Ch. 16/17: Anticonvulsants/Anti-Epileptics and Resp. Stimulants (Vickroy) Flashcards

1
Q

When is doxapram contraindicated?

A

animals with seizure disorders

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2
Q

most common spontaneous neuro disorder in dogs

A

seizures

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3
Q

Importany questions to ask when dog has seizures

A
  • is the reported event truly a seizure?

- can an underlying cause be identified and treated?

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4
Q

Things that can mimic seizures

A
  • cataplexy/narcolepsy
  • vestibular episode
  • encephalitis
  • exercise-induced collapse
  • drug-induced dyskinesias
  • cervical m. spasm
  • episodic NM dz
  • metabolic event
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5
Q

most (90%) of seizures are CNS or non-CNS?

A

CNS

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6
Q

causes of non-CNS induced seizures

A
  • metabolic/electrolyte imbalance (hypoxia, dec. Glu/Ca/Mg, inc. K)
  • liver dz
  • renal failure
  • drugs/toxins
  • hypothyroidism
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7
Q

causes on CNS induced seizures

A
  • organic brain disease (45%) (tumor, infection, head trauma) –> 2ary epilepsies
  • idiopathic epilepsy (45%) –>1ary epilepsies
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8
Q

idiopathic epilepsy

A

poorly char. CNS disorder that manifests as episodes of intermittent high neuronal activity

  • usually life-long*
  • can be focal or diffuse in brain
  • can be initiated by sensory or external stimuli
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9
Q

seizure

A

a clinical manifestation of excessive and/or hyper-synchronous neuronal discharges in the brain
-may present as episodic impairment or loss of consciousness accompanied by abnormal motor phenomena, psychic or sensory disturbances, ANS signs

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10
Q

convulsion

A

motor manifestation of seizures that involves involuntary contraction-relaxation of body muscles

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11
Q

epilepsy

A

commonly defined as 2+ seizures at least 24hrs aparts, resulting from a nontoxic/nonmetabolic cause

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12
Q

status epilepticus

A

continuous seizure activity lasting 30min or longer. Life-threatening

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13
Q

T/F: prolonged periods of seizure activity can produce irreversible brain damage and neuronal death and are char. by:

A
  • extremely high use of O2 and glucose
  • followed by prolonged CNS depression (unconsciousness)
  • requires some form of intervention**
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14
Q

anti-epileptic agent curative of seizures?

A

NO. Only reduces the symptoms

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15
Q

2 general mechs. by which anti-epileptics act:

A

1) suppress initiation of neuronal firing in epileptiform foci
2) inhibit spread of seizure activity into normal tissues

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16
Q

disadvantages of AEDs

A
  • high percentage of animals are refractory to AEDs
  • high incidence of side effects
  • devel. tolerance
  • loss of clinical efficacy over time
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17
Q

empirical use

A

to use what works in the patient as long as it works and is tolerated by the patient and o

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18
Q

phenobarb fx

A
  • long-acting barbiturate w/ anti-seizure properties

- sedative

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19
Q

barbiturates are classified according to:

A

duration of action

20
Q

phenobarb mech. of action

A

facilitates GABA activation of GABA-A receptor and opening of Cl channels –> CNS depression (i.e. cortical motor centers)

21
Q

all barbiturates are acids/bases

22
Q

T/F: phenobarb is DEA-controlled drug**

A

T. (class 4 agent)

23
Q

common side effect when starting phenobarb tx of seizures

A

sedation (however, tolerance to this builds up over time)

24
Q

long-term use of what two classes of drugs causes physical dependence?**

A

opiates, barbiturates. Severe withdrawal symptoms can result!

25
bioavailability of phenobarb
high oral bioavailability with low absorption
26
in most cases, signs of physical dependence are:
the opposite of the clinical effects of the drug
27
elim. of phenobarb
liver and kidney
28
Changes in pharmacokinetics following chronic administration of phenobarbital***
- tolerance leads to induction of liver microsomal enzymes: - shorter t1/2 - lower plasma drug lvls - must inc. maintenance dose** - hepatic metabolism of OTHER drugs also increased
29
chronic tx of phenobarb can result in what side effects?
- polyphagia, PU/PD - sedation, ataxia - elevated liver enzymes - restlessness and irritability
30
phenobarb drug interactions**
- binding of griseofulvin --> dec. drug absorption - attenuates action of vit. D - stimulation of hepatic enzyme activity --> inc. drug metabolism
31
phenobarb contraindications
pre-existing cardiac/resp. or liver dz
32
max. loading dose of phenobarb is limited by:
negative side effects it may produce
33
Is primidone a controlled drug?**
NO
34
primidone is classified as:
a deoxybarbiturate
35
primidone is contraindicated in what species
cats (hepato and neurotoxic)
36
T/F: primidone requires higher doses than phenobarb
T. (however, mech of action, elimination, interactions very similar to phenobarb)
37
Active ingredient in potassium bromide*
bromide anions
38
Is KBr controlled drug?
NO
39
Is KBr approved by FDA?
NO
40
KBr effects
sedation, anti-convulsant at higher doses. Only use when routine anticonvulsant therapy is ineffective!
41
KBr actions diminished by:
hyperchloremia
42
KBr is readily absorbed through:*
skin and mm. WEAR GLOVES
43
clorazepate class
-benzo
44
clorazepate fx
anti-convulsant (enhances GABA)
45
Is clorazepate controlled drug?
YES (class 4)
46
PK properties of clorazepate
- rapid oral absorb - active metabolites promote prolonged action - interacts with phenobarb hepatic metabolism
47
side effects of clorazepate
- physiological/psychological dependence - induces liver enzymes - tolerance to anti-seizure action with long-term tx