Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VET 433: Neurology > Seizures > Flashcards

Seizures Flashcards

1
Q

pyramidal neurons

A

excitatory neurons in the cerebral cortex

input comes from other neurons to stimulate or inhibit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

feedforward inhibition

A

neurons send excitatory signals to inhibitory neurons that block the pyramidal neurons

overall INHIBITORY effect on pyramidal neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

feedback inhibition

A

the effect of pyramidal neuron stimulation causes feedback inhibition on the same pyramidal neuron

overall INHIBITORY effect on pyramidal neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

EPSPs (excitatory synaptic potentials)

A

signals generated by surrounding cortical input

EPSPs converge to initiate an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

glutamate

A

main EXCITATORY neurotransmitter

fast transmission via ionotropic receptors (Na and Ca ion channels)

slow transmission via metabotropic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GABA

A

major INHIBITORY neuron

GABAa receptors: allows Cl- influx on the post-synaptic membrane

GABAb: mediated by K+ current; located on pre-synaptic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

epileptogenesis

A

the process by which a normal brain develops into an epileptic brain

due to genetic abnormalities or acute brain injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

intrinsic properties of seizure pathogenesis

A

focal zone of hyperexcitable neurons caused by a mutation in ion channels, receptors, second messengers, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

extrinsic properties of seizure pathogenesis

A

changes in extracellular ion concentration, modulation of glial cell function, transmitter metabolism/uptake, invasion of inflammatory cells, network changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

focal epileptic seizures

A

abnormal electrical activity arises in a localized group of neurons

only ONE cortical region is firing abnormally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

signs of focal epileptic seizures

A

ictal onset is consistent (signs stay the same in each seizure)

lateralized signs

  • motor: facial twitches, repeated jerking head movements, rhythmic blinking, repeated rhythmic jerks of one extremity
  • autonomic: dilated pupils, hypersalivation, vomiting
  • behavioral: anxiousness, restlessness, abnormal attention seeking, fear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

generalized epileptic seizures

A

abnormal electrical activity arises in bilateral hemispheres

MULTIPLE cortical regions are firing abnormally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

signs of generalized epileptic seizures

A

tonic, clonic, or tonic-clonic seizures

  • motor: bilateral
  • autonomic: hypersalivation, urination, defecation
  • behavioral: loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

myoclonus

A

sudden, brief, involuntary single or multiple contractions of muscle or muscle group of various locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

atonic

A

sudden loss or diminution of muscle tone without preceding myoclonic or tonic event

involves head, trunk, jaw, or limb musculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

automatism

A

a coordinated, repetitive motor activity

usually occurs when cognition is impaired and subject is amnesic afterwards
(resembles involuntary movement)

orofacial: lip. smacking/pursing, chewing, licking, swallowing

pedal: running movements in distal limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

focal to generalized epileptic seizures

A

abnormal activity arises in bilateral cerebral hemispheres

characterized by tonic, clonic, or tonic-clonic seizures (same as generalized)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the stages of seizures

A
  1. prodrome
  2. ictus
  3. post-ictus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

prodrome

A

changes in behavior (anxiety, withdrawal, vocalization)

not always apparent
lasts minutes to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ictus

A

rapid onset of tonic-clonic phases; can begin focally (facial twitches)

tonic: increased muscle tone/extension, loss of consciousness, pupils dilated
clonic: contraction and relaxation, jaw movements, autonomic signs

HIGH energy expenditure phase

lasts seconds to minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

post-ictus

A

disorientation, aggression, or restlessness following ictus

may be transiently blind or deaf
lasts hours to days

can take up to 2-3 days to become back to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

idiopathic epilepsy signalment

A

likely a genetic basis

breeds: spaniels, aussies, rotties, border collies, GSDs, dachshunds

age: 1-5 years (dogs), variable in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

idiopathic epilepsy history

A

seizure episodes reported by owner

may have a NORMAL interictal neurologic exam
- if seizure was a few days ago - should be neuro normal
- if seizure was within 2-3 days - may still be in post-ictus and have deficits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

structural epilepsy

A

epileptic seizures provoked by intracranial/cerebral pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

structural epilepsy signalment and history

A

age: <1 to >5 years (dogs), variable in cats

history: seizures, mentation changes, altered behavior, loss of learned responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

structural epilepsy presentation

A

normal neurological exam
- if abnormal - indicates signs of cerebral disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

syncope

A

NOT A SEIZURE
can mimic an epileptic event

caused by CV abnormalities
does not usually have tonic-clonic contractions

appears as falling to the ground and going limp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

characteristics of seizures

A
  1. abrupt onset and spontaneous cessation
  2. cannot be interrupted
  3. tonic-clonic movement
  4. altered mentation
  5. autonomic signs - salivation, urination, defecation, mydriasis
  6. post ictal obtundation
  7. present of intracranial/cerebral pathology
29
Q

what is the definitive diagnostic for seizures

A

electroencephalogram (EEG)

must be reading during the time of the abnormal brain activity - can do sedated or ambulatory

30
Q

indications for using EEG

A
  • age of epileptic seizure <6 months or >6 years
  • interictal neurologic abnormalities
  • status epilepticus or cluster seizures
  • idiopathic epilepsy not responding to medical management
31
Q

AED therapy indications

A
  1. identifiable structural lesions OR prior history of encephalopathy or trauma
  2. acute, repetitive seizures
    - >or= 3 generalized seizures in 24 hours
    - status epilepticus
  3. > or= 2 seizures in 6 months
  4. prolonged, severe, or unusual post-ictal periods
32
Q

what is the goal of AED therapy

A

reduce the frequency and severity of seizures

want to have a >50% reduction

33
Q

what drugs are AEDs

A
  1. potassium bromide
  2. levetiracetam (keppra)
  3. phenobarbital
  4. zonisamide
34
Q

phenobarbital MOA

A

increases neuron responsivity to GABA by activating GABAa channels

has an anti-glutamate effect by inhibiting Ca channels

35
Q

how is phenobarbital metabolized

A

hepatic - induces CYP450 and ALP

normal to see high ALP on serum chemistries

36
Q

time to reach steady state of phenobarbital

A

takes 10-14 days to reach steady state

37
Q

phenobarbital dosages

A

dogs: 3-5 mg/kg BID
cats: 1-2 mg/kg BID

38
Q

adverse effects of phenobarbital

A

PU, PD, PP
sedation
ataxia
weight gain
elevated ALP
pseudohypothyroid

39
Q

contraindications for phenobarbital

A

liver disease
concurrent CYP450 inhibiting drugs

40
Q

MOA of KBr

A

Br ion acts like a Cl ion and passes through Cl channels on post-synaptic GABAa receptors to hyperpolarize the membrane

41
Q

how is KBr metabolized

A

renal

42
Q

how long does it take KBr to reach steady state

A

very long - takes 3-4 months

43
Q

dosage for KBr

A

20-35 mg/kg SID

44
Q

adverse effects of KBr

A

PU, PD, PP
sedation
ataxia
weight gain
GI upset
hyperreactivity
bromism

45
Q

contraindications for KBr

A

NOT for use in cats
renal disease
pancreatitis
dogs that require rapid control of seizures

46
Q

zonisamide MOA

A

sulfonamide derivative

blocks Ca and Na channels on pre-synaptic side to reduce the amount of glutamate released into the synaptic cleft

also binds Cl channels on GABAa receptors

47
Q

how long does it take zonisamide to reach steady state

A

5-7 days

48
Q

dosage for zonisamide

A

dogs: 5 mg/kg BID

if concurrent phenobarbital: 10 mg/kg due to CYP450 induction

49
Q

adverse effects of zonisamide

A

sedation, ataxia, GI upset, KCS, polyarthropathy, decreased T4

50
Q

contraindications for zonisamide

A

pre-existing KCS

51
Q

keppra MOA

A

binds synaptic vesicular protein that carries glutamate in order to prevent it from binding to pre-synaptic membrane for release

52
Q

metabolism of Keppra

A

minimal hepatic metabolism
mostly excreted in urine

53
Q

time to reach steady state for Keppra

A

fast - reaches within 24 hours

54
Q

dosage for keppra

A

20 mg/kg QID

55
Q

adverse effects of keppra

A

well tolerated, very few adverse effects

56
Q

efficacy of keppra

A

poor when given alone
exception: feline audiogenic reflex seizures

57
Q

status epilepticus

A

ictus lasting > 5 minutes
OR
>2 minutes without regaining consciousness

requires IMMEDIATE intervention (causes primary brain injury –> neuronal cell death)

58
Q

phase 1 SE

A

compensated SE
increase in autonomic activity –> elevated catecholamines + steroids –> hypertension, tachycardia, hyperglycemia, hyperthermia, ptylatism

causes arrhythmias, poor renal perfusion, rhabdomyolysis

59
Q

phase 2 SE

A

uncompensated SE

~30 minutes following continuous ictus –> cerebrovascular autoregulation fails
- causes increased ICP –> hypotension, hypoglycemia, hypoxia –> resp. failure, metabolic acidosis, hyponatremia, hyperkalemia

RISK OF SUDDEN DEATH

60
Q

cluster seizures

A

> or = 3 generalized seizures in 24 hours

61
Q

when is it considered failure to regain consciousness

A

still unconscious 1-2 hours after ictus

62
Q

goal of emergency seizure management

A

terminate and prevent future seizure activity, manage complications and underlying conditions causing the seizures

63
Q

steps of emergency seizure management

A
  1. benzodiazepienes
  2. stabilize SE
  3. long acting AEDs
  4. diagnostics
  5. monitoring
64
Q

benzodiazepiene administration

A

midazolam: 0.2-0.5 mg/kg IV or IN

diazepam: 0.5 mg/kg IV or 1-2 mg/kg per rectum

65
Q

steps for stabilizing SE

A
  • IV access
  • obtain BW: lytes, glucose, calcium
  • flow by O2
  • BP (manage high ICP)
  • temperature (manage hyperthermia)

if seizures do not stop after benzo administration –> repeat dose

66
Q

when do you use long acting AEDs

A

once the benzodiazepienes have stopped the seizures

67
Q

what AEDs are used in emergency situations

A

phenobarbital - takes longer to reach steady state; high risk of doing loading dose

levetiracetam (keppra)

68
Q

monitoring after emergency seizure management

A

24 hr monitoring q4
monitor pupil size and reactivity, posture, EEG
general: temp, hydration, oxygenation, ventilation, HR, BP, recumbent care, bladder management

69
Q

what are negative prognostic indicators for seizures

A

inflammatory brain disease
loss of seizure control after 6 hr hospitalization
development of partial SE

VET 433: Neurology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions