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PSYC 3403 > Final Review > Flashcards

Final Review Flashcards

1
Q

Describe the mechanisms of caffeine. How does this mechanism explain the clinical effects of the drug?

A

Caffeine acts as an adenosine antagonist, blocking the effects of adenosine

It is a competitive inhibitor, meaning it competes for the same site and inhibits its actions

This explains its clinical effects because adenosine has sedative properties that increase throughout the day. It stimulates GABAergic neurons in the DA reward system, thus inhibiting DA rewards.

Since caffeine blocks adenosine it keeps people alert and it indirectly activates the reward system

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2
Q

What are the positive and negative effects of caffeine?

A

Positive aspects:
- Cardiovascular function: reduces disease, constricts cerebral vessels decreasing blood flow and reducing pressure, increases contractility & output
- GI: improves glucose metabolism, insulin secretion, and secretion of gastric acid
- Broncial relaxation (anti asthmatic)
- Reduces risk of cancer
- Neurological: protect against Parkinsons and symptoms of MS
Cognition/Mental Health: Reduces Alzheimers risk (polyphenols), improves memory, and decreases depression

Negative aspects:

  • Anxiogenic properties (can cause anxiety)
  • Tremors, rapid breathing
  • Sleep disturbances
  • Overdose can occur if drank too fast/too much
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3
Q

Caffeine is a _____ anlkaloid

A

Xanthine - stimulates the CNS, acts on kidneys to produce urine, stimulates cardiac muscles, and relaxes smooth muscles

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4
Q

How is caffeine absorbed and metabolized (pharmacokinetics) in the body?

A

99% of caffeine is taken into the blood within 45 min - it is absorbed quickly and freely throughout the body as it is lipid & water soluble

It is metabolized by the hepatic enzyme CYP1A2 and is broken down into 3 metabolites: Parazanthine (increases lipolysis), Theobromine (dilates blood v. and increases urine vol.), and Theophylline (relaxes bronchi)

2-3% of caffeine is excrete unchanged (not metabolized)

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5
Q

What effect for Flyvoxamine (SSRI) have of caffeine effects?

A

It inhibits CYP1A2 - people on this SSRI will have a harder time metabolizing caffeine

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6
Q

What is caffeine’s half life?

A

2-10 hours

It is extended in infants, pregnant women, and elderly people

The half life decreases while smoking a cigarette

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7
Q

What is caffenism and when does it occur?

A

Caffeinnism is a syndrome produced by overuse/overdose from caffeine - occurs at doses higher than 10mg (100 cups)

It causes:

  • CNS: anxiety/agistation/insomnia
  • PNS: tachycardia/hypertension/GI issues
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8
Q

What is the recommended caffeine intake for adults?

A

400mg

300 mg from pregnant women - but none is better

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9
Q

Does caffeine negatively impact pregnant women?

A

It can cause a moderate degree of getal growth restriction, can increase risk of mar carriage

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10
Q

What are the withdrawal symptoms of caffeine?

A

Headache, drowsiness, fatigue, impaired intellectual and motor performance, and negative mood state

Symptoms subside after 1-2 days

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11
Q

Can people become dependent on caffeine?

A

No. However, it is associated with habituation and tolerance with high doses (750-1200mg/day)

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12
Q

What are some health issues related to tobacco?

A
  • The single greatest cause of preventable death

- Accounts for 30% of all cancer deaths

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13
Q

What are the pharmacokinetics of nicotine?

A

It is absorbed rapidly and completely, reaching the brain in 7 seconds. It is saturated in the blood which results in the ‘head-rush’

It is metabolizes by hepatic enzyme CYP-2A6 and produces the metabolite cotinine which can remain in the blood for 48 hours

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14
Q

What is the half-life of nicotine?

A

2 hours

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15
Q

Describe the mechanism of action of nicotine.

A

Nicotine activates nicotinic acetylcholine receptors (nAChRs) which are found in the presynaptic terminals of DA neurons, ACh neurons, and Glu neurons

nAChR activation causes increase in BP & HR, releases epinephrine, and enhances GI

Nicotine acts as an agonist by stimulating the α2α4 nACh receptors which increases DA levels in the limbic system - critical for the rewarding effects

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16
Q

What are the pharmacological effects of nicotine?

A
  • May cause nauesa or vomitting
  • Stimulates hypothalamus which released ADH, causing fluid retention
  • Decreased muscle tone
  • Appetite suppression /weight loss
  • Increased blood flow to reward centres
  • Anti depressant effects
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17
Q

What can prenatal exposure to smoke cause?

A
  • 2-3-fold increase in being small for gestational age (SGA)
  • Pediatric asthma, SIDS, various immunological diseases
  • Fetal hypoxia (lack of O2) -> lower IQ
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18
Q

List the nicotine-replacement therapy options. Discuss their efficacy.

A
  1. Transdermal patch - nicotine plasma levels gradually increase so shouldn’t provide an individual with a ‘crash’
  2. Nicotine gum: nicotine plasma levels decrease quickly providing people with the urge to smoke
  3. Nicotine nasal spray: very low nicotine levels
  4. Nicotine inhalers
  5. E-cigarettes: very accessible, and are linked to less smoking cessation

All NRT treatments are essentially equally effective due to their overlap (besides varenicline which is the best)

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19
Q

What are the pharmacotherapeutic options for smoking cessation ?

A

Anti depressants:

  • Bupropion (wellbutrin, Zyban)
  • Varenicline (Champix) - most effective
  • CBT
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20
Q

What is a psychedelic drug?

A

Class of drugs that cause hallucinations and out-of-body experiences

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21
Q

List the major classes of psychedelic drugs, their associated drugs, and their mechanisms of action

A

Anticholinergic - scopolamine
- They are competitive muscarinic ACh antagonists

Catecholaminelike - mescaline, ecstacy
- 5-HT2A agonist

Serotoninlike or Monoaminergic - LSD
- 5-HT2A agonist

Glutaminergic NMDAR antagonist - Ketamine, phencyclidine
- noncompetitive antagonists of NMDAR

Opioid Kappa Receptor agonist - Salvinorin A

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22
Q

What is atropine?

A

Atropine is found the the Atropa belladonna plant and reverses cholinesterase inhibitors, increasing ACh production

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23
Q

What are the pharmacological effects of scopolamine?

A

Acts on the PNs to produce an anticholinergic syndrome: dry mouth, reduced sweating, dry skin, increased body temp, tachycardia

Acts on the CNS:
Low dose: drowsiness, profound amnesia, mental confusion, absence of REM

High(toxic) dose: delirium, coma, respiratory depression

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24
Q

Which two psychadelic drugs are found in nutmeg?

A

Myristin and Elemicin

Both catecholaminlike psychedelics

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25
Q

What is the origin of mescaline?

A

It is found in the peyote cactus and has a crown that is cut and dried into a hard brown disk called the mescal button

Can be chewed or soaked to make a drink

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26
Q

What are the effects of mescaline? How long do they last?

A

Produces an acute psychotomimetic state with prominent effects on the visual system

Single dose lasts up to 10 hours

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27
Q

Discuss the positive and negative symptoms of ecstasy?

A

Positive:
- Increased insight, empathy, enhanced communication, and transcendent religious experiences

Negative:

  • Hyperthermia (overheating)
  • Tachycardia
  • Convulsions
  • Kidney failure
  • Cardiac arrhythmia
  • Dealth (malignant hypothermia)
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28
Q

_________ can reverse malignant hypothermia in people who have taken MDMA

A

dantrolene

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29
Q

How does MDMA differ from mescaline?

A

MDMA is more potent and toxic as it inducesserotonergic neurotoxicity

MDMA is a releaser and/or reuptake inhibitor of monoamines

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30
Q

Which brain areas does LSD activate?

A

Medial prefrontal cortex and anterior cingulate cortex

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31
Q

What effects does LSD have on its user?

A
  • Alterations in perception
  • Temporal changes
  • Visual alteration
  • Euphoric mood
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32
Q

What is hallucination persisting perception disorder?

A

It is a flashback of a visual experience that occurs after the drug has passed - can occur after using LSD

They are often long-term, recurrent, and have an unpleasant dysphoric effect

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33
Q

What are the LSD-induced psychedelic experience phases?

A

Somatic phase: CNS stimulation and autonomic changes

Sensory (perceptual) stage: sensory distortions and pseudo hallucinations

Psychic phase: maximum drug effect: changes in mood, disruption of thought processes, altered time perception, possible ‘bad’ trip

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34
Q

How are Glutaminergic NMDAR Antagonists (PCP & Ketamine) different from other psychedelics?

A

They are structurally unrelated and do not have effects of 5-HT, ACh, or DA

The have psychotomimetic, analgesic, and amnestic properties

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35
Q

How does ketamine and PCP inhibit NMDA receptor’s?

A
  • Blockage of open channel by occupying a site within the channel of the receptor protein
  • Reduction in the frequency of NMDA channel opening by binding to second attachment site on the outside of the receptor protein
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36
Q

What psychological effects does ketamine and PCP have?

A

Induces a psychotic state: rigid, unable to speak, appear very drunk, amnesia, coma/stupor

Respiration does not become depressed in ketamine

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37
Q

What are the 3 primary goals of the cannabis law?

A
  1. Legalize, regulate, and restrict sale of recreational cannabis
  2. Restrict access of cannabis to youth
  3. Limit the illicit cannabis trade
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38
Q

What are the 3 psychoactive compounds produced by the cannabis sativa plant?

A
  • Delta-9-tatrahydrocannabinol (THC)
  • Cannabinol (minor component)
  • Cannabidiol (minor component)
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39
Q

Explain each term and put in order of potency: (a) Ganja, (b) hashish, and (c) marijuana

A
  1. hashish- dried resin of the female flower
  2. Ganja: dried tops of the female flower
  3. Marijuana: Dried remainder of plant
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40
Q

How is THC administered?

A

Joint, blunt, pipe, bong, and edibles

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41
Q

What is the mechanism of cannabis?

A

THC activates the cannabinoid receptors (CB1 and CB2) which are in the family of the G-protein-coupled receptors

G-protein-coupled receptors binds THC, inhitids adenylate cyclase and binds other cannabinoids

Activation causes inhibition of Ca2+ entry (depressing system) and facilitated K+ channels. This inhibits realize of other NTs, specifically GABA

42
Q

What are the endocannabinoids? How do cannabis and the endocannabinoid system work?

A

Endocannabinoids are endogenous and include:
Anandamide and 2-AG

They are partial agonists, like THC, but are weaker. They are produced, related, romped, and inactivated similar to those of other NTs

However, they are synthesized on demand, they move in a retrodrage direction to attach to the presynaptic terminal, and are taken into the neurons by an transporter

They are involved in the normal incentives elicited by pleasurable behaviour

43
Q

How is THC absorbed and metabolized?

A
  • 5-10mg is absorbed from a 75mg joint, depending on how people smoke

Absorption occurs rapidly and the ‘high’ is achieved quickly

It is distributed to various organs, especially those with sig. fatty material

The initial active metabolite, 11-hydroxy-THC is quickly broken down into the inactive compunt 11-nor-9-carboxy-THC (THC-COOH)

44
Q

What are the pharmacological effects of THC?

A
  • Analgesic properties
  • Decreases body temp
  • Calms aggression
  • temporal distortions
  • memory impairment
  • increased appetite
  • acute emory impairments paired with decreased blood flow
  • dose-dependent loss in memory
45
Q

Where are cannabinoid receptors found?

A

Throughout the body

Basal ganglia & cerebellum: movement and posture

Frontal cortex: psychoactive effects (senses, time)

Hippocampus: memory, memory storage

46
Q

What are the withdrawal symptoms of marijuana?

A
  • Depressed mood
  • Insomnia
  • Lower food intake
  • Irritability
47
Q

What two mechanisms occur during the development of THC dependence?

A
  • Down regulation of cannabinoid receptor

- Receptor internalization (minor)

48
Q

What is Dronabinol (Marinol) and what is its therapeutic use?

A

It is THC that can be consumed orally

It is used as an appetite stimulant for AIDS patients, anti-nauseant for against chemo, and reduce intra-ocular pressure

49
Q

What does a cannabinoid antagonist do?

A
  • Blocks marijuana induced intoxication
  • assist in marijuana abstinence
  • memory and learning enhancement
  • controlling obesity (rimonabant)
50
Q

What are the two different classifications of pain?

A

Acute pain: caused by soft tissue damage, infection, and inflammation

Chronic pain: linked with long-term illness or disease, may have no apparent cause, can trigger other issues, difficult to assess and diagnose

51
Q

What is nociception?

A

Nociception refers to the system that carries signals of damage and pain to the brain

Can detect mechanical, thermal, and chemical stimuli

52
Q

How are pain impulses transmitted and modulated within the CNS?

A

Pain transmission occurs when a noxious stimulus activates the primary afferent nociceptive neurons located in the dorsal root ganglia that send information to the dorsal horn of the spine

The pain signal ascends in the spinal afferent tract towards the thalamus, on the way sending information to the hindbrain and midbrain

Once it reaches the thalamus it projects to the cortex where it cues the subjective feeling of pain

The cortex then send signals in a bidirectional pathway back to the spinal centre that transmitted the pain message to either facilitate or inhibit the pain experience

53
Q

What is an opioid? Discuss all its sources

A

An opioid is any exogenous drug that binds to an opiate receptor, produces analgesia, and is blocked by an opiate antagonists

There are 3 sources:
- Natural: obtained from the resin of poppy seeds (morphine, codeine, and thebaine)

  • Semisynthetic: created from natural opioids (heron, oxycodone, hydromorphone)
  • Synthetic: derived in a lab (methadone, fentanyl)
54
Q

Describe the 3 types of opioid receptor. What happens when an opaite agonist activates its receptors?

A

There are 3 types of opioid receports, all are G-protein Coupled Receptos (GPCR)

mu receptors have analgesic effects and alter respiration

Kappa receptors may antagonize mu receptor activity. They have modest analgesic dysphoria and little to no respiratory depression

Delta receptors have no effect on emotional states, the modulate the activity of mu receptors, and they are poor analgesics

When an opiad agonist binds to a mu receptor the subunits dissociate and break into to components. These components interact to hyper polarize the neuron (increase K+, inhibit Ca2+, reduce cyclicAMP) making it less likely to dire and thus blocking the release of pain signals

55
Q

Define an opioid agonist, antagonist, mixed agonist-antagonist, and partial agonist. Give an example of each

A

A full/pure agonist has affinity for a opiate receptor and has an effect (ex. morphine)

A full/pure antagonist has affinity for a opiate receptor but elicits no change (ex. naltrexone)

A mixed-agonist-antagonist produces an agonistic effect at one receptor and an antagonistic at another (ex. pentazocine)

A partial agonist binds to receptor site but has lower efficacy than a full agonist (ex. buprenorphine)

56
Q

In addition to analgesia, what are the major physiological effects of opioid drugs?

A
  • Produces feelings of euphoria by increasing DA levels
  • Respiratory depression
  • Suppression of cough
  • Sedation, drowsiness, and reduces anxiety
  • Produces nausea and vomiting
  • Conspitation
  • Constricts pupils
  • Reduces libido
  • Releases histamine (allergies)
  • Reduce immense system
57
Q

How have opiate analgesics been reformulated to reduce their abuse potential?

A

Drugs that were highly abused to reformulated to be tamer proof. They are no longer able to be crushed and thus cannot be snorted or injected. This has resulted in the decrease of specific opiates as abused substances but caused an increase in other substances

58
Q

Which opiate is the most potent pain analgesic?

A

Morphine

59
Q

How is morphine administered? How is it absorbed in the body? How is it metabolized?

A

It can be administer by injection (epidural), inhalation, orally, or rectally

It is most commonly administered via i.v. injection

Morphine is mostly water-soluble and thus doesn’t pass through the BBB vary easily. Only 20% of morphine reaches the CNS

It is metabolized by various liver enzymes into the active metabolite morphine-6-glucornide

60
Q

What are opiate withdrawal symptoms?

A

Restlessness, dysphira, anxiety, insomnia, diarrhea

61
Q

Explain the purpose of rapid anethesisa-aided detoxification (RAAD)

A

RAAD is when someone is provided with an opiate antagonist (naloxone) and sympathetic blocker (clonidine) while unconscious. The purpose is to have someone fully detox and go through withdrawal while sleeping

They continue with psychotherapy and naltrexone but an opiate abstinence syndrome follows for up to 6 months

62
Q

Describe the pharmacokinetics of codeine. Why has it lost it’s popularity?

A

Codeine is less potent than morphine and must be metabolized by the CYP 2D6 enzyme in order to be active

It is metabolized to morphine

It is no longer popular as many people metabolize it rapidly, creating increased levels of morphine in the body. The metabolic conversion is also blocked by 4 out of 6 SSRIs

63
Q

Why is heroin such highly abused drug?

A

Heroin is 3x more potent than morphine

It has increased lipid-solubility with leads to faster penetration to brain, giving people an intense rush

64
Q

What are the problems with prescribing oxycodone? What are the two types?

A

Oxycodone is a semi-synthetic opioid similar in action to morphine.

It has a high abuse liability and it has an extremely high rate of increase

The two types are short-acting (Percodan) and long lasting/time-release (Oxycontin)

65
Q

Why is Fentanyl so deadly? How is it administered?

A

It is 80-500x more potent than morphine. It has severe respiration depression which results in respiratory failure

It is administered orally, skin patch, nasal spray, and IV

66
Q

What 3 factors mediate food intake?

A

Homeostatis - energy demands, you body works to keep in you this baseline/happy state

Emotional - stress, boredom

Hedonism - pleasure

67
Q

What is the biological model for food intake?

A

Hurmoral signals arise when hungry and they are sent to the hypothalamus which tells your body to eat food

Once you eat food your hormonal signals will tell the hypothalamus that you are full which will tell you to stop eating

This is a constant feedback loop of hunger and satiety

68
Q

Explain the differences between ghrelin and leptin. How does this influence our eating?

A

Ghrelin are GI peptides in the stomach and pancreas. They are an orexigenic agent that have a preprandial rise (increase before food consumption)

Leptin hormones of adipose tissue are anorexigenic agents. They antagonize the effects of neuropetide Y and anandamide to promote the synthesis of a-MSH which stimulates satiety and acts as an appetite suppressant

Ghrelin and Leptin levels are opposite: Grehlin is high before eating and Leptin is low before eating. Leptin has a postprandial rise

69
Q

How does insulin influence satiety?

A

Insulin is a peptide hormone in the pancreas that causes cells to take glucose from the blood

During periods of food abstinence your body will gain to use its fat source for energy. Insulin will stop the use of the fat during periods of glucose by inhibiting the release of glucagon

70
Q

Which two regions in the hypothalamus regulate food intake? Discuss it in terms of the dual-centre hypothesis

A

The lateral hypothalamus is the hunger centre

The ventromedial hypothalamic nucleus is the satiety centre

Humoral signals –> lateral hypothalamus –> eating on –> hormonal single –> Satiety –> ventromedial hypothalamus –> eating off -? Humoral signals –> etc…

71
Q

What are 3 factors that influence overconsumption of food?

A
  1. Disrupted neurobiology
  2. Poor impulse control
  3. Environmental factors
72
Q

What are the 3 levels of activity? Why does activity level matter during food consumption?

A

Sedentary, low active, and active

The more active you are the more calories you should consume

73
Q

How has personal food consumption increased ?

A
  • Increased serving size
  • Increased access
  • Social context (insta, outings)
  • Stress
74
Q

What is obesity?

A

When an individual has a BMI equal or greater than 30

It is a metabolic state where excess fat accumulates in peripheral tissues such ad adipose, muscle, and liver tissues

75
Q

Does food consumption activate reward centres?

A

Yes.

There is similar activation of brain meters in the dopamine-reward pathway: NA, PFC, VTA, and amygdala

76
Q

What are the physiological effects of food consumption?

A

It increases DA levels within the nucleus accumbens and the dopamine-reward pathway

Comfort/’trigger’ food can cause the release of 5-HT

In addicts, the DA release can be very significant

77
Q

What are symptoms of a food addiction?

A
  • Frequent periods of uncontrollable binges
  • Consume food beyond point of satiety
  • Feelings of guilt and depression
  • Excessive time and thought devoted to food
  • Preoccupation with body weight
78
Q

What are withdrawal symptoms from food addiction?

A
  • Mood swings
  • Agitation
  • Faintness
  • Headaches
  • Dysphoria
  • Hypoglycemia
79
Q

Does food addiction meet the criteria of an addiction?

A

Yes.

  1. Tolerance
  2. Withdrawal
  3. Investment
  4. Social change
80
Q

How was testosterone used in WWII?

A
  • Chronic wasting
  • Soilder supplement
  • Adolph Hitler
81
Q

How is testosterone synthesized?

A

Low levels of testosterone are detected by the hypothalamus receptors which causes the release of GRF (gonadtripin-releasing factor)

GRF stimulates the pituitary gland to produce two hormones: FSH (follicle-stimating hormone) and LH (luteinizing hormone)

The LH hormone stimulates synthesis and release of TS in the leydig cells of the testicle and the FSH hormone stimulates the production of spermatogenesis by the seminiferous tubules

The hypothalamus can now detect high levels of TS and stop the release of GRF. This creates a negative feedback loop

82
Q

What are the anabolic and androgenic effects of steroid use?

A

Anabolic effects:

  • increased protein synthesis
  • increased appetite
  • bone remodelling and growth
  • increased production of RBC

Androgenic effects:

  • increased hair growth
  • increased vocal cord
  • increased libido (but decrease of regular TS release, reducing spermatogenesis)
  • growth of clitoris
  • increased breast size in men
83
Q

What are the positive and negative effects of supratherapeutic steroid use?

A

Positive:

  • Increase tonic/burst muscle
  • Better strength and endurance

Negative?

  • Hypogoadal state (atrophy or testicles)
  • Lower HDL and increased LDL (cholesterol)
  • Risk of liver disorders
84
Q

What are therapeutic uses of steroids?

A

TS replacement for hypogonadism, blood anemias, muscle loss after trauma or disease

85
Q

What is the mechanism of action of steroids?

A

Steroids are rapidly absorbed by the GI tract, entering the blood and travelling to the liver

It is effectively metabolized by enzymes (first-pass) into an active metabolite androstanolone. IV bypasses first-pass metabolism

Steroids bind to the receptor, are taken into the nucleus where it binds to a DNA site and is transcript into mRNA. mRNA is then released from the nucleus where it is translated to a new protein

86
Q

What are the psychological effects of steroids?

A

Changes in behaviour and motivation - increases aggression

87
Q

What are withdrawal symptoms of steroids?

A
  • Depression
  • Fatigue
  • Restlessness
  • Insomnia
  • Loss of appetite
  • Decreased libido
  • Suicide ideation
88
Q

What does licensing/regulating gambling lead to?

A

Illegal gambling

Gambling tourism

89
Q

What forms of gambling are available?

A

Casinos, sports betting, quick-pick lotteries, scratch ‘n’ win, McDonald’s monopoly

90
Q

What is pathological gambling? What is the criteria?

A

Pathological gambling is when an individual begins to show biological symptoms related to their addiction and gambling

The criteria is:
- Preoccupation , Tolerance, Withdrawal symptoms, escape, chasing, lying, stealing, loss of control, illegal acts, risked significant relationships, and bail out

91
Q

What are characteristics of responsible gambling?

A
  • Entertainment not income, balance with other activities, never alone, accept losses as cost of entertainment, setting a budget, don’t borrow money, setting a time limit, taking breaks
92
Q

What are the phases in compulsive gambling decline?

A

Winning phase - increased frequency, unreasonable optimism
Losing phase - thoughts revolve around gambling, lying/stealing/debts
Desperation phase - panic/remorse, alienation

93
Q

What are the phases in recovery from compulsive gambling?

A

Critical phase - responsible thinking, reflection
Rebuilding- self-respect, regain trust
Growth - self-awareness, preoccupation decreased

94
Q

What is the mechanism of action of gambling addiction?

A

The nucleus accumbens fires the same when expecting a win vs. expecting a drug

It is linked to decreased NE and 5-HT

95
Q

What are the treatment options for a gambling addiction?

A

Medication: SSRI (paroxetine), bipolar meds (lithium), opiate antagonist (nalmefene) - typically used to treat an underlying disorder

Psychotherapy: counselling, step-based programs, peer support groups

96
Q

What are the symptoms of sex addiction?

A

Compulsivity - loss of ability choose freely whether to stop or continue

Continuation despite consequences

Obsession: other areas of their lives are neglected due to preoccupation of sex

97
Q

Which underlying disorders are typically associated with sex addiction?

A

Obsessive-compulsive disorder
Narcissistic personality disorder
Bipolar disorder

98
Q

Why do you think that the rates of gambling addiction are higher than sexual addiction?

A
  • Sex is normalized so often not discussed and when discussed people are less likely to view it as maladaptive
  • Depending on the type of sex addiction it can be highly stigmatized and thus not discussed with others
  • Easier to be a fully functioning sex addict as it doesn’t deplete your resources as quickly
  • There are not many health consequences related to sex addiction
  • Gambling can be a social activity and thus easier for a third-party to notice maladaptive trends
  • Having sex is less time consuming as people aren’t trying to win back what they lost
99
Q

What are types of sexual addictions?

A

Compulsive masturbation, sex with prostitutes, anonymous sex, multiple affairs outside relationship, habitual exhibitionism, habitual voyeurism, inappropriate ‘accidental’ sexual contact, child sexual abuse, rape

100
Q

What is the behaviour cycle for sexual addiction?

A
  1. preoccupation
  2. ritualization (‘the hunt’)
  3. compulsive sexual behaviour
  4. despair - not satisfied
101
Q

What is the cause for sex addiction?

A

Trauma
Impaired neurochemistry (Mesolimbic pathway, OCD, depression)
Developmental impairments

102
Q

What are treatment options for sex addiction?

A
  • Assessment and treatment for comorbid disorders
  • 12-step programs (SAA)
  • CBT

PSYC 3403 (3 decks)

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