Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mental Health/Psychiatry > Other Drugs of Abuse: Nicotine and Psychostimulants > Flashcards

Other Drugs of Abuse: Nicotine and Psychostimulants Flashcards

1
Q

Stimulants (AKA psychomotor stimulants) ______ activity of the CNS, causing the following symptoms: (4)

A

increase

  1. Excitement
  2. Euphoria
  3. Increased motor activity
  4. Decrease feelings of fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Therapeutic indications for some stimulants (4)

A
  1. ADHD
  2. Narcolepsy
  3. Anorexiant (obesity)
  4. Obstruction/sleep apnea (respiratory stimulant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Nicotine is the active component in ______. It is a ______ and ______ ______ stimulant.

A

Tobacco; CNS; autonomic ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

At concentrations achieved during recreational tobacco use, nicotine has ______ affinity for ______.

A

higher; NnAChR (Neuronal nicotinic acetylcholinergic receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nicotine exerts a combination of ______ and ______ effects. Nicotine can ______, then ______ neuronal nicotinic receptors.

A

Stimulatory; inhibitory; stimulate; desensitize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

At low doses in the CNS, nicotine stimulates: (4)

A
  1. Euphoria
  2. Arousal
  3. Relaxation
  4. Improves attention, learning, and problem solving
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

At high doses in the CNS, nicotine stimulates: (4)

A
  1. Tremors
  2. Convulsions
  3. Arrhythmias
  4. Respiratory paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Nicotine has a biphasic effect of transient stimulation and depression that occurs with all autonomic ganglia (esp. at high doses). Small doses ______ ganglion cells; large doses ______ ganglionic transmission.

A

Stimulate; block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In the adrenal medulla, small doses of nicotine ______ the discharge of ______. Large doses ______ ______ due to splanchnic nerve ______.

A

Discharge; catecholamines; prevent release; stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In the neuromuscular junction, ______ phase by nicotine is rapidly obscured by paralysis (toxic doses)

A

Stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nicotine also has affinity for: (4)

A
  1. Mechanoreceptors in the skin, mesentery, tongue, lung, and stomach
  2. Chemoreceptors in the carotid body
  3. Thermal receptors of the skin and tongue
  4. Pain receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Physiological effects of nicotine (3)

A
  1. Respiratory depression - central paralysis and paralysis of diaphragm/intercostal muscles
  2. Largely sympathomimetic: vasoconstriction, tachycardia, hypertension
  3. Parasympathomimetic in the GI tract and urinary system: nausea/vomiting (stimulation of chemoreceptors in the area postrema, vagal and spinal afferents), increased tone and motor activity of the bowel, and increased urinary voiding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acute nicotine toxicity (6)

A
  1. Fatal dose of 40 mg (amount in 2 cigarettes); toxicity is limited by emetic effects, so less absorption occurs if high doses are ingested
  2. If patient is experiencing CNS-stimulant actions (convulsions, coma, respiratory arrest) - treat with diazepam
  3. If patient is experiencing skeletal muscle end-plate depolarization blockade (respiratory paralysis of diaphragm and intercostal muscles) - treat with mechanical ventilation
  4. If patient is experiencing HTN and cardiac arrhythmias - treat with Atropine to control muscarinic excess
  5. Patients who survive the first 4 hours usually recover completely, assuming hypoxia and brain damage have not occurred
  6. Nicotine is rapidly metabolized and excreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pharmacokinetics and metabolism of nicotine (6)

A
  1. Metabolized by CYP2D6 and glucuronidation
  2. Nicotine INDUCES expression of CYP1A2 (caffeine) and CYP2E1 (alcohol)
  3. Eliminated by renal excretion of parent drug and metabolites
  4. Absorbed through multiple routes: skin, mucous membranes, lungs
  5. Administration via smoking (lungs) yields CNS affects in 7 seconds
  6. Positive reinforcement closely associated with the behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nicotine withdrawal (4)

A
  1. Symptoms: irritability, impatience, hostility, anxiety, dysphoric/depressed mood, difficulty concentrating, restlessness, increased heart rate, increased appetite or weight gain
  2. Urge to smoke correlates with low levels of nicotine in blood
  3. First-line medications reliably increase long-term smoking abstinence: nicotine replacement therapy (gum, inhaler, lozenge, nasal spray, transdermal patch), bupropion, varenicline (Chantix)
  4. Rimonabant - inverse agonist of CB1 receptor - improved smoking abstinence rates and reduced weight gain, but increased risk of suicidality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bupropion MOA

A

Antagonistic activity at neuronal nicotinic acetylcholine receptors and stimulant effects. Prevents effects of nicotine upon resumed smoking behavior.

17
Q

Varenicline (Chantix) MOA and ADRs

A

Partial agonist and full agonist of multiple nicotinic receptor subtypes. Variety of nicotinic receptor subtypes may mediate unpredictable effects.
FDA-issued warning: mood and behavioral changes, suicidal ideation.
Can cause vivid nightmares.
May increase cardiovascular risk.

18
Q

Nicotine replacement therapy (MOA and efficacy)

A

Delivery systems differ by patterns of exposure time. Can suppress the symptoms of nicotine withdrawal, enabling gradual abstinence.
More smokers achieve abstinence, but many resume smoking after weeks or months.
Improved efficacy with coupled with counseling and motivational therapy.

19
Q

Guidelines for treating nicotine dependance (5)

A
  1. Often involves repeated intervention and multiple cessation attempts
  2. Treatments are effective across a broad range of populations
  3. Combination of effective cessation medications can be used
  4. Individual, group, and telephone counseling: practical counseling (problem solving/skills training), social support, effective when in combination with pharmacotherapies, and motivational treatments can be effective in increasing future quit attempts
  5. Providing insurance coverage for these treatments increases quit rates
20
Q

Epidemiology of cocaine (4)

A
  1. Small percentage of total illicit drug abuse; 2x more common in men
  2. Intensity of euphoria and rapid onset is a powerful positive reinforcement (encourages escalating drug use)
  3. 10% of patients who use cocaine recreationally develop a use disorder
  4. Binge-use is common
21
Q

Cocaine MOA and general systemic effects (3)

A
  1. Effects occur due to blockage of catecholamine neurotransmitter re-uptake: increased dopamine concentrations in reward circuitry and norepinephrine in corticolimbic system (arousal, attention)
  2. CNS effects: improved performance on tasks requiring vigilance and alertness/arousal, sense of self-confidence and well-being, higher doses produce brief (5-30 minutes) euphoria, often followed by a desire for more drug
  3. Sympathomimetic effects: dose-dependent increase in heart rate and blood pressure
22
Q

Physiological effects of cocaine (4)

A
  1. Stimulant effects of increased catecholamines (and 5-HT): excitement, euphoria, increased motor activity, decrease feelings of fatigue
  2. Stimulant effects at HIGH DOSES: SEIZURE, premature labor, CARDIOVASCULAR COMPLICATIONS (arrhythmias, MI, myocarditis, aortic dissection, cerebral vasoconstriction)
  3. Behavioral risks: death from trauma while intoxicated, enhanced sexual experiences if taken prior to intercourse (increases compulsive and promiscuous sexual activity)
  4. Chronic cocaine use: reduced sexual drive, anxiety/depression/paranoia/psychosis, irritability and increased risk of violence, involuntary motor activity, and stereotyped behavior
23
Q

Acute cocaine toxicity (6)

A
  1. Psychiatric complaints (depression precipitated by cocaine dysphoria, agitation/paranoia)
  2. Seizure
  3. Hyperthermia (CNS stimulation increases heat production and vasoconstriction minimized heat dissipation) - major cause of FATALITY
  4. Chest pain (muscle or cardiac pain, pulmonary damage from impurities in cocaine)
  5. Treat with benzodiazepines! Calms agitated patient and helps cool patient. Treats and prevents convulsions.
  6. Other symptoms treated with short-acting antihypertensives, anticonvulsants, and supportive care
24
Q

Pharmacokinetics of cocaine (7)

A
  1. Absorbed rapidly from virtually all sites of administration; minimal oral bioavailability
  2. Euphoria from “snorting” lasts 15-30 minutes
  3. Smoking cocaine-base “crack” leads to instant absorption, intense euphoria compared to snorting (6x greater) and lasts 5-10 minutes followed by an intense dysphoria or “crash”
  4. Half-life = 50 minutes, but inhaled users typically crave more after 10-30 minutes
  5. Hydrolyzed by tissue esterases
  6. Benzoylecgonine (loss of methyl group) is a major urinary metabolite; can be found in urine 2-5 days after binge, up to 10 days with heavy use
  7. Drug abuse of cocaine and alcohol occurs frequently: alcohol reduced cocaine-induced irritability, cocaine may be transesterified to cocaethylene (equipotent with cocaine in blocking dopamine re-uptake)
25
Q

Cocaine (tolerance, dependance, withdrawal)

A

Tolerance: users are desensitized to euphoric effects; decreased intensity and duration of euphoria leads to compulsive use (dependence)

Withdrawal or “crash” is often a result of intermittent use. Symptoms include: dysphoria/depression, sleepiness/fatigue, cocaine craving, and bradycardia. Symptoms gradually diminish over 1-3 weeks. Withdrawal is generally mild and does not require pharmacotherapy. Biggest challenge is to prevent resumption of compulsive use.

26
Q

Cocaine use treatment (3)

A
  1. Behavioral therapy is the treatment of choice: individual and group psychotherapy
  2. Behavioral treatments with cocaine-free urine tests for accountability
  3. Combination with antidepressant agents or modafinil, a mild stimulant indicated for narcolepsy, may help reduce relapse
27
Q

Epidemiology of amphetamines (4)

A
  1. Among the most widely used illicit substances
  2. Subjective effects and use pattern similar to cocaine
  3. Binge-euphoria
  4. Clinical deterioration may progress more rapidly; behavioral therapies are the only available treatment for amphetamine abuse recovery
28
Q

Amphetamines MOA and effects (3)

A
  1. Amphetamine causes elevation of extracellular dopamine (dopamine efflux!)
  2. Depletion of dopamine stores occurs due to inhibition of VMAT and REVERSE TRANSPORT of dopamine by the dopamine transporter. Contributes to euphoria and reward.
  3. Exerts sympathomimetic effects: effects and toxicities are due to increased signaling by dopamine and norepinephrine
29
Q

Physiological effects of amphetamine (5)

A
  1. Amphetamine stimulates the entire cerebrospinal axis, cortex, brainstem, and medulla
  2. Increased alertness, decreased fatigue and appetite, and insomnia; performance enhancing
  3. Elevated NE and DA levels activate the adrenergic system
  4. High doses may cause arrhythmias and circulatory collapse
  5. Psychiatric effects of amphetamine depend on the personality and mental state of the individual
30
Q

Amphetamine intoxication (4)

A
  1. Acute toxicity may result in death - neurotoxic due to overstimulation of CNS
  2. Symptoms include: euphoria, increased wakefulness/physical activity/respiration, hyperthermia (FATAL), insomnia, decreased appetite, aggression, anxiety, confusion, irritability, paranoia, tachycardia/hypertension/stroke, tremors, convulsions (FATAL)
  3. Benzodiazepines may be indicated for control of SEIZURES
  4. Chronic use may result in psychosis
31
Q

Amphetamine withdrawal (4)

A
  1. Withdrawal symptoms: depression, altered mental status, drug cravings, sleep disturbances (dyssomnia), and fatigue
  2. Patients may experience withdrawal symptoms for several days, but are usually NOT in acute distress
  3. Supportive treatment for withdrawal (pharmacotherapy is no effective)
  4. Contraindicated with TCAs due to increased risk of CV events
32
Q

Amphetamine pharmacokinetics (4)

A
  1. 100% bioavailability
  2. Often administered by IV or smoking in substance abuse
  3. Hepatically metabolized by CYP2D6
  4. Methamphetamine can be produced from hydrolysis of ephedrine
33
Q

Methamphetamine pharmacokinetics and effects (5)

A
  1. Administered orally, intranasally, rectally, IV, and inhalation
  2. Causes brief, intense euphoric effect almost instantaneous after inhalation or IV injection (“rush” or “flash”) - escalation of drug intake occurs frequently in experimental users
  3. Continual use causes prolonged insomnia and an extremely irritable and paranoid state - brain damage and “meth mouth” are common in patients that smoke methamphetamine
  4. Long-lasting (2 days-several months) effects of discontinued use: depression, fatigue, anergia, cognitive impairments
  5. Dependence treatment is very difficult with a low success rate
34
Q

Therapeutic indications for amphetamines (4)

A
  1. FDA approved for ADHD and narcolepsy
  2. Off-label uses: obesity, depression, dysthymia, chronic fatigue syndrome, acquired immunodeficiency syndrome (AIDS), dementia, multiple sclerosis, fibromyalgia, neurasthenia
  3. Low doses allow therapeutic effects WITHOUT euphoric effect
  4. Emergence of dependence is always a risk
35
Q

Methylphenidate for ADHD (7)

A
  1. Structurally related to amphetamine; mild CNS stimulant that improves mental activities; high doses may lead to convulsions; abuse liability
  2. Low dopamine release is thought to result in diminished reward in children with ADHD; decreased interest in once-enjoyed activities may occur
  3. Readily absorbed after oral administration
  4. Hydrolyzed to ritalinic acid by CYP450, excreted renally
  5. DDIs: warfarin, phenytoin, phenobarbital, primidone, and TCAs
  6. ADRs: abdominal pain, nausea, anorexia, insomnia, nervousness, and fever. May increase seizure frequency in patients with epilepsy.
  7. Contraindicated in patients with glaucoma

Mental Health/Psychiatry (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions