Neuro and neuromuscular assessment Flashcards

1
Q

Basic Pathophysiology of MS

A

Diverse combinations of inflammation, demyelination and axonal damage in the CNS

-Loss of myelin followed by formation of plaques

-Peripheral nerves are not affected
Characterized by exacerbations and remissions

-Most common type: Primary-progressing
Unpredictable intervals

-Symptoms eventually persist leading to severe disability

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2
Q

Etiology of MS

A

genetically susceptible persons
No clear genetic, environmental, or infectious causes have yet been identified
Triggering event, e.g. virus
Pregnancy reduces exacerbation, increased risk of relapse postpartum

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3
Q

What are symptoms of MS from?

A

multifocal and always progressive, reflect sites of demyelination in the CNS

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4
Q

What are clinical manifestations of MS

A

Motor weakness/spasticity: issues with gait
Sensory disorders: numbness/tingling
Visual impairment: optic neuritis, diplopia
Bladder and bowel dysfunction
Autonomic instability
Increased incidence seizure disorders
Hyperthermia can exacerbate symptoms
Emotional instability/depression

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5
Q

How do you diagnose MS?

A

CSF and MRI

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6
Q

What is Optic neuritis (seen in MS?)

A

diminished visual acuity and defective pupillary reaction to light.

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7
Q

Main 5 symptom medications for MS?

A

Cortacosteroids, interferon, glatiramer, mitroxantrone, baclofen, methotrexate

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8
Q

Concerns with cortacosteroids

A

Acute exacerbations covers both immune and inflammatory response

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9
Q

Concerns with interferon?

A

Flu like symptoms. Alters inflammatory response, augments natural disease progression, may reduce relapse rates.

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10
Q

Concerns with Glatiramer

A

Noninterferon, nonsteroidal immune modulator

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11
Q

Big concern with Mitoxantrone

A

Severe cardiotoxicity
- functions as an immunosupressant

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12
Q

Baclofen anestesia concerns

A

prolongs sedation
Increases sensitivity to NDMR

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13
Q

Big concern for methotrexate

A

inhibits both cell-mediated an humoral response

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14
Q

MS anestesia implications

A

Assess and document neurologic deficits
Consider diagnostic testing based on medical management: CBC, BMP, LFTs
Consider stress dose corticosteroids
Take all MS meds up until DOS
Symptoms may be exacerbated postoperatively, respiratory muscle weakness increase likelihood ICU ventilatory support
Temperature management: Avoid hyperthermia!!!

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15
Q

What med do you avoid with MS in your anesthetic plan?

A

Avoid Succs Ch due to possible exaggerated release of K+

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16
Q

other anesthesia MS considerations?

A

Judicious NMB, possible prolonged effects or resistance
SAB implicated in postoperative exacerbations MS
MOA local anesthetic neurotoxicity?
Epidural and peripheral nerve block OK
Inform patient of the risk of postoperative MS exacerbation

17
Q

ALS patho

A

Progressive, incurable degenerative disease of upper and lower motor neurons
Weakness/atrophy and eventual paralysis of upper/lower extremities
Bulbar palsy, dysphagia, trismus, laryngospasm
Respiratory compromise, aspiration risk, exquisitely sensitive to sedating medications (anesthesia)

18
Q

Etiology of ALS

A

Genetic, environmental, autoimmune, and viral

19
Q

Patterns of progression

A

Time of survival after Dx ~ 3-5 yrs
Death results from ventilatory failure 2o to neuromuscular weakness

20
Q

What is the one ALS disease modification drug?

A

Riluzole: Na channel blocker , may increase glutamate uptake and slow progression of cellular destruction, Issues with potential liver dysfunction

21
Q

Why do you usually see an ALS patient?

A

Palliative procedures: PEG, tracheotomy
Elective or semi-elective procedures scheduled early in the disease process

22
Q

Preop testing?

A

Guided by patients’ comorbidities
An electrolyte panel and assessment of renal function is reasonable if the patient has severely impaired swallowing, weight loss, and is at risk for dehydration.

Creatine phosphokinase is typically elevated due to chronic muscle wasting and should not raise concerns for myocardial injury.

23
Q

ALS Anesthesia Implications

A

Risk for dehydration, aspiration and respiratory compromise

24
Q

What med should be avoided?

A

Succs

25
Q

Myasthenia Gravis Patho

A

Antibodies attack the postsynaptic ACh receptor at NMJ
90% have thymic hyperplasia (10% with tumor involvement)
Often found with other autoimmune disorders (RA)
Proximal muscle weakness alleviated by rest, exacerbated by activity
Bulbar muscle involvement: dysphagia,
diplopia, and ptosis

26
Q

What is Osserman staging system?

A

Osserman’s original classification divides adult myasthenia gravis into four groups based on the severity of the disease.

27
Q

MG treatment

A

First-line therapy: Anticholinesterase medications (pyridostigmine) +/- glucocorticoids
Immunosuppressant agents
Plasmapheresis +/- IV Ig: severe bulbar and respiratory compromise
Thymectomy: Patients with thymomas, < 45 yo, + serum anti-AChR antibody

28
Q

Myasthenic crisis

A

exacerbation of disease

29
Q

Cholinergic crisis

A

anticholinesterase overdose

30
Q

What can you give in preop to decreas risk of post op myasthenia crisis?

A

High dose glucocorticoids

31
Q

What one test might you do for an elective surgery with MG

A

Cardiopulmonary work up if functional capacity, dyspnea, and fatigue.

32
Q

Ways you can address MG patients increased risk of aspiration

A

Aspiration prophylaxis with H2 antagonists and metoclopramide

33
Q

In MG patients are there a normal or low number of postsynaptic Ach receptors?

A

Lower

34
Q

What is inhibited by anticholinesterase medications?

A

Plasma cholinesterase

35
Q

What is the effect of nondepolarizing NMB agents?

A

Increased sensitivity

36
Q

What is the effect of depolarizing NMB?

A

reduced, and more resistant… yet MORE PORLONGED