Brainscape's Knowledge GenomeTM

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


See full index

Neurology (inpt) > seizures > Flashcards

seizures Flashcards

1
Q

seizure

A

cortical events characterized by excessive or hypersynchonrnous discharge by cortical neruons

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

what are idiopathic sz?

A

usually begin bw 5-10 yrs old and have no specific cause

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

what are secondary sz?

A

may result from congenital abnormalities or pernatal injury, metabolic disorders, trauma, tumors, vascular dz, infex dz, or degenerative dz

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

generalized sz

A

sudden loss of consciousness; invovles both cerebral hemispheres w/ an alteration of consciousness

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

convulsive generalized

A

grand mal or tonic clonic; associated w. a postictal obtundation and confusion lasting for mins to hours

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

nonconvulsive generalized

A

absence; associated w/ only minor motor activity, such as blinking

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

absence is also called…

A

petit mal!

it begins in childhood, are often familial, and typically subside before adulthood

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

what are signs and sx of an absence sz?

A

brief, often unnoticable episodes of imparied consciouness, lasting only seconds and occuring up to hundreds of time sper day

**think staring spells

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

work up of an absence?

A

EEG

**3 per second generalized spike and wave tracing

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

how do you tx an absence sz?

A

ethosuximide is first line. valproic acid or zonisamide may be used

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

tonic clonic?

A

aka GRAND MAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

signs and sx of tonic clonic

A

begin suddenly w/ loss of consciousness and tonic extension of the back and extremities, continuing w/ 1-2 mins of repetitive, symmetric clonic movements

** classic sz incontinence and tongue biting

**pt may also appear cyanotic druing the ictal owing to poor respiratory fxn during sz

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

tx of grand-mal

A

emergent tx w/ benzo to abort thesz

-give antiepiliptics for seconary prevention-phenytoin, phenobarbital, valproate, lamotrigine, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

partial sz

A

simple or complex

arise from discrete region of 1 cerebral hemisphere

simple partial sz are NOT accompanied by an impariment of consciousness- may be an isolated tonic or clonic activity of a limb or transient altered 8

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

pediatric partial sz tx?

A

treat with phenobarbital

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

how do you tx intractable temporal lobe sz?

A

surgical options include anteriro temporal lobectomy or vagal nerve

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

Postictal?

A

Todd’s paralysis= wkness or paralysis that is often unilatral and resolves over 24 hrs

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

status epilepticus

A

can be convulsive or nonconvulsinve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is SE dx?

A

sz fail to cease spontaneously or recur so frequently that full consciousness is not restored between successive episodes

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

what are complications o SE?

A

possibility of permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage

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

how to tx SE?

A

Immediate management -ensure patent airway, including positioning the patient to prevent aspiration of stomach contents-Management of hyperthermia, related to increased motor activity and high levels of circulating catecholamines, may include a cooling blanket or induction of motor paralysis with a neuromuscular blocking agent-Diazepam or lorazepam is administered IV until the seizure stops; a loading dose of phenytoin or fosphenytoin is also given

22
Q

EEG findings in partial sz?

A

focal rhythmic discharge; but sometimes, no ictal activity will be seen

23
Q

EEG in complex partial?

A

interictal spikes or spikes associated w/ slow waves in the temporal or frontotemporal are

24
Q

what will EEG of epileptic sz show>

A

epileptiform

25
Q

what happens to the serum prolactin levels?

A

usually incrased after tru tonic-clonic zx, but are unaffected by psuedosz

26
Q

sz vs syncope (onset)

A

sz: sudden onset +/- preceding aura, focal sensory or motor phenomena, sensation of fear, smell, memor
syncope: progressive lightheadedness, diming of vision, faintness

27
Q

sz vs syncope course

A

sz: sudden loss of consciousness w/ tonic-clonic activity; tongue laceration, head trauma, bowel/urninary incontinence
syncope: gradual loss of consciousness limp or w/ jerking, rarely lasts > 14 sec

28
Q

sz vs syncope post spell

A

sz: postictal confusion and disorentation
syncope: typically immedicate return to lucidity

29
Q

tx for generalized convulsive, simple partial complex parital sx

A

carbamazepine, phenytoin, valproic acids, topiramates, lamotrigine, oxcarbazepine, levetiracetam, zonisamide

30
Q

potientialy side effects of felbamate?

A

aplastic anemia, hepatic failure

31
Q

tx for generallized nonconvulsive (absence) sz

A

valproic acid or ethosuximide

32
Q

Epilepsy

A

Disorder of the brain characterized by an enduring predisposition to generate epileptic seizures, and by the neurobiologic, cognitive, psychological, and social consequences of this condition

2 unprovoked sz occuring > 24 hrs apart

33
Q

what is a simple partial sz?

A

focal motor, no imparied cognition

34
Q

what is a complex partial?

A

dyscognitive focal seizure= impaired response

35
Q

what are all the types of generalized seizures?

A 
Absence
Tonic-clonic
Tonic
Clonic 
Myoclonic
Atonic (drop attack
36
Q

aura?

A

simple partial sz

Symptoms correspond to the area of brain affected by the abnormal electrical activity. Most commonly seen with complex partial seizures

37
Q

what is ictus?

A

what is seen/felt during abnormal lecctricl activity

38
Q

what is postictal?

A

what is seen/ felt until the brain recovers to baseline

-some pts don’t have one, others can e sleepy, confused, or have impaired awarness

39
Q

Todd’s paralysis

A

. Some patients who have seizures involving the motor strip may experience a paralysis of the arm or leg until that part of the brain recovers;

40
Q

when can you stop AEDs?

A 
Seizure free for 2 – 4 years
Depends on seizure type
Complete control within one year of onset
Onset btw ages 2 and 35
Normal neuro exam
Normal EEG
Withdraw slowly over at least 6 months
Relapse 25% after 1 yr, 29% after 2 years
41
Q

what is the Pathophys of a sz?

A

occurs when the message delivery systme becomes unbalanced

-normally, GABA keeps the system by triggering signals in the form of charged particles: causes large conentration of Cl ions to enter recieving neruon = stop message

when there isnt enough GABA, a sz can occur bc receiving neruons can be flooded with signals that say pass on message

-“go” messages are triggered by a diff type of Neurotransmitter that are postitive (sodium particles enter neuron)

42
Q

what are drugs that can inhivit the high frequency firing?

A

Carbamazepine, lamotrigine,phenytoin, andvalproic acid

43
Q

what is the brains major excitator NT?

A

glutamate

44
Q

what are the two groups of glutamate receptors?

A

1) Ionotropic—fast synaptic transmission
Three subtypes – AMPA, kainate, NMDA
Glutamate-gated cation channels
2) Metabotropic—slow synaptic transmission
G-protein coupled, regulation of second messengers (cAMP and phospholipase C)
Modulation of synaptic activity

45
Q

what is the mjor inhibitory NT?

A

GABA

46
Q

what are the 2 types of GABA receptors?

A

GABAA—post-synaptic, specific recognition sites, linked to CI- channel
GABAB —presynaptic autoreceptors that reduce transmitter release by decreasing calcium influx, postsynaptic coupled to G-proteins to increase K+ current

47
Q

what are the cellular mechanisms of seizure generation?

A 
Excitation (too much go) 
Ionic: inward Na+ and Ca++ currents
Neurotransmitter: glutamate, aspartate
Inhibition (too little stop)
Ionic: inward CI-, outward K+ currents
Neurotransmitter: GABA
48
Q

what is an ADR commont to all aeds?

A

suicidality

49
Q

what are some examples of blockers of reptitive activation of sodium channels?

A

phenytoin, carbamazepine, oxcarbazepine, valproate, felbamate, lamotrigine, topiramate, zonisamide, rufinamide , lacosamide

50
Q

carbamazepine is first line for what type of sz?

A

focal

*calso used for generalized tonic-clonic, mixed, pain control in trigeminal nerualgai

51
Q

what is carbamazepine CI in?

A

h/o bone marrow depression (risk of agranulocytosis, aplastic anemia)

MAOIs

HLA-B 1502

52
Q

majore ADR of carbamazepine?

A

-neruogocnitive (Drowsiness, diplopia, HA, ataxia, dizziness)
-GI
-leukopenis
hypona
rash
hepatitis, pancreatitis, aplastic anemai

PCD

Neurology (inpt) (10 decks)

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