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Therapeutics 3 Kappa Epsilon > Final- Van Rijn Learning Objectives > Flashcards

Final- Van Rijn Learning Objectives Flashcards

1
Q

Pain Transmission Pathway:

Ascending Pathway?

A

Periphery –> Spinal Cord –> CNS

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2
Q

Pain Transmission Pathway:

Descending Pathway?

A

CNS –> Spinal Cord –> Periphery/Site of injury

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3
Q

What receptors are involved in pain signaling of the PERIPERHY?

A 
Temperature sensitive (TRP/TRPM/TRPV)
Acid Sensitive (ASIC)
Chemical Irritant Sensitive (Histamine/Bradykinin)
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4
Q

Periphery Signaling:

What channel is involved with temperature sensitive

A

TRP
(TRPV - Vanniloid - HEAT)
(TRPM - Melastatin - COLD)

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5
Q

Periphery Signaling:

what ions are involved in the ASIC?

A

activated by H+
and
conducts Na+

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6
Q

Periphery Signaling:

what chemicals are involved with the chemical irritant sensitive

A

histamine
and
bradykinin

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7
Q

______ nerve goes toward spinal cord
and
_______ nerve goes toward muscle (from spinal cord)

A

afferent

efferent

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8
Q

Nerve Transmission from periphery to spinal cord:

involves _____ and _____ channels along the nerve to propagate the action til it reaches nerve terminal

A

Na+; K+

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9
Q

Nerve Transmission from periphery to spinal cord:

at nerve terminal ____ channels are present to further facilitate neurotransmitter release

A

Ca2+

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10
Q

Nerve Transmission from periphery to spinal cord:
release of neurotransmitters (main one is _______) and they work on ______ receptors/channels

(but also ______ neurons exist too..)

A

glutamate
glutametergic (AMPA, NMDA, mGlu)

GABA

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11
Q

there are how many different pain fibers (for us to know)?

A

3

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12
Q

what are the names of the 3 diff pain fibers

A

A-beta
A-delta
C-fibers

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13
Q

Rank the pain fibers from slowest to fastest

A

C fiber —> A-delta —> A-beta

slow —————————fast

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14
Q

which pain fiber is known as “second pain”

A

c fiber

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15
Q

which pain fiber is known as non-noxious

A

A-beta

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16
Q

which pain fiber is myelinated

A

A-delta and A-beta

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17
Q

which pain fiber is known as first pain

A

A-delta

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18
Q

which pain fiber is related to touch/pressure

A

A-beta

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19
Q

which pain fiber is known to have sharp/prickly feeling

A

A-delta (first pain)

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20
Q

which pain fiber is known to have dull aching pain

A

C-fiber (second pain)

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21
Q

which pain fiber is unmyelinated

A

C-fiber (why it is the slowest one!)

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22
Q

with pain transmission —- repeated stimuli will reduce firing threshold — thus _______ is used to heighten pain responding

A

substance P

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23
Q

what 4 things does substance P do to heighten pain response

A

vasodilation
degranulation of mast cells
release of histamine
inflammation and prostaglandins

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24
Q

What opioid drugs are phenanthrene structure

A 
morphine
codeine
hydrocodone
buprenorphine
levophanol
naloxone
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25
Q

what opioid drugs are non-phenanthrenes

A

tramadol
meperidine
fentanyl
methadone

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26
Q

what opioid is a partial agonist

A

buprenorphine

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27
Q

what opioid is an antagonist

A

naloxone

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28
Q

phenanthrene potency is altered mainly by changing substituents at the ____ and ____ position

A

3;6

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29
Q

Opioid antagonists (like naloxone) are created by having a ________ group

A

bulky side

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30
Q

T or F: Opioids do not experience much first pass metabolism

A

false!! hella first pass

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31
Q

since opioids do experience a lot of first pass metabolism… what is a concern about using the drugs

A

cant use same dose for IV and oral!!

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32
Q

Opioids are mainly _______ eliminated

A

renally (90%)

also CYP 2D6 and 3A4 stuff

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33
Q

what opioids are prodrugs

A

heroin codeine and tramadol

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34
Q

which opioid drugs are not prodrugs (the ones vanrijn points out…)

A

fentanyl and methadone

aka good if hepatic or renal dysfunction

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35
Q

what drugs are good for anesthesia (because reach peak plasma levels fast)

A

remifentanyl

sufentanil

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36
Q

CYP_____ makes opioids into inactive metabolites

A

CYP3A4 into NOR_______

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37
Q

Opioids are primarily metabolized by what CYPs

A

2D6 and 3A4

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38
Q

all opioid receptors are (Gs or Gi) couple

A

Gi (aka will inhibit adenylyl cyclase!)

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39
Q

what are 4 opioid receptors

A

Mu
Kappa
Delta
Nociceptin/orphanin

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40
Q

opioid receptors can be activated by the endogenous opioids —- these are known as?

A

endorphin
dynorphin
enkephalin
nociceptin

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41
Q

what receptor used to be known as an opioid receptor but actually isnt…

A

sigma receptor

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42
Q

all opioid receptors are Gi coupled but they also activate ________ channels to cause even more hyperpolarization

A

GIRK

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43
Q

opioid receptors are found presynaptically, postsynaptically, or both?

A

both!

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44
Q

Presynaptic inhibition happens via _______
and
Postsynaptic inhibition happens via_____

A

pre: inhibit Ca2+
post: induce hyperpolarization by GIRK

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45
Q

for mu opioids: _________ is assoc. w/ side effects

A

beta-arrestin (side effect of respiratory depression)

if a drug doesn’t use beta arrestin signaling - less/no chance of respiratory depression

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46
Q

______ is a natural ligand that binds to kappa opioid receptor

A

Dysnorphin

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47
Q

______ is a natural ligand that binds to delta opioid receptor

A

Enkephalin

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48
Q

Kappa or Delta Opioid Receptor?

Which one as potential use for treating addiction (because it may have a role in causing addiction…)

A

kappa

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49
Q

Kappa or Delta Opioid Receptor?

which one has role in preventing hypoxia/ischemia/stroke

A

delta

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50
Q

Kappa or Delta Opioid Receptor?

which one counterbalances the mu opioid receptor effects

A

kappa

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51
Q

Kappa or Delta Opioid Receptor?

which one reduces anxiety/depression

A

delta

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52
Q

Kappa or Delta Opioid Receptor?

which one may be involved in alcoholism

A

delta

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53
Q

list the drugs that are opioids but are non-analgesic

A

Dextromethorphan
Diphenoxylate w/ atropine
Loperamide
Eluxadoline (Viberzi)

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54
Q

sufentanil, remifentanil, alfetanil have v short half lives and are used for anestheia/sedation…
they have a short life because …?

A

they are broken down by esterases due to ester linkage

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55
Q

what Non-phenanthrene opioids are beneficial because they have SNRI antidepressant activities

A

tramadol
and
tapentadol

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56
Q

what opioid drugs have NMDA antagonism

A

methadone

levorphanol

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57
Q

what non phenanthrene opioid is not recommended due to being neurotoxic

A

meperidine

has active metabolite!!

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58
Q

Pentazocine and Butorphanol are

______ agonists and _____ partial agonists/antagonist

A

kappa

mu

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59
Q

Nalbuphine is a

full agonist at _____ and antagonist at ____

A

kappa

mu

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60
Q 
Buprenorphine is a 
partial agonist at \_\_\_\_\_\_ 
weak agonist at \_\_\_\_\_
and 
antagonist at \_\_\_\_\_
A

mu
kappa
delta

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61
Q

what does inflammatory pain feel like

A

throbbing / pulsating

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62
Q

what does neuropathic pain feel like

A

burning
tingling
shooting
electrical

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63
Q

what does visceral pain feel ike

A

deep
squeezing
compression

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64
Q

what does breakthrough pain feel like (??)

A

spontaneous
iodopathic
incidental

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65
Q

what pain is known as throbbing/pulsating

A

inflammatory

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66
Q

what pain is known as burning/tingling/shooting

A

neuropathic

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67
Q

what pain is known as deep/squeezing

A

visceral

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68
Q

what condition is known to be allodynia pain

A

fibromyalgia

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69
Q

Substance P or NMDA/AMPA are more related to peripheral sensitization?

A

Substance P

it heightens pain response

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70
Q

Substance P or NMDA/AMPA are more related to nerve transmission from periphery to spinal cord?

A

NMDA/AMPA(mGlur too)

these are the receptors at the spinal cord — receptors for the neurotransmitters that Ca2+ help release)

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71
Q

what pain related disease state is an example of central sensitization

A

fibromyalgia

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72
Q

tx options for fibromyalgias

A

Ca2+ blockers/TCAs/Anti-convulsants

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73
Q

Chronic pain is typiclly enhanced by _______ sensitization

A

central

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74
Q

opioid receptors are found in high expression in the ______ along the _______ pathway

A

brain stem

descending pathway

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75
Q

When opioid receptor is activated in brain — what are the results

A

altered mood
sedation
reduced emotional reaction

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76
Q

When opioid receptor is activated in brain stem — what are the results

A

increase activity of descending fibers

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77
Q

When opioid receptor is activated in spinal cord — what are the results

A

inhibit vesicle release

hyperpolarize postsynaptic membrane

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78
Q

When opioid receptor is activated in periphery — what are the results

A

reduce activation of primary afferent nerves

modulate immune activity by modulating inflammatory mediators

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79
Q

what drugs are known as “peripherally restricted mu opioid antagonists”

A

Relistor (Methylnaltrexone)
Entereg (Alvimopan)
Movantik (Naolxegol)
Symproic (naldemedine)

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80
Q

what are the “peripherally restricted mu opioid antagonists” drugs used for?

A

for opioid induce constipation

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81
Q

what is the MOA of drugs that are used for treating opioid induced constipation

A

they antagonize the mu opioid receptor in the ileus (peripherally restricted to the gut!)

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82
Q

preventative/acute management of opioid induced constipation?

A

senna
polyethylene glycol (Miralax)
Docusate

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83
Q

Therapeutic Use of the Mu Opioid Receptor

A

Analgesia (not chronic pain tho??)
sedation
antitussive

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84
Q

Kappa opioid receptors may have role in _______ and are typically known to cause ______

A

role in addiction

dysphoria

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85
Q

Delta opioid receptors are known to decrease _______ and ______
Delta opioid receptor will also treat ________

A

decrease anxiety/depression

treat alcoholism

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86
Q

mu, kappa, or delta is more related to chronic pain?

A

delta

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87
Q

what NSAID is a salicylate

A

aspirin

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88
Q

what NSAIDs are arylpropionic acids

A

ibuprofen

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89
Q

what NSAIDs are arylacetic acids

A 
indomethacin
diclofenac
ketorolac
etodolac
sulindac
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90
Q

what NSAIDs are Enolic acids

A

meloxicam

piroxicam

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91
Q

________ are the mediators of inflammatory pain – thye recruit inflammatory cells

A

Eicosanoids (aka arachidonic acid metabolites)

Prostaglandins, Thromboxanes, Leukotrienes, Cytokines

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92
Q

What are the types of eicosanoids?

A

Prostaglandins,
Thromboxanes,
Leukotrienes,
Cytokines

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93
Q

Inflammatory Response/Arachadonic Acid Pathway:

_______ are suggested to be the contributor to the painful response

A

prostaglandins

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94
Q

Inflammatory Response/Arachadonic Acid Pathway:

Inhibiting ________ leads to reduction in thromboxane

A

COX1

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95
Q

Inflammatory Response/Arachadonic Acid Pathway:

________ induces platelet aggregation

A

thromboxane

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96
Q

Inflammatory Response/Arachadonic Acid Pathway:

Inhibiting thromboxane = blood thinning or clotting?

A

thinning

duh, NSAIDS inhibit COX enzymes = decrease thromboxane = less aggregation = more bleeding

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97
Q

COX 1 or COX2 leads to protective mucosa effects?

A

COX1

why selective COX2 is good because then don’t worry about GI bleeds as much

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98
Q

Thromboxane or Prostacyclin will reduce platelet aggregation?

A

Prostacyclin

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99
Q

COX 1 or COX2 is induced when there is inflammation?

A

COX2

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100
Q

Thromboxane or Prostaglandins promote uterine motility?

A

prostaglandins

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101
Q

thromboxane causes vasodilation or vasoconstriction?

A

constriction!

Thromboxane = thrombosis = platelet aggregation AND constriction - aka asking for a thrombus..

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102
Q

COX 1 or COX 2 has bigger rule in nociception

A

cox 2!

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103
Q

PGI2 causes vasodilation or vasoconstriction?

A

vasodilation!

acts opposite of thromboxane

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104
Q

Aspirin Overdose/Poisoning looks like??

A

Metabolic Acidosis!! (seen when severe ASA toxicity)
(look at ABG and BMP)
N/V/sweating/fever
delirium
respiratory alkalosis (seen when moderate toxicity)

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105
Q

To treat Aspirin Overdose - what do you do?

A

want to get ASA excreted….

thus give dextrose, or Na+HCO3- or dialysis

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106
Q

what NSAID irreversibly inhibits COX?

A

ASA

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107
Q

Ibuprofen or Naproxen has longer half life

A

naproxen!(~14 hr)

[Ibuprofen (~2 hr)]

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108
Q

Diclofenac has increased risk for ________ and renal dysfunction with prolonged use

For protective effect —- use ________

A

risk: peptic ulcer
give: Misoprostol (PGE1 analog)

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109
Q

Arylacetic acid NSAIDs are really weak or strong inhibitors of prostaglandins?

A

strong!! why hella peptic ulcer risk

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110
Q

Enolic Acid NSAIDs have great ______ penetration

A

joint

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111
Q

At low doses of meloxicam it is __________ seletive

A

cox 2

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112
Q

Enolic acids — short or long half life?

A

long!
Meloxicam (~20 hours)
Piroxicam (~ 57 hours)

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113
Q

why should NSAIDs be avoided in pregnancy?

A

it inhibits uterine motility!!

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114
Q

when are NSAIDs sometimes helpful in pregancy?

A

used to DELAY preterm labor

because they inhibit uterine motility

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115
Q

NSAIDs cause diuresis or Peripheral edema?

A

edemaaaa (because NSAIDs lead to Na+ reabsorption)

why CV risk

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116
Q

Peripheral Edema risk with NSAIDs increase with shorter or longer acting NSAIDs?

A

longer!!

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117
Q

Advantages of APAP?

A

no GI toxicity
no effect on platelet aggregation
no reye’s syndrome crap

CAN still be used in liver disease – just do < 2 g/day

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118
Q

Disadvantages of APAP

A

hepatic necrosis if acute overdose

no anti-inflammatory effect

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119
Q

APAP is converted to _______ by _____ enzymes (which can form toxic reactions)

A

NAPQI; CYP

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120
Q

explain how APAP overdose happens

A

APAP –> NAPQI (which is a toxic fella)
NAPQI usually not a problem because it gets conjugation with GSH
BUT overdose = run out of GSH = more NAPQI

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121
Q

how does APAP and Alcohol a bad interaction?

A

Alcohol increases CYP Enzymes aka more NAPQI is made (still not enough GSH present to make NAPQI not a problem)

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122
Q

Biggest pro with COX2 Selective Inhibitors?

A

reduced ulcers and GI bleeds

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123
Q

Biggest con with COX2 Selective Inhibitors?

A

High chance of blood clots/strokes/heart attacks

because COX 1 not inhibited = more thromboxane (not in balance with PGI2) = hella more thrombosis/platelet aggregation

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124
Q

ALL NSAIDs should be avoided in patients with what 3 PMH/disease states?

A
  • CKD
  • Peptic Ulcer Disease
  • Hx of GI bleed
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125
Q

T or F: Not all NSAIDs carry a CV risk in pts with coronary heart disease in the short term

A

FALSE!!! they do!

(Diclofenac - highest risk
lowest risk - naproxen)

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126
Q

NSAIDs or APAP can cause asthma exacerbation

A

NSAIDs

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127
Q

what channel is an analgesic target (GOF and LOF mutations are big in this)

A

Na+

NaV1.7 and NaV1.8

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128
Q

Local anesthetics are _____channel blockers

A

Na+

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129
Q

what drugs are local anesthetics/Na+ channel blockers

A

lidocaine
Bupivicaine
Benzocaine

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130
Q

SNRIs w/out Na+ channel blocking properties can be used to treat chronic pain conditions because why?

A

they increase NE
more NE = able to activate alpha2 receptors in spinal cord = inhibit neutrotransmission bc receptors are GI coupled

*also why clonidine can work — works at alpha 2 receptor

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131
Q

(from VanRijn lectures)
which SNRIs have Na+ channel blocking power (#2)
and
which SNRIs do NOT have Na+ channel blocking power (but will still help with pain_

A

have Na+: Duloxetine and venlafaxine

No Na+: Milnacipran; Tapentadol

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132
Q

(from VanRijn lectures)

what drugs are Ca2+ blockers that can be possible analgesics

A

Gabapentin and PRegabalin
Ziconotide
Levetiracetam

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133
Q

Main points about general anesthesia

A

loss of consciousness

endotracheal tube needed

134
Q

main points of Neuraxial anesthesia

A

placed into spinal area/epidural

used for abdomen and lower back surgeries

135
Q

main points of peripheral nerve block (PNB)

A

local anesthetic

used for surgeries on extremities

136
Q

3 Main Components for Anesthesia

A

Muscle Relaxant
induce amnesia (loss of consciousness)
Analgesia/Sedation

(May need anxiolytic too)

137
Q

Propofol is a _________ modulator of ______ channels

Propofol is also a ______ agonist so it causes ______ at injection site

A

positive allosteric; GABA

TRPA; pain

138
Q

T or F: when trying to cause peripheral nerve block you should inject the drug directly into the nerves

A

Falseeee. NEVER inject directly into a nerve

139
Q

what drugs are typically used for peripheral nerve block

A

mepivacaine

ropivacaine

140
Q

which Na channel isoforms are expressed in the PNS in the afferent neuron?

A

Nav 1.7, 1.8, 1.9

aka have limited side effects because only in PNS

141
Q

which Na channel isoforms are expressed in the CNS?

A

Nav 1.1, 1.2, 1.3, 1.6

142
Q

which Na channel isoforms are expressed in the cardiac muscle?

A

Nav1.5

143
Q

which Na channel isoforms are expressed in the skeletal muscle

A

Nav1.4

144
Q

Cell Physiology:

At rest — Na+ is _____ of the cell and K+ is ______ the cell

A

Na+ – outside

K+ inside

145
Q

Process of Local Anesthetic (LA) Entering the Cell:

LA binds to ________ side of ______ channel

A

intracellular;

Na+

146
Q

Process of Local Anesthetic (LA) Entering the Cell:

LA is a weak acid or base?

A

weak base

147
Q

Process of Local Anesthetic (LA) Entering the Cell:

LA is a weak base thus it is or is not protonated at pH < 7.4

A

it is partly not protonated at a pH < 7.4 (thus can penetrate cells)
LA’s pKa = ~ 7.5 - 9..

148
Q

what are the 3 different moieties that make up local anesthetic?

A 
lipophillic group (aromatic ring(
intermediate linkage
ionizable group (terminal amine)
149
Q

Bicarbonate helps or inhibits Local anesthetics from penetrating the cell

A

helps!
since LA’s are weak bases - the higher the pH the increasing percentage that the LA is non-ionized and is more capable of crossing the membrane

150
Q

Local Anesthetics have a higher affinity for Nav channels when it is the non-ionized or ionized form?

A

ionized

when intracellular - pH is lower than extracellularly aka will be protonated

151
Q

Intracellular pH is lower or higher than the extracellular pH

A

LOWER aka more acidic aka will protonated local anesthetics (da weak bases)

152
Q

4 main factors that influence local anesthetics

A

frequency of transmission
size/class of peripheral axons
pH
Vascularity of target tissues

153
Q

______ pH reduces efficacy of LA

A

acidic

154
Q

Local anesthetics have faster/higher absorption when the blood flow is _______

A

greater

155
Q

LAs bind to the closed or open state of the Nav channel

A

open

156
Q

LAs work (aka block pain) better on small myelinated or large unmyelinated nerves

A

small/myelinated

because fire better and can move it faster

157
Q

Potency of LA is better when it is hydrophillic or lipophillic?

A

lipophillic

158
Q

For LA: lower or higher pKa leads to longer half life

A

lower pKa

lower pKa = more it resides in non-protonated form = cross plasma membrane faster also evades degradation

159
Q

Duration of action of a LA is is determined by _______ and _______

A

protein binding

hydrophobicity

160
Q

Adrenergic agonists or antagonists are used as adjuncts to local anesthetics — and why?

A

agonists!

they cause vasoCONSTRICTION and that prolongs duration of action by limiting diffusion of the drug

161
Q

Amide or Ester based LAs?

have fast onset

A

amide

162
Q

Amide or Ester based LAs?

have short to long duration

A

ester

163
Q

Amide or Ester based LAs?

have med to long duration

A

amide

164
Q

Amide or Ester based LAs?

have variable onset

A

ester

165
Q

Amide or Ester based LAs?

slow t1/2 (hours)

A

amides

166
Q

Amide or Ester based LAs?

rapid t1/2 (minutes)

A

esters

167
Q

Amide or Ester based LAs?

has fast hydrolysis by esterases

A

ester

168
Q

Amide or Ester based LAs?

has hydrolysis by CYP system

A

amide

169
Q

Amide or Ester based LAs?

caution of giving this kind of LA in hepatic disease

A

amide

bc its metabolized by CYPs

170
Q

Ester bond or amide bond is more rapidly metabolized

A

ester

171
Q

Metabolism of _____ bond containing LAs leads to formation of ______ which can cause an allergic rxn/dermatitis/asthmat attacks

A

ester bond

PABA (para-aminobenzoic acid)

172
Q

Main Local Anesthetic Toxicities

A

Neurotoxicity
Cardiovascular
Methemoglobinemia

173
Q

Local Anesthetics: Neurotoxicity
First CNS _______
then at high doses CNS _______

A

first: stimulation

high doses: depression

174
Q

Local Anesthetics: Neurotoxicity

When at first CNS is stimulated what is the result?

A

inhibit GABA neurons (aka = stimulation)

will induce seizures!!! ahhhh. treat w/ benzos

175
Q

Local Anesthetics: Cardiovascular

what are the outcomes of this toxicity?

A

Vasodilation/hypotension
Depress cardiac AP/Dysrhytmias
Cardiac arrest

176
Q

neuromuscular blockers work by blocking _______ or _________

A

block Ach transmission
or
block nicotinic receptors on skeletal muscle

177
Q

what are the 2 types of neuromuscular blockers

A

depolarizing
and
non-depolarizing

178
Q

what is an example of a depolarzing neuromuscular blocker

A

succinylcholine

179
Q

Avoid using depolarizing neuromuscular blockers in ______ because it could cause ______

A

HYPERkalemia;

cardiac arrest

180
Q

Succinylcholine is metabolized fast or slow and by what?

A

fast!!

by Butrylcholinesterase

181
Q

why should depolarizing agents be avoid if a patient has hyperkalemia

A

depolarizing agonists cause influx of K+ — adds to the current hyperkalemia = at high risk of cardiac arrest

182
Q

Non-depolarizing neuromuscular blockers MOA?

A

ACH/Nicotinic receptor ANTAGONIST

183
Q

example of non-depolarizing neuromuscular blocker

A

pancuronium

184
Q

Non-depolarizing neuromuscular blockers are _____-like

A

curare

185
Q

Non-depolarizing neuromuscular blockers are reversible or irreversible

A

reversible!! easily!

186
Q

how can you reverse non-depolarizing neuromuscular blockers

A

AchE inhibitors (neostigmine)

Cyclodextrin Scavenger (Suggamadex)

187
Q

naloxone or naltrexone?

has limited bioavailability

A

naloxone

why we do nasal spray

188
Q

naloxone or naltrexone?

has medium half life?

A

naltrexone (taken PO daily for abuse…)

189
Q

naloxone or naltrexone?

has faster onset?

A

naloxone

190
Q

what are the 3 main drug categories (for drugs that are abused)

A

stimulants
depressants
psychedelics

191
Q

what drugs of abuse are known as depressants

A 
opioids
alcohol
cannabis
GHB
inhalants
192
Q

what drugs of abuse are known as stimulants

A 
cocaine
amphetamine
meth
bath salts
ectasy
nicotine
193
Q

what drugs of abuse are known as psychedelics

A 
LSD
psilocybin
PCP
mescaline
ketamine
194
Q

per DEA: what schedule is this drug?

heroin

A

I

195
Q

per DEA: what schedule is this drug?

ketamine

A

III

196
Q

per DEA: what schedule is this drug?

BZDs

A

IV

197
Q

per DEA: what schedule is this drug?

lomitil

A

V (antidiarrheal - its an opioid used as an antidiarrheal)

198
Q

per DEA: what schedule is this drug?

marinol

A

III (its THC in capsule form)

199
Q

per DEA: what schedule is this drug?

Cocaine

A

II (!!!!!)

200
Q

per DEA: what schedule is this drug?

Ritalin

A

II

201
Q

per DEA: what schedule is this drug?

Marijuana

A

I

202
Q

per DEA: what schedule is this drug?

MDMA

A

I

203
Q

per DEA: what schedule is this drug?

PCP

A

II (!!!!!)

204
Q

per DEA: what schedule is this drug?

LSD

A

I

205
Q

per DEA: what schedule is this drug?

heroin

A

I

206
Q

per DEA: what schedule is this drug?

buprenorphine

A

III

207
Q

per DEA: what schedule is this drug?

psilocybin

A

I

208
Q

T or F: DEA drug scheduling is permanent

A

hell nah

209
Q

what 5 groups does VanRijn mention that are substances of abuse that act DIRECTLY on GPCRs?

A 
Opioids
LSD/mushrooms
Marijuana/K2/spice
GammaHydroxyButyyric ACid (GHB)
Caffeine
210
Q

Substances of abuse work on GPCRs:

Opioids work on what specifically?

A

opioid receptors (mu)

211
Q

Substances of abuse work on GPCRs:

LSD/mushrooms work on what specifically?

A

5HT receptors! (2A and 2C)

*LSD and Mushrooms aka psilocybin and psilocin?

212
Q

Substances of abuse work on GPCRs:

Marijuana/K2/Spice work on what specifically?

A

cannabinoid receptors (CB1)

213
Q

Substances of abuse work on GPCRs:

GHB works on what specifically?

A

GABA (B)!! receptor

GABA(A) is not a GPCR but is a channel

214
Q

Substances of abuse work on GPCRs:

caffeine works on what specifically

A

adenosine

215
Q

Substances of abuse work on GPCRs:
The drugs binding to their respective GPCR can modulate _______ or _______ channels — leads to increase or inhibiting release of excitatory/inhibitory neurotransmitters

A

Ca2+; K+

216
Q

what substances of abuse work INDIRECTLY on GPCRs

A

Cocaine/ampheamine

MDMA/Ectasy

Alcohol

217
Q

Substances of abuse work on GPCRs:

Cocaine/Amphetamine work on what specifically?

A

dopamine transporter (remember it is INDIRECTLY working on GPCRs)

218
Q

Substances of abuse work on GPCRs:

MDMA/Ecstasy work on what specifically?

A 
Monoamine transporter (DA/5HT)
(remember it is INDIRECTLY working on GPCRs)
219
Q

Substances of abuse work on GPCRs:

Alcohol works on what specfically?

A

GABA Channels!! (also 5HT, NMDAR, NACHR, KIR3) — WILL CAUSE ENDOGENOUS RELEASE OF OPIOIDS —

220
Q

what substances of abuse act on ION CHANNELS

A

Nicotine
PCP/Ketamine
BZDs/Barbitruates

221
Q

Substances of abuse working on Ion channels:

Nicotine works how?

A

AGONIST of ionotropic Ach receptors (Na+)

222
Q

Substances of abuse working on Ion channels:

PCP and Ketmaine work how?

A

ANTAGONIST to ionotropic NMDA receptor (Ca2+, K+, Na+)

223
Q

Substances of abuse working on Ion channels:

BZDs and Barbiturates work how?

A

Postive allosteric modulators (PAMs) for ionotropic GABA receptors (Cl-)

224
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
Cocaine

A

indirect on GPCRs (dopamine transporter)

225
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
Nicotine

A

ion channels (Ach receptor agonist)

226
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
Caffeine

A

direct on GPCRs (adenosine receptors)

227
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
BZDs

A 
ion channels
(PAM for GABA receptors)
228
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
MDMA/Ecstasy

A

indirect on GPCRs (monoamine transporter - DA and 5HT)

229
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
Alcohol

A

indirect on GPCRs (causes release endogenous opioids – GPCR)

230
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
amphetamine

A

indirect on GPCRs (dopamine transporter)

231
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
opioids

A

direct on GPCR (mu opioid receptor)

232
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
marijuana/K2/spice

A

direct on GPCRs - cannabinoid receptors (CB1)

233
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
GHB

A

direct on GPCRs (works on GABA(B))

234
Q

how does it work: direct on GPCRs, indirect on GPCRs, or on ion channels?
LSD/mushrooms

A

direct on GPCRs (works on serotonin receptors)

235
Q

Circuit related to dopamine neurons and abuse of drugs?

A

Limbic pathway!! (VTA –> Amygdala/Prefrontal cortex/Hippocampus)

236
Q

what brain region is important in reward sensation/valuation

A

nucleus accumbens

237
Q

what brain region is important in memory/learning

A

hippocampus

238
Q

what brain region is important in emotion/fear

A

amygdala

239
Q

what brain region is important in planning/judgement

A

prefrontaol cortex

240
Q

what brain region is the “source of dopamine”/dopamine neurons originate here

A

VTA (ventral tegmental area)

241
Q

drugs of abuse of diff. classes all are habit forming/addictive b/c they act on the same pathway of _______ release in the _______

A

dopamine;
nucleus accumbens

(they just may do it through different pathways that lead to DA release)

242
Q

why is the limbic system important for survival in humans?

A

limbic system makes you want to find food and procreate

243
Q

2 main hypothesis of addiction

A

dopamine hypothesis
and
glutamate hypothesis

244
Q

idea behind dopamine hypotehsis of addiction?

A

1) pleasurable events lead to release of DA
2) parkinson disease pts less likely to suffer from addiction – unless they are taking L-DOPA then they are more likely
3) dopamine is important in assigning “incentive salience”

245
Q

what is incentive salience

A

a particular item is a higher priority than other other things (ex: that dude dove in dirty toilet for opioid suppository b/c seemed like a v high priority for him)

246
Q

limits of dopamine hypothesis of drug abuse?

A

1) there is a distinction b/w like and want..

2) monkey experiment shows that DA neurons can fire in anticipation and evoke a drive to action (not always a response)

247
Q

Glutamate hypothesis of addiction?

A

1) Glu can increase DA activity in NAcc

2) destruction of Glu pathway to VTA = reduce drug reward

248
Q

Hypothesis of Addiction

______ controls_____ activity in amygalda

A

DA; Glu

249
Q

drug use iduces long term ______

A

plasticity

250
Q

what is LTP stand for (about drug use) and what does it mean

A

long term potentiation

means: persistent increase in synaptic strength following intense stimulation

251
Q

Drug Use: LTP:
Persistent stimulation causes strong release of ______ - this causes an enhanced expression of _______ receptors on post-synaptic membrane:
This leads to the ratio of _______ being increase

A

stimulation = major increase in Glu release
enhanced AMPA receptor expression

leads to higher ratio of: AMPA/NMDA

(higher ratio is known as CELLULAR MEMORY)

252
Q

T or F: Only unnatural substances lead to longer cellular memory (aka increase in AMPA/NMDA)

A

false!! natural (food, sucrose, sex) AND unnatural (cocaine, heroin, alcohol) both cause the increase ratio/longer prolonger memory
BUUUUUUUT
unnaturals’ ratio increase lasts longer!!

253
Q

T or F: when abstinence from a drug (after cellular memories have formed for the drug) - the drug addiction memories are not erased

A

truuue. - why people can relapse easily
BUT during abstinence time period — new cellular memories about abstinence are being created and are competing with the drug abuse cellularmemories

254
Q

Substance used disorder criteria: (how many pts?)
Mild:
Moderate:
Severe:

A

Mild: 2 - 3
Moderate: 4 - 5
Severe: > 6

255
Q

what are some of the emotional withdrawal symptoms

A 
anxiety/depression
restlessness/insomnia
irritability
poor concentration
(HA - vanrijn put this here but maybe physical??)
256
Q

what are some of the physical withdrawal symptoms

A 
sweating
racing heart
goose bumps
muscle spasms
tremors
N/VD
257
Q

what are some of the more dangerous withdrawal symptoms?

A

Grand Mal seizures
heart attacks/strokes
hallucinations/delirium tremens (DTs)

*these are seen a lot with alcohol and tranquilizers (bzds and barbiturates)

258
Q

difference/definitions of positive and negative reinforcements?

A

positive: keep taking because it is rewarding/pleasurable/giving satisfaction
negative: taking to escape a negative/painful stimulus or event

259
Q

3 main ways for pathway to addiction

A

1) Therapeutic use
2) recreational use
3) self medication

260
Q

Pathways to addiction:

Therapeutic use — (-) or (+) reinforcement?

A

(-) –> (+) –> (-)

261
Q

Pathways to addiction:

Recreational Use — (-) or (+) reinforcement?

A

(+) –> (-)

262
Q

Pathways to addiction:

Self Medication — (-) or (+) reinforcement?

A

(-)

263
Q

what are the primary psychoactive compounds in marijuana

A

THC
cannabidiol
cannabinol

264
Q

Cannabidiol oil — has low or high activity at CB receptors (thus also has low or high psychoactive effects)

A

low activty @ receptors

and low psychoactive activity (why starting to be used for seizures/legalized)

265
Q

Scheduling of Marijuana:
Plant: ____
Nabilone (synthetic cannabinoid): _____
Marinol (THC formulation) _____

A

I
II
III

266
Q

how is K2/Spice made?

A

synthetic marijauna/cannabinoids are sprayed onto plant material

267
Q

what are the physical effects of marijuana use?

A 
sedation
red eye 
tachycadria
angina (if hx of coronary insufficiency)
reduction in pulmonary vitality
268
Q

why does marijuana cause red eye

A

it dilates conjunctival vessels

269
Q

what are sxs of marijauna withdrawal

A

dysphoria
anxiety/depression
decreased appetite

270
Q

what is “cannabinoid hyperemesis syndrome” and how do you treat it?

A

it is N/V

relieved by hot shower and is dose dependent (so no smoking = no syndrome)

271
Q

overdose is uncommon but what are possible things seen with overdose on marijuana

A

anxiety/panic attacks

convulsions

272
Q

why can a fatal overdose not really happen with marijauan

A

there are no CB receptors in respiratory centers of brain stem

273
Q

PK of THC:
quick or slow absoprtion?
metabolized by ______
short or long half life?

A

quick absorption
liver (CYP2C9)
long 1/2 life

274
Q

PK of THC:
is an agonist to ______ which are GPCRs
are they Gi or Gs?

A

CB1/CB2

Gi

275
Q

since CB receptors are Gi – whent hey are activated they will _____ Ca2+ channels and _____ GIRK channels

A

inhibit Ca2+

activate GIRK

276
Q

THC will _____ release of GABA

A

inhibit

277
Q

CB1 or CB2 is of higher expression in brain?

A

CB1

278
Q

CB actions in the _______ lead to locomotor effects

A

cerebellum

279
Q

CB actions in the _______ lead to appeteite increase

A

hypothalamus

280
Q

CB actions in the _______ lead to effects on memory and coping with stress

A

hippocampus

281
Q

CB actions in the _______ lead to effects with pain

A

PAG, LC (locus coeruleus), SC (spinal cord)

282
Q

With marijuana ingestion: psyhcoactive cannabinoids will bind to _____ receptors found (pre or post) synaptically on _____ neurons

A

CB1 receptors

PRE-synapse

GABA neurons

283
Q

psychoactive CBs will promote or inhibit release of GABA neurotransmitters

A

INHIBIT

284
Q

with CBs inhibiting GABA release — the GABA receptors post synaptically have reduced activity — the post synaptic ones NORMALLY do what?

A

normally inhibit DA neurons

aka CB receptor activation leads to DISINHIBITION on DA neurons

285
Q

CB receptor activation leads to DISINHIBITION on DA neurons – this leads to dopamine _______ in the ______

A

release; nucleus accumbens

286
Q

CB1 or Cb2 is found in higher expression in the periphery

A

CB2

287
Q

CB1 or CB2 receptors are expressed on lymphocytes (B and T cells)

A

CB2

288
Q

Anandamide and 2-arachidonylglycerol (2-AG) are what ?

A

endogenous cannabinoids

289
Q

endogenous cannabinoids: for 2-AG
DAG lipase does _____ and is found ____
MAG lipase does ____ and is found _____

A

synthesis; post-synaptically

degradation; pre-synaptically

(not sure on locations 100% bc i think he contradicts himself later in the notes ………)

290
Q

endogenous cannabinoids: Anandamide
AEA does ______
FAAH does _______

A

AEA: synthesis

FAAH: degradation

291
Q

what route of marijuana ingestion is seen to be th emost efficacious

A

vaping

292
Q

what are the 2 FDA approved cannabinoid drugs

A

marinol

nabilone

293
Q

for FDA approved cannabinoid drugs:
Marinol or Nabilone?
acts as an anti-emetic

A

nabilone

294
Q

for FDA approved cannabinoid drugs:
Marinol or Nabilone?
is used to increase appetite (helpful for chemo pts o pts with HIV/AIDS)

A

Marinol

295
Q

for FDA approved cannabinoid drugs:
Marinol or Nabilone?
is synthetic THC in seasme oil

A

marinol

296
Q

Cannabinoids and Increasing Appetite:

activation of CB1 —> inhibits _____ neurons in the ______

A

POMC neurons

in hypothalamus

297
Q

Cannabinoids and Increasing Appetite:
NORMALLY when POMC neurons get stimulated (they are inhibited when CB is activated..) it leads to ________ which activates _______ which is involved in appetie suppression

A

release of alpha-MSh

activate MC4R (melanocortin)

298
Q

Cannabinoids and Increasing Appetite:

Normally POMC leads to appetite suppression or heightened

A

appetite suppression

POMC inhibited when marijuana in system thus leads to appetite being heightened

299
Q

Cannabinoids and Increasing Appetite:

when POMC is inhibited it shifts gene transcription of _____ (up or down) which leads to increase in appetite

A

beta endorphins (up!)

300
Q

Cannabinoids can reduce N/V:

CB1 receptors where allow this to happen?

A

CB1 in GI tract and in brain stem

super detailed:
in GI: submucsal plexus and myenteric plexus

in Brain stem:
NTS and AP

NTS: Nucleus of solitary tract; AP: Area Postrema

301
Q

CB1 presence in brain stem helps with reduce nausea with chemotherapy because it works at the NTS which affects ______ and AP which controls ______

A

NTS: gag reflex

AP: controls vomiting

302
Q

how do cannabinoids help with glaucoma?

A

CB1 receptors are on ciliary muscles can relax the muscle and reduce the fluid build up to reduce sxs of glaucoma

303
Q

Cannabinoids can help with MS: Ways that it helps:
Activating CB2 receptors on ____ cells
moving shift from _____ to _____ cells
there are also CB2 receptors on_____

A

on T cells
TH1 –> TH2 (aka goes towards anti-inflammatory)
glial cells

304
Q

how can cannibinoids be helpful in pain?

A

CB1 and Cb2 receptors are expressed in spinal cord and they can inhibit the release of substance P, inflammatory cytokines, and glutamate = reduce central pain sensitization

305
Q

psychedelics:

3 main classes?

A

hallucinogens
dissociateies
delirants

306
Q

t or f: hallucinogens are typically very addictive

A 
false actually
(biggest issue with these drugs is that they might hurt themselves while taking them)
307
Q

PCP and ketamine are usually used as?

A

veterinarion anestheetics

308
Q

Psilocybin and Psilocin:

these are in magic mushrooms
(less or more) potent than LSD
which one is a prodrug of the other?

A

less potent

Psilocybin is prodrug of psilocin

309
Q

Salvia:
acts fast or slow?
is a ____ opioid receptor agonist

A

works v fast

kappa

310
Q

what hallucinogen is known to be helpful in treating drug abuse because it allows for introspection?

*it is NOT legal in US

A

ibogaine

311
Q

what molecule is thought to be the cause of hallucinations

A

serotonin

312
Q

Serotonin Receptors:

G____?

A

Gi/o, Gs, AND Gq!!

313
Q

Presynaptic serotonin receptors tend to be G____
and
Postsynaptic serotonin receptors tend to be G____

A

Pre: Gi

Post: Gq

314
Q

LSD works on what serotonin G receptor?

A

Gq - 5HT2A

315
Q

serotonin/serotonin receptor binding molecules tend to have what common moiety?

A

tyrptamine

316
Q

Mescaline is found in peyote - it combines the action of what 2 other hallucinogens

A

LSD; MDMA

317
Q

LSD and MDMA (aka mescaline too) are known as _________ or ______ which makes these more hallucinogenic (rather than stimulatory)

A

empathogens; entactogens

318
Q

Mescaline has a ____ potency and _____ half life (and has cross tolerance with LSD)

A

LOW; long

319
Q

what hallucinogenic drugs are known to be glutamatergic NMDA receptor antagonists (this lead to inhibiting GABA release –> more glutamate release..)

A

Ketamine

PCP

320
Q

most of the dissociative psychedelics have what MOA?

A

NMDA receptor antagonist

321
Q

what are the 3 main medical uses of ketamine

A

anesthesia
chronic pain analgesia
anti-depressant (good for tx resistant)

322
Q

what are examples of dissociative psychedelics

A

Ketamine
PCP
Dextrmetorphan

Muscimol

323
Q

ketamine or PCP - which one has severe dissociation

A

PCP!

remember the PCP face being disgusting

324
Q

what is the MOA of muscimol

A

it is a true GABA(A) agonist

325
Q

what are examples of synthetic/designer drugs of psychedelics — of opioid class

A

krokodil (can cause gangrene)

Codeine derivs.

326
Q

what are examples of synthetic/designer drugs of psychedelics — of cannabinoid class

A

K2

Spice

327
Q

what are examples of synthetic/designer drugs of psychedelics — of stimulant class

A

Bath salts

designer steroids

328
Q

what are examples of synthetic/designer drugs of psychedelics — of psychedelics class

A

PCP

NBOMe

329
Q

NBOMe is a designer LSD like drug —- does this drug have a lower or higher chance of overdose

A

higher chance

most psychedelics don’t have this problem but this designer drug does

330
Q

Main ADEs with Inhalants

A

cerebral degradation/brain shrinkage
hypoxia
respiratory depression

331
Q

MOA of inhalants

A

inhibit excitatory transmission- NMDA antagonism
AND
stimulate inhibitory NTs

Therapeutics 3 Kappa Epsilon (20 decks)

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