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APEX-Neuro > NEURO-Brain > Flashcards

NEURO-Brain Flashcards

1
Q

Neurons purpose and primary role

A

The functional unit of the nervous system

Role=receive and send information

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2
Q

Which cells make up:
Grey matter
White matter

A

Grey matter = Cell bodies and nonmyelinated axons

White matter = Myelinated axons

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3
Q

What is the nucleus in the CNS

A

a collection of nerve cell bodies

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4
Q

Which cells support neuronal function

A

glial cells

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5
Q

What are the 4 types of glial cells

A

Astrocyte
Microglia
Ependymal cell
Oligodendrocyte

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6
Q

From which cell do most brain tumors arise

A

Glial

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7
Q

What are the 3 classifications of nerves in the CNS

A
  1. Multipolar
  2. Pseudounipolar
  3. Bipolar
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8
Q

Where are multipolar neurons found

A

Most of the CNS

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9
Q

Where are pseudounipolar neurons found

A
  1. Dorsal root ganglion

2. Cranial ganglion

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10
Q

where are bipolar neurons found

A
  1. Retina

2. Ear

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11
Q

What are 4 functions of the glial cells

A
  1. Creating healthy ionic environment
    2 Modulating nerve conduction
  2. controlling reuptake of neurotransmitters
  3. Repairing neurons following neuronal injury
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12
Q

What is are 2 functions of the astrocyte

A
  1. Regulate metabolic environment

2. Repair neuron after injury

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13
Q

What is the most abundant glial cell

A

Astrocyte

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14
Q

Where are ependymal cells located (3)

A

The roof of the 3rd and 4th ventricles

Spinal canal

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15
Q

What is the function of ependymal cells

A

Form the choroid plexus which produces CSF

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16
Q

What is the purpose of oligodendrocytes

A

Forming the myelin sheath in the CNS

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17
Q

Which cells form the myelin sheath in the peripheral nervous system

A

Schwann cells

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18
Q

Which is the function of microglia

A

To act as macrophages and phagocytize neuronal debris

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19
Q

What is the physiologic role of the dendrite

A

receives and processes signals

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20
Q

What is the physiologic role of the soma

A

Integrate signals

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21
Q

What is the physiologic role of the axon

A

Send signals

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22
Q

What is the role of the presynaptic terminal

A

Release NTs

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23
Q

Which 4 structures are contained in the cerebral hemispheres

A

Cerebral cortex
hippocampus
Amygdala
Basal ganglia

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24
Q

Which 2 structures are contained in the diencephalon

A
  1. Thalamus

2. Hypothalamus

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25
Q

Which 4 structures are contained in the brainstem

A
  1. Midbrain
  2. Pons
  3. Medulla
  4. Reticular activating system
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26
Q

What are the 3 divisions of the cerebellum

A
  1. Archicerebellum
  2. Paleocerebellum
  3. Neocerebellum
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27
Q

What structure connects the 2 cerebral hemispheres

A

Corpus callosum

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28
Q

What are the functions of each lobe

A 
Frontal = motor cortex
Parietal = somatic sensory cortex
Occipital = visual cortex
Temporal = auditory cortex and speech centers
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29
Q

What areas are in the temporal lobe that facilitate speech

Name their funciton

A

Wernicke’s area = understanding speech

Broca’s area = motor control of speech (connected via frontal lobe)

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30
Q

Where does cognition and movement take place in the cerebral cortex

A

Precentral gyrus of frontal lobe

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31
Q

Where does sensation take place in the cerebral cortex

A

Postcentral gyrus of parietal lobe

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32
Q

What is the function of the hippocampus

A

Memory and learning

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33
Q

What are 3 functions of the amygdala

A

Emotion
Appetite
Response to pain and stress

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34
Q

What is the function of the basal ganglia

A

Fine control of movement

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35
Q

What 2 structures are located in the basal ganglia

A
  1. Caudate nucleus

2. Globus pallidus

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36
Q

What is the function of the thalamus

A

Acts as a relay station that directs info to various cortical structures

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37
Q

What is the function of the hypothalamus

A

Primary neurohumoral organ

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38
Q

What function does the midbrain serve

A

Auditory and visual tracts

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39
Q

What is the function of the pons

A

autonomic integration

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40
Q

What 3 activities are controlled by the reticular activating system

A
  1. Control consciousness, arousal, and sleep
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41
Q

What is the function of the medulla

A

Autonomic integration

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42
Q

Where does autonomic integration occur in the brain

A

The pons and medulla in the brainstem

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43
Q

What are the functions of the following cerebellum

A 
Archicerebellum = maintains equilibrium
Paleocerebellum = regulates muscle tone
Neocerebellum = coordinates voluntary muscle movement
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44
Q

Which cranial nerves are sensory ONLY

A

CN 1, 2, 8

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45
Q

Which cranial nerves are motor ONLY

A

CN 3, 4, 6, 11, 12

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46
Q

Which cranial nerves have both motor and sensory function

A

CN 5, 7, 9, 10

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47
Q

What is the mnemonic for the function of CNs

A

Some Say Marry Money But My Brother Says Bad Business to Marry Money

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48
Q

Which cranial nerves function as motor nerves for the eyes

A

CN 3
CN 4
CN 6

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49
Q

Which muscles and direction does CN 3 control

A

Inferior oblique = extorsion, elevation

Inferior rectus = infraduction

Superior rectus = supraduction

Medial recuts = adduction

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50
Q

Which muscles and direction does CN 4 control

A

Superior oblique = intorsion, depression

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51
Q

Which muscles and direction does CN 6 control

A

Lateral recuts = abduction

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52
Q

Which cranial nerve is the only located centrally

A

The optic n

It is surrounded by dura

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53
Q

What is tic douloureux

A

Trigeminal neuralgia of CN 5

Generates excruciating neuropathic pain in face

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54
Q

What is a mnemonic for the 5 branches of the facial n (CN 7 )

A

Two Zebras Bit My Carrot

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55
Q

Which CN is injured in Bell’s Palsy and what is the result

A

CN 7

Ipsilateral facial paralysis

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56
Q

Which CN perform parasympathetic output

A

CN 3, 7, 9, 10

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57
Q

Which nerve is responsible for most parasympathetic activity

A

Vagus (CN 10)

Responsible for 75%

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58
Q

What are 3 functions of CSF

A
  1. Cushion
  2. Provides buoyancy
  3. Delivers optimal conditions for neuro fxn
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59
Q

Where is CSF located

A
  1. Ventricles (left and right laterals, third, and fourth)
  2. Cisterns around brain
  3. Subarachnoid space in brain and SC
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60
Q

What is the purpose of the BBB

A

To separate CSF from plasma

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61
Q

What is the structure of the blood brain barrier

A

Has tight junctions that restrict passage of large molecules and ions

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62
Q

How is the BBB affected by tumors, injury, infection or ischemia

A

It becomes dysfunctional

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63
Q

Where is the BBB not present in the brain (5)

A
  1. Chemoreceptor trigger zone
  2. Posterior pituitary gland
  3. Pineal gland
  4. Choroid plexus
  5. Parts of hypothalamus
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64
Q

Why are substances easier to pass the BBB in neonates

A

Because the BBB is poorly developed

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65
Q 
Key facts: 
CSF volume = 
Specific gravity = 
CSF pressure =
Rate of production =
A

CSF volume = 150 mL
Specific gravity = 1.002 - 1.009
CSF pressure = 5 - 15 mmHg
Rate of production = 30 mL/hr

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66
Q

Which structures connect the ventricles

Which ventricles are connected

A

Foramen of Monro
-Lateral to 3rd vent

Aqueduct of Sylvius
-3rd to 4th vents

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67
Q

What structures follow the 4th ventricle, draining CSF into the subarachnoid space

(list in order)

A

Foramen of Luschka

Foramen of Magendie

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68
Q

The mnemonic for CSF flow through the brain

A

Lover My 3 Silly 4 Lorn Magpies

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69
Q 
How do electrolyte levels of CSF compare to plasma
K+
pH
Glucose
Protein
A 
K+ = half of plasma level
pH = more acidic
Glucose = much lower (60)
Protein = exponentially lower
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70
Q

What are 2 types of hydrocephalus

A
  1. Obstructive

2. Communicating

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71
Q

What is the difference between obstructive and communicating hydrocephalus

A

Obstructive = CSF flow is obstructed (d/t mass, injury etc)

Communicating

  1. decreased absorption by arachnoid villi (i.e. hemorrhage)
  2. Overproduction
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72
Q

Define cerebral autoregulation

A

The brain’s ability to maintain constant BF over a wide range of MAPs
This ensures a steady state of BF in response to normal fluctuations

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73
Q

What is the equation for cerebral blood flow

A

CBF = CPP/ cerebral vascular resistance

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74
Q

What is the optimal global cerebral blood flow and % of CO

A

45 - 55 mL/100g tissue/min

15% CO

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75
Q

At what threshold of CBF does membrane failure and cell death occur

A

<15 mL/100g tissue/min

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76
Q

What are 5 determinants of CBF

A
  1. CMRO2
  2. CPP
  3. PaCO2
  4. PaO2
  5. Venous pressure
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77
Q

CMRO2 =

A

3.0 - 3.8 mL/O2/100g tissue/min

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78
Q

Describe the relationship between CMRO2 and CBF

A

They are coupled

If more O2 is needed the BF will increase

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79
Q

What is the utilization of O2 in the brain

A

60% for electrical activity

40% for cellular integrity

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80
Q

What factors decrease CMRO2

A
  1. Decreased temperature
  2. Halogenated anesthetics (uncoupled)
  3. Propofol
  4. Etomidate
  5. Barbiturates
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81
Q

What 4 factors increased CMRO2

A
  1. Hyperthermia
  2. Seizures
  3. Ketamine
  4. N2O
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82
Q

At what body temperature does EEG suppression occur

A

18 - 20*C

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83
Q

How much does CMRO2 decrease when temperature decreases

A

Decreased by 7% for every 1*C decrease

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84
Q

Which factor uncouples CMRO2-CBF

A

Halogenated anesthetics

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85
Q

At what MAP is CBF autoregulated

A

60 - 160 mmHg

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86
Q

What happens to CBF when CPP is below the level of autoregulation (2)

A
  1. CBF becomes pressure dependent

2. Increases risk of cerebral hypoperfusion

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87
Q

What is the range of CPP autoregulation

A

50 - 150 mmHg

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88
Q

What happens to CBF when CPP is above the level of autoregulation

A
  1. CBF becomes pressure dependent

2. Risk of cerebral edema and hemorrhage

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89
Q

What is the minimum MAP to maintain CPP with a normal ICP

A

55 - 65 mmHg

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90
Q

What 3 factors control cerebral autoregulation

A
  1. Local metabolism
  2. Myogenic mechanisms
  3. Autonomic innervation
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91
Q

What is CPP dependent on when autoregulation is impaired

A

Blood pressure

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92
Q

What are 3 variables that can reduce the effectiveness of autoregulation

A
  1. Intracranial tumor
  2. Head trauma
  3. Volatile anesthetics
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93
Q

How is autoregulation affected by HTN

A

The curve shifts right
The low threshold for autoregulation is increased, and pts become less tolerant of HoTN for CBF

Pt are at higher risk of cerebral ischemia with HoTN

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94
Q

What is normal CBF when PaCO2 is 40 mmHg

A

50 mL/100g tissue/min

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95
Q

How much does an increase or decrease in PaCO2 alter CBF

A

For every 1 mmHg increase in PaCO2, CBF increased by 1 - 2 mL/100g tissue/min

It is opposite for decrease in PaCO2

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96
Q

At what PaCO2 does maximal cerebral vasodilation occur

A

80 - 100 mmHg

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97
Q

At what PaCO2 does maximal cerebral vasoconstriction occur

A

25 mmHg

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98
Q

How is cerebral vascular resistance controlled

A

By the pH in the CSF around the arterioles

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99
Q

How does the pH of CSF alter cerebral vascular resistance (increased v decreased)

A

Increased CVR:
INC CSF pH (dec PaCO2) => INC CVR -> dec CBF
ex: resp alkalosis

Decreased CVR:
dec CSF pH (INC PaCO2) => dec CVR => INC CBF
ex: respiratory acidosis

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100
Q

Describe cerebral steal concept

A

Healthy brain tissue has vascular tone and can alter diameter

Ischemic or atherosclerotic areas are already maximally dilated

When healthy vessels vasodilate, the “steal” flow from the already maximally dilated ischemic areas

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101
Q

Describe the Robinhood effect in relation to cerebral blood flow

A

Use of hyperventilation to constrict health cerebral vessels to increase flow to ischemic regions

Hypocapnia could increase harm from left shift of O2 dissociation curve, which releases less O2

102
Q

How does PaO2 affect cerebral vessel diameter

A

PaO2 < 50 - 60 mmHg = vasodilation and INC CBF

PaO2 > 60 mmHg = CBF unaffected

103
Q

How does venous pressure affect cerebral volume

A

High venous pressures reduce venous drainage and INCREASE cerebral volume

104
Q

What is the consequence of increased venous pressure

A

Reduce drainage
Increase cerebral volume
Back pressure on the brain, reducing the arterial/venous gradient (difference between MAP - CVP)

105
Q

What conditions impair venous drainage (4)

A
  1. Jugular compression d/t head position (head flex or turned)
  2. Increased intrathoracic pressure d/t cough or PEEP
  3. Vena cava thrombosis
  4. Vena cava syndrome
106
Q

What is normal ICP

When does cranial HTN occur

A

5 - 15 mmHg

ICP > 20 mmHg

107
Q

What are 8 s/sx of intracranial HTN

A
  1. HA
  2. N/V
  3. Papilledema
  4. Pupil dilation
  5. Focal neuro deficits
  6. Decreased LOC
  7. Seizures
  8. Coma
108
Q

What is the Monro-Kelllie doctrine

A

The equilibrium of pressure-volume between brain, blood, and CSF within the cranium
Increase of one compartment must be countered by decrease in another to maintain normal pressure

109
Q

What is Cushing’s triad

A

HTN
Bradycardia
Irregular respirations

110
Q

Where is the most common site of herniation

A

Temporal uncus

Applies pressure to oculomotor nerve (CN 3)

111
Q

What is the pathophysiology of fixed, dilated pupil with cerebral herniation

A

Cerebral herniation at the temporal uncus puts pressure on the oculomotor n (CN 3) making it ischemic

112
Q

What is the gold standard of ICP measure

A

Intraventricular catheter

113
Q

How can ICP be measured

A

Intraventricular cath

Subdural bolt over cerebral cortex

114
Q

What 2 brain factors alter cerebral volume

A
  1. Cerebral swelling

2. tumor

115
Q

What 2 blood factors alter cerebral volume

A
  1. Increased CBF

2. Bleeding

116
Q

What 4 CSF factors alter cerebral volume

A
  1. INC CSF production by choroid plexus
  2. dec CSF removal by arachnoid villi
  3. Obstruction of reabsorption d/t bleed, infxn, tumor
  4. Passage of fluid across the BBB
117
Q

How does increased ICP affect CPP

A

CPP is reduced

118
Q

How is CPP preserved when ICP is increased

A

BP must increase

119
Q

What is the cause of irregular respirations with intracranial HTN in the Cushing’s triad

A

Compression of the medulla

120
Q

What are 6 types of brain herniations

A
  1. Cingulate
  2. Central
  3. Uncal
  4. Cerebellotonsillar
  5. Upward
  6. Transcalvarial
121
Q

Where is the most common site of brain herniation

A

Temporal uncus (transtentorial herniation)

122
Q

What are 7 methods to decrease cerebral blood volume

A
  1. Mild hyperventilation
  2. Avoid hypoxemia (PaO2<60 mmHg)
  3. Avoid vasodilators
  4. Use cerebral vasoconstrictors
  5. HOB >30*
  6. Avoid neck flexion
  7. Reduce intrathoracic pressure (dec PEEP/cough)
123
Q

What are 2 methods to decrease CSF

A
  1. Drain with intraventricular cath or VP shunt

2. Administer acetazolamide or furosemide

124
Q

What are 2 medications to decrease cerebral edema

A
  1. Diuretics

2. Steroids

125
Q

What method is used to decrease cerebral mass

A

Surgical debulking or hematoma evacuation

126
Q

What are 4 areas of ICP reduction

A
  1. Volume reduction
  2. CSF reduction
  3. Edema reduction
  4. Mass reduction
127
Q

How long does the effect of hyperventilation and dec PaCO2 on CBF last. Why

A

6 - 20 hrs

The pH of the CSF equilibrates with PaCO2

128
Q

What cerebral vasodilators should be avoided in pts with increased ICP

A

NTG, nitroprusside

129
Q

How is venous drainage facilitated

A
  1. HOB >30*
  2. Avoid neck flexion or extension which compresses jugular veins
  3. Avoid T-burg
  4. Reduce intrathoracic pressure
    - dec PEEP
    - avoid bucking, coughing, straining
130
Q

What 2 drugs can reduce CSF production

A

Acetazolamide

Furosemide

131
Q

What medication can reduce cerebral edema and mass

A

Mannitol

132
Q

Dose for mannitol

A

0.25 - 1.0 g/kg

133
Q

In which setting of increased ICP should steroids not be used

A

TBI

134
Q

What type of brain tumor should not receive steroids

A

Functional pituitary adenoma

135
Q

What is the primary function of the Circle of Willis

A

To provide redundancy of blood flow to brain

If one side is occluded, the other should be able to perfuse the affected area

136
Q

Which artery supplying the brain is unpaired

A

Basilar artery

137
Q

Where does the basilar artery supply

A

Posterior circulation, brainstem

138
Q

Which arteries arise from the basilar artery

A

Anterior inferior cerebellar a

Superior cerebellar a

139
Q

Describe the flow of blood from the aorta to structures in the posterior foss

A

Aorta => subclavian aa. =. vertebral aa. => basilar a => posterior fossa and spinal cord

140
Q

Where do the vertebral arteries enter the skull

A

Foramen magnum

141
Q

Describe the flow of blood from the aorta to the cerebral hemispheres

A

Aorta => carotid aa. => internal carotid aa. => circle of Willis => cerebral hemispheres

142
Q

Where does the anterior circulation enter the skull

A

Foramen lacerum

143
Q

How does venous blood drain from the cerebral cortex and cerebellum drain

A

Via the superior sagittal sinus and dural sinuses

144
Q

How does venous blood drain from the basal structures

A

Via the inferior sagittal sinus, great cerebral vein, and the straight sinuses

145
Q

Where do the cerebral venous pathways converge

A

The confluence of sinuses posterior to the occipital lobe

146
Q

How does blood drain from the confluence of sinuses out of the cranium

A

Via the transverse sinus, then sigmoid sinus and finally the paired jugular veins

147
Q

What are 6 risk factors for ischemic stroke

A
  1. HTN
  2. Smoking
  3. DM
  4. Hyperlipidemia
  5. Excessive EtOH
  6. Elevated homocysteine levels
148
Q

What must be ruled out prior to thrombolytic treatment for patients with suspected ischemic stroke

A

Intracerebral hemorrhage

149
Q

What is the time frame for receiving thrombolytic agents with suspected ischemic stroke

A

Within 4.5 hours after symptom onset

150
Q

What is the timeframe for embolectomy following ischemic stroke

A

Within 6 hours of symptom onset

151
Q

Why is HTN common following ischemic CVA

A

Elevated BP supports CPP and cerebral oxygenation

152
Q

What effect does HoTN have on patients experiencing an ischemic stroke

A

Worsens ischemia

153
Q

What is the goal BP for pts with ischemic stroke

A

185/110 mmHg

154
Q

How can elevated glucose impact outcomes for patients with ischemic stroke

A

During cerebral hypoxia (from ischemia), glucose is converted to lactic acid.

Cerebral acidosis destroys brain tissue and leads to poor outcomes

Monitor and treat elevated serum glucose

155
Q

Where does arterial bleeding occur in the brain

A

Subarachnoid space between the arachnoid and pia mater

156
Q

Where does venous bleeding occur in the brain

A

Between the dura and the arachnoid

157
Q

What causes aneurysm rupture

A

When there is increased transmural pressure (increased MAP over ICP)

158
Q

What are the causes of morbidity related to aneurysm rupture

A
  1. Obstructive hydrocephalus
  2. Rebleeding
  3. Vasospasm
159
Q

What are s/sx of aneurysm rupture

A
  1. Worse headache
  2. N/V
  3. Photophobia
  4. Focal Neuro deficits
  5. Photophobia
160
Q

How does SAH lead to meningismus

A

The meninges become irritated from blood spreading throughout the SA space

161
Q

How does a rupture aneurysm put someone at risk for hydrocephalus

A

The blood can block CSF flow causing obstructive hydrocephalus and increasing ICP

162
Q

What is the goal for intraoperative SBP during aneurysm surgery

A

120 - 150 mmHg

163
Q

What are the risks of HoTN technique during aneurysm surgery

A

CPP reduction may be inadequate

Autoregulation is impaired in pts following SAH so HoTN isn’t well tolerated for cerebral perfusion

164
Q

Why is cerebral vasospasm following SAH a major cause of morbidity and mortality

A

It causes delayed contraction of the cerebral arteries which can lead to infarction

165
Q

How are cerebral vasospasms monitored and when are they most likely

A

Most likely to occur 4 - 9 days after SAH

Monitored by frequent neuro checks and daily TCDs

166
Q

What is the gold standard of vasospasm diagnosis

A

Cerebral angiography

167
Q

What is the goal of vasospasm treatment

A

To maintain cerebral perfusion pressure

CPP = MAP - ICPorCVP

168
Q

Why is hypertension a goal for vasospasm prevention

A

Ischemic areas of the brain already have maximal dilation, so perfusion is pressure dependent, requiring increased MAP by 20 - 30 mmHg above baseline

169
Q

What are the components of triple H therapy

A

Hypervolemia
HTN
Hemodilution

170
Q

Why is hemodilution a goal of vasospasm and what is the target Hct

A

Liberal hydration supports blood pressure and CPP

Hemodilution reduces blood viscosity and cerebrovascular resistance

CBF improves

171
Q

Which CCB is used for vasospasm and by what mechanism does it attenuate vasospasm

A

Nimodipine

It increases collateral blood flow. It doesn’t actually relieve the spasm

172
Q

How are medically refractory vasospasm treated

A

With intra-arterial vasodilators (verapamil and nicardipine), papaverine, or milrinone

173
Q

Why are pts with aneurysmal SAH at risk for cerebral salt-wasting syndrome

Treatment

A

The brain releases natriuretic peptide, leading to volume contraction, hyponatremia, and sodium wasting by the kidneys

Treatment = isotonic crystalloids

174
Q

what are the 6 categories of motor response for GCS

A
  1. No motor response
  2. Abnormal extension to pain
  3. Abnormal flexion to pain
  4. Withdrawal from pain
  5. Localizes to pain
  6. Obeys command
175
Q

What re the 5 categories of verbal response for GCS

A
  1. No verbal response
  2. Incomprehensible sounds
  3. Inappropriate words
  4. Confused
  5. Oriented
176
Q

What are 4 categories of eye opening response for GCS

A
  1. no eye opening
  2. Eye opening to pain
  3. Eye opening to sound
  4. Spontaneous eye opening
177
Q

What are 8 additional anesthetic considerations for a patient with an acute TBI

A
  1. Full stomach
  2. Unstable c-spine
  3. Intracranial HTN
  4. Airway issues
  5. Unknown volume status
  6. Hypoxia
  7. Other injuries
  8. Intoxication
178
Q

What are 3 coagulant treatments for head injury in patients taking warfarin

A
  1. FFP
  2. PCC
  3. Recombinant factor 7a
179
Q

What are coagulant treatment options for head injury patients taking clopidogrel or aspirin

A
  1. Reverse with platelet transfusion

2. Us of recombinant factor 7a

180
Q

What 2 interventions can worsen neurological outcomes for patients with TBI

A
  1. Prolonged hyperventilation (low PaCO2)

2. Steroids

181
Q

How do hypertonic vs hypotonic solutions affect cerebral volume

A

Hypertonic saline = restores intravascular volume and decreases brain water

Hypotonic solution = increases cerebral edema

182
Q

Which IV fluids are linked to poor neurological outcomes and should be avoided in patients with TBI

A
  1. Hypotonic solutions
  2. Glucose-containing solutions
  3. Albumin
183
Q

Define partial or focal seizure

A

Activity is localized to a particular cortical region

184
Q

Define generalized seizures

A

Activity affects both hemispheres

185
Q

What is a Jacksonian march

A

When a partial seizure progresses to generalizes seizure

186
Q

What is tonic vs clonic movement with generalized seizure

A 
Tonic = whole body rigidity 
Clonic = repetitive jerking motions
187
Q

What is a surgical treatment for generalized seizures

A

Vagal nerve stimulator

Resection of foci

188
Q

What are criteria for status epilepticus

A
  1. Seizure duration >30 minutes

2. 2 grand mal seizures w/o regaining consciousness in-between

189
Q

What are 6 acute treatments for status epilepticus

A
  1. Phenobarbital
  2. Thiopental
  3. Phenytoin
  4. Benzos
  5. Propofol
  6. GA
190
Q

What are causes of new-onset seizures in an adult

A
  1. Structural brain lesion (tumor, head trauma, CVA)

2. Metabolic cause (hypoglycemia, drug toxicity, withdrawal)

191
Q

How do inhalation agents affect seizure activity

A

They tend to reduce EEG activity in a dose-dependent fashion

192
Q

Why are s/sx of seizure activity under GA

A
  1. Tachycardia
  2. HTN
  3. Increased EtCO2 d/t increased O2 consumption
193
Q

Which agents should be avoided in pts with history of seizure and why

A

Ketamine can induce seizure activity

Meperidine, the active metabolite accumulation is capable of producing sz activity

194
Q

Which 3 medications can be used to determine seizure location during cortical mapping.
Why

A
  1. Methohexital
  2. Etomidate
  3. Alfentanil

These drugs increase EEG activity and can help determine the location of szs

195
Q

Phenytoin effect on the liver

A

Induces hepatic enzymes

196
Q

How do carbamazepine and phenytoin affect nondepolarizing NMB metabolism

A

Contributes to resistance of nondepolarizing NMBD d/t hepatic enzyme induction

197
Q

Risk of phenytoin extravasation

A

Extravasation or arterial injection can cause significant tissue injury

Fosphenytoin avoids this

198
Q

What effect does valproic acid have on hepatic metabolism

A

Inhibits hepatic enzymes

199
Q

Which anticonvulsant drugs are hepatic enzyme inducers

A

Phenytoin

Carbamazepine

200
Q

Which anticonvulsant drugs are hepatic enzyme inhibitors

A

Valproic acid

201
Q

Carbamazepine effect on hepatic metabolism

A

Induces hepatic enzymes

202
Q

What 4 conditions can carbamazepine illicit

A
  1. Aplastic anemia
  2. Thrombocytopenia
  3. Liver dysfunction
  4. Hyponatremia
203
Q

What is the MOA of phenytoin

A

Blocks voltage-gated Na+ channels

Stabilizes membranes

204
Q

What type of kinetics does phenytoin follow

A

Zero order kinetics

205
Q

Valproic acid MOA

A

Blocks voltage-gated Na+ channels

Stabilizes membranes

206
Q

What effect does valproic acid have on phenytoin metabolism and plasma level

A

Slows metabolism
Displaces phenytoin from plasma proteins
Increases phenytoin levels

207
Q

Carbamazepine MOA

A

Blocks voltage-gated Na+ channels

Stabilizes membranes

208
Q

Gabapentinoid MOA

A

Inhibition of alpa 2-delta subunit of voltage-gated Ca++ channels in CNS

Decreases excitatory NT release

209
Q

What is the chemical structure of gabapentinoids

A

Chemical analogues of GABA but do not agonize GABA

210
Q

Which conditions are gabapentinoids useful

A
  1. Diabetic neuropathy
  2. Post-herpatic neuralgia
  3. Reflex sympathetic dystrophy
211
Q

6 side effects of phenytoin

A
  1. Dysrhythmias/HoTN
  2. Gingival hyperplasia
  3. Aplastic anemia
  4. Cerebellar-vestibular dysfunction
  5. Stevens-Johnson syndrome
  6. Birth defects
212
Q

Describe the pathophysiology of alzheimers

A

Development of diffuse beta-amyloid-rich plaques

Development of neurofibrillary tangles in the brain

213
Q

What are consequences of plaque formation in alzheimers

A
  1. Dysfunctional synaptic transmission
    - most common in ACh neurons
  2. Apoptosis
214
Q

What is the goal of Alzheimer treatment

A

To restore the concentration of ACh with cholinesterase inhibitors

215
Q 
What class of medications are used for Alzheimer's
Example drugs:
A

Cholinesterase inhibitor

Ex: tacrine, donepezil, rivastigmine, galantamine

216
Q

Pre-operative anesthetic considerations for patients with Alzheimer’s

A

Avoid preop sedation, which can worsen confusion

217
Q

Induction considerations for patients with Alzheimer’s

A

The use of succinylcholine can be prolonged in patients taking cholinesterase inhibitors

218
Q

Which anticholinergic is the best choice for an Alzheimer’s patient and why

A

Glycopyrrolate

It doesn’t cross the BBB

219
Q

What hemodynamic alterations and symptoms are patients taking cholinesterase inhibitors at risk for

A
  1. Bradycardia
  2. Syncope
  3. N/V
220
Q

What is Parkinson’s disease

A

chronic neurodegenerative disorder of the BASAL GANGLIA

With imbalance between dopamine and ACh

221
Q

Which neurotransmitters are out of balance in patients with Parkinson’s disease

A

Low dopamine levels

Elevated Ach levels

222
Q

What is the consequence of increased Ach in the basal ganglia

A

It increases GABA activity in the thalamus causing suppression (GABA = inhibitory)

223
Q

What is the result of thalamic inhibition from increased ACh

A

It suppresses the cortical motor system and motor areas in brainstem

Results in overactivity of the extrapyramidal system

224
Q

What is diagnosis of Parkinson’s based on

A

Requires 2 of 4 cardinal signs:

  1. Resting “pill-rolling” tremor
  2. Skeletal muscle rigidity
  3. Postural instability - loss of balance
  4. Bradykinesia - very slow movements and reflexes
225
Q

Why are 2 medications required to treat Parkinson’s disease

A

Levodopa is the precursor to dopamine. It is metabolized in the blood, however DA cannot cross BBB
Carbidopa prevents levodopa metabolism and allows more levodopa to enter the CNS

226
Q

What are 3 common side effects of levodopa-carbidopa

A
  1. Increase inotropy
  2. Tachycardia
  3. Orthostatic HoTN
227
Q

Selegiline class and MOA

A

MAO-B inhibitor that restores dopamine concentration by reducing dopamine metabolism in CNS

Doesn’t increase risk of tyramine-induced HTN crisis

228
Q

What are Parkinson’s patients at risk for with GA

A
  1. Autonomic instability
  2. Orthostatic HoTN
  3. Dysrhythmias
  4. Aspiration
229
Q

Should patients taking levodopa take it on the day of surgery

A

YES
It has a half-life of 6 - 12 hrs
It should be given during prolonged surgeries to prevent muscle rigidity

230
Q

How can antidopaminergic drugs impact Parkinson’s patients

Ex of drugs

A

They can exacerbate extrapyramidal s/sx

231
Q

Which drugs should be avoided in Parkinson’s patients

A

Antidopaminergic drugs

  1. Metoclopramide
  2. Butyrophenones (haldol, droperidol)
  3. Phenothiazine (phenergan)
232
Q

Which drug class can be used to treat acute exacerbation of Parkinsonian symptoms

A

Anticholinergics

Benadryl

233
Q

How is HoTN addressed in Parkinson’s patients

A

Volume expansion

Direct-acting agents (phenylephrine)

234
Q

What medication is held if a patient is undergoing deep brain stimulation

A

Levodopa

235
Q

Where are DBS electrodes inserted for Parkinson’s patients

A
  1. Subthalamic nucleus
  2. Globus pallidus
  3. Ventralis intermedius
236
Q

What medications are best suited for DBS surgery

A

Light sedation with opioids and dexmedetomidine

237
Q

Which medications should be avoided during DBS surgery and why

A 
GABA agnoists (propofol, bzds)
GABA plays crucial role in thalamus
Avoid these drugs b/c they interfere with electrophysiologic brain monitoring
238
Q

What is SBP goal for DBS surgery

A

<140 mmHg to avoid risk of intracranial hemorrhage

239
Q

What is the etiology of ischemic optic neuropathy

A

Inadequate blood supply to the optic nerve due to venous congestion in the optic canal, reducing ocular perfusion pressure

240
Q

Equation for ocular perfusion pressure

A

OPP = MAP - IOP

241
Q

What are the characterization of ION

A

Anterior ischemic optic neuropathy

Posterior ischemic optic neuropathy

242
Q

Which cranial nerve is affected in IOP

A

Optic nerve (CN 2)

243
Q

Describe anterior ischemic optic neuropathy

A

Located anterior to the lamina cribrosa and impaired perfusion through the posterior ciliary arteries is the most likely explanation

Swelling of the optic disc

244
Q

Describe posterior ischemic optic neuropathy

A

Occurs posterior to the lamina cribrosa and most likely d/t the pial vessel supply in the optic nerve

Normal optic disc (no swelling)

245
Q

When does vision loss typically occur with ION

A

24 - 48 hrs after surgery

246
Q

Which surgery is ION most common

A

after spinal surgery in prone position

247
Q

What are procedural risk factors for ION

A
  1. Prone position
  2. Wilson frame use
  3. Long duration of anesthesia
  4. Large blood loss
  5. Low ratio of colloid to crystalloid resus
  6. HoTN
248
Q

What are patient risk factors for ION

A
  1. Male
  2. Obesity
  3. DM
  4. HTN
  5. Smoking
  6. Old age
  7. Atherosclerosis
249
Q

What is the etiology of central retinal artery occlusion

A

Decreased perfusion of the central retinal artery (d/t reduced venous outflow from improper head position) leads to blindness

the artery arises from carotid and opthalmic aa.

250
Q

What is the typical presentation of central retinal artery occlusion

A

Sudden, painless, vision loss in one eye on emergence

Examination reveals cherry red macula with pale surrounding retina

251
Q

What are risk factors for central retinal artery occlusion

A
  1. Using horseshoe headrest in prone position
  2. Use of N2O following retinal detachment surgery with intraocular gas bubble
  3. Embolism
252
Q

Treatment for corneal abrasion

A 
Abx drops (erythromycin, tobramycin)
NSAIDs

APEX-Neuro (3 decks)

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