Chapter 5 Flashcards

1
Q

Identify the different stages of sleep and the neural activity in each

A

Awake: Alpha + **beta

Non-REM sleep:

  • Stage 1: Theta
  • Stage 2: Spindle + K complex
  • Stage 3 and 4 (slow wave sleep): Delta waves

REM sleep:
- high frequency, low amplitude waves that resemble wakefulness

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2
Q

Circadian rhythm

A
  • cyclical changes that occur on a roughly 24-hour basis in any biological processes
  • a 24 hour cycle scheduled by environmental cues
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3
Q

Biological clock

A

term for the suprachiasmatic nucleus (SCN) in the hypothalamus that’s responsible for controlling our levels of alertness

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4
Q

How do our bodies react to a disruption in our biological clocks?

A
  • sleep disruption

- increased risk of injuries

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5
Q

REM sleep

A
  • REM: darting of eyes underneath closed eyelids during sleep
  • REM sleep: stage of sleep during which the brain is most active and vivid dreaming most often occurs
  • increased heart rate and blood pressure
  • rapid, irregular breathing
  • dreams more frequent; tend to be emotional, illogical and prone to sudden shifts in plot
  • loss of muscle tone
  • activity increases to waking levels in many brain structures
  • some muscle activity
  • some degree of clitoral or penile erection
  • spend more time in REM prior to waking up
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6
Q

non-REM (NREM) sleep

A

stages 1 through 4 of the sleep cycle, during which rapid eye movements do not occur and dreaming is less frequent and vivid

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7
Q

hypnagogic imagery

A
  • scrambled, bizzare and dream-like images that flit in and out of consciousness
  • occurs in stage 1 sleep
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8
Q

myoclonic jerks

A
  • sudden jerks of our limbs as if being startled or falling

- occurs in stage 1 sleep

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9
Q

Free running rhythm

A
  • when not exposed to any environmental cues (ie. always dark/light)
  • still approximately a 24 hours cycle
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10
Q

List three theories for REM

A

(1) Those that say REM sleep is important for one’s mental health.
(2) Those that say REM sleep is necessary for the processing of memories.
These theories share one problem: Explaining why tricyclic antidepressant drugs are not debilitating

**(3) Default Theory

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11
Q

Default theory of REM

A
  1. REM is a break between bouts of NREM sleep.
  2. REM maintains a certain level of alertness that would not be possible in continuous NREM (REM keeps you alert to external stimuli).
  3. REM prepares us for wakefulness (hence the prominence of REM towards the end of a night’s sleep).
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12
Q

REM-sleep deprivation

A
  • A greater tendency for the person to initiate REM (they have to be woken more and more frequently).
  • Greater than normal amounts of REM sleep during subsequent nights of sleep. (REM rebound)
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13
Q

Dream theories

A
  1. Activation-Synthesis Hypothesis (Hobson, 1989)
    - It is our brain trying to make sense of it’s own sleep-related (random) activity
  2. It is a virtual trainer
    - The act of dreaming has a major role in early
    development (stimulation and simulation) and throughout life (simulation for prediction)
  3. Dreams result from the sleeper’s mind attempting to organize unconsciously reactivated memories. It organizes those reactivations into a narrative (Foulkes, 1982).
  4. Neurocognitive theory
    - dreams are a meaningful product of our cognitive capacities, which shape what we dream about
  • Scientists agree that acetylcholine turns on REM sleep and that the forebrain plays an important role in dreams
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14
Q

Lucid dreams

A

Somewhat akin to being “awake” in a dream: The dreamer is aware that they are dreaming and they can affect the course of the dream.

Support for their existence has come from studies of sleeping subjects who used a prearranged signal to communicate with the experimenter from their dreams.

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15
Q

Common beliefs about dreaming

A
  1. Many people believe external stimuli can become incorporated into their dreams.
    + Spraying water on sleeping subjects caused about half of the subjects to incorporate the water into their dreams.
    - However, most stimuli are neither incorporated into dream content nor elicit a behavioural response.
  2. Most people believe sleeptalking and sleepwalking (somnambulism) occur during dreams.
    - apparently false– paralyzed during REM sleep (although dreams can occur outside of REM sleep)
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16
Q

Why do we sleep?

A
  1. Recuperation theories of sleep
    - Being awake disrupts homeostasis
    - Sleep restores homeostasis
    - E.g. Energy levels
  2. Adaptation theories of sleep
    - May be no functional purpose
    - sleep is the result of a 24 hour timing mechanism
    - Protection from accidents & predation
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17
Q

Recuperation vs adaptation theory of sleep

Comparative studies of animals

A
  • more support for recuperation theory
  • comparative analysis of sleep
  • sleep DOES serve a physiological function
  • dolphins sleep with half a brain at a time
  • antelopes sleep 2-3 hours a day, even though this puts them at risk for predation
  • Sleep is not only for higher order human function
    • Doesn’t serve to release emotions to ensure good mental health
  • Sleep needed for survival but not in great amounts
    • Less during mating, migration, & short supply of food
  • No strong relationship between sleep length & body size, energy expenditure, body temperature
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18
Q

Physical, mental, and emotional health impacts of lack of sleep

A

Physical Health
Impaired immune system.
Hormone dysregulation (inc. appetite).

Mental Health
Cognitive impairment; attention deficits.
Memory lapses or memory loss.
Mental fatigue; hallucinations.

Emotional Health
Irritability; general anxiety.
Inability to handle stress.

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19
Q

Sleep deprivation: Human experiments

A

Moderate amounts of sleep deprivation–3-4 hours in one night–have been found to have 3 consistent effects:

  1. Subjects display an increase in sleepiness: They report feeling sleepier and fall asleep quickly if given the chance.
  2. They display disturbances on written tests of mood.
  3. They perform poorly on tests of vigilance.

**Microsleeps

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20
Q

What happens during the next sleep after sleep deprivation?

A

Sleep deprivation leads to increased efficiency to get stage 3&4 sleep, the next sleep

Regain most of stage 4 sleep
More slow wave sleep
Amount of slow wave sleep for 6H = 8H
Naps contain more slow waves if lack of sleep the previous night
Less stage 1&2 when less sleep
Waking during stages 3 & 4 cause sleepiness whereas waking during REM does not

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21
Q

Monophasic sleep

A
  • sleep once, nightly
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22
Q

Polyphasic sleep

A
  • take naps multiple times a day

- Most mammals and human infants regularly sleep more than once per day; they display polyphasic sleep cycles.

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23
Q

Gradual long-term sleep reduction experiment

A
  • In a study by Friedman et al. (1977), subjects reduced nightly sleep by:
  • 30 min every 2 weeks until they reached 6.5 h/night;
  • Then by 30 min every 3 weeks until they reached 5 h/night;
  • Then by 30 min every 4 weeks.
  • Once a subject indicated a lack of desire to reduce sleep further, they slept for 1 month at their shortest duration, then for 2 months at the shortest duration plus 30 min; then for a year at whatever duration they wanted.
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24
Q

Gradual long-term sleep reduction results

A
  • Increased sleepiness when less than 6hr/night
    • No notable changes in mood, physical health, or performance on tasks of vigilance or memory.
    • After 1 year, all subjects had reduced their sleep duration by between 1-2.5 h/night with no excessive sleepiness.
  • Subjective responses were often not in line with the objective measures, nor with their performance at work or school.
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25
Q

Stampi nap experiment results

A
  1. Subjects required a long time (~2 weeks) to adapt to the schedule.
  2. Once adapted, they were content and displayed no deficits on performance tests.
  3. Most displayed a strong preference for particular durations (e.g., 25 min);
  4. At first, most only showed slow-wave sleep. But eventually all subjects returned to their relative proportions of slow-wave- and REM-sleep–though rarely within the same nap.
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26
Q

How much sleep do we need?

A
  • 7 hours has the lowest mortality rate (correlation!)
  • in the gradual long-term sleep reduction experiment, sleeping for at least 6 hours resulted in no notable increased sleepiness or change in mood/physical health/performance on tasks of vigilance or memory.
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27
Q

List 3 types of sleep disorders

A
  1. Hypersomnia
    - Narcolepsy
  2. Insomnia
    - Sleep Apnea
    - Periodic limb movement syndrome
    - Restless leg syndrome
  3. Sleep walking
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28
Q

Hypersomnia

A
  • disorders of excessive sleep or sleepiness
  • ex. Narcolepsy
    Symptoms;
    1. Severe daytime sleepiness at inappropriate times
    2. Cataplexy – loss of muscle tone during wakefulness
    3. Sleep paralysis – can’t move as falling asleep or waking up
    4. Hypnagogic hallucinations – dreaming while awake
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29
Q

Narcolepsy

A
  • an example of hypersomnia
  • experience episodes of sudden sleep lasting anywhere from a few seconds to several minutes (less frequently, as long an hour)
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30
Q

Insomnia

A
  • difficult falling asleep
  • ex. Sleep apnea, periodic limb movement syndrome, restless leg syndrome
    Symptoms:
    1. Having trouble falling asleep (>30 minutes to doze off)
    2. Waking too early in the morning
    3. Waking during the night and having trouble returning to sleep
  • higher rates in people who suffer from depression/continual pain/stress
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31
Q

Sleep apnea

A
  • blockage of the airway during sleep
  • snore loudly, gasp, sometimes stop breathing for more than 20 seconds
  • rouses the person (several hundred times) during the night and interferes with sleep
  • no awareness of the awakenings
  • associated with being overweight
  • wear a facemask attached to a machine that blows air into the nasal passages
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32
Q

Night terrors

A
  • sudden waking episodes characterized by screaming, perspiring, and confusion followed by a return to deep sleep
  • occur almost exclusively in children
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33
Q

Sleepwalking

A
  • walking while fully asleep
  • not acting out their dreams
  • almost always occurs in non-REM (especially stage 3 or 4) sleep
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34
Q

Hallucinations

A
  • experience what isn’t there
  • realistic perceptual experiences in the absence of any external stimuli
  • occur in any sensory modality
  • 10-14% … or 39% of college/university students/general population report having hallucinated during the day at least once
  • some cultures view hallucinations as gifts of wisdom from the gods and incorporate them into their religious rituals
    • go out of their way to induce hallucinations (ie. fasting, praying, drugs)
  • oxygen and sensory deprivation, epilepsy, fever, dementia, and migraine headaches can cause visual hallucinations
  • auditory hallucinations occur when people attribute their thoughts/inner speech to an external source
35
Q

Deja vue

A
  • feeling of reliving an experience that’s new

- the more that scenes resemble previous scenes that they can’t recall, the more likely they are to report deja vue

36
Q

Mystical experiences

A
  • feelings of unity or oneness with the world, often with strong spiritual overtones
  • reliving mystical experience results in distinctive patterns of brain activation
37
Q

Out of body experiences

A
  • sense of our consciousness leaving our body
  • floating above their bodies, calmly observing themselves from above
  • people are not actually able to roam outside their body during an OBE
  • sometimes occur during a near death experience
38
Q

Near-death experiences

A
  • out-of-body experience reported by people who’ve nearly died or thought they were going to die
  • passing through a dark tunnel, experiencing a bright light, meeting spiritual beings/long-dead relatives, seeing our life flash before our eyes
39
Q

What is a drug?

A

1) A drug is assumed to affect physiological functioning in some way.
2) It is exogenous (rather than endogenous; e.g., insulin).

40
Q

Psychoactive drug

A

Drugs that influence the subjective experience and behaviour by acting on the central nervous system

41
Q

Four methods of drug administration and absorption

A
  1. Ingestion
    - Advantages: Easy and relatively safe.
    - Disadvantages: Unpredictable effects.
  2. Injection
    intramuscularly (IM; into muscle),
    intravenously (IV; into vein) ,
    subcutaneously (into fatty tissue below skin)
    Advantages: Speedy (and predictable) effects.
    Disadvantages: Speedy effects, infection potential.
  3. Inhalation
    Advantages: Speedy effects.
    Disadvantages: Unpredictable effects, damage to lungs.
  4. Absorption via mucous membranes
    Disadvantages: Damages membranes.
42
Q

How do drugs affect the CNS?

A
  • Some drugs (e.g., alcohol) act diffusely on neuron membranes throughout the CNS.

Others act in more specific ways:

  • Binding to particular synaptic receptors.
  • Influencing synthesis, transport, release, or deactivation of particular, neurotransmitters.
  • Influencing the chain of chemical reactions elicited in postsynaptic neurons by the activation of their receptors.
43
Q

Drug metabolism

A

the conversion of active drugs into non-active forms, usually by liver enzymes.

Many inactivated drugs can no longer pass through the blood brain barrier

44
Q

Drug excretion

A

elimination from the body

45
Q

Drug tolerance

A

Repeated exposures produce a diminished effect (or requires an increased dose to maintain a constant effect)

46
Q

Drug sensitization

A

Repeated exposures produce a heightened drug effect (or requires a smaller dose to maintain a constant effect)

47
Q

Specificity in drug tolerance/sensitization

A
  1. Cross-tolerance - One drug can produce tolerance/sensitization to other drugs that act by the same mechanism
  2. Tolerance/sensitization often develops to some effects of a drug, but not others
48
Q

Withdrawal syndrome

A

An adverse physiological reaction due to the sudden removal of a drug that an animal has been on for a significant period of time (i.e. days)

Individuals who suffer from withdrawal effects when they stop taking a drug are said to be physically dependent on that drug.

49
Q

Severity of withdrawal symptoms depends on

A

Type of drug
Duration of exposure
Degree of exposure
Speed of drug’s removal

50
Q

Classical conditioning and drugs

A
  • Learning has been shown to play a role in drug tolerance
  • UCS: Drug injection → UCR: Drug effects
  • After one or more administrations, we get the compensatory response (tolerance)
  • (Neutral stimulus) Conditioned Stimulus: Context (location/situation) → CCR/Conditioned compensatory response
  • Much tolerance is a result of a conditioned compensatory response
51
Q

Contingent drug tolerance

A
  • specific tolerance that develops only to drug effects that are actually experienced
  • experiment where if you take alcohol before convulsive stimulation vs after; only those who took it before became tolerant
52
Q

Addicts

A

habitual drug users who continue to use a drug despite its adverse effects (e.g., health, social life) and despite their repeated efforts to stop using.

53
Q

Models of addiction

A

1) Moral Model
2) Disease (Biomedical ) Model
3) Learning Models (behavioural, social, cognitive-behavioural)

54
Q

Moral Model of Addiction

A

Addiction is a choice made by individuals with low moral standards

Treatment = Punishment

55
Q

Biomedical (disease) Models

A
  1. Physical-dependence theories
    - Physical dependence traps addicts in a cycle of using and withdrawing
    - Criticisms: 1) Stop, restart after some time; 2) mild withdrawal drugs; 3) binge-detox pattern
  2. Positive-incentive theories
    - Primary factor in most addictions is the craving for the rewarding properties of the drug
    - Criticism: 1) Actual pleasure =/= anticipated pleasure
  3. Incentive-sensitization theory
    - The positive-incentive value of addictive drugs increases with repeated use

General criticisms

  • Exposure doesn’t always lead to addiction
  • Abstinence might not be necessary
  • Spontaneous “recovery”
  • Removes personal responsibility
56
Q

Behavioural learning model

A
  • Taste (alcohol) and immediate effects → Pleasure (positive reinforcement)
  • Effects of the drugs remove negative feelings (negative reinforcement)
  • Environmental cues associated with drug use (classical conditioning)
57
Q

Social learning model

A

Learn to do drugs by observing others (modelling)

Drug use is a learned behaviour

58
Q

Cognitive-behavioural model

A
  • both expectations and actual effects play a role
  • expectancy effects
  • if you expect alcohol, you will experience alcohol effects even if you’re just drinking tonic
  • if you expect tonic, you will not experience alcohol effects despite consuming alcohol
  • this is only true to a certain extent; if you drink a lot of alcohol, you will still become impaired
59
Q

Conditioned compensatory response

A
  • an automatic response that is opposite to the effect of alcohol or drug usage
  • triggered by physical environment, hearing the ice cubes poured into the glass, hearing alcohol poured over ice, preparation for injections (ie. preparing the needle)
60
Q

Influences for drug use/abuse

A
  • sociocultural influence (legal status+ culture may encourage/normalize consumption of drugs; unemployment)
  • personality (impulsivity)
  • learning and expectancies
  • genetic influences (asian glow, less likely to become alcoholic)
61
Q

4 general categories of drugs

A
  1. Stimulants (caffeine, cocaine)
  2. Psychedelics (marijuana)
  3. Depressants (alcohol)
  4. Narcotics (heroin/opiates)
62
Q

Opiates (Heroin)

A
  • Best analgesics (painkillers)
  • Effective treatment of cough & diarrhea
  • Highly addictive
63
Q

Heroin short term effects

A
Confusion
Slurred and slow speech
Slow breathing and heartbeat
Dry mouth
Tiny pupils
Reduced appetite and vomiting
Decreased sex drive
64
Q

Heroin overdose

A
Trouble concentrating
Irregular heartbeat
Cold, clammy skin
Slow breathing, blue lips and fingertips
Falling asleep (‘going on the nod’)
Passing out
Death
65
Q

Heroin chronic effects

A

Although opiates are highly addictive, the direct hazards of chronic exposure are relatively minor:

  1. Constipation
  2. Menstrual irregularity
  3. Reduced sex drive
66
Q

Heroin withdrawal effects

A

The withdrawal syndrome consists of the following symptoms, in roughly the following order:

  1. Increase in restlessness.
  2. Watery eyes, runny nose, yawning and sweating.
  3. Fitful sleep.
  4. Chills, shivering, profuse sweating, nausea, vomiting, diarrhea, cramps, pains, tremor, muscle spasms, gooseflesh.
67
Q

Other opiates (aside from heroin)

A

Oxycontin (Oxycodone)
semisynthetic prescription pain killer (1.5x stronger than morphine)

Fentanyl
synthetic prescription pain killer (50-100x stronger than morphine)

Carfentanyl
synthetic anesthetic for large animals (10,000x stronger than morphine)

68
Q

Alcohol short term effects

A

Alcohol molecules, because they are small and soluble, invade all parts of the body.

  1. Low doses: It can stimulate neural firing and facilitate social interaction.
  2. Moderate doses: Experience various degrees of cognitive, perceptual, verbal, and motor impairment, as well as a loss of control that can lead to a variety of socially unacceptable outcomes.
  3. High doses: Unconsciousness. If blood-alcohol levels reach 0.5%, there is a risk of death from respiratory depression.
  • Red flush: Produced by dilation of blood vessels in the skin–that dilation leads to a decrease in body temperature (hypothermia).
  • Diuretic: Alcohol increases the production of urine.
69
Q

Alcohol withdrawal effects

A

Alcohol withdrawal often produces a mild syndrome of headache, nausea, vomiting, and tremulousness, known as the hangover.

70
Q

Alcohol withdrawal syndrome

A
  1. Severe tremors, agitation, headache, nausea, vomiting, abdominal cramps, and profuse sweating (starts ~5 hours after last drink).
  2. Convulsive activity (starts ~ 15-30 hours after last drink). Potentially fatal.
  3. Delerium tremens (DTs). Characterized by disturbing hallucinations, bizarre delusions, agitation, confusion, fever, high blood pressure, and rapid heart rate (starts 1-2 days after last drink and lasts 3-4 days). Potentially fatal.
71
Q

Alcohol chronic effects

A
  1. Produces extensive brain damage. In some cases, can even lead to Korsakoff’s syndrome.
  2. Cirrhosis (extensive scarring) of the liver–the major cause of death amongst alcoholics.
  3. Irritation of the lining of the digestive tract–increasing the risk of oral and liver cancer, stomach ulcers, pancreatitis (inflammation of the pancreas), and gastritis (inflammation of the stomach).
  4. Other devastating effects: on the roads and in the home.
  5. Fetal alcohol syndrome (FAS): If alcohol is consumed by a pregnant mother, the child can suffer from some or all of the following: brain damage, mental retardation, poor coordination, poor muscle tone, low birth weight, retarded growth, and/or physical deformity.
72
Q

Caffeine short term effects

A
Increases alertness
Increased blood pressure
Increased breathing rate
Increased urination
Improved focus
Elevated alertness
Faster reaction time
Reduced perception of fatigue
Increased endurance
73
Q

Caffeine long term effects

A

Nervousness, insomnia, stomach irritation, fatigue

74
Q

Caffeine health implications (up to 400mg a day)

A

Not linked to risk of cancer
Not linked to risk of coronary heart disease
May protect from Parkinson’s, liver disease, diabetes 2
Caution for children and pregnant women

75
Q

Caffeine withdrawal effects

A
headaches, 
fatigue, 
drowsiness, 
irritability, 
difficulty concentrating 
depressed mood
76
Q

How much caffeine is safe?

A

Adults 400mg per day

Children 12-18 (100mg per day)

77
Q

Cocaine

A

Medicinal uses: → Surgical anesthetic for cataract removal

Many accidental overdoses

78
Q

Cocaine short term effects (low doses)

A

Euphoria
Extreme happiness and energy
Mental alertness
Hypersensitivity to sight, sound and tough
Sociability & confidence
Irritability
Paranoia — extreme and unreasonable distrust of others

79
Q

Cocaine short term effects (high doses)

A
Irregular heart rhythm
Tachycardia (elevated heart rate)
Heart attacks and/or strokes
Sweating, nausea, confusion
Seizures
Uncontrollable muscle movements such as shaking, jaw grinding or teeth chattering
Weak, shaky limbs
Death
80
Q

Cocaine long term effects

A

Snorting: Loss of sense of smell, nosebleeds, frequent runny nose, and problems with swallowing
Consuming by mouth: severe bowel decay from reduced blood flow
Needle injection: higher risk for contracting HIV, hepatitis C and other blood-borne disease

81
Q

Cocaine withdrawal effects

A
Difficulty concentrating/slower thinking
Fatigue or exhaustion
Inability to experience sexual arousal
Anhedonia, or the inability to feel pleasure
Increased appetite

(Milder than alcohol withdrawal syndromes!)

82
Q

Marijuana

A
  • Marijuana is the name commonly given to dried leaves and flowers of pistillate (“female”) Cannabis sativa
  • Main active ingredient: THC (delta-9-tetrahydrocannabinol)
  • Most of the cannbinoids can be found in a sticky resin covering the leaves and flowers of the plant; this can be extracted and dried to form a dark coloured solid called HASHISH

Medicinal uses

  • Pain, weight loss, and nausea from cancer
  • Chronic pain
  • Multiple sclerosis
  • Inflammatory bowel disease
  • Arthritis
  • Pain, weight loss, and/or nausea from HIV/AIDS infection
  • Seizures in epilepsy
  • Pain from spinal cord disease
83
Q

Marijuana short term effects

A

Low doses: Increased sense of well-being, alterations in the perception of space and time, and heightened sensations
High doses: Transient memory impairments, multistep goal-directed task impairments, speech production impairments. An acute transient psychosis occurs in some individuals.

84
Q

Marijuana chronic effects

A

Habitual smokers have dificts in respiratory function, and they are more likely to develop a chronic cough, bronchitis and asthma
Risk for dependence (~10% of users)