NeuroPharm Flashcards
what are some adverse drug reactions of KBr
Ataxia sedation Pu/Pd Polyphagia GI signs Pancreatitis
Why should you avoid if you can use of KBr in cats?
it can cause fatal respiratory distress in ~30-50% of cats
what is a big advantage to using KBr vs phenobarbitol
it is not metabolized by the liver
what are some considerations that should be remembered or addressed when a patient is on bromide
- furosemide enhaces excretion of bromide
- saline (fluid therapy enhaces excretion of bromide
- it will increase in dietary salt content
- Br is measured as Cl on a ClinPath panel. you can have alarming chemistry results - your CL may reach 200 mEq/L or more
how does Levetiracetam work?
it will interfere with presynaptic neurotransmitter release
how is levetiracetam eleminated
primarily via the kidneys, there is NO hepatic metabolism
what is the half life of levetiracetam
~4 hours in dog
~ 5-6 hours in cats
Have to administer TID
Why might you use a multimodal drug apporach when considering using KBr?
What drugs would you pair with KBr and why?
KBr has such a long half life it will take ~4 months to reach steady state.
Typically Phenobarbital is chosen initially however levetiracetam is a good choice as well.
Remember that you should max out the use of a drug before considering changing as over time it is possible that the patient may become resistant to it.
you have a patient that has been medically managed on Pheno and started having cluster seizures.
Why might this happen in spite of being on Pheno?
- subtherapeutic concentration of pheno
- refractory epilepsy
- progressive Dz (ie not idiopathic epilepsy
you have a patient that has been medically managed on Pheno and started having cluster seizures.
What would be your plan of attack for this patient?
TDM - through phenobarb level
- if 13 ug/mL you would need to increase dose
- if 35 ug/mL consider adding 2nd drug or reconsider diagnosis
What is the big NO GO number for phenobarb numbers, and why would you not want to exceed this?
DO NOT EXCEED
40 ug/mL
this WILL cause hepatic damage
T or F
It is ok to use Phenobarb if bile acids are elevated
FALSE
This will cause Liver damage!
DON’T DO IT
what is your go to drug/route for acute seizure management?
IV administration of diazepam
Oral should be avoided
- delayed absorption
- possible aspiration
- risk of injury
If IV access is not available for seizure management what is your next best option for administration of diazepam?
if IV access is not an option due to vascular collapse or active seizure,
Rectal is the best option. it is absorbed very quickly and easy to administer.
You can give an injectable dose to owners to have at home in case of emergency and have it given rectally
what is the MOA of diazepam
it enhances GABA activity which is an inhibitory neurotransmitter
what are the 3 main reasons that makes diazepam such a good emergency drug for seizures?
- highly lipid soluble
- fast distribution into CNS
- Short half life
- metabolism by liver
what is a rare but worthwhile adverse reaction in cats to diazepam?
idiosyncratic hepatic necrosis
- rare but fatal
- develops early in course of Tx
what are the 3 primary questions you need to ask to aid in your diagnosis of a seizure
what happened….
- prior to event
- during event (character, length and frequency)
- after event
what are some clinical signs for a behavioral seizure
- flybiting
- flank sucking
- tail biting
what 3 broad categories can a seizure cause be put into
- structural (symptomatic)
- metabolic (reactive)
- idiopathic
what are the top 5 DDX for structural causes of seizures
- Tumor
- Encephalitis
- Vascular event (stroke)
- Trauma
- Hydrocephalus
what are some DDX for metabolic causes of seizures
- toxins (lead, ethylene glycol, chocolate, metaldehyde, illicit drugs)
- liver Dz
- renal Dz
- hypoglycemia
- hypocalcemia
- hyperkalemia
- polycythemia
what is a notable difference between structural and metabolic causes of seizures
structural seizures will have interictal neurological deficits, whereas it is not typically seen in metabolic causes
what are some common clinical signs of idiopathic epilepsy
- onset of first seizure 1-5 years of age
- no interictal neurologic deficits
- diagnosis of rule out of other causes
what are the primary goals for short and long term treatment of seizures
Short term
- to end seizure activity as rapidly and effectively as possible with out causing significant respiratory and cardiac depression
Long term
- to decrease the frequency and severity of seizures
how many half lives does it take to both clear the drug from the body, and reach steady state
5 half lives
what are the 3 main anticonvulsants used in VetMed
- phenobarbital
- bromide
- levetiracetam
what is the MOA of phenobarbital
- acts on GABA gated chloride channels
- increases Cl- permeability
- hyperpolarizes neuronal cell
- inhibits glutamate activity (excitatory NT)
it is also metabolized by the liver (CYP 450)
what is the therapeutic level of phenobarbital that you should NEVER exceed
40 ug/ml
what 3 main systems should you monitor while using phenobarbital
- hepatic
- ALP»_space; ALT
- bile acids (don’t give if elevated)
- bone marrow
- immune mediated neutropenia or thrombocytopenia
- thyroid
- induces metabolism of both T4 and T3
- alters TSH levels
These drugs (__________) that inhibit CYP 450 will ________ the concentration of phenobarbital
- chloramphenicol
- ketaconazole
- cimetidine
will increase
Thyroxine, and theophylline which will induce/inhibit?? CYP 450 will ________ the concentration of phenobarbital
induce
decrease
