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APEX > Unit 7 - Neuro - Musculoskeletal > Flashcards

Unit 7 - Neuro - Musculoskeletal Flashcards

1
Q

patho of myasthenia gravis

A

Autoimmune destruction of post-junctional, nicotinic ACh receptors at NMJ via IgG

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2
Q

how does myasthenia gravis manifest

A

skeletal muscle weakness

Key: skeletal muscle weakness becomes worse later in the day

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3
Q

surgery that can relieve myasthenia gravis symptoms

A

thymectomy

↓ circulating Anti-AChR IgG in most patients

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4
Q

earliest signs of myasthenia gravis

A

diploplia, ptosis

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5
Q

how does bulbar muscle weakness manifest in myasthenia gravis

A

dysphagia, dysarthria, difficulty handling saliva

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6
Q

5 things that exacerbate myasthenia gravis symptoms

A
  1. pregnancy
  2. infection
  3. electrolyte abnormalities
  4. surgical/psychological stress
  5. aminoglycoside antibiotics
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7
Q

why might neonates of moms with myasthenia gravis require airway management

A

Anti-AChR IgG antibodies cross placenta & cause weakness in 15-20% of neonates for 2-4 weeks

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8
Q

1st line treatment of myasthenia gravis

A

PO pyridostigmine

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9
Q

what is the Tensilon test

A

To differentiate pyridostigmine overdose vs. myasthenic crisis, admin. edrophonium 1-2 mg IV

If muscle strength improves, pt had myasthenic crisis

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10
Q

immunosuppressants used in treatment of myasthenia gravis

A
  • corticosteroids
  • cyclosporine
  • azathioprine
  • mycophenolate
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11
Q

use of plasmapheresis in myasthenia gravis

A

temporary relief during myasthenic crisis or before thymectomy

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12
Q

how do pts with myasthenia gravis react to NMBs

A

Pts have fewer Nm receptors at NMJ
* Increased sensitivity to NDNMBs (reduce dose by 1/3 to 2/3)
* Decreased sensitivity to succs (also d/t impaired efficacy of pseudocholinesterase on pyridostigmine - 1.5-2 mg/kg for RSI)

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12
Q

how do pts with myasthenia gravis react to NMBs

A
  • Increased sensitivity to NDNMBs (reduce dose by 1/3 to 2/3)
  • Decreased sensitivity to succs d/t impaired efficacy of pseudocholinesterase on pyridostigmine (1.5-2 mg/kg for RSI)

Pts have fewer Nm receptors at NMJ

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13
Q

Increased risk for postop mechanical ventilation in myasthenia gravis pts

A
  • Disease duration > 6 years
  • Daily pyridostigmine > 750 mg/day
  • Vital capacity < 2.9 L
  • COPD
  • Surgical approach: median sternotomy > transcervical thymectomy
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14
Q

how do volatiles cause skeletal muscle relaxation

A

via action on ventral horn of spinal cord

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15
Q

patho of Eaton-Lambert syndrome

A

IgG-mediated destruction of presynaptic voltage-gated Ca2+ channel at presynaptic nerve terminal

reduces amount of ACh released into synaptic cleft

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15
Q

patho of Eaton-Lambert syndrome

A

IgG-mediated destruction of presynaptic voltage-gated Ca2+ channel at presynaptic nerve terminal

reduces amount of ACh released into synaptic cleft

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16
Q

how are postsynaptic nicotinic receptors affected in eaton lambert syndrome

A

present in normal quantity & function

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17
Q

presentation of eaton lambert syndrome

A
  • Proximal muscles most affected
  • Weakness generally worse in the morning and improves throughout the day
  • ANS dysfunction
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18
Q

s/s ANS dysfunction in eaton lambert syndrome

A
  • orthostatic hypotension
  • slowed gastric motility
  • urinary retention
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19
Q

treatment of eaton lambert syndrome

A

3,4-diaminopyridine (DAP)

increases ACh release from presynaptic nerve terminal & improves strengt

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20
Q

how do pts with eaton lambert syndrome react to NMBs

A

Sensitive to succs + NDNMBs

volatiles typically provide enough relaxation

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21
Q

diagnosis to consider when patient has suspected lung cancer undergoing mediastinoscopy, bronch, or thorascopy

A

up to 60% of pts with eaton lambert syndrome have small oat cell carcinoma

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22
Q

region affected by myasthenia gravis vs. eaton lambert sydrome

A

MG: postsynaptic Nm receptor
ELS: voltage gated Ca channel

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23
Q

ACh in myasthenia gravis vs. eaton lambert sydrome

A

MG = decreased response to ACh
ELS = decreased ACh release

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24
Q

NMJ region affected by myasthenia gravis vs. eaton lambert sydrome

A

MG: postsynaptic at motor end plate
ELS: presynaptic neuron

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25
Q

effectiveness of AChE inhibitors in region affected by myasthenia gravis vs. eaton lambert sydrome

A

MG: adequate
ELS: poor

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26
Q

patho of guillain barre syndrome

A
  • Peripheral polyneuropathy characterized by immunologic destruction of myelin in peripheral nerves
  • AP can’t be conducted
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27
Q

presentation of Guillain-Barre Syndrome

A
  • Flu-like illness usually precedes paralysis by 1-3 weeks
  • Typically persists ~2 weeks, full recovery in ~4 weeks
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28
Q

common etiologies of Guillain-Barre Syndrome

A
  • Common: Campylobacter jejuni bacteria, EBV, CMV
  • also: vaccinations, surgery, and lymphomatous disease
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29
Q

treatment of guillain barre syndrome

A

plasmapheresis and IVIG

steroids and interferon do NOT improve

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30
Q

s/s guillain barre syndrome

A
  • flaccid paralysis that begins in distal extremities and ascends bilaterally towards proximal extremities, face, & trunk
  • ANS dysfunction common
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31
Q

sensory deficits in guillain barre syndrome

A

paresthesia, numbness, pain

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32
Q

major anesthesia concerns with guillain barre syndrome

A

skeletal muscle denervation, impaired ventilation, ANS dysfunction

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33
Q

NMBs and guillain barre

A
  • Avoid succs (risk hyperkalemia from proliferation of EJRs)
  • Sensitivity to NDNMBs
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34
Q

why are guillain barre pts at high risk for HD instability under GA, position changes, PPV, and blood loss

A

ANS dysfunction

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35
Q

guillain barre pt response to indirect acting sympathomimetics

A
  • Exaggerated response d/t upregulation of postjunctional adrenergic receptors
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36
Q

patho of Familial Periodic Paralysis

A

Characterized by acute episodes of skeletal muscle weakness accompanied by changes in serum K+ concentration

Disorder of skeletal muscle membrane (↓ excitability), not NMJ

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37
Q

type of Familial Periodic Paralysis that’s a calcium channelopathy

A

hypokalemic periodic paralysis

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38
Q

type of Familial Periodic Paralysis that’s a sodium channelopathy

A

hyperkalemic periodic paralysis

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39
Q

how is Hypokalemic Periodic Paralysis diagnosed

A

if skeletal muscle weakness follows a glucose-insulin infusion (weakness with ↓ serum K+)

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40
Q

AVOID in Hypokalemic Periodic Paralysis

A
  • glucose containing solutions
  • K+ wasting diuretics
  • beta 2 agonists
  • succs
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41
Q

why should D5W be avoided in Hypokalemic Periodic Paralysis

A

D5W = insulin spike = K+ shifted into cells = hypokalemia

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42
Q

how is Hyperkalemic Periodic Paralysis diagnosed

A

if skeletal muscle weakness follows oral potassium admin (weakness after serum K+ increases)

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43
Q

AVOID in Hyperkalemic Periodic Paralysis

A
  • succs
  • K+ containing solutions like LR
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44
Q

treatment of Familial Periodic Paralysis

A

acetazolamide for both forms

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45
Q

why is acetazolamide used in treatment of familial periodic paralysis

A

creates non-anion gap acidosis
protects against hypokalemia & facilitates renal K+ excretion (protects against hyperkalemia)

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46
Q

AIs of familial periodic paralysis

A
  • Avoid hypothermia at all costs (even when on CPB)
  • Serum K+ monitoring indicated
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47
Q

how is MH characterized

A

disordered calcium homeostasis

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48
Q

how does Ca2+ enter myocyte when T-tubule is depolarized in MH

A

via dihydropyridine receptor

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49
Q

receptor activated by MH that instructs SR to release too much calcium

A

RyR1

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50
Q

why is there a substantial amount of ATP consumed in MH

A

More Ca2+ to engage with contractile elements + cell attempts to return excess to SR via SERCA2 pump

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51
Q

what causes hyperkalemia and myoglobinemia in MH

A

Sarcolemma breakdown = K+ and myoglobin to enter systemic circulation

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52
Q

effects of increased intracellular calcium in myocyte

A
  • Rigidity from sustained contraction
  • Accelerated metabolic rate, rapid ATP depletion
  • Increased O2 consumption
  • Increased CO2 and heat production
  • Mixed respiratory and lactic acidosis
  • Sarcolemma breaks down
  • K+ and myoglobin leak into systemic circulation
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53
Q

only 3 conditions definitively assoc with MH

A
  1. King-Denborough syndrome
  2. Central core disease
  3. Multiminicore disease
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54
Q

why should volatiles and succs be avoided in DMD

A

can have MH-like syndrome from rhabdo (not true MH)

absence of dystrophin destabilizes sarcolemma - more calcium can enter c

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54
Q

why should volatiles and succs be avoided in DMD

A

can have MH-like syndrome from rhabdo (not true MH)

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55
Q

patho of MH type reaction in DMD patients

A
  • Absence of dystrophin destabilizes sarcolemma during muscle contraction, ↑ membrane permeability
  • Extracellular Ca2+ free to enter cell (can ↑ rate of metabolism)
  • Intracellular K+ is free to exit cell (can result in hyperkalemic cardiac arrest)
  • Myoglobin free to exit cell
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56
Q

MH risk factors

A
  • Geography: families from Wisconsin, Nebraska, West Virginia, & Michigan at ↑ risk
  • Male sex
  • Youth
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57
Q

early s/s MH

A
  • tachycardia
  • tachypnea
  • masseter spasm
  • warm soda lime
  • irregular HR
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58
Q

late signs of MH

A
  • muscle rigidity
  • cola-colored urine
  • coagulopathy
  • irregular HR
  • hyperthermia
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59
Q

most sensitive indicator of MH reaction

A

EtCO2 that ↑ out of proportion to Vm

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60
Q

what is trimus

A

tight jaw that can still be opened (normal response to succs)

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61
Q

what is masseter rigidity

A

tight jaw that can’t be opened

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62
Q

what causes masseter spasm

A

↑ Ca2+ in myoplasm

site of action distal to NMJ so NMB will not relax jaw

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63
Q

gold standard for diagnosing MH

A

Caffeine-Halothane Contracture Test

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64
Q

who should have a Caffeine-Halothane Contracture Test

A

Anyone who has experienced MH or masseter spasm should be tested

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65
Q

who should have a Caffeine-Halothane Contracture Test

A

Anyone who has experienced MH or masseter spasm should be tested

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66
Q

MH differential

A
  • thyroid storm
  • neuroleptic malignant syndrome
  • sepsis
  • pheochromocytoma
  • serotonin syndrome
  • heat stroke
  • metastatic carcinoid
  • cocaine intoxication
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67
Q

how long should the machine be flushed for MH risk patient

A

20-100 min high flow (time depends on model)

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68
Q

charcoal filter prep for MH risk patient

A

Place Vapor-Clean charcoal filter on inspiratory and expiratory port of machine & flush with high FGF (>10 L/min) for 90 seconds prior to using machine on patient

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69
Q

external parts of machine that should be removed & replaced for MH risk patient

A

CO2 absorbent, circuit, bag

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70
Q

1st thing you should do with suspected MH reaction

A

Discontinue triggering agent (volatile or succs)

convert to TIVA

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71
Q

why should you hyperventilate when MH reaction suspected

A

facilitates CO2 elimination, enhances O2 delivery, drives K+ into cells

100% O2 at minimum FGF 10 L/min

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72
Q

why should you hyperventilate when MH reaction suspected

A

facilitates CO2 elimination, enhances O2 delivery, drives K+ into cells

100% O2 at minimum FGF 10 L/min

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73
Q

purpose of charcoal filters

A

Maintains halogenated anesthetic concentration < 5 ppm for up to 12 hours with FGF of 3 L/min

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74
Q

how often should Vapor-clean be changed during MH crisis

A

every hour

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75
Q

MOA of dantrolene

A

1) Reduces Ca2+ release from RyR1 receptor in skeletal myocyte
2) Prevents Ca2+ entry into myocyte, which ↓ stimulus for Ca2+ -induced- Ca2+ release

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76
Q

dantrolene dosing

A
  • 2.5 mg/kg IV repeated q5-10 minutes
  • Continued in ICU: 1 mg/kg q6H or 0.1-0.3 mg/kg/hr for 48-72 hours
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77
Q

common side effect of dantrolene admin

A

venous irritation

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78
Q

concentration & admin of Dantrium

A

20 mg/vial
reconstitute with 60 mL water

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79
Q

concentration & admin of Ryanodex

A

250 mg/vial
dilute in 5mL sterile water

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80
Q

when should you stop cooling pt with MH reaction

A

stop at 38 degrees C

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81
Q

treatment for lactic acidosis in MH

A

Bicarb 1-2 mEq/kg titrated to ABG and base deficit

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82
Q

treating hyperkalemia in MH

A

5-10 mg/kg CaCl
0.15 units/kg insulin + 1 mL/kg D50

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83
Q

how to prevent against dysrhythmias in MH

A

Class 1 antiarrhythmics
15 mg/kg procainamide, 2 mg/kg lidocaine

do NOT give CCBs

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84
Q

how to prevent against dysrhythmias in MH

A

Class 1 antiarrhythmics
15 mg/kg procainamide, 2 mg/kg lidocaine

do NOT give CCBs

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85
Q

desired UOP in MH

A

>2 mL/kg/hr
Protects against renal injury from free myoglobin

IV hydration, 0.25 mg/kg mannitol, 1 mg/kg Lasix

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86
Q

late, often fatal complication of MH

87
Q

etiology of DMD

A

X-linked, recessive disease that result from absence of dystrophin protein

88
Q

critical structural component of cytoskeleton of skeletal & cardiac muscle cells

A

dystrophin

89
Q

function of dystrophin

A

helps anchor actin & myosin to cell membrane

90
Q

consequence of absence of dystrophin in DMD

A
  • destabilizes sarcolemma during muscle contraction, ↑ membrane permeability
  • CK & myoglobin can enter systemic circulation
  • calcium enters cell and can cause inflammation, fibrosis, cell death
91
Q

why are pts with DMD predisposed to hyperkalemia with succs

A

destabilized sarcolemma allows EJRs to populate

92
Q

best practice for anesthesia in DMD pts

A

TIVA, avoid succs

93
Q

how does DMD present

A

atrophy and painless muscle degeneration

94
Q

respiratory effects of DMD

A
  • restrictive lung disease
  • ↑ secretions
  • risk PNA
  • Respiratory muscle weakness
95
Q

CV effects of DMD

A

Cardiac muscle degeneration = ↓ contractility, papillary muscle dysfunction, mitral regurg, cardiomyopathy, CHF

96
Q

s/s cardiomyopathy with DMD

A
  • resting tachycardia
  • JVD
  • S3/S4 gallop
  • displacement of PMI
97
Q

EKG changes in DMD

A

impaired conduction = sinus tach, short PR

Scarring of posterobasal aspect of ventricle = increased R wave in lead I, deep Q waves in limb leads

98
Q

why are DMD pts at increased risk aspiration

A

Impaired airway reflexes, GI hypomotility

99
Q

what should be included in preop workup of DMD pts

A

EKG, echo, cardiac MRI

100
Q

what is kyphoscoliosis

A

posterior curvature of spinal column

101
Q

T/F - patients with myasthenia gravis have decreased ACh

A

false - ACh is present in sufficient quantity but there aren’t enough receptors to translate extracellular signal to intracellualr response

102
Q

why are pts with myasthenia gravis at increased risk for aspiration

A

bulbar muscle weakness

103
Q

why are pts with myasthenia gravis at increased risk for aspiration

A

bulbar muscle weakness

104
Q

how should you ventilate a patient with suspected MH

A

hyperventilate with 100% FiO2 at minimum FGF 10 L/min

105
Q

med class that is contraindicated in MH reaction

A

calcium channel blockers

106
Q

if succs is indicated in a pt with myasthenia gravis, how should dose be adjusted

A

increase to 1.5-2 mg/kg

increased resistance to succs

107
Q

if succs is indicated in a pt with myasthenia gravis, how should dose be adjusted

A

increase to 1.5-2 mg/kg

increased resistance to succs

108
Q

another name for guillain barre

A

acute idiopathic polyneuritis

109
Q

another name for guillain barre

A

acute idiopathic polyneuritis

110
Q

how does paralysis normally present in GBS

A

Flaccid paralysis begins in the distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face.

112
Q

What changes should you make to the anesthesia machine if you suspect MH?

A
  1. Turn off the volatile anesthetic.
  2. Hyperventilate with 100% O2 at a minimum FGF of 10 L/min.
  3. Connect a charcoal filter to the inspiratory and expiratory limb of the circuit.
113
Q

respiratory changes that occur with DMD

A
  • Kyphoscoliosis decreases pulmonary reserve
  • Increased secretions and risk of pneumonia
  • Respiratory muscle weakness
114
Q

why are pts with DMD at risk for life-threatening hyperkalemia with succs admin

A

EJRs populate sacrolemma

115
Q

most common etiologies of scoliosis

A

80% idiopathic
congenital, myopathic, neuropathic, traumatic

116
Q

what does the Cobb angle describe

A

the magnitude of spinal curvature

117
Q

significance of Cobb angle 40-50 degrees

A

indication for surgery

118
Q

significance of Cobb angle 60 degrees

A

decreased pulmonary reserve

119
Q

significance of Cobb angle of 70 degrees

A

pulmonary symptoms present

120
Q

significance of Cobb angle of 100 degrees

A

gas exchange significantly impaired
higher risk of postop pulmonary complications

121
Q

Cobb angle assoc with higher risk of postop pulmonary complications

A

100 degrees

122
Q

early resp changes with scoliosis

A
  • restrictive ventilatory defect (decreased FEV1 and FRC)
  • decreased lung volumes and capacities (VC, TLC, FRC, RV)
123
Q

late resp changes with scoliosis

A

V/Q mismatch
hypoxemia
hypercarbia
pHTN
cardiorespiratory failure/cor pulmonale

124
Q

significance of hypercarbia in pts with scoliosis

A

impending respiratory failure

late respiratory change

125
Q

CV changes with scoliosis

A
  • increased PVR, RVH
  • MVP, mitral regurg, coarctation of aorta
126
Q

most common CV comorbidity with scoliosis

127
Q

nerve injuries assoc with prone positioning for scoliosis surgery

A

brachial plexus & ulnar
lateral femoral cutaneous (pressure on iliac crest)
peroneal (pressure lateral to fibula)

128
Q

complications of scoliosis surgery assoc with hip flexion

A

femoral vein occlusion, DVT

129
Q

which is better for pulmonary compliance in prone surgeries - Jackson or Wilson frame

130
Q

is decreased chest wall compliance an early or late complication of scoliosis

131
Q

What are 6 potential risks of a wake-up test?

A
  1. Inadvertant IV removal
  2. Extubation
  3. Awareness
  4. Pain
  5. Air embolism
  6. Damage to spinal instrumentation
132
Q

What region of the spinal cord do somatosensory evoked potentials monitor?

A

Posterior cord (dorsal column pathway)

133
Q

next action if pt can move hands but not feet during wake up test for scoliosis surgery

A

surgeon should decrease distraction on spinal rods

134
Q

AIs for scoliosis surgery

A
  • avoid N2O (increases PVR)
  • prepare for significant blood loss
  • monitor serial ABGs and UOP to assess end organ perfusion
135
Q

what do SSEPs assess

A

posterior spinal cord
sensory function

136
Q

pathway assessed by SSEPs

A

dorsal column pathway

137
Q

evoked potentials that monitor anterior spinal cord

A

MEPs (motor)

138
Q

3 anatomic airway structures impacted by RA

A
  1. TMJ
  2. cricoarytenoid joint
  3. C spine
139
Q

Patho of RA

A

autoimmune disease that targets synovial joints

140
Q

what causes systemic consequences of RA

A

infiltration of immune complexes into small and medium arteries
(leads to vasculitis)

141
Q

hallmark of RA

A

morning stiffness that generally improves with activity

142
Q

lymph node involvement in RA

A

enlargement of cervical, axillary, and epitrochlear lymph nodes

143
Q

joints affected by RA vs OA

A

RA: PIP and MCP in hands and feet
OA: weight-bearing joints

144
Q

4 airway risk factors assoc with RA

A
  1. limited mouth opening (TMJ synovitis)
  2. decreased diameter of glottic opening
  3. atlanto-occipital subluxation
  4. limited neck extension
145
Q

how does cricoarytenoid arthritis present

A

hoarseness
stridor
dyspnea

146
Q

DL findings that suggest cricoarytenoid arteritis

A

edema or erythema of vocal cords

147
Q

why should a smaller ETT be used in pts with RA

A

smaller glottic opening - prevent laryngeal trauma

148
Q

most common airway complication of RA

A

atlantoaxial subluxation & separation of atlanto-odontoid articulation

due to weakening of transverse axial ligament

149
Q

complication of neck movement in RA pts

A

risk for quadriparesis or paralysis

neck flexion worse than extension

150
Q

how is atlantoaxial subluxation & atlanto-odontoid articulation separation diagnosed in RA

A

distance between anterior arch of atlas and odontoid process is > 3 mm

151
Q

how to best assess for atlantoaxial subluxation & atlanto-odontoid articulation separation in RA pts

A

lateral c spine xray

152
Q

surgical correction of atlantoaxial subluxation & atlanto-odontoid articulation separation

A

odontoid decompression
posterior cervical fusion

153
Q

where does subaxial subluxation most commonly occur in RA pts

154
Q

what is the dens

A

superior bony projection of axis (C2)

155
Q

function of dens

A

provide pivot to facilitate head rotation

156
Q

borders of dens

A

anterior arch of atlas (C1) and transverse axial ligament

157
Q

most common hematologic complication of RA

A

anemia

other heme complications - plt dysfunction assoc with NSAIDs

158
Q

most common pulmonary complication of RA

A

pleural effusion

other pulm complications - interstitial fibrosis, limited chest wall expansion

159
Q

ventilatory defect assoc with RA

A

restrictive
(diffuse interstitial fibrosis)

160
Q

why are RA pts at risk of renal insufficiency

A

vasculitis
NSAIDs

161
Q

why are pts with RA at risk of peripheral neuropathies

A

nerve entrapment

162
Q

why can RA pts have limited chest wall expansion

A

costochondral involvement

163
Q

what causes aortic regurg in RA pts

A

dilation of aortic root

164
Q

CV complications of RA

A

pericardial effusion or tamponade
restrictive pericarditis
aortic regurg
valvular fibrosis
coronary artery arteritis

165
Q

labs assoc with RA

A
  • rheumatoid factor increased in 90% of pts
  • increased CRP, ESR
166
Q

MOA of antirheumetic drugs

A

inhibit TNF, interleukin-1 and 6, T cells, B lymphocytes

167
Q

AEs of methotrexate

A

liver dysfunction
bone marrow suppression

168
Q

med used in treatment of RA that prolongs duration of succs

A

cyclosporine

169
Q

meds used in treatment of RA

A
  • NSAIDs
  • steroids
  • immunosuppressants (methotrexate, cyclosporin, etanercept)
170
Q

why are RA pts at increased risk of cancer and infection

A

antirheumatic drugs suppress immune system

171
Q

most consequences of lupus are due to what?

A

antibody-induced vasculitis and tissue destruction

172
Q

most common problems assoc with lupus

A

polyarthritis
dermatitis

only 30-50% develop “classic” butterfly rash

173
Q

joints affected by lupus arthritis

A

can affect any joint but typically doesn’t involve spine

174
Q

airway complications assoc with lupus

A

cricoarytenoiditis
s/s: hoarseness, stridor, airway obstruction

175
Q

renal complications of lupus

A

nephritis with proteinuria

176
Q

pulmonary complications of lupus

A

restrictive pulmonary defect
pulmonary HTN
interstitial lung disease
pleural effusion
recurrent PEs

177
Q

CV complications of lupus

A

pericarditis (tamponade uncomon)
Raynaud’s
HTN
conduction defects
endocarditis

178
Q

heme complications of lupus

A

hypercoagulability
anemia
thrombocytopenia
leukopenia

179
Q

how does drug-induced lupus typically present and how long does it typically last

A

presents with mild s/s arthralgia, anemia, leukopenia, fever

typically lasts weeks to months

180
Q

most common offenders of induced lupus

A

“PISSED CHIMP”
Pregnancy
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide

181
Q

what causes hypercoagulability in lupus patients

A

development of antiphospholipid antibodies

risk DVT, stroke, PE

182
Q

treatment of lupus

A

aims to suppress immune system
NSAIDs, corticosteroids, immunosuppressants, antimalarials

183
Q

lab value if lupus pt develops antiphospholipid antibodies

A

prolonged aPTT

184
Q

what med may be taken by lupus patients and increase duration of succs

A

cyclophosphamide

inhibits plasma cholinesterase

185
Q

what is Marfan syndrome

A

autosomal dominant connective tissue disorder

186
Q

defining characteristic of Marfan syndrome

A

aortic insufficiency

aortic regurg, aortic dissection

187
Q

defining characteristic of Marfan syndrome

A

aortic insufficiency

aortic regurg, aortic dissection

188
Q

what does a pt with Marfan typically look like

A

very tall
pectus excavatum
kyphoscoliosis

189
Q

genetic musculoskeletal disorder assoc with high risk of spontaneous PTX

A

Marfan syndrome

190
Q

med given to Marfan syndrome pts to minimize wall stress

A

beta blockers

191
Q

what is Ehlers-Danlos syndrome

A

inherited disorder of collagen and procollogen

192
Q

common problems assoc with Ehlers-Danlos syndrome

A

arterial aneurysm
increased bleeding tendency

concerns: AAA, bleeding into joints

193
Q

what causes bleeding in Ehlers-Danlos syndrome pts

A

poor vessel integrity (not coagulopathy)

194
Q

anesthetic techniques to avoid in Ehlers-Danlos syndrome

A

regional, IM injection

d/t bleeding risk

195
Q

what is osteogenesis imperfecta

A

an autosomal dominant connective tissue disorder that causes brittle bones

196
Q

risks for pt with OI needing surgery/anesthesia

A
  • risk c spine fracture with airway management
  • risk fractures with positioning
  • risk fractures with NIBP cuff inflation or fasciculations with succs
197
Q

pulm complications assoc with OI

A

kyphoscoliosis and pectus excavatum
(decreased chest wall compliance = V/Q mismatch, arterial hypoxemia)

198
Q

lab increase in 50% of OI patients

A

serum thyroxine

199
Q

disease assoc with blue sclera

A

osteogenesis imperfecta

200
Q

what is multiple sclerosis

A

demyelinating disease of CNS

201
Q

why are MS pts aspiration risks

A

cranial nerve involvement can cause bulbar muscle weakness

202
Q

how is MS treated

A

steroids
interferon
azathioprine

203
Q

things that exacerbate MS

A

stress
body temp increase as little as 1 degree C

204
Q

is succs safe in MS

A

no - avoid (assoc with life threatening hyper K)

205
Q

what is myotonic dystrophy

A

prolonged contracture after voluntary contraction

result of dysfunctional calcium sequestration by SR

206
Q

things that increase risk of contractures in myotonic dystrophy

A

succs
NMB reversal with anticholinesterase (theoretical)
hypothermia

207
Q

myotonic dystrophy increases risk of:

A
  • aspiration
  • respiratory weakness
  • cardiomyopathy
  • dysrhythmias
  • sensitivity to anesthetics
208
Q

what is scleroderma

A

excessive fibrosis in skin and organs (particularly microvasculature)

209
Q

why is succs avoided in myotonic dystrophy

A

risk of sustained contractures - not MH

210
Q

what is CREST syndrome

A

Calcinosis
Raynaud’s
Esophageal hypomotility
Sclerodactyly
Telangiectasia

a type of scleroderma

211
Q

what is telangiectasia

A

spinder veins
increase mucosal bleeding

212
Q

why are scleroderma pts at risk for difficult airway

A

limited mouth opening and mandibular hypomotility assoc with skin fibrosis

213
Q

pulm complications of scleroderma

A

pulmonary fibrosis
pHTN

214
Q

why are scleroderma pts often hypertensive

A

decreased vessel compliance, renal artery stenosis

215
Q

why are scleroderma pts predisposed to corneal abrasions

A

eye dryness

216
Q

what is Paget’s disease

A

excess osteoblast and osteoclast activity
causes abnormally thick but weak bone deposits

217
Q

most common problem in Paget’s disease

A

fractures
pain

218
Q

pulmonary function measurements decreased with kyphoscoliosis

A
  • lung volumes
  • PaO2

APEX (54 decks)

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