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Pharmacology > Unit 4 Workbook > Flashcards

Unit 4 Workbook Flashcards

1
Q

DEPRESSION

  1. Hypothesis
  2. Pharmacological approaches
  3. Targets
A
  1. reduced central functioning of NA/serotonergic NT
  2. enhancement of synaptic NA/serotonin
  3. monoamine reuptake inhibitors, monoamine receptor antagonists, monoamine oxidase inhibitors
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2
Q

SCHIZOPHRENIA

  1. Hypothesis
  2. Pharmacological approaches
  3. Targets
A
  1. enhanced central functioning of dopaminergic NT
  2. reduction in dopamine receptor-mediated effects
  3. dopamine receptor antagonists, partial agonists
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3
Q

ANXIETY

  1. Hypothesis
  2. Pharmacological approaches
  3. Targets
A
  1. overactivity of central noradrenergic, underactivity of serotonergic and GABAergic systems
  2. restoration of normal activity of central transmitter systems
  3. benzodiazepine site of GABAA receptor complex, partial agonists of 5-HT1A receptors, serotonin reuptake inhibitors, noradrenergic receptor agonists
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4
Q

ALZHEIMER’S DISEASE

  1. Hypothesis
  2. Pharmacological approaches
  3. Targets
A
  1. neurodegeneration of central cholinergic neurons
  2. enhancement of synaptic ACh levels
  3. acetylcholinesterase inhibitors
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5
Q

PARKINSON’S DISEASE

  1. Hypothesis
  2. Pharmacological approaches
  3. Targets
A
  1. neurodegeneration of central dopaminergic neurons
  2. enhancement of synaptic dopamine levels
  3. increasing dopamine precursors, inhibition of MAO-B, dopamine receptor agonists
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6
Q

synaptosomes

A

a subcellular fraction obtained following the disruption and centrifugation of brain samples

The synaptosomes used in evaluating a drug’s binding are typically derived from rat brain

used to assess not only the affinity of the drug for the binding site of the target of interest (usually measured as a Ki, the dissociation equilibrium constant for an inhibitor) but also the relative affinity for a range of other proteins (including other receptors, neurotransmitter transport proteins, ion channels and enzymes) to determine selectivity

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7
Q

“classical” monoamine receptors

A

adrenergic (α1, α2, B1, B2);

dopamine (D1 -D5);

histamine (H1, H2);

muscarinic (M1-M5);

serotonin: (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3, 5-HT5A, 5-HT6, 5-HT7)

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8
Q

AA based receptors

A

GABA

benzodiazepine (BZD central, BZD peripheral)

phencyclidine (PCP) sits on NMDA receptor

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9
Q

neuropeptide receptors

A

angiotensin-II: AT1, AT2; bombesin; bradykinin (B2); calcitonin gene-related peptide (CGRP); cholecystokinin (CCKA, CCKB); endothelin (ETA, ETB); galanin: GAL1, GAL2); Growth factors, cytokines, chemokines: CXCR2, TNF-α, CCR1; melanocortin (MC4); neurokinin (NK1, NK2, NK3); neuropeptide Y (Y1, Y2); neurotensin (NT1, NT2); opiate: gamma, kappa, μ, orphanin: ORL1); PACAP (PAC1); somatostatin (Sst); vasopressin: (V1a); vasoactive intestinal peptide (VIP1)

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10
Q

other receptors

A

adenosine (A1, A2, A3); cannabinoid (CB1, CB2); prostanoid (P2X, P2Y); sigma σ

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11
Q

transporters

A

dopamine DA

noradrenaline NA

serotonin 5-HT

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12
Q

enzymes

A

Cyclooxygenase (COX-1, COX-2); acetylcholinesterase (AChE)

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13
Q

when is an affinity for more than 1 target desirable

A

dual reuptake inhibitor antidepressants (increase no. of patients that will respond)

D2/5-HT2 receptor antagonism that is a property of many of the more recently introduced antipsychotic agents (reduce adverse effects)

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14
Q

occupancy of a given concentration of a drug for its receptor equation

A
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15
Q

competitive antagonist

A

it should be able to displace the radioligand and generate a reverse sigmoid curve

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16
Q

IC50 value

A

The antagonist concentration that produces a 50% reduction in binding

similar to EC50

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17
Q

Cheng-Prusoff equation

A
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18
Q

3 mechanisms by which CNS drugs exert their effect

A

affinity for target

inhibition of reuptake

inhibition of enzyme activity

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19
Q

vilazodone

A

anti-depressant

In addition to 5-HT reuptake inhibition, vilazodone displays partial agonist properties at the 5-HT1A receptor, and these combined effects are believed to have antidepressant properties, whilst reducing the extent of serotonin-mediated adverse effects seen with SSRI antidepressants

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20
Q

3 AChesterase inhibitors

A
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21
Q

high affinity for H1 receptors

A

sedating and weight gain properties

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22
Q

α1 blockade

A

associated with a potential to produce postural (orthostatic) hypotension

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23
Q

fluoxetine

A

SSRI

selectivity for a single target, i.e. the 5-HT reuptake site and as a result has a “cleaner” safety profile than amitriptyline with most of its adverse effects associated with the serotonergic system

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24
Q

venlafaxine

A

roughly equivalent inhibition of noradrenaline and 5-HT reuptake and is known as a dual uptake inhibitor

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25
Q

mirtazapine

A

“atypical” profile in that has no affinity for reuptake sites, and instead exerts its antidepressant effects by blocking the α2 and 5-HT2A receptors

its sedating effects can be attributed to high affinity for the H1 receptor

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26
Q

in vitro profile for antidepressant drugs

A

darker colour => greater affinity for the target => low Ki value

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27
Q

face validity

A

how well the model simulates symptoms of the disease - core features of the disase to be modelled as identified in the diagnostic criteria

this is easier in some behaviours e.g. anhedonia, memory loss, than others (cognitive dysfunction)

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28
Q

predictive validity

A

How well the model responds to drugs that are effective clinically in the disease state, and only to these drugs, without there being either false positives or false negatives in the model

Moreover, the duration required for effective treatment should mirror that observed clinically

A consequence to emphasising the predictive validity is that the model is likely to produce active compounds that have a similar pharmacological profile to existing clinically effective drugs (i.e. “me-too” drugs that will have many of the same problems as far as efficacy and spectrum of activity are concerned), and that drugs with a truly novel mechanism of action may not be found to be active

29
Q

construct validity

A

The model possesses the same neurobiological substrates and involves similar pathophysiological mechanisms as the disease state, e.g. a perturbation in the same neural circuits and pathways

This validity is particularly challenging for animal models of CNS disorders to achieve, when we are uncertain of the specific underlying mechanisms (and moreover whether there is a single such mechanism) for the many CNS disorders

neuroimaging is helping to identify neuroanatomical landmarks - hippocampus, amygdala and frontal cortex are common across species

30
Q

mean and standard error of the mean

A

To determine whether drug treatment has had an effect, the data undergoes statistical testing and significant differences between drug treatments and the control group are denoted by the presence of symbols (most commonly asterisks) above the error bar

31
Q

drugs initially used to treat anxiety

A

barbituates - fatal in overdose

32
Q

benzodiazepines e.g.

treat…

A

anxiety

diazepam

33
Q

elevated plus maze (EPM)

A

Anxiolytic drugs will increase the number of entries and time spent in the open arms

34
Q

chlorpromazine

A

discovered by chance

35
Q

severe side effects of 1st generation antipsychotics

A

tardive dyskinesia and extrapyramidal symptoms (EPS)

36
Q

neurochemical MOA of amphetamine

A

release catecholamine neurotransmitters (particularly dopamine) from their presynaptic stores out into the synapse to activate postsynaptic receptors

It was observed that the consequences of administration of amphetamine and cocaine can resemble a psychotic episode

37
Q

amphetamine causes

A

an increase in locomotor activity

38
Q

acetylcholinesterase inhibitors treat

A

Alzheimers e.g. donepezil

39
Q

noncompetitive NMDA receptor antagonist treats

A

Alzheimer’s

e.g. memantine

40
Q

rotarod, 6-OHDA and zolpidem

41
Q

cocaine and diazepam

A

increase in locomotor activity with cocaine

then sedating effects of diazepam

anxiolytic effects

42
Q

extrapyramidal side effects

A

parkinson-like symptoms

may occur with 1st generation antipsychotics - excessive blockade of dopamine receptors

43
Q

catalepsy

what drug increases catalepsy

A

time taken for paws to be taken off ledge

haloperidol

44
Q

therapeutic effects of most CNS drugs

A

enhancement of the synaptic concentration of an endogenous NT (indirect agonist effect)

or by blocking or activating the postsynaptic receptors

45
Q

Pentylenetetrazole

A

a compound that induces seizures in mice

46
Q

L-DOPA

A

dopamine precursor

47
Q

Pramipexole

A

D2 receptor agonist

48
Q

Midazolam

A

GABA allosteric modulator

49
Q

Chlorpromazine

A

D2 receptor antagonist - 1st generation antipsychotic

50
Q

haloperidol

A

D2 receptor antagonist - 1st generation antipsychotic

51
Q

clozapine

A

D2 receptor antagonist - 2nd generation antipsychotic

52
Q

risperidone

A

D2 receptor antagonist - 2nd generation antipsychotic

53
Q

diazepam

A

GABA allosteric modulator

54
Q

busiprone

A

partial 5-HT1A agonist

55
Q

benzatropine

A

muscarinic antagonist

56
Q

mirtazapine

A

α2, 5-HT2A/5-HT2C antagonist

57
Q

selegeline

A

MAO-B inhibitor

58
Q

moclobemide

A

MAO-A inhibitor

59
Q

Phenelzine

A

non-selective MAO inhibitor

60
Q

donepezil

A

AChesterase inhibitor

61
Q

rivastigmine

A

AChesterase inhibitor

62
Q

Gallanthamine

A

AChesterase inhibitor

63
Q

fluoxetine

64
Q

escitalopram

65
Q

sertraline

66
Q

amitriptyline

A

serotonin/noradrenaline reuptake inhibitor (TCA)

67
Q

venlafaxine

A

serotonin/noradrenaline reuptake inhibitor

68
Q

vilazodone

A

SSRI and partial 5-HT1A agonist

Pharmacology (23 decks)

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