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Medicine - Year 1 > Block 6 - Psychological Medicine 1 > Flashcards

Block 6 - Psychological Medicine 1 Flashcards

1
Q

Define psychology

A

The scientific study of the behaviour of individuals and their mental processes

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2
Q

Define conciousness

A

The state of being aware ad responsive to sensory surroundings
The ability of memory, language, emotion, abstraction and attention

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3
Q

Why is consciousness hard to assess?

A

You need to be alert

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4
Q

How are sleep-wake cycles affected when you have a low level of consciousness?

A

You still have sleep-wake cycles until you are classed as ‘brain-dead’

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5
Q

What type of behaviour do you have when you are in a vegetative state?

A

Non-purposeful behaviour

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6
Q

What type of behaviour do you have when you are in a coma?

A

Reflex behaviour

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7
Q

What is a normal and abnormal loss of consciousness?

A

Normal: Sleeping
Abnormal: Loosing consciousness in situations where you shouldn’t (e.g. work)

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8
Q

10 pathology’s which cause a lack of consciousness?

A

Cardiovascular, dementia, diabetes, drugs, epilepsy, head injury, increased intracranial pressure, malaria, metabolic disorders, stroke

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9
Q

3 things to define brain stem death

A

No reflexes
Heart beat and breathing through machinery only
Clear evidence of brain damage through scans

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10
Q

4 examples of when people may not be brain stem dead

A

Drugs, reversible body disturbances, hypothermia, cervical cord injury

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11
Q

What 3 things does the Glasgow Coma scale look at?

What is each one scored out of?

A 
Eye opening (4)
Verbal response (5)
Motor response (6)
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12
Q

What are the 4 levels of eye opening in the Glasgow Coma scale?

A

Spontaneous
To loud voice
To pain
To nothing

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13
Q

What are the 5 levels of verbal response in the Glasgow Coma scale?

A 
Orientated
Confused/disorientated
Inappropriate words
Incomprehensible
Nothing
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14
Q

What are the 6 levels of motor response in the Glasgow Coma scale?

A 
Obeys commands
Localises pain
Withdraws from pain
Abnormal flexion
Extensor posturing
Nothing
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15
Q

What score does a fully conscious and comatised patient receive in the Glasgow Coma scale?

A

Fully conscious: 15

Comatised: 3

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16
Q

What is the Reticular Activating System?

A

A collection of nuclei and tracts in the midbrain that project to the pons, medulla and spinal cord

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17
Q

What 2 structures are needed for conciousness?

A

RAS System

Cerebral cortex

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18
Q

What are the 4 neurotransmitters involved in the reticular activating system?
What do they do?

A

Dopamine: Increases the will to do something
Noradrenaline: Increases when anxious/frightened (super conscious)
Acetylcholine: Sleep
Serotonin

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19
Q

What does damage to the anterior hypothalamus cause?

A

Decreased sleep

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20
Q

What does damage to the posterior hypothalamus cause?

How?

A

Increased sleep

Histamine activity –> drowsiness

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21
Q

What happens to acetylcholine levels when you are asleep?

What does this cause?

A

Increase

Activation of sensory thalamus –> Inhibition of reticular nucleus –> Increased thalamocortical neurones

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22
Q

What happens to the EEG when you are asleep and awake?

A

Asleep: Low frequency waves
Awake: High frequency waves

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23
Q

What is another name for synchronised sleep?

What are the EEG waves like?

A

non-REM sleep

Low frequency waves

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24
Q

What is another name for desynchronised sleep?

What are the EEG waves like?

A

REM sleep

High frequency waves

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25
Q

How often does REM occur?

A

Every 90-120 minutes

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26
Q

What happens to muscle tone during REM sleep?

A

It is lost

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27
Q

3 long term consequences of little sleep?

A

Obestiy, diabetes, increased blood pressure

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28
Q

What is narcolepsy?

A

Spontaneous transition from being awake to REM due to a mutation in the orexin receptor gene

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29
Q

How is the Circadian Rhythm established?

A

Light is detected by the retina and processed by the suprachiasmatic nucleus in the hypothalamus

Vasopressin is released to the pineal gland which releases the sleep promoting hormone melatonin

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30
Q

What are the EEG waves like for the 7 stages of sleep?

A 
Awake: low voltage high frequency BETA waves
Drowsy: ALPHA waves
Stage 1: THETA waves
Stage 2: Mixed EEG with sleep spindles
Stage 3+4: DELTA waves
REM: Low voltage and increased frequency
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31
Q

How does information get from the sensory stores to the long term memory?

A
  • Sensory stores of memory last milliseconds
  • Paying attention moves it to the short term store
  • Repeated attention changes the brain synapses causing it to be moved to the long term store
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32
Q

How can you decrease the chance of memory interference?

A

Remembering information in a meaningful way

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33
Q

2 things which patients with Amnesia find difficulty doing?

A

Forming new long-term memories

Recalling that information

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34
Q

5 causes of Alzheimer’s

A

Viral infection (herpes), Alcoholism (korsakoff’s), Head injury, Alzheimer’s, Anoxia

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35
Q

What is Anoxia?

A

When the hippocampus is deprived of oxygen

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36
Q

What is the memory loop that allows encoding and retrieval of memories?

A

Cortex - Hippocampus - Fornix - Mamillary bodies - Thalamus

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37
Q

What is the role of the para-hippocampal cortex

A

Provides spacial information and talks to the hippocampus

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38
Q

What is the temporal gradient?

A

A timeline of memories
Reterograde: Before the accident
Anterograde: After the accident

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39
Q

What happens to the reterograde and anterograde in Alzheimer’s patients?

A 
Reterograde = spared
Anterograde = lost
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40
Q

What is semantic memory?

A

Factual knowledge

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41
Q

What is non-declarative memory?

e.g.

A

Motor memories

e.g. if you draw image in a mirror you will improve over time even if you can’t remember drawing the previous images

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42
Q

Where are old memories stored?

Why is this possible?

A

Neocortex

The neocortex is next to the hippocampus so is able to cooperate with it

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43
Q

What two types of memory are spared in patients with amnesia?

A

Semantic and non-declarative memory

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44
Q

What is declarative memory?

A

Concious

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45
Q

What is non-declarative behaviour?

A

Non-conscious

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46
Q

Explain how the hippocampus forms a memory?

Where does it get its information from?

A

Combines 3 things:
PLACES: From the parahippocampal place
OBJECTS: From the inferior temporal cortex
PEOPLE: From the anterior temporal lobes

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47
Q

How does semantic dementia occur?

A

Damage to the neocortical store causes loss of conceptual knowledge and old memories

Loss of semantic memories

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48
Q

What is another name for semantic dementia?

A

Frontotemporal dementia (FTD)

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49
Q

What can people with semantic dementia still do?

A

Remember short term events
Non-verbal reasoning and intelligence is spared
Recognise simple animals but not complex ones
Copy an image well but can’t remember it as well after a minute

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50
Q

What memory is lost in amnesia?

What area of the brain is damaged?

A

New episodic memories

Hippocampus

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51
Q

What memory is lost in dementia?

What area of the brain is damaged?

A

Old semantic memories

Anterior temporal lobe

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52
Q

Define behavioural genetics

A

Casual links between genes, behavioural traits and neural mechanisms

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53
Q

Who founded behavioural genetics?

A

Francis Galton

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54
Q

What movement is behavioural genetics NOT linked to?

A

Eugenics

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55
Q

Define genome

A

A combination of alleles at a locus

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56
Q

Define behavioural phenotype

A

Observed trais

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57
Q

Define polygenic inheritance

A

Genes have small effects towards the heritability of a behavioural phenotype

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58
Q

Define heritability

A

The proportion of phenotypic variance that is accounted for by genetics

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59
Q

What do genome wide association studies do?

A

Link SNPs and CNVs to behavioural phenotypes

Unrelated individuals

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60
Q

What type of distribution does a large gene pool have?

A

A normal distribution

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61
Q

Which non-genetic environment has the biggest impact on siblings?

A

Non-shared

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62
Q

Define gene-environment correlation

A

Life experiences correlated with genetics

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63
Q

Define gene-environment interaction

A

Environmental effects depend on genetics
AND
Genetic effects depend on the environment

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64
Q

What type of research is human genetic research?

A

Observational

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65
Q

What is the difference between adoption studies and combination studies?

A

Adoption studies: Reared together vs apart

Combination studies: Twins adopted apart

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66
Q

What does TEDs stand for?
When did it start?
What did it examine?

A 
Twins Early Adoption Study 
1994
Language, behaviour and cognition
DNA analysis
Comparison between twins and parent
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67
Q

What happens to the inheritability of inheritance throughout development?

A

It increases

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68
Q

What type of neurotransmitter is glycine?

A

An amino acid

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69
Q

Neurotransmitters:

  • What are the vesicles like?
  • Where are they synthesised?
  • Where are they packaged?
A

Vesicle: Small, clear core
Synthesis: In the soma and transported down microtubule tracts in the axon
Packaged: In the presynaptic neurone

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70
Q

Neuropeptides:

  • What are the vesicles like?
  • Where are they synthesised?
  • Where are they packaged?
  • What happens in the pre-synaptic neurone?
A

Vesicle: Large, dense core
Synthesis AND packaged: In the soma and transported down microtubule tracts in the axon
Pre-synaptic neurone: Modified

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71
Q

What are co-transmitters?

A

Make, store and release more than one neurotransmitter/peptide?

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72
Q

What is the difference between low and high frequency stimulation?

A

Low: Neurotransmitters
High: Neurotransmitters AND neuropeptides

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73
Q

What is the difference between inotropic and metabotropic receptors?

A

Inotropic: Ion channel, agonist causes conformational change, fast
Metabotropic: Trans-membrane receptor, agonist signals through intracellular intermediates, slow

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74
Q

4 ways of identifying neurotransmitters?

A

Immunocytochemistry: Antibody

In-situ hybridisation: Synthetic probe with nucleotides that binds to mRNA in tissue

Microiontophoresis: Inject drug and pass an electric current to stimulate axon and record voltage

Radioactive binding assay: Calculate radiation level

75
Q

7 things ACh is involved in in the brain

A

Arousal, biorhythms, learning, memory, sexual behaviour, sleep and thermoregulation

76
Q

What 5 areas of the brain is ACh found in?

A

Basal forebrain, cortex, hippocampus, pons and midbrain

77
Q

Where are nicotinic ACh receptors found? (4)

A

Autonomic ganglia, adrenal medulla, CNS and NMJ

78
Q

Where are muscarinic ACh receptors found? (2)

A

CNS and peripheral tissues

79
Q

What are the 2 types of nicotinic receptors and where are they found?

A

Nn: Postgabglionic neurones, presynaptic cholinergic terminals
Nm: Skeletal motor end plates

80
Q

What are the 5 types of muscarinic ACh receptors and what are their structure?

A

M1, M2, M5: Stimulatory G protein

M2, M4: Inhibitory Gi protein and K+ channels

81
Q

Which ACh receptor is blocke by curare?

A

Nicotinic

82
Q

How is ACh formed? (+ enzyme)

A

Choline + acetyl CoA –> ACh

Enzyme: Choline acetyl transferase (chAT)

83
Q

How is ACh broken down? (+ enzyme)

A

ACh –> Choline + Acetate/Acetyl Acid

Enzyme: Acetylcholinesterase (AchE)

84
Q

What is glutamate a reduced form of?

Name 2 other molecules it can be synthesised by

A

Glutamic acid

Glucose and aspartame

85
Q

Which organ’s functioning does glutamate regulate?

A

The brain

86
Q

Explain what happens to glutamate in glial cells

A

Glutamate –> Glutamine
(Enzyme: Glutamine synthetase)

It is then transported to mitochondria in the synapse where Glutamine –> Glutamate
(Enzyme: Glutaminase)

87
Q

How can glutamate cause neurone death?

A

If there are too high extraneuronal levels

88
Q

How is glutamate packaged into vesicles?

A

By the action of a proton pump

89
Q

What are the 3 types of glutamate receptors?

A

AMPA
NDMA
Kainite

90
Q

Which glutamate receptors are decreased in epilepsy?

A

AMPA

91
Q

Which glutamate receptors are decreased in strokes and memory problems?

A

NDMA

92
Q

Explain how the receptors AMPA and NDMA co-exist

A

Glutamate binds to AMPA and causing partial depolarisation and a confrontational change which removes the Mg ions that are blocking the NDMA receptor

93
Q

How is GABA made? (+ enzyme)

Name 2 other molecules that GABA can be made from

A

Glutamine –> Glutamate (Enzyme: Glutaminase)
Glutamate –> GABA (Enzyme: Glutamic acid decarboxylase)

Glucose and pyruvate

94
Q

What 2 ions can GABA neurones activate?

A

Chloride and calcium

95
Q

What happens in epilepsy?

A

Increased GABA inhibition causes uncontrolled brain excitation

96
Q

How is glycine produced? (+ enzyme)

Where is it produced?

A

Serine –> Glycine
(Enzyme: SHMT)
In the mitochondria

97
Q

Where are glycine receptors found?

A

Brainstem

Spinal cord

98
Q

What do glycine receptors do in the spinal cord?

A

Inhibit skeletal muscle

99
Q

What causes hyperreflexia?

4 symptoms

A

Glycine receptor defects

Increase in muscle tone, exaggerated startle reflex, rigidity and decreased balance

100
Q

What causes stiff person syndrome?

1 symptom

A

Decreased GABA

Stiff muscles

101
Q

What 2 groups do all catecholamines have?

A

Catechol and amine group

102
Q

What is the rate limiting step for catecholamine production?

A

Tyrosine –> L-DOPA

103
Q

What is the role of MAO-A?

Where does it occur?

A

Oxidises serotonin in the liver

104
Q

What is the role of MAO-B?

Where does it occur?

A

Oxidises dopamine in the liver

105
Q

What are the four dopamine pathways and what are they involved in?

A

Mesolimbic: Reinforcement and reward
Mesocortical: Planning, emotions, cognition, motivation
Nigrostriatal: Movement
Tuberoinfundibular: Inhibits prolactin release from pituritary gland

106
Q

Which pathway is disrupted in Parkinson’s disease?

A

Nigrostriatal

107
Q

How is dopamine broken down?

A

Dopamine –> DOPAC –> Homovanillic Acid

108
Q

What are the 2 classes of dopamine receptors?
Which receptors do they include?
What are they coupled to?

A

D1-like receptors: positively coupled to adenylate cyclase via Gs proteins (D1+D5)

D2-like receptors: negatively coupled to adenylate cyclase via Gi proteins (D2,D3+D4)

109
Q

Where is noradrenaline released from in the brain?

A

Locus Coeruleus in the brainstem

110
Q

What do decreased and increased levels of noradrenaline lead to?

A

Decreased: Depression
Increaded: Mania

111
Q

2 pathways by which noradrenaline is broken down

A

Nordrenaline –> Normetanephrine (Enzyme: COMT)

Noradrenaline –> VMA/MHPG (Enzyme: MAO)

112
Q

How is serotonin produced? (+enzyme)

A

Tryprophan –> 5HTP (Enzyme: Tryptophan hydroxylase)

5HTP –> Serotonin (Enzyme: 5HTP decarboxylase)

113
Q

What is another name for serotonin?

A

5HT

114
Q

Where do serotenergic neurones project from?

A

The Raphe Nuclei in the brainstem

115
Q

What do decreased levels of serotonin lead to?

A

Depression

116
Q

How is serotonin taken up by neurones?

A

SERT transporters

117
Q

How is serotonin taken up into vesicles?

A

VMAT

A monoamine transporter

118
Q

How many classes of serotonin receptors are there?
What word describes them all?
Which is the odd one out?

A

7 receptor classes: metabotropic

5-HT3 = inotropic

119
Q

2 ways that serotonin is degraded

A

MAO oxidises it to 5-HIAA

Pineal gland converts it to melatonin

120
Q

What family is Substance P in?

A

Tachykinin family

121
Q

What does substance P bind to and what are its two effects?

A

Neurokinin 1,2,3

Smooth muscle contraction and pain transmission

122
Q

What 7 brain regions is substance P involved in?

A

Amygdala, Cerebral Cortex, Dorsal horn, Hypothalamus, Medulla, Striatum, Substantia Nigra

123
Q

Define stress

A

An imbalance between demands, and personal resources to deal with these demands

124
Q

How can life events trigger stress through appraisals?

A

Life event –> Primary appraisal –> Secondary appraisal –> Stress

125
Q

Define primary appraisal

A

Assessment of event

126
Q

Define secondary appraisal

A

Assessment of coping abilities

127
Q

Give an example of a physiological response to stress

A

Fight or flight

128
Q

Give 4 examples of emotional responses to stress

A

Sad, irritable, tearful, over-reacting

129
Q

Give 5 examples of behavioural responses to stress

A

Activity changes, diet changes, decreased sleep, increased smoking and drinking

130
Q

Give 5 examples of cognitive responses to stress

A

Difficulty concentrating, hard to make decisions, self-critical, sensitive to criticism, switching off

131
Q

What does the individual illness response depend on?

A

Appraisal and coping style, childhood factors, mental illness, previous illness experience, worrying

132
Q

What can stress cause to happen to existing illnesses?

A

Relapses

133
Q

How does stress increase levels of cortisol?

A

Activates the hypothalamic-pituritary adrenocorticol axis

134
Q

How does stress increase levels of catecholamines?

A

Activates the sympathetic-adrenal medullary system

135
Q

3 changes that bereavement causes in the heart?

A

ECG changes
Increased vascular resistance
Ventricular dysfunction

136
Q

What does the disease illness response depend on?

A

Is the disease life-threatening or controllable
Is the disease ambiguous?
Does the disease have undesirable treatment?

137
Q

What is emotional discharge?

A

When you talk to other people about how you are feeling

138
Q

What are illness cognition’s?

What does it influence?

A

The patient’s own common sense beliefs about their illness

It influences their response

139
Q

What 6 things affect illness cognition?

A
  • How the patient identifies the disease
  • The perceived duration of the disease
  • The expected outcome for the disease
  • Whether the disease can be controlled or cured
  • The personal ideas about what may have caused the disease
  • How the patient appraises the pain
140
Q

Define pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

141
Q

How long does pain have to occur for before it is classed as chronic?

A

6 months

142
Q

6 impacts of chronic pain on patients

A

Negative attitude, fear avoidance, decreased activity levels, depressive symptoms, social issues, unrealistic expectations

143
Q

What is central sensitisation?

How does it occur?

A

When the pain threshold is decreased so sensitivity to pain is increased
Changes to the receptors in the dorsal horn

144
Q

5 reasons why pain gates open?

A

Anxiety, decreased activity (e.g. stiff joints), depression, focusing on pain, stress

145
Q

Explain how persistent pain can be made worse

A

Persistent pain decreases activity causing muscle and joint weakness. This causes fatigue and frustration causing social issues and depression –> more pain

146
Q

5 examples of social treatments for pain

A

Communication, goal setting, pacing, relaxing, return to work

147
Q

5 examples of psychological treatment for pain

A

Acceptance, CBT, fear-avoidance, mindfulness, psychoeducation

148
Q

3 examples of physical treatment for pain

A

Exercise, pain education, homeopathy

149
Q

What 5 categories are in the ‘Holistic model of pain’?

Give 2 examples for each category

A 
Behaviour: Work, hobbies, resting
Environment: Relationships, home
Mood: Depressed etc.
Physical: Weight increase, medication side effects
Thoughts: Isolated, useless
150
Q

What 2 things does CBT develop?

A

New behaviours and thoughts

151
Q

What is mindfulness?

A

Meditative techniques that soothe brain patterns

152
Q

Three examples of third wave cognitive therapies

A

Compassion therapy
Acceptance and commitment therapy
Mindfulness

153
Q

Define somatisation

A

Physical expression of psychological pain

154
Q

Define stress

A

Condition that challenges the maintenance of homeostatsis

155
Q

Give examples of external, internal, psychological and physiological stressors

A

External: Physical environment, society, life events,
Internal: Lifestyle, self-appraisal, personality
Psychological: Unemployment, relationships, work, money, health
Physiological: Health

156
Q

What is the general adaptation syndrome?

A

The physiological response to stress to regain homeostasis

157
Q

What are the 4 phases of the stress response?

A

Alarm phase: ST - fight or flight
Resistance phase: LT - adapting
Exhaustion phase: Body depletes resources
Recovery

158
Q

What does the short term stress response activate?

A

Sympathetic nervous system

Catecholamine release

159
Q

How is stress activated in the brain?

A

Cerebral cortex –> Hypothalamus –> ST/LT

160
Q

What does the long term stress response activate?

A

Hypothalamic-Pituritary-Adrenal Axis

161
Q

Give an example of a glucocorticoid
When is it secreted
6 roles

A

Cortisol
Secreted during stress
Activates CNS, anti inflammatory, decreases B and T cells, increase glucose, increases memory, maintains blood pressure

162
Q

Give an exmaple of a mineralocoritocoid
Where is it released
3 roles

A

Aldoesterone
Released by the adrenal cortex
Sodium and water retention, increases blood pressure and immune supression

163
Q

13 symptoms of excessive stress

A

Ageing, anxiety, asthma, blood pressure increase, cancer, depression, diabetes, GI issues, immune dysfucntion, migraine, muscle breakdown, psychosis, sex hormone decrease

164
Q

What can persist after the stress response?

A

Pathological changes

165
Q

What does acute and chronic stress do to the immune system?

A 
Acute = Increases the immune system
Chronic = Decreases the immune system
166
Q

Define psychoneuroimmunology

A

Nervous and immune system interactions

167
Q

4 methods to decrease stress

A

Counselling, exercise, meditation, relaxation

168
Q

What does activation of the Periaqqueductal grey matter lead to? (in regards to stress)

A

Avoidance behaviour

169
Q

What does activation of the diffuse modulatory systems lead to? (in regards to stress)

A

Increased vigilance

170
Q

What does cortisol enhance?

A

Memory

171
Q

What are relaxation and exercise examples of?

A

Psychological treatments

172
Q

Define anxiety

A

Inappropriate expression of fear in unrealistic situations

It is anticipated and affects ADL

173
Q

Define fear response

A

Realistic response to a known and threatening stimulus

174
Q

Define anxiety disorder

A

Psychological disorder with unrealistic fear

175
Q

4 symptoms of anxiety disorder

A

Tension, stimulation of the nervous system, GI issues, insomnia

176
Q

Give 5 examples of anxiety disorders

A 
Generalised anxiety disorder
Panic Disorder
Phobias
Obsessive Compulsive disorder
Post Traumatic Stress disorder
177
Q

What is Generalised anxiety disorder?

A

6+ months of anxiety, panic or worry

178
Q

What is Panic Disorder

A

Panic attacks - brief periods of intense fear

Increased blood pressure, hyperventilation, heart palpitations, tight chest, dizzy, tingling

179
Q

What are Phobias?

A

Strong fears of specific things/situations

180
Q

What is Obsessive Compulsive disorder?

A 
Intrusive thoughts (obsessions) that cause anxiety
People have specific compulsions (repetitive behaviours) to decrease their anxiety
181
Q

What is Post Traumatic Stress disorder?

2 brain changes during this condition?

A

Anxiety triggered by recall of past/stressful life events
Re-lived through flashbacks and nightmares
Causes avoidance, detachment and insomnia

Decreased size of the hippocampus and abnormal amydala activation

182
Q

4 actions of noradrenaline in the brain?

A

Attention, behaviour, feeding and sleep

183
Q

3 actions of serotonin in the brain?

A

Emotion, mood and sleep

Medicine - Year 1 (20 decks)

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