B6 W3 Flashcards by Sumaya L

Persistent pain cycle

Less active, loss of fitness, sleep problems, stress, medication side effects which leads to more persistent pain

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Regulation of the HPA axis

Cortisol feedback which binds to glucocorticoid receptors of the hippocampus to suppress the hypothalamus release of CRH

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Emotional response to stress

Tearful, irritability, over-reacting

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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

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Illness cognition

A patients implicit beliefs about their illness and how they cope with it.

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Salience

What makes something stand out- the more positive something seems, the more desirable it is, dependent on emotional response. Connected to identity

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Ventral tegmental area

Dopaminergic and dopamine binds to the accumbens nucleus and prefrontal cortex, causing pleasure

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Properties of addictive substances

Salience, mood modification, tolerance, withdrawal, causes neglect of other activities and relapse

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Factors which contribute to alcoholism

Genetic, social, upbringing

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Effect of glucoorticoid

Proteolysis, lipolysis, gluconeogenesis, Increase blood glucose levels, maintain blood pressure,

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Behavioural response to stress

Comfort eating/loss of appettite, excess drinking.smoking, excess activity/underactivity and disturbed sleep, poor medication compliance

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Stages of change

Precontemplative, contemplative, preparation, action, maintenance and relapse

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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

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Glucocorticoids

Molecules with potent anti-inflammatory and immunosuppressive properties used to treat autoimmune conditions

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Central sensitisation

Development and maintenance of chronic pain, where the CNS is in a state of high reactivitiy which lowers the pain threshold

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Effect of acute stressors on the immune system

Upregulation

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Short term stress response

Increases HER, BP, divert blood to heart and skeletal muscles, increase metabolic rate

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What is preserved in semantic dementia?

Memory of recent events, phonology and syntax, visual-spaital skills

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What stage in the cycle of change does the patient make changes?

Action

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Addiction maintenance

Long term memory encoding of substance-taking behaviours and reduced frontal inhibition

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Somatisation

Physical expression of psychological pain with no organic/physical basis- common compaints are headaches, GI pain, back pain

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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

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Positive reinforcer of addiction

Substance like drugs or alcohol

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Negative reinforcer of addiction

Withdrawal symptoms

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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