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Flashcards in Anticonvulsants Deck (33)
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1
Q

How does binding GABA receptors elicit an inhibitory response?

A

hyperpolarizes the neuron by causing Cl influx

2
Q

What are two GENERAL mechanisms of seizure generation?

A

1) altered membrane function

2) altered neurotransmitters

3
Q

T/F: One misfiring neuron is enough to cause a seizure

A

False (must recruit surrounding neurons and propagate the signal)

4
Q

To reach the CNS anticonvulsants must be ______ ______

A

lipid soluble

5
Q

If dosing interval is greater than half life, what is the best way to address therapeutic failure

A

shorten the dosing interval

6
Q

When does a drug accumulate

A

When dosing interval is shorter than the half-life

7
Q

with a drug that accumulates, what is the best way to address therapeutic failure

A

increase the dose

8
Q

With which relation of dosing interval to half-life is a missed dose likely to be less important?

A

When dosing interval is less than half-life

9
Q

What should you not use when collecting samples to measure anticonvulsant concentrations?

A

Serum separator tube (can bind drug and artificially lower concentration)

10
Q

The loading dose for a drug that accumulates is based on what

A

the drug’s half-life (longer half-life=larger loading dose)

11
Q

Phenobarbital MOA

A

binds GABA receptors and inhibits glutamate and Ca influx

12
Q

For which drug does the oral dose=IV dose

A

Phenobarbital

13
Q

Important interaction of phenobarbital at the liver?

A

POTENT enzyme inducer (rapidly increases clearance of other drugs that go through hepatic metabolism…including itself)

14
Q

Diazepam MOA

A

GABA agonist

15
Q

which drug is first choice for status epilepticus and why?

A

Diazepam; rapidly penetrates the CNS

16
Q

When giving phenobarb, seeing an increase in serum alk phos means what

A

induction (NOT disease)

17
Q

What is phenobarb’s schedule?

A

Class IV

18
Q

Why can’t diazepam be used long-term?

A

development of tolerance

19
Q

The use of diazepam is contraindicated in which spp.?

A

Cats

20
Q

Name 2 reasons KBr is a good choice for add-on therpay

A

1) it doesn’t share a mechanism of action

2) renally excreted (no hepatic concerns

21
Q

Unique interaction of KBr?

A

competes with Cl…will be more readily excreted with high Cl (NaCl) diets

22
Q

And indication for use of KBr as the sole anticonvulsant?

A

P with liver disease

23
Q

Which drug is associated with GI upset?

A

KBr

24
Q

Zonisamide MOA

A

decreases positive ion influx (targets Na and T Ca channels)

25
Q

Why might dogs be at a greater risk when taking zonismaide?

A

it undergoes acetylation during metabolism (dogs are deficient)

26
Q

How could phenobarb impact zonisamide?

A

could increase its clearance

27
Q

Zonisamide unique adverse event?

A

can cause hypothyroidism (inhibits hormone synthesis)

28
Q

What does “Lev” tell us

A

the drug is an enantiomer

29
Q

Levetriacetam MOA

A

unknown; may bind synaptic vesicles to prevent NT release

30
Q

Which two drugs have a relatively short half-life

A

Diazepam

Levetiracetam

31
Q

What 3 locations does Leve undergo metabolism?

A

Renal (most), hepatic and plasma

32
Q

Limitations on Leve dosing?

A

minimum weight of 15kg

33
Q

When should you evaluate response to therapy?

A

3 half-lives and one seizure interval