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;
32 Cards in this Set
- Front
- Back
|
phenytoin
|
mneum: Sean
MOA: *Prolong state of sodium channel inactivation Tx: *DOC for generalized tonic clonic seizures (Grand Mal) *Status epilepticus (given iv) *Fosphenytoin = water-soluble pro-drug of phenytoin S/E: *Hirsuitism *Gingival hyperplasia *Osteomalacia *Megaloblastic anemia *All S/E result from CYP450 that destroys vit D & folate *Teratogenic effects – “Fetal Hydrantoin syndrome" |
|
|
DOC Tx of multiple seizure types
|
valproate
|
|
|
DOC for atonic
|
valproate
|
|
|
DOC for myoclonic
|
valproate
|
|
|
Tx wide-spectrum seziures
|
valproate & lamotrigene
|
|
|
Tx epilepsy
|
1. phenytoin
2. ethotoin 3. valproate 4. carbamazepine 5. lamotrigene 6. zonisamide 7. ethosuximide 8. phenobarbital 9. diazepam (valium) 10. clonazepam 11. gabapentin |
|
|
Tonic-Clonic (Grand Mal):
|
manifest as sudden loss of consciousness, w/ tonic contraction of body musculature followed by rhythmic jerking of the extremities & then depression of CNS function for varying periods.
|
|
|
Absence (petit mal):
|
characterized by brief loss of awareness, sometimes w/ eye blinking or lip smacking, but w/o loss of consciousness or body tone. This form of epilepsy is almost always seen in young children
|
|
|
valproate?
|
MOA: *prolong state of sodium channel inactivation
Tx: *Wide spectrum *DOC for atonic & myoclonic *DOC Tx of multiple seizure types S/E: *Hepatotoxicity: esp when other anti-seizure drugs are administered concurrently (makes sense b/c if have multiple sizures, you’re probly on multiple drugs) |
|
|
*DOC for ALL Partial seizures
|
Carbamazepine
|
|
|
DOC for trigeminal neuralgia
|
carbamazepine
|
|
|
what epilepsy Tx causes BM depression?
|
carbamazepine
mneum: “carbam” sounds like carbon, so it depresses your BM until all you have is a carbon skeleton |
|
|
carbamazepine
|
MOA: *prolong state of sodium channel inactivation
Tx: *DOC for ALL Partial seizures *DOC for trigeminal neuralgia S/E: BM depression |
|
|
lamotrigene
|
MOA: *prolong state of sodium channel inactivation
*metab by Glucoronide (not CYP450) Tx: *Wide spectrum of anti-seizure activity S/E: *safe for pregnancy *No cognitive impairment *less S/E + interactions b/c doesn't affect CYP450 |
|
|
phenobarbital: MOA?, Tx?
|
MOA: *Enhance GABA mediated incr in chloride conductance
==>incr DURATION of Cl channel opening mneum: Barbie (Barbiturates, i.e. phenobarbital) is the one who never leaves the party (incr duration) Tx: epilepsy |
|
|
*DOC for Status epilepticus
|
Diazepam (Valium)
|
|
|
Diazepam
|
=Valium
Tx: *DOC for Status epilepticus MOA: *BZ (diazepam is prototype benzodiazapam) *Enhances the GABA-mediated increase in chloride conductance ==>incr FREQ of Cl channel opening |
|
|
typical antipsychotics--ex's?
|
-chlopromazine
-haloperidol |
|
|
chlorpromazine-MOA, Tx, SE?
|
=typical antipsychotic
MOA: *D2 antagonist *greater potency at blocking D2 than 5-HT receptors Tx: decr positive symptoms of schizophrenia (hallucination, delusions, conceptual disorganization in speech & behavior, agitation) SE: *incr prolactin- gynecomastia, galactorrhea, amenorrhea, wt gain *EPS- dystonia, psuedoparkinsonism, akathisia (motor restlessness), tardive dyskinesias *low potency (chlorpromazine)- more likely to be more antichol, sedative & produce orthostatic hypotension *high potency (Haloperidol)- more EPS -antiadrenergic -anticholingergic -antihistamine |
|
|
what gives SE:
-gynecomastia -EPS |
typical antipsychotics
|
|
|
what are the atypical antipsychotics?
|
-clozapine
-olanzapine -risperidone -quetiapine -ziprasidone |
|
|
olanzapine?
|
same as all atypical antipsychotics
*5HT2/D2 antagonist *5HT2 block > D2 block Tx: *decr + Sx of schizo *decr - Sx of schizo- b/c they work to incr DA in prefrontal cortex SE: *greater weight gain (d/t blocking 5-HT) (development of type II diabetes & hyperlipidemia) *Neuroleptic Malignant Syndrome tx: dantrolene + bromocriptine (Park Rx: DA-analog) *relatively similar antiadrenergic, anticholinergic & antihistamine profile as typicals, except: *Clozapine- 1-3% incidence of granulocytopenia or agranulocytosis, Thus check CBC weekly *Olanzopine is VERY antihistaminic Mneum: sounds like you’re going to sneeze, so givce an antihistamine -Risperidone -NOT anticholingergic -less neuro/EPS -↑ PRL *Quetiapine- NOT anticholinergic |
|
|
Acute Tx of mania
|
lithium
|
|
|
DOC as prophylaxis for bipolar
|
lithium
|
|
|
S/E of lithium
|
BAD S/E!
*CV: non-specific T wave changes *GI-diarrhea *Endocrine: direct antithyroid- cause hypothyroidism & goiter |
|
|
Summary of effect desired to treat schizophrenia
|
tract 1 = do not change D2-receptor stimulation
tract 2 = decreased D2-receptor stimulation (alleviates + Sx) tract 3 = increase D2-receptor stimulation (alleviates - Sx) tract 4 = do not change D2-receptor stimulation |
|
|
effect of typical antipsychotics on DA tracts
|
You can already see the problem with the typical antipsychotic drugs:
they block D2-receptors everywhere! So, let's see what happens when you block D2-receptors in all four tracts. tract 1 = nigrostriatal tract = EPS = BAD, schlimm, malo tract 2 = mesolimbic tract = prevents positive symptoms = GOOD, gut, bueno tract 3 = mesocortical = does not help negative symptoms and may even make them worse because negative symptoms appear to result from a lack of D2-receptor stimulation here = BAD tract 4 = TI = hyperprolactinemia = gynecomastia, amenorrhea = BAD |
|
|
effects of atypical antipsychotics on DA tracts
|
First, the atypical drugs are able to block D2-receptors, but they
are much more potent in blocking serotonin 5-HT2-receptors. This fact is significant because 5-HT stimulation of 5-HT2 receptors in the nigrostriatal (Tract 1) and mesocortical (Tract 3) tracts inhibits the rate of firing of DA neurons. Thus, blockade of 5-HT2-receptors in the nigrostriatal and mesocortical tracts enhances the release of DA. The increased DA release evidently overrides the blockade of D2-receptors, so the atypical drugs do NOT cause EPS and may actually increase D2-receptor stimulation in the cortex (Tracts 1 & 3). The latter effect would account for the fact observation that the atypical drugs improve the negative symptoms of schizophrenia. Second, 5-HT does not inhibit DA release in the mesolimbic pathway, so the atypical antipsychotic drugs cannot increase DA release in the mesolimbic pathway. Rather, they block D2-receptors to prevent the positive symptoms of schizophrenia. Last, the atypical drugs appear to have insufficient activity to block D2-receptors in the Tubloinfundibular tract, so plasma prolactin does not change. Summary of the effects of the atypical antipsychotic drugs: tract 1 = nigrostriatal = no effect on neurotransmission = no EPS tract 2 = mesolimbic = block of D2-receptors = no positive symptoms tract 3 = mesocortical = enhanced D2-stimulation = improved negative symptoms tract 4 = Tubuloinfundibular = so effect = no hyperprolactinemia |
|
|
DA tracts in CNS
|
tract 1: SN tract=mvmt (nl in schizo)
tract 2: mesolimbic=emotion/motivation/reward (increase-->psychosis) *pos Sx tract 3: mesocortical=cognition, motivation *- Sx Tract 4: Tuberoinfundibular (DA stimulates D2 receptors to inhibit PRL release, nl in schizo) |
|
|
DOC for absence seizures
|
ethosuxamide
|
|
|
gabapentin
|
(GABApentin)
MOA: promote release of GABA Tx: *partial & generalized tonic clonic *postherpetic neuralgia |
|
|
fosphenytoin
|
=water-soluble pro-drug of phenytoin
Tx: status epilepticus, prevent and Tx seizures occurring during neurosurgery |
