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Neuropharmacology > Drugs > Flashcards

Drugs Flashcards

1
Q

psychotropics

A

drug capable of affecting the mind, emotions, and behavior

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2
Q

what is noradrenaline involved in

A 
receptors all throughout brain so impact all brain systems
arousal, wakefulness
alertness in forebrain
mood in amygdala/hippocampus
pain in spinal cord
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3
Q

what is dopamine involved in

A

more restricted distribution
prominent in prefrontal cortex - decision, judgement, risk
nigrostriatal system (from substantia nigra to striatum) - motor control
mesolimbic/mesocortical system - behaviour, mood
tuberohypophyseal system - endocrine control

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4
Q

what is serotonin (5-HT) involved in

A

widespread distribution throughout brain
sleep, wakefulness, mood, feeding, sensory transmission, pain
Raphe nuclei - primary source of serotonergic fibres

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5
Q

monoamine uptake

A

NET - noradrenaline
SERT - serotonin
DAT - dopamine

transporters remove NT from synaptic cleft

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6
Q

drugs that cause monoamine uptake inhibition and some clinical uses

A

Cocaine - act on DAT
MDMA (ecstasy) - act on SERT, also on VMAT (transport into vesicles)
Amphetamine - target NET and VMAT and inhibit MAO

clinical uses - ADHD, narcolepsy (sleep), reduce apetite, PTSD, depression, weigth control

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7
Q

amphetamines

A 
increase motor activity
euphoria, excitement, insomnia, anorexia
given to troops in war to be less sleepy and hungry (Benzedrine)
can cause dependence
high doses can cause psychosis

clinically: Adderall for ADHD
Ritalin for ADHD/narcolepsy
Methedrine for obesity

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8
Q

Cocaine (HCl form or free-base crack) effects

A

increased motor activity
euphoria, excitement, garrulousness (talkative), increased BP/HR
shorter lasting than amphetamines
strong dependence

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9
Q

Modafinil

A

increased wakefulness for narcolepsy
vigilance, improve cognitive performance (likely from wakefulness)
bind DAT and NET with low affinity, displaces cocaine for DAT
and other NT systems
low abuse potential because no ‘high’

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10
Q 
cognitive enhancers (limitless)
\+ study
A

caffeine, modafinil, methyphenidate, ampakines

hopes to reduce mental fatigue, increase motivation, attention, concentration, memory, normalise behaviour like sch./autism

chess study: takes longer on moves and thinks more if took enhancers but chance of winning decreased as game progressed, bad effect if there’s a time limit

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11
Q

Ampakines

+ study

A

cognitive enhancers
activate glutamate AMPA receptors
epileptic seizures if activate too much

Skinner box study: mice improve performance of pressing bar to get food, maintained high performance when stopped drug so new brain connections (limitless ending??)

promote release of BDNF so plasticity and growth

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12
Q

Depression monoamine theory

A

evidence: drugs like reserpine reduce monoamine (MA) levels and cause depression
but not clear how monoamine links to symptoms (take weeks to change)

drug classes:
monoamine oxidase inhibitors (phenelzine) prevent MA breakdown
monoamine uptake inhibitors (tricyclics, imipramine) target NET, SERT
selective monoamine uptake inhibitors (citalopram, fluoxetine=Prozac) target SERT (SSRI)
reboxatine target NET
duloxetine target NET and SERT (SNRI)

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13
Q

Schizophrenia (dopamine)

A

increased D2 receptor activity (+ve symptoms)
decreased D1 receptor activity (negative symptoms)

drug classes:
Chlorpromazine (1st generation, typical) - target D1, D2 and other
Clozaine/Risperidone (2nd, atypical) - more at D2 but also D1

side effects: motor, tardive dyskinesia (less with 2nd), gynecomastia (man breasts), weight gain, drowsy

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14
Q

Parkinson’s (less dopamine)

A

loss neurones in substantia nigra (less black substance)

suppression of voluntary movement, cognitive impairment

treatment:
Levodopa with carbidopa or benserazide
inhibit COMT so more levodopa in periphery to cross blood-brian barrier and converted to dopamine
target receptors to prevent dopamine metabolism too
deep-brain stimulation to cause DA release and trigger pathways

can cause schizo

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15
Q

local anaesthetics vs general anaesthetics

A

act locally to block nerve conduction

act in brain to cause loss of consciousness for operation/experiments - inhalation gases/IV infusion

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16
Q

structure of general anesthetics

A

variety of chemical structures with no specific one, nothing in common
(apart form opioids)

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17
Q

Stages of anaesthesia

A

how deep (need to know to get to right stage)

1) awake but drowsy, distorted perception, analgesia the end of stage
2) dangerous stage so need to move through it quickly, excitation, inhibitory neurones affected 1st, motor reflexes, unconscious, shouldn’t eat before, uncontrolled movement, lose temp control, irregular breathing, cardiac dysrhythmia
3) surgical anaesthesia, regular breathing, depressed cough/vomit reflex, pupils constrict then dilate, skeletal muscles relax, drop BP, loss corneal reflex
4) not good, deep, shallow breathing, fall BP, feeble pulse, wide pupils, no ventilation from depression of medulla oblongata so die

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18
Q

what is the best stage of anaesthesia?

A

plane 3 of stage 3
deep, shallow breathing, weak pulse, no response to surgery, dilated pupils, reduced muscle tone, absent/diminished reflexes

but difficult to measure because no movement

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19
Q

EEG and anaesthesia

A

can monitor depth
as deepens - amplitude of high frequency components fall and lower frequency amplitude increases

large amplitude slow frequency waves

changes are agent dependent

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20
Q

theories of general anaesthesia (GA)

A

lipid theory
protein theory
combination

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21
Q

Lipid theory of GA (mechanism, evidence, correlation, problems)

A

GA dissolve in membrane and change bilayer thickness/curvature/order of chains/elasticity so change protein properties

evidence: no defined structure, push GA out w/ pressure

Meyer-Overton correlation: more lipid soluble GA=more potent

problems: stereoisomers same solubility but 1 active 1 not
new compounds don’t fit correlation
more carbons more soluble but too long stops working (cut off effect)
non-immobilisers soluble but not anaesthetic
temp changes bilayer but not anaesthetic

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22
Q

Protein theory of GA (target proteins, evidence)

A

specific membrane proteins: GABAa receptor (inhibitory), 2 pore K channel (control resting pot.), NMDA receptor (excitatory)

evidence: mutate and look at potency
GABAa mutant - propofol not work, no change w/ alphaxalone
2PK mutant - halothane and isoflurance not work
NMDA mutant - xenon and isoflurane not work

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23
Q

identifying relevant anaesthetic protein targets

A

right place
work in same conc as used clinically
stereo selective effects - work in vivo and vitro
appropriate sensitivity and insensitivity to other compounds

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24
Q

ideal anaesthetic

A

rapid action and recovery
minimal irritant
miscible with air/O2 so no explosion
analgesic, muscle relaxant

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25
Q

anaesthetic potency

A

MAC (minimum alveolar concentration

alveolar partial pressure of inhaled anaesthetic which prevents movement to pain in 50% patients

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26
Q

what does a greater solubility of an inhaled agent in blood mean?

A

solubility in blood determined by bloog/gas co-efficient

greater solubility means reduced rate of rise of alveolar partial pressure so reduced rate rise of brain partial pressure and slower rate anaesthetic onset (slower activation if more soluble)

lower solubility means quicker to affect pass to and affect brain, because drug in alveoli need to fill arterial blood before go to brain

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27
Q

rate of equilibrium

A

brain (lean) has fast perfusion so rapid equilibrium

fat has less blood so slow perfusion and slow equilibrium

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28
Q

how does increased cardiac output affect anaesthetics?

A

delay induction because remove anaesthetic from area so conc/ can’t build up, prevent overdose

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29
Q

recovery from anaesthetic

A

rate of reduction of alveolar partial pressure determines rate of recovery (how quick breathe)

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30
Q

intravenous anaesthetics

A

Propofol
thiopental
etomidate
ketamine

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31
Q

propofol (MJ overdose)

A 
GABAa receptor
liver metabolised
lipid soluble
in fatty tissue
pleasant
antiemetic (stop vomit)
apnoea (respiratory depression) and decrease BP
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32
Q

thiopental

A 
dangerous
barbiturate (CNS depressant)
GABAaR
lipid soluble
cross blood-brain barrier rapidly
distribute to other tissues
live metabolised
poor analgesic and muscle relaxant
cardiorespiratory depression
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33
Q

etomidate

A

rapid recovery without hangover

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34
Q

ketamine

A 
hallucinations
not used apart from horses and battlefield
child anaesthesia
abuse/dependence
treat depression
irreversible effects in bladder
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35
Q

inhalation anaesthetics

A

depress respiration, increase artierial CO2, impair O2 exchange, decrease brain metabolic rate, even though increase cerebral blood flow
relax skeletal muscles
machine to breathe it in and out goes to scavenger not air

halothane, isoflurancce, NO, neuromuscular blacking drugs

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36
Q

halothane

A

potent, smooth induction, non-irritant, moderate muscle relaxation, hepototoxicity for surgeon

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37
Q

isoflurance

A

less potent than halothane, decrease BP, depress respiration, muscle relax, less hepatotoxicity

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38
Q

nitric oxide

A

maintain anaesthesia, analgesic, need with other anaesthetics, for labour pain

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39
Q

neuromuscular blocking drugs

A

muscle relax, lighter anaesthetic, relax vocal cords, respiration assistance

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40
Q

pain

A

unpleasant sensory and emotional experience to real or potential tissue damage and depends on distraction, previous exp., expectation, context etc.

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41
Q

pain pathways

A

peripheral nociceptive afferent neurones activated by stimuli

central mechanisms generate pain sensation

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42
Q

neuropathic pain

A

pain without tissue damage

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43
Q

peripheral pain pathways (fast and slow pain)

A

pass info from periphery

1) fast pain - A.delta fibres, myelinated, 1-5um diameter, fast conductance, mechanosensitive and temp sensitive
2) slow pain - C fibres, unmyelinated, 0.1-1.5um diameter, slow, mechanosensitive and temp sensitive and chemical stimuli

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44
Q

mutations so no pain

A

in Na channels in Ad or C fibres

45
Q

what is slow pain pathway for?

A

to immobilise so don’t damage further

46
Q

spinothalamic tract

A

carry pain to CNS

pain to afferent fibres (C/Adelta) which come in dorsal root ganglia to dorsal horn of spinal cord then crosses to other side and go up tract to thalamus to sensory cortex and then feel pain

47
Q

Gate theory of pain

A

2 signals like pain and distraction can’t pass through ‘crossing’ at the same time so large peripheral fibres with distraction can stop pain going to brain

48
Q

descending pathways

A

modulate pain signal
parallel pathways modulate affective dimensions of pain (emotional) and control autonomic activity

pathways include Raphe nuclei, reticular formation, pathway from cortex

PAG (periaqueductal gray) key in system, if activate can cause analgesia

49
Q

opiate (opioid) analgesics

A

most potent painkillers
from opium poppy
opioid is opiates + synthetic substances

50
Q

opioid effects

A

CNS: analgesia w/o unconsciousness, respiratory depression, nausea/vomit from activate chemotrigger zone in medulla

sensitivity to CO2: breathing centre in medulla, CO2 drives breathing, respiratory depression reduces CO2 sensitivity so stop breathing and die of overdose

other CNS effects: euphoria, dry mouth, drowsy, no cough reflex, pupils constrict

other effects: increase tone in GI tract (less store), less gut motility, constipation, delay emptying so slow drug absorption

histamine release so urticaria, bronchoconstriction, hypotension

51
Q

how were opioid receptors discovered and explain

A

through binding studies

opiates labelled with radioisotopes so see receptors

52
Q

what does the presence of opioid receptors suggest?

A

must be natural endogenous opioids in body

53
Q

endogenous opioid peptides

A

enkephalins, endorphins (endogenous morphine)

in areas associated with nociception (pain) e.g. PAG, rostral ventral medulla, substantia gelantosa
beta endorphin in hypothalamus, send projections to PAG and noradrenergic nuclei in brain stem

role in pain perception, reward, stress, autonomic control

54
Q

multiple opiate receptors

A

there are multiple ligands to 1 receptor, under different circumstances 1 is more effective

55
Q

opioid receptor subtypes (names, distribution, functions)

A

u mu
d delta
k kappa
with diff ligands and distributions

MOP (u) widely in CNS and periphery, cortex, thalamus, PAG, substantia gelatinosa (SG)
KOP (k) hypothalamus, PAG, SG
DOP (d) pontine nuclei, amygdala, cortex

functions: analgesia, k no respiratory depression and dysphoria, only u euphoria, d no pupil constrict and no sedation
ligands: enkephalins for M/D, morphine for M

56
Q

opioid receptor mechanisms

A

G-protein coupled so inhibit adenylate cyclase, reduce NT release, activate K and inhibit Ca channels

opioids stored as large propeptides cleaved at presynaptic terminal

directly inhibit pain by reducing transmission to spinal cord
OR
increase descending inhibition so enhance descending pathway and block GABA release

57
Q

tolerance

A

increased dose required for same effect, occurs in a few days (no effect on constipation and pupils)

agonist and receptor internalised, beta arrestin binds, receptor removed and destroyed so less effect because less receptors

58
Q

dependence

A

physical - reset homeostatic mechanisms from repeated use and adaptation, withdrawal if abrupt termination
psychological - craving

psychological outlasts physical

59
Q

pharmacokinetics

A

morphine analogues not absorbed well orally so injection for pain
2ndary metabolism - conjugated with glucoronide
hepatic metabolism - to gut with bile and retaken up
most excreted in urine

60
Q

types of opioid drugs

A

morphine

fentanyl - acute pain and anaesthetic, very potent, rapid onset, short, used to stop heroin/cocaine use

codeine - less potent, methyl ester of morphine, weaker, less side effects, combine with paracetamol and over the counter because below therapeutic dose

pethidine - short, less potent, child birth, respiratory depression, dry mouth, blurry, less constipate than morphine

methadone - chronic pain, no euphoria, less sedation, slow recovery, useful for withdrawal and addicts

61
Q

opioid antagonists

A

nalorphine, naloxone, naltrexone
most are competitive except nalorphine
treat overdose, treat respiratory depression in babies

62
Q

partial opioid agonist

A

buprenorphine (Temgesic) at MOP
sublingual/injection/intrathecal
similar to morphine but less respiratory depression
for chronic pain/dependence

63
Q

history of cannabinoids

A

lecture 11

64
Q

main part of cannabinoids

A

THC

65
Q

THC (tetrahydrocannabinol) central effects

A

impaired STM and motor coordination, sense of time, mood, cognition, catalepsy (trance), hypothermia, analgesia, antiemetic, increase apetite

experiment: pilots decrement in performance even 24hrs later - applies to cars

66
Q

THC peripheral effects

A

tachycardia, vasodilation, IOP falls (intraocular pressure in eye), bronchodilator

67
Q

THC pharmacokinetics

A

rapid onset from smoking
oral takes longer but lasts longer (4-8 hrs instead of 30mins to 2hrs)
conjugation and enterohepatic circulation prolongs duration
highly lipophilic so accumulate slowly in fat and can detect weeks after

68
Q

cannabinoids mode of action

A

CB1 receptor: main, ligand binding of THC, GPCR (binding decreased by non-hydrolysable GTP analogue)
wide distribution in brain lots in cerebral cortex because decisions
inhibit Ca channels, activate K channels so inhibit PKA less cAMP inhibit transmission

CB2 (also GPCR) on immune cells, inhibit adenylyl cyclase

69
Q

endogenous ligands for CB1/CB2 receptors

A

anandamide (1st found)
2-AG (2nd found)

various others

70
Q

where does anandamide and 2-AG come from?

A

not stored in vesicles but made on demand when calcium increases and 2 calcium sensitive enzymes cleave them from membrane phospholipids

EMT (endocannabinoid membrane transporter) releases ligands from pre/post synaptic neurones so can go post to pre (retrograde)

71
Q

enzymes that break down CB endogenous ligands

A

FAAH (fatty acid amide hydrolase) breaks down anandamide
(knockout in mice means reduced pain and more sensitive to exogenous ligand because can’t break it down)

MAGL (monoacylglycerol lipase) breaks down 2-AG

72
Q

FABP5

A

transporter of cannabinoids

deletion stops eCB-mediated control of synaptic transmission in dorsal raphe nucleus

73
Q

retrograde signalling of cannabinoids

A

depolarise post-synaptic will inhibit pre-synaptic (DSI)
and same for excitation (DSE)
so post affecting pre

depolarise means Ca open so make cannabinoids and come out EMT and bind receptors so inhibit transmitter release into cell

74
Q

cannabinoids and glial cells

A

release NT like ATP activates microglia in immune response

75
Q

synthetic cannabinoids

A

JWH - very potent, leaked to black market as ‘spice’
synthetic chemical are dried and shredded so smoked or liquids to vaporise
more severe adverse effects like peripheral effects
turn into zombies
hard to know what’s in drug you buy

76
Q

medical uses of cannabinoids

A

none so need license to work
some derivatives on market like CBD oil

antiemetic effects for chemotherapy (Nabilone for unresponsive to conventional antiemetics)
desirable side effects - sedation, drowsy, euphoria
undesirable - dizzy, dysphoria, depression, hallucinations, paranoia, hypotension

analgesia - CB1 in pain processing areas so agonist cause analgesia

appetite - VTA reward, desire to eat, hard to study

MS - reduce pain, not cost effective

anti-cancer - inhibit growth, weak evidence

77
Q

CBD (cannabidiol)

A

no THC so no psychoactive effects
lacks evidence

for pain, depression, anxiety, acne, cardiac health, antipsychotic, for abuse, anti-diabetic, for extreme epilepsy

anandamide uptake inhibitor, activate TRPV1 receptor and GOR55 R and 5-HTIA, modify adenosine uptake

78
Q

marijuana

A

hallucinations, paranoia, depression, anxiety, long term effects, gateway drug

79
Q

why are drugs addictive?

A

rewards from dopamine/serotonin release
drug affects VTA nuclei, release dopamine so reward/motivation
drugs block uptake of 5-HT from Raphe nuclei so increase wellbeing

incentive salience - cognitive process for desire because reward, hi-jacked by drugs

80
Q

top-down control

A

normal brain motivated through pathway: orbital frontal cortex make decision, regulated in prefrontal cortex in central gyrus, memory
drugs override self regulation and strong memory for reward so overcome natural pathways

81
Q

addiction study in animals

A

sweet liquid vs drugs and measure preference with pusing lever no. of times
heroine push lever a lot more compared to nicotine

82
Q

innate tolerance

A

genetic sensitivity, after 1st dose

83
Q

acquire tolerance

A

pharmacokinetic, changes in metabolism and absorption as take more
e.g. reduce systemic conc. with enzyme that breaks drug down
OR change in receptor/systems reduce response

84
Q

cross tolerance

A

less response if taking another because work through same mechanism
e.g. cocaine and amphetamines

85
Q

treatment criteria for addiction

A 
quick and easy access
help mental health
stay in treatment
behavioural therapy
medication
monitoring
test for diseases
86
Q

pharmacological approaches to treating addiction

A

withdrawal symptoms - substitute drug (methadone for heroin addicts)

long term substitution - methadone/buprenorphine/legal heroin

block response to drug - Naltrexone blocks opioid

aversive therapy - Disulfiram

reduced continued drug use - treat underlying e.g. mental health

87
Q

Disulfiram

A

antabuse
unpleasant effect to ethanol because blocks breakdown
not used often
take daily orally but why would you if you want alcohol
small amounts in mouthwashes can trigger reaction

some antibiotics block pathway so can’t drink alcohol

88
Q

cocaine mode of action

A

blocks uptake transporters for dopamine and 5-HT
NAc (nucleus accumbens) released dopamine
everything rewired over time
changes AMPAR levels, impaired cystine-glutamate exchange, change intrinsic membrane excitability of MSN (medium spiny neurones) so more spines

89
Q

cocaine withdrawal and treatment

A

crash 1-4 days after binge
withdrawal 1-10 weeks after
extinction - still low mood and episodic cravings

no treatment apart from contingency management (CM) which is rewards for not taking drug
CBT prevent relapse and avoid situation when likely to take drug

90
Q

opioid addiction, mechanism, withdrawal, treatment

A

rush (45s) - intense pleasure
nod (15-20min) - sleepy, detached
high (hrs) - well being
straight (up to 8hrs) - no high no withdrawal (then withdraw)

activate receptors on GABA neurones in VTA so not inhibited and release more dopamine

chronic: reduce cAMP but slowly recover (increases adenylyl cyclase so more cAMP) and decrease dopamine receptors so tolerance
withdraw: more adenyl cyclase than normal so lots cAMP and hyperactivity within 8hrs

methadone alleviate withdrawal symptoms

91
Q

methadone

A

long 1/2 life
take for 4 weeks as impatient and 12 weeks in community
lose tolerance and may overdose if miss days
likely taking heroine if missed more than 5 days

92
Q

buprenorphine

A

less sedating than methadone
given on alternative days
2 forms: alone (subutex) or combination with opioid receptor antagonist naloxone (suboxone)

naloxone has no effect if taken orally but block it if injected

93
Q

naltrexone

A 
opioid receptor antagonist
no tolerance, precipitates withdrawal
only used in overdose because instant withdrawal
insufficient evidence of effectiveness
prevents relapse when no longer on drug
94
Q

nicotine

A

carcinogens in smoke
lots of deaths (41% lung cancer)
nicotinic Rs in neuromuscular junction/brain
areas in reward (hippocampus, VTA, amygdala, NAc, PFc)
changes synapses after long use

treat with nicotine replacements - poorly absorbed orally, transdermal patches, E-cigarettes
Varenidine (partial nicotine agonist)
Bupropion (nicotine antagonist)

95
Q

ethanol

A

4-5% population are alcoholics
affect many NT synapses

treatment with Acamprosate calcium SR tablets and counselling to stop relapse
weak NMDAR antagonist reduce cravings
Disulfiram
alleviate withdrawal with various drugs

96
Q

how do all addictive drugs work?

A

VTA reward pathway

97
Q

ego dissolution

A

melt away as a person
at one with everything
dream like but clear consciousness

98
Q

3 major psychedelic agents

A

Lysergics (like LSD) target 5-HT2 receptor agonists, depression, addiction

Empathogen like MDMA (ecstasy) monoamine uptake inhibitor which affects serotonin

Dissociatives (like Ketamine=special K, phencyclidine-angel dust) target NMDARs
special k linked to depression

99
Q

psychoactive monoamines

A

amphetamine
tryptamine
dopamine/serotonin/norepinephrine

psychedelics - mescaline, psilocin, psilocybin, LSD

serotonin folded into LSD structure

100
Q

LSD

A

synthesised
interacts with 5-HT2 receptor (mutated lid means bind less)
structure keeps LSD in place in receptor

diff networks recruited depending on task and LSD disrupts networks
more brain regions talking to each other with higher intensity

can treat depression, anxiety, alcohol abuse
reduce anxiety in patients with terminal illness

101
Q

ego inflation

A

alcohol and cocaine cause you to be more talkative, more about you, more aware of ourselves, not ego dissolution where you seize to be who you are

102
Q

psilocybin

A

alleviates symptoms of depression
study in cancer patients
quick onset and long lasting
long study better (may be spontaneously get better)

103
Q

MDMA

A

for PTSD
less rumination (dwelling)
reduced communication of hippocampus + prefrontal cortex so reduce traumatic memory
amygdala better communication so contextualise fear

study makes solitary octopus more sociable

104
Q

forest plot

A

all studies summed up

105
Q

dissociative psychedelics and schizophrenia

A

ketamine/PCP

glutamate theory of sch. is reduced activation of NMDAR (reduced NR1 subunit)
symptoms of psychedelics similar to sch.

Abs to NMDAR caused psychosis so could be from autoimmune disease

106
Q

ketamine anaesthetic

A

intravenous horse tranquiliser
awake but detached
bronchodilator, anti-inflammatory

107
Q

ketamine antidepressant

A

IV infusion
improve mood and decrease suicide
short lived high
disrupt areas in rumination (dwelling)

108
Q

mechanism of ketamine antidepressant

A

NMDAR antagonist
targets NMDAR on inhibitory interneurones so reduce activity and fewer AP
less GABA so less inhibition of glutamatergic neurones
more glutamate
release BDNF
new synapses, synaptic strength, networks rearranged so stop depression

Esketamine nasal spray for treatment-resistant depression

109
Q

correctly using psychedelics in psychiatry

A

pure drugs
correct dose
correct mindset
correct setting

Neuropharmacology (3 decks)

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