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Neuropharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what is pain?

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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2
Q

what is nociception?

A

the neural process of encoding noxious stimuli

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3
Q

Name and describe the neural steps in processing of pain signals

A

transduction: noxious stimuli are converted to electrical signals in sensory nerve endings

transmission: neural events which relay the information from the periphery to the cortex

modulation: the nervous system can selectively inhibit the transmission of pain signals

perception: subjective interpretation by the cortex of the noxious stimulus (sensory and affective component)

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4
Q

the therapeutic goal of pain treatment is to

A

eliminate abnormal pain without interfering with normal protective pain

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5
Q

activation of nociceptors sends signals to many parts of the brain including:

A

anterior cingulate cortex, basal ganglia, hypothalamus, parabranchial nucleus of dorsolateral pons, posterior cingulate cortex, posterior parietal complex, supplementary motor area

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6
Q

the ascending pain system…

A

transmits information from nerve endings to the brain

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7
Q

the descending pain system….

A

allows the brain to modulate incoming information by sending projections down to the spinal cord

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8
Q

afferent fibers synapse in the —- and project —- separate pathways to the —-. One pathway is for —— —— aspects of pain and the other is for the —– aspects of pain

A

dorsal horn, up, brain, sensory discriminative, emotional

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9
Q

Name and describe the three categories of primary afferent fibers

A

Alpha beta fibers: myelinated non-nociceptive, very fast conduction, convey light touch/vibration, may become nociceptive after nerve injury

Alpha delta fibers: myelinated nociceptors, fast conduction, convey fast pricking pain, cold, thermal

Nociceptive C fibers: unmyelinated nociceptors, slow conduction, convey slow burning and aching pain, polymodal (high threshold mechanical, thermal, cold)

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10
Q

first pain is characterized by —- fibers while second pain is characterized by — fibers

A

A delta, C fibers

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11
Q

Fibers are typically referred to by the stimuli they respond to an example would be CPM, CM, CH which stand for ——

A

Polymodal, mechano, heat

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12
Q

TRP channels are —– in nociceptors and other sensory neurons

A

thermosensors

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13
Q

what is allodynia?

A

perception of pain from a normally non-painful stimulus

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14
Q

what is hyperalgesia?

A

exaggerated perception of pain from a normally painful stimulus

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15
Q

today —- and other —– are commonly used for —— pain while —- and —- are gold standard for moderate to severe pain

A

aspirin, NSAIDS, inflammation-induced, morphine, opioid

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16
Q

what are opioids?

A

peptides that bind to the same postsynaptic receptors as bioactive opium extracts

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17
Q

name the 3 groups of endogenous opioid receptor ligands

A

endorphins (endogenous morphine), enkephalins, dynorphins

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18
Q

name and describe the 3 major GPCRs that bind opioid peptides

A

mu opioid receptors: major analgesic target, also responsible for addictive effects, bind endorphins

delta opioid receptors: minor analgesic target, bind enkephalins

kappa opioid receptors: possible pro-nociceptive effect, cause dysphoria, bind dynorphin

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19
Q

Describe how opioids are highly effective analgesics presynaptically and postsynaptically

A

presynaptic: block calcium influx, open potassium channels (potassium efflux), decreases excitatory neurotransmitter release

postsynaptic: open potassium channels, hyper polarize 2 order neuron, inhibit action potential generation

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20
Q

describe analgesics for acute pain

A

local anesthetics, blockage of voltage gated sodium channels, drugs end with Caine, side effects include respiratory depression, cardiovascular problems, seizures

acetaminophen: cox inhibition but different than NSAIDs, side effects kidney and liver failure

NSAIDs: inhibits COX1 & COX2, ends with in/en/ac/ib, side effects include ulcers, kidney failures, prolonged bleeding, reye syndrome

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21
Q

describe analgesics for acute-chronic pain

A

opioids: reduce activity of pain fibers and increase central modulation of pain, end with Eine/yl/one, side effect include vomiting, constipation, confusion, respiratory depression, abuse

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22
Q

Name and describe centrally acting analgesics

A

opioids, cannabinoids (sim to opioids in analgesic profile)

alpha 2 adrenergic agonists: used as opioid holiday during chronic opioid therapy

NE reuptake inhibitors: increase NE and activate alpha 2

selective ion channel blockers: Calcium and sodium ion channels modulate neuronal excitation and antagonists specific for channels subtypes may have few side effects

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23
Q

anxiolytic drugs can also treat —– and in high doses can cause —- and ——- from —— and ——-

A

insomnia, unconsciousness, death, respiratory , cardiavascular depression

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24
Q

acute anxiety can be treated by

A

benzodiazepines

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25
Q

panic disorder can be treated by

A

SSRI/SNRI and behavioral therapy

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26
Q

OCD can be treated by

A

long term antidepressants along with behavioral therapy

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27
Q

PTSD can be treated by

A

behavioral therapy, ketamine, prazosin, propranolol

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28
Q

Name and describe the classification of anxiolytic and hypnotic drugs

A

benzos: most important class used for treating anxiety and insomnia

5HT1A receptor agonists: showing anxiolytic activity with little sedation

barbiturates: now obsolete but still occasionally prescribed

Beta adrenoreceptor antagonists: mainly to reduce physical symptoms of anxiety such as tremors and palpitations

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29
Q

—— was the 1st benzodiazepine and some benzodiazepines like —– show anticonvulsant activity with less marked sedative effects

A

chlordiazepoxide, clonazepam

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30
Q

describe the mechanism of action for benzodiazepines

A

they act selectively on GABA A receptors

enhance the response to GABA by facilitating the opening of GABA-activated Cl- ion channels

do not affect receptors for other amino acids such as glycine or glutamate

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31
Q

name the main effects of benzodiazepines

A

-reduction of anxiety and aggression
-sedation and induction of sleep
-reduction of muscle tone and coordination
-anticonvulsant activity
-anterograde amnesia

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32
Q

with the exception of —— benzodiazepines do not have antidepressant effects

A

alprazolam

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33
Q

Benzodiazepines in acute overdose are —— dangerous than other anxiolytic drugs

A

less

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34
Q

in overdose, benzodiazepines cause

A

prolonged sleep without serious depression of respiration or cardiovascular function

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35
Q

what are the main side effects of benzodiazepines?

A

drowsiness, confusion, amnesia, impaired coordination

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36
Q

tolerance of benzodiazepines appears to represent a change at the —– level

A

receptor

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37
Q

stopping benzodiazepine treatment after weeks or months causes —–, —–, and —–

A

increase in symptoms of anxiety, tremor, dizziness

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38
Q

withdrawal of benzodiazepines after chronic administration causes physical symptoms similar to those that follow —- withdrawal, namely —–, —-, —–, and sometimes ——

A

opioid, nervousness, tremor, loss of appetite, convulsions

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39
Q

benzodiazepine clinical uses include

A

treatment of anxiety, status epilepticus, muscle spasm alcohol withdrawal, preoperative sedation, light anesthesia, anterograde amnesia

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40
Q

describe the pharmacokinetics of benzodiazepines

A

given orally, intravenously, intramuscularly

metabolized in liver and excreted in urine

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41
Q

benzodiazepines can have interactions with

A

alcohol and other CNS depressants by having an additive effect

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42
Q

SSRIs and SNRIs often have —— efficacy and —- incidence of side effects compared to —- and —–

A

greater, lower, benzos, barbituates

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43
Q

SSRIs and SNRIs can —– anxiety before anxiolytic effects can begin

A

worsen

44
Q

side effects of SSRIs and SNRIs include

A

agitation, nausea, diarrhea, decreased sex drive, anorgasmia, weight gain, hypertension, tachycardia

they can also produce SSRI discontinuation syndrome

45
Q

describe the pharmacology of Buspirone

A

-its a 5-HT1a receptor agonist
-it relieves anxiety without sedation
-takes a week to become effective, used for chronic anxiety
-low potential for addiction
-no muscle relaxation or anticonvulsant activity
-not as effective as benzos or SSRIs

46
Q

Vilazodone is a ——/——- agonist for depression

A

SSRI/5HT1a

47
Q

describe the pharmacology for Flumazenil

A

-completely blocks benzodiazepine binding sites
-counteracts adverse effects of benzodiazepine such as respiratory depression from intravenous administration or overdose
-intravenous use only, action lasts only 1-2 hours, repeated doses may be necessary for heavily sedated patient to remain alert
-use cautiously in persons with history of seizures or head injury
-no significant interactions with other drugs

48
Q

drug dependence describes the human condition in which

A

drug taking becomes compulsive and takes precedence over other needs, often with serious consequences

49
Q

drug abuse is a more —- term meaning….

A

general, recurrent use of substances that are illegal or that cause harm to the individual

50
Q

drug addiction can be described as

A

a chronic condition centering around an intense desire to obtain increasing amount of a particular substance to the exclusion of all other activities

it involves the progression of acute drug use to the development of drug seeking behavior, the vulnerability to relapse, and the decreased slowed ability to respond to naturally rewarding stimuli

51
Q

drug dependence refers to the body’s…

A

physical need for a specific agent, it represents a stable change in brain function

52
Q

if someone becomes drug dependent they will develop —– or —– withdrawal symptoms after use of the substance is stopped

A

physiological, psychological

53
Q

dependence is characterized by ——. this occurs when the body becomes —— ——- to a specific amount of a substance thereby causing the person to —– the amount of drug intake to achieve the previous effect

A

tolerance, less responsive, increase

54
Q

several psychotropic drugs including —- and —– produce withdrawal symptoms but are not —- so it is important to distinguish between —- and —–

A

antidepressants, antipsychotics, addictive, dependence, addiction

55
Q

—– dependence is not a major factor in sustaining long term drug dependence as —– ——– is more important

A

physical, psychological reinforcement

56
Q

positive reinforcement is the —– felt from the ——– being ——-

A

pleasure, reward pathway, stimulated

57
Q

negative reinforcement is the —— to drug cessation (—— ——) that subjects attempt to —– by ——- the drug

A

aversion, withdrawal symptoms, escape, self administering

58
Q

—— also plays a role is sustaining drug dependence. Antecedents associated with drug taking themselves evoke a ——-. Or reversely those associated with drug cessation become ——

A

conditioning, pleasurable response, aversive

59
Q

virtually all dependence-producing drugs activate the —— —- pathway, even though their primary sites of activation are generally elsewhere

A

mesolimbic dopamine

60
Q

the reward pathways begins in the —— —– —- of the —– and connects to the —– —- via the ——– ——, the —–, and the —– as well as to the —— ——-

A

ventral tegmental area, midbrain, limbic system, nucleus accumbens, amygdala, hippocampus, prefrontal cortex

61
Q

name the warning signs of drug abuse

A

-secrecy or withdrawal
-depressed or maybe even suicidal
-loss of focus on customary activities
-change in spending habits
-trouble with the law
-cycles of increased energy, restlessness, and inability to sleep
-abnormally slow movements, speech or reaction time
-confusion or disorientation
-sudden weight loss or gain
-cycles of excessive sleep

62
Q

the controlled substances act created —- schedules which regulates the manufacture, importation, possession, and distribution of certain drugs and two federal departments —– and ——- determine which drugs are added or removed from the various scheduled. ——, —–, —–, and —– are explicitly exempt from the controlled substances act

A

5, department of justice, department of health and human services, tobacco, beer, wine, and caffeine

63
Q

Schedule 1 drugs are those where….

A
  • the drug or other substance has a high potential for abuse
    -the drug or other substance has no currently accepted medical use in treatment
    -there is a lack of accepted safety for use of the drug or other substance under medical supervision
    -no prescriptions may be written for schedule 1 substances
64
Q

schedules 2-4 all include drugs with —— —. Five is the least restrictive such as ——- while two is the most restrictive such as —–, —-, —–

A

medical uses, cough medicines with codeine, morphine, cocaine, methadone

65
Q

examples of schedule 1 drugs include

A

cannabis, heroin, MDMA, LSD

66
Q

pharmacological approaches to treating drug dependence include which 3 strategies?

A

substitution to alleviate withdrawal symptoms, long term substitution, blocking therapies

67
Q

substitution to alleviate withdrawal symptoms include

A

-methadone used short term to blunt opiate withdrawal
-benzodiazepines to blunt alcohol withdrawal
-alpha 2 adrenoreceptor agonists (clonidine) to diminish withdrawal

68
Q

long term substitution includes

A

-methadone substitution for opioid addiction
-nicotine patches or chewing gum

69
Q

blocking therapies include

A

-nalterxone to block opioid effects
-mecamylamine to block nicotine effects
-immunisation against cocaine and nicotine to produce circulating antibody

70
Q

CNS stimulants include which 3 drugs

A

amphetamines/methamphetamines, cocaine, nicotine

71
Q

amphetamine and methamphetamine produce feelings of —- and —– ——

A

alertness, increased energy

72
Q

name the different ways meth users ingest meth and the effects it brings

A

-smoking or injecting which gives an immediate rush that lasts for only a few minutes but is extremely pleasurable
-snorting which after 3-5 minutes produces euphoria high but no intense rush
-swallowing which after 15-20 minutes produces euphoria high but no intense rush

73
Q

as with similar stimulants, meth users often go through a binge abuse cycle which consists of…..

A

rush, high, binge, tweaking, crash, normal and withdrawal

74
Q

describe the rush that comes with meth use

A

-last 5-30 minutes
-the addicts heartbeat races
-metabolism blood pressure and pulse soar
-feelings of pleasure

75
Q

describe the high that comes with meth use

A

-lasts 4-16 hours
-the addict often feels aggressively smarter and becomes argumentative

76
Q

describe the binge that comes with meth use

A

-lasts 3-15 days
-the addict maintains the high for as long as possible and becomes hyperactive, both mentally and physically

77
Q

describe the tweaking that comes with meth use

A

-most dangerous stage of the cycle
-tweaker has probably not slept in 3-15 days and is irritable and paranoid
-often behave or react violently and if they are using alcohol or another cans depressant, their negative feelings and associated dangers intensify
-craves more meth but no dosage will help recreate the euphoric high which causes frustration and leads to unpredictability and potential for violence
-eyes are moving 10 times faster than normal, voice has a slight quiver, and movements are quick and jerky

78
Q

high intensity abusers of meth experience…

A

extreme weight loss, very pale facial skin, sweating, body odor, discolored teeth, scars or open sores on their bodies

scars are the results of abusers hallucination of bugs on their skin and attempts to scratch the bugs off

79
Q

describe the withdrawal that comes with meth use

A

-no immediate symptoms are evident but the user will first become depressed and then lethargic
-the craving for meth hits and they may become suicidal
-fatigue, excessive sleeping, agitation, psychosis

80
Q

describe the treatment for meth addiction

A

-must want to give up amphetamine/methamphetamine
-need to avoid all stimulants including caffeine and tobacco
-self help groups or treatment program
-prescribed medication including antidepressants for depression and craving, sedatives for anxiety and trouble sleeping, and antipsychotics for paranoia and cravings

81
Q

describe the ways cocaine users ingest cocaine

A

-injecting where after 15-30 seconds an intense rush is produced
-snorting where it is absorbed via nasal membranes then into the brain within 3-5 minutes with peak effects a few minutes after that. self limiting ad the more cocaine that is absorbed the slower the absorption
-smoking where after 5-8 seconds an intense rush is produced

82
Q

name and describe the different forms of cocaine

A

-cocaine hydrochloride (water soluble, suitable for drinking, snorting, or injecting)
-freebase cocaine (water insoluble, suitable for smoking)
-crack cocaine a freebase form made using sodium bicarbonate (water insoluble, suitable for smoking)

83
Q

cocaine side effects include

A

anhedonia, loss of motivation, nightmares, hunger, emotional depression, insomnia

84
Q

describe cocaine overdose

A

-most often not fatal but does feel like it
-overly sweaty, cold and clammy sensation, feeling of impending death

85
Q

describe deaths from cocaine use

A

result from cardiac arrest, seizure, respiratory failure, extra high body temperature (severe hyperthermia)

86
Q

describe treatment of cocaine addiction

A

no medications available, treatment programs, behavior modification

87
Q

CNS depressants include which 3 drugs?

A

benzodiazepines, barbiturates, methaqualone

88
Q

benzodiazepine withdrawal symptoms can be similar to….

A

alcohol withdrawal

89
Q

benzodiazepine addiction treatment includes

A

transferring the physically dependent patient to an equivalent dose of diazepam then gradually weaning the patient off

90
Q

barbiturates produce similar intoxication to ——. recreational user report that a barbiturate high gives them feelings of —— —– and ——. the main risk of barbiturate abuse is ——- ——–

A

ethanol, relaxed contentment, euphoria, respiratory depression

91
Q

withdrawal symptoms from barbiturates include

A

anxiety, elevated cardio and respiratory rates, nausea, hallucinations, seizures, irritability, muscle pain, tremors, confusion

92
Q

barbiturates decrease —- —– so withdrawal often results in disruptions such as ——, —–, or ——-

A

REM sleep, nightmares, insomnia, vivid dreaming

93
Q

treatment for barbiturates addiction includes

A

transferring the physically dependent patient to an equivalent dose of diazepam then gradually weaning the patient off

94
Q

generally describe methaqualone

A

sedative drug that is similar in effect to barbiturates

95
Q

describe the recreational and overdose effects of methaqualone

A

-relaxation, euphoria, drowsiness, reduced heart and respiratory rate, increased sexual arousal, numbness of fingers and toes
-larger doses use depression muscular miscoordination, slurred speech, headache, photophobia
-overdose can cause delirium, convulsions, hypertonia, hyperreflexia, vomiting, renal insufficiency, coma and death through cardiac or respiratory arrest

96
Q

describe treatment of methaqualone addiction

A

transferring the physically dependent patient to an equivalent dose of diazepam then gradually weaning

97
Q

CB1 receptors are the…… in the human brain

A

most abundant GPCRs

98
Q

CB2 receptors are largely found in —– —- and other —— —–

A

immune cells, peripheral tissues

99
Q

CB1 receptors are highly expressed in the ——–, ——-. ——– ——, ——-, and —–. This distribution account for the effects of cannabis on ——, ——, and ——-

A

hippocampus, cortex, basal ganglia, cerebellum, and spinal cord, memory, cognition, and movement

100
Q

describe the cellular mechanism of action of cannabinoid receptors

A

-directly inhibit N and P/Q type Ca++ channels
-indirectly inhibit A type Ca++ channels via adenylyl cyclase
-activate inwardly rectifying K+ channels
-directly inhibit Na+ channels
-activate the mitogen activated protein (MAP) kinase signaling pathway

101
Q

describe the overall mechanisms of action of cannabinoids

A

THC acts as an agonist at CB1 and CB2 receptors

102
Q

describe the effects of cannabinoids

A

euphoria, drowsiness, relaxation, impairs short term memory and mental activity, decreases muscle strength, impairs high skilled motor activity, catalepsy, analgesia, antiemetic action, increased appetite, xerostomia, hallucinations, delusions, enhancement of sensory activity

103
Q

describe the clinical use of cannabinoids

A

-dronabinol is an appetite stimulant
-rimonabant which is a CB1 antagonist is an antiemetic, obesity treatment
-nabilone is a synthetic cannabinoid, used as an antiemetic, an analgesic for neuropathic pain, appetite stimulant
-sativex to alleviate neuropathic pain and spasticity

104
Q

describe the pharmacokinetics of cannabinoids

A

-lipid soluble
-effects appear immediately but take about 20 minutes to reach maximum
-effects gone after 3 hours
-read more on the slide idk im in a rush

105
Q

describe there adverse effects from cannabinoids

A

-increased heart rate, decreased blood pressure, reddening of the conjunctiva and sclera, reduced intraocular pressure, bronchodilation
-high doses cause toxic psychosis develops, tolerance and mild physical dependence

106
Q

describe the tolerance of cannabinoids

A

tolerance develops rapidly

107
Q

describe withdrawal of cannabinoids

A

-lack of immediate withdrawal symptoms has led people to incorrectly conclude withdrawal does not occur
-symptoms include anger irritability aggression, depression, slight tremors, decreased appetite, craving, aches pains chills, inability to concentrate, sleep disturbance, sweating

Neuropharmacology (2 decks)

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