Muscle Contraction - Trachte Flashcards

1
Q

Somatic motor neurons

A

emanate from the ventral region of the spinal cord

innervate skeletal muscle

release Acetylcholine

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2
Q

The acetylcholine interacts with ________ receptors on skeletal muscle

A

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

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3
Q

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

A

lidocaine

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4
Q

Botox

A

botulanotoxin (lasts 6 weeks).

blocks fusing of vessicle to membrane.

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

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5
Q

Neuromuscular blocking

A

Used for muscle paralysis in surgery or mechanical ventilation.

Selective for motor (vs. autonomic) nicotinic receptor.

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6
Q

Myosenetha gravis treatment

A

treat with anticholinesterase–boosts ACh concentration

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7
Q

ryanidine receptors are also known as

A

(aka calcium release channels)

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8
Q

Ryanodine

A

binds to calcium release channels

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9
Q

What molecule would you look for in a MI?

A

troponen I and T;

a better acute measurement is ECG.

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10
Q

Calcium is released from

A

the sarcoplasmic reticulum.

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11
Q

Interaction of _____ and ____ produce force in contracting skeletal muscle

A

actin and myosin

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12
Q

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

A

lighter areas become shorter (I band);

actin fillaments.

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13
Q

Myosine bridges have two binding sites…

A

ATP binding site and actin binding site

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14
Q

What causes the power stroke in muscle?

A

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).

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15
Q

What allows the release of the myosin head from actin?

A

ATP binding

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16
Q

What is the most common disorder causing muscle weakness?

A

Amyotropic lateral sclerosis (Lou Gehrig’s Disease).

Degeneration of motor neurons.

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

17
Q

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

A

Myasthenia gravis (autoimmune disease)

18
Q

Malignant hyperthermia

A

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

Usually triggered by anesthetics.

19
Q

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

A

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

20
Q

Muscle contraction resulting in shortening is termed?

A

concentric

21
Q

Muscle contraction resulting in lengthening is termed?

22
Q

How does cardiac muscle differ from skeletal muscle?

A

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.

23
Q

How does smooth muscle differ from skeletal muscle?

A

Not striated.

Contraction not controlled by troponin or tropomyosin.

Has autorhythmicity.

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

24
Q

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

A

Troponen C

25
Key word for calcium-induced calcium release...
ryanodine receptors
26
Speed of contraction is dependent on what?
**myosin ATPase activity**
27
Somatic nerves release what?
acetylcholine
28
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.
29
Acetylcholinesterases do what?
**degrade ACh**. Use *_anticholinesterase_* to treat Myasthenia gravis!
30
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.\
31
What drug is used to diagnose myasthenia gravis?
**Edrophonium**. Administered i.m.
32
What are the toxicities of anticholinesterases?
**SLUDGE**: increases sweating. lacrimation, urination, diarrhea, GI distress, emesis (can exacerbate COPD, asthma, peptic ulcers)
33
How do you reverse a competitive inhibitor of nicotinic receptors?
anticolinesterase.
34
succinylcholine
**deplarizing** agent. Causes chronic Na+ influx causing depolarization. **Overstimulates nicotinic receptor**. Short acting. Don't use in burns.
35
If you want to paralyze via the nicotinic receptor, what drugs could you use?
**competitive** (prevents action potential): **tubocurarine**, **mivacurium**. **depolarizin**g (simply depolarizes RMP): **succinylcholine**.
36
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.
37
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.
38
What receptor mediates skeletal muscle contraction?
nicitinic receptor.