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Apex > Musculoskeletal Diseases > Flashcards

Musculoskeletal Diseases Flashcards

1
Q

What is myasthenia Gravis?

A

Autoimmune disease ~ igG antibodies destroy post-junctional, nicotinic, acetylcholine receptors at the neuromuscular junction

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2
Q

What is a key feature of Myasthenia Gravis?

A

Skeletal weakness that becomes worse later in the day (periods of rest allow for muscular recovery)

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3
Q

What are some S&S of Myasthenia Gravis?

A

Diplopia, ptosis (EARLIEST sign)
Bulbar muscle weakness (muscles of the throat and mouth)
Dyspnea with exertion

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4
Q

What are some things that make myasthenia Gravis worse?

A

Pregnancy
Infection
Electrolyte imbalances
Stress
Aminoglycoside abx

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5
Q

What is the treatment for myasthenia Gravis?

A

Oral pyridostigmine (anticholinesterase inhibitor) is first line treatment

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6
Q

How can you tell if a patient with myasthenia crisis is having a cholinergic crisis (they are on anticholineresterases) or if they are having myasthenia crisis?

A

Tensilon test!

Diagnose with edrophonium (1-2 mg IV)

If muscle weakness worsens ~pt is with cholinergic crisis

If muscle weakness improves ~ myasthenia crisis

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7
Q

What type of surgery can a patient with myasthenia Gravis have that may relieve symptoms?

A

Thymectomy

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8
Q

What can provide temporary relief during myasthenia crisis or before thymectomy?

A

Plasmapharesis

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9
Q

A patient with myasthenia Gravis has what reaction to NMB?

A

Increased sensitivity to non-depolarizing NMBs (ROC)

Decreased sensitivity to depolarizing NMBs (SUX)

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10
Q

Patients with myasthenia Gravis who may need postoperative ventilation include:

A

Disease duration > 6 years
Daily pyridostigmine > 750 mg/day
Vital capacity < 2.9
COPD
Surgical approach ~ median sternotomy > transcervical thymectomy

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11
Q

What is Eaton-Lambert Syndrome associated with?

A

Destruction of presynaptic voltage gated calcium channels

Increased sensitivity to succinylcholine

Small lung carcinoma

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12
Q

In Eaton-Lambert Syndrome, when are symptoms the worst?

A

Worse in the morning and get better throughout the day.

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13
Q

What is the treatment for eaton-Lambert Syndrome?

A

3,4-diaminopyridine (DAP) ~ increases Ach release from presynaptic terminal

**anticholinesterases are NOT helpful

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14
Q

How does a patient with Eaton-Lambert Syndrome response to NMB?

A

Sensitive to BOTH! Doses should be reduced.

They are a high risk for postoperative ventilatory failure

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15
Q

What is the most common cause of acute, generalized paralysis?

A

Guillian-Barre syndrome

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16
Q

What is Guillian Barre?

A

Acute idiopathic polyneuritis ~ immunologic assault on myelin in the peripheral nerves

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17
Q

How does Gillian barre present?

A

Flu-like symptoms 1-3 weeks before

Most common etiologies are campylobacter jejuni bacteria, Epstein-barr, and cytomegalovirus

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18
Q

What are the S&S of Gillian Barre?

A

Flaccid paralysis that begins in distal extremities and ascends bilaterally towards the proximal extremities

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19
Q

What is the treatment for Gillian Barre?

A

Plasmapheresis and IV IgG

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20
Q

How does patients with Guillian Bare react to NMB?

A

Sensitive to BOTH! Avoid Sux.

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21
Q

What is familial Periodic Paralysis?

A

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

Two variants: hypokalemic vs. hyperkalemic

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22
Q

Hypokalemic periodic paralysis is associated with what?

A

Calcium channelopathy

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23
Q

Hyperkalemic periodic paralysis is associated with what?

A

Sodium channelopathy

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24
Q

What do you know if a patient has hypokalemic periodic paralysis?

A

Patient gets weak following a glucose-insulin infusion ~ becomes weak after the serum K+ decreases

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25
Q

How do you know if a patient has hyperkalemic periodic paralysis?

A

Patient becomes weak following oral potassium administration ~ weakness following a rise in serum K

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26
Q

What is the treatment for both hypokalemic AND hyperkalemic periodic paralysis?

A

Acetazolamide

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27
Q

What are TWO major anesthetic considerations?

A

HYPOTHERMIA must be avoided
Serial K+ monitoring is recommended

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28
Q

What is safe to administer for HYPOkalemic periodic paralysis? What is not safe!?

A

Safe: acetazolamide and Nondepolarizers

Not safe: glucose containing solutions, potassium wasting diuretics, beta 2 agonists, Sux

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29
Q

What is safe to administer for HYPERkalemic periodic paralysis? What is not safe!?

A

Safe: glucose containing solutions, potassium wasting diuretics, beta-2 agonists, nondepolarizers, acetazolamide

Not safe: sux and potassium containing solutions (LR)

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30
Q

What is MH?

A

Inherited disease of skeletal muscle that is characterized by disordered calcium homeostasis.

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31
Q

What two drugs stimulate MH?

A

Halogenated agents
Succinylcholine

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32
Q

what is the pathophysiology of MH?

A

T-tubule depolarized > Ca influx > activation of RyR1 receptor > increase in Ca (can’t be “turned off”) > SERCA2 tried to help but it take a LOT of ATP > increase O2 consumption > breakdown in sarcolemma > K+ and myoglobin leak

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33
Q

What are the only three co-existing diseases with MH?

A

King-Denborough
Central core
Multiminicore

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34
Q

What are early signs of Malignant hyperthermia?

A

Tachycardia, increased EtCO2, and masseter spasm, tachypnea, warm soda lime

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35
Q

What are late signs of MH?

A

Hyperthermia, cola-colored urine, and DIC, muscle rigidity

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36
Q

What is the most sensitive indicator of MH?

A

EtCO2 the rises out of proportion to minute ventilation

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37
Q

What is the different b/t trismus and masseter spasm?

A

Trismus: tight jaw that CAN still be opened
(Normal response to sux)

Masseter spasm: tight jaw the CANNOT be opened
(If patient experiences this, assume MH until proven otherwise)

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38
Q

What is the gold standard for diagnosing MH?

A

Caffeine-halothane contracture test (requires a LIVE muscular biopsy sample)

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39
Q

What are some differential diagnoses for MH?

A

Pheochromocytoma
Thyroid storm
Malignant neuroleptic syndrome
Serotonergic syndrome
Heatstroke
Cocaine intoxication

40
Q

What medications are contraindicated in the treatment of MH?

A

Calcium channel blockers

(Life-threatening hyperkalemia may result when a CCB is co-administered with dantrolene)

41
Q

How should a provide prep for a patient with MH?

A

Anesthesia gas machine must be flushed with high-flow oxygen ~ (can be for 20-100 minutes)

All external parts should be removed

Vaporizers should be physically removed from the machine

Patient should be monitored for 1-4 hours in PACU.

42
Q

As an alternative to purging guideline for MH, what can you use?

A

Charcoal filter

43
Q

How much fluid does each vial of dantrolene need to be reconstituted with?

A

60 mL of FREE WATER (not NS)

44
Q

What is the order in which you treat MH?

A
  1. Discontinue triggering agent
  2. Call for help
  3. Hyperventilate with 100% FiO2 at FGF of 10L/min
  4. Administer Dantrolene or Ryanodex (2.5 mg/kg)
  5. Cool the patient
  6. Correct lactic acidosis (bicarb 1-2 mEq)
  7. Treat hyperkalemia (Ca-DI ~ calcium, Dextrose, insulin)
  8. Protect dysrhythmias (lido/procainamide)
  9. Maintain urine output (>2 mL/kg/hr)
  10. DIC is a baaaad sign ~ impending demise
45
Q

What is the most common skeletal muscle myopathy?

A

Duchenne muscular dystrophy

46
Q

What is Duchenne muscular dystrophy?

A

X-linked recessive disease that results from the absence of the dystrophin protein

47
Q

What is dystrophin?

A

Structural component of the cytoskeleton of skeletal and cardiac cells. ~ helps anchor actin and myosin to the cell membrane

48
Q

Why does Succinylcholine carry a black box warning?

A

Risk of cardiac arrest and sudden death secondary to hyperkalemia in children with undiagnosed skeletal muscle myopathy

49
Q

What are some resp considerations for Duchenne?

A

Kyphoscoliosis (restrictive lung disease) > decreases FRC (decreased reserve) > increased secretions and risk of pneumonia.

50
Q

What are some cardiac considerations for Duchenne’s?

A

Degeneration of cardiac muscle > reduced contractility, papillary musc dysfunction, mitral regurge and CHF

(These pts may have resting tachycardia, JVD, S3/S4 gallop)

**must have cardiac work up before surgery (EKG, ECHO, MRI)

51
Q

What are some EKG changes you may see with Duchenne’s?

A

Sinus tach with short PR

Due to scarring, LV manifests as increased R wave amplitude in lead I and deep Q waves

52
Q

What are some GI considerations for Duchenne’s?

A

Impaired airway reflexes and GI hypomotility ~ increased risk for aspiration

53
Q

What is the Cobb angle?

A

Describes the magnitude of spinal curvature in a patient with scoliosis

54
Q

What does a Cobb angle of 40-50 indicate?

A

Surgery

55
Q

What does a Cobb angle of 60 indicate?

A

Decreased pulmonary reserve

56
Q

What does a Cobb angle of 70 indicate?

A

Pulmonary symptoms present

57
Q

What does a Cobb angle of 100 indicate?

A

Gas exchange impairment. Very high risk of post-operative pulmonary complications.

58
Q

What are some early resp complications with scoliosis?

A

Restrictive vent defect
FEV1 and FRC are decreased
FEV1/FVC ration = normal
Decreased lung volumes
And decreased chest wall compliance

59
Q

What are some late resp complications of scoliosis?

A

V/Q mismatch
Hypoxemia
Hypercarbia
Pulmonary HTN
Cor Pulmonale

60
Q

What are some cardiovascular changes due to scoliosis?

A

RV hypertrophy (d/t PHTN)

61
Q

A vital capacity of what correlates with the requirements for post-op ventilation?

A

VC < 40%!

62
Q

What is a “wake up” test?

A

Method of assessing neurological integrity during complex spine surgery

**turn off agent and allow patient to wake up.

( Risks of wake up include: pain, awareness, air embolism, tracheal extubation, damage to surgical instrumentation, line removal)

63
Q

What three areas does Rheumatoid Arthritis affect the airway?

A

Temporomandibular joint (limited mouth opening)
Cricoarytenoid Joints (decrease glottic opening)
Cervical spine (limited neck extension)

64
Q

What is the most common airway complication of RA?

A

Atlantoaxial subluxation and separation ~ this ultimately allows the atlanto-odontoid process to compress the spinal cord at the level of the foramen magnum

65
Q

What is Rheumatoid Arthritis?

A

Autoimmune disease that targets the synovial joints. In addition, there is infiltration of immune complexes in the small and medium arteries leading to vasculitis.

66
Q

What is the hallmark of RA?

A

Stiffness in the morning that generally improves with activity

Primarily affects proximal interphalangeal and metacaepophalangeal joints.

67
Q

How does RA affect the pulmonary system?

A

Pleural effusion
Interstitial fibrosis ~ limited chest wall expansion and restrictive vent pattern

68
Q

how does RA affect the cardiac system?

A

Pericardial effusion/tamponade
Aortic regurge
Vascular fibrosis
Coronary artery arteritis

69
Q

How does RA affect the hematological system?

A

Anemia
Platelet dysfunction (d/t asa)

70
Q

What labs are increased in RA?

A

C-reactive cells protein
Erythrocyte sedimentation rate.

(Both labs test for inflammation)

71
Q

What is the treatment for RA?

A

Antirheumatics (think methotrexate)
Glucocorticoids
NSAIDS

72
Q

How does RA affect the renal system?

A

Insufficiency d/t vasculitis and NSAIDs

73
Q

How does RA affect the CNS?

A

Peripheral neuropathy

74
Q

What is Systemic Lupus Erythematosus?

A

Autoimmune disease characterized by the proliferation of antinuclear antibodies

Antibody induced vasculitis and tissue destruction

75
Q

Who does Lupus primarily target?

A

Young women

76
Q

How does lupus affect the airway?

A

Cricoarytenoiditis ~ airway obstruction, stridor, and hoarseness

77
Q

How does Lupus affect the Nervous system?

A

Stroke
Psychosis
Neuropathies

78
Q

How does Lupus affect the kidneys?

A

Nephritis with proteinuria

79
Q

How does Lupus affect the pulmonary system?

A

Restrictive dx process
PHTN
Interstitial lung disease
Pleural effusion
**Recurrent PE

80
Q

How does Lupus affect your heart?!

A

Pericarditis
Raynaud’s disease
HTN
Conduction defects
Endocarditis

81
Q

How does Lupus affect your Hematologic system?

A

Antiphospholipid antibodies
Hypercoagulability
Anemia
Thrombocytopenia
Leukopenia

82
Q

What are some things that can exacerbate Lupus symptoms? Think of the mnemonic

A

PISSED CHIMP

P: pregnancy
I: infection
S: surgery
S: stress
E: enalapril
D: d-penicillamine

C: captopril
H: hydralazine
I: isoniazid
M: methyldopa
P: procainamide

83
Q

What is the medical treatment for Lupus? Similar to RA

A

Corticosteroids
NSAIDs
Immunosuppressants (methotrexate, cyclophosphamide)
Antimalarials

84
Q

Which immunosuppressant increases the duration of succinylcholine? This immunosuppressant is used for both RA and Lupus.

A

Clycophosphamide

85
Q

What is the defining characteristic of Marfan’s disease?

A

Aortic insufficiency

(Also remember AAA)

86
Q

What is the definitely characteristic of Ehler’s Danlos syndrome?

A

Bleeding into joints

(Result of poor vessel integrity)

87
Q

What is the definitely characteristic of osteogenesis imperfecta?

A

Blue sclera

(Also think weak bones ~ fx can occur from BP or Sux)

88
Q

What is Multiple Sclerosis?

A

Demyelination disease of the CNS (can cause sensory, motor and autonomic instability)

Can be exacerbated by stress and hyperthermia

NO sux

89
Q

What is myotonic dystrophy?

A

Prolonged contracture following voluntary contracture ~dysfunction in calcium sequestration

90
Q

What are 3 things that increase the risk of contractures in myotonic dystrophy?

A

Sux
NMB reversal with anticholinesterases
Hypothermia

91
Q

What is Scleroderma?

A

Excessive fibrosis in the skin and organs ~ particularly the microvascular.

92
Q

What is CREST syndrome?

A

Type of scleroderma

C: calcinosis
R: Raynaud’s phenomenon
E: esophageal hypomotility
S: sclerodactyly
T: telangiectasia (spider veins)

93
Q

What is Paget’s disease?

A

Excessive osteoblastic and osteoclastic activity that causes abnormally thick, but weak, bone deposits

94
Q

What is Paget’s disease caused by?

A

Excessive parathyroid hormone or calcitonin deficiency

Pain and fx are the most common problems.

95
Q

How does scleroderma complicate airway management?

A

Ski fibrosis > limits mouth opening
Telangiectasis > increases the risk for mucosal bleeding

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