Exam IV: Musculoskeletal Diseases Flashcards

1
Q

Skeletal Muscle

A

voluntary control and striated

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2
Q

Smooth Muscle (most internal organs) but not the heart

A

involuntary autonomic control and nonstriated

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3
Q

cardiac muscle

A

intrinsic pacemaker - autonomic nervous system and striated

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4
Q

The force generated dependant on intracellular _____ and activation of _____ and _____ filaments

A

calcium
actin and myosin

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5
Q

Skeletal Muscle Include:
(voluntary control; striated)

A

Muscles of the tongue and soft palate
Extrinsic eye muscles
Muscles that move the scalp
All muscles attached to the skeleton
Muscles of pharynx
Muscles of upper 1/3 of esophagus
Lips * Anus* - serve as sphincters

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6
Q

Skeletal Muscle - Innervated by myelinated efferent motor nerve fibers to make _____ ____ _____

A

alpha motor neurons

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7
Q

At the muscle, divides into branches and ends on individual muscle cells called “____ _____.”

A

muscle fibers

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8
Q

Motor unit = 1 motor neuron + ____ ____ in it

A

all fibers

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9
Q

When motor nerve fires, all _____ in motor unit contract at the ___ ____.

A

fibers
same time

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10
Q

Acetylcholine (Ach)

increased Ca++ that comes in…. ____________

A

increased ACh that is released

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11
Q

Acetylcholine (Ach)

150-200 _____ _____ (_____) released with each nerve impulse

A

ACh vesicles (quanta)

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12
Q

Acetylcholine (Ach)

Each _____ has 10, 000 molecules of Ach

A

quantum

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13
Q

Acetylcholine (Ach)

Big ____ _____ — lots of ACh and many receptors available

A

safety margin

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14
Q

Aminoglycoside and Polymyxin antibiotics —- _____ ______ ______

A

inhibit ACh release

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15
Q

Lambert Eaton syndrome –

A

associated with small cell carcinoma of lung; autoimmune derangement in presynaptic Ca++ channels ; decreases Ach release

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16
Q

Botulinum toxin (clostridium botulinum) inhibit ACh release causing ____ ____

A

flaccid muscle

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17
Q

Mg++ competes with Ca++ at voltage-gated channel; ____ ____ release

A

decreases ACh

18
Q

Calcium Channel Blockers block Ca++ conductance mostly through ____ ____ _____ in heart

A

“slow” (L) channels

19
Q

ACh Receptor—–Post junctional

NMJ - each has estimated 50 million tightly packed _____ _____ sites

A

nicotinic AChR

20
Q

ACh Receptor—–Post junctional

Located at crests of ____ ____ ____ ____ folds

A

motor end plate junctional

21
Q

ACh Receptor—–Post junctional

Made in the _____ cells and then pushed to the end plate membrane and ______ face protrudes a bit

A

muscle
junctional

22
Q

ACh Receptor—–Post junctional

Activation requires ________ ACh binding at each of the alpha subunits

A

SIMULTANEOUS

23
Q

ACh Receptor—–Post junctional

Once occupied, cation channel will open, increased conductance to + ions (especially Na+) = ________________________

A

a net depolarizing potential (EPP)

24
Q

ACh Receptor—–Post junctional

If one ACh molecule leaves the subunit the channel _____ and _____ stops and membrane resets or repolarizes

A

closes
current

25
WAR at alpha subunit-KING OF THE HILL! Cholinergic agonist (ACh) VS receptor antagonist (NDMR)
transmission vs blockade
26
WAR at alpha subunit-KING OF THE HILL! All dependent on concentration of ____ and concentration/binding properties of _____
ACh antagonist
27
Drugs that block the ACh receptor at the NMJ Curare-like muscle relaxants:
vecuronim pancuronium cisatracurium rocuronium
28
Drugs that inactivate acetylcholinesterase Muscle relaxant reversal agents (Compete with ACh for a subunit binding sites):
neostigmine edrophonium pyridostigmine ACh not hydrolyzed so it increases quantity of ACh at synapse Used to reverse muscle relaxants - *also used to treat myasthenia gravis
29
Cholinergic receptors ______, too
prejunctionally
30
Prejunctional Receptors Thought that they may _____ neurotransmitter movement and release
enhance
31
Prejunctional Receptors Antagonist effects at prejunctional area = decrease in release of ____ leading to _____
ACh FADE
32
Prejunctional Receptors Fade (with tetany and train of four) may be reflecting the blockade of prejunctional receptors by the _____ and ACh release is not fast enough to keep up with _____ _____
NDMR rapid stimulation
33
Acetylcholinesterase Rapidly hydrolyzes ACh to _____ + _____ in the junctional cleft
choline + acetate
34
Acetylcholinesterase Choline back into prejunctional nerve terminal to make ____ ____
new ACh
35
Acetylcholinesterase Reversal of NDMR (neostigmine, etc)- ANTI CHOLINESTERASE-inhibits breakdown of ACh and increases the amount of ACh at the NMJ ---->
*Agonist (ACh) >antagonist (NDMR); transmission restored
36
Acetylcholinesterase Pseudocholinesterasen- also hydrolyzes ACh; metabolizes ____ _____ and _____
ester LA and Succinylcholine
37
Extrajunctional Receptors (EJR) In utero--- _____ _____ _____. Muscle cells have EJRs and are over entire length of muscle cell. (yAChR and alpha7 subunits)
no muscle innervation
38
Extrajunctional Receptors (EJR) ___ ____, nerve-muscle contact fully mature — ACh receptors only in NMJ; EJRs disappear from ______ part of muscle
Age 2 peripheral
39
Extrajunctional Receptors (EJR) If neural activity ____ or _____ — muscle goes back to fetal like synthesis of yAChR and alpha 7 receptors (stroke, spinal cord transection, burn, direct muscle damage, prolonged immobility) ***Can develop with ____ _____ from “injury”. Can also return to normal
decreased or removed 48 hours
40
Extrajunctional Receptors (EJR) EJR – resistant to NDMR, _____ _____ required
large doses
41
Extrajunctional Receptors (EJR) EJR — more sensitive to ACh, _____ causes channel to stay open, Na into cell and K+ out
succinylcholine
42
EJR—more sensitive to ACh, succinylcholinechannel stays open, Na into cell and K+ out ***No Sux (even as low as _____) with these type of patients—dangerous _____ ***Hyper-K+ because prolonged ______ and too much ____ out
20mg hyper-K+ depolarization K+