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S5 - Advanced Patho > Neuro Diseases > Flashcards

Neuro Diseases Flashcards

1
Q

normal CBF

A

50 mL/100 g brain tissue when CPP 50-150 mmHg

approx 750 mL/min (15-20% of CO)

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2
Q

factors that govern CBF (5)

A
  1. CMRO2
  2. CPP
  3. PaCO2/O2 tension
  4. various meds (esp. volatiles)
  5. intracranial abnormalities
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3
Q

rate of CMRO2

what % of total body O2?

A

3-3.8 mL O2/100 g brain tissue/minute

20% of total body O2

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4
Q

what is most cerebral O2 consumption used for?

A

to generate ATP for neuronal electrical activity

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5
Q

result of high O2 consumption + low O2 reserve

what happens if not restored ASAP?

A

unconsciousness in 10 seconds if perfusion stopped

if not restored in 3-8 min - ATP stores depleted, cellular injury and death can occur

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6
Q

2 things that decrease CMRO2

A

hypothermia

anesthetic agents

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7
Q

2 things that increase CMRO2

A

hyperthermia

seizures

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8
Q

CPP =

what is a normal value?

A

MAP - ICP

normally 60-110 mmHg

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9
Q

T/F - if a pt has an ICP > 30 but normal MAP, CPP won’t change

A

false - CPP and thus CBF can change (whatever that means)

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10
Q

effect of CPP on EEG:

  • CPP < 50 mmHg
  • CPP 25-40 mmHg
  • CPP < 25 mmHg
A
  • < 50 = slowing on EEG
  • 25-40 = flat EEG
  • < 25 = possible irreversible brain damage
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11
Q

what determines CPP beyond 50-150 mmHg

A

pressure-dependent

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12
Q

how do increases and decreases in BP impact arteries?

A

increased BP = arterial constriction

decreased BP = arterial dilation

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13
Q

Effects of CBF in normotensive pt:

  • CBF 35 mmHg
  • CBF 150 mmHg

(shouldn’t this be in mL or something? sos)

A
  • CBF 35 mmHg = ischemia (nausea, dizziness)
  • CBF 150 mmHg = vessels maximally constricted, fluid forced out of vessel = cerebral edema
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14
Q

how does HTN affect autoregulation curve

A

shifts to right

chronic HTN - lower limit shifts upward

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15
Q

autoregulation lost or impaired with (3):

A
  • intracranial tumors
  • head trauma
  • volatile anesthetics
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16
Q

most important extrinsic influence of CBF

A

PaCO2

(directly proportional)

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17
Q

how does CBF change with PaCO2 changes

A

CBF changes approx 1-2 mL/100 g/min per mmHg change in PaCO2

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18
Q

what PaCO2 is associated with shifting the PaCO2/CBF curve to the left

A

< 20

may have EEG changes

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19
Q

how does decreased PaCO2 affect:

  • CSF pH
  • vessels
  • ischemia
  • ICP
A
  • increased CSF pH
  • vasoconstriction
  • increased cerebral ischemia
  • decreased ICP
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20
Q

how does increased PaCO2 affect:

  • CSF pH
  • vessels
  • ischemia
  • ICP
A
  • decreased CSF pH
  • vasodilation
  • decreased cerebral ischemia
  • increased ICP
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21
Q

CBF is not significantly affected by decreased PaCO2 until threshold of ____

A

50

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22
Q

3 major effects of hypocapnia that lead to tissue hypoxia

(picture on slide 10)

A
  1. vasoconstriction
  2. increased neuronal excitability
  3. CSF alkalosis
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23
Q

how does CSF alkalosis r/t hyperventilation lead to tissue hypoxia

A

alkalosis → oxyhgb dissociation curve L shift → decreased O2 delivery → tissue hypoxia

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24
Q

how does neuronal excitability r/t hyperventilation lead to tissue hypoxia?

A

increased excitatory amino acids → increased O2 consumption → tissue hypoxia

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25
Q

how does vasoconstriction r/t hyperventilation lead to tissue hypoxia?

A

vasoconstriction → decreased CBF → decreased O2 supply → tissue hypoxia

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26
Q

how does vasoconstriction r/t hyperventilation affect ICP

A

vasoconstriction → decreased CBF → decreased CBV → brain relaxation/decreased ICP

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27
Q

how does hypocapnia impact TBI or brain bleed

A

~unclear~

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28
Q

how does temp change affect CBF

A

CBF changes 5-7% per 1° C

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29
Q

how does hypothermia affect CMRO2 and CBF

A

both decrease

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30
Q

how does hyperthermia affect CMRO2 and CBF

A

both increase

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31
Q

how does hct affect viscosity

A

decreased Hct = decreased viscosity (also decreases O2 carrying capacity)

increased Hct = increased viscosity, decreased CBF

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32
Q

suggested optimal Hct for cerebral O2 delievry

A

30%

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33
Q

how do brain blood vessels create a blood-brain barrier?

(pic on slide 13)

A

tight junctions (no pores) create the barrier

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34
Q

what things move easily across the BBB?

what things are restricted?

A

lipid-soluble things move easily - CO2, O2, H2O, most anesthetics

restricted: ionized or large molecular weight

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35
Q

conditions that disrupt BBB (8)

A
  • severe HTN (chronic or acute, new onset)
  • strokes
  • trauma
  • tumors
  • infection
  • hypercapniea
  • hypoxia
  • sustained seizures
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36
Q

if the BBB is disrupted, what is fluid movement dependent on?

A

hydrostatic pressure (not osmotic gradient)

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37
Q

major function of CSF

A

protect CNS against trauma

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38
Q

where is CSF formed?

A

choroid plexus of cerebral ventricles (mostly lateral)

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39
Q

2 ways CSF is produced

A
  1. ultrafiltration and secretion by cells of choroid plexus
  2. passage of water, electrolytes, and other things across BBB
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40
Q

she said she wouldn’t ask specifics about CSF flow through the brain but to be familiar with it? so peek at the pic on slide 16

A

:)

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41
Q

how much CSF do adults produce

A

21 mL/hr (500 mL/day)

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42
Q

total CSF volume

A

150 mL

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43
Q

what % of the cranial vault is made up by:

  • brain
  • blood
  • CSF
A
  • brain - 80%
  • blood - 12%
  • CSF - 8%
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44
Q

where is ICP measured?

A

lateral ventricles or over cerebral cortex

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45
Q

what is the Monroe-Kellie Doctrine?

A

any increase in one compartment (brain, blood, CSF) must be offset by equal reduction in another to avoid increased ICP

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46
Q

ICP values:

  • normal
  • mild increase
  • moderate increase
  • severe increase
A
  • normal: 5-10 mmHg
  • mild: 20-30 mmHg
  • moderate: 30-40 mmHg
  • severe: > 40 mmHg
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47
Q

blood pressure effects of cerebral blood volume are dependent on?

A

autoregulation of CBF

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48
Q

where is a subfalcine herniation?

what are the adverse effects?

A

cingulate gyrus under falx cerebri

compression of anterior cerebral artery → midline shift

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49
Q

where is a transtentorial herniation?

what are the adverse effects?

A

uncinate gyrus through tentorium cerebelli

brainstem compression → altered consciousness, gaze defects, ocular reflex defects, hemodynamic and resp failure → death

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50
Q

what is a transcalvarial herniation?

A

any area beneath a defect in the skull

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51
Q

what can herniate through foramen magnum

A

cerebellar tonsils

stupid question sry

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52
Q

where is an uncal herniation?

adverse effect?

A

medial portion of temporal lobe

causes oculomotor nerve dysfunction → pupil dilation, ptosis, lateral deviation of affected eye

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53
Q

s/s cerebral tonsils herniating through foramen magnum

A

cardiac and resp dysfunction indicating medullary dysfunction

leads to death

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54
Q

s/s increased ICP

A

HA, nausea, pupil dilation, blurred vision, decreased LOC, seizures, coma, blah blah

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55
Q

Cushing’s Triad

A

irregular respirations

increased BP

decreased HR

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56
Q

how do brain tumors directly and indirectly increase ICP?

A

directly d/t size

indirectly d/t edema in surrounding tissue

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57
Q

inner brain things that increase ICP (5)

A
  • brain tumors
  • brain bleeds
  • brain hematoma
  • infection (meningitis, encephalitis)
  • aqueductal stenosis
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58
Q

inner brain things that increase ICP (5)

A
  • brain tumors
  • brain bleeds
  • brain hematoma
  • infection (meningitis, encephalitis)
  • aqueductal stenosis
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59
Q

what is aqueductal stenosis?

what disorder is seen in ⅓ of these pts?

A

congenital narrowing of cerebral aqueduct connecting 3rd and 4th ventricles

⅓ have seizures

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60
Q

interventions to decrease ICP (9)

a bunch of ish but we already know this

A
  • elevate HOB
  • head neutral
  • hyperventilation
  • CSF drainage
  • hypothermia
  • hyperosmotic drugs
  • corticosteroids
  • cerebral vasoconstrictors
  • HTN control
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61
Q

dose of mannitol to decrease ICP

A

20% mannitol

0.25-1 g/kg IV

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62
Q

cerebral vasoconstrictors that can decrease ICP

A

barbiturates

propofol

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63
Q

MAP goal when giving antihypertensives to decrease ICP

A

> 70

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64
Q

underlying mechanisms of seizure disorders

A
  • loss of inhibitory activity
  • enhanced release of excitatory amino acids
  • enhanced neuronal firing d/t voltage-mediated Ca2+ current
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65
Q

a bunch of shit can cause seizures. we know that

A

examples:

  • genetic predisposition
  • brain tumor/trauma
  • infection/febrile illness
  • hypoxia
  • drug OD/withdrawal
  • fatigue, stress
  • methohexital
  • ketamine
  • demerol
  • metabolic defects
66
Q

metabolic defects that precipitate seizures

A
  • hyper/hyponatremia
  • hypomagnesemia
  • hypocalcemia
  • hypoglycemia
  • alkalosis
67
Q

anesthesia drugs that can precipitate seizures

A
  • methohexital
  • ketamine
  • demerol
68
Q

manifestations of partial seizures

A

motor, sensory, autonomic, or psych symptoms

69
Q

where do generalized seizures originate

(plz reword)

A

bilaterally symmetric electrical activity

70
Q

what is a petit mal seizure?

A

aka absence seizure

transient lapse in consciousness

71
Q

manifestations of a grand mal seizure

A

aka tonic-clonic seizures

loss of consiousness → clonic activity → tonic motor activity

72
Q

status epilepticus is a medical emergency

A

next

73
Q

focus of preop eval for pts with seizures

A
  • cause/triggers
  • type of seizure
  • medications
  • last seizure
74
Q

T/F - if a pt just has partial seizures it’s not as important that they continue AEDs throughout periop period

A

false - even a partial sz can progress to generalized sz

75
Q

meds to avoid in pts with seizure disorders

A
  • ketamine
  • methohexital
  • demerol
  • atracurium/cisatracurium in large doses (metabolites)
76
Q

NMB dosing considerations for pts with seizure disorders

A

probably will need to increase dose d/t hepatic enzyme induction (from sz meds)

77
Q

meds and doses to terminate a seizure

A
  • 50-100 mg Propofol
  • 500-1000 mg Dilantin (slowly)
  • 1-5 mg midazolam
78
Q

most common causes of adult seizures

A
  • mostly structural lesions (head trauma, tumors, stroke)
  • metabolic abnormalities (liver failure, uremia, hypoglycemia, hyopcalcemia, drug tox, drug/ETOH withdrawal)
79
Q

pt population assoc. with idiopathic seizures

A

kiddos (can carry into adulthood)

80
Q

what is Parkinson’s disease

A

most common disorder involving motor tracts of EPS (controlled by basal ganglia and cerebellum)

81
Q

what is primary parkinson’s?

A

degenerative disorder of substantia nigra

interferes with dopamine pathways to basal ganglia

onset > 50 yrs old

82
Q

what causes secondary parkinson’s?

A

trauma, drugs, infection, toxins

(usually reversible)

83
Q

principle feature of Parkinson’s

A

degeneration of dopaminergic pathways (inhibitory) and relative excess of cholinergic activity (excitatory)

84
Q

classic signs of Parkinson’s

~trigger warning~

A
  • skeletal muscle tremors
  • rigidity
  • akinesia of facial muscles
  • often oily skin, seborrhea
  • diaphragmatic spasms
  • eventually includes muscles of chewing/swallowing
  • upper airway involvement may restrict airflow
85
Q

where does rigidity first occur in Parkinson’s

A

neck muscles

86
Q

describe skeletal muscle tremors with Parkinson’s

A

rhythmic, usually at rest

usually disappear with voluntary movement

pill-rolling tremor

87
Q

goal of parkinson’s treatment

A

increase concentration of dopamine in basal ganglia or decrease effects of ACh

88
Q

side effects of L-dopa (Sinemet, Parcopa)

A
  • dyskinesias
  • confusion
  • headache
  • hallucinations
  • orthostatic hypotension
  • increased contractility
89
Q

MOA of decarboxylase inhibitors for Parkinson’s

A

prevents conversion of levodopa to dopamine in periphery to optimize conversion in CNS

90
Q

3 general med classes used to treat Parkinson’s

A
  1. Levodopa-dopamine precursors
  2. decarboxylase inhibitor
  3. anticholinergics
91
Q

surgical treatment of Parkinson’s

A

deep brain stimulation - stimulates various nuclei in basal ganglia to relieve/help with tremor

92
Q

intraop anesthesia concerns for deep brain stimulation treatment of Parkinson’s

A
  • they’re awake :(
  • sitting position - VAE risk
  • avoid propofol/benzos
  • avoid oversedation (little access to airway)
93
Q

why should propofol and benzos be avoided with deep brain stimulation (Parkinson’s treatment)

A

alter recordings of nuclei and thus stimulation of appropriate place (brain area?)

94
Q

meds to avoid in pts with Parkinson’s

A
  • ketamine
  • metoclopramide
  • phenothiazines (Compazine, Thorazine)
  • butyrophenones (Haldol, Droperidol)
  • opioids (use carefully? predisposed to rigidity)
  • succs (rare reports of hyperkalemia)
95
Q

dosing considerations for nondepolarizing NMBs in Parkinson’s

A

generally normal

96
Q

most common neurodegenerative disease

A

Alzheimer’s

97
Q

how is Alzheimer’s characterized

A

slow decline in intellectual function (5 + years)

affects memory, judgment, decision making, emotional lability

98
Q

late signs of Alzheimer’s

A

extrapyramidal symptoms

apraxias

aphasia

99
Q

why do pts with Alzheimer’s have altered responses to many anesthetic drugs?

A

loss of gray matter

100
Q

how does Alzheimer’s affect brain?

A

marked cortical atrophy with ventricular enlargement

101
Q

patho of Alzheimer’s

A

proteins in neurons become twisted and distorted “neurofibrillary triangle”

“senile plaques” deposit that disrupt impulse transmission, esp. in cerebral cortex & hippocampus

102
Q

consent considerations for Alzheimer’s pts

A

must get from someone legally able to provide - pt may not have cognitive ability to consent

103
Q

pts with Alzheimer’s can have new-onset, temporary impairment after anesthesia that lasts how long?

A

1-3 days

104
Q

considerations for giving anticholinergics to Alzheimer’s pts

A

avoid centrally acting (atropine, scopolamine) - add to confusion

use glycopyrrolate if needed

105
Q

use of regional anesthesia in Alzheimer’s pt

A

no contraindications but consider how you will give anxiolysis and potential side effects

106
Q

what is multiple sclerosis?

A

reversible demyelination at random and multiple sites in brain and spinal cord

inflammation eventually causes scarring

107
Q

causes and etiology of MS

A

may be autoimmune initiated by a virus

primarily affects females 20-40 yrs old (2:1 vs. males)

108
Q

central symptoms of MS

A
  • fatigue
  • cognitive impairment
  • depression
  • unstable mood
109
Q

GI/GU symptoms of MS

A
  • incontinence
  • diarrhea or constipation
  • urinary frequency or retention
110
Q

airway symptoms of MS

A
  • dysarthria
  • dysphagia
111
Q

visual symptoms of MS

A
  • nystagmus
  • optic neuritis
  • diplopia
112
Q

musculoskeletal symptoms of MS

A
  • weakness
  • spasms
  • ataxia
113
Q

sensation symptoms of MS

A
  • pain
  • hypoesthesias
  • parasthesias
114
Q

how is MS diagnosis confirmed?

A

CSF or MRI

115
Q

if a pt with MS comes in for elective surgery and they just got over an exacerbation yesterday, is it ok to proceed?

A

nah - give them a biscuit

116
Q

considerations for NMBs in pts with MS

A

if paresis or paralysis - no succs

117
Q

can peripheral nerve blocks be used on pts with MS?

A

yup

118
Q

can conduction still occur across demyelinated axons in MS pts?

A

yes - but affected by many things, including temperature

119
Q

what is ALS?

A

neurodegenerative, rapidly progressive weakness of both upper and lower motor neurons

120
Q

when does ALS typically present?

symptoms?

A

usually present in 50s or 60s

muscular weakness, atrophy, fasciculations, spasticity

121
Q

anesthesia concerns for ALS pts

A
  • aspiration risk
  • no Succs (hyperkalemia risk)
  • after 2-3 years, progresses to all skeletal muscles and pt has ventilation failure
122
Q

what is Guillain Barre syndrome

what can cause it?

A

immunologic reaction against myelin sheath of peripheral nerves → sudden onset of paralysis, areflexia, and paresthesias

assoc. with URI/GI infections, Hodgkin’s disease, HIV

123
Q

s/s Guillain Barre

A

weakness or paralysis that starts in the legs and spreads cephalad over several days

124
Q

types of Guillian Barre

A
  • acute inflammatory demyelinating polyneuropathy (75%)
  • acute motor axonal neuropathy
  • acute motor and sensory axonal neuropathy
125
Q

peak disability of GBS

A

10-14 days

126
Q

treatment of GBS

A

some respond to plasmapheresis

127
Q

anesthesia concerns for GBS pts

~trigger warning, feel free to break this up~

A
  • labile ANS - prepare for dysrhythmias and ANS instability
  • respiratory insufficiency/paralysis, pharyngeal muscle weakness
  • no succs
  • regional is controversial
  • hypotension with position change or small blood loss
  • exaggerated HTN with laryngoscopy
128
Q

common autonomic dysfunctions in GBS pts

A
  • wide change in BP
  • profuse diaphoresis
  • gastroparesis
  • tachycardia
  • dysrhytmias
129
Q

cycle of events leading to CVA

A

cell hypoxia → edema → activation of excitatory amino acids → creation of free radicals → calcium influx → (cell hypoxia)

130
Q

what causes a CVA?

A

cerebral perfusion is interrupted, depriving brain of O2 and glucose

131
Q

most common surgeries r/t CVA

A
  • open heart for valve disease
  • surgery on thoracic aorta
132
Q

mortality with intraop stroke

A

25%

133
Q

risk for periop stroke with GA + history of CV disease

A

0.4-3%

134
Q

***prior stroke or hx of TIA = increased risk of periop CVA***

A

:|

135
Q

risk factors for CVA (10)

A
  • HTN
  • diabetes
  • cigarettes
  • drug abuse
  • age > 75
  • CAD
  • hyperlipidemia
  • Afib
  • hereditary
  • prior stroke/hx TIA
136
Q

conditions assoc. with thrombotic CVA

A
  • atherosclerosis
  • diabetes
  • hypercoagulability
  • dehydration
  • arteritis
  • polycythemia vera
  • HTN
137
Q

what causes a thrombotic CVA?

A

arterial occlusion caused by thrombi in carotid or cerebral vessels

138
Q

what causes an embolic CVA?

A

fragments break from thrombi formed outside brain

139
Q

conditions assoc. with embolic CVA

A
  • Afib
  • endocarditis
  • prosthetic valve
  • carotid disease
  • valvular and aortic surgeries
140
Q

most common cause of hemorrhagic CVA

other causes?

A

HTN (60-80%)

also - ruptured aneurysm, AVM, bleeding tumor, coag defects

141
Q

headaches often assoc. with what type of CVA?

A

hemorrhagic

142
Q

treatment of a thrombotic or embolic stroke

A

IV fibrinolytic within 3 hours of symptom onset

143
Q

T/F - a pt with a suspected thrombotic or embolic stroke should be given a fibrinolytic ASAP

A

(this seems like an issue for the ER but)

false - don’t give until CT scan has r/o hemorrhage

144
Q

when should a suspected stroke pt not be given fibrinolytics

A
  • hx or evidence of bleed
  • known AVM, aneurysm, neoplasm
  • plt < 100
  • INR > 1.7
  • stroke, NSGY, or head trauma within past 3 months
145
Q

NMB considerations for CVA

A

resistance in paretic limb

monitor TOF in nonparetic limb

no succs

146
Q

effects of CVA in the area of infarct

A
  • loss of autoregulation
  • loss of CO2 responsiveness
  • loss of BBB integrity
147
Q

BP goal for HTN pt with CVA

A

keep slightly higher than normal

148
Q

pts with cerebrovascular disease at greatest risk for stroke

A
  • open heart procedures with valvular diseases
  • CAD with ascending aortic atherosclerosis
  • diseases of thoracic aorta
149
Q

risks for pts with cerebrovascular disease in noncardiac surgeries

A

risks assoc. with hyper or hypotension

150
Q

effects of pulse pressures > 80 mmHg

A

endothelial injury → hypoperfusion or embolism

151
Q

how does HTN affect BBB

A

sustained HTN = BBB breakdown

152
Q

how long does it take for blood flow abnormalities, BBB, and CO2 responsiveness to heal/resolve after a stroke?

A

blood flow abnormalities - 2 wks

BBB/CO2 responsiveness - 4 wks

153
Q

consults required before proceeding with elective surgery in pts with hx TIA

A

neuro and CV

154
Q

cases we might see pts with cerebrovascular diseases

A
  • emboli removal
  • carotid endarterectomy
  • endovascular procedures
  • hematoma evacuation
  • decompressive crani
155
Q

things to have ready for a pt with cerebrovascular disease

A

art line

IV vasodilators

beta blockers

156
Q

symptoms of spinal cord disorders

A
  • loss of sensation
  • weakness/paralysis of extremities
  • reflex changes (hyper or hypo)
  • bladder/bowel incontinence
  • back pain
  • muscle spasms
157
Q

causes of spinal cord disorders (3)

A
  • trauma
  • infection/abscess
  • autoimmune disorders
158
Q

airway considerations for spinal cord disorders

A
  • keep head neutral
  • possible obstruction/edema
  • RLN damage
159
Q

CV issues in pts with spinal cord disorders

A
  • reflex bradycardia
  • arrythmias
  • hyper and hypotension
160
Q

which CN is responsible for each of these s/s of increased ICP?

  • blurred vision
  • inability to adduct eyes
  • inability to abduct eyes
A
  • blurred vision - CN II
  • adduct - CN III
  • abduct - CN VI
160
Q

what are watershed infarcts?

A

hypoperfusion and necrosis in areas most distal to arterial blood supply

(??? sos her explanation didn’t really make sense to me so I googled it and its kinda different from what she said)

S5 - Advanced Patho (6 decks)

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