Psych Flashcards
1
Q
What are the two patterns of depression?
A
Unipolar: dysthymia (chronic low mood), melancholia (major depression), atypical depression (with other symptoms eg weight gain)
Bipolar: Bipolar Disorder and Cyclothymia
2
Q
What are the key symptoms of depression?
A
Persistent sadness or low mood
and/or marked loss of interests or pleasure
3
Q
What are the additional symptoms beyond the key ones which are pRt of a diagnosis for depression?
A
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
4
Q
What circuitry is involved in depression?
A
Decreased activity: Prefrontal cortex, Hippocampus (reward pathways)
Increased activity: Amygdala, Hypothalamus (HPA) (stress pathways)
5
Q
What are the 4 theories for depression?
A
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
6
Q
Describe the role of 5HT in depression
A
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
7
Q
Describe the role of NA in depression
A
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
8
Q
What structural changes are seen in a depressed brain?
A
Decreased arborisation
Decreased synapses
Restored by AD/BDNF (brain derived neurotrophic factor)
Overproduction of receptors due to under production of transmitter
9
Q
How can inflammation lead to depression?
A
Inflammatory mediators lead to:
Microglia activation, Cell dysfunction, Cell death
Leads to spectrums of disorders
10
Q
What are treatment options for depression?
A
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)
11
Q
Describe the placebo effect in depression treatment
A
30% of patients respond to placebo
Can change neuronal activity levels
Different effects to ADs
Works even if told
12
Q
Describe electroconvulsive therapy
A
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
13
Q
Describe transcranial magnetic stimulation
A
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
14
Q
What are Side-effects of SSRIs/5HT modulation?
A
Slow onset Nausea Sleep disorders Sexual dysfunction Drug interactions may lead to ‘serotonin syndrome’ (hyperthermia, cardiovascular problems, aggression, tremor and rigidity)
15
Q
What atypical antidepressants can be used for depression?
A
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
16
Q
Name 4 SSRIs that can be used for depression
A
Fluoxetine
Citalopram
Sertraline
Paroxetine
17
Q
How can light therapy help in depression?
A
Light therapy can enhance mood
Sleep pattern disruption depresses mood
Agomelatine: Melatonin agonist, Increases slow-wave sleep, Currently in use for depression
18
Q
What are the 5 main actions of TCAs?
A
5HT reuptake blocker NA reuptake blocker α1 adrenoreceptor antagonist H1 receptor antagonist M1 receptor antagonist
19
Q
What are Side-effects of TCAs?
A
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
20
Q
How are MAOI As used in depression?
A
Increases NA/5HT levels by inhibiting enzymatic breakdown
Moclobemide - reversible
21
Q
What are side effects of MAOI A drugs?
A
Similar to TCAs Many cross drug reactions - DO NOT USE WITH SSRIs/TCAs Postural hypotension Restlessness Convulsions Sleep disorders ‘cheese reaction’
22
Q
Describe Presynaptic modulation of NA and 5HT by α-adrenoceptors
A
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
23
Q
What are Side-effects of adrenoceptor antagonists?
A
Decreased vascular flow in extremities Postural hypotension Fatigue Bronchoconstriction Cardiac failure Bradycardia Sleep disorders Impotence Depression
24
Q
How is lithium used?
A
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
25
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
26
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
27
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
```
28
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
```
29
What are 5 alternative counselling approaches?
```
Psychodynamic Therapy
Humanistic Approach
Systemic Approach
Transactional Analysis
Integrative Approach
```
30
What are the 5 factors that are assessed in CBT?
```
Thoughts
Feelings
Behaviour
Body
Environment
```
31
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
32
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)
33
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
34
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
35
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
36
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
37
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
38
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
39
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)
40
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
41
What are the 4 phases of herniation (coning) syndrome?
Subfalcine (F)
Central (C)
Transtentorial (U)
Tonsillar (T)
42
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
```
43
In what 3 ways can you assess the level of herniation syndrome?
Size and reactions of pupils
Vestibulo-ocular reflex
Response to painful stimulus
44
What are normal pupils like?
3 – 4mm diameter, equal, brisk reaction to light
45
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
46
What effect would midbrain compression have on pupils?
Fixed dilated >7mm diameter, IIIrd nerve lesion. Edinger Westphal nucleus probably affected. No pupil light reflex
47
What effect would a major brainstem compression have on pupils?
Fixed mid-size 5mm diameter, IIIrd nerve plus sympathetic lesion. No reaction to light
48
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
49
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
50
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
51
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
52
What is the AVPU scale?
A – Alert and oriented in place/time/person
B – Responsive to verbal stimulation
C – Responsive to pain
D – Unresponsive
53
What are the five dimensions of symptoms shown by Schizophrenic sufferers?
```
Positive symptoms
Negative symptoms
Cognitive symptoms
Aggressive symptoms
Anxiety/Depression
```
54
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
55
What are positive symptoms of schizophrenia?
Delusions - generally persecutory
Hallucinations - generally auditory and third person
Agitation
Exaggerated/disorganised speech
Exaggerated/disorganised and bizarre behaviour
56
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
57
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
58
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
59
What are the 2 groups of antipsychotics?
Classical (first generation) antipsychotics
| Atypical (second generation) antipsychotics
60
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
61
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
62
What is Clozapine?
Prototype atypical antipsychotic, it is a serotonin-dopamine antagonist with high efficacy but has the most side effects associated with its use of all the atypicals
63
What is Risperidone?
Biphasic activity, atypical at low doses and more conventional at higher doses
Used to treat other disorders including dementia, and also for children and adolescent use
64
What is a main advantage of atypical antipsychotics?
Lower incidence of extrapyramidal symptoms which is a major side effect associated with classical antipsychotics
65
What major side effects are seen with antipsychotic drugs?
Extrapyramidal symptoms
Seen in up to 75% of patients - altering activity in nigrostriatal pathways
Dystonias, akathisia, parkinsonism, sedation, seizures, hypotension, hypothermia, hypersensitivity, weight gain. Agranulocytosis is a problem with clozapine and requires regular monitoring.
66
What is Agranulocytosis?
problem with clozapine and requires regular monitoring
| Leukopenia
67
Why do atypical antipsychotics have less side effects than classical?
Atypical have a higher affinity for the mesolimbic and cortical pathways than the nigrostriatal dopaminergic pathways
68
What is Neuroleptic malignant syndrome?
side effects associated with use of antipsychotics in patients with a genetic polymorphism of the D2 receptor (which may account for 12-15% of patients). High fever, autonomic problems and altered consciousness
69
What is Tardive dyskinesia?
Prolonged classical use, high risk which in many cases is irreversible.
Disabling involuntary movements, including: tongue protruding, choreiform movements, grimacing and twisting of the face and limbs
Spontaneously remit in 30% of presentations, disabling voluntary
movements are difficult to treat
Caused by oxidative neurodegeneration caused by increased glutamatergic transmission which results from a down-regulation of the dopamine system
70
What class of drug is haloperidol? And What is its primary mechanism of action?
Classical antipsychotic
| Dopamine (D2) receptor antagonist
71
What disorders was haloperidol commonly used to treat?
```
Schizophrenia
Acute psychosis, such as Alcohol/drug-induced psychosis
Delirium
Agitation
Hyperactivity
Aggression
```
72
What would you do to reduce the symptoms and occurrence of tardive dyskinesia?
Reduce/Stop drug use, switch to Atypical Antipsychotic, stop any anticholinergics immediately
73
What supplements/drugs may aid with symptom relief of tardive dyskinesia?
Vitamin E&B6, Benzodiazepines, β-blockers
74
Name the signs/symptoms of parkinsonism
```
Tremor, pill rolling/10Hz
Stiffness, cog wheel rigidity
Clumsiness
Festinant gait
Postural changes, mask-like face
Speech problems (monotonous, aprosodic)
Micrographia
Sleep disturbances
Skin problems
```
75
Which of the dopamine pathways are involved in the pathogenesis of (a) schizophrenia and (b) parkinsonism?
(a) Mesolimbic and mesocortical
| (b) Striatonigral
76
Many other substances can induce iatrogenic parkinsonism; name some of these
Antiemetics: Droperidol, Metoclopramide
Antiepileptics: Valproate
Cardiovascular Agents: Alpha-methyldopa, Reserpine
Vestibular Sedatives: Cinnarizine, Flunarizine
Miscellaneous: Tetrabenazine, MPTP/MPP+, CO/CO2
77
Which imaging technique may be useful in determining specific types of parkinsonism?
FMRI or PET
78
What is the name of the late stage side effects associated with long term treatment for parkinsonism?
On off effects
79
What are the two forms of memory?
Procedural and declarative
80
Which areas are involved in procedural memory?
cerebellum, basal ganglia and pre-motor cortex
| difficult to form but onceformed are long lasting and can be performed without conscious recollection
81
Where are declarative memories stored?
rapidly learnt but also rapidly forgotten, depend upon connections between the hippocampus and widespread regions of the cerebral cortex
82
What does the ability to form long term memories require?
Repetition and consolidation, the process by which immediate experiences are converted first into short term then into long term memories appears to depend upon physical changes in synaptic connections. The act of remembering refers to the process whereby
information is retrieved from long term storage into consciousness (declarative memory) or is expressed as motor skill (procedural memory)
83
What are anterograde and retrograde amnesia?
Anterograde: inability to form new memories following an accident because of fault in the consolidation of new experience into long term memory. Associated with damage to the temporal lobes, particularly the hippocampal gyrus
Retrograde: inability to recall events prior to some precipitating event. This type of amnesia is a failure of long term memory. As such memories are distributed throughout the cerebral cortex, retrograde amnesia may follow generalised lesions such as those produced by Alzheimer's disease
84
What is episodic memory?
autobiographical events (times, places, associated emotions, and other contextual who, what, when, where, why knowledge) that can be explicitly stated. It is the collection of past personal experiences that occurred at a particular time and place
85
Which types of memory are declarative?
Episodic and semantic
86
Which form of memory, procedural or declarative appears first in development?
Procedural
87
What sub-cortical structure is involved in many aspects of procedural memory?
Cerebellum and basal ganglia
88
What is aphasia?
Loss of ability to use language
89
What abnormalities would you expect a CT scan of an Alzheimers brain to show?
Cortical atrophy and enlarged ventricles
90
Drug dependence is characterised by three components, what are these?
Psychological dependence – emotional distress caused by withdrawal of the drug
Physical dependence – physical symptoms of withdrawal of the drug
Tolerance – a requirement for increasing amount of drug to maintain the ‘high’
91
Why would someone on heroin have miosis? Which cranial nerve controls pupil constriction?
Heroin (diamorphine) is an opioid drug which acts to reduce sympathetic tone, enhancing parasympathetic activity. Pupillary constriction one of the side effects of opioid administration and is the result of unopposed activity of the parasympathetics, carried by the oculomotor nerve (CNIII)
92
Which opioid antagonist could be given to help with relapse in addictive behaviour. How does it work? What other addiction is this drug also used for?
Naltrexone is a long-lasting competitive opioid antagonist, used in relapse prevention - prevent action of administered opioids, reducing positive reinforcement of opioid ‘high.’ Naltrexone can also reduce the ‘highs’ associated with alcohol addiction
93
Why might heroin addicts gums look swollen and lose a few teeth?
Opioids do not directly cause tooth decay or damage to the gums but reduce salivary secretions, so dry mouth - bacteria and waste products not washed away and can lead to increasing acidity levels around the teeth and gum-line
Opioids also activate chemotactic trigger zone in the brainstem, so increased vomiting, exposing teeth to high levels of acid
Heroin users have cravings for sweet, sugary foods so higher risk of tooth decay. Regular brushing, good oral hygiene programme and frequent dental checkups help. However, motivation for self-care and grooming is low
94
Name the three main approaches taken in addiction management
Abstinence based - detoxification, rehabilitation
Harm-reduction - advice on safe sex and injecting, needle exhange program etc
Recovery-oriented- for those who wish to be drug-free: to create effective exit routes out of specialised drug treatment, including
community detoxification and efficient access to Tier 4 provision. for those in maintenance treatment: to be well integrated with primary care and other systems of support and care
95
What are the main psychosocial interventions available for addiction management?
```
Brief Interventions
Motivational Interviewing
Structured Counselling
CBT
Contingency Management
Relapse Prevention
AA/NA/CA
```
96
What can you do to help reduce lapses in compliance with addiction interventions?
Random urinalysis
Daily pick-up/Instalment prescriptions
Titrate dose against symptoms
Offer various psychosocial support
97
What is FRANK?
National initiative and support group, enabling confidential and open discussion of drug misuse, treatments and a way to find additional support
98
If methadone does not suit the patient, what other opioid is licensed for use in addiction management?
Buprenorphine
If neither methadone nor buprenorphine work, it is possible to use dihydrocodeine or slow-release opioids as alternatives
99
What is Valium?
Trade name for Diazepam - Benzodiazepine
Increasing inhibitory activity in the nervous system - co-agonists at the GABAA-receptor, increasing the movement of chloride ions through this channel, acting on the γ-subunit
100
What drug could be used alas benzo antagonist to reverse overdose?
Flumazenil - competitive antagonist
101
Why are benzos generally only prescribed for short-term use?
Dependence and tolerance develop very quickly so usage kept to a minimum. Long lag time and severe withdrawal effects so long-term users should be weaned off very gradually
102
What class of drug acts in a similar way to valium, but on the β-subunit of the GABAA receptor? What are these drugs most commonly used for in the clinic?
Barbiturates are most commonly used as anaesthetics, but are also associated with euthanasia
103
The CAGE questionnaire is a quick tool for determining actual, or potential, problems with alcohol misuse. What are the 4 questions used in this questionnaire?
Have you ever felt you should Cut down on your drinking?
Have people Annoyed you by criticizing your drinking?
Have you ever felt bad or Guilty about your drinking?
Have you ever had an Eye opener (drink first thing in the morning) to steady your nerves or to get rid of a hangover?
104
When you consider using the CAGE questionnaire what should you avoid before starting the questions?
You should not discuss alcohol use before you start the CAGE questions as the sensitivity of the test is significantly reduced if the patient is primed for questions about alcohol use
105
What CAGE score indicates clinical significance?
Greater than 2
106
What AUDIT score should be considered clinically significant for harmful dependence and behaviour in men? And in women?
A score of 8 of more indicates potential alcohol problems in men, in women a score of 4 is clinically significant
107
Chronic alcoholics generally suffer from severe dietary insufficiencies as a result of malabsorption, what are they?
Fat, nitrogen, sodium, water, thiamine, folic acid, vitamin B12 and D-xylose
108
What type of gait would you associate with vitamin B12 deficiency and why?
You would see a heavy stamping type of gait due to loss of proprioceptive inputs resulting from loss/degeneration of the dorsal columns. Have to stamp to activate pain pathways in order to determine where feet/legs are in the mental body image required for conscious movement
109
One of the most problematic of the dietary insufficiencies seen in alcoholics is Thiamine. What is the alternative name for this vitamin and which element of Wernicke-Korsakoff syndrome could be attenuated by providing thiamine supplements?
Vitamin B1
Wernicke-Korsakoff syndrome - two elements
Wernicke’s encephalopathy: abnormal gait and posture, paralysis of eye movement and deranged mental function. If symptoms are not too pronounced and long-term they can be alleviated with vitamin B1 supplements
Korsakoff syndrome (or alcoholic amnestic disorder)mdescribes the later stages of this disorder and is irreversible, and includes confabulation and deterioration in higher conceptual functions, and spontaneity/initiative. It is also linked with marked amnesia, both anterograde and retrograde
110
What are addictive behaviours?
Repetitive habit pattern that increases the risk of diseases and/or associated personal and social problems. The individual has a loss
of control, immediate gratification with deleterious effects, and experiences relapses when trying to quit
111
What is addiction as a disease?
A chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences
Considered a brain disease because drugs change the brain structure and how it works
These changes can be long lasting, and can lead to the harmful behaviours seen in people who abuse drugs
112
What is addiction as an attachment disorder?
Induced by a person's misguided attempt at self-repair because of deficits in psychic structure
113
What is substance misuse?
Drug and/or alcohol taking which causes harm to the individual, their significant others or the wider community. By definition those requiring
drug or alcohol treatment are substance misusers
114
What is dependence syndrome?
3 or more of the following present together during the previous year:
Strong desire or compulsion to take the substance
Difficulties in controlling substance taking behaviour in terms of its onset, termination or levels of use
A physiological withdrawal state
Evidence of tolerance
Progressive neglect of alternative pleasure or interests
Increased amount of time necessary to obtain or take the substance or recover from its effects
Persisting with substance abuse despite clear evidence of overtly harmful consequences
115
What is a dual diagnosis?
Patients suffering from psychiatric disorders and addictive behaviours especially drug and alcohol misuse
116
What is addictive gambling?
Persistently repeated gambling which continues and increases despite adverse social consequences such as impoverishment, impaired family relationships, disruption of personal life
Differentiated from recreational gambling and betting, when done by manic patients and when part of the sociopathic personality
117
Which pathway is involved in addiction?
Meso Limbic dopaminergic reward pathway
| From nucleus accumbens to ventral tegmental area and prefrontal cortex
118
What transmission do drugs of abuse target?
Directly or indirectly target the brain’s reward system by flooding the circuit with dopamine
A neurotransmitter present in regions of the brain that regulate movement, emotion, cognition, motivation and feelings of pleasure
Overstimulation of this system, which rewards our natural behaviours, produces the euphoric effects sought by people who abuse drugs and teaches them to repeat the behaviour
119
Describe the survival instinct theory of addiction
Life-sustaining activities such as food, water, sex and nurturing associated with pleasure or reward
Any activity inducing pleasure is associated with sustaining life and needs to be remembered, and repeated
Drugs and alcohol can release 2 to 10 times the amount of dopamine that natural rewards do which can occur almost immediately (as when drugs are smoked or injected)
The effects can last much longer than those produced by natural rewards.The resulting effects on the brain’s pleasure circuit dwarf those produced by naturally rewarding behaviours
Brain mistakenly interprets that taking these pleasure inducing drugs is
essential for survival
120
What impact does increased rewarding behaviour (drug taking) have on the addict?
Leads to increase in pleasure threshold because of neuroadaptation
Normal pleasure inducing activities get boring
Brain directs its normal drives away from natural reinforcers and towards the more pleasurable drugs
For heroin and cocaine all natural drives are subsumed by an overwhelming search for and use of drugs
Addicts give up sex, grooming, hygiene, and work and hardly eat or drink and ignore health problems
121
What psychosocial factors can affect addiction?
Pleasure seeking: Having high or buzz, feeling comfortably numb, pleasantly drowsy, full of energy and confidence
Self-medicating for anxiety, strong emotions such as anger, for pain, boredom, lack of motivation and self confidence and withdrawal symptoms
Pressure from peers or others
Addictive personality: Sensation seeking or impulsive behaviour traits or extroverts: predisposed to experiment
Persons with obsessional, dependent or anxious characteristics find it hardest to stop
122
What is anxiety?
Abnormal and pathological fear and worry
123
What is Generalised Anxiety Disorder?
Range of anxiety disorders including panic disorder (with and without
agoraphobia), PTSD, OCD, social phobia, specific phobias (for example of spiders) and acute stress disorder
124
What are features of GAD?
```
Worry (difficult to control) – could lead to decreased occupational and social functioning
Interrupted sleep
Poor concentration
Increased sensitivity to noise
Sweating
Dry mouth
Urinary frequency
Hyperventilation (shortness of breath and dizziness)
Palpitations
```
125
What definition allows diagnosis of GAD?
```
Excessive anxiety and worry occurring more days than not, for at least 6 months, about a number of events or activities
3 or more of:
Restlessness or feeling on edge
Easily fatigued
Difficulty concentrating
Irritability
Muscle tension
Sleep disturbance
```
126
What options are available to help people cope with anxiety?
Pharmacological treatments
Relaxation-Mindfullness
Cognitive Behavioural Therapy: learning link between the physiological changes and psychological responses
Thought dairy – emotions associated with physical symptoms of anxiety
127
What 3 ways do people with anxiety poorly cope with their symptoms?
Selective attention: seeing only the negative features of an event
Magnification: exaggerating the importance of undesirable events
Overgeneralisation: drawing broad negative conclusions on the basis of a single insignificant event
128
What are the 4 categories of the effects of stress?
Affective: shock, distress, anxiety, fear, depression etc
Behavioural: smoking, alcohol, help seeking delay, poor adherence etc
Cognitive: poor attention, errors in decision-making, hypervigilance for threats, see ambiguous events as threatening, memory loss etc
Physiological: activation of nervous system, hormone production, metabolic function, immune function, fatigue, disease and illness
129
What physiological effects can stress have on the body?
```
Slower wound healing
More post-surgery complications
Longer in-patient stay
More analgesia use
Longer recovery, e.g. return to work
More service use, e.g.related symptoms
Less use of rehabilitation services
Increased risk of co-morbidity and early mortality
```
130
What are the Three perspectives to understand stress?
Stimulus: stressor, cause
Response: effect, physiological
Process: personal, environment interaction (transaction)
131
What effect does the fight or flight response have on the body?
Increased: HR, BP, RR, peripheral diversion of blood and cortisol
Decreased: immune surveillance, gut function, kidney function, fat
stores, sex steroids
132
What are 3 stages of general adaptation syndrome?
Alarm: fight or flight response - nervous, endocrine and immune
systems activated for defence against threat
Resistance: conservation response initiated to return homeostasis, but becomes counterproductive if alarm continues
Exhaustion: depletion of physiological resources - collapse of adaptive responses, immune failures and disease outcomes
133
What are 3 dimensions of stressors?
Chronicity: discrete sudden traumas to continuous chronic stressors
Magnitude: life changing events to daily hassles
Inclusiveness: individuals to societies
134
What is the transactional model of stress?
```
Stimulus Event: potential stressor
Primary Appraisal: event demands
Secondary Appraisal: ones self
Response: Coping
Health-Related Outcome: Stress
```
135
Describe how coping can be hierarchically ordered
Activities: cognitions and behaviours directed towards management of stressor demands
Strategies: related coping activities clustered into meaningful groups e.g. Planning, or Mental disengagement
Dimensions: related strategies clustered into one of two inclusive dimensions according to focus, e.g. problem-focussed coping
and emotion-focussed coping
136
What is problem focused coping?
Attempts to manage or change concrete aspects of the stressor, most effective when the stressor is amenable to change
137
What is emotional focused coping?
Attempts to remove or reduce the emotional distress, most effective when the stressor cannot be changed
138
What is cognition?
Mental action or process of acquiring knowledge and understanding through thought, experience and senses
Conscious mental activities such as thinking, understanding, learning, and remembering
Mental act or process by which knowledge is acquired, including perception, intuition and reasoning
139
What are Areas of Cognition?
Memory: Working, Anterograde, Retrograde, not short-term memory, Reading, praxis, Attention/Concentration, Calculation, Visuospatial, Language, Executive functioning, Writing
140
What types of memory are there?
Working memory: short-term, Immediate recall of small amounts of verbal or visual material (7 +/- 2 – nb chunking)
Anterograde memory: Acquisition of new information
Retrograde memory: Recall of previously learnt information
Explicit memory: episodic & semantic
Implicit: procedural
141
What are components of attention?
Concentration
Vigilance
Persistence
142
What is Dyspraxia?
Inability to carry out complex motor actions despite intact motor and sensory, coordination, comprehension & co-operation
143
What is Executive Functioning?
Frontal lobe = executive, behaviour, personality
higher order cognitive functioning
Adaptation, abstraction, mental flexibility, problem-solving, planning, initiation, sequencing, judgement, goal-setting
144
What are Principles of cognitive assessment?
Should assess all patients - Degree will vary depending on presentation
Can be screened through observation – memory, attention/concentration, language
Formal bedside testing if history or screening indicates Eg poor memory, head injury, reduced attention at interview
Many tests are not ‘pure’
Use of assessment schedules ≠ cognitive assessment
145
How can assessment of working memory be carried out?
Observation: Coherent history, Repetitive, Forgetful
Bedside Testing: Working Memory
Digit span forwards (7) / backwards (5)
Immediate recall of 10 item list
Immediate recall of name and address (7) Nb not 3 items eg apple, table, penny
146
How would you assess anterograde memory?
Delayed recall of 10 item list
Delayed recall of name and address
Delayed recall of 3 items
147
How would you assess retrograde memory?
Dates of wars
Recall of Prime Ministers / Presidents / Monarchs
Recall of personal information (need informant)
148
How would you do an Assessment of Attention / Concentration?
Observation: Ability to maintain conversation, Distractability
Bedside Testing: Orientation in time / place (also memory), Digit span forwards / backwards (also workingmemory), Serial subtraction eg 100-7, 20-3, Spelling backwards eg WORLD, Days of week or months of year backwards
149
How would you assess use of language?
Observation: Able to express fluently and appropriately, word finding difficulties (semantic dysphasia), understand questions / instructions
Bedside Testing: Naming objects and parts (watch, strap, winder,
pen, nib), Repetition of complex words or sentences (Statistician, Hippopotamus, Constitutional), (Above, beyond and below, No ifs, ands or buts), Comprehension of instructions eg 3 stage command, pen-watch-keys test (Put pen on watch, Put pen between watch and keys, Pick up watch and give me pen, Before you touch the keys, touch the pen)
150
How would you assess executive functioning?
Bedside testing: Verbal fluency eg 1 min - animals, supermarket, FAS
Abstraction eg proverb interpretation (People in glass houses, One swallow doesn’t make a summer), similarities/differences (apple/banana, coat/dress, table/chair, poem/statue, praise/punishment), cognitive estimates (Camels in Holland, How fast does a horse gallop)
Response inhibition / set shifting eg alternating sequence test, go-no go test, Luria, trail-making test
151
How would you assess Visuospatial function?
Observation: Positioning on chair, bumping into furniture
Bedside Testing: Intersecting pentagons, Cube, Clock face (Ask to draw face, put in numbers, then set hands to ten past eleven)
152
How could you assess functions such as reading, writing, calculation, praxis?
Reading: Read aloud complex words (pint, tomb, dough) or a sentence Follow written instructions eg “close your eyes”
Writing: Write a simple sentence
Calculation: Addition, subtraction, multiplication, division
Praxis: Mime a common action eg cleaning teeth
153
What are the 4 aims of CBT
Identify thinking that causes problematic feelings and behaviours
Question individuals negative thinking
Identify unwanted behaviour patterns
Plan behavioural goals and steps to achieve goals
154
What are the 3 types of depression?
Mild depression: Few, if any, symptoms in excess of the 5 required to make diagnosis, symptoms result in only minor functional impairment
Moderate depression: Symptoms or functional impairment are between ‘mild’ and ‘severe’
Severe depression: Most symptoms, and the symptoms markedly interfere with functioning. Can occur with or without psychotic symptoms
