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Neuro > Neuro Exam 2 > Flashcards

Neuro Exam 2 Flashcards

1
Q

Tripans mechanism

A

agonist for 5HT receptor to cause
vasoconstriction of cerebral vessels
inhibition of peptide release to cause vasodilation, inflammation, pain
prevent activation of pain fibers in trigeminal n.

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2
Q

Sumatripan

A

first line tripan used to treat moderate to severe migraine

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3
Q

Absorption route of triptans

A

Oral, nasal, sc (only sumatriptan)

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4
Q

distribution Triptans

A

low lipid solubility, poor CNS penetration. newer ones are more liophilic

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5
Q

half life tripans

A

2-4 hours

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6
Q

Adverse effects - Triptans

A

Paresthesia, flushing, dizziness, drowsy.

Seriouds: coronary vasospasm, agina, MI, arrhythmia.

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7
Q

Precautions with Triptans

A

coronary, arterial disease, uncontrolled htn

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8
Q

Drug interactions - triptan

A

not with 24 hours of Ergot Alkaloid due to additive vasoconstriction
Not at same time of MAO I, SSRIs, or SNRIs - serotonin syndrome.

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9
Q

Ergot Alkaloids mechanism

A

agonist of 5Ht receptor - similar to triptan mechanism

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10
Q

Dihydroergotamine

A

ergot alkaloid

intranasal, parenteral.

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11
Q

ergotamine

A

ergot alkaloid
Oral, sublingual, rectal.
Poor oral bioavalibiliy - slow onset - long duration.

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12
Q

ergotamine+caffine

A

ergot alkaloid

added to increase absorption, still less than tripans.

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13
Q

Ergot Alkaloid uses

A

terminating moderate to severe migraines.
less effective and more toxic than triptans - 2nd line.
Used in pts with duration >48 hrs or frequent recurrence

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14
Q

Adverse effects of ergot alkaloids

A

mild: N, V, D, parasthesias, vertigo
Severe: vascular occlusion, gangrene (due to alpha1 AR receptors stimulated) - associated with overdose.

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15
Q

Drug interactions - ergot alkaloid

A

avoid use with nonselective Beta blockers - severe peripheral ischemia
not used within 24 hrs of tripan
contraindicated with CYP3A4

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16
Q

Migraine Prevention treatment

A

prophylaxis for severe frequent (>4 month), long lasting (>12 hours), or disabling.
No single med is a clear choce, and takes 3-4 weeks to take effect.

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17
Q

Migraine Prophylaxis

A 
Antihypertensives - BB, calcium channel, ACEI
Antidepressants
anticonvulsants
Botox
Metbysergide
NSAIDs
Dietary Supplements
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18
Q

Beta Blocker

A

Propanolol - migraine prevention first line.

used for continuous prophylaxis

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19
Q

Beta Blocker - side effects

A

fatigue, exercise intolerance, depression, orthostatic hypotension.
contraindicated - asthma, diabetes, CHF

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20
Q

Calcium channel blockers

A

Verapamil - Third line prophylaxis for migraines
effectivness is limited.
Should not be used with BB

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21
Q

ACE I

A

Second or third line for Migraine prophylaxis

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22
Q

Tricyclic Antidepressants

A

Amitriptyline - second line for migraine prophylaxis. and can be given to pts with insomnia or depression.
SE: sedation.

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23
Q

Anticonvulsants

A

Valproate and topiramate - first line - similar to propanolol
Gabapentin - third line for migraine prophylaxis.

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24
Q

Valproate

A

anticonvulsant used for migraine prevention

causes nasuea, tremor, eight gain, hair loss

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25
Q

Topiramate

A

anticonvulsant for migraine prevention

causes parasthesias, langauage and cognitive impariment, weight loss

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26
Q

Botox

A

second line treatment for chronic migraine (>15 per month)

causes HA, neck pain, muscle weakness, ptosis

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27
Q

Methysergide

A

serotonin receptor antagonist - 5HT blocker to block vasoconstriction to iniate migraine.
effective but high toxicity - N, V, D, retroperitoneal, heart valve fibrosis.

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28
Q

NSAIDs - migrain prophylaxis

A

short term migraine pregention

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29
Q

Dietary supplements in migraine prophylaxis

A

Riboflavi - Vit B2
Butterbur - antispasmatic vascular wall, anti-inflammatory
Feverfew

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30
Q

Sources of Opiods

A 
Plants - opium poppy
Animals
1) Enkephalin 
2) endorphins
3) dynorphin
4) endomorphins
5) nocicptin
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31
Q

Enkephalin

A 
endogenous opioid
modulates NT at synpase (short distance) with rapid breakdown.
Found in brain and spinal cord.
Met-Enkephalin
Leu-Enkephalin
Derived from pro-enkephalin
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32
Q

Endorphin

A

endogenous opioid that acts on NT and as a hormone
derived from proopiomelatocortin
Found in hypothalamus and pituitary

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33
Q

Beta - Endorphin

A

a 31 AA, most active endorphin that contains a Met-Enkephalin a amino terminal

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34
Q

Dynorophin

A

endogenous opioid
unsure of role
derived from pre-dynorphin

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35
Q

Dynorphin A

A

biologically kappa selective

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36
Q

Endomorphins

A

new endogenous opioids, not well characterised.
variation on opioid motif
Tyr-Pro-Trp/Phe-Phe
Mu receptor selective

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37
Q

Nociceptins

A

regulate pain tranmission but act on different receptors

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38
Q

Naloxone

A

blocks opioids

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39
Q

Mu receptors

A

cause analgesia and respiratory depression.
endo: beta endorphin and enkephalins
Morphine

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40
Q

Delta receptor

A

analgesia only
Endo: beta endorphin and enkephalins
NO drugs

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41
Q

Kappa receptor

A

spinal analgesia
dynorphin A
drug: pentazocine

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42
Q

Mechanism of mu receptor

A

1) via B-gamma cose VGCC on presynaptic Neuron to decrease NT release
2) via beta-gamma activate GIRK - K channels - to hyperpolarize Pre or Post
3) via Gi/o decrase cAMP

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43
Q

Analgesic actions of opioids

A

1) inhibition of ascending pain pathway
2) activation of descending pain pathway
3) subjective response to pain

44
Q

how do opioids inhibit ascending pain pathway

A

decrease presynaptic NT release in Dorsal horn of Substance P and glutamate
Inhibit excitatory post synaptic spinothalamic neurons

45
Q

how to opioids excite descending pain pathway

A

activate inhibitory neurons to medulla, PAG, locus coerulus

46
Q

how do opioids control subjective pain?

A

euphoria, feel less pain, limbic system

47
Q

Do opioids releive 2nd or 1st pain better

A

2nd - dull, constant

48
Q

Behavioral consequences of opioids

A

Euphoria (mu receptors to active reward pathway), dysphoria (K receptors), sedation, behavioral excitation (acute toxicity)

49
Q

Respiratory consequences of opioids

A

decrease RR at therapuetic doses

due to decrases CO2 sensitivity in brainstem to cause incrased CO2 in blood, cerebral vasodilation –> and increased ICP

50
Q

GI effects of opioids

A

N,V - ambulatory pts.
Constipation - no tolerance
Urinary retention

51
Q

Cough effects of opioids

A

acts on cough center in medulla

Codeine - at low does as to not cause analgesic or respiratory affect.

52
Q

Dextromethorphan

A

non-analgesic opiod preffered over codeine for cough suppresion due to decrease potential for abuse, blocks NMDA recpetor - so acts like PCP or ketamine… so restricted

53
Q

Cardiovascular risks of Opioids

A

minimal, but occur indirectly through histamine - vasodilaton and decrases BP.
O decrease cardiac workloud and inhibit barorecpetor effect.
used to treat pulmonary embolism with cardiac dysfunction

54
Q

Contraindicaitons of opioids

A 
respiratory dysfunction - severe
high iCP
hypotension
shock - endogenous agents already active
hypothyroidism
impaired hepatic function
55
Q

Drug interactions of opiates

A

CNS depressants - Barbiturates - additive to CNS depression and increase in metabolism
Phenothiazine - atnipsychotic - increased risk of respiratory depression, decreased BP
MAO I and tricyclic antidepressants

56
Q

which opioid agents cross BBB

A

heroine and codeine

57
Q

Metabolism of opioids

A

liver metabolism to form morphine-6-glucuronide

58
Q

Morphine

A

mu agonist

II: used for post op and acute traumatic pain

59
Q

Heroine

A

mu agonist

I - highly lipophilic, rapid onset, high abue

60
Q

Codeine

A

II or III with tylenol, mu agonist
10% of caucasians are deficient in CYP2D6 - so not as effecitve
antitussive, high toxicity in high doses

61
Q

Oxycodone

A

II
mu agonist
equipotent to morphine - high abuse rate. good oral

62
Q

Hydrocodone

A

Vicodin III

antitussive, weak analgesic - equivalent to codeine.

63
Q

Tramadol

A

U receptor agonist

blocks monoamine uptake to potentiate descending pain pathways

64
Q

Fentanyl

A 
U receptor agonist
II
100X more potent than morphine
short duration of 1 hr (morphine is 4-6 hr)
requires ventilatory support. 
has transdermal patch
65
Q

Loperamide

A

imodium
antidiarrheal
low solubility so stays in GI

66
Q

Buprenorphine

A

partial mu agonist
precipitates mild withdrawal symptoms
long acting

67
Q

Methadone

A

mu receptor agonist - use to treat opioid withdrawal symptoms

68
Q

Naloxone

A

Mu receptor ANTAGONIST to block effects of endogenous opioids.

69
Q

Tolerance is due to..

A

frequence, dose, duration

70
Q

Physical Dependence

A

usually mild, and can be uliminated by taper

71
Q

psychological dependence

A

addiction - craving or desire.

due to adaptations in neuronal circuits

72
Q

Opiate withdrawal

A

flu like symptoms
dilated pupils, insomnia, rhinorrhea, sweat, N, D, cramps, chills.
Precipitated by antagonists and mixed agonists.
Tx clonidine to decreases SNS (alpha 2 agonist)
not life threatening.

73
Q

Evaluation of pain experience

A 
Severity 
Behavior - learned
Cognitive - thinking process
cultural
Suration
Origin - nocicpetive vs neuropathic
74
Q

Acute v chronic pain

A

acute - resolution or healing of damaged tissue
Chronic - pain persisting longer than expected - beyond normal healing, chornic disease, without identifiable cause, cancer

75
Q

neuropathic pain

A

disengaged from noxious or healing process. caused from nerve damage

76
Q

Functional pain

A

abnormal operation of nervous system - fibromyalgia, IBS, tension type HA - hyperalgesia and allodynia

77
Q

spinobulbar tract

A

carries pain info to limbic system - emotional and motivational pain experience

78
Q

mu opioid receptors in PAG….

A

block GABA release and remove inhibition to activate PAG outfluw

79
Q

PAG activates

A

spinal enkephalin and spinal monoamine release (5HT and NE)

80
Q

mu opioid receptrs in spinal cord..

A

are activated by enkephalins to decrease glutamate and substance P release and hyperpolarize post synatpic neuron to cause analgesia

81
Q

alpha 2 ARs…

A

are located presynpatically. Activation by NE attenuates excitation of 2nd order neuron and cause analgesia.

82
Q

Drugs involved in Pain Transduction

A

NSAIDS

83
Q

Drugs involved in Pain Transmission

A

Local Anesthetics

NMDA receptor antagonists

84
Q

NMDA receptor antagonists

A

Ketamine

block glutamate receptor deplolarization - decrease transmission of nociceptive stimuli

85
Q

Modulation of transmission drugs

A

mu opioid agonsts

alpha2 AR agonists - block substance P release from primary neuron

86
Q

NSAID - action

A

inhibit COX2 and PG synthesis

transduction of pain

87
Q

LA - action

A

block VSSC

tranmission

88
Q

NMDA antagonists - action

A

block glutamate depolarization at 2nd order neurons.

Transmission to pain blocker

89
Q

Mu opioid receptor agonists - action

A

block glutamate and substance P from primary neuron
Hyperpolarize 2nd order neuron
Modulation of transmission and perception

90
Q

Alpha2 adrenergic agonist - action

A

block glutamate and substance P from primary neuorn

Modulation of tranmission

91
Q

Management of mild pain

A

non opioid +/- adjuvant analgesic

92
Q

Moderate acute pain

A

immediate release short-acting opioids with slow titration + non-opioid +/- adjuvant analgesics

93
Q

Severe acute pain

A

immediate release short acting opioids with RAPID titration + non opioid +/- adjuvant analgesics

94
Q

Multimodal analgesic

A

benefits by synergistic actions to allow lower doses and limit dose related side effects

95
Q

`Formulations of Opioids

A

Immediate release - parenteral and oral opioids
Sustained release - for morphine extended duration
Transdermal patch

96
Q

NSAIDs

A

COX2 inhibitors to interefere with inflammatory cascade at peripheral and central sites.

97
Q

Side effects of NSAIDs

A

GI ulceration, increased bleeding risk, renal dysfunction

98
Q

Acetaminophen

A

COX2 inhibitor to block central sensitization

99
Q

Alpha 2 AR agonists

A

Clonidine
acts on dorsal horn and cells and locus ceruleus to modulate tranmission
can cause hypotension, bradycardia, sedations

100
Q

Ketamine

A

NMDA antagonist in ascending pain modulatory pathway.

reduces development to tolerance in long term opioid use .

101
Q

Peripheral sensitization

A

type of neuropathic pain
damaged peripheral nerves synthesize proinflammaotry mediators to activate terminal and produce pain or render hypersensitive.

102
Q

Central sensitization

A

neuropathic pain

amplification of synaptic transfer from terminal to dorsal horn neurons by BDNF and substance

103
Q

Chronic Pain Management

A

mechanistic approach rather than therapuetic class stratification.
Enhance descending inhibitory
Decrease central sensitization and peripheral sensitization

104
Q

What drugs enhance desending inhbitiory pain pathway

A

Opioids, antidepressants (block NE, serotonin reuptake)

105
Q

What decreaeses central sensitization

A

anticonfulstants, ketamine

106
Q

what decreases peripheral sensitization

A

anticonvulsants, LA

Neuro (5 decks)

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