B6 W3 Flashcards
Persistent pain cycle
Less active, loss of fitness, sleep problems, stress, medication side effects which leads to more persistent pain
Regulation of the HPA axis
Cortisol feedback which binds to glucocorticoid receptors of the hippocampus to suppress the hypothalamus release of CRH
Emotional response to stress
Tearful, irritability, over-reacting
Stores of memory
Sensory- unprocessed for 0.5 to 3 seconds but a large capacity
Short term- for a few seconds or longer. More limited capacity than sensory but lasts longer.
Long-term: hours-> years with unlimited capacity
Illness cognition
A patients implicit beliefs about their illness and how they cope with it.
Salience
What makes something stand out- the more positive something seems, the more desirable it is, dependent on emotional response. Connected to identity
Ventral tegmental area
Dopaminergic and dopamine binds to the accumbens nucleus and prefrontal cortex, causing pleasure
Properties of addictive substances
Salience, mood modification, tolerance, withdrawal, causes neglect of other activities and relapse
Factors which contribute to alcoholism
Genetic, social, upbringing
Effect of glucoorticoid
Proteolysis, lipolysis, gluconeogenesis, Increase blood glucose levels, maintain blood pressure,
Behavioural response to stress
Comfort eating/loss of appettite, excess drinking.smoking, excess activity/underactivity and disturbed sleep, poor medication compliance
Stages of change
Precontemplative, contemplative, preparation, action, maintenance and relapse
Aspects of illness cognition
Identity- Label the illness and symtpoms
Timeline- perceived duration of symptoms
consequences of illness
cause about the ideas- punishment, eg
Control/cure
Glucocorticoids
Molecules with potent anti-inflammatory and immunosuppressive properties used to treat autoimmune conditions
Central sensitisation
Development and maintenance of chronic pain, where the CNS is in a state of high reactivitiy which lowers the pain threshold
Effect of acute stressors on the immune system
Upregulation
Short term stress response
Increases HER, BP, divert blood to heart and skeletal muscles, increase metabolic rate
What is preserved in semantic dementia?
Memory of recent events, phonology and syntax, visual-spaital skills
What stage in the cycle of change does the patient make changes?
Action
Addiction maintenance
Long term memory encoding of substance-taking behaviours and reduced frontal inhibition
Somatisation
Physical expression of psychological pain with no organic/physical basis- common compaints are headaches, GI pain, back pain
Amygdala
Located in the temporal lobe. Receives sensory information via the basolateral nucleus from the hippocampus and temporal lobes. Sends signals through its central nucleus to the:
-> hypothalamus stimulate the HPA axis for long term stress.
-> the periaqueductal grey matter to increase avoidance behaviour.
-> diffuse modulatory system to increase vigilance
Positive reinforcer of addiction
Substance like drugs or alcohol
Negative reinforcer of addiction
Withdrawal symptoms
What causes low white blood cell count in stress?
Aldosterone
Effects of aldosterone
Causes immune suppression and sodium and water retention to increase BP
Anterior temporal lobe
Long term semantic memory and non-declarative memory
What heightens pain/causes more pain gates to be open?
Stress, psychological factors, boredom, lack of activity
Hippocampus
Suppresses the HPA axis
Temporal gradient
Childhood memories are preserved but events before and since brain damage are not remembered
Glucocorticoids
Mobilising lipids and adipose stores, glycogenolysis and gluconeogenesis
Stress- effects
Ulcers, high BP and cortisol,, low WBC , blood sugar fluctuation, susceptibility to cancer
Generalised anxiety disorder
Anxiety over 6 months
Episodic memory
Hippocampus- located in the medial temporal lobe . It has LTM stores.
Dependence
Compulsive need for a drug
Addictive substances
Pleasure-producing potency, rapid onset of action, short duration of action, tolerance and withdrawal
Adrenocorticotropin hormone
Acts on the adrenal glands above the kidneys
Reverse temporal gradient
Impaired recall of facts and distant events- occurs in semantic dementia
Cognitive stress response
Difficulty concentrating, making decisions, self-criticism, sensitivity to criticism
Sleep for memory consolidation
Slow-wave sleep
Stages of encoding memory
Acquisition (into STM)
Secondary stress appraisal
Of personal coping abilities or personal resources and immediate social network
Non-declarative memory
Procedural memory, classical conditioning and priming
Panic disorder
Brief periods of intense terror and apprehension with shortness of breath and hyperventilation
Nucleus accumbens
Sub cortical structure in the forebrain. Involved in the dopaminergic pathway for pleasure as part of the mesolimbic system. It is invovled in drug addiction via glutamate transmission which is associated with relapse due to increased prefonrtal drive of the cortex to drug associated stimuli
SSRI uses
Anxiety and depression
Decay theory
When we learn something new, a neurochemical physical trace is formed
Periaqueductal grey matter
Midbrain region surrounding the cerebral aqueduct. Receives signals from the central nucleus of the amygdala to increase avoidance behaviour in stress and pain. Responsible for descending modulation of pain perception via both inhibition of pain perception and facillitation of pain perception
Periaqueductal grey matter- descending pain pathways
Projects to the ventromedial medulla which contains serotenergic raphe nuclei to inhibit neurons in the dorsal horn of the spinal cord of the spinothalamic pathway. This pathway is modulated by serotonin and noradrenaline
What neurotransmitters are involved in pain?
Glutamate which acts on ionotropic AMPA, NMDA or kainate receptors on the a-delta myelinated pain afferents transmitting to the dorsal horn of the spinal cord from the nociceptors. Substance P is released by nerves and inflammatory cells and acts on neurokinin receptors on unmyelinated C fibres in the dorsal horn of the spinal cord. It is inhibited by the periaqueductal grey matter descending pain pathway via serotonin.
Where do third order neurons terminate of the spinothalamic pathway?
From the thalamus to the somatosensory cortex and periaqueductal grey matter
What inhibits the periaqueductal descending pain pathways?
Mu opioid receptors, GABA
Endogenous opioid receptors
G protein coupled receptors which arise from terminals of the amygdala and hypothalamus. They regulate neurotransmission of pain by causing hyperpolarisaiton of cells in the dorsal horn. It reduces the release of susbtance P from first order neurons and causes hyperpolarisation of second order neuorns which reduces action potentials
How do endogenous opioid receptors act on the periaqueductal grey matter?
Enhance descending inhibition of the pain pathway where it is found in the periaqueductal grey matter and raphe nucleus of the ventromedial medulla
Prefrontal cortex
Involved in higher thinking. implicated with low dopamine levels in mesocortical pathway
Motivational interviewing
Promotes change via:
Empathy thorough reflecting listening, determine discrepancy between client’s goals and current behaviour, avoid confrontation, adjust to resistance and support self-efficacy
Physical management of pain
Graded exercise, medication management, pain education, intrathecal device
Gradual loss of memory- organic
Alzheimer’s, amnesia and dementia
Final common pathway for drug seeking
Release of glutamate from the nucleus accumbens in response to increased excitability of neurons from the prefrontal cortex . This is due to reduced inhibitory presynaptic regulation of excitatory glutamate transmission as a result of consistent drug use that causes changes in prefrontal cortex.
Short-term stress response
Mobilises glucose reserves, increases HR, metabolic rate and circulation
Dopamine in substantia nigra
Pars compacta projects onto the striata, concerned with motor functioning
How are brain structures affected in PTSD?
Reduced size of the hippocampus and abnormal activation of the amygdala.
How does the amygdala act on the diffuse modulatory systems?
Via central nucleus for increased vigilance
