Behaviour Modifying Drugs Flashcards by Giselle Carter

what are the 5 key neurotransmitters for behaviour modification

NE
dopamine
serotonin
GABA
acetylcholine

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T/F the current drugs used to modify behaviour in vetmed are extra-label use of human drugs

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what is the effect of behaviour modifying drugs on behaviour modifying techniques

it can decrease latency to responses

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what are the two types of aggression? which is more common and which is more of a concern?

offensive and defensive; offensive more of a concern but defensive more common

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what are some subtypes of aggression

fear
dominance
territorial
possessive
maternal

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drugs that do what can reduce aggression

drugs that increase central serotonergic activity

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what general category of drugs (3) can reduce compulsive behaviour

TCA’s, SSRIs, opioid antagonists

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what types of drugs can help fear/anxiety/phobias

anxiolytics

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treatment of behaviour disorders with drugs will vary in duration with:

drug class
the individual/species
the unwanted behaviour
the owner’s compliance

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how are most behaviour modifying drugs given (constantly or as needed)

most are NOT given as needed

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how do we ideally want to manage behaviour modifying drug dosage

gradually reduce (taper) the dose based on the animals response; identify the lowest effective dose

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what is an important consideration re. pharmacokinetics and pharmacodynamics if you think a behaviour modifying drug is not working

It takes time! approx 5 half-lives before reaching steady state; receptor modification also takes time

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what can you do if the behaviour modifying drug is not working

adjust dose (consider ADRs)
switch drug class
combination drug therapy

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Are behaviour modifying drugs good transdermal

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many behaviour drugs used in vet med are weak (acids/bases)

what does this mean?

bases

good lipophilicity
low protein binding
good CNS penetration

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most behaviour drugs are metabolized by

liver

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what are the principal anxiolytics in vetmed

benzodiazepines

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how do benzodiazepines work? where is the anxiolytic effect coming from

stimulate GABA-A receptors; believed that the anxiolytic effect is due to modulation of 5-HT and NE neurons in the CNS

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T/F the anxiolytic effects of benzos can be immediate and increase with dosing

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what is the use of benzodiazepines for anxiolysis

separation anxiety and general anxiety

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why should we avoid using benzodiazpines in aggressive dogs

can cause disinhibition

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what are some potential adverse effects of benzodiazepines as an anxiolytic drug

what can we use to reverse these effects

disinhibition
excitement and amnesia
hepatotoxicity in cats with diazepam
sedation
mm relaxation
ataxia
hyperphagia

flumazenil

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is the half life of diazepam higher in dogs or cats and what does that mean

cats (5.5h vs 1h in dogs); can be used chronically in cats only

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what are some caveats of diazepam as a behaviour modifying drug

disappointing for immediate effects; daily use better than as needed use; may need higher doses in panic states

what is a benefit of alprazolam over diazepam

more potent so it produces better results in dogs with panic disorders where a rapid response is needed

what is a benefit of lorazepam over alprazolam and diazepam

lower hepatic metabolism before excretion, making it better for liver dz patients, geriatric patients, and cats

what is the MoA of buspirone

5-HT receptor partial agonist

what is the use of buspirone

for generalized anxiety

what are the pros and cons of buspirone

pros: - less sedation and side effects vs BZDs - less abuse potential - no withdrawal cons: - poor immediate effects

the general category of antidepressants includes many classes of drugs including:

- selective serotonin re-uptake inhibitors: SSRIs - tricyclic antidepressants: TCAs - monoamine oxidase inhibitors: MAOI

what is the general property (effect) of all antidepressants

altering NE and 5-HT levels in the CNS

what is the MoA of tricyclic antidepressants

inhibit 5-HT and NE re-uptake in the CNS (produces the anxiolytic and decreased arousal) also anticholinergic and antiadrenergic effects some also inhibit histamine receptors

what are some ADRs associated with tricyclic antidepressants

- CVS effects - GI effects - urinary effects - sedation

when are tricyclic antidepressants contraindicated

- KCS - glaucoma

what is a benefit of tricyclic antidepressants over BZDs

tricyclic antidepressants do not produce disinhibition

what is the MoA of clomipramine

primarily blocks 5-HT re-uptake but a metabolite (desmethyl clomipramine) blocks NE re-uptake

what are the uses of clomipramine (4)

- anti-anxiety - treatment of stereotypies - storm and noise phobias - aggression

what is the MoA of amitriptyline

more selective for 5-HT re-uptake over NE reuptake both decreased arousal/calming and pain management

what is the most common use of amitriptyline in cats

idiopathic interstitial cystitis

T/F SSRIs are classified as anti-depressants but display a wide array of effects

what are the main safety concerns with SSRIs

generally considered very safe - anorexia and sedation - serotonin syndrome

serotonin syndrome is more likely when SSRIs are combined with:

- 5-HT agonists - TCAs: also decrease 5-HT reuptake - MAOI: decrease SSRI metabolism - OTC herbal supplements

what is the MoA of fluoxetine

5-HT reuptake inhibition

fluoxetine is metabolized to

norfluoxetine

what are the consequences of fluoxetine metabolism to norfluoxetine

creates a 6 week washout as norfluoxetine is an active metabolite; there is a long elimination half-life of both drugs as accumulation occurs with multiple doses

T/F transdermal fluoxetine exists

T but poor and variable bioavailability

what is the idea behind opiate receptor antagonists for behaviour disorders

believed that some stereotypies are a coping mechanism that is reinforced by endorphin release; these drugs block that reinforcement by blocking the opioid receptor

what is naltrexone and what are its pros and cons

opiate receptor antagonist; expensive; not a controlled substance

what is the MoA of antipsychotics

inhibit dopamine D2 receptors

what are pros and cons of antipsychotics

pros: - quieting - transquilizers cons: - inhibit learning - lower bp - sedation - extrapyramidal effects - ataraxia - poor anxiolytics

what are some examples of low potency antipsychotics

acepromazine, chlorpromazine

what are the major side effects of acepromazine and chlorpromazine

greater cholinergic (sedation) and a-adrenergic (hypotensive) blocking effects

when are acepromazine and chlorpromazine mainly used

as needed for noise and thunderstorm phobia (max effect 1h after dosing)

what is the MoA of medroxyprogesterone acetate

acts on GABA-A receptors, increases endogenous opioid release, stimulates central steroid receptors

what are the uses of medroxyprogesterone acetate

mostly in males to reduce aggression, urine marking and roaming

what are some adverse effects of medroxyprogesterone acetate

- mammary enlargement - BM suppression - diabetes mellitus - addisons dz - liver damage - hyperphagia

where are pheremones extracted from in dogs and in cats

dogs: intermammary sebaceous gland cats: facial pheremone glands

how can anticonvulsants be used to manage behaviour? name 3 examples

behaviour with a neurological basis only - gabapentin - trazadone - dexmedetomidine

what is the MoA of trazadone and how is it used

5-HT and NE reuptake inhibition; used for thunderstorms and as an adjunct for TCA and SSRI treatment