Block 6 W2 Flashcards

1
Q

What is addiction?

A

The continued repetition of a behaviour despite adverse consequences. May continue to point of death.
It is ambivalence.
Affects 2mill

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2
Q

Outline the cycle of addiction.

A

Social drinking -> problem/abusive drinking -> dependence and altered brain function -> excessive and uncontrolled drinking -> abstinence -> acute/protracted withdrawal symptoms -> relapse.

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3
Q

Describe end-stage addiction.

A

Overwhelming desire to take the drug, diminished ability to control drug seeking, reduced pleasure from biological rewards -> drug becomes most salient (important) thing in their life.

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4
Q

What structural changes occur in the brain in addiction?

A

Addicts take alcohol/drugs so often it becomes an automatic habit due to changes in the prefrontal cortex -> over learning of drug-related cues and can be triggered by cues years after abstinence.

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5
Q

Outline dependence syndrome.

A
  1. Salience - use of substance is high priority.
  2. Tolerance
  3. Withdrawal symptoms - body’s homeostasis disrupted.
  4. Relief from symptoms with further use.
  5. Compulsion to use substance
  6. Narrowing of repertoire - neglect of other interests
  7. Reinstatement after abstinence - 1 drink ruins it all
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6
Q

Define pre-contemplation.

A

Not ready.

People are not intending to take action and can be unaware that their behaviour is problematic.

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7
Q

Define contemplation.

A

Getting ready.
People are beginning to recognise that their behaviour is problematic and start to look at the pros and cons of their continued actions.

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8
Q

Do some people have a vulnerability to addiction?

A

The alcohol gene - 25% of the sons of alcoholics develop alcohol problems themselves -> definite genetic risk of alcoholism but no single gene.
Twin studies - 4 good studies show increased concordance for monozygotic over dizygotic.
Adoption studies - 3 - 4x increase in risk in adoptees raised apart.

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9
Q

Describe the asian flush.

A

Flush reaction in 50% of asians due to variant of acetaldehyde dehydrogenase gene -> slow metabolism of alcohol.
There is a genetic contribution to heavy drinking but affected heavily by social, upbringing and personality factors.

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10
Q

What maintains addiction?

A
  1. Personality factors - thrill seeking, impulsive, mood dysregulation.
  2. Social factors - substance use amongst family and friends.
  3. Altered physiology in continuous presence of drug - homeostasis altered so can’t function properly without the drug.
    Unpleasant effects when drug is absent - withdrawal -> strong negative reinforcement.
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11
Q

Discuss the environmental influences on addiction.

A

Vietnam war - 1/2 soldiers used heroin, when they returned to US, only 7% were addicted -> shows addiction is high dependent on circumstances.
Rat park - caged rats consume more morphine compulsively and rats in park prefer plain water.
Severely distressed animals like people will relieve their distress pharmacologically if they can.

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12
Q

How does addiction occur?

A

Drugs have highly positive reinforcing effect - high.

Negative reinforcement - feeling hungover/withdrawal - helped by more drinking.

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13
Q

Describe Skinner’s box.

A

Answers question - how is behaviour conditioned? As we go down the list, behaviour increases:

  1. rat presses lever to get food - positive reinforcement
  2. fixed interval schedule - food comes out every 5mins
  3. variable interval schedule - food comes every random number of presses (gambling)
  4. rat presses level to turn off electric shock - negative reinforcement.
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14
Q

What have studies on rats shown?

A

Rat in a cage will repeatedly self-administer heroin/cocaine even to point of death -> directly activating the dopamine reward system.
Electrodes implanted in the nucleus accumbens have the same effect.

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15
Q

What is the role of dopamine in addiction?

A

Dopamine levels spike with many pleasurable activities i.e. sex, eating.
All addictive drugs lead to increased dopamine levels in nucleus accumbens.
DA system linked to salience of an activity -> things that activate dopamine reward system become more important.
Addicts become less sensitive to natural reinforcers and substances become more salient.

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16
Q

What can you get addicted to?

A

Alcohol, drugs (legal - benzodiazepines, opiates, illegal - heroin, cocaine), gambling.
Activities associated with pleasure and activates dopamine reward system - sex, eating, porn, video games, shopping, exercise.

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17
Q

What makes a substance addictive?

A
  1. pleasure producing potency
  2. rapid onset of action
  3. short duration of action
  4. tolerance and withdrawal
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18
Q

What are the social and cultural attitudes to addiction?

A

Factors that influence societal consumption of alcohol:
- price
- availability
Alcohol has become more available and cheaper.
Education about dangers doesn’t make much difference.

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19
Q

Define motivational interviewing.

A

Counselling method that helps people resolve ambivalent feelings and insecurities to find the internal motivation they need to change their behaviour.
Interviewer evokes a conversation about change and commitment and listens and reflects back the patient’s thoughts so that the patient can hear their reasons and motivations.

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20
Q

How does life events cause stress?

A

Imbalance between the demands made on us and our personal resources to deal with these demands. Not the life events themselves that cause stress but the interpretation and the meaning to the individual.
Life events -> appraisal -> stress.

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21
Q

Define primary and secondary appraisal.

A

Primary - appraisal of the event.

Secondary - appraisal of personal coping abilities or personal resources and resources in the immediate social network.

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22
Q

What are the stress responses?

A

Emotional response - feeling on edge, irritability, tearful.
Cognitive response - difficulty concentrating, self-critical, difficulty making decisions.
Behavioural response - comfort eating, drinking/smoking, activity/underactivity.
Physiological response - increased HR, BR, perspiration.

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23
Q

Outline the links between a stress response and misinterpretation of physiological symptoms.

A

Stress -> physiological response -> physical symptoms -> misinterpretation -> anxiety -> physiological response -> cycles.
e.g. HR -> palpitations -> heart attack

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24
Q

Define medically unexplained symptoms.

A

Physical symptoms not explained by organic disease which cause distress and impair functioning and for which there is positive evidence or a strong assumption that the symptoms are linked to psychological factors e.g. stress, mental illness.
Patients have varying degrees of insight that some symptoms are due to psychological factors.

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25
Q

Define somatoform disorders.

A

Severe, chronic psychiatric disorders where patients have chronic and multiple MUS and are excessively disabled.

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26
Q

What are medically descriptive terms?

A

IBS, chronic fatigue syndrome, fibromyalgia, atypical non-cardiac chest pains.

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27
Q

How is stress linked to MUS?

A

Some MUS arise from normal bodily sensations (physiological processes) with misinterpretation.
Some MUS arise from minor pathology and are exaggerated at times of stress.

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28
Q

What is the biopsychosocial model of MUS?

A

Bodily sensations i.e. minor pathology, stress, physiological processes -> misinterpretation fed by beliefs/childhood experience and personality/mental state -> MUS and this is maintained by reaction of other iatrogenic secondary gains.

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29
Q

What is the impact of stress on physical illness?

A

Relates to relapse, control of chronic disease and morbidity.
Indirect - via behavioural changes e.g. poor compliance with medication, increased alcohol intake -> epilepsy and heart disease, reduced exercise -> heart disease.
Direct - stress activates HPA axis causing cortisol secretion and the sympathetic-adrenal-medullary system causing catecholamine secretion.

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30
Q

How does stress impact on heart disease?

A

Increased risk of death after loss of spouse - CVD accounts for 20-53% of excess deaths.

  1. acute bereavement associated with heightened SNS activation -> haemodynamic changes -> causing increases vascular resistance -> ischaemia.
  2. takotsubo cardiomyopathy - broken heart syndrome -> left ventricular dysfunction and ECG changes due to high levels of circulating catecholamines in post menopausal women.
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31
Q

How does stress impact mental illness?

A

Significant association between stressful life events and mental illness. 3-6 months preceding depressive illness, 50-80% patients will have experienced a significant life event.
6 fold excess of adverse life events in the months preceding the onset of depressive disorder.

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32
Q

What are the individual factors that lead to stress?

A

Premorbid personality - worrier, obsessive.
Prior experience of illness.
Mental state.
Childhood difficulties - early trauma, difficult interactions with health professionals.
Appraisals and coping styles.

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33
Q

Define illness appraisal.

A
Leventhal illness cognitions - a patient's own implicit common sense beliefs about their illness - provides framework around which a patient understands and copes with their illness.
5 dimensions:
1. identity - label and symptoms
2. timeline - perceived duration
3. consequences - expected outcome
4. cause - personal ideas about cause
5. control/cure - how to recover.
Using this framework, patients make an interpretation of their illness, select a coping style and appraises the coping style.
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34
Q

Define emotion focused model of coping.

A

Involves managing emotions and maintaining emotional equilibrium - works well transiently so reserved of brief stress or where nothing realistically can modify stress.

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35
Q

Define problem focused model of coping.

A

Controlling the problem and reconstructing it as manageable.

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36
Q

Describe ways of emotion focused coping.

A

Emotional discharge - talking about problems.
Making and maintaining supportive friendships.
Gaining emotional support from religion.
Resigned acceptance - coming to terms with it.

37
Q

Describe ways of problem focused coping.

A

Seeking info and support, learning new procedures and behaviours i.e. lifestyle changes, identifying alternative activities, developing a realistic action plan.

38
Q

Define pain.

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage.
Short-term pain - acute pain e.g. sprained ankle
Long-term pain - persistent chronic pain e.g. back ache. Pain extends beyond the expected period of healing and frequently has no identifiable cause.

39
Q

What is the epidemiology of chronic pain?

A

10% in Yorkshire living with chronic pain, 1,200 new patients/year. Majority managed in primary care.

40
Q

Describe the epidemiology of back pain.

A

12% sick days in UK, 116 mill days lost production, 3.1 mill adults in UK, 9.4% GP consultations.

41
Q

What are the red flags of LBP?

A

Cauda equina, cancer, infection, fracture, inflammatory arthopathy.
Other specific diagnoses - lumbar radicular syndrome, pain arising from facet joints and discs, spinal stenosis.

42
Q

Define non-specific LBP.

A

Tension, soreness, stiffness in the lower back region for which it is not possible to identify a specific cause of pain.

43
Q

What are the yellow flags of non-specific LBP?

A

Negative attitude that back pain is harmful or potentially disabling, fear avoidance behaviour, reduced activity level, expectation that it is passive, tendency to depression, low morale and social withdrawal, social and financial problems.

44
Q

What is the pain gate theory?

A

The spinal cord has a series of gate into which messages about pain arrive from all over the body via nerves. These can sometimes be more open than at other times thus the more you think about pain, the worse it feels.

45
Q

What can open the gates more?

A

Stress and anxiety
Psychological factors - focusing attention on it and boredom.
Lack of activity - stiff joints, reduced fitness.

46
Q

Define central sensitisation.

A

Condition of the NS that is associated with the development and maintenance of chronic pain. When CS occurs, the NS goes through a process “wind up” and gets regulated in a persistent state of high reactivity - this lowers the threshold for what causes pain and subsequently comes to maintain pain even after the initial injury might have healed.

47
Q

What are the 2 characteristics of CS?

A
  1. allodynia - at pain with things that isn’t normally painful - nerves in the area are in heightened state of reactivity.
  2. hyperalgesia - stimulus is more painful than it should be - heightened reactivity.
48
Q

What are the causes of CS?

A

Changes in dorsal horn of spinal cord and in the brain - at cellular level, receptors sites.
Strokes and spinal injuries can cause damage to CNS -> CS.

49
Q

How is chronic pain managed?

A

NICE recommendation - paracetamol, NSAIDs, tricyclic antidepressants and opioids only if low and intermittent.
Multimodal approach is recommended:
- behavioural/social -> pacing, goal setting, relaxation, return to work.
- psychological -> acceptance, CBT, mindfulness, psychoeducation.
- physical -> graded exercise, medication management, TENS, acupuncture.

50
Q

Describe the chronic pain MDT.

A

Medic/anaesthetists - medication, injections, spinal cord stimulators.
Specialist nurses - TENS, medication knowledge
Physiotherapists - TENS, strengthening and fitness exercises, posture.
OTs - pacing, goal setting, adaptations for functioning.
Psychologists - 1:1, group, risk management.

51
Q

What are the psychological factors in chronic pain?

A

Psychological threat can increase sensitivity to potential physical threats -> possibility of increased pain.
Pain can be a protective response to psychological stimuli and pain can be activated by non-physical elements e.g. memory.

52
Q

What is the holistic model of pain?

A

Looking at behaviour, thoughts, environment, moods and physical factors that could affect the patients chronic pain.

53
Q

What did Lazarus and Folkman say about chronic pain?

A

The meaning that people give to an event determines their response to it.
So people with negative beliefs about their pain can experience greater suffering.
e.g. if you think the LBP is due to a muscular strain from gardening -> paracetamol and hot shower. If you think something is really wrong -> significant worry and visit GP.

54
Q

What are the cognitive behavioural model of pain and depression?

A

Patient appraisals of the impact of their pain on their lives and their sense of control over their pain determines the pain-depression relationship.
Patients who believe they could still function despite pain and believed had some control - didn’t become depressed.

55
Q

What are the psychological approaches of managing chronic pain?

A

CBT
Third wave cognitive therapies - mindfulness, acceptance and commitment therapy (ACT) and compassion-focused therapy (CFT).

56
Q

How does CBT work?

A

Challenge thoughts + develop more helpful thoughts + develop and experiment new behaviours.

57
Q

How does mindfulness work?

A

Based on Buddhist meditative techniques.
Imaging studies have shown that mindfulness can soothe the brain patterns underlying pain.
Significantly reduces anxiety, stress, depression, irritability, insomnia that can arise from living with chronic pain.

58
Q

How is childhood trauma a risk factor for chronic pain?

A

Research shows prolonged anxiety, hyper-vigilance and fearfulness associated with early trauma leads to pain behaviour. 49% chronic pain patients report childhood physical and sexual abuse.
Morison found 55% of women being treated for somatic disorders also had history of childhood sexual abuse.

59
Q

Define somatisation.

A

The physical expression of psychological pain e.g. headaches, GI pain, pelvis and abdominal pain, back and neck pain.

60
Q

Define stress.

A

Any condition that actually or potentially poses a challenge to the body’s abilities to maintain homeostasis.

61
Q

Differentiate between eustress and distress.

A

Eustress - good, helpful, prepares us to meet challenges and improves performance.
Distress - bad, unpleasant, disease producing stress, impairs performance.

62
Q

Define stressors.

A

Any stimulus that produces a stress response.

63
Q

What are the different types of stressors?

A

External - physical environment, social interaction, major life events, daily hassles.
Internal - lifestyle choices, personality traits, negative self-talk.
Psychosocial events - unemployment, marriage, divorce, bereavement, work problems, money concerns.
Physiological events - blood loss, low blood glucose, cold or flu, surgery.

64
Q

Describe the stress response.

A
  1. alarm phase - initial fight or flight response (short-term)
  2. resistance or adaptation phase - body attempts to cope with prolonged stress (long-term).
  3. exhaustion phase - resources depleted and body unable to maintain function.
65
Q

Describe the alarm phase.

A

Fight or flight, rapid reaction to acute stress, short lived, activates the sympathetic branch of ANS.
Controlled by chemicals called catecholamines - adrenaline and NA.

66
Q

What is the sympathetic response to stress?

A

Increased HR, BP, blood diverted to heart and skeletal muscles, away from non-essential organs i.e. digestive, reproductive tracts.
Dilation of airways, conversion of glycogen to glucose in liver, increases alertness and sweating.

67
Q

Describe the HPA axis.

A

Resistance/adaptive phase:
Stress activates HPA axis - hypothalamic-pituitary-adrenal.
1. neurosecretory cells in hypothalamus releases corticotropin releasing hormone (CRH)
2. CRH activates anterior pituitary gland
3. anterior pituitary secretes adrenocorticotropic hormone (ACTH)
4. ACTH travels through blood to adrenal glands
5. ACTH stimulates cells in adrenal cortex to release cortisol (glucocorticoid).

68
Q

What are the effects of cortisol?

A

Lipids released into blood
Amino acids/proteins released from muscles to blood
Increase in blood glucose
Aldosterone released by adrenal cortex causes retention of Na+, increased water retention and increased BP
Immune suppression

69
Q

Differentiate between short-term stress response and long-term stress response.

A

Short term:
- increased HR and BP
- increased blood glucose
- muscles become energised
Long term:
Cortisol -> protein and fat metabolism instead of glucose breakdown and inflammation and immune cells suppressed.
Aldosterone -> Na+ and water retention and increased blood volume and BP.

70
Q

Define glucocorticoids.

A

Group of hormones of the adrenal cortex secreted during stress i.e. cortisol.

71
Q

What are the effects of excessive stress?

A

Anxiety, depression, high BP, ulcers, immune dysfunction, ageing, cancer, increased migraines and suppresses sex steroids.

72
Q

Describe the exhaustion phase.

A
Resources of the body become so depleted, they can't sustain the resistance phase.
Prolonged exposure to high cortisol:
- muscle breakdown
- IR suppression
- ulceration
- depression/psychosis
- failure of pancreatic beta cells
- ageing
73
Q

How is the amygdala and hippocampus involved in stress?

A

Involved in fear responses - activation of the central nucleus leads to stress response.

  • amygdala and hippocampus regulate CRH neurons in hypothalamus
  • amygdala activation stimulates HPA axis
  • hippocampal activation suppresses HPA axis
74
Q

Describe the cortisol feedback mechanism.

A

Circulating cortisol binds to glucocorticoid receptors in hippocampus -> activates hippocampus, which suppresses CRH released by hypothalamus -> reduces HPA activation -> less cortisol released by adrenals.

75
Q

Describe the role of stress in memory.

A

Emotionally salient events are remembered better than at neutral as amygdala and stress hormones involved.
Injecting cortisol enhances memory whereas propranolol and amygdala lesions reduces memory.

76
Q

What is the role of stress on the immune system?

A

Acute stressors upregulate IS
Chronic stress inhibits IS - mediated by glucocorticoid:
- cortisol decreases B and T cell numbers
e.g. widows have dampened IS
Glucocorticoid have a potent anti-inflammatory and immunosuppressive properties i.e. prednisolone used to treat arthritis.

77
Q

Define anxiety.

A

Inappropriate expression of fear - unrealistic and unfounded.
Fear response occurs in an anticipatory manner - interferes with daily life.
Psychological disorder.

78
Q

What are the typical symptoms of anxiety?

A

Tension, overactivity of ANS, upset stomach, expectation of an impending disaster, continuous vigilance, insomnia.

79
Q

List the types of anxiety disorders.

A
Generalised anxiety disorder
Panic disorder
Phobias
OCD
PTSD
80
Q

Describe GAD.

A

Ongoing state of anxiety lacking any reason or focus.
Duration - at least 6 months
Worrying excessive about many issues i.e. money, health, family.

81
Q

Describe panic disorder.

A

Brief periods of intense terror and apprehension.
Symptoms - SOB, hyperventilation, heart palpitations, chest tightness, trembling, dizziness - misinterpreted as heart attack.

82
Q

Describe phobias.

A

Strong fear of specific things or situations i.e. open spaces, flying, snakes.

83
Q

Describe OCD.

A
Intrusive thoughts (obsessions) cause anxiety i.e. contamination with germs. 
Compulsions are repetitive behaviours that try to neutralise anxiety i.e. frequent hand washing.
84
Q

Describe PTSD.

A

Anxiety triggered by recall of past stressful experiences i.e. military combat, serious accidents.
People relive the experience through nightmares and flashbacks and have difficulty sleeping and feel detached.
Increased arousal and avoidance of stimuli associated with trauma.
Hippocampus size reduced and abnormal activation of amygdala.

85
Q

What treatment options are there for anxiety?

A

Psychological - first line i.e. CBT

Pharmacological - second line but in combo with psychotherapy i.e. benzodiazepines, SSRIs, beta-blockers.

86
Q

Describe the MoA of benzodiazepines.

A

GABA agonists - bind to regulatory sites on GABA receptors to enhance the inhibitory effects of GABA in the brain.
Increases the influx of negatively charged Cl- into neurones -> hyper polarisation and inhibits AP.
Causes suppression of brain circuits in stress response.

87
Q

What are the effects, examples and side effects of benzodiazepines?

A

Effect - reduces anxiety, sedative for insomnia, muscle relaxant. Effective in short-term for acute anxiety.
e.g. diazepam, temazepam, clonazepam
Side effects - drowsiness, confusion, amnesia, impaired concentration, withdrawal symptoms and addictive with long-term use.

88
Q

Describe the use of SSRIs for anxiety.

A

e.g. fluoxetine (prozac)
Used to treat mood disorders - antidepressants but also used for anxiety e.g. GAD and OCD.
Prolonged action of serotonin by blocking reuptake.

89
Q

Describe the use of beta-blockers for anxiety.

A

e.g. pronanolol

Reduces sympathetic symptoms of anxiety i.e. tremor, palpitations and sweating.