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S5 - Advanced Patho > Musculoskeletal Disease > Flashcards

Musculoskeletal Disease Flashcards

1
Q

skeletal muscle has what type of control and what type of characteristics?

A
  • voluntary control
  • striated
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2
Q

smooth muscle has what type of control and what type of characteristics?

where is it located?

A
  • involuntary autonomic control
  • nonstriated
  • located in most internal organs (not heart)
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3
Q

cardiac muscle has what type of control and what type of characteristics?

A
  • autonomic nervous system - its the intrinsic pacemaker
  • striated
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4
Q

the generation of muscular force is dependent on what two things?

A
  • intracellular Ca
  • activation of actin and myosin filaments
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5
Q

where is skeletal muscle found?

A
  • tongue and soft palate
  • extrinsic eye muscles
  • muscles that move the scalp
  • all muscles attached to the skeleton
  • pharynx
  • upper 1/3 of esophagus
  • lips *
  • anus*

**serve as sphincters

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6
Q

what innervates skeletal muscles?

A

myelinated efferent motor nerve fibers

“alpha motor neurons”

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7
Q

muscle divides into branches and ends on individual muscle cells called what?

A

“muscle fibers”

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8
Q

what is one “motor unit” composed of?

A

1 motor neuron + all fibers in it

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9
Q

T/F: when a motor nerve fires, all fibers in the motor unit contract at the same time

A

true

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10
Q

normal neuromuscular transmission begins with what?

A

an action potential

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11
Q

the action potential reaches the nerve terminal and activates what?

A

the calcium channel

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12
Q

as an action potential comes down and activates the ion channels, what NT is released into the synaptic cleft?

A

acetylcholine

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13
Q

ACh that is released into the synaptic cleft bind to what receptors?

where are these located?

A
  • bind to ACh receptors - obvi
  • muscle plasma membrane
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14
Q

after ACh receptors are activated, what two things happen?

A
  • ACh receptors open and allow Na+ to enter into the muscle
  • rapid decline in ACh levels
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15
Q

what is the sequence of events after the ACh receptors open?

A
  • Na+ into muscle generating action potential
  • voltage-gated Na+ channels open and allow more Na+ into cell
  • action potential leads to muscle contraction
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16
Q

what are the two causes of the rapid decline in ACh levels?

A
  • ACh diffusion
  • ACh deactivation by AChE within the synaptic cleft

~this prevents multiple reactivation of ACh receptors

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17
Q

how many ACh vesicles are released with each nerve impluse?

A

150-200

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18
Q

each ACh vessicle (quanta) has how many molecules of ACh?

A

10,000

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19
Q

what two types of antibiotics inhibit ACh release?

A

aminoglycosides

polymixin

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20
Q

how does Lambert Eaton Syndrome, associated with small cell carcinoma in the lungs, impact ACh release?

what other impact does it have regarding muscle action potential?

A
  • decreases ACh release
  • autoimmune derangement in presynaptic Ca2+ channels
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21
Q

how does botulinum toxin impact ACh?

A

decreases release

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22
Q

how does Mg impact ACh?

A
  • Mg competes with Ca2+ at the voltage-gated channels
  • decrease ACh release
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23
Q

how do calcium channel blockers impact ACh release?

A

block Ca2+ conductance through “slow” (L) channels in heart

decreased calcium = decreased ACh release

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24
Q

each neuromuscular junction has how many nicotinic ACh receptor sites?

A

estimated 50 million

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25
Q

where are ACh receptors located?

where are they made?

A
  • located at crests of motor endplate junctional folds
  • made in the muscle cells → pushed to the endplate membrane, junctional face protrudes a bit
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26
Q

T/F: activation of postjunctional receptors requires ACh binding at both of the alpha subunits

A

true

~must be simultaneous binding~

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27
Q

what happens once both alpha-subunits are occupied?

A
  • cation channel opens →
  • increased conductance to cations (especially Na+) =
  • a net depolarizing potential (EPP)
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28
Q

what happens to the ACh receptor after an ACh molecule leaves?

A

channel closes →

current stops →

membrane resets or repolarizes

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29
Q

what determines whether ACh or our muscle relaxants has an effect?

~pls reword

A

dependent on concentration of ACh and concentration/binding properties of the antagonist

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30
Q

examples of drugs that block the ACh receptors

A

curare-like muscle relaxants

  • vecuronim
  • pancuronium
  • cisatracurium
  • rocuronium

and like all the other muscle relaxants…

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31
Q

examples of drugs that inactivate acetylcholinesterase

A

muscle relaxant reversal agents - compete with ACh for a subunit binding sites

  • neostigmine
  • edrophonium
  • pyridostigmine
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32
Q

how do ACh reversal agents work?

A
  • muscle relaxant reversal agents - compete with ACh for a subunit binding sites
  • ACh not hydrolyzed so it increases quantity of ACh at synapse
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33
Q

what type of receptors are the prejunctional receptors?

A

cholinergic

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34
Q

what is thought to be the function of prejunctional receptors?

A

enhance neurotransmitter movement and release

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35
Q

what is seen from antagonist effects at the prejunctional area?

A

decrease in release of ACh

  • can see a FADE on train-of-four*
  • **Fade (with tetany and train of four) may be reflecting the blockade of prejunctional receptors by the NDMR and ACh release is not fast enough to keep up with rapid stimulation
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36
Q

MOA of AChE

A
  • rapidly hydrolyzes ACh to choline + acetate in the junctional cleft
  • choline goes back into prejunctional nerve terminal to make new Ach

cause God was the first recycler :)

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37
Q

how do muscle relaxant reversal agents - anticholinesterases (neostigmine) work?

A
  • inhibits breakdown of ACh
  • thus increasing the amount of ACh at the NMJ
  • ACh antagonizes muscle relaxant
  • transmission restored
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38
Q

what enzyme hydrolyzes ACh, metabolizes ester LAs, and SCh?

A

pseudocholinesterase

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39
Q

tell me about muscles in little uterus babies?

A
  • no muscle innervation in utero
  • muscle cells have extrajunctional receptors over the whole muscle cell

(yAChR and alpha7 subunits)

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40
Q

what age do muscle nerves become fully mature?

what receptors are seen/not seen at this point?

A
  • 2 years
  • ACh receptors only in neuromuscular junction
  • extrajunctional receptors disappear from peripheral part of muscle
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41
Q

what occurs to muscle receptors if neural activity is decreased or removed?

A
  • extrajunctional receptors formed
  • muscle goes back to fetal like synthesis of yAChR and alpha 7 receptors
  • can develop within 48 hrs post injury
  • can later return to normal

(stroke, spinal cord transection, burn, direct muscle damage, prolonged immobility)

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42
Q

how do extrajunctional receptors respond to non-depolarizing muscle relaxants?

A
  • resistant to NDMR
  • large doses required
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43
Q

how do extrajunctional receptors respond to succs?

considerations?

A
  • more sensitive to SCh (and ACh)
  • channel stays open - Na+ into cell and K+ out

***no Sux (even small doses) —dangerous hyper-K+

***hyper-K+ bc prolonged depolarization and too much K+ out

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44
Q

examples of patients with increased extrajunctional receptors

med considerations?

A

stroke, spinal cord transection, burn, direct muscle damage, prolonged immobility

no succs ever (potential hyperkalemia/death)

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45
Q

what is myasthenia gravis?

A

chronic disease

decreased number of working postsynaptic ACh receptors

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46
Q

causes of myasthenia gravis

A
  • autoimmune: 80-85% have IgE antibodies
  • thymus seems to play a role
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47
Q

what organ might be removed in a pt with myasthenia gravis

A

thymus (improves symptoms but not curative)

lol remember how isla got a freaking thymus transplant

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48
Q

T/F - pts with myasthenia gravis have cognitive dysfunction

A

false - only a motor disease

:(

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49
Q

hallmark of myasthenia gravis

A

generalized weakness that improves with rest

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50
Q

severity of myasthenia gravis symptoms

A

range from slight ptosis to resp failure

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51
Q

muscles most often affected in myasthenia gravis

A

eyes, mouth, pharynx, proximal limb, shoulder girdle muscles

52
Q

considerations for pregnant pts with myasthenia gravis

A

33% have exacerbation

the bebe may have transitory symptoms

53
Q

myasthenia gravis exacerbating factors

A
  • infection
  • stress
  • surgery
  • electrolyte imbalances
  • some meds
53
Q

myasthenia gravis exacerbating factors

A
  • infection
  • stress
  • surgery
  • electrolyte imbalances
  • some meds
54
Q

treatment of myasthenia gravis

A
  • anticholinesterases (pyridostigmine)
  • immunosuppressants
  • plasmapheresis
  • thymemectomy
55
Q

IV equivalent of 60 mg TID pyridostigmine

A

2 mg

this is very confusing to me but i simply do not care enough to figure it out

56
Q

2 complications of myasthenia gravis

what do they both present with?

A

cholinergic crisis

myasthenic crisis

both present with weakness and resp failure

57
Q

what causes cholinergic crisis

what are the symptoms

A

giving too much anticholinesterase

excessive salivation & tearing, diarrhea, bradycardia, miosis, weakness, resp failure

58
Q

what causes myasthenic crisis?

symptoms?

A

underdosing anticholinesterase

ptosis, weakness, resp failure

59
Q

what should you expect if a pt with myasthenia gravis takes their meds DOS?

A

increased vagal reflex, interferes with NMBs, inhibits plasma cholinesterase

60
Q

what should you expect if your myasthenia gravis pt doesn’t take their meds DOS?

A

possible deterioration with advanced disease

~whatever that means~

61
Q

electrolyte imbalances especially important to correct preop for pt with myasthenia gravis

A

hypokalemia - can potentiate muscle weakness

62
Q

induction conisderations for pt with myasthenia gravis

A
  • may have pharyngeal or laryngeal weakness
  • aspiration risk
  • RSI
63
Q

induction considerations for pt with myasthenia gravis

A
  • may have pharyngeal or laryngeal weakness
  • aspiration risk
  • RSI
64
Q

preferred anesthetic technique for pts with myasthenia gravis

A

regional or local

65
Q

anesthetic technique if GA is used for myasthenia gravis

A

inhalation induction can decrease muscle tone enough for intubation & avoid need for NMBs

66
Q

postop consideration for myasthenia gravis

A

muscle strength may seem adequate in early recovery but deteriorate a few hours later

67
Q

predictors for postop ventilation in myasthenia gravis pt

A
  • transsternal thymectomy
  • having disease > 6 yrs
  • daily pyridostigmine dose > 750 mg
  • COPD
  • preop VC < 2.9 L
68
Q

NMB considerations in myasthenia gravis

A
  • 10-100x more sensitive to NDNMBs
  • treated MG: resistant to succs
  • untreated MG: sensitive to succs

i thought it was untreated they are resistant and treated they are sensitive but idk which is up and which is down at this point

consulted TC via pharm I notes and she said if MG is untreated, they’re resistant to succs and sensitive to NDNMBs

treated = sensitive to succs, resistant to NDNMBs

69
Q

where should TOF be assessed in pt with myasthenia gravis

A

orbicularis oculi

may overestimate degree of relaxation but best place to avoid undetected residual weakness

70
Q

antiarrhythmics that worsen myasthenic weakness

A
  • quinidine
  • procainamide
  • beta blockers (systemic and ocular)
  • calcium channel blockers
71
Q

antibiotics that worsen myasthenic weakness

A
  • aminoglycosides (gentamicin)
  • quinolones (cipro, levofloxacin)
  • macrolides (erythromicin, azithromycin)
72
Q

couldnt think of a way to ask this and combining it all was too damn long BUT

quinine, Mg salts, and iodine contrasts worsen myasthenic weakness

A

who cares

73
Q

how do anticholinesterases affect LAs

A

may impair hydrolysis of ester LAs and cause prolonged block

amide class is ok

74
Q

what causes Lambert-Eaton Myasthenic Syndrome

A
  • autoimmune
  • usually with small cell carcinoma of bronchi
75
Q

age and gender Lambert-Eaton Myasthenic Syndrome is common in

A

men 50-70 yrs old

76
Q

goal of Lambert-Eaton Myasthenic Syndrome treatment

A

improve strength, decrease ANS deficits (plasmapheresis, steroids, IVIG, immunosuppressants, ¾-diaminopyridine)

77
Q

when should Lambert-Eaton Myasthenic Syndrome be suspected?

A

pts with muscle weakness and suspected diagnosis of lung carcinoma

78
Q

diagnosis to suspect in pts with muscle weakness and possible lung carcinoma

A

Lambert-Eaton Myasthenic Syndrome

79
Q

patho of Lambert-Eaton Myasthenic Syndrome

A
  • presynaptic calcium channels damaged by autoantibodies
  • reduced calcium-mediated exocytosis of ACh at NMJ
80
Q

patho difference in myasthenia gravis vs lambert eaton myasthenic syndrome

A

LEMS - postjunctinoal AChRs unaffected

MG - postjunctional AChRs decreased

81
Q

what disease is simular to botulism or mag tocxicity

A

Lambert-Eaton Myasthenic Syndrome

82
Q

main symptoms of Lambert-Eaton Myasthenic Syndrome

A
  • muscle weakness
  • fatigue
  • hyporeflexia
  • proximal limb muscle aches
83
Q

s/s ANS dysfunction with Lambert-Eaton Myasthenic Syndrome

A

orthostatic hypotension

impaired gastric motility

urinary retention

84
Q

NMB considerations with Lambert-Eaton Myasthenic Syndrome

A

very sensitive to both succs and non-depolarizers

can use volatiles alone for tracheal relaxation

85
Q

important pre-op discussion to have with a pt with Lambert-Eaton Myasthenic Syndrome

A

may need postop ventilation

and also prob all these damn diseases

86
Q

what is true about all “myotonias”

A

all have inability of skeletal muscles to relax after stimulation (chemical or physical)

87
Q

typical age of myotonic dystrophy onset

A

20-30 yrs

88
Q

patho of myotonic dystrophy

A

skeletal muscles are hypotonic, dystrophic, and weak yet persistently contract

89
Q

what is myotonia?

A

persistent contracture of muscle after stimulation

90
Q

meds used to treat myotonic contractures

A

phenytoin, procainamide, tocainamide

91
Q

how is muscle weakness assoc. with myotonic dystrophy treated?

A

it isnt :(

92
Q

T/F - NDNMBs help with myotonic dystrophy symptoms

A

nope

93
Q

s/s myotonic dystrophy

A
  • hypoplastic, weak skeletal muscles of neck and face
  • sleep apnea
  • v sleepy (aka hypersomnolence)
  • conduction defects
  • intestinal hypomotility
94
Q

conduction defects seen in myotonic dystrophy

A
  • 1st degree AV block common
  • bradycardia
  • A fib/flutter
95
Q

respiratory complications of myotonic dystrophy

A

pharyngeal/respiratory muscle weakness

restrictive-type disease

96
Q

what general complication of anesthesia/surgery should def be avoided in pts with myotonic dystrophy

A

hypothermia - makes contractions worse

97
Q

pre-op intervention for myotonic dystrophy

A

EKG

98
Q

NMB use in myotonic dystrophy

A

avoid succs

NDNMBs are ok but recognize muscle wasting

99
Q

what is duchenne’s muscular dystrophy (DMD)?

A

X-linked recessive progressive, painless degeneration and necrosis of muscle fibers

infiltration of fat and fibrous tissue in muscle

100
Q

muscles affected first in DMD

A

pelvic girdle and muscles of thigh or calf depending on which slide you look at

:)

101
Q

common age of presentation for DMD

A

2-6 yrs old

102
Q

cardiac complications of DMD

A

cardiomyopathy

mitral regurg

ventricular dysrhythmias

103
Q

EKG changes you might see in pt with DMD

A

tall R waves

deep Q waves

104
Q

ideal anesthetic plan for DMD pt

A

local or regional

consider TIVA over GA

105
Q

chronic med use in DMD that may need to be addressed intra op

plz reword my brain hurts

A

steroids

106
Q

why is it v important to carefully titrate fluids in pts with DMD

A

CHF risk

107
Q

why might you consider an NG tube in a pt with DMD

A

aspiration risk

108
Q

what is the most chronic inflammatory disease in adults

A

rheumatoid arthritis

109
Q

possible etiologies of RA

A

genetic

environmental

autoimmune (circulating autoantibodies in 70-80%)

110
Q

joints typically affected in RA

A

PIP/MCP joints of hands and feet

111
Q

when might an RA pt be on TNF inhibitors

A

systemic involvement

112
Q

what is Felty’s syndrome

A

RA, splenomegaly, neutropenia

113
Q

CV complications of RA

A

aortic or mitral valve regurg

pericardial effusion/inflammation

114
Q

most common peripheral neuropathy in RA pts

A

carpal tunnel

115
Q

musculoskeletal symptoms in RA pts

A
  • dislocation and dissolution of skeletal structures
  • deformed joints with no stability and minimal or no ROM
  • severe pain
  • crippling joint deformities
116
Q

random s/s in RA pts

A
  • constant low-grade fever
  • photosensitivity
  • muscle aches
  • mucosal ulcers
  • poor circulation
  • pleural inflammation
  • fatigue
  • loss of appetite
117
Q

most important joints involved in RA

A

TMJ

cricoarytenoids

atlantoaxial joint

118
Q

what should you suspect in RA pt with hoarse voice?

A

swollen/inflamed cricoarytenoids

119
Q

s/s c spine involvement in RA

A

limited neck movement

severe laryngeal deviation

120
Q

most common site of c spine involvement in RA pts

A

C1-C2

20-40% have atlantoaxial subluxation

121
Q

things about RA pts that makes careful positioning super important

A

osteopenic

steroid use

122
Q

common med hx in RA pts

A

NSAIDs

steroids

methotrexate

TNF inhibitors

123
Q

post-extubation complications to watch for in RA pts

A

laryngeal edema

stridor

124
Q

pre-op consideration for RA pts with advanced disease

A

c-spine xray

125
Q

RA + dry eyes =

A

sjogren’s syndrome

who gives a single shit*

*not me

S5 - Advanced Patho (6 decks)

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