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Clinical Neuroscience 2 > Pharm- 11 > Flashcards

Pharm- 11 Flashcards

1
Q

Which sensations do A(delta) fibers transmit for pain?

A

myelinated transmit impulses much faster, used for first pain, noxious cold below 5 degrees C and injurious force on the skin

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2
Q

Which sensations do C-fibers transmit for pain?

A

nonmyelinated transmit impulses slower, used for second pain, temperatures above 45 degrees C and chemical and mechanical stimuli

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3
Q

Describe the pathway of pain peception from the periphery to the thalamus?

A

Impulses from the skin generated by the nociceptors activation are conducted to the dorsal horn of the spinal cord
In the dorsal horn the nociceptors form synapses with interneurons and second order neurons
Second order neurons travel in the lateral areas of the spinal cord (ALS from pain, temp crude touch), and project mainly to the thalamus

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4
Q

Where does the thalamus then project pain fibers in the CNS?

A

somatosensory Cx of the parietal lobe

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5
Q

Which fibers transmit the first pain signals?

A

transmitted by the Aδ fibers and is quick sharp (pinprick-like) in quality, and is perceived as highly localized on the body

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6
Q

Which fibers transmit the second pain signals?

A

transmitted by C-fibers and is slower to develop but longer lasting, feels dull, throbbing, or burning (the clap), and only diffusely localized, and endures after the stimulus ends

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7
Q

Are Aδ or C fibers more susceptible to local anesthetics?

A

Aδ

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8
Q

Define analgesics

A

are specific inhibitors of pain pathways

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9
Q

How does codeine work?

A

signals the cell to increase K+ conductance in postsynaptic neurons and decrease Ca entry into presynatpic neurons –> double whammy decrease in NT action/release

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10
Q

What is local anesthesia?

A
  • are nonspecific inhibitors of peripheral sensory (including pain), motor, and autonomic pathways
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11
Q

How does lidocaine work?

A

inhibits conductance of AP’s in all afferent and efferent nerve fibers in the PNS

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12
Q

How do all local anesthetics block pain perception?

A

Inhibiting Na-channels –> prevents AP’s on pain fibers

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13
Q

Procaine, tetracaine, and cocaine are example of what type of local anesthetics?

A

ester-linked

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14
Q

Lidocaine, prilocaine, bupivacaine, articaine, and EMLA are example of what types of local anesthetics?

A

amide-linked

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15
Q

What happens to ester-linked local anesthetics in the presence of water and esterases?

A

easily hydrolyzed to carboxylic acid and alcohol

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16
Q

Do amide or ester linked local anesthetics have a longer duration of action?

A

Amide LA’s

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17
Q

What is the role of the aromatic group in the local anesthetic (LA)?

A

Hydrophobicity –> passage through cell membranes

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18
Q

What happens if there is too much hydrophobicity in the LA?

A

It’s bad cuz the drug wont leave the hydrophobic interior of the cell –> continually acting

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19
Q

What are the 2 forms the amine group of the LA exist in?

A

protonated (+) or deprotonated (0)

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20
Q

What is the range of pKa for LAs?

A

8-10 (theyre weak bases)

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21
Q

So at physiological pH (7.4), are LA’s protonated or unprotonated?

A

almost equal amts of both

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22
Q

Which form (+ or 0) crosses the cell membrane?

A

neutral form

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23
Q

Which form (+ or 0) binds stronger to the voltage-gated Na channel?

A

+ form

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24
Q

Procaine (novocain)- use

A

epidural for delivery, dentists

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25
Q

Procaine- plasma T1/2

A

low b/c of hydrophobicity and rapid removal

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26
Q

Procaine- potency

A

Low b/c of rapid dissociated from Na channel

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27
Q

Tetracaine- use

A

topical and spinal anesthesia

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28
Q

tetracaine- plasma T1/2

A

logn b/c of high hydrophobicity, can stay in tissues for a while

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29
Q

Tetracaine- potency

A

high because of high hydrophobicity and longer binding to Na channel

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30
Q

Cocaine- use

A

;-), mucosal and opthalmic local anesthetic, Dx of Horners

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31
Q

Cocaine- plasma T1/2

A

medium

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32
Q

Cocaine- potency

A

medium

33
Q

Lidocaine- use

A

infiltration anesthesia, peripheral nerve block, epidural, spinal, topical anesthesia

34
Q

Lidocaine- plasma T1/2

A

medium duration, rapid onset

35
Q

Lidocaine- potency

A

moderate

36
Q

Prilocaine- use

A

dental work

37
Q

Prilocaine- plasma T1/2

A

medium

38
Q

Prilocaine- potency

A

moderate

39
Q

Bupivacaine- use

A

infiltration, regional, epidural, and spinal anesthesia

40
Q

Bupivacaine- plasma T1/2

A

long

41
Q

Bupivacaine- potency

A

high

42
Q

Articaine- use

A

dental work

43
Q

Articaine- plasma T1/2

A

short because rapidly metabolized in liver and plasma

44
Q

EMLA- use

A

combo od lidocaine and prilocaine, local anesthetic as a patch for dental prodecures in kids.

45
Q

What is the “ideal” hydrophobicity of LA’s for clinical use?

A

moderate hydrophobicity

46
Q

What exacly is the LA’s mechanism to inhibit the Na channel?

A

It prevents it from opening (major role) and physically blocks the pore (minor role)

47
Q

What are the 2 favorable forms of the Na channel that the LA prefers?

A

they have a higher affinity for the open and inactivated states of the sodium channel than for the resting state

48
Q

The degree of inhibition of sodium current by LA depends on what factor?

A

frequency of impulses in then nerve so you have tonic and phasic inhibition

49
Q

When does tonic inhibition occur?

A

occurs when the time between action potential is long compared to the time of dissociation of LA from the sodium channel

50
Q

Give an example why the degree of inhibiton from a LA depends on the freuqency of AP’s

A

assume before AP arrives an equilibrium has been established where 5% of Na channels are bound with LA. When the AP arrived the other 95% of channels can open and then go to inactivate state. During the brief impulse some of these channels become bound by LA . However, b/c of the long time before the next AP arrives the bound LA can dissociate from the sodium channel allowing it to return to the resting state. Thus the equilibrium of only 5 % bound by LA is reestablished before the next AP arrives and the next AP will be blocked to the same extent as the previous one

51
Q

When does phasic inhibiton occur?

A

occurs when there is NOT enough time between action potentials for the equilibrium to be reestablished –> only some of the Na channels can return to the resting state

52
Q

What is a differential functional blockade?

A

during onset of local anesthesia, different fiber types within a peripheral nerve are blocked at different times due to their intrinsic susceptibility to blockade

53
Q

What is the general order of a differential functional blockade?

A

1st pain –> 2nd pain –> temp –> touch –> proprioception –> SkM tone

54
Q

What is the role of substance P and glutamate in the spinal cord for pain?

A

mediate the transmission of nociceptive impulses between primary and second afferent neurons in the dorsal horn of the spinal cord

55
Q

What do epidural anesthetics do to substance P and glutamate in the spinal cord?

A

inhibit their receptors directly –> increasing the pain threshold –> decreasing pain perceptions

56
Q

What is “pharmacokinetics?”

A

what the body does to the drug

57
Q

When a LA is injected into the tissues, what are the 4 properties of the tissues to clear the drug?

A

Vascularity of the injection site, the drug concentration, the co admin of a vasoconstrictor, and propertires fo the injected solution (viscosity) all influence rate and extent of systemic absorption of LA

58
Q

Why is epinephrine often given with LA’s?

A

it reduces blood flow to the area of injection by causing smooth muscle of the vessles to contract and thereby slow the rate of removal of LA

59
Q

Which organ has a large LA binding capacity and express biotransformation pathways that can metabolize amide linked LAs?

A

Lungs

60
Q

What are the 2 plasma proteins that LA’s can bind to in the blood?

A

α-1 glycoprotein and albumin

61
Q

What happens to the LA’s binding to α-1 glycoprotein and albumin if the pH decreases?

A

it decreases as the pH decreases suggesting that the neutral form binds these proteins with high affinity

62
Q

What is the fast elimination of ester-linked LA’s done by?

A

by tissue and plasma esterases (pesuedocholinesterases)

63
Q

What metabolizes amide-linked LA’s?

A

primarily in the liver by P450 enzymes, which does aromatic hydroxylation, N-dealkylation, and amide hydrolysis

64
Q

What is topical anesthesia?

A

provided short term pain relief when applied to mucous membranes or skin

65
Q

What is infiltration anesthesia?

A

used to numb an area of skin (or mucosal surface) via an injection

66
Q

Why does infiltration anesthesia provide numbness faster than topical anesthesia?

A

b/c LA doesn’t have to cross the epidermis

67
Q

What are minor blocks?

A

blocking a single nerve, like the radial n

68
Q

What are major blocks?

A

blocking a big ass nerve, like the brachial plexus, which blcoks the whole arm

69
Q

Why does the injection for a peripheral nerve blockade only have a limited amt of drug reach the nerve?

A

The LAs must cross several layers of membranes before it reaches the target site and most of the drug is partitioned elsewhere into perinerural fat, and muscle, or removed by the local circulation

70
Q

What is a central nerve blockade?

A

drug is delivered near the spinal cord includes both epidural anesthesia and intrathecal (spinal) anesthesia

71
Q

What happens in an intravenous regional anesthesia (Bier block)?

A

Both a tourniquet and a distally located elastic band are applied to an elevated extremity leading to partial exsanguination of the limb

The tourniquet is then inflated and the band removed and the LA is then injected into a vein in the extremity to provide local anesthesia and the tourniquet prevents systemic toxicity by limiting blood flow to and from the extremity

72
Q

When are bier blocks used?

A

arm and hand surgery

73
Q

What are the damages of LAs to local tissues?

A
  • LAs can cause local irritation with skeletal muscle being the most sensitive to irritation
  • Plasma levels of creatine kinase are elevated after intramuscular injection of LAs indication damage to muscle cells
74
Q

What do LA’s do to peripheral vasculature?

A

• Lidocaine for example initially causes vasoconstriction but at later times produces vasodilation
Bronchial smooth muscle is also affected in a biphasic manner initially LAs cause vasoconstriction but at later times they cause bronchorelaxation

75
Q

What do LA’s do to cardiac muscles?

A
  • Cardiac effects of LAs are complex due to their action on Na K and Ca channels
  • Early effect is to reduce the conduction velocity of the cardiac action potential through both conducting and nodal tissues
76
Q

Why can LA’s (like lidocaine) act as a class I antiarrythmatic?

A

At very low concentrations LAs can act as antiarrhythmic drugs b/c can prevent ventricular tachycardia and ventricular fibrillation

77
Q

How can LA’s help with reducing cardiac contractility?

A

• LAs can also directly inhibit calcium channels in the plasma membrane and this combined with reduced intracellular calcium storage can reduce myocardial contraction

78
Q

What are the effects of LA’s on the CNS?

A

• Initially LAs produce signs of CNS excitement including tremors, tinnitus (ring in ear), shivering, twitching, and sometimes generalized convulsions
o Caused by LAs selectively blocking inhibitory pathways in the cerebral cortex
• As the concentration of LAs increase in the CNS all neuronal pathways excitatory and inhibitory are blocked leading to CNS depression
• Death is ultimately results from respiratory failure

Clinical Neuroscience 2 (16 decks)

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