Muscle Contraction - Trachte

Question 1

Somatic motor neurons

Answer 1

emanate from the ventral region of the spinal cord

innervate skeletal muscle

release Acetylcholine

Question 2

The acetylcholine interacts with ________ receptors on skeletal muscle

Answer 2

nicotinic receptors; Nicotinic ACh receptors are ligand-gated Na+/K+ channels; NN (found in autonomic ganglia) and NM (found in neuromuscular junction) subtypes.

Question 3

What can you use to block Na+ channels on neurons for anesthesia?

Answer 3

lidocaine

Question 4

Botox

Answer 4

botulanotoxin (lasts 6 weeks).

blocks fusing of vessicle to membrane.

toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions –> Faccid paralysis

Question 5

Neuromuscular blocking

Answer 5

Used for muscle paralysis in surgery or mechanical ventilation.

Selective for motor (vs. autonomic) nicotinic receptor.

Question 6

Myosenetha gravis treatment

Answer 6

treat with anticholinesterase–boosts ACh concentration

Question 7

ryanidine receptors are also known as

Answer 7

(aka calcium release channels)

Question 8

Ryanodine

Answer 8

binds to calcium release channels

Question 9

What molecule would you look for in a MI?

Answer 9

troponen I and T;

a better acute measurement is ECG.

Question 10

Calcium is released from

Answer 10

the sarcoplasmic reticulum.

Question 11

Interaction of _____ and ____ produce force in contracting skeletal muscle

Answer 11

actin and myosin

Question 12

When skeletal muscle contracts, the ____ bands get shorter and ____ is pulled toward the midline.

Answer 12

lighter areas become shorter (I band);

actin fillaments.

Question 13

Myosine bridges have two binding sites…

Answer 13

ATP binding site and actin binding site

Question 14

What causes the power stroke in muscle?

Answer 14

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).

Question 15

What allows the release of the myosin head from actin?

Answer 15

ATP binding

Question 16

What is the most common disorder causing muscle weakness?

Answer 16

Amyotropic lateral sclerosis (Lou Gehrig’s Disease).

Degeneration of motor neurons.

Caused by defect in superoxide dismutase 1. Progressive and Fatal.

Question 17

What disease is caused by autoantibodies against nicotinic receptors in skeletal muscle?

Answer 17

Myasthenia gravis (autoimmune disease)

Question 18

Malignant hyperthermia

Answer 18

caused by mutation of ryanodine receptor allowing excessive release of calcium.

Usually triggered by anesthetics.

Question 19

The amount of force generated by a muscle is directly proportional to …

Answer 19

the number of actin-myosin crossbridges per cross-sectional area (length doesn’t matter, thickness does)

Question 20

Muscle contraction resulting in shortening is termed?

Answer 20

concentric

Question 21

Muscle contraction resulting in lengthening is termed?

Answer 21

eccentric

Question 22

How does cardiac muscle differ from skeletal muscle?

Answer 22

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.

Question 23

How does smooth muscle differ from skeletal muscle?

Answer 23

Not striated.

Contraction not controlled by troponin or tropomyosin.

Has autorhythmicity.

Involves DAG–>PL-C–>IP3–>induces calcium release.

Question 24

Calcium binding to ____ releases inhibition of actin-myosin interactions.

Answer 24

Troponen C

Question 25

Key word for calcium-induced calcium release…

Answer 25

ryanodine receptors

Question 26

Speed of contraction is dependent on what?

Answer 26

myosin ATPase activity

Question 27

Somatic nerves release what?

Answer 27

acetylcholine

Question 28

acetylcholine interacts with what?

Answer 28

Nicotinic ACh receptors are ligand-gated Na+/K+ channels; NN (found in autonomic ganglia) and NM (found in neuromuscular junction) subtypes.

Question 29

Acetylcholinesterases do what?

Answer 29

degrade ACh.

Use anticholinesterase to treat Myasthenia gravis!

Question 30

Mechanism of muscle contraction…

Answer 30

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.\

Question 31

What drug is used to diagnose myasthenia gravis?

Answer 31

Edrophonium.

Administered i.m.

Question 32

What are the toxicities of anticholinesterases?

Answer 32

SLUDGE: increases sweating. lacrimation, urination, diarrhea, GI distress, emesis (can exacerbate COPD, asthma, peptic ulcers)

Question 33

How do you reverse a competitive inhibitor of nicotinic receptors?

Answer 33

anticolinesterase.

Question 34

succinylcholine

Answer 34

deplarizing agent.

Causes chronic Na+ influx causing depolarization.

Overstimulates nicotinic receptor. Short acting.

Don’t use in burns.

Question 35

If you want to paralyze via the nicotinic receptor, what drugs could you use?

Answer 35

competitive (prevents action potential): tubocurarine, mivacurium.

depolarizing (simply depolarizes RMP): succinylcholine.

Question 36

If you want to paralyze via inhibiting acetylcholine release, what drug would you use?

Answer 36

Botulanotoxin (lasts 6 weeks).

blocks fusing of vessicle to membrane.

toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions –> Faccid paralysis.

Question 37

If you want to prevent contraction and malignant hyperthermia, what drug would you use?

Answer 37

Dantrolene.

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

Question 38

What receptor mediates skeletal muscle contraction?

Answer 38

nicitinic receptor.