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drugs Flashcards

1
Q

Tetrodoxins

A

NaV
toxin found in marine species
Bind to external alpha subunit in S5-S6 loop region
Block pore
Used to isolate effects of channel in vitro

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2
Q

Phenytoin and Carbamazepine

A

NaV
Treatment epilepsy by preventing seizures
Slow recovery from inactivated state which limits firing rate of neurons

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3
Q

local anaesthetic (cocaine, lidocaine, procaine)

A

Non-ionised form crosses membrane e.g. procaine diffuse in and then go through fenestrations
Bind Na channel at sites exposed to lipid membrane and block channel
Bind inactivated state of channel creating use dependent blocker

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4
Q

tetraethylammonium (TEA)

A

Inhibits most K+ channels

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5
Q

Cs+

A

inhibits delayed rectifiers K(Ca), K(IR), K(ATP)
Stops repolarisation of channel = extended hyperpolarisation

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6
Q

Gabapentin and Pregabalin

A

Treat chronic pain and epilepsy by regulating Nt release in sensory neurons
Bind a2/20 subunit and disrupt trafficking of channel to membrane
Selective for CaV2.2 (N type)
pregabalin is better as has more reliable absorption and bioavailability and is less effected by food consumption can cause dizziness, sedation, incoordination and memory effects. May be some abuse potential due to euphoria, sedation, dissociation and relaxation at sub-therapeutic dose
Gabapentin reduces VGCC trafficking, tethering and activation
take time to produce effect and aren’t effective for all patients

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7
Q

Bicuculline

A

Competitive antagonist of most GABA(A) receptors
Not therapeutic but first used to define GABA(A) receptors
Causes extensive excitation so not great

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8
Q

Benzodiazepine (diazepam and temazepam)

A

enhance action GABA by increase frequency of channel opening
selective for GABA(A)R containing
a1 = sedation and impaired motor coordination
a2 = anxiolysis and muscle relaxation
a3 = muscle relaxation and impaired motor coordination
a5 and gamma subunits (30%)
Bind interface between alpha and gamma subunit
Binding site contains crucial histidine residue

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9
Q

Barbiturate (pentobarbitone)

A

May act alone or enhance action of GABA
Act on all GABA(A)R
Cause channel to stay open longer
Don’t always need GABA as can act to increase Cl- entry (makes them more dangerous)

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10
Q

Ethanol

A

enhance action of GABA
Prolong open time of channel
Bind with transmembrane domain

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11
Q

General anaesthetics (propofol)

A

Enhance action of GABA
Directly stimulation receptors at high concentrations
Bind interface between alpha and beta subunits within transmembrane region

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12
Q

Neurosteroids (allopregnanolone)

A

Promote opening of GABA(A) receptor channel
Receptors containing a delta subunit are most sensitive

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13
Q

Strychnine

A

Antagonist poison at glycine receptors
Causes paralysis
Bind at subunit interface like glycine

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14
Q

Ivermectin

A

Allosteric enhancer of glycine channels
Bind transmembrane domains

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15
Q

5HT3 antagonists

A

Alosteron used for IBS
Ondasetron antiemetic - competitive antagonist with serotonin
Act on gut
Act at the interfaces between subunits and altering how the subunits trigger opening and closing of the channel

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16
Q

L-DOPA

A

Precursor to dopamine and synthesised by dopa-decarboxylase
Increases dopamine synthesis
Nigrostriatal dopamine pathway

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17
Q

Dietary tryptophan

A

Precursor to serotonin
Increase serotonin synthesis
Increase mood

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18
Q

MDMA (methylenediethylmethamphetamine)

A

Inhibit 5HT reuptake through the transporters (SERT, NET, DAT) which increases available serotonin in synaptic cleft
Affect mood, appetite and sexual behaviours
Can inhibit tryptophan hydroxylase and reduce serotonin synthesis

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19
Q

Amphetamine

A

disrupt vesicular monoamine storage by competing for VMAT with monoamines
Reverse vesicular uptake of monoamines by dissipating H+ gradients
Reverse monoamine transport increase release of monoamine into the synapse
Increase arousal and vigilance, reward and mood where monoamines released

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20
Q

Methamphetamine

A

Same as amphetamine but produces greater effects
Higher effective dose
More likely to cause addiction
Do more which causes more side effects

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21
Q

Reserpine

A

disrupts storage of noradrenaline in vesicular monoamine transporter by disrupting the H+ gradient (proton gradient)
Range of areas where noradrenaline stored and released to affect mood, blood pressure regulation

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22
Q

Bromocriptine

A

D2 receptors
Agonist to treat Parkinsons
Nigrostriatal dopamine pathway

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23
Q

Clozapine

A

D2 receptors
Antagonist to treat psychosis
mesolimbic/mesocortical dopamine pathway

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24
Q

Clonidine

A

a2 adrenoceptor
Partial agonist for hypertentsion
Brainstem nuclei that release noradrenaline and centrally control BP

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25
Q

Mirtazepine

A

a2 adrenoceptor
antagonist to treat depression
range of areas where noradrenaline stored
Released to regulate mood

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26
Q

buspirone

A

5HT(1A) receptor
agonist for anxiety
range of areas where noradrenaline stored and released

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27
Q

Naratriptan

A

5HT(1A/D/F) receptor
Agonist to treat migrane
Trigeminocerebrovascular system involved in migrane generation

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28
Q

Cocaine

A

Block dopamine transporter to prevent reuptake also at NET and SERT
Prolong dopamine action
Dopamine mesolimbic pathway
Ventral tegmental area of midbrain to nucleus accumbens of forebrain
Also Na channel blocker

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29
Q

Amitriptyline

A

Antidepressant
Block noradrenaline and serotonin transporters
prevent dopamine re-uptake to prolongs dopamine action in synapse
Range of areas where noradrenaline and serotonin are stored and released
affect mood and vegetative behaviours

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30
Q

Bupropion

A

Block dopamine transporter to prevent dopamine reuptake
Prolong dopamine action in synapse
Dopamine mesolimbic pathway to reduce nicotine craving

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31
Q

Moclobemide

A

Inhibit MAO-A to reduce monoamine degradation
Increases cytoplasmic monoamine concentration and spontaneous leakage into synapse
Range of areas where noradrenaline and serotonin stored and released
Affect mood and vegetative behaviour
Used for depression

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32
Q

Selegeline

A

Inhibit MAO-B to reduce dopamine degradation
Increase available dopamine
Nigrostriatal
Used for parkinsons

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33
Q

TBOA

A

blocks all EAATs
Has benzene ring

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34
Q

buprenorphine

A

opioid that binds tightly which inhibits agonist and antagonist binding
produces weak signal
improves safety
low intrinsic efficacy

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35
Q

tramadol and tapentadol

A

syngerist between opioid and NA or 5HT pathways
Tramadol = u-receptor and SERT
Tapentadol = u-receptor and NET
means need less morphine for similar effect
The modulate descending pathways

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36
Q

NSAIDS (aspirin and ibuprofen)

A

inhibit COX1 and COX2
Inhibits prostaglandin release which reduces nociceptors sensitivity
Reversible inhibition

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37
Q

NSAIDS (aspirin and ibuprofen) in migranes

A

release arachidonic acid which is broken down in COX into thromboxane, prostacyclin and prostaglandin (pro-inflammatory mediators)
aspirin blocks COX enzymes
Inhibits prostaglandin release which decreases inflammation
Work best when given early in an attack
Act on trigeminal system

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38
Q

Morphine

A

activates opioid receptors to reduce Ca2+ influx
Reduces Nt release which reduces transmission
it can also directly inhibit
Addiction, tolerance and overdose common

39
Q

Ziconotide

A

only N type VGCC blocker approved for chronic pain treatment
Mediates Nt release by block Ca2+ influx
widely expressed which leads to severe side effects
Spinal delivery
less tolerance issues

40
Q

Ergotamine for migrane

A

5HT(1D) partial agonist
Act at other monoamine receptors
Cause vasoconstriction (including coronary vessels)
Block trigeminal nerve transmission
Adverse effect = nausea and vomiting
Not first line

41
Q

Triptan for migrane

A

5HT(1B/1D/1F) agonists
inhibit trigeminal nerve transmission peripherally (ganglia) and centrally (trigeminal nucleus caudalis)
Inhibit release of vasoactive peptide from meningeal blood vessels
Stimulate 5HT1B receptors causes vasoconstriction (can’t use in CVD)
Inhibit release of neuropeptides that cause inflammatory soup
Relieve the pain and nausea

examples include Sumaptriptan, zolmitriptan, rizatriptan, eletriptan, naratriptan

42
Q

B-adrenoceptor antagonists for migrane

A

propranolo and metoprolo
have an unknown MOA
Side effects are fatigue and bronchoconstriction
Contraindications include asthma

43
Q

5HT2 receptor antagonists for migrane

A

pizotifen, cyproheptadine and methysergide
prevent 5HT2 receptor induced vasodilation and consequent inflammation
Side effects are weight gain, antimuscarinic effects

44
Q

Anticonvulsants for migranes

A

sodium valproate, gabapentin and topiramate
Reduce cortical excitability and alter ion channel activity
decrease trigeminal transmission
decreased cortical spreading depression
Cannot take if pregnant (teratogens)
reduce excitability to reduce migrane

45
Q

Ca2+ channel antagonists for migrane

A

Nifedipine and verapamil
Decrease Ca2+ entry which reduces cellular excitability
Increase reduced sensitisation threshold

46
Q

TCAs for migrane

A

5HT and NA transport inhibitors which lead to an increase in available 5Ht and NA which increases inhibition of spinothalamic neurons
Block serotonin transport in to have more serotonin binding to reduce pain

47
Q

CGRP monoclonal antibodies for migrane

A

CGRP receptor antagonists
Compete at sites to prevent CGRP binding which reduces vasodilation
can cause live toxicity

48
Q

What makes heroin (opioid) addictive

A

Efficacious agonist
Its metabolite 6-monoacetylmorphine is more lipophilic than morphine
Therefore gets into the brain faster and causes a greater rush
inhibit cell that the mu-opioid receptor is on in the brain
Get more dopamine release because you are inhibiting the inhibitor (GABA)

49
Q

Methadone

A

mu-agonist which long half life
stops withdrawal and craving of heroin without overdose
Not as satisfying for abusers
combine use with social support to help ween off opioids
Still OD risk

50
Q

Buprenorphine for opioid abusers

A

occupies opioid receptor and prevents full agonists like heroin having an effect
Partial agonism
less OD risk than methadone but not all patients are stable on this drug
combine with naltrexone to prevent injection

51
Q

Naltrexone for opioid abusers

A

Orally active antagonist
Occupies receptor to prevent agonist binding
Need to detox before use
Poor compliance as does not reduce craving
High relapse rate

52
Q

Nicotine

A

Agonist at nicotinic receptors
Increases release of adrenaline from adrenal glands
Get increased BP, HR, respiration and blood glucose
Increases alertness, reduces anxiety and tension
Increases dopamine release in reward centres
Acts at nucleus accumbens and prefrontal cortex
Fast response is what allows the association to be drawn

53
Q

Agonist therapy for nicotine

A

Patch, gum, nasal spray or inhaler
Eliminates smoke exposure
Agonist at receptor therefore reduces craving
Breaks the cue of cigarette with hit
Should be done with CBT

54
Q

Partial agonists for nicotine

A

Varenicline (alpha 4 veta 2) and cytisine
Reduce craving and smoking satisfaction
Side effects like nausea, sleep issues
May be better than nicotine replacement therapies

55
Q

Antagonist for nicotine

A

mecamylamine
block nicotine reward but no effect on craving
Side effects include drowsiness, dizziness and constipation
May help reduce smoking when combined with nicotine replacement therapy

56
Q

Vaccine for nicotine

A

antibodies produced that bind nicotine and prevent it crossing the BBB
No effect on craving and no better than placebo
May have a role in at risk groups and prevention

57
Q

Bupropion for nicotine

A

antidepressant with an unclear MOA
some reduction in craving (may be due to inhibiting dopamine uptake)
lowers seizure threshold and causes sedation
similar effect to replacement therapy

58
Q

Alcohol

A

Enhances GABAergic and glycinergic synaptic transmission
Leads to increased inhibition
Inhibition of Ca channels and activation of K+ channels
Get inhibition of glutamate receptor function and inhibition of adenosine transport
Effects occur everywhere
Individual genetic differences in these proteins contribute to addiction potential
may stimulate reward pathway by reducing GABA transmission and allowing dopamine to be more active
acts in PFC, amygdala, hippocampus and cerebellum

59
Q

disulfam for alcohol

A

causes unpleasant flush, palpitations and nausea when consuming alcohol
Take before high risk events
does not effect craving

60
Q

Acamprosate for alcohol

A

may act inhibition of NMDA or may change GABA or glutamate synaptic transmission

61
Q

Topiramate for alcohol

A

Antiepileptic and may alter phosphorylation of Na+,Ca2+, GABA and glutamate receptors/channels
May increase GABA and reduce glutamate synaptic transmission
reduces drinking but results vary

62
Q

Paracetamol and NSAIDs have what effect on ENDOCB systems

A

Increase EndoCBs as they are inhibitors of FAAH which degrades anandamide
Therefore have more anandamide around which is an endocannabinoid

63
Q

Phenytoin, carbamazepine ad lamotrigine (anti-seizure)

A

Modulate voltage gated ion channels
Inhibition and enhancement of inactivation

64
Q

Diazepam and tiagabine (anti-seizure)

A

enhance GABA mediated inhibition
Tigabine inhibits GABA transporter 1
positive allosteric modulators
May boost GABA in synapse to increase inhibition
Benzodiazepines

65
Q

Levetiracetam (anti-seizure)

A

Interact with synaptic release machinery
Bind synaptic vesicle glycoprotein (SV2A)

66
Q

Perampanel (anti-seizure)

A

Block ionotropic glutamate receptors (AMPA)

67
Q

Gabapentin and pregabalin (anti-seizure)

A

inhibit Ca2+ channel which block them and stop the release of neurotransmitter
Can reduce excitation

68
Q

CBD (epidiolex) (anti-seizure)

A

Not sure if this works - they assume it just increased the actions of clobazam which led to greater inhibition thus leading to reduces seizures

69
Q

Monoamine reuptake inhibitors MOA

A

block NA or 5HT transporters which increases levels of NA and 5HT in the synapse
TCAs - block mACh, 5HT, histamine and a-adrenoceptors. Have a narrow TI and they strongly potentiate alcohols effects (high anticholinergic and CVD side effects)
SSRI - some action on mACh and histamine. Main action on 5HT (high CNS and GIT side effects and cause increased violence, aggression and suicide behaviours - decrease overtime)

70
Q

Monoamine oxidase inhibitors (MAO-I) MOA

A

inhibit breakdown of NA, 5HT and DA which increases available monoamines
Increase leakage of monoamines into synapse and extracellular space
Can cause cheese reaction which is fatal
Irreversible and non-selective

71
Q

Tetracyclic antidepressant MOA

A

block a2 adrenoceptors which increases NA and 5HT release
Preferred action on 5HT1

72
Q

St John’s Wort (hypericum perforatum)

A

effective for mild-moderate depression
short term = inhibit 5HT, NA, DA, GABA and glutamate reuptake. Reduces NA gradient reduces transport
Long term = downregulate postsynaptic ß-adrenoceptors and increase post-synaptic 5HT1A and 5HT2 receptors
Induces CYP34A so cannot take drugs metabolised by this enzyme or will cause OD

73
Q

5HTP

A

5-hydroytryptophan used for depression
precursor to 5HT to boost serotonin levels

74
Q

benzodiazepine and insomnia

A

can promote onset of sleep
Selective (increased affinity) for GABA(A) receptors and increases the number of channels open and opening time which allows more GABA out and more inhibition
May act at amygdala, PFC, hypothalamus, striatum, bed nucleus of striatum and hippocampus
acts at a1, a2, a3 and a5 (a1 is sedative, a2 and 3 anxiolytic and a3 and a5 myorelaxant
Should really only use for one month and should be tapered off

75
Q

Z-drugs

A

Zolpidem, Zaleplon and Eszopiclone
less memory/cognition side effects than BZ
Some preference for a1
May produce bizarre sleep behaviours
Don’t cause daytime sedation
But when you stop taking them insomnia may get worse

76
Q

Antihistamines for insomnia

A

histamine is arousing
H1 inverse agonists block this effect
Cross BBB (lipophilic), have low molecular weight and are not PGP target
less effective than BZ as don’t target all systems
Get more daytime sedation, fog, memory issues and lots of side effects

77
Q

Melatonin for insomnia

A

Has a role in circadium rhythm
2 GPCR receptors (m1 activates sleep onset and m2 shifts circadium rhythm)
can cause endocrine issue in high doses
Ramelteon (synthetic analogue) has less rebound insomnia and is used for issues with sleep onset

78
Q

Benzos for anxiety

A

not first line
Act rapidly but can cause drowsiness
a2 and a3 subunit are what are important
Acts in the amygdala
alprazolam and clonazepam have higher a2 affinity

79
Q

SSRIs for anxiety

A

Bind and stop reuptake which elevates 5HT outside the cell = greater activation
5HT released from raphe nucleus
Fluoxetine and paroxetine have less side effects but can be slow acting with some side effects

80
Q

Other anxiety drugs include

A

Pregabalin - acts at alpha2delta subtype of VGCC to increases GABA levels
Buspirone - partial 5HT1a agonist for treatment of generalised anxiety disorder. Gi/o coupled receptor with strong expression in amygdala, hippocampus, cortex, DR and septum (targets range of regions)
Sometimes use TCAs and MAOIs or SNRIs (duloxetine and venlafaxine)

81
Q

Typical antipsychotics

A

ameliorate pos symptoms but have little effect on neg and cognitive symptoms
potent D2 receptor antagonists with moderate affinity for a-adrenergic and 5HT2 receptors (80% receptor occupancy)
Weak to moderate affinity for D1 and D4 receptors, histamine H1 and mACh receptors
e.g. phemothiazines, butyrophenones and thioxanthenes

82
Q

Atypical antipsychotics

A

diazepines, dibenzothiazepines, benzamides, benzisoxazols and quinolinone
Ameliorate both pos and neg symptoms
Greater therapeutic efficacy with fewer side effects
effective in treatment resistant patients
antagonise D2 receptors with high affinity and/or selectivity (60% receptor occupancy)
high affinity for 5HT2 receptors (except benzamides)
moderate affinity for a-adrenergic (except benzamides) and D3 receptors
Clozapine and olanzapine have high affinity for D4 receptors

83
Q

L-DOPA for parkinsons

A

Crosses the BBB and can be taken up by neurons and converted into dopamine (however can be converted in periphery)
Take with inhibitor of dopa decarboxylase to prevent conversion in periphery
AADC (Benserazide and carbidopa) allow more L-DOPA to cross BBB
COMT (Entacapone, opicapone, tolcapone) helps with BBB crossing and can also make sure synaptic dopamine sticks around for longer in central system so stops breakdown in synaptic cleft
MAOB (rasagiline, selegiline and safinamide) stop dopamine breakdown in synaptic cleft
can cause dyskinesia

84
Q

Dopamine agonists for Parkinsons

A

Directly stimulate DA receptors
Use dependent on surviving DA neurons (can’t give L-DOPA when neurons are dead)
D2R (pramipexole, ropiniole ad piribedil)
D1R (apomorphine and rotigotine)
Side effects include impulse control disorders, cardiac fibrosis, excessive daytime sleepiness and hallucinations

85
Q

anticholinergics for parkinsons

A

antagonise the mAChR
can be associated with delirium and confusion
Amantadine (symmetrel) is a NMDA receptor antagonist which leads to a reduction in glutamatergic overactivity in STN

86
Q

What types of drugs may be used for alzheimers

A

cholinesterase inhibitors and NMDA antagonists
May use antidepressants and neurleptics (modulate NA and 5HT neurotransmission to help with cognition)
just used to halt the symptoms but do not effect the disease pathology

87
Q

What is the future of drugs for AD

A

SS-secretase inhibitors or Y-secretase inhibitors to target pathology
APOE - cholesterol transport and reuptake
antibiotic clioquniol and lipoic acid chelate zinc reduce plaque formation in animal studies
immunisation with ß-amyloid to reduce plaque formation

88
Q

Nootropics

A

enhance learning and memory and facilitate flow of information between hemispheres
enhance resistance to chemical or physical assault
Piraxetam and pramiracetam enhance release of ACh which has shown cognitive enhancement in rats

89
Q

tryptamines

A

looks like serotonin
indul core with 2 carbon chain and amine on tail
Psilocybin and psilocin which are 5HT2A/2C and 1A agonists that produce perceptual distortion (may help with depression)
DMT short psychedelic trips with vivid hallucinations and ego death they agonise various 5HT receptors

90
Q

phenthylamine

A

looks like dopamine
potent 5HT2A agonists
Mescaline 5HT1A/2A/2C agonist with effects like altered sense of time, thinking processes and closed eye visual hallucinations
2C-B combination of MDMA and LSD. Entactogen hallucination effects vary dependent on dose
Bromo-dragonfly long lasting 2-3 days and selective for 5HT2A

91
Q

Lysergamides

A

combination of phenthylamine and tryptamine
LSD is very potent and produces euphoria, auditory and visual hallucinations, vibrant colours etc. With high doses causing ego death and perceptual distortions
LSB less potent than LSD
Ergotamine 5HT2A full agonist but acts at 5HT2B/2C and some 5HT1 receptors as well. Also dopamine D2. not psychoactive and used to treat migranes (but can be made into LSD so heavily controlled)

92
Q

MDMA

A

stimulant, entactogen, empathogen with psychedelic properties
causes neurons to dump serotonin
May help with PTSD

93
Q

Ketamine

A

dissociative anaesthetic with hallucinogenic, euphoric and psychedelic properties
May help with depression as it adjusts the signalling

PCOL drugs (1 decks)

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