TRACHTE

Question 1

How many efferent fibers come from spinal cord in somatic nervous system?

Answer 1

1

Question 2

neurotransmitter in somatic nervous system

Answer 2

acetylcholine

Question 3

receptor in somatic nervous system

Answer 3

nicotinic

Question 4

What can activate nicotinic receptor

Answer 4

acetylcholine or nicotine

Question 5

6 steps that activation results in - step 1

Answer 5

Na influx

Question 6

6 steps that activation results in - step 2

Answer 6

depolarization

Question 7

6 steps that activation results in - step 3

Answer 7

muscle action potential

Question 8

6 steps that activation results in - step 4

Answer 8

opening of voltage sensitive calcium channel

Question 9

6 steps that activation results in - step 5

Answer 9

release of calcium from sarcoplasmic reticulum

Question 10

6 steps that activation results in - step 6

Answer 10

contraction

Question 11

efferent nerves from the spinal column virtually always release..

Answer 11

acetylcholine

Question 12

toxin from krait that blocks neuromuscular nicotinic ion channel

Answer 12

alpha - bungarotoxin or cobra venom

Question 13

Do somatic nerves have a synapse outside the spinal cord?

Answer 13

No (that’s autonomic nerves)

Question 14

Nerve activation leads to 9 things….1

Answer 14

acetylcholine release

Question 15

Nerve activation leads to 9 things….2

Answer 15

nicotinic receptor activation

Question 16

Nerve activation leads to 9 things….3

Answer 16

sodium influx

Question 17

Nerve activation leads to 9 things….4

Answer 17

muscle endplate depolarization

Question 18

Nerve activation leads to 9 things….5

Answer 18

muscle action potential

Question 19

Nerve activation leads to 9 things….6

Answer 19

calcium influx

Question 20

Nerve activation leads to 9 things….7

Answer 20

calcium induced calcium release from sarcoplasmic reticulum

Question 21

Nerve activation leads to 9 things….8

Answer 21

calcium interaction with troponin

Question 22

Nerve activation leads to 9 things….9

Answer 22

myosin-actin interaction (muscle contraction)

Question 23

What drugs could prolong acetylcholine actions?

Answer 23

anticholinesterases: neostigmine, pyridostigmine, edrophonium

Question 24

If something blocks acetylcholine release, what is prevented (2 things)

Answer 24

1. muscle depolarization

Question 25

Something that blocks nicotinic receptors will prevent.. (2 things)

Answer 25

muscle depolarization

Question 26

drug that prevents AcH release

Answer 26

botulinum toxin

Question 27

drugs that block nicotinic receptors (useful in surgery)

Answer 27

mivacurium

Question 28

Something that blocks calcium induced calcium release will block...

Answer 28

contraction! (but not depolarization)

Question 29

drug that blocks calcium induced calcium release

Answer 29

dantrolene

Question 30

What is useful for treating myasthenia gravis

Answer 30

anticholinesterases

Question 31

What do anticholinesterases do?

Answer 31

increase acetylcholine concentrations in the vicinity of the nicotinic receptor (outside the somatic nerve)

Question 32

charge of acetylcholine

Answer 32

negative (comes from aspartic acid)

Question 33

what does acetylcholine get broken down to?

Answer 33

acetic acid and choline

Question 34

2 carbamate drugs

Answer 34

neostigmine

Question 35

stimulates nicotinic receptors, useful for myasthenia gravis, abdominal distension or atony of detrusor muscle. More often used in the hospital only though.

Answer 35

Neostigmine (quaternary ammonium)

Question 36

delivery of neostigmine

Answer 36

oral or parenteral

Question 37

Used in myasthenia gravis or to reverse competive neuromusclar antagonism; can also be used prophylactically to prevent action of nerve gas.

Answer 37

Pyridostigmine

Question 38

Why is pyridostigmine used more in patients?

Answer 38

It is better absorbed orally.

Question 39

Why can pyridostigmine be used with nerve gas/

Answer 39

It could occupy some sites of Ach and prevent acetylcholinesterases from binding there

Question 40

Therapeutic idea in myasthenia gravis

Answer 40

increase Ach concentrations to increase interactions with nicotinic receptors. Nicotinic receptors are depleted in MG so must increase Ach to get interaction w/Nic receptor.

Question 41

On a response vs acetylcholine concentration plot, what way would it shift if neostigmine was administered?

Answer 41

left shift

Question 42

Reversilbe anticholinesterase that is administered parenterally and is very SHORT ACTING

Answer 42

Edrophonium

Question 43

What is edrophonium good for?

Answer 43

diagnosing myasthenia gravis and treating paraoxysmal supraventricular tachycardia

Question 44

If an increase in strength is seen after administering edrophonium...

Answer 44

myastenic crisis

Question 45

if a decrease in strength is seen after administering edrophonium...

Answer 45

cholinergic crisis

Question 46

cholinergic crisis

Answer 46

If there person is getting too much acetycholinesterase, the edrophonium will make them weaker.

Question 47

unique property of acetylcholine related to activation:

Answer 47

excessive stimulation desensitizes the organ to further stimulation (principle behind cholinergic crisis)

Question 48

Acetycholinesterase toxicity

Answer 48

Sludge

Question 49

S

Answer 49

sweating

Question 50

L

Answer 50

lacrimation

Question 51

u

Answer 51

urination

Question 52

D

Answer 52

diarrhea

Question 53

G

Answer 53

GI distress

Question 54

E

Answer 54

emesis (vomiting)

Question 55

What causes SLUDGE

Answer 55

stimulation of organs in body that respond to parasympathetic innervation, lung constriction, pinpoint pupils

Question 56

Where are neuromuscular blockers used?

Answer 56

surgery

Question 57

2 types of neuromuscular blockers

Answer 57

competitive and depolarizing

Question 58

Mechanism of neuromuscular competitive blockers

Answer 58

competitively compete for nicotinic receptor sites

Question 59

What parts of contraction, etc. are blocked w/neuromuscular competitive blockers?

Answer 59

Na influx (compete for nicotinic sites)

Question 60

How do depolarizing agents work?

Answer 60

depolarize END PLATE OF MUSCLE - leads to chronic Na influx

Question 61

How do competitive agents work on muscles..

Answer 61

affect smaller muscles first then larger ones

Question 62

What can reverse competitive blockers?

Answer 62

acetylcholinesterase (neostigmine, etc)

Question 63

What is most sensitive to depolarizing agents?

Answer 63

chest and abdomen

Question 64

What does acetylcholinesterase do to depolarizing agents/

Answer 64

may augment block (increase intensity)

Question 65

What do you see with depolarizing agents?

Answer 65

twitching before paralysis

Question 66

What effects occur from neuromuscular blockers (4)

Answer 66

paralyze skeletal muscle

Question 67

When don't you want to use neuromuscular blockers

Answer 67

burn patients

Question 68

Examples of competitive blockers

Answer 68

d-tubocurarine

Question 69

examples of depolarizing agents

Answer 69

succinylcholine

Question 70

what can enhance competitive block?

Answer 70

ether

Question 71

What has slight ability to reverse competitive blockade due to beta 2 receptors on muscle

Answer 71

epinephrine

Question 72

toxic effects of neuromuscular blockers

Answer 72

apnea

Question 73

what can cause malignant hyperthermia

Answer 73

halothane

Question 74

treatment for malignant hyperthermia

Answer 74

dantrolene

Question 75

what does dantrolene do?

Answer 75

inhibits calcium release from sarcoplasmic reticulum by blocking the Ryanodine receptor

Question 76

What does dantrolene prevent?

Answer 76

CONTRACTION

Question 77

Absorption of neuromuscular blockers

Answer 77

intravenously (quaternary ammonium)

Question 78

How are neuromuscular blockers usually excreted

Answer 78

kidneys

Question 79

what drug is not excreted by the kidneys

Answer 79

atracurium

Question 80

uses of neuromuscular blockers

Answer 80

anesthetics

Question 81

What are resistant to succinylcholine

Answer 81

myasthenics

Question 82

what potentiates succinylcholine effects

Answer 82

anticholinesterases

Question 83

What should you check for in patient before giving succinylcholine

Answer 83

butyrylcholinesterase

Question 84

What does butyrylcholinesterase do?

Answer 84

degrades succinylcholine (gives short duration due to rapid metabolism)

Question 85

Other side effects of succinylcholine

Answer 85

can produce malignant hyperthermia

Question 86

when is succinylcholine used

Answer 86

shorter procedures

Question 87

what does succinylcholine do to the contraction/acetylcholine concentration curve

Answer 87

flat lines (no contraction occurs)

Question 88

what does tubocarine do to the contraction/acetylcholine concentration curve

Answer 88

shifts curve to the right - decreases contraction of muscle (need higher Ach for contraction to occur)

Question 89

prevents acetylcholine release by cleaving proteins (SNAP25) necessary for acetylcholine exocytosis

Answer 89

botulinum toxin A (botox)

Question 90

where is botox injected

Answer 90

region of spastic muscle

Question 91

how long does botox last

Answer 91

3 months

Question 92

what can botox treat

Answer 92

spasms of eye

Question 93

most potent lethal toxin known (8 serotypes, only 3 have antisera)

Answer 93

botulinum toxin

Question 94

Prevents CONTRACTION and malignant hyperthermia

Answer 94

dantrolene

Question 95

Potentiate contraction w/antichoinesterases

Answer 95

neostigmine

Question 96

What drug would BLOCK action potential from occuring

Answer 96

tubocurarine (competitive)