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73 Cards in this Set
- Front
- Back
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muscle cell membrane
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sarcolemma
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muscle fibers are made up of
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myofibrils
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myofibrils are made up of
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myosin and actin
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think filaments, dark bands
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myosin
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thin filaments, light bands
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actin
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Light muscle bands (actin) builds up in who? and Why?
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marathon runners because they are more resistant to fatigue
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the striated appearance of muscle fibers is due to what?
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alternating bands of dark and light filaments
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Energy is needed for the skeletal muscle contraction to occur and this is derived from the breakdown of
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ATP
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filaments which bind actin and myosin together
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z discs
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portion of myofibrils between tow z discs making up a skeletal muscle cell
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sarcomere
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this contains K+, mag, and phosphate, and enzymes and mitochondria
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sarcoplamic recticulum
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what does the sliding filament theory say
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actin and myosin will slide over one another in order to cause a contraction
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where is Ca+ released
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scaroplasmic recticulum
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when ca enters the myofibrils what happens
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actin and myosin slide over each other causing a contraction
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what three proteins make up the actin filament
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actin, tropomyosin, and troponin
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in the resting state this covers the actins active sites so that a contraction cannot occur
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tropomyosin
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this binds calcium and initiates contraction
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troponin
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3 types of troponin
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Troponin C
Troponin T Troponin I |
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what does troponin I do?
Troponin C Troponin T |
keeps tropomysin next to actin
strongly attracted to calcium strongly attracted to tropomyosin |
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explain the process of a muscle contraction
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Ca released for sarcoplasmic reticulum, Ca binds to troponin C, troponin C deactivates the troponin-trypomysin complex exposing myosin binding sites, myosin binds to actin and pivots pulling the actin causing a contraction
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compartment syndrome acts similarly to ICP in what way?
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monroe kellie doctrine
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compartment syndrome can lead to _____ causing renal failure
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myoglobin urea
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what is virchows triad
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hypercoaguability,
hemodynamic changes (statius, turbulence) endothelial injury or dysfunction |
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what is pascals law
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change in pressure=density X force of gravity X (change in height of the fluid column)
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Pascals law helps to explain what in terms of compartment syndrome
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decreased perfusion to elevated extremities (legs, arms etc)
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what do you use when a patient is in the lateral position to reduce the risk of extremity ischemia ?
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axiallary roll
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what is compressed in the lithotomy position that could lead to compartment syndrome
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popliteal artery, use foot straps instead of things that hold under the knees if long procedure
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what are the 6 P's of compartment syndrome
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pain, palor, pulselessness, paresthesia, paralysis, poikelthermia (cold)
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hyperesthesia and allodynia define what
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extreme pain when something is being done that doesn't usually hurt, seen with compartment syndrome, bush of the area causes extreme pain
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pressure greater than ____ equals compartment syndrome
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30
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acetylcholine is hydrolized into _____ and_____ by acetylchlinesterase
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choline and acetate
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______ provide acetol co enzyme A which gets put together with choline by acethycholitransferase to make new Ach
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mitochondria
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what is the make up of a nicotinic cholinergic receptor
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2 alpha, 1 beta, 1 epsilon, 1 delta
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NMJ has a large margin of safety so effects of a non depolarizing muscle relaxant not seen until what % of receptors are blocked
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75
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NDMR=
SUCCS or DMR= |
competitive antagonist
agonist |
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what are the pre synaptic effects of NDMR
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decreases the amount of Ach at the NMJ
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which NDMR drugs are thought to have pre synaptic effects
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benxylisoquinolines
curare, atracurium, cisatracurium |
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pre synaptic effects are thought to be responsible for what
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The fade seen on the nerve stimulator
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what will happen if you mix a benzylisoquinoline what a aminosteroid?
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synergism
So if you give 1/4 roc with 1/4 atracurium it will give you a dose stronger than 1 dose of either. |
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why is there not an ongoing contraction at the motor end plate when using suxs
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because succs stays on the end plate keeping it depolarized...kind of like a refractory period
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where is the one place that Succs leads to tonic contraction?
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extraocular muscles
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how long will the extraoccular tonic contraction occur and how much with the IOP be increased with the use of Succs
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8min 8mmhg
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what are the aminosteroid NDMR
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vecuronium, rocuronium, pancuronium
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how are the aminosteorids (Rock, vec, and pancuronium) metabolized
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liver/kindey
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the benzylisoquinolines have what type of degradation
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enxymatic, humoral (hoffmans elimination)
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if you give roc before succs to decrease the faculations would you need more or less succs?
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more
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what things increase the likelyhood of channel blocking preventing open receptors
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aminoglycosides, tricyclic antidepressants, cocaine
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NMB reversals are what type of drugs
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anti-acetylcholinesterase drugs
allow ach to be more competitive at receptor sites |
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neostigmine is given with what anticholonergic? how long is its onset
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glycopyrrolate
8 min |
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edrophonium (tensolon) is given with what anticholinergic? how long is its onset
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atropine
1 min |
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edrophonium if better paired with what NDMR and why
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benzylisoquinolines because they both have presynaptic effects.
Benzylisoquinolines decrease the amount of ach at the NMJ and edrophonium will increase ach from the terminal |
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of the reversals which has less muscurinic effects
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edrophonium
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what things can desensitize (make pt weaker) receptor to the action by ach
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volatile, antibiotics, local anesthetics, phenothiazines, ca channel blocker, ach agonist
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what antibiotics cause desensitation of receptors to action by ach (make pt weaker)
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aminoglycosides, clindamycin, and mostly polymixin
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when succ is used in doses greater than ____ or prolonged infusion what can occur.
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2mg/kg
phase two block, also known as desensitization block or dual block |
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what is the first sign of a phase II block
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tachyphylaxis
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in extrajunctional receptors the epslion subunit is replaced by what...what does this mean?
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gamma, receptor stays open longer allowing more K out leading to Hyperkalemia
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review slide on hyperkalemia following sux, 20
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all leading toward vtach also look at list that causes extrajunctional receptors
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autoimmune disease which reduces the number of ach receptors
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myasthenia gravis
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is release of ach normal in myasthenia gravis
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yes, it is post junctional problem with decreased number of ach receptors
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what drug is used for diagnose and treatment of myasthenia gravis
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tensolon (edrophonium)
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Myasthenia gravis only effects what muscles
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skeletal
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Hyperplasia of what may cause myasthenia gravis
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thymus
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do you need more or less NDMR for a patient with myasthenia gravis. More or less Succs?
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less
more because less receptors to act on |
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what drug are most patients with myasthenia gravis treated with and what is a side effect that may make reversal tricky
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pyridostigmine decrease plasma cholinesterase
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what happens to patients with myasthenic syndrome as they exercise
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symptoms improve
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What patients would you be on the look out for myasthenic syndrome?
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Pts who are having a lung resection because oat cell CA associated with this disease process
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if your patient has myasthenic syndrome what drug is ineffective
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neostigmine
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what is the most common demyelinating disease of the CNS
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multiple sclerosis
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what is the most common motor neuron disease
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ALS
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what will succs do to a patient who has mytonia congentia?
Where is the mutation in this diesase |
gives a prolonged contraction
voltate gated cl channels |
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can you give patients with myastenia gravis succs?
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yes
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which paralysis has a normal response to NDMRs
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HYPOkalemic periodic paralysis
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