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Veterinary Clinical Pharmacology > NeuroPharm > Flashcards

NeuroPharm Flashcards

1
Q

what are some adverse drug reactions of KBr

A 
Ataxia
sedation
Pu/Pd
Polyphagia
GI signs
Pancreatitis
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2
Q

Why should you avoid if you can use of KBr in cats?

A

it can cause fatal respiratory distress in ~30-50% of cats

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3
Q

what is a big advantage to using KBr vs phenobarbitol

A

it is not metabolized by the liver

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4
Q

what are some considerations that should be remembered or addressed when a patient is on bromide

A
  • 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
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5
Q

how does Levetiracetam work?

A

it will interfere with presynaptic neurotransmitter release

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6
Q

how is levetiracetam eleminated

A

primarily via the kidneys, there is NO hepatic metabolism

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7
Q

what is the half life of levetiracetam

A

~4 hours in dog
~ 5-6 hours in cats

Have to administer TID

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8
Q

Why might you use a multimodal drug apporach when considering using KBr?

What drugs would you pair with KBr and why?

A

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.

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9
Q

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?

A
  • subtherapeutic concentration of pheno
  • refractory epilepsy
  • progressive Dz (ie not idiopathic epilepsy
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10
Q

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?

A

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
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11
Q

What is the big NO GO number for phenobarb numbers, and why would you not want to exceed this?

A

DO NOT EXCEED
40 ug/mL

this WILL cause hepatic damage

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12
Q

T or F

It is ok to use Phenobarb if bile acids are elevated

A

FALSE

This will cause Liver damage!

DON’T DO IT

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13
Q

what is your go to drug/route for acute seizure management?

A

IV administration of diazepam

Oral should be avoided

  • delayed absorption
  • possible aspiration
  • risk of injury
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14
Q

If IV access is not available for seizure management what is your next best option for administration of diazepam?

A

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

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15
Q

what is the MOA of diazepam

A

it enhances GABA activity which is an inhibitory neurotransmitter

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16
Q

what are the 3 main reasons that makes diazepam such a good emergency drug for seizures?

A
  • highly lipid soluble
    • fast distribution into CNS
  • Short half life
  • metabolism by liver
17
Q

what is a rare but worthwhile adverse reaction in cats to diazepam?

A

idiosyncratic hepatic necrosis

  • rare but fatal
  • develops early in course of Tx
18
Q

what are the 3 primary questions you need to ask to aid in your diagnosis of a seizure

A

what happened….

  • prior to event
  • during event (character, length and frequency)
  • after event
19
Q

what are some clinical signs for a behavioral seizure

A
  • flybiting
  • flank sucking
  • tail biting
20
Q

what 3 broad categories can a seizure cause be put into

A
  • structural (symptomatic)
  • metabolic (reactive)
  • idiopathic
21
Q

what are the top 5 DDX for structural causes of seizures

A
  • Tumor
  • Encephalitis
  • Vascular event (stroke)
  • Trauma
  • Hydrocephalus
22
Q

what are some DDX for metabolic causes of seizures

A
  • toxins (lead, ethylene glycol, chocolate, metaldehyde, illicit drugs)
  • liver Dz
  • renal Dz
  • hypoglycemia
  • hypocalcemia
  • hyperkalemia
  • polycythemia
23
Q

what is a notable difference between structural and metabolic causes of seizures

A

structural seizures will have interictal neurological deficits, whereas it is not typically seen in metabolic causes

24
Q

what are some common clinical signs of idiopathic epilepsy

A
  • onset of first seizure 1-5 years of age
  • no interictal neurologic deficits
  • diagnosis of rule out of other causes
25
Q

what are the primary goals for short and long term treatment of seizures

A

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

26
Q

how many half lives does it take to both clear the drug from the body, and reach steady state

A

5 half lives

27
Q

what are the 3 main anticonvulsants used in VetMed

A
  • phenobarbital
  • bromide
  • levetiracetam
28
Q

what is the MOA of phenobarbital

A
  • 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)

29
Q

what is the therapeutic level of phenobarbital that you should NEVER exceed

A

40 ug/ml

30
Q

what 3 main systems should you monitor while using phenobarbital

A
  • hepatic
    • ALP&raquo_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
31
Q

These drugs (__________) that inhibit CYP 450 will ________ the concentration of phenobarbital

A
  • chloramphenicol
  • ketaconazole
  • cimetidine

will increase

32
Q

Thyroxine, and theophylline which will induce/inhibit?? CYP 450 will ________ the concentration of phenobarbital

A

induce

decrease

Veterinary Clinical Pharmacology (6 decks)

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