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joeli unit 3 > seizures and LOC > Flashcards

seizures and LOC Flashcards

1
Q

Activation of NMDA receptors leads to influx of

A

Na+ and Ca2+

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2
Q

Activation of Kainate and AMPA receptors leads to influx of

A

Na+
Variable Ca2+

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3
Q

Activation of NMDA, Kainate, and AMPA receptors leads to efflux of

A

`K+

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4
Q

postsynaptic kainate receptor allows for

A

excitation

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5
Q

presynaptic kainate receptor allows for

A

inhibition by inhibiting the release of GABA

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6
Q

IPSP for GABA-A receptor

A

-70 mV

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7
Q

IPSP for GABA-B receptor

A

-100 mV

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8
Q

binding of GABA-A receptor leads to influx of

A

Cl-

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9
Q

binding of presynaptic GABA-B receptor leads to

A

decreased Ca2+ influx

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10
Q

binding of postsynaptic GABA-B receptor leads to

A

increased K+ efflux

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11
Q

what med binds to GABA-A receptor

A

BZDs

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12
Q

what cardiac issues do we see in status epilepticus

A

high output cardiac failure
ventricular arrhythmias

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13
Q

ventricular arrhythmia in status epilepticus is due to

A

incongruent signals from parasympathetic and sympathetic

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14
Q

skeletal muscle contractions during status epilepticus and effect on metabolism

A

skeletal muscle contractions increase metabolism

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15
Q

increased metabolism in status epilepticus leads to

A

increased lactic acid production

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16
Q

muscle breakdown in status epilepticus causes

A

hyperkalemia

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17
Q

hyperkalemia in status epilepticus causes

A

potassium is unable to efflux from neurons so the cell is unable to hyper polarize

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18
Q

muscle breakdown can also damage what organ

A

kidneys

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19
Q

is the diaphragm contracted or relaxed in status epilepticus

A

diaphragm contraction

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20
Q

do we see hyper or hypoventilation during status epilepticus

A

hypoventilation

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21
Q

hypoventilation causes us to switch to

A

anaerobic metabolism

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22
Q

anaerobic metabolism increases

A

lactic acid

23
Q

does hypoventilation cause respiratory acidosis or alkalosis

A

hypoventilation causes respiratory acidosis

24
Q

increased pulmonary pressure causes

A

pulmonary edema

25
Q

why do we have hypoglycemia in later stages of status epilepticus

A

insulin > available glucose

26
Q

how does vasodilation affect cerebral blood flow

A

vasodilation –> decreased cerebral blood flow

27
Q

if parasympathetic is activated in status epilepticus, what will we see in terms of our bowels

A

detrusor muscle contraction –> urination
defecation reflex activation –> defecation

28
Q

what lowers the threshold and causes a seizure after a stroke

A

changes in ions related to ischemia
excessive glutamate
alteration in penumbra tissue

29
Q

what type of stroke has a greater risk of seizure

A

multi-infarct stroke

30
Q

patients who develop seizure 2 weeks post stroke are more likely to develop epilepsy. this may be related to

A

glial scarring

31
Q

where is the reticular activating system located

A

brainstem

32
Q

in decorticate posturing, where is the lesion located

A

above the red nuclei = above midbrain

33
Q

in decerebrate posturing, where is the lesion located

A

below the red nuclei = below midbrain

34
Q

which has a worse prognosis between decerebrate and decorticate posturing

A

decerebrate posturing has a worse prognosis

35
Q

what pathways are damaged in both decerebrate and decorticate posturing

A

descending motor pathways

36
Q

if descending motor pathways are damaged in decerebrate and decorticate posturing, what does this mean in terms of our muscle tone?

A

increased tone due to decreased inhibition from those pathways

37
Q

is brainstem function present in decorticate and decerebrate posturing?

A

yes, some brainstem function is present in both

38
Q

what cranial nerves are connected through MLF

A

3, 4, 6

39
Q

what else is connected through MLF besides cranial nerves

A

vestibular nuclei
upper cervical nuclei

40
Q

what does the MLF do

A

yokes eye movements (conjugate gaze)

41
Q

before checking the oculocephalic reflex, what should you check FIRST

A

make sure no cervical injury!!!!

42
Q

how to perform oculocephalic reflex

A

hold eyelids open
move head from side to side

43
Q

during the oculocephalic reflex, if the brainstem is intact, what would we expect

A

eyes will move in opposite direction of head rotation

44
Q

if brainstem is intact for oculocephalic reflex, what is this reflex called (street name)

A

doll’s eye response/reflex

45
Q

for oculocephalic reflex, if brainstem is injured, what would we expect

A

eyes are fixed in MIDPOSITION and will move with head

46
Q

can an awake and non-injured person overcome oculocephalic reflex?

A

YES – no doll’s eye reflex in awake and uninjured patient

47
Q

oculovestibular testing: cold calorics has two components. what are they

A

fast component
slow component

48
Q

fast component of oculovestibular testing: cold calorics

A

nystagmus is directed AWAY from ear stimulated

49
Q

slow component of oculovestibular testing: cold calorics

A

eye movement TOWARD cold

50
Q

what would a normal response be fore oculovestibular testing: cold calorics

A

both components present
both are in appropriate directions

51
Q

in an unconscious patient, and the brainstem is intact, what would we expect for oculovestibular testing: cold calorics

A

slow response is PRESENT toward cold
fast response is ABSENT
BOTH eyes respond

52
Q

why do both eyes respond in oculovestibular testing: cold calorics in an unconscious patient when brainstem is intact

A

MLF is intact

53
Q

what would you expect for oculovestibular testing: cold calorics in unconscious patient who has a brainstem lesion

A

both components are ABSENT
eyes remain in fixed position

54
Q

why do eyes remain in fixed position for oculovestibular testing: cold calorics in patient who is unconscious and brainstem is injured

A

MLF is not intact

joeli unit 3 (7 decks)

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