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Assessment > Exam 2 - Musculoskeletal Diseases > Flashcards

Exam 2 - Musculoskeletal Diseases Flashcards

1
Q

Systemic Sclerosis is another name for?

A

Scleroderma

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2
Q

What are the 3 processes that characterize scleroderma?

A
  1. Autoimmune-mediated inflammatory vasculitis
  2. Fibrosis of skin and internal organs from abnormal deposition of extracellular collagen
  3. Microvascular changes produce tissue fibrosis and organ sclerosis
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3
Q

What are the 3 main forms of scleroderma?

A
  • Localized (just skin)
  • Limited cutaneous
  • Diffuse cutaneous (rapidly progressing with CV complications)
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4
Q

What mnemonic guides the main symptoms associated with scleroderma?
Expound on the mnemonic.

A
  • Calcinosis
  • Raynaud’s
  • Esophageal reflux
  • Sclerodactyly
  • Telangiectasia’s
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5
Q

What skin and musculoskeletal abnormalities might be seen with scleroderma?

A
  • Taut skin
  • Contractures & myopathy
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6
Q

What can happen to nerves with scleroderma?

A

Compression

Careful when placing lines

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7
Q

What are the CV changes seen in scleroderma?

A
  • Systemic and Pulmonary HTN (careful on induction; etomidate)
  • Dysrhytmias
  • Vasospasms of small arteries in fingers
  • CHF
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8
Q

What is keratoconjunctivitis sicca?

A

Dry, red eyes from keratin deposits

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9
Q

What severe kidney issue can be caused by scleroderma?
Treatment?

A

Renal crisis - precipitated by steroids
Tx: ACEi

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10
Q

Pulmonary complications with scleroderma?

A
  • Diffuse pulmonary fibrosis
  • Decreased compliance
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11
Q

What are the GI symptoms with scleroderma?
What treatments are/are not effecive?

A
  • Decreased motility
  • Xerostomia (mouth dryness)
  • Malabsorption syndrome
  • Pseudo obstruction

Tx: Hypomotility - Octreotide; Reglan does not work

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12
Q

What treatments are used for scleroderma and their effects?

A
  • Symptom alleviation
  • ACE-inhibitors - renal protection
  • PDE inhibitors - decrease pulm HTN
  • Digoxin - improve CO
  • Steroids/Immunosupressive therapy - target organ involvement
  • PPIs - reflux
  • CCB - Raynauds
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13
Q

What airway and pulmonary anesthetic considerations exists for scleroderma?

A
  • Pulmonary fibrosis (↓ compliance/reserve)
  • Decreased ROM for airway
  • Oral bleeding (can give TXA topically)
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14
Q

What CV anesthetic considerations exists for scleroderma?

A
  • Difficult IV/arterial access
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15
Q

What non-airway/CV anesthetic managements can we do for patients with scleroderma?

A
  • Regional anesthesia
  • Pre-warm and keep warm
  • VTE prophylaxis (3x more prone to embolism)
  • Stress dose their steroids
  • Positioning d/t contractures
  • Pulse ox difficulty
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16
Q

What is Duchenne’s Muscular Dystrophy (DMD)?
What initial symptoms are present at 2-5 years of age?

A
  • X-linked dystrophin mutation resulting in muscle atrophy.
  • (Ages 2-5) = waddling gait, frequent falling, can’t climb stairs, Gower’s sign.
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17
Q

What s/s are seen with DMD?

List:
CNS
Musculoskeletal
CV
Pulm
GI

A
  • CNS - intellectual disability
  • MS - kyphoscoliosis, muscle atrophy, ↑ CK
  • CV - ↑ HR, cardiomyopathy, short PR & tall R-wave in V1, deep Q wave in limb leads
  • Pulm - weakened respiratory muscles and weak cough (related to 30% of deaths), OSA
  • GI - hypomotility & gastroparesis
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18
Q

What is pseudohypertrophic DMD?

A

Fatty infiltration, making muscles appear larger - most severe and and common form of childhood muscular dystophy

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19
Q

What are the anesthetic concerns and interventions relevant to DMD patients?

  • Airway
  • Pulmonary
  • CV
  • GI
A
  • Airway - weak laryngeal reflexes & cough
  • Pulm - weakened muscles, increased secretions (may need vent support post op)
  • CV - Get pre-op EKG & echo
  • GI - delayed gastric emptying
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20
Q

What drug should be avoided with DMD patients?

A
  • Succinylcholine (Rhabdo, ↑K⁺, increased risk of MH)

use NDMBs

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21
Q

What type of anesthesia is prefereable for a DMD patient?

A

Regional (vs GA)

But not easy to do on a child

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22
Q

Why might one use less volatile gasses with DMD patients?

A
  • DMD patients have ↑risk of malignant hyperthermia.

Ensure you have Dantrolene

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23
Q

What is the pathophysiology of myasthenia gravis?

A
  • ↓ function of NMJ post-synaptic ACh receptors.
  • Results in muscle weakness and rapid exhaustion of voluntary muscles

αlpha sub-units of ACh receptor are bound by antibodies.

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24
Q

What organ is linked with the production of anti-ACh antibodies?

A
  • Thymus
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25
Q

Which condition is characterized by partial recovery with rest?

A

Myasthenia Gravis

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26
Q

What are MuSK antibodies?

A
  • Muscle-specific kinase; present in 10% of MG patients
  • Loss ofAChreceptors and a changein the structure of the post-synaptic folds
  • No thymic involvement
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27
Q

What is type 1 and 4 MG classifications?

A

Type 1: limited to involvement of extraocular muscles
Type 4: Severe from of skeletal muscle weakness

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28
Q

What are the initial s/s of MG?

A
  • Ptosis
  • Diplopia
  • Dysphagia
  • Dysarthria (trouble speaking)
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29
Q

What may a patient with MG present to the ED for?

A

Isolated respiratory failuire

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30
Q

What autoimmue disorders are associated with MG?

A
  • RA
  • SLE
  • Pernicious anemia (B12 deficiency)
  • Hyperthyroidism
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31
Q

What abx can trigger MG symptoms?

A

Mycins (gentamicin, streptomycin, tobramycin)

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32
Q

Differentiate Myasthenic Crisis and Cholinergic Crisis.

A
  • Myasthenic Crisis - Insufficient drug therapy resulting in severe muscle weakness and respiratory failure.
  • Cholinergic Crisis - too much -stigmine drug (excess ACh) = SLUDGE-M symptoms.
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33
Q

What test is used to diagnose myasthenia gravis?

A

Edrophonium/Tensilon Test
- 1-2 mg IVP
- Myasthenia symptoms improve with injection
- If cholinergic crisis, symptoms will worsen

34
Q

What drugs are the firstline treatment for Myasthenia Gravis?
What would be done if drugs were ineffective?

A
  • Pyridostigmine (max dose 120 mg q3h)
  • Surgical Thymectomy
35
Q

What drugs/treatments other than pyridostigmine or surgery could be used for myasthenia gravis?

A
  • Corticosteroids
  • Azathioprine
  • Cyclosporine
  • Mycophenolate
  • Plasmapheresis
  • Immunoglobulin
36
Q

What is the most commmonly used/most effective treatment for MG?

A

Corticosteroids - used when muscle weakness is not controlled by anticholinesterase tx

37
Q

What anesthetic considerations exist for myasthenia gravis?

A
  • Aspiration risk & weakened respiratory muscles. (Give H2 antagonist and reglan)
  • Sensitivity to NMBs (intubate without if possible - should be easier d/t intrinsic muscle weakness)
  • No succinylcholine (resistant to it from pyridostigmine )
38
Q

Which muscle should you not not check TO4 on MG patients?

A
  • Adductor Pollicis
  • Orbicularis Oculi will overestimate degree of blockade
39
Q

What is osteoarthritis (OA)?
What makes the pain better?

A
  • Degeneration of articular cartilage with minimal inflammation.
  • Pain better at rest.
  • Pain is worse with motion.
40
Q

What are Heberden nodes?
What disease process do they indicate?

A
  • Bony swellings of the distal interphalangeal joints.
  • Osteoarthritis
41
Q

What spinal complications occur from osteoarthritis?

A
  • Vertebral degeneration
  • Nucleus pulposus herniation
  • Nerve root compression
42
Q

What are the treatments for osteoarthritis?

A
  • PT & exercise
  • Maintenance of muscle function
  • Pain relief
  • Joint replacement surgery
  • No corticosteroids
43
Q

What anesthetic considerations exist for OA?

A
  • Limited airway ROM - may require fiberoptic or video laryngoscopy
44
Q

What is rheumatoid arthritis?
What hand condition is often seen on inspection?

A
  • Auto-immune systemic inflammatory disease
  • Swelling of the Proximal Interphalangeal, metocarpophalangeal, and elbow joints.
  • 2-3x higher in women than men
45
Q

What type of swelling presents with RA?

46
Q

What joints are usually spared by rheumatoid arthritis?

A
  • Thoracic & Lumbosacral spine
47
Q

With this condition it is common to have synovitis of the temporomandibular joint.

A

Rheumatoid Arthritis

48
Q

Patients with this disorder have morning stiffness that gets better throughout the day?

49
Q

Why would the sniffing position and thus intubation be affected in a patient who has rheumatoid arthritis?

A
  • Atlantoaxial subluxation (odontoid process pushes on spinal cord)
  • Cricoarytenoid arthritis (hoarseness, dyspnea, and upper airway obstruction may be present)
50
Q

What cardiac symptoms can be seen with RA?
Pulmonary?

A
  • CV: Pericarditis and accelerated CAD
  • Pulm: Restrictive lung changes, rheumatoid nodules (resembles TB on xray)
51
Q

What two facial symptoms are often seen with RA?
These are manifestations of what syndrome?

A
  • Keratoconjunctivitis sicca (dry eye)
  • Xerostomia (dry mouth)
  • Sjogren syndrome
52
Q

What hematologic symptoms are seen in RA?

A
  • Anemia of chronic disease
  • neutropenia
  • elevated platelets
53
Q

What drugs are used to treat rheumatoid arthritis?

A
  • NSAIDs
  • Corticosteroids
  • DMARDs
  • TNF-α inhibitors & Interleukin-1 inhibitors
54
Q

What are the side effects of COX-1 and COX-2 inhibitors?

A

COX-1 inhibitors: GI irritation and platelet inhibition;decrease renal blood flow and GFR
COX-2 inhibitors: fewer GI side effects and do not interfere with platelet function; decrease renal blood flow and GFR
Increase risk of CVA and CAD

55
Q

Compare and contrast DMARDs vs TNF-α inhibitors & Interleukin-1 inhibitors in how they treat rheumatoid arthritis.

A
  • DMARDs (methotrexate) slow disease progression but can take 2-6 months to see effects
  • TNF-α & IL1 inhibitors generally work better than DMARDs (IL1’s are slower onset and less effective than TNF)
56
Q

What drug can be given to prevent methotrexate toxicity?

A

Folic acid

57
Q

What anesthesia considerations exist for rheumatoid arthritis?

A
  • Airway complications by atlantoaxial subluxation or TMJ.
  • Severe RA lung disease
  • Stress dose steroids may be necessary
58
Q

What pathology is this and what are these lesions called?

A
  • Discoid lesions characteristic of SLE.
59
Q

What type of rash is depicted below? What pathology is it characteristic of?
What often causes it?

A
  • Maculopapular rash characteristic of SLE and exposure to the sun.
60
Q

What CV symptoms are seen with SLE?

A
  • Pericarditis (most common)
  • CAD
  • Raynaud’s
61
Q

What type of arthritis is seen with SLE?

A
  • Symmetrical w/ no spinal involvement but involves avascular necrosis of femoral head
62
Q

What pulmonary symptoms are characteristic of SLE?

A
  • Lupus pneumonia
  • Vanishing Lung syndrome (elevated diphragm, recurrent atelectasis)
  • Restrictive lung disease
63
Q

What are the CNS s/s in SLE?

A
  • Cognitive dysfunction
  • Anxiety/depression
  • Atypical migraines
64
Q

What are the renal s/s in SLE?

A
  • Glomerulonephritis
  • Hematuria
  • Decreased GFR (oliguric renal failure)
65
Q

What treatment can accelerate death via coronary athersclerosis in patients with SLE?

A

Corticosteroids

66
Q

Hematologic s/s in SLE?

A
  • Thromboembolism
  • Thrombocytopenia
  • Hemolytic anemia
67
Q

GI s/s in SLE?

A
  • Abd pain
  • Pancreatitis
  • ↑ Liver enzymes
68
Q

What drugs are utilized to treat SLE?

A
  • NSAIDs or ASA
  • Antimalarials (HCQ & quinacrine)
  • Corticosteroids (major cause of morbidity)
  • Immunosuppressants (methotrexate, azathioprine)
69
Q

What anesthesia considerations exist for SLE patients?

A
  • Recurrent laryngeal nerve palsy (difficulty speaking)
  • Cricoarytenoid arthritis
  • Stress dose steroids likely necessary
70
Q

What pathophysiology causes malignant hyperthermia?
Mortality rate?

A
  • Genetic mutation of ryanidine and dihydropyridine receptor
  • 50%
71
Q

What patho causes rhabdo in MH?
Hyperthermia?

A
  • Sustained high levels of sarcoplasmic Ca2+that rapidly drives skeletal muscle into a hypermetabolic state
  • Increased activity of pumps and exchangers trying to correct the increase in sarcoplasmic Ca2+associated with triggered MH increases the need for ATP, which in turn produces heat
72
Q

What are the early signs of malignant hyperthermia?

A
  • ↑CO₂
  • ↑HR
  • ↑RR
  • Jaw muscle spasm (biting down on ETT)
  • Peaked T waves
  • Acidosis
  • Muscle rigidity
73
Q

What are the late signs of malignant hyperthermia?

A
  • Hyperthermia
  • Rhabdo & cola-urine
  • ↑CPK
  • VTach/Vfib (from hyperkalemia)
  • Acute renal failure
  • DIC
74
Q

Can you give nitrous to someone with a history of MH?

A

Yes
Just not succ or volatiles

75
Q

What is initial Dantrolene dosing?
What is the max dose?
How does it help MH?

A
  • Initial: 2.5mg/kg
  • Max: 10mg/kg
  • Reduces the concentration of sarcoplasmic Ca2+to below contractile threshold
76
Q

What should be done immediately if MH is suspected?

A
  • Stop all triggering agents
  • Hyperventilate with 100% O2 at 10 L/min
  • Change breathing circuit and soda lime
77
Q

What other drugs besides dantrolene are used to treat the effects of MH?

78
Q

What should be done post op for MH patients?

A
  • Transfer to ICU
  • Report to MH registry
  • MH testing for pt and family members (muscle biopsy contracture testing w/ halothane and caffiene)
79
Q

Kahoot

2 MH triggers?

A
  • Isoflurane
  • Anectine (succinylcholine)
80
Q

Kahoot

Horners syndrome occurs as a result of which blockade?

A

Stellate ganglion

Assessment (8 decks)

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