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b. princip. exam 2 (w13) > neuromuscular disorders > Flashcards

neuromuscular disorders Flashcards

1
Q

what systems are affected in patients with neuromuscular disorders?

A

respiratory, nutritional balance and cardiovascular systems

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2
Q

name the 6 major neuromuscular disorders that cause issues with anesthesia?

A
  1. muscular dystrophy
  2. rheumatoid arthritis
  3. myasthenia gravis
  4. systemic lupus erythematosus
  5. multiple sclerosis
  6. paralysis agitans (aka parkinsons)
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3
Q

organ dysfunction in Neuro musc. disease:
Respiratory:
1.respiratory insuffeciency is major cause of what in patients with neuromusc. disorder?
2. ventilatory performance…
3. how does loss of skeletal muscle control impair respiratory compensation in NM disease patients?
4. what increases work of breathing and causes muscle fatigue and ventilatory insuffeciency in these patients?

A
  1. major cause of death
  2. depends entirely on skeletal muscle
  3. it causes a loss of ventilatory reserve and loss of ability to increase minute ventilation on demand (these are costal and accessory muscle manuvers)
  4. periopertive changes in lung function and incrased metabolic rate
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4
Q
  1. what are early responses to increased respiratory work?

2. what do these responses cause?

A

1a. frequent changes in respiratory pattern to alternate work between fatiguing muscles and accessory respiratory muscles
1b. increased respiratory rate to allow more effecient use of weakened muscles resulting in increased respiratory inspiratory time and increased ratio of dead space to tidal volume
2. decrease ventilatory effeciency and increase risk of ventilatory failure

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5
Q
  1. what does expiratory muscle dysfunction cause (2 things)?

2. what does continued perfusion of non-ventilated lung segments result in?

A

1a. impairs ability to cough and further exacerbates reductions in forced expiratory capacity (seen even more with abdominal and thoracic procedures)
1b. inablilty to expectorate secretions leads to collapsed lung segments and predisposes patients to bacterial contamination and pneumonia
2. arterial hypoxemia

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6
Q

NMD patient:
1. what causes the impaired gas exchange in these patients while asleep?
2]. how would these patients compensate for this?

A
  1. decreased central drive mechanisms

2. voluntary hyperventilation

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7
Q

changes with laryngeal and glottic muscle function d/t weakness:

A
  1. frequently impaired-which causes recurrent aspiration and airflow obstruction (when severe) d/t weakness of tongue, jaw, retro pharynx, glottis and larynx muxcles.
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8
Q

changes with laryngeal and glottic muscle function d/t cranial nerves:

A

cranial nerves may be affected by disease process specifically to brainstem and lower cranial nerves 9,10 & 12.

  • -9,10 &12 supply most of airway motor function
  • -9 & 10 supply sensory
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9
Q

what are the effects of residual anesthesia and muscle relaxants on the laryngeal and glottic muscle function in these patients?

A

exacerbate upper airway muscle dysfunction

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10
Q

what type of cardiac dysfunction might NM disease patients have with:

  1. neuropathic disease?
  2. myopathic disease?
A
  1. autonomic dysfunction with neuropathic disease

2. myocardial failure with myopathic disease

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11
Q
  1. what signs and symptoms might be seen with neuropathic diseases?
  2. what disease is common for cardiac changes?
A
  1. auronomic cardiac involvement:
    - loss of beat to beat variability in heart rate (the most sensitive indicator)
    - resting tachycardia
    - postural hypotension
  2. dysautonomia
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12
Q
  1. what other disorders accompany dysautonomia?

2. why is this?

A
  1. volume and electrolyte disorders
  2. autonomic system controls distribution of:
    - systemic blood flow by modulation of blood flow thru sodium retention (via aldosterone) which also limits insensible loss volume
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13
Q

myopathic dysfunctions from NM disease:

  1. what do they do?
  2. what does this cause?
A
  1. directly affect cardiac muscle

2. CHF, complex cardiac dysrhythmias and formation of mural thrombi in the heart

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14
Q

respiratory assessment for MD disease (1-5)

A
  1. sob
  2. orthopnea, posturing, kyphosis, scoliosis
  3. rapid shallow breathing
  4. uncoordinated ventilatory muscles
  5. paradoxical upward motion of abdomen during inspiration indicative of profound diaphragm weakness
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15
Q

lab assessment for NM disease patient

A
  1. depend on patient hx and severity of disease
  2. abgs, cxr
  3. PFTs (forced vital capacity is good estimate of ventilatiory muscle strength and chest wall compliance)
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16
Q

what signs would you see:

  1. autonomic dysfunction CV/ GI / skin/ eye signs:
  2. heart issues:
  3. what may you need prior to procedure?
A
  1. orthostatic hypotension, resting tachycardia, paralytic ileus, anhidrosis (lack of sweating), miosis
  2. cardiomyopathy is common; left ventricular dysfunction, mitral valve prolapse, papillary muscle dysfunction
  3. may need EKG prior
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17
Q

what drugs might you want to avoid d/t dysautonomia

A

adrenergically active or blocking drugs (ketamine or beta blockers)

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18
Q
  1. what are the nutritional effects of NM disorders?

2. what would be the side effect of poor nutrition?

A
  1. hypoalbuminemia, anemia, hypocalcemia,

2. increased incidence of wound infection and impaired healing

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19
Q
  1. name a myopathic disease:

2. name a neuropathic disease:

A
  1. myopathic=muscular dystrophy

2. neuropathic=multiple sclerosis

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20
Q

a patient with MD may have CHF, what would you use to monitor this patient?

A

central line (CVP)

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21
Q

what affects to general anesthetics have on NM disease patients?

A

decrease muscle contraction up to 50% (=increased weakness)

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22
Q
  1. what effect do NDMRs have on denervated muscle patients?

2. what is the best way to use NDMRs?

A
  1. have normal effects on patients with denervated muscle, but clinical response may be PROLONGED
  2. small doses and careful monitoring with TOF
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23
Q

succinylcholine effect on NM disease patients.

A
  1. succ should be avoided if possible
  2. may need more succ for Myasthenia Gravis (d/t less nicotinic receptors)
  3. can cause pathological muscle contracture and lethal hyperkalemia in denervated and immobile patients (>4 days immobile) d/t increased # of EJRs.
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24
Q

Muscular dystropyies:

  1. what is it?
  2. Duchenne’s (aka)
  3. what systems does Duchenne’s affect?
A
  1. heredity (autosomal dominant) disease characterized by painless degeneration and atrophy of skeletal muscles in males (women are carriers); progressive and symmetrical skeletal muscle wasting with sensation and reflexes intact.
  2. aka pseudohypertrophic
  3. affects cardiac and pulmonary
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25
Q

Duchenne’s MD

1. what causes it, and what are effects and life expectancy?

A
  • most common and most severe form of MD
  • x-linked, recessive gene
  • affected individuals produce abnormal DYSTROPHIN (a protein found in the sarcolemma of muscle fibers). also have increased plasma CK which reflects increased muscle permeability.
  • becomes apparent in males age 2-5 yes old; intially affects proximal skeletal muscles in pelvis which become pseudo-hypertrophic as a result of fatty infiltration
  • wheelchair bound by age 8-11
  • death usually occurs by age 15-25 (d/t chf or pneumonia).
26
Q

cardiac dysfunction from Duchenne’s MD:

A
  • degeneration of cardiac muscle
  • ekg shows tall R wave in V1, deep Q in limb leads
  • short PR and sinus tach
  • mitral regurg d/t papillary muscle dysfunction
  • decreased myocardial contractility
  • diagnosed by muscle bx
27
Q

pulmonary dysfunction from Duchenne’s MD:

A
  • chronic inspiratory muscle weakness (decreased ability to cough, increased accumulation of secretions=pneumonia).
  • sleep apnea leads to pulm htn
  • kyphoscoliosis contributes to RESTRICTIVE respiratory pattern
  • 30% of duchenne’s deaths are respiratory caused
28
Q

treatment for duchenne’s:

A

there is no real treatment, glucocorticostreoids are given to help though.

29
Q

anesthesia for duchenne’s:

  1. best technique?
  2. drugs to avoid?
  3. can you use other muscle relaxants?
  4. what else is a good technique?
  5. what does rhabdo affect?
  6. what should you monitor (for rhabdo or MH)?
  7. what is a side effect of may present after surgery?
  8. can you use VAs?
  9. what should you have available then?
  10. what other anesthetic choice is good?
A
  1. best technique is narcotic
  2. worst is sux (causes rhabdo, hyperkalemia & cardiac arrest)
  3. generally respond normally to NDMR (but may have prolonged response)
  4. local, regional or spinal is best if possible (averts problems that MRs and gas cause), but give doses you would give to a 90 y/o (d/t loss of muscle)
  5. rhabdo also affects GI muscle, decreasing motility and increasing chance for aspiration (gastrokinetics; NGT if gastric issues)
  6. monitor ETCO2 and temp
  7. may have delayed pulmonary insuffectincy (may present 36 hours later)
  8. can use VAs in very low mac (but VAs cause rhabdo and myocardial depression)
  9. have dantrolene available (although may not develop MH)
  10. (non trigger) TIVA is good choice
30
Q

Rheumatoid arthritis:

  1. what is it?
  2. what else is affected by RA?
A
  1. most comon chronic inflammatory arthritis; affects 1% of adults; 2-3x more prevalent in women.
  2. can be symmetrical polyarthropathy and have significant systemic involvement.
31
Q

systemic affects of RA:

  1. vessels?
  2. heart?
  3. lungs?
  4. blood issues?
  5. skin issues?
  6. liver and kidney issues?
A

1-affects small and medium sized arteries, causes vasculitis d/t immune complex deposits
2-cardiac issues include: pericarditis, myocarditis, rheumatoid nodules in conduction system, pericardial effusion in 1/3 of patients
3-resp effects: pleural effusions (most common) may mimic TB or CA on cxr; pulmonary fibrosis (restrictive lung changes= decreased pulmonary volumes/ vital capacity). VQ abnormalities d/t decreased arterial oxygenation
4- blood issues: Felty’s syndrome (anemia) is RA with splenomegaly and leucopenia
5- Keraconjunctivitis (dry eyes) seen in 10% of patients with RA
6. liver and kidney issures related to drug therapy for RA
-

32
Q

treatment for RA:

A
  1. nsaids
  2. DMARDS (disease modifying antirheumatic drugs)
  3. corticosteroids are bridgh therapy to decrease inflammation until dmards kick in
33
Q

what are DMARDS?

A
  1. drugs like methotrexate, antimalarials (chloroquine), azathioprine, sulfasalazine that change the course of RA
  2. methotrexate is preferred (given 1x week, monitor liver fxn and CBC).
34
Q

other therapy:

  1. what is the action of other RA therapy drugs ? what are side effects?
  2. Name 2 of them:
A
  1. drugs that interfere with tumor necrosis factor alpha and interlukin-1, act more rapidly than DMARDS but can cause demyelinating syndromes and infection
  2. Remicaide (infliximab), Enbrel (etanercept)
35
Q

Systemic lupus erythmatosus (SLE)

  1. what is it?
  2. who does it affect?
  3. exacerbated by what?
A
  1. multisystem chronic inflammatory disease with antinuclear antibody production
  2. typically seen in young women 1 in 1000 females; also in slow acetylators
  3. exacerbated by stress; also can be drug induced by procainamide, pcn, methyldopa, hydralazine, isioniazid are most common.
36
Q

lupus signs/symptoms:

  1. integumentary
  2. blood
  3. kidneys
  4. cardiac
  5. musculoskeletal
  6. serosa
A
  1. maculopapular rash (butterfly rash)
  2. anemia, leucopenia, thrombocytopenia
  3. nephritis
  4. hypertension
  5. arthralgia
  6. serositis (inflammation of serous linings of heart, lungs, abdomen etc.).
37
Q

diagnosis of lupus is done by:

A

presence of ana antibodies in > 95% of patients

along with presence of butterfly rash, thrombocytopenia, serositis and nephritis

38
Q

what issues can be directly related to lupus:

  1. joints:
  2. systemic:
A
  1. avascular necrosis to head or condyle of femur (need hip replacement).
  2. -CNS
    - heart (pericarditis, chf, valve issues),
    - lungs (pneumonia, restrictive pulmonary disease, lung hemorrhage (pulmonary angiitis)
    - kidneys-(glumerulonephritis)
    - neuromuscular-(myopathy)
    - skin- (rashes)
39
Q

treatment of lupus:

A
  • corticosteroids

- immunosuppressive therapy (cyclophosphamide, azathioprine, myophenolate mofetil)

40
Q

anesthetic management in lupus:

  1. what are common surgeries for lupus patients?
  2. how is anesthesia managed?
  3. what is a good technique for simpler surgeries (especially if pulmonary issues)
A
  1. AV shunts (renal failure); joint replacements
  2. depends on the systemic involvement of the disease
  3. spinal is ok (spares pulmonary issues)
41
Q

myasthenia gravis:

  1. what is it?
  2. what are the side effects?
  3. which nerves are affected
  4. whom does it affect?
  5. what virus may be associated with MG, also rheumatoid arthritis and multiple sclerosis?
A
  1. chronic autoimmune disease involving the NMJ caused by a decrease in acetylcholine receptors
  2. weakness with rapid exhaustion of voluntary skeletal muscles with repetitive use; with partial recovery with rest.
  3. cranial nerves that innervate skeletal muscles are affected most; EYES (diplopia, ptosis are initial symptoms).
  4. 1:7500 adults; females usually at age 20-30; males over 60
  5. epstein barr virus is possibly cause of those 3
42
Q

pathophysiology of Myasthenia Gravis

A
  • destruction of POST SYNAPTIC neuromuscular junction ach receptors by circulating antibodies
  • 70-80% of functional receptors are lost (nicotinic)
  • increased sensitivity to NDMRs
  • 70% of MG patients have Thymus gland dysfunction (hyperplasia) d/t reaction to muscle end plate fragments (within the thymus) which causes the production of anti-muscle antibodies.
  • removal of thymus causes remission in 75% of MG patients
  • usually die from resp failure
43
Q 
classification of MG:1
I
IIA
IIB
III
IV
A

I. –extraocular muscles (10% of patients)
IIA. –slowly progressive and mild form of skeletal muscles in respiration. they respond well to corticosteroids and anticholinesterases
IIB.– more severe skeletal muscle weakness, poor drug therapy response and respiratory muscles are involved
III. –acute onset with rapid deterioration of skeletal muscle; high mortality
IV. –severe skeletal muscle weakness; progression of type I or IIA or IIB

44
Q

s/s of MG

  1. how is it characterized?
  2. what affects or exacerbates it?
  3. what are common initial complaints?
  4. what happens in the throat?
  5. what is common after activity?
  6. what cardiac issues are common?
  7. frequently associated with what other issues?
A
  1. periods of exacerbation and remission
  2. affected by environmental, physical and emotional changes (pregnancy, infection, lyte imbalances, animoglycoside abx)
  3. ptosis and diplopia are common initial complaints
  4. weakness of pharyngeal and laryngeal muscles results in dysphagia and poor handling of oral secretions
  5. weakness after exercise
  6. cardiomyopathy
  7. frequently associated with other autoimmune diseases: hyperthyroidism, RA, lupus (SLE)
45
Q

treatment for MG? (5 things)

A
  1. anticholinesterase drugs
  2. thymectomy
  3. corticosteroids
  4. plasmaphoresis
  5. immunosuppressants (azathioprine (imuron))
46
Q
  1. drugs used to treat MG?
  2. what is the goal of drugs with MG?
  3. name 2 of the drugs and doses (a,b)
A
  1. anticholinesterase drugs
  2. goal: to increase neuromuscular transmission by increasing the neurotransmitter (Ach) at the NMJ
    3.
    a)- neostigmine-15 mg oral ; 1.5 mg IM (lasts 3-6 hours)
    b)-pyridostigmine aka. mestinon (most common)-60 mg oral; 2 mg IM
  3. pyridostigmine has fewer muscarenic side effects (i.e. heart rate, gi, salivary etc).
47
Q

cholinergic crisis:

  1. what is it?
  2. cause?
  3. how is it diagnosed?
  4. how is it done?
A
  1. increased weakness with excessive muscarenic effects (bradycardia, salivation, diarrhea, GI cramping, resp distress, miosis).
  2. overdose of anticholinesterase drugs
  3. edrophonium (tensilon) test: 1-2 mg (up to 10 mg)
  4. FIRST give the atropine (edrophonium works in 30 seconds and causes MARKED BRADYCARDIA!!). If weakness gets worse, it is cholinergic crisis; if it gets better is is MG.
48
Q

MG:

action, dose and S/E of immunosuppressant: (Imuron)

A
  • interferes with production of Ach-R antibodies
  • causes severe hemopoetic depression
  • infection and malignancy rare
  • dose=100-200 mg/day
49
Q

MG:

action of steroids, remission rates, best steroid for the job:

A
  • 80% remission
  • reduces Ach-R antibody levels
  • facilitates neuromuscular junction transmission
  • prednisone (corticosteroid) best d/t interference with antibodies
50
Q

plasmaphoresis for MG:

action:

A
  • separates plasma from blood to remove circulating antibodies, reinfused with non toxic antibodies
  • if VC is less than 2L, reduces time to extubation if done preopertively
51
Q

thymectomy for MG
how effective?
time frame?

A
  • becoming the first line treatment for MG
  • most are done on patients that have thymomas, thymus hyperplasia or therapy resistant MG
  • 75-96% of patients improve (but it takes 2-5 years to reach remission).
52
Q

anesthesia for MG-Preop:

  1. should these persons be outpatients?
  2. what should they be advised of?
  3. what med treatment intra op should be individualiazed?
  4. should they take their MG meds preopertively?
A
  1. they should be inpatients (admitted the night before)
  2. that they will probably wake up intubated
  3. individualize anticholinesterase drugs (reversal) and steroids
  4. may hold meds only if disease is mild; if severe DO TAKE MEDS.
53
Q

Induction for MG patient:

  1. what type meds?
  2. what drugs will be difficult to predict?
  3. what 3 drugs have an effect on anesthesia meds? what do they do?
  4. if severe disease, intubation should be done without what meds?
  5. what medication may have to be given at a higher dose?
  6. why should you not pretreat with NDMR?
  7. when using MRs always use the…?
A
  1. use only short acting drugs
  2. muscle relaxants can be difficult to predict d/t resistance of NDMRs and needing higher doses of sux (2-3x higher dose=1.5-2 mg/kg)
  3. corticosteroids may cause resistance to aminosteroidal MRs (vec & roc); aminoglcoside abx potentiate aminosteroid MRs, calcium channel blockers increase weakness with MRs.
  4. consider intubation without MRs if severe disease (breathe them down with sevo or do awake fiberoptic)
  5. sux may need to be given at 1-1.5 mg/kg (maybe even 2 mg/kg)
  6. pretreating with NDMR may cause paralysis
  7. peripheral nerve stimulator (get a baseline before MR)!!!
54
Q

MG:
anesthesia maintainance:
1. what drug is good d/t fact that it decreases need for more MR?
2. how much should NDMRs be reduced?
3. what drugs have prolonged effects?
4. what muscle is the best to test for blockade? why?
5. what reversal med should be done in small increments? what are the increments? why?
6. what is the preferred anesthetic means?

A
  1. volatile agents good (but may cause severe resp depression d/t already weakened muscles)
  2. reduce NDMR dose by 1/10, 1/2, or even 2/3
  3. may have prolonged effect from narcotic or barbs
  4. titrate pyridostigmine in 1 mg increments (to avoid cholinergic crisis)
  5. obicularis oculi muscle; it overestimates blockade (prevents you from giving too much)
  6. regional preferred if possible
55
Q

obstetrics and MG

  1. how does pregnancy affect MG patients?
  2. what can happen to the neonates?
  3. what is the treatment for the neonates?
A
  1. pregnancy and early post partum period can exacerbate MG
  2. 15-20% of neonates born to MG mothers exhibit neonatal myasthenia within 1-21 days post birth
  3. they are treated with anticholinesterases and mechanical ventilation
56
Q
  1. myasthenic syndrome aka…?
  2. what is it?
  3. what diseases is it associated with?
A
  1. eaton-lambert syndrome
  2. antibodies developed at PRE-SYNAPTICALLY calcium channels leads to channel destruction and decreased levels of Ach.
  3. usually associated with carcinomas (particularly lung), sarcoidosis, autoimmune disease, metastatic cancers
57
Q

myasthenic syndrome:

  1. signs and symptoms:
  2. treatment:
  3. s/e of treatment
  4. anesthetic implications:
A
  1. s/s: muscle weakness, fatigus, hyporeflexia, proximal limb aches, diaphragm and costal muscle weakness, autonomic system dysfunction (impaired gastric motility, orthostatic hypotension, urinary retention), STRENTGH IMPROVES with exercise, does not respond to anticholinergic agents.
  2. TX: drugs from aminopyridine group which promote calcium influx and calcium dependent release of acetylcholine (guanidine hydrochloride)
    - plasmaphoresis and imunosuppressant drugs (good results)
  3. guanidine s/e: severe toxic effects; interstitial, intractable vomiting, bone marrow depression)
  4. sensitive to NDMR and DMR, reduce dosages and titrate using peripheral nerve stim.
58
Q
  1. what is myotonic dystrophy?
  2. what does it cause?
  3. treatment?
  4. what are clinical manifestations?
  5. what stimiulus worsens the condition
  6. cardiac effects (8 things)
  7. pulmonary effects (7 things)
A
  1. myotonic dystrophy is an autosomal dominant trait; characterized by a slow progressive deterioration of skeletal, cardiac and smooth muscle resulting in death d/t skeletal muscle wasting and cardiac conduction defects.
  2. usually occurs in 2nd and 3rd decade of life (most common and severe inherited, late onset MD). skeletal muscles are unable to relax after stimulation. membrane excitablilty caused by sodium and chloride channel defects.
  3. treatment includes dilantin, procainamide, tocainide and mexiletine (which delay return of membrane excitablilty by blocking Na+ influx back into muscle cells). no treatment available for muscle weakness with this disease.
  4. expressionless face, ptosis, distal limb weakness, frontal balding, testicular atrophy, cataracts, insulin resistance
  5. worsened by pressure, touch, cold, shivering
  6. cardiac disturbances occur in most patients. usually conduction defects (1st degree AV block most common), also sinus brady, afib, aflutter, complete heart block and sudden death may occur. also left ventricle systolic dysfunction, mitral valve prolapse and wall abnormality
  7. weak thoracic muscles, diaphragm and intercostals; sleep apnea and hypersomnolence cause hypoventilation and decreased ventilatory response to CO2.
59
Q

anesthesia for myotonic dystrophy:

  1. drugs not to use?
  2. what drugs or methods are best?
  3. what about anticholinesterases and train of 4?
  4. why is aspiration of high risk?
  5. temperature?
A
  1. NO SUX or etomidate (cause prolonged contractions and myoclonus (respectively)). opiates, benzos and VAs can cause severe resp depression (use judiciously).
  2. may use NDMRs with dose adjusted according to muscle wasting; regional is best if possible.
  3. reversal agents and peripheral nerve stimulators may stimulate contractions (use short acting NDMRs).
  4. succeptible to aspiration d/t palate, pharynx and esophageal muscle dysfunction with gastric hypomobility.
  5. avoid hypothermia by warming
60
Q 
Which would u avoid in MS patients?
A. Bair hugger
B. rocuronium
C. Sevo
D. Regional
A

A. Bair hugger; Uhtoff’s syndrome is a heat intolerance seen in MS patients that exacerbates symptoms

b. princip. exam 2 (w13) (5 decks)

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