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Joeli lectures > Seizures and LOC > Flashcards

Seizures and LOC Flashcards

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1
Q

NMDA receptor responds to

A

Glutamate
Glycine

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2
Q

What must be dislodged from NMDA receptor before the channel can open?

A

Magnesium

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3
Q

Open NMDA receptor

A

Influx of sodium and calcium
Efflux of potassium

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4
Q

Activation of NMDA receptor leads to

A

ion changes the facilitate depolarization

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5
Q

AMPA receptor activated by

A

binding of neurotransmitter

Glutamate is the example in lecture

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6
Q

Activation of AMPA receptor leads to

A

influx of sodium
efflux of potassium

influx of calcium is variable –

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7
Q

Kainate receptor activated by

A

neurotransmitters

glutamate is example in lecture

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8
Q

Activation of Kainate receptor leads to

A

influx of sodium
efflux of potassium

variable influx of calcium

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9
Q

Post synaptic kainate receptor

A

allows for excitation

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10
Q

pre synaptic kainate receptor

A

inhibition

inhibits the release of GABA

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11
Q

is GABA-A receptor a post synaptic or presynaptic receptor

A

post synaptic receptor

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12
Q

Binding of GABA-A leads to

A

influx of chloride –> IPSP of -70 mV (hyper polarization)

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13
Q

What type of receptor is GABA-B

A

metabotropic receptor that affects ion channels

leads to hyperpolarization

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14
Q

Presynaptic GABA-B receptor

A

decreased calcium influx

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15
Q

Postsynaptic GABA-B receptor

A

increased potassium efflux

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16
Q

Voltage gated ion channels —- how it works

A

stimulus –> conformation changes of Na+ channels –> influx of sodium (fast response) –> depolarization –> delayed potassium opening –> potassium efflux –> hyper polarization

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17
Q

Most pharmacotherapy for seizure is directed at

A

regulating the voltage gated ion channels

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18
Q

What medications target the GABA receptors

A

Benzodiazepines

Bind to GABA A receptor to open chloride channels

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19
Q

Hypocalcemia and seizure

A

low serum calcium level increases our membrane resting potential meaning that it doesn’t require as much for that action potential to be reached so we need little change for that action potential to happen –> so we are in a hyper excitable state

Can also lead to decreased inhibition of sodium channels which allows more sodium to come in which allows more depolarization

Normally, K+/Ca2+ channels are activated by intracellular Ca2+ so if low Ca2+, then channels won’t open which prevents K+ from leaving so the cell won’t be able to hyper polarize

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20
Q

Hypomagnesemia and seizures

A

No Mg2+ blocking NMDA receptor —> ability for Ca2+ influx –> more depolarization

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21
Q

Hyponatremia and seizures

A

if intracellular fluid of sodium is greater than extra cellular fluid then we know that water will follow and will cause edema which lowers the threshold

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22
Q

Status epilepticus definition

A

greater than or equal to five minutes of continuous seizures
OR
greater than or equal to 2 discrete seizures between which there is incomplete recovery of consciousness in a 30 min window

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23
Q

Early in status epilepticus

A

cerebral auto regulation is turn off which is the ability of the brain to maintain the same blood flow pressure in a wide range of blood pressures

leads to increased systemic blood pressure –> increased cerebral blood flow

Allows for oxygen and glucose delivery to neuronal cells

Able to sustain aerobic metabolism

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24
Q

During status epilepticus

A

increased ion pumping –> increased metabolic demand –> increased ventilation and oxygen delivery –> switch to anaerobic respiration –> lactic acid build up

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25
Late status epilepticus
lactic acid build up --> peripheral vasodilation decreased systemic blood pressure --> decreased cerebral blood flow decreased oxygen and glucose delivery to neuronal cells
26
cardiac issues in status epilepticus
high output heart failure autonomic nervous sytem activation (PNS and SNS) --> incongruent signals --> ventricular arrhythmia
27
skeletal muscle contractions in status epilepticus
increased metabolism --> increased lactic acid production --> acidic environment for neuronal cells muscle breakdown --> K+ release --> hyperkalemia --> increased extracellular K+ --> inability for K+ to efflux from neuronal cells --> unable to hyper polarize muscle breakdown --> rhabdomyolysis --> damage to kidneys --> renal tubular necrosis hyper pyrexia (high fever) due to excessive muscle contractions
28
Pulmonary issues in status epilepticus
diaphragm contraction --> hypoventilation --> decreased oxygen availability --> anaerobic metabolism --> increased lactic acid diaphragm contraction --> hypoventilation --> CO2 excess --> respiratory acidosis increased pulmonary pressure --> fluid leak from vessels --> pulmonary edema aspiration
29
EARLY autonomic nervous system and glucose
increased insulin (brings down blood sugar) and increased glucagon (increases blood sugar) glycogenesis in liver --> release of glucose stores net effect = available glucose to use for energy
30
LATE autonomic nervous system and glucose
insulin secretion > available glucose stores --> hypoglycemia (bc insulin lowers blood glucose)
31
Parasympathetic activation in status epilepticus
detrusor muscle contraction --> urination defecation reflex activation --> defecation increased secretions including ion bronchial tree
32
lactic acid in status epilepticus
all of energy usage, muscle contractions, increase lactic acid --> vasodilation --> further decreased cerebral blood flow decreased pH including in brain --> neuronal cell death
33
cellular level in the brain for status epilepticus
decreased ATP --> Na+/Ca2+ pump failure --> increased intracellular Ca2+ --> Ca2+ mediated cell damage free radical release --> neuronal cell death mitochondria dysfunction --> apoptotic factors released --> neuronal cell damage
34
Overall status epilepticus
increased muscle activity leads to decreased oxygen and glucose supple increased energy utilization by neurons and brain leads to decreased oxygen and glucose supply to the brain further damaging neurons anaerobic respiration causes lactic acid build up and decreased pH --> damaging neurons widespread organ dysfunction also note that lack of oxygen and glucose causes us to switch to anaerobic metabolism
35
Post-stroke seizure has
high morbidity and mortality
36
Changes in ions related to ischemia, excessive glutamate, and alteration in penumbra tissue lead to
lowering the threshold and increased excitability
37
what stroke has higher risk of seizure
multi-infarct stroke
38
for post stroke seizures, morbidity and mortality increased as
time of onset from initial stroke decreases
39
when are patients more likely to develop epilepsy after stroke
patients who develop seizure 2 weeks post stroke may be related to glial scarring
40
Where is reticular activating system located
brainstem
41
reticular activating system function
maintains consciousness, alertness, and arousal functions in sleep/wake filters sensory info efferent connections to the autonomic NS --> helps control breathing and heart rate provides inhibitory influence from external stimuli by reducing sensory activity during sleep
42
Glasgow Coma Scale is composed of three parameters
best eye response, best verbal response, best motor response
43
Best eye response (4)
4 - eyes open spontaneously 3 - eye opening to verbal command 2 - eye opening to pain 1 - no eye opening
44
Best verbal response (5)
5 - oriented 4 - confused 3 - inappropriate words 2 - incomprehensible sounds 1 - no verbal response
45
Best motor response (6)
6 - obeys commands 5 - localizing pain 4 - withdrawal from pain 3 - flexion to pain (decorticate response) 2 - extension to pain (decerebrate response) 1 - no response
46
GCS 13 or higher
mild brain injury
47
GCS 9-12
moderate injury
48
GCS 8 or less
severe brain injury
49
Decorticate posturing
lesion above red nuclei = above midbrain forearms flexed, LE's extended
50
Decerebrate posturing
lesion below red nuclei = below midbrain UE's extended, pronated, hands flexed, LE's extended implies more complete disconnect between higher centers and brainstem more severe, extensive brainstem injury worse prognosis
51
Medial longitudinal fasciculus (MLF)
longitudinal fiber bundle --> runs through medullar, pons, midbrain connects six ocular motor nuclei (3 pairs) (III, IV, VI), vestibular nuclei, upper cervical nuclei Yokes eye movements; conjugate gaze
52
Oculocephalic reflex first most important
make sure no cervical injury
53
Oculocephalic reflex: how to do it
hold eyelids open and move head from side to side
54
Oculocephalic reflex if brainstem intact
eyes will move in opposite direction of head rotation dolls eyes response = reflex is present
55
Oculocephalic reflex is brainstem is injured
eyes are fixed in mid position and will move with head more severe injury = worse prognosis
56
Oculocephalic reflex is patient is awake and non-injured
able to "track" or overcome reflex
57
Oculovestibular testing fast component
nystagmus is directed away from ear stimulated
58
Oculovestibular testing slow component
eye movement toward cold
59
Normal response for oculovestibular testing
both components are present both are in appropriate directions for cold stimulus
60
Oculovestibular testing response in unconscious patient, brainstem intact
slow response is present toward cold, fast response absent both eyes respond
61
Oculovestibular testing response in unconscious patient, lesion of brainstem
both components are absent eyes remain in fixed position

Joeli lectures (18 decks)

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