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Musculoskeletal Diseases Flashcards

1
Q

What is the pathophysiology of myasthenia gravis?

A

Enough acetylcholine is present, but post-junctional nicotinic acetylcholine receptors are destroyed by IgG antibodies.

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2
Q

What SS present with myasthenia gravis?

A

First: diplopia and ptosis
bulbar weakness
dyspnea with exertion
proximal muscle weakness

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3
Q

What antibiotic can exacerbate myasthenia gravis? Why?

A

Aminoglycosides - they prevent normal Ach release presynaptically and block Ach receptors post-synaptically

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4
Q

What other situations exacerbate myasthenia gravis?

A

pregnancy (babies can be weak too for 2-4 weeks (lifespan of IgG))
infection
surgical stress
psychological stress
electrolyte abnormalities

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5
Q

What medication is used to treat myasthenia gravis? Why?

A

pyridostigmine - is an cholinesterase inhibitor (anitcholinesterase) -> increases parasympathetic neurotransmission by inhibiting Ach breakdown

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6
Q

What is the Tensilon test? How is it conducted?

A

Used to determine if acute weakness is due to pyridostigmine overdose (cholinergic crisis) or exacerbation of myasthenic SS (myasthenic crisis)

Administer 1-2 mg Edrophonium

If muscle weakness worsens, is cholinergic crisis (more Ach at NMJ made weakness worse). Treat with anticholinergic.

If muscle weakness improves, was myasthenic crisis. Increasing Ach at the NMJ improved the muscle strength.

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7
Q

What surgical treatment is indicated for myasthenia gravis?

A

Thymectomy - reduces circulating Anti-AchR IgG in most patients

Via median sternotomy or transcervical approach

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8
Q

What medications are used for immunosuppression in a patient with myasthenia gravis?

A

corticosteroids
cyclosporine
azathioprine
mycophenolate

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9
Q

Which patients with myasthenia gravis should be counseled on potential need for postop ventilation?

A

disease duration > 6 years
daily pyridostigmine > 750 mg/day
vital capacity < 2.9L
COPD
surgical approach: median sternotomy > transcervical thymectomy

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10
Q

In what disease is muscle weakness worse in the morning and improves through the day?

A

Eaton-Lambert syndrome aka myasthenic syndrome aka Lambert-Eaton Myasthenic syndrome

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11
Q

What is the pathophysiology surrounding Eaton-Lambert syndrome?

A

IgG mediated destruction of presynaptic voltage-gated Ca channels (normal receptors postsynaptically)

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12
Q

What treatment is indicated for Guillain Barre?

A

plasmapheresis
IV IgG

steroids and interferon not useful! contrary to multiple sclerosis

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13
Q

What is another name for Guillain Barre?

A

acute idiopathic polyneuritis

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14
Q

What is the treatment for both hypo- and hyper-kalemic periodic paralysis? Why?

A

Azetazolamide
creates non-gap acidosis = protection for hypokalemic
facilitates renal K excretion = protection for hyperkalemic

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15
Q
A
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16
Q

How should you manage body temperature in hypo/hyperkalemic periodic paralysis?

A

normothermia
avoid hypothermia at all costs!! even on CPB

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17
Q

Discuss the pathophysiology of malignant hyperthermia:

A

T-tubule is depolarized -> Ca enters myocyte via dihydropyrodine receptor
defective ryanodine receptor (RYR1) is active -> instructs sarcoplasmic reticulum to release way too much Ca
cell attempts to return Ca to sarcoplasmic reticulum via SERCA2 pump
+ more Ca to engage cardiac myocytes
substantial amount of ATP is used
increased O2 consumption
increased CO2 production
damaged sarcolemma allows potassium and myoglobin to escape (these are renal toxic) and enter systemic circulation

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18
Q

What are consequences of increased intracellular Ca in the myocyte?

A

rigidity from sustained contraction
accelerate metabolic rate and rapid depletion of ATP
increased O2 consumption
increased CO2 and heat production
mixed respiratory and lactic acidosis
sarcolemma breaks down
potassium and myoglobin leak into systemic circulation

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19
Q

What conditions ARE associated with MH?

A

King-Denborough syndrome
Central core disease
Multiminicore disease

20
Q

Which conditions are NOT associated with MH?

A

Duchenne Muscular Dystrophy
Becker Muscular Dystrophy
Myotonic dystrophy
Myotonia congenita
Neuroleptic malignant syndrome
Osteogenesis imperfect

21
Q

What are the risk factors for MH?

A

Geographical - Wisconsin, Nebraska, West Virginia, and Michigan
Male sex
Youth

22
Q

What are early signs of MH?

A

increased EtCO2 disproportionate to minute ventilation
tachycardia
tachypnea
masseter rigidity
warm soda lime
irregular heart rhythm

23
Q

What are intermediate signs of MH?

A

cyanosis
patient warm to touch
irregular heart rhythm

24
Q

What are late signs of MH?

A

muscle rigidity
overt hyperthermia
cola-colored urine
coagulopathy
irregular heart rhythm

25
Q

What are differential diagnoses to MH?

A

neuroleptic malignant syndrome
serotonergic syndrome
thyroid storm
pheochromocytoma
sepsis
cocaine intoxication
heatstroke
metastatic carcinoid

26
Q

What is the sequence of MH treatment?

A
  1. DC triggering agent
  2. Call for help
    3a. Hyperventilate with 100% FiO2 and min 10L FGF
    3b. Apply charcoal filters, then new breathing circuit and reservoir bag
  3. Administer Ryanodex or dantrolene
  4. Cool the patient (til 38C)
  5. Correct lactic acidosis
  6. Treat hyperkalemia
  7. Protect against dysrhythmias
  8. Maintain UOP > 2 mL/kg/hr
  9. DIC - late sign, impending demise
27
Q

Discuss dantrolene or Ryanodex administration:

A

2.5 mg/kg IV every 5-10 min
stop dantrolene when signs of hyper metabolism subside
continue in ICU at 1 mg/kg q 6 hr or 0.1-0.3 mg/kg/hr for 48-72 H
(can reoccur up to 36 hours)
use largest vein possible (venous irritation is common)
if require >20 mg/kg, reconsider MH diagnosis

28
Q

MH meds:

A

hyperthermia: cold IVF, cold fluid lavage stomach and bladder, ice packs

lactic acidosis: NaHCO3 1-2mEq/kg IV titrated to ABG and base deficity

hyperkalemia: CaCl 5-10 mg/kg IV, insulin 0.15 unit/kg + glucose 1mL/kg, hyperventilation

dysrhythmias: procainamide 15 mg/kg IV, lidocaine 2 mg/kg IV, NO CCB

maintain UOP: IV hydration, mannitol 0.25 g/kg IV, furosemide 1 mg/kg IV

hyperventilation: facilitates CO2 elimination, increases O2 deliver, drives K into cells

29
Q

Discuss the pathophysiology of muscular dystrophy:

A

absence of dystrophin (anchor of actin and myosin to cell membrane) destabilizes sarcolemma during muscle contraction and increases membrane permeability
sarcolemma breakdown allows creatine kinase and myglobin to enter systemic circulation
calcium freely enters the cell, activating proteases which destroy contractile elements and lead to inflammation, fibrosis, and cell death

30
Q

Discuss the respiratory considerations of muscular dystrophy:

A

kyphoscoliosis - restrictive -> decreased pulmonary reserve -> increased secretions and risk of pneumonia

respiratory muscle weakness

31
Q

Discuss the cardiac considerations of muscular dystrophy:

A

degeneration of cardiac muscle -> reduced contractility, papillary muscle dysfunction, mitral regurgitation, cardiomyopathy, CHF

cardiomyopathy signs: resting tachycardia, JVD, S3/S4 gallop, point of maximal impulse displacement

32
Q

Discuss the EKG changes of muscular dystrophy:

A

impaired cardiac conduction -> sinus tach and short PRI
scarring of posterobasal aspect (back/bottom) of LV -> increased R wave amplitude in Lead I, deep Q waves in limb leads

33
Q

Discuss the GI considerations of muscular dystrophy:

A

impaired airway reflexes and GI hypomotility -> increased aspiration risk

34
Q

Which type of scoliosis is most common? What other types exist?

A

idiopathic (80%)
congenital
myopathic (muscular dystrophy and amyotonia congenita)
neuropathic (cerebral palsy, syringomyelia, Friedreich’s ataxia)
traumatic

35
Q

What Cobb Angle is indicative of surgery?

A

40-50 degrees

36
Q

What early respiratory changes accompany scoliosis?

A

Restrictive: decreased FEV1 and FVC (FEV1/FVC ratio normal)

Decreased VC, TLC, FRC, RV

Decreased chest wall compliance

37
Q

What CV changes accompany scoliosis?

A

RV hypertrophy (due to increased pulmonary vascular resistance)
mitral valve prolapse (most common)
mitral regurgitation
coarctation of the aorta

38
Q

What vital capacity indicates postop ventilation in a patient with scoliosis?

A

<40%

39
Q

How does rheumatoid arthritis affect the airway?

A

temporomandibular joint
cricoarytenoid joints
cervical spine

40
Q

What is the most common airway complication of RA?

A

AO subluxation and separation of the atlanto-odontoid articulation

40
Q

What late respiratory changes accompany scoliosis?

A

V/Q mismatch
hypoxemia
hypercarbia (impending respiratory failure)
reduced response to hypercapnia
pulmonary hypertension
cor pulmonale
cardiorespiratory failure

41
Q

What stressors and drug exposures are known to exacerbate systemic lupus erythema?

A

PISSED CHIMP
Pregnancy
Infection
Stress
Surgery
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide

42
Q

Which immunosuppressant increases the duration of succinylcholine?

A

Cyclophosphamide - inhibits plasma cholinesterase

43
Q

What disorder has an increased bleeding tendency due to poor vessel integrity?

A

Ehlers-Danlos syndrome

44
Q

What type of anesthesia is not safe in multiple sclerosis?

A

spinal (epidural okay)

45
Q

What three things increase the risk of contractures in myotonic dystrophy?

A

sux - use nondepolarizer
NMB reversal with anticholinesterases - use sugammadex
hypothermia - shivering -> sustained contractions

46
Q

What is CREST syndrome and which condition is it associated with?

A

scleroderma

Calcinosis
Raynaud’s
Esophageal hypomotility
Sclerodactyly
Telangiectasia

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