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Neurology Exam > Neurology PP 2 > Flashcards

Neurology PP 2 Flashcards

1
Q

Epilepsy is defined as

A

Recurrent unprovoked seizures

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2
Q

In important to avoid prolonged fasting as

A

Low glucose can increase seizures

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3
Q

Long acting barbs may be problematic due to

A

Prolonged sedation & respiratory depression

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4
Q

Which medication should be avoided due to its pro convulsant properties

A

Tramadol

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5
Q

Which NMB can induce seizures

A

Atracurium’s metabolite LAUDANOSINE (esp in hepatic failure)

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6
Q

LAs have the potential to

A

Cause seizure at high doses

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7
Q

Which antiemetic should be avoided

A

Dopamine antagonist like Regland, since it can increase the severity of the seizures

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8
Q

When is a seizure likely to happen?

A

On induction or emergence

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9
Q

Increased GABAergic inhibition can

A

Make the cortex more susceptible to seizures

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10
Q

Which anesthetics can induce seizure

A

Enflurane

Etomidate

Sevo

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11
Q

What is Multiple Sclerosis

A

Chronic autoimmune disease that affects the CNS

Inflammation, demyelination & neurodegeneration

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12
Q

A lumbar puncture for MS looks for

A

Oligclonal bands in CSF

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13
Q

What is the treatment for MS

A

Disease modifying treatment

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14
Q

What is the goal of disease modifying treatments

A

Prevent relapse

Slow progressive worsening

(injectables, orals, monoclonal antibody treatments)

Treatment for relapse: corticosteroids, plasmapheresis or IVIG

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15
Q

Symtomatic treatment of MS includes

A

Muscle relaxants

Potassium channel blockers

Botox

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16
Q

What happens to Myelin during MS?

A

Immune response targets myelin & nerve fibers

Plaque forms where there is myelin loss & inflammation

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17
Q

What is Axonal Transection

A

In NS, the axons are damaged or severed, contributing to permanent Neuro deficits

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18
Q

MS requires demonstration of at least

A

2 CNS lesions or spinal cord

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19
Q

What can aggravate MS

A

Hyperthermia

Spinal anesthesia

Local anesthetics due to increased sensitivity of demyelinated axons

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20
Q

What MS medication potentates NDMA

A

Baclofen

Must use reversal

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21
Q

Demyelinated axons are

A

More sensitive to heat

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22
Q

GBS starts & ends

A

Starts in lower extremities & moves up

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23
Q

GBS affects

A

The peripheral nervous system

Rapid onset of muscle weakness

Sometimes paralysis

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24
Q

Who’s at higher risk of GBS

A

Males

Adults

Onset can last up to 6 months

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25
Q

Common infections that cause GBS

A

Cytomegalovirus (CMV)
Epstein Barr Virus (EBV)

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26
Q

GBS effects on immune cells

A

T & B cells activate & produce antibodies against these nerves

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27
Q

What are the subtypes of GBS

A

Demyelinating

Axonal

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28
Q

With GBS, there is a risk for

A

Autonomic dysfunction

Respiratory Failure

Aspiration

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29
Q

GBS will have an exaggerated response to

A

Indirect acting vasopressors

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30
Q

Wha drug should be avoided in GBS

A

Sux due to hyperkalemia

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31
Q

Which non depolarizers can be used with GBS

A

Cis

Vec

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32
Q

In GBS, compensatory CV response

A

May be absent

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33
Q

Postpolio sequelae manifest as

A

Fatigue
Skeletal muscle weakness
Joint pain
Cold intolerance
Dysphasia
Sleep & breathing problems

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34
Q

Poliomyelitis is sensitive to

A

Sedative effects of anesthesia

Sensitive to nondepolarizers

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35
Q

Poliomyelitis my experience

A

Delayed awakening

Sensitivity to cold

Abnormal pain perception

PNA so suction!!

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36
Q

Cerebral palsy affects

A

Motor system & results in progressive spasticity & hypertonicity

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37
Q

What is chorea

A

Rapid jerky movements

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38
Q

What happens when a baclofen pump is abruptly stopped

A

Rebound spasticity

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39
Q

What is the standard procedure for CP

A

Tendon release

Selective dorsal rhizotomy to reduce spasticity

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40
Q

PeriOp considerations for CP

A

GERD

increased salvation

PNA

Imparied swallowing

Reactive airway disease ( will bronchospasm)

Seizures

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41
Q

CP are at higher risk risk for

A

Latex Allergy

Hypothermia

Excessive secretions

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42
Q

Are CP sensitive to IA

A

Yes

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43
Q

CP is resistant to

A

Non depolarizers

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44
Q

In CP, emergence

A

May be delayed

May also see irritability (precedex)

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45
Q

ALS (Lou Gehrigs) disease is characterized as

A

Loss of motor neurons in brainstem & spinal cord

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46
Q

Majority of ALS is

A

Sporadic

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47
Q

ALS involves dysfunctional

A

Mitochondria

Oxidative damage to protein, lipids & DNA

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48
Q

Activation of microbial & astrocytes release

A

Proinflammatory cytokines & neurotoxic factors, contributing to motor neuron damage

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49
Q

Patient with Bulbar symptoms may have

A

Difficulty protecting their airway increasing aspiration risk due

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50
Q

How does Sux cause hyperkalemia

A

Due to upregulation of Ach receptors on enervated muscles, leading to life threatening potassium release

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51
Q

ALS may have an increase sensitivity to

A

Non depolarizers

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52
Q

Alzheimer’s disease involves multiple molecular & cellular mechanisms including

A

Amyloid beta plaque formation, tau protein hyperphosphorylation, neuroinflammation, synaptic dysfunction & neuronal loss

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53
Q

AD patients are at an increased risk of

A

Agitation & confusion , so it is best to stay away from benzos

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54
Q

What are the biomarkers in AD

A

CSF analysis total tau & phosphorylation tau

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55
Q

What medications help manage AD

A

Chokinesterase inhibitors

NMDA receptor antagonist

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56
Q

In patient with AD, anticholinergics can

A

Further suppress ACh

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57
Q

What is Parkinson’s disease

A

Loss of Dopaminergic neurons in basal ganglia

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58
Q

Dopamine deficiencies can cause

A

Activation of GABA neurons, resulting in cortical inhibition

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59
Q

In Parkinson’s disease, an increase in glutamate NT

A

Causes increased cholinergic activity

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60
Q

What is the hallmark finding of Parkinson’s

A

Lewy Bodies

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61
Q

What is the treatment of Parkinson’s

A

Levodopa combined with Carbidopa

Dopamine Agonist (bromocriptine, pergolide, cabergoline, ropinirole, pramipexole, Amantadine,apomorphine)

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62
Q

What are examples of Dopamine metabolism inhibitors

A

MAO-B inhibitors (selegelline)

COMT inhibitors (entacapone, tolcapone)

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63
Q

What are examples of centrally acting anticholinergics

A

Trihexphenidyl

Benztropine

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64
Q

If a patient has vocal tremor, then they are at an increased risk of

A

Aspiration

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65
Q

Which medications would be avoided in Parkinson’s

A

Regland, Driperidol & phenothiazines due to them being anti dopaminergics

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66
Q

With Parkinson’s, meperidine taken with Selegiline can cause

A

Neuroleptic Malignant Syndrome

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67
Q

In patients with Parkinson’s, wha twill you see when given fentanyl

A

Rigid chest

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68
Q

What is Neuroleptic Malignant Syndrome

A

Results from the lack of dopamine

Dopamine receptor blockade

Inadequate dopamine production

Occurs with sudden withdrawal of antiparkinsonian therapy (metoclopramide)

Give bromocriptine or Haldol to treat

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69
Q

What is the diagnostic criteria for NMH

A

Temperature 38 C

Extra pyramidal effects >2

Autonomic dysfunction >2

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70
Q

When treating NMS, what is the dose of Bronocriptine

A

2.5 mg Q8H up to 5mg Q4H

Continued for 7-10 days

71
Q

When treating NMS, what is the dose of Dantrolene

72
Q

What is the difference between GBS & Myasthenia Gravis

A

GBS is ascending

MG is descending

73
Q

MG is caused by autoimmune disruption of

A

Postsynaptic Ach receptors at the NMJ

74
Q

With MG, muscle strength improves with

A

Rest

Deteriorates rapidly with exertion

75
Q

What can exacerbate MG

A

Infection
Surgery
Pregnancy
ABX

76
Q

How’s MG graded

A

On the Osserman grading system

Classes 1, 1A, 2A, 2B, 3 (intubate), 4

77
Q

With a thymectomy, you will seen an

A

Increase in T cells

78
Q

What is the most sensitive test for MG

A

Single fiber electromyography

79
Q

What will be seen with MG patients

A

Phase 2 block

80
Q

Plasmapheresis depletes plasma esterase, which will prolong the effects of

A

Suxs
Mivacurium
Ester-linked LAs

81
Q

With MG, patients may be resistant to

A

Depolarizers due to reduced receptor activity, requiring increased dose

Increased risk of non depolarizing phase 2 block

82
Q

MG treatment includes

A

Plasmapheresis + IVIG for 5 days

83
Q

Excessive anticholinesterase drugs can lead to

A

Cholinergic Crisis

84
Q

What is SLUDGE

A

Acronym for cholinergic crisis

Salvation
Lacrimation
Urination
Defication
GI disturbance
Emesis

85
Q

With the SLUDGE acronym, you can also have

A

Bradycardia
Miosis
Bronchospasm

86
Q

Cholinergic crisis is due to

A

Excess Ach at NMJ

87
Q

How do you treat cholinergic crisis

A

Atropine
Mechanical Ventilation

88
Q

Can sux be used with MG

89
Q

With MG & nondepolarizing mumble relaxants

A

Patient will have increased sensitivity

90
Q

Suds & MG

A

Resistant to blockade & delayed onset

91
Q

MG & locals

A

Prolonged action & increased toxicity or ester linked agents

92
Q

MG & ABX

A

Neuromuscular blockade is increased with aminoglycoside & erythromycin

93
Q

Lambert Eaton is associated with

A

Small cell Carcinoma

94
Q

Lambert Eaton is caused by a

A

Reduction in the release of Ach due to antibodies attacking voltage gates calcium channels at NMJ

95
Q

What can & cannot help patients with Lambert Eaton

A

Exercise helps

Anticholinesterase DOES NOT REVERSE IT

96
Q

Lambert Eaton patients are sensitive to

A

Depolarizers

Non depolarizers

97
Q

Lambert Eaton affects which gender

98
Q

MG is associated with what coexisting pathology

99
Q

MG responds well to

A

Anticholinesterase

100
Q

What is Myotonic Dystrophy

A

Persistent contractures of skeletal muscle after voluntary contraction or following electrical stimulation

Abnormality in intracellular ATP system that fails to return calcium to the SR

101
Q

In Myotonic Dystrophy, what is the cardiac involvement

A

Mitral valve prolapse in 20% of individuals

Deterioration of the bundle of HIS leading to 1st degree AV block

102
Q

In Myotonic Dystrophy, what is the pulmonary involvement

A

Restrictive lung disease

Impaired response to hypoxia & hypercarbia

103
Q

In Myotonic Dystrophy, what is a common eye finding

A

Cataracts/Christmas tree

104
Q

In Myotonic Dystrophy, what are typical GI s/s

A

Gastric stony

Intestinal hyper-motility

Pharyngeal muscle weakness with impaired airway protection

Cholelithiasis

105
Q

In Myotonic Dystrophy, what should be avoided

A

Premedications with sedatives

Etomidate (due to myoclonus)

Suxs (exaggerates contractures & elevated K)

Anticholinesterase (may precipitate contraction)

Hypothermia

Exaggerated MI effects

106
Q

In Myotonic Dystrophy, patients are susceptible to

107
Q

In Myotonic Dystrophy, which tests should be performed

A

Cardiac & pulmonary

108
Q

In Myotonic Dystrophy, what is likely to aggravate s/s

109
Q

Which muscular dystrophy diseases are Xlinked

A

Duchennes

Beckers

110
Q

With muscular dystrophy, dead muscle cells are replaced by

A

Fat tissue & fibrous scars

111
Q

In muscular dystrophy, the muscles

A

Cannot contract normally, which leads to weakness

112
Q

What is the most common muscle dystrophy seen in children

A

Duchenne

Beckers

113
Q

What is the most common cause of death in DMD

A

Respiratory insufficiency

114
Q

How does scoliosis affect DMD

A

With every 10th degree, FBC decreases by 4%

115
Q

DMD can cause this cardiac problem

A

Mitral regurgitation due to papillary muscle dysfunction

116
Q

Which method of anesthesia should be considered with DMD

A

TIVA to prevent cardiac depression

117
Q

What has been associated with DMD

118
Q

Signs of MH

A

Muscle rigidity (master muscle)

Rapid unexplained increase in end tidal

Fever

Increased creative phosphate

Cola urine

119
Q

MH is cause by mutations in the

A

RYR1 gene

Results in high intracellular level of Ca+

120
Q

What are MH triggers

A

Depolarizing relaxants (Suxs)

Inhalation agents

121
Q

How is MH treated

A

Discontinue agent

Hyperventilate with 100% oxygen

Dantrolene 2.5 mg/kg IV to a total dose of 10mg/kg Q5-10min

Correct metabolic acidosis

Control fever

Monitor UO

Treat hyperK

122
Q

What’s the gold standard for preventing MH

A

Screening with caffeine contracture test on muscle biopsy

GOLD STANDARD

123
Q

How long should MH be monitored

124
Q

Metabolic myopathies are at an extreme risk of

125
Q

Mitochondrial Myopathies can lead to

A

AV block

Difficult anesthetic since most drugs depress mitochondria

126
Q

What is the most common spinal injury

A

Hyperextension

127
Q

In trauma, what can increase swelling

A

Methylprednisone

128
Q

Spinal shock is characterized by

A

Flaccid muscle paralysis & loss of sensation below injury

129
Q

What is neurogenic shock

A

Results from autonomic nervous system impairment following CNS injury

130
Q

What is ASIA classification

A

Extent of injury with A being total loss of motor & sensory function below lesion

131
Q

Bradycardia occurs due to

A

Loss of T1 through T4 sympathetic innervation

132
Q

Should fiber optic be used in head trauma

133
Q

Plain c ray imaging is

A

Not sensitive for ligamentous injury

134
Q

Suxs is safe within

A

24h post injury

135
Q

With spinal cord injuries, what is the goal MAP?

A

Above 85-90mmHg for at least 7 days to prevent further injury

136
Q

What are risk factors for POVL

A

Make
Obese
Wilson frame
Longer surgery
High blood loss

137
Q

What is anterior spinal artery syndrome

A

Caused. Y sustained hypoperfusion of the anterior spinal artery

Leads to motor weakness

138
Q

When does Autonomic dysreflexia occur

A

Weeks to months after complete SCI (starts at 10 days)

Will have systemic HTN, HA, swearing & flushing above injury level

Triggered by stimulus below injury (bladder dissection)

139
Q

With spinal cord injury, you’ll see ___ above & trigger points____ injury

A

S/s above

Below

140
Q

What is the acute management of autonomic dysreflexia

A

Remove stimulus

Deepen anesthesia

Vasodilators

141
Q

What type of anesthetic is preferred for spinal surgery

A

GA or spinal (to reduce triggers)

142
Q

SSEP monitors integrity of

A

Peripheral nerves

Spinal cord

Brainstem

Sensory cortex

143
Q

MEP monitors

A

Motor cortex & anterolateral spinal cord

144
Q

ENG is sensitive to

A

Mechanical & thermal injury

145
Q

What inhibits SSEP signals

A

Potent volatile anesthetics & nitrous

Decrease amplitude & increase latency

146
Q

During SSEPs, muscle relaxants are useful for

A

Eliminating myotonic interference

147
Q

MEPs is highly sensitive to

A

Anesthesia, especially volatile

Caution use of muscle relaxers

148
Q

What can impair or abolish EMG signals

A

Muscle relaxants

Inhaled & IV have minimal effects

149
Q

Injury at or above C5 may cause

A

Apnea due to diaphragm deneevation

150
Q

What can happen during tracheobronchial suctioning

A

Bradycardia & cardiac arrest

151
Q

During anesthesia for chronic spinal cord injury, what should be avoided

A

Autonomic hyperreflexia

152
Q

With a baclofen pump, make sure to watch out for

153
Q

Chronic spinal cord patients are at an increase risk of

A

Dehydration

Hyperkalemia

Stones

154
Q

Autonomic Hyperreflexia appears after

A

Spinal shock & with the return of spinal cord reflexes

155
Q

Autonomic Hyperreflexia is triggered by

A

Cutaneous or visceral stimulation below the level of injury

156
Q

Autonomic Hyperreflexia causes vasoconstriction

A

Below the injury level due to lack of inhibitory impulses from higher CNS centers

157
Q

Autonomic Hyperreflexia s/s

A

Reflex bradycardia

Cutaneous vasodilation above injury

Severe HTN include HA & blurred vision

Nasal stuffiness due to vasodilation

158
Q

Autonomic Hyperreflexia complications

A

Cerebral, retinal, subarachnoid hemorrhage

Increased operative blood loss

Loss of consciousness

Seizure

Arrhythmias

Pulmonary edema

159
Q

Autonomic Hyperreflexia can cause pulmonary edema, which indicates

A

Acute left ventricular failure due to increased after load

160
Q

What percentage exhibit Autonomic Hyperreflexia

A

85% with lesions above T6

Unlikely when below T10

161
Q

What testing should be performed for scoliosis

A

Pulmonary & cardiac

162
Q

What should you look for cardiac wise for scoliosis

A

Signs of right ventricular hypertrophy or cor pulmonale

163
Q

Contraindications for TXA

A

DVT
PE
Recent stent
Chronic Afib

164
Q

What should be available when administering blood

A

Ca+ & FFO for every 2-3 units of blood

165
Q

How should scoliosis vent be managed

A

Lower tidal volumes & higher RR

166
Q

Can you side cell saver for metastatic cases

167
Q

What should be checked if a patient is prone

A

Cuff leak to assess airway edema

168
Q

Myelomeningocele is associated with

A

Maternal folate deficiency
Trisomy 13 & 18
Type 2 Chiari malformation

At increased risk for latex allergies

169
Q

What can occur, especially with Tyoe 2 Chiari malformations

A

Hydrocephalus

170
Q

Ulnar nerve

Facial nerve

A

Recovery

Onset

171
Q

What should be avoided in tethered spinal cord syndrome

A

Spinal anesthesia to prevent cord injury

172
Q

Kennedys disease is

Friedreich disease is

A

X linked

Autosomal

173
Q

Autonomic Hyperreflexia is common in

A

Ethical & thoracic injuries

Neurology Exam (2 decks)

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