Muscle Contraction - Trachte Flashcards
Somatic motor neurons
emanate from the ventral region of the spinal cord
innervate skeletal muscle
release Acetylcholine
The acetylcholine interacts with ________ receptors on skeletal muscle
nicotinic receptors; Nicotinic ACh receptors are ligand-gated Na+/K+ channels; NN (found in autonomic ganglia) and NM (found in neuromuscular junction) subtypes.
What can you use to block Na+ channels on neurons for anesthesia?
lidocaine
Botox
botulanotoxin (lasts 6 weeks).
blocks fusing of vessicle to membrane.
toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions –> Faccid paralysis
Neuromuscular blocking
Used for muscle paralysis in surgery or mechanical ventilation.
Selective for motor (vs. autonomic) nicotinic receptor.
Myosenetha gravis treatment
treat with anticholinesterase–boosts ACh concentration
ryanidine receptors are also known as
(aka calcium release channels)
Ryanodine
binds to calcium release channels
What molecule would you look for in a MI?
troponen I and T;
a better acute measurement is ECG.
Calcium is released from
the sarcoplasmic reticulum.
Interaction of _____ and ____ produce force in contracting skeletal muscle
actin and myosin
When skeletal muscle contracts, the ____ bands get shorter and ____ is pulled toward the midline.
lighter areas become shorter (I band);
actin fillaments.
Myosine bridges have two binding sites…
ATP binding site and actin binding site
What causes the power stroke in muscle?
release of phosphate causes the angle of the myosin head to revert to 45 degrees and pull the actin in toward the M-line (center).
What allows the release of the myosin head from actin?
ATP binding
What is the most common disorder causing muscle weakness?
Amyotropic lateral sclerosis (Lou Gehrig’s Disease).
Degeneration of motor neurons.
Caused by defect in superoxide dismutase 1. Progressive and Fatal.
What disease is caused by autoantibodies against nicotinic receptors in skeletal muscle?
Myasthenia gravis (autoimmune disease)
Malignant hyperthermia
caused by mutation of ryanodine receptor allowing excessive release of calcium.
Usually triggered by anesthetics.
The amount of force generated by a muscle is directly proportional to …
the number of actin-myosin crossbridges per cross-sectional area (length doesn’t matter, thickness does)
Muscle contraction resulting in shortening is termed?
concentric
Muscle contraction resulting in lengthening is termed?
eccentric
How does cardiac muscle differ from skeletal muscle?
Both striated.
Gap junctions between cardiac cells easily disseminates electric impulses. Has autorhythmicity (contracts on its own). More dependent on extracellular calcium to cause calcium-induced calcium release.
Much longer action potential.
How does smooth muscle differ from skeletal muscle?
Not striated.
Contraction not controlled by troponin or tropomyosin.
Has autorhythmicity.
Involves DAG–>PL-C–>IP3–>induces calcium release.
Calcium binding to ____ releases inhibition of actin-myosin interactions.
Troponen C
Key word for calcium-induced calcium release…
ryanodine receptors
Speed of contraction is dependent on what?
myosin ATPase activity
Somatic nerves release what?
acetylcholine
acetylcholine interacts with what?
Nicotinic ACh receptors are ligand-gated Na+/K+ channels; NN (found in autonomic ganglia) and NM (found in neuromuscular junction) subtypes.
Acetylcholinesterases do what?
degrade ACh.
Use anticholinesterase to treat Myasthenia gravis!
Mechanism of muscle contraction…
ACh release –> nicotinic receptor activation –> sodium influx –> muscle endplate depolarization –> muscle action potential –> Ca++ influx –> Ca++ release (from SR) –> Ca++ interaction with troponin –> myosin-actin interaction resulting in force.\
What drug is used to diagnose myasthenia gravis?
Edrophonium.
Administered i.m.
What are the toxicities of anticholinesterases?
SLUDGE: increases sweating. lacrimation, urination, diarrhea, GI distress, emesis (can exacerbate COPD, asthma, peptic ulcers)
How do you reverse a competitive inhibitor of nicotinic receptors?
anticolinesterase.
succinylcholine
deplarizing agent.
Causes chronic Na+ influx causing depolarization.
Overstimulates nicotinic receptor. Short acting.
Don’t use in burns.
If you want to paralyze via the nicotinic receptor, what drugs could you use?
competitive (prevents action potential): tubocurarine, mivacurium.
depolarizing (simply depolarizes RMP): succinylcholine.
If you want to paralyze via inhibiting acetylcholine release, what drug would you use?
Botulanotoxin (lasts 6 weeks).
blocks fusing of vessicle to membrane.
toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions –> Faccid paralysis.
If you want to prevent contraction and malignant hyperthermia, what drug would you use?
Dantrolene.
Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
What receptor mediates skeletal muscle contraction?
nicitinic receptor.
