Musculoskeletal-Assessment Exam 2 Flashcards
1
Q
Scleroderma is characterized by what 3 interrelated processes?
Another name for scleroderma?
A
systemic sclerosis
- Autoimmune-mediated inflammatory vasculitis
- Fibrosis of skin and internal organs from abnormal deposition of extracellular collagen
- Microvascular changes produce tissue fibrosis and organ sclerosis
2
Q
T/F
Vascular structures do not regenerate
A
True
3
Q
What are the 3 main forms of scleroderma?
A
Localized
Limited cutaneous
Diffuse cutaneous
4
Q
Describe localized scleroderma
A
Involvement of the skin of the face, trunk, and distal limbs
5
Q
Describe limited cutaneous scleroderma
A
Usually a combination of scleroderma features; CREST syndrome
6
Q
Describe diffuse cutaneous scleroderma
A
Rapidly progressive disease, with generalized skin involvement and cardiovascular complications with vascular involvement, coronary artery disease, cardiomyopathy, and hypertension
7
Q
Scleroderma is what type of disease?
A
Autoimmune
8
Q
Why is it important to understand that autoimmune diseases follow the same patterns (meaning a lot of pts might have multiple)?
A
Polypharmacy, long term opiods
9
Q
What is CREST an acronym for?
What does it stand for?
A
All symptoms of scleroderma
C: Calcinosis
R: Raynaud’s
E: Esophageal dysfunction
S: Sclerodactylyl
T: Telangiectasias
10
Q
What is CREST syndrome?
A
Vascular endothelial cell injury results in widespread capillary loss and vascular obliteration and leakage of serum proteins into the interstitial space
- Tissue edema, lymphatic obstruction, and fibrosis
poor prognosis d/t extent of visceral involvement (the kidney, the lung, the heart and the gastro-intestinal tract)
11
Q
Scleroderma S/S of the skin
A
mild thickening and diffuse non-pitting edema
taut skin
calcium deposits
12
Q
Scleroderma S/S of the MS system
A
Limited mobility/contractures (taut skin)
skeletal muscle myopathy (weakness, proximal skeletal muscles)
plasma CK increased
mild inflammatory arthritis
13
Q
Scleroderma S/S of the nervous system
A
Nerve compression
trigeminal neuralgia (facial pain)
keratoconjunctivitis sicca (dry, red eyes)
14
Q
Scleroderma S/S of the CV system
A
Systemic and pulmonary HTN
dysrhythmias
cardiac conduction abnormalities
CHF
pericarditis
pericardial effusion w/ or w/o cardiac tamponade
vasospasm in small arteries of fingers
15
Q
Where is the nerve compression usually in scleroderma?
A
Distally (i.e radial, ulnar)
16
Q
S/S of pulmonary HTN
A
Venous distention (JVD)
pulmonary edema on chest xray
dilated RV
17
Q
Management of pulmonary HTN
A
- Keep them euvolemic or a little dry
- Use flo-lan or sildenafil
- Slow induction! Take your time. See how they react hemodynamically to meds.
- Can also sedate these patients first then start volatile anesthetics
18
Q
Induction DOC for pulmonary HTN
A
Etomidate
19
Q
Scleroderma S/S of the pulm. system
A
Diffuse interstitial pulmonary fibrosis
arterial hypoxemia
decreased pulmonary compliance
20
Q
Scleroderma S/S of the renal system
A
Decreased renal blood flow and systemic HTN
21
Q
Renal crisis is precipitated by _______ and the treatment is _______
A
Corticosteroids
Ace inhibitors
22
Q
Scleroderma S/S of the GI system
A
Xerostomia
poor dentition
fibrosis of GI tract (esophageal and small intestine hypomotility)
dysphagia
reflux
malabsorption syndrome
coagulation disorders
pseudo-obstruction
**reglan/metoclopramide does not work
23
Q
What does renal crisis by steroids look like?
A
dryness of the oral mucosa
malabsorption syndrome - small intestine bacteria overgrowth (broad spectrum ABX)
vitamin k malabsorption,
pseudo-obstruction (intestine hypomotility)
24
Q
Scleroderma treatment includes:
A
PPIs (reflux)
CCB
Ace inhibitors (renal crisis)
Arbs
For pulm. HTN:
Prostacyclins
Phosphodiesterase inhibitors
Oxygen
Antiocoagulation
Diuretics
Digoxin (improve CO)
25
_____ such as ______ are effective in improving small intestine hypomotility, whereas prokinetic drugs such as metoclopramide are not.
Somatostatin analogues
Ocreatide
26
If someone who takes ACE/ARBS are hypotensive in OR, what is the DOC?
Vasopressin
27
Scleroderma anesthesia management of the airway
Mandibular motion, small mouth opening, neck ROM, oral bleeding
28
Scleroderma anesthesia management of the CV system
IV/arterial line access
- may be difficult d/t contracted intravascular volume
- may want to do femoral line instead
29
Scleroderma anesthesia management of the pulm. system
Decreased pulmonary compliance and reserve, avoid increasing PVR
30
Scleroderma anesthesia management of the GI. system
Aspiration
- Give PPIs, H2 blockers
31
Scleroderma anesthesia management of the eyes
Corneal abrasions
32
Other considerations for scleroderma anesthesia management:
Regional anesthesia (want to avoid intubation)
Keep warm
VTE prophylaxis
Positioning: increased risk of motor/nerve injury
Pulse ox difficulties
33
VTE is how much more common in scleroderma pts?
3 times
34
Treat oral bleeding in scleroderma pts with:
Phenylephrine spray
Gauze in phenylephrine or vasopressin
TXA
Vit. K
Calcium
35
Ways to keep pts warm in OR
Bair hugger
warm fluids
blankets
turn up the air
36
What are the VTE prophylaxis methods?
Mechanical
- SCD: sizing can be problematic
- Walking
Chemical: 5000 units sub-q heparin on the morning of sx
37
A lot of the scleroderma pts will be on steroids so we need to give:
100 of hydrocortisone every 6-8 hours
38
What is the most common and most severe form of childhood progressive muscular dystrophy?
Pseudohypertrophic muscular dystrophy
39
______ is a large protein that plays a major role in stabilization of the muscle membrane and signaling between the cytoskeleton and extracellular matrix.
Dystrophin
40
muscular dystrophy is caused by:
a mutation in the dystrophin gene located on the X chromosome (X-linked recessive trait)
Fatty infiltration = pseudohypertrophic
41
Initial symptoms of muscular dystrophy:
waddling gait, frequent falling, difficulty climbing stairs
42
In MD pts, death usually occurs at _____ due to ______
20-25 years
CHF or pneumonia
43
MD pts are usually wheelchair bound by _____ years old
8-10
44
Duchenne muscular dystrophy is a ______ disorder and starts in _____
Progressive
Childhood
45
DMD occurs more in young ____ than young _____
Boys
Girls
46
CNS s/s of Pseudohypertrophy Muscular Dystrophy
Intellectual disability
47
MS s/s of Pseudohypertrophy Muscular Dystrophy
Kyphoscoliosis
skeletal muscle atrophy: can lead to long bone fractures
serum CK 20-100x normal (increased permeability of skeletal muscle membranes and skeletal muscle necrosis)
48
CV s/s of Pseudohypertrophy Muscular Dystrophy
Sinus tachycardia
cardiomyopathy
EKG abnormalities
Short PR interval
V1 – tall R waves
Limb leads – deep Q waves
49
Pulm. s/s of Pseudohypertrophy Muscular Dystrophy
weakened respiratory muscles and cough
loss of pulmonary reserve and increased secretions (pneumonia)
OSA
pulmonary HTN
50
What percent of deaths in PMD pts occur for pulm. reasons?
30%
51
PMD anesthesia mangement by systems
Airway: weak laryngeal reflexes and cough (avoid neuromuscular blockers)
Pulmonary: weakened muscles, increased secretions
CV: Pre-op EKG and/or echo based on severity
GI: Delayed gastric emptying
52
Pts with PMD can be on ventilatory support post op for ____
36 hours
53
General PMD anesthesia management
- Avoid succinylcholine
- Pharyngeal and respiratory muscle weakness
- Rhabdomyolysis
- MH – increased incidence (use Dantrolene)
- Regional > GA
54
If you use succs in a PMD pt, they are at risk for:
Rhabdo
Hyperkalemia
MH
Cardiac arrest (VF)
55
Triggers of malignant hyperthemia
Succs
Volatiles
56
What is your short term sedation option for MD pts?
Ketamine, precedex (prefer ketamine first)
57
MG is characterized by _____ and ______
what type of disorder is it?
Exacerbations
Remissions
Autoimmune
58
Define myasthenia graves
Decrease in functional post-synaptic ACh receptors at the neuromuscular junction d/t destruction or inactivation by circulating antibodies
- postsynaptic α subunit of muscle-type acetylcholine receptors
- 80% of receptors can be lost
59
MG is muscle weakness without _____, _______, or ____ dysfunction
Peripheral
Central
Autonomic
60
Describe muscle specific kinase antibodies (MuSK)
a tyrosine kinase specifically present at the neuromuscular junction and crucial in the formation and maintenance of the postsynaptic membrane
- Loss of ACh receptors and a change in the structure of the post-synaptic folds
- No thymic involvement
61
Describe the different classifications of MG
*Per Cornelius, only have to know 1 and 4)
Type 1: limited to involvement of the extra ocular muscles
- if confined to the yes for 2 years, unlikely disease progression
Type 4: severe form of skeletal muscle weakness
62
MG s/s
- Ptosis, diplopia, and dysphagia – initial
* Ocular, pharyngeal, and laryngeal muscle involvement
- Dysarthria
- Pulmonary: isolated respiratory failure; occasional presenting manifestation
- MS: Arm, leg, or trunk muscle weakness; asymmetric
- CV: Myocarditis – A Fib, heart block, or cardiomyopathy
63
Autoimmune diseases associated with MG:
RA
SLE
Pernicious anemia
Hyperthyroidism
64
what percent of MG patients present with ptosis and/or diplopia?
60%
65
T/F
Skeletal muscles innervated by cranial nerves (which ones?) are especially vulnerable with MG pts
True
Ocular, pharyngeal, largyngeal
66
Difference in myasthenia crisis vs cholinergic crisis
Myasthenic crisis
- Drug resistance or insufficient drug therapy
- S/S: severe muscle weakness and respiratory failure
Cholinergic crisis
- Excessive anticholinesterase treatment
- S/S: muscarinic side effects – profound muscle weakness, salivation, miosis, bradycardia, diarrhea, abdominal pain
67
What is the edrophonium/tensilon test?
1-2 mg IVP of edrophonium
- Improves myasthenic crisis, makes cholinergic crisis worse
68
Common meds that we give that has cholinergic effects
Atropine
Scopolamine
Robinul
Serotonin inhibitors
zofran
phenergan
69
First line of treatment for MG?
What does it do?
Anticholinesterases
- inhibits Cholinesterase which are responsible for breakdown of acetylcholine and increases the amount of ACh available at the neuromuscular junction
70
Do we prefer pyridostigmine or neostigmine? Why?
What is the max dose?
Pyridostigmine
Lasts longer, less side effects
Max dose: 120 mg Q3 H
71
Thmectomy induces _____ and allows for reduced use of _______.
It specifically reduces _________
Remission
Immunosuppressive medications
ACh receptor antibody levels post procedure
72
What are other treatment options for MG?
Immunosuppression
- Corticosteroids, azathioprine, cyclosporine, mycophenolate
Immunotherapy
- Plasmapheresis: removes antibodies from circulation
- Immunoglobulin: temporary effect
73
Repeated treatment of plasmapheresis increases risk of:
infection, hypotension, and pulmonary embolism
74
MG anesthesia management considerations:
- Aspiration risk
- Weakened pulmonary effort
- Marked sensitivity to nondepolarizing muscle relaxants
- Resistance to succinylcholine
- Intermediate-acting muscle relaxant
- Intubate without NMBD
75
Other meds we can give to MG pts that have the same effects w/o depolarization:
Remifentanil in high doses
- use if need high neuromuscular blockade
76
Why do MG pts have a resistance to succs?
pyridostigmine inhibits true cholinesterase and impairs plasma cholinesterase
77
What is the most common join disease and a major cause of disability?
Explain it
Osteoarthritis
Degenerative process that affects articular cartilage w/ minimal inflammatory reaction in the joints
78
Joint trauma can include:
Biomechanical stresses
Joint injury
Abnormal joint loading
Neuropathy
Ligament injury
Muscle atrophy
Obesity
79
Osteoarthritis pain is present with ___ and relieved by ______.
However, you can see stiffness in the _____
Motion
Rest
Morning
80
Where are the most common places to see OA?
Knees, hips, shoulders
81
Causes of OA
Repetitive mechanical stress/overuse
Genetics
Obesity
Occupations with a lot of physical labor
82
Herberden nodes:
Distal interphalangeal joints
- red marks on the ends of fingers
83
In OA of the vertebral bodies/discs, there is protrusion and compression of what?
Protrusion:
- nucleus pulposus
Compression:
- nerve roots
84
OA treatment
PT and exercise
Maintaining muscle function
Pain relief: no opiods
Joint replacement surgery
Stem cell therapy
PRP
85
OA anesthesia management considerations
Airway
Limited ROM
* pre op eval should document the extent of limitation (particularly in c-spine), baseline severity of pain, all pain mangement interventions
86
RA is _____ mediated and is a _______ disease
autoimmune
Systemic inflammatory
87
RA is _____ x higher in women than men
2-3
88
RA includes involvement of what joints in the hands and feet?
proximal interphalangeal and metacarpophalangeal joint
89
Rheumatoid factor is present in ____% of pts
90
90
RA usually affects the ____ and ____
Hands
Feet
91
Describe fusiform swelling
typical when involvement of the proximal interphalangeal joints
- Swollen distal interphalangeal joints
- As it progresses, they may not be able to use hands – may have mobility assist devices
92
RA onset is ____ and involves _____/_____ joints
acute
single/multiple
93
S/S of RA
**this card is stupid long too, I'm sorry lol*
Atlantoaxial subluxation
- Odontoid process protrudes into the foramen magnum
- Pressure on the spinal cord or impairs 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
NM: Weakened skeletal muscles
Peripheral neuropathies
CV: Pericarditis, accelerated coronary atherosclerosis
Pulmonary: Restrictive lung changes, pleural effusion
Hematology: Anemia, neutropenia, elevated platelets
Keratoconjunctivitis sicca and xerostomia (manifestations of Sjogren syndrome)
94
RA coincides with:
trauma, surgery, childbirth, or exposure to temperature extremes
95
What is synovial inflammation?
Big joints
96
What is the difference with how symptoms progress with RA vs OA?
RA tends to feel the worst in the morning
OA gets worse throughout the day
97
With atlantoaxial subluxation, what is usually the distance of the anterior margin of the odontoid process from the posterior margin?
3 mm
98
With atlantoaxial subluxation, think:
RA
Down syndrome
99
Why do we care about atlatnoaxial subluxation?
Spinal cord goes through foramen magnum
- When head is rotated, the odontoid process will put pressure on the vertebral arteries and this can cause stroke like symptoms
100
Most common cause of atlanto-occipital instability is:
Bone issues in c-spine at the atlas/axis bone
101
RA treatment
Relieve pain, preserve joint function and strength, prevent deformities, and attenuate systemic complications
- Drug therapy, PT, OT, and/or orthopedic surgery
102
Drug therapy for RA
NSAIDS
- Use with DMARDs
* Decrease joint swelling, relieve stiffness, provide analgesia
- COX-1 inhibitors – s/e: GI irritation and platelet inhibition; decrease renal blood flow and GFR
- COX-2 inhibitors – s/e: fewer GI side effects and do not interfere with platelet function; decrease renal blood flow and GFR
* Increase risk of CVA and CAD
Corticosteroids
- Decrease joint swelling, pain, and morning stiffness
- Bridge therapy while DMARDs are starting to work
- Dosages >10 mg/day maybe needed to treat vasculitis
- S/E: osteoporosis, osteonecrosis, susceptibility to infection, myopathy, hyperglycemia, and poor wound healing
103
______ inhibitors and ______ inhibitors are more effective then DMARDS but _____ onset
TNF
IL-1
Slower
104
It takes ______ months to achieve effects with DMARDS on RA
2-6
105
S/E of DMARDS
risk of bone marrow suppression and cirrhosis; monitor hematologic parameters and liver function tests
Folic acid can reduce methotrexate toxicity
106
S/E of TNF alpha inhibitors
toxicities – infection (TB) and demyelinating syndromes
107
RA anesthesia management considerations:
Airway → what we worry about:
- Atlantoaxial subluxation
- TMJ limitation: May not be able to open mouth enough for us to look at airway
-Cricoarytenoid joints
Severe rheumatoid lung disease
Protect eyes
Stress dose steroids will be needed for these patients
108
Lupus is usually present in _____ women, ages _____ years.
African American
15-40
109
Typical manifestations of SLE
Antinuclear antibodies
Characteristic malar rash
Thrombocytopenia
Serositis
Nephritis
110
Describe SLE
A multisystem chronic inflammatory disease characterized by antinuclear antibody production
- Antibodies in 95% of pts
111
SLE manifestations are a result from:
- Tissue damage from vasculopathy mediated by immune complexes
- Direct result of antibodies to cell surface molecules or serum components
112
Onset of SLE can be drug induced by which drugs?
What are the mild symptoms associated?
procainamide, hydralazine
arthralgias, a maculopapular rash, fever, anemia, and leukopenia
113
SLE can be exacerbated by:
infection, pregnancy, and surgery
114
What syndrome is common with SLE?
What is it?
HELLP
a serious complication of pregnancy that can occur in women who have preeclampsia. HELLP stands for Hemolysis, Elevated Liver enzymes, and Low Platelets.
115
What is a maculopapular rash?
Discoid lupus lesions, which are thick and disk-shaped. They often appear on the scalp or face and can cause permanent scarring. They may be red and scaly, but they do not cause pain or itching.
116
S/S of SLE
Polyarthritis and dermatitis
Symmetrical arthritis
- No spinal involvement
- Avascular necrosis of femoral head or condyle
CNS: Cognitive dysfunction, psychological changes
CV: Pericarditis (most common), coronary atherosclerosis, Raynaud’s
Pulmonary: Lupus pneumonia, restrictive lung disease, vanishing lung syndrome (decreased lung volumes, elevated diaphragm)
Renal: Glomerulonephritis, decreased GFR
GI/Liver: ABD pain, pancreatitis, elevated liver enzymes
NM: Skeletal muscle weakness
Hematology: Thromboembolism, thrombocytopenia, hemolytic anemia
Skin: Butterfly-shaped malar rash, discoid lesions, alopecia
117
in SLE, CNS problems can be related to:
vasculitis and fluid/electrolyte imbalances, fever, HTN, uremia, infection, and drug-induced effects
118
Pericarditis S/S
chest pain, friction rub, ECG changes, pericardial effusion
119
Death during the course of SLE may be due to:
Coronary atherosclerosis
120
Deep sulcus sign:
large volume of air in pleura, shoves diaphragm down
121
SLE management:
NSAIDS or ASA
Anti-malarial (dermatologic) – initial treatment
- Most common: Hydroxychloroquine
- others: quinacrine
Corticosteroids
Immunosuppressants
- Methotrexate, azathioprine
- Starts with methotrexate
122
SLE anesthesia management
Based upon manifestations and organ dysfunction
- Get CBC, BMP, ECG
Airway: recurrent laryngeal nerve palsy, cricoarytenoid arthritis
- upper airway obstruction
Stress dose of corticosteroids
123
If you have recurrent laryngeal nerve palsy, how does this present?
What about bilateral laryngeal nerve palsy?
Difficulty talking, stridor
Difficulty breathing
124
MH is a _____ syndrome.
Describe MH:
Hypermetabolic, genetic mutation
The 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
It is the sustained high levels of sarcoplasmic Ca2+ that rapidly drives skeletal muscle into a hypermetabolic state that may proceed to severe rhabdomyolysis.
125
MH non-triggering agents
126
S/S of MH
Elevated end-tidal CO2
Tachypnea and/or tachycardia
Generalized muscle rigidity
Mixed metabolic and respiratory acidosis
127
How do differentiate between someone biting on the ETT and possibly having massager muscle spasm from MH?
You may think sedation is light if airway pressure is high, so you give more sedation, but peak pressure will stay up if MH
If increased peak pressures, will think tube is kinked off.. But co2 would also go up … need to differentiate between simply kinked ETT or MH
128
MH treatment:
D/C all triggering gas/drugs
Hyperventilate with 100% O2 at 10 L/min
Change breathing circuit and soda lime
Dantrolene
- 20 mg + 3 G mannitol
*Mix with 60 mL sterile water
- Initial dose 2.5 mg/kg→ continue to redose until 10
- Max upper limit 10 mg/kg
Treat arrythmias
Monitor urine output
Cool the patient
- gastric lavage, cold compress, arctic sun
129
Why is dantrolene an effective treatment for MH?
it reduces the concentration of sarcoplasmic Ca2+ to below contractile threshold.
130
MH diagnosis relies on what?
the caffeine–halothane contracture test, measuring contraction forces upon exposure of muscle to caffeine or halothane
131
What other med is present in the dantrolene vial?
Mannitol
132
What is the purpose of soda lime?
absorbs co2 but leaves oxygen – it can be exposed to volatile agent or even absorb it – so it can release it as well
133
MH post op considerations
Transfer to ICU 24-48 hours
Report to MH registry
www.mhaus.org
1-800-MH-HYPER (644-9737)
MH testing for pt and family members
- Muscle biopsy contracture testing
- Halothane plus caffeine contracture test
