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207 Cards in this Set
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what are the 3 primary mechanisms of axn for Antiepileptic drugs?
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1. Enhance inhibitory neurotransmission via GABA stimulation
2. Stabilize cell membranes & surrounding cells (Na/Ca/K channels) 3. Reduce excitatory neruotransmission via antagonism of Glutamate |
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According to AAN guidelines, what "new" AED drugs are recommended as initial therapy for newly diagnosed Epilepsy?
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Lamotrigine (LAMICTAL), Gabapentin (Neurontin), Oxcarbazepine (Trileptal)& Topiramate (TOPAMAX)
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La Neu Tri Top
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Which old AED's are recommended for intial use of newly diagnosed Epilepsy?
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Cabamazepine (TEGRETOL), Phenytoin (DILANTIN), Valproic Acid (DEPAKOTE)& Phenobarbital
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Which new AED's are used primarily as adjunct therapies & why?
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Tiagibine (GABITRIL), Zonisamide (ZONEGRAN), Levetiracetam (KEPPRA); b/c insufficient evidence to be used as primary tx for new pts.
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What steps should be taken before changing to a 2nd AED choice when pt has failure with 1st AED therapy?
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Check diagnosis, Check compliance, Check for drug &/or alcohol abuse, check for underlying neoplasm (eg. CA or brain tumor)
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What were all "new" AEDs originally approved for?
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As adjunct treatment of partial or General Tonic Clonic (GTC) seizues.
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_____ &_____ Can be used as monotherapy for refractory partial epilepsy according to AAN guidelines (HINT: New)
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Oxcarbazepine (TRILEPTAL) & Topiramate (TOPAMAX); Went back and got approved as monotherapies
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What drugs can be used as adjuncts in CHILDREN with refractory partial seizures?
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Gabapentin (NEURONTIN), Lamotrigine (LAMICTAL), Oxcarbazemine (TRILEPTAL) & Topiramate (TOPAMAX)
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What pregnancy category are the NEW AEDs?
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Pregnancy Category C
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What pregnancy category are the OLD AEDs?
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Pregnancy Category D
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What drugs should be used w/ Lennox- Gastaut Syndrome?
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Topiramate (TOPAMAX) & Lamotrigine (LAMICTAL)
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Which AEDs do not markedly increase metabolism of birth control pills?
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VPA (DEPAKOTE), Topiramate (TOPAMAX) & Oxcarbazepine (TRILEPTAL)
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What is the drug of choice for treatment of neonatal seizures?
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Phenobarbital
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What is Phenobarbitals Mechanism of Axn?
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It increases seizure threshold & stimultes GABA
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What is a unique feature of Carbamazepine?
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It is an autoinducer; Hepatic enzyme inducer of its own metabolism.
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What are the CONCENTRATION related adverse effects of Carbamazepine?
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Diploplia, nausea, sedation, ataxia & dizziness
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What are the IDIOSYNCRATIC adverse effects of Carbamazepine?
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HYPOnatremia, blood dyscrasias, aplastic anemia & rash--> Stevens Johnson Syndrome
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What is Carbamazepine's MOA?
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Modulates Na+ ion channels
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What is Phenytoins MOA?
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Modulates Na/ Ca ion channels-- Has nonlinear pharmacokinetics!!
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Estrogen is considered to be seizure ______, while Progestrin is considered to be seizure ______.
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Activating, Protective.
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What was the first treatment for Epilepsy?
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Potassium Bromide (1857)
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What AED was discovered accidentally as an effective treatment in the 1960's?
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Valproic Acid-- originally used as a solvent to clean floors.
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What are the 3 major electrolytes that are involved w/ seizure activity?
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Na, Ca, & K
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Which are inhibitory & which are excitatory?
GABA, Glutamate, Aspartate |
Inhibitory, Excitatory, Excitatory
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What is the name of the receptor where Glutamate binds?
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NMDA receptor; when constantly exposed to glutamate can "burn" out.
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What are the 2 major classifications of seizures?
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Partial & Generalized
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Name the types of partial seizures and how they differ.
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Partial originates in 1 hemisphere--
*Simple partial: Consciousness is NOT impaired *Complex partial: Consciousness IS impaired |
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What type of seizure involves both hemispheres of the brain and where consciousness is ALWAYS impaired?
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Generalized
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What is another name for partial seizures?
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FOCAL seizures
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What is the most important predictor of remission in epilepsy?
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Number of seizures within the first 6 months of treatment
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What percentage of seizure patients are started on AED after their 2nd seizure?
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80-90% b/c seizure reoccurence is only about 30-60% after 1st seizure.
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What is the goal of treatment for epilepsy?
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No Seizures and No side effects.
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Which AED is a potent enzyme INHIBITOR & can double the half-life of Lamotrigine (LAMICTAL)?
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Valproic Acid/ Divalproex Sodium (DEPAKOTE)
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What is Lamotrigine's (LAMICTAL) MOA?
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Modulates Na/ Ca channels, aspartate/ glutamate activity (excitatory neurotransmitters)
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What is Levetiracetam's (KEPPRA) MOA?
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Modulates Ca & K channels & GABA (Inhibitory neurotransmitter)
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Which AED is considered relatively non-toxic and has virtually no side effects?
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Levetiracetam (KEPPRA)
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What is the advantage or using Oxcarbazepine (TRILEPTAL) over Carbazepine (TEGRETOL)?
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Oxcarbazepine is not an autoinducer as Carbazepine is.
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HYPOnatremia is reported more with Oxcarbazepine or Carbazepine?
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Oxcarbazepine-- especially in at risk patients eg. Elderly
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Which "new" AED causes the most cognitive impairment?
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Topiramate (TOPAMAX)
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What are the 4 common Concentration- related side effects of Phenytoin (DILANTIN)?
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Nystagmus, Ataxia, Confusion & DEATH
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What does GCSE stand for?
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Generalized Convulsive Status Epilepticus
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What is the number one cause of GCSE?
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Non compliance or abrupt withdrawal from drugs-- esp Antiepileptic drugs.
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What are the 4 immediate goals of treatment of GCSE?
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1. Stabilize pt & maintain ABC's
2. Make dx & identify te precipitating factors 3. Terminate seizure ASAP 4. Prevent seizure recurrence |
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What are some nonpharmacological treatments for GCSE?
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Air (O2) administration, correct metabolic acidosis if necessary, Check EEG for electrical disturbances, Give 100 mg Thiamine then glucose (50cc dextrose to adults)
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What are the most commonly used drug classes for treatment of GCSE?
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Hydantoins (Phenytoin), Benzodiazepines & Barbituates
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What is the benzodiazepine of choice according to the Epilepsy Foundation of America?
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Lorazepam (ATIVAN)-- not as lipophilic as diazepam but has longer duration of axn!
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What is a major consideration when utilizing Diazepam (VALIUM) & Lorazepam (ATIVAN) in IV form?
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Both contain propylene glycol-- a cardiac depressant; can cause cardiac arrythmias & hypotn is used too rapidly
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Why is the history of the seizure important when diagnosing GCSEs?
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Gives nature & duration of seizure
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What are the major pathophysiological markers of Phase I GCSEs?
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*Increse in Epinephrine, NorEpi, cortisol
*Metabolic demands are increased *HTN, tachycardia, arrythmias *Cerebral perfusion & blood flow preserved *Increased secretions/ airway obstruxn |
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What are the major pathophyiological markers of Phase II GCSEs?
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*Glucose is low- normal
*Hyperthermia, Hypoxia & possible respiratory failure developemt *Increase in sweating, salivation, prolactin, GH & ACTH *Motor activity may cease but electrical activity will persist |
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With regard to Status Epilepticus patients, what drug do some recommend as first line out of hospital treatment? And why?
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Midazolam (VERSED)b/c well tolerated, doesn't need to be diluted, causes minimal changes in BP, RR & has no cardiac depressant effects
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Why must Phenytoin (DILANTIN) be diluted in normal saline?
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b/c it precipitates in glucose containing solutions.
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What are some advantages of Fosphenytoin (CELEBYX) over Phenytoin (DILANTIN)? (3)
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1.Is water soluble ester form of phenytoin, more compatible w/ IV fluids
2. NO propylene glycol,less likely to cause arrythmias & Hypotn 3. Can administer more rapidly & is rapidly converted to Phenytoin after IM/IV administration. |
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What population is Phenobarbital typically used in?
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Neonatal
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Seizure termination most likely involves _______.
_______ controls Cl Channels & causes post synaptic hyperpolarization while______ (pre & post synaptic) inhibits release of excitatory amino acids |
GABA
GABA-a receptor GABA-b receptors |
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Define Chorea
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Ongoing, rapid & irregular flitting movements that appear willful but are involuntary & dancelike.
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What is a festinating gait?
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Involuntary acceleration of ones gait (walk)
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Micrographia
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Handwritting that decreases in size
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Substantia Nigra
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Dopamine producing nerve cells located in the brain stem that control voluntary movement.
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Stratum
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Mass of gray matter that includes the putamen & caudet
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Hypomimia
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A mask-like face with little expression
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Dyskinesia
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Abnormal involuntary movements that typically are medication induced.
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What are thought to be the environmental contributing factors in the development of Parkinson disease?
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Rural living, drinking well water, heavy metal & hydrocarbon exposure
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What are thought to be protective factors in the development of Parkinson disease?
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Cigarette smoking, caffeine consumption & NSAID use.
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MTPT is broken down by this enzyme producing this damaging ion.
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Monamineoxidase B & MPP ion
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MPP ion is damaging because...?
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It interferes with Mitochondrial Metabolism of neurons in the Substantia Nigra.
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What are the hallmark signs of Parkinson disease?
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TRAP= Tremor (at rest) Rigidity, Akinesia & Postural Changes.
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What is the difference between Essential tremor and tremor at rest?
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Essential tremor occurs when not at rest.
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GABA is a/an_________ neurotransmitter.
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INHIBITORY
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Glutamates is a/an __________ neurotransmitter.
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EXCITATORY
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Loss of D2 receptor function in the brain is responsible for loss of this type of muscle control.
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Voluntary.
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Caudate Nucleus
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Affects coordinated movement
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Putamen & Caudate Nucleus
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(Both responsible for movement) Comprise the Striatum
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Substantia Nigra
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Generates DOPAMINE which regulates reward and movement
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Basal Ganglia
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Comprised of Striatum, putamen, caudate nucleus, globus pallidus, subthalmic nucleus & substantia nigra
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Thalamus
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Responsible for relaying auditory, sensory, visual signals & movements into cerebral cortex
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Cerebral Cortex
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Manages higher brain function such as voluntary movements, sensation, reasoning and memory
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Globidus Pallidus
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group of nerves deep in the brain affecting movement, balance and walking
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Dopamin
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regulates movements; adrenaline is a derivative of dopamine. Decreased dopamine is assoc'd w/ PD; lose ihibitory effect--> Tremor at rest.
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GABA
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functions as INHIBITORY neurotransmitter; regulates sleep and anxiety
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Glutamate
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functions as EXCITATORY neurotransmitter
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Substance P
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Transmits pain impulses from body to CNS
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Hormones release from the brain that bind certain receptors to supress pain and effect emotion.
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Endorphins
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Acetylcholine
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manufactured in CNS & parasympathetic nervous system & is important for memory and learning
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With a decrease in Dopamine, Acetylcholine has a ________ effect.
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GREATER effect--> Tremor at rest.
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What is Allodynia?
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Painful response to what is normally nonpainful stimuli, eg. light touch, change in temp. etc.
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List 3 examples of Neuropathic pain.
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1.Post herpetic neuralgia
2. Phantom limb pain 3. Diabetic neuropathy |
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Neuropathic pain is generally less responsive to ______ alone.
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OPIOIDS.
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With acute pain, its intesity is usually_____ to the degree of damage.
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PROPORTIONAL.
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What are the beneficial effects of the acute injury response? (4)
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1. Maintain perfusion
2. Enhanced energy produxn 3. Immobilization; minimizing further tissue injury 4. Learned avoidance |
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What are the adverse effects of acute injury response? (7)
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1.Hypertension
2.Cardiac Issues 3.Hypercoagulable state 4.Hyperglycemia 5.Reduxn in respiration volumes & rates 6.Mental/ Emotional 7. Prolonged convalescence |
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What are some agents used in the treatment of Chronic pain & their mechanism of axn?
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Capsaicin- depletes substance P
TCAs- block serotonin/ NorEpi Uptake Other antidepressants- may decrease neuronal excitation |
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What is considered to be the hallmark of Multiple Sclerosis? (Hint: MRI)
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Plaques of scar tissue in multiple areas of CNS
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What are the possible contributing factors of MS
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*Genetic predisposition
*Geography *Age *Environmental Triggers *Vitamin D deficiency |
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What are the two "major" theories of etiology for MS?
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1. Autoimmune theory-immune attack vs 1 or more self mylen/oligodentrocyte antigens
2. Antimicrobial theory- virus/infexn |
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T Cells are involved with cell- mediated immunity.
Type 1 are_________, while Type 2 are_________. |
PRO-Inflammatory-- produce interferon gamma, implicated in MS.
ANTI- Inflammatory. |
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B- Cells are responsible for _________ Immunity & are also known as?
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Humoral immunity and are also known as ANTIBODIES eg. IgG, IgM, IgA, etc.
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These proteins act as signally molecules that modulate the inflammatory response.
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Cytokines
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What do cytokines trigger?
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Expression of adhesion molecules on endothelial cells & leukocytes & Migration of WBS's across the endothelial wall of brain & spinal cord.
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_________ are a family of adhesion molecules that mediate attachment and signal transduction.
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Integrins
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Interferons are naturally occuring proteins produced by ________ & ________.
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Fibroblasts & Macrophages
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Interferons largely act in these 3 ways.
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1. Immunomodulatory
2. Antiviral 3. Antiproliferative |
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What cells appear to initiate myelin destruction?
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T-helper cells (CD4)-- activated in the periphery following Antigen processing and presentation by macrophage or APC
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According to the Autoimmune theory of MS, activated T- cells are responsible for these 2 actions.
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1. Express adhesion molecules
2. Produce matrix metalloproteinases that chew up and poke holes in the BBB allowing for entry of T-cells. |
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There is a(n) INCREASE or DECREASE in T-supressor cells reported in patients with active and progressive MS.
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DECREASE
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What are the 2 primary ways that microbial infexn may cause or contribute to MS?
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1. Infection itself triggers the autoimmune response
2. Bacteria/ virus directly attacks myelin sheath |
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Which virus is implicated 20x's more than others to the development of MS?
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Epstein Barr Virus-- elevated Ab titers are measured
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Demyelination & Inflammation lead to the ______?
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Characteristic lesions found in CNS, spinal cord &/or optic nerves
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What are some primary symptoms of Multiple Sclerosis? Remember Primary symptoms are directly caused by the disease.
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Fatigue, Sensitivity to heat, bladder & bowel dysfn, gait problems, visual disturbances, abnormal sensations, cognitive dysfn, dizziness, spasticity and pain, impaired speech and swallowing & emotional disturbances
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What are some secondary symptoms of MS? Secondary symptoms are classified as complications brought on by the primary symptoms of the disease.
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UTI, bed sores, muscle contractures, Respiratory tract infexns.
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What are some tertiary symptoms of MS? Remember that these symptoms affect the Quality of Life for the patient
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Social withdrawal, Personal life issues, Emotional disturbances & financial problems.
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How much higher is the rate of suicide among MS patients compaired to the general population?
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7 times higher in MS patients
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What does KEDSS stand for and what does it represent?
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Kurtzke Expanded Diability Status Scale-- it's a common assessment tool used to assess MS disease severity.
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The 1st attack in MS is commonly called the __________?
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CIS= Clinically Isolated Syndrome
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This type of MS is associated w/ period of disease remission and little or no progression of the disease. It accounts for approximately 85% of MS cases.
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Relapsing Remitting MS (RRMS)
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After the 2nd attack, this form of MS just become progressively worse due to little or no remission.
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Secondary Progressive MS (SPMS)
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This form of MS is progressive from the onset. More males initially present with this form and there are NO drugs labelled to treat this form of the disease.
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Primary Progressive MS (PPMS)
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This form of MS is know to be steadily worsening from onset with acute 'flare-ups'. It accounts for a low percentage of patients but they have a worse long term prognosis than RRMS patients do.
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Progressive Relapsing MS
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After 2 or more attacks and 2 or more objective lesions have been identified, what additional data is needed to obtain a clinical MS diagnosis?
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NONE= clincal diagnosis.
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With 1 attack & 2 or more objective lesions what else is needed to obtain a clinical MS diagnosis?
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DISSEMINATION IN TIME demonstrated by MRI or 2nd Clinical attack
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With 1 attack and 1 objective lesion what is needed to obtain a clinical MS diagnosis?
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DISSEMINATION IN SPACE & TIME demonstrated by MRI or + CSF or 2 or more lesions consistant w/ MS or MRI or 2nd clinical attack
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With 2 or more attacks and objective lesion what is needed to obtain a clinical MS diagnosis?
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DISSEMINATION IN SPACE demonstrated by MRI or + CSF & 2 or more MRI lesions or Clinical attack involving different site.
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What does the ABCR TM stand for in the treatment of MS?
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They are the disease modifying therapies; stands for Avonex, Betaseron, Copaxone, Rebif & Tysabri & Mitoxantrone.
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________ are naturally occurring cytokines that exhibit antiviral, anti-proliferative & anti-inflammatory effects. They are also indicated in relapsing forms of MS
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Beta Interferons
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What are the 4 points of efficacy for Beta Interferons?
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1. Reduce relapse rate in patients w/ MS; ~30%
2. Reduce T2 MRI lesion burden; ~50-80% 3. Slow sustained disability progression. 4. Improve measures of QOL & cognitive function. |
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What MS patient populations should be treated with Beta Interferons?
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Any patient w/ Relapsing Remitting MS OR patients with Secondary Progressive MS that are still experiencing relapses & those at high risk for developing MS
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What is the most recognizable post-injection side effect of Beta Interferons?
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FLU-LIKE SYMPTOMS; fatigue, muscle aches, fever, chills etc. Occurs in ~ 50% of pts; can be avoided/ reduced by premedicating w APAP or NSAIDS prior to injection.
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When using Beta Interferons what side effects should the health care provider monitor for?
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Depression or psyche worsening, Injection site reaxn, Worsening spasticity, Thrombocytopenia (reduced blood counts), hepatotoxicity & seizures.
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In the EVIDENCE trial, which group had a greater percentage relapse- free patients after 24 weeks? Rebif or Avonex
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Rebif- 75%- had fewer MRI lesions also-- but also had injexn site reaxns & more leukocyte abnormalities!
Avonex- 63% |
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What is Interferon Beta- 1a (Avonex) indicated for?
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Relapsing forms of MS to slow accumulation of physical disability & decrease frequency of exacerations.
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What is unique about Avonex?
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Only Interferon given IM; injexns may be painful!
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What pregnancy category are the Interferons?
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Pregnancy category C
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How is Interferon Beta 1b given?
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SubQ injexn 3 times per weeks; if dose skipped doses should be given at least 48hrs apart!
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Name the oldest Interferon Beta 1b.
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Betaseron
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What is Betaseron indicated for?
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Indicated in treatment of relapsing forms of MS.
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What is Glatiramer (COPAXONE) Mechanism of action?
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NOT CLEARLY DEFINED; was designed to mimic & compete w/ myelin basic protein but may induce t-supressor cells in periphery.
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How is Copaxone administered?
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SUBQ injexn of 20mg ONCE DAILY.
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What 3 things is Copaxone shown to do in treatment of MS?
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*Reduce clinical attack rate in RRMS
*Reduce MS lesion burden on MRI *Slow time to sustained disability progression in pts w/ RRMS |
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Unlike Beta Interferons, Glatiramer (COPAXONE) is not associted with this side effect.
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Flu like symptoms; don't have to pretreat
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What pregnancy category is Copaxone?
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Pregnancy category B
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What is Copaxone's place in therapy?
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Should be considered for treatment of ANY patient with RRMS; it may be helpful in those w/ progressive disease as well-- only small trials so far.
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What is Mitoxantrone (NOVANTRONE)?
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Anti-neoplastic & immunosuppressive; shown to reduce clinical attack rate and MRI lesion burden in Relapsing MS
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This drug is indicated for use in Secondary Progressive MS & clinically worsening Relapsing Remitting MS.
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Mitoxantrone (NOVANTRONE); 1st and only drug w/ this approval in US.
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What is the main adverse side effect associated with use of Novantrone?
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Cumulative dose-related cardiotoxicity; manifests as cardiomyopathy, reduced EF or irreversible CHF; Limits total use to 2-4 years.
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Generic name Mitoxantrone
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What pregnancy category is Mitoxantrone (NOVANTRONE)?
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pregnancy category X
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What is a unique feature of Natalizumab (TYSABRI)?
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Fully humanized monoclonal antibody vs. Alpha-4 integrins
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What is Bacolofen's (LIORESAL) mechanism of action?
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GABA Analog; for treatment of reversible spasticity associated with MS or spinal cord lesions
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What is Tizanidine's (ZANAFLEX) mechanism of action?
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Short acting a-agonist; enhances presynaptic inhibition of motor neurons. Has compararble efficacy vs Baclofen (LIORESAL)
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What class of drugs is largely used for treatment of Urinary incontinence in MS pts?
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Anticholinergics; Oxybutynin, tolterodine, probantheline, dicyclomine & amitriptyline
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What type of drugs are used to treat fatigue in MS patients?
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Stimulants; Amantidine, Pemoline (CYCLERT), Methylphenidate (CONCERTA) & dextroamphetamine (DEXEDRINE) & Modafanil (PROVIGIL)
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What type of drugs is commonly used to treat the tremor in MS patients?
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Beta Blockers-- Propranolol; Non selective B-blocker
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What type of drugs are used to treat the sensory symptoms of MS?
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TCA's, antidepressants, anticonvulsants.
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What is the enzyme responsible for the conversion of tyrosine to levadopa?
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Tyrosine Hydroxylase
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What is the enzyme responsible for the conversion of Levadopa to Dopamine?
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Dopa decarboxylase
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What is the name of the enzyme found throughout the body and can metabolize dopamine?
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COMT; catechole methyltransferase
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Symptoms of PD appear only after 60-80% of dopamine neurons in the substantia nigra have died or have been impaired. True or False?
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True
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What is the catalyst that converts Tyrosine into Levodopa?
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Tyrosine Hydroxylase
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What are the 4 core symptoms of PD?
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TRAP: tremor, rigidity, akinesia & postural changes
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What is a clinical sign of PD that appears in 75% of patients?
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TREMOR
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Dyskinesia may be induced by the use of antiparkinsonism medications. True or False?
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True
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A response to _______ may help confirm Parkinson Disease diagnosis.
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L-Dopa (Levo/carbidopa)
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Psychiatric disorders such as depression, bipolar disorders addiction and schitzophrenia can cause PD. True or False?
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FALSE
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Dopamine production peripheral to the brain can cause...?
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Nausea & low blood pressure
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In regards to dose failures, a patient's "delayed ons" or the time in which a medication seems to "kick in" can be exacerbated by...?
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Consumption of high protein foods
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A common side effect of Amantadine (SYMMETREL) is...?
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Insomnia, swelling legs and SPLOTCHY SKIN a.k.a LIVEDO RETICULARIS
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LIVEDO RETICULARIS is associated with what PD treatment drug?
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Amantadine (SYMMETREL)
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Name the present preferred surgery for treatment of moderate to advanced Parkinson Disease.
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Subthalmic Surgery; can stimulate the cerebral cortex to work again.
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The lack of which neurotransmitter is thought to be primarily responsible for Parkinson Disease?
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Dopamine
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A physician prescribed Amantadine for PD-- what does it effectively treat?
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Tremor
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In the __________ researchers discovered an association between PD and low levels of dopamine in the striaum of the brain.
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1950's
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Some evidence exists that suggest that the onset of PD before the age of 40 may be cause by genetic factors. True or False
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True
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Parkinson disease is associated with a loss of dopaminergic neurons in the _______.
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Substantia Nigra
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The most common treatment for Parkinson disease is?
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Levodopa
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Transplants of fetal cells into the brains of humans w/ PD have been consistently successful in treating PD. True or False?
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FALSE
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Falls commonly occure early in the course of Parkinson disease. True or False?
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FALSE
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What drugs are substrates for CYP2C9?
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Phenobarbital, Phenytoin, Valproic Acid, Carbamazepine, Warfarin, Diazepam & Tricyclic Antidepressants.
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What drugs are inducers of CYP2C9?
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Carbamazepine (AUTOINDUCER), Phenobarbital, Rifampin
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What drugs are inhibitors of CYP2C9?
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Valproic Acid, Cimetidine, Tamoxifen, Verapamil
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What drugs are substrates for CYP2C19?
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Phenobarbital, Phenytoin, Valproic Acid, SSRIs, Diazepam and Tricyclic Antidepressants
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What drugs are inducers of CYP2C19?
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Phenytoin, Phenobarbital and Rifampin.
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What drugs are inhibitors of CYP2C19?
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Topiramate, Azoles, Omeprazole
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What drugs are substrates for CYP3A4?
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Carbamazepine, Tiagibine, Zonisamide, Statins, Amkio, CCBs, Theophylline, Macrolides
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What drugs are inducers of CYP3A4?
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Carbamazepine, Phenobarbital, Phenytoin,
Felbamate (FELBATOL), Rifampin |
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What drugs are inhibitors or CYP3A4?
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Azoles, Cimetidine, Amiodarone, Macrolides, CCBs, SSRIs
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What drugs are substrates of UDP glucuronyl transferase?
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Lamotrigine, Carbamazepine
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What drugs are Inducers of UDP glucuronyl transferase?
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Lamotrigine, Phenobarbital and Phenytoin
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What drugs are Inhibitors of UDP glucuronyl transferase?
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Valproic Acid
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To ameliorate pain is to....?
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Make it more tolerable.
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Many cancer patients are undermedicated for pain because... (9)
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*Fear of addiction
*Fear of possibly hastening death *Lack of knowledge *Poor pain assessment *Fear of DEA *Pt reluctance to report pain *Compliance issues *Reimbursement schedules *Formularies |
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What are the principles of therapy for MILD pain??
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1. Assess the frequency/ duration/ etiology of pain routinely
2. If bone present, use of NSAID should be routine 3. Always dose a med to max before reverting to next step unless pain is out of control 4. If pain is constant or recurring always dose ATC |
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When treating chronic pain what is the maximum dosage for Carbamazepine (TEGRETOL)?
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Titrated slowly up to max of 1000mg/qd
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What is the mechanism of action for Oxcarbazepine (TRILEPTAL)?
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Inhibits voltage-dependent Na+ channels & inhibits high-threshold N-Type Ca++ channels
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What is the mechanism of action or Carbamazepine (TEGRETOL)?
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Enhances inactivation of voltage-gated Na+ channels, increases release of serotonin & enhances dopaminergic transmission.
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The FDA has approved Carbamazepine (TEGRETOL) for ____ (HINT: treatment of chronic pain)
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Treatment of Trigeminal Neuralgia
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How does modulation of Na+ decrease pain?
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Prevents spontaneous ectopic discharges at concentrations lower than needed to block or inhibit impulse generation eg. w/ pain due to injury of the peripheral nervous system (Diabetes, severe accident)
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What is the MDD for Oxcarbazepine (TRILEPTAL)?
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Typically 600-1200 mg/day up to a max of 2400mg/day
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How does Gabapentin work?
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Does not influence synthesis or uptake of GABA--binds to voltage gated Ca++ channels presynaptically;may modulate release of excitatory neurotransmitters.
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What is the MDD for Gabapentin (NEURONTIN)?
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3600mg/day; above 3600, it inhibits its own absorption.
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What is Lamotrigine's (LAMICTAL)mechanism of action?
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*Stabilizes Na channels
*Inhibits release of glutamate *Modulated high-threshold N-Type Ca channels |
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What is the max daily dose for Lamotrigine (LAMICTAL)?
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25 mg/ day w/ a max daily dose of 400mg/day
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What are the major adverse effects of Opioid analgesics?
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Mood changes, somnolence, respiratory depression, decreased GI motility, stimulation of chemoreceptor trigger zone (N/V) Histamine release, tolerance & dependence
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What are some common drug interactions of NSAIDS?
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*Increases [warfarin]
*Increases nephrotoxicity risk; esp if on Diuretics or ACEI *Hyperkalemia; esp if on K-sparing diuretics or K supplements |
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According to the WHO, what are the STEP I agents for pain treatment
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*APAP-
*NSAIDS *ASA *+/- adjuvants |
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According to the WHO, what are the adjuvants used for treatment of neuropathic pain?
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TCAs & Anticonvulsants
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When treating a person suspected for abusing opioids for pain what type of agent should never be used?
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Mixed agonist-antagonist
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Which pure agonist primarily activates the mu receptor in treatment of pain?
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OPIOID AGONISTS
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Which agent for pain should NEVER be used in end stage renal patients due to its harmful metabolite that are renally excreted?
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Meperidine (DEMEROL) should never be given and Normederidine, it's metabolite can accumulate or be cleared via the kidneys
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