Module 6

generalized and partial seizures and bipolar disorder (mental disorder)

by suppressing sodium and calcium influx and by potentiating GABA

generalized, partial, and abscence seizures
Bipolar disorder and prophylaxis of migraine HA's

moderately hepatoxic

used to treat absence seizures by reducing the synaptic nerve response to low-frequency repetitive stimulation

clinics only

monitor seizure activity, watch for drowsiness when giving sedating agents, monitor therapeutic blood levels, monitor liver enzymes and assess weakness, fatigue and muscle pain

thought to be a depletion of the neurotransmitters serotonin, dopamine, and norepinephrine

due to excessive reuptake or by excessive breakdown by monoamine oxidase (MAO)

symptoms does not improve for about 4 weeks

therapeutic responses vary

Anti-seizure agents raise the seizure threshold by inhibiting excitatory activity in the motor cortex of the brain

1) suppression of sodium influx,
2) suppression of calcium influx or
3) potentiation of gamma aminobutyric acid (GABA) in the brain

Hydantoins
Iminostilbenes
Barbituates
Benzodiazepines
Valporic Acids
Succinides

potentiating GABA and decreasing the conduction of impulses

seizures and are sedating

may be used in conjunction with other anti-convulsants

(Romazicon) may be given IV, will work within 2 min.

potentiating GABA

have less residual effect and are thought to cause less physiological and psychological dependence

decrease food bioavailability

short term anesia

Binds to serotonin and dopamine receptors in the CNS resulting in decreased transmission of these neurotransmitters

monitor for (EPS) extrapyramidal side effects
abnormal movements, eg. Parkinson
dystonia
tardive dyskinesia

synthesized from serotonin and is secreted by the pineal gland

darkness and suppressed by light received through the retina

act very rapidly
decreases food bioavailability
short-term amnesia i awakened
alcohol increase action causing psycho-motor impairments

opiods

bind with opiate receptors in the central nervous system altering the perception of and the emotional response to pain

can be used to suppress cough, slow respiratory rate and decrease peristalsis, pre-medication before surgery

given before the pain becomes severe

Chronic pain is better managed by scheduled doses around the clock rather than by PRN administration

hyperpyrexia

location,
intensity (use intensity scale)
quality
pattern
precipitating factors
alleviating factors
associated symptoms
coping mechanisms

a lower addiction potential because of their antagonistic properties

less likely to cause respiratory depression

withdrawal symptoms, opiod dependent

shouldnt be given in head trauma(can mask symptoms)
shouldnt be given in shock (decrease BP)
shouldnt be given in respiratory depression
use caution in clients with history of addition (dont deny pain control)
use cautiously in pt with urinary retention/asthma
cause constipation
dont crush SR preparations-respiratory distress

for opioid overdoses

Opioid Antagonists

anxiolytics and somnifacients

anxiolytics and somnifacients

anxiolytic and somnifacients

anxiolytic and somnifacients

decrease excitability in the motor cortex of the brain by suppressing sodium influx through the sodium channels

decreases the neuronal action potential
highly protein bound
narrow therapeutic index
hepatoxic

(TCA's) Tricyclic Anti-Depressants
(MAOI's) Monamine Oxidase Inhibitors
(SSRI's) Selective Serotonin Reuptake Inhibitors

reuptake of serotonin 5HT and norepinephrine by the pre-synaptic region

1) sedation 2) lowered seizure threshold 3) heart block with large doses 4) orthostatic hypotension 5) anti-cholinergic effects 6) increased appetite with weight gain and 7) inorgasmia.

at bedtime

increase the level of serotonin in the brain by decreasing presynaptic neuronal reuptake

SSRI's

loss of appetite and decrease sexual function

4-6 weeks

should be seen at least 6 months to 1 year

4-6 weeks to see effects
therapy is 6 months -1year
increase suicidal ideation in teenagers
avoid taking meds with grapefruit and grapefruit juice

bipolar disorder by blocking release of dopamine and norepinephrine

has a very narrow therapeutic index
fluid intake of 2500-3500 per day
adequate NA intake

D

CNS depression by potentiating GABA and inhibiting impulses subcortically in the limbic system, thalamus and hypothalamus

NSAIDS
Acetaminophen
Salicytes

anti-depressants & anti-convulsants

a degenerative disorder of the CNS caused by the destruction of the neurons in the substantia nigra that produce the neurotransmitter dopamine

balance, posture and involuntary muscle movement

Dopaminergic drugs are used to increase dopamine levels

1. Administer anti-Parkinson medications on time to avoid a worsening of symptoms.
2. Abrupt discontinuation of these drugs can lead to a Parkinsonian crisis.
3. Foods high in pyridoxine (vitamin B6) can decrease the effects of these drugs.
4. Change positions slowly to avoid faintness or dizziness.

1. Monitor for anti-cholinergic effects such as blurred vision, dry mouth, urinary retention, constipation and tachycardia