Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Adv Pharm 1 > Neuro Drugs from Textbook Chart > Flashcards

Neuro Drugs from Textbook Chart Flashcards

1
Q

What is the MOA for Phenytoin/Fosphenytoin?

A

Na Channel Blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the kinetics of Phenytoin/Fosphenytoin?

A

*Decreases synaptic release of glutamate and increases release of GABA
*At therapeutic levels, the major action is to block Na+ channels and inhibit the generation of rapidly repetitive Aps

Oral absorption nearly 100%
IM absorption unpredictable
Fosphenytoin is well absorbed IV
Highly protein bound
Accumulates in the brain, liver, muscle, and fat
No active metabolites (all inactive)
Excreted in urine
Elimination is dose-dependent (FIRST ORDER KINETICS, increases in the dose after the liver has reached max capacity can result in toxicity)
Half-life: 12-36 hrs
Average 24 hrs for most pts
5-7 days to reach a steady state after each dose change (4 half-lives to reach steady state)
At high doses, it may take as long as 4-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the clinical applications for Phenytoin/Fosphenytoin?

A

*Partial seizures
*Generalized tonic-clonic seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the S/Sx of toxicity associated with Phenytoin/Fosphenytoin?

A

nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism

Nystagmus and loss of ocular movements are early signs (do not indicate need to decrease dose)

Diplopia and ataxia are most common dose related adverse effects requiring dose adjustments

Sedation occurs only at considerably high levels
Gingival hyperplasia
Hirsutism (male patterned hair growth in women)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the S/sx associated with long-term use of Phenytoin/Fosphenytoin?

A

Coarsening of facial features, mild peripheral neuropathy (diminished deep tendon reflexes in the lower extremities), osteomalacia, vitamin D deficiencies, low folate levels, megoblastic anemia (inhibition of DNA synthesis during RBC production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drug interactions occur with Phenytoin/Fosphenytoin?

A

Interactions with phenobarbital, carbamazepine, topiramate, steroids, oral contraceptives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the MOA for Carbamazepine?

A

Na Channel Blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the kinetics for Carbamazepine?

A

Rapidly absorbed orally (bioavailability 75-85%)
Peak levels in 4-5hrs
Metabolized in the liver
Half-life: 25-65hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical applications for Carbamazepine?

A

Focal seizures
Focal-to-bilateral tonic-clonic seizures
Trigeminal neuralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the toxicity S/Sx for Carbamazepine?

A

nausea, diplopia, ataxia, hyponatremia, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drug interactions occur with Carbamazepine?

A

Interactions with phenytoin, valproate, fluoxetine, verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the MOA for Valproate?

A

Unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the kinetics for Valproate?

A

Nearly complete (>90%) absorption
Metabolized in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical applications for Valproate?

A

Generalized tonic-clonic seizures
Focal seizures
Absence seizures
Myoclonic seizures
Other generalized seizure types
Migraine prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the toxicity S/Sx for Valproate?

A

nausea, tremor, weight gain, hair loss, teratogenic, hepatotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the drug interactions associated with Valproate?

A

Interactions with phenobarbital, phenytoin, carbamazepine, lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the MOA for Lamotrigine?

A

Na Channel Blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the Kinetics associated with Lamotrigine?

A

Nearly complete (>90%) absorption
Peak levels in 1-3hrs
Extensively metabolized, no active metabolites
T1/2 = 8-35hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical applications for Lamotrigine?

A

Focal seizures
Generalized tonic-clonic seizures
Absence seizures
Other generalized seizures
Bipolar depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the toxicity S/Sx of Lamotrigine?

A

dizziness, headache, diplopia, rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What drug interactions occur with Lamotrigine?

A

Interactions with valproate, carbamazepine, phenytoin, phenobarbital

22
Q

What is the MOA for Levetiracetam?

A

SV2A ligand

23
Q

What are the kinetics for Levetiracetam?

A

Nearly complete (>95%) absorption
Peak levels in 1-2hrs
Not bound to plasma proteins
Minimal metabolism in blood, most excreted unchanged in the urine

24
Q

What are the clinical applications for Levetiracetam?

A

Focal seizures
Generalized tonic-clonic seizures
Myoclonic seizures

25
Q

What are the toxicity s/sx for levetiracetam?

A

nervousness, dizziness, depression, seizures

26
Q

What drug interactions occur with Levetiracetam?

A

Minimal interactions with other drugs

27
Q

What is the MOA for Topiramate?

A

Multiple actions

28
Q

What are the kinetics for Topiramate?

A

Half-life decreases when used with other drugs (usually 20-30 hours)
20-70% excreted unchanged in urine
No active metabolites

29
Q

What are the clinical applications for Topiramate?

A

Focal seizures
Generalized seizures
Lennox-Gastaut syndrome
Migraine prophylaxis

30
Q

What are the toxicity S/Sx for Topiramate?

A

somnolence, cognitive slowing, confusion, paresthesia

31
Q

What drug interactions occur with Topiramate?

A

Interactions with phenytoin, carbamazepine, oral contraceptives, lamotrigine, Lithium

32
Q

What is the MOA for Chlorpromazine?

A

Typical

D2 and 5-HT2A receptor antagonism (D2 > 5HT2A)

33
Q

What are the kinetics for Chlorpromazine?

A

Long half-life with metabolism dependent elimination
*May be excreted in urine weeks after last dose of chronically administered drug

34
Q

What are the clinical applications for Chlorpromazine?

A

Schizophrenia (alleviates positive symptoms)
Bipolar disorder (manic phase)
Antiemetics
pre-op Sedation
Pruritus

35
Q

What are the toxicity S/Sx associated with Chlorpromazine?

A

S/sx r/t effects on alpha adrenergic blockade (hypotension) & muscarinic blockade (anticholinergic 🡪 dry mouth, etc.) & histamine blockade (CNS depression, sedation, decreased seizure threshold, QT prolongation)

S/sx r/t dopa receptor blockade (akathisia, dystonia, parkinsonian symptoms, tardive dyskinesia, and hyperprolactinemia)

36
Q

What is the MOA of Haloperidol?

A

Typical

D2 and 5-HT2A receptor antagonism (D2 > 5HT2A)

37
Q

What are the kinetics for Haloperidol?

A

Metabolism-dependent elimination

38
Q

What are the clinical applications for Haloperidol?

A

Schizophrenia (alleviates positive symptoms)
Bipolar disorder (manic phase)
Tourette syndrome

39
Q

What are the toxicity S/sx associated with Haloperidol?

A

Some alpha blockade (hypotension), but minimal muscarinic & histamine blockade (less sedation**)
S/sx: extrapyramidal dysfunction

40
Q

What is the MOA for Clozapine?

A

Atypical

D2 and 5-HT2A receptor antagonism (5HT2A > D2 )

41
Q

What are the kinetics for Clozapine?

A

*For other antipsychotics, relapse is variable after d/c… but NOT for Clozapine.
*Relapse after d/c of Clozapine is rapid and severe

42
Q

What are the clinical applications for Clozapine?

A

Schizophrenia (alleviates both positive and negative symptoms)
Agitation in Alzheimer and Parkinson patients

43
Q

What are the toxicity s/sx associated with Clozapine?

A

Some alpha blockade and some muscarinic blockade, variable H1 blockade
S/sx: agranulocytosis, diabetes, hypercholesteremia, weight gain

44
Q

What is the MOA for Lithium?

A

Unclear
Suppresses inositol signaling and inhibits glycogen synthase kinase-3 (GSK-3)

45
Q

What are the kinetics for Lithium?

A

Narrow therapeutic window
Oral absorption, renal elimination
Half-life: 20 hours

46
Q

What are the clinical applications for Lithium?

A

Bipolar affective disorder (prophylactic use can prevent mood swings between mania and depression)

47
Q

What are the toxicity s/sx associated with Lithium?

A

No specific antagonistic actions on autonomic nervous system receptor or specific CNS receptors, no sedative effects
S/sx: tremor, edema, hypothyroidism, renal dysfunction, dysrhythmias, pregnancy category D
-Polyuria, polydipsia,
-C/I in SSS due to SA node depression

48
Q

What drug interactions occur with Lithium?

A

Interactions: clearance decreased by thiazides and some NSAIDs

49
Q

What is the MOA for Carbamazepine (Tegretol) - (Antipsychotic use)

A

Unclear

50
Q

What are the kinetics for Carbamazepine (antipsychotic use)

A

Oral absorption
Once daily dosing
Forms active metabolite

51
Q

What are the clinical applications for Carbamazepine (antipsychotic use)

A

Bipolar disorder (acute mania and prophylaxis in depressive phase)

52
Q

What are the toxicity S/sx associated with Carbamazepine (antipsychotic use)

A

Hepatotoxicity and induction of P450 drug metabolism, tremor, liver dysfunction, weight gain

Adv Pharm 1 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions