Basic Neurophysiology Flashcards

1
Q

Glutamate Receptors

A

NMDA
AMPA
Kainate

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2
Q

GABA-A Receptor Mechanis

Drugs acting on GABA-A

A
  • opens chloride channels–>hyperpolarization

- BZs, barbs, prop, and etomidate

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3
Q

GABA-B Receptor Mechanism

A

2nd messenger system

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4
Q

Opioid Receptor Mechanism

A

Increased potassium and decreased calcium conductance resulting in hyperpolarization

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5
Q

Impact of volatiles on CBF

A

CBF increases as concentration of volatiles increase (so then ICP increases)
*iso>des>sevo

  • direct cerebral arterial vasodilators (except N20)
  • interrupt autoregulation (including N20)
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6
Q

CBF and CMR effect

  • fentanyl
  • ketamine
  • volatile anesthetics
  • prop/etomidate/barbs/BZs
A
  • fentanyl: minimal reduction in CBF and CMR
  • ketamine: increases CBV, variable effects on CMR
  • volatiles: decrease CMR and increase CBF
  • prop/etomidate/barbs/BZs: decrease CBF and CMR

*IV agents do not disrupt cerebral auto regulation or CO2 responsiveness

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7
Q

Drugs that decrease CSF production

A

Acetazolamide, furosemide, spironolactone, corticosteroids, isoflurane, vasoconstrictors

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8
Q

Class A nerves

A

large, myelinated peripheral nerves

A-delta: myelinated, low threshold for activation, and conduct fast
*nociception

A-alpha: motor and prorioception
A- beta and A-gamma: cutaneous touch, pressure and muscle spindles

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9
Q

Class C fibers

A
  • non-myelinated or lightly myelinated nerves w/slow conduction velocities
  • slow-pain and post-ganglionic autonomic system
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10
Q

Pain pathway and 1st, 2nd, and 3rd order neurons

A
  • 1st order neuron: cell body in DRG w/fibers to the periphery, synapses on 2nd order neuron in dorsal horn of spinal cord
  • 2nd order neuron: cell body in dorsal horn of spinal cord, sends transmission to contralateral hemisphere of spinal cord and sends signals up to STT and synapses in a variety of places (most important: thalamus, PAG, and reticular formation)
  • 3rd order neuron: cell body in thalamus, signals to the sensory cortex
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11
Q

Hormonal response to pain

A

Increased:

  • cortisol
  • angiotensin II
  • ADH
  • catecholamines
  • cytokines
  • ACTH
  • growth hormone
  • glucagon
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12
Q

Role in pain:

  • post-central gyrus
  • anterior cingulate gyrus
  • insular cortex
A
  • Post-central gyrus: sensory
  • Anterior cingulate gyrus: emotional response to pain
  • Insular cortex: prioritizing pain and judging its degree
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13
Q

Postganglionic sympathetic fibers

A

Adrenergic (except sweat glands and some blood vessels)

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14
Q

Sympathetic nervous system pathway

A

Preganglionic fibers arising from the spinal grey matter in the thoracic and lumbar region exit the ventral rami (like motor neurons) and synapse after a short distance on a paired bilateral paravertebral sympathetic ganglion chain

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15
Q

Beta 2 effects

A

Bronchodilation
Smooth muscle relaxation
Insulin secretion
Glycogenolysis (lysis of glycogen in liver)

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16
Q

Creation and metabolism of norepinephrine

A

Tyrosine–>Dopa–>Dopamine–>Norepi–>Epi

Norepinephrine metabolism: MOA and COMT

17
Q

Post-operative Cognitive Decline or Dysfunction (POCD)

A

Central cholinergic insufficiency

-other theory: anesthetic associated beta-amyloid phosphorylation, like that of Alzheimer’s

18
Q

Risk Factors for POCD

A
  • Age *by far most significant
  • type and duration of surgery
  • substance use
  • low education
  • physical infirmary
  • hearing and visual impairments
  • sleep deprivation
  • high ASA status
  • male gender
19
Q

Benefits of mild intraoperatively hypothermia

A
  • decreases neuronal oxygen demand while preserving energy sources (normal ATP and phosphocreatine levels)
  • decreased CMR and CBF

*NO improvement in outcomes

20
Q

CBF constant over what MAP range

A

60-160 mm Hg

21
Q

CBF change per 1°C change in temperature

A

6% decrease in CBF with every 1°C decrease in temp

*50% decrease in CBF for every 10°C decrease in temp

22
Q

Normal CSF production per hour and per day

A

21 ml/hr

500 ml/day

23
Q

CSF flow

A

Lateral ventricles–>intraventricular foramina (of Monro)–>3rd ventricle–>cerebral aqueduct (of Sylvius)–>4th ventricle–>median aperture of 4th ventricle (foramen of Magendie) and lateral apertures of 4th ventricle (foramina of Luschka)–>cerebellomedullary cistern (cistern magna)–>subarachnoid space around brain and spinal cord

24
Q

Total CSF volume

A

150 ml

25
Q

Cranial volume mass composition

A

80% brain
15% blood
5% CSF

26
Q

Normal ICP

A

<10 mm Hg

27
Q

Which inhalation agent increases CBF the most?

A

Halothane

  • up to 200% increase (20% for iso)
  • hyperventilation can blunt this effect
28
Q

Luxury Perfusion

Circulatory Steal Phenomenon

A

Luxury Perfusion: Combination of a decrease in neuronal metabolic demand w/an increase in CBF (metabolic supply) caused by volatile agents

Circulatory Steal Phenomenon: occurs in setting of focal ischemia- volatile agents can increase blood flow in normal areas of the brain, but not in ischemic areas, where arterioles are already maximally vasodilated. The end result may be a redistribution (“steal”) of blood flow away from ischemic to normal areas.

29
Q

Robin Hood or Reverse Steal Phenomenon

A
  • cerebral vasoconstriction in normal areas of brain, redistributing blood flow from normal to ischemic areas
  • occurs with barbiturates because they cause vasoconstriction only in normal areas of brain tissue
30
Q

Effect of barbiturates on CNS physiology

A
  • decrease CMR, CBF, CBV (blood volume)
  • increase CSF absorption
  • all in all–>lower ICP
31
Q

Ketamine and CNS effects

A
  • only IV agent that dilates cerebral vasculature and increases CBF (50%), but no change in CMR
  • increases in CBF, CBV, and CSF volume can potentially increase ICP in patients with decreased intracranial compliance
  • may offer neuroprotective effects: NMDA blockade during periods of increased glutamate concentrations, as occurs during brain injury, may be protective against neuronal cell death (NMDA blockade reduces Ca2+ entry)
32
Q

Effect of lidocaine

A
  • decreases CMR, CBF, and ICP (but less than other agents) without significant hemodynamic effects
  • may be neuroprotective
33
Q

IV agents capable of producing burst suppression

A
  • barbiturates, etomidate, and propofol

- NOT benzos, opioids, or ketamine

34
Q

Anesthetic effect on evoked potentials

A
  • IV agents generally have minimal effects

- Volatiles have marked effects