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
why do we have hypoglycemia in later stages of status epilepticus
insulin > available glucose
26
how does vasodilation affect cerebral blood flow
vasodilation --> decreased cerebral blood flow
27
if parasympathetic is activated in status epilepticus, what will we see in terms of our bowels
detrusor muscle contraction --> urination defecation reflex activation --> defecation
28
what lowers the threshold and causes a seizure after a stroke
changes in ions related to ischemia excessive glutamate alteration in penumbra tissue
29
what type of stroke has a greater risk of seizure
multi-infarct stroke
30
patients who develop seizure 2 weeks post stroke are more likely to develop epilepsy. this may be related to
glial scarring
31
where is the reticular activating system located
brainstem
32
in decorticate posturing, where is the lesion located
above the red nuclei = above midbrain
33
in decerebrate posturing, where is the lesion located
below the red nuclei = below midbrain
34
which has a worse prognosis between decerebrate and decorticate posturing
decerebrate posturing has a worse prognosis
35
what pathways are damaged in both decerebrate and decorticate posturing
descending motor pathways
36
if descending motor pathways are damaged in decerebrate and decorticate posturing, what does this mean in terms of our muscle tone?
increased tone due to decreased inhibition from those pathways
37
is brainstem function present in decorticate and decerebrate posturing?
yes, some brainstem function is present in both
38
what cranial nerves are connected through MLF
3, 4, 6
39
what else is connected through MLF besides cranial nerves
vestibular nuclei upper cervical nuclei
40
what does the MLF do
yokes eye movements (conjugate gaze)
41
before checking the oculocephalic reflex, what should you check FIRST
make sure no cervical injury!!!!
42
how to perform oculocephalic reflex
hold eyelids open move head from side to side
43
during the oculocephalic reflex, if the brainstem is intact, what would we expect
eyes will move in opposite direction of head rotation
44
if brainstem is intact for oculocephalic reflex, what is this reflex called (street name)
doll's eye response/reflex
45
for oculocephalic reflex, if brainstem is injured, what would we expect
eyes are fixed in MIDPOSITION and will move with head
46
can an awake and non-injured person overcome oculocephalic reflex?
YES -- no doll's eye reflex in awake and uninjured patient
47
oculovestibular testing: cold calorics has two components. what are they
fast component slow component
48
fast component of oculovestibular testing: cold calorics
nystagmus is directed AWAY from ear stimulated
49
slow component of oculovestibular testing: cold calorics
eye movement TOWARD cold
50
what would a normal response be fore oculovestibular testing: cold calorics
both components present both are in appropriate directions
51
in an unconscious patient, and the brainstem is intact, what would we expect for oculovestibular testing: cold calorics
slow response is PRESENT toward cold fast response is ABSENT BOTH eyes respond
52
why do both eyes respond in oculovestibular testing: cold calorics in an unconscious patient when brainstem is intact
MLF is intact
53
what would you expect for oculovestibular testing: cold calorics in unconscious patient who has a brainstem lesion
both components are ABSENT eyes remain in fixed position
54
why do eyes remain in fixed position for oculovestibular testing: cold calorics in patient who is unconscious and brainstem is injured
MLF is not intact