Nur 638; Neuromuscular Blocking Agents Part 1

Front 1

What is the principal pharmalogical effect of neuromuscular blocing agents (NMB)?

Back 1

to interrupt transmission of nerve impulses at the neuromuscular junction (NMJ).

Front 2

What is the MOA of nondepolarizers?

Back 2

interfere or antagonize the actions of acetylcholine.

Front 3

What is the MOA of depolarizers?

Back 3

mimic the action of acetylcholine.

Front 4

Where are motor cammands generated?

Back 4

CNS

Front 5

Where do the cell bodies of the cranial motor neurons lie?

Back 5

in the branistem

Front 6

The axons of the cranial motor neurons have axons that extend through ________ _______ to control muscles in the head and neck.

Back 6

cranial nerves

Front 7

The cell bodies of the spinal motor neurons lie in the _______ ______.

Back 7

spinal cord

Front 8

The spinal cord neurons control the ________ and _______ in our lower body.

Back 8

muscles; glands

Front 9

What is the main part of the neuron?

Back 9

cell body

Front 10

What does the cell body contain?

Back 10

nucleus(DNA); endoplasmic reticulum; ribosomes (for building proteins); mitochondria (for energy).

Front 11

What is the purpose of the axon?

Back 11

to carry nerve impulses along the length of the cell.

Front 12

The ________ is the actual end of the nerve or nerve ending.

Back 12

dendrite

Front 13

What is the function of the dendrite?

Back 13

to allow thecell to communicate with other cells or to perceive the environment

Front 14

Motor neurons exit from the ______ ______ of the spinal cord, while sensory neurons exit from the _______ _____.

Back 14

anterior horn; posterior horn

Front 15

What is the area called where nerves and the muscle meet?

Back 15

neuromuscular junction

Front 16

An impulse travels along the nerve axon until it reaches the _______ _______ of the axon.

Back 16

terminal end

Front 17

At the end of each axon, there are ________ which contain a neurotransmitter called__________.

Back 17

vesicles; acetylcholine

Front 18

What is the ion that is responsible for the release of acetylcholine from the vesicle?

Back 18

Ca++

Front 19

By entering the _________ _________, calcium causes release of acetylcholine into the synaptic cleft.

Back 19

pre-synaptic terminal

Front 20

Acetylcholine enters the pre-synaptic terminal in packages called ________.

Back 20

quanta

Front 21

Each quanta of acetylcholine contains how many molecules af Ach?

Back 21

5,000-10,000 molecules

Front 22

Acetylcholine diffuses across the synaptic cleft and binds with the Ach ________ that is on the post-synaptic muscle fiber.

Back 22

receptor

Front 23

What action does Ach have on the post-synaptic receptor?

Back 23

It causes the receptor to become permeable to Na+

Front 24

What happens when the ion channel becomes permeable to Na+?

Back 24

Na+ goes rushing into the cell while K+ leaks out and the inside of the cell becomes more positive then the outside of the cell. Because for every 3 Na+ in 2 K+ go out. (Also, the membrane is more permeable to K+ so, K+ is continuously leaking out of the cell willy nilly!!)

Front 25

What is the name of the enzyme that breaks down acetylcholine?

Back 25

acetylcholinesterase

Front 26

What 2 substances are formed when acetylcholinesterase breaks Ach down?

Back 26

acetic acid and chlorine

Front 27

What happens to chlorine that is formed from Ach?

Back 27

it is reabsorbed back into the presynaptic vesicles to be stored and reused.

Front 28

Skeletal muscles are made of ________ _________.

Back 28

striated fibers

Front 29

What are the contractible subunits of the muscle fibers?

Back 29

myofibrils

Front 30

Myofibrils are made up of subunits called ________. These subunits connected end to end are called a ________ ______.

Back 30

sarcomere; functional unit

Front 31

What is the name of the junction where sarcomeres are attached to each other?

Back 31

Z-lines

Front 32

Where is calcium stored and released from in the muscle?

Back 32

sarcoplasmic reticulum

Front 33

What are the thin filaments of a sarcomere? thick filaments?

Back 33

actin; myosin

Front 34

What is the name of the cytoplasm found in muscle cells?

Back 34

sarcoplasm

Front 35

What does calcium release from the sarcoplasmic reticulum do to the actin and myosin?

Back 35

Calcium binds to the muscle protein and causes contraction; the actin and myosin slide on each other to shorten the muscle fiber.

Front 36

What gives myosin the energy to move along the actin filament?

Back 36

ADP and troponin

Front 37

Calcium's retreat back into the SR causes the muscle to ________.

Back 37

relax

Front 38

The ending "urium" indicates that the muscle relaxant is a __________.

Back 38

Benzylisoquinoline (these are histaminergic)

Front 39

The ending "onium" indicates that the muscle relaxant is a _________.

Back 39

steroid

Front 40

__________ and _________ are metabolized by pseudocholinesterases (also known as plasmacholinesterases).

Back 40

Succinylcholine; mivacurium

Front 41

Which NMB's are metabolized by hoffman's elimination?

Back 41

Atracurium and Cis-atracurium

Front 42

When the 4th twitch is eliminated, what percentge of block might the patient still have?

Back 42

75-80%

Front 43

The nerve stimulator is useful in determining ______ ______ ________.

Back 43

onset of blockade.

Front 44

What is the "gold standard" for extubation after NMB use and reversal?

Back 44

head lift for > 5 seconds

Front 45

All skeletal muscles have ________ _________ receptors.

Back 45

cholinergic nicotinic

Front 46

Name in order the most resistant to least resistant to NMB blockade: facial muscles, upper airway, diaphragm, peripheral and abdominal muscles.

Back 46

Diaphragm (most resistant) > other resp, upper airway & facial muscles > peripheral & abdominal (least resistant)

Front 47

What kind of regulationto receptors (up or down) is a spinal cord transection?

Back 47

Denervation injury (i.e. spinal cord transection)
Receptors increase or up-regulate
More receptors so need more drug to block
Need more NDMR
More receptors so need less drug to stimulate
Need less sux

Front 48

What kind of regulation to receptors (up or down) occurs in myasthenia gravis?

Back 48

Myasthenia gravis
Body destroys receptors so see decrease or down-regulation
Need less drug to block
Less NDMR
Need more drug to stimulate
More sux

Front 49

What kind of regulation to receptors is seen in chronic opiod use?

Back 49

Chronic high levels of drug cause decrease in receptors or down-regulation
Fewer receptors so see less and less effect
Tolerance develops