Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
157 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Name the four types of glutamate receptors.
|
NMDA, Kainate, AMPA, mGluR - (all are ligand-ion except mGluR is g-protein)
|
|
|
|
In alzheimer's patients, what neurotransmitter are they deficit in and what is in excess?
|
DEFICIENT= decrease in acetylcholine because of loss of cholinergic cells in the nucleus basalis which leads to loss of cognitive function; EXCESS= increase in glutamate; excess glutamate accumulates outside the neurons and causes Ca2+ to enter via the NMDA receptor channels, leading to neuronal damage and eventual cell death.
|
|
|
|
What are the two main categories of treatments for AD?
|
acetylcholinesterase inhibitors and NMDA (ion channel) receptor antagonist; (muscarinic and nicotinic receptor agonists are under development)
|
|
|
|
Name four acetylcholinesterase inhibitors that treat AD.
|
Tacrine (liver tox), donepezil, rivastigmine, galantamine - Ach-ase inhibitors are best used in early stages of AD
|
|
|
|
Name an NMDA receptor antagonist that is used in treating AD.
|
memantine (Namenda) - protects the neurons from the excitotoxic effects of glutamate
|
|
|
|
Name some alternative treatments for AD.
|
Ginkgo, curcumin, folic acid, (omega3, Bvitamins, and exercise - trials)
|
|
|
|
Abnormalities in what gene can increase the risk for AD? This gene (when normal) controls the distribution of APP (amyloid precursor protein) inside nerve cells in the brain and prevents APP from breaking down into a toxic byproduct called amyloid beta peptide(which is responsible for the plaques).
|
SORL1
|
|
|
|
What chromosomes(if mutated) are involved in rare, early-onset AD?
|
1,14,21
|
|
|
|
What chromosomes(if mutated) are involved in late-onset AD?
|
19
|
|
|
|
Chromosome 19 houses this allele that increases the risk for late-onset AD and may be responsible for plaque formation.
|
ApoE4
|
|
|
|
What is tau's normal role and what is the problem in AD?
|
tau proteins normally keep the microtubules straight allowing nutrients to enter the neuron, in AD the enzyme (Pin-1) causes the tau protein is problematic and allows the microtubules to curl and tangle; thus neurofibrillary tangles
|
|
|
|
In AD, plaques form from the inappropriate cleavage of APP (amyloid precusor protein) into amyloid-beta-peptide. What are the enzymes called that create the amyloidogenic forms of amyloid-beta-protein consisting of 40-42 amino acids?
|
beta and gamma secretase (the alpha secretase doesn't form amyloid)
|
|
|
|
What cholinesterase inhibitor (tx AD) is good for delaying nursing home placement and progression?
|
donepezil
|
|
|
|
What cholinesterase inhibitor (tx AD) is good for maintaining global functioning and ADLs?
|
rivastigmine
|
|
|
|
What cholinesterase inhibitor (tx AD) comes in an extended release version?
|
galantamine
|
|
|
|
make sure not to give an AD patient this type of drug?
|
anti-cholinergics (asthma-bronchodilators) and major and minor tranquilizers and hypnotics
|
|
|
|
What do you give to treat dementia associated psychosis?
|
atypical antipsychotics (aripiprazole, olanzapine, quetiapine, risperidone, clozapine, ziprasidone); however black box warning says no
|
|
|
|
Define Huntington's disease.
|
rare, autosomal dominant dz, caused by a trinucleotide repeat of CAG on chromosome 4; clinically: chorea, athetosis, dementia, and death
|
|
|
|
What is the neurotransmitter problem in HD?
|
decreased GABA that causes increased dopamine that stimulates D2 receptors in the corpus striatum (basal ganglia) and induces involuntary movements or chorea
|
|
|
|
What are the symptomatic treatments for HD?
|
Dopamine antagonists (haloperidol, chloropromazine) or GABAb receptor agonist (baclofen)
|
|
|
|
How does a HD brain grossly differ from a normal brain?
|
the caudate is missing
|
|
|
|
If you were holding the brain of someone with fungal encephalitis, what parts would feel abnormal?
|
limbic and frontal softening
|
|
|
|
What syndrome is caused by a deficiency in thiamine (B1)
|
Wernicke-Korsakoff's syndrome - usually in alcoholics (bilateral damage to mamillary bodies)
|
|
|
|
What are the benefits of taking omega 3 FA?
|
prevent and tx CA, CV disease, neurological dz (depression, OCD, ADD, Alzheimers), inflammatory dz
|
|
|
|
Where is the vomiting center located?
|
lateral medullary reticular formation in the MEDULLA
|
|
|
|
Where is the chemoreceptor trigger zone receptors located?
|
floor of the fourth ventricle (lies outside the BBB)
|
|
|
|
the chemoreceptor trigger zone maintains what types of receptors?
|
dopamine D2, 5-HT3, opioid, muscarinic, and substance P
|
|
|
|
What types of receptors do the vestibular nuclei have?
|
muscarinic and H1
|
|
|
|
In the GI system, what types of receptors does vagus have?
|
serotonin (5-HT3)
|
|
|
|
what part of the vestibular system is responsible for maintaining balance while stationary?
|
utricle and saccule
|
|
|
|
what part of the vestibular system is responsible for detecting changes in position?
|
semicircular canals
|
|
|
|
What are the treatments for motion sickness?
|
H1 antagonist, anticholinergics (anti-muscarinic) - inhibit the vestibular nuclei from releasing glutamate that would activate the Nucleus Tractus solitarius and induce vomiting
|
|
|
|
What is the new emetogenic and what drug has it replaced?
|
activated charcoal and replaced ipecac
|
|
|
|
Name the highly emetogenic chemo drug?
|
cisplatin
|
|
|
|
What are the 3 types of emesis involved with chemotherapy?
|
acute, delayed, and anticipatory
|
|
|
|
Explain the process of acute emesis.
|
take chemo drug (cisplatin) --> enterochromaffin cells are irritated and release serotonin --> the serotonin activates the 5-HT3 receptors on the vagus afferents and activate the nucleus tractus solitarius --> emesis
|
|
|
|
What are the preventative treatments for acute emesis in chemotherapy?
|
5-HT3 receptors antagonist with a corticosteroid (dexamethasone)
|
|
|
|
Explain the process of delayed emesis in chemo.
|
cisplatin is still in the system 24hours later --> the serotonin metabolites have already been urinated out --> can't use 5-HT3 antagonist. delayed emesis involves the non-BBB area postrema and presence of substance P. In order for substance P to be active and induce vomiting it needs its endogenous ligand, neurokinin 1; so block neurokinin-1, block emesis
|
|
|
|
What are the treatments for delayed emesis in chemo?
|
neurokinin-1 receptor antagonist; combination metoclopromide and corticosteriods; (cannabinoids: dronabinol and nabilone - chemo sickness in general)
|
|
|
|
What drug prevents both acute and delayed emesis in chemo?
|
Aprepitant; it has 5-HT3 antagonist plus corticosteroid for acute emesis and a neurokinin-1 blocker for delayed emesis
|
|
|
|
how do you treat anticipatory emesis?
|
try and prevent the 1st occurance by ensuring patient has anti-emetics; otherwise, benzodiazapines may work - difficult to tx
|
|
|
|
Name some serotonin 5-HT3 receptor antagonist.
|
Ondansetron, Granisterone, Dolasteron, palonosetron, and ramosetron - beware of prolongation of QT interval
|
|
|
|
name some D2 receptor antagonist and of them which has less side-effects?
|
metoclopramide(cross BBB - may have extrapyramidal effects) and domperidone (can't cross - less CNS effects); both are 5-HT4 agonist and are GI promotility drugs; and Phenothiazines (promethazine)- antipsychotics with potent D2 antagonism; butyrophenone
|
|
|
|
what are H1 blockers used for and name some.
|
motion sickness - promethazine, diphenlhydramine (benadryl), demenhydrinate, cyclizine, meclizine
|
|
|
|
describe scopolamine and its uses.
|
anticholinergic (blocks Ach/muscarinic receptor) transdermal patch for motion sickness
|
|
|
|
What is the pathophysiology of PD?
|
loss of dopamine in the nigrostriatal pathway that causes the thalamus to become overstimulated with GABA
|
|
|
|
What is the first line drug choice in PD?
|
levodopa (metabolic precursor of dopamine) - can cross the BBB to get in basal ganglia and be converted to dopamine; extremely short half-life (plasma levels drop and cause on-off phenomenon, person gets sudden tremors, etc)
|
|
|
|
What is the disadvantage of levodopa and how is it remedied?
|
large doses are required because the drug gets decarboxylated in the periphery to dopamine; remedy situation by using carbidopa (blocks GI and peripheral tissue metabolism of DOPA to dopamine- doesn't get by BBB- doesn't hurt the dopamine in the CNS)
|
|
|
|
What receptor and pathway are most involved in Parkinson's?
|
D2; D2 activation inhibits the indirect pathway (causes more GABA to be released from the striatum leading to more GABA release at the thalamus (causing a net inhibition at the thalamus)
|
|
|
|
How many dopamine receptors are there and what do they each do to cAMP?
|
D1,2,3,4,5; D1 and D5 cause in increase in cAMP; D2,3,4 cause a decrease in cAMP
|
|
|
|
What Dopamine receptor do the anti-Parkinson's dopamine agonists largely activate?
|
D2
|
|
|
|
Name the four dopamine agonist used in parkinson's treatment
|
bromocriptine -ergoline-D2; also used for hyperprolactinemia), ropinirole (non-ergoline-D2), pramipexole (non-ergoline-D3),pergolide (ergoline D2,D1) (hint: old parkinson's pts BuRPP)
|
|
|
|
Name the benefits and limitations to dopamine agonists.
|
BENEFITS:directly stimulates the dopa receptor, independent of viable dopamine cells, reduces risk of dyskinesia, not affected by dietary proteins(like levadopa), delays motor complications; LIMITS:have to titrate individual dose, s/e:N/dizzy, halluncinations, illusions, somnolence, edema, compulsions
|
|
|
|
Using what drug with l-dopa (levadopa) will prevent what?
|
carbidopa + L-dopa will prevent the levadopa from being broken down in the periphery by dopa decarboxylase (carbidopa is an inhibitor of dopa decarboxylase)
|
|
|
|
What two enzymes can metabolize levadopa into dopamine in the periphery?
|
COMT and DDC (dopa decarboxylase)
|
|
|
|
What is the role of MAOb?
|
break-down dopamine in the presynaptic channel
|
|
|
|
what is the role of COMT?
|
break-down dopamine in the periphery
|
|
|
|
Name all the major categories of drugs that can treat Parkinsons.
|
precursor of dopamine(levadopa); dopamine agonists (4), MAOb inhibitors, COMT inhibitors, anti-viral(amantadine), antimuscarinics (BTB), apomorphine
|
|
|
|
Name the 3 anti-muscarinic drugs used in PD treatment.
|
BTB - benztropine, trihexyphenidyl, biperiden (decrease in dopamine causes an increase in Ach)
|
|
|
|
Name the COMT inhibitors that are used to treat PD.
|
entacapone and tolacapone (hepatotoxic) - think of al capone
|
None
|
|
|
Name the MAOb inhibitors.
|
selegiline(metabolized to weak amphetamine) and rasagiline(irreversible blocking)
|
|
|
|
What would you need to give with apomorphine to prevent a common side-effect?
|
anti-emetic - acute emesis 5-HT3 antagonist like Tigan
|
|
|
|
Name the anti-PD drug that is a combo levadopa/carbidopa that is orally dissolvable.
|
parcopa
|
|
|
|
what is an essential tremor?
|
a neurological disorder characterized by shaking of (usually) the hands, evoked by intential movements; very common; incidence and prevalence increases with age; 95% upper limbs, 34% head, benign condition
|
|
|
|
how do you treat essential tremor?
|
pharm - non-selective b-blocker, propanolol and/or anticonvulsant primidone; SURGICAL: DBS(deep brain stimulation), Thalamotomy, gamma knife thalamotomy.
|
|
|
|
Name the disorder that is characterized by leg dysthesias that are exacerbated by inactivity, relieved by movement?
|
RLS Restless Leg Syndrome
|
|
|
|
Name the disorder that is characterized by brief, repetitive jerking of lower limbs while in stage 1 and 2 sleep; causes awakening.
|
PLMD - Periodic Limb Movement Disorder
|
|
|
|
Who commonly gets RLS Restless Leg Syndrome?
|
19% of pregnant women
|
|
|
|
Restless leg syndrome and Periodic Limb Movement Disorder is exacerbated by what?
|
caffeine, TCAs, SSRIs, anemia, family history
|
|
|
|
How do you diagnose Restless leg syndrome and PLMD?
|
RLS- clinically; PLMD- sleep study
|
|
|
|
What is the FDA approved med for RLS?
|
ropinirole (dopamine agonist)
|
|
|
|
What are the two major types of anesthesia?
|
General (inhaled and intravenous) and Local (injected nerve blocks)
|
|
|
|
Define General anesthesia.
|
reversible changes in neurological function that cause: 1. inhibition of stimulatory systems 2. stimulation of inhibitory systems, 3. balace between systems; mechanism poorly understood (there are 4 stages- 1.analgesia, 2.excitement, 3.surgical anesthesia, 4.medullary paralysis - not in handout)
|
|
|
|
What are the 3 major problems with understanding anesthesia?
|
1. the definition is unclear and doesn't describe the neurobiology, 2. neurobiology of consciousness is not understood, 3. there are multiple differences and unknowns in the anesthesia pharm agents
|
|
|
|
Give a general overview of how one would use general anesthesia during surgery.
|
use an intravenous agent for induction of anesthesia and use an inhalational agent for maintenance of anesthesia.
|
|
|
|
Why would you give other medications before surgey? Name some and their action.
|
Benzodiazepines (midazolam,deazepam, reduce anxiety); barbituates (pentobarbital, sedation); antihistamines (diphenhydramine, prevent allergic rxn); opioid (fentanyl, provide analgesia); anticholinergics (scopolamine, amnesia, prevent bradycardia, and fluid secretion); Antiemetics (ondansetrone, prevent aspiration, reduce post-op N/V)
|
|
|
|
Name the intravenous agents that one would utilize for induction of anesthesia.
|
Barbituates, Benzodiazepines, etomidate, ketamine, propofol
|
|
|
|
Name the inhalational agents one would use to maintain anesthesia.
|
volatile agents (isoflurane, halothane, Sevoflurance, desflurane,enflurane); Nitrous oxide and Xenon
|
|
|
|
What is the mechanism of action of anesthetics?
|
Increase GABA's effect on GABAa's receptors; block nicotinic receptors, activate K+ channels, inhibit NMDA (glutamate) receptors, inhibit synaptic proteins (decrease NT release-amnesia); enhance glycine effect on glycine receptors (immobility, since glycine is inhibitory - controls Cl- channel)
|
|
|
|
What is the Mechanism of action for benzodiazepines, etomidate, and propofol?
|
enhance GABA's effect on GABAa receptors - enhance inhibition
|
|
|
|
what is the mechanism of action for anesthetic nitrous oxide?
|
activating K+ channels and blocking nicotinic receptors
|
|
|
|
what is the mechanism of inhaled anesthetics and barbiturates?
|
enhance GABA's effect on GABAa receptors - enhance inhibition
|
|
|
|
what is the mechanism of action for ketamine and xenon?
|
inhibit NMDA (glutamate) receptors - block excitation and activates K+ channels
|
|
|
|
What anesthetics work by enhancing GABA's effect on GABAa receptors?
|
BZDs, Barbs, inhaled anesthetics, etomidate, propofol
|
|
|
|
in regard to inhaled anesthetics, how would one measure the concentration of the Gas?
|
measure the partial pressure or the "tension"
|
|
|
|
the inspired gas' partial pressure, ventilation rate, and gas solubility tell you what about the inhaled anesthetic?
|
these factors will determine the speed of induction or the time it takes from administration to teh achievement of surgical anesthesia
|
|
|
|
less soluble gas =
|
faster induction and elimination
|
|
|
|
what inhalational anesthetics smell good?
|
sevoflurane and halothane
|
|
|
|
what inhalational anesthetics smell bad?
|
desflurane and isoflurane
|
|
|
|
what is the MAC?
|
Minimum Alveolar concentration or minimum anesthetic concentration = the concentration of an anesthetic that produces immobility in 50% of patients exposed to it
|
|
|
|
What is the relationship with MAC, potency and lipophilicity?
|
the lower the MAC, the higher the potency and more lipophilic
|
|
|
|
If you mix gases together, how do you measure MAC?
|
add the MACs together (nitrous oxide is commonly mixed with other agents)
|
|
|
|
Why is MAC useful?
|
helps compare anesthetic agents; easily measured, consistent and reproducible
|
|
|
|
since MAC is changed by many diseases, drugs, physiological states, What happens to MAC in pregnancy, elderly, acute alcohol poisoning, chronic alcoholism?
|
pregnancy, elderly, acute alcohol poisoning = all DECREASE; chronic alcoholism INCREASES (cross tolerance)
|
|
|
|
What happens to MAC in hyperthermia?
|
MAC increases in hyperthermia
|
|
|
|
What happens to MAC in hypernatremia?
|
MAC increases in hypernatremia
|
|
|
|
What happens to MAC in hypothermia?
|
MAC decreases in hypothermia
|
|
|
|
What happens to MAC in shock?
|
MAC decreases in shock
|
|
|
|
What happens to MAC in elevated CNS catecholamine NT release?
|
MAC increases
|
|
|
|
What happens to MAC in CNS depressant drugs?
|
MAC decreases
|
|
|
|
What happens to MAC in acute cocaine use?
|
MAC increases in acute cocaine use
|
|
|
|
Name the inhaled anesthetics in order of increasing potency or decreasing MAC.
|
nitrous oxide, desflurane, sevoflurane, ether, enflurane, isoflurane, halothane
|
|
|
|
nitrous oxide, Halothane, desflurane, isoflurane, and sevoflurane all _________ cerebral blood flow.
|
increase cerebral blood flow
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ cerebral oxygen consumption.
|
decrease cerebral oxygen consumption
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ intracranial pressure.
|
increase ICP
|
|
|
|
What does a decreased cardiac output do to induction speed of an inhaled anesthetic?
|
a decreased CO will speed up the induction time
|
|
|
|
What type of tissue in the body will hold an anesthetic the longest?
|
fat, has low flow and high capacity
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ tidal volume.
|
decrease
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ respiratory rate.
|
increase
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ airway resistance.
|
decrease
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ ventilatory response to hypercarbia/hypoxemia.
|
depresses it
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ renal blood flow.
|
decrease
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ GFR.
|
decrease
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ hepatic blood flow.
|
decrease
|
|
|
|
Halothane, desflurane, isoflurane, and sevoflurane all _________ uterine smooth muscle.
|
decrease
|
|
|
|
What inhaled anesthetic increases nausa and vomiting?
|
nitrous oxide
|
|
|
|
what is the relationship of blood:gas partitioning coefficient to speed of induction and elimination?
|
the lower the number, the faster the induction and elimination
|
|
|
|
Name the inhaled anesthetic. MAC>100%.
|
Nitrous Oxide
|
|
|
|
Name the inhaled anesthetic. rapid onset and recovery and a good analgesic.
|
Nitrous oxide.
|
|
|
|
Name the inhaled anesthetic. not pungent (used for induction with children), rare induction of hepatitis, medium rate of onset and recovery, and sensitizes the heart to epi-induced arrhythmias.
|
halothane
|
|
|
|
Name the inhaled anesthetic. most rapid onset of action and recovery (low PC), poor induction agent, used for maintaince, used for outpatient surgery, irritates the airway and stinks.
|
desflurane
|
|
|
|
Name the inhaled anesthetic. used for out-patient surgery, smells good and is not irritating to the airway, useful induction agent, esp. in children.
|
sevoflurane
|
|
|
|
Name the inhaled anesthetic. smells bad, replaced by desflurane, potent, medium rate of onset and recovery, least likely to cause nausea.
|
isoflurane
|
|
|
|
Name the inhaled anesthetic. considered obsolete; slow onset and recover (large PC), releases F-ions causing renal dysfunction.
|
methoxyflurane.
|
|
|
|
used in conjunction with succinylcholine, this inhalant can cause malignant hyperthermia. what is your antidote?
|
any halogenated GA (halothane); rescue: dantrolene
|
|
|
|
this inhalant can cause megoblastic anemia after prolonged exposure.
|
nitrous oxide
|
|
|
|
many anesthetics cause nausea and vomiting by affecting the chemoreceptor zone in the base of the 4th ventricle. name some Rx.
|
ondansetron, avoid N2O, droperidol, metaclopromide and dexamethasone
|
|
|
|
Name the two types of partial (focal) seizures and define.
|
SIMPLE PARTIAL: involves a focal neurological symptom that can be motor, sensory, or psychomotor. consciousness is always retained. COMPLEX PARTIAL: the initial focus of abnormal discharge spreads to both hemispheres (patient loses consciousness) and experiences postictal (postseizure) confusion. majority of complex originate in teh temporal lobe
|
|
|
|
Name the seizure that involves 1st a LOC, rigidity, loss of bowel and bladder, then jerking movements of the entire body.
|
Generalized Tonic-Clonic or Grand Mal seizure
|
|
|
|
Name the seizure that involves: usually children, very brief LOC, 3Hz spike-and-wave discharge on EEG, may occur dozens of times a day, and involves a low threshold of Ca2+ in the thalamic neurons.
|
absence seizures (Petite Mal)
|
|
|
|
Name the seizure that involves rhythmic jerking of all muscles, LOC, marked autonomic manifestations.
|
Clonic seizures
|
|
|
|
Name the seizure that involves non-rhythmic, rapid jerking with brief bursts of multiple spikes in the EEG.
|
myoclonic seizures
|
|
|
|
Name the epileptic syndrome that is characterized by brief recurrent myoclonic jerks fo the body with sudden flexion or extension of the body and limbs; attacks are fragmentary and often bilateral; also known as West Syndrome.
|
Infantile Spasms
|
|
|
|
Define Epilepsy.
|
group of chronic syndromes characterized by recurrent seizures with periods of consciousness.
|
|
|
|
Define seizures.
|
sudden,transitory, and uncontrolled episodes from abnormal discharging of neuronal cells with associated motor, sensory,or behavioral changes; excessive firing of neurons
|
|
|
|
Convulsions appear in what types of seizures?
|
all Generalized Tonic-Clonic Seizures and Simple Partial and Complex Partial Seizures if the focal neuronal discharge includes motor centers. Convulsion are MOTOR manifestations
|
|
|
|
Explain the tonic and clonic phases of the Grand mal or Generalized Tonic-Clonic seizure.
|
TONIC: sustained powerful muscle contraction (involves all body musculature) which arrests breathing. EEG: rhythmic high freq., high voltage discharges; CLONIC PHASE: alternating contraction and relaxation, EEG: groups of spikes and periodic neuronal depolarizations with clusters of action potentials.
|
|
|
|
The older epileptic drugs are targeted toward what?
|
Na+ channels blocking
|
|
|
|
The newer anti-epileptic drugs are targeting what?
|
Glutamate (NMDA, AMPA, Kainate) inhibitors and GABA agonists
|
|
|
|
What is the drug of choice for Partial seizures?
|
both simple and complex partial seizures are treated with Phenytoin and Carbamazepine; alternative options: valproic acid, phenobarbital, primidone
|
|
|
|
What is the drug of choice for absence seizures?
|
1st: Ethosuximide(inhibits Ca influx through T-type channels in thalamus) 2nd: Valproic Acid(inactivates Na+ and increases GABA; not to be used in children - possible hepatic failure)
|
|
|
|
What is the drug of choice for Myoclonic seizures?
|
Valproic acid (enhances GABA)
|
|
|
|
What is the primary treatment for status epilepticus?
|
use diazepam then phenytoin
|
|
|
|
What is the drug of choice for Febrile seizures in kids?
|
Phenobarbital
|
|
|
|
What is the drug of choice for Generalized Tonic Clonic (grand mal)?
|
Phenytoin or Valproic acid
|
|
|
|
Name this drug. the oldest anti-epileptic that's main S/E is sedation. MOA prolongs opening of Cl- channels, blocks GLU and Ca2+.
|
Phenobarbital
|
|
|
|
These drugs all inhibit vitamin K and may cause hemorrhage in a fetus.
|
Carbamazepine, Phenobarbital, Phenytoin, and Primidone (CP3)
|
|
|
|
Do not use these drugs during pregnancy for fear of congenital defects.
|
valproic acid (spina bifida), topiramate (limb agenesis and hypospadias) and zonisamide (teratogenic in animals)
|
|
|
|
These drugs not only induce the cytochrome P-450 mechanism and cause certain drugs (warfarin, vitamins, TCAs, theophylline, and steroid hormones) to become less potent (shorter T1/2), but they also cause vitamin K deficiencies.
|
Carbamazepine, Phenobarbaital, Phenytoin, and Primidone and cigarettes
|
|
|
|
These drugs cause an increase in availability of drugs that are metabolized by the P-450 system; aka. they inhibit the P-450 enzyme system.
|
erythromycin, verapamil, trimethoprim/sulfa, propoxyphene, cimetidine. - given with drugs that utilize the P-450 system can cause drug overdose
|
|
|
|
What are the anti-epileptic drugs main MOA?
|
to block the intitiation of abnormal electrical discharge and prevent the spread of abnormal discharge to other areas
|
|
|
|
Anti-epileptic drugs are used in many other neuropsychiatric disorders including:
|
tremor, spasticity, movement disorder; Migraines; Psychiatry; and Chronic pain
|
|
|
|
List the 3 Glutamate receptors in the brain.
|
NMDA, AMPA, and Kainate
|
|
|
|
Name the new AED that has many times replaced Carbamazepine because of less side-effects.
|
Lamotrigine (inhibits glutamate, blocks Na channels, prevents repetitive firing); however possible s/e is Stevens Johnson syndrome.
|
|
|
|
What benzodiazepine is efficacious in treating absence seizures and myoclonic seizures by increasing the frequency of Cl- channels? Its biggest S/E: sedation.
|
clonazepam
|
|
|
|
What is the main side-effect of benzodiazepines?
|
sedation
|
|
|
|
what is the difference in partial and generalized seizures?
|
partial start in one area (if its complex partial it will go from the focal area and migrate to both hemispheres and cause LOC); generalized start in both hemispheres and have LOC too
|
|
