Antidepressants and antianxiety Flashcards by Iseoluwa Ojo

Biologic hypothesis of depression

________
_____________ theory
_______ – _______

Genetics
Monoamine theory
Hormonal – Neuroendocrine

How well did you know this?

Not at all

Perfectly

Monoamine theory of depression

Due to a deficit in the monoamine transmitters –___________ and _________ in some regions of the brain

norepinephrine and serotonin

How well did you know this?

Not at all

Perfectly

Monoamine theory of depression

Supportive evidence
•The monoamines play a role in _________

•Antidepressants act by facilitating __________

•Drugs that ______________

arousal and mood

noradrenergic and serotonergic transmission

block monoaminergic synthesis and storage

How well did you know this?

Not at all

Perfectly

Examples of drugs that block monoaminergic synthesis and storage

???

reserpine, alpha-methyltyrosine, methyldopa

How well did you know this?

Not at all

Perfectly

Monoamine hypothesis
Research evidence against monoamine hypothesis

Although levels of norepinephrine and serotonin are increased immediately,
therapeutic effects are seen at _____
Likely a trophic factor

2-3 weeks

How well did you know this?

Not at all

Perfectly

Neuroendocrine

Depressed patients have a (low or high?) level of cortisol and does not (rise or fall?) when _______________________ test is carried out

This is thought to occur as a result of a deficiency of _____________ to the __________

High; fall

dexamethasone suppression

noradrenergic and serotonergic input

hypothalamus

How well did you know this?

Not at all

Perfectly

Neuroendocrine

Hypothalamus secretes corticotrophin releasing hormone (CRH) which stimulates the pituitary gland to produce ACTH and this further stimulates cortisol

________ level is also increased
_______ hormone is reduced

Prolactin

Growth

How well did you know this?

Not at all

Perfectly

Other hypothesis of depression

Low levels of brain derived __________ factors

Increased cortical _______ levels

____________________

neurotrophic

glutamate

Neurodegeneration

How well did you know this?

Not at all

Perfectly

What antidepressants are?

Drugs used to treat depression- by ___________

Mainly (inhibitory or excitatory?) to increase monoaminergic transmission

elevate mood

excitatory

How well did you know this?

Not at all

Perfectly

Classification of antidepressants

Reversible monoamine oxidase inhibitor (RIMA) –_________,_______

Selective serotonin reuptake inhibitor –_____,_______,_______,_______,________,_______,________

moclobemide, clorgyline

fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram, dapoxetine

How well did you know this?

Not at all

Perfectly

Classification of antidepressants

____________(RIMA)

_________ antidepressant
Selective ____________ inhibitor

Serotonin and ———————-

______ antidepressants

Reversible monoamine oxidase inhibitor

Tricyclic antidepressant

Selective serotonin reuptake inhibitor

Serotonin and noradrenaline reuptake inhibitors

Atypical

How well did you know this?

Not at all

Perfectly

Atypical antidepressants – ______,_______,_________,______,______,_____________

trazodone, mianserin, mirtazapine, bupropion, atomoxetine, tianepine

How well did you know this?

Not at all

Perfectly

Serotonin and noradrenaline reuptake inhibitors – ________,_______

venlafaxine, duloxetine

How well did you know this?

Not at all

Perfectly

Monoamine oxidase

MAO – a ___________ enzyme , ________________________ of amines like adrenaline, noradrenaline , dopamine, serotonin

mitochondrial

oxidative deamination

How well did you know this?

Not at all

Perfectly

Monoamine oxidase

Two type
MAO –A – Present in _____ nerve endings, _________ and human ______. Preference for _______ and _______

MAO –B –Present in _________ areas in the ________ and ________. Preferentially deaminates _________.

adrenergic; intestinal mucosa; placenta
5-HT and NA.

serotonergic

brain and platelets

phenylethylamine

How well did you know this?

Not at all

Perfectly

Monoamine oxidase

___________ is degraded equally by MAO –A and MAO-B

Dopamine

How well did you know this?

Not at all

Perfectly

Monoamine oxidase inhibitors

Irreversible – _______ ,———,_______

Reversible
MAO –A __________,__________

MAO –B _____________

phenelzine, tranylcypromine, isocarboxazid

Moclobemide, Clorgyline

Selegiline

How well did you know this?

Not at all

Perfectly

Selegiline is not used in depression.

T/F

Antidepressant only at high doses

How well did you know this?

Not at all

Perfectly

Irreversible monoamine oxidase inhibitors

(Selective or Non-selective?)

No longer in use because of _________ and _____________

Non-selective

drug drug interactions and drug –food interaction (cheese) etc

How well did you know this?

Not at all

Perfectly

Irreversible monoamine oxidase inhibitors

Inhibits the enzyme irreversibly – action lasts about ________ until new enzymes are synthesised

3 weeks

How well did you know this?

Not at all

Perfectly

Irreversible monoamine oxidase inhibitors

Cheese reaction – reaction with ______, some ___,________,_________ extracts.

Release (small or large?) amount of _____ from adrenergic neurons

Leading to dangerous ______________

cheese

beers, wine and yeast

Large ; noradrenaline

hypertensive crises

How well did you know this?

Not at all

Perfectly

Reversible inhibitors of MAO –A

Moclobemide –

•reversible and (selective or non-selective?)
•Duration of action is ______
•Indicated for ____________ depression

•Less adverse reaction – can be displaced by _______ from enzyme binding site

•Adverse effects – nausea , dizziness

•Drug interactions – rare, caution when prescribing with _____________ and _________

selective; 1-2 days

mild to moderate

tyramine

other antidepressants and pethidine

How well did you know this?

Not at all

Perfectly

Tricyclic antidepressants

Uptake blocker – inhibit ————- and _________ at the ——— and ——— membranes.

Prolonged accumulation of the monoamines lead to the _______ of the inhibitory presynaptic ______,_______, and _________ auto receptors.

There is also an adaptive change in the postsynaptic receptors leading to _________ noradrenergic and serotonergic transmission.

norepinephrine and serotonin transporter

neuronal and platelet ; desensitization

alpha 2, 5HT1A and 5HT1D

enhanced

How well did you know this?

Not at all

Perfectly

Tricyclic antidepressants

Inhibits other receptors
_____ adrenergic,

________ receptors

histaminergic effects H__

5-HT__ and 5-HT___

D___ -

Alpha

Muscarinic

5-HT1 and 5-HT2

D2 -

How well did you know this?

Not at all

Perfectly

Pharmacological actions of Tricyclic antidepressants CNS - Clinical effects seen within _________ of treatment because there is upregulation of the ________ and _______ receptors in the CNS. Improved ______ pattern.

2 -3 weeks serotonin and Noradrenaline sleep

Pharmacokinetics of Tricyclic antidepressants (Poorly or Well?) but (slowly or rapidly?) absorbed (Mildly or Highly?) plasma and tissue protein bound (Small or Large?) vol. of distribution Metabolism – hepatic microsomal enzyme

Well; slowly Highly ; Large

Pharmacokinetics of Tricyclic antidepressants Imipramine is ________ to an (active or inactive?) metabolite called __________ Amitriptyline is similarly ________ to __________ (Short or Long?) half-lives

demethylated Active ; desipramine demethylated; nortriyptyline Long

Adverse effects of Tricyclic antidepressant ________,___________,__________ _____eased appetite and weight ____

Sedation, mental confusion , weakness Incr; gain

Adverse effects of Tricyclic antidepressant Anticholinergic effects –____ mouth, bad taste , (constipation or Diarrhea?) , urinary _______, ________ vision Lowers ______ threshold and causes ______ in cases of overdose. – less likely with _______ and ________

dry; constipation; retention; blurred seizure; seizures amitriptyline and imipramine.

Adverse effects of of Tricyclic antidepressant CVS – ______cardia ECG changes and cardiac arrhythmias – disturbs ___________ especially in the ______ postural _________ –_____ blockade and inhibition of ________

Tachy intraventricular conductance elderly hypotension; alpha 1 CVS reflexes

Tolerance and dependence of Tricyclic Antidepressant Tolerance to ________ and ________ Dependence (low or high?).

anticholinergic and hypotensive Low

Drug interactions of Tricyclic antidepressants Potentiates the action of _____________ Abolishes the antihypertensive effect of _______ and _______ by preventing their _____________________ Potentiates _____ depressants _____ ,________ displaces TCA from their binding sites causing toxic effects

direct sympathomimetics guanethidine and clonidine; transport into adrenergic nerves CNS Phenytoin , aspirin

Selective serotonin reuptake inhibitors Selectively inhibit membrane associated serotonin transporter T/F

Selective serotonin reuptake inhibitors (More or Less ?) efficacy compared to TCA especially in severe depression (more or less?) tolerable (more or less?) sedative, cognitive, psychomotor effects ______ anticholinergic and alpha adrenergic effects _____ effect on seizure threshold.

Less; more Less no no

———- are the First line drugs in depression

Selective serotonin reuptake inhibitors

Selective serotonin reuptake inhibitors is also used for other conditions like anxiety, phobia and obsessive and compulsive disorders T/F

Adverse effects of Selective serotonin reuptake inhibitors Nausea – _____________ stimulation Nervousness, restlessness, headache, (constipation or diarrhoea?) Epistaxis, ecchymosis and increased NSAIDS associated blood loss – impairment of _________

5HT3 receptor diarrhoea platelet function

Adverse effects of Selective serotonin reuptake inhibitors _______– 5HT3 receptor stimulation Nervousness, restlessness, headache, diarrhoea _______,_________ and increased ____________ associated blood loss – impairment of platelet function

Nausea Epistaxis, ecchymosis NSAIDS

Drug interactions - SSRI SSRI are enzyme (inducers or inhibitors ?) leading to ______ levels of TCAs, haloperidol, clozapine, warfarin Serotonin syndrome – when a patients takes a ____________________ with SSRI. ______,_________,________, and _______

inhibitors elevated serotonergic drug Restlessness, agitation, sweating and convulsions

Serotonin norepinephrine reuptake inhibitors Include _______ and _________ More specific for ________ and ________ transporter

venlafaxine and duloxetine serotonin and norepinephrine

Serotonin norepinephrine reuptake inhibitors More likely to cause ____tension compared to SSRI

hypo

Which is more likely to cause hypotension SNRI or SSRI

Serotonin norepinephrine reuptake inhibitors are More likely to cause hypotension compared to SSRI

Atypical antidepressants Includes _______,__________,__________ ________ mechanism of action

trazodone, mianserin, bupropion Variable

Uses of antidepressants Endogenous and major ________ ___________ disorders ______ disorders ____________ pain ______________ disorder ______ Migraine Pruritus

depression; Obsessive compulsive Anxiety ; Neuropathic Attention deficit hyperactivity Enuresis

Antianxiety drugs Anxiety disorders are _________ _______ characterized by _______,_________ and concerns or fear about some defined or undefined future threat

unpleasant emotional statesm uneasiness, discomfort

Antianxiety drugs Drugs used to treat these disorders have ___________ effects

CNS depressive

Classification of antianxiety drugs List 5

Benzodiazepines Azapirone Sedative antihistamines Beta blocker Selective serotonin reuptake inhibitors

Classification of antianxiety drugs Benzodiazepines – ______,_____,_____,____, and _____ Azapirone –_______,_____,______ Sedative antihistamines- _________ Beta blocker – _________ Selective serotonin reuptake inhibitors

diazepam, alprazolam, lorazepam, oxazepam and chlordiazepoxide Buspirone, Gebiprone, Ispapirone Hydroxyzine Propanolol

Buspirone No ______ action (More Or Less?) likely to cause sedation , cognitive impairment No ________ or ____________ effect (More or Less ?) likely to cause tolerance or dependence

GABA Less anticonvulsant or muscle relation Less

Versus SSRI _______,________ _______,_________,_______,_________ SNRI _______,_____,———-,_________,_________

Fluoxetine, Paroxetine, Sertraline, Citalopram, Escitalopram, Fluvoxamine Venlafaxine Duloxetine Desvenlafaxine Levomilnacipran Milnacipran

TCA :Secondary amines List 4 TCA: Tertiary amines List 5 MAOl List 5

– Nortriptyline – Desipramine – Protriptyline -Amoxapine Amitriptyline Imipramine Trimipramine Clomipramine Doxepin Tranylcypromine Phenelzine Moclobemide Selegiline Isocarboxazid

SARI ________,__________ Atypical ______,———,_______,———-,_______

Trazodone Nefazodone Mirtazapine Bupropion Vilazodone Vortioxetine Varenicline

MECHANISM OF ACTION SSRI __________ of ____________ in synaptic cleft – Thus ______ease in _______ levels SNRI _________ of ___________________ in synaptic cleft – Thus ____eased ___________________________ levels

Inhibition of serotonin reuptake Increased ; SEROTONIN Inhibition of norepinephrine reuptake reuptake Increased; SEROTONIN and NOREPINEPHRINE

Mechanism of Action TCA –________ of __________ in synaptic cleft – Thus _____ease in _______ and _______ levels MAOI – (Selective or Nonselective?) inhibition of _________________ – Thus ____eased ______ and _____eased accumulation of, ————-,______,———

Inhibition; norepinephrine reuptake Increase in SEROTONIN and NOREPINEPHRINE Nonselective ; monoamine oxidase enzyme Decreased; breakdown; increased NOREPINEPHRINE, SEROTONIN, epinephrine

Mechanism of action SARI and Atypical – Block _________________ receptors leading to ____eased activity of _______________ receptors in the CNS

postsynaptic type 2 serotonin Increased SEROTONIN of type 1 receptors

Mechanism of action – SARI (Weak or Strong?) inhibition of ___________ leading to ______ease in ______ levels – Atypical (Selective or Non-selective?) ______________ causing ___eased ________________________________

Weak; serotonin reuptake Increase; SEROTONIN Selective; α2-adrenergic antagonist Increased; SEROTONIN and NOREPINEPHRINE release

Adverse effects SSRI –_________ disturbance – ______ dysfunction –________ – _______ – ____________ syndrome

Gastrointestinal Sexual Insomnia Sedation Serotonin

Serotonin syndrome occurs when SSRIs are _____________________

combined with MAOI

Serotonin syndrome List the characteristics

S hivering H yperreflexia I ncreased temperature V ital signs instability E ncephalopathy R estlessness S weating

ADVERSE EFFECT SNRI – Similar side effect to _____ – _____tension – ____lytics – Insomnia – Hyper______

SSRI Hyper Anxio lipidemia

ADVERSE EFFECT TCA –____________/________ ———— – _____toxicity – Tremor – Weight _____ – _____pyrexia – ______ dysfunction –_____________ effects

Orthostatic/ Postural hypotension Cardio Gain Hyper ; Sexual Anti-muscarinic

ADVERSE EFFECT MAOI – ________ ——-tension – _____toxicity – Insomnia –_____ dysfunction –______— syndrome – __________ crisis

Orthostatic hypo Hepato Sexual; Serotonin Hypertensive

Hypertensive crisis can occur when you combine MAOI with _______ containing foods Also called __________ interaction

TYRAMINE WINE-CHEESE

ADVERSE EFFECT Atypical – Mirtazapine Increase ________ Weight _____ – Bupropion Seizure Weight _____ ___________ DYSFUNCTION

appetite; gain loss; NO SEXUAL

ADVERSE EFFECT SARI –________ –_______ – Orthostatic hypotension – Nausea

Priapism Sedation