Psych Flashcards
What are the two patterns of depression?
Unipolar: dysthymia (chronic low mood), melancholia (major depression), atypical depression (with other symptoms eg weight gain)
Bipolar: Bipolar Disorder and Cyclothymia
What are the key symptoms of depression?
Persistent sadness or low mood
and/or marked loss of interests or pleasure
What are the additional symptoms beyond the key ones which are pRt of a diagnosis for depression?
Disturbed sleep (decreased or increased compared to usual)
Decreased or increased appetite and/or weight
Fatigue or loss of energy
Agitation or slowing of movements
Poor concentration or indecisiveness
Feelings of worthlessness or excessive or inappropriate guilt
Suicidal thoughts or acts
What circuitry is involved in depression?
Decreased activity: Prefrontal cortex, Hippocampus (reward pathways)
Increased activity: Amygdala, Hypothalamus (HPA) (stress pathways)
What are the 4 theories for depression?
Neurotransmitters– Monoamines: Serotonin (5HT) Noradrenaline. NTs involved in arousal are decreased
Neurohormones - Steroids, HPA axis (Stress, Anxiety)
Immune - inflammatory response has knock on effect on other systems
Circadian - change in sleep wake cycle induces inflammation
Describe the role of 5HT in depression
Main site of production are raphé nuclei in medulla
Acts centrally in multiple areas
Involved in: Mood, agitation, OCD, anxiety, appetite, insomnia, sexual function, nausea and vomitting, GI function
Large interaction between 5HT and NA neurons centrally
Interactions in the brainstem speed activity, Interactions in the cortex slow activity
Describe the role of NA in depression
Main site of NA production in CNS is the Locus Coeruleus
Acts Centrally and peripherally (particulalry ANS transmission)
Multiple Functions: depression, attention, energy homeostastis, agitation, emotions, blood pressure, heart rate, bladder control, motor function
Large interaction between 5HT and NA neurons centrally
Interactions in the brainstem speed activity, Interactions in the cortex slow activity
What structural changes are seen in a depressed brain?
Decreased arborisation
Decreased synapses
Restored by AD/BDNF (brain derived neurotrophic factor)
Overproduction of receptors due to under production of transmitter
How can inflammation lead to depression?
Inflammatory mediators lead to:
Microglia activation, Cell dysfunction, Cell death
Leads to spectrums of disorders
What are treatment options for depression?
Pharmacological: SSRIs, TCAs, MAOI-A, Atypical Antidepressants, e.g. NASSA (Noradrenergic and specific serotonergic antidepressants), NRI (NA re uptake inhibitor)
Cognitive Behavioural Therapy
Transcranial Magnetic Stimulation (TMS)
Electroconvulsive Therapy (ECT)
Describe the placebo effect in depression treatment
30% of patients respond to placebo
Can change neuronal activity levels
Different effects to ADs
Works even if told
Describe electroconvulsive therapy
High frequency activity to cortex - epileptiform activity
Gold standard for severe depression, non responsive to other treatment
50% show improvement
Side effects: Memory loss, Addiction
Describe transcranial magnetic stimulation
Good for severely depressed patients who don’t respond to antidepressants
Significantly less stigma that ECT
Magnetic pulses targeted at: Prefrontal cortex, Limbic system, Increased activity so improve cognition, Fewer side effects
What are Side-effects of SSRIs/5HT modulation?
Slow onset Nausea Sleep disorders Sexual dysfunction Drug interactions may lead to ‘serotonin syndrome’ (hyperthermia, cardiovascular problems, aggression, tremor and rigidity)
What atypical antidepressants can be used for depression?
NRIs work in the same way as SSRIs- Reboxetine
SNRI - combined 5HT and NA reuptake inhibitors - Venlafaxine
5HT partial agonists reduce activity to increase transmitter levels- Buspirone, Trazodone
Name 4 SSRIs that can be used for depression
Fluoxetine
Citalopram
Sertraline
Paroxetine
How can light therapy help in depression?
Light therapy can enhance mood
Sleep pattern disruption depresses mood
Agomelatine: Melatonin agonist, Increases slow-wave sleep, Currently in use for depression
What are the 5 main actions of TCAs?
5HT reuptake blocker NA reuptake blocker α1 adrenoreceptor antagonist H1 receptor antagonist M1 receptor antagonist
What are Side-effects of TCAs?
Accumulation may lead to slowly developing side effects
Sedation due to antihistamine effects
Postural hypotension
Confusion
Visual problems
Cardiac dysrhythmia due to alpha receptor action
Mania
Many drug interactions, from aspirin to alcohol
How are MAOI As used in depression?
Increases NA/5HT levels by inhibiting enzymatic breakdown
Moclobemide - reversible
What are side effects of MAOI A drugs?
Similar to TCAs Many cross drug reactions - DO NOT USE WITH SSRIs/TCAs Postural hypotension Restlessness Convulsions Sleep disorders ‘cheese reaction’
Describe Presynaptic modulation of NA and 5HT by α-adrenoceptors
α-1 receptors act to accelerate
α-2 receptors act as a brake, inhibiting release presynaptically,
α-1 agonists speed transmission up and α-2 antagonists cut the brake cable eg. Mirtazapine - α-2 antagonist
What are Side-effects of adrenoceptor antagonists?
Decreased vascular flow in extremities Postural hypotension Fatigue Bronchoconstriction Cardiac failure Bradycardia Sleep disorders Impotence Depression
How is lithium used?
General mood stabiliser
Acts to reduce G-protein function and inhibits IP pathway signalling,
inhibits various kinases
Suppresses gene function
Increases neurogenesis
Salt used
Slow absorption, modified release form often used
Side effects various depending on intoxication levels
What are aims of CBT?
Identify thinking that causes problematic feelings and behaviour
Question the individual’s negative thinking in order to enable positive change in thought processes
Identify unwanted behaviour patterns
Plan behavioural goals and the step by step process for the achievement of the goals
How might you Identify and dysfunctional thoughts using CBT?
Shoulds- a set of expectations concerning one’s own behaviour and the behaviour of others
Catastrophising - expecting the worst, and interpreting situations as evidence of looming disaster
Filtering- focussing on negative aspects of a situation, and ignoring the positives
Polarisation - extreme view – people and circumstances must be categorised, with no shades of grey
Over-generalisation - reaching conclusions from a single incident, or a limited range of events
Personalisation - tending to assume that people are negatively referring to oneself; always comparing oneself with others
Mind-reading - assuming that you know what others are thinking, without asking them
Heaven’s reward - expecting that pain and sacrifice will be rewarded – feeling dismayed when this does not happen
What syndromes can CBT be useful for?
Depression Anxiety and panic attacks Addictions such as pathological gambling Obsessive-compulsive disorder Drug or alcohol problems Eating Disorders Phobias Chronic Fatigue Syndrome
What is REBT – Rational Emotive Behaviour Therapy?
This involves the ABCD approach where A = Activating Event B = Belief (about the event) C = Consequences (of the event) D = Disputing the belief/anticipated consequences of the event
What are 5 alternative counselling approaches?
Psychodynamic Therapy Humanistic Approach Systemic Approach Transactional Analysis Integrative Approach
What are the 5 factors that are assessed in CBT?
Thoughts Feelings Behaviour Body Environment
What is consciousness?
An individual’s state of awareness of his internal and external environments and of his mental state which enables him if necessary to manipulate meaningfully the situation in which he finds himself at any
point in time
What 3 factors does a normal state of consciousness depend on?
Upper brainstem reticular formation – wakefulness (Alertness)
Limbic system and frontoparietal association areas – affect, mood, attention and motivation (Attention)
Cerebral cortex – state of awareness and interaction with environment (Awareness)
What are the 4 levels of consciousness?
Normal – fully oriented in place, time and person
Lethargy (Somnolence) – awareness impaired bunormal on arousal; speech slow; voluntary movements diminished and slow; EEG mildly abnormal with some sleep pattern
Stupor – no real awareness; speech in response to pain; voluntary movements minimal/mass movement response to pain; EEG abnormal
but distinguishable from normal sleep pattern
Coma (Unconsciousness) – no awareness; speech absent; movements absent or only reflex in response to pain; EEG grossly abnormal or absent
What is persistent vegetative state?
Reticular formation is intact but cerebral cortex is non-functional
Person is awake - eyes are open and move around and sleep-awake cycles are present
Awareness is absent
Meaningful response to verbal command or pain is absent
EEG contains rhythmic activity resembling sleep cycles
What is minimally conscious state?
A sub-group of patients with severe alteration of consciousness who do not meet diagnostic criteria for coma or PVS
Inconsistent but discernable behavioural evidence of consciousness, eg. response to command, verbalisation, visual pursuit
May be temporary or permanent but overall prognosis more favourable than that of Persistent Vegetative State
What is locked in syndrome?
Sensation, reticular formation and cortical function are intact
Person is fully awake and aware
Motor function is absent but vertical eye movements and eyelid elevation may be spared
Usually due to infarct in ventral pons involving corticobulbar and corticospinal tracts
What 2 things physiologically produce coma?
Damage to brain stem reticular formation
Extensive cortical damage, especially if bilateral, but sometimes involving only the dominant hemisphere
What things may cause coma?
Supratentorial lesion – usually tumour or haemorrhage having mass lesion effect
Infratentorial lesion – tumour, haemorrhage or infarction, often with mass lesion effect
Toxic/Metabolic disorders – infection, drugs,hypoglycaemia, hyperglycaemia, uraemia, anoxia
What effects do intracranial mass lesions have on the brain?
Expansion of a lesion within the fixed volume cavity of the cranium may cause a rise in intracranial pressure
Expansion of a lesion may displace structures from one intracranial compartment to another (herniation)
Compression and destruction of brain adjacent to a lesion may cause neurological abnormalities (localising symptoms and signs)
Why might a mass lesion caused increased intracranial pressure?
Cranium is not distensible, Brain, CSF and blood are incompressible
Small expansile lesions can be accommodated by decrease in
amounts of intracranial CSF and blood
Larger lesions overcome this compensatory mechanism and cause
rise in intracranial pressure
Made worse by oedema of brain around lesion. As pressure rises cerebral perfusion falls and is partly compensated by hypertension and bradycardia
Symptoms and signs include headache, nausea and vomiting,
altered mental status, localising signs, pupillary changes, papilloedema, visual loss and irregular respiration. Death may result from brain ischaemia
What are the 4 phases of herniation (coning) syndrome?
Subfalcine (F)
Central (C)
Transtentorial (U)
Tonsillar (T)
Describe symptom progression in herniation (coning) syndrome
Headache/nausea/vomiting Hypertension, bradycardia and widened pulse pressure Pupillary changes Hemiparesis and/or hemisensory loss Somnolence Stupor Coma Cheyne-Stokes (periodic)/abnormal breathing pattern Death
In what 3 ways can you assess the level of herniation syndrome?
Size and reactions of pupils
Vestibulo-ocular reflex
Response to painful stimulus
What are normal pupils like?
3 – 4mm diameter, equal, brisk reaction to light
What effect would a thalamic lesion have on the pupils?
2 – 3mm diameter - constricted
react to light but difficult to see as parasymp connections still in tact
reduced sympathetic activity
What effect would midbrain compression have on pupils?
Fixed dilated >7mm diameter, IIIrd nerve lesion. Edinger Westphal nucleus probably affected. No pupil light reflex
What effect would a major brainstem compression have on pupils?
Fixed mid-size 5mm diameter, IIIrd nerve plus sympathetic lesion. No reaction to light
What may pin point pupils be a sign of? Non drug related
1 - 2mm diameter, react to light but difficult to assess, isolated sympathetic lesion in pons
How can you assess the vestibulo occular reflex?
Doll’s Head Test – turning head results in conjugate movement of eyes in opposite direction
Caloric Test – ice cold water in ear causes nystagmus with slow phase towards test ear
Normal tests indicate integrity of brainstem from pons(vestibular nuclei) to midbrain (III nucleus)
Response of only one eye suggests unilateral III or VI nerve lesion
No response indicates major brainstem damage
How can you assess an unconscious patients response to painful stimulus?
Strong pressure applied to supraorbital ridge or sternum
Localising response indicates moderate dysfunction
Flexion of arms and extension of legs (Decorticate response) indicates thalamic compression
Extension and medial rotation of arms and extension of legs (Decerebrate response) indicates lower brain stem compression involving the red nucleus and below
What are the 3 assessment criteria on the Glasgow coma scale?
Eye opening: spontaneous, verbal command, response to pain, None
Verbal response: Oriented in place/time/person, Confused but uses sentences, Inappropriate use of words, Uses only non-speech sounds, No vocalisation
Motor response: Obeys commands, Localises response to pain, Semi-purposeful flexion withdrawal response to pain, Non-purposeful flexion response to pain, Extensor response to pain, No response to pain
What is the AVPU scale?
A – Alert and oriented in place/time/person
B – Responsive to verbal stimulation
C – Responsive to pain
D – Unresponsive
What are the five dimensions of symptoms shown by Schizophrenic sufferers?
Positive symptoms Negative symptoms Cognitive symptoms Aggressive symptoms Anxiety/Depression
What is schizophrenia?
Fundamental and characteristic distortions of thinking and perception, and affect that is inappropriate or blunted
Diagnosis requires disturbance over six months with at least one month of classical symptoms: delusions, hallucinations, disorganised or catatonic behaviour or negative symptoms
What are positive symptoms of schizophrenia?
Delusions - generally persecutory
Hallucinations - generally auditory and third person
Agitation
Exaggerated/disorganised speech
Exaggerated/disorganised and bizarre behaviour
What are the negative symptoms of schizophrenia?
4 A’s
Affective Blunting
Anhedonia and Associality - loss of pleasure, lack of motivation to engage in social interaction
Alogia - poverty of speech
Apathy/Avolition - lack of drive for goals
What anatomical alterations can be seen in schizophrenic patients?
Degeneration occurs within grey matter, particularly medial temporal lobes, enlarged ventricles and sulci
Cerebral blood flow is reduced in the basal ganglia and frontal lobes
What is a major problem with antipsychotic drugs?
Less effect on the negative symptoms, 60% of patients still suffer these even when the positive symptoms are under control
What are the 2 groups of antipsychotics?
Classical (first generation) antipsychotics
Atypical (second generation) antipsychotics
What are classical antipsychotics?
Antagonists at the D2 receptor, but they also act on muscarinic (M1), histamine (H1) and adrenergic (α1) receptors. However, they have a low efficacy and 30% of patients are non-reponders
What are atypical antipsychotics?
Multiple receptor subtypes of 5HT, Dopamine muscarinics, histminergic
and aderenergic receptors and may also inhibit reuptake mechanisms. Atypical antipsychotics are better at dealing with negative symptoms than classical
