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BVetMed - Animal Behaviour > Introduction to Psychopharmacology > Flashcards

Introduction to Psychopharmacology Flashcards

1
Q

What are the major drug psychoactive classes?

A 
- Sedatives- 
Benzodiazepines 
Barbituates 
Azapirones 
- Antidepressives and anxiety - 
TCA
SSRI
MAO inhibitors 
- Neuroleptic/Antipyschotics eg. ACP, chlorpromazine, haloperidol 
- epilepsy and mania 
Anti-convulsants 
-Sedative 
Antihistamines
B Blockers
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2
Q

When may B blockers be used?

A

Combat the somatic signs of aniety which could be detected by body -> feelings of fear

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3
Q

Which drugs are used as anti depressive in humans/ anxiety in animals? Which other condition may one of these be useful for?

A

TCAs
SSRIs
MAO Inhibitiors
- may also be useful in age related cog decline (dementia)

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4
Q

Give examples of drugs acting at the cell membrane

A

Adrenaline

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5
Q

Give examples of drugs acting at a nuclear receptor and impacting protein synthesis

A

Sex hormones, GH (Steroids)

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6
Q

Give examples of drugs acting on intracellular enzymes

A

MAO inhibtiors

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7
Q

Define drug

A

A substance that induces a biological response

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8
Q

Define receptor

A

A cellular drug target

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9
Q

Define pharmacokinetics and pharmacodynamics

A

Kinetics - What the body does to the drug

Dynamics - What the drug does to the body

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10
Q

Define affinity, efficacy and specificity

A

Affinity - ability to interact with a receptor
Efficacy - ability to induce a biological response
Specificity - NO drug is truly specific - as the conc^ will exert other actions

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11
Q

How do antagonists and agonists differ in functionality?

A

Agonist - affinity and efficacy

Antagonist - has affinity but NEVER efficacy (always =0)

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12
Q

What are the different types of agonist?

A

Full
Partial
Inverse

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13
Q

What is digoxin used for?

A

Congestive heart failure - +inoptrope

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14
Q

Define threshold concentration

A

Lowest dose to give an effect

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15
Q

Define max dose

A

Maximum dose before side effects begin to majorly increase

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16
Q

Give examples of a partial agonist

A
  • Buspirone - 5-HT modulator used for feline urinary issues, separation anxiety and feather pecking
  • Buprenorphine - partial opioid agonist -> less risk of reparatory depression associated with analgesia and harder to OD
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17
Q

What is the outcome of a partial agonist dependant upon?

A

The [endogenous agonist]
- if ^ -> antagonism
- if v -> agonism
Therefore acts as a MODULATOR of neurotransmission

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18
Q

What are the 6 types of antagonism?

A

Competitive (reverisble)
Competitive (Irreversible) - usually enzymes (enzyme “suicide”)
Non-competitive - inhibits the way enzymes function
Physiological
Pharmacokinetic
Chemical

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19
Q

Give a use of an antagonist

A

Dexometodine -> Aneasthesia
Competitive antagonist shifts concentration of active anaesthetic and stops it from working, thus reversing effects of anaesthesia
(Shifts dose response curve to the right)

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20
Q

How does non-competitive antagonism affect the shape of the dose-response curve?

A

MAY shift curve -> right
Decreases gradient of slope
Decreases maximum possible response

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21
Q

What are the two types of receptor adaptation that occur in response to drug use?

A 
Short term - desensitisation 
-> rapid
uncoupling from effector mechanism eg. G protein 
internalisation of receptor 
inactivation of ion channels 
temporary efect 
rapidly reversed 
Long term - down-regulation 
-> slow 
changes in protein expression levels 
adaptive response to long term agonist activation 
secondary to other mechanisms eg. chronic stress 
influenced by multiple factors 
slow to reverse
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22
Q

What phenomena may receptor adaptation underlie?

A 
Antidepressants 
Antipyschotics 
Mood stabilising drugs 
Tolerance
Side effect profiles 
-> May also be the therapeutic action of the drug!!
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23
Q

Give an example of receptor adaptation?

A

Exogenous steroid use -> endogenous steroid production by negative feedback (can occur with any long term medication)

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24
Q

Outline the different aspects of pharmacokinetics

A 
What the body does to the drug
Administered->
Absorption->
Systemic blood circulation->
Distribution->
Tissues ->
Elimination (metabolised or excreted)
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25
Q

Which factors can affect absorption?

A

Route, frequency of dosing, half life

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26
Q

Which factors can affect distribution?

A

Plasma protein binding, lipid solubility, rate of blood flow

27
Q

Which factors can affect elimination?

A

Half life, frequency of dosing, disease

28
Q

Why do heavy metal and DDT poisoning occur?

A

The elimination pathway of their pharmacokinetics is not functional!

29
Q

When do drug interactions occur?

A

Build up of substrate and insufficient enzyme -> interactions
eg. dysfunctional P450 hepatic enzyme system which can occur genetically

30
Q

What must be remembered about psychiatric drugs?

A

Many have active metabolites which can build up
Most drug interactions are more for academic or marketing interest than clinically relevant
Some have low Tis eg. TCAs like clomipramine

31
Q

Give 5 pharmacological targets for neurotransmission

A
  1. Post-synaptic receptors eg. buspirone (5-HT1a), diazepam (GABAa)
  2. Auto/hetero receptors - negative feedback from the synapse stimulated by tonic NT levels eg. mirtazipine (a2-adrenoceptor) appetite stimulus, antidepressant and sleep disorder drug
  3. Enzymes eg. selegeline (MAOb inhibitor) neuroprotective action
  4. Reuptake transporters eg. clomipramine (TCA), fluvoxetine (SSRI)
  5. Ion channels
32
Q

What actions do successful/effective drugs tend to have?

A

Broad effects at multiple sites (this -> ^risk of side effect though)

33
Q

Give a psychoactive drug with a low TI

A

Clomipramine (TCA) for separation anxiety

  • > cardiotoxicity with arrythmias
  • no antidote
  • delayed onset
34
Q

Give the 6 drug classes used in the treatment of anxiety

A

1- Benzidiazepines - amnesic, anxiolytic, hypnotic, NOT LONGTERM, tolerance and dependence)
2- Barbituates - anticonvulsant, anaesthetic, v TI (Petabarbitone = euthanasia) CNS depressant
3- Azapirones - antipyschotic, motor sedative (voluntary movement only, reflexes still work) DA antag. eg. Stresnil (pig aggression,) Fluoperidol SHORT TERM behaviour control
4-Buspirone - nonsedating anxiolytic 5-HT1a partial agonist
5- Antihistmines (sedative) eg. piritone
6- B-blockers - treat somatic signs of anxiety

35
Q

What are the actions of ACP

A

Sedative but REFLEXES ARE NOT AFFECTED - give analgesia too

36
Q

What are the 3 GABA receptors?

A

GABAa - ligand gated ion channel, pentameric, Cl- channel
GABAb - G-protein coupled receptor, activting K+ channels
GABAc - ligand gated ion channel Cl-

37
Q

What is the mechanism of action of benzodiazepines?

A

Enhance response of GABA - facilitate opening of GABA activated Cl- channel
Bind to regulatory site
^affinity for GABA
^frequency of opening
Do not affect conductance or mean opening time
- potentiates GABA effectiveness essentially

38
Q

What ar the effects and uses of Benzodiazepines?

A

-v anxiety and aggression
- sedation, hypotic
- reduced muscle tone and coordination
- anticonvulsant
- retrograde amnesia
- paradoxical increase in irritability and aggression (DISINHIBITION)
unwanted effects
- acute overdose
- tolerance and dependance
- side effects during therapy eg. sedation when wanted as an anxiolytic

39
Q

What may underlie anxiety neurologically?

A

> Distribution of GABA receptors (potentially)
Serotonin
-Dense 5-HT input to locus coerulus and amygdala which spark a fear response before visual recognition of the stimulus itself
-Low 5-HT activity may -> dysregulation of other neurotransmitters eg. NA
-Reciprocal interactions eg. medial PFC connected wit hamygdala, allowing regulation of affect and modulation of autonomic and neuroendocrine function allowing cognitive control of anxiety response
-STEIN’S theory suggests ^5-HT -> anxiety disorders

40
Q

What is the main use of Azaperones?

A

Anxiolytic and aggression

41
Q

What is the pharmacological activity of azaperones like?

A

Chemical straightjacket! - Multiple actions at multiple receptors

42
Q

Give an example of an azaperone

A

Buspirone - partial 5-HT1a agonist

43
Q

How does endogenous ligand concentration affect the actions of partial agonists?

A

If endogenous ligand conc is high, acts as an antagonist by competing for receptors (thus moves curve -> right)
If endogenous ligand conc is low, acts as an agonist but can only produce a sub maximal response

44
Q

Following the onset of a shock or fear response, what should happen?

A

NA and 5-HT increase, then are Downregulated by prefrontal cortex

45
Q

How is histamine related to the brain?

A

Present in low levels in the CNS
- hypothalamc neurones with widespread axonal innervations
- H1 in cortex and reticular activating system aontribute to arousal and wakefulness (therefore H1 antags are sedative)
Also involved in emesis, regulation of food and water intake, thermoreg

46
Q

What pathological state occurs when the serotonin system fails to function correctly?

A

Depression

47
Q

Which are the monoamine NTs?

A

Serotonin (IMPULSE,) Noradrenaline (VIGILANCE,) Dopamine (DRIVE) - interactions as outlined by Healy and MacMonagle 1997

  • implicated in the control of mood, emotion and behavioural responses
  • regulate and are influenced by endocrine systems
48
Q

Which part of the neurone does buspirone act on?

A

The cell body (usually in the brainstem) Downregulates 5-HT system

49
Q

Why is dopamine not usually targeted for drug use in antidepressant field?

A

Link with cocaine/amphetamine

50
Q

Give 7 drugs used in the treatment of affective disorders (OCD, depression, anxiety disorders)

A

TCAs eg. clomipramine, amytryptaline
SSRIs eg. Fluoxetine, paroxetine
5HT and NA reuptake inhibs eg. Venlafaxine
5HT and NA repecific antagonist eg. Mirtazapine
- both of these ^NA and 5HT
NA SRIs eg. Reboxetine
Mixed uptake inhibitors and antagonists eg. nefazedone
MAO inhibitors eg. Selegeline
ALL ACT TO INCREASE MONOAMINE TRANSMISSION

51
Q

What does the increased [synaptic monoamine] act to do?

A
  1. Activation of somatodendritic autoreceptors - v firing rate -> hippocampal neurogenesis
  2. Receptor adaptation up/down regulation (plasticity) -> ^[synaptic] and cognitive effects
  3. Activation of pre-synaptic auto receptors - v NT release -> Post-synaptic receptor adaptation
    * Remember there are multiple causes of anxiety
52
Q

Which drugs are safer, TCAs or SSRIs?

A

SSRIs! TCAs have a sedative muscarinic effect and give you dry mouth and blurred vision

53
Q

How selective are most uptake inhibitors for 5HT or NA?

A

Ranges from Citalopram (most selective for 5HT) to Reboxetine (most selective for NA)
VENLAFAXINE VERY GOOD DRUG EQUAL NA AND 5HT SELECTIVITY

54
Q

What are antipyschotics/neuroleptics used for?

A 
controlling aggression (scizophrenia in humans)
- chemical straight jacket
55
Q

What are the two classes of antipyschotics/neuroleptics?

A

Typical - DA untags (Extrapyramidal, muscarinic and Motor side effects)
- Treat + symptoms of schizophrenia, multiple sites of action all D2 receptors, multiple side effects (may induce depression and parkinsons or catalepsy in animals)
Atypical - DA and 5HT antags (No motor side effects, but weight gain, insomnia, sedation side effects)
- More selective targeting D2 and 5HT2 Rs, reduced side effects and therapeutic profile

56
Q

Outline the antiphyschotic drug D2 R blockade

A
  1. mesolimbic - reduces positive symptoms
  2. Mesocortical - Incresases negative symptoms, cognitive deficits
  3. Nigrostriatal - induces motor side effects (parkinsons)
  4. Tuberoinfundibular - Effects on hormone secretion (hyperPRLeamia)
57
Q

High doses of what type of drug can provide chemical restraint?

A

Antipyschotics eg. Aceptapromazine

58
Q

What is another name for Atypical antipyschotics?

A

2nd generation

  • D2 and 5HT antagonists (hypothesised improved efficacy and reduced side effects compared to typical antipyschotics but limited evidence)
  • Fast off theory (fast kinetics)
  • R5HT2a receptors expressed in cortical, hippocampal regions especially
59
Q

How can the best efficacy be achieved when formulating a drug?

A

Multiple therapeutic mechanisms, without multiple extra mechanisms which will evoke side effects

60
Q

What physiological use do anticonvulsants have?

A

Mood stabilising - eg. for bipolar

  • enhanced GABA action eg. phenobarbital
  • Inhibition of sodium channels eg. Carbamazepine, phenytoin
  • Inhibition of calcium channels eg. Ethosuximide, gabapentin
  • reduce electrical excitability of cell membranes through USE DEPENDANT Na channel blockade
61
Q

What type of drug is Selegeline?

A

MAOb inhibitor

  • enhance DA reelase and blockade of reuptake
  • does not induce food interactions
62
Q

Where does MAob predominate?

A

DA rich areas of CNS

63
Q

How may MAOb be neuroprotective? (i.e. for use in dementia in dogs and cats)

A

Reduces oxygen free radical production (up regulates superoxide dismutase)
Delays apoptosis
- sows decline, does NOT prevent

BVetMed - Animal Behaviour (35 decks)

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