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Psychopharmacology > Exam 2: Psychostimulants > Flashcards

Exam 2: Psychostimulants Flashcards

1
Q

What is a monoamine?

A

Catecholamines AND indoleamines

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2
Q

What is a catecholamine?

A

Dopamine, Norepinephrine, Epinephrine

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3
Q

Catecholamine synthesis enzymes

A

TH (+OH)
AADC (-COOH)
DBH (-H –> - OH)
PNTM (add -CH3)

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4
Q

How and why are catecholamines stored in vesicles?

A

VMAT2 transporter
ion trapping- proton pump acidifies vesicles ionizing catecholamines,
which are WEAK BASES. low pH in vesicle = ion trapping

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5
Q

how does reserpine affect vesicular storage of catecholamines

A

Reserpine= inhibits vesicularization of monoamines.

Frees monoamines degraded by enzyme (MAO). Depletes monoamines

Induces sedation, low bp

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6
Q

What are the subtypes of noradrenergic receptors?

A

1) alpha 1
2) alpha 2
3) Beta 1

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7
Q

What role do receptor subtypes (noradrenergic) play in mediating effects of catecholamines (e.i. autonomic activity)

A

1) alpha 1- increase phosphoinositide, muscle contraction, activating
2) alpha 2- inhibiting, low cAMP
3) beta 1- activating, increase cAMP

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8
Q

What is the difference between reuptake transporters and autoreceptors?

A

Reuptake= brings NE and DA back into the cell for degradation/reuptake into vesicles

Autoreceptor: binds to cause decrease in vesicular release

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9
Q

Norepinephrine/Epinephrine degradation

A

COMT and MAO, doesn’t matter the order, leads o Vanillylmadnelic Acid (VMA)

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10
Q

Norepinehprine: alpha 2 vs. beta 1

A

Beta 1: Gs, increase cAMP

alpha 2: Gi, low cAMP

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11
Q

NE and heart rate stuff

A

Beta 1 vs. Ach’s M2 to increase heart rate with adenyl cyclase

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12
Q

Autonomic control of bladder

A

Beta 2 (NE)- relax bladder
M3 - contracts bladder
Alpha 1- contracts sphincter
M1- relax sphincter

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13
Q

Autoreceptors

A

D2 - DOPAMINE
Alpha 2= NE

1) Bind DA/NE
2) Close Ca2+ channels
3) Reduce vesicular transmitter release

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14
Q

Free base vs. Hydrochloride cocaine

A

Free base: unionized, LS, Base, vaporizes.

Hydrochloride: Ionized, WS, Salt, purified, degraded before vape

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15
Q

Cocaine is an (acid/base)

A

Base

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16
Q

Cocaine HCL (stable salt)–> Free base or crack?

A

Free base: mix with ammonia, extra with ether, then evaporate

Crack: Mix with baking soda, heat, filter and wash

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17
Q

Cocaine HCL (stable salt)–> Free base or crack?

A

Free base: mix with ammonia, extra with ether, then evaporate

Crack: Mix with baking soda, heat, filter and wash

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18
Q

Kinetics of cocaine? (- admin, other card)

2) Absorption
3) Distribute
4) Metabolize
5) Excretion

A

2) Weak base, increase absorption by increase pH

3) Cross BBB
4) via liver, 1st order
metabolites: benzoylecgonine & cocaethylene

5) after ~4 hr. metabolites may persist up to 3-5 days.

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19
Q

What is the primary pharmacodynamic mechanism by which cocaine is proposed to
affect neuronal activity? (Binding/action)

A

Blocks REUPTAKE of DAT

Blocks UPTAKE of SERT/NET

Blocks local sodium channels

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20
Q

What evidence implicates dopamine in cocaine craving as experienced by heavy users?

A

Cocaine blocks DA reuptake in mesolimbic pathway.

Cocaine rats: want paired compartment, unless DAT KO.

Also, increased dendrite spines in NA

21
Q

Mechanisms of toxic/lethal effects of cocaine admin?

A

increases heart rate/bp by decreasing NE reuptake

Also constricts coronary artery, reduces oxygen to heart.

22
Q

What is the only approved therapeutic use of cocaine?

A

Local anesthetic, block Na+ channels for surgeries and reduce blood flow to site

(e.i. procaine and lidocaine)

23
Q

What are the different chemical forms of amphetamine? Parent compound?

A

??

24
Q

Desired effects associated with amphetamine/cocaine admin?

A

Arousal, alert, wake, energy, concentrate, no distraction, confidence, euphoria, physical performance

25
Q

How does renal pH affect 1/2 life of amphetamine?

A

??

26
Q

Amphetamines and vesicular storage: primary mechanism

A

Enters vesicle by VMAT2

Increases pH in vesicle

reduces ionization/ion trapping, so molecules leak out

27
Q

Mechanisms behind toxic/lethal effects of amphetamine admin?

A

increases heart rate/bp by increasing NE release

28
Q

What are approved/off label therapeutic applications of amphetamine?

A

FDA: narcolepsy/ADHD

Off-Label: Obesity/Depression

29
Q

How are stimulant/non-stimulants proposed to manage ADHD symptoms?

A

Improve attention/focus, no distraction, etc.

Increase DA/NE from VTA/LC to PFC regions for inhibition of motor, basal ganglia, and cerebellum.

30
Q

What are some important features/consequences of psychostimlant tolerance?

A

Slow tolerance in ADHD/narcolepsy

Tolerance to therapeutic effects fast for other disorders.

Reverse tolerance possible for some effects (brain seizures).

31
Q

Psychostimulant dependence.

A

Withdrawal: fatigue, sleep, depression, hunger

Positive reinforcement: craving, anhedonia

32
Q

Effect of drugs of abuse on synaptic dopamine levels: 11C-raclopride

A

1) baseline density
2) density after drug abuse
3) (1-2), decrease in 11C-R binding=

A) Decrease in D2/D3 receptors
B) increase in synaptic dopamine

33
Q

Cocaine adminstration

A

Internasal: onset min, duration 60 min
Inhalation: onset sec, duration 15 min

34
Q

Adminstration: Coco Leaves

A

Buccal

35
Q

Admin: Cocaine HCL or Speed

A

intranasal/intravenous

36
Q

Admine: Cocaine base or Ice

A

inhalation

37
Q

What amphetamine is racemic and less potent?

A

dextrolevoamphetamine (Benzedrine)

38
Q

What amphetamine is an active isomer?

A

dextroamphetamine (Dexedrine)

39
Q

What amphetamine is more potent in CNS?

A

dextromethamphetamine (Desoxyn)

40
Q

Amphetamine adminstration (uppers)

A

Uppers: Oral

41
Q

Amphetamine onset and duration of action: Oral vs. inhalation

A

Oral: Onset in 30 Minutes, Variable Duration

– Inhalation: Onset in Seconds, Duration of 15 Minute

42
Q

Amphetamine elimination

A

Half-life between 6-36 hours depending on renal pH

Metabolites persist up to 3-5 days after last
administration in urine and saliva, 90 days in hair

Detection is affected by amount and duration of
use, route of administration, metabolism, hydration,
body size, percent body fat, age

43
Q

Cocaine is ___ than amphetamine

A

larger

44
Q

Amphetamine stimulates what?

A 
Release DA/NE 
1) enter by reuptake
2) leaky vesicles (primary)
3) inhibits MAO
4) High Concentration of
 DA and NE in Cytoplasm
 Reverses the Transport
 of DA and NE into Synapse
45
Q

sympathomimic effects

A

dilation airway/pupils
inhibit digestions
urinary retention
increase body temp

46
Q

Toxic effects

A 
Headache
• Dizziness
• Confusion
• Agitation
• Fatigue
• Insomnia
• Seizures
• Cardiac Arrest
• Stimulant Psychosis
• Dental Disease (Amphetamine)
• Neurotoxicity (Amphetamine)
47
Q

stimulant psychosis

A

paranoia, hallucination, delusion, stereotypy

48
Q

reverse tolerance for amphetamines can occur for

A

brain seizures

49
Q

cocaine vs. amphetamine in mesolimbic pathway

A

cocaine- blocks DA reuptake

amphetamine- stimulates DA release

Psychopharmacology (16 decks)

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