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MSK diseases Flashcards

1
Q

pathophysiology of MG

A

IgG antibodies destroy post junctional nicotinic Ach receptors at NMJ
-aka theres enough Ach just not enough functional receptors which is why it presents as skeletal muscle weakness

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2
Q

key feature of MG

A

gets worse throughout day or after exercise. rest allows for recovery

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3
Q

surgical option for MG

A

thymus gland plays a role and a thymectomy brings relief to patients

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4
Q

sx of MG
(earliest: 2)

A

earliest signs: diplopia, ptosis
bulbar muscle weakness (muscles of mouth and throat). dysphagia, dysarthria, difficulty handling saliva. dyspnea with exertion, proximal muscle weakness.

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5
Q

situations that exacerbate sx of MG (5)

A

pregnancy
infection
electrolyte abnormalities**
surgical and psychological stress
aminoglycoside abx**

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6
Q

MG antibodies and neonates
(including how long it lasts)

A

anti AchR IgG antibodies cross placenta and cause weakness in 15-20% of neonates.
-can persist for up to 2-4 weeks, consistent with half life of these antibodies
-neonates may need aw management

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7
Q

tx for MG (4)

A

-anticholinesterases: PO pyridostigmine is first line
-immunosuppression: corticosteroids, cyclosporine, azathioprine, mycophenolate
-surgery: thymectomy (reduces anti AchR IgG- median sternotomy OR trans cervical approach)
-plasmapharesis: temporary relief for MG crisis before thymectomy

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8
Q

MG and pyridostigmine OD (cholinergic crisis) sx, dx, tx

A

-pt with MG on pyridostigmine becomes acutely weak
-dx via tensilon test (edrophonium 1-2mg IV). if sx get worse, patient is in cholinergic crisis–> tx with anticholinergics
if sx improve, patient had MG crisis

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9
Q

MG and ND NMB’s

A

increased sensitivity
-potency is increased so reduce dose by 1/2-2/3

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10
Q

MG and depolarizing NMB’s

A

decreased sensitivity
-if RSI required, dose should be 1.5-2mg
-since pyridostigmine is mainstay of medical management, it descreases pseudocholinesterase and increases DOA of succ

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11
Q

postop concerns for a patient with MG

A
  1. residual NMB/muscle weakness
  2. bulbar dysfunction- difficulty handling PO secretions
  3. educate on plausible need for postop MV and what increases their risk (disease duration >6y, daily pyridostigmine >750mg/day, VC <2.9L, COPD, if the surgical approach was the median sternotomy> trans cervical thymectomy
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12
Q

lambert eaton syndrome or LEMS pathophysiology

A

-IgG mediated destruction of presynaptic Vg Ca channels at the pre synaptic nerve terminal
-for this reason, Ca entry via depol is limited and so is Ach released into synaptic cleft
-post synaptic nicotinic receptor is present in normal quantity and functions normally

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13
Q

clinical presentation of LEMS

A

-proximal muscles are most affected and weakness is worst in the AM but gets better throughout the day (probs because more Ach can say hello)
-resp musculature and diaphragm become weak
-ANS dysfunction causes orthostatic HoTN, slowed gastric mobility, urinary retention

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14
Q

LEMS tx

A

3,4 diaminpyridine (DAP) increases Ach release from presynaptic nerve terminal and improves strength of contraction.
-acetylcholinesterase are not helpful and tensilon test does not aid in dx

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15
Q

anesthetic considerations for LEMS patient

A

-reversal with acetylcholinesterase may be inadequate despite proper dosing
-at high risk for postop vent failure
-~60% of LEMS patients have small cell (oat cell) carcinoma of lung.

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16
Q

LEMS response to succ

A

sensitive

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17
Q

LEMS response to ND NMB’s

A

sensitive

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18
Q

Guillian Barre syndrome

A

aka acute idiopathic polyneuritis
-immunologic assault on myelin in peripheral nerves
-AP cant be conducted to motor end plate never receives the signal

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19
Q

clinical presentation of Guillian barre (acute idiopathic polyneuritis)

A

-flu like illness usually precedes paralysis by 1-3w
-GBS usually persists for 2 weeks with full recovery in ~4w
-about 2% affected with GBS will develop chronic inflammatory demyelinating polyneuropathy

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20
Q

common etiologies of Guillian barre

A

campylobacter jejuni bacteria, epstein barr, and cytomegalovirus. other causes include vaccines, surgery, and lymphomatous disease

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21
Q

s/sx of GBS

A

-flaccid paralysis begins in distal extremities and ascends bilaterally towards proximal extremities, trunk, and face
-intercostal muscle weakness impairs ventilation
-facial and pharyngeal weakness causes difficulty swallowing
-sensory deficits include parasthesias, numbness, and pain
-autonomic dysfx is common- tachycardia or bradycardia, HTN or HoTN, diaphoresis or anhidrosis, orthostatic HoTN

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22
Q

tx of GBS

A

plasmapheresis and IV IgG
(-in contrast to MS, steroids and interferon do not improve this condition)

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23
Q

anesthetic considerations for GBS
(resp, steroids?, adrenergic drugs, type of anesthesia)

A

-facial and pharyngeal weakness causes difficulty swallowing and increases risk of aspiration
-may require postop MV
-with autonomic dysfunction youre at risk for hemodynamic variability and should do aline
- exaggerated response to indirect sympathomimetics due to up regulation of post junctional adrenergic receptors
-regional anesthesia is controversial
-steroids are not useful
-immobility increases risk of DVT

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24
Q

succ and GBS

A

sensitive, avoid. up regulation of post junctional receptors

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25
Q

ND NMB’s and GBS

A

increased sensitivity

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26
Q

is familial periodic paralysis a disease of the NMJ

A

no its a DO of the skeletal muscle membrane (reduced excitability)

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27
Q

hypokalemic periodic paralysis is associated with which type of channelopathy

A

calcium

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28
Q

dx of hypokalemic periodic paralysis

A

present if skeletal muscle weakness follows a glucose insulin infusion. patient becomes weak as serum k decreases

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29
Q

dx of hyperkalemic periodic paralysis

A

if skeletal muscle weakness follows PO potassium administration.

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30
Q

tx for either hyper or hypokalemic periodic paralysis

A

acetazolamide. creates non anion gap acidosis (HCO3- fall is matched by Cl- rise) which protects against hypokalemia while facilitating renal K excretion which guards against hyperkalemia

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31
Q

anesthetics considerations for familial periodic paralysis: temperature

A

hypothermia avoided at all costs. normothermia even on CPB bro

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32
Q

with hypokalemic periodic paralysis, what drugs are safe to administer

A

non depolarizers, acetazolamide

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33
Q

with hypokalemic periodic paralysis, what drugs are NOT safe to administer (4)

A

glucose containing solutions
K wasting diuretics
B2 agonists
succ

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34
Q

with hyperkalemic periodic paralysis, what drugs are safe to administer (5)

A

glucose containing solutions
K wasting diuretics
B2 agonists
non depolarizers
acetazolamide

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35
Q

with hyperkalemic periodic paralysis, what drugs are NOT safe to administer (2)

A

succ
K containing solutions

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36
Q

hypokalemic periodic paralysis and succ

A

association between this and MH, dont admin

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37
Q

hyperkalemic periodic paralysis and succ

A

no association with MH BUT at much higher risk for hyperkalemic issues r/t succ

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38
Q

ND NMB’s and familial periodic paralysis

A

slight increased sensitivity but safe to use. use shorter acting if possible

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39
Q

2 classes of drugs known to trigger MH

A

halogenated agents and depolarizing NMB’s

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40
Q

MH pathophys

A
  1. when T tubule is depolarized, Ca enters myocyte via dihydropyridine receptor
  2. activates defective receptor RYRY1, which instructs SR to release way too much Ca into cell.
  3. not only is there more Ca for contraction, SERCA2 pump is trying to pump Ca back in
  4. both increase O2 consumption, take a lot of ATP
  5. breakdown of sarcolemma allows K and myoglobin (toxic to the kidneys) to enter the system circulation
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41
Q

consequences of increased intra cellular calcium in myocyte

A

-rigidity from sustained contraction
-accelerated metabolic rate and rapid depletion of ATP
-increased O2 consumption
-increased CO2 and heat production
-mixed resp and lactic acidosis
-sarcolemma breaks down
-K and myoglobin leak into systemic circulation

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42
Q

3 diseases definitively associated with MH

A
  1. king den borough syndrome
  2. central core disease
  3. multi mini core disease
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43
Q

DMD in comparison to MH

A

absence of dystrophin destabilizes sarcolemma during muscle contraction and increases membrane permeability. This allows myoglobin to exit cell. Creates MH like syndrome but it is due to rhabdo not true MH

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44
Q

halogenated agents/depolarizing NMB’s and DMD

A

creates MH like syndrome (and really rhabdo) so still avoid

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45
Q

any DMD or muscular dystrophy who has cardiac arrest on induction should be treated as if

A

if its hyperkalemic and should receive CaCl immediately

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46
Q

conditions NOT associated with MH include (5)

A

Becker muscular dystrophy
neuroleptic malignant syndrome
myotonia congenita
myotonic dystrophy
osteogenesis imperfecta

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47
Q

factors that increase risk of MH include

A
  1. geography (families in wisconsin, nebraska, WV, michigan)
  2. male sex
  3. youth
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48
Q

earliest signs of MH include

A

tachycardia
masseter spasm
increased EtCO2
warm soda lime
irregular heart rhythm

49
Q

intermediate signs of MH include

A

cyanosis
irregular heart rhythm
patient warm to touch

50
Q

late signs of MH include (5)

A

muscle rigidity
cola colored urine
coagulopathy
irregular heart rhythm
overt hyperthermia

51
Q

most sensitive indicator of MH

A

EtCO2 that rises out of proportion to MV

52
Q

MH can occur as late as how many hours after exposure to triggering agent?

A

6 hours

53
Q

core temperature usually (but not always) rises how many minutes after exposure to triggering agent?

A

15 minutes

54
Q

trismus versus masseter spasm

A

trismus describes a tight jaw that can be opened
masseter spasm describes a tight jaw that cannot be opened

55
Q

when will you see trismus

A

succ admin

56
Q

why will a NMB not relieve a spasm

A

muscle rigidity is due to increased calcium in the myoplasm which is distal to NMJ

57
Q

if a patient experienced masseter muscle rigidity, what should you do

A

assume MH until proven otherwise

58
Q

describe halothane contracture test

A

requires a liver muscle biopsy
gold standard for dx of MH
anyone who has experienced MH or masseter spasm should be referred to for this test
this test has a high sensitivity and a low specificity

59
Q

differential dx to consider with MH

A

thyroid storm
malignant neuroleptic syndrome
sepsis
pheo
serotinergic syndrome
heat stroke
metastatic carcinoid
coke intoxication

60
Q

what class of drugs are contraindicated with MH tx

A

CCB, co administration with dantrolene can cause life threatening hyperkalemia

61
Q

how long to flush anesthesia machine with MH and what else to do

A

20-200 minutes depending on machine
-all external parts should be removed and replaced
-includes CO2, absorbent, circuit, breathing bag
-physically remove vaporizers

62
Q

monitoring for MH intra op and PACU when suspected/known

A

if they dont develop MH within 1 hour of procedure starting, then they probably won’t
monitor for 1-4h in PACU

63
Q

charcoal filters and MH

A

will keep halogenated anesthetic concentration below 5ppm for up to 12h with a minimum FGF of 3L/min
-flush anesthesia machine with high FGF (10L/min) for 90 seconds with filters on prior to using machine on patient.

64
Q

2 MOA’s of dantrolene

A
  1. reduces Ca release from RYRY1 receptor in skeletal myocyte
  2. prevents calcium entry into myocyte which reduces stimulus for calcium induced calcium release
65
Q

each vial of dantrolene contains

A

20mg of dantrolene and 3mg of mannitol

66
Q

how to reconstitute a vial of dantrolene

A

60mL of preservative free water

67
Q

MH tx acute phase

A
  1. d/c triggering agent and continue anesthesia with IV technique
  2. call for help
  3. hyperventilate with 100% FiO2 and FGF > or = 10L/min
  4. if you have charcoal filters, apply them and new circuit/reservoir bag
  5. administer dantrolene/ryanadex
  6. cool patient until under 38 (cool IVF, cold lavage of stomach and bladder, ice packs)
  7. correct acidosis (NaHCO3 1-2mEq/kg IV titrated too ABG and base deficit)
  8. tx hyperkalemia (CaCl 5-10mg/kg IV, until .15 units/kg +D50 1mL/kg)
  9. protect against dysrhythmias with class 1 antiarrhythmics (procainamide 15mg/kg IV, lidocaine 2mg/kg IV. NO CCB’s)
  10. maintain UOP >2mL/kg/h (mannitol .25g/kg IV, furosemide 1mg/kg IV, fluids)
  11. check coag panels. DIC is indicative of impending demise
68
Q

benefits of hyperventilation during acute phase of MH tx

A

CO2 elimination
O2 delivery
drives K into cells

69
Q

how often to change vapor clean charcoal filters intra op

A

every hour

70
Q

review administration of dantrolene/ryanadex in acute phase of MH and tx continuation to ICU

A

2.5mg/kg IV and repeat q5-10m
-stop dantrolene when sx of hyper metabolism subside
-continue in ICU at 1mg/kg q6h or 0.1-0.3mg/kg/h for 48-72h
-venous irritation is common, use largest vein possible
-if patient requires more than 20mg/kg, reconsider MH dx

71
Q

ryanodex contains

A

250mg dantrolene and requires 5mL of sterile water dilutent

72
Q

after stabilization they should be monitored for reoccurrence of MH in the ICU for up to

A

36h

73
Q

for DMD, the breakdown of sarcolemma allows what into the blood stream

A

creatinine kinase and myoglobin enters circulation. calcium also freely enters the cell which activates proteases that destroy contractile elements and cause inflammation, fibrosis, and cell death

74
Q

clinical presentation of DMD

A

more common in males, presents with atrophy and painless muscle degeneration. profound weakness in 1st decade of life.
often require surgical tx of scoliosis and contractures and rarely live past 30y

75
Q

respiratory considerations for DMD

A

-kyphoscoliosis (posterior curvature of spine) and therefore restrictive lung disease–>decreased p.reserve–> increased secretions and risk of PNA
-respiratory muscle weakness

76
Q

cardiac considerations for DMD

A

degeneration of cardiac muscle–> reduced contractility–>papillary muscle dysfunction, mitral regurg, cardiomyopathy, congestive heart failure
-signs of cardiomyopathy include resting tachycardia, JVD, S3/S4 gallop, displacement of PMI (point of maximal impulse)
-patients should receive cardiac work up before surgery (EKG, echo, cardiac MRI)

77
Q

EKG changes and DMD

A

impaired cardiac conduction- ST and short PR interval
scarring of posterobasal aspect (back/bottom) of LV manifests as increased R wave amplitude in lead I, and deep Q waves in the limb leads

78
Q

GI considerations and DMD

A

impaired aw reflexes and GI hypo motility = increased risk of aspiration

79
Q

etiology of scoliosis (lateral and rotational curvature of spine) (5)

A

-idiopathic (incidence 80%)
-congenital
-myopathic (MD and amyotonia congenita)
-neuropathic (CP, syringomyelia, Friedrichs ataxia)
-traumatic

80
Q

how to measure cobb angle

A

two most displaced vertebrae are ID’d
line is drawn parallel to each
perpendicular line is drawn from each these lines
angle where they intersect is the cobb angle

81
Q

degree of cobb angle and significance:
40-50
60
70
100

A
82
Q

early respiratory complications of scoliosis

A

-restrictive ventilatory defect (FEV1 and FRC are decreased but FEV1/FVC is normal
-decreased VC, TLC, FRC, RV
-decreased chest wall compliance

83
Q

late respiratory complications of scopliosis

A

VQ mismatching
hypoxemia
hypercarbia (sign of impending resp failure)
p.HTN
reduced response to hypercapnea
cor pulmonale
cardiorespiratory failure

84
Q

CV changes with scioliosis

A

EKG may show RV strain and right atrial enlargement r/t increased PVR

85
Q

complications of the prone position:
airway
neck
eyes
UE’s
LE’s
abdomen

A
86
Q

thoracic correction of scoliosis higher than _____ may require one lung ventilation with DLT or bronchial blocker

A

T8

87
Q

anesthetic considerations for scoliosis patient

A

-assess resp reserve with exercise tolerance, ABG, VC. <40% predicted VC correlates with postop ventilation
-cervical scoliosis may cause difficult intubation
-N2O increases PVR
-prep for significant blood loss
-deliberate HoTN to MAP 60mmHg carries risk of hype-perfusion and ION
-monitor end organ perfusion with ABG and UOP
-use active warming such as forced air, fluids, etc
-VAE risk
-wake up test v monitoring SSEP/MEP’s

88
Q

if, during wake up test, patient can move hands and not feet, what is the next step

A

reduce distraction on spinal rods

89
Q

2 names for the structure in this image

A

odontoid process (dens)

90
Q

3 ways RA impacts aw

A
  1. limited mouth opening (TMJ r/t synovitis)
  2. decreased diameter of glottic opening- use smaller tube (cricoaretynoid joints)
  3. cervical spine (Atlanta occipital subluxation with flexion and limited extension)
91
Q

s/sx cricoaretynoid arthritis

A

hoarseness, stridor, dyspnea, may result in aw obstruction
edema or erythema of vocal cords suggests it
also at risk for post extubation aw obstruction

92
Q

how to dx AO subluxation for RA

A

lateral x ray to assess if distance between anterior arch of atlas and odontoid process is >3mm

93
Q

surgical correction of AO subluxation r/t RA entails

A

odontoid decompression and posterior cervical fusion

94
Q

pathophysiology of RA

A

autoimmune disease that targets synovial joints
-cytokines (TNF and interleukin 1) play a large role in this
-infiltration of immune complexes into small and medium arteries resulting in vasculitis
-RA affects proximal interphalangeal and metacarpophalangeal joints (whereas osteoarthritis typically affects weight bearing)

95
Q

complications of RA
eyes
aw
nervous system
endocrine
renal
pulmonary
cardiac
GI
heme

A
96
Q

lab testing of RA

A

rheumatoid factor is an anti immunoglobulin antibody that is increased in 90% of RA patients
-c reactive protein and erythrocyte sedimentation is also increased

97
Q

medical management of RA

A

-reducing inflammation, anti rheumatics, glucocorticoids, NSAIDS

98
Q

RA and DMARDS
(3 drug examples)

A

-disease modifying anti rheumatic drugs
-inhibit TNF and IL-1 and IL-6 and T cells and B lymphocytes
-suppress immune system and increase risk of infx and CA
-examples: methotrexate, cyclosporine, etanercept

99
Q

SE of methotrexate

A

causes liver dysfunction and suppresses bone marrow

100
Q

cyclosporine and succ

A

prolongs DOA of succ

101
Q

pathophysiology of SLE

A

autoimmune disease characterized by proliferation of anti nuclear antibodies
-most consequences are r/t antibody induced vasculitis and tissue destruction

102
Q

systemic manifestations of SLE
aw
nervous system
renal
pulmonary
cardiac
hematologic

A
103
Q

exacerbation of SLE: PISSED CHIMP

A
104
Q

medical tx for SLE (4)

A

aimed at suppressing immune system
-corticosteroids
-nsaids
-immunosuppression (cyclophosphamide, azathioprine, methotrexate, mycophenylate)
-antimalarials (hydroxychloroquine and quinacrine)

105
Q

anesthetic considerations for SLE

A

-cricoaretynoid arthritis may present as hoarseness, stridor, aw obstruction. risk of post extubation laryngeal swelling and aw obstruction, necessitating steroids, consider smaller ETT for cricoaretynoiditis
-antiphospholipid antibodies may develop. although aPTT is prolonged, theyre at risk for hyper coagulability and thrombosis. at risk for stroke, DVT, PE

106
Q

what exacerbates sx of SLE

A

pregnancy, stress, infection, surgery

107
Q

cyclophosphamide and succ

A

inhibits plasma cholinesterase and increases DOA of succ

108
Q

marfan syndrome pathophysiology

A

connective tissue DO with autosomal dominance and inheritance (think AAA and aortic insufficiency)

109
Q

marfan syndrome sx/risk

A

-dilated aortic root that sets the stage for aortic insufficiency and dissection (minimize wall stress with BB)
-AAA, cardiac tamponade (if aortic dissection), mitral prolapse, spontaneous PTX (careful with PIP)
-pregnancy increases risk of CV complications

110
Q

marfan syndrome and patient stature/appearance

A

tall with pectus excavatum (sunken chest), kyphoscoliosis, and hyperreflexive joints (careful with positioning)

111
Q

Ehlers danlos syndrome

A

inherited DO of pro collagen and collagen (think spontaneous bleeding into joints and AAA)
-common problems include arterial aneurysms, increased bleeding tendency (due to poor vessel integrity not coagulopathy)
-due to bleeding risk, avoid regional anesthesia and IM injections. excessive bleeding can also occur during invasive line placement and trauma during aw management

112
Q

osteogenesis imperfecta

A

connective tissue DO with autosomal dominant inheritance (think weak bones)
-brittle bones (careful during positioning). even BP cuff can fx bones.
-careful with aw management (cspine fx risk increased, cervical ROM decreased)
-kyphoscoliosis and pectus excavatum reduce chest wall compliance and VC which creates VQ mismatch and hypoxemia
-serum thyroxine is increase in 50% of patients (increased BMR and VO2–> hyperthermia)
-risk of MH not increased *
-blue sclera….which are susceptible to fx

113
Q

MS

A

-demyelinating disease of CNS
-CN involvement causes bulbar muscle dysfx (increases aspiration risk)
-patients are tx with corticosteroids, interferon, azathioprine
-s/sx can be exacerbated by stress and increased body temp
-literature (is weak but suggests) epidural is safe but spinal is not ?
-NO SUCC!!!!! hyperkalemia city

114
Q

myotonic dystrophy
(and can they get halogenated anesthetics)

A

-prolonged contracture after voluntary contraction
-result of dysfunctional calcium sequestration by SR
-succ, NMB reversal with anticholinesterases, hypothermia r/t shivering and sustained contractions increased risk of contractions
-also at risk for: aspiration, resp muscle weakness, cardiomyopathy and dysrhythmias, sensitivity to anesthetic agents
-can get halogenated anesthetics, not at risk for MH

115
Q

scleroderma

A

excessive fibrosis in skin and organs, particularly in microvasculature
-aw: skin fibrosis limits mouth opening and mandibular mobility (FOI)
-lungs: p.fibrosis and p.HTN
-heart: dysrhythmias and CHF
-BV: decreased compliance, HTN
-kidneys: renal failure and renal artery stenosis- HTN
-peripheral cranial nerves: nerve entrapment by tight connective tissue- neuropathy
-eyes: dryness predisposes to corneal abrasion
-telangiectasiasis: spider veins that bleed easily and can become an aw issue- consider FOI

116
Q

CREST and scleroderma

A

calcinosrs, raynauds, esophageal hypo motility, sclerodactyly, telangiectasia

117
Q

Pagets disease

A

excess osteoblastic and osteoclastic activity that causes abnormally thick but weak bone deposits
-excessive PTH or calcitonin deficiency
-pain and fx are most common problems
-peripheral nerve entrapment can occur
-no vascular involvement (yay one win!)

118
Q

common drugs that cause drug induced SLE (CHIMP)

A

hydralazine and isoniazid

119
Q

which immunosuppressant increases DOA of succ

A

cyclophosphamide (plasma cholinesterase inhibitor)

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