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RUSVM Pharmacology > Muscle Relaxants and AEDs > Flashcards

Muscle Relaxants and AEDs Flashcards

1
Q

What are the anti-tremorogenic and sedating drugs

A

Methocarbamol
Guaifenasin
Dantrolene

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2
Q

What re the antiepilieptic drugs

A 
Diazepam and midazolam 
Phenobarbital 
Bromide 
Levetricetam 
Zonisamide
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3
Q

What is the site of action of dantrolene?

A

Peripheral -muscle cells

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4
Q

What is the site of action of guaifensin?

A

Central -> spinal cord

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5
Q

What is the site of action of methocarbamol

A

Central -> spinal cord

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6
Q

What is the MOA of dantrolene?

A

Peripherally acting muscle relaxant -> acts on the muscle cell

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7
Q

T/F: dantrolene crosses the BBB

A

F

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8
Q

What is the drug of choice for treatment of malignant hyperthermia (hypermetabolic syndrome)

A

Dantrolene

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9
Q

What is hypermetabolic syndrome

A

Idiosyncratic drug reaction
Hyper metabolic rxn on skeletal muscle -> rhabdomyolysis

Life threatening hyperthermia, hyperkalemia, and cell death
Multiple organ dysfunction syndrome (MODS)

Often fatal

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10
Q

__________ are very toxic to dogs and can lead to malignant hyperthermia

A

Hops

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11
Q

What are the clinical uses of dantrolene

A

Malignant hyperthermia

Tetanus –> cause muscle relaxation

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12
Q

What is the MOA of methocarbamol?

A

Blockade of nerve impulse transmission in the spinal cord

Cross the BBB

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13
Q

What is the main clinical use of methocarbamol?

A

Reduce muscle spasm (approved in cat, dog, and horse)

  • > tetanus
  • > intoxication (tremorogenic)

Treatment of acute inflammatory or traumatic conditions (eg intervertebral disk disease )

Functional urethral obstruction/urinary retention (less common use)

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14
Q

What is the half life of methocarbamol

A 
Relatively short (1-2hrs) 
Shorter when given IV
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15
Q

How is methocarbamol administered

A

Oral or IV

Irritating if administered IM/SQ -> not recommended

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16
Q

Strychnine, metaldehyde, pyrethrin(cat) and some toxic molds are treated with ____________ to reduce treorogenic toxins

A

Methocarbamol

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17
Q

What are the side effects of methocarbamol ?

A

Sedation, salivation, weakness, lethargy, and ataxia

Caution using injectable form with renal disease

Avoid extravasation and administer IV slowly

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18
Q

What is the MOA of Guaifensin

A

Centrally-acting muscle relaxant and expectorant (break up a cough)

Blocks nerve impulse transmission in spinal cord, brain stem and subcortical areas of the brain -> cross BBB

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19
Q

What is the onset and duration of guaifensin

A

Rapid onset and short duration (10-20min)

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20
Q

What are the clinical uses of guaifensin ?

A

Intubation -> relax pharyngeal and laryngeal muscles

Procedural sedation in horse and cattle
-> Guaifensin + Xylazine + ketamine (triple drip)

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21
Q

What are precautions to using guaifensin

A

High concentration causes hemolysis

Cattle more sensitive than horse

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22
Q

______________ drug is contraindicated in horse receiving guaifensin

A

Physostigmine

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23
Q

________ is a clinical manifestation of abnormal electrical activity in the brain (uncontrolled firing of neurons)

A

Seizure

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24
Q

_________ is a chronic syndrome of seizures occurring intermittently over months to years

A

Epilepsy

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25
Q

__________________ is ‘true epilespy’ and is genetic

A

Idiopathic

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26
Q

______________ epilepsy has intracranial vs extra-cranial causes

A

Acquired/symptomatic

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27
Q

________________ seizures is when more than one seizure occurs within a 24hr period with recovery inbetween

A

Cluster

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28
Q

____________________ is when you have repeated seizures without full recovery between them or a single seizure that lasts > 5mins

A

Status epilepticus (SE)

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29
Q

_____________ drugs prevent or treat seizures

A

Anticonvulsants

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30
Q

_______________ drugs generally refers to maintenance management of epileptic seizures

A

Antiepileptic drugs (AED)

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31
Q

_____________ seizures do not respond to therapeutic doses of AEDs

A

Refractory

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32
Q

_______________ seizures occur at periodic intervals during treatment course with AEDs

A

Breakthough

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33
Q

What are the types of seizures

A

Generalized

  • convulse
  • non-convulsive (absent)

Partial

  • simple (lateralizing motor activity, no loss of consciousness)
  • complex (altered motor activity and consciousness)
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34
Q

What is the major excitatory neurotransmitter in the brain?

A

Glutamate -> depolarization

-interact with NMDA, AMPA and kainate receptors

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35
Q

What is the major inhibitory neurotransmitter in the brain

A

GABA (hyperpolarization)

-interact with GABA receptor (Gprotein coupled)

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36
Q

Pyrethrum, rhododendrons, spider, and scorpion bites effect the ___________ channels and will cause (excitation or inhibition) of neurons

A

Sodium (inhibits inactivation of Na channel)

Excitation

37
Q

Organophosphate and carbamate cause ___________________ stimulation leading to increased neuronal excitation

A

Cholingergic

38
Q

Clads, amanita mushrooms, and algae cause _____________stimulation that leads to increased neuronal stimulation

A

Glutamtergic

39
Q

Caffeine, therophyline, aminophylleine, and theobromine cause ________________ toxicosis leading to increased neuronal excitation

A

Methylxanthine

40
Q

Strychnine has _______________ antagonism causing decreased neuronal inhibition

A

Glycine -> a inhibitory neurotransmitter

41
Q

What are the three main ways of AED action?

A

Reduction of excitatory transmission
Enhancement of inhibitory process
Modulation of membrane cation conductance

42
Q

How can an AED reduce excitatory transmission?

A

Decrease excitatory neurotransmitters: Glutamate

Na channel blockade

43
Q

How can an AED enhance inhibitory processes ?

A

Increase inhibitory neurotransmitter : GABA

Hyperpolarize postsynaptic membrane (GABAa: chloride permeability)

44
Q

How can an AED modulate membrane cation conductance

A

Block voltage-gated inward positive currents: Na or Ca

Increase outward positive current: K

45
Q

What are the therapeutic goals of an AED

A

Emergency (acute) treatment

  • seizure in progress
  • risk of kindling seizures

Maintenance (chronic) treatment

  • reduce frequency or severity of seizures
  • reduce time between breakthrough seizures (if occurring) and reduce severity/duration
46
Q

What is the drug of choice to stop a seizure in progress?

A

Diazepam (intranasal or per rectum)

47
Q

What is the onset and duration of diazepam?

A 
Rapid (immediate) 
Short duration (2-4hrs)
48
Q

What drug can be used to stop a seizure in progress if there is not IV access?

A

Midazolam (IM)

49
Q

What two benzodiazepines can be used in acute therapy of seizures

A

Diazepam

Midazolam

50
Q

What drug can be used in acute therapy of a seizure that is neuroprotective, but it will have a slower onset but a longer duration than benzodiazepines

A

Phenobarbital (IV)

Will also have sedative effect because it is a barbiturate

51
Q

What drugs will mask seizure activity but does not have true anticonvulsant effects?

A

Propofol or Alfaxalone (IV)

52
Q

What is a con to using propofol to control seizures

A

Very rapid but short acting

Airway protection required -> intubate

53
Q

How can seizures be controlled at home?

A

Diazepam intranasally or rectally

Controlled substance-> legalities to consider
Cannot be stored in a plastic container/syringe (will bind plastic)

54
Q

When should a patient receive maintenance therapy for seizures?

A

Treatable underlying cause of seizure has been ruled out

Status epilepticus

Cluster seizures

Seizure starts within a week of head injury

More than 2-3 seizures in 6-12months

55
Q

Why can diazepam not be given orally to cats?

A

Hepatotoxicity

56
Q

Cats give bromide are at risk for developing _________

A

Asthma/ pneumonitis

57
Q

T/F: dantrolene crosses the BBB

A

F

Peripherally active muscle relaxant

58
Q

What is given to treat tremorogenic toxicity, such as topical permethrin in cats?

A

Methocarbamol

59
Q

What are the 3 main causes of a seizure?

A 
Intracranial lesion (symptomatic epilespy) 
Extracrainial lesion (reactive epilepsy)
Primary disorder (idiopathic disorder)
60
Q

What features does the ideal AED have?

A

Effective -> broad spectrum regardless of underlying cause

Safe

Long half life-> SID or BID

Anti-epileptogenic effects

Enteral and parenteral

Affordable/sustainable for long time use

61
Q

What are the AEDs?

A

Phenobarbital
Bromide
Levetricetam
Zonisamide

62
Q

What is the most common first-line AED for chronic therapy?

A

Phenobarbital (oral and IV)

63
Q

What is the MOA of phenobarbital?

A

GABA agonist

-> potentiates the inhibitory effects of GABA by binding and prolonging opening of Cl- channels

64
Q

how is phenobarbital metabolized?

A

Liver
POTENT inducer of hepatic microsomal enzymes (cytochrome P450) and metabolized through this system

May develop tolerance due to enzyme induction (monitor levels) and may increase rate of degradation of other drugs using this pathway

65
Q

What are precautions to using phenobarbital ?

A 
PU/PD/PP
Sedation(transient) 
Elevated liver enzymes 
- high ALP-> induced by steroid and phenobarbital 
- high ALT -> liver damage
66
Q

What AED is the least appropriate for a patient with liver damage/dysfunction

A

Phenobarbital

67
Q

What is the MOA of bromide?

A

Alters Cl- transport across neuronal cell membranes

Anticonvulsant -salt/chemical powder

68
Q

Who is bromide use contraindicated in and why?

A

CAT

Asthma like change that can cause acute respiratory distress

69
Q

How is bromide excreted?

A

Unchanged by kideny

70
Q

What is the duration of bromide

A

Long half life (24days)-> 2-3months to reach steady state (shortened if loading dose used)

71
Q

What are precautions to bromide use?

A

Interfere with Cl- on serum chemistry-> reads as false high

Changes in Cl- ion concentration can significantly interfere with bromide levels (increased Cl- causes increased Br excretion in kidney) -> keep salt intake constant

Asthma like change (contraindicated in cats!)

Plasma drug concentration monitoring

72
Q

What can be seen with bromism?

A

Bromism= toxicity with overdose of bromide

Severe sedation and neurological signs
-> treat with 0.9%NaCl to promote excretion

Pancreatitis (range of GI signs)

73
Q

What is the MOA of Levetricetam?

A

We think it binds to synaptic vesicle protein SV2A -> decrease neurotransmitter release

But we dont really know so.. just FYI

74
Q

What is the duration of action of levetricetam ?

A

Very short half life (3-4hrs)

75
Q

How is levetricetam excreted?

A

Unchanged in the urine

76
Q

What is the preferred treatment of seizures due to hepatic encephalopathy ?

A

Levetricetam

77
Q

Is therapeutic blood level monitoring required for levetricetam ?

78
Q

What are the clinical uses of levetricetam ?

A

IV for acute seizure treatment
Oral dose for maintenance therapy
Pulse therapy around breakthrough seizures -> given 3-5days following a breakthrough seizure

Tolerated in cats and doggos

79
Q

What are precautions to using levetricetam ?

A

Sedation/ataxia-> dose dependent (transient with oral therapy)
Inappetence, salivation, lethargy in cats
Caution with decreased renal clearance
Tolerance

80
Q

What is the MOA of Zonisamide

A

Inhibits voltage-gated sodium channels ->stabilize neurons

NOT on GABA receptors

81
Q

Where is zonisamide excreted

A

Urine (80%)

Liver

82
Q

Do you need to monitor therapeutic blood levels of zonisamide?

83
Q

What are the clinical uses of zonisamide?

A

Oral capsule only
Adjunct AED agent (2nd or 3rd line add-on drug) for maintenance therapy

In Cato and doggo

84
Q

What are precautions to using zonisamide ?

A

Well tolerated overall

  • hepatopathy
  • GI signs and somnolence (depression) in cats

Sulfonamides chemical structure

  • idiosyncratic rxn
  • monitor CBC after initiating treatment
85
Q

What drugs do we monitor therapeutic drug levels?

A

Phenobarbital and bromide (kBr)

86
Q

What drug has anticonvulsant effects through inhibition of voltage-gated sodium channels in the CNS

A

Zonisamide

87
Q

What AED has the shortest and longest half life in doggo?

A

Longest- bromide

Shortest- levetiracetam

88
Q

Why is bromide contraindicated for use in cats?

A

Bronchopulmonary changes

RUSVM Pharmacology (18 decks)

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