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2 - BB/HD > BB CAL > Flashcards

BB CAL Flashcards

1
Q

Sodium ion concentrations

A

Axoplasm = 15

Interstitial fluid = 150

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2
Q

Potassium ion concentrations

A

Axoplasm = 150

Interstitial fluid = 5

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3
Q

Chloride ion concentrations

A

Axoplasm = 9

Interstitial fluid = 125

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4
Q

Anion concentrations

A

Axoplasm = high

Interstitial fluid = very low

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5
Q

Resting membrane potential

A

-65mV

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6
Q

Depolarised membrane potential

A

+40mV

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7
Q

Equilibrium potential for sodium

A

+58mV

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8
Q

Fast vs slow axonal transport

A 
Fast = 400mm/day 
Slow = 2.5mm/day
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9
Q

Typical synaptic delay

A

0.5ms

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10
Q

Number of vesicles in a nerve terminal

A

10,000

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11
Q

Number of NT molecules stored in each vesicle

A

3000

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12
Q

How manyy vesicles fuse for each action potential?

A

1-10

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13
Q

What is the effect of autoreceptors?

A

Depends if they are excitatory or inhibitory

Control how much NT is released in subsequent APs

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14
Q

Examples of retrograde NTs

A

NO

Endocannabinoids

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15
Q

In a GCPR, which subunit is GTP attached to?

A

Alpha

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16
Q

What is the approximate threshold value/

A

-55mV

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17
Q

Structure of a ligand gated ion channel

A

Hetero-oligomeric proteins

4-5 subunits

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18
Q

Structure of a GCPR

A

Single polypeptide chain

Crosses the membrane 7 times

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19
Q

What can cause depolarisation?

A

Influx of Na+
Influx of Ca2+
Closing of K+ channels
Efflux of Cl-

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20
Q

What causes hyperpolarisation?

A

Opening of K+ channels

Influx of Cl-

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21
Q

Which amino acid is tyrosine synthesised from?

A

Phenylalanine

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22
Q

What is the first step of dopamine synthesis from tyrosine?

A

Tyrosine –> L-Dopa
By tyrosine hydroxylase
This is the rate limiting step
Requires THB as a cofactor

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23
Q

What is the second step of dopamine synthesis from L-Dopa?

A

L-Dopa –> dopamine
By dopamine decarboxylase
Uses vitamin B6 as a cofactor
Also catalyses the final synthetic steps of 5-HT, histamine, tyramine and tryptamine synthesis

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24
Q

What is the molecule responsible for dopamine transport into vesicles?

A

VMAT2
Vesicular monoamine transporter 2
Requires ATP

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25
Q

Which type of calcium channels open in response to terminal bouton depolarisation?

A

N type

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26
Q

What happens when dopamine binds to D2 autoreceptors?

A

Inhibits dopamine synthesis

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27
Q

Two fates of dopamine

A
  • -> homovanilic acid by COMT then MAO
  • this is the major pathway
  • can be used to monitor dopamine turnover

–> 3,4-dihydrophenylacetic acid (DOPAC) by MAO and aldehyde dehydrogenase

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28
Q

D1 receptor family

A

D1 and D5
GCPRs
Postsynaptic
Activate adenylate cyclase

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29
Q

D2 receptor family

A 
D2, D3 and D4
GCPRs 
Mostly postsynaptic but some presynaptic 
Inhibit adenylate cyclase 
Activate K+ channels 
Decreased Ca2+ conductance
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30
Q

Where are D1 and D5 channels found?

A 
D1 = basal ganglia 
D5 = hippocampus and hypothalamus
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31
Q

Where are D2, D3 and D4 channels found?

A 
D2 = basal ganglia 
D3 = limbic areas 
D4 = frontal cortex, midbrain and medulla
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32
Q

What are the 3 dopamine pathways in the brain?

A

Nigrostriatal

  • 75% of brains dopamine
  • cell bodies in SNPC
  • axons terminate in corpus striatum
  • involved in motor control
  • death leads to PD

Mesolimbic

  • cell bodes in VTA of midbrain
  • axons terminate in the NA and olfactory tubercle
  • involved in Schizophrenia

Mesocortical

  • cell bodies in the VTA of midbrain
  • axons project to the frontal and cingulate cortices
  • involved in memory, motivation, reward, addiction
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33
Q

Alpha methyl-p-tyrosine

A

Inhibits tyrosine hydroxylase

Blocks dopamine synthesis

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34
Q

Reserpine and tetrabenazine

A

Inhibits VMAT2
Inhibits vesicular storage of dopamine
Used in Huntingdon’s disease

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35
Q

Dopamine agonists

A 
Pergolide 
Quinpirole 
Bromocriptine 
Apomorphine
Used in PD
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36
Q

Dopamine receptor antagonists

A

Antipsychotics –> schizophrenia
Chlorprozamine, haloperidol, clozapine (D4 mainly)
Also have affinity for ACh , H1 and 5-HT2 receptors

37
Q

Amantadine

A

Causes dopamine release
Blocks dopamine reuptake
Used in PD

38
Q

Selegiline

A

MAOb inhibitor
+ rasagiline
Used in PD

39
Q

Entacapone, tolcapone

A

COMT inhibitors
Used in pD
Used alongside L-Dopa

40
Q

Antimuscarinics

A

Benzhexol, benztropine
Can be used in PD
Increase release and inhibit reuptake

41
Q

How is 5-HT synthesised?

A

Tryptophan taken up into nerve terminal

Tryptophan –> 5-hydroxytyptophan 5-HTP b

  • by tryptophan hydroxylase
  • required tetrahydrobiopterin
  • rate limiting step

5-HTP –> 5-HT
- by DOPA decarboxylase

42
Q

What is needed for 5-HT storages

A

Vesicles
ATP
Na+

43
Q

How is 5-HT inactivated?

A

Degraded by MAO initially

  • -> 5-HIAA by aldehyde dehydrogenase (predominant) = oxidation
  • -> 5-hydroxytryptophol by alcohol dehydrogenase = reduction
44
Q

What type of receptors are 5-HT receptors?

A

All GCPRs

Except 5-HT3 which are ligand gated ion channels

45
Q

5-HT1

A 
Negatively coupled to adenylate cyclase 
Activate K+ channels 
A = anxiety + pain  
B = cranial blood vessels 
F = uterus
46
Q

5-HT2

A

Coupled to inositol phosphate
A = anxiety, depression, pain, vascular, tracheal and bronchial smooth muscle contraction
B = rat fundic strip contraction
C = spinal distribution –> CSF formation rate

47
Q

5-HT3

A

Ligand gated ion channels

Role in emesis

48
Q

5-HT4

A

Positively coupled to adenylate cyclase
Relax oesophageal smooth muscle
Increase heart rate and force

49
Q

5-HT6&7

A

Positively coupled to adenylate cyclase

Low peripheral expression

50
Q

Which receptors affect serotonin release?

A

Inhibitory 5-HT1a receptors

Inhibition 5-HT1b/d autoreceptors

51
Q

Buspirone, ipsapirone

A

5-HT1a partial agonists
Desensitise 5-HT1a receptors
Increase firing rate and 5-HT release
Used to treat anxiety

52
Q

Sumatriptan

A

5-HT1b/d agonist
Used for migraine and cluster headache treatment
Induces cerebral blood vessel vasoconstriction and reduces release of neuropeptides

53
Q

Ondansetron

A

5-HT3 antagonist

Anti-emetic

54
Q

LSD

A

Agonist of 5-HT1 receptors

55
Q

Irreversible MAOIs

A 
Phenelzine, isocarboxazid 
Non-selective 
Cheese reaction (with tyramine ingestion)
56
Q

Moclobemide

A

Reversible MOAIs
More selective for MAOa
Much less severe risk effects and Cheese reaction

57
Q

Drugs that do not give rise to dependence

A

Cannabinoids

LSD

58
Q

Psychological effects of withdrawal

A 
Produced by all drugs of dependence 
Due to effects on the limbic system
Mood changes 
Anxiety 
Agitation 
Feeling unable to cope
59
Q

Drugs that only produce psychological withdrawal

A

Cocaine
Amphetamine
Nicotine
Caffeine

60
Q

Physical dependence

A

Clear cut syndrome of physical symptoms

Relatively short lived –> 2 weeks

61
Q

Opiate withdrawal

A 
Diarrhoea 
Nausea/vomiting 
Abdominal discomfort
Convulsions 
Sweating
62
Q

Barbiturate withdrawal

A 
Anxiety 
Insomnia 
Epileptic fits 
Sweating 
Tremors 
Delirium, delusions and hallucinations
63
Q

Benzodiazepines withdrawal

A

Convulsions
Panic attacks
Anxiety

64
Q

Alcohol withdrawal

A

Convulsions
Sweating
Tremors
Anxiety

65
Q

Which drugs develop tolerance but not dependence?

A

LSD
GYN
Anticholinesterases

66
Q

What is acute tolerance?

A

Tachyphylaxis –> densitisation
Occurs when a receptor becomes desensitisied after the first dose
Occurs with nicotine

67
Q

Types of chronic tolerance

A 
Cellular = pharmacodynamic 
Pharmacokinetic = metabolic
68
Q

What is cellular tolerance?

A

Due to neuroadaptive changes that produce diminished responses to drugs
Follows chronic exposure
Major contributor to drug tolerance

69
Q

What is pharmacokinetic tolerance?

A

Due to an increase in metabolism of a drug
Caused by induction of liver enzymes
Overcome by taking a larger dose

70
Q

Psychomotor stimulants

A

Nicotine
Amphetamine
Cocaine
Caffeine

71
Q

CNS depressants

A

Alcohol
Opiates
Barbiturates
Benzodiazepines

72
Q

Nicotine tolerance

A

All 3 types
Acute - to HR changes
Cellular - to nausea, dizziness
PK - only to a small degree

73
Q

Where does nicotine act?

A

NA and VTA –> dependence and reward
Hippocampus –> increased attention
Reticular formation –> increased alertness

74
Q

BZ tolerance

A

Cellular type

To antipsychotic effects more than anxiolytic effects

75
Q

Where do BZs and barbiturates act?

A

Raphe nuclei –> increase 5-HT transmission

Reticular formation –> sedation

76
Q

Barbiturate tolerance

A

PK –> p450 enzyme induction

Some cellular tolerance

77
Q

Alcohol tolerance

A

Acute - in one session
Cellular = in regular drinking
PK = only in severe alcoholics –> p450

78
Q

Opiate tolerance

A

Early = nausea and vomiting
Medium = euphoria, analgesia and respiratory depression
No tolerance = constipation, pupillary constriction

79
Q

Opiate receptors

A

Mu –> euphoria, analgesia, resp depression, constipation
Kappa –> analgesia
Delta –> analgesia

80
Q

Where do opiates act?

A

VTA and NA –> euphoria and dependence
PAG –> analgesia
Reticular formation –> sedation and respiratory depression
Area postrema = nausea and vomiting

81
Q

Cocaine dependence

A

Psychological but not physical

82
Q

Cocaine tolerance

A

Euphoria is lost

Cardiovascular effects do not show tolerance easily

83
Q

Cocaine MoA

A

Inhibition dopamine reuptake

84
Q

Where does cocaine act?

A

NA –> euphoria and dependence
Hypothalamus –> increased temperature and decreased food consumption
Reticular formation –> increased alterness

85
Q

Caffeine tolerance

A

Fast = unpleasant effects

Little tolerance = psychostimulant effects

86
Q

Caffeine MoA

A

Inhibits adenosine A1 receptors

Inhibits PDE which inactivates cAMP

87
Q

Amphetamine tolerance

A

Cellular type

Means overdose is likely –> psychosis

88
Q

Amphetamine MoA

A

Stimulate release of catecholamines (DA, NA, A)
Inhibit reuptake
Inhibit MAO

89
Q

Where do amphetamines act?

A

NA –> euphoria and dependence
Hypothalamus –> increased temperature and decreased food consumption
Reticular formation –> increased alterness

2 - BB/HD (8 decks)

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