406 E2 - Myasthenia Gravis Flashcards
what type of disease is myasthenia gravis
an autoimmune disorder (type II)
myasthenia gravis
characterized by fluctuation weakness of certain muscle groups (ocular, bulbar, limb, & respiratory)
myasthenia gravis course of disease
spontaneous case that goes into remission -> back to baseline -> stabilization -> relapse -> severe relapse w/ progression
what causes weakness in myasthenia gravis
antibody mediated immunological attack directed in the postsynaptic membrane of the neuromuscular junction
breakdown in communication between the nerves and the muscles
myasthenia gravis risk factors
-gender (women)
-age: 10 to 65yrs
myasthenia gravis etiology
possibly a genetic component that is gets triggered
myasthenia gravis pathogenesis
antibodies attack ACh receptors -> decrease in ACh receptor sites at the neuromuscular junction -> this prevents ACh molecules from attaching and stimulating muscle contraction
body is producing enough AHc but not enough receptor sites
myasthenia gravis: CM
insidious onset
-fluctuating weakness of skeletal muscle
-strength comes back after resting
-difficulty swallowing
-drooling
-impaired nutrition / aspiration
-impaired ventilation
-muscle fatigue after exercise
what muscles are involved in myasthenia gravis
-eyes/eyelids
-facial
-speaking (mouth, face)
-breathing (neck)
when do clinical manifestations typically first appear w/ myasthenia gravis
pregnancy, postpartum, or after some anesthesias
myasthenic crisis
acute exacerbation of muscle weakness
myasthenic crisis triggers
infection, surgery, emotional distress, pregnancy/menses, inadequate pharmacotherapy or other drugs
what is our biggest concern w/ a myasthenic crisis
weakness of respiratory muscles leading to respiratory depression which puts pt at high risk for respiratory arrest
myasthenia gravis pharmacotherapy
-immunosuppressants (steroids)
-cholinesterase inhibitors
how do cholinesterase inhibitors work
-prevent inactivation of ACh by cholinesterase
-intensify the effects of ACh released from motor neurons, increases muscle strengthen
cholinesterase inhibitor nursing considerations
-give 30 minutes prior to eating to strengthen swallowing muscles
-not a cure, sx relief
what class is neostigmine
cholinesterase inhibitor (anti cholinesterase)
neostigmine indication
myasthenia gravis
neostigmine MOA
enhances cholinergic action by facilitating transmission of impulses across neuromuscular junctions
neostigmine, in therapeutic doses, affects which receptors
muscarinic and nicotinic receptors
cholinergic SE (GI, mouth, bladder, heart, lungs, eyes)
GI: increased motility, diarrhea
Mouth: increased secretions
Bladder: urinary urgency
Heart: bradycardia
Lungs: bronchial constriction
Eyes: miosis (constriction)
anticholinergic SE (GI, mouth, bladder, heart, lungs, eyes)
GI: decreased motility, constipation
Mouth: dry mouth
Bladder: urinary retention
Heart: tachycardia
Lungs: bronchial dilation
Eyes: mydriasis (dilation)
atropine can be used for what
comfort care to dry up secretion so they don’t choke on it
neostigmine SE: muscarinic
-increased secretions, GI motility
-urinary urgency
-bradycardia
-bronchial constriction
-miosis (near sighted)
neostigmine SE: neuromuscular
-therapeutic: increased muscle contraction
-toxic doses: reduced contraction
-cholinergic crisis w/ toxicity
cholinergic crisis
-extreme muscle weakness or paralysis
-S/s of excessive muscarinic stimulation
treatment for cholinergic crisis
-mechanical ventilation
-antidote: atropine
individuals w/ myasthenia gravis should always wear what
med alert bracelet
MG crisis vs Chol crisis
MG: not enough stimulation (muscles are weak bc no stim)
Chol: too much ACh or nystigmine (muscles overstim and wear out)
both lead to respiratory failure
differentiating between MG and Chol crisis
give edrophonium (a short acting cholinesterase inhibitor that will temporarily increase ACh) -> if they’re in MG they will improve and if they’re in chol they will worsen