Chapter 14 Flashcards by Rachel Kelly

bipolar mood disorder

mood disorder where episodes of mania and depression occur alternately

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depression

mental state characterized by depresssed mood, with feelings of frustration and hopelessness

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exogenous, or reactive, depression

depression caused by external factors or life events

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lithium

an element similar to sodium that is used in the treatment of mania and bipolar mood disorder

reduces hyperactivity and excitement

allows better organization of thought patterns

MOA- chemical properties are similar to sodium

decreases nerve tissue excitability

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major depressive disorder (MDD)

depression that arises from within an individual and requires psychotherapy and drug treatment

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mania

mental state of excitement, hyperactivity, and excessive elevation of mood

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MAOIs

monoamaine oxidase inhibitors, antidepressant drugs that inhibit MAO

decrease the amounts of norepinephrine and serotonin that are destroyed

permit the levels of norepinephrine and serotonin in the brain to increase

ex- isocarboxazid
phenelizine
tranycypromine

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monoamine oxidase (MAO)

enzyme that inactivates (breaks down)norepinephrine and serotonin

found in adrenergic and serotonergic nerve endings

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monoamine theory of mental depression

theory that mental depression is caused by low brain levels of norepinephrine and serotonin (monamines)

high levels may result in mania

endocrine and neurotropic deficiencies can also play a role in mental depression

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psychomotor stimulant

amphetamine or related drug that increases mental and physical activity

not true anti depressant and have limited use in depression

MOA- helps our bodies make more norepinephrine and dopamine by stimulating the CNS (produce mood elevation)

Increase neurotransmitter activity by inhibiting neuro transmitter reuptake

produce drug tolerance and drug dependence

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SNRIs

serotonin-norepinephrine reuptake inhibitors, a class of antidepressant drugs

MOA- Block the reuptake of noepinephrine and serotonine

ex- desvenlafaxine
duloxetine
venlafaxine

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SSRIs

selective serotonin reuptake inhibitors, a class of antidepressant drugs

MOA- block the reuptake of serotonin into the serotonergic nerve endings

increase stimulation of seretonin receptors

drugs vary in the degree of activation

ex- fluozetine, fluvoxamine, paroxetine,sertraline, escitalopram, citalapram

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TCAs

tricyclic anti depressants, a class of antidepressant drugs

MOA- block reuptake of norepinephrine and serotonin into the neuronal nerve endings

increased serotonin and noepinephrine levels contributed to the anti depressant effect

ex- nortriptyline
amitriptyline
doxepin
imipramine
desipramine
clomipramien

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Anti Depressants increase levels of what?

norepinephrine or serotonin

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Lithium and Anticonvulsant drugs

used to treat depression/bipolar disorder

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Clinical Indications of SSRIS

preferred therapy for treatment of jamor depression and most anxiety disorders

administered 1-2 times a day

treatment for PTSD and OCD

premenstural dysphoric disorder

ex - fluoxetine and sertraline

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Adverse Effects

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GI disturbances (nausea, diarrhea, dry mouth and anorexia

sexual dysfunction

CNS effects (head ache, nervousness, insomnia and tremors)

overdose leads to serotonin syndrome (confusion, fever, tremor agitation,restlessness and occasionally, seizures

sudden discontinuation may lead to discontinuation syndrome (dizziness, nausea, anxiety and insomnia-patients must be tapered off med

Clinical Features of SNRIs

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venlafazine- moderately activating
desvenlafazxine- active metabolite of venlafazine
duloxetine- causes low incidences of CNS activation
other uses- treatment of GAD, chronic pain disorders, and fibromyalgia

Adverse effects of SNRIs

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increased blood pressure, heart rate, and CNS stimulation

sudden discontinuation can lead to discontinuation syndrome

What are the major differences between SSRIS and SNRIS?

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SSRIs are preferred for the treatment of major depression, there are lower incidences of adverse and toxic effects with SSRIs. SSRIS do not cause significant anticholinergic alpha adrenergic blocking, or histaminic reactions. this is the main reason why they are preferred over TCAs

TCAs and MAO inhibitors are used as alternatives when SSRIS and SNRIS are contradicted or ineffective

Pharmacological Actions of TCAs

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produce varying degrees of sedation, anticholinergic effects, and alpha-adrenergic blockade

drug effects are evident for 2 weeks after the termination of drug therapy

Adverse and toxic effects of TCAs

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anticholinergic- dry mouth constipation, urinary retention and rapid heartbeat

alpha-blocking-postural hypotenion blurred vision and drowsiness

toxic effects may be produced in the heart and liver

overdosing can result in lethal cardiac arrhythmia, seizures, and death

Interactions with TCAs

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alcohol- increaded sedation

TCAs interactions with amphetamines

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amphetamines-increased CNS stimulation

TCAs interactions with Anticholinergics,

dry mouth constipation, urinary retention, blurred vision

TCAs interactions with Anticonvulsants

increased possibility of seizures

TCAs interactions with Bariturates

increased metabolism of tricyclics (decreased effectiveness) increased sedation

TCAs interactions with MOA inhibitors

increased CNS stimulation, hyperpyrexia, seizures

TCAs interactions with Phenothiazines

anticholinergic effects, CNS depression

TCAs interactions with SSRIs, SNRIs

increased CNS stimulation, serotonin syndrome

Drug Interactions with MAOIs

caution must be exercised with the use of other drugs

Dietary Restrictions with MAOIs

foods contain tyramine (wine beer herring and certain cheeses) sympathetic drugs used to treat cold symptoms must be avoided- decongestants and bronchodilators

Adverse Effects of MAOIs

dry mouth, urinary retention, constipation, blurred vision, hypotension, weight gain, sexual dysfunction and CNS disturbances

Nefazodone and Trazadone

week inhibitors of seotonin and norepinephrine reuptake effectively antagonized 5HT2A serotonin receptors

bupropion

useful in the treatment of bipolor disorder reduces CNS effect of nicotine withdrawal

mirtazapine

antagonises serotonin 5HT2 and 5HT3 receptors acts as a sedative

why do we use psychomotor stimulants

because MAOIS and tricyclic antidepressants have a delayed therapeutic response psychomotor stimulates are occasionally used to elevate mood and increase psychomotor activity amphetamines used to treat narcolepsy and hyperkinesis in children can calm down hyper activity stimulate motor or physical activity

Adverse and Toxic Effects of psychomotor stimulants

dry mouth, rapid heartbeat, increased blood pressure, restlessness and insomnia toxic doses may produce severe agitation and psychosis

Pharmacokinetics of lithium

administered as a salt, lithium carbonate blood levels are regularly measured decreased sodium intake and hyponatremia can lead to toxicity

Adverse and toxic effects

nausea, tremors, and disturbances of the thyroid gland overdose can cause vomiting, diarrhea, drowsiness. loss of equilibrium, ringing in the ears, and frequent urination toxic levels can lead to development of cardiac arrythmias or nephritits occasionally produces disturbances of the contraindicated in patients with an existing thyroid condition pregnancy category D should not be used in pregnancy

Preferred therapy for Depression, Mania, and Bipolor Disorder

major depression is treated using SSRIs lithium and valproate are considered first-line mood stabilizers valporate, carbamazepine, lurasidine and lamotrigine are used to treat bipolor disorder

Chapter 14 Flashcards

(41 cards)