PSYCHIATRY Flashcards

(245 cards)

1
Q

Describe the aetiology of ADHD.

A

ADHD is most likely caused by a complex interplay of factors:
neurobiologic (neuroanatomical and neurochemical)
genetic influences
environmental/psychosocial factors
CNS insults (such as perinatal factors, CNS infections, FAS or premature.)
Research repeatedly demonstrates that ADHD runs in families

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2
Q

What are the 3 core behaviours of ADHD?

A
  1. Hyperactivity.
  2. Inattention.
  3. Impulsivity.
    (HII)

These symptoms occur in every child from time to time but when they are persistent and impact on daily functions, more investigation is needed

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3
Q

ADHD core behaviours: give 3 signs of impulsivity.

A
  1. Blurts out answers.
  2. Interrupts.
  3. Difficulty waiting turns.
  4. When older, pregnancy and drug use.
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4
Q

ADHD core behaviours: give 3 signs of inattention.

A
  1. Easily distracted.
  2. Not listening.
  3. Mind wandering.
  4. Struggling at school.
  5. Forgetful.
  6. Organisational problems.

Does not appear to be listening when spokento directly
Makes careless mistakes
Looses important items

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5
Q

What is the diagnostic criteria for ADHD? According to DSM-5 (Diagnostic and Statistical Manual of Mental Disorders)

A

ADHD definition <17 Years

6/9 inattentive symptoms and 6/9 hyperactivity/impulsivity.

Present before 12 years
Developmentally inappropriate
Several symptoms in 2 or more settings
Clear evidence symptoms interfere/reduce the quality of social/academic/occupational function
.

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6
Q

What are some differentials of ADHD?

A

Age-appropriate behaviour in active children;
attachment disorder; hearing impairment; learning difficulty; a high IQ child
insufficiently stimulated/challenged in mainstream school; behavioural
disorder; anxiety disorder; medication side-effects (e.g. antihistamines).

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7
Q

What tools can be used in order to diagnose ADHD?

A
  1. Clinical interview - are there any RF’s for ADHD?
  2. ADHD nurse classroom observation.
  3. Questionnaires (SNAP), Conor’s questionaire
  4. Quantitative behavioural (QB) analysis.

Brown attention deficit disorder scale
WHO adult ADHD self-report scale

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8
Q

Describe the nn pharmalogical treatment for ADHD.

A
  1. Education.
  2. Parenting programmes and school support.
    Behavioural interventions, e.g. encouraging realistic expectations, positive reinforcement of desired behaviours (small immediate rewards), consistent contingency management across home and
    school, break down tasks, reduce distraction.

Implementing Routines
Evidence base for fish oils in diet
Learning support

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9
Q

What are some medicine for ADHD?

A

Methylphenidate (ritalin, concerta, Equasym)
Atomoxetine (Strattera®) A non-stimulant NE reuptake inhibitor licensed for the treatment of ADHD.

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10
Q

What are some things you need to consider/ SE of ADHD medication?

A

headache, insomnia, loss of appetite, stomach ache, dry mouth, nausea

Can stunt growth
Need to Monitor weight, height and BP
Methyphenidate is Not recommended to take during pregnancy

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11
Q

What are the 3 main features of the deficits seen in ASD?

A

They can be categorised as deficits in social interaction, communication and behaviour

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12
Q

Outline some social interaction issues often seen in those with ASD

A

NO DESIRE TO INTERACT WITH OTHERS
BEING INTERESTED IN OTHERS TO HAVE NEEDS MET
LACK OF MOTIVATION TO PLEASE OTHERS
AFFECTIONATE ON OWN TERMS

Touches inappropriately
Poor Eye contact
Plays alone
Finds it stressful to be with other people

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13
Q

Outline some communication issues often seen in those with ASD

A

Repetitive use of words or phrases
Delay, absence in language development
Lack of appropriate non-verbal communication such as smiling, eye contact, responding to others, and sharing interest
Lack of desire to communicate at all
PEDANTIC LANGUAGE, VERY LITERAL, POOR OR NO UNDERSTANDING OF IDIOMS AND JOKES

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14
Q

Outline some behavioural issues seen in Autism

A

USING TOYS AS OBJECTS
INABILITY TO PLAY OR WRITE IMAGINATIVELY
RESISTING CHANGE
PLAYING SAME GAME OVER AND OVER
OBSESSIONS/RITUALS
There may be self-stimulating movements that are used to comfort themselves, such as hand-flapping or rocking.
Extremely restricted food preferences

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15
Q

Describe the treatment for ASD.

A
  • Education and games to encourage social communication.
  • Visual aids and timetables.
  • Parenting workshops and school liaison.
    Manage Comorbidity

There are no medications available for ASD

Diagnosis should be made by a specialist in autism. This may be a paediatric psychiatrist or paediatrician with an interest in development and behaviour. A diagnosis can be made before the age of 3 years. It involves a detailed history and assessment of the child’s behaviour and communication..

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16
Q

Outline some of the people within the MDT for dealing with ASD.

A

Child psychology and child and adolescent psychiatry (CAMHS)
Speech and language specialists
Dietician
Paediatrician
Social workers
Specially trained educators and special school environments
Charities such as the national autistic society

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17
Q

What are some risk factors for depression?

A

Prior depression
Family Hx depression
Female
Hx abuse
Drug and alcohol use
Low socioeconomic status
Recent bereavement, stress or medical illness, traumatic life event
Co-existing medical conditions (chronic disease)

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18
Q

What are the 3 key symptoms of depression?

ys. According to ICD-10 criteria, how long must symptoms last to be classified as a depressive episode?

A

Low mood
Loss of energy (anergia)
Anhedonia (loss of enjoyment of formerly pleasurable activities)

The correct answer is 2 weeks. The ICD-10 criteria for depressive illness are as follows:

In typical depressive episodes, individuals usually suffer from depressed mood, loss of interest in things you would normally find pleasure in (anhedonia), and reduced energy levels (anergia).

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19
Q

What are some things you may find on consulation/examination/investigations for depression?

A

Carry out mental state examination
- Appearance may be normal, or evidence of self beglect. substnace abuse, tearfulllness, anxious, fidegty

Speach may be monotonic and slow - patient may appear distracted

Psychotic features - eg auditory hallucinations, loss of insight

Baseline tests for FBC and TFT may be useful for ruling out anaemia and hypothyroidism, that can lead to depression

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20
Q

What is the name of the questionaire used in depression?

A

The Patient Health Questionnaire-9 (scored out of 27) is used to grade depression

– It asks patients to report over the last 2 weeks how often they have been experiencing symptoms

– Made of 9 items which is scored from 0-3

– Mild = 5-9 – Moderate = 10-14 – Moderate/Severe = 15-19 – Severe = >19

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21
Q

What is the non pharmalogical measurements for mild depression?

aka PHQ-9 less than 15

A

Mild depression
* Watchful waiting (GP monitoring progress post diagnosis)
* Guided self-help: workbook/online course + therapy support
* Exercise
* Talking therapies - CBT, interpersonal therapy (IPT), psychodynamic psychotherapy
○ CBT:
§ Aim to help understand thoughts/behaviour + how they affect you
§ Recognises events in past but concentrates on how can change thinking/feeling/behaviour in present
§ Available on NHS for depression/mental health problems
○ IPT:
§ Focus on relationships with others and problems within them
§ E.g. issues with communication, coping with bereavement

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22
Q

What is the treatment for moderate/severe depression? aka PHQ-9 of more than 15 - How long for remission of symptoms before tapering off?

A

Moderate/severe depression
* Antidepressants (SSRIs, TCAs) - continued for 6+ mths after Sx stop
* Combination therapy e.g. meds + talking therapy

SSRI - Selective serotonin reuptake inhibitors eg Sertraline, paroxetine, fluoxetine, citalopram
Fluoxetine 1L in children

TCAs (Tricyclic antidepressants):
Imipramine, amitriptyline

SNRIs (Serotonin-noradrenaline reuptake inhibitors):
Venlafaxine, duloxetine,

NARI - Non adrenergic receptor inhibitor - Mirtazapine

Antidepressants should be continued for at least 6 months after remission of symptoms to decrease risk of relapse

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23
Q

What is some treatment for very severe depression

A

Resistant depression Tx w/ combo of antidepressants +
Lithium
Atypical antipsychotic
Another antidepressant

ECT very effective in severe cases (Electroconvulsive Therapy)

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24
Q

Outline what bipolar disorder consists of - what is the ICD-10 definition

A

Bipolar affective disorder - recurrent episodes of altered mood and activity

Involving upswings and downswings (hypomania/mania + depression)

Hx of 2 mood disorders, at least one:
Hypomania < 4d
Mania >7 d

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25
What are some of the causes/risk factors for bipolar disorder?
Genetic links + environmental stressors/triggers -> mood disorder A number of studies have reported abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis in bipolar disorder which are consistent with reduced HPA axis feedback Prolonged psychosocial stressors during childhood, such as neglect or abuse, are associated with HPA axis dysfunction in later life, which may result in hypersensitivity to stress. People with a history of childhood sexual or physical abuse appear to be more at risk and to have a worse prognosis
26
types of bipolar, according to DSM-5 - outline what is seen in bipolar I disorder, and bipolar II disorder
Bipolar 1 - mania & depression, sometimes more episodes of mania Bipolar 2 - more episodes of depression and only mild hypomania (easy to miss, always ask Sx of mania in person presenting w/ typical depression Sx)
27
Types of bipolar - outline what is seen in cyclothymia - What differentiates mania from hypomania?
Cyclothymia - chronic mood fluctuations over 2+ yrs, episodes of depression and hypomania (not mania). Rapid cycling, episodes only lasting few days **presence of psychotic Sx e.g. auditory hallucinations/grandiose delusions differentiates mania from hypomania
28
What are some things you might see in an episode of hypomania? How long do these tend to last?
Lasts about 4 days Elevated mood Increased energy, talkativeness Poor concentration Mild reckless behaviour (overspending) Sociability/overfamiliarity Increased libido/sexual disinhibition Increased confidence Decreased need to sleep Change in appetite
29
What are some things you might see in an episode of mania? How long do these tend to last?
Sx mania (lasting atleast 1wk, more extreme than hypomania) Uncontrollable elation Overactivity Pressure of speech (words can't get out fast enough, and cannot be interupted) Impaired judgement Extreme risk-taking behaviour Social disinhibition Inflated self-esteem, grandiosity Psychotic Sx can occur **Insight often absent during episodes**
30
What are some differentials that you need to rule out in bipolar disorder?
Substance abuse (amphetamines, cocaine) Endocrine disease - Cushing's, steroid-induced psychosis Schizophrenia Schizoaffective disorder - Dx when affective and first rank schizophrenic Sx equally prominent Personality disorders - emotionally unstable, histrionic ADHD in younger people
31
What is the first management of bipolar disorder, for episodes of mania
Treatment options for an acute manic episode (as per the NICE guidelines updated 2023) include: Antipsychotic medications (e.g., olanzapine, quetiapine, risperidone or haloperidol) are first-line Existing antidepressants are tapered and stopped
32
What is the 2nd line management for episodes of mania seen in bipolar, and what cna be used in v acute attacks that are severe
First ensure that the patient stops taking any antidepressant, or at least ween them off, and then give **Lithium** Anti Convulsnants - Carbamazepine, Valporate, and Lamotrigine Valporate can affect fertility in men (so only give over 65,) and tetragenic in women (only give over 55) Benzodiazepines may be used in the short term for acute behavioural disturbance. Lorazepam and antipsychotics may be useful for rapid tranquillisation
33
What is the treatment of bipolar, for a depressive episode?
– For depression –> Treat with antipsychotics alone or in combination with SSRI’s – 1st line is **Olanzapine, Lamotrigine or Quetiapine and Fluoxetine** – Do not just prescribe SSRIs by themselves as they can precipitate mania If a patient is taking an antidepressant at the onset of an acute manic episode, the antidepressant should be stopped.
34
Clinically, lithium is the most effective long-term mood stabiliser for preventing both manic and depressive episodes in bipolar disorder. - What are some side effects of lithium
L - leukocytosis I - insipidus diabetes (nephrogenic) T - tremors (if coarse, think toxicity) H - hydration (easily dehydrates, need to drink lots, is renally cleared) I - increased GI motility U - underactive thyroid M - metallic taste (warning of toxicity), mums beware - teratogenic Lithium + diuretics -> dehydration Lithium + NSAIDs -> kidney damage & weight gain, hypothyroidism
35
What are some investigations you would want to do to rule out other causes of symptoms seen in GAD?
depression and obsessive compulsive disorder Hyperthyroidism - do TFTs Pheochromocytoma Lung disease - excessive salbutamol use Congestive HF - heart meds -> anxiety Hypoglycaemia Do Bloods, and BP
36
What are some risk factors/causes of developing GAD?
Family Hx anxiety Aged 35- 54 Being divorced or separated Living alone Being a lone parent Physical/emotional stress Financial, bereavement etc Hx physical/sexual/emotional trauma (in childhood) Chronic physical health condition Worries about physical health Female 2:1 Male
37
Outline some neuropathology that is thought to be linked to GAD
Low levels of GABA, contribute to anxiety. Been seen that frontal cortex and amygdala undergo structural remodelling induced by the stress of maternal separation and isolation, which alters behavioural and physiological responses in adulthood. * Heightened amygdala activation occurs in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia and specific phobia Basically overfiring/activation of the amygdala
38
What is the non pharmalogical management of GAD?
Mild anxiety can be managed with watchful waiting and advice about self-help strategies (e.g. meditation), diet, exercise and avoiding alcohol, caffeine and drugs. Moderate to severe anxiety can be referred to CAMHS services to initiate: Counselling Cognitive behavioural therapy
39
What is the pharmacological management of GAD?
SSRI (sertraline is first-line SSRI) – Be careful in young people as the SSRI increases anxiety initially and can lead to suicidal thoughts - ***Patients ≤ 25 years who have been started on an SSRI should be reviewed after 1 week*** Pre-gabalin If a first line SSRI such as sertraline is ineffective or not tolerated, try another SSRI or an SNRI for GAD eg duloxetine or venafalexine – If acutely anxious –> Benzodiazepine (but not for > 4 weeks) Beta blockers e.g. bisoprolol for physical Sx
40
OCD - Define what is meant by Obsessions, and give some examples of some Obsessions relieved by compulsion (1), recognised as irrational (1), and has an impact on daily function (1)
Obsessions = unwanted/uncontrolled thoughts and intrusive images, pt finds difficult to ignore aggressive impulses e.g. - images of hurting a child or parent contamination e.g. – becoming contaminated by shaking hands with another person need for order e.g. – intense distress when objects are disordered or asymmetric religious e.g. – blasphemous thoughts, concerns about unknowingly sinning repeated doubts e.g. – wonder if a door was left unlock
41
OCD - Define what is meant by Compulsions
repetitive actions pt feels they must do, generating anxiety if not done - often way to handle the obsessions checking e .g. – repeatedly checking locks, alarms, appliances cleaning e.g. – hand washing hoarding e.g. – saving trash or unnecessary items mental acts e.g. – praying, counting, repeating words silently
42
What are some causes/Risk factors for developing OCD?
Genetic predisposition (twins, especially monozygotic) Developmental factors Emotional/physical/sexual abuse Neglect Social isolation Teasing, bullying Parental over protection Psychological factors Over-inflated sense of responsibility Intolerance of uncertainty Belief in controllability of intrusive thoughts Stressors Pregnancy Postnatal period Family Hx Stressful life events Environmental factors Rarely In adults: neurological conditions e.g. brain tumour, Huntington's chorea, frontotemporal dementia, complication of brain injury to frontal lobe/basal skull
43
What is the non pharmalogical treatment for OCD?
Mild functional impairment Offer short CBT (<10h), including **exposure-response prevention (ERP)** or group therapy CBT ERP * Moderate functional impairment Offer more intensive CBT (>10h)
44
What is the pharmacological treatment of OCD?
or drug therapy (SSRI, e.g. fluoxetine 20–40mg od) When treating OCD, **compared to depression, the SSRI usually requires** a higher dose and a longer duration of treatment (at least 12 weeks) for an initial response * Severe functional impairment Offer psychological therapy + drug treatment. If inadequate response at 12wk, offer a different SSRI or **clomipramine (a TCA that also acts as a serotonin reuptake inhibtior).** Refer if symptoms persist
45
What are some causes/risk factors for developing phobias?
animals (spides, snakes, worms) Blood/injection/injury Situational (lifts, flying, enclosed space) Natural environment (storms, heights, water) Other: choking, vomiting, clowns Amygdala, anterior cingulate cortex and insula hyperactivity involved in underlying mechanism of action
46
What are the 3 types of Phobias?
Simple phobia Inappropriate anxiety in the presence of ≥1 object/situation, e.g. flying, enclosed spaces, spiders Social phobia Intense/persistent fear of being scrutinized or negatively evaluated by others leads to fear and avoidance of social situations (e.g. using a telephone, speaking in front of a group). Agoraphobia fear of fainting and/or loss of control are experienced in crowds, away from home, or in situations from which escape is difficult. Avoidance results in patients remaining within their homes where they know symptoms will not occur.
47
What are the general treatments for phobias?
For simple phobias - Treatment is only needed if symptoms are frequent, intrusive, or prevent necessary activities. Exposure therapy is effective. For social and agoraphobia - drug therapy SSRIs, and TCAs eg **Clomipramine** Psychological therapies CBT (cognitive restructuring) +/- exposure
48
What is meant by baby blues? How long does it last for?
a period of low mood and irritability, which normally starts three to four days after birth, and lasts for 1-2 weeks. Symptoms are usually mild, only last a few days and resolve within two weeks of delivery. No treatment is required. Happens in over 50% of mothers
49
What is seen in Postnatal depression? How long must symptoms be going on before a diagnosis can be made?
a depressive episode within the first twelve months postpartum, peak incidence is 2 months after birth Postnatal depression is similar to depression that occurs outside of pregnancy, with the classic triad of: Low mood Anhedonia (lack of pleasure in activities) Low energy Symptoms should last at least two weeks before postnatal depression is diagnosed.
50
What is some of the treatment for post natal depression? What would be the medication of choice
self-help strategies and non-directive counselling (‘listening visits’ by a health visitor). Moderate to severe depression usually requires treatment with antidepressant medication and/or psychotherapy (CBT). Breast-feeding is not a contraindication for antidepressant treatment, but drugs with low excretion in breastmilk, such as sertraline, are preferred. *High levels of Fluoxetine can transfer in breast milk*
51
What is seen in postpartum psychosis?
Postpartum psychosis – 1-2:1000 Depression Mania Psychosis
52
What is the treatment of puerperal psychosis?
Admission to the mother and baby unit Cognitive behavioural therapy Medications Electroconvulsive therapy (ECT)
53
What is the problem with SSRIs in pregnancy?
Can lead to neonatal abstinence syndrome (also known as neonatal adaptation syndrome). It presents in the first few days after birth with symptoms such as irritability and poor feeding.
54
Define PTSD
Post traumatic stress disorder Develop (immediately/delayed) post exposure to stressful event/threatening, catastrophic situation
55
What are some common causes of PTSD?
Serious accident e.g. RTA Witness of violence - school, domestic, torture, terrorist attack, rape Combat exposure Natural disaster Sudden death of loved one Multiple major life stressors
56
What are the clinical feautres of PTSD? How long must they be present for?
Symptoms – **These must be present >1 month** – Persistent intrusive thoughts and re-experiencing –> flashbacks, nightmares and intrusive images – Autonomic hyperarousal –> persistent activation gives startle, hypervigilance, insomnia – Avoidance –> patient avoids situations and stimuli associated with the event – Emotional detachment –> feeling detached from people and lack of ability to experience feelings – Higher risk of depression, substance misuse, unexplained physical symptoms
57
What are some non pharmalogical managements for PTSD
CBT - eg education about the nature of PTSD, selfmonitoring of symptoms, anxiety management, breathing techniques Eye movement desensitization and reprocessing (EMDR): Using voluntary multi-saccadic eye movements to reduce anxiety associated with disturbing thoughts Stress management Hypnotherapy
58
What are some pharmaogical managments for PTSD
**SSRIs (e.g. paroxetine 20–40mg/day; sertraline 50–200mg/day)** are licensed for PTSD, or **Venlafaxine, a SNRI** It may be helpful to target specific symptoms: * Sleep disturbance (including nightmares): may be improved by mirtazapine (45mg/day), * Anxiety symptoms/hyperarousal: consider use of BDZs (e.g. clonazepam 4–5mg/day), buspirone, antidepressants, propranolol. * Intrusive thoughts/hostility/impulsiveness: some evidence for use of carbamazepine, valproate, or lithium. * Psychotic symptoms/severe aggression or agitation: may warrant use of an antipsychotic (some evidence for olanzapine, risperidone etc)
59
What are some primary causes of insomia?
Fear/anxiety about falling asleep Change of environment (adjustment disorder) Inadequate sleep hygiene Idiopathic insomnia (rare, lifelong inability to sleep) Behavioural insomnia of childhood
60
What are some secondary causes of insomia?
Sleep-related breathing disorder e.g. sleep apnoea Circadian rhythm disorders Shift work REM behavioural disorder e.g. Lewy body dementia, PD Medication conditions causing pain -> awake Psychiatric disorders - depression (early morning waking), anxiety (early/middle insomnia) Drugs/alcohol - steroids, antidepressants, stimulants
61
What are some nonpharmacological management options for insomnia?
Encourage good sleep hygiene, routines Remove noise, light, and distractions Wind down before bed Avoid caffeine/stimulation Sleep restriction Prevent naps during day to promote sleeping @ night
62
What are some pharmalogical management options for insomnia?
Medication (once good sleep hygiene proved unsuccessful) Z drugs 1L - zopiclone, zolpidem, zapeplon - *enhances the effect of the neurotransmitter gamma-aminobutyric acid (GABA), a GAGA agonist* Sedating antidepressants - mirtazepine Melatonin Side effects of Zopiclone - agitation, bitter taste in mouth, constipation, decreased muscle tone, dizziness, dry mouth, and increased risk of falls (especially in the elderly)
63
What is paraphrenia?
psychotic illness characterized by delusions and hallucinations, without changes in affect (although there may be reactive anxiety), a form of thought, or personality. it's the most common form of psychosis in old age - aka late-onset schizophrenia
64
What are some things you'd see in paraphrenia?
*no evidence of dementia w/ later onset cases - no memory problems Delusions, hallucinations - often about neighbours Paranoid - often re. neighbours spying, taking things can also be misidentification, hypochondraical, religious Partition delusion - believe people/objects can go through walls Less -ve Sx (blunting/apathy) and formal thought disorder compared to early onset
65
What is the treatment steps in paraphrenia?
Relieve isolation and sensory deficits. Low-dose atypical antipsychotics preferred as elderly are very sensitive to side-effects, but non-compliance secondary to lack of insight is often an issue.
66
Broadly speaking, what is seen in a cognitive impairment?
Minor problems w/ cognition - mental abilities: memory, thinking Not severe enough to interfere w/ everyday life Mild cognitive impairment = pre-dementia condition in some people
67
What are some causes of a cognitive decline, particulary in the elderly?
Depression, anxiety, stress Sleep apnoea and other sleep disorders Physical illness (constipation, infection) Poor eyesight/hearing Vitamin/thyroid deficiencies e.g. Vit B12 SE of medication: CCBs, anticholinergics, benzodiazepines Drug/alcohol abuse Uncontrolled health conditions like high BP, high cholesterol, diabetes, obesity
68
What are teh symptoms of cognitive decline?
Not severe enough to interfere w/ daily life -> not defined as dementia (dementia Dx = 2/more of problems with: memory, reasoning, language, coordination, mood, behaviour) Memory - forgetting recent events/repeating same question Reasoning, planning, problem solving - struggling to think things through Attention - v easily distracted Language - taking longer than usual to find right word for something Visual depth perception - struggling to interpret 3D object, judge distances, navigate stairs
69
What are some investigations for a cognitive decline
Take a thorough, collateral history Review of medications MSE Input from family/collateral Hx Bloods/urine if suspect infection/another clinical cause
70
What is the management for a cognitive impairment>
Prophylaxis/Mx of precipitative Sx: Poorly controlled heart condition/diabetes/strokes -> ^ risk MCI So control e.g. prevent high BP Medication management of depression/anxiety Good sleep hygiene Preparation for the future when memory may get worse Power of attorney etc
71
What are some causes of delirium?
Infection - UTI, pneumonia, septicaemia Toxicity - substance misuse, intoxication withdrawal (d.tremens), opioids Vascular - CVA (stroke), haemorrhage, head trauma Epileptic Metabolic - hyper/othyroidism, hyper/oglycaemia, hypoxia, hypercortisolaemia Medications - anticholinergics, parkinson's meds, benzodiazepines, drug accumulation, polypharmacy, postsurgery, steroids Nutritional/dehydration - thiamine B1 deficiency, B12 deficiency, folate deficiency
72
What are some causes of Psychosis, that can be differentials to schizophrenia?
Bipolar disorder – often may present with symptoms of schizophrenia Psychotic Depression Alcohol hallucinations, due to withdrawal Drugs - **especially Cannabis**, Cocaine, LSD, magic Mushrooms (Psilocybin) Dopamine Agonists, like Levo Dopa in Parkinsons Other health conditions, like Encephalitis Epilspeys (temporal lobe seizure,) Dementia, and Parkinsons B12 def, hypoglycaemia, Trauma Brief Psychotic disorder – symptoms are present for less than a month, then disappear.
73
Outline what schizophrenia is - what are the 4 main things seen in it, as well as in psychosis in general?
Schizophrenia, a form of psychosis, is characterised by distortion to thinking and perception and inappropriate or blunted affect. See Hallucinations, and delusions, Thought and speech disorders and negative symptoms
74
Schizophrenia and psychosis - define hallucinations
Hallucinations: hallucinations can be defined as perceptions in the absence of stimuli. Most commonly auditory but may be visual or affect smell, taste, or tactile senses.
75
Schizophrenia and psychosis - define delusions
Delusions: a fixed, false belief not in keeping with cultural and educational background.
76
Outlien what is thought to be some of the pathogenesis behind schizophrenia
increased size of the ventricles and reduced whole-brain volume, in those with Schizophrenia **Increased activity of dopamine** in the mesolimbic region is associated with symptoms of psychosis.
77
what are some risk factors for developing schizophrenia?
fHx/genetic link Affected brain development in early life (trauma, epilepsy, developmental delay, perinatal infection) Smoking cannabis in adolescence Severe childhood bullying/physical abuse Socioeconomic deprivation Adverse life events Social isolation Typical age onset 20-30s
78
What are some general things you may see in schizophrenia, and how may they be categorized?
Positive: - Delusions, Hallucinations, Disorganised speech and behaviour, and Catatony Negative: - Less emotions, Loss of interest, Poverty/decreased speech, less motivation Cognitive - Decline in cognition, memory, learning
79
How may a diagnosis of schizophrenia be made? in line with the ICD-10
ICD-10 Diagnosis of schizophrenia made when: * At least 1 first-rank Sx * Or at least 2 second-rank Sx For 1+ months
80
What are the first rank symptoms for schizophrenia, according to Schneider, in line with the ICD-10 Diagnosis
First rank Sx: **Delusional preceptions** *(a delusion that arises from a real perception )* **3rd person auditory hallucinations** (running commentary, hears people talking about them, not to them) **Thought disorder/alienation** (broadcast, withdrawal, insertion, deletion) **Passivity phenomena** (made to do/feel things against their will - someone controlling thoughts, feelings, actions)
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What are the second rank symptoms of schizophrenia, according to Schneider, in line with the ICD-10 Diagnosis
**Any other type of hallucination,** not third person auditory **Formal thought disorder** (words come out wrong, thoughts muddled) *Second-rank thought disorders indicate disturbances in logical structure or coherence of thought but generally do not involve the delusional sense of intrusion or control by external forces, like first order thought disorder symptoms.* **Catatonic** behaviour - excitement, posturing or waxy flexibility, negativism, mutism and stupor. **Negative symptoms** - marked apathy, paucity of speech, and blunting or incongruity of emotional responses (it must be clear that these are not due to depression or to neuroleptic medication).
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What are some tests you would do on someone w schizophrenia?
Bloods for organic causes psychosis - brain tumours, cysts, PD, Huntington's, brain injury, severe systemic infection FBC LFT TFT Syphillis serology Bloodborne Virus screen Autoimmune causes -anti–NMDA receptor antibodies for autoimmune encephalitis,ANA, anti-DS DNA for Lupus Collateral Hx from someone else Blood, hair or urinary screens may be used for illicit drugs and alcohol, particularly in those presenting with acute psychosis of unknown cause. MSE, risk assessment
83
What are some atypical anti psycotics, and how do they work?
Atypical anti-psychotics – work by blocking dopamine (but not as strongly as typical antipsycotics) and also are **Serotonin 5-HT2A Receptor Antagonists** (block serotonin) Quetiapine Olanzapine Risperidone Clozapine Aripiprazole Atypical are first line now (other than clozapine) not concordant w antispycotics? switch to depot medication
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What are some typical anti-psychotics, and how do they work? When should they be tried?
Typical anti-psychotics – work by dopamine blockade (D2 receptors): Haloperidol Chlorpromazine
85
When should you trail clozapine as an antipsychotic? What do you need to do with it?
If **two other anti-psychotics have not been effective,** then clozapine should be considered. ***can be effective at helping reduce negative symptoms*** Second line – Clozapine – atypical antipsychotic – this is not included as a first line treatment, as requires close monitoring as it has a tendency to cause **aplastic anaemia,** which can be fatal. **If two other anti-psychotics have not been effective**, then clozapine should be considered. CPMS – Clozepine monitoring system. A national service in the UK, that gives advice on the drug dosage to use, depeninding on the blood test results you send to them. Compulsory for anyone on clozepine. Only consultant psychiatrists can prescribe clozapine
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What are some adverse effects of clozapine
agranulocytosis (1%), neutropaenia (3%) reduced seizure threshold - can induce seizures in up to 3% of patients constipation myocarditis: a baseline ECG should be taken before starting treatment arrhythmias hypersalivation
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What checks need to be done regulary for people on antipsychotic medications?
ECG – as QTC prolongation can occur **Glucose and lipids** – antipsychotics can lead to **diabetes and metabolic syndrome** If on CLOZAPINE – regular FBCs to check for AGRANULOCYTOSIS ---> Once a week for 18 weeks, then fortnighlty for rest of year, and then monthly thereafter
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What are some other side effects of antipsyhcots?
Diabetes/insulin resistance and dyslipidaemia QT segment changes on ECG - prolonged, can lead to Torsades De Pointes Agranulocytosis – clozapine Extra-pyramidal side effects due to the dopamine blockade - Urinary retention Blurred vision Dry mouth Weight gain Hyperprolactinaemia (due to dopamine blockade and dopamine down regulates prolactin)
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What are some assossciated spefici side effects of the following atypical antipsycotics - olanzapine, quetapine, risperidone. What atypical is least likely to increase prolactin levels and cause side effects?
Olanzapine is notorious for its associations with dyslipidemia and weight gain, and is also associated with diabetes and sedation. It is for this reason that some patients are purposefully given olanzapine if they are underweight and cannot sleep. Quetiapine is also associated with weight gain and dyslipidemia. However, one of the most notable side effects of this drug is postural hypotension. Risperidone can increase the likelihood of developing extrapyramidal side effects, as well as cause postural hypotension and sexual dysfunction. All atypical antipsychotics can cause weight gain and hyperprolactinemia. However, generally speaking, aripiprazole has a good side effect profile and is less likely to increase prolactin levels or cause other side effects. not concordant w antispycotics? switch to depot medication
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What are some extra pyrimidial side effects of antipsycotics, and how can they be treated?
Acute dystonic reaction (hours) Muscle spasm, acute torticolis, *(neck muscles contract involuntarily, causing the head to twist or tilt to one side.)* eyes rolling back Parkinsonism (days) Tremor, bradykinesia Akathisia (days to weeks) “inner restlessness, pacing and agitated, often intolerable. They literally can’t stop moving e.g. shaking legs, touching table Massive RF for suicide in young males with schizophrenia Tardive dyskinesia (months to years) - *eg can be oral facial, tongue rolling* Grimacing, tounge protrusion, lipsmacking Very difficult/impossible to treat as you’ve upregulated all the D2 receptors These side effects are worse and more common in the older antipsychotics Treat with Procyclidine, an anticholinergic drug
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What are some other medications used for treating side effects of anti pyscotics, and what are these side effects?
Procyclidine: Used for acute dystonia Propranolol: Used for akathisia (a restlessness syndrome caused by antipsychotics) TARDIVE DYSKINESIA (few months later, motor uncoordination and slow odd movement) → Tx w TETRABENAZINE PARKINSONISM → consider LDOPA
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What are some non pharmacological treatments of schizophrenia?
Individual CBT: normally consists of at least 16 one-on-one sessions. It helps patients create links between their thoughts, feelings and actions with their experience of schizophrenia. Family intervention: should include the patient suffering from schizophrenia if possible as well as their main carer. Normally consists of 10 sessions over 3 months - 1 year. Art therapies can be particularly helpful for negative symptoms. Self-help groups and forums (e.g. Hearing Voices groups) enable people with psychosis to share experiences and ways to cope with symptoms This should be done alongisde antipyscotic
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Outline some differential diagnosis for medically unexplainable symptoms
Factitious, symptoms are fabricated and not experienced as real by the patient Somatoform disorder - Symptoms are unconsciously generated by the mind, but experienced as real by patient Undiagnosed - symptoms are arising from a physical cause that hasn't been identified yet
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What is a somatisation disorder? How is it classified?
Characterised in ICD-10 by at least two years of multiple physical symptoms with no physical explanation (symptoms are felt as real by pt) patients persistently refuse to accept the advice of doctors that there is no physical explanation, and their social and family functioning is impaired as a result of the illness
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What are some causes/risk factors for somatisation disorder?
MC in women Hx sexual or physical abuse Adverse childhood events Hx trauma related disorders ?psychological stress Physical injury Surgery Another neurological disorder
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What are some clinical signs of a somatisation disorder, and what are the most common symptoms?
Speech disturbance Swallowing disturbance Distractable Sx e.g. tremor that stops when pt asked to walk/perform cognitive task **Often GI/skin complaints** Cognitive complaints - forgetfulness, short term memory problems Refusing to believe no organic cause
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What is the management of a somatisation disorder?
Treatment should begin by ruling out all organic illnesses. Acknowledge symptom severity and experience of distress as real but emphasize negative investigations and lack of structural abnormality. Reassure patient of continuing care Some evidence for the effectiveness of patient education in symptom re-attribution, brief contact psychotherapy, group therapy, or CBT if the patient can be engaged in this.
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What is seen in a conversion disorder?
Physical signs! Presents with neurological SIGNS (rather than symptoms) But the examination is inconsistent The patient is not faking it consciously, but there is no evidence of underlying pathology
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What are some signs seen in conversion disorders?
paralysis Loss of speech Sensory loss Seizures Amnesia Examination and investigations are inconsistent
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What is the management of conversion disorders?
Management: – First exclude organic cause –> then therapies like hypnosis, psychotherapy, stress management treating any underlying mood disorder and exploring with the patient and the family any ‘secondary gain’ (such as sympathy or avoidance of family conflict) that might be maintaining symptoms.
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Whats the difference between somatisation and conversion disorders?
Dissociative disorders differ from somatisation in that they more often present with signs rather than only symptoms and are often acute in their presentation.
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Outline what is seen in hypochondrial disorder Where is it most common in?
This is a disorder where patients believe they have a serious underlying disease e.g. cancer, HIV, AIDS – Similarly, to before, there is no physical or organic explanation – Patients don’t accept negative test results and instead feel great distress and worry – It is more common in men and people who have more contact with disease (e.g. health workers)
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What is hypochondrial disorder also asscoated with ?
Dysmorphophobia is related to hypochondriacal disorder. It is an excessive preoccupation with imagined or barely noticeable defects in physical appearance. For example, patients may become preoccupied by the size of their nose, believing an objectively normal nose to be ugly and deformed Many think it is on a spectrum with obsessive–compulsive disorder.
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what is the management of hypochondrial disorder?
Allow patient time to ventilate their illness anxiet-ies. Clarify that symptoms with no structural basis are real and severe. Explain negative tests and resist the temptation to be drawn into further exploration Uncontrolled trials demonstrate antidepressant benefit, even in the absence of depressive symptoms. Try fluoxetine 20mg, and CBT
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What are dissociative disorders? What is seen in them
(PSYCHIATRIC SIGNS) Dissociative Disorders involve **disruptions in memory, identity, or perception as a response to psychological stress** occur in the absence of pathology and these are more common in women According to the psychoanalytic view of psychiatry, painful memories are “cut-off” from conscious self and instead “converted” into more bearable - It is seen as a way to cope with previous emotional trauma
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Give some different types of dissociative disorders
**Dissociative amnesia** – A condition where the patient has no recollection of upsetting and personal information **Dissociative fugue** – A form of dissociative amnesia in which the patient flees away from their home – They display amnesia for their identity, memories, personality and this can last hours to days **Dissociative identity disorder** –It is a condition where the patient develops multiple personalities which can take over. – It is strongly linked to early childhood trauma e.g. sexual abuse – Patient has amnesia for when the different personalities take over, but maybe aware of their existence
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What is the management fo disassociative disorder?
First involves checking if there is an organic cause – Psychotherapy is main line to explore trauma and recall true identity - Potential EMDR
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Other delusional disorders - Outline what is seen in Cortards syndrome
holds the delusional belief that they are dead, do not exist, are putrefying, or have lost their blood or internal organs
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What is Charles - Bonnet Syndrome? What conditions are known to cause it
Complex visual hallucinations in a person with partial or severe blindness (macular degeneration, diabetic retinopathy) Patients understand that the hallucinations are not really and often have insight compared to other disorders For those experiencing CBS, knowing that they have this syndrome and not a mental illness seems to be the most comforting treatment so far, as it improves their ability to cope with the hallucinations.
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Outline what is seen in Muchausens syndrome
This is a condition where patients will produce physical or psychological symptoms to attain a patient’s role – Patients can feign the symptoms, exaggerate them or deliberately hurt themselves to produce symptoms – Typically, patients take hallucinogens, inject faeces to make abscesses and contaminate urine samples.
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Outline what is seen in malingering
Malingering (FINANCIAL GAIN) This is when a patient feigns or exaggerates their symptoms purely for a financial reward or other gain. – Unlike Munchanhausen syndrome, it is not to play a patient’s role but to **receive compensation, personal damages or get off work** – It is not a medical diagnosis, but can lead to a large economic burden on health care systems
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Give some other types of delusional disorders
Erotomanic - believe another person (often famous/important) is in love with them, may attempt to contact/stalking behaviour Grandiose - overinflated sense self worth, power, identity, believe have talent/made important discovery Jealous - spouse/sexual partner unfaithful without any concrete evidence Persecutory - believe someone/something is mistreating/spying on/attempting to harm them, may repeatedly contact legal authorities Somatic - physical issue/medical problem e.g. parasite, bad odour
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Give the definition of personality
The characteristics and relatively permanent sets of behaviours, cognitions, and emotional patterns that evolve from biological and environmental factors ‘Characteristic lifestyle and mode of relating to others’ (ICD – International Classification of Diagnosis)
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What is a personality disorder?
Deeply ingrained, repetitive patterns of behaviour abnormal in a particular culture Increase distress and risk to self/others Decrease function typically apparent by the time of adolescence Causes long-term difficulties in personal relationships or in functioning in society”
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What are the 3 clusters of personality disorders?
Split into cluster A, B, C - **Mad, Bad and Sad** Split into cluster A, B, C Cluster A - mad - paranoid, schizoid, schizotypal Cluster B - bad - borderline (emotionally unstable), histrionic (centre of attention, making everything a drama), narcissist, antisocial Cluster C - sad - avoidant/anxious, dependant, anankastic (obsessive compulsive)
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What are some risk factors/aeitology for personality disorders?
Childhood sexual abuse - strong link to borderline PD Adverse events during pregnancy/birth/neonatal period Poor parenting and adverse childhood Conduct disorder as a child Cognitive theory suggests that people with PDs developed ways of coping with early life adversity (e.g. turning anger against oneself rather than expressing it if this could result in parental violence) that manifest as maladaptive traits later in life (e.g. problems in interpersonal relationships).
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What are some features of symptoms seen in personality disorders?
**Persistent**: o Starts in Childhood o Present for at least;2 years **Problematic:** o Leads to significant personal distress that may only become apparent at a later stage o Associated with significant difficulties with social relationships **Pervasive:** o Applies to various personal and social situations o Significant distress or impairment must occur across ALL settings
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Give some specific persoanility disorders group in Cluster A personalty disorder
Paranoid Schizoid Schizotypal
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Define paranoid personality disorder and list some of its features (A)
unwarranted tendency to interpret the actions of others as demeaning or threatening Thinks the world is – a conspiracy Think people are – devious Acts as if – always on guard, suspicious
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Define schizoid personality disorder and list some of its features (A)
pervasive pattern of indifference to social relationships and a restricted range of emotional experience and expression ***aloof*** Thinks the world is – uncaring Thinks people are – pointless, replaceable Thinks they are the only person they can depend on Commonest behaviour – withdrawal Least likely to be – emotionally available and close Schizoi**D** - = **Distant**
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deifne schizotypal personality disorder and list some of its features (A)
pervasive pattern of deficits in interpersonal relatedness and peculiarities of ideation, experience, appearance and behaviour Strong desire to have relationships, unable to maintain them - poor at gauging others perception of them Schizo**T**ypical - magical **t**hinking
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What are some similarities and differences between cluster A personality disorder and schizophrenia?
Similarities - can have paranoia, and will experience the negative symptoms - of flat affect, and blunted emotions *indeed, maybe a genetic link between the two?* ask about FH of one in relatives when taking a history for the other* Differences - Paranoia is more intense in schizophrenia, and in schizophrenia, you have delusions, as well as positive symptoms like hallucinations and racing thoughts
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What are the personality disorders grouped together in Cluster B?
**Bad** borderline (emotioanlly unstable) antisocial, histrionic narcissist, BAHN
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Define borderline (emotionally unstable) personality disorder and list some of its features
Aka emotionally unstable - intense joy <--> rage Most common type Definition = pervasive pattern of instability of mood, interpersonal relationships and self-image * Self-damaging impulsivity (spending, sex, substance abuse, reckless driving, binge-eating) Thinks people are – untrustworthy Ashamed of themselves Commonest behaviour – self-harm Terrified of abandonment - might do extreme things to keep from leaving Least likely to be – able to show self-compassion Charlotte from Strike?
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Define antisocial personality disorder and list some of its features
* Gross irresponsibility * Incapacity for maintaining relationships * Irritability - Disregard for moral values, - manipulative - Often charming * Low threshold for frustration and aggression * Incapacity for experiencing guilt * Deceitfulness * Disregard for personal safety *Have to be over 18 to get the diagnosis of this, with a history of conduct disorder* *Overrepresented in the prison population*
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Define histrionic personality disorder and list some of its features
Definition = pervasive pattern of excessive emotionality and attention seeking Thinks the world is – their audience Thinks people are – in competition for attention Thinks they are vivacious (attractively lively and animated) Commonest behaviour – exhibitionism Least likely to be – able to listen to others Few meaningful relationships, v superficial
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Define narcissistic personality disorder and list some of its features
pervasive pattern of grandiosity, lack of empathy and hypersensitivity to the evaluation of others Thinks the world is – a competition Thinks people are – inferior Thinks they are – special Commonest behaviour – competitiveness Least likely to be – humble
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Name some other conditions that are thought to have a genetic link with personality disorders seen in Cluster B?
Depression Bipolar Substance abuse disorder
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What personality disorders can be seen in Cluster C?
Obsessive-Compulsive Personality Disorder (ICD), or Anankastic (DSM) Anxious (ICD) or Avoidant (DSM) Dependant PD OAD
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Define anankastic/obsessive compulsive personality disorder and list some of its features How can it be distinguished from OCD (obsessive compulsive disorder)
pervasive pattern of perfectionism and inflexibility * Excessive doubt, caution, rigidity and stubbornness * Preoccupation with details, rules, lists, order * Perfectionism interfering with task completion
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Define avoidant/anxious personality disorder and list some of its features How is it different to social phobia
pervasive pattern of social discomfort, fear of negative evaluation and timidity Persistent feelings of tension and inadequacy * Social inhibitions * Unwillingness to become involved with people unless certain of being liked * Restriction in lifestyle to maintain physical security Social phobia is ansiexty related to specific things, like crowded spaces, public speaking etc - but Anxious persoanality disorder is more general and widespread
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Define dependant personality disorder and list some of its features
Definition = pervasive pattern of dependent and submissive behaviour Thinks the world is – overwhelming Thinks people are – stronger and more competent than themselves, wants people to make decisions for them They are - needy Commonest behaviour – clinging V vunverable to getting in abuse, controlling relationships,
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Outline some of the management optiosn seen in helping those with personality disorders
Structure, consistency and clear boundaries (i.e. agreement of behaviour that is acceptable and unacceptable) help with housing and other social matters Drugs are sometimes used to treat specific PD traits, e.g. mood stabilisers for impulsivity (not generally recommended because of lack of evidence). Continuity of care very important – changes in doctors etc. may invoke strong emotional reactions
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What is some additional treatment you can give for treatment for an boarderline personality disorder?
Medications – mood stabilisers, sedatives during borderline PD crises Mood stabilising medication Topiramate Lithium Valproate Lamotrigine Adapted CBT for borderline PD
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Outline some different examples of SSRIs
Sertraline Citalopram Fluoxetine
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Outline the method of action for SSRIs
SSRIs inhibit the reuptake of serotonin. As a result, the serotonin stays in the synaptic gap longer than it normally would, and may repeatedly stimulate the receptors of the recipient cell
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What are some side effects of SSRIs?
Nausea, indigestion Worsening of sexual dysfunction Weight gain Suicidal thoughts in younger people Serotonin syndrome
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What are some drugs that SSRIs interact with, that you would need to provide w PPI cover?
NSAIDs, Aspirin and Heparin - give a PPI cover NB - fluoxetine and paroextine have higher risk of interaction, as particulary good at inhibiting Liver enzymes
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What are some drugs that can precipitate serotonin syndrome in people with SSRIs?
Linezolid Monoamine oxidase inhibitors (MAOIs) Lithium MDMA Tramadol St. John's wort Tricyclic antidepressants (TCAs) Serotonin-norepinephrine reuptake inhibitors (SNRIs) Triptans (eg sumartriptan) NB - fluoxetine and paroextine have a higher risk of interaction, as particularly good at inhibiting Liver enzymes
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Give some roles of Serotonin in the brain
CNS Modulates thermoregulation, behaviour and attention PNS Regulates GI motility, vasoconstriction, bronchoconstriction, uterine contraction Other Promotes platelet aggregation (combined use with antiplatelet can increase bleeding risk
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What is serotonin syndrome?
Serotonin syndrome (SS) is a group of symptoms that may occur with the use of certain serotonergic medications or drugs. Diagnosis is based on a person's symptoms and history of medication use. Other conditions that can produce similar symptoms such as neuroleptic malignant syndrome, malignant hyperthermia, anticholinergic toxicity, heat stroke, and meningitis should be ruled out
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What are some symptoms of serotonin syndrome
The symptoms are often present as a clinical triad of abnormalities: Cognitive effects: headache, agitation, mental confusion, hallucinations, coma Autonomic effects: shivering, sweating, hyperthermia, vasoconstriction, tachycardia, nausea, diarrhea. Neuromuscular hyperactivity : myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor.
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What is the management of serotonin syndrome?
IV fluids, cooling measures Benzodiazepines Stop offending agent If Sx persist after stimulus removed, consider cyproheptadine (serotonin antagonist)
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Outline examples of SNRIs
Venlafaxine Duloxetine
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what are some common features of SSRI discontinuation syndrome? How do you avoid this?
Discontinuation symptoms increased mood change restlessness difficulty sleeping unsteadiness sweating gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting paraesthesia - **brain zaps/eletric shock symptoms** When stopping a SSRI the dose should be gradually reduced over a 4 week period to avoid this
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What is the MOA of SNRIs?
Leads increased concentration of norepinephrine in the synaptic cleft. - Inhibits 5HT reuptake pumps and NAd transporter At low doses, they act like an SSRI - noradrenaline changes don’t occur much at low doses
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What are some side effects of SNRIs?
aise BP, contraindicated in heart disease Similar to SSRIs Similar to SSRI = Sweating Dose-dependant hypertension
148
Outline some examples of tricyclic antidepressants
Amitriptyline Imipramine Clomipramine Dosulepin Higher Dose **depression, lower dose - used for pain**
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Outlline the MOA of tricyclic antidepressants
Action on the presynaptic neurone - inhibit the uptake of monoamines at the presynaptic membrane (bind to ATPase monoamine pump) Increase serotonin, noradrenaline **Decrease acetylcholine, histamine, sodium and calcium**
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What are some side effects of tricyclic antidepressants? What are some of them CI in?
Dangerous in overdose due to It affecting sodium and calcium - very cardiotoxic CHECK ECG IF THE PATIENT IS ON THESE Look for - **Wide QRS - more than 3 small squares** - **Sinus tachycardia** Anticholinergic side effects: Blurred vision - pupil dilation Urinary retention Dry mouth Constipation Confusion agitation *(dilated pupil, tachycardia, urinary retention - sympathetic NS side effects)?* *CI in narrow angle glucoma, as can worsen it as it interferes w BP in eye*
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When would you consider using Monoamine Oxidase inhibitors?
MAOIs are seldom used, and then only in treatment - resistant depression or atypical depression **old fashioned** (depression with increased sleep, increased appetite, and phobic anxiety). Basically, in atypical depression
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How do monoamine oxidase inhibitors work?
MAOIs inactivate monoamine oxidase enzymes that oxidise the monoamine neurotransmitters, such as **dopamine, noradrenaline, serotonin (5 - HT), and tyramine.** - more of them in the CNS
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What are some side effects of Monoamine oxidase inhibitors? Give some examples of them
Can cause v. v. high BP if taken with tyramine (aged cheese, cured meats, broad beans). **Tyramine reaction crisis** can lead to SAH anticholinergic side - effects, weight gain, insomnia, postural hypotension, tremor, paraesthesia of the limbs, and peripheral oedema eg Selegiline, Phenelzine
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Give some side effects of atypical antidepressants, like Mirtazapine What are they CI in ?
Drowsiness Weight gain CI in narrow angle glucoma, as can worsen it as it interferes w BP in eye
155
Define Phenomenology - how does it shape psychiatric practise?
the direct investigation and description of phenomena as consciously experienced by an individual, namely a patient Pysch, emphasises that psychiatric symptoms should be diagnosed according to their form rather than according to their content. This means, for example, that a delusion is a delusion not because it is deemed implausible by a person in a position of authority, such as a doctor, but because it is ‘ an unshakeable belief held in the face of evidence to the contrary, and that cannot be explained by culture orreligion ’ <3 xxxx
156
When would you perscribe lithium?
acute manic episodes and in the long-term prophylaxis of Bipolar affective disorder Lithium should only be started if there is a clear inten ion to continue it for at least three years, as poor complince and intermittent treatment may lead to rebound mania. The starting dose of lithium should be cautious
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What are some side effects of lithium at lower dose? How long post dose should a sample be taken for checking lithium levels?
Side effects - at lower doses 0.4-1 mmol/L * Nausea * Fine tremor * Weight gain * Oedema * Polydipsia and polyuria * Hypothyroidism **Long-term lithium use can result in hyperparathyroidism and resultant hypercalcaemia** When checking lithium levels, the sample should be taken 12 hours post-dose
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What are some side effects of lithium toxicity? Above 1.0 mmol/L How long post dose should a sample be taken for checking lithium levels?
Above 1.0 mmol/L Signs of toxicity * Vomiting * Diarrhoea * Coarse tremor * Slurred speech * Ataxia Seizures * Drowsiness and confusion **Long-term lithium use can result in hyperparathyroidism and resultant hypercalcaemia** Lithium **is Teratrogenic!!** When checking lithium levels, the sample should be taken 12 hours post-dose
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How often should lithium be checked, when starting it or changing the dose, and when stable? What side of things should be monitored on it and how often?
Lithium has a half-life of approximately 24 hours. Therefore, one can expect serum lithium concentrations to reach steady state after approximately 5-7 days (when circa 97-99% of the drug has been metabolised). Hence, serum lithium levels should be checked 7 days after a dosage change. Lithium levels measured one week after starting treatment or changing dose, weekly until stabilized once stable measured every 3 months. BMI, U&E, eGFR, Calcium and Thyroid levels measured every 6 months
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What pyschiatric disorder could you use sodium valporate and carbamazepine, and lamotrigeine for?
Bipolar, prophylactically They are **Teratrogenic!!**
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What are some side effects of Sodium valporatte and lamotrigine ?
Lamotrigine Skin reactions (including Stevens– Johnson syndrome) aseptic meningitis drowsiness diplopia leucopenia insomnia Sodium valpoarate Nausea Gastric itrartaion diarrhoea Weight gain They are **Teratrogenic!!**
162
Name 3 broad kinds of psychological therapies
1 Supportive therapy *Explorative pyschotherapies=* 2 Cognitive and Behavioural therapies 3 Psychodynamic therapies
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Outline what is seen in supportive therapy - for what may it be used?
Explanation and reassurance establishing rapport, facilitating emotional expression, reection, reassurance * Non-directive problem-solving, e.g. for adjustment disorders, stress, bereavement * Mild depression or anxiety Counselling is similar to supportive therapy in that it involves explanation, reassurance, and support.
164
Outline what is seen in CBT
This is a therapy with works on the interplay between thoughts, emotions and behaviours. Its aim it to tackle both negative the cognitive thinking and behaviour in mental illness. a) Cognitive –> Aim is to help people identify and challenge automatic negative thoughts and abnormal beliefs b) Behaviour –> This is based on learning theory of operant condition (positive and negative reinforcement) – If people have habitual wrong behaviours (e.g. avoidance in anxiety) it teaches people relaxation techniques and gradual exposure with positive reinforcement to change their behaviour.
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For what things can CBT be used to treat?
CBT is used to treat depression, anxiety, eating disorders and some personality disorders. It can also be used to treat psychosis
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Outline what is seen in psychodynamic/pyshcoanalyitc therapies
psychoanalysis stems from the work of Sigmund Freud. - views human behaviour as determined by unconscious forces derived from primitive emotional needs. Therapy aims to resolve longstanding underlying conflicts and unconscious defence mechanisms (e.g. denial, repression). Helping the person to become more aware of the unconscious processes which are giving rise to symptoms or to difficult repeating patterns Helping the person construct a narrative of their life and give meaning to symptoms
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What is the general procedure seen in Psychodynamic therapies? e. g. Psychoanalysis + Psychodynamic Psychotherapy
– The patient explores their subconscious by using free association (says whatever is on their mind) – The therapist interprets these statements to **link the patient’s past experience with their current life** and their relationship with the therapist. This uses 2 skills: Transference - when patient projects feelings they have for someone else (from past, say parent or ex partner) onto the therapist = These feelings can provide insights into the client’s past relationships and unresolved emotions. Countertransference is when the therapist, often unconsciously, projects their own feelings onto the client. This could be triggered by something the client says or does that reminds the therapist of someone in the therapists own life. **The relationship heals!!!!!!**
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Outline what is seen in Cognitive Analytic Therapy (CAT) For what can it be used?
Short time, cheaper pyschological treatment – It looks at the ways an individual think and feels and the events and relationships underlying experiences. – They key of this therapy is reflection after – therapist writes a goodbye letter and asks patient to respond - **gets patients to find new nad better ways of coping with established problems** Used in 'Personality Disorder’, Eating disorders
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What is seen in Dialetcai ldehvaiour therapy? When may it be used?
similar to CBT and also provides group skills training to equip the individual with alternative coping strategies Skills such as mindfulness (bringing one’s attention back to thepresent moment), which is **derived from Buddhist meditation.** Used for those with Boarderline personality disorders, eating disorders
170
Outline what is seen in Eye movement desensitization and reprocessing
– Patients then recall the disturbing events and the emotion they felt at the time (e.g. sexual abuse and feeling powerless – They then work together to create a positive belief about the event (“I am stronger now and so not powerless”) – The therapist then activates both sides of your brain using Dual Activation Stimulation (DAS) by making they do eye movements usually involves the therapist directing the patients’ lateral eye movements by asking them to look first one way then the other (saccadic eye movements) – This allows the brain to reprocess the upsetting memories by removing the old emotion and replacing it with the more positive, empowering emotion – This means the memory is no longer experienced as a traumatic.
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What is seen in interpersonal psychotherapy, and for what may it be used for?
IPT is a talking treatment that helps people with depression **identify and address problems in their relationships with family, partners and friends.** The idea is that poor relationships with people in your life can leave you feeling depressed, it gets the patient to **view their emotions in terms of their interpersonal network** e.g. a close member may have died (causing grief) The rest of the session then involves work on how to cope and change their views of these events and transform their relationship into a positive one used for moderate and severe depression IPT is usually offered for 16 to 20 sessions.
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What is ECT? For what can it be used for?
Electroconvulsive Therapy - uses electrodes to induce a modified cerebral seizure Severe depression Prolonged or severe episode of mania that has not responded to treatment Cataonia ECT should be used to induce fast and short-term improvement of severe symptoms after all other treatment options have failed, or when the situation is thought to be life-threatening (because of high risk of suicide or not eating and drinking).
173
How is ECT thought to work?
This is a treatment option which uses electrodes to induce a modified cerebral seizure in the brain – This leads to massive amounts of neurotransmitter release, hormone secretion and a transient increase in blood brain barrier permeability. – It is used to induce fast improvement after all other treatment options have failed
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When does English Mental Health Act permit ECT to be given?
Patient gives informed consent (before every treatment) The patient lacks capacity, and it does not conflict with advance decision AND It’s an emergency, and the independent consultant has not yet assessed (Section 62 of Mental Health Act) OR An Independent Consultant (appointed by Mental Health Act Commission) agrees to it **IF A PATIENT HAS CAPACITY AND REFUSES, IT CANNOT BE GIVEN**
175
Outline the procedure of ECT
Procedure: – Patient is nil-by-mouth for 4 hours before intervention – Patient is given short-acting anaesthetic + muscle relaxant drug – Preoxygenation is given to increase SpO2 – A shock is delivered to the scalp either bilaterally or unilaterally Bitemporal ECT is typically used for faster and more robust results but comes with higher risks of cognitive side effects. Unilateral ECT is chosen for a more cautious approach with fewer cognitive impacts, especially in less severe cases or when **cognitive preservation is critical.** – This evokes a 20-60s seizure within the brain
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What are some contraindications for ECT
– Raised intracranial pressure (absolute) – Stroke and MI, pregancy, phaemchromocytoma (relative contraindication
177
What are some side effects of ECT?
Patients have reported that ECT causes cognitive impairment. Therefore cognitive function should be assessed prior to, during and after a course of treatment. Assessment should include: * orientation and time to reorientation after each treatment, * new learning, * retrograde amnesia, * subjective memory impairment. * dysrhythmias due to vagal stimulation, postictal headache, * confusion, * retrograde and anterograde amnesia with difficulties in registration and recall that may persist for several weeks
178
What is Neuroleptic malignant syndrome?
Psychiatric emergency caused by excess of neuroleptic medication (aka both typical and atypical antipsychotics) or acute withdrawal from Parkinson's medication Cocaine and ectasy can also cause it
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Why does Neuroleptic malignant syndrome happen? What are some symptoms of it?
NMS results from as dopaminergic hypothalamic spinal tracts are blocked, so they can't tonically inhibit preganglionic sympathetic neurons as usual Occurs over hrs-days (within 10d) - gradual Hyperpyrexia Hyporeflexia Fluctuating consciousness Diffuse rigidity Raised CK - Rhabdomyolysis can occur Leukocytosis May have high K+ and low Ca
180
What is the management of Neuroleptic malignant syndrome?
The mainstay of treatment involves stopping the drug and supportive measures such as oxygen, IV fluids, and cooling blankets Drugs - **dantrolene and lorazepam** may also be used to decrease muscle rigidity.
181
What are some symptoms of opiate overdose
Acute presentation = drowsiness Respiratory depression -> resp acidosis CO2 retention) Hypotension Tachycardia Pinpoint pupils Chronic = constipation
182
What is the management of an opiate overdose?
ABCDE approach **Naloxone IM** - blocks opioid receptors in the brain * Methadone (opioid agonist) or buprenorphine (opioid partial agonist) are first line; they are less euphoriant and have a relatively long half-life than opioids of abuse. * Lofexidine is sometimes used for short detoxification treatments or where abuse is mild or uncertain Naltrexone (opioid antagonist) blocks the euphoric effects and is occasionally used to help prevent relapse.
183
What are some signs of opioid withdrawal? What drug do you give to treat it?
Clinical features of withdrawals are mediated by noradrenaline overactivity: * Dilated pupil * Tachycardia + hypertension * Insomnia, restlessness, anxiety, irritability, tremor * Abdo pain, nausea, vomiting, diarrhoea * Watering eyes * Muscle aches Treatment **Lofexidine** - *It does not act on opioid receptors but instead reduces the body's physical withdrawal symptoms by dampening the sympathetic nervous system, which becomes overactive during opioid withdrawal.*
184
In both ICD - 10 and DSM - IV the first step in diagnosis is to specify the substance or class of substance - what kind of substances are commonly involved in substance abuse?
ICD - 10 F10 Alcohol F11 Opioids F12 Cannabinoids F13 Sedatives or hypnotics F14 Cocaine F15 Other stimulants, including caffeine F16 Hallucinogens F17 Tobacco F18 Volatile solvents F19 Multiple drug use and other
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The second step in diagnosis is to specify the type of disorder involved, according to the ICD 10 - what types of substance abuse disorders are there?
ICD - 10 .0 Acute intoxication .1 Harmful use .2 Dependence syndrome .3 Withdrawal state .4 Withdrawal state with delirium .5 Psychotic disorder .6 Amnesic syndrome .7 Residual and late-onset psychotic disorder .8 Other mental and behavioural disorders
186
Give some risk factors for a substance abuse disorder
Addiction liability - depends on: How substance taken: orally, injection, inhaling Rate substance crosses blood brain barrier and triggers reward pathway in brain Time takes to feel effect of substance Substance ability to induce tolerance ± withdrawal symptoms Male Aged ~ 18-25 Mental health conditions: ADHD, bipolar, depression, GAD, panic disorder, PTSD Adverse childhood experiences: childhood abuse/neglect, witnessing domestic violence, family members with SUD
187
what is the MOA of benzodaizapines?
– They facilitate and enhance the binding of GABA to the GABAA receptors [Benzodiazepines]- Benzodiazepines target the γ-aminobutyric acid type A (GABAA ) receptor --> GABAA is the main inhibitor neurotransmitter in the brain --> benzodiazepines facilitate and enhance the binding of GABA to the GABAA receptors --> results in desired anxiolytic effect
188
How many g and ml is one unit of alchohol
One unit of alcohol is equivalent to 10ml or 8g of pure alcohol
189
Outline some of the physiological effects that alcholol has on the body
* Alcohol increases GABA function (GABA-A receptor activation) * GABA is the main inhibitory neurotransmitter in the brain - calming effect * Alcohol reduces glutamate function - inhibitory action at NMDA glutamate receptors ○ Glutamate is the major excitory neurotransmitter that is involved in brain processing such as learning and memory ○ Effects on glutamate lead to amnesia and sedation
190
What are some signs of alchohol dependance?
CANT STOP C - compulsion to drink A - aware of harms but persists N - neglect of other activities T - tolerance to alcohol S - stopping causes withdrawal T - time preoccupied with alcohol O - out of control use P - persistent, futile wish to cut down Withdrawal Tremors Anxiety Nausea, vomiting Headache Tachycardia Irritability, aggression Delirium
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What are some investigations/questionaires to screen for alcohol dependency?
CAGE questionnaire screening C - do you ever think about cutting down A - do you get annoyed when others comment on drinking habit G - ever feel guilty about drinking E - ever drink in morning (eye-opener) AUDIT questionnaire Developed by WHO Multiple choice for harmful alcohol use screen
192
What are some blood tests results you would see in an alcoholic?
Bloods Raised MCV Raised ALT and AST (AST:ALT ratio above 1.5 suggests ALD) Raised GGT Raised ALP later in disease Raised bilirubin in cirrhosis Low albumin (reduced synthetic function of liver, reduced clotting factor production) Deranged U&Es in hepatorenal syndrome
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What is the management for someone who is alcohol dependant?
Management – Patients are often referred to an alcohol dependence programme to help them quit. – They can use a mixture of behavioural interventions (e.g. CBT) and pharmacological treatment – Disulfiram –> this **inhibits acetaldehyde dehydrogenase**, so people feel hungover as soon as they drink alcohol (avoid in ischaemic heart disease) – Acamprosate –> **this is a weak NMDA antagonist** which is used to reduce alcohol craving - **works on glutamate**
194
outline the order of symptoms seen in alcohol withdrawal
symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety peak incidence of seizures at 36 hours peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
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Outline the pathophysiology behind delirium tremens
Alcohol boosts GABA, which inhibits the brain and dampens excitatory glutamate receptors. Over time, the brain adapts, becoming more sensitive to excitatory signals. When alcohol stops, the brain becomes overactive, causing symptoms like confusion and agitation.
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what are some symptoms of delerium tremens? What is the management?
Symptoms – Together they are called delirium tremens – Early on –> increased anxiety, with sweating and agitation – After 24 hours –> Seizures with visual hallucinations – From 48-72 hours –> Course tremors, agitation, delusions and severe visual hallucinations (lilliputian, seeing small people) Management – 1st line is benzodiazepine chlordiazepoxide
197
What is the management of alcohol withdrawal?
Pharmacological management of alcohol withdrawal and detoxification * **Chlordiazepoxide** - benzodiazepine commonly used in the UK (long acting) * Diazepam (long acting) * Lorazepam (short acting) -Lorazepam is preferred to chlordiazepoxide in patients with **liver cirrhosis/hepatic failure** due to the way it is metabolised, Oxazepam (short acting)
198
What is a detox regime? What are the two types?
Detox protocol: Typically involves the use of benzodiazepines to reduce the risk of withdrawal complications, alongside monitoring of vital signs and symptom management. Shouldn't take any longer than 10 days, so you don't risk getting a new addiction to benzodiazepines * Community detox: This might be appropriate if he has a supportive home environment, no history of severe withdrawal, and no other medical or psychiatric comorbidities. Inpatient detox: Inpatient care would be necessary if he is at high risk for severe withdrawal (DTs or seizures), has a lack of social support, coexisting psychiatric disorders (like PTSD), or medical conditions (e.g., liver disease).
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How can we gauge the severity of alcohol withdrawal?
The CIWA-Ar is used to guide the pharmacological management of alcohol withdrawal. Clinicians add up scores for all ten criteria. The total CIWA score can be used to assess the presence and severity of alcohol withdrawal: Absent or minimal withdrawal: score 0-9 Moderate withdrawal: score 10-19 Severe withdrawal: score > 20 The total CIWA score influences the frequency at which further observations are made: Initial score is ≥ 8: repeat hourly for 8 hours. Then if stable 2-hourly for 8 hours. Then if stable 4-hourly. Initial score < 8: assess 48-hourly for 72 hours and if score < 8 for 72 hours, discontinue assessment. The total CIWA score guides clinicians with regards to the need for pharmacological management of alcohol withdrawal: Symptom-triggered regimen (not prescribed regular withdrawal medication): give PRN medication when CIWA score is ≥ 8 Fixed-dose reducing regime with PRN medication (prescribed regular withdrawal medication): give additional PRN medication if CIWA score is ≥ 15
200
what are some blood tests used to screen for alcohol dependance?
Gamma Glutamyl Transpeptidase (accept GGT) b. Red blood cell mean corpuscular volume (accept rbc MCV or MCV) c. Carbohydrate deficient transferrin (CDT) ALL raised
201
Define Wernicke's Encephalopathy
is a neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations.
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What is Korsakoff's Syndrome? How is it related to Wernickes?
Hypothalamic damage & cerebral atrophy due to thiamine (vitamin B1) deficiency (eg in alcoholics). Wernicke's encephalopathy is the acute, reversible stage of the syndrome, and if left untreated it can later lead to Korsakoff syndrome, which is chronic and irreversible.
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How can chronic alcoholism lead to a thiamine deficiency?
It **block the phosphorylation of thiamine**, stopping it from being converted into its active form Ethanol **reduces gene expression of Thiamine transporter**, so can stop it getting absorbed in the duodenum. Alcoholic tend to have a poor diet, relying on alcohol for calories so will not get enough Thiamine (b1) anyway
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How can a lack of thiamine (vit B1) affect the brain?
- Thiamine deficiency impairs glucose metabolism and this leads to a decrease in cellular energy. - The brain is particularly vulnerable to impaired glucose metabolism since it utilises so much energy.
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What is the classical triad seen in Wernicke's encephalopathy?
1 confusion 2 ataxia (wide-based gait; fig 2) 3 **ophthalmoplegia** (nystagmus, lateral rectus or conjugate gaze palsies).
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What does Wernicke - Korsakoff syndrome predominantly target? What symptoms does this cause?
- Mainly targets the limbic system, causing severe memory impairment: - **Anterograde amnesia:** inability to create new memories - **Retrograde amnesia:** inability to recall previous memories. - **Confabulation:** creating stories to fill in the gaps in their memory which they believe to be true. - **Behavioural changes**
207
What investigations would you do in suspected Wernicke's encephalopathy?
- Diagnosis is typically made **based on clinical presentation** - **Bloods including LFTs**: measure thiamine levels, measure blood alcohol levels, liver function may be deranged in alcoholism - **Red cell transketolase test:** rarely done, thiamine is a co-enzyme to transketolases so transketolase activity will be low - **MRI/CT:** can confirm diagnosis by showing degeneration of the mammillary bodies Lumbar puncture to rule out other causes of the symptoms of wernickes
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What is the management for Wernicke's encephalopathy?
Urgent replacement to prevent irreversible Korsakoff’s syndrome (p718). Give thiamine (Pabrinex®) Oral supplementation (100mg OD) should continue until no longer ‘at risk’, *give other B vitamins as well* Correct Magnesium deficiency as well If there is coexisting hypoglycaemia, correct it
209
Why do you need to give Thiamine before you give glucose in a patient with Wernicke's?
it’s important to normalise the thiamine levels first, because without thiamine pyrophosphate, **most of the glucose will become lactic acid and that can lead to metabolic acidosis.** (often the case in this group of patients), make sure **thiamine is given before glucose**, as Wernicke’s can be caused by glucose administration to a thiamine-deficient patient - ***NOT GIVING THIAMINE AS YOU JUST THINK ITS HYPOGLYCAEMIA IS A COMMON MISTAKE DOCTORS MAKE***
210
How do cocaine and ampethamines work?
These drugs block the reuptake of dopamine and noradrenaline (and 5-HT) increasing transmission at synapses
211
What are some signs of a cocaine/amphetmanie overdose?
Main effect – Increased energy and concentration, euphoria and hyperactivity Side effects: – Cardiovascular –> Increased pulse, blood pressure, hyperthermia, can lead to aortic dissection – Heart –> QRS widening and QT prolongation – GI –> Reduced appetite and ischaemic colitis – Psychological –> Insomnia, agitation and hallucinations e.g. formication (sensation of ants under the skin) – If you take a prolonged large dose, the euphoria can turn to depression and anxiety – Can get psychosis –> delusions, visual and auditory hallucinations
212
What is the management of a cocaine overdose?
– IV benzodiazepines + treat complications (heart attack, aortic dissections) + antipsychotics
213
What are the 5 key principles you must consider when assessing mental capacity
i) A person is **assumed to have capacity** until it is established that the person lacks it ii) A person should not be treated as unable to decide **unless all practicable steps to help them have failed** iii) A person should **not** be treated as unable to decide **just because it is unwise** iv) Decisions made on **behalf of an incapable person must be in their best interests** v) Regard should be taken to **find the solution which is least restrictive of the person’s rights and freedom of action**
214
Under the MCA, what are the 3 reasons why you may provide treatment for someone who does not have capacity?
– If a valid advanced decision to refuse treatment exists – If a valid Lasting Power of Attorney for Health and Welfare exists – If neither exists, the person providing treatment should act in the patient’s best interests.
215
In order to section someone *(forcibly admit someone to hospital/secure setting)*, for **assessment** what is grounds/personal is required and for how long? What part of the MHA?
Under section 2 of the mental health act Need 2 Drs: one section 12 approved, one ideally previous contact w/ pt, and then approval from approved mental health professional (AMHP) to confirm the section. Patient suffering from mental disorder to degree that warrants detention in hospital for assessment Pt should be detained for own health/safety or the protection of others **Lasts 28 days, cannot be Cannot be renewed**
216
In order to section someone *(forcibly admit someone to hospital/secure setting)*, for **treatment** what is grounds/personal is required and for how long? What part of the MHA?
Under section 3 of the mental health act Again, Need 2 Drs: one section 12 approved, one ideally previous contact w/ pt, and then approval from approved mental health professional (AMHP) to confirm the section. Patient suffering from mental disorder to degree that warrants detention in hospital for treatment. Pt should be detained for own health/safety or the protection of others The treatment needed cannot be effectively provided unless the patient is detained. Appropriate medical treatment is available to them. lasts 6 months, can be renewed
217
What is outlined in section 4 of the MHA?
Patient suffering from mental disorder to degree that warrants detention in hospital for assessment Pt detained for own safety/safety of others Not enough time for 2nd Dr to attend i.e. due to risk 1 Dr (does not need to be section 12 approved) Can only last 72 hours - used only in emergencies (in A+E)
218
What is outline in section 5 of the mental health act, both in 5(2) and 5(4)
For pt already admitted (to psychiatric/general hospital) but wanting to leave section 5(4) says Nurses can detain patients in hospital (this is their holding power until a Dr can attend,) for **6 hours** Section 5(2) says Doctors (this is their holding power until section 2/3 can be put in place) NB - has to be Dr on a specific ward, cannot be done in A&E, for **72 hours**
219
What is outlined in section 135 and 136 of the mental health act
135 - allows police to enter house and mreove a patient to a place of safety 136 allows police to take someone to a place of safety for an assessment Both can be done by a police, but the should try and confirm this with a doctor or nurse Both for a duration of 72 hours
220
If a patient has been detained under section 2,3,35,36 or 37, is consent required for treatment
Consent to Treatment As a general rule, once a patient is detained under S2, 3, 35, 36 or 37 of the MHA, consent is not required for the administration of psychiatric treatment. – The justification for treatment is provided by S63 which states that: “The consent of a patient shall not be required for any medical treatment given to him for the mental disorder from which he is suffering” Treatments are Covered by S63 All medical treatment for the mental disorder, including: Treatments for the disorder itself (e.g. antipsychotics for schizophrenia) Treatments for conditions causing the disorder (e.g. hypothyroidism causing depression) Treatments for the physical consequences of the disorder (e.g. NG in anorexia) Safe holds and physical control and restraint (when necessary)
221
Define what self harm is - what are some reasons for it?
Intentional non-fatal self-inflicted harm * a desire to interrupt a sequence of events seen as inevitable and undesirable * a need for attention * an attempt to communicate/express themselves * a true wish to die Used to express something hard to put into words, change emotional pain into physical pain, have a sense of being in control, punish themselves for feelings/experiences…
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What are some risk factors for self harm
Unlike completed suicide, DSH is more frequent in women, the under-35s, lower socia l classes and the single or divorced. * Like suicide, DSH is associated with psychiatric illness, particularly depression and personality disorder
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What are some clinical signs of self harm?
Cuts/scratches on arms/legs Picking at skin Burns Bruising Weight loss/weight gain Hair loss (pulling at hair)
224
When assessing self harm/suicide attempt, what are the 3 domains you should split factors into?
Before During After
225
Suicide and self-harm risk assessment - what things should you try to find out about BEFORE they attempted suicide/self-harm?
Precipitants - specific event/build up? Planned/impulsive? Precautions taken against discovery? (left the house, turned off phone etc) Alcohol/recreational drugs at time of event? - suggests more impulsive
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Suicide and self-harm risk assessment - what things should you try to find out about DURING they attempted suicide/self-harm?
Method (if drugs - what did they take, how much) Was pt alone Where was it - more remote = higher risk What went through mind at the time Did they think their self-harm would end their life? What did they do straight after the self-harm?
227
Suicide and self-harm risk assessment - what things should you try to find out about AFTER they attempted suicide/self-harm?
Did pt call anyone? Go to A&E? Who were they found by How they felt when help arrived Current mood Still feel suicidal? - would they attempt again
228
What are some management options for self harm?
A good first step is to agree with patients what their problems are and what immediate interventions are both feasible and acceptable to them. * Ensure that they know who they can turn to if suicidal intent returns (e.g. A & E). * Crisis Resolution Team referral may be necessary if suicidal ideation is present. * Think about reducing access to means of suicide if possible – for example, by encouraging patients to dispose of unneeded tablets from the home, and by prescribing antidepressants of lower lethality (e.g. SSRIs rather than tricyclics) and in small batches. * Consider psychological therapy and encouraging engagement in self-help and community social and support organisations.
229
What are some risk factors for suicide?
SAD PERSONS Sex (male) Age <19 or >45 Depression Previous suicide attempt - **one of the strongest risk factors for future sucide completion** Excess alcohol or substance use Rational thinking loss Separated or single Organised plan No social support Sickness
230
What are some clinical signs of suicidal behaviour?
Warning signs: * Obsessive thinking about death * Feelings of hopelessness, worthlessness, helplessness * Behaviours suggestive of absolute death wish: ○ Put financial affairs in order ○ Visiting people to say goodbye in community, awareness of pts who: Frequently, repeatedly attend Disengaged w/ services Prescribed several antidepressants Heightened concern from family members
231
what are some principles around suicide prevention?
* Detect and treat psychiatric disorders. * Be alert to risk and respond appropriately to it. * Prescribe safely * Give urgent care at appropriate level of patients with suicide intent – refer to Crisis Resolution and Home Treatment Teams. - Can also admit for hospitalization (consider detention under the Mental Health Act) if patients considered unsafe outside hospital even with intensive support. *Provide careful management of deliberate self-harm (DSH) * Act at the population level, tackling unemployment and reducing access to methods of self-harm.
232
What are the domains assessed in a Mental State Examination?
Appearance and behaviour Speech Mood and affect Thoughts Perception Insight and judgement Risk
233
What is a functional neurological disorder?
sometimes called conversion disorder, involves sensory and motor symptoms that are not explained by any neurological disease and may be caused by underlying psychosocial factors.
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What are some typical symptoms seen in a conversions disorder
Symptoms can include weakness, gait disturbance, seizures, sensory loss and vision disturbances. There may be a history of significant trauma or stress. Glove distribution sensory loss
235
what is the treatment of a paracetamol overdose? What is the defintion of a staggered overdose?
Activated charcoal within one hour (stops reabsorption) **Activated charcoal (within 1 hour of ingestion).** N-acetylcysteine (NAC) based on serum paracetamol level and clinical presentation. N acetylcysteine Replenishes body stores of glutathione Glutathione is needed to detoxify a toxic intermediary product of paracetamol metabolism (NAPQI). . A staggered overdose is defined as the first and last paracetamol ingested being more than 1 hour apart.
236
Abnormalities of thought flow and coherence - define Loose associations
moving rapidly from one topic to another with no apparent connection between the topics. Similar to - Knight's move, or derailment, is a pattern of thought in which ideas lack logical progression. For example, 'I live in a flat, I had juice at breakfast, and my mother is from Wales.'
237
Abnormalities of thought flow and coherence - define Circumstantial thoughts
these are thoughts which include lots of irrelevant and unnecessary details but do eventually come back to the point. *(stereotype - old person in GP consultation, tells you about family/dogs etc then finally comes back to talking about dizziness etc)*
238
Abnormalities of thought flow and coherence - define Tangential thoughts
digressions from the main conversation subject, introducing thoughts that seem unrelated, oblique, and irrelevant. Tangentiality is the act of wandering from a topic without returning to it Each topic links to one another in this case (home to breakfast to the cafe to the village), however, they did not answer the question asked.
239
Abnormalities of thought flow and coherence - define flight of ideas, and thought blocking
Flight of ideas: seen with fast, pressured speech. Ideas run into one another, making it difficult for the observer to follow the flow of speech.] Thought blocking: sudden cessation of thought, typically mid-sentence, with the patient unable to recover what was previously said.
240
Abnormalities of thought flow and coherence - define Neologisms and word salad
Neologisms: words a patient has made up which are unintelligible to another person. Word salad: speaking a random string of words without relation to one another.
241
Outline some features of addictive behaviour, and what's needed for a diagnosis?
Features of substance misuse: * Acute intoxication, hazardous use (puts individual at risk), use despite harmful effects to physical/mental health, tolerance to substance, withdrawal, dependence, residual disorder, compulsion to take, prioritising over commitments * 3 or more symptoms from ICD-10 Criteria for >1 month
242
What are some medications used to help with smoking addiction, (stop smoking, reduce cravings, reduce pleasure)
NRT (stop smoking cigarettes), Champix/Varenicline (reduce cravings), Bupropion/Zyban (reduce pleasure Bupropion can lower the seizure threshold, so CI in epilepsy
243
outline the difference between mood and effect
Mood and affect Mood and affect both relate to emotion, however, they are fundamentally different. Affect represents an immediately expressed and observed emotion (e.g. the patient’s facial expression or overall demeanour). Mood represents a patient’s predominant subjective internal state at any one time as described by them. Affect is what you observe, and mood is what the patient tells you (as an analogy, mood is the climate whilst affect is the current weather).
244
Give some differences in the presnetation of neuroleptic malingacy syndrome and serotonin syndrome
Hyporeflexia, Serotonin Syndrome: Rapid onset; **hyperreflexia, clonus**, myoclonus, tremor, agitation, diarrhea, **dilated pupils**, and diaphoresis. Triggered by serotonergic drugs. Neuroleptic Malignant Syndrome: Gradual onset; **muscular rigidity**, **hyporeflexia**, autonomic instability (e.g., fluctuating BP), altered mental status, **hyperthermia**, and elevated CK. Triggered by antipsychotics or dopamine withdrawal.
245
describe what panic disorder is
Panic disorder is a type of anxiety disorder that involves sudden, intense episodes of fear or discomfort, often accompanied by physical symptoms: Palpitations Sweating Trembling Shortness of breath Dizziness Chest pain Choking sensations Feelings of unreality (depersonalization or derealization) Fear of dying, losing control, or going mad Panic attacks are unpredictable and have no specific trigger. They can happen anytime, anywhere, and without warning