Week 2 Flashcards

Question

How do benzodiazepines reduce anxiety?

Answer 1

Increase the effectiveness (affinity) of **GABA at GABA-A** receptors This allows for more influx of chloride ions, which hyperpolarises membranes and results in **inhibition of postsynaptic potential** Can also produce mild muslce relaxation due to action on GABA receptors in spinal cord, cerebellum and brain stem

Answer 2

Fairly safe in overdose, as by themselves they are unlikely to cause respiratory depression May cause paradoxical aggression Can cause anterograde amnesia, impaired coordination and sedation Can lead to tolerance and dependence - **addiction** May show withdrawal symptoms

Answer 3

CBT including response prevention (confronting the anxiety-provoking stimulus and not performing the associated ritual) SSRIs (fluoxetine, sertraline, citalopram, escitalopram, paroxetine)/TCAs (clomipramine)

Answer 4

Rapid action and well-tolerated but dependence can develop in as little as 3 weeks, so use no more than 2 weeks Can cause sedation/psychomotor impairment Problems with discontinuation/withdrawal Alcohol interaction Can worsen co-morbid depression

Answer 5

Type 1 - single, unexpected incident Type 2 - could be repetitive, ongoing, betrayal of trust, developmental etc. **Type 2 holds a x3 risk for developing PTSD**

Answer 6

Cortisol levels are **low**

Answer 7

MHA - about treating a mental disorder (18+ year olds). People may be physically restrained by physical components of disease cannot be treated under this act AwIA - about treating a physical disorder (16+ year olds) in someone with a mental disorder or inability to communicate. Cannot use force

Answer 8

ED - lasts 72 hours from admission, can be done by any qualified doctor but needs MHO approval as well. **Can only assess the patient** SD - can be done at home, needs go ahead from an approved medical practitioner (section 22), psychiatrist, ST4 and above, and lasts for 28 days. **Can both assess and treat**

Answer 9

BPD - 9-20 years Schizophrenia - 10-20 years Drug and Alcohol abuse - 9-24 years Recurrent depression - 7-11 years

Answer 10

LITHIUM **LT** - low thyroid **I** - diabetes Insipidus **H** - heart **UM** - unwanted movements

Answer 11

**Withdrawal symptoms** Presents with confusion, toxic psychosis, convulsions, insomnia, subjective anxiety, loss of appetite and body weight, tremor, perspiration etc. Mechanism: **neuroadaptation of GABA response**. Chronic treatment with BZDs causes a reduced response to GABA, and withdrawal may result in symptoms due to decreased density of BZD receptors

Answer 12

1. switch patient to equivalent dose of **diazepam/chlordiazepoxide**, preferably taken at night 2. reduce dose every 2-3 weeks 3. reduce dose further, in even smaller steps if necessary 4. stop altogether

Answer 13

SSRIs - panic disorders, OCD, PTSD, phobias, GAD Tricyclics - 2nd line for panic disorders, OCD Venlafaxine (SNRI) - GAD Moclobemide (MAO inhibitor)- social anxiety disorder

Answer 14

Midazolam Lorazepam Oxazepam Temazepam Diazepam Chlordiazepoxide

Answer 15

**Glutamine** - major **excitatory** neurotransmitter in the brain **GABA** (and Glycine in the spinal cord) - major **inhibitory** neurotransmitter in the brain

Answer 16

Serotonin Histamine Dopamine (a catecholamine) Adrenaline (a catecholamine) Noradrenaline (a catecholamine)

Answer 17

GABA is used to **control** feelings of fear and anxiety In stress, excitatory signals fire rapidly and are sent from the amygdala to other areas of the brain. This causes feelings of fear/anxiety **Inhibitory interneurones** in the amygdala release GABA which binds to postsynpatic GABA receptors and inhibits the excitatory signals, reducing these feelings - **GABA has a calming, tranquilizing effect**

Answer 18

a) acutely, SSRIs are **angiogenic** b) chronically, SSRIs are **anxiolytic** Mechanism is not fully understood

Answer 19

**Pregabalin** (calcium channel blocker and GABA enhancer) - only used if patient is unresponsive to other treatments Beta-blockers e.g. **Propranolol** - best for treatment of somatic symptoms e.g. tremor, palpitations etc. **Buspirone** (5-HT_1A receptor partial agonist, works **antagonistically** on **D₂, D₃, D₄** receptors as well as partially **agonistically** on **Alpha₁**) - suppresses serotonergic activity while noradrenergic and dopaminergic activity is enhanced

Answer 20

1. psychoeducation 2. Self help/education groups 3. CBT or drug treatment (SSRIs) 4. SNRIs 5. Pregabalin 6. Combination of CBT and drug treatment

Answer 21

1. CBT 2. SSRI (escitalopram or sertraline) - review after 12 weeks 3. SSRI plus CBT 4. alternative SSRI or SNRI (venlafaxine) 5. MAOI (moclobemide)

Answer 22

1. self help 2. CBT or SSRI if long-standing/no benefit from CBT 3. Tricyclics (clomipramine, desipramine, imipramine, lofepramine) - continue for 6 months

Answer 23

1. If mild and \<4 weeks from trauma - watchful waiting 2. Within 3 months - trauma focused CBT and hypnotic medication if sleep disturbances 3. More than 3 months after trauma - trauma focused CBT or EMDR (eye movement desenitisation and reprocessing) 4. Drug treatment (limited evidence) - paroxetine (SSRI) or mirtazepine (MAOI)

Answer 24

1. low intensity psychological interventions - CBT, self help groups etc. 2. more intensive psychological intervention or SSRI 3. consider an increased SSRI dose after 4-6 weeks if indicated 4. SSRI plus CBT & ERP 5. Clomipramine (TCA) 6. augmentation with antipsychotic, or clomipramine plus citalopram

Answer 25

Physical symptoms which after investigation are not fully explained by a physical disease process or injury Symptoms are **real**, and not imagined

Answer 26

"Partial loss of the normal integration between memories, awareness of identity, immediate sensations and control of bodily movements" - Dissociative amnesia - Dissociative fugue - Dissociative stupor - Trance and possession disorders - Dissociative disorders of movement and sensation (motor, sensory and/or convulsions)

Answer 27

Repeated presentation of physical symptoms and persistent requests for investigations, in spite of negative findings and reassurances Usually resist attempts to discuss psychological basis, "**attention-seeking behaviour**" Symptoms can be multiple, recurrent and frequently changing

Answer 28

Functional weakness | (or Malingering)

Answer 29

Tonic-clonic fitting in someone without epilepsy (although 10% of sufferers also have epilepsy!) More common in women and is commonly seen as a comorbidity with depression, anxiety and PTSD. 90% of sufferers report previous traumatic experiences, especially in childhood (e.g. abuse, neglect) Requires **EEG monitoring** to differentiate from epilepsy

Answer 30

IBS Chronic Fatigue Syndrome, Fibromyalgia, ME Chronic Regional Pain Syndrome Hypochondriasis

Answer 31

Factitious disorders (previously called Munchausen's Syndrome) - feigning illness, disease or psychological trauma **to draw attention, sympathy or reassurance** Malingering - feigning illness for **secondary gain**

Answer 32

Autosomal dominant Child risk - 50% Genetic sequence - **CAG repeats** encoding polyglutamine, causing neuronal loss

Answer 33

Anticipation

Answer 34

- Depression and anxiety - Compulsions - Suicidal ideas - Aggression - Blunted affect - Psychosis

Answer 35

- Choreiform movements - Writhing movements - Gait disturbances - Problems chewing, swallowing, speaking - Rigidity

Answer 36

- Decline in executive functions - Short and long term memory deficits

Answer 37

PSEN1, PSEN2 and APP are associated with EOFAD Early onset familial disease accounts for 2% of Alzheimer's cases

Answer 38

Hypomania is a less intense version of Mania Energy levels will be higher than normal but not to the extent of Mania, and there will be an **absence of psychotic symptoms** Crucially, there is no distinct functional impairment in people with Hypomania and they may not require hospitalisation

Answer 39

2nd trimester viral illness Obstetric problems - pre-eclampsia, foetal hypoxia, emergency C section **Risk increased by 50% by childhood viral CNS infection** Substance abuse - cannabis, amphetamines, cocaine

Answer 40

Reduced frontal lobe volume Reduced frontal lobe grey matter Enlarged lateral ventricles

Answer 41

Reduction in the volume of **grey matter.** NB - these changes are present early in the disease and are likely pre-morbid - temporal cortex (especially the superior temporal gyrus) - medial temporal lobe (especially the hippocampus) - possibly also the orbitofrontal cortex, parietal cortex and basal ganglia

Answer 42

**Fractional anisotropy (FA)** - higher numbers indicate **healthy** white matter tracts **Mean diffusivity (MD)** - higher numbers indicate **less healthy** white matter tracts

Answer 43

**Dopamine** - it is assumed that schizophrenia is related to overactivity of dopamine pathways in the brain **Dopamine receptor antagonists** are therefore used to treat the symptoms of schizophrenia (**atypical antipsychotics** such as quetiapine, risperidone or olanzapine, **typical antipsychotics** like haloperidol, **antiemetics** like metoclopramide or domperidone, **TCAs** etc.)

Answer 44

Nigrostriatal - extrapyramidal motor system Tuberoinfundibular - control of prolactin release (**dopamine is inhibitory to prolactin**) Mesolimbic/Cortical - motivation and reward systems

Answer 45

a) amphetamines - **extra release of dopamine vesicles into synapse** b) antipsychotics - **blocks D2 receptor family on postsynaptic receptors**

Answer 46

D1 receptor family (**D1 and D5**) - **stimulates cAMP** D2 receptor family (**D2, D3, D4**) - **inhibits adenylyl cyclase, inhibits voltage gated Ca²⁺ channels and opens K⁺ channels**

Answer 47

**Neuregulin** - signaling protein that mediates cell-cell interacitons and plays critical roles in the growth and development of multiple organ systems **Dysbindin** - essential for adaptive neural plasticity **DISC-1** - involved in neurite outgrowth and cortical development through its interaction with other proteins

Answer 48

Haloperidol (high potency), Chlorpromazine (low potency), Fluphenazine Important to remember that the **dose of the drug correlates with the degree of D2 receptor blockade** i.e. giving a higher dose of the drug will produce a greater effect Associated with **extrapyramidal side effects**

Answer 49

Olanzapine, Quetiapine, Risperidone, Clozapine

Answer 50

The **nigrostriatal pathway**

Answer 51

Acute dystonic reaction - painful involuntary spasms Parkinsonism Akathisia - mental and/or motor restlessness Tardive dyskinesia - typically affects face and mouth e.g. tongue rolling, lip smacking. Results from long term use

Answer 52

**Hyperprolactinaemia** - inhibition of dopamine allows prolactin levels to rise May present with **sexual dysfunction**

Answer 53

**Metabolic syndrome** as a result of serotonin blockade Cluster of conditions that increase risk of heart disease, stroke and T2DM Includes hypertension, raised blood glucose, raised triglycerides, excess body fat etc.

Answer 54

Olanzapine - **histamine blockade** Could cause sedation and increased appetite

Answer 55

Typicals - **dopamine** Atypicals - have a greater degree of affinity for **serotonin (5-HT)**

Answer 56

**Clozapine** (atypical) Major side effects is **agranulocytosis** Clozapine use requires **monthly blood tests** (even though agranulocytosis is unlikely to occur outside of the initial beginnings of treatment) - weekly tests for the first 6 months, fortnightly for the next 6 months then every 4 weeks thereafter (including for one month after cessation)