Exam 2 Musculoskeletal Spring 2024 Flashcards
What is scleroderma?
Inflammation and autoimmune disease that causes vascular injury and vascular obliteration. Chronic hardening and tightening of the skin and connective tissues.
Tissue fibrosis and organ sclerosis.
What are the 3 forms of scleroderma?
- Localized scleroderma- skin, face, distal limb
- Limited cutaneous systems sclerosis - CREST syndrome, has prominent skin manifestations
- Diffuse cutaneous system sclerosis- generalized skin involvement and cardiac complications.
The limited symptoms of scleroderma are referred to as CREST. What does CREST stand for?
S/S of Scleroderma
Skin:
MS:
Nervous System:
CV:
Skin: Taut skin
MS: Limited mobility/contractures, skeletal muscle myopathy
Nervous System: Nerve compression
CV: HTN, PAH, dysrhythmias, vasospasm in small arteries of fingers, CHF,CAD,
S/S of Scleroderma
Pulmonary:
Renal:
GI:
Pulmonary: Diffuse interstitial pulmonary fibrosis, decreased pulmonary compliance (stiff lungs)
Renal: Decreased renal blood flow and systemic HTN
GI: Xerostomia, poor dentition, fibrosis of GI tract (no Reglan, will not stimulate fibrotic GI tract), reflux
Scleroderma Treatment?
for reflux?
for Raynauds?
for PH?
- PPIs for reflux
- CCBs for Raynaud’s & vasospasms
- ACEIs for Renal protection (The only tx shown to alter the course of scleroderma is ACE inhibitors to treat scleroderma renal crisis)
(note: ACE-I cause angioedema & increased coughing)
- Prostacyclins or phosphodiesterase inhibitors, oxygen, anticoagulation, and diuretics for Pulmonary HTN
- Digoxin to Improve CO
- Immunosuppressive and steroid therapy targeted toward affected organ involvement: Skin, lung, cardiac, and muscle
SclerodermaAnesthesia Management and Considerations
Airway:
IV:
Pulmonary:
GI:
Eyes:
Other:
Airway: Mandibular motion, small mouth opening, neck ROM (do not manipulate neck while asleep), oral bleeding
CV: IV/arterial line access may be difficult, use US.
Pulmonary: Decreased pulmonary compliance and reserve, avoid increasing PVR (do not make them hypoxic)
GI: Aspiration
Eyes: tape eyes, ointment, gauze, goggles
Other: Regional anesthesia may be best for these patients, keep patient warm, VTE prophylaxis, Positioning with care, Pulse ox difficulties (ear probe)
What is Pseudohypertrophy Muscular Dystrophy/ Duchenne Muscular Dystrophy (DMD)
Mutation in the dystrophin gene (x-linked recessive) causes fatty infiltration leading to pseudohypertrophic muscles.
Common in 2-5 y/o boys
By age 8-10 Wheelchair bound
Usually live until ages 20-25 years (CHF, pneumonia)
large protein that plays a major role in stabilization of the muscle membrane and signaling between the cytoskeleton and extracellular matrix
Dystrophin
Initial symptoms of Duchenne Muscular Dystrophy
Initial symptoms: waddling gait, frequent falling, difficulty climbing stairs, tiptoes.
Duchenne Muscular DystrophyS/S
CNS:
MS:
CV:
Pulmonary:
GI:
CNS: Intellectual disability
MS: Kyphoscoliosis, skeletal muscle atrophy, serum CK 20-100x normal d/t increase muscle permeability
CV: Sinus tachycardia, cardiomyopathy, EKG abnormalities (tall R-wave in V1)
Pulmonary: OSA, weakened respiratory muscles, and cough
GI: Hypomotility, gastroparesis
Duchenne Muscular DystrophyAnesthesia Management
Airway:
Pulmonary:
CV:
GI:
Airway: weak laryngeal reflexes and cough - consider increased secretions, possible ventilatory support
Up to 36 hours post-op
Pulmonary: weakened muscles, Will need Oral airways or nasal airways. Need to be woken up on CPAP or BIPAP
CV: Pre-op EKG and/or echo based on the severity
GI: Delayed gastric emptying, aspiration risk
Other anesthesia management for Duchenne Muscular DystrophyAnesthesia:
What drug do you want to avoid?
When do you want to extubate these patients?
What type of incidence are higher in these patients?
What type of anesthesia may be best?
Avoid succinylcholine can cause hyperkalemia and rhabdomyolysis. Use NDMR (Rocuronium).
Pharyngeal and respiratory muscle weakness, secure the airway. Make sure the patient is fully awake.
MH – increased incidence. Have Dantrolene ready. Use TIVA as an alternative
Regional Anesthesia may be best than GA.
What is Myasthenia Gravis?
A chronic autoimmune disorder involving the NMJ. There will be decreased functional post-synaptic AChreceptors.
Muscle weakness w/ rapid exhaustion of voluntary muscles. Partial recovery with rest.
ACh receptor-bindingantibodies are linked to thymus abnormalities.
Myasthenia GravisS/S
Eyes:
Oral:
Pulmonary:
Skeletal:
Heart:
Endocrine:
Ptosis (droopy eyelid), diplopia (double vision)
Dysarthria (slurred speech), dysphagia, and difficulty handling saliva
Isolated respiratory failure (rare)
Arm, leg, or trunk muscle weakness
Myocarditis
Autoimmune diseases associated
RA, SLE, pernicious anemia, hyperthyroidism
Myasthenic Crisis vs Cholinergic Crisis?
What is the effect of the Edrophonium/Tensilon Test in each condition?
Myasthenic crisis:
D/t drug resistance or insufficient drug therapy
S/S: severe muscle weakness and respiratory failure
Cholinergic crisis (SLUDGE):
D/t excessive anticholinesterase treatment
S/S: muscarinic side effects – profound muscle weakness, salivation, miosis, bradycardia, diarrhea, abdominal pain
Edrophonium/Tensilon Test:
1-2 mg IVPof edrophonium will improve the myasthenic crisis and makes the cholinergic crisis worse.
Myasthenia GravisTreatment
(first-line treatment): ?
surgical ?
Anticholinesterases:
The first line of treatment
Pyridostigmine last longer than neostigmine
Thymectomy:
Induces remission
Reduced use of immunosuppressives
Reduces ACh receptor antibody levels
Full benefit delayed (2-6 months)
MG treatment immunosuppression-wise?
Immunosuppression:
Corticosteroids, azathioprine, cyclosporine,mycophenolate
Indicated when skeletal muscle weakness is notadequately controlled by anticholinesterase drugs
Corticosteroids–most commonly used and most consistently effective treatment
Immunotherapy :
Plasmapheresis: short-term clinical improvement
Removes antibodies from circulation . Repeated tx increases risk of infection, hypotension, and pulmonary embolism
Immunoglobulin: short term, No effect on circulating concentrations of ACh receptor antibodies
What is Osteoarthritis?
The most common joint disease in the ____?
OA is characterized by _________ inflammation.
Does stiffness fade throughout the day?
Degenerative process affecting articular cartilage, the most common joint disease in the elderly.
Characterized by minimal inflammation usually a result of chronic joint trauma (sports), biomechanical stresses, joint injury, abnormal joint loading, neuropathy, ligament injury, muscle atrophy, and obesity.
Pain present with motion,relieved by rest. Morning stiffness fades throughout the day. (T-rex)
What joints will osteoarthritis affect?
Weight-bearing and distal interphalangeal joints.
Heberden nodes- Distal interphalangeal joints,
Protrusion of the nucleus pulposus (herniated disc) can lead to compression of nerve roots.
Degenerative disease – vertebral bodies and intervertebral disks. OA will affect the breakdown of the cartilage of the joints and discs in the neck and lower back. Middle to lower C-spine and L-spine.
Heberden nodes?
Heberden nodes- Distal interphalangeal joints, first knuckle (pictured)
What is Rheumatoid Arthritis?
which joints affected?
IG present in how many pts
An autoimmune-mediated, systemic inflammatory disease that usually affects the proximal interphalangeal and metacarpophalangeal joints
2-3x higher in woman than men
Rheumatoid nodules at pressure points (elbows)
Rheumatoid factor (IG antibody present in 90% of patients with RA)
Rheumatoid Arthritis
morning stiffness is like?
what kind of joint swelling?
what joints not affected?
Single or multiple joints
Painful synovial inflammation, swelling, and increased fluid
Morning stiffness like OA, but remains stiff throughout the entire day.
Symmetrical distribution of several joints.
Fusiform swelling - Joints become enlarged and the fingers crooked (pictured)
Synovitis of the temporomandibular joint (decrease mouth opening)
Affects nearly all joints (except the t-spine and lumbosacral spine)
Rheumatoid Arthritis S/S
Atlantoaxial subluxation:
Cricoarytenoid arthritis:
Osteoporosis
NM
Atlantoaxial subluxation instability (C1 and C2) (>3 mm separation): Odontoid process (dens) protrudes into the foramen magnum. The instability can place pressure on the transverse ligament and spinal cord. Instability can also impair vertebral artery blood flow.
Cricoarytenoid arthritis:
Acute – hoarseness, dyspnea, and stridor w/ tenderness over the larynx; swelling and redness of arytenoids
Chronic – asymptomatic or variable degrees of hoarseness, dyspnea, and upper airway obstruction
Osteoporosis: More common in women than men
NM: Weakened skeletal muscles (peripheral neuropathies)
What is Systemic Lupus Erythematosus?
Typical Manifestation:
Multisystem chronic inflammation characterized by antinuclear antibody production.
- Common in young women & African Americans; ages 15 to 40
Typical manifestations (Usually will have 3 out 5 of the following):
1. Antinuclear antibodies
2. Malar rash (butterfly rash)
3. Thrombocytopenia
3. Serositis- inflammation of a serous membrane around the organ
5. Nephritis
Systemic Lupus ErythematosusS/S
GI/Liver:
NM:
Hematology:
Skin:
GI/Liver: ABD pain, pancreatitis, elevated liver enzymes
NM: Skeletal muscle weakness
Hematology: Thromboembolism, thrombocytopenia, hemolytic anemia,
Skin: Butterfly-shaped malar rash, **Discoid lupus lesions, which are thick and disk-shaped. **
Malignant HyperthermiaNon-triggering Agents
Malignant HyperthermiaS/S
Early Sign:E
levated end-tidal CO2
Tachypnea and/or tachycardia
Generalized muscle rigidity
Mixed metabolic and respiratory acidosis
MASSETER SPASM – muscle for mastication Masseter spasm if succinylcholine has been used
- also caused by etomidate
