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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
anaesthetic potency
MAC (minimum alveolar concentration alveolar partial pressure of inhaled anaesthetic which prevents movement to pain in 50% patients
26
what does a greater solubility of an inhaled agent in blood mean?
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
27
rate of equilibrium
brain (lean) has fast perfusion so rapid equilibrium | fat has less blood so slow perfusion and slow equilibrium
28
how does increased cardiac output affect anaesthetics?
delay induction because remove anaesthetic from area so conc/ can't build up, prevent overdose
29
recovery from anaesthetic
rate of reduction of alveolar partial pressure determines rate of recovery (how quick breathe)
30
intravenous anaesthetics
Propofol thiopental etomidate ketamine
31
propofol (MJ overdose)
``` GABAa receptor liver metabolised lipid soluble in fatty tissue pleasant antiemetic (stop vomit) apnoea (respiratory depression) and decrease BP ```
32
thiopental
``` 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 ```
33
etomidate
rapid recovery without hangover
34
ketamine
``` hallucinations not used apart from horses and battlefield child anaesthesia abuse/dependence treat depression irreversible effects in bladder ```
35
inhalation anaesthetics
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
36
halothane
potent, smooth induction, non-irritant, moderate muscle relaxation, hepototoxicity for surgeon
37
isoflurance
less potent than halothane, decrease BP, depress respiration, muscle relax, less hepatotoxicity
38
nitric oxide
maintain anaesthesia, analgesic, need with other anaesthetics, for labour pain
39
neuromuscular blocking drugs
muscle relax, lighter anaesthetic, relax vocal cords, respiration assistance
40
pain
unpleasant sensory and emotional experience to real or potential tissue damage and depends on distraction, previous exp., expectation, context etc.
41
pain pathways
peripheral nociceptive afferent neurones activated by stimuli central mechanisms generate pain sensation
42
neuropathic pain
pain without tissue damage
43
peripheral pain pathways (fast and slow pain)
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
44
mutations so no pain
in Na channels in Ad or C fibres
45
what is slow pain pathway for?
to immobilise so don't damage further
46
spinothalamic tract
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
Gate theory of pain
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
descending pathways
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
opiate (opioid) analgesics
most potent painkillers from opium poppy opioid is opiates + synthetic substances
50
opioid effects
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
how were opioid receptors discovered and explain
through binding studies | opiates labelled with radioisotopes so see receptors
52
what does the presence of opioid receptors suggest?
must be natural endogenous opioids in body
53
endogenous opioid peptides
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
multiple opiate receptors
there are multiple ligands to 1 receptor, under different circumstances 1 is more effective
55
opioid receptor subtypes (names, distribution, functions)
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
opioid receptor mechanisms
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
tolerance
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
dependence
physical - reset homeostatic mechanisms from repeated use and adaptation, withdrawal if abrupt termination psychological - craving psychological outlasts physical
59
pharmacokinetics
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
types of opioid drugs
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
opioid antagonists
nalorphine, naloxone, naltrexone most are competitive except nalorphine treat overdose, treat respiratory depression in babies
62
partial opioid agonist
buprenorphine (Temgesic) at MOP sublingual/injection/intrathecal similar to morphine but less respiratory depression for chronic pain/dependence
63
history of cannabinoids
lecture 11
64
main part of cannabinoids
THC
65
THC (tetrahydrocannabinol) central effects
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
THC peripheral effects
tachycardia, vasodilation, IOP falls (intraocular pressure in eye), bronchodilator
67
THC pharmacokinetics
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
cannabinoids mode of action
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
endogenous ligands for CB1/CB2 receptors
anandamide (1st found) 2-AG (2nd found) various others
70
where does anandamide and 2-AG come from?
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
enzymes that break down CB endogenous ligands
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
FABP5
transporter of cannabinoids | deletion stops eCB-mediated control of synaptic transmission in dorsal raphe nucleus
73
retrograde signalling of cannabinoids
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
cannabinoids and glial cells
release NT like ATP activates microglia in immune response
75
synthetic cannabinoids
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
medical uses of cannabinoids
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
CBD (cannabidiol)
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
marijuana
hallucinations, paranoia, depression, anxiety, long term effects, gateway drug
79
why are drugs addictive?
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
top-down control
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
addiction study in animals
sweet liquid vs drugs and measure preference with pusing lever no. of times heroine push lever a lot more compared to nicotine
82
innate tolerance
genetic sensitivity, after 1st dose
83
acquire tolerance
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
cross tolerance
less response if taking another because work through same mechanism e.g. cocaine and amphetamines
85
treatment criteria for addiction
``` quick and easy access help mental health stay in treatment behavioural therapy medication monitoring test for diseases ```
86
pharmacological approaches to treating addiction
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
Disulfiram
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
cocaine mode of action
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
cocaine withdrawal and treatment
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
opioid addiction, mechanism, withdrawal, treatment
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
methadone
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
buprenorphine
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
naltrexone
``` 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
nicotine
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
ethanol
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
how do all addictive drugs work?
VTA reward pathway
97
ego dissolution
melt away as a person at one with everything dream like but clear consciousness
98
3 major psychedelic agents
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
psychoactive monoamines
amphetamine tryptamine dopamine/serotonin/norepinephrine psychedelics - mescaline, psilocin, psilocybin, LSD serotonin folded into LSD structure
100
LSD
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
ego inflation
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
psilocybin
alleviates symptoms of depression study in cancer patients quick onset and long lasting long study better (may be spontaneously get better)
103
MDMA
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
forest plot
all studies summed up
105
dissociative psychedelics and schizophrenia
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
ketamine anaesthetic
intravenous horse tranquiliser awake but detached bronchodilator, anti-inflammatory
107
ketamine antidepressant
IV infusion improve mood and decrease suicide short lived high disrupt areas in rumination (dwelling)
108
mechanism of ketamine antidepressant
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
correctly using psychedelics in psychiatry
pure drugs correct dose correct mindset correct setting

Neuropharmacology (3 decks)

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