Case 8 Flashcards

Question

what is a delusion? what are the different types?

Answer 1

• Delusion – “a fixed, false belief, unshakeable by superior evidence to the contrary, and out of keeping with a person’s cultural norms”. • Patients may persist with different types of delusions:  Reference – e.g. people are always talking about ‘me’.  Persecution – e.g. people are out to kill me.  Control – e.g. my body is not under my control, I am a puppet.  Bizarre and impossible – e.g. think you are a tree. - grandiosity (mania in bipolar disorder) – you have special powers - hypochondriacal or somatic (various, often depression) – referred to your body – I believe I have a rat inside by leg - nihilistic (usually psychotic depression) – I’m dead, my head is empty - guilt (usually psychotic depression) – look back on little things and they develop such a huge presence that they start to believe that they don’t deserve to live because of that, or they think they are responsible for all the evil in the world

Answer 2

* Hallucination – a perception, internally generated, in the absence of an external stimulus. * Hallucinations can occur in any sensory modality: hearing (auditory –most common), vision (visual), taste (gustatory), smell (olfactory), somatosensory (tactile), kinaesthetic (body position), temperature, pressure.

Answer 3

 Paranoid Schizophrenia – dominated by delusions and hallucinations (positive symptoms).  Residual Schizophrenia – predominant negative symptoms. Paranoid schizophrenia: - Most common - Largely defined by the presence of auditory hallucinations or delusional thoughts about persecution or conspiracy - Often diagnosed late into illness because they often look normal to others – only when experience a major stressful event in your life that exposes your paranoid thoughts to family Disorganised or hebephrenic schizophrenia: - Confused thought process - Ability to maintain logical thinking is largely affected Catatonic schizophrenia: - Catatonic stupor: dramatic reduction in activity – waxy flexible may develop as well - Catatonic excitement: hyperactivity and presence of stereotypic behaviour – repetitive but purposeless actions Undifferentiated schizophrenia: - May have some signs of paranoid, hebephrenic or catatonic schizophrenia, but doesn’t obviously fit into one of these types alone Residual schizophrenia: - Predominantly negative symptoms Schizoaffective disorder: - Mixture of schizophrenia and either depression or bipolar disorder - Mental illness in its own right

Answer 4

* Constant prevalence around the world = 1%. * No significant influence of culture, ethnic background or socio-economic group. There is a slightly increased prevalence in urban areas. * No overall difference exists between the sexes. * The average age of onset appears to be earlier in men (15-25 years) than in women (20-30 years). * Men have a poorer response to treatment than women, and a worse long-term outcome.

Answer 5

ICD-10 Diagnostic Criteria:  At least 1 first-rank symptom (for at least 1 month): 1. Thought echo, thought insertion or withdrawal, or thought broadcasting. (Thought echo – a voice repeating your thoughts after you think it) (Thought insertion – your thoughts belong to someone else) (Thought broadcasting – others can hear your thoughts) 2. Delusions of control, influence or passivity, clearly referred to body or limb movements or specific thoughts, actions or sensations. 3. Auditory hallucinations giving a running commentary or discussing the patient between themselves, hallucinatory voices from parts of the body. 4. Persistent delusions that are completely impossible.  Or at least 2 second-rank symptoms (at least 1 month): 1. Other persistent hallucinations in any modality. 2. Thought disorder (neologisms, loosening or breaks in the train of thought resulting in incoherent or irrelevant speech). 3. Catatonic behaviour (posturing, waxy flexibility, mutism, stupor, catatonic excitement). 4. Negative symptoms, not due to depression or medications.

Answer 6

• Schizophrenia has a significant genetic component.  Relatives of schizophrenic patients have a higher risk of developing the illness compared to the 1% rate in general population. • There is a higher risk of schizophrenia for people born in winter months and also after viral epidemics, which may affect development in utero. Genetics: - Tends to run in families but no single gene thought to be responsible - Different combinations of genes make people more vulnerable to the condition - In identical twins, if one twin develops schizophrenia the other twin has a one in two chance of developing it too Pregnancy and birth complications: - People who develop schizophrenia are more likely to have experienced complications before and during their birth, such as: a low birth weight, premature labour, a lack of oxygen (asphyxia) during birth Triggers: - Stress – main psychological triggers of schizophrenia are stressful life events - Drug abuse – particularly cannabis, cocaine, LSD or amphetamines, may trigger symptoms of schizophrenia in people who are susceptible - Studies shown teenagers under 15 who use cannabis regularly, especially ‘skunk’ and other more potent forms of the drug, are up to four times more likely to develop schizophrenia by the age of 26

Answer 7

Dopamine neurons have 4 major projections: 1. Nigrostriatal pathway  Substantia nigra → caudate and putamen. It has 2 main branches which are:  Dorsal striatum - motor (involuntary) control Parkinson's Disease.  Associative striatum - learning, habituation, memory, attention, motivation, emotion, and volition. 2. Mesolimbic pathway  Ventral Tegmental Area in midbrain to limbic regions associated with reward, motivation, affect and memory.  Include ventral striatum (nucleus accumbens), amygdala, hippocampus & medial prefrontal cortex. 3. Mesocortical pathway  VTA to frontal cortex, including dorsolateral prefrontal cortex (DLPFC).  Cognitive function, motivation & emotional response. 4. Tuberoinfundibular pathway  Tuberal region to median eminence (infundibular region at top of pituitary stalk).  DA acts to inhibit prolactin release from pituitary.

Answer 8

Dopamine neurons have 4 major projections: 1. Nigrostriatal pathway  Substantia nigra (SNc) → caudate and putamen. It has 2 main branches which are:  SNc -> Dorsal (sensorimotor) striatum - motor (involuntary) control Parkinson's Disease.  SNc -> Associative (mid) striatum - learning, habituation, memory, attention, motivation, emotion, and volition. (PD) 2. Mesolimbic pathway  Ventral Tegmental Area in midbrain to limbic regions associated with reward, motivation, affect and memory.  Include ventral striatum (nucleus accumbens), amygdala, hippocampus & medial prefrontal cortex. 3. Mesocortical pathway  VTA to frontal cortex, including dorsolateral prefrontal cortex (DLPFC).  Cognitive function, motivation & emotional response. 4. Tuberoinfundibular pathway  Tuberal region to median eminence (infundibular region at top of pituitary stalk).  DA acts to inhibit prolactin release from pituitary.

Answer 9

• There are a few postsynaptic dopamine receptors. • Dopamine receptors are divided in two families: D1 receptors and D2 receptors.  D1 receptors activate adenylyl cyclase.  D2 receptors inhibit the formation of cAMP by inhibiting adenylyl cyclase. * D2 receptor is divided into long and short versions depending on whether it is a pre-synaptic autoreceptor which is a short version, or postsynaptic receptors on other neurones which are long. * Each ‘D’ receptor is region specific with some overlap. * D2 receptors affect dopamine synthesis, metabolism and release. * D3 receptors affect dopamine release. D1-like receptor family: - D1 - D5 D2-like receptor family: - D2 (L+S) - D3 - D4 D1 receptor family: - D1 – motor striatum, associative striatum, ventral striatum, cerebral cortex - D5 – hippocampus, hypothalamus D2 receptor family: - D2 (L+S – long and short depending on whether presynaptic autoreceptors or postsynaptic receptors) – motor striatum, associative striatum, ventral striatum - D3 – ventral striatum, associative striatum, hippocampus, amygdala - D4 – frontal cortex, medulla, midbrain, amygdala

Answer 10

* Usually, if there is a decrease in dopamine in the DLPFC, it feeds back to the striatum, causing an increased release of dopamine there. * The same is for the reverse – if there is an increase in the release of dopamine at the striatum, it causes a decrease in the dopamine in the DLPFC. * In schizophrenia, this creates a vicious cycle, where, first, there is a decrease in the levels of dopamine in the DLPFC, which leads to an increase in the striatal dopamine, which then causes a further decrease in the dopamine levels in the DLPFC. • It is important to note that these DA dysregulation are secondary to another dysfunction of the brain.  Rather, it is secondary to a more proximal abnormality e.g. in GABA or glutamate systems.

Answer 11

* Usually, if there is a decrease in dopamine in the DLPFC, it feeds back to the striatum, causing an increased release of dopamine there. * The same is for the reverse – if there is an increase in the release of dopamine at the striatum, it causes a decrease in the dopamine in the DLPFC. * In schizophrenia, this creates a vicious cycle, where, first, there is a decrease in the levels of dopamine in the DLPFC, which leads to an increase in the striatal dopamine, which then causes a further decrease in the dopamine levels in the DLPFC. • It is important to note that these DA dysregulation are secondary to another dysfunction of the brain.  Rather, it is secondary to a more proximal abnormality e.g. in GABA or glutamate systems.

Answer 12

* The current version of the hypothesis proposes that psychosis is associated with increased dopamine presynaptic function in the nigrostriatal pathway (particularly the part that projects to the associative subdivision of the striatum) rather than the mesolimbic system. * Dopamine abnormalities are believed to be secondary or ‘knock-on’ effects of a more primary abnormality perhaps in the glutamate or GABA systems in dorsolateral prefrontal cortex. - Excessive DA release in striatum during illness exacerbations (during psychosis) - positively correlated with positive symptoms – the more dopamine, the more symptoms - correlated with good treatment response to antipsychotic drugs - Inadequate DA in frontal cortex (all the time) - associated with deficits in cognitive function e.g. working memory

Answer 13

* Glutamate is the most abundant excitatory neurotransmitter in the CNS. * Receptors: NMDA, AMPA, kainate, mGluR1-8 * NMDA receptor hypofunction is a model for positive, negative and cognitive symptoms of schizophrenia. * It predicts that hypoactivity of NMDA receptor function → excessive glutamate release which leads to glutamate excitotoxicity → impaired neuronal development → worsening of schizophrenia and disease progression. - Decrease NMDA receptor function:  glu excitotoxicity -> impaired neuronal development -> disease progression  DA dysregulation via glu-DA interactions

Answer 14

``` Genetic factors: - neuroregulin - dysbindin - DAAO/G72 - isolated variants Environmental factors: - pre/perinatal insult - developmment neurotoxicity - activity/nutritional status - metabolic variation ``` Effects: - sensory deficits - generalised cognitive deficits - impaired learning & memory - thought disorder - negative symptoms - position symptoms - gaiting deficits - executive dysfunction - dopamine dysregulation -> positive symptoms, gating deficits, executive dysfunction

Answer 15

* Relapse of positive symptoms associated with ↑ DA in associative striatum. This increase can be detected up to 3 years before onset of first episode schizophrenia. * Can’t currently predict conversion to schizophrenia with adequate sensitivity and specificity by PET. * Cognitive deficits (e.g. WM) associated with ↓mesocortical DA (in the DLPFC). * Ideal antipsychotic would reduce associative striatum DA release without impairing DA function in mesocortical (cognitive impairment), sensorimotor striatum (EPS) or limbic striatum (worsening of negative symptoms) regions.

Answer 16

* In schizophrenia, antipsychotic medications are proven effective in treating acute psychosis and reducing the risk of future psychotic episodes. * The treatment of schizophrenia thus has two main phases: an acute phase, when higher doses might be necessary in order to treat psychotic symptoms, followed by a maintenance phase, which is usually life-long.

Answer 17

• The treatment is aimed to decrease dopamine binding to the D2 dopamine receptor. • The drugs can be divided into:  Typical (old) antipsychotics - chlorpromazine  Atypical (new) antipsychotics – resperidone • Antipsychotics all reversible antagonists at D2 dopamine receptors.  They block the excessive production & release of dopamine in psychosis. • Dopamine is released by nigrostriatal neurones and moderates striatal function. Side effects of typical - Shaking, trembling, muscle twitches, muscle spasms Side effects of both - Drowsiness, weight gain (particularly atypical), blurred vision, constipation, lack of sex drive, dry mouth

Answer 18

65% D2 receptor occupancy different antipsychotics can provide this efficacy at different doses

Answer 19

 Resperidone and olanzapine D2R occupancy is relatively sustained over 24 hours. - Clozapine and quetiapine D2R occupancy declines more quickly - Means you don’t need to block them all day - For antipsychotic efficacy, a drug must block more than 65% of D2 receptors in the associative striatum for an adequate proportion of the time - This does not need to be continuous (i.e. 24 hr/day) – some APs (e.g. clozapine, quetiapine) only achieve this intermittently – the optimum duration is not yet known  Typical antipsychotics have a narrow dose range for efficacy vs overdose.  Atypical antipsychotics have a wide dose range for efficacy vs overdose.

Answer 20

• The increase in dopamine levels occur in the associative striatum, yet D2R occupancy occurs in the limbic (ventral) striatum.  D2 receptor occupancy in striatum treats positive psychotic symptoms but not negative symptoms. • Extrastriatal D2 receptor occupancy is not associated with any measures of treatment response or side effects. D2 receptor occupancy in unwanted regions is currently unavoidable.

Answer 21

• D2 receptor antagonism in the dopaminergic pathways gives rise to a range of related side effects ( at >72% D2 receptor occupancy): 1. Nigrostriatal motor pathway – Parkinsonism and other extrapyramidal side effects (EPSE) 2. Mesolimbic pathway – excessive blockade leads to worsening of the negative symptoms. 3. Mesocortical pathway – may exacerbate low dopamine, leading to deterioration in cognitive function. 4. Tuberoinfundibular pathway – hyperprolactinaemia secondary to antipsychotics.  It is clinically difficult to achieve efficacy without hyperprolactinaemia. • These antipsychotics can also antagonise other receptors (muscarinic, alpha-2-adrenergic and 5-HT2 receptors), leading to receptor-mediated side effects. - Threshold for raised prolactin: >72% D2 receptor occupancy - EPSE: >78% D2 receptor occupancy - Clinically difficult to achieve efficacy without hyperprolactinaemia - Second-generation antipsychotics easier to achieve efficacy without EPSE

Answer 22

* Atypical antipsychotic drug with high affinity for 5-HT and dopamine D2 receptors. * Risperidone is effective for treating the positive and negative symptoms of schizophrenia owing to its “loose” binding affinity for dopamine D2 receptors and additional 5-HT antagonism compared to first generation antipsychotics, which are strong, non-specific dopamine D2 receptor antagonists. • Mechanism of Action:  Blockade of dopaminergic D2 receptors in the ventral striatum, alleviating positive symptoms of schizophrenia such as hallucinations and delusions.  Blockade of serotonergic 5-HT2 receptors in the mesocortical tract, causes an excess of dopamine, resulting in an increase in dopamine transmission, and an elimination of core negative symptoms.  Dopamine receptors in the nigrostriatal pathway are not affected by risperidone and extrapyramidal effects are avoided.  Like other 5-HT2 antagonists, risperidone also binds at alpha(1)-adrenergic receptors and, to a lesser extent, at histamine H1 and alpha(2)-adrenergic receptors. • Side Effects:  Hypotension, weight gain, rash, vomiting, constipation.

Answer 23

• Atypical antipsychotic. - Licensed for treatment resistant schizophrenia (TRS) - TRS if two antipsychotics fail or can’t be tolerated at full dose - About 20% of early Sz, maybe 30% eventually eligible - Weight gain – sometimes the thinnest people gain the most weight • Mechanism of Action:  Combination of antagonistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex.  D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms. • Side Effects:  Sedation, hunger, hypersalivation, diabetes ('dirty drug') - Rare side effect: agranulocytosis - Hence rigorous blood monitoring regime -meds can’t be dispensed without clear FBC -no depot (injections), needs specialist service

Answer 24

* Elevated serum prolactin levels – antagonism of dopamine receptors in the tuberoinfundibular pathway * Parkinsonian symptoms – antagonism of dopamine receptors in the nigrostriatal pathway * Weight gain – antagonism of histamine H1 and serotonin 5-HT2c receptors plus effects on leptin * Deterioration in working memory – antagonism of dopamine receptors in the mesocortical pathway * Blurred near vision – antagonism of muscarinic M1 acetylcholine receptors * Sedation – antagonism of H1 and alpha-adrenergic receptors

Answer 25

* Cannabis is a dried female flower of Cannabis sativa. * The plant contains several psychoactive substances, the most significant being the terpenoid Δ-9-tetrahydrocannabinol (THC). • There are two types of cannabinoid receptors involved in the role of cannabis in psychosis:  CB1 receptors – mediate most effects of cannabinoids on the CNS (also in the lungs, liver and kidneys).  These are involved in physiological processes such as appetite, pain-sensation, mood and memory.  These receptors are responsible for the euphoric and anticonvulsive effects of cannabis.  CB2 receptors – found in the PERIPHERY and are expressed mainly in the immune system and in hematopoietic cells. • Cannabinoid receptors are activated by: 1. Plant cannabinoids (produced by the cannabis plant) – THC – through the production of an endocannabinoid (a ligand known as anadamide) 2. Endocannabinoids (produced by humans)

Answer 26

Plant Cannabinoids (THC) and Ligand (Anandamide): * As THC enters the brain, it causes the user to feel euphoric – or high – by acting on the brain’s reward system. * THC activates the reward system by stimulating brain cells to release dopamine. • Mode of action of THC (Euphoria):  Increases the release of dopamine in the brain.  This causes stimulation of the D2 dopamine receptors in the striatum.  This causes an increase in the formation and release of a ligand called anandamide.  Anandamide activates cannabinoid receptors.  This leads to the euphoria. • THC also disrupts coordination and balance by binding to CB1 receptors in the cerebellum and basal ganglia.

Answer 27

• Endocannabinoids are substances produced in the brain. • They are used in retrograde signalling between neurons, in to temporarily reduce the amount of conventional neurotransmitter released.  Their production is Ca2+ dependent.  They are produced in post-synaptic GABA neurons. • Mode of action of Endocannabinoids (Euphoria):  GABA is released into the synaptic cleft and binds to the ‘endocannabinoid source’ (where the endocannabinoids are produced).  This leads to the production of endocannabinoids.  Endocannabinoids released from the depolarised post-synaptic GABA neuron bind to CB1 receptors in the pre-synaptic GABA neuron and cause a reduction in GABA release.  This causes a decrease in the inhibitory effects in the brain, thus leading to euphoria.  This is called “endocannabinoid-mediated depolarisation-induced suppression of inhibition”. • Mode of action of Endocannabinoids (Anticonvulsive):  Cannabinoids are thought to have regulatory role in the striatum in terms of glutamatergic signals from the corticostriatal fibres.  Intense firing of corticostriatal neurones leads to release of glutamate which causes as influx of Ca2+ ions in the post-synaptic membrane.  Constant glutamate release causes Ca2+ ions to build up in the post-synaptic membrane.  This accumulation causes Ca2+ ions to synthesise endocannabinoids in the medium-sized striatal spiny neurones.  These stimulate CB1 receptors on the pre-synaptic corticostriatal fibres leading to a decreased release of glutamate.

Answer 28

Mental Health Act 1983 (Sections 2 and 3) • The Mental Health Act covers the reception, care and treatment of mentally disordered persons, the management of their property and other related matters. • It provides legalisation by which people diagnosed with a mental disorder can be detained in hospital or police custody and have their disorder assessed or treated against their wishes, unofficially known as “sectioning” (detainment). • The Act has been reviewed and amended by the Mental Health Act 2007.

Answer 29

• For detainment to happen, certain professionals must agree that the patient has a mental disorder that requires them to stay in hospital.  Assessment and treatment is given if needed.  Only carried out when own safety or someone else’s is at risk.

Answer 30

the patient must be: 1. Suffering from a mental disorder 2. At risk to his/her health or safety and/or other people’s safety 3. Unwilling to accept hospitalization voluntarily

Answer 31

• The patient is placed under Section 2 if they have not been assessed in hospital before or if they have been assessed in hospital for a long time. • An application for admission to hospital under section 2 must be made by an Approved Mental Health Professional (AMHP) AND your nearest relative.  Must be seen within 14 days of making application.  Must be signed by TWO APPROVED HEALTH PROFESSIONALS + NEAREST RELATIVE/ OTHER APPROVED HEALTH PROFESSIONAL.  One of the two AMPH must be approved under ‘section 12’. • Doctors must have seen you within 5 days of each other (if the other health professional is a doctor). • Admission to hospital must be arranged within 14 days of the last medical examination. * The length of detainment is up to 28 days. * Section 2 can’t be renewed but the patient may be transferred onto Section 3.

Answer 32

 Appeal against detention to a Tribunal during the first 14 days of detainment.  Appeal to the Mental Health Act managers.  Ask for the help of an Independent Mental Health Advocate.  A Patient Rights Leaflet informing them about their legal rights. * THE PATIENT CAN’T REFUSE TREATMENT. * However, some treatments can’t be given without consent unless certain criteria are met, such as electro-convulsive therapy (ECT).

Answer 33

 Responsible Clinician  Mental Health Act managers  Nearest relative (although this can be overruled by the Responsible Clinician)  Tribunal (court of Justice)

Answer 34

* Before discharging, a care plan should be made under the Care Programme Approach (CPA) which will look at how the patient’s needs will be met. * Many hospitals contact within 7-14 days of discharge.

Answer 35

* You are detained in hospital for treatment. * This treatment is necessary for health, safety or protection of other people. • The patient can be detained under Section 3 for two reasons: 1. If the patient has a known mental health illness and therefore assessment, under Section 2, is not needed. 2. If the patient is transferred from Section 2.

Answer 36

• A Community Treatment Order allows someone discharged from Section 3 to be readmitted if they don’t obey specific conditions (usually adherence to medication). • To be detained, the same procedure as in section 2 (above) is followed – application.  Must be signed by TWO APPROVED HEALTH PROFESSIONALS + NEAREST RELATIVE/ OTHER APPROVED HEALTH PROFESSIONAL.  One of the two AMPH must be approved under ‘section 12’. • The length of detainment is up to 6 months. • Detention can be renewed for a further 6 months  This can only be done by a responsible doctor, 2 months before due date.  After that, detention can be renewed for further periods of one year at a time.

Answer 37

• The patients have the right to:  Appeal against detention to a Tribunal once during the first 6 months of detainment.  Appeal once during the second six months if section 3 renewed.  Appeal to the Mental Health Act managers for discharge.  Ask for the help of an Independent Mental Health Advocate.  A Patient Rights Leaflet informing them about their legal rights. • THE PATIENT CAN’T REFUSE TREATMENT.  They can be treated against their will for 3 months after which they have to be seen by a second opinion appointed doctor (SOAP) which then decide on treatments.  However, some treatments can’t be given without consent unless certain criteria are met such as electro-convulsive therapy (ECT)

Answer 38

* Under the Mental Capacity Act, a patient without “capacity” can be admitted and treated for general medical or psychiatric illness in order to sustain life or prevent a serious deterioration in their condition; can restrain or threaten to restrain to protect from harm, in proportion to the risk and severity of harm. * It must be assumed that the patient has capacity and if in doubt, take all steps to support decision making, act only in best interests of patient but take least restrictive approach. • The mental health law does not specifically mention lack of decisional competence/capacity. • Possible justification for this are:  Use of coercion justified because of risk to self or others:  Coercion - the practice of forcing another party to act in an involuntary manner by use of intimidation or threats or some other form of pressure or force.  Use of coercion justified because having a mental disorder (automatically) entails lack of competence to make decisions.  Mental disorder is qualitatively different from physical disorder.  Tradition - The Mental Capacity Act is an example of case law consolidated into statute

Answer 39

* While atypical antipsychotics have demonstrated improvements in psychotic symptoms, insight and cognition, these may not be enough to ensure compliance with oral daily medication. * Long-acting risperidone may therefore bring together the benefits of the atypical antipsychotics with the long-acting injection delivery system required to build a platform for improved outcomes. memory and understanding -> satisfaction -> compliance

Answer 40

* Early intervention services (EIS) have been developed to address the needs of individuals (aged 14-35 years) with early psychosis. * Typically, there is a delay between the onset of the first episode of psychosis and receiving an effective treatment – a period of untreated psychosis. * Reducing this duration of untreated psychosis (DUP) for people with schizophrenia may lead to an improved prognosis. • Early Intervention Services (EIS) for psychosis aim to:  Detect emergent symptoms  Reduce the duration of untreated psychosis (DUP)  Improve access to effective treatments, particularly in the ‘critical period’ (first 3-5 years following onset). ``` • Early Intervention Services reduce:  Hospital admission  Relapse rates  Symptom severity • Early Intervention Services improve:  Access to treatment  Engagement with treatment ```

Answer 41

Components other than medication:  CBT – target negative cognitions.  Family Intervention  Psychotherapy (Milieu Therapy) – patients join a support group.  Assertive Community Treatment - aims to help mentally ill patients who suffer from areas of life such as work, social relationships and physical health.  Cognitive Remediation (Behavioural intervention) - training activities that aim to improve cognitive skills, social cognition, memory, attention and processing speed in everyday life

Answer 42

Care coordinator: responsible for making sure that everyone is working together to identify patient needs and investigate resources available to meet those needs.  Likely to be a community psychiatric Nurse (CPN), an occupational therapist (OT) or a social worker.  OT: help people with mental, physical or social disabilities to independently carry out everyday tasks or occupations.  CPN: experienced, trained mental health nurses who work with people affected in the community and their families. Approved Mental Health Practitioners:  Trained and experienced in mental health.  Makes decisions about whether a person should be compulsorily admitted to hospital for assessment and treatment. Psychiatrists:  A doctor who specialises in the diagnosis and treatment of people who are mentally ill.  May diagnose illness, prescribe medication. Psychologists:  They have special training in psychology (study of human behaviour and mind) and in mental health.  They are not medical doctors.  Use their specialist skills to assess mental health problems and can provide talking therapies, psychotherapy and counselling. Support Time Recovery Workers:  They provide support and time to you the service user to help in patients recovery process.

Answer 43

Prodromal (withdrawn) -> active (severe symptoms) -> residual (cognitive symptoms)

Answer 44

Most people with schizophrenia are treated by community mental health teams (CMHTs) - Goal of the CMHT is to provide day-to-day support and treatment while ensuring you have as much independence as possible After your fist episode of schizophrenia, you should initially be referred to an early intervention team Care programme approach (CPA): - People with complex mental health conditions are usually entered into a treatment process known as a care programme approach (CPA) - Essentially a way of ensuring you receive the right treatment for your needs - Four stages: assessment, care plan, key worker appointed, reviews Crisis resolution teams (CRT) - Treat people with serious mental health conditions who are currently experiencing an acute and severe psychiatric crisis - Without the involvement of the CRT, these people would require treatment in hospital

Answer 45

- 18F-DOPA is an analogue of the DA precursor DOPA - Uptake provides an index of presynaptic DA function - 18F-DOPA uptake directly correlated with severity of prodromal symptoms and neuropsych impairment - ‘at risk mental state’ (ARMS) = prodromal, mild symptoms – AKA ultra-high risk (UHR) - DA function elevated in patients with prodromal signs of schizophrenia, although they did not yet have the disorder - This elevation approached that seen in patients with established schizophrenia

Answer 46

- Elevated DA function in associative, not limbic or sensorimotor subdivision - Dopamine significantly elevated in the sensorimotor striatum and particularly in the associative striatum (i.e. nigrostriatal pathway), but normal in ventral striatum (found after two studies)

Answer 47

Most likely explanation is abnormal DLPFC function, possibly secondary to abnormal glutamate NMDA receptors affecting GABA and glutamate function

Answer 48

1. Neurodevelopmentally hypofunctional NMDA receptor mediated synapse on parvalbumin-containing GABA interneurons 2. GABA release is low and doesn’t adequately suppress cortico-brainstem glutamate outflow 3. Excessive direct glutamate stimulation of SNc DA neuron cell bodies leads to increase DA in AST and SMST 4. Excessive indirect glu stimulation of mesocortical DA neuron cell bodies in VTA 5. Decrease cortical DA release

Answer 49

Inadequate release of DA in the VTA is what gives you negative symptoms Inadequate release of DA in the cortex in mesocortical system which gives you your cognitive symptoms All of this happens because the NMDA receptors on the GABA interneuron aren’t working adequately

Answer 50

- Psychosis is strongly associated with overactivity of presynaptic DA function (synthesis and synaptic release) in nigrostriatal pathway, particularly associative division - opposite of PD - what would we like? To selectively attenuate this pre-synaptically - what do we have? The ability to block the action of the increased DA post-synaptically at D2 receptors - Cognitive impairment is associated with decreased DA release in PFC (mesocortical system) - Negative symptoms not well explained by DA, but some evidence they may be worse if DA release is decreased in limbic (ventral) striatum (i.e. mesolimbic pathway) (VTA)

Answer 51

- Abnormally high levels of prolactin in blood ``` Sexual dysfunction: - Diminished libido - Decreased arousal - Orgasmic dysfunction Breast pathology: - Galactorrhoea - Breast enlargement - Slight increased risk of breast cancer Reproductive dysfunction: - Anovulation - Oligomenorrhoea - Amenorrhoea - Subfertility - False pregnancy tests Hypogonadism: - Decreased BMD - Hip fracture Miscellaneous: - Acne and hirsutism ```

Answer 52

People that go on to develop schizophrenia generally develop later – they walk and talk later, potty train later, perform less well at school, perform less well on IQ tests – starting to get onset of negative symptoms - Then start to develop anxiety, depression - Then start full psychotic symptoms (not everyone)

Answer 53

- >60% occupancy of D2 in associative striatum has an antipsychotic effect - >75% occupancy of other D2 causes motor SE & hyperprolactinaemia

Answer 54

- Legal and not medical concept - Ability to make a decision - Related to a particular decision - Relates to a particular time - Person may be able to make some decisions but not others - Can vary over time

Answer 55

- The Mental Capacity Act 2005 provides the legal framework for acting and making decisions on behalf of individuals who lack the mental capacity to make particular decisions for themselves - Everyone working with and/or caring for a person over the age of 16 who may lack capacity to make specific decisions must comply with this Act when making or acing for that person - The same rules apply whether the decisions are life changing events or everyday matters THE PRINCIPLES - A person must be assumed to have capacity unless it is established that he lacks capacity - A person is not to be treated as unable to make a decision unless all practicable steps to help fim to do so have been taken without success - A person is not to be treated as unable to make a decision merely because he makes an unwise decision - An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his best interests - Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is less restrictive of the person’s rights and freedom of action

Answer 56

- Understand information related to the decision - Retain information related to the decision - Use or weigh that information as part of the process of making the decision - Communicate the decision (whether by talking, using sign language or any other means)

Answer 57

- Section 1(3) of the Act states that dependence on alcohol or drugs is not considered to be a disorder or disability of the mind for the purposes of the definition of mental disorder in the Act - Alcohol or drug dependence may be accompanied by, or associated with, a mental disorder which does fall within the Act’s definition - Learning disabilities and autistic spectrum disorders are forms of mental disorder as defined in the Act - But a person with learning disability shall not be considered by reason of that disability to be: a) Suffering from a mental disorder…for the purposes of the provisions Act b) Requiring treatment in hospital for a mental disorder…unless that disability is associated with abnormally aggressive or seriously irresponsible conduct on his part

Answer 58

- Section 2 = assessment, lasts for up to 28 days - Section 3 = treatment, lasts for up to 6 months, renewable for another 6 months and then 12 months - Section 4 = emergencies, lasts for up to 72 hours - Section 5(2) = doctors holding power, lasts for up to 72 hours - Section 5(4) = nurses holding power, lasts for up to 6 hours - Community Treatment Orders