Neuromuscular (Exam III) Flashcards

1
Q

Multiple Sclerosis pathophys

A

progressive, autoimmune demylelination of central nerve fibers

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2
Q

onset of MS

A

20-40

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3
Q

risk factors for MS

A

1st degree relative
EBV
other autoimmune disorders
smoking

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4
Q

triggers for MS

A

stress
elevated temps
postpartum period

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5
Q

s/s of MS

A

motor weakness, sensory disorders, visual impairment, autonomic instability
varies based on site of demyleination

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6
Q

treatment for MS

A

no cure
managed by corticosteroids, immune modulators, targeted antibodies

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7
Q

pre-anesthetic considerations for MS

A

assess existing deficits
if respiratory compromise - consider PFTs
Labs: CBC with platelets, BMP w/wo LFT
consider preop steroids
temperature management is crucial
avoid succinycholine

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8
Q

why might you draw a BMP with LFT on a MS patient

A

on dantrolene and azathioprine - causes bone marrow suppression, liver function impairment
*close attention to glucose and electrolyes as steroids may impact levels

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9
Q

what anesthetic plan might you have for a MS patient

A

General, regional, peripheral nerve block are acceptable options

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10
Q

what RSI agent would you avoid in MS

A

succinycholine - may induce HyperK+

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11
Q

what might hyperthemia do to an MS patient

A

preciptate an exacerbation of MS symptoms

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12
Q

when is maysthenia gravis (MG) muscle weakness exacerbated

A

w/ exercise

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13
Q

thymic hyperplasia in myasthenia gravis is common at _____% with _____% of patients improving with thymectomy

A

thymic hyperplasia in myasthenia gravis is common at 10% with 90% of patients improving with thymectomy

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14
Q

what can cause symptom exacerbation with myasthenia gravis

A

pain, insomnia, infection, surgery

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15
Q

treatment of myasthenia gravis

A

ACh-E inhibitors (pyridostigmine), immunosuppressive agents, steroids, plasmapharesis, IVIG
*90% of patients improve with thymectomy

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16
Q

MG preanesthetic considerations

A

assess existing deficits
if respiratory compromise, consider PFTs
optimize respiratory function
Labs: CBC, BMP +/- LFT
counsel pt on increased risk of postop vent support until fully recovered from anesthesia

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17
Q

4 medication considerations with MG

A

reduce NMB dose to avoid prolonged muscle weakness
caution with opioid to avoid respiratory compromise
ACh-E inhibitors prolong succinycholine and ester LAs (X-caine)
preop steroid with anyone on long term steroids

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18
Q

when would you add an LFT to MG chem panel

A

if the patient is on azathiporine

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19
Q

eaton-lambert syndrome pathophysiology

A

autoantibodies against VG Ca++Channels
-reduce Ca++ influx decreasing ACh release

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20
Q

60% of eaton lambert syndrome cases are associated with what

A

small cell lung carcinoma

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21
Q

s/s of Eaton Lamber Syndrome

A

progressive limb-girdle weakness, dysautonomia, oculbulbar palsy

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22
Q

treatment for eaton lambert syndrome

A

Selective K+ channel blocker
“3-4 diaminopyridine”
ACh-E inhibitors
Aziathioprine (immunologics)
Steroids
Plasmapheresis, IVIG

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23
Q

preanesthetic considerations for ELS (Eaton Lambert Syndrome)

A

assess exsisting deficits
if respiratory compromise - PFTs
optimize respiratory functoin
*extreme caution with NMB and opioid dosing
may need post-op respiratory support until fully recovered from anesthesia

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24
Q

ELS and neuromuscular blockers

A

VERY SENSITIVE to ND-NMB and D-NMB
*significantly more sensitive to ND-NMB than MG patients

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25
Q

muscular dystophy pathophysiology

A

hereditary disorder of msucle fiber degerneration caused by breakdown of the dystophin-glycoprotein complex
- leading to myonecrosis, fibrosis, and skeletal membrane permeability

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26
Q

what is the most common and severe form of muscular dysrophy
who does it affect- onset & lifespan

A

Duchenne (DMD)
occurs only on boys, onset 2-5y
Wheelchair bound by 8-10 y
lifespan 20-25 d/t cardiopulm complications

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27
Q

s/s of muscular dystrophy

A

progressive skeletal muscle wasting without motor/sensory abnormalities, kyphoscolosis, long bone fragility, respiratory weakness, frequent PNE, EKG changes

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28
Q

what lab is elevated in muscular dystrophy and why?

A

creatine kinase due to muscle wasting

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29
Q

what is myotonia

A

prolonged contractions after muscle stimulation, seen in several muscle disorders

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30
Q

most common myotonia

A

myotonic dystrophy
onset: 20-30 y
muscle wasting in face, masseter, hand, pre-tibial muscles & may effect pharyngeal, laryngeal, diaphragmatic muscles
cardiac conduction may be effected

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31
Q

what valvular disorder is seen in myotonic dystrophy

A

20% have mitral valve prolapse

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32
Q

myotnia congenita involves what muscles

A

skeletal.
smooth and cardiac muscles are spared
(milder form)

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33
Q

what is central core disease

A

rare. core muscles cells lack mitochondrial enzymes
- proximal muscle weakness & scoliosis

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34
Q

what triggers myotonias

A

stress and cold temps

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35
Q

treatment for myotonias

A

no cure
managed with quinine, procainamide, steroids

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36
Q

preanesthetic condiserations for muscular dystrophies

A

CBC, BMP, PFTs, consider CK
preop EKG, ECHO - elvaluate for cardiomyopathy

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37
Q

drug condiserations for muscular dystrophies

A

caution with Non-depolarizing NMB (careful montiroing throughout)
hypermetabolic syndrome - similar to MH seen with sux and volatile anesthetics
life threatrening HyperK+ and arrythmias seen with sux
Sux and VA may exacerbate instability of muscle membrane

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38
Q

pre anesthetic considerations for muscular dystrophy (9)

A
  • assess extent of CV and pulmonary abnormalities
  • assess breath and heart sounds
  • GI hypomotility (aspiration risk)
  • high reactio of endocrine abnormalities (check thyroid and glucose levels)
  • keep warm to avoid flares
  • avoid Depolarizing NMB b/c fasiculations trigger myotonia
  • caution with opioids
  • optimize respiratory status
  • incerased risk of postop respitatory weakness
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39
Q

3 major dementia syndromes

A

alzheimers (70%)
Vascular dementia (25%)
parkinsons (5%)

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40
Q

basic preop consierations with dementia patients

A

assess level of cognitive dysfunction
if patient unable to give informed consent look to medical POA
investigate any advanced directives for medical decision making
basic labs and pertinent test/imaging
potential aspiration risk (may be full stomach)
increased risk for postop delirium

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41
Q

which preop meds need to be reviewed prior to anesthetic with dementia patients

A

ACh-I, MAOIs, psych meds

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42
Q

preferred anesthetic plan on dementia patietns

A

regional - decreased opioid requirement
*balance opioids to meet analgesic requirement without exacerbating delirium

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43
Q

parkinson’s disease pathophysiology

A

degeneration of dopaminergic fibers of basal ganglia
unknown case. advanced age is the biggest risk factor

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44
Q

dopamine regulates the _________ by ____ _____ stimulation, which is stimulated by _______

A

dopamine regulates the extrapyramidal motor system by inhibiting exess stimulation, which is stimulated by ACh

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45
Q

T/F in parkinsons the motor neurons are under stimulated

A

false, in parkinon’s motor neurons are over stiumulated

46
Q

triad of symptoms with parkinsons

A

skeletal muscle tremor, rigitidity, akinesia, posture
TRAP

47
Q

other symptoms of parkinsons

A

pill roll tremor, facial rigidity, slurred speech, difficulty swallowing, respiratory difficutlty, depression, dementia

48
Q

treatment for parkinsons

A

Levadopa (cross BBB), anticholinergics, MAOIs (inhibit dopamine degredation), deep brain stimulator

49
Q

preanesthetic considerations for parkinsons

A

assess severity with special attetention to respiratory compromise
review home meds (MAOIs)
basic labs along with PFT if respiratory symptoms
EKG, ECHO if indicated
increased aspiration risk (dysphagia, or possible dementia)

50
Q

mediations to avoid in parkinsons patients

A

avoid reglan, phenothiazines, butyrophenones
avoid demerol if on MAOI

51
Q

parkinsons home med to continue prior to surgery

A

PO levadopa must be continued to avoid unstable extrapyramidal effects such as chest wall rigidity

52
Q

parkinsons patient with Deep brain stimulator considerations

A
  • may need to be disabled to avoid interaction with cautery
  • if cautery used, biopolar recommended
53
Q

primary, most common brain tumor

A

gliomas (~45%)
types based on histologic cell-type
subclasses based on oncogenic mutations

54
Q

benign mengiomas

A

15%, arise from dura or archnoid tissue

55
Q

pituitary adenomas

A

7%, noncancerous, majority found on autopsy

56
Q

metastatic carcinoma

A

6%, can vary widely in origin and symptoms

57
Q

other types of brain tumors

A

schawnnomas, craniopharyngiomas, dermoid tumors

58
Q

in regards to brain tumors what can cause neurologic deficits

A

the mass!
increases ICP, papilledema, headache, mental impairment, mobility impairment, vomiting, autonomic dysfunction, seizures

59
Q

brain tumors - pre anesthesia considerations

A

history, previous therapies, presenting symptoms
radiation damage may lead to lethargy and AMS
chemoteraphy may also have neuro effects
CBC, BMP (glucose), EKG
CT/MRI
preop steroids and antiseizure per surgeon

60
Q

why are patients w brain tumors on steroids

A

minimize cerebral edema
*continue steroids and monitor glucose

61
Q

what diuretic is used to reduce ICP and pressure

A

mannitol

62
Q

autonomic dysfunction from brain tumor may manifest on

A

EKG
labile HR and BP

63
Q

anticonvulsants are common with which lesions

A

supratentorial lesions

64
Q

cerebrovascular disease preop considerations

A
  • review history, deficits, imaging, treatments, and co-existing disease
  • assess orientation, pupils, bilateral grip stregnth, LE strength
  • ask about headache, tinnitus, vision/memory loss, bathroom issues
  • assess cause of CVA - vascular, embolic
  • Imaging- carotid U/S, CT/MRI head and neck and ECHO
  • preop EKG
  • CBC, BMP (including glucose)
65
Q

causes of embolic CVA

A

afib, prostethic valve, right to left shunt, PFO

66
Q

new anticoagulant use for cardiac thrombus means what

A

no elective cases within 3 months

67
Q

if pt is on anticoagulant for CVA prophylaxis

A

consult prescriber to establish protocol

68
Q

high risk patients on long acting anticoags need what to bridge the gap

A

short acting anticoagulants (LMWH, IV unfractionated heparin)
*close monitoring of coagulation status is required

69
Q

can you do regional anesthesia on a pt with CVA history and anticoags

A

if anticoags have been D/Cd for sufficient time to perform block

70
Q

clincal manifestations of regional strokes - anterior cerebral artery

A

contralateral leg weakness

71
Q

1.

clincal manifestations of regional strokes - middle cerebral artery

A

contralateral hemiparesis and hemisensory deficits (face and arm more than legs)
aphasia (dominant hemisphere)
contralaterral visual defect

72
Q

clincal manifestations of regional strokes - posterior cerebral artery

A

contralateral visual vield defect
contralateral hemiparesis

73
Q

clincal manifestations of regional strokes - penetrating arteries

A

contralateral hemiparesis
contralateral hemisensory deficits

74
Q

clincal manifestations of regional strokes - basilar artery

A

oculomotor deficits and or ataxia with crossed sensory and motor deficits

75
Q

clincal manifestations of regional strokes - veterbal artery

A

lower cranial nerve deficits and or ataxia with crossed senory deficits

76
Q

majority of aneurysms not diagnosed before _____

A

rupture
* only 1/3 aneursyms pts have sx before rupture

77
Q

s/s of cerebral aneursym

A

headache, photophobia, condusion, hemiparesis, coma

78
Q

risk factors for cerebral aneursym

A

HTN
smoking
female
oral contraceptive
cocaine use

79
Q

diagnosis of cerebral aneursym

A

CT/angio
MRI
lumbar puncture with CSF analysis (if rupture suspected)

80
Q

intervention for cerebal aneurysm should be preformed within how many hours of rupture for best outcome

A

72 hours

81
Q

pre-anesthesia considerations for cerebral aneursyms

A

CT/MRI, EKG, ECHO, CBC, BMP, T&C with blood available
*BP control, mannitol (avoid rupture)
seizure prophylaxis, CVC

82
Q

surgical treatment of cerebral aneursyms

A

coiling, stenting, trapping, bypass (very large aneursyms)
*Neurosurgery on standby incase of intraop rupture/SAH

83
Q

T/F pts with cerebral aneurysms may be on steroids

A

True, monitor glucose

84
Q

when are vasospasms likely to occur post Sub archonid hemorrage (SAH)

A

3-15 days post SAH

85
Q

triple H therapy for SAH vasospasm

A

hypertension
hypervolume
hemodilution
*to avoid complications of hypervolemia, HTN is the initial main treatment

86
Q

interventional treatment for post SAH vasospasm

A

balloon dilation
direct injection of vasodilators to relieve the vasospasm

87
Q

aneursym grading for prognosis

A

Hunt & Hess
0- unruptured
1- reputrued with minimal headdache and no neuro deficits
2- moderate to sever headache, no deficit other than cranial nerve palsy
3- drowsiness, confusion, mild focal motor deficit
4- stupor, significant hemiparesis, early decebration
5 - deep coma, decebrate rigidity

88
Q

what is an AVM

A

aterial to venous connection without intervening capillaries
*high flow, low resistance shunting
*believed to be congetinal

89
Q

symtpoms of AVM

A

range from mass-effects to hemorrhage

90
Q

where are majority of AVM located

A

supratentorial

91
Q

diagnosis of AVM

A

angio, MRI

92
Q

treatment of AVM

A

angio-guided embolization
surgical resection (higher mortality)

93
Q

pre anesthesia considerations for AVM

A

H&P, review meds, imaging, CBC, BMP, T&C, EKG, ECHO
*BP control, seizure prophalyxsis
*large bore IV access x2, Aline

94
Q

traumatic brain injury “TBI” severity is categorized by

A

GCS - glasco-coma scale

95
Q

primary injury -TBI

TBI (traumatic brain injury)

A

occurs at time of insult

96
Q

intubation is required in severe TBI

A

GCS <9
AW trauma
respiratory distress

97
Q

mild hyperventilation to control

A

ICP

98
Q

pre anesthesia considerations for TBI

A

do not delay emergent surgery
review co-morbidities, degree of injury, imaging, labs, gross neuro exam
*C-Spine stabilization, IV access, CVC, ALine, possible uncrossmatched blood if no time for T&C
*intraop ISTAT, pressors, bicarb, Calcium

99
Q

why to refrain from NGT/OGT in TBI

A

potential basal skull fracture

100
Q

chari malformation

A

congential displacement of cerellum
C/o Headache, extending to shoulders/arm, visual disturbances, ataxia
Tx= surgical decompression

101
Q

pre-anesthesia considerations for Chari malformation

A

Review H&P, deficits, imaging, CBC, BMP, T&C
May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline

102
Q

classifications of Chiari Malformation

A
103
Q

Pre-anesthesia considerations for seizures

A

Determine source of seizures (if known) and how well they are controlled. Want anti-seizure drugs on board before incision.
Review drugs and pharmacokinetic/pharmacodynamic actions

104
Q

May be called to intubate post-seizure

A

RSI w/cricoid pressure

105
Q

seizure
& causes

A

transient, paroxysmal, and synchronous discharge of neurons in the brain
caused by transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
-In these cases, treating the underlying cause is curative

106
Q

Epilepsy

A

recurrent seizures d/t congenital or acquired factors

107
Q

Antiepileptic drugs decrease ____ excitability/enhance _____

A

Antiepileptic drugs decrease neuronal excitability/enhance inhibition

108
Q

which seizure drugs cause drug-drug interactions

A

Phenytoin, Tegretol, Barbiturates are enzyme-inducers

109
Q

secondary injuries- TBI (6)

TBI (traumatic brain injury)

A

neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, neurogenic shock

110
Q

which cranial nerves are commonly affected by myasthenia gravis? what effects do they have?

A

ocular (common) - diplopia, ptosis
bulbar - laryngeal/pharyngeal weakness leading to respiratory insuffienccy, aspiration risk

111
Q

Myasthenia Gravis Pathophysiology

A

autoimmune: antibodies generated against N-ACh-receptors at skeletal motor endplate
*no effect on smooth or cardiac muscle