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Neuro Quiz 9 > Cocaine and Stimulants > Flashcards

Cocaine and Stimulants Flashcards

1
Q

**Behavioral Stimulants

A 
Cocaine
Amphetamines
Methylphenidate (ritalin)
Pemoline (Cylert)
Phenmetrazine (preludin)
MOA- Increased levels of NE and DA
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2
Q

**Antidepressants

A

Imipramine and amitriptyline (MOA: block NE/5-HT reuptake)

Tranylcypromine (MOA: MAOi)

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3
Q

**Legal Recreational Drug

A

Caffeine (blocks adenosine receptors)

Nicotine (stimulates ACh receptors)

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4
Q

Cocaine Chemistry

A

Local anesthetic
Hydrochloride crystal or snow is inhaled (NOT suitable to be smoked because it decomposes at high temperatures)
Extracted in ether to make free base cocaine which can be smoked

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5
Q

Cocaine Routes

A

Oral: Chewing Coca Leaves (~75% lost to first pass; 25% reach the brain)
Intranasal (snorting)
Inhalation (smoking or free basing)
Intravenous (mainlining)

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6
Q

Cocaine Routes Onset

A

Oral: more than 1 hour
Intranasal: 30-60 minutes
Inhalation: Within seconds
IV: Delayed-onset about 30-60 seconds

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7
Q

**Major Metabolite of Cocaine

A

Benzoylecgonine (in urine for 3 days and much longer in chronic user)

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8
Q

3 Main Effects of Cocaine

A

Local anesthetic
Blood vessel constrictor
Psycho-stimulant (STRONG reinforcing qualities)

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9
Q

Cocaine MOA

A

Block reuptake of DA, NE and 5HT

Increases DA in the VTA and NA (psycho-stimulant effects and behavior-reinforcing properties)

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10
Q

Cocaine Psychological Changes

A 
Mood elevation
Enhanced cognition, drive states (hunger, sex, thirst)
Talkative
Suppressed appetite
Delayed Sleep
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11
Q

Cocaine Delayed Effects

A

60-90 minutes after administration: mild euphoria with anxiety followed by long-lasting anxiety (cravings)
High dose: loss of coordination, tremors and seizures

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12
Q

Cocaine Toxic Symptoms

A

Anxiety, sleep deprivation, hyper-vigilance

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13
Q

High dose, long-term use of Cocaine Symptoms

A 
Dysphoria
Paranoia
Severe depressive
Schizo
CV/Neurovascular: strokes
Fetal: difficulty in unstructured play and easily frustrated, cognitive problems and ADHD is common
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14
Q

Amphetamine was used to treat:

A

narcolepsy and then later 39 conditions like smoking, schizo, hypotension
WWII fight fatigue and enhance preformance

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15
Q

Amphetamine MOA

A

Increase in the levels of monoamine (inhibit reuptake of NE and DA10 fold and is partly degraded into ROS which increase oxidative stress and neurotoxicity

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16
Q

Low Dose Effects of Amphetamine

A

Behavioral and psychomotor stimulation
Appetite supressant effects
Agression in adults
Inhibits aggression and causes ADHD behavior in children
Increased BP followed by reflector bradycardia and bronchodilatio

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17
Q

High Dose Effects of Amphetamine

A

Aggression and paranoid delusions
Severe anorexia
Amphetamine psychosis = acute schizophrenic attack

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18
Q

Chronic Dose Effects of Amphetamine

A

Severe depletion of DA
Depletion of tyrosine hydroxylase
Less of DA receptors
Loss of responsiveness to natural reinforcers

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19
Q

Amphetamine Tolerance

A

Develops rapidly with dysphoria, sedation, and lethargy

20
Q

Caffeine Blackout in a Can

A

Energy drinks + Alcohol

  • Caffeine effects goes away faster than the alcohol, person would pass out due to the alcohol effects
  • Caffeine also covers the effects of alcohol so drink more but you don’t think you are
21
Q

Caffeine MOA

A

Regular concentration: antagonist of adenosine receptor
High concentration: Increased intracellular Ca (increased strength and duration of contractions in skeletal and cardiac muscles)
Blocks both A1 and A2alpha receptors

22
Q

A1 Receptors

A

Abundant in the brain

Decreased release of neurotransmitters which leads to decreased neuronal firing

23
Q

A2alpha Receptors

A

DA rich regions of the brain
Increased GABA release
Decreased affinity of DA

24
Q

Caffeine Halflife

A

2.5-4.5 hours but increases with decreased age

Smokers: 30-50% reduction due to CYP1A2

25
Q

Caffeine Physiological Effects

A

Bronchodilation, increased gastric acid secretion and BP, and decreased RR (peripheral)
Increased: alertness, cognitive performance and auditory vigilance (CNS)

26
Q

Caffeine Symptoms of Intoxication (>250 mg)

A 
Restlessness, nervousness, rambling
Excitement, anxiety
Flushed face
Tachycardia, arrhythmia
GI
Insomnia
Psychomotor, agitation, low seizure threshold
27
Q

Cigarette Chemicals

A

> 4000 compounds in cigarette smokes (43 known cancer-causing agents)
Nicotine is the main compound with regards to addiction

28
Q

Nictonine PK

A

Readily crosses plasma membrane
Readily absorbed through skin, lungs, mucous membrane
High first pass metabolism

29
Q

Smoking + Nicotine

A

Sharp increase leading to lots of DA release to the NA

30
Q

**Nicotine Metabolite

A

Cotinine (80%)

Excreted in the urine and has a 24 hour plasma half-life

31
Q

Nicotine + Reward System

A 
Nicotine causes DA release in the NA by binding alpha4beta2 in the VTA (post)
Nicotine binds to alpha 7 in the VTA (pre) which causes dopamine release in the NA
Desensitize alpha4beta2 (post) on GABA interneurons in the VTA
32
Q

What does GABA do?

A

Reduced GABA disinhibits mesolimbic dopamine neurons and thus enhances dopamine release in NA

33
Q

Nicotine + CNS Stimulation

A

Activates brain nicotinic ACh receptors

34
Q

Low Dose Nicotine + CNS Stimulation

A 
	Increased alertness and cognitive functioning
	Feelings of pleasure and relaxation
	Reduced depression, anxiety and hunger
	Stimulated respiration
	Induced vomiting
35
Q

High Dose Nicotine + CNS Stimulation

A

Induces tremors and convulsions followed by depression and death

36
Q

Nicotine + Cardiovascular

A

Increased HR, cardiac output, oxygen consumption and BP

37
Q

Nicotine + GI Tract

A

Increased bowl activity and tone

Causes N/V/D (through PS/S)

38
Q

Nicotine + Exocrine Glands

A

Initial stimulation and then inhibition

39
Q

Nicotine Patch and Gum

A

Nicotine levels increase sharply to pleasurable reinforcing levels
Between puffs, this level falls
As nicotine levels fall, receptors begin to re-sensitize and cause craving

40
Q

Nicotinic Partial Agonists

A

Varenicline

41
Q

Varenicline MOA

A

Stabilize nicotinic receptors in an intermediate state

42
Q

Smoking while on Varenicline

A

If they smoke while on NPA, it will still compete with nicotine for the receptor and cause a drop in the DA which blocks the euphoria and brings DA back down

43
Q

Transdermal Delivery of nicotine

A

Steady level of nicotine which can desensitize some receptors and relieve some craving
Does NOT induce euphoria NOR does is it sufficient to eliminate all cravings

44
Q

Buproprion MOA

A

Increased amounts of DA through the synaptic cleft, it will only be enough to cover the craving not causing euphoria

45
Q

ACh and Nicotine

A

ACh is a full agonist of alpha4beta2 nicotinic receptors but it is short acting due to AChE (short pulses of DA release)
Nictonine is a full agonists of alpha4beta2 nicotinic receptor (prolong opening of these channels until they desensitize - prolong burst of DA release)

46
Q

NPA (Nicotinic Partial Agonists) MOA

A

Causes sustained small increases in frequency of opening of alpha4beta2 nicotinic receptors in the VTA leading to small sustained increases in DA release

47
Q

NPA vs Bupropion

A

NPA is more effective than bupropion

Neuro Quiz 9 (4 decks)

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