Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/32

Click to flip

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