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101 Cards in this Set
- Front
- Back
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What are seizures a sign of?
How do you definitively diagnose them? |
forebrain dysfunction
-electroclinical coorelation (brain dysrythmia) |
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What are cluster seizures?
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2 or more seizures occuring within a short time period, usually separated by minutes to hours, but regains consciousness in between ictal events
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What are generalized seizures assoicated with?
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loss of consiousness and bilateral motor manifestations
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Can a partial seizure become generalized?
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yes
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What is the definition of status epilpticus?
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-20-30 minutes of continuous seizure activity (will result in brain damage) SO...
-practically > or equal to 5 minutes |
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What is epilepsy and what are the 3 classifications?
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-chronic, recurrent seizures
1 - idiopathic (primary) -- mainly due to functional neuronal defects 2 - symptomatic (secondary) - due to a primary brain disease 3 - cryptogenic - can't prove there is a brain disease |
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What are the 4 stages to a seizure?
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1 - prodrome
2 - aura - assoicated with EEG abnormalities 3 -ictus 4 - post-ictal period |
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What happens during the tonic and clonic stage of a tonic-clonic seizure?
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tonic - sustained contra ction of all muscles
clonic - rhythmic contraction of muscles resulting in paddling of the limbs and repetitive chewing |
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Neuronal hypersynchrony results from predominance of what?
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excitatory influences on neurons
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What is kindling?
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a focus of epileptogenic neurons recruits neighboring neurons --> enlarges seizure focus
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What is mirror focus?
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a focus of epileptogenic neurons in one hemisphere recruits homologous neurons in the contralateral cortex
-results in partial seizure with secondary generalization |
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What is the most common veterinary neurological disorder?
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epilepsy
-canine = 0.5-5 % of population -feline - 0.5% -genetic predispositions |
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Does a normal interictal EEG exclude seizure disorder?
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no
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What paroxysmal events can mimic seizures?
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1 - syncope
2 - narcolepsy/catalepsy 3 - behavior sterotypy 4 - vestibular signs 5 - sleep movements 6 - pain 7 - myasthenia gravis |
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How do you distinguish a idiopathic epilepsy evet?
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-MRI/CT scan and CSF normal
-no cause of reactive seizures found on history, CBC, biochem, UA -normal interictal exam -may or may not be interictal EEG abnormalites |
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What is the normal signalment in dogs and for idiopathic epilepsy?
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-9 months and 3 years
-familial |
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What types of seizures are seen with idiopathic epilepsy?
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generalized OR partial
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What is the most common epilepsy seen in cats?
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symptomatic (secondary)
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What age does symptomatic epilepsy manifest as?
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any age
usually <6 months or > 6 years |
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What type of seizures are common with reactive seizures?
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partial
+/- secondary generalized |
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Are MRI/CT imaging of brain and CSF normal or abnormal with symptomatic epilepsy?
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abnormal, but normal does not rule it out
-in this case, could be inflammatory (menigoencephalitis), neurodegenerative disease |
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What are the parts of epilepsy treatment philosophy?
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1 - educate
2 - empathize, enable, engage 3 - experimentation 4 - economics |
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When is chronic therapy for seizures recommended?
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1 - patient has history of status epilepticus
2 - patient has 3 or more seizures in 6 weeks 3 - patient has new of previous structural intracranial disease 4 - patient has had ictus > 2 minutes in duration 5 - prior to supratentorial intracranial surgery |
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What is the general mechanism of action of GABA?
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1 - potentiation of GABA post-synaptic inhibition (GABA is the most potent inhibitory NT in the NS)
2 - facilitation of pre-synaptic GABA receptors 3 - reduction in high-frequency neuronal firing via Na channel blockade 4 - modulation of neuronal membrane cation conductance |
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How is modulation of neuronal membrane cation conductance achieved?
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-calcium channel blockage
-antagonism of excitatory neurotransmitters |
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What drugs are used for primary ACD of dogs and cats?
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cats = phenobarb, primidone, bromide, diazepam
dogs = same as above BUT not diazepam |
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What is the MOA of phenobarb - a barbituate?
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GABA receptor mediated post-synaptic neuronal hyperpolarization
-inhibits glutamine-dependent EPSP -reduces Ca channel conductance |
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What is phenobarb metabolized by?
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liver - P450 enzymes
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What happens after long term use of phenobarb?
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metabolic tolerance - need higher doses to maintain same serum concentration
-usually BID dosing is ok, unless severe |
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When is phenobarb steady state achieved?
true biological? |
10-14 days (canine half life is 37-73 hours and feline half life is 34-43 hours) -- you will want to check up at this point
30-90 days |
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How much should you reduce the dose of phenobarb with hepatic insuffiencey?
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25%
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How often should you monitor an animal with phenobarb?
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6 months after steady state is achieved
-CBC, chem, UA, serum PB, bile acids |
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What is the efficacy in dogs of phenobarb?
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effective monotherapy in 60-90%
-montly drug cost in a 30kg dog is $7-15 |
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What are common adverse effects to phenobarb?
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-PU/PD/polyphagia
-transient sedation -subclinical hepatic enzyme elevation -pseudohypothyroidism -paradoxixal hyperexcitability |
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What are uncommon adverse effects to phenobarb?
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-clinical hepatic failure
-dose dependent hepatocutanous syndromw -pancytopenia -dyskinesia |
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What kind of drug is primidone?
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barbituate - so it has the same MOA of phenobarb and same adverse effects
-may be a bit more hepatotoxic |
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What is the drug of choice to control seizures in the face of hepatic disease?
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bromides because excreted via the kidney
KBr or NaBr salts |
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What is the half life of bromide in the dog and cat?
What does this allow for? |
-dog - average 25 days
-cat - average 8 days -LONG -allows for once per day dosing |
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When should you set your appointment for steady state monitoring when using bromide?
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dog - 6-12 weeks
cat - 4-8 weeks |
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Elimination of bromide relys on what?
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dietary chloride content and hydration status
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Is dosing the same with KBr and NaBr?
What form are these available? |
no
liquid or capsule |
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What is bromides efficacy in IE as a monotherapy?
-What is the cost? |
80% in dogs
Cost is similar to phenobar and is more efficacious therefore choice for most clinicians |
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What are common SE with bromide?
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-PU/PD/polyphagia
- nausa/vomiting -transient sedation -ataxia/paresis -derm changes -aggression -pseudohypochloremia |
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What are rare SE of bromides?
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-pancreatitis
-bronchial-asthma syndrome in cats -bromism - reversible with diuresis; risk factor if >2.5 mg/ml in serum, neurotoxic signs |
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What is the MOA of diazepam?
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-GABA receptor mediated post-synaptic neuronal hyperpolarization
-reduces Ca channel conductance |
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Why is diazepam not effective in dogs?
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- poor bioavailability
-pharmocodynamic tolerance common seizure risk with withdrawel |
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How do you dose diazepam in cats?
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to effect - no monitoring needed
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What are adverse effects of diazepam?
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-sedation
polyphagia paradoxical excitement -fatal idiosyncratic necrotizing hepatopathy |
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HOw do you know if ACD is working?
-need to read the seizure diary to determine this |
1 -BEST = prologation of interictal interval
(> 50% is excellent response and < 25 % is only fair; no change or decreases is POOR) 2 - reduction in length of ictus 3 - change in phenotypic severity of ictus |
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What are the 2 reasons for medically refractory epilepsy?
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1 - pharmocoresistant epilepsy - most common
2 - adverse effects of drugs are clinically intolerable |
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What are the 2 general mechanisms of pharmacoresistnace?
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1 - pharmacokinetic (metabolic) tolerance
2 - pharmacohynamic (functional) tolerance |
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What are the mechanisms for pharmacokinetic resistance?
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-impaired drug penetration of BBB - not major in dogs
- hepatic/renal metabolic enzyme induction (mixed function oxidases) common with barbituates, but can be overcome with increased dosage |
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What is the MOA of pharmacodynamic resistnace?
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reduction in pharmacological sensitivity of ion channels or NT receptors that are molecular targets of anticonvulsants
-chronic drug exposure -progressive epileptogenesis -genetic predisposition |
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What is the incidence of true medically refractory epilepsy?
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20-30% of IE cases
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What are common sources for therapeutic failure?
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-DVM origin-->
1 - inadequate therapeutic monitoring 2 - wrong diagnosis 3 - wrong dose 4 - bad communication - Client 1 - compliance |
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When is a second anticonvulsant drug recommended?
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1 - seizures unacceptable despite adequate serum ACD concentration
2 - adverse drug effects intolerable (can first try reducing the dose by 15-20% if seizure control is accepable) |
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80% of dogs that are refractory to PB or BR monotherapy will respond to what?
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PB/BR combination
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50% of dogs on PB will be able to PB dose reduced or discontinued whrn on what drug?
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BR - and vica versa
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What percentage of case are cured with ACD?
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30-40%
-weaning therapy 10% will have spontaneous remission |
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What is negatively associated with survival?
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SE
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When should you attempt to wean ACD?
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-seizure free for 6-12 months
-GRADUAL weaning is crucial |
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How do you wean PB and BR?
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20% dose reduction every 3-4 weeks
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What seizures are considered emergency?
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1- SE
2 - single ictus > 2 minutes 3 - 3 or more seizures in a 24 hour period 4 - failure to regain consciousness within 1 hour of ictus |
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What is the therapy for emergency seizures in a:
-puppy or toy breed with low glucose? |
50% dextrose
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What is the therapy for emergency seizures in a:
-pregnant or lactating bitch with low Ca? |
10% Calcium gluconate
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What is the therapy for emergency seizures in a:
-does not have low Ca or glucose? |
-diazepam IV, IN, or per rectum
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What are the first line drugs for emergent seizures?
Why? |
benzodiaepens
-rapid entry into CNS (minutes) -parental administration via non-IV routes possible - short-acting -minimal CV depression -available and inexpensive |
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What should be the CRI duration of diazepam, propofol or ketamine?
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at least 4 hours
-then wean dose/rate 25% every hour until off as long as seizure free |
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What re SE to SE?
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1 - hyperthermia induced change (DIC, SIRS/MODS
2 - progressive and irreversible brain damage and intracranial hypertension (non-cardiogenic pulmonary edema, brain-heart syndrome, cushings reflex) |
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How do you treat intracranial hypertension?
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-maintain MaBP
-O2 mannitol -furosemide (also for non-cardiogenic pulmonary edema) |
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What are treatments at home for ermgent seizures?
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rectal diazepam/intranasal
-manual vagal manuvers such as ocular compression or carotid massage |
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What are two methods for administering chronic ACD?
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continual maintenance
pulse therapy |
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What drugs can be used at home for pulse therapy of emergent seizures?
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1 - clonazepam
2 - chlorazepate -both converted to nordiazepam |
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What can be implanted to help with treating seizures?
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electrical generator for vagal stimulation
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What surgical procedures can be done for seizures?
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- cortical resection
- corpus callosotomy -hemispherectomy - children only |
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What diets can help with seizures?
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-ketogenic diet - not effective (pancreatitis)
-hypoallergenic |
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What are advantages of felbamate?
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-non-sedating drug
-don't need to monitor -ischemic neuroprotection -more economic than ZNS or LEV |
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What are indications for using felbamate as a monotherapy?
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-symptomatic epilepsy with altered consciousness or from cerebrovascular disease
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When is felbamate used as an add-on drug?
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-partial seizure manifestation - atonic seizures
- large of giant breed dogs |
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What are SE with felbamate?
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- GI - anorexia, vomiting, diarrhea
-decreased hepatic metabolism of PB -aplastic anemia/myelosuppression (reversible) -hepatotoxicity -generalized tremors -KCS |
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What is the half life of gabapentin?
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3-4 hours
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What are the advantages with gabapentin?
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wide MOS
-no therapeutic monitoring -more economic than ZNS or LEV |
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What is gabapentin efficacious for treating other than seizures?
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-neuropathic pain
-movement disorders |
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What are SE to gabapentin?
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-sedation
-ataxia -hepatotoxicity -polyphagia with weight gain -efficancy? |
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How often do you have to dose gabapentin in responders?
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q 6 hours
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What is the half life of levetiracetam?
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4 hours
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Is there hepatic metabolism with levetiracetam?
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no
-wide MOS |
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Do you need to therapeutically monitor with Levetiracetam?
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no
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What are levetiracetam's neuroprotective properties especially good for?
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seizure induced brain injury
antikindling effect on progressive epileptogenesis |
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How is levetiracetam good as a emerceny seizure treatment?
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-parenteral formaulation is available
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What are indications for use of levetiracetam?
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-heaptic dysfunction
-prolonged ictus recurrent SE -severe cluster seizures -epileptic cats -refractory epileptic with severe BR or PB adverse effects |
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What are adverse SE with levetiracetam?
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-RARE
-sedation GI (ptyalism, vomiting) ataxia |
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What is the half life of zonisamide?
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15 hours
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How is zonisamide metabolised?
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in liver
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When is zonisamide indicated?
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-add ons for all types of pharmacoresistant seizures
-monotherapy for when PB or BR should be avoided or small breeds |
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Can zonisamide be used in cats?
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yes
-has a high MOS |
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How is zonisamide dosed?
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BID
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When should you monitor with zonisamide?
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-7-14 days after dose change
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What are some of the adverse effects of zonisamide related to?
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sulfonamides
-interference with thyroid -KCS |
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Is therapeutic monitoring needed when treating with zonisamide?
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yes
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What are 2 main disadvantatges with zonisamide?
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1 - more expensive
2 - transient, clinical adverse effects more common such as vomiitng, ataxia and sedation |
