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
Q

WAR at alpha subunit-KING OF THE HILL!

Cholinergic agonist (ACh) VS receptor antagonist (NDMR)

A

transmission vs blockade

26
Q

WAR at alpha subunit-KING OF THE HILL!

All dependent on concentration of ____ and concentration/binding properties of _____

A

ACh
antagonist

27
Q

Drugs that block the ACh receptor at the NMJ
Curare-like muscle relaxants:

A

vecuronim
pancuronium
cisatracurium
rocuronium

28
Q

Drugs that inactivate acetylcholinesterase
Muscle relaxant reversal agents (Compete with ACh for a subunit binding sites):

A

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
Q

Cholinergic receptors ______, too

A

prejunctionally

30
Q

Prejunctional Receptors

Thought that they may _____ neurotransmitter movement and release

A

enhance

31
Q

Prejunctional Receptors

Antagonist effects at prejunctional area = decrease in release of ____ leading to _____

A

ACh
FADE

32
Q

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 _____ _____

A

NDMR
rapid stimulation

33
Q

Acetylcholinesterase

Rapidly hydrolyzes ACh to _____ + _____ in the junctional cleft

A

choline + acetate

34
Q

Acetylcholinesterase

Choline back into prejunctional nerve terminal to make ____ ____

A

new ACh

35
Q

Acetylcholinesterase

Reversal of NDMR (neostigmine, etc)-
ANTI CHOLINESTERASE-inhibits breakdown of ACh and increases the amount of ACh at the NMJ —->

A

*Agonist (ACh) >antagonist (NDMR); transmission restored

36
Q

Acetylcholinesterase

Pseudocholinesterasen- also hydrolyzes ACh; metabolizes ____ _____ and _____

A

ester LA and Succinylcholine

37
Q

Extrajunctional Receptors (EJR)

In utero— _____ _____ _____. Muscle cells have EJRs and are over entire length of muscle cell. (yAChR and alpha7 subunits)

A

no muscle innervation

38
Q

Extrajunctional Receptors (EJR)

___ ____, nerve-muscle contact fully mature — ACh receptors only in NMJ; EJRs disappear from ______ part of muscle

A

Age 2
peripheral

39
Q

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

A

decreased or removed
48 hours

40
Q

Extrajunctional Receptors (EJR)

EJR – resistant to NDMR, _____ _____ required

A

large doses

41
Q

Extrajunctional Receptors (EJR)

EJR — more sensitive to ACh, _____ causes channel to stay open, Na into cell and K+ out

A

succinylcholine

42
Q

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

A

20mg
hyper-K+
depolarization
K+