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

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

A

acids

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
Q

bioavailability of phenobarb

A

high oral bioavailability with low absorption

26
Q

in most cases, signs of physical dependence are:

A

the opposite of the clinical effects of the drug

27
Q

elim. of phenobarb

A

liver and kidney

28
Q

Changes in pharmacokinetics following chronic administration of phenobarbital***

A
  • 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
Q

chronic tx of phenobarb can result in what side effects?

A
  • polyphagia, PU/PD
  • sedation, ataxia
  • elevated liver enzymes
  • restlessness and irritability
30
Q

phenobarb drug interactions**

A
  • binding of griseofulvin –> dec. drug absorption
  • attenuates action of vit. D
  • stimulation of hepatic enzyme activity –> inc. drug metabolism
31
Q

phenobarb contraindications

A

pre-existing cardiac/resp. or liver dz

32
Q

max. loading dose of phenobarb is limited by:

A

negative side effects it may produce

33
Q

Is primidone a controlled drug?**

A

NO

34
Q

primidone is classified as:

A

a deoxybarbiturate

35
Q

primidone is contraindicated in what species

A

cats (hepato and neurotoxic)

36
Q

T/F: primidone requires higher doses than phenobarb

A

T. (however, mech of action, elimination, interactions very similar to phenobarb)

37
Q

Active ingredient in potassium bromide*

A

bromide anions

38
Q

Is KBr controlled drug?

A

NO

39
Q

Is KBr approved by FDA?

A

NO

40
Q

KBr effects

A

sedation, anti-convulsant at higher doses. Only use when routine anticonvulsant therapy is ineffective!

41
Q

KBr actions diminished by:

A

hyperchloremia

42
Q

KBr is readily absorbed through:*

A

skin and mm. WEAR GLOVES

43
Q

clorazepate class

A

-benzo

44
Q

clorazepate fx

A

anti-convulsant (enhances GABA)

45
Q

Is clorazepate controlled drug?

A

YES (class 4)

46
Q

PK properties of clorazepate

A
  • rapid oral absorb
  • active metabolites promote prolonged action
  • interacts with phenobarb hepatic metabolism
47
Q

side effects of clorazepate

A
  • physiological/psychological dependence
  • induces liver enzymes
  • tolerance to anti-seizure action with long-term tx

Pharmacology (21 decks)

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