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    DRUGS AFFECTING THE CENTRALNERVOUS SYSTEM

    ANATOMY OF THE NEUROLOGICAL SYSTEMBy: Ms. Louradel M. Ulbata, RN, MAN

    PHYSIOLOGY OF THE NEUROLOGICSYSTEMOrganization of the Nervous SystemA. Central nervous system (CNS).1. Brain

    2. Spinal Cord

    B. Peripheral nervous system (PNS).1. Twelve pairs of cranial nerves

    2. Thirty-one pairs of spinal nerves

    B.1. Autonomic nervous systema. Sympathetic system

    b. Parasympathetic system.

    B.2. SOMATIC NERVOUS SYSTEMa. Afferent Nerves

    b. Efferent Nerves

    CELLS OF THE NERVOUS SYSTEM

    A. Neuron-the functional cell of the nervoussystem.

    1. Common characteristics.a. Responds or reacts to stimuli

    b. Conducts impulses

    c. Influences other neurons.

    2. Structurea. Cell body-contains the cell nucleus whichcontrols cellular activity.

    b. Axon-conducts impulses away from the cellbody

    c. Dendrites-receive incoming stimuli andtransmit them to the axon of another neuron.

    3. Function/classification.a. Afferent neurons (sensory) transmitinformation towards the CNS.

    b. Efferent neurons (motor)transmit informationaway from the CNS.

    REMEMBER: S MESensory= Afferent; M otor = Efferent

    c. Somatic system1). Afferent are sensory neurons that transmit

    impulses from the skeletal muscles and skin to

    the CNS.

    2). Efferent are motor neurons that transmit

    impulses that lead to contraction and control of

    skeletal muscle.

    d. Visceral system.1). Afferent are sensory neurons that transmit

    impulses from smooth muscle and cardiac

    muscle to the CNS.

    2) Efferent are motor neurons that transmit

    impulses to the glands, cardiac muscle, and

    smooth muscle.

    e. Synapse or synaptic terminals are areas of

    chemical transmission of an impulse from the

    axon of one neuron to the dendrites of another

    neuron.

    Functional Properties of Neurons

    Irritabilityability to respond to stimuli Conductivityability to transmit an

    impulse

    NERVE FUNCTION is NERVECONDUCTION

    ACTION POTENTIALNerve Cell undergoes:

    1. Resting Membrane Potential2. Action Potential / Depolarization3. Repolarization / Restabilization

    1. RESTING MEMBRANE POTENTIAL Sodium predominates outside the cell,

    potassium inside the cell.

    Inside of the cell is relatively negativewith the presence of potassium and

    large amounts of negative ions.

    2. Action Potential / Depolarization When a cell is stimulated, cell

    membranes become permeable to

    sodium ions.

    Sodium moves inside the cell andpotassium moves out.

    Inside of the cell becomes positivelycharged.

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    Sudden change in the charge of the cellfrom negative to positive is called action

    potential.

    3. REPOLARIZATION The sodium-potassium pump restores

    the original configuration

    This action requires ATP Sodium is pumped out of the

    cell and potassium back into the

    cell.

    B.Supporting cells provide support,nourishment, and protection to the neuron.

    1. Neurilemmaprotective cells whichsurround the axons in the PNS.

    a. Provide for effective regeneration ofPNS nerve fibers.

    b. Form the myelin sheath in the PNS.c. No neurilemma present in the CNS.

    2. Glial cells protective cells in the CNS;responsible for the formation of the

    myelin.

    3. Myelin sheath.a. Dense membrane or insulator around

    the axon.

    b. Facilitates function of the neuron,c. Contributes to the blood-brain barrier to

    protect the central nervous system

    against harmful molecules.

    4. nodes of Ranvier- Intermittent gaps between the

    myelin sheath that allow

    communication between nerve

    fibers.

    - Signals jumping from node to

    node travel hundreds of

    times faster than signals travelingalong the surface of the

    axon.

    D. Impulse conduction.SALTATORY CONDUCTION An action potential excites one section

    of the nerve membrane and electrical

    impulse then SKIPS from one node to

    the next generating an action potential.

    These node-to-node mode ofconduction is termed SALTATORY OR

    LEAPING TRANSMISSION

    ADVANTAGES OF SALTATORY OfLEAPING TRANSMISSIONMembranes are forming fewer action

    potentials so:

    1. The speed of conduction is much faster2. The nerve is protected from exhaustion

    or using up energy to form multiple

    action potentials

    Synaptic transmission:TRANSMISSION OF ELECTRICALIMPULSES FROM ONE NEURON TOANOTHER

    a. A chemical synapse maintains a one-way communication link between

    neurons

    synapse -junction between twoneurons.

    NERVE SYNAPSE IS MADE UP OF:

    1. presynapticnerve -ends BEFOREspecific synapse

    2. synaptic cleft -separates synapse bya tiny gap (less than one-

    millionth of an inch)

    3. Post synaptic Nerve- begins AFTERsynapse

    b. Chemical neurotransmitters (neuro-mediators) facilitate the transmission ofthe impulse across the synapse.

    1). Acetylcholine.

    2). Norepinephrine.

    3). Dopamine.

    4). Histamine.c. Impulses pass in only one direction.

    Impulses are able to cross the synapseto another nerve

    Neurotransmitter is releasedfrom a nerves axon terminal

    The dendrite of the next neuronhas receptors that are

    stimulated by the

    neurotransmitter

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    An action potential is started inthe dendrite

    To return the effector to a resting state sothat it can be stimulated again, the actionsof these neurotransmitter must be stoppedby one or more of these processes:

    1. Reuptake by the presynaptic nerve- neurotransmitters are reabsorbed by

    the presynaptic nerve to reuse/recycle

    2. Inactivation by an enzyme

    3. Broken down by enzymes in the area

    4. Diffusion out of the synaptic cleft and

    removal by the vascular system

    d.Nerve regenerationentire neuron is unableto undergo complete regeneration.

    1. The axons of the PNS may regenerate via the

    connective tissue neurilemma, providing the cell

    body of the neuron remains viable.

    2. Neuron regeneration in the CNS is very

    limited, possibly due to the lack of neurilemma.

    3. Scar tissue is a major deterrent to successful

    cellular regeneration.

    CENTRAL NERVOUS SYSTEM

    The brain and the spinal cord within the

    vertebral column make up the central nervous

    system.

    A. The brain and the spinal columnare protected by the rigid bony

    structure of the skull and the

    vertebral column.

    B. Meningesprotectivemembranes that cover the brain

    and are continuous with those ofthe spinal cord. (DAP)

    1. Dura mater-a tough membraneimmediately outside the

    arachnoid; provides protection

    to the brain and spinal cord.

    2. Arachnoid-a delicatenonvascular, waterproof

    membrane that encases the

    entire CNS; the subarachnoid

    space contains the cerebral

    spinal fluid.

    3. Pia mater-a delicate vascularconnective tissue layer that

    covers the surfaces of the brain

    barrier.

    C. Cerebral spinal fluid (CSF).

    1. Serves to cushion and protectthe brain and spinal cord; brain

    literally floats in CSF.

    2. CSF is clear, colorless, wateryfluid; approximately 100 to 200

    cc total volume, with a normal

    fluid pressure of 70 to 150 mm

    of water 9average-125 cm water

    pressure).

    3. Formation and circulation ofCSF.

    a. Fluid is secreted by the choroidsplexus located in the ventricles

    of the brain.

    b. CSF flows through the lateralventricles into the third ventricle,

    flows through the Aqueduct of

    Sylvius into the fourth ventricle

    where the central of the spinal

    column opens.

    c. From the fourth ventricle, thereare openings into the cranial

    subarachnoid space; CSF flows

    around the spinal cord ad brain.

    d. Since CSF is formedcontinuously, it is reabsorbed at

    a comparable rate by the

    arachnoid villi.

    D. Brain.I. FOREBRAIN Prosencephalon - Pro Die & Te ll Diencephalon => Thalamus,

    Hypothalamus Telencephalon => Cerebrum

    1. Cerebrumseat ofconsciousness

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    - convolutions or gyri & grooves:

    sulci or fissures which

    expands or increases the surface

    area of the brain

    - is divided into left and right

    hemispheres connected to

    each other by the corpus

    callosum

    - the cerebral cortex is the

    surface layer of each

    hemisphere.

    A. Major lobes of thecentral cortex.

    a. Frontal.1). Coordination of voluntary

    skeletal muscle movement.

    2). Abstract thinking, morals,

    judgment.

    3). Speech area, motor speech area

    (Brocas area) located in only one

    hemisphere.

    b. Parietal.1. Interprets sensory nerve impulses

    (pain, temperature,

    touch).

    2. Maintains proprioception.

    3. Recognition of size, texture, and

    shape of objects.

    c. Temporal.1. Auditory area- interprets meaning

    of certain sounds.

    2. Wernickes area- comprehension

    and formulation of

    speech.

    d.Occipital area-interprets visionand controls ability to understand

    written words.

    e. The limbic lobeis thought to bea link bet emotional & cognitive(thought) mechanisms.

    f. Thecentral lobe (insula)isthought to be involved in both

    autonomic & somatic activities.

    2.Thalamus.1. relay station for all sensory

    information

    2. Activities related to

    consciousness.

    3. . Hypothalamus.1. Regulation of visceral

    activities-body temperature,

    motility and secretions of the GI

    tract, arterial blood pressure.

    2. Nerve connections with the

    thalamus and the cerebral

    cortex make it possible for our

    emotions to influence visceral

    activity.

    3. Regulation of endocrine

    glands via influence on the

    pituitary gland.

    4. Neurosecretion of antidiuretic

    hormone (ADH) which is stored in

    the pituitary

    3. Motor areas of the cerebralcortex.a. Primary function is coordination

    and control of skeletal muscle

    activity.

    b. Corticospinal tracts (pyramidaltracts).

    1. Descending tract from the

    motor area of the

    cerebral cortex to the spinal

    cord.

    2. Majority of nerves cross in the

    medulla to the opposite

    side before descending into

    the spinal cord.

    3. These pathways do not cross

    over.

    c. Brain cells and the nerve fibers in

    the descending tracts of the central

    nervous system are called uppermotor neurons.

    II. MIDBRAIN (MESENCEPHALON)- Consists of 4 rounded bodies, the corpora

    quadrigemina:

    Paired upper bodies: serve asvisual reflex centers for head &

    eyeball movements

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    Paired lower bodies: serve asrelay centers for auditory

    information

    III. HINDBRAIN (RHOMBENCEPHALON) Brainstem

    Pons Medulla oblongata

    CerebellumA.. Pons- respiratory apneustic center,

    nucleus of cranial nerves-

    5,6,7,8

    B. Medulla oblongata-a continuation of thespinal cord as it enters into the cranial

    vault in the brain.

    - respiratory and cardiovascular centers,

    nucleus of cranial nerves 9,10,11,12

    1. Conduction center and crossing

    center for the upper motor neurons.

    2. Maintains control of cardiac rate.

    3. Vasomotor center for constriction

    and dilation of vessels.

    4. Respiratory center for changes in

    rate and depth of breathing.

    5. Vomiting reflex center.

    6. Swallowing reflex center.

    C. The Cerebellum 2nd largest part of the brain w/c consists

    of 2 hemispheres& a connecting

    portion, the vermis

    responsible for coordination of musclemovements

    functions:1. helps make muscular movement

    smooth instead of jerky &

    trembling

    2. helps maintain muscle tone &posture

    3. impulses from the vestibularapparatus are continuously

    delivered to the cerebellum tohelp maintain equilibrium

    RETICULAR FORMATION Nerve fibers arising from the central

    core of the medulla and lower pons

    Reticular Activating System- arises from reticular formation.

    - essential for arousing from

    sleep and remaining alert.

    - Injury to RAS can cause

    anesthesia and coma

    Basal ganglia (cerebral nuclei)regulate and program muscle

    activity coming from the cerebral

    cortex.

    Movement is controlled by:

    a. Cerebral cortexvoluntaryinitiation of motor activity.

    b. Basal ganglia-assist to maintainposture.

    c. Cerebellum-coordinates musclemovement.

    CEREBRAL CIRCULATIONa. The internal carotid arteriesenter the

    cranial vault at the temporal area

    b. Vertebral arteriesarise from the

    subclavian artery and enter the brain at

    the foramen magnum.

    c. The Circle of Willisis an arterial

    anastomosis at the base of the brain.

    The circle ensures continued circulation if

    one of the main vessels is

    disrupted.

    THE SPINAL CORD1. The spinal cord is continuous with the

    medulla and extends down the vertebral

    columns to the level of the first and

    second lumbar vertebra.

    2. Each column is divided into functional

    groups of nerve fibers.

    a. Ascending tractstransmit impulses tothe brain (sensory pathway).

    b. Descending tractstransmit impulsesfrom the brain to the various levels of the

    spinal cord (motor pathways).3. Structure.

    a. Closely approximately vertebrae

    provide protection from the spinal cord

    and nerve roots.

    b. Intervertebral discslie between each

    vertebra to provide flexibility to the

    spinal column.

    c. Nucleus pulposusis a gelatin

    substance in the vertebral disc.

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    5. Upper motor neurons-originate in the

    brain, transmit impulses to the

    muscles and organs.

    6. Lower motor neuronsoriginate in

    the spinal cord, transmit impulses

    to the muscles and organs.

    4. Reflex activity.a. The reflex arch must be intact, the

    spinal cord serves as the connection

    between the afferent pathway (sensory), and

    the efferent pathway (motor).

    b. By testing the reflex arc (deep tendon

    reflexes), the lower motor neuron and the

    sensory/motor fibers from the spinal

    column can be evaluated.

    Reflex arc

    a. Reflexare is the functional unit whichprovides pathways over which nerve

    impulses travel.

    b. Passage of impulses over a reflex arc

    is called a reflex act or a reflex.

    c. Reflex arcThe afferent neuroncarries the stimulus to the spine; integrates

    it into and through the spine (CNS) to the

    efferent neuron; crosses the synapse

    with the message from the CNS to the

    organ or muscle which responds to the

    stimuli. This is the sequence of events

    when testing the deep tendon

    reflexes.

    PERIPHERAL NERVOUS SYSTEM(PNS)

    Cranial nerves

    1. Twelve pairs of cranial nerves.2. Originate from under the surface

    of the brain.

    A. Spinal nerves.1. Each pair of nerves is

    numbered according to

    the level of the spinal

    cord from which it

    originates.

    2. Each spinal nerve is connectedto the cord by two roots.

    A. DORSAL (PoSterior)root- receives SENSORYinput from sensory

    receptors throughout the

    body.

    B. Ventral (anterior root)amotor nerve carrying neuron

    messages to glands and to

    the peripheral area.

    REMEMBERDORSAL ROOT/ POSTERIOR=SENSORY

    VENTRAL ROOT/ ANTERIOR

    = MOTOR

    3. The roots fuse at the exit fromthe vertebra to form a mixed

    spinal nerve.

    4. SPINAL NERVEPLEXUSES

    - network of interwoven spinal

    nerves

    MAJOR PLEXUSES:A. CERVICAL PLEXUSES

    a. sends motor impulses to the

    NECK muscles

    b. Sends out PHRENIC nerve,

    activating the diaphragm

    c. Receives sensory impulses from

    neck snd back of the head

    B. BRACHIAL PLEXUSES- Innervates shoulder, arm,

    forearm, wrist and hand

    c. LUMBOSACRAL PLEXUS- Innervates the lower

    extremities.

    - Sends out the large SCIATICNERVE

    C. Somatic nervous systemassociated withthevoluntarycontrol of body movements via

    skeletal muscles,and withsensoryreceptionof

    externalstimuli(e.g.,touch,hearing,andsight

    http://en.wiktionary.org/wiki/voluntaryhttp://en.wiktionary.org/wiki/voluntaryhttp://en.wiktionary.org/wiki/voluntaryhttp://en.wikipedia.org/wiki/Skeletal_muscleshttp://en.wikipedia.org/wiki/Skeletal_muscleshttp://en.wikipedia.org/wiki/Sensehttp://en.wikipedia.org/wiki/Sensehttp://en.wikipedia.org/wiki/Sensory_receptorhttp://en.wikipedia.org/wiki/Sensory_receptorhttp://en.wikipedia.org/wiki/Sensory_receptorhttp://en.wikipedia.org/wiki/Stimulus_(physiology)http://en.wikipedia.org/wiki/Stimulus_(physiology)http://en.wikipedia.org/wiki/Stimulus_(physiology)http://en.wikipedia.org/wiki/Tactitionhttp://en.wikipedia.org/wiki/Tactitionhttp://en.wikipedia.org/wiki/Tactitionhttp://en.wikipedia.org/wiki/Hearing_(sense)http://en.wikipedia.org/wiki/Hearing_(sense)http://en.wikipedia.org/wiki/Hearing_(sense)http://en.wikipedia.org/wiki/Sighthttp://en.wikipedia.org/wiki/Sighthttp://en.wikipedia.org/wiki/Sighthttp://en.wikipedia.org/wiki/Sighthttp://en.wikipedia.org/wiki/Hearing_(sense)http://en.wikipedia.org/wiki/Tactitionhttp://en.wikipedia.org/wiki/Stimulus_(physiology)http://en.wikipedia.org/wiki/Sensory_receptorhttp://en.wikipedia.org/wiki/Sensehttp://en.wikipedia.org/wiki/Skeletal_muscleshttp://en.wiktionary.org/wiki/voluntary
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    D. autonomic nervous systemregulatesinvoluntary activity (cardiovascular, respiratory,

    metabolic, body temperature, etc.)

    1. Consists of two divisions that have

    antagonistic activity.

    2. Parasympathetic divisionmaintains

    normal body functions.

    - REST & DIGEST

    3. Sympathetic division-prepares the

    body to meet a challenge or an emergency

    (preparation for fight/flight).

    SYMPATHETIC VS PARASYMPATHETIC

    Parasympathetic:

    REST ANDIGEST

    Sympathetic:FIGHT

    LIGHT

    unction: => slows stuffown

    => speed stuffp

    ontrol Craniosacral:brain + belowhe belt

    Thoracolumbar:bove the belt

    Neurotransmittr

    ACETYLCHOLIE

    EPINEPHRINENE

    "DUMBBELS":DiarrheaUrinationMiosis"constrict"BradycardiaBronchoconstrictErection "point"Lacrimation

    alivation

    Opposite of

    Parasympatheti

    cs:

    Constipation

    Urinary retention

    Mydriasis "eyes

    wide with fright"

    Tachycardia

    Bronchodilate

    Ejaculation

    "shoot"

    Xerophthalmia

    (dry eyes)

    Xerostomia (dry

    mouth)

    CRANIAL NERVES

    arenerveswhich start directly from thebrainsteminstead of thespinal cord.

    Only the first and the second pairemerge from thecerebrum;the

    remaining 10 pairs emerge from the

    brainstem.

    NUMBER NAME FUNCTION

    I.

    II.

    III.

    IV.

    V.

    VI.

    VII.

    Olfactory

    Optic

    Oculomotor

    Trochlear

    Trigeminal:

    Opthalmic

    Macillary

    Mandibular

    Abducens

    Facial

    Sense of smell

    Vision-conducts

    information from

    the retina

    Down and outward

    movement of the

    eye

    Pupillary

    constriction and

    accommodation

    Muscle of the

    upper eyelid (ability

    to keep the eye

    open)

    Movement of the

    eye

    Corneal reflex

    Sensory fibers of

    the face

    Motor nerves for

    chewing and

    swallowing

    Inward movement

    of the eye

    Facial expression

    Sense of taste on

    anterior tongue

    Muscle of the

    eyelid (ability to

    close the eye)

    VIII.

    IX.

    X.

    Acoustic

    Glossopharyngeal

    Vagus nerve

    Reception of

    hearing and

    maintenance of

    equilibrium

    Sense of taste on

    posterior tongue

    Salivation

    Swallowing or

    gag reflex

    Assists in

    http://www.wordiq.com/definition/Nervehttp://www.wordiq.com/definition/Nervehttp://www.wordiq.com/definition/Nervehttp://www.wordiq.com/definition/Brainstemhttp://www.wordiq.com/definition/Brainstemhttp://www.wordiq.com/definition/Spinal_cordhttp://www.wordiq.com/definition/Spinal_cordhttp://www.wordiq.com/definition/Spinal_cordhttp://en.wikipedia.org/wiki/Cerebrumhttp://en.wikipedia.org/wiki/Cerebrumhttp://en.wikipedia.org/wiki/Cerebrumhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Brainstemhttp://en.wikipedia.org/wiki/Cerebrumhttp://www.wordiq.com/definition/Spinal_cordhttp://www.wordiq.com/definition/Brainstemhttp://www.wordiq.com/definition/Nerve
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    XI.

    XII.

    Accessory (Spinal)

    Hypoglossal

    swallowing action

    Motor fibers to

    larynx for speech

    Innervation of

    organs in thorax

    and abdomen

    Important in

    respiratory,

    cardiac, and

    circulatory

    reflexes

    Ability to rotate

    the head and

    raise the shoulder

    Muscles of the

    tongue

    PSYCHOTROPIC DRUGS

    Drugs that affect mental function Cannot cure psychiatric illness but

    they can modify or lessen

    symptoms

    Classification of Psychotropic Drugs

    1. Tranquilizers- decrease anxiety and

    hyperactivity causing a marked decrease

    in the level of consciousness

    1. Antidepressants- Used to treat depression that has

    become severe enough to interfere with a

    persons ability to function normally.

    TRANQUILIZERS

    1. Major Tranquilizers- also known as

    ANTIPSYCHOTICS

    - used to treat psychoses

    2. Minor Tranquilizers

    - also knows as

    ANXIOLYTICS

    - used to treat the less

    severe neurotic and psychosomatic

    MAJOR TRANQUILIZERS/

    ANTIPSYCHOTICS

    Psychotic Disorders

    Definition: Psychotic disorders are

    defined as mental disorders in which the

    personality is severely altered and a

    persons contact with reality is impaired.

    Characteristics: delusions, hallucinations,

    odd behavior, and incoherent or

    disorganized speech

    Schizophrenia

    literal translation splitmind

    separate emotional sidefrom intellectual side

    emotional &cognitive processes

    don't function

    together

    Positive schizophrenia

    symptoms are caused by an excess

    or distortion of normal functions.

    The positive symptoms of schizophrenia

    include:

    Delusions. Delusions are inflexiblemisleading beliefs. They appear as

    a result of exaggerations or

    distortions of reasoning, as well as

    false interpretations of things andevents. For example, one can think

    that some book was written

    especially for him/her.

    Hallucinations. False sensoryperceptions or perceptual

    experiences that do not exist in

    reality.

    Ambivalence.Holding seeminglycontradictory beliefs or feelings

    about the same person, event , or

    situation

    Echopraxia. Imitation of themovements and gestures of

    another person whom the client is

    observing.

    Flight of ideas. Continuous flow ofverbalization in which the person

    jumps rapidly from one topic to

    another.

    Ideas of Reference. Falseimpressions that external eventshave special meaning for the

    person.

    Perseveration. Persistentadherence to a single idea or topic

    ; verbal repetition of a sentence,

    word or phrase.

    Associative Looseness.Fragmented or poorly related

    thoughts or ideas

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    Negative Symptoms of Schizophrenia

    Negative schizophrenia symptoms are

    those that reflect a decrease in normal

    functions, or a loss of them

    Affective flattening ( Flat affect) isusually expressed by the absenceor reduction of emotional

    expression, such as mimicry, voice

    tone, eye contact and body

    language.

    Alogiais the tendency to speakvery little or to convey little

    substance of meaning ( poverty of

    content)

    Avolition (Lack of volition) is theabsence of goal-oriented behavior,absence of will, ambition, or drive

    to take action or accomplish task.

    A person loses interest to the

    surrounding world, doesn't do

    anything, and sits doing nothing

    for long periods of time.

    Apathy. Feelings of indifferencetoward people, activities and

    events.

    Anhedonia. Feeling no joy orpleasure from life or any activitiesor relationships.

    Blunted Affect. Restricted range ofemotional feeling, tone or mood.

    Catatonia. Psychologically-inducedimmobility occasionally marked by

    periods of agitation or excitement;

    the client seems motionless, as if in

    a trance.

    ETIOLOGY OF SCHIZOPHRENIA

    NEUROCHEMICAL FACTORSThe dopamine and serotonin

    hypothesis:

    - schizophrenia is caused by an excess

    of dopamine and serotonin activity in the

    brain.

    Dopamine Pathways

    1. Mesolimbic

    Projects from brainstem to limbicareas.

    Mesolimbic- mesocortical (behavior )

    Overactivity produces delusions and

    hallucinations

    2. Mesocortical

    - May be associated with both

    positive and negative symptoms

    - Blockade may help increase

    negative symptoms of schizophrenia

    3. Nigrostriatal

    - Projects from thesubstania nigra to the basal

    ganglia

    A part of theextrapyramidal system

    Thus side effects arecalled extrapyramidal Extrapyramidal

    -> part of the

    nervous system that regulates muscle

    reflexes.

    Types of movement disorderscaused by this pathway include:

    Akathisia Dystonia Tardive dyskinesia Tremor, rigidity,

    bradykinesia

    Drug-inducedParkinsonism

    4. Tuberoinfundibular

    Tuberoinfundibular- pituitarysystem (endocrine)

    Endocrine control - tubero-infundibular system.

    - Dopamine and dopamineagonists suppress prolactin release,

    dopamine antagonists may stimulate it

    leading to increased prolactin

    Blockade produces galactorrhea

    Antipsychotic drugs

    -block DA receptors in both systems and

    therefore Parkinsonian symptoms and

    EPS are side effects.

    CATEGORIES OF ANTIPSYCHOTIC

    1. CONVENTIONAL/ TRADITIONAL/TYPICAL ANTIPSYCHOTIC DRUGS

    - are dopamine

    antagonists

    - targets only the

    positive signs of schizophrenia

    2. ATYPICAL/ NEWER

    ANTIPSYCHOTIC DRUGS

    - are both dopamine

    and serotonin antagonist

    - targets both

    positive and negative signs of

    schizophrenia

    Traditional/ Conventional

    /Typical Antipsychotics

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    Phenothiazines chlorpromazine

    (Chlorpromazine Mixture,

    Chlorpromazine Mixture

    Forte, Largactil)

    fluphenazine(Anatensol,Modecate) flupenthixol(Fluanxol) pericyazine(Neulactil) pimozide(Orap) thioridazine(Aldazine) trifluoperazine(Stelazine) zuclopenthixol(Clopixol)

    Butyrophenones haloperidol(Haldol,

    Serenace)

    droperidol(DroleptanInjection) Chlorpromazinewas the

    first anti-psychotic drug developed

    Mechanism of Action of

    Phenothiazines

    The drugs found in this class areantagonists.

    They work by blocking theDopamine receptors in the

    dopamine pathways of the brain;

    thus, decreasing the normal effect

    of dopamine release.

    Blocking the dopamine receptorsin the mesolimbic pathway results

    in the antipsychotic effect.

    Butyrophenones

    Butyrophenones are high-potencyantipsychotics (potency refers not

    to effectiveness but rather to the

    ability to bind to dopamine

    receptors)

    Haloperidol (Haldol) is the most

    common of the butyrophenones

    Mechanism of Action

    All the butyrophenones work inthe same manner as the

    phenothiazines.

    They block the dopaminereceptors in the dopamine

    pathways, thus, thwarting any

    possible over excitation of the

    dopamine receptors.

    Typical Antipsychotics

    Phenothiazines andButyrophenonesare typical

    antipsychotics

    These drugs are no longerregarded as the best practice for

    treating psychotic disorders, eventhough they are still commonly

    utilized in emergency treatments.

    The reason for this is that they arenot very selective. They do not

    only block the D2 receptors of the

    mesolimbic pathway but also

    block the D2 receptors in the

    nigrostriatal pathway,

    mesocortical zone, and

    tuberoinfundibularpathway.

    The fact that they are not veryselective causes the extrapyramidal symptoms such as

    tardive diskinesia

    Atypical Anti-psychotics

    Were developed in an attempt tominimize the side effects of typical

    anti-psychotics

    They have proven to cause fewerextra

    pyramidal symptoms (EPS) when

    compared

    to typical anti-psychotics.

    They produce fewer EPS becausethey are

    more selective.

    Atypical agents aripiprazole(Abilify) clozapine(CloSyn, Clopine,

    Clozaril)

    risperidone(Risperdal) quetiapine(Seroquel) amisulpride(Solian) olanzapine(Zyprexa) ziprazidone(Zeldoxx)

    Mode of Action

    Dopamine and serotoninAntagonists

    Atypical antipsychotic drugs havea similar blocking effect on

    dopamine receptors but appear to

    be more selective in targeting the

    intended pathway to a larger

    degree than typical antipsychotics.

    They also interact with otherneurotransmission systems,

    particularly with the serotonergic

    and noradrenergic pathways.

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    SIDE EFFECTS OFANTIPSYCHOTIC DRUGS

    A. NEUROLOGIC SIDE EFFECTS

    1. EXTRAPYRAMIDAL SIDE EFFECTS(EPS)

    2. TARDIVE DYSKENISIA3. SEIZURES4. NEUROLEPTIC MALIGNANT

    SYNDROME

    EXTRAPYRAMIDAL SIDE

    EFFECTS (EPS)

    - Are reversible movementdisorders induced by neurolepticmedication.

    - Include:a. Dystonic reactions

    b.

    Pseudoparkinsonism

    c. Akathisia

    1. DYSTONIA- characterized by spasms in

    discrete muscle groups such as theneck muscles (torticollis) or eye

    muscles ( oculogyric crisis)

    - these may also be accompanied

    by protrusion of the tongue,

    dysphagia, and laryngeal spasms

    - extremely frightening and painful

    to the pt

    - Treatment:

    Diphenhydramine (Benadryl)

    Benztropine (Cogentin)

    2. Pseudoparkinsonism

    - Neuroleptic-induced

    parkinsonism

    - characterized by:

    a. shuffling gait

    b. masklike facies

    c. muscle stiffness

    d. rigidity

    e. drooling

    f. akinesia ( slowness and

    difficulty

    initiating movement)

    g. tremors

    Treatment:

    -Benztropine Sulfate

    (Cogentin)

    - Biperiden ( Akineton)

    3. AKATHISIA

    - characterized by restlessness,

    movement, pacing, inability to

    remain still.

    Treatment:

    Propranolol (Inderal)

    Benzodiazepines

    TARDIVE DYSKINESIA

    - a late appearing

    side effect of antipsychotic

    medications

    - characterized by

    abnormal, involuntary movements

    such as lip smacking, tongue

    protrusion, chewing, blinking,

    grimacing.

    - Irreversible once ithas appeared

    CLOZAPINE atypical

    antipsychotic has not not been

    found to have this effect

    SEIZURE

    - Clozapine is a

    notable exception

    - associated with

    high dosage of med

    NEUROLEPTIC MALIGNANT

    SYNDROME ( NMS)

    - serious and fatal side

    effect

    - characterized by:

    FFever AAutonomic instability LLeukocytosis TTremor EElevated enzymes (elevated

    CPK)

    RRigidity of muscles- treated by stopping the medication- Prescribe bromocriptine and

    dantrolene (dopaminergic

    agonists)

    NON-NEUROLOGIC SIDE

    EFFECTS

    Blurred visionConstipationUrinary retentionMemory dysfunctionDry mouthSinus tachycardiaSedation, drowsinessWeight gainHypotension

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    aminobutyric acid (GABA) more

    effective causing interference with

    neuron firing.

    OTHER ANXIOLYTIC ANDHYPNOTIC DRUGS

    1. Paraldehyde ( Paral)

    - A very old drug used orally andrectally to sedate patients with

    delirium tremens or psychiatric

    conditions characterized by

    extreme excitement

    - Has distinctive odor- Cannot be stored in plasticcontainers or dispensed with a

    plastic spoon or syringe

    - Dilute first before using, use foodto improve taste, keep away from

    heat and flame, discard any

    unused portion

    2. Buspirone ( Buspar) A newer antianxiety agent Has no sedative, anticonvulsant or

    muscle relaxant properties

    It reduces the signs and symptomsof anxiety w/o many of the CNS

    effects and severe adverse effects

    associated with other anxiolytic

    drugs.

    Rapidly absorbed by the GI Metabolized in the LIVER Excreted in the URINE Caution in pts with hepatic or

    renal impairment and elderly

    patients

    May cause dry mouth andheadache

    3. Ramelteon ( Rozerem)

    Introduced in 2005 First of a new class of

    sedatives/hypnotics, MELATONIN

    RECEPTOR AGONISTS

    Stimulates the melatonin receptorwhich are thought to be involved

    in the maintenance of circadian

    rhythm and the sleep-wake cycle

    Used for treatment of insomniacharacterized by difficulty with

    sleep onset

    Metabolized in the LIVER Excreted in FECES and URINE Should be administered 30minutes before bed; allow 8 hours

    of sleep

    Patients should be monitored fordepression and suicidal ideation

    NURSING IMPLICATION FOR

    PSYCHOTROPIC DRUGS

    1. Careful initial assessment of ptsbehavior

    2. Pts with psychiatric disturbancesshould watched as they take their

    meds

    - stay w/ them as

    they take the meds and check the

    mouth if it has been swallowed

    3. MAJOR TRANQUILIZERS: Close

    observation and reporting of the

    earliest signs of EPS.

    Earliest sign of TD : AbN

    movt of tongue muscles

    4. Caution pt not to drive or

    perform potentially dangerous

    activities

    5. POSTURAL HYPOTENSION :

    Warn not to change body position

    quickly.

    6. PHOTOSENSITIVIY: Warn not to

    stay outside in bright sunlight as

    this can lead to eye damage and

    skin pigmentation.7. Warn pt & family bwt changes in

    body appearance and sexual

    function (eg; weight gain,

    gynecomastia, changes in mens,

    galactorrhea, decreased libido)

    8. inform client of side effects and

    encourage to report problems

    instead of discontinuing

    medication

    teach client methods of managing

    or avoiding unpleasant side effects

    and maintaining medication

    regimen:

    dry mouth sugar-freefluids and sugar-free hard

    candy

    * client should avoid calorie-ladenbeverages and candy

    constipation exercise,increase water and bulk-

    forming foods; stool

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    softener permissible but

    avoid laxatives

    photosensitivity sunscreen

    10. Report signs of infection (fever,

    sorethroat

    ANTIDEPRESSANTS

    DEPRESSION

    - Is an affective disordercharacterized by overwhelming

    sadness, despair and hopelessness

    that is inappropriate with respect

    to the event or events that

    precipitated the depression.-

    BIOGENIC AMINE THEORY OF

    DEPRESSION

    States that depression is caused bydeficiency of biogenic amines

    norepinephrine (NE), serotonin (

    5HT) and dopamine in certain

    areas of the brain

    Causes of Deficiency of Biogenic

    Amine

    1. Monoamine Oxidase ( MAO) maybreak them down to be recycled or

    restored in the neuron

    2. Rapid fire of the neurons may leadto their depletion

    3. Numbers or sensitivity ofpostsynaptic receptors may

    increase depletingneurotransmitter levels

    DRUG THERAPY FOR

    DEPRESSION

    ANTIDEPRESSANT DRUGS

    - most effective

    means of treating depression

    - counteracts the

    effects of neurotransmitter

    deficiencies

    - Increases the level

    of biogenic amines in the brain

    in three ways:

    a) may inhibit the

    effects of MAO

    b) block reuptake by

    the releasing nerve

    c) may regulate

    receptor sites and breakdown

    of neurotransmitters

    THREE (3) GROUPS: 1. TRICYLIC ANTIDEPRESSANTS

    (TCAs)

    2. MONOAMINE OXIDASEINHIBITORS (MAOIs)

    3. SELECTIVE SEROTONINREUPTAKE INHIBITORS (SSRIs)

    MONOAMINE OXIDASE INHIBITORS

    (PANAMA)

    1. Tranylcypromine (Parnate)2. Phenelzine ( Nardil)3. Isocarboxacid ( Marplan)

    THERAPEUTIC ACTIONS

    - Inhibit MAO, an enzyme found innerves and other tissues that

    breaks down the biogenic amine

    NE, dopamine and 5GT.

    It takes 2-3 weeks before initial

    therapeutic effects become

    noticeable

    DRUG FOOD INTERACTIONS

    Patients taking MAOIs shouldavoid TYRAMINE-CONTAINING

    FOODS

    Tyramine and other amines thatare found in food which are

    normally metabolized by MAO

    enzymes in the GI may be

    absorbed in high concentrations in

    the presence of MAOIs, resulting in

    increased blood pressure (

    HYPERTENSIVE CRISIS)

    Tyramine causes the release ofstored NE in the nerve terminals

    which further contributes to high

    BP

    HYPERTENSIVE CRISIS

    - characterized by:a. Occipital

    Headache

    b. Palpitations

    c. Neck stiffness

    d. N& V

    e. sweating

    f. dilated pupils

    g. photophobia

    h. tachycardia

    i. chestpain

    j. may progress to

    intracranial bleeding and stroke

    TYRAMINE CONTAINING FOODS

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    A VOCADO B ANANA C HEDDAR and AGED CHEESE S OY SAUCE & PRESERVED

    FOODS

    DRUG-DRUG INTERACTIONS

    MAOIs w/ TCAs:- hypertensive crisis

    - coma

    - severe convulsions MAOIs with SSRI :

    - Serotonin

    Syndrome

    - rapid

    changes in vital signs (fever,

    oscillations in blood pressure),

    sweating, nausea, vomiting,

    rigid muscles, myoclonus,

    agitation, delirium, seizures,

    and coma.

    - A period of 6 weeks should elapseafter stopping an SSRI before

    beginning therapy with a MAOI

    TRICYCLIC ANTIDEPRESSANTS

    (TCAs)

    - All reduces the reuptake of 5HTand NE into the nerves

    - It takes 2-3 weeks before initialtherapeutic effects become

    noticeable.

    THERAPEUTIC ACTIONS

    Inhibit presynaptic reuptake of the

    neurotransmitters NE and 5HT

    which leads to the accumulation of

    these neurotransmitters in the

    synaptic cleft and increased

    stimulation of the postsynaptic

    receptors.

    TRICYCLIC ANTIDEPRESSANTS

    Imipramine (Tofranil) Amitriptylline Amoxapine (Asendril) Clomipramine (Anafranil) Desipramine (Nopramin) Doxepin (Sinequan)

    TCA:

    CHECK:

    1. BP it causes HYPOTENSION2. HEART RATE it causes CARDIAC

    ARRYTHMIAS

    SELECTIVE SEROTONINREUPTAKE INHIBITORS

    Newest group of antidepressantdrugs

    Specifically blocks the reuptake of5HT, with little to no known effect

    on NE

    Do not have the many adverseeffects associated with TCAs and

    MAOIs so they are a better choice

    for many patients

    THERAPEUTIC ACTIONS

    Specifically blocks the reuptake of5HT, with little to no known effect

    on NE, increasing the levels of 5HT

    in the synaptic cleft.

    SELECTIVE SEROTONIN

    REUPTAKE INHIBITORS

    FLUOXETINE (prozac)- first SSRI

    - Indicated to treat

    depression, obsessive-

    compulsive d/o, bulimia, panic

    disorders and premestrual

    dysphoric disorder

    Fluvoxamine (Luvox) Paroxetine (Paxil) Sertraline (Zoloft) Citalopram (Celexa)

    SIDE EFFECTS OF

    ANTIDEPRESSANTS

    Dry mouth -it is helpful to drinksips of water; chew sugarless gum;

    brush teeth daily.

    Constipation -bran cereals, prunes,fruit, and vegetables should be in

    the diet.

    Bladder problems -emptying thebladder completely may be

    difficult, and the urine stream may

    not be as strong as usual. Older

    men with enlarged prostate

    conditions may be at particular

    risk for this problem. The doctor

    should be notified if there is any

    pain.

    Sexual problems -sexualfunctioning may be impaired; if

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    this is worrisome, it should be

    discussed with the doctor.

    Blurred vision -this is usuallytemporary and will not necessitate

    new glasses. Glaucoma patients

    should report any change in visionto the doctor.

    Dizziness -rising from the bed orchair slowly is helpful.

    Drowsiness as a daytime problem -this usually passes soon. A person

    who feels drowsy or sedated

    should not drive or operate heavy

    equipment. The more sedating

    antidepressants are generally

    taken at bedtime to help sleep andto minimize daytime drowsiness.

    Increased heart rate -pulse rate isoften elevated. Older patients

    should have an electrocardiogram

    (EKG) before beginning tricyclic

    treatment.

    NURSING IMPLICATION

    Arrange for lower dosage inelderly patients and in those withrenal or hepatic impairment bcoz

    of the potential for severe adverse

    effects

    Monitor for patients for up to 4weeks to ascertain onset of full

    therapeutic effect before adjusting

    dosage

    Establish suicide precautions forseverely depressed patients and

    limit the quantity of the drug

    dispensed to decrease the risk ofoverdose

    Administer the drug once a day in

    the morning to achieve optimal

    therapeutic effects. If the dosage is

    increased or if the patient is having

    severe GI effects, the dosage can be

    divided

    MAOI:

    Monitor BP and signs of HPN Crisis Have phentolamine or another

    adrenergic blocker on standby as

    treatment in case of hypertensive

    crisis

    Provide a list of potential drug-food interactions that can cause

    severe toxicity to decrease the risk

    of a serious drug-food interaction.

    Provide a diet low in tyramine.

    Inform pt that these foods mustnot be eaten while the medication

    is being taken or 2-3 weeks after it

    has been discontinued.

    Anti- manic agent

    LITHIUM CARBONATE

    Decreases pts HYPERACTIVITY Best taken after meals Takes 10-14 days before

    therapeutic effect becomes

    evident.

    - Antipsychotic is

    administered during the first two

    (2) weeks to manage the acutesymptoms of mania until lithium

    takes effect.

    Instruct pt to increase fluid intake(3L/ day) and sodium intake

    (3gm/day)

    Monitor serum levelNormal : .5 -

    1.5 meq/ L

    LITHIUM TOXICITY

    - Nausea, Anorexia,

    Vomiting, Diarrhea, AbdominalCramps

    Mannitol administered if toxicity

    occurs

    ANTI-EPILEPTIC DRUGS

    I. Epilepsy

    - Is characterized by seizures thatresult from sudden discharge ofexcessive electrical energy from

    nerve cells in the brain

    Pathological Basis: Abnormal electrical discharge in the

    brain. Imbalances occur between

    glutamate-mediated excitatory

    neurotransmission and gamma-

    aminobutyric acid (GABA) mediatedinhibitory neurotransmission.

    Changes in ion channels

    TYPES OF SEIZURES

    2 BROAD CATEGORIES:

    1.generalized

    - are produced by electrical impulsesfrom throughout the entire brain,

    2. partial (also called local or focal).

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    - are produced (at least initially) by

    electrical impulses in a relatively small part

    of the brain.- The part of the brain generating the

    seizures is sometimes called the FOCUS

    Generalized seizures

    1. Grand-mal seizure- also known as tonic-clonic

    seizure

    - involve dramatic tonic-clonic

    muscle contractions, loss of consciousnessand a recovery period characterized

    by confusion and exhaustion.

    2. Absence seizures( Petit mal)- involve abrupt, brief (3-5 seconds)

    periods of loss of consciousness.

    - The patient typically interrupts an activity

    and stares blankly.

    - Patients are usually not aware that they arehaving a seizure, except that they

    may be aware of "losing time."

    - occurs more frequently in children anddisappears at puberty

    3. Myoclonic seizures- consist of sporadic periods of

    muscle contractions, usually on both sides of

    the body.

    - Patients sometimes describe the jerks asbrief electrical shocks. When violent, these

    seizures may result in dropping or

    involuntarily throwing objects.

    4. FEBRILE SEIZURES

    - are related to very high fevers and usually

    involve convulsions.- most frequently occur in children

    - usually self-limited and do not reappear

    5. STATUS EPILEPTICUS- the most dangerous of all seizure

    conditions- a state in which seizures rapidly recur

    again and again

    Partial Seizures

    Partial seizures are divided into:

    1. simple

    2. complex

    1. SIMPLE- awareness is retained- occur in a single part of the brain and may

    involve a single muscle movement or

    sensory alteration

    2. Complex partial seizures- by definition, include impairment of

    awareness.- involve complex sensory changes such as

    hallucinations, mental distortion, changes in

    personality, loss of consciousness and lossof social inhibition

    ANTIEPILEPTIC DRUGS

    A drug which decreases the frequencyand/or severity of seizures in people withepilepsy

    Treats the symptom of seizures, not theunderlying epileptic condition

    Goal

    maximize quality of life byminimizing seizures and adverse drug

    effects

    Basis of Pharmacological Rx

    Most anti-epileptic agents act either by

    blockade of depolarization channels (Na+and Ca++)

    OR

    Enhancing the activity of GABA

    (neurotransmission inhibition)

    DRUGS FOR TREATING TONIC-

    CLONIC SEIZURES

    1. HYDANTOINS

    2. BARBITURATES ANDBARBITURATE-LIKE DRUGS

    3. BENZODIAZEPINES

    THERAPEUTIC ACTION

    - all stabilize nerve membranesthroughout the CNS to decrease excitability

    and hyperexcitability to stimulation.

    - BENZODIAZEPINES- Decrease excitability and

    conduction

    HYDANTOINS & BARBITURATES- Stabilize the nerve membraneby influencing ionic channels in

    the cell membranes

    HYDANTOINS* promote the exit of sodium ions from the

    cell, returning the cell to a stable restingmembrane potential

    * less sedating than many other

    antiepileptics

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    - Phenytoin ( Dilantin)

    - Ethotoin ( Peganone)

    - Fosphenytoin (Cerebyx)

    PHENYTOIN (DILANTIN)

    Although an effective and well triedantiepileptic, it is not the first line intreatment of partial or generalized

    epilepsy due to its toxicity

    Limited water solubility not giveni.m.

    Slow, incomplete and variableabsorption..

    Metabolized by liver Therapeuticplasma concentration:

    10-20 g/ml

    CONTRAINDICATION

    Those who are allergic to Dilantin,phenytoin, or any inactivecomponents used to make the

    medication.

    DRUG INTERACTIONS

    Alcohol- Alcohol can interfere with the way

    the body handles Dilantin.

    - Chronic alcohol intake candecrease the level of Dilantin in the

    blood, while short-term intake of a large

    amount of alcohol can increase the level

    of Dilantin in the blood.

    SIDE EFFECTS:

    Confusion. Dizziness Insomnia Twitching Headaches Nausea,vomiting, or constipation Larger or fuller lips Excessive body or facial hair. High blood sugar (hyperglycemia) Signs of liver damage, such as

    yellow skin or eyes (jaundice)

    Unexplained bruising or bleeding Swollen or tender lymph nodes Bending of the penis (which makes

    intercourse difficult)

    Suicidal thoughts or behavior Signs of an allergic reaction,

    including unexplained rash, hives,

    itching, and unexplained swelling.

    Gingival Hyperplasia Sexual-Endocrine Effects:

    Osteomalacia- softening of the bones due

    to defective bone mineralization.

    Hirsutism- excessive hairiness on

    humans in those parts of the body whereterminal hair does not normally occur or is

    minimal

    Hyperglycemia

    Teratogenic effects

    Fetal hydantoin syndrome Cleft lip Cleft palate Congenital heart disease Mental retardation

    NURSING RESPONSIBILITIES:

    Dilantin comes in extended-releasecapsules, chewable tablets, and an

    oral suspension. These products are

    not interchangeable. It can be taken with or without food.

    If it upsets the stomach, it may be

    taken with food. It is important thatpt takes it consistently the same way

    (either with food or without food).

    The medication should be taken atthe same time each day to maintain

    even levels of the drug in the blood.

    It should not be stopped without firstdiscussing with thehealthcare

    provider.

    Seizure medications, includingDilantin, may increase the risk ofsuicidal thoughts or behavior. If pt

    feels depressed or has any suicidal

    thoughts, let the healthcare provider

    know right away Dilantin may increase blood sugar.

    This is especially important for

    people with diabetes. Dilantin may cause bone weakness,

    because it affects the way the body

    deals with vitamin D (which isimportant for strong bones).

    * As with all seizure medications, Dilantin

    should not be stopped suddenly.* Because Dilantin can cause gum problems,

    good dental care is very important while pt

    is taking Dilantin

    BARBITURATES & BARBITURATE-

    LIKE DRUGS

    Phenobarbital (Luminal)- Primidone (Mysoline)

    - Mephobarbital (Mebaral)

    PHENOBARBITAL(SOLFOTON, LUMINAL)

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    - available in oral and parenteral

    forms

    - used for emergency control ofstatus epilepticus and acute

    seizures

    - TSL: 15-40 mcg/ml

    BENZODIAZEPINES

    DIAZEPAM (VALIUM) CLONAZEPAM ( KLONOPIN) Potentiate the effects of GABA, an

    inhibitory neurotransmitter

    DIAZEPAM (VALIUM)

    - not used for long term management

    of epilepsy- well absorbed from the GI tract

    - metabolized in the liver

    - excreted in the urine

    DRUGS FOR TREATING ABSENCE

    SEIZURES

    1. SUCCINAMIDES

    Modulate the inhibitoryneurotransmitter GABA

    a. Ethosuximide (Zarontin)

    B. Methsuximide (Celontin)

    ETHOSUXIMIDE (ZARONTIN)

    DOC for treating absence seizures Has fewer adverse effects compared

    with many other antiepileptic drugs

    Available for oral use TSL: 40-100 mcg/ml

    METHOSUXIMIDE (CELONTIN)

    Oral drug used to treat absenceseizures that are resistant to other

    drugs

    Associated with bone marrowsuppression

    THERAPEUTIC ACTION:

    Suppress the abnormal electricalactivity in the brain that is assoc with

    absence seizure

    Ethosuximide should be tried first;methosuximide should be reserved

    for the tx of seizures that are

    resistant to other agents because it isassociated with more severe adverse

    effects

    OTHER DRUGS FOR TREATING

    ABSENCE SEIZURES

    1. VALPROIC ACID (DEPAKENE)

    - reduces abnormal electrical activity

    in the brain and may also increase GABA

    activity at inhibitory receptors- DOC for the treatment of

    myoclonic seizures

    - 2nd DOC for the treatment ofabsence seizures because it is associatedwith hepatic toxicity and has more SE.

    2. Acetazolamide (Diamox)

    - sulfonamide drug

    - tx of absence seizures- also used to tx open-angle and

    secondary glaucoma, acute mountain

    sickness, decrease edema assoc with CHF

    3. ZONISAMIDE (Zonegram)- newer agents that inhibit voltage-

    sensitive sodium and calcium channels, thus

    stabilizing nerve cell membranes- should be tapered over 2 weeks

    when discontinuing as this could increase

    the risk of seizure.- pt should increase fluid intake

    because of the risk of renal calculi

    DRUGS FOR TREATING PARTIAL

    (FOCAL)SEIZURES

    1. CARBAMAZEPINE (TEGRETOL)

    MECHANISM OF ACTION It works by blocking sodium

    channels in the brain. By blocking

    sodium channels, the medicationmay decrease the activity of nerve

    cells, preventing them from firing

    abnormally.

    SIDE EFFECTS

    dizziness upset stomach headache unsteadiness double vision N& v

    ADVERSE EFFECTS:

    Anemia or other blood disorders- Aplastic anemia

    - Agranulocytosis

    Unusual bruising or bleeding Worsening of seizures Hallucinations Depression Suicidal thoughts or behaviors Increased infections or infections

    that do not go away

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    Water retention, swelling, ordifficulty breathing, which can be

    signs of (CHF)

    HBP (HPN) or LBP (hypotension) An irregular heart rhythm

    (arrhythmia) Yellowing of the whites of the eyes

    or skin (jaundice), which may be a

    sign of liver damage, including liver

    failure or hepatitis Difficulty passing urine or a sudden,

    unexplained decrease in urine

    production (which can be a sign ofkidney damage)

    Low sodium levels in the blood(hyponatremia),which may cause

    symptoms such as:

    Loss of appetite Nausea or vomiting Irritability Excessive tiredness Confusion Hallucinations Muscle weakness Muscle spasms or cramps

    Signs of an allergic reaction,including:

    An unexplained rash Hives Itching Unexplained swelling

    Stevens-Johnson syndrome (SJS) ortoxic epidermal necrolysis (TEN).

    - very dangerous skin

    reactions

    - These problems start outas skin rashes but can progress

    to permanent disfigurement or

    even loss of life.

    CONTRAINDICATIONS:

    Those who: Are allergic to carbamazepine or any

    of the inactive components used to

    make carbamazepine.

    Have had bone marrow depression inthe past. Bone marrow depression is

    a blood disorder in which the bone

    marrow does not function properly toproduce blood cells.

    Are allergic to TCAs Have taken a monoamine oxidase

    inhibitor (MAOI) within the past twoweeks.

    2. Oxacarbazepine

    derivative of carbamazepine Similar mechanism of action and

    toxicity to carbamazepine

    No report of hepatic failure or bonemarrow suppression

    less drug interactions Partial seizure

    3. LAMOTRIGINE (LAMICTAL)

    Indications Partial seizures +/- secondary

    generalization Lennox-Gastaut Syndrome Also used in primary

    generalized epilepsy(absence, myoclonic)

    Lennox-Gestaut syndrome Childhood epileptic encephalopathy(Lennox-Gastaut syndrome [LGS])

    is a devastating pediatric epilepsysyndrome

    Child-onset epilepsy (4-6 years) 5 % of epileptic attacks in children Severe and difficult to treat Multiple attacks daily

    ADVERSE EFFECTS Signs of a dangerous allergic

    reaction, including:

    Hives or any rash Fever Swollen lymph nodes

    (swollen "glands")

    Painful sores in or around themouth or eyes

    Swelling of the lips or tongue Suicidal thinking or behavior Lamictal can cause very serious skin

    rashes and allergic reactions.

    - These rashes can cause

    large sections of the skin to dieand can cause disfigurement or

    even loss of life

    - SJS and TEN- Gradual administration

    decreases the risk