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ana 410G > exam2 > Flashcards

exam2 Flashcards

1
Q

describe the 2 phases in a generalized motor onset seizure

A
  • tonic-clonic: bilateral stiffening and jerking (1-3min)
  • post ictal (min to hrs) : lethargic, deep/slow breaths
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2
Q

describe the symptoms of a non-motor generalized onset seizure

A
  • absence phase (s): behavioral arrest
  • no post ictal phase
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3
Q

which type of generalized onset seizure is most often occuring in children?

A

non-motor/absent seizures

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4
Q

what are the 2 types of focal onset seizures?

A
  • aware/motor
  • unaware/non motor
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5
Q

a focal motor onset seizure….
- occurs in?
- symptoms ?
- post ictal phase
- duration

A
  • frontal lobe
  • unilateral arm/face/leg jerking activity and stiffened posture
  • none
  • 45s to 4min
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6
Q

which type of seizure is associated with the jacksonian march

A

focal motor

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7
Q

a focal non-motor onset seizure….
- occurs in?
- symptoms ?
- post ictal phase
- duration

A
  • temporal lobe
  • aura/automatism/non-purposeful movements
  • confusion and amnesia to event
  • 45s to 4min
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8
Q

why is it hard to diagnose a seizure correctly if its onset is unilateral but spreads bilaterally

A

symptoms will mimic a generalized onset seizure and potentially be misdiagnosed

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9
Q

what are the three main childhood epilepsy syndromes? at what ages do they typically occur?

A

infancy - west syndrome
infancy/early childhood - dravet syndrome
childhood - lennox gastaut syndrome

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10
Q

list some key concepts about lennox gastaut syndrome

A
  • can be many seizure types
  • cognitive impairment occurs
  • slow spikes on EEG signify presence of syndrome
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11
Q

list some key concepts about dravet syndrome

A
  • Na+ channel mutation
  • cardiac morbidities
  • worsens with fever
  • can be many seizure types
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12
Q

lennox gastaut and dravet syndromes are associated in what way?

A

they are both ineffective with most medicine, but have similar symptoms that can be improved with CBD

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13
Q

name the seizure type that is typically resolved by early adolescence and describe some key features

A

childhood absence seizures
- normal neurodevelopment
- treated with Ethosuximide
- 5-7yrs old
- generalized non motor seizures
- 3Hz spike on EEG is present

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14
Q

name the seizure type that is typically resolved by mid teenage years and describe some key features

A

Rolandic Epilepsy (centrotemporal)
- 7-8yrs old
- nocturnal, focal hemi-clonic seizures
- treatment is a risk benefit discussion

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15
Q

Juvenile Myoclonic Epilepsy symptoms include?

A
  • tonic clonic phase
  • occasional absence seizures
  • photsensitivity
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16
Q

Juvenile Myoclonic Epilepsy is triggered by and describe the medication.

A

triggered by:
- sleep deprivation
- alcohol

medications are effective but life long

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17
Q

febrile seizures can be ___1.___ if theyre less than 15 minutes long or ___2.____ if they are longer than 15 minutes. This peaks at __3.____. Treatments are typically __4._____. Children who have febrile seizures have a ____5.____ % chance of developing epilepsy if they have ___6.___ seizures.

A
  1. simple non-focal
  2. complex focal
  3. 18 months
  4. supported
  5. 2-5
  6. complex
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18
Q

Which childhood epilepsy syndromes do not resolve as children get older

A

lennox gastaut, dravet, west

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19
Q

west syndrome is a type of childhood epilepsy syndrome that can be described by

A
  • infantile spasms
  • developmental aggression
  • hypsarrhythmia (extreme disorganization)
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20
Q

seizures fall into which two categories

A

provoked and unprovoked

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20
Q

which type of seizure (provoked/unprovoked) are more likely to recur

A

unprovoked

20
Q

describe a provoked seizure

A
  • acute symptoms
  • less than 7 days between
  • caused by stroke, infection, TBI
21
Q

describe an unprovoked seizure

A
  • remote symptoms
  • more than 7 days between
  • caused by random events or tumors
22
Q

if someone has 2 unprovoked seizures, their chances of recurring are up to _____%

A

60

23
Q

what are the 4 etiologies of seizures?

A
  • metabolics
  • substances
  • structural insults
  • genetics
24
Q

genetic factors are involved in about how many seizure cases?

A

2/3

25
Q

Whole exome sequencing is helpful….

A

for precision medicine

26
Q

describe seizure progression

A

Aura, ictal, post ictal, interictal, repeat

27
Q

describe the DSM-5 criteria for diagnosing someone with schizophrenia

A
  1. must experience at least two - delusions, hallucinations, disorganized speech, catatonic behavior, negative symptoms
  2. decrease in level of function
  3. continuous signs of disturbance for more than 6 months
  4. ruled out schizoaffective and mood disorders
  5. not caused by substances or other medical conditions
  6. diagnosis only if prominent delusions or hallucinations are present in patients with autism
28
Q

what percent of people are diagnosed with schizophrenia?

A

1%

29
Q

what 4 pathways play a role in schizophrenia - describe each

A
  1. mesolimbic - behavior regulation + cause delusions/hallucinations when overactive
  2. nigrostriatal - controls movement, EPS when dopamine is blocked
  3. mesocortical - executive fxn, - symptoms when dopamine is blocked
  4. tuberoinfundibular - regulates prolactin release, increases w/dopamine blocked and is where side effects originate from treatments
30
Q

what are some generalized side effects from schizophrenia treatments and which drug groups treat them

A
  1. parkinsonism - tremor - treated w/anticholinergic meds
  2. acute dystonia - involuntary spasm - treated w/ intramuscular benztropine
  3. akathisia - restlessness - treated w/hydrophobic b-blockers
31
Q

the dopamine hypothesis suggests

A
  1. dopamine mimetics worsen symptoms (cocaine)
  2. dopamine receptor antagonists improve symptoms
  3. schizophrenia is caused by overabundance of dopamine
32
Q

what are some key receptors involved in schizophrenia and what generally do each do

A

D2, D3, D4 - inhibitory
D1, D5 - stimulatory

33
Q

describe how epilepsy differs in women

A

estrogen is a proconvulsant and progesterone is an anticonvulsant so medications need to be monitored and adjusted

34
Q

describe how epilepsy differs in eldery

A
  • mostly focal and staticus seizures with prolonged post-ictal phases
  • 1.7 year average time from symptom onset to diagnosis due to misinterpretation of symptoms in elderly
35
Q

what are some treatment challenges with elderly epilepsy

A
  • removing or adding inhibitory/inducing medications impacts everything
  • medicine interactions and efficacy in elderly are impacted
36
Q

what are some of the genes susceptible to mutation in schizophrenia

A

DISC1, dysbindin, neureglin

37
Q

what are the big ideas behind glutamate drug treatments for schizophrenia

A

they looked promising in clincal phases early, but the most promising even failed in phase 3

38
Q

describe a general overview of the progression of treatment for schizophrenia

A
  • 1900-1950s frontal lobotomy and ECT were main treatments
  • in the 1950s chlorpromazine was the first drug to be productive at treatments
  • in 1960s typical antipsychotic drugs were developed but had bad side effected
  • in the 1990s atypical antipsychotic drugs were developed but some side effects prolonged after usaged
  • 2000s developed next gen atypical antipsychotics that are used today
39
Q

typical antipsychotics
- which receptors
- induce what side effects
- example
- relationship with dopaminergic neurons

A

-D2
- induced EPS and tardive dyskinesia - elevate serum prolactin
- haloperidol
- induce depolarization blockade of S.Nigra and VTA dop neurons

40
Q

atypical antipsychotics
- which receptors
- induce what side effects
- example
- relationship with dopaminergic neurons

A
  • 5HT2A/D2
  • no EPS or tardive dyskinesia or serum elevation - longer lasting than typical
  • clozapine
  • induce depolarizations blockade of VTA dop neurons
41
Q

what does the glutamatergic deficiency tell us about schizophrenia

A

the decrease in dendritic spines, increase in glutamatergic tone leading to cell death, and decreased inhibition of GABA causing excessive stimulation could be the closest thing to pathology for schizophrenia

42
Q

key differences because epilepsy and orthostatic hypertension

A

OH- triggered by position changes, quick recovery, negative motor and brief myoclonus, light headed vague aura and orthostatic vital signs, low volume status and autonomic dysfunction history

43
Q

key differences because epilepsy and transient ischemic attack

A

TIA- lasts min to days, negative motor and sensory, no aura, vascular risk factors

44
Q

key differences because epilepsy and PNES

A

PNES- anxiety or stress inducing, last 5-30min, headache following, forced eye closure, prior history of trauma or psychiatric disease

45
Q

key differences because epilepsy and migraines

A

M - triggered by food or smells, last hours to days, aura followed by headache, family history of migraines

46
Q

key differences because epilepsy and vasovagal syncope

A

VS- triggered by needles, negative motor symptoms and myoclonus for a few seconds, vague aura of light headedness and palpitations, no neurological risk factors

47
Q

key differences because epilepsy and cardiac arrhythmia

A

CA- negative motor symptoms, family history of cardiac syndromes, last seconds to minutes and similar recovery time

48
Q
A

ana 410G (10 decks)

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