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NS_BTRAN > UNIT4_Pharm > Flashcards

UNIT4_Pharm Flashcards

1
Q

What are the sturtures that are involved in the brain rewards pathway? (6)

A
  • Nucleus Accumbens
  • Ventral Tegmental area (VTA)
  • Amygdala
  • Hippocampus
  • Lateral Hypothalamus
  • Prefrontal Cortex
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2
Q

_______________ is a major component of ventral striatum.

A

Nucleus Accumbens: major component of ventral striatum

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3
Q

What structure is the midbrain structure with dopaminergic cells innervating all the rewards pathway structures?

A

Ventral Tegmental Area (VTA)

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4
Q

What is the structure that integrates and projects to VTA and nucleus accumbens?

A

Amygdala;

Thought to be important to formation of stimulus-rewards associations.

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5
Q

What brain structure is critical for the executive function in providing control of impulses from destructive behaviors.

A

Prefrontal cortex;

Impairment following chronic drug abuse important mediator in loss of control over drug intake (Addiction)

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6
Q

What neural system is a dopamine pathway that is the final common pathway of reinforcement and rewards called?

A

Mesolimbic system

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7
Q

Stimulation of ____ neurons by natural reinforcers → dopamine release in nucleus accumbens

A

VTA

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8
Q

Stimulation of VTA neurons by natural reinforcers → ________ release in nucleus accumbens

A

dopamine

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9
Q

Stimulation of VTA neurons by natural reinforcers → dopamine release in ______ _______.

A

nucleus accumbens

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10
Q

ALL drugs with dependence liability share What final common pathway of increasing synaptic dopamine levels in nucleus accumbens?

A

Mesolimbic system;

More intense/direct effect drug has on dopamine neurons, the greater addiction potential

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11
Q

TA (dopamine cell bodies) + nucleus accumbens (where DA neurons project) + amygdala (connects VTA and NA).

This system is called?

A

Reactive Rewards System

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12
Q

What is the function of the Reactive Rewards System?

A

signal immediate prospect of pleasure or pain and provides motivational and behavioral drive to achieve that pleasure or avoid that pain

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13
Q

Learning conditioned in the amygdala. The amygdala connects to the VTA how?

The amygdala connects to the Nucleus Accumbens how?

A

→ connects back to VTA as a relevance detector (for anything relevant to previous drug abuse experience).

→ connects to nucleus accumbens to signal emotional memories triggered by internal or external cues → initiate impulsive-automatic-obligatory actions to find/take more drugs.

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14
Q

Drugs of abuse: repeated exposure to drugs of abuse results in _______ ________ to trigger drug-seeking behaviors when presented with internal (craving, withdrawal) or external (environmental associations) cues

A

pathologic “learning”

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15
Q

Reflective reward system connects what to what?

A

Reflective reward system: connects PFC to nucleus accumbens.

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16
Q

This the reflective rewards system

  • Orbitofrontal projections → ?
  • Dorsolateral PFC → ?
  • VMPFC → ?
A
  • Orbitofrontal projections → regulate impuls
  • Dorsolateral PFC → analysis of situation
  • VMPFC → integration of impulsiveness and cognitive flexibility with its regulation of emotions
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17
Q

Describe the interaction of drugs of abuse with brain reward pathways in the development of addictive behaviors.

A
  1. Repetitive drug-induced rewarding experiences → alter reward circuits so drug ingestion and cues that merely predict pleasure will activate mesolimbic dopamine release.
  2. Amygdala learns that drug causes pleasure and drug cues with pleasure.
  3. Drug cues → dopamine release in NAc → GABA output from NAc → thalamus → prefrontal cortex.
  4. Absence of activity in reflective reward system → drug seeking behavior initiated.
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18
Q

What routes of drugs admin are associated with most rapid rise in brain levels of drug and greater likelihood to produce addiction

A

IV and Inhalation

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19
Q

Withdrawal effects more severe for drugs with ______ half-lives → continued drug administration just to prevent withdrawal

A

short half-lives

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20
Q

How does the tendency for abuse of a drugs change with a faster onset of action?

A

faster onset of action = increase liability for drug abuse

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21
Q

What brain pathway is central to the reinforcing actions of dopaminergic drugs?

A

VTA → Nucleus Accumbens

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22
Q

Are both of these statements True or False?

Produces motivational states that modulate physiological-behavioral responses ensuring survival and reproduction.

Complementary pathway to networks for learning about dangerous stimuli (fear).

A

Both are True!

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23
Q

____?____: Stimulus interpreted as intrinsically positive – something to be approached

A

Reward

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24
Q

Drug-induced pleasurable states are strong motivators of ____ drug use.

A

initial

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25
Q

____?____ : Increases probability that behaviors paired with it will be repeated.

A

Reinforcing stimulus

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26
Q

What pathway functions as interface between limbic emotional-motivational information and extrapyramidal regulation of motor behavior.

A

Ventral Tegmental Area [VTA] → Nucleus Accumbens [NA]

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27
Q

VTA activation releases _________ onto NA neurons → pleasure perceived and identifies stimulating activity as one to be repeated .

A

Dopamine

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28
Q

VTA activation releases DA onto _________ _______ → pleasure perceived and identifies stimulating activity as one to be repeated .

A

NA neurons

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29
Q

T/F?

Drugs of abuse - act via one NT systems - a pathway that increases DA release in the nucleus accumbens?

A

FALSE!!!

Drugs of abuse - acting via MULTIPLE NT systems - share final common pathway and also increase DA release in the nucleus accumbens.

The more intense and more direct this effect on DA release  greater the addiction potential of the drug

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30
Q

What Neurotransmitter is central to pathologic learning in reward pathway?

A

Dopamine & Glutamate.

Both are involved in physiological survival & pathological learning.

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31
Q

Signals from the Pre-Frontal Cortex → Nucleus Accumbens is the __________ rewards system.

A

Reflective Reward System - PFC → NA

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32
Q

Prefrontal cortex to nucleus accumbens:

Orbitofrontal → ?

Dorsolateral → ?

Ventromedial → ?

A

Prefrontal cortex to nucleus accumbens

Orbitofrontal → regulating impulses

Dorsolateral → analysis of situation

Ventromedial → integration with emotions

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33
Q

In the Relative Risk of Addiction scale, which class of drugs is a 5?

A

5 = highest risk of addiction.

5 = stimulants (cocaine, meth)

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34
Q

In the Relative Risk of Addiction scale, which class of drugs is a 4?

A

4 = high addiction risk

4= Nicotine, Opiates,

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35
Q

Which mechanism of drug action is associated with the greatest risk for development of addictive behaviors?

A

Increased release of Dopamine

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36
Q

Withdrawal effects more severe for drugs with ____?____ half-lives

A

short

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37
Q

What is the DA hypothesis of Schizophrenia?

A

overactivity of brain dopaminergic pathways (especially mesolimbic pathway)

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38
Q

In general, what is the MOA for most antipsychotic drugs?

A

CNS dopamine receptor blockers

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39
Q

___________ pathway: integration of sensory input and motor responses with affective or emotional data

A

Mesolimbic pathway: integration of sensory input and motor responses with affective or emotional data
□ Hyperactivity → Positive symptoms
□ Antipsychotic agents (via D2 block) are most effective in reducing positive symptoms (delusions, hallucinations, disordered cognition).

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40
Q

___________ pathway: DLPFC and VMPFC involved in communication and social abilities

A

Mesocortical pathway: DLPFC and VMPFC involved in communication and social abilities.
□ Hypoactivity due to cell loss in PFC → negative symptoms (poverty of speech, anhedonia, lack of motivation, social isolation).

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41
Q

__________ pathway: dopaminergic tract (substantia nigra → striatum)

A

Nigrostriatal pathway: dopaminergic tract (substantia nigra → striatum)

□ Plays central role in planned and coordinated movement.

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42
Q

_________________ pathway: hypothalamic neuronal release of DA in pituitary → inhibit prolactin release

A

Tuberoinfundibular pathway: hypothalamic neuronal release of DA in pituitary → inhibit prolactin release.

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43
Q

Activation of 5HT-2A receptors leads to _________

A

hallucinantory effects

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44
Q

Where are 5HT2A-receptors located?

A

Glutamate pyramidal neurons in cortical regions

&

Dopamine nerve terminal in striatum

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45
Q

Activation of 5HT2A receptors on _______ neurons in the on the Pre-Frontal Cortex → decrease DA → NEGATIVE SX.

A

Dopamine;

Blockage of these receptors by ATYPICAL agents results in increased DA release, and alleviation of negative symptoms of schizophrenia

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46
Q

Activation of 5HT2A receptors on Dopamine neurons in the on the Pre-Frontal Cortex → ________ DA release → NEGATIVE SX.

A

decrease;

Blockage of these receptors by ATYPICAL agents results in increased DA release, and alleviation of negative symptoms of schizophrenia

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47
Q

Activation of 5HT2A receptors on Dopamine neurons in the on the Pre-Frontal Cortex → decrease DA release→ _______ SX.

A

NEGATIVE Sx;

Blockage of these receptors by ATYPICAL agents results in increased DA release, and alleviation of negative symptoms of schizophrenia

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48
Q

Blocking 5HT2A receptors on DA neurons in the PFC by _______ agents results in increase DA release and alleviation of negative Sx of Schizophrenia.

A

Atypical

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49
Q

Activation of 5HT2A receptors on ___________________ in PFC → stimulation of DA neurons in VTA → increase DA release in mesolimbic pathway → POSITIVE Sx.

A

glutamate pyramidal cells

50
Q

Activation of 5HT2A receptors on glutamate pyramidal cells in PFC → ______________________ → increase DA release in mesolimbic pathway → POSITIVE Sx.

A

stimulation of DA neurons in VTA

51
Q

Activation of 5HT2A receptors on glutamate pyramidal cells in PFC → stimulation of DA neurons in VTA → increase DA release in ________ pathway → POSITIVE Sx.

A

mesolimbic

52
Q

Activation of 5HT2A receptors on glutamate pyramidal cells in PFC → stimulation of DA neurons in VTA → increase DA release in mesolimbic pathway → _________ Sx.

A

POSITIVE

53
Q

Glutamate Neuronal Systems:

Hypofunction of __________________ in PFC → diminished inhibitory influences on mesolimbic and mesocoritical DA pathways → POSITIVE and NEGATIVE Sx.

A

NMDA receptor on GABAergic interneurons

54
Q

Glutamate Neuronal Systems:

Hypofunction of NMDA receptor on GABAergic interneurons in PFC → _______________ on mesolimbic and mesocoritical DA pathways → POSITIVE and NEGATIVE Sx.

A

diminished inhibitory influences

55
Q

Glutamate Neuronal Systems:

Hypofunction of NMDA receptor on GABAergic interneurons in PFC → diminished inhibitory influences on _________________ pathways → POSITIVE and NEGATIVE Sx.

A

mesolimbic and mesocoritical Dopamine

56
Q

Glutamate Neuronal Systems:

Hypofunction of NMDA receptors on GABAergic interneurons in PFC → diminished inhibitory influences on mesolimbic and mesocortical dopamine pathways → ?

A

Both positive and negative symptoms

57
Q

What is the brain glutamate pathway also called?

A

Cortical-Brainstem VTA:

Increased cortical output due to loss of cortical GABA inhibition→ increase mesolimbic DA release → Positive symptoms.

Increased cortical output due to loss of cortical NMDA-glu neurons→ loss of cortical GABA inhibition → increased activity of cortical glutamate neurons → decreased mesocortical DA release → Negative symptoms

58
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to _____________ → INCREASE mesolimbic DA releases → POSITIVE Sx.

A

loss of cortical GABA inhibition

59
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to loss of cortical GABA inhibition → _________ mesolimbic DA releases → POSITIVE Sx.

A

INCREASE

60
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to loss of cortical GABA inhibition → INCREASE mesolimbic DA releases → ____________ Sx.

A

POSITIVE

61
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to _______________ → loss of cortical GABA inhibition → increase activity of cortical glutamate neurons → DECREASE mesocortical DA release→ NEGATIVE Sx.

A

loss of cortical NMDA-Glu neurons

62
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to loss of cortical NMDA-Glu neurons → loss of cortical GABA inhibition → ___________________________ → DECREASE mesocortical DA release→ NEGATIVE Sx.

A

increase activity of cortical glutamate neurons

63
Q

Brain Glutamate Pathways: Cortical-Brainstem VTA:

Increased cortical output due to loss of cortical NMDA-Glu neurons → loss of cortical GABA inhibition → increase activity of cortical glutamate neurons → _______________ DA release→ NEGATIVE Sx.

A

DECREASE mesocortical

64
Q

wrt. to DA and 5HT2 receptors, what is the dopamine theory of schizophrenia?

A

Blockage of D2 receptors explains most significant pharmacologic effects of anti-psychotic agents BUT efficacy found in anti-psychotic agents that block 5HT2 receptors without blockage of D2 receptors.

65
Q

Typical (1st Gen.) anti-psychotic drugs = __1__ D2/5HT2A ratio.

Atypical (2nd Gen.) anti-psychotic drugs = ___2___ D2/5HT2A ratio.

A
  1. Typical = HIGH DA/Serotonin ratio

2. Atypical (2nd gen) = LOW Dopamine/5HT2A ratio.

66
Q

Which type of Anti-psychotic drugs has good efficact against positive Sx but a high incidence of extrapyramidal toxicity?

A

Typicals (1st gen.)

67
Q

Which type of Anti-psychotic drugs are better for Pt. with negative Sx and cognition deficits & helps to decrease risk of EPSE Sx.

A

Atypical (2nd gen)

68
Q

Name Atypical (2nd gen) anti-psychotics). (4)

A
  • Aripiprazole
  • Clozapine
  • Olanzapine
  • Quetiapine
69
Q

Name some Typical Anti-Psychotic agents. (2)

A
  • Chlorpromazine

- Haloperidol

70
Q

List Antimanic agents. (3)

A
  • Lithium
  • Valproic Acid
  • Carbamazepine
71
Q

List the classes of antidepressants we learned. (8)

A
  • TCADs
  • Trazodone
  • SSRIs
  • Mirtazapine
  • Bupropion
  • MAOi (Phenelzine)
  • Venlafaxine
  • Electroconvulsive therapy
72
Q

In the Monoamine therory of depression, all effective antidepressants drugs what what properties?

A

Enhancing NE-5HT-DA availability in synapse. (low 5HT can induce depression)

This theory does not explain the whole etiology of depression. shift in NT and receptors fucks with downstream signalling.

73
Q

What is the neurodegenerative hypothesis of depression?

A

Depression associated with neuronal loos in PFC and Hippocampus and anti-depressant Tx act by inhibition this loss by stimulating neurogenesis.

74
Q

Neurodegenerative hypothesis of depression:

_____________ pathway: stress-induced activation of Hypothalamus-Pituitary-Adrenal axis switches on gene expression that promotes neuronal apoptosis and neuronal cell death due to excitotoxic actions of glutamate via NMDA receptors.

A

Pro Depressive

75
Q

Neurodegenerative hypothesis of depression:

_____________ pathways: monoamines (NE and 5-HT) act on G-protein coupled receptors and brain-derived neurotrophic factor (BDNF) act on kinase-linked receptor to switch on genes that promote neurogenesis and protect against apoptosis

A

Antidepressive

76
Q

What are the two sedative-hypontic agents?

A

Benzos and Barbiturates;

  • Graded dose-dependent CNS depressant effects.
  • Augment GABA inhibition and/or inhibit glutamate excitation.
  • Sedative drugs → decrease activity, moderate excitement, and calm recipient.
  • Hypnotic drugs → produce drowsiness, facilitate onset + maintenance of sleep.
77
Q

MOA of:

Benzos?

Barbiturates?

A

Benzos bind alpha or gamma subunits and facillitate channel opening, but do NOT directly initiate Cl- current.

Barbiturates PROLONGS GABA effects. Enchnaces Cl- channel opening ONLY in presence of GABA

78
Q

What is the MOA of Z-drugs?

A

interact with Benzos binding sites as agonist.

Only binds to A1 subunit of GABA channels.

79
Q

What drugs reverses the effects of Benzos?

A

Flumazenil; antagonist of benzo binding site.

Not effective in Barbiturate or Ethanol toxicity.

80
Q

T/F?

Flumazenil can also be used in the Tx of Barbiturate overdose.

A

FALSE!!

Flumazenil is for benzos only!!!

81
Q

What drug class has an MOA that is a 5HT1A partial Agonist?

A

Buspirone

82
Q

How do you Tx an Opiod OD?

A

Naloxone (Narcan); opiod Antagonist, short acting.

Make sure to est. airway and stabilize CV

83
Q

T/F?

You can die from Opioid Withdraw.

A

FALSE

84
Q

3 ways (drugs) to Tx opioid withdraw?

A

Clonidine → alleviate SNS overactivity symptoms (nausea, vomiting, cramps, sweating tachycardia, increased BP) in acute withdrawal.

Methadone → substitute opioid, long DOA.

Buprenorphine → partial mu agonist

85
Q

List common/major OPioid drugs:

A
  • heroin
  • morphone
  • oxycodone
  • methadone
  • fentanyl
  • hydrocodone
  • codeine
  • loperamide (anti-diarrhea)
86
Q

What are the major drug (drug classes) in CNS stimulants?

A
  • amphetamine
  • methamphetamine
  • cocaine

*MDMA = hallucinogen + CNS depressant

87
Q

In general, what is the MOA of CNS stimulants?

A

interacts with catecholamines NTs (DA) to cause release or block reuptake of catecholamines.

88
Q

Which of the following antipsychotics is considered to be the most potent and thus have the highest risk of extrapyramidal symptoms?

Thioridazine
Chlorpromazine
Haloperidol
Clozapine
Olanzapine
A

Haloperidol

89
Q

Which of the following antipsychotics has been shown to be a partial agonist at the dopamine D2 receptor?

Thioridazine
Risperidone
Haloperidol
Aripiprazole
Quetiapine
A

Aripiprazole

90
Q

What are the major classes of CNS DEPRESSANTS?

A
  • alcohol
  • benzos
  • barbiturates
91
Q

What is the MOA of ethanol?

A

GABA-A ch. enhancement + NMDA receptor blocker → disinhibition & excitation.

92
Q

In terms of CNS depressants drugs, which drug class most rapidly develops tolerance:

A

Most rapid to dev. tolerance > slowest:

Barbiturates > ethanol > Benzos

93
Q

What are the major classes of Hallucinogens?

A
  • Indoleamines: LSD, DMT, mushrooms (psilocybin)

- Phenylethylamines: Mescaline, MDMA, MDA, DMA

94
Q

What is the MOA of Hallucinogens in the CNS?

A

agonist at the 5HT2 postsynaptic serotonin receptor

Phenylethnlamines also induce dopamine release with effects on DA receptors.
MDMA: SERT reverse transporter leads to 5HT release.

95
Q

What is the MOA of weed in the CNS?

A

CB1 agonist

96
Q

What are the main classes of dissociative Anesthetics?

A
  • phencyclidine

- Ketamine

97
Q

Describe the metabolism of ethanol?

A

a. 2-10% out unchanged in air and urine
b. 1st pass metabolism: gastric mucosa

c. 90-98% in liver: ethanol → acetaldehyde → acetic acid.
~ AHD & CYP2E1

98
Q

Where is ADH at?

A

liver cytosol and mitochondria

99
Q

what order kinetics is the metabolism of ethanol?

A

Zero-Order! happens at a constant rate.

100
Q

What is the general MOA of Ethanol?

A

inhibits Glutamate binding to NMDA receptor

101
Q

What is Antabuse (disulfiram)?

A

inhibits Aldehyde Dehydrogenase → 5-10x increase in acetaldehyde → N/V, resp & CVD collapse, convulsions.

102
Q

What are the effects of Etanhol on;

  • CNS
  • Liver
  • Kidney
  • GI Tract
  • CV
  • Fetus
A
  • CNS: Sedative-Hypnotic: CNS depressant effect (similar to barbiturates)
    Increase GABA + decrease glutamate
    Anxiolysis
    Anticonvulsant: BUT hyperexcitability upon withdrawal
    May precipitate convulsions
    Analgesic effects, sleep effects
    Emetic effect → stimulate CTZ → induce vomiting
  • Liver: damage due to increased NADH + direct toxicity
    Fatty liver
    Alcoholic hepatitis → jaundice, ascites, vomiting, anorexia
    Alcoholic cirrhosis → jaundice, portal HTN, esophageal varices
  • Kidney: diuresis (decreased ADH secretion, increased fluid intake)
  • GI tract: Esophagitis, ulcers, gastritis (due to inflammatory effect of alcohol) → epigastric pain, vomiting, hematemesis
    Pancreatitis (due to secretory effect of alcohol) → weight loss, blood loss, abdominal pain, shock
  • Cardiovascular:
    Vasodilation, heart disease, HTN
    Can be CARDIOPROTECTIVE due to decreased platelet aggregation and increased HDL levels
  • Fetus: Fetal Alcohol Syndrome
    Prenatal or postnatal growth retardation and altered morphogenesis (especially facial dysmorphology)
    Small head, epicanthal folds, low nasal bridge, small eye openings, short nose, thin upper lip, flat midface, smooth philtrum, underdeveloped jaw.
103
Q

How do you Tx Ethanol withdraw?

A
  • Benzos: actions at GABA receptors prevents emergence of CNS hyperexcitability following withdraw.
  • Clonidine: effective signs of autonomic hyperactivity
104
Q

There is cross-tolerance in ethanol use with what other drug classes?

A

Sedative-hypnotic and general anesthetics

105
Q

With ethanol use, there can be additive effects with all _____1_____, promotion of GI bleeding with taken with ____2____, and increase risk of hepatotoxicity with _____3_____.

A
  1. CNS depressants
  2. aspirin
  3. acetaminophen
106
Q

Using ethanol with what other drugs leans to disulfiram-like Sx?

A

Metronidaziole (ABX)

107
Q

Name 2 drugs that are mood stabilizers.

A

Lithium and Valproate

108
Q

What is the MOA of Lithium?

A

enhance 5HT action and/or diminish NE and DA effects.

Blocks PIP recycling (GPCR, IP3 and DAG)

109
Q

nitrous oxide, halothane, and other halogenated “fluranes” are examples of what class of anesthetic?

A

Inhaled anesthetics

110
Q

barbiturates, benzodiazepines, ketamine, opioids, and propofol are examples of what class of anesthetic?

A

Intravenous anesthetics

111
Q

procaine, lidocaine, bupivacaine, tetracaine, mepivacaine, and cocaine are examples of what class of anesthetic?

A

Local anesthetics`

112
Q

Which Intravenous anesthetics is notable for its rapid redistribution into skeletal muscle and fat?

A

Thiopental

Thiopental is a barbiturate used for induction of general anesthesia and short surgical procedures. In addition to potentiating GABA-A,

it decreases cerebral blood flow and intracranial pressure.

Thiopental is highly lipid soluble, causing a rapid onset. Its actions are short-lived due to redistribution into skeletal muscle and fat.

113
Q

What drug is a barbiturate used for induction of general anesthesia and short surgical procedures. In addition to potentiating GABA-A,

A

Thiopental

114
Q

What is a notable side effect of bupivacaine?

A

Severe cardiovascular toxicity can occur with bupivacaine.

115
Q

What is the proposed MOA of inhaled anesthetics?

A

There are many theories explaining the mechanism of action of inhaled anesthetics, including action on cortical centers and inhibition of excitatory transmission in the spinal cord, but the exact mechanism of action is unknown.

116
Q

____________ is a NMDA-receptor antagonist that is categorized as a dissociative anesthetic. It is an analog of phencyclidine (PCP).

A

Ketamine

117
Q

____________ can prolong QT interval (progressing to Torsades de pointes and ventricular fibrillation). This is a Black Box warning.

A

Droperidol

118
Q

What are the 4 agents that can be used for the induction of general anesthesia?

A

Propofol,
Etomidate,
Thiopental
Ketamine

119
Q

The rates of onset and recovery of inhaled anesthestics is dependent on the __________ ratio.

A

Blood:Gas ratio.

High value of blood:gas = slow onset and slow recovery

120
Q

anesthetics with low blood-gas ratios have a what rate of onset and recovery.

A

FAST!

121
Q

What is Valproic acid is also indicated for?

A

myoclonic seizures, bipolar disorder, and migraine prophylaxis.

NS_BTRAN (21 decks)

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