Psychological And Sociological Principles Flashcards
Mind and body dualism
What is the difference between the mind and brain
Advantages of classifications in health
Facilitate reporting and inform public health issues such as allocation of resources
•Facilitate meaningful communication and debate between patients, professionals, organisations and legislators
•Promote a feeling of being understood (“we’ve seen this before – your problems are not unique”)
•Provide a framework for research
•Offer evidence for treatment options and some information about natural history and prognosis
Disadvantages of classifications in health
Improved scientific understanding makes a mockery of previous attempts to classify (e.g. phrenology)
•Categorisation means defining thresholds which are arbitrary
•depression / dysthymia / fed up
•obese / well built / chubby / slender
•Categorisation can lead to stigma and prejudice
•Economy of thought may lead to oversimplification, reductionism and ultimately inhumane action
What is used to classify mental disorders
ICD 10
Role of emotion
Motivator for learning
Means of best obtaining rewards/avoiding punishment = stimulus-reinforcer association and instrumental (action-outcome) learning
Emotion
A strong feeling deriving from one’s circumstances, mood or relationship with others
Movement and emotion
Ability or inability to act determines which cluster of emotions is felt
Theories of emotion
Basic
Appraisal
Psychological constructionist
Bayesian model
Theories of emotion: appraisal
Meaningful interpretation of an object/situation by individual
Action readiness
May be automatic
Theories of emotion: psychological constructionist
Psychical compounds of basic ingredients (affect + ideational component)
Internal state subject of meaning analysis
Theories of emotion: basic
Biologically privileged emotion automatically triggered by objects/events
Hard-wired circuits
Variability: cultural ‘display rules’
Models of emotional categorisation
Discrete
Dimensional (valence and arousal)
Componential
Eckman’s 6 basic emotions
Anger
Disgust
Fear
Joy
Sadness
Surprise
Orbitofrontal cortex- appraisal
Input - ventral cortical streams (identity)
Orbitofrontal cortex: medial -reward
Activation: subjective pleasantness
Orbitofrontal cortex: lateral - punishment/ non-reward
Negative reward predictions error
Expectation of punishment
Mesolimbic pathway
Important in reward/behaviour responses
Connected to amygdala and orbitofrontal cortex
Ventral tegmental area
Amygdala- appraisal
Conditioned responses to stimuli predicting harm
Facial expression recognition
Slower response in reversal learning tasks
Little involved in subjective emotional experience
Identification of emotions
Sight- V1, V2, V4, inferior temporal visual cortex
Taste- nucleus of the solitary tract, thalamus, insular taste cortex
Smell- olfactory bulb
Touch- thalamus VPL, somatosensory cortex and insula
Auditory- temporal auditory cortex
Appraisal of emotions
Amygdala
Orbitofrontal cortex
Regulation of emotions
Cognitive and attentional top-down bias
Dorsal and ventrolateral frontal lobes
Reactivity of emotions
Cingulate cortex
Striatum/basal ganglia
Lateral hypothalamus, insula
Medial and ventromedial prefrontal cortex
Reactivity: cingulate cortex
Action-outcome learning
Anterior: outcome
Posterior: action
Mid: output to premotor areas
Posterior cingulate cortex inout
Parietal lobes- spatial/action related information
Posterior cingulate cortex output
Hippocampus
Anterior cingulate cortex
Outcome
Subgenual: reward signals from medial OFC
Supracollosal: punishment/non-reward data from lateral OFC
Mid cingulate cortex
Output to premotor areas (eg SMA)
Reactivity: ventromedial prefrontal cortex
Reward related decision making
Synaptic networks signal value of chose offer
Reactivity: hypothalamus and insula
Modulated by:
OFC via anteroventral insula and subgenual cingulate cortex
Amygdala- hypothalamus and Periaqueductal grey
Feedback from autonomic output not needed for emotional behaviour/feelings
Suppression of emotions
Autonomic and endocrine responses
What part of the brain is involved in stimulus-response habit learning
Striatum/ basal ganglia
What part of the brain is involved in action-outcome learning
Cingulate cortex
What part of the brain is involved in choice value and decision making
Medial prefrontal cortex
What does OFC stand for
Orbitofrontal cortex
Sensation
A mental process resulting from the immediate external stimulation of a sense organ
I.e. touch smell taste sight hearing
Perception
The ability to become aware of something or understand something following sensory stimulation
I.e. tactile olfactory gustatory visual auditory
Bottom up processing
Sensation
Top down processing
Perception
Bottom up processing-visual
Nasal/temporal retina
Optic nerve
Optic chiasma
Lateral geniculate nucleus
Top down processing -visual
Primary visual cortex- brain begins to process what you have seen and make connections
2 forms of retina
Temporal
Nasal
Bottom up processing - auditory
Everything up to auditory cortex
Perceptual set
The psychological factors that determine how you perceive your environment
What adds to perceptual set
Context
Culture
Expectations
Mood and motivation
Illusion
An instance of a wrong or misinterpreted perception of a sensory experience
Hallucinations
Experiences involving the apparent perception of something not present
Features of bottom up processing
Immediate response before processing what has happened eg jumping when scared
Features of top down processing
After brain processes what has happened
Gestalt theory effect
Used in advertising
Subconscious top down processing to engage audience with advertising more
different ways individuals group stimuli together in order to make a whole that makes sense to them.
Gestalt theory mechanisms
Proximity
Common fate (parallel lines)
Continuity
Closure
Symmetry
Thatcher effect
phenomenon where it becomes more difficult to detect local feature changes in an upside-down face, despite identical changes being obvious in an upright face
Hallucinations in psychiatry
Schizophrenia
Depression with psychosis
Bipolar affective disorder
Schizoaffective disorder
Drug induced psychosis
Acute transient psychosis
How many people experience hallucinations within their lifetime
1 in 20
Prevalence of schizophrenia
1 in 100
What investigation is used to investigate hallucinations
fMRI
What can cause hallucinations
Neurological
Drugs
Sensory deprivation
Abnormal physiological deprivations- eg sleep deprivation
Infections - delirium
Psychiatric illnesses
Hallucinations are …
Top down processing
Expectations and hallucinations
PTSD
Expecting certain emotions
Bio-psycho-social model of treatment
Bio = medications
Psycho = psychologists - therapy
Social= social networks, connections, friends, family
Delivery of raw data
Sensatiom
Interpretation of raw data
Processing of raw data
How many categories of mental illness/conditions are there
9
9 categories of mental illness/conditions
The organic illnesses
The dependency states – alcohol; drugs
The mood disorders
The anxiety states
The psychoses
The behavioural disorders
Neurodiversity
Childhood disorders
Personality disorders
The organic illnesses
The dementias
Delirium
Examples of rarer forms of organic presentations:
B12 and Folate deficiency
Cushing’s disease
Thyrotoxic storm
Wilson’s disease
And many more physical illnesses
Examples of rarer forms of organic presentations:
Examples of rarer forms of organic presentations:
B12 and Folate deficiency
Cushing’s disease
Thyrotoxic storm
Wilson’s disease
And many more physical illnesses
The dementias
Alzheimer’s
Vascular dementia
Lewy body
Frontotemporal
Types of Alzheimer’s
Rx- acetylcholine esterase inhibitors
Rx- glutamate bloackade
Types of Vascular dementia
Subcortical
Stroke related
Multi-infarct
The dependency states
Drugs eg heroin, cocaine, marijuana, amphetamines
Alcohol
Mood disorders
Depressive illness (unipolar)
Mania (unipolar)
Bipolar
Cyclothymia- extreme mood swings
Low mood (adjustment disorders, burnout , life setting)
The anxiety states
Generalised anxiety disorder
Panic attacks
OCD
Derealisation-depersonalisation
The psychoses
Schizophrenia
Acute and transient psychosis
Monosymptomatic delusion
Post-natal (puerperal) psychosis
Drug induced psychosis
The behavioural disorders
Sleep
Sex
Eating
Hanits
Neurodiversity
The developmental disorders:
Autism
ADHD
learning disability
Conditions related to childhood
Separation anxiety
General anxiety states
School refusal
Other behavioural problems
Sexual, psychological and physical abuse
Personality disorders
Borderline PD
Dissocial PD
Causes of delirium
Infection
Temperature
What is delirium
Acute onset of confusion
Dementia vs delirium
Onset
- acute onset = delirium
- progressive = dementia
How long does alcohol withdrawal take
2 weeks
How long heroin withdrawal take
72 hours
Symptoms and signs to look for in alcohol withdrawal
Epileptic fits
Panicking anxiety
Craving
Physical tremors
Vomiting
Gastritis
Red face
Clinical depression symptoms
Serotonin stimulated pathways:
Loss of appetite
Loss of sex drive
Early morning waking (can get to sleep but wake up earlier than usual feeling awful- throughout the day begin to feel better)
When does a predisposition to alcohol attachment arise
25 years old
How many young men suffer with OCD
1 in 10
Which brain centre is stimulated with anxiety
Bed nucleus- anticipation of something going wrong
Predictive behaviour
Role of the bed nucleus
Anxiety
Gender identity
Appetite
Dampens startle response- in men only (somatostatin)
Social recognition
Parental bonding
What drives sexual orientation
Hypothalamus
Eustress
Positive stress which is beneficial and motivating
- typically the experience of striving for a goal which is within reach
Distress
Negative stress which is damaging and harmful
- typically occurs when a challenge (or threat) is not resolved by coping or (rapid) adaptation
Physical stressors
Insults or injuries that produce direct physiological effects, eg damage of body rid due and/or bodily threat (pain, haemorrhage or inflammation)
Where are physical stressors processed
Brainstem and hypothalamus- reflexive
Stressors
Causes
Stress response
Physiological or psychological- mediated by the brain
Psychological stress
Stimuli that are perceived as excessively demanding or threatening, often involving anticipation
What areas of the brain are involved in psychological stress
Prefrontal cortex
Amygdala
Hippocampus
3 phases of stress response
Alarm
Adaptation
Exhaustion
Alarm
Threat identified- body’s response is state of alarm (fight or flight)
Adaptation
Body engages defensive countermeasures
Exhaustion
Body runs out of defences and resources are depleted
Homeostasis
Maintaining internal environment necessary for cell function
Allostasis
How complex systems adapt (eg via HPA axis) to changing environments by changing set-points
Allostatic load
Cumulative exposure to stressors , which if unrelieved leads to systems ‘wearing out’
Acute stress
Brief response to a novel but short-lived situation experienced by the body as a danger
Conscious perception of threat is not always involved
Healthy and adaptive and necessary for survival = fight or flight
Causes of acute stress
Noise
Short-term danger eg fire
Brief physiological change eg hunger or cold
Brief illness
Chronic stress
Arises from repeated or continued exposure to threatening or dangerous situations, especially those that cannot be controlled
More likely to involve appraisal and conscious perception
Examples of chronic stressors
Physical illness, disability and pain
Physical or sexual abuse
Poverty including poor housing, hunger, cold or damp, debt
Unemployment
Bullying or discrimination
Caregiving
5 elements of human stress response
Biochemical
Physiological
Behavioural
Cognitive
Emotional
How are stress responses mediated
Via autonomic nervous system and hypothalamo-pituitary axis (HPA)
Lead to changes that influence future responses to stress also reflecting brain plasticity
Sympathomedullary pathway
Hypothalamus activates the adrenal medulla
Adrenal medulla (controlled by ANS) releases adrenaline and noradrenaline into the bloodstream
Body prepares for fight or flight- adrenaline and noradrenaline reinforces the pattern of sympathetic activation eg increased heart rate and blood pressure
Energy
Hormones involved in sympathomedullary pathway
Adrenaline
Noradrenaline
The pituitary-adrenal system
Higher brain centres activate hypothalamus
Hypothalamus releases corticotrophin (CRF)
Pituitary gland releases adrenocorticotrophic (ACTH)
Adrenal cortex releases corticosteroids
Corticosteroids causes changes-liver releases energy and the immune system is suppressed
Action of corticosteroids
Liver releases energy
Immune system suppressed
Hormone the hypothalamus releases in response to stress
Corticotrophin (CRF)
Hormone the adrenal cortex releases in response to stress
Corticosteroids
Hormones the Adrenal medulla releases in response to stress
Adrenaline and noradrenaline
Hormone the pituitary gland releases in response to stress
Adrenocorticotrophin (ACTH)
Catecholamines
Adrenaline
Noradrenaline
Biochemical and molecular stress response
Steroids especially glucocorticoids (cortisol)
Catecholamines (adrenaline & noradrenaline)
The so-called sympathetic nervous system (SNS) ‘fight-or-flight’ chemicals
Inflammation and immune response are important & complex, mediated and modified by adrenaline and cortisol. Effects can be pro- and anti-inflammatory, and GCCs also have direct effects on the CNS.
Acute stress: immune suppression (anti-inflammatory)
Chronic stress: partial immune suppression + low-grade chronic inflammatory response, possibly through epigenetic effects on gene expression
Balance between immune activation & autoimmunity disrupted in chronic stress response (NB reduced vaccination response)
Immunosenescence?
Acute stress and immune response
Immune suppression- anti-inflammatory
Chronic stress and immune response
partial immune suppression + low-grade chronic inflammatory response, possibly through epigenetic effects on gene expression
Balance between immune activation & autoimmunity disrupted in chronic stress response (NB reduced vaccination response)
Immunosenescence?
Fight or flight chemicals
Steroids= glucocorticoids (cortisol)
Catecholamines = adrenaline and noradrenaline
Inflammation and immune response and stress
important & complex, mediated and modified by adrenaline and cortisol.
Effects can be pro- and anti-inflammatory, and GCCs also have direct effects on the CNS.
Hormones involved in stress and immune response
Adrenaline
Cortisol
Fast physiological stress response
Breathing more rapid to increase oxygen
Blood flow increases up to 400%, directed to heart & muscles
Increased heart rate & blood pressure
Muscles tense
Glucose released, insulin levels fall: boost energy to muscles
Red blood cells discharged from the spleen
Mouth becomes dry & digestion is inhibited
Sweating
Cytotoxic & surveillance WBCs go where injury & inflammation may occur i.e. bone marrow, skin, lymph nodes
Immunosenescence
Rapid aging of the immune system as a response to chronic stress
Physical (somatic) effects of chronic stress
Headache
Chest pain
Stomach ache
Musculoskeletal pain
Low energy
Loss of libido
Colds & infections
Cold hands & feet
Clenched jaw & grinding teeth
Behavioural responses to stress
Easily startled & hypervigilant
Change in appetite – both directions
Weight gain (obesity) or weight loss
Procrastinating and avoiding responsibilities
Increased use of alcohol, drugs & smoking
Nail biting, fidgeting and pacing
Sleep disturbances especially insomnia
Withdrawal
Cognitive responses to stress
Constant worrying
Racing thoughts
Forgetfulness and disorganisation
Inability to focus
Poor judgement
Being pessimistic or seeing only the negative side
Altered learning
Emotional responses to stress
Depression & sadness
Tearfulness
Mood swings
Irritability
Restlessness
Aggression
Low self-esteem and worthlessness
Boredom & apathy
Feeling overwhelmed
Rumination, anticipation & avoidance
What can modify the perception of threat
Context
Appraisal
Vulnerability
Learning (past experiences)
Stress and illness
related to a host of illnesses, esp of cardiovascular and GI systems, ie those with strong ANS connections.
Stress exacerbates physical illnesses and slows recovery and increases susceptibility to infection.
Strong evidence of association between depression and mortality following an MI.
Evidence of causal association between stress and physical illness is still limited, though note emerging evidence that chronic stress increases ‘immune ageing’.
Exposure to stress (trauma) is greater in those experiencing deprivation and with less healthy lifestyles.
Stress and cancer
Stress linked to survival rather than incidence
Stress and cardiovascular disease
High blood pressure
Abnormal heart rhythms
MI
Stroke
Stress and gastrointestinal problems
Inflammatory bowel disease
Irritable bowel syndrome
Stress and illness
Cancer: stress linked to survival rather than incidence
Cardiovascular disease: high blood pressure, abnormal heart rhythms, MI and stroke
Obesity & eating disorders
Infertility, recurrent miscarriage & menstrual problems
Rheumatoid arthritis
Skin & hair problems eg acne, psoriasis, eczema
Gastrointestinal problems: inflammatory bowel disease, irritable bowel syndrome.
Medically unexplained symptoms (MUS)
Infectious diseases especially covid-19
Stress and skin + hair problems
Acne
Psoriasis
Eczema
Post traumatic stress disorder
Vivid flashbacks & nightmares
Intrusive thoughts and images
Sweating
Nausea
Trembling
Hypervigilance & increased startle response
Agoraphobia
Insomnia
Irritability
Impaired concentration
Stress management
Shiatsu, T’ai Chi, Yoga
Mindfulness
Meditation
Exercise
Sleep hygiene
Friends and family
Healthy diet
Exposure to natural environments
Aromatherapy
Cognitive Behavioural Therapy
6 reasons why natural selection left us vulnerable to disease
Mismatch
Infection
Constraints
Trade-offs
Reproduction
Defensive responses
Routine health data
Collected, collated and disseminated on a regular basis
Health data
Data to describe population health status eg mortality or morbidity
Data about health care
Data on factors influencing health
Why collect routine health data
Monitor health of the population- descriptive epidemiology
Generate hypotheses in causes of ill health —>further research —> possible prevention
Inform planning of services and policy to meet health needs, including resource allocation
Evaluate and assess performance of policies and services including quality and outcomes
Generate research statistics to be included in summaries for research dissemination and in funding applications
Types of health information
Mortality
Morbidity (diseases)
Use and quality of health care
Health status/ quality of life
Individual lifestyle (health related behaviour)
Wider determinants (socio-economic, cultural and environmental conditions)
Population demographics
Mortality statistics
- Doctor completes certificate of cause of death
- ‘Informant’ takes certificate to local registrar and registers death
- Copy of registration sent to ONS where causes of death are coded
- ONS compile and publish mortality statistics
Cause of death recording
Underlying cause of death according to WHO:
A. Disease or injury that initiated the train of events directly leading to death, or
B. The circumstances of the accident or violence that produced the fatal injury
Data quality - CART
Completeness
Accuracy
Relevance and/or representativeness
Timeliness
Health information - morbidity
State of being diseased
Degree of severity of disease
Incidence of disease
Prevalence of disease
Incidence
Number of new cases in a particular population during a particular time interval
Prevalence
Total number of cases in a particular population at a particular point in time
Incidence rate
Number of new cases/ population at risk
Point prevalence
Number of cases at a point in time/ total population
Health benefits of green space
Improved relaxation and restoration
Improved social capital
Improved functioning of the immune system
Enhanced physical activity, improved fitness and reduced obesity
Anthropogenic noise buffering and production of natural sounds
Reduced exposure to air pollution
Reduction of the urban heat island effect
Enhanced pro-environmental behaviour
Optimised exposure to sunlight and improved sleep
Mitigation of harm- urban green
Reduce air pollution
Noise reduction
Temperature regulation
Conducive to the restoration of depleted capacities - urban green space
Reduction of stress
Increases in positive emotions
Facilitation of recovery from attentional fatigue
Mechanisms by which green space benefits health and well-being
Mitigation of harm
Restoration of depleted capacities
Building new capacities
Microbial diversity
Biological symptoms of depression
Poor sleep
Poor appetite
Reduced libido
Poor concentration
What is depression
Low mood
Anhedonia
Low energy
Neurodegenerative disease of impaired plasticity
Cognitive symptoms of depression
Worthlessness (poor self esteem)
Guilt
Hopelessness
Suicidal thoughts
HPA axis and depression
Increased corticotropin releasing hormone
Enlarged adrenals and pituitary
Reduced negative feedback
Reduced glucocorticoid receptor expression in the brain
HPA axis
Hypothalamus —> corticotropin releasing hormone
Anterior pituitary—> adrenocorticotropic hormone
Adrenal cortex —> cortisol
Negative feedback loop = cortisol inhibits release of other 2 hormones
History of childhood maltreatment
Increased adrenocorticotropic hormone release in response to stress
Effect of cortisol (stress) on the brain
Neurotoxic
Causes neuro-vulnerability
Affects dendrite formation
Reduces neurogenesis
Causes changes to the EEG
Particularly affects frontal lobes and hippocampus
Medial pre-frontal cortex
Evaluating emotional state
Social cognition
Dorsolateral prefrontal cortex
Working memory
Problem solving
Which part of the frontal lobe has a larger volume loss in depression
Dorsolateral prefrontal cortex > medial prefrontal cortex
Hippocampus
Important for memory
Effect of depression on hippocampus
Reduced size - up to 20% volume loss
Dose related effect- correlates with number of and length of previous episodes
Associates with learning based cognitive deficits
Much of the volume loss is irreversible
Neurogenesis
Grow axons and dendrites and integrate into existing networks
Stress and neurogenesis
Down regulates
Restraint and shock stress causes reduced neurogenesis - particularly when learned helplessness is induced
‘Social dominance stress’ reduces the number of surviving new cells (same rate)
Stress and dendrites
Mediated by reduced neurotrophins eg brain derived neurotrophic factor
Brain derived neurotrophic factor
Stress decreases BDNF
Low BDNF in unmedicated depressives
How do antidepressants work
Increase glucocorticoid receptor expression (regulating HPA activity)
Increase neurogenesis
Increase BDNF synthesis- improve connectivity and increase number of synapses
Affect gene expression
Monoamines in the brain
Serotonin
Noradrenaline
Dopamine
What can lead to depression
Acute stress
Previous trauma eg early adversity and parenting
MDD
Major depressive disorder
Function of the default mode network
Daydreaming, internal ‘flow’ of consciousness- resting state
Automatically details- self’s place in time and space, projecting to other places in time and space
Self reference- referring to traits or states, emotional and moral reasoning
Thinking about others- theory of mind, social judgements/evaluations
Default mode network in depression
Depressed people find it hard to appropriately switch off their DMN in response to a task - excessive rumination
Entropy
Measure of disorder/chaos
How does the brain attempt to reduce entropy
Top-down processing- makes predictions to reduce surprises
Initially visual predictions and other basic sensory functions
Eventually words, concepts and core beliefs
Functional MRI scans
Based on oxygen or glucose take up
Functional connectivity- spatially distinct areas of the brain showing similar activity at similar times
Functional connectivity
Spatially distinct areas of the brain showing similar activity at similar times
Allows the study of networks
Default mode network contains
Medial prefrontal cortex
Precuneus including the hippocampus
Acute psychedelic state
Reduced activity in the default mode network- metabolism and functional connectivity
Reduced alpha power in PCC
Ego dissolution
Correlated with reduction in default mode network
“Inexperienced a decrease in my sense of self-importance”
High entropy- high disorder, flexible states
Psychedelic state
Infant consciousness
REM sleep/dreaming
Early psychosis
Sensory deprivation
Near death experience
Magical thinking
Dreamy state of temporal lobe epilepsy
Divergent- thinking/creativity
Low entropy- low disorder, rigid states
Come
Anaesthesia
Sedation
Deep sleep
Seizure
Depression
OCD
Addiction
Rigid/narrow thinking
Mindfulness meditation
Short (8 week) course of daily mindfulness practice reduces activity in the default mode network
And treats and prevents depression
Focus on breath- increasing attention and being more aware of one’s own mind
Depression is
A disease of reduced plasticity- reduced connectivity at cellular level
A disease of increased self-referential thinking- reduced connectivity at the interpersonal level
Social rank theory
After a prolonged fight for dominance there is a role for submission
Social risk theory
Sensitivity to social risk
Inhibition of confident behaviour
‘Cry for help’
Depressogenic modern society
Over-emphasis on the self and one’s ‘rank’
Self-referential ruminations
Fear of social threat
5 pillars of wellbeing
Physical activity
Connect with others
Learn something new
Practice mindfulness
Acts of generosity
Some psychiatric diagnoses are associated with issues of either ‘over-control’ or ‘under-control’. Which of the following behaviours would be typical of an individual with ‘over-control’ traits?
Good at delayed gratification
