Musculoskeletal (2) Flashcards

1
Q

Most common chronic inflammatory arthritis, 2-3x higher in women than men

A

Rheumatoid arthritis

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2
Q

What is an IG antibody that is present in 90% of RA patients?

A

Rheumatoid factor

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3
Q

Where do rheumatoid nodules appear?

A

Pressure points; under elbows

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4
Q

When is fusiform swelling typical?

A

When there is involvement of the proximal interphalangeal joints?

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5
Q

What are some characteristics of Rheumatoid arthritis?

A
  • painful synovial inflammation, swelling, and increased fluid
  • morning stiffness
  • symmetrical distribution of several joints
  • fusiform swelling
  • synovitis of temporomandibular joint
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6
Q

what are symptoms of acute cricoarytenoid arthritis?

A

hoarseness, dyspnea, and stridor with tenderness over the larynx; swelling and redness of arytenoids

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7
Q

What are symptoms of chronic cricoarytenoid arthritis?

A

Asymptomatic or variable degrees of hoarseness, dyspnea, and upper airway obstruction

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8
Q

What are s/s of rheumatoid arthritis?

A
  • atlantoaxial subluxation
  • cricoarytenoid arthritis
  • osteoporosis
  • NM: weakened skeletal muscles and peripheral neuropathies
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9
Q

What are CV concerns for rheumatoid arthritis?

A

Pericarditis, accelerated coronary atherosclerosis, cardiac valve fibrosis, conduction defects

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10
Q

What are pulmonary concerns for rheumatoid arthritis?

A

Restrictive lung changes, pleural effusion, rheumatoid nodules (resembles TB or CA on CXR)

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11
Q

What is another name for scleroderma?

A

Systemic Sclerosis

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12
Q

What is Scleroderma?

A
  • Inflammation and autoimmunity
  • Vascular injury with vascular obliteration
  • Tissue fibrosis and organ sclerosis
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13
Q

What is CREST syndrome in association with Scleroderma?

A

Calcinosis: Ca++ deposits in skin

Raynauds Phenomenon: Spasms of blood vessels in response to cold or stress

Esophageal Dysfunction: GERD, Decrease motility

Sclerodactyly: Thickening and tightening of skin on fingers and hands

Telangiectasis: Dilation of capillaries causing red marks on skin surface

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14
Q

What diagnostic test can be used to help ID pulmonary HTN?

A

CXR: Enlarged RV

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15
Q

If a patient has pulmonary HTN fro Scleroderma what med would you want to use for induction?

A

Etomidate

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16
Q

How does the skin look in pts with scleroderma?

A

Taut

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17
Q

How does Scleroderma affect musculoskeletal system?

A

Limited mobility/ contractures and skeletal muscle myopathy

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18
Q

How is the nervous system effected by Scleroderma?

A

Nerve compression

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19
Q

How is CV system impacted by scleroderma?

A

Systemic and pulmonary HTN, dysrhythmias, vasospasm in small arteries of fingers, CHF

Increased risk for pericarditis and pericardial effusion

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20
Q

How does scleroderma affect GI?

A

*Xerostomia (dry mouth)
*Poor dentation
*Fibrosis of GI tract
* Reflux

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21
Q

How does scleroderma affect renal system?

A
  • Decreased RBF and systemic HTN
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22
Q

What are the treatment options for Scleroderma?

A

Alleviate Symptoms

  • ACE-inhibitors
  • PPI
  • CCB
  • Want to have recent echo
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23
Q

What is the drug of choice for patients on ace-inhibs who go hypotensive?

A

Vasopressin

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24
Q

Airway considerations for someone with Scleroderma:

A
  • Mandibular motion
  • Small mouth opening
  • Oral bleeding
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25
Q

What can you do if patient with scleroderma is bleeding in their mouth post intubation (keeps oozing)?

A
  • Local phenylephrine
  • IV TXA
  • Vitamin K
  • Ca++
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26
Q

Where would be the best site if you have to place an art line in a patient that has scleroderma?

A

Larger vessel

want to prevent vaso-occlusive crisis

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27
Q

What are some consideration when a patient with scleroderma is intubated?

A
  • Decreased pulm compliance and reserve
  • Avoid increasing PVR
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28
Q

_____ is 3x more common in patients with Sclerodema.

A

VTE

  • Prophylaxis with SQ hep 5000u
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29
Q

What is a concern with the eye for patient with scleroderma?

A

Corneal abrasions (from dry eyes)

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30
Q

What is another term for pseudohypertrophy muscular dystrophy?

A

Duchenne Muscular Dystrophy

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31
Q

Pseudohypertrophy Muscular Dystrophy is a ______ linked _______ trait

A

X-linked recessive

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32
Q

What gene has the mutation for duchenne MD?

A
  • Mutation in the dystrophin gene (large protein that stabilizes muscle membrane)
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33
Q

What does the term Pseudohypertrophic mean?

A

Muscle appear enlarged but its actually being replaced by fatty infiltrations

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34
Q

Duchenne MD most common in girls or boys? What are the initial symptoms?

A

Boys

Waddling gait, frequent falls, difficulty climbing stairs

Usually WC bound by 8-10 y/o
Usually don’t live past 20-25y/o

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35
Q

What is the primary complication that causes premature death in duchenne MD?

A

CHF and/or PNA (pulmonary complications)

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36
Q

What are CNS S/S for Pseudohypertrophy MD?

A

Intellectual disability

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37
Q

What are musculoskeletal issues that occur with Pseudohypertrophy MD progression?

A
  • Kyphoscoliosis
  • Skeletal muscle atrophy
  • Increase serum CK (20-100x norm–renal fx)
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38
Q

What are CV issues in patients with pseudohypertophy MD?

A
  • Sinus Tachycardia
  • Cardiomyopathy
  • Short PR, tall R waves (V1), deep Q waves

Preop EKG/echo

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39
Q

What are pulmonary complications in patient with duchenne MD?

A
  • Weak respiratory muscles
  • Weak cough
  • Increased secretions
  • Loss of pulm reserve

probably want to avoid NMB with these guys

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40
Q

If you do have to give NMB to patient with duchenne MD, what would you anticipate?

A

*Potential they wont be able to get off vent
* Full reversal with Sugammadex

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41
Q

GI consideration for pt with duchenne MD:

A

Delayed gastric emptying (Aspiration risk)

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42
Q

Why is Succinylcholine avoided in patients with Duchenne MD?

A

Increases risk of rhabdo, hyperkalemia, MH, and cardiac arrest

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43
Q

What type of anesthesia would be a better option for Duchenne MD patients?

A

Regional Anesthesia: avoids risks of GA, provides post op analgesia, and facilitates chest physiotherapy

would maybe need Ketamine or Precedex to facilitate Regional

44
Q

What causes Myasthenia Gravis?

A
  • Chronic autoimmune disorder
  • Decreased functional post-synaptic ACh receptors
  • ACh receptor-binding antibodies and thymus abnormalities
45
Q

What are classic S/S of Myasthenia Gravis?

A
  • Muscle weakness with rapid exhaustion of voluntary muscles (exhaustion with basic activities)
  • Partial recovery with rest
  • Ptosis, Diplopia, Dysphagia
  • Dysarthria
  • Isolated resp failure
  • arm, leg, trunk weakness
  • Myocarditis
46
Q

How is Myasthenia Gravis classified?

A

Type 1-4

  • Type 1: Limited involvement of the extraocular muscles (unlikely disease progression)
  • Type 2: slow progression
  • Type 3: acute onset (< muscle strength in 6 months)
  • Type 4: Severe skeletal muscle weakness
47
Q

What autoimmune diseases are associated with Myasthenia Gravis?

A
  • RA
  • SLE
  • Pernicious anemia
  • Hyperthyroidism
48
Q

What is a common reason for myasthenia crisis? What are the symptoms?

A
  • Drug resistance or Insufficient drug therapy
  • Severe muscle weakness and respiratory failure
49
Q

What is a cholinergic crisis? What are S/S?

A
  • Excessive Anticholinergic treatment
  • Muscarinic side effects: profound muscle weakness, salivation, miosis, bradycardia, diarrhea, abdominal pain (SLUDGE-M)
50
Q

What test is used to diagnose MG?

A

Tensilon test: Edrophonium 1-2mg IVP

  • Improved MG
  • Worsens cholinergic crisis
51
Q

What is first line therapy for Myasthenia Gravis?

A

Anticholinesterases: increase ACh at NMJ
* Pyridostigmine > Neostigmine
* Could cause pt to have tolerance to NMB (maybe avoid NMB)

52
Q

What surgical treatment can be considered with MG type 2 or 3?

A

Thymectomy:
* Induces remission or allows reduction of immunosuppressive drugs
* Recudes ACh antibody levels
* Full benefit delayed a few months postop

53
Q

When is immunosuppression indicated for patient with MG?

A

When skeletal muscle weakness is not controlled by anticholinergics

Immunosuppression: Steroids, azathioprine, cyclosporin, mycophenolate

54
Q

What are options for immunotherapy for patients with MG?

A
  • Plasmapheresis: removes antibodies
  • Immunoglobulin injections: temporary effect if on verge of crisis
55
Q

What are anesthesia management considerations for patients with MG?

A
  • Aspiration risk
  • Weakened pulmonary effort
  • Marked sensitivity to non-depolarizing NMB (or no response to NMB at all)
  • Resistant to Succyinylcholine
    *Intubate without NMB or use intermediate-acting NMB
56
Q

What med can be used for induction instead of succinylcholine in patients with MG?

A

Remifentanil

or can intubate using volatile agent

57
Q

What is the most common joint disease and leading chronic disease of the elderly population?

A

Osteoarthritis

58
Q

How is osteoarthritis pain characterized?

A

Pain present with motion, relieved with rest

*morning stiffness disappears with movement

59
Q

What is the degenerative process that affects articular cartilage with minimal inflammatory reaction in the joints?

A

Osteoarthritis

60
Q

How does osteoarthritis cause joint trauma?

A
  • Biomechanical stresses
  • Joint injury
  • Abnormal joint loading
  • Neuropathy
  • Ligament injury
  • Muscle atrophy
  • Obesity** (Often not surgical candidate until lose weight)
61
Q

Which areas are most commonly affected by osteoarthritis?

A

Weight-bearing and distal interphalangeal joints

  • Knees and hips most common
62
Q

What are Heberden nodes and what are they associated with?

A

Bony growths that develop on the distal interphalangeal joints

Associated with Osteoarthritis

63
Q

Which parts of the spine are commonly affected by osteoarthritis?

A

Middle to lower cervical and lumbar spine

*If c-spine usually C6-C7; more commonly lumbar

64
Q

What is primary treatment for osteoarthritis?

A
  • PT/exercise
  • Maintaining muscle function
  • Pain relief
  • Joint replacement therapy

NO STEROIDS– causes joints to fail faster

65
Q

What are we concerned about from anesthesia standpoint for patients with OA?

A
  • Airway: worry about neck extension ability
  • Limited ROM of extremities
66
Q

What are hematologic concerns for rheumatoid arthritis?

A

Anemia, neutropenia, elevated platelets - get a CBC preop

67
Q

Other s/s of RA that resemble Sjogren syndrome:

A

Keratoconjunctivitis sicca (dry eyes) and xerostomia

68
Q

Treatment of RA:

A

NSAIDs, corticosteroids, DMARDs, tumor necrosis factor inhibitors and interleukin inhibitors, surgery

69
Q

How do NSAIDs help with RA?

A

Decrease joint swelling, relieve stiffness, provide anesthesia - COX 1 and COX 2 inhibitors

70
Q

How do corticosteroids help with RA?

A

decrease joint swelling, pain, and morning stiffness

  • bridge therapy while DMARDs are starting to work
71
Q

How do DMARDs help with RA?

A

Halt or slow disease progression - methotrexate

72
Q

How does surgery help with RA?

A

Intractable pain, impairment of joint function, joint stabilization; total replacement

73
Q

How does TNF-alpha inhibitors and IL-1 inhibitors compare to DMARDs?

A

TNF-alpha inhibitors act more rapidly than other DMARDs;
IL-1 inhibitors have a slower onset and are less effective than TNF inhibitors

74
Q

Anesthesia considerations for a patient with RA:

A
  • Airway: Atlantoaxial subluxation, TMJ limitation, cricoarytenoid joints
  • Severe rheumatoid lung disease
  • Protect eyes
  • Stress dose
75
Q

Typical manifestations of Systemic Lupus Erythematosus:

A
  • Antinuclear antibodies
  • Characteristic malar rash
  • Thrombocytopenia
  • Serositis
  • Nephritis
76
Q

SLE manifestations are a result of:

A
  • Tissue damage from vasculopathy mediated by immune complexes
  • Direct result of antibodies to cell surface molecules or serum components
77
Q

What characterizes SLE?

A
  • Multisystem chronic inflammatory
  • Antinuclear antibody production
  • antibodies in 95% of patients
78
Q

What population is SLE common in?

A

Young women and African Americans; ages 15 to 40

79
Q

CNS S/S of Lupus:

A

cognitive dysfunction, physiological changes - related to vasculitis and fluid/electrolyte imbalances, fever, HTN, uremia, infection and drug-induced effects

80
Q

CV s/s of Lupus:

A

Pericarditis (most common), coronary atherosclerosis, Raynaud’s

81
Q

Pulmonary s/s of Lupus:

A

Lupus pneumonia (pulmonary infiltrates, pleural effusion, dry cough, dyspnea, arterial hypoxemia), restrictive lung disease, vanishing lung syndrome (rare, decreased lung volumes, diaphragm elevated)

82
Q

Renal s/s of Lupus:

A

glomerulonephritis w/ proteinuria, hematuria, decreased GFR (oliguric renal failure)

83
Q

GI/liver s/s of lupus:

A

ABD pain, pancreatitis, elevated liver enzymes

84
Q

Hematology s/s of Lupus:

A

Thromboembolism, thrombocytopenia, hemolytic anemia

85
Q

Other s/s of Lupus:

A

Skeletal muscle weakness, butterfly-shaped malar rash, discoid lesions, alopecia

86
Q

Treatment for SLE:

A
  • NSAIDs or ASA
  • Anti-malarial: hydroxychloroquine and quinacrine
  • Corticosteroids
  • Immunosuppressants: methotrexate, azathioprine
87
Q

Anesthesia management for SLE:

A
  • Based on manifestation and organ dyfunction
  • Airway: recurrent laryngeal nerve palsy, cricoaryteniod arthritis, upper airway obstruction
  • Stress dose of corticosteroids
88
Q

Malignant hyperthermia is considered a ____ syndrome

A

Hypermetabolic

89
Q

What is the genetic mutation in malignant hyperthermia?

A
  • Ryanodine receptor - RYR1 gene
  • Dihydropyridine receptor
90
Q

What is the mortality rate for malignant hyperthermia?

91
Q

What produces the heat in malignant hyperthermia?

A

The increased activity of pumps and exchangers trying to correct the increase in sarcoplasmic Ca++ associated with triggered MH increases the need for ATP, which produces heat

92
Q

What leads to rhabdomyolysis in malignant hyperthermia?

A

Sustained high levels of sarcoplasmic Ca++ that rapidly drives skeletal muscle into a hypermetabolic state that may proceed to severe rhabdomyolysis

93
Q

What causes the rigidity in malignant hyperthermia?

A

Result of the inability of the Ca++ pumps and transporters to reduce the unbound sarcoplasmic Ca++ below the contractile threshold

94
Q

Triggers for malignant hyperthermia:

A

Volatile anesthetics and succinylcholine (anectine)

95
Q

EARLY s/s of MH:

A
  • hypercarbia
  • tachypnea
  • sinus tachycardia
  • masseter muscle spasm
  • generalized muscular rigidity
  • peaked T waves
  • metabolic and respiratory acidosis
96
Q

LATE s/s of MH:

A
  • hyperthermia
  • cola-colored urine/rhabdo
  • Elevated CPK
  • Cardiac dysrhythmia (VT/VF)
  • Acute renal failure
  • CV collapse
  • DIC
97
Q

Treatment for MH:

A
  • D/C all triggering gas/drugs
  • hyperventilate with 100% at 10 L/min
  • change breathing circuit and soda lime
  • Dantrolene
  • Treat arrhythmias
  • Monitor urine output
98
Q

How does Dantrolene work? What is the dosage?

A

It reduces the concentration of sarcoplasmic Ca++ to below contractile threshold - inhibits release

  • 20 mg + 3 G mannitol
  • initial dose 2.5 mg/kg
  • max upper limit 10 mg/kg
99
Q

Post-op care for MH:

A
  • transfer to ICU for 24-48 hours
  • report to MH registry
  • MH testing for pt and family members - muscle biopsy contracture testing; halothane plus caffeine contracture test
100
Q

CREST syndrome is commonly associated with what disease?

A

Scleroderma

101
Q

Tensilon test with edrophonium improves with?

A

Myasthenia Gravis

102
Q

RA results in increase pain at what time of day?

103
Q

Airway concerns in RA include:

A

TMJ movement limitation
Atlantoaxial subluxation

104
Q

Which of the following is not common manifestation of SLE?

A

Asymmetric arthritis

105
Q

Horner’s syndrome occurs as a result of which blockade?

A

Stellate Ganglion (over flow from inter-scalene)

106
Q

Newer treatment for MH that is less volume than Dantrolene: