Classification: Beta 2 agonist

MOA:Binds to beta 2 receptors in the bronchioles and causes vasodilation. Has the same effect of NE. May  increase in electrogenic sodium pump, increase in CAMP

Classification:NET and DAT inhibitor. Weak inhibitor of MAO

MOA:Increases release of MONOAMINES (DA and Norepinephrine) in the synapse by displacing the NT from storage vesicles and inducing their release into the synapse, blocks re-uptake by NET and DAT. Also, blocks the breakdown of NTs by blocking MAO.

Classification:β1 Antagonist

MOA:block the increase in CAMP and the decrease in K

Indication/Clinical Application: Hypertension, Angina

SE and AED's:Bradyarrhthmia, AV Block, Bronchospasm

Contraindications: Asthma, COPD, Shock

Classification:Muscarinic antagonist

MOA:Competitively blocks all M subtypes

(M1- postsynaptic):Blocks the decrease in K+ conductance and increase in IP3 and DAG in excitatory

(M2- presynaptic): blocks the increase in K+ conductance and decrease in cAMP in inhibitory

Classification:GABA-B agonist

MOA:Binds to GABA-B causing the either inhibition of calcium channels (presynaptic) or activation of K+ channels depending on the location of the receptor. (postsynaptic)

Indication/Clinical Application: Antispasmatic

Classification:Dopamine 2 receptor agonist

MOA:Binds to dopamine receptor to stimulate activity. Presynapse= decrease Ca2+ Postsynapse= increase K+ and decrease CAMP

Indication/Clinical Application: Adjunct for Parkinson's

Classification:Alteration of the release of transmitter.(agonist?)

MOA:Causes the release of the peptide substance P from sensory neurons. Eventually depletes Substance P

Indication/Clinical Application: Pain.

Classification:α2-agonist

MOA:Selectively activates central α2-adrenergic autoreceptors and thereby inhibit sympathetic outflow from CNS.

Inhibitory Reponse (presynaptic)= decrease the ca2+ conductance

uses: anti-hypertensive

opioid withdrawal

cancer pain

Classification: NET blocker (blocks reuptake of DA and NE); ester-linked local anesthetic.

MOA: Inhibits the NE transporter, (blocks the reuptake) allowing released catecholamines (DA and NE) to remain in adrenergic synaptic clefts for a longer period of time.

Classification: Opioid peptide antagonist

MOA: Antagonist at mu, delta, and kappa opoid receptors- NOTE, these are INHIBITORY RECEPTORS

Mu (presynaptic,beta endorphin)- Blocks the decrease of Ca2+ and CAMP

Delta (postsynaptic, enkephalin)-Blocks the increase in K+ and decrease in CAMP

Kappa (dynorphin) 

Classification: Nm and NN (motorneuron nicotinic) receptor agonist

MOA:excitatory receptor: binding increases cation conductance (influx of ions)

Classification: 5-HT3 (serotonin receptor) Antagonist

MOA: blocks serotonin binding preventing increase in cation conductance

Indication/Clinical Application: antimimetic/antinausea, used primarily in chemotherapy

Classification: alpha 1 agonist w/ NE

MOA: Agonist at the 1 receptor at: Cell bodies in pons and brain stem project to all levels.Excitatory receptor:Decrease K+ conductance (more depolarization), increase IP3, DAG .

Indication/Clinical Application: Common Cold

Classification: Antagonist alpha1 w/ NE

MOA:Cell bodies in pons and brain stem project to all levels.Excitatory receptor: BLOCKS the Decrease K+ conductance (more depolarization),and increase IP3, DAG .

Indication/Clinical Application: BPH, HTN

SE and AED's:dizziness

Classification: H2 (excitatory receptor) antagonist

MOA: lead to an Blocks the decrease in K+ conductance, and increase in cAMP (compared to agonist)

Indication/Clinical Application: GERD, PUD

Classification: Inhibits NE storage

MOA: VMAT inhibitor (depletes catecholamines at symp nerve endings and brain) interferes with the intracell storage

Indication/Clinical Application: HTN

Classification: Glycine receptor (inhibitory receptor) antagonist

MOA: Blocks the increase in Cl-, Significant decreases in Cl-conductance which causes a severe excitation

Indication/Clinical Application: pesticide, particularly small vertebrates such as birds and rodents

SE and AED's: Convulsant action 

Therapeutic Considerations: High mortality (NOT Therapeutic)

Classification: alpha2 (inhibitory receptor) antagonist

MOA: block of alpha2 regulatory receptor on presynaptic neuron leads to an increase in ca+, thus increase in NE release.

Block the increase in K+ and the decrease in CAMP

Indication/Clinical Application: impotence/ED

Classification: AED

MOA:Main: Decreases Glutamate release by inactivation of Fast Na+ Channels and increase release of GABA.

but, prob works with combo MOA's

Also mentioned:Alters Na+, K+, Ca++ Conductance. Alters membrane potentials and inhibits the generation of rapidly firing action potential. Alters concentrations of amino acids, norepinephrine, ACh and γ-aminobutyric acid.

Indication/Clinical Application:

•  Main: Partial seizures (simple, complex and Partial with generalized tonic-clonic) + Tonic Clonic Seizures. Also mentioned: Effective against attacks that are either primary or secondary to another seizure type.(Everything EXCEPT: Absence and myoclonic )
• Drug of choice for STATUS EPILEPTICUS
• Arrhythmia induced by cardiac glycosides
  
• Neuralgia
  

SE and AED's:

• Gingival Hyperplasia.
• Neuropathy
• Agranulocytosis
  
• RASH (Non-genetic link).
• Diplopia.
• Ataxia (uncoordinated)
• hirsutism.
• nystagmus.

Contraindications: Hydantoin hypersensitivity. Hydantoin refers to a chemical structure present in phenytoin

Therapeutic Considerations: 

• can interact with many other Rx.
• Lower dose= t1/2 is 24 hours
• anti-folate affects of antiseizure drugs
  
• Can exacerbate absence seizures
  
• superior to phenytoin
  

PK:

Broad spectrum inducer
Absorption= formulation dependent
Highly Protein Bound -90%
Because it has saturable, nonlinear PK, small changes in dose lead to big changes in plasma concentration and therefore causing increased side effects.
Dose dependent elimination
t1/2= 12 to 36 hours
Metabolized by 2c9/10/19

VPA decreases metabolism

Can be displaced by: VPA, phenybutazone, sulfonamides

levels increased by: cimetidine, disulfiram, felbamate, isoniazid, rufinamide, topiramate (may),
Levels decreased by: CBZ and pb
Increases the metab of: CBZ, Lamotrigine, levodopa, OC, quinidine, and Warfarin
Decreases levels of Tiagabine
induces 2C/3A & UGT

Classification: AED

MOA:Fosphenytoin is Phenytoin pro-drug. Same MOA.

Indication/Clinical Application: Same as phenytoin 

SE and AED's:Same as phenytoin

Contraindications: Same as phenytoin

Therapeutic Considerations: More soluble prodrug of phenytoin. Can be given IM and IV. You need esterases to cleave produrg

Classification: Tricyclic

MOA:Blocks sustained high frequency firing of neurons through action on VG Na channels, Decreases synaptic release of glutamate. Blocks repeptitive firing of cultured spinal cord neurons, Likely involved in blocking the VG Na channels. (Interacts with Adenosine receptors (we don't know how) affect neuronal morphology by depleting inositol.

Indication/Clinical Application: 

• GTC seizures, partial seizures,(Every seizure EXCEPT: absence and myoclonic)
  
• trigeminal neuralgia
• bipolar disorder (acute mania, prevention of recurrence of mania & prophylactixis of depressive phase)- reasonable alternative to lithium (OXC -not as effective)
• FDA approved for bipolar disorder

SE and AED's:

• Toxicity:
•  Nausea,
  
• diplopia (dose related)
• ataxia (dose related)
•  hyponatremia
  
• water intoxication
•  headache
• blood disorders: aplastic anemia, leukopenia (not p-lem w/ use as mood stablizer)
•  agranulocytosis
•  rash (OXC less so than CBZ)
• (no greater & sometimes less than those associated w/ lithium for bp)

Contraindications: concomitant use of MAOIs

Therapeutic Considerations:  Linear metabolism of carbamazepine makes it a more attractive choice than phenytoin for patients with potential drug interactions.

very close imipramine and other antidepressants. Superior to primidone

may be used alone or in combination w/ Lithium in refractory bipolar patients (rarely used w/ VPA); Use as a mood stabalizer is similar to its use as an anticonvulsant; May work equally as well as Lithium when added to an antipsychotic drug

OVERDOSE: Major emergency - managed like overdoses of TCAs

Alters neuronal morphology - through inositol depletion mechanism;

PK:

• Linear metabolism
• Induces its own metabolism
• can increase the metabolism of PHT, PRM, ETH, VPA and clonazepam
• drugs that inhibit clearance include propoxyphene, VPA
• drugs that decrease concentrations include PB and PHT
  
• Metabolized by 1A2, 2CA, 2C9 ,3A4
  
• Induces 2c9, 3A, UGT
• well absorbed orally
• peak levels 6-8 hours
• Metabolized to active 10,11 epoxide!
• T1/2 8-12 in treated pnts, 36 in normal subjects
  

Classification: AED

MOA:Substituted monosaccharide (structurally different than the other antiseizure drugs) , Blocks repeptitive firing of cultured spinal cord neurons, Likely involved in blocking the voltage gated sodium channels. potentiates inihbitory effect on GABA. Depresses excitatory action of kainate on glutamate receptors. Alters the phosphorylation of voltage gated and ligated ion channels. Blocks the posynaptic AMPA receptor of the presynaptic nerve terminal

( Summary=*May inhibit sodium channel *May potentiate GABA activation of GABAA channel

*May antagonize AMPA receptor)

Indication/Clinical Application: 

• Monotherapy to treat partial seizures, Generalized seizure (tonic clonic). (used for everything cept for myoclonic)
  
• Lennox-Gastaut syndrome
• West's syndrome
•  Absence seizures
•  Approved for treatment of migraine
• Acute MANIA (in bipolar, not approved but used for)

SE & ADE's:

• NO diosyncratic rxn 
• dose effects happen in first 4 weeks:
• somnolence
•  cognitive slowing
•  nervousness
•  confusion
•  acute myopia &
• glaucoma (may prompt drug withdrawal)
• D/C rate ~ 15% only

Therapeutic Considerations: *One of the newer antiseizure medications made*start low and go slow *not bound to plasma proteins,

PK:

• t1/2= 20h (less)
•  extenstive metab but 40% excreted unchanged in the urine
• inihibits 2c19
• well absorbed

• Topiramate may increase the plasma-levels of phenytoin
• Carbamazepine can increase the elimination of topiramate

Classification: AED

MOA:Sulfonamide derivative. primary action appears to be on the sodium channel. Blocks high-frequency firing via action on VG Na+ channels. May act on voltage gated ca2+ channel.

Indication/Clinical Application:Generalized tonic-clonic seizures, partial seizures, myoclonic seizures, infantile spasms

(everything except absence)

SE and AED's:

• Toxicity
• Drowsiness
•  cognitive impairment
• skin rashes

PK:

• 70% Bioavailable orally
• minimally bound
• greater than 50% metab by UGT and 3A4
  

Classification: AED

MOA:Triazole derivative with little similarity to other antiseizure drugs. Decreases sustained high-frequency firing neurons in vitro. Throught to prolong the inactive state of Na+ channel. May inhibit mGlur5 glutamate receptors. No significant interactions with GABA systems or metabotropic glutamate receptors.

Indication/Clinical Application: May be useful in difficult to treat epilepsy symptoms. Approved in the USA for Lennox-Gastaut syndrome for pnts 4 yrs and older. Adjunct treatment. Effective against all seizure types in this syndrome. Specific against tonic-atonic seizures and may be effective against partial seizures.

SE and AED's:Common: Somnolence, vomiting, pyrexia(fever), diarrhea * dizziness, fatigue, diplopia

Therapeutic Considerations: Should be given with food.

PK

• modestly induces cyp 3A4, Cyp2c9/19
• Extensively Metabolized by UGT
• well absorbed
• Plasma concentration peak between 4-6 hours
• Half life is 6-10 hours,
• minimal plasma protein binding(25%).
• Most of the drug excreted in the urine (acid metabolite in 2/3rd of dose)
• only 2% excreted unchanged in urine

• Rufinamide increases levels of phenobarbital and phenytoin

Indication: acute mania in bipolar (good for a small group of refractory patients but not for maintenance or depression) Not FDA approved for bipolar

Contraindication: Maoi's 

Therapeutic Considerations: Interactions: Similar to CBZ but less enzyme induction than CBZ so fewer drug interactions Therapeutic Considerations: fewer hypersensitivity reactions than CBZ, may cause hyponatremia more often than CBZ

PK:

• induces 3A4, UGT
• induces its OWN metabolism by UGT
• inhibits 2C19, UGT (weak)
• shorter half life
• active metabolite with longer duration
  

Classification:AED

MOA:Enhances phasic GABAA receptor responses, prolongs open of Cl channels, Reduces excitatory synaptic responses

May selectively suppress abnormal neurons. Exact mech not really known. Inhibit the spread and firing of FOCI. @ higher doses- suppresses fast Na+ channels, blocks L/N type Ca2+

Indication/Clinical Application: Generalized tonic-clonic seizures, partial seizures, myoclonic seizures, generalized seizures, neonatal seizures, status epilepticus. every seizure type esp when diff to control. little evidence for effect of generalized seizures.

SE and AED's:Sedation, cognitive issues, ataxia, hyperactivity

Contraindications: Porphyria (improper synthesis of heme), Severe liver dysfunction, Respiratory disease

Therapeutic Considerations:  Drug of choices for seizures in infants.

PK:

Phenobarbital induces numerous P450s increasing valproate, carbamazepine, felbamate, phenytoin and lamotrigine metabolism, Phenobarbital levels can be increased by valproic acid, rufinamide, or phenytoinDecreases Benzo levels. induces 2C and 3A. Inhibits CYP. metabolized by 2C19 and 2C9

. ***Barbiturates may exacerbate absence seizure. Phenobarbital is used

Antiseizure Drugs
primarily as an alternative drug in the treatment of focus seizures and tonic-clonic seizure (extremely long half life but verrrrrry variable) Active metabolite of primidone, sedation when given with VPA.

Classification:

MOA:Similar to phenytoin.

Indication/Clinical Application: Generalized tonic-clonic seizures, partial seizures

SE and AED's:Sedation, cognitive issues, ataxia, hyperactivity

Therapeutic Considerations: Interactions: Similar to phenobarbital. Originally looks like phenytoin. CBZ and Phenytoin are superior (for complex PARTIAL). Anticonvulsant properties before metabolized (Metabolize to pb and PEMA). Peak conc in 2-6 hours. T1/2 10-25.

2C, 3A, and UGT (broad spectrum). Inhibit CYP. Metabolized by 2C9 and 2C19

Classification:

MOA:produces a voltage & use dependent inactivation of Na+ channels. inhibits vg n & PQ type channels. Acts presynaptically on VG-Ca2+ channels, Decreases glutamate release. Suppresses the sustained rapid firing of neurons.

Indication/Clinical Application: Generalized tonic-clonic seizures, generalized seizures, monotherapy for partial seizures, absence seizures and myoclonic seizures in children, (it is used for EVERY SEIZURE). Focal epilepsy. FDA approved for BIPOLAR DISOrDER (acute mania, prevention of recurrence of mania, & prophylaxis in depressive phase that follows mania)- One of the few shown for the depressive phase

SE and AED's:Dizziness, HA ,nausea, somnolence, diplopia, rash (pediatric high risk)

Therapeutic Considerations: Interactions: Phenytoin and phenobarbital increases the metabolism of lamotrigine. Valproate decreases the clearance of lamotrigine (increase blood level conc).

Therapeutic Considerations: Lamotrigine is a useful alternative to phenytoin and carbamazepine as a treatment for tonic-clonic seizures, Lamotrigine is the third drug of choice for absence seizures. Antifolate properties. induces UGT and metabolized by UGT. it induces its own metabolistm

Classification:Glutamate receptor inhibitor

MOA:Produces a use-dependent block of the NMDA receptor

(NR1-2B). Potentiates GABA-A receptor responses.

Indication/Clinical Application:used as adjunct. Refractory epilepsy, especially focal and tonic-clonic seizures, partial seizures, lennox gausaut

SE and AED's:Photosensitivity, gastrointestinal irritation, abnormal gait, dizziness,

aplastic anemia,hepatic failure.= high rates!

Contraindications: Blood dyscrasia, liver disease

Therapeutic Considerations: Felbamate has been associated with fatal aplastic anemia and liver failure and its use is restricted to patients with refractory epilepsy (esp focal and tonic clonic) . Felbamate

40-50% excreted unchanged in the POOP.

increases phenytoin and valproic acid levels and decreases levels of carbamazepine..

metabolized to not 1, not 2, but 3 active metabolites!!!!!!! 20-25% protein bound. t1/2= 13-23

Classification:GABA derivative.

MOA:Decreases excitatory (glutamate) transmission by acting on VG Ca2+ channels (N-Type) presynaptically (α2δ subunit). Transported into the brain by the L-amino acid transporter.

Indication/Clinical Application: Adjunct partial seizures, generalized seizures, diabetic peripheral neuropathy, postherpetic neuraglia, prophylaxis of migraines. Acute Mania (in bipolar, not approved but is used for)

SE and AED's:Somnolence, dizziness, ataxia, tremor, HA

Therapeutic Considerations: Although gabapentin increases GABA content in neurons and glial cells in vitro, its main antiseizure effect appears to be through its inhibition of Ca2+ channels most patients. Originally planned as a spazmolytic. F is 50%. decreases with increasing dosage. Not bound to plasma proteins. NOT metabolized. t1/2= 6-8. not very effective as AED

Classification:AED; GABA derivative

MOA:Decreases excitatory transmission by acting on VG Ca2+ channels in presynaptic ntype channels (α2δ subunit)

Indication/Clinical Application: Partial seizures (adjunct treatment w/ or w/o secondary generalization), Diabetic peripheral neuropathy, Fibromyalgia, & Postherpetic neuralgia

SE and AED's:Somnolence, dizziness, ataxia, tremor

Therapeutic Considerations: Structurally similar to gabapentin but more potent. Used for treatment of focal seizures in patients with hepatic dysfunction.Available only in oral form! not bound, not metabolized. t1/2=6-7 hrs. minimal interactions. Does not induce, inhibit, or metabolized by ANYTHING! fuck you liva!!!!

Classification: AED

MOA:Enhances slow inactivation of Na+ channels, Blocks effect of neurotrophic factors BDNF& NT3 (via CRMP-2). Prevents axonal dendritic growth (so seizure wont spread to other other parts of the brain)

Indication/Clinical Application: Generalized tonic-clonic seizures, partial seizures (adjunct therapy, w/ or w/o secondary generalization; pts 16 or older).Used in pain syndromes

SE and AED's:Toxicity: Dizziness, headache, nausea, diplopia

Therapeutic Considerations: Typically given twice a day. PK: Well absorbed, Minimal protein binding, One major nonactive metabolite, t1/2= 12–14 h. *Does NOT induce/inhibit CYP or UGT. Metabolized by CYP2C19.*

"i'm kinda a big deal"

Classification:AED,

selective modifier of SV2A function

MOA:binds to synaptic vesicular protein SV2A (protein not well understood) to modify release of GABA and glutamate

Metabolite has some inhibition of histone deacetylase

*Function of SV2A unknown-->possibly modifies synaptic release of glutamate and GABA

Indication/Clinical Application: Partial seizures (kids and adults) ,

generalized myoclonic seizure(of juvenile myoclonic epilepsy), generalized tonic-clonic seizure (everything except absence)

SE and AED's:somnolence,

asthenia (weakness)
ataxia (loss of muscle coordination)
dizziness

@toxic levels: nervousness, depression, seizures and all of the above

some agitation or anxiety

rare: idiosyncratic rxns

Therapeutic Considerations: t1/2 =6-11 hrs

high fu
3 inactive metabolites
Inhibits burst firing without affecting normal neuronal excitability
Dosage forms: PO and IV
MINIMAL drug interactions.
Not metabolized by enzymes.
*Ineffective for induced max electroshock and induced pentylenetetrazol seizures

prominent activity in the kindling model

Classification: AED

MOA:inhibits GABA reuptake transporter GAT-1 in forebrain, neurons and glia increases extracellular GABA in forebrain and hippocampus to prolong inhibitory action of syn release GABA. derivative of nipecotic acid.

Indication/Clinical Application: partial seizures

Potent against kindled seizures in rodents
weak against max electroshock (model) seizures

SE and AED's:Excessive confusion, somnolence (drowsy) or ataxia (these may require DC)

Dose related: nervousness, dizziness, tremor, difficulty in concentrating and depression

Can cause seizures in some Pt, especially pts taking for nonseizure reasons

rare: psychosis, rash (idosyncratic)

Therapeutic Considerations:

 t1/2 = 4-8 hrs

well absorbed

extensively metabolized
low fu
0 active metabolites

may enhance GABA activity by blocking GABA reuptake into presynaptic neurons

metabolized by CYP3A4, therefore decreased levels seen with use of phenytoin, carbamazepine, or phenobarbital

Classification:Cyclic Ureide

MOA:Reduces low threshold Ca2+ currents (T-type) (thus inhibiting currents that generate cortical discharge of an absence attack in thalamic neurons); w/o altering the voltage dependence or recovery kinetics of Na channels

Indication/Clinical Application: Absence Seizures (1st line)

SE and AED's:GI disturbances, pain

behavior changes are usually in the direction of improvment]

idiosyncratic aed-very uncommon  

Therapeutic Considerations: VPA causes a decr. in ethosuximide clearance; little activity against maximal electroshock; considerable efficacy against pentylenetetralzol seizures ('pure petit mal' drug). completed metabolized. Not protein bound.Not sure what metabolized by.Doesn't induce or inhibit anything!!!

Classification:Gaba Derivative

MOA:irreversibly inhibits GABA-transaminase

Indication/Clinical Application: Partial Seizures, infantile spasms

SE and AED's:Toxicity: Common: drowsiness, dizziness, & weight gain; Serious: agitation, psychosis, visual field loss (long term therapy)

Contraindications: preexisting mental illness

Therapeutic Considerations: F=0.7; not metabolized, t1/2~6-8 hrs; Interactions minimial; Indirectly enhances GABA activity; may also inhibit the vesicular GABA transporter; leads to some desensitization of synaptic GABAa receptors; Causes prolonged activation of non synaptic GABAa receptors (provide tonic inhibition); decr. in brain glutamine synthetase activity (2nd to incr. [GABA]); Marketed as racemate; S(+) is active. Not bound

Classification:AED,

MOA:Blocks high-frequency firing of neurons; Modifies amino acid metabolism; Blockade of NMDA excitation; Increases activity of glutamic acid decarboxylase (GAD-turns glutamic acid into GABA) ; Inhibits activity of GAT; Inhibits histone deacetylase; indirect inhibition of GSK-3 , can upregulate gene expression through inhibition of histone deacetylase, inhibits inositol signaling thru an inositol depletion mechanism

Indication/Clinical Application: Generalized tonic-clonic seizures, partial seizures, generalized seizures, absence seizures (2 line) (verry effective, used when ethosux doesn't work), myoclonic seizures; (does pretty much everything)

*Management of bipolar disorder (either phase); migraine prophylaxis FDA approved for maintance and acute mania

SE and AED's:Pain and GI disturbances. idiotox limited to hepatotox - reversible (2 yr or multiple meds) spina bifida woman

Contraindications: Liver disease; Urea cycle disorders

Therapeutic Considerations: Valproate displaces phenytoin from plasma proteins; VPA inhibits (2C9 and UGT) the metabolism of several drugs (Phenobarbital, phenytoin and carbamazepine); VPA can dramatically decrease the CL of lamotrigine, ethosuxamide.

Often preferred when pnt has GTC w/ absence. well absorbed. Highly bound to plasma proteins.Metabolism increased by CBZ. Inhibits CBZ CL. Blood plasma levels are increased by felbamate.

extensively metabolized.

*Combinations of VPA w/ other psychotropic meds - used in management of biplar (generally well tolerated); effective for acute (MANIC) *1st choice*, prevention of recurrence of mania, unclear about maintenance; often combined w/ Lithium

Classification:Benzodiazepines

MOA:Potentiates GABA A response

Indication/Clinical Application: Generalized focal and tonic-clonic status epilepticus, seizure cluster, anx and etoh withdrawal

SE and AED's:Sedation, tolerance, ataxia, fatigue

Contraindications: Acute narrow-angle glaucoma; Untreated open-angle glaucoma

Therapeutic Considerations: Benzodiazepine levels are decreased by carbamazepine or phenobarbital.

well absorbed orally. many formulations: oral, IV, rectal (gel). peak conc- 1 hour. highly protein bound and extensively metabolized. min interactions. only used to get rid of acute seizures. More potent against electroshock. highly effective stopping continuous seizure activity. ocasionally given long term but not really since rapid build up of tolerance.

Classification:Benzodiazepines

MOA:Potentiates GABAA response

Indication/Clinical Application: treatment of status epilepticus, focal and tonic clonic, seizure clusters, anx and etoh withdrawal

SE and AED's:Sedation, tolerance, ataxia, fatigue

Contraindications: Acute narrow-angle glaucoma; Untreated open-angle glaucoma

Therapeutic Considerations: May be more effective and longer acting than diazepam;

Benzodiazepine levels are decreased by carbamazepine or phenobarbital. Well absorbed, IV and rectal. May be more effective and longer active for status epilepticus. peak conc= 1 hr, highly protein bound, extensive metabolized

Classification:Benzodiazepine

MOA:Potentiates GABA response

Indication/Clinical Application: Absence and myoclonic generalized seizures, infantile spasms, anxiety and EtOH withdrawl.

SE and AED's:sedation(esp @ start), tolerance and lethargy

Contraindications: narrow angle or untreated open angle glaucoma.

Therapeutic Considerations: [Benzo] and decreased by cocomitant carbamazepine or phenobarbital use;

long acting drug, start at low dose. documented efficacy against absence and infantile spasms. Starting doses should be small (sedation). 4th drug of choice in absence

Classification:Benzodiazepine

MOA:Potentiates GABA A response

Indication/Clinical Application:  (pretty much only used anx and etoh withdrawal) adjunct for complex partial in adults

SE and AED's:sedation, tolerance and lethargy

Contraindications: dependence, suicidal thoughts/behaviors, somnolence, sedation, etc. Many more in notes

Therapeutic Considerations: approved for pts age 2 or older. Schedule IV drug - abuse potential. Well absorbed orally. Minimal enzyme interation. [Benzo]

decreased by carbamazepine or phenobarbital. peak conc 1 hr

start low go slow

Classification:Benzodiazepine

MOA:Potentiates GABA response

Indication/Clinical Application: add on therapy for Lennox-Gastault Syndrome, absence and myoclonic seizures, infantile spasms

SE and AED's:dependence, suicidal thoughts/behaviors, somnolence, sedation, fever, drooling, constipation, cough, UTI infection, insomnia, aggression, fatigue, URT, irritable,vomitting, trouble swallowing, probs with coordination, bronchitis, pnemonia, increase risk of suicidal thought

Contraindications: narrow angle or untreated open angle glaucoma

Therapeutic Considerations: approved for pts age 2 or older. Schedule IV drug - abuse potential. Well absorbed orally. Minimal enzyme interation.

[Benzo] decreased by carbamazepine or phenobarbital. May cause delayed psychomotor development and behavioral disorders.NOT USED FOR ANX and ETOH withdrawal. Granted an oral drug designation. FDA requires med guide

Classification:Anti-manic and Mood Stabilizer

MOA:Suppresses inositol signaling by 1. depletion of intracellular inositol. 2. Direct Inhibition--> inhibition of glycogen synthase kinase 3 (GSK-3) by competing w/ Mg++. 3. Effect on 2nd messenger: acts on inositol phosphates. Lithium inhibits inositol monophosphatase (IMPase) and inositol polyphosphate 1- phosphatase, resulting in depletion of substrate for IP3 production...Lithium can inhibit NE-sensitive adenylyl cyclase (gives lithium antidepressant and anitmanic effects). Effect on G proteins: Lithium uncouples receptors from their G proteins. MAJOR WORKING HYPOTHESIS ON MOA: Lithium reduces myoinositol in brain, which alters protein kinase C-mediated signaling causing alteration in gene expression. Lithium also alters production of proteins implicated in long-term neurplastic events, which gives lithium long-term mood stabilization effect.

Indication/Clinical Application: Bipolar Disorder: anti-manic & mood stabilizer. Treats acute phase & prevents recurrent manic & depressive episodes. Recurrent endogenous depression with a cyclic pattern. Adjunct in Schizoaffective disorder treatment. Adjunct in unipolar depression.

SE and AED's:Tremor. Polyuria. Sub-clinical hypothyroidism. choreathetosis(involuntary movements), motor hyperactivity, ataxia, dysarthria(inability to pronounce words), and aphaxia(inability to understand language). Decr. thyroid function. Polydipsia(thirst). Edema. sick sinus "brady-tachycardia". Transient acneiform eruptions. Folliculitis. Leukocytosis.

Contraindications: 

sick sinus "brady-tachycardia"

Therapeutic Considerations: 1.Schizophrenia:useful only as adjunct. 2.Complete absorption in 6-8 hrs w/ peak plasma levels in 30mins-2 hrs 3. No hepatic metabolism --> excreted in urine (T1/2 = 20 hours) 4. Pts on lithium must obtain TSH levels q6-12 months. 5.Slow onset of action. 6. 80% success rate for remission from manic phase & 60% success rate for maintenance treatment. 7. Propranolol & atenolol alleviate lithium induced tremor. 8. Incr. renal CL during pregnancy. 9. Low teratogencity 10.Some sequestration in bone 11.No protein binding

Classification: phenothiazine Antipsychotic (typical) 

MOA:

Blockade of D2 receptors >> 5HT2a receptors (this is associated with hallucinations)

Blockade of:

Alpha receptor

Muscarinic (M) receptor

H1-receptor

CNS depression (sedation)

Indication/Clinical Application: treatment of manic phase of bp

Side effects: Sedation, CNS depression 

Name whether excitatory or inhibitory receptor

Nn & Nm
M1, M3, M5
M2, M4
Mu and Delta
H2

Alpha 1
Alpha 2

Beta 1

Beta 2

GABA B

D 1 and 2

Glycine

Nn & Nm excitatory
M1, M3, M5 excitatory
M2, M4 inhibitory
Mu and Delta are inhibitory
H2 is stimulatory

Alpha 1Excitatory

Alpha 2 inhibitory

Beta 1 Excitatory

Beta 2 Inhibitory

Gaba B Inhibitory

D1 and 2 Inhibitory

Glycine Inhibitory

Classification: Atypical Antipsychotic

MOA: Blockade of 5HT2a > blockade of D2

A-receptor blockade

Variable H1-receptor blockade

Indication/Clinical Application: 

manic phase (of bipolar)

Classification: Atypical antipsychotic

MOA:

Blockade of 5HT2a > D2

Variable H1-receptor blockade

Indication/Clinical Application: 

Manic phase (of biploar)

Classification:

Atypical Antipsychotic

MOA:

Blockade of 5Ht2a > D2

M-receptor blockade

variable H1-receptor blockade

Indication/Clinical Application: 

manic phase of bipolar

bipolar disorder maintenance

Therapeutic Considerations: 

Olanzapine plus fluoxetine in combo approved for treatment of bipolar depression and maintenance therapy 

Classification: Atypical Antipsychotic

MOA:

Blockade of 5HT2a > D2

variable H1-receptor blockade

Indication/Clinical Application: 

manic phase of bipolar &

bipolar depression &

bipolar disorder maintenance 

Classification: Atypical Antipsychotic

MOA:

Blockade of 5HT2a > D2

A-receptor Blockade

variable H1-receptor blockade

Indication/Clinical Application: 

manic phase of bipolar