synthesis of DA
Tyrosine --> L-DOPA --> DA
L-DOPA --> DA
Functions = behavioral activation, MOTION
codes for REWARD, salience, novelty - 138are DA and learning related? why or why not?1) DA neurons fire in response to rewarding stimuli
2) DA neurons fire in response to novel/intense stimuli
3) this means DA neurons learn to fire in response to reward-predicting stimuli
REWARD-LEARNING - 139what happens to DA neuron firing in the absence of a predicted reward?firing is reduced
DA neurons provide a reward prediction-error signal
DA neurons code for absence of reward - 140VTApart of midbrain
neurons of the VTA synthesize DA, and and distribute them widely to diff areas of brain
VTA axons then send DA to the nucleus accumbens - 141DA pathways (2)Nigrostriatal = Implicated in voluntary motion --> Parkinson's (too little DA)
Mesocorticolimbic = Implicated in reward, learning, and ADDICTION - 142DA receptorsall are METABOTROPIC
D1 = D1, D5
D2 = D2, D3, D4 - 143D1 receptorsdepolarizes
striatum, VS/nucleus accumbens, everywhere
G protein Gs --> stimulates Adenylyl Cyclase --> cAMP synthesis (2nd mess.)
Second messenger: Indirectly depolarizes/excites membrane potential
pro-cAMP synth. - 144D2 receptorshyperpolarizes
striatum, VS/nucleus accumbens, everywhere
Post & pre synaptic receptor
G protein Gi --> inhibits Adenylyl Cyclase --> inhibits cAMP synthesis
anti-cAMP synth.
ALSO: Indirectly opens K+ channels/hyperpolarizes
post-syn inhibition - 145which DA receptor is pro-cAMP synthesis?pro-cAMP = D1
- 146which DA receptor is anti-cAMP synthesis?anti-caMP = D2
- 147What enzymatically breaks down DA?Monoamine Oxidase (MAO)
Catechol-O-methyltransferase (COMT)
Monoamine oxidase inhibitors (MAOIs) - 148what protein eliminates DA thru reuptake?DA transporter (DAT)
- 149what happens if you block DA?no movement
paralysis
DA antagonists - 150what happens if you ^ DA?movement
tho these are dose-dependent effects
DA agonists - 151triptophan is related to which NT?5-HT
- 152how is triptophan related to __(NT)__?5-HT is synthesized from dietary triptophan
- 153what is 5-HT responsible for the function of?Functions in motor output, mood, anxiety, and feeding
- 154where is 5-HT produced?very locally in Raphe Nuclei
- 155where is 5-HT distributed?forebrain and PNS
- 156how is the 5-HT(3) receptor different from all the other 5-Ht receptors?it's ionotropic
it's excitatory for Na+ (depolarizes post-syn neuron) - 1575-HT(1A) receptormetabotropic
Common in amygdala, hippocampus, & dorsal raphe nucleus
Auto-receptor - 158what does 5-HT(1A) binding ultimately do in terms of ion channels?Binding ultimately opens K+ channels
OR
Changes protein synthesis via second messenger - 159what behaviors result from 5-HT(1A) binding?Reduced anxiety (BuSpar), eating, and aggression
- 1605-HT(2A) receptormetabotropic
Common in cortex, striatum, accumbens - 161what does 5-HT(2A) binding ultimately do in terms of ion channels?Binding ultimately opens Ca2+ channels,
OR
Changes protein synthesis via second messenger - 162what behaviors result from 5-HT(2A) binding?Movement, hallucinations! LSD, shrooms
- 163how is 5-HT eliminated?reuptake
or
enzymatic degradation - 164what do autoreceptors do to 5-HT?reuptake 5-HT into the pre-syn neuron
- 165example of a 5-HT autoreceptorDAT (DA transporter)
- 166what drugs affect 5-HT reuptake?SSRIs
tricyclic antidepressants - 167what does Monoamine Oxidase (MAO) do to 5-HT?enzymatically breaks down 5-HT
- 168what drugs affect enzymatic degradation?Monoamine oxidase inhibitors (MAOIs)
- 169norepinephrine (NE) is another name for what?noradrenaline (NA)
- 170NE is what type of monoamineCatecholamine
- 171what is NE synthesized from?synthesized from DA
- 172where is NE synthesized?locus coeruleus (pons)
- 173is NE locally or widely distributed?widely
- 174what are the functions of NE?Functions:
– Wakefulness/arousal (sympathetic!)
– Cognition/memory
– Emotional memory - 175how is NE eliminated?reuptake and enzymatic degredation
(like DA) - 176epinephrine is also known as what?adrenaline
- 177define pharmacodynamicsThe study of the mechanisms of drug effects = what the drug does to the body/brain
how drugs interact w/ systems in the brain - 178define pharmacokineticsThe study of the factors that determine bioavailability
How drugs are processed by your body - 179(in terms of pharmacokinetics) the way the body processes drugs determines ___ & ___?time course
&
bioavailability - 180the onset and duration of effects defines what term?time course
- 181how much of the drug actually reaches target defines what term?bioavailability
- 182how are pharmacokinetics relative?Relative to how much was
consumed/administered (DOSE)
In some cases, very small %! - 183what is RADME? how does this relate to the way the body handles drugs?Route of administration – how we take it
Absorption – how it gets into blood stream
Distribution – how it gets around the body and into brain
Metabolism – how drugs are broken down
Elimination – of drug or metabolic waste product - 184what does the R in RADME stand for? why is this important?Routes of Administration
“How the drug gets into body”
Can have a huge influence on:
drug effects, reinforcement, abuse potential - 185how does the R in RADME affect the A in RADME?routes of administration contribute to absorption
- 186what are the 4 types of R in RADME?1. Oral administration (PO)
2. Inhalation
3. Mucus membranes/skin
4. Injection (IV, IP, IM, SC) - 187how safe is oral administration?Safe, uncomplicated, can be tasty
- 188how fast is oral administration of drugs?Slow and very complicated/unpredictable from the drug’s perspective
~0.5 - 3 hours - 189what makes oral administration so unpredictable?Must survive stomach acid (e.g., insulin, cocaine)
Must dissolve in stomach fluid (liquid ≠ tablet)
Potential enzymatic degradation (alcohol)
Potentially delayed by food (e.g., fatty)
Penetrate stomach lining/intestine
Lipid solubility
Pass into bloodstream – ‘first pass’ at liver Might metabolize some of the drug further - 190how fast is the inhalation of drugs?Fast(est) and most direct.
1. Lung area + bloodflow
2. Lungs capillaries --> left heart --> brain - 191what are some problems with inhalation?hard to judge proper dose
effects dependent on drug type
very irritating to lungs
rapid offset - 192what is included in mucus membranes/skin? Why is this relevant to routes of absorption?Skin, sublingual, intranasal (snorting or
nasal spray), vaginal, rectal
Membranes moist and rich in blood
supply --> rapid bloodstream absorption - 193how fast are drug effects felt thru use of mucus membranes?~1- 30 minutes
- 194what are some issues with using mucus membranes as a route of administration?Dosing (can be hard to judge)
Local effects on membrane (e.g., cocaine)
Some molecules absorb better than others (e.g. aspirin – not so well) - 195how fast is the injection route of administration?~10-30 seconds
- 196what are some pros about intravenous injection as a route of administration?Rapid, accurate dosing
High doses
Strong/fast high
Goes through the heart (the only thing that slows down the speed drug effects) - 197what are some cons about intravenous injection as a route of administration?Most dangerous for OD or reaction
Infections (Hep, HIV)
Blood vessels collapse - 198the routes of administration affect the time course of blood levels. How does the conc. of drug in the brain and time elapsed change based on drugs and their route of administration?
- 199Route of administration affect ___. This in turn impacts the ___.1. blood level
2. speed and intensity of the psychoactive effects/high - 200route of administration ultimately affects ___.reinforcement/abuse potential
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- Non-exhaustive list of terms that may appear on the Midterm exam
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- Lauren Delgadillo
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