Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When may B blockers be used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give examples of drugs acting at the cell membrane

A

Adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Sex hormones, GH (Steroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give examples of drugs acting on intracellular enzymes

A

MAO inhibtiors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define drug

A

A substance that induces a biological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define receptor

A

A cellular drug target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define pharmacokinetics and pharmacodynamics

A

Kinetics - What the body does to the drug

Dynamics - What the drug does to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do antagonists and agonists differ in functionality?

A

Agonist - affinity and efficacy

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the different types of agonist?

A

Full
Partial
Inverse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is digoxin used for?

A

Congestive heart failure - +inoptrope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define threshold concentration

A

Lowest dose to give an effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define max dose

A

Maximum dose before side effects begin to majorly increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Which factors can affect absorption?
Route, frequency of dosing, half life
26
Which factors can affect distribution?
Plasma protein binding, lipid solubility, rate of blood flow
27
Which factors can affect elimination?
Half life, frequency of dosing, disease
28
Why do heavy metal and DDT poisoning occur?
The elimination pathway of their pharmacokinetics is not functional!
29
When do drug interactions occur?
Build up of substrate and insufficient enzyme -> interactions eg. dysfunctional P450 hepatic enzyme system which can occur genetically
30
What must be remembered about psychiatric drugs?
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
Give 5 pharmacological targets for neurotransmission
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
What actions do successful/effective drugs tend to have?
Broad effects at multiple sites (this -> ^risk of side effect though)
33
Give a psychoactive drug with a low TI
Clomipramine (TCA) for separation anxiety - > cardiotoxicity with arrythmias - no antidote - delayed onset
34
Give the 6 drug classes used in the treatment of anxiety
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
What are the actions of ACP
Sedative but REFLEXES ARE NOT AFFECTED - give analgesia too
36
What are the 3 GABA receptors?
GABAa - ligand gated ion channel, pentameric, Cl- channel GABAb - G-protein coupled receptor, activting K+ channels GABAc - ligand gated ion channel Cl-
37
What is the mechanism of action of benzodiazepines?
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
What ar the effects and uses of Benzodiazepines?
-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
What may underlie anxiety neurologically?
> 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
What is the main use of Azaperones?
Anxiolytic and aggression
41
What is the pharmacological activity of azaperones like?
Chemical straightjacket! - Multiple actions at multiple receptors
42
Give an example of an azaperone
Buspirone - partial 5-HT1a agonist
43
How does endogenous ligand concentration affect the actions of partial agonists?
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
Following the onset of a shock or fear response, what should happen?
NA and 5-HT increase, then are Downregulated by prefrontal cortex
45
How is histamine related to the brain?
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
What pathological state occurs when the serotonin system fails to function correctly?
Depression
47
Which are the monoamine NTs?
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
Which part of the neurone does buspirone act on?
The cell body (usually in the brainstem) Downregulates 5-HT system
49
Why is dopamine not usually targeted for drug use in antidepressant field?
Link with cocaine/amphetamine
50
Give 7 drugs used in the treatment of affective disorders (OCD, depression, anxiety disorders)
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
What does the increased [synaptic monoamine] act to do?
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
Which drugs are safer, TCAs or SSRIs?
SSRIs! TCAs have a sedative muscarinic effect and give you dry mouth and blurred vision
53
How selective are most uptake inhibitors for 5HT or NA?
Ranges from Citalopram (most selective for 5HT) to Reboxetine (most selective for NA) VENLAFAXINE VERY GOOD DRUG EQUAL NA AND 5HT SELECTIVITY
54
What are antipyschotics/neuroleptics used for?
``` controlling aggression (scizophrenia in humans) - chemical straight jacket ```
55
What are the two classes of antipyschotics/neuroleptics?
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
Outline the antiphyschotic drug D2 R blockade
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
High doses of what type of drug can provide chemical restraint?
Antipyschotics eg. Aceptapromazine
58
What is another name for Atypical antipyschotics?
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
How can the best efficacy be achieved when formulating a drug?
Multiple therapeutic mechanisms, without multiple extra mechanisms which will evoke side effects
60
What physiological use do anticonvulsants have?
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
What type of drug is Selegeline?
MAOb inhibitor - enhance DA reelase and blockade of reuptake - does not induce food interactions
62
Where does MAob predominate?
DA rich areas of CNS
63
How may MAOb be neuroprotective? (i.e. for use in dementia in dogs and cats)
Reduces oxygen free radical production (up regulates superoxide dismutase) Delays apoptosis - sows decline, does NOT prevent

BVetMed - Animal Behaviour (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions