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Mental Health > Nicotine And Psychostimulant Abuse > Flashcards

Nicotine And Psychostimulant Abuse Flashcards

1
Q

psychomotor stimulants

A

MOA: all increase activity of the CNS

- leads to excitement, euphoria, increase motor activity and feelings fatigue

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2
Q

Therapeutic indications for stimulants

A

ADHD

Narcolepsy

Anorexiant (suppress hunger)

OSA

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3
Q

Nicotine MOA

A

Agonists at the neuronal nicotinic receptors

  • there are 16 in the autonomic ganglion, therefore a lot of ADRs and effects occur here
  • there is 1 nicotinic receptor type in the neuromuscular junction*
  • concentrations >200nM (normal smoking of cigarettes), nicotine has higher affinity at neuronal nicotinic receptors*
  • more affinity for Nm Receptors in higher concentrations

has dose dependent stimulation (low doses) or inhibition(high doses) effects

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4
Q

Symptoms of higher vs low doses of nicotine

A

Low doses = euphoria, arousal, relaxation

  • activates within normal limits
  • activation/stimulation of nicotinic receptors

High doses = tremors, convulsions, arrhythmias

  • activates well outside normal limits
  • down-regulation and desensitization of nicotinic receptors
  • adrenal medulla effects:
  • small doses = releases catecholamines (NE/E)
  • large doses = disables release due to inhibitory stimulation of splanchnic nerves*
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5
Q

Other than CNS/PNS/medulla and NMJ, where else are nicotinic receptors seen?

A

Mechanoreceptors in:

  • skin
  • mesentery
  • tongue
  • lung
  • stomach

Chemoreceptors in the carotid body

Thermal receptors in the skin/tongue

Pain receptors

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6
Q

Respiratory depression

A

Occurs in overdose of nicotine by paralysis of the CNS and the NMJs of the diaphragm and intercostal muscles

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7
Q

Cardiac effects of nicotine

A

In high doses = Vasoconstriction, tachycardia, HTN

effects are largely mediated by sympathetics

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8
Q

GI tract and urinary system effects of nicotine

A

Nausea/vomiting

Diarrhea

Bladder voiding

effects are predominantly parasympathetic

also increase emesis due to stimulation of vagus and area postrema in the medulla oblongata

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9
Q

Acute nicotine toxicity

A

Fatal dose = 40-50 mg

  • roughly two- three cigarettes if digested
  • 40-50 cigarettes if smoked
OD effects: 
- CNS = convulsions/coma/respiratory arrest (tx = diazepam) 
- Respiratory paralysis 
(tx = mechanical ventilation) 
- HTN/cardiac arrhythmias 
(Tx = atropine and wait out)

needs to survive first 4 hrs and have oxygen in brain at all times. If this occurs, near 100% chance to survive

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10
Q

Pharmacokinetics of nicotine

A

Metabolizes via CYP2D6 and glucuronidation

Induces CYP1A2 and CYP2E1
- metabolizes caffeine and alcohol easier*

Ways to use tobacco in order of how fast they reach peak concentration in blood:

1) cigarettes (5 min and 15 mg)
- metabolize very quickly though
2) snuff (10 minutes and 15 mg)
- metabolizes slower
3) chewing tobacco (60 minutes and 15 mg)
- metabolizes slower
4) nicotine gum ( 30 minutes and 7 mg)
- metabolizes slowest

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11
Q

What kind of learning theory is used in smoking?

A

Positive reinforcement that is reinforced over 200 times a day on average
- makes extinction very challenging

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12
Q

Nicotine withdrawal

A

low blood levels of nicotine = cravings to smoke

Symptoms

  • anxiety
  • dysphoria/ depressed mood
  • difficulty in concentration
  • restlessness
  • tachycardia
  • increased sedation and weight gain
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13
Q

First-line therapies for nicotine cessation

A

Nicotine replacement therapies
- gum, inhaler, lozenge, nasal spray, patch

Sustained release via bupropion patch
- antagonist of NAChRs

Varenicline (partial agonist and full agonist of nicotine receptors) use

  • depends on receptors it hits, and can cause increase suicidal thoughts and vivid nightmares
  • also increases cardiovascular risks

Counseling and motivational therapy

not first line but rimonabant (inverse agonist of CB1 receptors) is experimental for smoking cessation

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14
Q

Cocaine MOA

A

Blocks DAT and NET reuptake receptors

  • increases dopamine in reward circuitry
  • increase NE in cortiolimbic system
  • *also indirectly increases 5-HT levels as well
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15
Q

Effects of cocaine

A

Low doses:

  • increased arousal/attention
  • increased self-confidence
  • euphoria (30 min only)
  • dose dependent tachycardia and BP
  • decreases fatigue

High doses:

  • seizures
  • cardiovascular complications
  • increased risk of self-induced trauma
  • risky sexual behavior

Chronic use:

  • anxiety/depression/paranoia
  • irritability and increased aggression
  • psychosis
  • involuntary motor activity
  • stereotyped behavior (moves predictably based on situation)
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16
Q

Acute cocaine toxicity symptoms

A

Psychiatric complaints
- paranoia and delusions/psychosis

Seizures

Hyperthermia (#1 cause of death)

Chest, heart and pulmonary pains

Treatment =

  • benzos (calms patients and treate hyperthermia)
  • symptomatic treatments
  • group and individual psychotherapy
17
Q

Cocaine metabolism

A

Hydrolysis by tissue esterases
- results in benzoylecgonine metabolite (which can be tested for in urine)

Cocaine and ethonal abuse together

  • cocaine is metabolized to cocaethylene (essentially another dose of cocaine)
  • OD is very likely

Ways to take cocaine:
smoked
Snorted
Ingested

18
Q

Cocaine withdrawal symptoms

A

Dysphoria

Depression/sleepiness/fatigue

Cravings

Bradycardia

symptoms gradually go away over 1-3 weeks and are usually mild

challenge is to prevent resumption of binge cocaine use. This can lead to increased risks of OD

19
Q

Amphetamines MOA

A

Both inhibits VMAT receptor and reverses the transport of DAT and NET receptors
- DAT and NET-receptors now efflux dopamine and NE out into presynaptic clef

This leads to mass elevation of dopamine NE and mass depletion after about 24 hrs
- toxic and withdrawal effects are worse as a result

20
Q

Physiological effects of amphetamines

A

Simulates entire cerebrospinal axis, cortex, brainstem, medulla
- this is why its used in performance enhancing

Symptoms

  • increased alertness
  • decreased fatigue and appetite
  • insomnia
  • elevates BP and Bradycardia
  • urine retention
  • tachypnea

High doses
- cardiac arrthymias

21
Q

Acute toxicity of amphetamines

A

Is more dangerous than cocaine

Symptoms

  • Euphoria
  • hyperthermia (fatal if left unchecked)
  • insomnia
  • aggression and paranoia
  • tachycardia HTN and strokes
  • tremors
  • seizures/ convulsions (fatal if left unchecked)

Treatments:

  • benzos (seizures and hyperthermia)
  • symptomatic treatment
22
Q

Amphetamine withdrawal

A

Symptoms:

  • depression
  • AMS
  • sleep disturbances
  • extreme for fatigue

Treatment:

  • supportive only and symptomatic
  • very rarely fatal though*

Note: CANT use TCAs for depression since it increases CV event risks (which amphetamines do by themselves)

23
Q

Amphetamine therapeutic indications

A

ADHD

Narcolepsy

Off-label uses: (low doses ONLY)

  • AIDS/MS/dementia
  • fibromyalgia
  • dysthymia
  • obesity
  • depression
24
Q

What class of antidepressants are contraindicated for depression seen in amphetamine withdrawal?

A

TCA’s

- high risk of CV events

Mental Health (46 decks)

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