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Joeli lectures > Seizures and LOC > Flashcards

Seizures and LOC Flashcards

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
Q

Late status epilepticus

A

lactic acid build up –> peripheral vasodilation

decreased systemic blood pressure –> decreased cerebral blood flow

decreased oxygen and glucose delivery to neuronal cells

26
Q

cardiac issues in status epilepticus

A

high output heart failure

autonomic nervous sytem activation (PNS and SNS) –> incongruent signals –> ventricular arrhythmia

27
Q

skeletal muscle contractions in status epilepticus

A

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
Q

Pulmonary issues in status epilepticus

A

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
Q

EARLY autonomic nervous system and glucose

A

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
Q

LATE autonomic nervous system and glucose

A

insulin secretion > available glucose stores –> hypoglycemia (bc insulin lowers blood glucose)

31
Q

Parasympathetic activation in status epilepticus

A

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

increased secretions including ion bronchial tree

32
Q

lactic acid in status epilepticus

A

all of energy usage, muscle contractions, increase lactic acid –> vasodilation –> further decreased cerebral blood flow

decreased pH including in brain –> neuronal cell death

33
Q

cellular level in the brain for status epilepticus

A

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
Q

Overall status epilepticus

A

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
Q

Post-stroke seizure has

A

high morbidity and mortality

36
Q

Changes in ions related to ischemia, excessive glutamate, and alteration in penumbra tissue lead to

A

lowering the threshold and increased excitability

37
Q

what stroke has higher risk of seizure

A

multi-infarct stroke

38
Q

for post stroke seizures, morbidity and mortality increased as

A

time of onset from initial stroke decreases

39
Q

when are patients more likely to develop epilepsy after stroke

A

patients who develop seizure 2 weeks post stroke

may be related to glial scarring

40
Q

Where is reticular activating system located

A

brainstem

41
Q

reticular activating system function

A

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
Q

Glasgow Coma Scale is composed of three parameters

A

best eye response, best verbal response, best motor response

43
Q

Best eye response (4)

A

4 - eyes open spontaneously
3 - eye opening to verbal command
2 - eye opening to pain
1 - no eye opening

44
Q

Best verbal response (5)

A

5 - oriented
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - no verbal response

45
Q

Best motor response (6)

A

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
Q

GCS 13 or higher

A

mild brain injury

47
Q

GCS 9-12

A

moderate injury

48
Q

GCS 8 or less

A

severe brain injury

49
Q

Decorticate posturing

A

lesion above red nuclei = above midbrain
forearms flexed, LE’s extended

50
Q

Decerebrate posturing

A

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
Q

Medial longitudinal fasciculus (MLF)

A

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
Q

Oculocephalic reflex first most important

A

make sure no cervical injury

53
Q

Oculocephalic reflex: how to do it

A

hold eyelids open and move head from side to side

54
Q

Oculocephalic reflex if brainstem intact

A

eyes will move in opposite direction of head rotation

dolls eyes response = reflex is present

55
Q

Oculocephalic reflex is brainstem is injured

A

eyes are fixed in mid position and will move with head

more severe injury = worse prognosis

56
Q

Oculocephalic reflex is patient is awake and non-injured

A

able to “track” or overcome reflex

57
Q

Oculovestibular testing fast component

A

nystagmus is directed away from ear stimulated

58
Q

Oculovestibular testing slow component

A

eye movement toward cold

59
Q

Normal response for oculovestibular testing

A

both components are present
both are in appropriate directions for cold stimulus

60
Q

Oculovestibular testing response in unconscious patient, brainstem intact

A

slow response is present toward cold, fast response absent
both eyes respond

61
Q

Oculovestibular testing response in unconscious patient, lesion of brainstem

A

both components are absent
eyes remain in fixed position

Joeli lectures (18 decks)

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