central nervous system depressants. cns depressants sedatives drugs that have an inhibitory effect...
TRANSCRIPT
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Central Nervous System Depressants
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CNS Depressants
Sedatives• Drugs that have an inhibitory effect on the
CNS to the degree that they reduce:– Nervousness
– Excitability
– Irritability
– without causing sleep
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CNS Depressants
Hypnotics• Calm or soothe the CNS to the point that they
cause sleep
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CNS Depressants
Sedative-Hypnotics—dose dependent:• At low doses, calm or soothe the CNS
without inducing sleep• At high doses, calm or soothe the CNS• to the point of causing sleep
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Sedative-Hypnotics: Barbiturates
• First introduced in 1903, standard agents for insomnia and sedation
• Habit-forming
• Only a handful commonly used today due in part to the safety and efficacy of: BENZODIAZEPINES
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Sedative-Hypnotics: Barbiturates
Four categories:• Ultrashort
– mephobexital, thiamylal, thiopental
• Short– pentobarbital, secobarbital
• Intermediate– aprobarbital, butabarbital
• Long– phenobarbital
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Sedative-Hypnotics: Barbiturates
Barbiturates have a very narrow therapeutic index.
Therapeutic Index• Dosage range within which the drug is effective
but above which is rapidly toxic.
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Sedative-Hypnotics: Barbiturates
Mechanism of Action• Site of action:
– Brain stem (reticular formation)– Cerebral cortex
• By inhibiting GABA, nerve impulses traveling in the cerebral cortex are also inhibited.
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Sedative-Hypnotics: Barbiturates
Drug Effects• Low doses: Sedative effects
• High doses: Hypnotic effects(also lowers respiratory rate)
Notorious enzyme inducers
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Sedative-Hypnotics: Barbiturates
Therapeutic Uses• Hypnotics• Sedatives• Anticonvulsants• Surgical procedures
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Sedative-Hypnotics: Barbiturates
Side Effects
Body System EffectsCNS Drowsiness, lethargy, vertigo
mental depression, coma
Respiratory Respiratory depression, apnea, bronchospasms, cough
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Sedative-Hypnotics: Barbiturates
Side Effects
Body System EffectsGI Nausea, vomiting,
diarrhea
Other Agranulocytosis, vasodilation, hypotension, Stevens-Johnson
syndrome
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Sedative-Hypnotics: Barbiturates
Toxicology• Overdose frequently leads to respiratory
depression, and subsequently, respiratory arrest.• Can be therapeutic:
– Anesthesia induction– Uncontrollable seizures: “phenobarbital coma”
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Sedative-Hypnotics: Barbiturates
Drug Interactions• Additive effects:
– ETOH, antihistamines, benzodiazepines, narcotics, tranquilizers
• Inhibited metabolism:– MAOIs will prolong effects of barbiturates
• Increased metabolism:– Reduces anticoagulant response, leading to
possible clot formation
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CNS Depressants: Benzodiazepines
Most frequently prescribed sedative-hypnotics• Most commonly prescribed drug classes• Favorable side effects• Efficacy• Safety
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CNS Depressants: Benzodiazepines
Classified as either:
• Sedative-hypnotic or Anxiolytic
(Medication that relieves anxiety)
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CNS Depressants: Benzodiazepines
Sedative-Hypnotic Type• Long-Acting:
– flurazepam (Dalmane), quazepam (Doral)
• Short-Acting:– estazolam (Prosom), temazepam (Restoril),– triazolam (Halcion)
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CNS Depressants: Benzodiazepines
Anxiolytic Type
• alprazolam (Xanax)
• chloridiazepoxide (Librium)
• diazepam (Valium)
• lorazepam (Ativan)
• midazolam (Versed)
zolpidem (Ambien) and zaleplon (Sonata)
(nonbenzodiazepine hypnotic agents, share characteristics)
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CNS Depressants: Benzodiazepines
Mechanism of Action• Depress CNS activity• Affect hypothalamic, thalamic, and limbic
systems of the brain• Benzodiazepine receptors
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CNS Depressants: Benzodiazepines
Drug Effects
• Calming effect on the CNS
• Useful in controlling agitation and anxiety
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CNS Depressants: Benzodiazepines
Therapeutic Uses• Sedation
• Sleep induction
• Skeletal muscle relaxation
• Anxiety relief
• Treatment of alcohol withdrawal
• Agitation
• Depression
• Epilepsy
• Balanced anesthesia
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CNS Depressants: Benzodiazepines
Side Effects
• Mild and infrequent
Headache DrowsinessDizziness VertigoLethargyParadoxical excitement (nervousness) “Hangover effect”
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CNS Depressants: Nursing Implications
• Before beginning therapy, perform a thorough history regarding allergies, use of other medications,health history, and medical history.
• Obtain baseline vital signs and I & O, including supine and erect BPs.
• Assess for potential disorders or conditions that may be contraindications, and for potential drug interactions.
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CNS Depressants: Nursing Implications
• Give 15 to 30 minutes before bedtime for maximum effectiveness in inducing sleep.
• Most benzodiazepines (except flurazepam) cause REM rebound and a tired feeling the next day; use with caution in the elderly.
• Patients should be instructed to avoid alcohol and other CNS depressants.
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CNS Depressants: Nursing Implications
• Check with physician before taking any other medications, including OTC medications.
• It may take 2 to 3 weeks to notice improved sleep when taking barbiturates.
• Abruptly stopping these medications, especially barbiturates, may cause rebound insomnia.
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CNS Depressants: Nursing Implications
• Safety is important
– Keep side rails up
– Do not permit smoking
– Assist patient with ambulation (especially the elderly)
– Keep call light within reach
• Monitor for side effects
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CNS Depressants: Nursing Implications
• Monitor for therapeutic effects– Increased ability to sleep at night– Fewer awakenings– Shorter sleep induction time– Few side effects, such as hangover effects– Improved sense of well-being because of
improved sleep
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Anticonvulsants and Drugs to Treat Other CNS Disorders
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Chapter 8 Topics
• Epilepsy• Parkinson’s Disease• Myasthenia Gravis• Attention-Deficit Disorders• Amyotrophic Lateral Sclerosis (ALS)• Multiple Sclerosis (MS)• Alzheimer’s Disease
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Learning Objectives
• Develop an understanding of the physiologic processes that occur in epilepsy.
• Classify seizures and the goals of their therapy.
• Understand that specific drugs are used in different classes of seizures.
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Learning Objectives
• Be familiar with Parkinson’s disease and the drugs used in its treatment.
• Know the symptoms and treatments of– myasthenia gravis– attention-deficit disorders– amyotrophic lateral sclerosis– multiple sclerosis– Alzheimer’s disease
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Epilepsy
• Common neurologic disorder with sudden and recurring seizures
• Caused by abnormal electrical impulses in the brain
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Epilepsy
• In the U.S., 2.5 million people are affected.
• Not all seizure disorders are epilepsy.
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Epilepsy
SeizureAbnormal electrical discharges in the cerebral cortex caused by sudden, excessive firing of neurons
– Result in a change in behavior of which the patient is not aware
– While conscious, the patient may or may not lose movement control
– Loss of body control may affect one area or the entire body
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Epilepsy
Causes of Seizures • Imbalance of excitatory and inhibitory
neurotransmitters:– Glutamate – inhibitory– GABA – excitatory– Other neurotransmitters can be involved
• Neurotransmitter levels are controlled by enzymes• Disruption in enzymes = disruption of
neurotransmitters
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Epilepsy
Causes of Seizures• ETOH withdrawal• Cardiovascular disease• High fever• Hypocalcemia• High or low blood
sugar• Hypoxia
• Infection (meningitis)• Metabolic
abnormalities• Brain tumor• Toxic substances• Trauma or injury to
the head
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Epilepsy
Classes of Seizures• Partial
• Generalized
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Epilepsy
Classes of Seizures• Partial
– Simple-partial– Complex-partial
• Generalized
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Epilepsy
Classes of Seizures• Partial
– Simple-partial– Complex-partial
• Generalized– Tonic-clonic or grand mal– Absence or petit mal– Myoclonic– Atonic
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Epilepsy
Partial Seizures• Localized in a specific area of the brain
• Occurs with 65% of epileptic patients
• Can progress to generalized seizures
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Epilepsy
Partial Seizures• Simple-Partial
• Complex-Partial
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Epilepsy
Partial Seizures• Simple-Partial
– No loss of consciousness– May have muscle twitching or sensory
hallucinations
• Complex-Partial
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Epilepsy
Partial Seizures• Simple-Partial
– No loss of consciousness– May have muscle twitching or sensory
hallucinations
• Complex-Partial– Impaired consciousness– With confusion, blank stare, and postseizure
amnesia
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Epilepsy
Generalized Seizures• Involves both hemispheres of the brain, not
one specific location• Types
– Tonic-Clonic– Absense– Myoclonic– Atonic
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Generalized Seizures
Tonic-Clonic Seizures• Tonic – body becomes rigid, lasts a minute
or less
• Clonic – initiated with muscle jerks, and may be accompanied by shallow breathing, loss of bladder control, and excess salivation
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Generalized Seizures
Absence• Interruption of activities by blank stare, rotating
eyes, uncontrolled facial movements, rapid eye blinking, and/or jerking of an arm or leg
• No generalized convulsions• Usually lasts 30 seconds or less• Many times it progresses to tonic-clonic as the
patient gets older
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Generalized Seizures
Myoclonic• Occurs with sudden, massive, brief muscle
jerks or non-massive, quick jerks
• Consciousness is not lost
• Can occur during sleep
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Generalized Seizures
Atonic• Begins with sudden loss of muscle tone and
consciousness
• Muscles relax, limbs go limp
• Lasts a few seconds to a minute, then patient can resume standing and walking
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Generalized Seizures
Status Epilepticus• Continuous tonic-clonic seizures with or
without return to consciousness
• High fever and lack of oxygen severe enough to cause brain damage or death
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Discussion
What percentage of status epilepticus patients die, regardless of treatment?
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Discussion
What percentage of patients status epilepticus patients die, regardless of treatment?
Answer: 10%
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Antiepileptic Drug Therapy
Goals of Therapy1. Seizure control or lessen the frequency
2. Prevent emotional and behavioral changes
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Discussion
Note: 30% of patients are not compliant due to side effects (sedation and loss of cognitive processes).
What are some possible strategies health care providers can use to help improve drug therapy compliance?
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Antiepileptic Drug Therapy
Neuronal Activity
1. Polarized (resting)
2. Depolarized (firing)1. Sodium and calcium enter the cell
2. When sufficient amounts cross, neurotransmitters are released
3. Neurotransmitter release leads to firing of the neuron
3. Repolarization (return to resting)
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Antiepileptic Drug Therapy
Abnormal Neuronal Activity
• DepolarizationIf excessive neurotransmitters are released it leads to uncontrollable firing of the neuron = seizure
• TreatmentBlock the firing of the neuron by raising the threshold of depolarization
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Antiepileptic Drug Therapy
• Start with monotherapy at a low dose and titrate up slowly
• Medication must be maintained at steady therapeutic levels (no missed doses)
• Polytherapy can be used if sufficient response is not seen with monotherapy
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Antiepileptic Drug Therapy
Problems with Therapy
• Wrong medication is used for the seizure type
• Side effects may cause problems with patient compliance
• If doses are missed, there is an increased risk of seizure activity
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Anticonvulsants
• carbamazepine (Epitol, Tegretol)• clonazepam (Klonopin)• diazepam (Valium)• divalproex (Depakote)• ethosuximide (Zarontin)• Fosphyenytoin (Cerebyx) • gabapentin (Neurontin)
Drug List
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Anticonvulsants
• lamotrigine (Lamictal)
• levetiracetam (Keppra)
• lorazepam (Ativan)
• oxcarbazepine (Trileptal)
• phenobarbital (Luminal Sodium)
• phenytoin (Dilantin)
Drug List
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Anticonvulsants
• primidone (Mysoline)
• topiramate (Topamax)
• valproic acid (Depakene)
• zonisamide (Zonegran)
Drug List
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Therapeutic Regimens for Seizures
Seizure Type 1st Line 2nd Line 3rd Line
Partial Tegretol or Dilantin
Neurontin or Lamictal
Luminal, Mysoline, or Depakene
Absence Zarontin or Depakene
Klonopin
Atonic, Atypical Absence, Myoclonic
Depakene Klonopin or Lamictal
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Therapeutic Regimens for Seizures
Seizure Type 1st Line 2nd Line 3rd Line
Tonic-Clonic, Tonic, Clonic
Tegretol, Dilantin, or Depakene
Luminal or Mysoline
Status Epilepticus Valium, Ativan, or Dilantin
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valproic acid (Depakene) and divalproex (Depakote)
• Increases the availability of GABA (inhibitory)
• Take with water, not a carbonated drink
• Do not use aspirin
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Dispensing Issues
• Depakote and Depakene can easily be confused.
• Be careful with Depakote and Depakote ER.
• Depakote ER is only once a day.
Warning!
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phenytoin (Dilantin)
• May be used to prevent seizures
• Promotes sodium outflow from cells – stabilizes the neuronal membrane
• Be cautious of drug interactions
• Intravenous phenytoin must be mixed carefully
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Phenytoin Side Effects
Dose Related– Ataxia– Diplopia– Dizziness– Drowsiness– Encephalopathy– Involuntary movements
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Phenytoin Side Effects
Non-Dose-Related– Gingival hyperplasia– Peripheral neuropathy– Vitamin deficiencies
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Cerebyx (anticonvulsant)
– Celexa (antidepressant)
– Celebrex (for pain and arthritis)
Warning!
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carbamazepine (Epitol, Tegretol)
• Has effect on sodium channels which may alter synaptic transmission.
• Blood monitoring must be done regularly.
• Be cautious of interactions and side effects.
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gabapentin (Neurontin)
• Used in conjunction with other medications
• No significant drug interactions
• Used for many other disorders, particularly neuropathic pain
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Dispensing Issues
Neurontin (anticonvulsant) and Noroxin (antibiotic) are sound-alike drugs, but they are easy to distinguish by strength.
Warning!
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clonazepam (Klonopin)
• Only indication is prophylaxis of seizures
• Depresses nerve transmission in the motor cortex
• C-IV controlled substance (benzodiazepine)
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Lamictal (anticonvulsant)
– Lamisil (antifungal)
– Lomotil (for diarrhea)
Warning!
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topiramate (Topamax)
• Is thought to alter sodium channels and thereby increases GABA activity and decreases glutamine activity
• Causes significant cognitive effects
• Drink fluids to decrease risk of kidney stones
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Kaletra (antiviral for HIV)
– Keflex (antibiotic)
– Keppra (anticonvulsant)
Warning!
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Discussion
Which neurotransmitters play the greatest role in seizures?
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Discussion
Which neurotransmitters play the greatest role in seizures?
Answer
• Glutamate (excitatory)
• GABA (inhibitory)
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Parkinson’s Disease
• Characteristic Signs– Resting tremor– Rigidity– Akinesia
• Usually affects people over 60
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Parkinson’s Disease
Physiology
• Result of pathologic alterations in the extrapyramidal system (part of the CNS that controls motor activities)
• Distinguishing feature: Lewy bodies (protein masses) found in the midbrain
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Parkinson’s Disease
Physiology• Normal muscle movement requires balance of
dopamine (inhibitor) and ACh (stimulator)• In the substantia nigra, enough dopamine is
released to counteract the effects of ACh• In parkinsonism, enough dopamine is not released
which leads to excessive motor nerve stimulation
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Cutaway View of the Brain
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Substantia Nigra
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Parkinson’s Disease
Drug Therapy• Improves the functional ability and clinical
status of patients• Aims at symptomatic relief, does not alter
the disease process• Patients may have temporary or prolonged
remission• Side effects can be a problem
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Anti-Parkinson Agents
• amantadine (Symmetrel)
• benztropine (Cogentin)
• bromocriptine (Parlodel)
• entacapone (Comtan)
• levodopa (Dopar)
• levodopa-carbidopa (Sinemet)
Drug List
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Anti-Parkinson Agents
• levodopa-carbidopa-entacapone (Stalevo)
• pergolide (Permax)
• pramipexole (Mirapex)
• ropinirole (ReQuip)
• selegiline (Eldepryl)
• tolcapone (Tasmar)
Drug List
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levodopa (Dopar)
• Metabolized to dopamine in the brain, but the brain does not receive a full dose
• Drug has very undesirable effects
• After about 5 years of therapy, 2/3 of patients experience “on-off” phenomenon
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levodopa-carbidopa (Sinemet)
• Probably the most common drug used for parkinsonism
• Carbidopa allows for lower doses of levodopa to be used which decreases side effects
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Amantadine (for Parkinson’s)
– Ranitidine (for the stomach)
– Rimantadine (for the flu)
Warning!
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entacapone (Comtan)
• Indicated for patients who have a deteriorating response to levodopa
• Less toxic than tolcapone
• Take without regard to food
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Discussion
What are the two primary neurotransmitters involved in Parkinson’s disease and what role do they play?
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Discussion
What are the two primary neurotransmitters involved in Parkinson’s disease and what role do they play?
Answer• ACh (excitatory)• Dopamine (inhibitory)
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Myasthenia Gravis
• Autoimmune disorder of the neuromuscular junction
• ACh receptors are destroyed at the motor end plate
• Characterized by weakness and fatigability, especially of the skeletal muscles
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Motor End Plate
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Myasthenia Gravis
Presenting Signs
• Ptosis (drooping eyelid)
• Diplopia (double vision)
• Dyarthria (speech)
• Dysphagia (swallowing)
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Myasthenia Gravis
Treatment
Blocking the destruction of ACh causes improvement for the patient
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Myasthenia Gravis Agents
• azathioprine (Imuran)
• cyclophosphamide (Cytoxan)
• edrophonium (Enlon, Reversol)
• neostigmine (Prostigmin)
• pyridostigmine (Mestinon)
Drug List
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pyridostigmine (Mestinon)
• Blocks destruction of ACh
• Allows for ACh accumulation at the synaptic junction
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cyclophosphamide (Cytoxan)
• Prevents cell division by targeting the auto-immune portion of the disease
• Use chemotherapeutic precautions
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Attention-Deficit Disorders
• Attention-Deficit Hyperactivity Disorder (ADHD)
• Attention-Deficit Disorder (ADD)
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Attention-Deficit Disorders
Attention-Deficit Hyperactivity Disorder (ADHD)Characterized by purposeless, chronic, pervasive, driven behavior that affects a child in social, emotional, and academic settings.
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Attention-Deficit Disorders
Attention-Deficit Hyperactivity Disorder (ADHD)Characteristics for Assessment
– Hyperactivity– Impulsivity– Distractibility
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Attention-Deficit Disorders
Attention-Deficit Disorder (ADD)• Has less hyperactivity
• Child is more lethargic and more easily distracted
• Both disorders are more common in boys than girls
• Some symptoms can persist into adulthood
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Attention-Deficit Disorder Agents
• atomoxetine (Strattera)
• clonidine (Catapres, Catapres-TTS)
• desipramine (Norpramin)
• dexmethylphenidate (Focalin), C-II
• dextroamphetamine-amphetamine (Adderall), C-II
Drug List
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Attention-Deficit Disorder Agents
• imipramine (Tofranil)
• methylphenidate (Concerta, Metadate, Ritalin, Ritalin-SR), C-II
• nortriptyline (Aventyl, Pamelor)
• pemoline (Cylert), C-IV
Drug List
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methylphenidate (Concerta, Metadate, Ritalin, Ritalin-SR)
• C-II controlled substance• Drug of choice to treat ADD, ADHD, and
narcolepsy• Increases levels of neurotransmitters in the brain• Concerta is a QD dose – outer shell dissolves to
release medication immediately, then drug is slowly released through pores in the tablet
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dextroamphetamine-amphetamine (Adderall)
• C-II controlled substance
• Effects last about 6 hours
• Primary side effect is depression
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Adderall (ADD, ADHD)
– Inderal (anxiety, hypertension)
Warning!
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atomoxetine (Strattera)
• Nonstimulant inhibitor of norepinephrine reuptake
• Controls impulsivity and activity
• Not a controlled substance, so refills can be called in
• Side effects: weight loss and slowed growth
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Dispensing Issues
Look-Alike and Sound-Alike Drugs
– Clonidine (ADD, ADHD)
– Klonopin (seizures)
Warning!
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Discussion
Compare and contrast ADHD and ADD.
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Discussion
Compare and contrast ADHD and ADD.
Answer• ADHD – hyperactivity, impulsivity, and
distractability• ADD – more lethargic and easily
distracted
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Amyotrophic Lateral Sclerosis (ALS)
• Known as Lou Gehrig’s disease
• Progressive degenerative disease of the nerves
• Leads to muscle weakness, paralysis, and eventually death
• Caused by excessive levels of glutamate
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ALS Agent
• riluzole (Rilutek)
Drug List
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riluzole (Rilutek)
• First drug approved for ALS
• Inhibits release of glutamate
• Shown to improve survival rate by 3 months is some patients
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Multiple Sclerosis (MS)
• Autoimmune disease in which myelin sheaths degenerate
• Patient loses use of muscles and often eyesight is affected
• Some drugs can slow progression, but there is no cure
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MS Agents
• baclofen (Lioresal)
• glatiramer acetate (Copaxone)
• interferon beta-1a (Avonex, Rebif)
• interferon beta-1b (Betaseron)
• mitoxantrone (Novantrone)
• tizanidine (Zanaflex)
Drug List
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interferon beta-1a (Avonex, Rebif)
• Used for ambulatory patients
• Reduces frequency of attacks
• Delays disability
• Drug should be taken at night with APAP to prevent flu-like side effects
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baclofen (Lioresal)
• Skeletal muscle relaxant
• Inhibits transmission of reflexes at the spinal cord
• Onset requires three to four days
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Alzheimer’s Disease
• Degenerative disorder of the brain that leads to progressive dementia and changes in personality and behavior
• Progression1. Minor forgetfulness
2. Inability to complete complex tasks
3. Complete incapacitation, disorientation, and failure to thrive
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Alzheimer’s Disease
• There are no treatments that can reverse this disease
• Depression should be treated according to symptoms
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Alzheimer’s Agents
• donepezil (Aricept)
• galantamine (Reminyl)
• ginkgo
• memantine (Namenda)
• rivastigmine (Exelon)
• tacrine (Cognex)
Drug List
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donepezil (Aricept)
• Convenient with few side effects
• Improves memory and alertness
• Give once a day at bedtime
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memantine (Namenda)
• May have fewer side effects than other drugs
• Approved for moderate to severe conditions
• Evidence that the drug does slow disease
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rivastigmine (Exelon)
• Has fewer interactions than Aricept
• More difficult to dose and administer
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Discussion
How does Alzheimer’s disease affect patients’ families? Has the disease affected someone in your family?
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Discussion
Several of the diseases presented in this chapter are degenerative and there is yet no known cure. How might this affect patients with a diagnosis of one of these conditions?