Chapter 14 Flashcards
bipolar mood disorder
mood disorder where episodes of mania and depression occur alternately
depression
mental state characterized by depresssed mood, with feelings of frustration and hopelessness
exogenous, or reactive, depression
depression caused by external factors or life events
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
major depressive disorder (MDD)
depression that arises from within an individual and requires psychotherapy and drug treatment
mania
mental state of excitement, hyperactivity, and excessive elevation of mood
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
monoamine oxidase (MAO)
enzyme that inactivates (breaks down)norepinephrine and serotonin
found in adrenergic and serotonergic nerve endings
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
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
SNRIs
serotonin-norepinephrine reuptake inhibitors, a class of antidepressant drugs
MOA- Block the reuptake of noepinephrine and serotonine
ex- desvenlafaxine
duloxetine
venlafaxine
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
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
Anti Depressants increase levels of what?
norepinephrine or serotonin
Lithium and Anticonvulsant drugs
used to treat depression/bipolar disorder
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
Adverse Effects
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
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
increased blood pressure, heart rate, and CNS stimulation
sudden discontinuation can lead to discontinuation syndrome
What are the major differences between SSRIS and SNRIS?
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
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
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
alcohol- increaded sedation
TCAs interactions with amphetamines
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
