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ALS > Block 6 > Flashcards

Block 6 Flashcards

1
Q

what is consciousness?

A

state of being aware of and responsive to ones surroundings

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2
Q

what is the psychological definition of consciousness?

A

a persons awareness of perception of something

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3
Q

what are the levels of consciousness? (14)

A
  1. fully conscious
  2. clouding of consciousness
  3. confusional state
  4. delirium
  5. lethargy
  6. obtundation
  7. stuper
  8. hypersomina
  9. minimally responsive state
  10. unresponsive wakefulness syndrome
  11. akinetic mutism
  12. locked in syndrome
  13. coma
  14. brain death
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4
Q

what is a normal loss of consciousness?

A

sleep

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5
Q

what is an abnormal loss of consciousness? (3)

A
  • coma
  • anaesthesia
  • unresponsive wakefulness syndrome
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6
Q

what is the most common cause of unconsciousness worldwide?

A

Malaria (cerebral)

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7
Q

what is the most common cause of unconsciousness in the UK?

A

stroke

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8
Q

what ways can you assess consciousness? (4)

A
  • ABC
  • history
  • screening
  • glasgow coma scale
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9
Q

what are the 3 domains of the Glasgow coma scale?

A
  • eye opening
  • verbal response
  • motor response
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10
Q

what Glasgow coma scale score does a fully conscious patient have?

A

15

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11
Q

what Glasgow coma scale score does a deep coma patient have?

A

3

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12
Q

what do the scores on the Glasgow coma scale show? (3)

A
  • 13-15 - mild head injury
  • 9-12 - moderate head injury
  • 3-8 - severe head injury
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13
Q

what % of cases of Unresponsive Wakefulness Syndrome were misdiagnosed?

A

40%

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14
Q

what are the features brainstem death? (3)

A
  • person must be unconscious and fail to respond to stimulation
  • heartbeat and breathing maintained by a ventilator
  • clear brain damage has occurred - incurable
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15
Q

what is the definition of brainstem death?

A

the irreversible cessation of the function of the brainstem and loss of capacity for consciousness

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16
Q

how do we test for brainstem death? (6)

A
  • pupil response - shine torch
  • corneal reflex - stroke cornea
  • vestibule-occular reflex - ice-cold water in ear
  • cranial nerve response - supraorbital pressure to elicit motor response
  • cough/gag reflex - Catheter down trachea
  • respiratory effort - disconnect ventilator for 5 mins
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17
Q

what regulates consciousness?

A

Reticular Activating System (RAS)

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18
Q

what is the reticular formation?

A

collection of nuclei found throughout midbrain and extends into the hindbrain

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19
Q

what four nuclei make up the Reticular Activating System?

A
  1. locus coeruleus
  2. raphe nuclei
  3. ventral tegmental area
  4. cholinergic nuclei
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20
Q

what is the main neurotransmitter of the locus coeruleus?

A

noradrenaline

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21
Q

what is the main neurotransmitter of the raphe nuclei?

A

seretonin

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22
Q

what is the main neurotransmitter of the ventral tegmental area?

A

dopamine

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23
Q

what is the main neurotransmitter of the cholinergic nuclei?

A

acetylcholine

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24
Q

what two other areas are considered to be involved in consciousness?

A
  • anterior hypothalamus
  • posterior hypothalamus
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25
Q

what is the main neurotransmitter of the anterior hypothalamus?

A

GABA

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26
Q

what is the main neurotransmitter of the posterior hypothalamus?

A

histamine

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27
Q

what is the Reticular Activating System involved with? (3)

A
  • sleep-wake cycle
  • arousal
  • attention
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28
Q

what areas are involved in sleep? (3)

A
  • cerebral cortex
  • reticular nucleus
  • thalamus
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29
Q

what happens to cholinergic fibres when awake?

A

increase firing

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30
Q

what happens to cholinergic fibres when asleep?

A

decrease firing

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31
Q

what are features of the wake cycle when awake? (4)

A
  • Ach active
  • sensory thalamus facilitated
  • reticular nucleus inhibited
  • EEG desynchronous
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32
Q

what are features of the wake cycle when asleep? (4)

A
  • Ach inactive
  • sensory thalamus inhibited
  • reticular nucleus active
  • EEG synchronous
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33
Q

what three neurons interact to form oscillations in EEGs?

A
  • thalamocortical
  • reticular
  • corticothalamic
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34
Q

what are the two main types of sleep?

A
  • non-REM
  • REM
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35
Q

what are the EEG waves in NREM sleep? (2)

A

slow and synchronised

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36
Q

what are the EEG waves in REM sleep?

A

high frequent activity

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37
Q

which sleep is associated with dreams?

A

REM

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38
Q

how long does each sleep cycle last?

A

90 minutes

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39
Q

what are some common sleep disorders? (3)

A
  • sleep apnoea
  • enuresis
  • epilepsy
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40
Q

what are the short term consequences of sleep deprivation? (6)

A
  • slower reflexes
  • memory disorder
  • muscle fatigue
  • mood swings
  • aggressive behaviour
  • disorientation
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41
Q

what are the long term consequences of sleep deprivation? (4)

A
  • obesity
  • diabetes
  • high BP
  • CVD
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42
Q

what is antisocial behaviour?

A

behaviour that transgresses a society’s rules, norms and laws that is likely to cause harm to others

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43
Q

what does the 2003 Anti-Social Behaviour define antisocial behaviour as?

A

behaviour by a person which causes or is likely to cause harassment, alarm or distress to person not of the same household

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44
Q

how many 5-19yr olds present antisocial behaviour?

A

4.6%

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45
Q

what is the % difference for boys and girls displaying antisocial behaviour?

A
  • boys - 5.8%
  • girls - 3.4%
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46
Q

how much does conduct disorder cost per young person?

A

£103k

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47
Q

where in society does antisocial behaviour affect? (5)

A
  • policing
  • social work
  • education provision
  • impact of crime
  • criminal justice process
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48
Q

what are examples of antisocial behaviour syndromes? (3)

A
  • Oppositional Defiant Disorder - younger children <10
  • Conduct Disorder - adolescents
  • Antisocial Personality Disorder - adults
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49
Q

what is conduct disorder? (2)

A
  • persistent behavioural problems
  • defiant, disobedient, provocative, spiteful behaviours
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50
Q

what are the three domains of Limited Prosocial Emotions?

A
  • daring impulses
  • callous unemotional
  • grandiose manipulative
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51
Q

what are some common learning difficulty co-morbidities with conduct disorder? (6)

A
  • learning problems
  • literacy issues
  • speech & language problems
  • global learning disability
  • autism spectrum conditions
  • ADHD
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52
Q

what are some common mental health co-morbidities with conduct disorder? (7)

A
  • depression
  • anxiety
  • psychosis illness
  • substance misuse
  • PTSD
  • attachment issues
  • personality disorder
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53
Q

how do we assess young people with conduct issues? (6)

A
  • NICE guidelines
  • multidisciplinarys
  • cognitive assessment
  • info from different sources
  • developmental history
  • mental health assessment
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54
Q

what are some examples of adverse childhood experiences? (8)

A
  • physical abuse
  • verbal abuse
  • sexual abuse
  • alcoholic parent
  • physical neglect
  • emotional neglect
  • family members in jail
  • family members diagnosed with illness
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55
Q

what did Kendler’s (2014) Scandinavian adoption studies show? (2)

A
  1. risk for all conduct behaviour was higher in the adopted offspring of biological parents with conduct behaviour
  2. risk higher if there are environmental risk factors in adoptive home
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56
Q

what is the environmental argument for antisocial behaviour?

A
  • ‘warrior gene’
  • Monoamine oxidase A gene
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57
Q

what is the role of the monoamine oxidase A gene?

A

breaks down MA neurotransmitters (dopamine, serotonin, etc…) in synaptic cleft

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58
Q

what happens to MAOA in antisocial behaviour individuals?

A

low activity results in higher aggression

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59
Q

what are the psychosocial management techniques for conduct disorder? (3)

A
  • Parent-Management Training (PMT)
  • Cognitive Behavioural Therapy (CBT)
  • Multi-Systemic Therapy
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60
Q

what are the two major groups of neurotransmitters?

A
  1. small molecules
  2. neuropeptides
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61
Q

what are four classes of neurotransmitters?

A
  • Ach
  • Biogenic amines
  • Amino acids
  • Gases -
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62
Q

what is co-transmission?

A

releasing more than one neurotransmitter at the same time

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63
Q

what is low frequency stimulation?

A

release of small vesicles

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64
Q

what is high frequency stimulation?

A

release of small and large vesicles

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65
Q

what are the characteristics for a chemical messenger to be a neurotransmitter? (5)

A
  1. chemicals must be synthesised in the neuron
  2. when released, must produce a response in target cell
  3. specific receptors are on post synaptic cell
  4. induce the same response when on target
  5. must be removed from synaptic cleft
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66
Q

what are two main receptors on the post-synaptic cell?

A
  • ionotropic - ion channels
  • metabotropic - binds to G proteins
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67
Q

what is the most common neurotransmitter in the PNS?

A

acetylcholine

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68
Q

where is acetylcholine found?

A

neurons of the hippocampus and cerebral cortex

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69
Q

how does acetylcholine transmission work? (4)

A
  1. choline and acetyl coA bind to form Ach
  2. Ach packaged with vesicle
  3. fuse with membrane and release Ach
  4. Ach broken down by acetylcholine-esterase
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70
Q

what are the two types of cholinergic receptors?

A
  • nicotinic receptors
  • muscarinic receptors
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71
Q

what type of receptor is the nicotinic receptor?

A

ionotropic

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72
Q

what type of receptor is the muscarinic receptor?

A

metabotropic

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73
Q

what are the three amino acids involved in neurotransmission?

A
  • glutamate
  • GABA
  • Glycine
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74
Q

how does glutamine transmission work? (4)

A
  1. glutamine converted to glutamate by glutaminase
  2. glutamate processed in vesicle, released into synapse
  3. binds to receptors OR gets taken back up by cell to be released
  4. Glial cells reuptake and process back to glutamine for the presynaptic cell
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75
Q

what are the three subtypes of glutamate receptor?

A
  • AMPA
  • NMPA
  • Kainate
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76
Q

How do the glutamate receptors work? (5)

A
  1. release glutamate into synaptic cleft
  2. glutamate binds to ADMA receptor
  3. AMDA receptor opens, allow Na+ entry, depolarises cell
  4. NMDA receptors release Mg+, allowing calcium entry
  5. This drives the signal
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77
Q

How does GABA transmission work? (3)

A
  1. glutamate is converted to GABA by glutamate decarboxylase
  2. released into synaptic cleft
  3. uptake by glial cell, turned back to glutamine, re-enters the pre-synaptic cell
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78
Q

what type of receptor are GABA receptors?

A

ionotrophic

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79
Q

how many subunits do glutamate receptors have?

A

3

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80
Q

how many subunits do GABA receptors have?

A

5

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81
Q

what do benzodiazapams treat?

A

Epilepsy

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82
Q

how do benzodiazapams work to treat epilepsy?

A

enhances the inhibition, this controls the excessive excitation

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83
Q

in the postsynaptic cell, what does acetylcholine get converted back to? (2)

A

choline and acetic acid

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84
Q

in the presynaptic cell, what does glutamine get converted to? (2)

A

glutamate by glutaminase

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85
Q

in the presynaptic cell, how is glycine produced? (2)

A

serin converted to glycine by SHMT

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86
Q

in the glial cell, what does glycine get broken down into? (2)

A

CO2 and NH3

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87
Q

how does glycine work? (2)

A
  1. Renshaw cells use Glycine to link to the reccurent neuron
  2. Neuron acts as inhibitor, switches off motor neuron
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88
Q

what are examples of biogenic amines? (2)

A
  • catecholamines (noradrenaline, adrenaline, dopamine)
  • seretonin
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89
Q

how are catecholamines inactivated? (3)

A
  1. uptake
  2. enzymatic breakdown
  3. diffusion away from receptors
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90
Q

how is dopamine synthesised? (2)

A
  1. tyrosine converted to L-DOPA by tyrosine hydroxase
  2. L-DOPA converted to dopamine by dopa decarboxylase
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91
Q

what three pathways is dopamine involved in? (3)

A
  • mesolimbic - reinforcement
  • mesocortical - planning
  • nigrostriatal - movement
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92
Q

how is noradrenaline synthesised? (1)

A

Dopamine converted to noradrenaline by dopa-B-hydroxylase

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93
Q

how is serotonin synthesised? (2)

A
  1. tryptophan converted to 5-Hydroxtytophan by tryptophan hydroxylase
  2. 5-Hydroxtytophan converted to 5 Hydroxytryptamine by 5-HTP decarboxylase
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94
Q

what can serotonin be broken down into?

A

melatonin

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95
Q

which serotonin receptor is involved in anxiety?

A

5-HT1a

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96
Q

what is a neuromodulator?

A

neurotransmitters that do not conform to their actions

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97
Q

what is substance P?

A

peptide neurotransmitter

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98
Q

which receptor does substance P bind strongest to?

A

NK1

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99
Q

what is a mental state exam?

A

covers psychiatric symptomatology shown at interview

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100
Q

how do you start a mental state exam?

A
  • private space
  • quiet space
  • face towards patient
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101
Q

what are the components of the mental state exam? (7)

A
  1. appearance and behaviour
  2. speech
  3. mood
  4. thought content
  5. abnormal beliefs
  6. cognitive state
  7. insight
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102
Q

what do you look for appearance of the mental state exam? (2)

A
  • general appearance
  • facial appearance
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103
Q

what are the features of appearance in schizophrenic patients? (5)

A
  • echopraxia
  • tics
  • poor eye contact
  • increased movements
  • restlessness
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104
Q

what is stupor?

A

mute, immobile but fully conscious

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105
Q

what is depressive retardation?

A

a lesser form of psychomotor retardation

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106
Q

what is obsessional slowness?

A

secondary to repeated doubts and compulsive rituals

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107
Q

what is psychomotor agitation?

A

overactivity usually unproductive

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108
Q

what is compulsion?

A
  • repetitive and stereotyped
  • seemingly purposeful
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109
Q

what do you look for speech of the mental state exam? (4)

A
  • rate
  • quality
  • articulation
  • form
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110
Q

what is poverty of speech?

A

restricted amount of speech

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111
Q

what is pressure of speech?

A

increased rate & quantity

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112
Q

what is dysarthria?

A

difficulty in articulation of speech

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113
Q

what is neologism?

A

new words being constructed

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114
Q

what is echolalia?

A

automatic imitation by patient of another persons speech even when they dont understand it

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115
Q

what is thought blocking?

A

sudden interruption in train of thought leaving a blank

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116
Q

what is knights move thinking?

A

odd associations between ideas leading to disruption in continuity

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117
Q

what two assessments should be carried out for mood in a mental health exam?

A
  • objective assessment
  • subjective assessment
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118
Q

what is dysphoric mood?

A

unpleasant mood

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119
Q

what is anhedonia?

A

loss of ability and interest in regular activities

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120
Q

what is euphoria?

A

elevation of mood

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121
Q

what is irritable mood?

A

annoyed and provoked to anger

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122
Q

what is anxiety?

A

feeling of apprehension, tension or uneasiness owing to anticipation of an external/internal danger

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123
Q

what is affect?

A

pattern of observable behaviours that is the expression of emotion

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124
Q

what is an inappropriate affect?

A

appearing cheerful when talking about recent bereavement

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125
Q

what is a flat affect?

A

total absence of signs of expression of affect

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126
Q

what is a delusion?

A

fixed, false personal belief based on incorrect inference about external reality

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127
Q

what is a primary delusion?

A

arises fully formed without any discernible connection with previous events

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128
Q

what is secondary delusion?

A

arises when trying to make sense of their experiences

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129
Q

what is an illusion?

A

false perception of a real external stimulus

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130
Q

what is a hallucination?

A

false sensory perception in the absence of a real external stimulus

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131
Q

what do you look for cognitive of the mental state exam? (4)

A
  • orientation - time, place, person
  • attention and concentration - spelling backwards
  • memory - recall
  • general knowledge - current news event
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132
Q

What is episodic memory?

A

Memory of events

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133
Q

What is semantic memory?

A

Factual knowledge

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134
Q

Why are childhood memories spared in amnesia?

A

Through a process of consolidation, memories lose their reliance on the hippocampus

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135
Q

What are the two stores of long-term memory?

A
  • Hippocampus
  • Anterior temporal lobes
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136
Q

What type of memory does the anterior temporal lobe store?

A

Sematic memory

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137
Q

What condition is there damage to the anterior temporal lobe?

A

Semantic dementia

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138
Q

What is amnesia?

A

Inability to learn new long-term memories

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139
Q

What is semantic dementia?

A

Loss of knowledge

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140
Q

What are positive symptoms of schizophrenia? (2)

A
  • Hallucinations
  • Delusions
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141
Q

What are first-rank symptoms of schizophrenia? (3)

A
  • Thought interference
  • Delusion of control
  • 3rd person auditory-verbal hallucinations
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142
Q

What are negative symptoms of schizophrenia? (4)

A
  • Lack of motivation
  • Reduced speech
  • Reduced emotion
  • Social withdrawal
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143
Q

What two factors contribute to neurodevelopment abnormality?

A
  • Genetic component
  • Environmental factors
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144
Q

What are the arguments for the dopamine hypothesis? (3)

A
  • Antipsychotics block postsynaptic dopamine receptors
  • PET and SPECT scans show increase dopamine activity in ppl with schizophrenia
  • Evidence of elevated presynaptic dopamine synthesis and release
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145
Q

What are the arguments against the dopamine hypothesis? (3)

A
  • Cause of schizophrenia may be upstream
  • Antipsychotics take 2+ weeks to work on symptoms
  • Other transmitters appear to be involved with psychosis e.g. glutamate
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146
Q

What is the aim of treatment for negative schizophrenia symptoms? (2)

A
  • Increase dopamine transmission
  • Via mesocortical pathway
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147
Q

What is the aim of treatment for positive schizophrenia symptoms? (2)

A
  • Decrease dopamine transmission
  • Via mesolimbic pathway
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148
Q

Which receptor do antipsychotics target? (2)

A
  • Antagonise D2 receptors
  • In mesolimbic system
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149
Q

Which receptors do first generation antipsychotics target?

A

D1 and D2

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150
Q

Which receptors do second generation antipsychotics target?

A

D2 and seretonin, less on D1

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151
Q

How does a partial agonist exert it’s effect on dopamine? (2)

A
  • Act as a D2 antagonist where there is too much dopamine
  • Act as a D2 agonist where there is too little dopamine
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152
Q

What is depression?

A

Persistent low mood/self-esteem with reduced enjoyment/interest

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153
Q

What is depression a result of?

A

Deficient in brain monoamine neurotransmitters - noradrenaline, serotonin and dopamine

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154
Q

What does serotonin influence? (3)

A
  • Mood
  • Emotional behaviour
  • Sleep
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155
Q

What does noradrenaline influence? (4)

A
  • Sleep
  • Wakefulness
  • Attention
  • Feeding behaviour
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156
Q

What does dopamine influence? (2)

A
  • Motivation
  • Reward
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157
Q

What are the arguments of the Monoamine theory of depression? (3)

A
  • Antidepressants increase the available of monoamine at synapses
  • Reserpine which depletes MOA transmission causes depression
  • People with depression have lower levels of MOA precursors in the blood
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158
Q

What are the arguments against the Monoamine theory of depression? (2)

A
  • Take 2+ weeks to work
  • Cocaine and amphetamine mimic serotonin but do not act as antidepressants
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159
Q

What are examples of antidepressant therapies? (4)

A
  • Tricyclic antidepressants
  • SSRIs
  • Monoamine Oxidase Inhibitors (MAOIs)
  • Serotonin Noradrenaline reuptake inhibitors (SNRI)
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160
Q

What are the side effects of tricyclics to treat depression? (4)

A
  • Antagonises H1 receptors - sedation
  • Antagonises muscarinic receptors - dry mouth, blurred vision
  • Antagonises alpha adreno receptors - postural hypotension
  • Toxic in overdose
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161
Q

What are the side effects of SSRIs to treat depression? (5)

A
  • Nausea and vomiting
  • Sexual dysfunction
  • Inhibit metabolism of other drugs
  • Withdrawal reaction
  • Safer in overdose
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162
Q

Why do antidepressants take two weeks to work? (3)

A
  • Initial increase in 5HT is cancelled out by presynaptic auto-receptors reducing 5HT release and more reuptake of the extra 5HT in the synapses
  • After couple of weeks auto receptors desensitize and block reuptake transporters
  • Eventual 5HT increase in synapse
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163
Q

What happens when GABA receptors are stimulated? (2)

A
  • GABA receptors allow flux of Cl ions across post synaptic membrane
  • Hyperpolarises the neurone
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164
Q

What do benzodiazepines bind to?

A

GABA receptor allosteric site

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165
Q

What is the effect of benzodiazepines?

A

Increases Cl- flux and more inhibition

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166
Q

What are the side effects of benzodiazepines? (4)

A
  • Drowsiness
  • Confusion
  • Forgetfulness
  • Impaired motor control
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167
Q

What is the enteric system responsible for?

A

Gastric system

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168
Q

How does vesamicol presynaptically block nerve function?

A

Blocks Ach uptake into vesicles

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169
Q

How does Hemicholinium presynaptically block nerve function?

A

Blocks reuptake of Ach into presynaptic cell

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170
Q

How does Botulinium presynaptically block nerve function?

A

Blocks release of Ach vesicles into the cleft

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171
Q

What are the two types of cholinesterase inhibitors? (2)

A
  • Reversible
  • Irreversible
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172
Q

How do reversible cholinesterase inhibitors work? (2)

A
  • Bind to the enzyme for a period of time
  • Enzyme inhibited until inhibitor is removed
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173
Q

How do irreversible cholinesterase inhibitors work?

A

Covalent bond preventing reactivation

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174
Q

How do non-depolarising agents work as post synaptic inhibitors? (3)

A
  • Act as competitive antagonists
  • Does NOT cause an action potential
  • Causes muscle relaxation
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175
Q

How do depolarising agents work as post synaptic inhibitors? (2)

A
  • Bind to Ach receptors and generate an AP
  • Causes muscle fasculations
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176
Q

What are antagonist muscarinic receptor drugs used for?

A

Reverse non-depolarising neuromuscular blocking agents

177
Q

What is atropine used for?

A

Reverse effects of organophosphate poisoning

178
Q

What is scopolamine used for?

A

Nausea and vomiting

179
Q

What is pilocarpine used for?

A

Reduce pressure in eye (glaucoma)

180
Q

What are some examples of catecholamines? (4)

A
  • Noradrenaline
  • Adrenaline
  • Dopamine
  • Isoprenaline
181
Q

What are the three noradrenaline transport systems?

A
  • Neuronal
  • Extraneuronal
  • Vesicular
182
Q

What does tyramine convert to and release into the synaptic cleft?

A

Noradrenaline

183
Q

How do drugs target synaptic MAO inhibitors? (3)

A
  • Non selective MAO inhibitors
  • MAO A inhibitors
  • MAO B inhibitors
184
Q

What are physical symptoms of anxiety? (3)

A
  • Muscle tension
  • Hyperventilation
  • Sympathetic overactivity
185
Q

What are psychological symptoms of anxiety? (3)

A
  • CNS - poor conc, memory
  • Mood - fear, panic
  • Thoughts - future danger
186
Q

What are unhelpful behaviours of anxiety? (5)

A
  • Pacing room
  • Attempts at coping - caffeine, smoking
  • Avoiding fear stimulations
  • Safety behaviours
  • Asking for reassurance
187
Q

What are the treatments for anxiety? (7)

A
  • Education
  • Relaxation
  • Advice on sleep
  • CBT
  • SSRIs
  • Benzodiazepines
  • Beta blockers
188
Q

What are the 5 key questions of a clinical assessment of anxiety? (5)

A
  1. Normal reaction to stress?
  2. Secondary to physical/mental illness?
  3. Lifelong personality trait?
  4. Triggered by a specific object?
  5. Is it present from time to time or all the time?
189
Q

What are the three stages of the simple cognitive model for panic disorder?

A
  1. Sensation - e.g. heart racing
  2. Interpretation - having heart attack
  3. Panic
190
Q

What is Clarke’s Cognitive Model (1986)? (6)

A
  1. Trigger
  2. Viewed as a threat
  3. Anxiety and panic
  4. Leads to physical and mental symptoms
  5. Leads to safety behaviours, avoidance, selective attention
  6. Leads to misinterpretation - catastrophic thoughts - back to 3
191
Q

What is learning?

A

Relatively permanent change in behaviour that occurs because of experience

192
Q

What does learning enable humans to do?

A

Adapt to environment and increase chances of survival

193
Q

What is the brain structure is involved in learning?

A

Amygdala

194
Q

What are the types of learning? (4)

A
  • Associative
  • Vicarious
  • Factual transmission
  • Complex learning
195
Q

What is associative learning?

A

Learning that certain events go together

196
Q

What is an example of associative learning?

A

Classical and operant conditioning

197
Q

What is vicarious learning?

A

Learning by direct observation

198
Q

What is an example of vicarious learning?

A

Modelling

199
Q

what is an example of complex learning? (2)

A
  • Social learning
  • Emotional intelligence
200
Q

Who described classical conditioning?

A

Pavlov (1927)

201
Q

Who described operant conditioning?

A

Skinner (1938)

202
Q

What are the two types of associative learning models?

A
  • Classical conditioning
  • Operant conditioning
203
Q

What is the definition of classical conditioning?

A

A learning process where a previously neutral stimulus becomes associated with another stimulus by repeated pairing

204
Q

What is the definition of operant conditioning?

A

The alteration of behaviour by reward or punishment e.g. certain responses are learned because they affect the environment

205
Q

What is an example of classical conditioning?

A

Pavlov’s dogs

206
Q

What are examples of operant conditioning? (4)

A
  • Positive reinforcement (praise)
  • Negative reinforcement (picking up crying baby)
  • Punishment (smacking)
  • Extinction (time out)
207
Q

What are the stages of Pavlov’s dogs? (4)

A
  1. Unconditioned stimulus (food) leads to unconditioned response (saliva)
  2. Conditioned stimulus (bell) leads to no stimulation
  3. Conditioned stimulus presented with UCS (food) leads to UCR (saliva)
  4. Conditioned stimulus leads to conditioned response (saliva)
208
Q

What are some examples of classical conditioning? (5)

A
  • Food cues - salivation
  • Music in films - enhances emotions
  • Meeting an old friend - old memories
  • Visit to doctors’ surgery - pain/anxiety
  • Chemotherapy - nausea entering room
209
Q

Which operant conditioning types increase the likelihood of desired behaviour? (2)

A
  • Positive reinforcement
  • Negative reinforcement
210
Q

Which operant conditioning types decrease the likelihood of desired behaviour? (2)

A
  • Punishment
  • Extinction
211
Q

What does positive reinforcement involve?

A

Presenting a pleasant stimulus after a desire behaviour has occurs

212
Q

What does negative reinforcement involve?

A

Removing an unpleasant stimulus after an undesired behaviour occurs

213
Q

What does punishment involve?

A

Presenting an unpleasant stimulus after an undesired behaviour occurs

214
Q

What does extinction involve?

A

Removing a previously pleasant stimulus

215
Q

What is an example of positive reinforcement?

A

Praise for a good exam result

216
Q

What is an example of negative reinforcement?

A

Picking up a crying baby

217
Q

What is an example of extinction?

A

Time out for toddlers

218
Q

What did Thorndike’s Law of Effect (1911) argue?

A

Successful behaviour will be repeated (vice versa)

219
Q

What are the types of reinforcers in Thorndike’s Law of Effect? (2)

A
  • Primary (food, water, escape from pain/cold)
  • Secondary (money, praise, attention, success)
220
Q

What must be needed for reinforcers to work?

A

Immediate/linked to the act

221
Q

What are the two types of positive reinforcement?

A
  • Continuous
  • Partial
222
Q

What are the types of partial reinforcement? (2)

A
  1. Ratio schedules - depends on the number of responses e.g. paid after every 3 shirts made
  2. Interval schedules - depends on the time interval e.g. paracetamol every 4 hours
223
Q

What can partial reinforcement be?

A
  • Fixed - predictable
  • Variable - unpredictable
224
Q

Which reinforcement do people work harder under?

A

Partial

225
Q

What is shaping?

A

Rewarding behaviours which increasingly approximate to the desired more complex behaviour e.g. learning to walk, talk, drive

226
Q

What is chaining? (3)

A
  • Breaking down complex behaviours into series of simple acts
  • Each reinforces next in chain
  • E.g. holding spoon, later to put spoon in bowl to get praise
227
Q

What is negative reinforcement?

A

Removal of an aversive stimulus after a desired behaviour has occurred

228
Q

What is an example of negative reinforcement? (4)

A
  1. Baby cries
  2. Mum picks baby up
  3. Baby stops crying
  4. Mum negatively reinforced (do it next time)
229
Q

What is a phobia? (2)

A
  • A marked persistent fear triggered by a specific object/situation
  • Leads to avoidance of that situation
230
Q

What are the types of phobias? (3)

A
  • Agoraphobia - public places, crowds, shops
  • Social phobia - eating, speaking, performing
  • Specific phobia - animals, heights, needles
231
Q

How is a phobia maintained? (4)

A
  1. Phobic stimulus
  2. Anxiety
  3. Avoidance or escape
  4. Anxiety reduced - back to 1
232
Q

What is graded exposure?

A

The deliberate confrontation of a feared object or situation until the anxiety evoked reduces

233
Q

What are the treatments of phobias? (2)

A
  • Graded exposure
  • SMART targets
234
Q

What is punishment?

A

Presentation of an unpleasant stimulus after an undesired behaviour occurs

235
Q

What must punishment be to be effective? (3)

A
  1. Link response to consequences
  2. Be consistently applied
  3. Sufficiently applied the first time
236
Q

What are the problems with punishment? (4)

A
  • Physical or emotional harm
  • Paradoxical attention
  • Teaches aggression as a model to solve difficulties
  • Leads to fear/dislike of person
237
Q

What is extinction?

A

A decrease in behaviour by withholding a previous reward

238
Q

What is an example of extinction?

A

Time out for toddler tantrums

239
Q

What are the 10 symptoms for recognising depression?

A
  • D - depressed mood
  • E - energy loss
  • P - pleasure lost
  • R - retardation
  • E - eating changed
  • S - sleep changed
  • S - suicidal thoughts
  • I - I’m a failure
  • O - only me to blame
  • N - not able to function
240
Q

How many number of symptoms are needed to recognise depression? (3)

A
  • Mild depression - 4
  • Moderate - 5-6
  • Severe - 7
241
Q

How does CBT work to treat depression? (3)

A
  • Cognitive - challenge unhelpful and extreme ways of thinking
  • Behavioural - behavioural activation e.g. goal setting
  • Therapy - talking treatment
242
Q

What is Beck’s Cognitive Triad (1976)?

A

Depression is caused and maintained by negative views of…
- The Self… as worthless
- The World… as unfair
- The Future… as hopeless

243
Q

What are the aims of behavioural activation? (3)

A
  • Do something, not nothing
  • Stop avoiding and ruminating
  • Reverse the vicious cycle
244
Q

What is dementia?

A

An acquired, chronic and progressive cognitive impairment, sufficient to impair ADLs

245
Q

What age do you tend to develop dementia?

A

65+

246
Q

What does dementia often begin with?

A

Forgetfulness

247
Q

What does dementia lead to after forgetfulness?

A

Disorientation in time, then place, then person

248
Q

What does the risk of dementia increase with?

A

Age

249
Q

What is the % risk of dementia over the age of 65?

A

5%

250
Q

What is the % risk of dementia over the age of 80?

A

20%

251
Q

Which gender does dementia affect more?

A

Females

252
Q

What are types of dementia? (4)

A
  • Alzheimer’s
  • Vascular
  • Lewy body
  • Frontotemporal
253
Q

What is the most common type of dementia?

A

Alzheimer’s

254
Q

What is the cause of Alzheimer’s dementia?

A

Abnormal protein deposits lead to neuronal death

255
Q

How can you categorise symptoms of Alzheimer’s? (3)

A
  • Mild - wondering and getting lost, repeating questions
  • Moderate - problems recognising friends and family
  • Severe - expressive and receptive aphasia
256
Q

What is the second most common dementia?

A

Vascular

257
Q

What is the cause of vascular dementia?

A

Disrupted blood flow to the brain e.g. blood clots

258
Q

What are the symptoms of vascular dementia? (4)

A
  • Forgetting current or past events
  • Trouble following instructions or learning new info
  • Hallucinations or delusions
  • Poor judgement
259
Q

What is the cause of Lewy body dementia?

A

Abnormal deposits of the alpha-synuclein protein

260
Q

What are the symptoms of Lewy body dementia? (4)

A
  • Cognitive decline
  • Movement problems
  • Sleep disorders
  • Visual hallucinations
261
Q

What is the cause of frontotemporal dementia?

A

Abnormal tau protein deposits in temporal and frontal lobes

262
Q

What are the symptoms of frontotemporal dementia? (3)

A
  • Behavioural and emotional - difficulty planning/organizing
  • Language problems - difficulty producing or understanding speech
  • Movement problems - shaky hands/problems with balance
263
Q

What are some ways you can help someone with dementia? (6)

A
  • Encourage regular exercise
  • Help maintain good diet
  • Reduce noise
  • Encourage social contact
  • Use a calendar
  • Create a dementia friendly environment
264
Q

what does the sympathetic nervous system do? (5)

A
  • Increases HR, BP and BR
  • Diverts blood towards skeletal muscle
  • Dilation of pupils
  • Inhibits peristalsis
  • Constricts intestinal and urinary sphincters
265
Q

what does the parasympathetic nervous system do? (5)

A
  • Decrease HR, BP and BR
  • Maintains even blood supply throughout body
  • Constriction of pupils
  • Stimulates peristalsis
  • Relaxes intestinal and urinary sphincters
266
Q

What type of outflow does the parasympathetic nervous system have?

A

Craniosacral outflow

267
Q

What type of outflow does the sympathetic nervous system have?

A

Thoracolumbar outflow

268
Q

Which nerves give parasympathetic responses? (2)

A
  • Cranial nerves 3, 7, 9, 10
  • Sacral nerves S2, 3, 4
269
Q

Where do the short pre-ganglionic neurons arise from in the sympathetic nervous system?

A

T1-L2

270
Q

Where are ganglia found in the sympathetic nervous system?

A

Para and pre vertebral chains

271
Q

What is the size of the post-ganglionic neurons in the sympathetic nervous system?

A

Long

272
Q

What is the size of the post-ganglionic neurons in the parasympathetic nervous system?

A

Short

273
Q

Where do the autonomic nerves arise from?

A

Lateral horn of grey matter

274
Q

What do the autonomic nerves enter the sympathetic chain by?

A

White ramus

275
Q

Where can the pre-synaptic neuron go after entering the sympathetic chain? (2)

A
  1. Synapse in sympathetic chain, out through grey ramus, becomes spinal nerve
  2. Synapse in sympathetic chain, ascending or descend inside the chain
276
Q

Which axons are highly myelinated?

A

Preganglionic

277
Q

Which axons are unmyelinated?

A

Postganglionic

278
Q

Which nerves arise from the greater splanchnic nerve?

A

T5-T9

279
Q

Which nerves arise from the lesser splanchnic nerve?

A

T10-T11

280
Q

Which nerves arise from the least splanchnic nerve?

A

T12

281
Q

Which nerves arise from the lumbar splanchnic nerve?

A

L1 to L2

282
Q

Which neurotransmitters are released in the sympathetic nervous system? (2)

A
  • Pre-ganglionic neuron to post-ganglionic neuron = Ach
  • Post-ganglionic neuron to effector tissue = noradrenaline
283
Q

Which neurotransmitters are released in the parasympathetic nervous system? (2)

A
  • Pre-ganglionic neuron to post-ganglionic neuron = Ach
  • Post-ganglionic neuron to effector tissue = Ach
284
Q

What is the exception to which neurotransmitters are released in the sympathetic nervous system? (2)

A
  • Pre-ganglionic to adrenal medulla - Ach
  • Adrenal medulla to blood - noradrenaline
285
Q

What is a health psychology?

A

Understanding psychological influences on how people stay healthy, why they become ill and how they respond when they do get ill

286
Q

What is a health behaviour (2)

A
  • Any activity people perform to maintain or improve their health
  • Regardless of their perceived health status or whether the behaviour achieves that goal.
287
Q

What is Matarazzo (1984)’s definition of health behaviour?

A

Behaviours that are related to the health status of the individual

288
Q

What is Matarazzo (1984)’s definition of health behaviour?

A

Behaviours that are related to the health status of the individual

289
Q

What are some examples of Matarazzo (1984)’s health behaviours? (2)

A
  • Health impairing behaviours/habits - smoking, eating high fat diet
  • Health protective behaviour - attending health check/screenings
290
Q

Why is it important to study health behaviour? (4)

A
  • Find relationship with life expectancy
  • Behaviour engaged in because of disease
  • Treatment schedules involve behaviours
  • Lifestyle change involve behaviours
291
Q

What are the theories of health belief? (5)

A
  • Attribution theory
  • Locus of control
  • Leventhal’s model of illness representation
  • Self-efficacy
  • Transtheoretical model/stages of chance
292
Q

What is attribution theory? (2)

A
  • Theory deals with how the social perceiver uses information to arrive at causal explanations for events
  • Examines what information is gathered and how it is combined to form a causal judgement
293
Q

What are the components of the attribution theory? (4)

A
  • Internal vs external
  • Stable vs unstable
  • Global vs specific
  • Controllable vs uncontrollable
294
Q

What is the theory of locus of control?

A

People differ to the degree in which they believe they can control their lives

295
Q

What are the components of locus of control? (3)

A
  • Internal vs external
  • Behavioural control
  • Cognitive control
296
Q

What are the components Leventhal’s model of illness representation? (5)

A
  • Identity - what am I dealing with?
  • Timeline - how long has it been?
  • Consequence - is there bleeding?
  • Cause - got it from someone?
  • Control - can I self-medicate?
297
Q

How can a healthcare practitioner use Leventhal’s model in practice? (2)

A
  • Can provide the framework/checklist to guide understanding how patients psychologically represent the illness
  • Can then correct inaccuracies that might affect their decision-making process or management of their medical conditions
298
Q

What is the theory of self-efficacy?

A

People’s beliefs in their capability to exercise some measure of control over their own functioning and over environmental events

299
Q

What are the two types of expectancy in the theory of self-efficacy?

A
  • Outcome expectancy - behaviour will lead to a favourable outcome
  • Self-efficacy expectancy - one can perform the behaviour properly
300
Q

What is the transtheoretical model/stages of change? (2)

A
  • Consider individuals to be at different ordered stages
  • Describes how they move through the stages with changes to their behaviour
301
Q

What are the steps in the transtheoretical/stages of change model? (6)

A
  1. Pre-contemplative - sees no problem but others disapprove
  2. Contemplative - weighing up pros and cons
  3. Determinism - to carry on as before or to change
  4. Active change - putting the decision into practice
  5. Maintenance - actively maintaining change
  6. Relapse - return to previous behaviour
302
Q

What also influences behaviour change in the transtheoretical model? (4)

A
  • Decisional balance
  • Self-efficacy
  • Process of change - cognitive/behavioural
  • Temptation
303
Q

How can a healthcare practitioner use the transtheoretical model in practice? (3)

A
  • Listening and hearing the position of the patient
  • Use a role model to demonstrate how certain behaviours are done
  • Mastery through practice/rehearsal - behaviour in supervision to independent self-regulation
304
Q

What are examples of theories of predictors of health behaviours? (3)

A
  • Health belief model
  • Protection motivation theory
  • Theory of planned behaviour
305
Q

The health belief model argues people are more likely to adhere to health behaviours when they… (7)

A
  1. view their physical problem as severe
  2. perceive themselves to be susceptible to further negative health effects if they fail to adhere
  3. consider the likelihood of treatment to be effective as high
  4. identify few barriers to adherence
  5. experience few rewards for failing to adhere
  6. encounter environmental cue supporting the decision to adhere
  7. believe that they can change
306
Q

The protection theory assumes protection motivation is maximised when… (6)

A
  1. the threat to health is severe
  2. the individual feels vulnerable
  3. the adaptive response is believed to be an effective means for averting the threat
  4. the person is confident in their abilities to successfully complete the adaptive response
  5. the rewards associated with the maladaptive behaviour are small
  6. the costs associated with the adaptive response are small
307
Q

What are the two types of appraisals involved in the protection motivation theory? (2)

A
  1. Threat appraisal
  2. Coping appraisal
308
Q

What four components make up the maladaptive response in the protection motivation theory?

A
  • Severity and vulnerability
  • Intrinsic and extrinsic rewards
309
Q

What three components make up the adaptive response in the protection motivation theory?

A
  • Response efficacy and self-efficacy
  • Response costs
310
Q

In the theory of planned behaviour, what 3 aspects contribute to the strength of an individual’s intentions to change?

A
  • Attitudes
  • Subjective norm
  • Perceived behavioural control
311
Q

What does the theory of planned behaviour identify?

A

Salient beliefs to be able to target the intervention appropriately

312
Q

What must be targeted in the theory of planned behaviour? (4)

A
  • Target
  • Action
  • Time
  • Context
313
Q

How can a healthcare practitioner use the theories of behaviour models in practice? (2)

A
  • Provide insight into variables that facilitate/hinder behaviour change
  • Provide info to support successful, tailored interventions
314
Q

What is the definition of medically unexplained symptoms?

A

Physical symptoms not explained by organic disease-causing distress and impairing function

315
Q

What is MUS most likely to be associated with?

A

Psychiatric disorder

316
Q

Which risk groups present with MUS? (5)

A
  • Increasing age
  • Lower social class
  • History of Trauma
  • Concrete thinkers who struggle with abstract ideas - ASD
  • Personal history or family history of physical illness that’s become significant to patient
317
Q

What % of patients in GP surgeries have MUS?

A

25%

318
Q

What is the cost of MUS to the NHS each year?

A

£3.25 billion

319
Q

What are common physical symptoms in relation to depressive disorder? (5)

A
  • Fainting
  • menstrual problems
  • headache
  • chest pain
  • dizziness
320
Q

MUS has a poor prognosis if…? (4)

A
  • Symptoms last more than 2 years
  • History of childhood abuse
  • History of long duration of untreated psychiatric disorder
  • Ongoing unresolvable, severe psychosocial stressors
321
Q

What are the two key diagnoses for MUS in the ICD-10?

A
  • Dissociative disorders
  • Somatoform disorders
322
Q

What is dissociative disorder? (2)

A
  • Presented with a biological problem but does not match any test results
  • Psychological factors play a role
323
Q

What is somatoform disorder?

A

Expressing psychological disorders through physical means

324
Q

What is dissociation?

A

Partial or complete loss of integration between memories and identity

325
Q

What is conversion?

A

When there is loss of, or altered; motor, cognitive, or sensory function which are usually under voluntary control

326
Q

What are types of functional neurological disorders? (5)

A
  • Motor (tremor, paresis, paralysis)
  • Sensory (Vertigo, functional blindness, altered sensations)
  • Axial (abnormal gait, posture, knee-buckling)
  • Speech (Dysarthria, Stutter, whisper)
  • Paroxysmal (Non epileptic attacks)
327
Q

What is involved in a dissociative disorder? (2)

A
  • Disorders of physical functions under voluntary control
  • loss of sensations
328
Q

What is involved in somatoform disorder? (2)

A
  • Disorders involving pain
  • Other autonomic functions
329
Q

What is the most common area on the body for somatoform disorders? (3)

A
  • Gastro
  • MSK
  • Dermatological
330
Q

Which gender are somatoform disorders more common in?

A

Females

331
Q

What is the process of somatisation?

A

Emotional distress is expressed in the form of physical symptoms

332
Q

What is the diagnostic criteria of somatoform disorder? (3)

A
  • At least 2 years of multiple and variable physical symptoms with no adequate explanation
  • Persistent refusal to accept the advice
  • Some degree of impairment of social and family functioning
333
Q

What are some predisposing factors of MUS? (4)

A
  • Genetics
  • Personality traits
  • Familial transmission
  • Trauma
334
Q

What can trigger the onset of MUS? (3)

A
  • Periods of stress
  • Psychological, social or physical illness
  • Increased vulnerability
335
Q

What is an illness behaviour?

A

How individuals respond to bodily indications

336
Q

What is an abnormal illness behaviour?

A

Illness denial

337
Q

What is the meaning of a sick role?

A

Exemptions from usual responsibilities

338
Q

What are the treatments for MUS? (3)

A
  • Screen for psych comorbidities, understand motive, repeated pattern of presentation
  • Mental health and psychological support
  • Explain / Challenge unclear diagnosis / Accept ambiguity
339
Q

What MUS symptoms does stress lead to?

A

MSK pains

340
Q

What MUS symptoms does panic lead to?

A

Difficulty breathing/chest pains

341
Q

What is stress?

A

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

342
Q

What is eustress? (2)

A
  • Mild stress that is useful
  • E.g Revising for exams
343
Q

What is distress? (2)

A
  • Unpleasant stress
  • E.g. death of family
344
Q

What is a stressor?

A

Any stimulus that produces a stress response

345
Q

What are the types of stressors? (4)

A
  • External
  • Internal
  • Psychosocial events
  • Physiological events
346
Q

What are examples external stressors? (5)

A
  • Physical environment e.g. noise
  • Social interactions e.g. rudeness
  • Daily hassles e.g. commuting
  • Organisational e.g. deadlines
  • Major life events e.g. lost job
347
Q

What are examples of internal stressors? (3)

A
  • Lifestyle choices e.g. schedule
  • Mind e.g. unrealistic expectations
  • Personality traits e.g. perfectionist
348
Q

What are examples of psychosocial stressors? (4)

A
  • Unemployment
  • Marriage
  • Divorce
  • Work problems
349
Q

What are examples of physiological events? (4)

A
  • Blood loss
  • Breaking an arm
  • Surgery
  • Catching an infection
350
Q

What is general adaptation syndrome?

A

Physiological response to stressors to regain homeostasis

351
Q

What are the 3 stages of the stress response?

A
  1. Alarm phase
  2. Resistance/adaptation phase
  3. Exhaustion phase
352
Q

What is the alarm phase in the stress response? (2)

A
  • short-term stress response
  • Initial ‘fight-or-flight’ response
353
Q

What is the resistance/adaptation phase in the stress response? (2)

A
  • Long term stress response
  • Body attempts to cope with prolonged stress
354
Q

What is the exhaustion phase in the stress response? (2)

A
  • Resources are depleted
  • Body is unable to maintain function
355
Q

What is the order of structures involved in short term stress response? (6)

A
  1. Stress
  2. Cerebral cortex
  3. To hypothalamus
  4. To sympathetic nervous system
  5. To adrenal medulla
  6. Release adrenaline, noradrenaline
356
Q

What is the order of structures involved in long term stress response? (6)

A
  1. Stress
  2. Cerebral cortex
  3. To hypothalamus
  4. To pituitary gland
  5. To adrenal cortex
  6. To glucocorticoids
357
Q

What is the sympathetic responses to short term stress? (5)

A
  • Increaser HR, BP
  • Blood diverted to head and skeletal muscles
  • Dilation of airways - increase O2
  • Alertness increases
  • Sweating
358
Q

Describe the mechanism of the HPA axis in the adaptation phase of the long-term stress response? (6)

A
  1. Stress activates the HPA axis
  2. Neurosecretory cells in hypothalamus to release CRH (corticotropin releasing hormone)
  3. CRH activates anterior pituitary gland
  4. Anterior pituitary secretes ACTH (adrenocorticotropic hormone)
  5. ACTH travels through blood to adrenal glands
  6. ACTH stimulates cells in adrenal cortex to release cortisol
359
Q

Describe the mechanism of cortisol in the adaptation phase of the long-term stress response? (5)

A
  1. Lipids released into blood
  2. Amino acids/proteins released from muscles into blood
  3. Increase in glucose in blood, through synthesis
  4. Aldosterone released by adrenal cortex - causes retention of sodium, increased water retention, increased blood pressure
  5. Immune suppression
360
Q

What are glucocorticoids?

A

A group of hormones of the adrenal cortex secreted during stress

361
Q

What is an example of a glucocorticoid?

A

Cortisol

362
Q

What effect do glucocorticoids have on the body? (6)

A
  • Increase blood glucose levels
  • Maintain blood pressure
  • Break down protein and convert to glucose
  • Help make fats available
  • Activate the CNS
  • Allows the body to cope with stress
363
Q

What is psychoneuroimmunology?

A

Interactions between the nervous system, behaviour and the immune system

364
Q

What can acute stressors upregulate?

A

The immune system

365
Q

What can chronic stress inhibit?

A

The immune system

366
Q

What does cortical increase/decrease the numbers of? (2)

A
  • B-cells
  • T-cells
367
Q

What are abnormal levels of stress involved in? (6)

A
  • Anxiety
  • Depression
  • High BP
  • Ulcers
  • Aging
  • Cancer
368
Q

What does prolonged exposure to high levels of cortisol cause? (6)

A
  • Muscle breakdown
  • Suppression of immune response
  • Ulceration of gastrointestinal tract
  • Depression / psychosis
  • Failure of pancreatic beta cells
  • Aging
369
Q

What response is the amygdala involved in?

A

Fear

370
Q

Activation of ____ leads to the stress response

A

Central nucleus

371
Q

What does the amygdala and hippocampus regulate?

A

CRH (corticotropin releasing hormone) neurons in the hypothalamus

372
Q

What affect do the amygdala and hippocampus have on the HPA axis? (2)

A
  • Amygdala activation stimulates HPA axis - more stress
  • Hippocampal activation suppresses HPA axis – less stress
373
Q

How does the cortisol feedback mechanism work? (3)

A
  • Circulating cortisol binds to glucocorticoid receptors in hippocampus
  • Activations hippocampus, which suppresses CRH release by hypothalamus
  • Reduces HPA activation – less cortisol release by adrenals
374
Q

What is anxiety disorder?

A

A psychological disorder characterised by unrealistic, unfounded fear

375
Q

What is fear?

A

Realistic response to a threatening stimulus that is known

376
Q

What is generalised anxiety disorder? (2)

A
  • Ongoing state of anxiety lacking any reason or focus
  • At least 6 months duration
377
Q

What is panic disorder?

A

Brief periods of intense terror and apprehension (panic attacks)

378
Q

What is a phobia?

A

Strong fears of specific things or situations e.g. open spaces, flying, snakes, social interactions

379
Q

What is obsessive-compulsive disorder?

A

Intrusive thoughts (obsessions) cause anxiety

380
Q

What is post-traumatic stress disorder?

A

Anxiety triggered by recall of past stressful experiences

381
Q

What are the treatments of anxiety disorders? (2)

A
  • Psychological - CBT
  • Pharmacological - benzodiazepines
382
Q

What are the effects of benzodiazepines? (3)

A
  • Reduce anxiety by
  • Sedative
  • Muscle relaxant
383
Q

What happens with long term use of benzodiazepines? (2)

A
  • Reduces effectiveness
  • Become addictive
384
Q

How do benzodiazepines work to treat anxiety? (3)

A
  • bind to a regulatory site on the GABAA-receptor
  • Enhances the inhibitory effect
  • Suppressing brain circuits in stress response
385
Q

How do beta blockers work to treat anxiety?

A

Reduce physical symptoms of anxiety such as tremor, palpitations, sweating

386
Q

How do SSRIs work to treat anxiety?

A

Prolong action of serotonin by blocking uptake

387
Q

What is addiction?

A

Continued repetition of a behaviour despite adverse consequences

388
Q

What is addiction characterised by? (3)

A
  • Loss of control over the substance
  • Compulsion to use substance
  • With/without withdrawal phenomena
389
Q

What is the ICD-11 Criteria for alcohol dependence? (3)

A

Two or more of the following in last year:
* Impaired control over alcohol use
* Increasing precedence of alcohol use over other aspects of life, including maintenance of health, and daily activities and responsibilities, such that alcohol use continues or escalates despite the occurrence of harm or negative consequences
* Physiological features indicative of neuroadaptation to the substance, including:
– Tolerance to alcohol
– Withdrawal state upon cessation of alcohol
– The use of alcohol to avoid withdrawal symptoms

390
Q

How long do withdrawal acute effects last?

A

5-10 days

391
Q

What are the different pathways to dependence? (2)

A
  • Environmental
  • Neurobiology
392
Q

What factors affect environmental and dependence?

A
  • Prevalence trends - affordability, intoxication promoted by media, easily accessible
  • Individual - influence of peers
  • Other factors - adverse childhood experiences, poor family support
393
Q

What factors affect neurobiology? (3)

A
  • Developing the cycle of addiction
  • Interaction with dopamine, opioid and cannaboid transmissions
  • Suppression of CNS
394
Q

What are the steps in the cycle of addiction? (6)

A
  1. Salience
  2. Mood modification
  3. Tolerance
  4. Withdrawal
  5. Conflict - neglect of other activities
  6. Recovery, relapse
395
Q

What % of people with alcohol dependence make serious quit attempts?

A

40%

396
Q

What did Edwards (1983) discover in alcohol addiction? (2)

A
  • 11 years follow up of alcohol dependant patients
  • Found 27% stable remission
397
Q

What did Valliant (1983) discover in alcohol addiction? (2)

A
  • 8 years follow up of detoxified alcohol dependant patients
  • Found 34% stable remission
398
Q

What % of people in England complete their alcohol dependence treatment?

A

60%

399
Q

What factors are associated with poorer outcomes of relapse after treatment? (5)

A
  • Social instability
  • Having an alcohol-free network
  • Family history of dependence
  • Mental ill health
  • Previous treatment and failed attempts
400
Q

What are examples of low impact alcohol strategies? (5)

A
  • Unit labelling
  • Sensible drinking campaigns
  • Public education
  • School based education
  • Voluntary advertising
401
Q

What are examples of medium impact alcohol strategies? (4)

A
  • Brief interventions
  • Treatment
  • Safer drinking environment
  • Heavier enforcement
402
Q

What are examples of high impact alcohol strategies? (2)

A
  • Taxation and pricing
  • Restricting availability
403
Q

What are the 5 main principles of motivational interviewing?

A
  1. Express empathy through reflective listening.
  2. Develop discrepancy between clients’ goals or values and their current behaviour.
  3. Avoid argument and direct confrontation.
  4. Adjust to client resistance rather than opposing it directly.
  5. Support self-efficacy and optimism.
404
Q

What is behaviour change counselling? (2)

A
  • A constructive conversation about change in which the practitioner tries to understand how the patient feels about change,
  • Uses open questions and empathetic listening statements.
405
Q

How does behaviour change counselling work? (3)

A
  • Many health problems are influenced by personal behavior
  • For health improvements to occur the person’s behavior will need to change
  • For change to take place the person needs to be active (ready/motivated)
406
Q

What are the prerequisites for change in behaviour change counselling? (5)

A
  1. Belief that change sis a good idea
  2. Importance of change
  3. Confidence to change
  4. Knowledge of what to do
  5. Ready to attempt change
407
Q

What are the principles of motivational interviewing? (5)

A
  • Express empathy
  • Develop discrepancy
  • Avoid argumentation
  • Roll with resistance
  • Support self-efficacy
408
Q

what is pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

409
Q

What is recurrent pain?

A

Pain that comes and goes

410
Q

What is short term pain?

A

Acute pain

411
Q

What is long term pain? (2)

A
  • Chronic pain
  • Lasts longer than 3 months
412
Q

What % of sick days in the UK are from back pain?

A

12%

413
Q

What is a homunculus?

A

A distorted map of our surface body in the brain

414
Q

How is the homunculus relevant to pain?

A

Shows areas of the body that have denser receptors are more sensitive to pain

415
Q

What is neuroplasticity?

A

Ability of neural networks to change through growth and reorganisation

416
Q

What is the Pain Gate Theory (1960)?

A

Explains that different factors influence our experience, including our own thoughts and feelings

417
Q

What factors can influence pain perception? (3)

A
  • Stress and tension
  • Psychological factors
  • Lack of activity
418
Q

What is central sensitisation?

A
  1. usually pain would activate our ‘top-down’ pain suppressing capacity
  2. in central sensitisation, the system is malfunctioning
  3. more ‘bottom-up’ info arrives in the brain, not enough ‘top-down’ suppression

This persistent state of reactivity lowers the threshold for what causes pain, eventually maintains pain even after injury has healed

419
Q

What is hyperalgesia?

A

Stimulus that is typically pain is perceived as more painful than it should

420
Q

What is included in pain management strategies? (3)

A
  • Behavioural - pacing, goal setting, relaxation
  • Psychological - acceptance, CBT, fear avoidance
  • Physical - graded exercise, medication, management
421
Q

Which areas of life can pain affect? (5)

A
  • Behaviour - work, hobbies, chores
  • Moods - down, depressed, frustrated
  • Physical - put on weight, sleep, walking
  • Environment - relationships, children
  • Thoughts - isolated, vulnerable
422
Q

How do beliefs and interpretations influence pain?

A

People with negative beliefs about their pain can experience greater suffering

423
Q

What does the cognitive behavioural model of pain argue?

A
  • Patient’s appraisals of the impact of their pain on their lives determines the pain-depression relationship
  • E.g. patients who believed they could still function despite their pain did not become depressed compared to those who believed they couldn’t
424
Q

What are the psychological approaches to working with chronic pain? (4)

A
  • CBT
  • Mindfulness
  • Acceptance and commitment therapy (ACT)
  • Compassion focused therapy (CFT)
425
Q

How can childhood trauma affect chronic pain? (3)

A
  • Trauma triggers prolonged anxiety and fearfulness
  • Makes the nervous system persistently reactive
  • Leading to pain behaviour
426
Q

What is primary appraisal?

A

Appraisal of the event

427
Q
A
428
Q

What are the 4 domains of stress? (4)

A
  • Emotional - crying
  • Cognitive - difficult to concentrate
  • Behavioural - comfort eating
  • Physiological - increase HR, BR
429
Q

Give an example of a misinterpretation of physiological symptoms

A
  1. Increased breathing rate
  2. Difficulty breathing
  3. Thinks they are having a HA
430
Q

What is indirect impact of stress? (5)

A

Impact via behavioural changes
- Poor compliance with medication
- Increase alcohol intake
- Increase smoking
- Reduced exercise
- Poor diet

431
Q

What is direct impact of stress? (2)

A
  1. Activation of the HPA axis
  2. causing cortisol secretion
432
Q

What is the impact of mental illness on existing physical illness? (2)

A
  • Increased mortality rates
  • Increased morbidity rates
433
Q

What is Leventhal’s (1984) dimensions to illness cognition? (5)

A
  • Identity
  • Timeline
  • Consequences
  • Cause
  • Control
434
Q

What are coping strategies for stress? (2)

A
  • Problem solving
  • Emotion focused coping
435
Q

What do you have to rule out before diagnosing an eating disorder? (6)

A
  • IBD
  • Hyperthyroidism
  • Malignancy
  • Iron deficiency anaemia
  • Focus of infection
  • Low vitamin D
436
Q

What is an eating disorder?

A

Abnormal attitude towards food that causes someone to change their eating habits and behaviour

437
Q

What is the criteria for anorexia nervosa? (4)

A
  • Rapid weight loss >15% below expected
  • BMI of 17.5
  • Body image distortion
  • Avoidance of fattening foods
438
Q

What are the criteria for bulimia nervosa? (4)

A
  • Recurrent episode of over-eating - >2/week for 3+ months
  • Persistent pre-occupation with eating
  • Attempts to counteract by; self-induced vomiting
  • Self-perception of being too fat
439
Q
A

ALS (10 decks)

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