psycho pharmacology - final

8/6/2019 Psycho Pharmacology - Final

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Presented by :Cantos Peter Cinco, CarlaCorpus, Blaine Maxine

Cruz, Kimberly Anne B.De Borja , Jose Paolo

Psychopharmacology


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Psychopharmacology

Is the use of medications to treat mental

illness.


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Neurotransmitters

are chemical substance manufactured in the neuron to aidin transmission of information throughout the body.

D opamine generally excitatoryS erotonin mostly inhibitoryAc etyl ch oline synthesized in dietary holine found inred meat and vegetables. Found to affect sleep/wakecycles and signal muscles to be active.Norepinep h rineGABA (Gamma-amino butyri c a c id) major inhibitoryneurotransmitter. Found to modulate other neurotransmitters rather than to provide direct stimulus


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Efficacy-maximal therapeutic effect that adrug can achieve

Potency describes the amount of the drugneeded to achieve the maximum effect.

Half-life is the time it takes for half of thedrug to be removed in the blood stream.


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Off label use- A drug that proves effective for adisease that differs from the one involved in the

original testing and FDA approval.

e.g. anticonvulsants approved to prevent seizuresare prescribed for their effects in stabilizing themoods fo clients with bipolar disorder ( off label )

B lack box warning ( black label warning ) a typeof warning that appears on the package insert forprescription drugs that may cause serious adverseeffects. It is so named for the black border thatusually surrounds the text of the warning.


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AntipsychoticDrugs

Prepared by : Cruz, Kimberly Anne B.


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Psychosis- inability to recognizereality, complicatedsevere thoughtdisorder and inability to relate with others.


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A ntipsychotics

A lso known as N euroleptics

U sed to treat symptoms of psychosis such as delusions andhallucinations seen inschizophrenia, schizoactivedisorders, and manic phase of bipolar disorders.


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O ff label uses : Anxiety and insomnia ;aggressive behavior and other disruptivebehaviors that sometimes accompany Alzheimers disease


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D1 - Motor neurons in t h e basal ganglia and may beprin c ipal dopamine stimulating re c eptor for motor fun c tions

- influen c e D2 fun c tion- h as no dire c t role in c ontrolling psy ch oti c symptoms

D2 overa c tivation c auses positive symptoms ( e.g.h allu c inations ). It is modulated w h en D1 is blo ck ed (ex c ept in s ch izop h renia

D3and

D4- overstimulation of

D3may be asso

c. wit

h negative symptoms. D4 may be related to positive

symptoms.

D5 -found only in limbi c regions. May be an importantdopamine-stimulating re c eptor for be h avior.


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M ode of Action:

B locking receptors of neurotransmitter dopamine(Neurochemical Theory of Schizophrenia ).

Dopamine generally excitatory neurotransmitterClassified into subcategories : D1 D2 D3 D4 and D5D2 D3 D4 have been associated with mental illness.

Typical antipsychotic drugs are potent antagonists of D2 D3 D4 , making an effective treatment of targetsymptoms however extrapyramidal side effects may be produced. This is due to the blockage of D2receptors.


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Dopamine system stabilizers (DSS ) are drugs thatstabilize dopamine output.

Preserve and enhance when dopaminergictransmission is too low and reduce it where it is

too high.

Depot injection is a time-release form of medicationfor maintenance therapy.

Vehicle : sesame oil . M edication is absorbed slowly over time thus less frequent administration isneeded to maintain desired therapeutic effects .


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Typical AntipsychoticL ow poten c yC hlorpromazine (Largactil, T horazine)T hioridazine (Mellaril)Mesoridazine

Medium poten c yLoxapine (Loxapac, Loxitane)Molindone (Moban)Perphenazine (T rilifon)T hiothixene (Navane)T rifluoperazine (Stelazine)H ig h poten c yH aloperidol (H aldol, Serenace)Fluphenazine (Prolixin)DroperidolZuclopenthixol (C lopixol)Prochlorperazine


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Chlorpromazine ( Thorazine)-considered the first antipsychoticdrug. It was synthesized in 1950 by French scientists while attempting todevelop a new antihistamine. It camefrom phenothiazine family of drugs, is


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Thioridazine (M

ellaril)Also used for short-term marked

depression accompanied by

anxiety,tension, sleep disturbance

M aximum upper limit of 800 mg due topigementary retinopathy( pigment depositson the fundus characterized by decreasedvisual acuity and impaired night vision )


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Trifluoperazine (Stelazine)

I: Excessive anxiety,tension, agitation aswell as for psychotic manifestation

Perphenazine ( T rilafon )I: Depression and psychotic


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Butyrophenone : HaloperidolHaloperidol ( Haldol ) high potency that tends to cause more EPSEs andfewer anticholinergic side effects thando low potency drugs.Can be used alone or in combination

with benzodiazepine, lorazepam(Ativan )Is a long-acting form can be given at

2-4 weeks intervals


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Atypical antipsychotic drugsH ave greater effect on negative symptomsBlockade of serotonin receptors that , inturn, is thought to liberate dopamine incortex explaining the reduction of negativesymptoms.


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Atypical antipsychotic drugsAmisulpride (Solian)Aripiprazole (Abilify)Asenapine (Saphris)B

lonanserin (Lonasen)Clotiapine (Entumine)Clozapine (Clozaril)Iloperidone (Fanapt)M osapramine (Cremin)O lanzapine (Zyprexa)Paliperidone (Invega)Perospirone (Lullan)Quepin (Specifar)Quetiapine (Seroquel)Remoxipride (Roxiam)


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Dibenzodiazepine: ClozapineClozapine ( Clozaril ) was the first new anHas greater affinity to Dopamine D-1,Dopamine D-4 , and serotonin(5H2T)receptors

Agranulocytosis

Benzisoxazole : RisperidoneGreater affinity to D2 receptor and similar antagonism to serotonin 5 HT

Doesnt appear to cause agranulocytosis,

EPSE, tardive dyskenisia or NMS


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Sertindole (Serlect )

Potent Dopamine D2 and serotonin 5HT2antagonismB oth positive and negative schizophreniaProlonged QT intervalWithdrawn from the market due to number

of cardiac arrythmia and deaths caused.12-24 mg /day


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Side effects

Extrapyramidal side effectsNeuroleptic M alignant Syndrome

Tardive dyskinesiaAnticholinergic side effects


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weight gainmild ECG changes


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Extrapyramidal Side

EffectsSerious neurologic

symptoms caused by blockage of Dopamine (D2)

receptor located in themidbrain.

They are major side effectsof antipsychotic drugs.

A cute dystoniaP seudoparkinsonisA kathisia


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A cute dystonia (most likely1 st week of treatment)

Acute muscular rigidity andcrampting, a stiff or thick tongue withdifficulty swallowing, in severe caseslaryngospasm and respiratory difficulties

T orticolis twisted head and neckO pisthotonus tightness of entire

body with head back and arched neckO culogyric crisis eyes rolled back

and in locked position.

Treatment:B enztropine mesylate(Cogentin)Dophenhydramine ( B enadryl )


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Torticolis

OpisthotonusOpisthotonus

Oculogyric crisisOculogyric crisis


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P seudoparkinsonism Also known as drug-induced ParkinsonismSymptoms resemble Parkinsonism:

Stiff stoop postureM asklike faciesDecreased arm swingA shuffling, festinating gait ( with small steps)Cogwheel rigidity (ratchet-like movements of joints)Drooling

TremorB radycardiaCoarse pin-rolling movement of the thumb and fingers while at rest


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T reatment :

C hanging antipsychotic medication that haslower incidence of EPS

Additional oral anticholinergic agent or Amantadine ( Dopamine agonist )


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A kathisia

Inform client about the types of sideeffects and encourage to report suchproblems.

Drink sugar free fluids and eatingsugar free candy ( dry mouth )

Sunscreen ( photosensitivity )Avoid driving and performingpotentially dangerous activities

If missed a dose, client can take it if

its 3-4 hours late.


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T reatment :

C hanging antipsychotic medication that has

lower incidence of EPS

Additional oral agent such as beta-blocker ,anticholinergic or benzodiazepine


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T ardive dyskinesia ( TD )

Tardive means late appearing ( usu. Aftermonths or years)D yskinesia refers to abnormal voluntary

skeletal muscle movements whichusually produce a jerky motion.Anticholinergic drugs such astrihexyphenidyl and benztropine may

aggravate TD. Three times more likely to have animpaired gag reflex

Treatment : B romocriptine ( Parlodel )


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Signs and Symptoms

Lip smackingGrinding of teethRolling or protrusion of tongue

TicsDiaphragmatic movements

Note :I nvoluntary movements are generally coordinated ,

fluctuate in severity and disappear during sleep.

T D is IRREVER S IBLE .D iscontinuing antipsychotic can arrest its progression


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Prevention of T

D

Keeping medication dosages as low as possibleC hanging medicationsMonitoring periodically for signs of T D usingstandardized assessment tool such as A IMS

( Abnormal Involuntary Movement Scale )

O nce the client have acquired T D he/she may be given

atypical antipsychotic which does not have been foundto cause T D


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N euroleptic Malignant Syndrome(N MS)

Typical onset : 3-9 days after initiation of therapy

S/Sx: increased temperature ( chief sign )

muscular rigidity , tremors , impairedventilation, muteness, altered consciousness,autonomic hyperactivity

Treatment: Dantrolene ( Dantrium)B

romocriptine ( Parlodel )Note :Antipsychotics should not be reinstituted for atleast 2 weeks after complete resolution N M S

symptoms


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D roperidol ,T hioridazine,Mesoridazine

M ay lengthen QT interval leading to

potentially life treatening cardiacdysrhythmias or CARDIAC ARREST.


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C lozapine

A granulocytosis - P OT E N TI ALLY F A T AL

D evelops suddenly characterized by:A . feverB. malaiseC . U lcerative sore throatD . L eukopenia

N OT E : D rug must be discontinued I MM E DI A T ELY if WB C count drops by 50% or to less than

3,000


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B efore initiation of treatment:

M ust have a baseline W B C count anddifferential

Throughout the treatment and 4 wks afterdiscontinuation :WB C count every week


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Inform client about the types of side effects andencourage to report such problems.

Drink sugar free fluids and eating sugar free candy ( dry mouth )Sunscreen ( photosensitivity )Avoid driving and performing potentially dangerous

activitiesIf missed a dose, client can take it if its 3-4 hourslate.


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A nti ch olinergi c S ide effe c ts

O ften occur with the use of antipsychotic

drugs

O rthostatic hypotension, dry mouth,constipation, urinary hesitance / retention,blurred near vision, dry eyes ,photophobia ,nasal congestion and decreased memory.


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S ide effect Nursing intervention

Peripheral Nervous S ystem

Constipation Encourage high dietary fiber and increasedwater intake ; give laxatives as ordered

Dry mouth Advise to take sips of water frequently ,

Nasal congestion Give over the counter nasal congestants if

approved by physicianBlurred vision Advise to avoid potentially dangerous

tasks,. Reassure that normal vision returnsin few weeks, when tolerance in side

effects develops .

Mydriasis Advise to report eye pain immediatelyPhotophobia Advise to wear sunglasses outdoors

Hypotension/ Orthostatichypotension

Advise the patient to get out of the bed or chair slowly. Sit on the side of the bed for 1full minute whle dangling feet , then slowly

rise. Measure BP before each dose.


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Tachycardia Is usually a reflex response to hypotension.With clozapine, hold dose if PR>140 bpm

Urinary Retention Encourage frequent voiding and voiding whenurge is present. Monitor I and O

Urinary hesitation Provide privacy. Run water in sink. Run warmwater in the perineum

Sedation H elp patient get up early and get the daystarted

Weight gain H elp patient order an appropriate diet; diet pillsshould not be taken

Agranulocytosis If WB C


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C entral Nervous system

Akathisia Be patient and reasssure the patient who is jittery that you

undersand the need to move. Switching to new antipsychotic drugmay be necessary for compliance since akathisia is a chief causeof this.

Dystonias If severe, give antiparkinson drugs immediately as needed or antihistamine and offer assurance. More likely an order for intramuscular administration will not have been written so call thephysician at once to obtain order.

Pseudoparkinsonism Assess for tremors , rigidity and bradykinesia and report physician. Antiparkinsonism drugs will probably indicated

Tardive dyskinesia Assess using A IMS.

NMS Be alert for this is potentially fatal. Routine temperature taking.Encourage adequate water intake.Assess for rigidity , tremor andsimilar symptoms

Seizures Discontinue drugsSeizure precautions


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Thank You !


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A nti D epressants or Mood Elevators

Used to treat depressive disorders caused byemotional or environmental stressors,frustrations, losses, drugs.

T h ese drugs are c lassified as T ric yc lic A ntidepressants, Monoamine OxidaseInh ibitors (M A OIs) and A typi c alA ntidepressants .


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T ric yc lic A ntidepressants

Increase the level of neurotransmitters, serotoninor norepinephrine in the space between nerveendings.Used to treat symptoms of depression such asinsomia, decreased appetite, decrease libido,excessive fatigue, indecisiveness, difficultthinking and concentrating, somatic symptoms,irritability and feeling of worthlessness.C onsidered effective in 85% of those who exhibitsymptoms of depression


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T hose receiving tricyclic agents generallyshow an increase mental alertness and

physical activity with mood elevationwithin a few days after initial therapy isbegun.

C O NT RA IND IC ATI O NS :Pregnant and lactating womenPersons recovering from myocardialinfarctionPersons with severe liver disease andkidney disease


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S IDE EFFE CT S :Dry mouthBlurred visionT achycardiaUrinary retentionC onstipationIncrease intraocular pressureIncrease seizure susceptibility in epilepticpatients

Acute toxicity due to overdose.


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NURS ING IMPL IC ATI O NS : Assess the level or severity of patient'sdepression.Monitor for drug interactionsNote any side effects

Avoid excessive exercise and hightemperatures on patientInstruct patient to take drug as prescribed.No attempt should be made to alter the

dosage.


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Monoamine Oxidase In h ibitor (MA OIs)

Antidepressants that prevents metabolism of neurotransmitters.Effective in treating depression with acute anxietyattacks, phobic attacks, or many physicalcomplaints or patients who fail to respond totricyclic agents and patients who are indepressive phase of manic depressive illness.


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C ON

TRA

IND

IC A

TI ONS

:

AsthmaC ongestive heart failureH

ypertensionC ardiac ArrhythmiasImpaired kidney functionH

ypernatremiaC erebral Vascular DiseaseH yperthyroidism

Liver Disease


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S IDE EFFE CT S :

Abnormal heart rateO rthostatic hypotensionNausea and Vomiting

Drowsiness or InsomiaH eadache

Vertigo

Blurred VisionC onstipationWeakness

Loss of appetite


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PA TI EN T EDU C ATI O N:

Avoid tyramine rich food, caffeinecontaining foods or alcoholic beveragesDo not alter dosage or discontinue the drug

H ave vision checked periodically Avoid overactivity


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First line agents to treat anxietyProbably the most effective, as well as thesafest, agents for prophylaxis and long-termtreatment of panic attacks


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V enlafaxine (Effexor, Effexor XR)

First drug approved for both GAD and major

depression At lower doses : blocks the reuptake of serotonin

At medium to higher doses : blocks thereuptake of norepinephrineDoses at higher range are believed to bemore effective


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H ave four basic clinical uses

1. For chronic anxiety2. For time-limited periods in people going through

crises3. For presurgery nervousness

4. For treatment of panic disorder


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Mode of Ac tion

Enhance the effects of the inhibitory

neurotransmitter GABA GABA attaches to GABA receptors, which trigger theopening of chloride channels.

C hloride has a hyperpolarizing effect on the neuron,which makes the neuron less responsive to excitatoryneurons.

Inhibit the anxiety response to stressors


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O verall effect : slowing down or halting of

neuronal firing

Neuronal inhibition : a brain without the inhibitionof GABA can produce th oug h t a cc eleration,

autonomi c dysfun c tion, ex c essive anxiety,pani c , or even seizure a c tivity.


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P harma

cologi

cEffe

cts

Depressing effect on the C NS

5 major effects1. Reduce anxiety2. Relax muscles3. Promote sleep

4. Prevent seizures5. Produce amnesia


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Because benzodiazepines depress the reticular

activating system, incoming stimuli are mutedand evoke less reaction. As the antianxiety agent decreasesenvironmental input, a general relaxing effect

takes places.T he ability to mute incoming stimuli gives agreat potential for abuse


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C an cause several levels of C NS depression,from sedation to anesthesia.

Accomplished by depressing the inhibitoryneurons that affect the arousalC

auses a state of disinhibition, which results infeelings of euphoria and excitement that, in turn,can lead to poor judgment.


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Inhibiting effect accounts for their anticonvulsive

activity.Intravenous diazepam ( V alium) andlorazepam ( A tivan) are first-line agents for status epilepticus

clonazepam (Klonopin) is regularly prescribedorally


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P h arma c o k ineti c s Absorption :

Readily absorbed after oral ingestion Slow and inconsistent IM administration (except for

lorazepam [Ativan])

Distribution : highly lipid-soluble, therefore,readily cross the blood-brain barrier Metabolism : liver Active metabolites can exert an effect for up to

10days

Excretion:

urine


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Sh ort h alf-lives

20 hours or less

Preferable for use in older adults lorazepam (Ativan) oxazepam (Serax) temazepam (Restoril)


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L ong h alf-lives

Longer than 20 hours

T herefore, has an extended duration of action clorazepate ( T ranxene) chlordiazepoxide (Librium) diazepam (Valium)


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PNS SEs C

onstipation Double vision H ypotension Incontinence

Urinary retention C an exacerbate narrow-angle glaucoma


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Side Effe

ctsC NS SEs

Sedation and mental alertness (a 20-mm H g drop of systolic level while the patient is standing warrantswithholding the drug and notifying the physician)

Drowsiness Fatigue Ataxia Mental impairment

Slowing of reflexes C onfusion Depression H eadache


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Relatively safe drugs when taken alone butcan be deadly if mixed with other C NS

depressants (alcohol)Signs and symptoms of overdose: Somnolence, confusion, coma, diminished

reflexes and hypotensionT reatment: emptying the stomach withinduced vomiting and gastric lavage,followed by activated charcoal. Monitor BP,PR and RR and provide supportive care


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B enzodiazepine Re c eptor A ntagonist

Flumazenil (Romazi c on) blocks thebenzodiazepine-binding site on the GABA

receptor It selectively blocks benzodiazepinereceptors but does not block adrenergic or cholinergic receptor T hus, because it does not stimulate the C NSand does not block other receptors, it can begiven when benzodiazepine overdose issuspected


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If patient responds to flumazenil, thebenzodiazepines are present

Response typically occurs within 30-60 secs.2 important considerations :

1. Does not speed up metabolism or excretion of benzodiazepines

2. H as a short duration of actionT hus, repeated doses of flumazenil as thebody eliminates benzodiazepines from thesystem is neededFurthermore, it might not reversebenzodiazepine-induced respiratorydepression and can precipitate seizures


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U se duringpregnan c y

Might be associated withcleft lip and cleft palate in

1 st trimester Floppy infant syndromehas been asc. with

benzodiazepine useduring labor Also known to be foundin breat milk

! Discontinue or taper tolowest possible dose


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5. Alcohol and other C NS depressants

exacerbate the effects of benzodiazepines6. H ypersensitivity to one benzodiazepine

might mean hypersensitivity to another 7. T hese drugs should not be stopped abruptly


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Buspirone (BuSpar) is a first-line agent Advantages :

It is not sedating It is not a drug that causes a high, so it has no

abuse potential It has no cross-tolerance with sedatives or

alcohol It does not produce dependence, withdrawal or

tolerance It does not cause muscle relaxation

Disadvantages : It takes 1 to 6 weeks to be effective


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Provides relief from anxiety within 7-10 days,but maximal therapeutic gain in notachieved until 3 to 6 weeks after treatment isinitiatedH as a relatively short half-life

Effective in reducing symptoms of worry,apprehension, difficulties with concentrationand cognition, and irritabilityDoes not depress the C NS


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S ide Effe c ts

Dizziness

NauseaH eadacheNervousnessLight-headednessExcitement


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IMPL ICA T IONS FOR N U RS INGA CT IONS

Before administering :

1.T

he nurse should assess the persons mentaland physical status to avoid the risk of adverseside effects

2. Pregnant women or those breast-feeding should

not be placed on antianxiety agents because of the risk of these side effects


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3. If a patient complains of sleep disturbance, thecausative factor should be identified if possible.

4. Appropriate nursing measures to promoterelaxation such as a warm drink or a backrub,should be first be tried as alternatives to the

administration of hypnotics.


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When administering, the nurse should :1.

Give the daily dose at bedtime to promotesleep, minimize adverse reactions, and allowmore normal daytime activities to occur.

2. Administer IM dosages deeply and slowly

into large muscle masses because they areirritating to tissues and can cause pain at thesite of injection. T he Z-track method isgenerally used to avoid irritation of tissue.


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3. O bserve for therapeutic effects.4. O bserve for side effects such as

oversedation, hypotension, pain at theinjection site, skin rashes, and paradoxicexcitement. Symptoms of paradoxicexcitement include hostility, rage, confusion,depersonalization, or hyperactivity. Rare sideeffects include G I discomfort, nausea,vomiting, menstrual irregularities, blooddyscrasias, photosensitivity andnonthrombocytopenic purpura


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1. Avoid mixing alcoholic beverages,antihistamines, or antipsychotic drugs withantianxiety agents because they can increasethe depressant effects of those agents,possibly causing death.

2. Avoid ingesting large amounts of beveragescontaining caffeine, a stimulant, because it candecrease the effects of hypnotic agents.


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3. Report symptoms of fever, malaise, sorethroat, petechiae, easy bruising or bleeding and skin rash.

4. Sudden cessation of these agents cancause REM or rebound effects of insomnia, dreams, nightmares,hyperexcitability, agitation or convulsions.

5. Avoid excessive use of these drugs toprevent the onset of substance abuse or addiction.

6. H ypnotics are ineffective as analgesics.


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A ntimani c A gents(L ith ium S alts)


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Administration of lithium is considered thetreatment of choice for the manic phase of the bipolar disorder formerlytermed manic-depressive illness and for thelong-term prophylaxis of this bipolar disorder.

It has also been used in the treatment of depressive andschizoaffective disorders, aggression, anduncontrolled rage reaction.


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W h at is L ith ium?Exact therapeutic effects : unknownNot metabolized in the body80% of lithium dose is reabsorbed in the proximal renaltubules and excreted by the kidneys.Believed to level out the activity of neurotransmitters inthe areaof the brain that controls emotions, thus preventing adecreasedactivity of nerve impulses, resulting in depression, or anincreasedactivity, resulting in anemiamaintains a constant sodium concentration in the brain,regulation in mood swings as well as impulses travelingalong nerve cells


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TYP ES OF A NT IMA NIC D RU GS


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LITHI UM C ARB O NAT E

A.) Mode of Action

*T he precise mechanism by which lithiumproduces its therapeutic effect is complex andpoorly understood.


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B.) Indications1. T reatment of depressive disorders :

(i) T reatment can be justified in the acute stages of depressive disorders, whenother measures have failed.(ii) T reatment of resistant depression- ex : effective in patients who have failed torespond to cyclic antidepressant drug.(iii) Enhances the effects of TC As and MA O Is.(iv) Enhances the effects of of SSR Is- however, lithium should be introducedcautiously because of the risk of the serotonin syndrome developing (owing toenhanced serotonergic activity); this risk appears to be lowest with fluvoxamine.

2. Preventing relapse of depressive disorders:

(i) In unipolar affective disorders :Lithium reduces the rate of relapse

After the first episode- treatment should be prolonged for 6 months post-clinicalrecovery.

After 2 or more episodes- treatment should be prolonged for several (1-3) yearspost-clinical recovery; lithium is particularly useful in the prophylaxis of recurrentunipolar depression.C ontinuing treatment with lithium reduces the rate of relapse after treatment of ECT .(ii) In bipolar affective disorders- prolonged administration of lithium (5 years)prevents relapses into depression.


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3. T reatment of mania : Lithium is effective in high doses(1000 mg nocte), but the therapeutic response usuallyonly occurs in the second week of treatment; thus, theresponse to lithium is slower than the response toantipsychotic drugs.

4. Preventing relapse of mania : In bipolar affectivedisorders, prolonged administration of lithium (5 years)prevents relapses into mania.

5. T reatment of mixed affective states.6. Prophylaxis of schizoaffective disorders- in combination

with an antipsychotic depot injection.7. T reatment of aggressive or self-mutilating behaviour.


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C .) Adverse effects1.Short-term side-effects :

(i) G I disturbances (N/V, diarrhea)

(ii) Fine tremor (iii) Muscle weakness(iv) Polydipsia

2. Long-term side-effects :(i) Nephrogenic diabetes insipidus(ii) H ypothyriodism(iv) C ardiotoxicity(v) O edema

(vi) Weight gain(vii) T ardive dyskinesia and other movement disorders.

3. T oxic effects :(i) Increasing G I disturbances (anorexia, vomiting, diarrhea).(ii) Increasing C NS disturbances (coarse tremor, drowsiness, ataxia, nystagmus,incoordination, slurring of speech, convulsions, coma).(iii) T he effects of lithium overdosage may be fatal- hence it is important that the serum lithiumlevel be closely monitored to ensure that it lies within the therapeutic range of 0.4-1.0 mmol/L(the lower end of this range is for maintenance therapy; the higher end of this range is for treatment in the acute stages of illness) in blood samples taken 12 hours after the last dose of lithium; serum lithium levels over 1.5 mmol/L may be fatal.(iv) O nce stabilized on lithium carbonate, the following should be monitored :- Every 3 months- serum lithium levels and serum urea and electrolytes.-Every 6 months- thyroid functions test-Every 12 months- E C G.


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4.) Drug interactions :

(i) Na + depletion raises the serum lithium levels and may result inlithium toxicity- therefore the concurrent use of diuretics (particularly

thiazides) should be avoided.

(ii) T he concurrent use of carbamazepine with lithium may result inneurotoxicity without raising the serim lithium level- hence if carbamazepine is added to lithium, it should be done so withcaution.

(iii) NSA IDs raise the serum lithium levels and may result in lithiumtoxicity- therefore their concurrent use with lithium should beavoided.

(iv) AC E inhibitors raise the serum lithium level.


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5.) C ontraindications :

(i) Pregnancy(ii) Breast feeding(iii) Renal impairment


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L ith ium toxi c ity o cc urs w h en serum lit h ium levels ex c eeds1

.5

to2

.0mEq/liter and in c ludes t h e following symptoms:

DrowsinessSlurred speechMuscle spasmsBlurred visionDiarrhea

DizzinessStupor C onvulsionsC omaDeath


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Implic

ations for NursingAc

tions:Lithium therapy should be given during or after meals to decrease gastric irritation.

Serum lithium levels should be taken at leasttwice a week during the initiation of therapybefore stabilization of the manic intervals.Serum samples should be drawn 12 hours after a dose is administered; desired levels shouldreach 1.0 to 1.5 mEq/L.Patient should be observed for decreases inmanic behavior and mood swings, adverse sideeffects, and drug interactions.


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P atient Edu c ation: ( L ith ium T h erapy)

Regular blood lithium levels are necessary for safe, effectivetherapy. Blood samples should be taken 12 hours after previous dose of lithium; therefore, do not take the morning dose until the serumsample has been taken.

Avoid taking other medications without the physician's knowledge

because these may increase or decrease the effects of lithium.

Report any unusual symptoms, illness, or loss of appetiteimmediately to the physician.

C ontinue to take the drug despite an occasional relapse. Somepatients respond slowly to lithium therapy.

Notify the doctors whenever a change in diet occurs because thismay affect the lithium level.

Women should not breast-feed while taking lithium.

Schedule an annual physical examination.

C arry a Medic Alert card or wear a Medic Alert bracelet.


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D aily D osage of L ith ium S alts:

Generic NameGeneric NameLithium carbonateLithium carbonate

Lithium citrateLithium citrate

Trade Name Trade NameEskalithEskalith

LithaneLithaneLithobidLithobidEskalith CR Eskalith CR

CibalithCibalith--ss

Dosage Range (mg/day)Dosage Range (mg/day)900900--1800 mg in divided1800 mg in divideddoses until serum levelsdoses until serum levelsreach 1.0reach 1.0--1.51.5 mEq mEq/L/L

Begins with 300 mg BIDBegins with 300 mg BIDand gradually increase by and gradually increase by 300 mg increments to300 mg increments toachieve desired serumachieve desired serumlithium levellithium level


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A nti c onvulsantsUsed to treat seizure disorders, which are notuncommon amongindividuals with psychiatric disorders.For example, individuals experiencing acute substanceabuse withdrawal are given sedatives and anticonvulsantmedications to prevent or treat seizures and deliriumtremens.O ther examples include individuals with organic mentaldisordersassociated with Axis III physical disorders or conditions

such asbrain tumor, history of head injury, explosive personality,or epilepsy.

According to Maxmen, 1991, it can also treat bipolar disorders,especially mania.


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Commonly used anti c onvulsantsDepakene (valproic acid)Dilantin (phenytoin)

Klonopin (clonazepam)Mysoline (primidone)T egretol (carbamazepine)

Zarontin (ethosuximide)


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CA RBA MAZ EP INE

Available as standard formulation requiring threetimes a day dosing, and a modified-releaseformulation ( T egretol Retard) to allow twice dailydosing up (up to 800 mg B ID).


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A.) Mode of Action- Structurally similar to the tricyclic antidepressant

imipramine, however, carbamazepine has noeffect on monoamine reuptake.

- T hought to mediate its therapeutic effect byinhibiting kindling phenomena in the limbicsystem.


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B.) Indications1.) T reatment of depressive disorders- T reatment of resistant depression, i.e. worth a

trial in patients who have failed to respond to acyclic antidepressant drug and lithium

carbonate.- Enhances the effects of TC As and SSR Is.


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3.) T reatment of mania-C arbamazepine is effective in high doses (600 mg

bd- 800 mg bd), but the therapeutic responseusually only occurs in the second week of treatment; thus, the response to carbamazepineis slower than the response to antipsychoticdrugs.


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5.) T reatment of all forms of epilepsy- exceptabsence seizures.

6.) T reatment of trigeminal neuralgia.7.) T reatment of behavioral disorders secondary to

limbic epileptic.

8.) T reatment of aggressive behavior (includingafter head injury).

9.) T reatment of acute alcohol withdrawal.


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C .) Adverse Reactions1.) Side-effects :

-Dizziness and drowsiness-Generalized erythematous rash (3%)-Visual diturbances (esp. double vision)-G I disturbances (anorexia and constipation)-Leucopenia and other blood disorders-H yponatremia


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2.) C arbamazepine should be initiated at a dosageof 200 mg bd and increased after 1 week to theusual therapeutic dosage of 200 mg mane, 400mg nocte required for prophylaxis (somepatients may require 400 mg bd)-carbamazepine is a less toxic drug than lithiumcarbonate and regular serum level estimationappears to be unnecessary; however, becauseof the slight risk of leucopenia and other blooddisorders, it is important that full blood count ismonitored periodically.


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3.) C arbamazepine is an inducer of the liver enzyme cytochrome P450 2D6- thus it lower

plasma haloperidol levels by half.4.) It also decreases the plasma concentrationof :

-O ral contraceptives

-Warfarin


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5.) T he plasma concentration of carbamazepine isincreased by :

-Erythromycin-C imetidine-C alcium channel blockers

-Isoniazid


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A.) Mode of Action-Sodium vaproate is thought to mediate its

therapeutic effect through indirect effects of GABA-ergic succinic semialdehydedehydrogenase), implying a possible underlyingbiochemical disturbance of GABA deficiency insome affective disorders.

-Valproate semisodium is thought to permeate theblood-brain barrier more easily.


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B.) Indications1.) T reatment of depressive disorders2.) Preventing relapse of depressive disorders :3.) T reatment of mania

-effective in high doses- 600 mg bd-1200 mg bd)

4.) Preventing relapse of mania5.) T reatment of all forms of epilepsy.


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C .) Adverse Effects1.) Side-effects :

-Recent concern over severe hepatic andpancreatic toxicity.

-H aematological disturbances (thrombocytopenia,

inhibition of platelet aggregation).-Drowsiness, weight gain and hair loss.


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2.)Sodium valproate is initiated at a dosage of 200mg bd and increased after 1 week to 400 mg bdand again after another week to 600 mg bd, theusual theraeutic dosage required for prophylaxis(some patients may require 800 mg bd)- sodium

valproate is a less toxic drug than lithiumcarbonate and regular serum level estimationappears to be unnecessary, however, becauseof the slight risk of severe hepatic andpancreatic toxicity, and haematologicaldisturbance of platelet function, it is importantthat liver function test s, serum amylase leveland full blood count are monitored periodically.


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P ic tures of valproi c a c id

Can be in a form of a c apsule, syrup, or a tablet


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Implic


tions: Abrams (1991) cites the following nursing actions for anticonvulsantdrug therapy :

1. Give on a regular schedule to maintain therapeutic blood levels.

2. Give oral anticonvulsant drugs with meals or fluid to reducegastric irritation and decrease G I side effects. Zantac (ranitidine)is often prescribed to eliminate gastric irritation.

3. O bserve for therapeutic effects, which occur approximately seven toten days after drug therapy is started.

4. Monitor for adverse effects including C NS changes (drowsiness,sedation, ataxia), G I irritation, skin disorders, blood dyscrasias,respiratory depression, liver damage, gingival hyperplasia,hypocalcaemia, and lymphadenopathy.

5. O bserve for drug interactions.


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Patient Edu

cation:

Patient receiving anticonvulsant drug therapy should be instructed to

1. Inform the physician/psychiatrist of any known physical illnessesor pregnancy.

2.Inform the physician/psychiatrist of any medication or

O TCdrug heor she is presently taking.

3. T ake medications with food or glass of fluid at the same time eachday.

4. Ask for the same brand and form of drug when renewing prescriptions.

5. Follow directions when taking a liquid preparation of phenytoin(Dilantin).

6. Discuss monitoring blood levels of type prescribed drug to avoidreaching toxic levels.

7. Report any adverse side effects to physician/psychiatrist

D aily D osage of U sed


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D aily D osage of U sedA

ntic

onvulsantsGeneric NameGeneric Name

CarbamazepineCarbamazepineClonazepamClonazepamEthosuximideEthosuximidePhenytoinPhenytoinPrimidonePrimidone

Valproate Valproate Valproic Valproic acidacid

Trade Name Trade Name Tegretol TegretolKlonopinKlonopinZarotoninZarotoninDilantinDilantinMysolineMysolineDepakoteDepakoteDepakeneDepakene

Dosage Range (mg/day)Dosage Range (mg/day)600600--1200 mg 1200 mg 1.51.5--20 mg 20 mg 500500--1500 mg 1500 mg 500500--625 mg 625 mg 500500--2000 mg 2000 mg 60 mg/kg in divided doses60 mg/kg in divided doses10001000--3000 mg 3000 mg


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A ti ch li i c /A ti k i


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A nti ch olinergi c /A ntipar k insonA

gents

An anticholinergic agent is a substance thatblocks the neurotransmitter acetylcholine inthe central and the peripheral nervoussystem. An example of an anticholinergic isgabapentindicyclomine, and the classicexample is atropine. Anticholinergics areadministered to reduce the effects mediatedby acetylcholine on acetylcholine receptors inneurons throughcompetitive inhibition.T herefore, their effects are reversible.


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Indic

ations

Anticholinergic/antiparkinson agents are thedrugs of choice to treat extra pyramidaldisorders, to treat idiopathic or postencephalitic Parkinsons disease, or to useas an adjunct to levodopa. Anticholinergicdrugs are utilized to decrease salivation,spasticity, and tremors in people who haveminimal symptoms or cannot toleratelevodopa. T hey may also be prescribed incombination with other antiparkinson drugs.


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Contraindic

ations

Anticholinergic drugs are contraindicated inthe presence of glaucoma, myastheniagravis, gastrointestinal obstruction, prostatichypertrophy, and urinary bladder neckobstruction. T hey must be used in cautionwith patients exhibiting symptoms related tocardiovascular disorders.


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Implic


tions

Give antiparkinson agents with or immediately following food intake to preventor reduce gastrointestinal stress.O bserve for therapeutic effects such as

decreased salivation, tremor, and drooling(anticholinergic effects).O bserve for improvement in gait, balance,posture, speech, and self-care ability.


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Monitor for adverse effects due toanticholinergic drugs (atropine like effects)such as dry mouth, drowsiness, andconstipation.Monitor for adverse reactions toantiparkinson agents.


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Patient Edu

cation

Maintain an adequate amount of fluid intake(unless contraindicated) to prevent excessivedryness of the mouth. T aking the medication

just before meal, chewing gum, or sucking onhard candies may alleviate this side effect.

Avoid operating potentially hazardousmachinery or driving an automobile if symptoms of blurred vision or drowsinessoccur.


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H ave routine vision examinations to eliminatethe possibility of the presence of glaucoma.Limit use of alcohol, high protein foods, andvitamin B6 as they decrease therapeuticeffect of levodopa.

psycho pharmacology - final

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